Heart Attack Pathology
- What is a Heart Attack?
- What are the structures and functions of a normal coronary artery?
- What happens to the coronary artery in atherosclerosis?
- Who gets coronary artery plaques and what happens to the plaques?
- What causes a Heart Attack?
- What happens to the heart muscle after a person survives a Heart Attack?
- Can a person have more than one Heart Attack?
What is a Heart Attack?
A heart attack is a layperson's term for a sudden blockage of a coronary artery. This blockage, which doctors call a coronary artery occlusion, may be fatal, but most patients survive it. Death can occur when the occlusion leads to an abnormal heartbeat (severe arrhythmia) or death of heart muscle (extensive myocardial infarction). In both of these situations, the heart can no longer pump blood adequately to supply the brain and other organs of the body. Almost all heart attacks occur in people who have coronary artery disease (coronary atherosclerosis). So, this photo essay will review the structure (anatomy) of the normal coronary artery, the structural abnormalities (pathology) of the coronary artery in atherosclerosis, and the effect of these abnormalities on the heart.
What are the structures and functions of a normal coronary artery?
The coronary arteries carry blood to the heart to supply oxygen and necessary nutrients. As seen in Figure 1, the wall of a coronary artery has 3 distinct layers: the inner (intima), middle (media), and outer (adventitia) layers. The wall of the artery surrounds the lumen of the artery, which is the channel through which blood flows.
Figure 1: Normal Coronary Artery
Cross-sectional Microscopic View
In Figure 1, smooth muscle is red, and connective (supporting) tissue is black (elastic) or blue (collagen)
The intima is best seen in the close-up view in Figure 1. It is composed of a layer of so-called endothelial cells that covers the artery's inner (lumenal) surface, connective (supporting) tissue (collagen and elastin), and a layer of compact elastic tissue called the internal elastic lamina (IEL). In the past, the intima was thought to be simply a passive layer whose major purpose was to serve as a barrier. Now, however, we know that the endothelial cells actually keep track of the pressure, flow, and "health" of the artery. Moreover, endothelial cells secrete chemicals that can adjust the function of the artery (e.g., vasodilator chemicals to widen and vasoconstrictors to narrow it) and growth of the artery wall (e.g., growth factors).
The media (M) is a layer made up primarily of smooth muscle cells (SMCs). The muscle can contract and relax to control the blood pressure and flow in the artery. Elastic tissue and collagen in the media, along with elastic tissue in the IEL, increase the elasticity and strength of the wall of the artery, as the artery contracts and relaxes. The adventitia is a layer of connective tissue and cells (e.g., SMCs) that produce this connective tissue. The adventitia contains potent factors, including one called tissue thromboplastin, that promote blood clotting. The clots are useful when the artery becomes injured because they can limit excessive bleeding from the injured artery.
What happens to the coronary artery in atherosclerosis?
In coronary artery disease (coronary atherosclerosis), injury to the intima of the artery leads to the formation of plaques, which are regions of thickening on the inner lining of the artery. How then do the plaques form? In response to the injury, the smooth muscle cells (SMCs) from the media and perhaps from the adventitia move (migrate) into the intima. In the intima, these SMCs reproduce themselves (divide) and make (synthesize) connective tissue. These processes of migration, division, and synthesis, which collectively are referred to as intimal proliferation (buildup), cause thickening of the intima. When cholesterol, other fats, and inflammatory cells, such as white blood cells, enter the proliferating, thickened intima, the result is an atherosclerotic plaque. Then, as these plaques grow, they accumulate scar (fibrous) tissue and abundant calcium. (Calcium is the hard material in our teeth and bones.) Hence, the plaques are often hard, which is why atherosclerosis is sometimes referred to as "hardening of the arteries."
Who gets coronary artery plaques and what happens to the plaques?
Most adults in industrialized nations have some plaques (atherosclerosis) on the inner (lumenal) surface of their coronary arteries. Autopsy studies of young soldiers who died in World War II, the KOrean War, and the Vietnam War showed that even young adults in their 20s usually have coronary arteries that exhibit localized (focal) thickening of the intima. This thickening is the beginning of intimal proliferation and plaque formation. The distribution, severity (amount of plaque), and rate of growth of the plaques in the coronary arteries vary greatly from person to person. Figure 2 shows a coronary artery with an uneven (asymmetric), stable atherosclerotic plaque. A stable plaque may grow slowly, but has an intact inner (lumenal) surface with no clot (thrombus) on this surface.
Figure 2: Coronary Artery with Stable Atherosclerotic Plaque
Cross-sectional Microscopic View
What causes a Heart Attack?
Rupture of a stable plaque in a coronary artery is the initial pathological event leading to a heart attack. When the rupture occurs, a clot suddenly forms in the lumen (channel) of the artery at the site of the rupture. Bleeding into the plaque often accompanies the rupture. The clot then blocks (occludes) the artery and thereby decreases the blood flow to the heart. This sequence of events in the coronary arteries is the basic problem in over 75% of people who suffer a heart attack. In some patients, more often women, there is just an erosion or ulceration of the plaque surface, rather than a full rupture that leads to clot formation in the coronary artery. Figure 3 shows an atherosclerotic plaque rupture and a clot in a coronary artery.
Figure 3: Rupture of Atherosclerotic Plaque in Coronary Artery
Cross-sectional Microscopic View
What happens to the heart muscle after a person survives a Heart Attack?
According to medical studies, 50% to 75% of people survive their first heart attack The others die during the heart attack because the decreased coronary blood flow causes a severe abnormal heart rhythm or extensive death of heart muscle. Figure 4 shows the heart of a patient who died 5 days after a heart attack. The photos show his myocardial infarction as it appears on the surface of the left ventricle and when the heart is sliced to view the muscle wall. About 90% of myocardial infarctions involve only the left ventricle (LV), which pumps oxygen-rich blood that comes from the lungs to the entire body. The other 10% also involve the right ventricle (RV), which pumps the blood to the lungs.
Figure 4: Myocardial Infarction Caused by Heart Attack
Views of Heart Surface and Slice Across Heart
If a person survives a heart attack, the heart muscle may return to normal or become a region of dead heart muscle (the myocardial infarction). The amount and health of the remaining heart muscle is the major determinant of the future quality of life and longevity for a patient after a heart attack. A heart attack can interrupt the normal electrical wiring of the heart, leading to abnormal heart rhythms. The heart attack can also weaken the pumping action of the heart causing shortness of breath due to heart failure. Each of these complications of a heart attack can occur at any time during the recovery period as a result of dead, dying, or scarring heart muscle.
Can a person have more than one Heart Attack?
Yes. Not uncommonly, people with coronary artery disease have more than one heart attack over the years. In fact, by looking at the heart tissue at autopsy, pathologists can tell when myocardial infarctions occurred. Thus, very recent (acute, hours old) infarctions may appear as a pale brown region, infarctions days old (subacute) appear yellow, and healed (weeks to years old) infarctions appear as white scars in the heart muscle. Figure 5 shows three myocardial infarctions of different ages in the muscle of a left ventricle.
Figure 5: Three Myocardial Infarctions of Different Ages
Slice Across Heart Ventricles
Pediatric Epilepsy Surgery
- What is epilepsy?
- What are the different types of clinical seizures?
- What causes epilepsy in children?
- Are seizures bad for children?
- How is epilepsy treated?
- Who is a candidate for epilepsy surgery?
- What tests are used to determine if a child is a candidate for epilepsy surgery?
- Who performs pediatric epilepsy surgery?
- What are the types of epilepsy surgery?
- Resective epilepsy surgery
- Corpus callosotomy
- Vagus nerve stimulator (VNS)
- Find a local Pediatric Surgeon in your town
- What are the risks of epileptic surgery?
- Pediatric Epileptic Surgery At A Glance
What is epilepsy?
An epileptic seizure is a sudden and transient occurrence of signs and/or symptoms that are the result of an abnormal activity of the brain. Epileptic seizures are the common and defining component of the disorder that is referred to as epilepsy. The diagnosis of epilepsy implies that there is an abnormality in the brain and that this abnormality will result in more epileptic seizures. That is, an individual that has an isolated seizure as a result of an acute transient insult to the brain, for example a metabolic disorder, or a seizure observed after an acute trauma to the brain, would not be diagnosed as having epilepsy. In other words, epilepsy is the tendency to have repeated spontaneous seizures.
That are the different types of clinical seizures?
There are different types of seizures, which traditionally have been categorized as either generalized seizures or partial seizures. Generalized seizures are those in which the clinical manifestations indicate that the whole brain is involved from the beginning of the seizure. Partial seizures (local, focal) are those in which the epileptic event is limited to one part of the body or to a particular function of the brain, indicating that the epileptic seizure started in one limited area of the brain. Partial seizures may remain focal or may expand to the rest of the brain. When seizures expand to the rest of the brain these are referred to as secondary generalized seizures. Consciousness is always impaired in generalized seizures; however, in the case of partial seizures consciousness may be preserved , as in the so-called simple partial seizures, or it may be impaired, as is the case with the complex partial seizures.
Among the generalized seizures, the generalized tonic clonic seizure (traditionally recognized as a grand mal seizure) is the most common type. In this seizure there is a succession of muscle contractions (tonic component), more obvious in the extremities but affecting almost every muscle of the body, followed by sudden relaxation (clonic component) and further followed by another tonic component. This succession of events is repeated several times.
Simultaneously, there are other signs and symptoms including dilatation of the pupils, increased heart rate, and increased blood pressure. Cyanosis (skin and lips turning blue-purple) is also seen due to persistent contraction of the diaphragm muscle and holding of the breath. These convulsions are usually followed by a period of confusion. In most instances these seizures, as well as most of the epileptic seizures, last for a few seconds or at the most for 2-3 minutes. Occasionally the seizure event may be prolonged, lasting several minutes. By definition, when the event lasts more than 30 minutes, it is described as status epilepticus.
Another well known generalized seizure is the absence seizure, also called petit mal seizure, because the clinical symptoms are not as dramatic as with the generalized tonic clonic seizures. In the absence seizures, as the name implies, the patient looks absent, like "not being here." With this type of seizure there is a sudden interruption of activities, and the patient becomes unresponsive. Usually these seizures, particularly when they last longer than a few seconds, are associated with other subtle clinical signs such as eye blinking or twitching in the face or upper body. There is almost no confusion after these seizures, and the patient returns to his/her activities without even acknowledging that a seizure has occurred.
In the atonic seizures (drop attacks) there is a sudden loss of muscle activity, like a sudden paralysis. The patient will collapse like a marionette when all its strings are cut at once. If these seizures happen when the individual is walking, a fall will result, or if the patient is seated, he/she will experience a sudden drop of the head, usually without the motor reflexes that help people to prevent injuries. These seizures are very brief and might result in serious injuries, most often to the forehead, mouth, and/or face.
The myoclonic seizures consists of rapid, jerky contractions of isolated muscles or group of muscles which may or may not result in body movements.
The tonic seizures consists of a brief stiffening of the muscle groups, resulting most often in extension of the arms or legs or arching of the trunk. Some of these seizures might be associated with a forced exhalation of air, due to a sudden contraction of the expiratory muscle through partially contracted vocal cords, resulting in a loud sound.
Partial (focal, local) seizures
With partial (focal, local) seizures, the clinical events originate in a limited area of the brain. The clinical manifestations depend upon the area of the brain that is abnormal. Many different clinical events can be seen with this type of seizure.
For example, with simple partial seizures (consciousness is not impaired) if the focal area of the brain involved is the motor area, the patient might have rhythmic contractions in one arm or leg. If the areas compromised are more involved with the visual system then the patient might complain of visual illusions.
Other abnormal sensations might be the result of lesions in the auditory, olfactory, or gustatory areas. Some other symptoms might include:
- epigastric pain,
- pallor (paleness),
- pupillary dilatation,
- a sense of "déjá vu,"
- fear or anger, and
These patients are conscious when the symptoms occur, and their description of the symptoms can be very useful in determining which area of the brain is involved in the seizure. This has important implications for the selection of the appropriate treatment, especially for the decision about the need for surgery.
The complex partial seizures (sometimes called "temporal lobe seizures" or "psychomotor seizures"), in which consciousness is impaired, have a greater array of symptoms. The symptoms already described in the simple partial seizures might be present and might be followed by complex automatic behaviors such as manipulating objects, walking around the room, or answering questions, usually done in a rumbling, difficult-to-understand language.
What causes epilepsy in children?
Many different disorders of the brain may be associated with epilepsy.
For some patients the epileptic disorder is congenital, that is, the child is born with the predisposition to have epilepsy. In other patients the epileptic disorder is acquired, as a result of brain damage that occurred after birth.
The congenital epilepsies could be the result of the child having a gene that is responsible for the epileptic disorder; these are the genetic types of epilepsy. Alternatively, congenital epilepsy may be the result of factors that interfere with the development of the brain during gestation, resulting in brain malformations.
In acquired epileptic disorders, the damage might occur at the time of birth, for example the case of newborns that have oxygen deprivation during labor and delivery; or intracranial bleeding, as seen in some children born prematurely. Also, the brain damage may occur any time after birth. For example, epilepsy could be a complication of infections in the brain (meningitis, encephalitis), head injuries with brain damage, brain tumors, or intracranial bleeding.
Are seizures bad for children?
Presently there is no indication that short-lasting seizures will result in any brain damage. However, prolonged seizures, especially generalized tonic-clonic seizures, in some cases could result in brain damage, but this is very unusual.
Although brain damage is not likely, children can be injured at the time of the seizures. For example, in the atonic seizures there is a sudden loss of muscle power and, if this happens when the patient is standing, it is followed by a fall that might result in injuries to the face and/or mouth. Similar types of physical injuries can happen with other seizures.
How is epilepsy treated?
The main line of treatment is with antiepileptic drugs, which are effective in controlling seizures in 70%-80% of patients with epilepsy. There are several antiepileptic medications. Since certain medications are much better for some seizures, the choice of the medication should be made by a physician who is familiar with these medications. If possible, the child should be evaluated in a center specializing in epilepsy. If this is not feasible, usually pediatric neurologists have training in epileptic disorders and are a good source for a referral.
When antiepileptic drugs fail to control the seizures, the patients may improve with surgical procedures.
Who is a candidate for epilepsy surgery?
Surgery is indicated in a small group of children.
It usually takes the failure of two or three antiepileptic medications before a child would be considered as a potential candidate for surgery. In general, this happens at least after two or three years of continuous treatment with medications. The failure might be due:
- to a resistance to the antiepileptic medications that are available,
- to the presence of intolerable side effects to the antiepileptic medication,
- or to a combination of both.
Since surgical procedures might be very effective in some children, once it is clear that the child's epileptic disorder is not responding to treatment with antiepileptic medications, surgery should be considered. Young age is not a contraindication for surgery, and there is no benefit in waiting for the child to be older. In fact, there is considerable evidence that the younger a child is at the time of surgery, the better his/her potential will be for good function after the surgery. There is a certain degree of plasticity in the brain that helps with the recovery of functions that can be damaged at the time of surgery. This plasticity is higher in younger than in older children.
What tests are used to determine if a child is a candidate for epilepsy surgery?
As previously mentioned, surgery is only preferred once it is clear that the child is resistant to or does not respond well to antiepileptic medications. Many tests are used to make this determination.
Electroencephalograms (EEG) are very important in determining the type of epileptic seizures as well as the area of the brain that is responsible for the seizure disorder. When the routine EEG (usually one hour long) does not give enough information, then the child might need to be hospitalized (usually in special EEG wards) for a prolonged EEG with video monitoring. During the hospital admission (which may last several days) the EEG is recorded continuously throughout the entire day. The goal is to record epileptic events for further analysis. In some children it is necessary to stop the antiepileptic medications while the child is in the hospital to facilitate the emergence of an epileptic event.
Neuroimaging studies are very important to help determine the presence of brain lesions. A CT scan and an MRI, in some cases, might be helpful to point to the specific area of the brain that is abnormal. These tests are very effective to identify developmental abnormalities, brain tumors, scars due to prior bleeding events, or the presence of vascular malformations that might be responsible for the epileptic seizures.
In some children, functional MRI (fMRI), positron emission tomography (PET), single photon emission computed tomography (SPECT), magnetoencephalography (MEG), or ictal SPECT (an SPECT obtained at the time of the epileptic event) might also be indicated in order to determine the area of the brain to be excised.
In some cases the localization of the epileptogenic area requires invasive monitoring. In these children, electrodes that record the brain activity are placed either inside the brain (intracerebral electrodes) or directly on top of the brain (subdural electrodes). This procedure may be done at the time of the surgery or days before, in which case it requires a small operation and admission to the hospital for several days for continuous EEG recording.
Resective surgery (removing specific areas of brain tissue) may result in functional deficits. The functional deficits relate to the area of the brain involved in the surgery. For example, operations near the motor area might result in motor paralysis; surgery in the posterior area of the brain (the occipital lobe) might result in visual deficiencies. Of particular importance is the surgery that is performed in or near the temporal lobe which, among other functions, is responsible for language comprehension and memory. In such cases a special test, called the WADA test, is performed to ensure that removal of the local lesion does not result in severe memory or language functional deficits.
Once the evaluation is completed the team will decide if the patient is a viable candidate for surgery and in that case, what type of surgery is indicated.
It is worthwhile to mention that not all of the above-mentioned tests are necessary in all patients.
Who performs pediatric epilepsy surgery?
The actual surgery is performed by a neurosurgeon with specialized training and experience in pediatric epilepsy surgery. However, prior to the surgery the patient must be evaluated by a team of epileptologists, neuroradiologists, neuropsychologists, and neurosurgeons with specialized training in patients with refractory epilepsy. Most of these teams are in large academic medical centers with affiliations to medical schools. The team will tailor the surgery for each child on an individual basis.
What are the types of epilepsy surgery?
The following are the surgical interventions that are performed to control epileptic disorders. These procedures can be done directly on the brain, (resective surgery or corpus callosotomy), or by implanting a stimulator of the vagus nerve in the neck (vagal nerve stimulation).
- In resective surgery the part of the brain that causes the seizures is removed.
- In corpus callosotomy the major connection between the two sides of the brain is severed (cut).
- Vagus nerve stimulation is a procedure in which a small wire is attached to the vagus nerve in the neck. This wire is used to electrically stimulate the vagus nerve.
Resective epilepsy surgery
Resective surgery is the best indication for those children with epilepsy that is resistant to the antiepileptic medications and in whom a focal area of the brain was identified as the cause of the seizures. Most of these children have focal seizures rather than generalized seizures. In this procedure, the portion of the child's cerebral cortex that is causing seizures is removed. In some children the epileptic area is restricted to one discrete area of the brain, for example the temporal lobe; in other children several areas of the brain might be involved. The type and the extent of the surgery depends upon the size and location of the epileptogenic area. When the lesion is very discrete, a small area of the brain might be removed, a procedure known as partial lobectomy. If the lesion is more extensive, the child might need a bigger resection, known as multilobar resection. In some extreme cases a full half of the brain might need to be removed, known as a hemispherectomy.
Since resective surgery will result in the elimination of an area of the brain that might still be functioning before the operation is performed, it must be determined that the area in question can be removed without unacceptable problems, such as a loss of language capacity or a severe motor (movement) insufficiency.
In some children resective surgery could be the most effective form of treatment. For example, in children with mesial temporal sclerosis, a condition in which there is a well-localized lesion in the temporal lobe, the resection of the lesion can result in up to 80% of patients being seizure-free. Fifty percent of children with extensive malformations involving one hemisphere may be seizure-free after hemispherectomy.
In general, for the selective group of children with well-localized lesions, resective surgery will be beneficial in most of them.
The corpus callosum is a structure composed of nerve fibers that allows for communication between both sides of the brain. Corpus callosotomy consist of cutting the corpus callosum. In partial callosotomy, one section of the corpus callosum is cut, whereas in total callosotomy the whole length of the corpus callosum is cut. Since the fibers that go from one half of the brain to the other half are cut, the communication between the two halves of the brain is impaired. This is precisely the goal of the callosotomy. By limiting the communication between the two sides of the brain the callosotomy prevents the rapid spreading of the epileptic event from one half of the brain to the other.
The indication for this operation is rather limited, mostly to children who have frequent drop attacks, and at the present time is not frequently performed.
Vagus nerve stimulator (VNS)
The vagus nerve is a nerve that connects the brain with several internal organs such as the lungs, heart, stomach, and other organs. Stimulation of the vagus nerve sends information to the brain. Studies have shown that electrical stimulation of the vagus nerve results in an inhibition of seizure activity. However, the reasons for this improvement are not clear.
The vagus nerve stimulator (VNS) is a device that consists of a wire attached to an electrical stimulator. The wire is wrapped around the left vagus nerve in the neck, and the electrical stimulator is implanted in a pouch under the skin in the upper chest. The stimulator is programmed to send electrical signals continuously. The strength and the frequency of the electrical stimulation is adjusted as needed by professionals with special training in this technique. Additionally, the system has a magnetic hand-held device that can be used by the patient. Patients who can recognize the beginning of their seizures, for example those who have auras, can use this device to activate the system and abort the seizure. Also, since the stimulator can be activated at any time, if needed, it could be useful to shorten long-lasting seizures and also in the prevention of status epilepticus.
VNS seems to be effective in a variety of seizure disorders and epileptic syndromes. It has also proven to be effective in epileptic disorders that are resistant to antiepileptic treatment. Studies show that in many individuals with refractory seizures, VNS significantly reduced seizure activity, and some people have been rendered seizure-free.
VNS is indicated in children with epileptic disorders resistant to medication that are not candidates for surgery.
In the USA, VNS is approved for children older than 12 years of age; however, there is no age limit in the European Union.
What are the risks of VNS implantation?
Potential side effects of VNS implantation are those from general anesthesia, the failure of the implant to work and infection at the implant site. Additionally, stimulation of the vagus nerve may cause hoarseness, coughing, and may even change the heart rate. Because the VNS is implanted outside the skull, there is little possibility of additional neurological damage.
What are the risks of epilepsy surgery?
Some of the risks associated with epilepsy surgery are related to the presurgical evaluation. Some of the tests performed require the use of contrast material that might result in severe allergic reactions. Implanting electrodes in the brain or placing electrodes on the surface of the brain for continuous monitoring requires surgical procedures that are not very complicated but may be associated with bleeding or infections.
Many tests, as well as the different surgical procedures, require the use of heavy sedation or general anesthesia. General anesthesia has a very small risk of death.
There are several risks inherent to the surgery, for example, bleeding inside the brain. Bleeding inside the brain might result in additional brain damage, besides; the accumulation of blood might increase the pressure inside the cranium resulting in severe complications, including death. Also the operation may be complicated by infections that can result in meningitis. A later complication of these events could be the development of hydrocephalus, which may require another surgical procedure.
As described before, resective surgery implies the removal of a piece of the brain that in some instances could be as much as the whole hemisphere. This resective surgery may aggravate prior functional deficits or may result in new ones. These complications may occur even after very careful evaluation.
The range of complications varies with the extent of the surgery and the area removed. For example:
- operations near the motor areas might result in paralysis or weakness in the arms or legs, or loss of fine motor coordination in the hands;
- operations near the language areas might result in language disorders;
- operations near the cortical visual areas might result in visual deficits.
In the particular case of the callosotomy, since there is some degree of disconnection between the right and the left side of the brain, besides the complications already mentioned, some annoying subtle deficiencies may be experienced. For example, some patients may be able to identify, by visual recognition, objects presented to one side of the brain, but might not be able to name them because the memory of the name is in the other side of the brain. In general there are fewer complications with callosotomies than with resective surgery.
Yet, as in the case with all surgeries, there is always the risk of failure. In the case of epilepsy surgery this means recurrence of the epileptic seizures after the operation. Depending upon the type of pre-existing lesion, the failure rate may be as high as 50%. However, even in these cases, the seizures may be easily controlled with medications after the surgery.
In general there are very few complications observed after surgery. Approximately 3% of children who have had epilepsy surgery experience complications, and less than 1 % have neurological complications. Mortality (death) is very rare.
As previously mentioned, there is plasticity in the brain of young children, mostly up to the age of 7 to 9 years. The plasticity helps in the recovery of deficits that can be the result of surgery. For example, for children in whom the language areas were affected by the surgery there is remarkable recovery of language functions. Therefore, young children with intractable seizures who are candidates for surgery are much better off when the surgery is done sooner than later.
Pediatric Epileptic Surgery At A Glance
- Pediatric epilepsy surgery can be used to treat a highly selected group of patients whose seizures are not controllable by standard means.
- The appropriate candidate for epilepsy surgery must meet several criteria.
- There are currently three major categories of epilepsy surgery: resective surgery, corpus callosotomy, and implantation of the vagus nerve stimulator.
- In patients that meet the requirements for epilepsy surgery the results, in terms of seizure control, can be very positive with minimal side effects and complications.
Previous contributing medical author
Epilepsy: Surgical Options for Epilepsy
- What is epilepsy surgery?
- Who is a candidate for epilepsy surgery?
- What surgical options are available?
- How effective is epilepsy surgery?
- What are the risks of epilepsy surgery?
- Find a local Neurosurgeon in your town
What Is Epilepsy Surgery?
Most people with epilepsy can control their seizures with medication. But they aren't effective for about 30% of patients. In some cases, brain surgery may be an option.
Epilepsy surgery is an operation on the brain to control seizures and improve the person's quality of life. There are two main types of epilepsy surgery:
- Surgery to remove the area of the brain producing seizures.
- Surgery to interrupt the nerve pathways through which seizure impulses spread within the brain.
Surgery is considered only if the area of the brain where the seizures start, called the seizure focus, can be clearly identified, and if the area to be removed is not responsible for any critical functions, such as language, sensation and movement. Extensive evaluation and testing are necessary to determine if surgery is appropriate.
Who Is a Candidate for Epilepsy Surgery?
Surgery may be an option for people with epilepsy whose seizures are disabling and/or are not controlled by medication, or when the side effects of medication are severe and greatly affect the person's quality of life. Patients with other serious medical problems, such as cancer or heart disease, usually are not considered for epilepsy surgery.
What Surgical Options Are Available?
Different surgical procedures are available to treat epilepsy. The type of surgery used depends on the type of seizures and the area of the brain where the seizures start. The surgical options include:
- Lobe resection: The largest part of the brain, the cerebrum, is divided into four paired sections, called lobes -- the frontal, parietal, occipital and temporal lobes. Temporal lobe epilepsy, in which the seizure focus is located within the temporal lobe, is the most common type of epilepsy in teens and adults. In a temporal lobe resection, brain tissue in the temporal lobe is resected, or cut away, to remove the seizure focus. The anterior (front) and mesial (deep middle) portions of the temporal lobe are the areas most often involved. Extratemporal resection involves removing brain tissue from areas outside of the temporal lobe.
- Lesionectomy: This is surgery to remove isolated brain lesions -- areas of injury or defect such as a tumor or malformed blood vessel -- that are responsible for seizure activity. Seizures usually stop once the lesion is removed.
- Corpus callosotomy: The corpus callosum is a band of nerve fibers connecting the two halves (hemispheres) of the brain. A corpus callosotomy is an operation in which all or part of this structure is cut, disabling communication between the hemispheres and preventing the spread of seizures from one side of the brain to the other. This procedure, sometimes called split-brain surgery, is for patients with extreme forms of uncontrollable epilepsy who have intense seizures that can lead to violent falls and potentially serious injury.
- Functional hemispherectomy: This is a variation of a hemispherectomy, a radical procedure in which one entire hemisphere, or one half of the brain, is removed. With a functional hemispherectomy, one hemisphere is disconnected from the rest of the brain, but only a limited area of brain tissue is removed. This surgery generally is limited to children younger than 13 years old who have one hemisphere that is not functioning normally.
- Multiple subpial transection (MST): This procedure is used to help control seizures that begin in areas of the brain that cannot be safely removed. The surgeon makes a series of shallow cuts (transections) in the brain tissue. These cuts interrupt the movement of seizure impulses but do not disturb normal brain activity, leaving the person's abilities intact.
How Effective Is Epilepsy Surgery?
The effectiveness varies, depending on the type of surgery. Some people are completely free of seizures after surgery. For others, the frequency of seizures is significantly reduced. In some cases, surgery may not be successful and a second surgery (re-operation) may be recommended. Most patients will need to continue taking anti-seizure medication for a year or more after surgery. Once seizure control is established, medications may be reduced or eliminated.
What Are the Risks of Epilepsy Surgery?
The risks of epilepsy surgery include:
- Risks associated with surgery: These include infection and bleeding, as well as the risk of an allergic reaction to the anesthesia.
- Risk of neurological deficits: Surgery can worsen existing problems or create new problems with the way the brain functions. Neurological deficits include loss of functions such as vision, speech, memory or movement.
- Risk of surgery failure: Even with careful pre-surgical evaluation, surgery may not eliminate or reduce seizures. Before undergoing surgery your doctor will discuss the potential risks and benefits of the procedure.
- Before undergoing surgery your doctor will discuss the potential risks and benefits of the procedure.
In some cases, isolated seizures may occur immediately following surgery. This does not necessarily mean the operation was not successful. Occasionally, a second operation, or re-operation, is needed to remove brain tissue that is later found to be a source of seizure activity.
WebMD Medical Reference
Reviewed by Brunilda Nazario, MD on October 29, 2009 © 2009 WebMD, LLC. All rights reserved.
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*Dementia Facts Medically Edited by:
Charles P. Davis, MD, PhD
- Dementia is a term that describes a collection of symptoms that include decreased intellectual functioning that interferes with normal life functions and is usually used to describe people who have two or more major life functions impaired or lost such as memory, language, perception, judgment or reasoning; they may lose emotional and behavioral control, develop personality changes and have problem solving abilities reduced or lost.
- There are different classification schemes for dementias roughly based (and with overlap) on observed problems; some frequently used are cortical (memory, language, thinking, social) , subcortical (emotions, movement, memory), progressive (cognitive abilities worsen over time), primary (results from a specific disease such as Alzheimer's disease and secondary (occurs because of disease or injury).
- Alzheimer's disease (AD): is the most common cause of dementia in people over age 65 with cause possibly related to amyloid plaques and neurofibrillary tangles; almost all brain functions, including memory, movement, language, judgment, behavior, and abstract thinking, are eventually affected.
- Vascular dementia: is the second most common cause of dementia caused by brain damage from cerebrovascular or cardiovascular problems (strokes) or other problems that inhibit vascular function; symptoms similar to AD but personality and emotions effected only late in the disease.
- Lewy body dementia: is common and progressive where cells in the brain's cortex die and other contain abnormal structures (Lewy bodies); symptoms overlap with Alzheimer's disease but also include hallucinations, shuffling gait, and flexed posture with symptoms that may vary daily.
- Frontotemporal dementia: is dementia linked to degeneration of nerve cells in the frontal and temporal brain lobes and some evidence for a genetic factor (many have a family history of the disease); symptoms in patients (usually ages 40 – 65) have judgment and social behavior problems such as stealing, neglecting responsibilities, increased appetite, compulsive behavior and eventual motor skill problems and memory loss.
- HIV-associated dementia: is due to infection of the brain with HIV virus; symptoms include impaired memory, apathy, social withdrawal, and concentration problems.
- Huntington's disease: is a heredity disorder caused by a faulty gene and children of a person with the disorder have a 50% chance of getting the disease; symptoms begin in 30-40 year old people with personality changes such as anxiety, depression and progress to show psychotic behavior severe dementia and chorea - involuntary jerky, arrhythmic movements of the body.
- Dementia pugilistica: is also termed Boxer's syndrome, is due to traumatic injury (often repeatedly) to the brain; symptoms commonly are dementia and parkinsonism (tremors, gait abnormalities) and other changes depending where brain injury has happened.
- Corticobasal degeneration: is a progressive nerve cell loss in multiple areas of the brain; symptoms begin at about age 60 on one side of the body and include poor coordination and rigidity with associated visual-spatial problems that can progress to memory loss, hesitant speech and dysphagia (difficulty swallowing).
- Creutzfeldt-Jakob disease: is a rare disease that seems related to a gene mutation that causes rapid (death about one year after symptoms begin to develop) degenerative and fatal brain disease in people usually over 60 years old; personality changes and reduced coordination develop, rapidly followed by impaired judgment and vision and many patients develop a coma before they die.
- Other rare hereditary dementias: – Most of these diseases develop in people between 50 – 60 years old and most have variable symptoms of poor reflexes, dementia, hallucinations, paralysis and most develop coma before death; some of the names of these diseases are Gerstmann-Straussler-Scheinker disease, familial British dementia, familial Danish dementia and fatal familial insomnia.
- Secondary dementias: These dementias occur in patients with other disorders of movement such as Parkinson's disease or multiple sclerosis and may because by one or more problems listed above; these dementias may share symptoms with any of the above mentioned dementias but researchers are unsure if this is due to disease overlap or other causes.
- Dementias in children: While infections, trauma and poisoning can lead to dementia in both children and adults, there are some dementias that are unique to children but may result in mental problems, seizures, reduction or loss of motor skills, blindness, neurodegeneration and death; many are inherited disorders such as Niemann-Pick disease, Batten disease, Lafora disease and mitochondrial abnormalities.
- Other conditions that may cause dementia: Reactions to medications, endocrine and metabolic problems, nutritional deficiencies, infections, subdural hematomas, poisoning, brain tumors, anoxia (lack of oxygen), heart and lung problems.
- What conditions are not dementia: Although these conditions may resemble some aspects of dementia, they have different causes, usually are treatable and have better outcomes; examples are depression, delirium, mild cognitive impairment and age-related cognitive decline.
- Dementia causes: All causes of dementia result from death and damage of nerve cells in the brain; genetics and possibly the formation of different types of inclusions in the brain cells are likely the major causes, although some researchers suggest that certain inclusions may be only side effects of an underlying disorder.
- Risk factors for dementia include advancing age, genetics (family history), smoking, alcohol use, atherosclerosis, high cholesterol, diabetes, high plasma homocysteine levels, mild cognitive impairment, Down syndrome
- Dementia is diagnosed by using many methods such as patient's medical and family history, physical exam, neurological evaluations, cognitive and neuropsychological testing, CT's, MRI's and other brain scans, mental status exams, electroencephalograms, blood tests, psychiatric evaluations, and even some pre-symptomatic tests are available for some patients that may have a genetic link to dementia.
- Most treatments for dementia will neither reverse or stop the disease; however, there are treatments and medications that may reduce the symptoms and slow the disease progression; they are tight glucose control by persons with diabetes, intellectual stimulating activities, lowering cholesterol and homocysteine levels, regular exercise, education, controlling inflammation of body tissues, using NSAID's and possibly other medications.
Introduction to Dementia
A woman in her early 50s was admitted to a hospital because of increasingly odd behavior. Her family reported that she had been showing memory problems and strong feelings of jealousy. She also had become disoriented at home and was hiding objects. During a doctor's examination, the woman was unable to remember her husband's name, the year, or how long she had been at the hospital. She could read but did not seem to understand what she read, and she stressed the words in an unusual way. She sometimes became agitated and seemed to have hallucinations and irrational fears.
This woman, known as Auguste D., was the first person reported to have the disease now known as Alzheimer's disease * (AD) after Alois Alzheimer, the German doctor who first described it. After Auguste D. died in 1906, doctors examined her brain and found that it appeared shrunken and contained several unusual features, including strange clumps of protein called plaques and tangled fibers inside the nerve cells. Memory impairments and other symptoms of dementia, which means "deprived of mind," had been described in older adults since ancient times. However, because Auguste D. began to show symptoms at a relatively early age, doctors did not think her disease could be related to what was then called "senile dementia. "The word senile is derived from a Latin term that means, roughly, "old age."
It is now clear that AD is a major cause of dementia in elderly people as well as in relatively young adults. Furthermore, we know that it is only one of many disorders that can lead to dementia. The U. S. Congress Office of Technology Assessment estimates that as many as 6.8 million people in the United States have dementia, and at least 1.8 million of those are severely affected. Studies in some communities have found that almost half of all people age 85 and older have some form of dementia. Although it is common in very elderly individuals, dementia is not a normal part of the aging process. Many people live into their 90s and even 100s without any symptoms of dementia.
Besides senile dementia, other terms often used to describe dementia include senility and organic brain syndrome. Senility and senile dementia are outdated terms that reflect the formerly widespread belief that dementia was a normal part of aging. Organic brain syndrome is a general term that refers to physical disorders (not psychiatric in origin) that impair mental functions.
Research in the last 30 years has led to a greatly improved understanding of what dementia is, who gets it, and how it develops and affects the brain. This work is beginning to pay off with better diagnostic techniques, improved treatments, and even potential ways of preventing these diseases.
What Is Dementia?
Dementia is not a specific disease. It is a descriptive term for a collection of symptoms that can be caused by a number of disorders that affect the brain. People with dementia have significantly impaired intellectual functioning that interferes with normal activities and relationships. They also lose their ability to solve problems and maintain emotional control, and they may experience personality changes and behavioral problems such as agitation, delusions, and hallucinations. While memory loss is a common symptom of dementia, memory loss by itself does not mean that a person has dementia. Doctors diagnose dementia only if two or more brain functions - such as memory, language skills, perception, or cognitive skills including reasoning and judgment - are significantly impaired without loss of consciousness.
There are many disorders that can cause dementia. Some, such as AD, lead to a progressive loss of mental functions. But other types of dementia can be halted or reversed with appropriate treatment.
With AD and many other types of dementia, disease processes cause many nerve cells to stop functioning, lose connections with other neurons, and die. In contrast, normal aging does not result in the loss of large numbers of neurons in the brain.
What Are the Different Kinds of Dementia?
Dementing disorders can be classified many different ways. These classification schemes attempt to group disorders that have particular features in common, such as whether they are progressive or what parts of the brain are affected. Some frequently used classifications include the following:
- Cortical dementia: dementia where the brain damage primarily affects the brain's cortex, or outer layer. Cortical dementias tend to cause problems with memory, language, thinking, and social behavior.
- Subcortical dementia: dementia that affects parts of the brain below the cortex. Subcortical dementia tends to cause changes in emotions and movement in addition to problems with memory.
- Progressive dementia: dementia that gets worse over time, gradually interfering with more and more cognitive abilities.
- Primary dementia: dementia such as AD that does not result from any other disease.
- Secondary dementia: dementia that occurs as a result of a physical disease or injury.
Some types of dementia fit into more than one of these classifications. For example, AD is considered both a progressive and a cortical dementia.
Alzheimer's disease is the most common cause of dementia in people aged 65 and older. Experts believe that up to 4 million people in the United States are currently living with the disease: one in ten people over the age of 65 and nearly half of those over 85 have AD. At least 360,000 Americans are diagnosed with AD each year and about 50,000 are reported to die from it.
In most people, symptoms of AD appear after age 60. However, there are some early-onset forms of the disease, usually linked to a specific gene defect, which may appear as early as age 30. AD usually causes a gradual decline in cognitive abilities, usually during a span of 7 to 10 years. Nearly all brain functions, including memory, movement, language, judgment, behavior, and abstract thinking, are eventually affected.
AD is characterized by two abnormalities in the brain: amyloid plaques and neurofibrillary tangles. Amyloid plaques, which are found in the tissue between the nerve cells, are unusual clumps of a protein called beta amyloid along with degenerating bits of neurons and other cells.
Neurofibrillary tangles are bundles of twisted filaments found within neurons. These tangles are largely made up of a protein called tau. In healthy neurons, the tau protein helps the functioning of microtubules, which are part of the cell's structural support and deliver substances throughout the nerve cell. However, in AD, tau is changed in a way that causes it to twist into pairs of helical filaments that collect into tangles. When this happens, the microtubules cannot function correctly and they disintegrate. This collapse of the neuron's transport system may impair communication between nerve cells and cause them to die.
Researchers do not know if amyloid plaques and neurofibrillary tangles are harmful or if they are merely side effects of the disease process that damages neurons and leads to the symptoms of AD. They do know that plaques and tangles usually increase in the brain as AD progresses.
In the early stages of AD, patients may experience memory impairment, lapses of judgment, and subtle changes in personality. As the disorder progresses, memory and language problems worsen and patients begin to have difficulty performing activities of daily living, such as balancing a checkbook or remembering to take medications. They also may have visuospatial problems, such as difficulty navigating an unfamiliar route. They may become disoriented about places and times, may suffer delusions (such as the idea that someone is stealing from them or that their spouse is being unfaithful), and may become short-tempered and hostile. During the late stages of the disease, patients begin to lose the ability to control motor functions. They may have difficulty swallowing and lose bowel and bladder control. They eventually lose the ability to recognize family members and to speak. As AD progresses, it begins to affect the person's emotions and behavior. Most people with AD eventually develop symptoms such as aggression, agitation, depression, sleeplessness, or delusions.
On average, patients with AD live for 8 to 10 years after they are diagnosed. However, some people live as long as 20 years. Patients with AD often die of aspiration pneumonia because they lose the ability to swallow late in the course of the disease.
Vascular dementia is the second most common cause of dementia, after AD. It accounts for up to 20 percent of all dementias and is caused by brain damage from cerebrovascular or cardiovascular problems - usually strokes. It also may result from genetic diseases, endocarditis (infection of a heart valve), or amyloid angiopathy (a process in which amyloid protein builds up in the brain's blood vessels, sometimes causing hemorrhagic or "bleeding" strokes). In many cases, it may coexist with AD. The incidence of vascular dementia increases with advancing age and is similar in men and women.
Symptoms of vascular dementia often begin suddenly, frequently after a stroke. Patients may have a history of high blood pressure, vascular disease, or previous strokes or heart attacks. Vascular dementia may or may not get worse with time, depending on whether the person has additional strokes. In some cases, symptoms may get better with time. When the disease does get worse, it often progresses in a stepwise manner, with sudden changes in ability. Vascular dementia with brain damage to the mid-brain regions, however, may cause a gradual, progressive cognitive impairment that may look much like AD. Unlike people with AD, people with vascular dementia often maintain their personality and normal levels of emotional responsiveness until the later stages of the disease.
People with vascular dementia frequently wander at night and often have other problems commonly found in people who have had a stroke, including depression and incontinence.
There are several types of vascular dementia, which vary slightly in their causes and symptoms. One type, called multi-infarct dementia (MID), is caused by numerous small strokes in the brain. MID typically includes multiple damaged areas, called infarcts, along with extensive lesions in the white matter, or nerve fibers, of the brain.
Because the infarcts in MID affect isolated areas of the brain, the symptoms are often limited to one side of the body or they may affect just one or a few specific functions, such as language. Neurologists call these "local" or "focal" symptoms, as opposed to the "global" symptoms seen in AD, which affect many functions and are not restricted to one side of the body.
Although not all strokes cause dementia, in some cases a single stroke can damage the brain enough to cause dementia. This condition is called single-infarct dementia. Dementia is more common when the stroke takes place on the left side (hemisphere) of the brain and/or when it involves the hippocampus, a brain structure important for memory.
Another type of vascular dementia is called Binswanger's disease. This rare form of dementia is characterized by damage to small blood vessels in the white matter of the brain (white matter is found in the inner layers of the brain and contains many nerve fibers coated with a whitish, fatty substance called myelin). Binswanger's disease leads to brain lesions, loss of memory, disordered cognition, and mood changes. Patients with this disease often show signs of abnormal blood pressure, stroke, blood abnormalities, disease of the large blood vessels in the neck, and/or disease of the heart valves. Other prominent features include urinary incontinence, difficulty walking, clumsiness, slowness, lack of facial expression, and speech difficulty. These symptoms, which usually begin after the age of 60, are not always present in all patients and may sometimes appear only temporarily. Treatment of Binswanger's disease is symptomatic, and may include the use of medications to control high blood pressure, depression, heart arrhythmias, and low blood pressure. The disorder often includes episodes of partial recovery.
Another type of vascular dementia is linked to a rare hereditary disorder called CADASIL, which stands for cerebral autosomal dominant arteriopathy with subcortical infarct and leukoencephalopathy. CADASIL is linked to abnormalities of a specific gene, Notch3, which is located on chromosome 19. This condition causes multi-infarct dementia as well as stroke, migraine with aura, and mood disorders. The first symptoms usually appear in people who are in their twenties, thirties, or forties and affected individuals often die by age 65. Researchers believe most people with CADASIL go undiagnosed, and the actual prevalence of the disease is not yet known.
Other causes of vascular dementia include vasculitis, an inflammation of the blood vessel system; profound hypotension (low blood pressure); and lesions caused by brain hemorrhage. The autoimmune disease lupus erythematosus and the inflammatory disease temporal arteritis can also damage blood vessels in a way that leads to vascular dementia.
Lewy body dementia (LBD)
Lewy body dementia (LBD) is one of the most common types of progressive dementia. LBD usually occurs sporadically, in people with no known family history of the disease. However, rare familial cases have occasionally been reported.
In LBD, cells die in the brain's cortex, or outer layer, and in a part of the mid-brain called the substantia nigra. Many of the remaining nerve cells in the substantia nigra contain abnormal structures called Lewy bodies that are the hallmark of the disease. Lewy bodies may also appear in the brain's cortex, or outer layer. Lewy bodies contain a protein called alpha-synuclein that has been linked to Parkinson's disease and several other disorders. Researchers, who sometimes refer to these disorders collectively as "synucleinopathies," do not yet know why this protein accumulates inside nerve cells in LBD.
The symptoms of LBD overlap with AD in many ways, and may include memory impairment, poor judgment, and confusion. However, LBD typically also includes visual hallucinations, parkinsonian symptoms such as a shuffling gait and flexed posture, and day-to-day fluctuations in the severity of symptoms. Patients with LBD live an average of 7 years after symptoms begin.
There is no cure for LBD, and treatments are aimed at controlling the parkinsonian and psychiatric symptoms of the disorder. Patients sometimes respond dramatically to treatment with antiparkinsonian drugs and/or cholinesterase inhibitors, such as those used for AD. Some studies indicate that neuroleptic drugs, such as clozapine and olanzapine, also can reduce the psychiatric symptoms of this disease. But neuroleptic drugs may cause severe adverse reactions, so other therapies should be tried first and patients using these drugs should be closely monitored.
Lewy bodies are often found in the brains of people with Parkinson's and AD. These findings suggest that either LBD is related to these other causes of dementia or that the diseases sometimes coexist in the same person.
Frontotemporal dementia (FTD)
Frontotemporal dementia (FTD), sometimes called frontal lobe dementia, describes a group of diseases characterized by degeneration of nerve cells - especially those in the frontal and temporal lobes of the brain. Unlike AD, FTD usually does not include formation of amyloid plaques. In many people with FTD, there is an abnormal form of tau protein in the brain, which accumulates into neurofibrillary tangles. This disrupts normal cell activities and may cause the cells to die.
Experts believe FTD accounts for 2 to 10 percent of all cases of dementia. Symptoms of FTD usually appear between the ages of 40 and 65. In many cases, people with FTD have a family history of dementia, suggesting that there is a strong genetic factor in the disease. The duration of FTD varies, with some patients declining rapidly over 2 to 3 years and others showing only minimal changes for many years. People with FTD live with the disease for an average of 5 to 10 years after diagnosis.
Because structures found in the frontal and temporal lobes of the brain control judgment and social behavior, people with FTD often have problems maintaining normal interactions and following social conventions. They may steal or exhibit impolite and socially inappropriate behavior, and they may neglect their normal responsibilities. Other common symptoms include loss of speech and language, compulsive or repetitive behavior, increased appetite, and motor problems such as stiffness and balance problems. Memory loss also may occur, although it typically appears late in the disease.
In one type of FTD called Pick's disease, certain nerve cells become abnormal and swollen before they die. These swollen, or ballooned, neurons are one hallmark of the disease. The brains of people with Pick's disease also have abnormal structures called Pick bodies, composed largely of the protein tau, inside the neurons. The cause of Pick's disease is unknown, but it runs in some families and thus it is probably due at least in part to a faulty gene or genes. The disease usually begins after age 50 and causes changes in personality and behavior that gradually worsen over time. The symptoms of Pick's disease are very similar to those of AD, and may include inappropriate social behavior, loss of mental flexibility, language problems, and difficulty with thinking and concentration. There is currently no way to slow the progressive degeneration found in Pick's disease. However, medication may be helpful in reducing aggression and other behavioral problems, and in treating depression.
In some cases, familial FTD is linked to a mutation in the tau gene. This disorder, called frontotemporal dementia with parkinsonism linked to chromosome 17 (FTDP-17), is much like other types of FTD but often includes psychiatric symptoms such as delusions and hallucinations.
Primary progressive aphasia (PPA) is a type of FTD that may begin in people as early as their forties. "Aphasia" is a general term used to refer to deficits in language functions, such as speaking, understanding what others are saying, and naming common objects. In PPA one or more of these functions can become impaired. Symptoms often begin gradually and progress slowly over a period of years. As the disease progresses, memory and attention may also be impaired and patients may show personality and behavior changes. Many, but not all, people with PPA eventually develop symptoms of dementia.
HIV-associated dementia (HAD)
HIV-associated dementia (HAD) results from infection with the human immunodeficiency virus (HIV) that causes AIDS. HAD can cause widespread destruction of the brain's white matter. This leads to a type of dementia that generally includes impaired memory, apathy, social withdrawal, and difficulty concentrating. People with HAD often develop movement problems as well. There is no specific treatment for HAD, but AIDS drugs can delay onset of the disease and may help to reduce symptoms.
Huntington's disease (HD)
Huntington's disease (HD) is a hereditary disorder caused by a faulty gene for a protein called huntingtin. The children of people with the disorder have a 50 percent chance of inheriting it. The disease causes degeneration in many regions of the brain and spinal cord. Symptoms of HD usually begin when patients are in their thirties or forties, and the average life expectancy after diagnosis is about 15 years.
Cognitive symptoms of HD typically begin with mild personality changes, such as irritability, anxiety, and depression, and progress to severe dementia. Many patients also show psychotic behavior. HD causes chorea - involuntary jerky, arrhythmic movements of the body - as well as muscle weakness, clumsiness, and gait disturbances.
Dementia pugilistica, also called chronic traumatic encephalopathy or Boxer's syndrome, is caused by head trauma, such as that experienced by people who have been punched many times in the head during boxing. The most common symptoms of the condition are dementia and parkinsonism, which can appear many years after the trauma ends. Affected individuals may also develop poor coordination and slurred speech. A single traumatic brain injury may also lead to a disorder called post-traumatic dementia (PTD). PTD is much like dementia pugilistica but usually also includes long-term memory problems. Other symptoms vary depending on which part of the brain was damaged by the injury.
Corticobasal degeneration (CBD)
Corticobasal degeneration (CBD) is a progressive disorder characterized by nerve cell loss and atrophy of multiple areas of the brain. Brain cells from people with CBD often have abnormal accumulations of the protein tau. CBD usually progresses gradually over the course of 6 to 8 years. Initial symptoms, which typically begin at or around age 60, may first appear on one side of the body but eventually will affect both sides. Some of the symptoms, such as poor coordination and rigidity, are similar to those found in Parkinson's disease. Other symptoms may include memory loss, dementia, visual-spatial problems, apraxia (loss of the ability to make familiar, purposeful movements), hesitant and halting speech, myoclonus (involuntary muscular jerks), and dysphagia (difficulty swallowing). Death is often caused by pneumonia or other secondary problems such as sepsis (severe infection of the blood) or pulmonary embolism (a blood clot in the lungs).
There are no specific treatments available for CBD. Drugs such as clonazepam may help with myoclonus, however, and occupational, physical, and speech therapy can help in managing the disabilities associated with this disease. The symptoms of the disease often do not respond to Parkinson's medications or other drugs.
Creutzfeldt-Jakob disease (CJD)
Creutzfeldt-Jakob disease (CJD) is a rare, degenerative, fatal brain disorder that affects about one in every million people per year worldwide. Symptoms usually begin after age 60 and most patients die within 1 year. Many researchers believe CJD results from an abnormal form of a protein called a prion. Most cases of CJD occur sporadically - that is, in people who have no known risk factors for the disease. However, about 5 to 10 percent of cases of CJD in the United States are hereditary, caused by a mutation in the gene for the prion protein. In rare cases, CJD can also be acquired through exposure to diseased brain or nervous system tissue, usually through certain medical procedures. There is no evidence that CJD is contagious through the air or through casual contact with a CJD patient.
Patients with CJD may initially experience problems with muscular coordination; personality changes, including impaired memory, judgment, and thinking; and impaired vision. Other symptoms may include insomnia and depression. As the illness progresses, mental impairment becomes severe. Patients often develop myoclonus and they may go blind. They eventually lose the ability to move and speak, and go into a coma. Pneumonia and other infections often occur in these patients and can lead to death.
CJD belongs to a family of human and animal diseases known as the transmissible spongiform encephalopathies (TSEs). Spongiform refers to the characteristic appearance of infected brains, which become filled with holes until they resemble sponges when viewed under a microscope. CJD is the most common of the known human TSEs. Others include fatal familial insomnia and Gerstmann-Straussler-Scheinker disease (see below).
In recent years, a new type of CJD, called variant CJD (vCJD), has been found in Great Britain and several other European countries. The initial symptoms of vCJD are different from those of classic CJD and the disorder typically occurs in younger patients. Research suggests that vCJD may have resulted from human consumption of beef from cattle with a TSE disease called bovine spongiform encephalopathy (BSE), also known as "mad cow disease."
Other rare hereditary dementias
Other rare hereditary dementias include Gerstmann-Straussler-Scheinker (GSS) disease, fatal familial insomnia, familial British dementia, and familial Danish dementia. Symptoms of GSS typically include ataxia and progressive dementia that begins when people are between 50 and 60 years old. The disease may last for several years before patients eventually die. Fatal familial insomnia causes degeneration of a brain region called the thalamus, which is partially responsible for controlling sleep. It causes a progressive insomnia that eventually leads to a complete inability to sleep. Other symptoms may include poor reflexes, dementia, hallucinations, and eventually coma. It can be fatal within 7 to 13 months after symptoms begin but may last longer. Familial British dementia and familial Danish dementia have been linked to two different defects in a gene found on chromosome 13. The symptoms of both diseases include progressive dementia, paralysis, and loss of balance.
Dementia may occur in patients who have other disorders that primarily affect movement or other functions. These cases are often referred to as secondary dementias. The relationship between these disorders and the primary dementias is not always clear. For instance, people with advanced Parkinson's disease, which is primarily a movement disorder, sometimes develop symptoms of dementia. Many Parkinson's patients also have amyloid plaques and neurofibrillary tangles like those found in AD. The two diseases may be linked in a yet-unknown way, or they may simply coexist in some people. People with Parkinson's and associated dementia sometimes show signs of Lewy body dementia or progressive supranuclear palsy at autopsy, suggesting that these diseases may also overlap with Parkinson's or that Parkinson's is sometimes misdiagnosed.
Other disorders that may include symptoms of dementia include multiple sclerosis; presenile dementia with motor neuron disease, also called ALS dementia; olivopontocerebellar atrophy (OPCA); Wilson's disease; and normal pressure hydrocephalus (NPH)
Dementias in Children
While it is usually found in adults, dementia can also occur in children. For example, infections and poisoning can lead to dementia in people of any age. In addition, some disorders unique to children can cause dementia.
Niemann-Pick disease is a group of inherited disorders that affect metabolism and are caused by specific genetic mutations. Patients with Niemann-Pick disease cannot properly metabolize cholesterol and other lipids. Consequently, excessive amounts of cholesterol accumulate in the liver and spleen and excessive amounts of other lipids accumulate in the brain. Symptoms may include dementia, confusion, and problems with learning and memory. These diseases usually begin in young school-age children but may also appear during the teen years or early adulthood.
Batten disease is a fatal, hereditary disorder of the nervous system that begins in childhood. Symptoms are linked to a buildup of substances called lipopigments in the body's tissues. The early symptoms include personality and behavior changes, slow learning, clumsiness, or stumbling. Over time, affected children suffer mental impairment, seizures, and progressive loss of sight and motor skills. Eventually, children with Batten disease develop dementia and become blind and bedridden. The disease is often fatal by the late teens or twenties.
Lafora body disease is a rare genetic disease that causes seizures, rapidly progressive dementia, and movement problems. These problems usually begin in late childhood or the early teens. Children with Lafora body disease have microscopic structures called Lafora bodies in the brain, skin, liver, and muscles. Most affected children die within 2 to 10 years after the onset of symptoms.
A number of other childhood-onset disorders can include symptoms of dementia. Among these are mitochondrial myopathies, Rasmussen's encephalitis, mucopolysaccharidosis III (Sanfilippo syndrome), neurodegeneration with brain iron accumulation, and leukodystrophies such as Alexander disease, Schilder's disease, and metachromatic leukodystrophy
What Other Conditions Can Cause Dementia?
Doctors have identified many other conditions that can cause dementia or dementia-like symptoms. Many of these conditions are reversible with appropriate treatment.
Reactions to medications. Medications can sometimes lead to reactions or side effects that mimic dementia. These dementia-like effects can occur in reaction to just one drug or they can result from drug interactions. They may have a rapid onset or they may develop slowly over time.
Metabolic problems and endocrine abnormalities. Thyroid problems can lead to apathy, depression, or dementia. Hypoglycemia, a condition in which there is not enough sugar in the bloodstream, can cause confusion or personality changes. Too little or too much sodium or calcium can also trigger mental changes. Some people have an impaired ability to absorb vitamin B12, which creates a condition called pernicious anemia that can cause personality changes, irritability, or depression. Tests can determine if any of these problems are present.
Nutritional deficiencies. Deficiencies of thiamine (vitamin B1) frequently result from chronic alcoholism and can seriously impair mental abilities, in particular memories of recent events. Severe deficiency of vitamin B6 can cause a neurological illness called pellagra that may include dementia. Deficiencies of vitamin B12 also have been linked to dementia in some cases. Dehydration can also cause mental impairment that can resemble dementia.
Infections. Many infections can cause neurological symptoms, including confusion or delirium, due to fever or other side effects of the body's fight to overcome the infection. Meningitis and encephalitis, which are infections of the brain or the membrane that covers it, can cause confusion, sudden severe dementia, withdrawal from social interaction, impaired judgment, or memory loss. Untreated syphilis also can damage the nervous system and cause dementia. In rare cases, Lyme disease can cause memory or thinking difficulties. People in the advanced stages of AIDS also may develop a form of dementia (see HIV-associated dementia, page 14). People with compromised immune systems, such as those with leukemia and AIDS, may also develop an infection called progressive multifocal leukoencephalopathy (PML). PML is caused by a common human polyomavirus, JC virus, and leads to damage or destruction of the myelin sheath that covers nerve cells. PML can lead to confusion, difficulty with thinking or speaking, and other mental problems.
Subdural hematomas. Subdural hematomas, or bleeding between the brain's surface and its outer covering (the dura), can cause dementia-like symptoms and changes in mental function.
Poisoning. Exposure to lead, other heavy metals, or other poisonous substances can lead to symptoms of dementia. These symptoms may or may not resolve after treatment, depending on how badly the brain is damaged. People who have abused substances such as alcohol and recreational drugs sometimes display signs of dementia even after the substance abuse has ended. This condition is known as substance-induced persisting dementia.
Brain tumors. In rare cases, people with brain tumors may develop dementia because of damage to their brains. Symptoms may include changes in personality, psychotic episodes, or problems with speech, language, thinking, and memory.
Anoxia. Anoxia and a related term, hypoxia, are often used interchangeably to describe a state in which there is a diminished supply of oxygen to an organ's tissues. Anoxia may be caused by many different problems, including heart attack, heart surgery, severe asthma, smoke or carbon monoxide inhalation, high-altitude exposure, strangulation, or an overdose of anesthesia. In severe cases of anoxia the patient may be in a stupor or a coma for periods ranging from hours to days, weeks, or months. Recovery depends on the severity of the oxygen deprivation. As recovery proceeds, a variety of psychological and neurological abnormalities, such as dementia or psychosis, may occur. The person also may experience confusion, personality changes, hallucinations, or memory loss.
Heart and lung problems. The brain requires a high level of oxygen in order to carry out its normal functions. Therefore, problems such as chronic lung disease or heart problems that prevent the brain from receiving adequate oxygen can starve brain cells and lead to the symptoms of dementia.
What Conditions Are Not Dementia?
Age-related cognitive decline. As people age, they usually experience slower information processing and mild memory impairment. In addition, their brains frequently decrease in volume and some nerve cells, or neurons, are lost. These changes, called age-related cognitive decline, are normal and are not considered signs of dementia.
Mild cognitive impairment. Some people develop cognitive and memory problems that are not severe enough to be diagnosed as dementia but are more pronounced than the cognitive changes associated with normal aging. This condition is called mild cognitive impairment. Although many patients with this condition later develop dementia, some do not. Many researchers are studying mild cognitive impairment to find ways to treat it or prevent it from progressing to dementia.
Depression. People with depression are frequently passive or unresponsive, and they may appear slow, confused, or forgetful. Other emotional problems can also cause symptoms that sometimes mimic dementia.
Delirium. Delirium is characterized by confusion and rapidly altering mental states. The person may also be disoriented, drowsy, or incoherent, and may exhibit personality changes. Delirium is usually caused by a treatable physical or psychiatric illness, such as poisoning or infections. Patients with delirium often, though not always, make a full recovery after their underlying illness is treated.
What Causes Dementia?
All forms of dementia result from the death of nerve cells and/or the loss of communication among these cells. The human brain is a very complex and intricate machine and many factors can interfere with its functioning. Researchers have uncovered many of these factors, but they have not yet been able to fit these puzzle pieces together in order to form a complete picture of how dementias develop.
Many types of dementia, including AD, Lewy body dementia, Parkinson's dementia, and Pick's disease, are characterized by abnormal structures called inclusions in the brain. Because these inclusions, which contain abnormal proteins, are so common in people with dementia, researchers suspect that they play a role in the development of symptoms. However, that role is unknown, and in some cases the inclusions may simply be a side effect of the disease process that leads to the dementia.
Genes clearly play a role in the development of some kinds of dementia. However, in AD and many other disorders, the dementia usually cannot be tied to a single abnormal gene. Instead, these forms of dementia appear to result from a complex interaction of genes, lifestyle factors, and other environmental influences.
Researchers have identified several genes that influence susceptibility to AD. Mutations in three of the known genes for AD - genes that control the production of proteins such as amyloid precursor protein (APP), presenilin 1, and presenilin 2 - are linked to early-onset forms of the disease.
Variations in another gene, called apolipoprotein E (apoE), have been linked to an increased risk of late-onset AD. The apoE gene does not cause the disease by itself, but one version of the gene, called apoE epsilon4 (apoE E4), appears to increase the risk of AD. People with two copies of the apoE E4 gene have about ten times the risk of developing AD compared to people without apoE E4. This gene variant seems to encourage amyloid deposition in the brain. One study also found that this gene is associated with shorter survival in men with AD. In contrast, another version of the apoE gene, called apoE E2, appears to protect against AD.
Studies have suggested that mutations in another gene, called CYP46, may contribute to an increased risk of developing late-onset sporadic AD. This gene normally produces a protein that helps the brain metabolize cholesterol.
Scientists are trying to determine how beta amyloid influences the development of AD. A number of studies indicate that the buildup of this protein initiates a complex chain of events that culminates in dementia. One study found that beta amyloid buildup in the brain triggers cells called microglia, which act like janitors that mop up potentially harmful substances in the brain, to release a potent neurotoxin called peroxynitrite. This may contribute to nerve cell death in AD. Another study found that beta amyloid causes a protein called p35 to be split into two proteins. One of the resulting proteins triggers changes in the tau protein that lead to formation of neurofibrillary tangles. A third study found that beta amyloid activates cell-death enzymes called caspases that alter the tau protein in a way that causes it to form tangles. Researchers believe these tangles may contribute to the neuron death in AD.
Vascular dementia can be caused by cerebrovascular disease or any other condition that prevents normal blood flow to the brain. Without a normal supply of blood, brain cells cannot obtain the oxygen they need to work correctly, and they often become so deprived that they die.
The causes of other types of dementias vary. Some, such as CJD and GSS, have been tied to abnormal forms of specific proteins. Others, including Huntington's disease and FTDP-17, have been linked to defects in a single gene. Post-traumatic dementia is directly related to brain cell death after injury. HIV-associated dementia is clearly tied to infection by the HIV virus, although the exact way the virus causes damage is not yet certain. For other dementias, such as corticobasal degeneration and most types of frontotemporal dementia, the underlying causes have not yet been identified.
What Are the Risk Factors for Dementia?
Researchers have identified several risk factors that affect the likelihood of developing one or more kinds of dementia. Some of these factors are modifiable, while others are not.
Age. The risk of AD, vascular dementia, and several other dementias goes up significantly with advancing age.
Genetics/family history. As described in the section "What Causes Dementia?" researchers have discovered a number of genes that increase the risk of developing AD. Although people with a family history of AD are generally considered to be at heightened risk of developing the disease themselves, many people with a family history never develop the disease, and many without a family history of the disease do get it. In most cases, it is still impossible to predict a specific person's risk of the disorder based on family history alone. Some families with CJD, GSS, or fatal familial insomnia have mutations in the prion protein gene, although these disorders can also occur in people without the gene mutation. Individuals with these mutations are at significantly higher risk of developing these forms of dementia. Abnormal genes are also clearly implicated as risk factors in Huntington's disease, FTDP-17, and several other kinds of dementia. These dementias are described in the section "What are the different kinds of dementia?"
Smoking and alcohol use. Several recent studies have found that smoking significantly increases the risk of mental decline and dementia. People who smoke have a higher risk of atherosclerosis and other types of vascular disease, which may be the underlying causes for the increased dementia risk. Studies also have found that drinking large amounts of alcohol appears to increase the risk of dementia. However, other studies have suggested that people who drink moderately have a lower risk of dementia than either those who drink heavily or those who completely abstain from drinking.
Atherosclerosis. Atherosclerosis is the buildup of plaque - deposits of fatty substances, cholesterol, and other matter - in the inner lining of an artery. Atherosclerosis is a significant risk factor for vascular dementia, because it interferes with the delivery of blood to the brain and can lead to stroke. Studies have also found a possible link between atherosclerosis and AD.
Cholesterol.High levels of low-density lipoprotein (LDL), the so-called bad form of cholesterol, appear to significantly increase a person's risk of developing vascular dementia. Some research has also linked high cholesterol to an increased risk of AD.
Plasma homocysteine.Research has shown that a higher-than-average blood level of homocysteine - a type of amino acid - is a strong risk factor for the development of AD and vascular dementia.
Diabetes. Diabetes is a risk factor for both AD and vascular dementia. It is also a known risk factor for atherosclerosis and stroke, both of which contribute to vascular dementia.
Mild cognitive impairment. While not all people with mild cognitive impairment develop dementia, people with this condition do have a significantly increased risk of dementia compared to the rest of the population. One study found that approximately 40 percent of people over age 65 who were diagnosed with mild cognitive impairment developed dementia within 3 years.
Down syndrome. Studies have found that most people with Down syndrome develop characteristic AD plaques and neurofibrillary tangles by the time they reach middle age. Many, but not all, of these individuals also develop symptoms of dementia.
How Is Dementia Diagnosed?
Doctors employ a number of strategies to diagnose dementia. It is important that they rule out any treatable conditions, such as depression, normal pressure hydrocephalus, or vitamin B12 deficiency, which can cause similar symptoms.
Early, accurate diagnosis of dementia is important for patients and their families because it allows early treatment of symptoms. For people with AD or other progressive dementias, early diagnosis may allow them to plan for the future while they can still help to make decisions. These people also may benefit from drug treatment.
The "gold standard" for diagnosing dementia, autopsy, does not help the patient or caregivers. Therefore, doctors have devised a number of techniques to help identify dementia with reasonable accuracy while the patient is still alive.
Doctors often begin their examination of a patient suspected of having dementia by asking questions about the patient's history. For example, they may ask how and when symptoms developed and about the patient's overall medical condition. They also may try to evaluate the patient's emotional state, although patients with dementia often may be unaware of or in denial about how their disease is affecting them. Family members also may deny the existence of the disease because they do not want to accept the diagnosis and because, at least in the beginning, AD and other forms of dementia can resemble normal aging. Therefore additional steps are necessary to confirm or rule out a diagnosis of dementia.
A physical examination can help rule out treatable causes of dementia and identify signs of stroke or other disorders that can contribute to dementia. It can also identify signs of other illnesses, such as heart disease or kidney failure, that can overlap with dementia. If a patient is taking medications that may be causing or contributing to his or her symptoms, the doctor may suggest stopping or replacing some medications to see if the symptoms go away.
Doctors will perform a neurological examination, looking at balance, sensory function, reflexes, and other functions, to identify signs of conditions - for example movement disorders or stroke - that may affect the patient's diagnosis or are treatable with drugs.
Cognitive and neuropsychological tests
Doctors use tests that measure memory, language skills, math skills, and other abilities related to mental functioning to help them diagnose a patient's condition accurately. For example, people with AD often show changes in so-called executive functions (such as problem-solving), memory, and the ability to perform once-automatic tasks.
Doctors often use a test called the Mini-Mental State Examination (MMSE) to assess cognitive skills in people with suspected dementia. This test examines orientation, memory, and attention, as well as the ability to name objects, follow verbal and written commands, write a sentence spontaneously, and copy a complex shape. Doctors also use a variety of other tests and rating scales to identify specific types of cognitive problems and abilities.
Doctors may use brain scans to identify strokes, tumors, or other problems that can cause dementia. Also, cortical atrophy -degeneration of the brain's cortex (outer layer) - is common in many forms of dementia and may be visible on a brain scan. The brain's cortex normally appears very wrinkled, with ridges of tissue (called gyri) separated by "valleys" called sulci. In individuals with cortical atrophy, the progressive loss of neurons causes the ridges to become thinner and the sulci to grow wider. As brain cells die, the ventricles (or fluid-filled cavities in the middle of the brain) expand to fill the available space, becoming much larger than normal. Brain scans also can identify changes in the brain's structure and function that suggest AD.
The most common types of brain scans are computed tomographic (CT) scans and magnetic resonance imaging (MRI). Doctors frequently request a CT scan of the brain when they are examining a patient with suspected dementia. These scans, which use X-rays to detect brain structures, can show evidence of brain atrophy, strokes and transient ischemic attacks (TIAs), changes to the blood vessels, and other problems such as hydrocephalus and subdural hematomas. MRI scans use magnetic fields and focused radio waves to detect hydrogen atoms in tissues within the body. They can detect the same problems as CT scans but they are better for identifying certain conditions, such as brain atrophy and damage from small TIAs.
Doctors also may use electroencephalograms (EEGs) in people with suspected dementia. In an EEG, electrodes are placed on the scalp over several parts of the brain in order to detect and record patterns of electrical activity and check for abnormalities. This electrical activity can indicate cognitive dysfunction in part or all of the brain. Many patients with moderately severe to severe AD have abnormal EEGs. An EEG may also be used to detect seizures, which occur in about 10 percent of AD patients as well as in many other disorders. EEGs also can help diagnose CJD.
Several other types of brain scans allow researchers to watch the brain as it functions. These scans, called functional brain imaging, are not often used as diagnostic tools, but they are important in research and they may ultimately help identify people with dementia earlier than is currently possible. Functional brain scans include functional MRI (fMRI), single photon-emission computed tomography (SPECT), positron emission tomography (PET), and magnetoencephalography (MEG). fMRI uses radio waves and a strong magnetic field to measure the metabolic changes that take place in active parts of the brain. SPECT shows the distribution of blood in the brain, which generally increases with brain activity. PET scans can detect changes in glucose metabolism, oxygen metabolism, and blood flow, all of which can reveal abnormalities of brain function. MEG shows the electromagnetic fields produced by the brain's neuronal activity.
Doctors may use a variety of laboratory tests to help diagnose dementia and/or rule out other conditions, such as kidney failure, that can contribute to symptoms. A partial list of these tests includes a complete blood count, blood glucose test, urinalysis, drug and alcohol tests (toxicology screen), cerebrospinal fluid analysis (to rule out specific infections that can affect the brain), and analysis of thyroid and thyroid-stimulating hormone levels. A doctor will order only the tests that he or she feels are necessary and/or likely to improve the accuracy of a diagnosis.
A psychiatric evaluation may be obtained to determine if depression or another psychiatric disorder may be causing or contributing to a person's symptoms.
Testing people before symptoms begin to determine if they will develop dementia is not possible in most cases. However, in disorders such as Huntington's where a known gene defect is clearly linked to the risk of the disease, a genetic test can help identify people who are likely to develop the disease. Since this type of genetic information can be devastating, people should carefully consider whether they want to undergo such testing.
Researchers are examining whether a series of simple cognitive tests, such as matching words with pictures, can predict who will develop dementia. One study suggested that a combination of a verbal learning test and an odor-identification test can help identify AD before symptoms become obvious. Other studies are looking at whether memory tests and brain scans can be useful indicators of future dementia.
Is There Any Treatment for Dementia?
While treatments to reverse or halt disease progression are not available for most of the dementias, patients can benefit to some extent from treatment with available medications and other measures, such as cognitive training.
Drugs to specifically treat AD and some other progressive dementias are now available and are prescribed for many patients. Although these drugs do not halt the disease or reverse existing brain damage, they can improve symptoms and slow the progression of the disease. This may improve the patient's quality of life, ease the burden on caregivers, and/or delay admission to a nursing home. Many researchers are also examining whether these drugs may be useful for treating other types of dementia.
Many people with dementia, particularly those in the early stages, may benefit from practicing tasks designed to improve performance in specific aspects of cognitive functioning. For example, people can sometimes be taught to use memory aids, such as mnemonics, computerized recall devices, or note taking.
Behavior modification - rewarding appropriate or positive behavior and ignoring inappropriate behavior - also may help control unacceptable or dangerous behaviors.
Most of the drugs currently approved by the U. S. Food and Drug Administration (FDA) for AD fall into a category called cholinesterase inhibitors. These drugs slow the breakdown of the neurotransmitter acetylcholine, which is reduced in the brains of people with AD. Acetylcholine is important for the formation of memories and it is used in the hippocampus and the cerebral cortex, two brain regions that are affected by AD. There are currently four cholinesterase inhibitors approved for use in the United States: tacrine (Cognex), donepezil (Aricept), rivastigmine (Exelon), and galantamine (Reminyl). These drugs temporarily improve or stabilize memory and thinking skills in some individuals. Many studies have shown that cholinesterase inhibitors help to slow the decline in mental functions associated with AD, and that they can help reduce behavioral problems and improve the ability to perform everyday tasks. However, none of these drugs can stop or reverse the course of AD.
A fifth drug, memantine (Namenda), is also approved for use in the United States. Unlike other drugs for AD, which affect acetylcholine levels, memantine works by regulating the activity of a neurotransmitter called glutamate that plays a role in learning and memory. Glutamate activity is often disrupted in AD. Because this drug works differently from cholinesterase inhibitors, combining memantine with other AD drugs may be more effective than any single therapy. One controlled clinical trial found that patients receiving donepezil plus memantine had better cognition and other functions than patients receiving donepezil alone.
Doctors may also prescribe other drugs, such as anticonvulsants, sedatives, and antidepressants, to treat seizures, depression, agitation, sleep disorders, and other specific problems that can be associated with dementia. In 2005, research showed that use of "atypical" antipsychotic drugs such as olanzapine and risperdone to treat behavioral problems in elderly people with dementia was associated with an elevated risk of death in these patients. Most of the deaths were caused by heart problems or infections. The FDA has issued a public health advisory to alert patients and their caregivers to this safety issue.
There is no standard drug treatment for vascular dementia, although some of the symptoms, such as depression, can be treated. Most other treatments aim to reduce the risk factors for further brain damage. However, some studies have found that cholinesterase inhibitors, such as galantamine and other AD drugs, can improve cognitive function and behavioral symptoms in patients with early vascular dementia.
The progression of vascular dementia can often be slowed significantly or halted if the underlying vascular risk factors for the disease are treated. To prevent strokes and TIAs, doctors may prescribe medicines to control high blood pressure, high cholesterol, heart disease, and diabetes. Doctors also sometimes prescribe aspirin, warfarin, or other drugs to prevent clots from forming in small blood vessels. When patients have blockages in blood vessels, doctors may recommend surgical procedures, such as carotid endarterectomy, stenting, or angioplasty, to restore the normal blood supply. Medications to relieve restlessness or depression or to help patients sleep better may also be prescribed.
Some studies have suggested that cholinesterase inhibitors, such as donepezil (Aricept), can reduce behavioral symptoms in some patients with Parkinson's dementia.
At present, no medications are approved specifically to treat or prevent FTD and most other types of progressive dementia. However, sedatives, antidepressants, and other medications may be useful in treating specific symptoms and behavioral problems associated with these diseases.
Scientists continue to search for specific treatments to help people with Lewy body dementia. Current treatment is symptomatic, often involving the use of medication to control the parkinsonian and psychiatric symptoms. Although antiparkinsonian medication may help reduce tremor and loss of muscle movement, it may worsen symptoms such as hallucinations and delusions. Also, drugs prescribed for psychiatric symptoms may make the movement problems worse. Several studies have suggested that cholinesterase inhibitors may be able to improve cognitive function and behavioral symptoms in patients with Lewy body disease.
There is no known treatment that can cure or control CJD. Current treatment is aimed at alleviating symptoms and making the patient as comfortable as possible. Opiate drugs can help relieve pain, and the drugs clonazepam and sodium valproate may help relieve myoclonus. During later stages of the disease, treatment focuses on supportive care, such as administering intravenous fluids and changing the person's position frequently to prevent bedsores.
Can Dementia be Prevented?
Research has revealed a number of factors that may be able to prevent or delay the onset of dementia in some people. For example, studies have shown that people who maintain tight control over their glucose levels tend to score better on tests of cognitive function than those with poorly controlled diabetes. Several studies also have suggested that people who engage in intellectually stimulating activities, such as social interactions, chess, crossword puzzles, and playing a musical instrument, significantly lower their risk of developing AD and other forms of dementia. Scientists believe mental activities may stimulate the brain in a way that increases the person's "cognitive reserve" - the ability to cope with or compensate for the pathologic changes associated with dementia.
Researchers are studying other steps people can take that may help prevent AD in some cases. So far, none of these factors has been definitively proven to make a difference in the risk of developing the disease. Moreover, most of the studies addressed only AD, and the results may or may not apply to other forms of dementia. Nevertheless, scientists are encouraged by the results of these early studies and many believe it will eventually become possible to prevent some forms of dementia. Possible preventive actions include:
- Lowering homocysteine. In one study, elevated blood levels of the amino acid homocysteine were associated with a 2.9 times greater risk of AD and a 4.9 times greater risk of vascular dementia. A preliminary study has shown that high doses of three B vitamins that help lower homocysteine levels - folic acid, B12, and B6 - appear to slow the progression of AD. Researchers are conducting a multi-center clinical trial to test this effect in a larger group of patients.
- Lowering cholesterol levels. Research has suggested that people with high cholesterol levels have an increased risk of developing AD. Cholesterol is involved in formation of amyloid plaques in the brain. Mutations in a gene called CYP46 and the apoE E4 gene variant, both of which have been linked to an increased risk of AD, are also involved in cholesterol metabolism. Several studies have also found that the use of drugs called statins, which lower cholesterol levels, is associated with a lower likelihood of cognitive impairment.
- Lowering blood pressure.Several studies have shown that antihypertensive medicine reduces the odds of cognitive impairment in elderly people with high blood pressure. One large European study found a 55 percent lower risk of dementia in people over 60 who received drug treatment for hypertension. These people had a reduced risk of both AD and vascular dementia.
- Exercise. Regular exercise stimulates production of chemicals called growth factors that help neurons survive and adapt to new situations. These gains may help to delay the onset of dementia symptoms. Exercise also may reduce the risk of brain damage from atherosclerosis.
- Education. Researchers have found evidence that formal education may help protect people against the effects of Alzheimer's disease. In one study, researchers found that people with more years of formal education had relatively less mental decline than people with less schooling, regardless of the number of amyloid plaques and neurofibrillary tangles each person had in his or her brain. The researchers think education may cause the brain to develop robust nerve cell networks that can help compensate for the cell damage caused by Alzheimer's disease.
- Controlling inflammation. Many studies have suggested that inflammation may contribute to AD. Moreover, autopsies of people who died with AD have shown widespread inflammation in the brain that appeared to be caused by the accumulation of beta amyloid. Another study found that men with high levels of C-reactive protein, a general marker of inflammation, had a significantly increased risk of AD and other kinds of dementia.
- Nonsteroidal anti-inflammatory drugs (NSAIDs). Research indicates that long-term use of NSAIDs - ibuprofen, naproxen, and similar drugs - may prevent or delay the onset of AD. Researchers are not sure how these drugs may protect against the disease, but some or all of the effect may be due to reduced inflammation. A 2003 study showed that these drugs also bind to amyloid plaques and may help to dissolve them and prevent formation of new plaques.
The risk of vascular dementia is strongly correlated with risk factors for stroke, including high blood pressure, diabetes, elevated cholesterol levels, and smoking. This type of dementia may be prevented in many cases by changing lifestyle factors, such as excessive weight and high blood pressure, which are associated with an increased risk of cerebrovascular disease. One European study found that treating isolated systolic hypertension (high blood pressure in which only the systolic or top number is high) in people age 60 and older reduced the risk of dementia by 50 percent. These studies strongly suggest that effective use of current treatments can prevent many future cases of vascular dementia.
A study published in 2005 found that people with mild cognitive impairment who took 10 mg/day of the drug donepezil had a significantly reduced risk of developing AD during the first two years of treatment, compared to people who received vitamin E or a placebo. By the end of the third year, however, the rate of AD was just as high in the people treated with donepezil as it was in the other two groups.
What Kind of Care Does a Person with Dementia Need?
People with moderate and advanced dementia typically need round-the-clock care and supervision to prevent them from harming themselves or others. They also may need assistance with daily activities such as eating, bathing, and dressing. Meeting these needs takes patience, understanding, and careful thought by the person's caregivers.
A typical home environment can present many dangers and obstacles to a person with dementia, but simple changes can overcome many of these problems. For example, sharp knives, dangerous chemicals, tools, and other hazards should be removed or locked away. Other safety measures include installing bed and bathroom safety rails, removing locks from bedroom and bathroom doors, and lowering the hot water temperature to 120°F (48. 9°C) or less to reduce the risk of accidental scalding. People with dementia also should wear some form of identification at all times in case they wander away or become lost. Caregivers can help prevent unsupervised wandering by adding locks or alarms to outside doors.
People with dementia often develop behavior problems because of frustration with specific situations. Understanding and modifying or preventing the situations that trigger these behaviors may help to make life more pleasant for the person with dementia as well as his or her caregivers. For instance, the person may be confused or frustrated by the level of activity or noise in the surrounding environment. Reducing unnecessary activity and noise (such as limiting the number of visitors and turning off the television when it's not in use) may make it easier for the person to understand requests and perform simple tasks. Confusion also may be reduced by simplifying home decorations, removing clutter, keeping familiar objects nearby, and following a predictable routine throughout the day. Calendars and clocks also may help patients orient themselves.
People with dementia should be encouraged to continue their normal leisure activities as long as they are safe and do not cause frustration. Activities such as crafts, games, and music can provide important mental stimulation and improve mood. Some studies have suggested that participating in exercise and intellectually stimulating activities may slow the decline of cognitive function in some people.
Many studies have found that driving is unsafe for people with dementia. They often get lost and they may have problems remembering or following rules of the road. They also may have difficulty processing information quickly and dealing with unexpected circumstances. Even a second of confusion while driving can lead to an accident. Driving with impaired cognitive functions can also endanger others. Some experts have suggested that regular screening for changes in cognition might help to reduce the number of driving accidents among elderly people, and some states now require that doctors report people with AD to their state motor vehicle department. However, in many cases, it is up to the person's family and friends to ensure that the person does not drive.
The emotional and physical burden of caring for someone with dementia can be overwhelming. Support groups can often help caregivers deal with these demands and they can also offer helpful information about the disease and its treatment. It is important that caregivers occasionally have time off from round-the-clock nursing demands. Some communities provide respite facilities or adult day care centers that will care for dementia patients for a period of time, giving the primary caregivers a break. Eventually, many patients with dementia require the services of a full-time nursing home.
A list of caregiver organizations and support groups is included at the end of this booklet.
What Research Is Being Done?
Current research focuses on many different aspects of dementia. This research promises to improve the lives of people affected by the dementias and may eventually lead to ways of preventing or curing these disorders.
Causes and prevention
Research on the causes of AD and other dementias includes studies of genetic factors, neurotransmitters, inflammation, factors that influence programmed cell death in the brain, and the roles of tau, beta amyloid, and the associated neurofibrillary tangles and plaques in AD. Some other researchers are trying to determine the possible roles of cholesterol metabolism, oxidative stress (chemical reactions that can damage proteins, DNA, and lipids inside cells), and microglia in the development of AD. Scientists also are investigating the role of aging-related proteins such as the enzyme telomerase.
Since many dementias and other neurodegenerative diseases have been linked to abnormal clumps of proteins in cells, researchers are trying to learn how these clumps develop, how they affect cells, and how the clumping can be prevented.
Some studies are examining whether changes in white matter - nerve fibers lined with myelin - may play a role in the onset of AD. Myelin may erode in AD patients before other changes occur. This may be due to a problem with oligodendrocytes, the cells that produce myelin.
Researchers are searching for additional genes that may contribute to AD, and they have identified a number of gene regions that may be involved. Some researchers suggest that people will eventually be screened for a number of genes that contribute to AD and that they will be able to receive treatments that specifically address their individual genetic risks. However, such individualized screening and treatment is still years away.
Insulin resistance is common in people with AD, but it is not clear whether the insulin resistance contributes to the development of the disease or if it is merely a side effect.
Several studies have found a reduced risk of dementia in people who take cholesterol-lowering drugs called statins. However, it is not yet clear if the apparent effect is due to the drugs or to other factors.
Early studies of estrogen suggested that it might help prevent AD in older women. However, a clinical study of several thousand postmenopausal women aged 65 or older found that combination therapy with estrogen and progestin substantially increased the risk of AD. Estrogen alone also appeared to slightly increase the risk of dementia in this study.
A 2003 study found that people with HIV-associated dementia have different levels of activity for more than 30 different proteins, compared to people who have HIV but no signs of dementia. The study suggests a possible way to screen HIV patients for the first signs of cognitive impairment, and it may lead to ways of intervening to prevent this form of dementia.
Improving early diagnosis of AD and other types of dementia is important not only for patients and families, but also for researchers who seek to better understand the causes of dementing diseases and find ways to reverse or halt them at early stages. Improved diagnosis can also reduce the risk that people will receive inappropriate treatments.
Some researchers are investigating whether three-dimensional computer models of PET and MRI images can identify brain changes typical of early AD, before any symptoms appear. This research may lead to ways of preventing the symptoms of the disease.
One study found that levels of beta amyloid and tau in spinal fluid can be used to diagnose AD with a sensitivity of 92 percent. If other studies confirm the validity of this test, it may allow doctors to identify people who are beginning to develop the disorder before they start to show symptoms. This would allow treatment at very early stages of the disorder, and may help in testing new treatments to prevent or delay symptoms of the disease. Other researchers have identified factors in the skin and blood of AD patients that are different from those in healthy people. They are trying to determine if these factors can be used to diagnose the disease.
Researchers are continually working to develop new drugs for AD and other types of dementia. Many researchers believe a vaccine that reduces the number of amyloid plaques in the brain might ultimately prove to be the most effective treatment for AD. In 2001, researchers began one clinical trial of a vaccine called AN-1792. The study was halted after a number of people developed inflammation of the brain and spinal cord. Despite these problems, one patient appeared to have reduced numbers of amyloid plaques in the brain. Other patients showed little or no cognitive decline during the course of the study, suggesting that the vaccine may slow or halt the disease. Researchers are now trying to find safer and more effective vaccines for AD.
Researchers are also investigating possible methods of gene therapy for AD. In one case, researchers used cells genetically engineered to produce nerve growth factor and transplanted them into monkeys' forebrains. The transplanted cells boosted the amount of nerve growth factors in the brain and seemed to prevent degeneration of acetylcholine-producing neurons in the animals. This suggests that gene therapy might help to reduce or delay symptoms of the disease. Researchers are now testing a similar therapy in a small number of patients. Other researchers have experimented with gene therapy that adds a gene called neprilysin in a mouse model that produces human beta amyloid. They found that increasing the level of neprilysin greatly reduced the amount of beta amyloid in the mice and halted the amyloid-related brain degeneration. They are now trying to determine whether neprilysin gene therapy can improve cognition in mice.
A clinical trial called the Vitamins to Slow Alzheimer's Disease (VITAL) study is testing whether high doses of three common B vitamins - folic acid, B12, and B6 - can reduce homocysteine levels and slow the rate of cognitive decline in AD.
Since many studies have found evidence of brain inflammation in AD, some researchers have proposed that drugs that control inflammation, such as NSAIDs, might prevent the disease or slow its progression. Studies in mice have suggested that these drugs can limit production of amyloid plaques in the brain. Early studies of these drugs in humans have shown promising results. However, a large NIH-funded clinical trial of two NSAIDS (naproxen and celecoxib) to prevent AD was stopped in late 2004 because of an increase in stroke and heart attack in people taking naproxen, and an unrelated study that linked celecoxib to an increased risk of heart attack.
Some studies have suggested that two drugs, pentoxifylline and propentofylline, may be useful in treating vascular dementia. Pentoxifylline improves blood flow, while propentofylline appears to interfere with some of the processes that cause cell death in the brain.
One study is testing the safety and effectiveness of donepezil (Aricept) for treating mild dementia in patients with Parkinson's dementia, while another is investigating whether skin patches with the drug selegiline can improve mental function in patients with cognitive problems related to HIV.
How Can I Help Research?
People with dementia and others who wish to help research on dementing disorders may be able to do so by participating in clinical studies designed to learn more about the disorders or to test potential new therapies. Information about many such studies is available free of charge from the Federal government's database of clinical trials, clinicaltrials.gov (http://clinicaltrials.gov).
Information about clinical trials specific to Alzheimer's disease is available from the Alzheimer's Disease Clinical Trials Database (www.alzheimers.org/trials), a joint project of the U. S. Food and Drug Administration and the National Institute on Aging (NIA) that is maintained by the NIA's Alzheimer's Disease Education and Referral Center.
For clinical trials taking place at the National Institutes of Health, additional information is available from the following office:
Patient Recruitment and Public Liaison Office
National Institutes of Health
Building 61, 10 Cloister Court
Bethesda, Maryland 20892-4754
TTY: 301-594-9774 (local), 866-411-1010 (toll free)
Another important way that people can help dementia research is by arranging to donate their brains to brain and tissue banks after they die. Tissue from these banks is made available to qualified researchers so that they can continue their studies of how these diseases develop and how they affect the brain. Brain banks accepting donations include the following:
UM/NPF Brain Endowment Bank
University of Miami Dept. of Neurology
1501 N.W. 9th Ave., Rm. 4013 (D 4-5)
Miami, FL 33136
Tel: 305-243-6219 800-UM-BRAIN (862-7246)
People who have more than one family member affected by AD also may be able to help research by contributing blood samples to a gene bank. A large initiative to collect such samples was announced in 2003. This large gene bank should accelerate research efforts to identify genes that play a role in AD. People interested in participating in this gene bank can learn more about it at the address and telephone numbers below:
Where can I get more information?
For more information on neurological disorders or research programs funded by the National Institute of Neurological Disorders and Stroke, contact the Institute's Brain Resources and Information Network (BRAIN) at:
Information also is available from the following organizations:
National voluntary health organization committed to finding a cure for Alzheimer's and helping those affected by the disease.
Works to provide optimal care and services to individuals confronting dementia and to their caregivers and families thruogh member organizations dedicated to improving quality of life.
Generates funds for Alzheimer's research targeted at areas of research typically not supported by Federal agencies.
Non-profit organization that promotes and funds research into finding the cause and cure for frontotemporal dementias (FTD); provides information, education, and support to those affected by FTD and their caregivers; and sponsors professional health education programs related to FTD.
Federation of voluntary health organizations dedicated to helping people with rare "orphan" diseases and assisting the organizations that serve them. Committed to the identification, treatment, and cure of rare disorders through programs of education, advocacy, research, and service.
Supports and assists families and caregivers of adults with debilitating health conditions. Offers programs and consultation on caregiving issues at local, state, and national levels. Offers free publications and support online, including a national directory of publicly funded caregiver support programs.
Nonprofit, tax-exempt, charitable organization that offers information about care for patients with Alzheimer's-type dementia. Publishes and distributes a newsletter, cookbook, and the Caregiver's Information Pack.
Grassroots organization dedicated to supporting and improving the lives of America's family caregivers. Created to educate, support, empower, and advocate for the millions of Americans who care for their ill, aged, or disabled loved ones.
Supports those affected by Lewy body dementias and promotes research for a cure. Sponsors education and outreach programs.
Public charity whose mission is to accelerate the discovery and development of drugs to prevent, treat, and cure Alzheimer's disease, related dementias, and cognitive aging.
Non-profit, volunteer foundation that promotes research, education, and awareness of CJD and reaches out to people affected by CJD.
Non-profit organization established for support, information sharing, and advocacy.
International non-profit organization whose mission is to provide emotional support to, raise consciousness about, and advocate for the spouses/partners and children of the chronically ill and/or disabled.
Information and referral service that assists and promotes the development of quality respite and crisis care programs; helps families locate respite and crisis care services in their communities; and sponsors advocacy and awareness efforts concerning respite care.
Non-profit charitable organization dedicated to funding research and educating the public on Alzheimer's disease, glaucoma, macular degeneration, heart disease, and stroke. Provides emergency financial assistance to Alzheimer's disease patients and their caregivers.
Non-profit membership organization representing hospice and palliative care programs and professionals. Provides free referrals to the public for hospice listings across the United States and internationally. Distributes free packets of general information describing hospice services and the Medicare Hospice Benefit.
Cortisone Injection (Corticosteroid Injection)
of Soft Tissues & Joints
- What are corticosteroids?
- Is a cortisone injection merely a pain reliever or temporary remedy?
- For what conditions are cortisone injections used?
- What are the advantages of cortisone injections?
- What are the disadvantages and side effects of cortisone injections?
- Are there special advantages in using cortisone injections for joint inflammation (arthritis)?
- Are there special side effects that can occur with cortisone joint injections?
- How are cortisone injections of soft tissues given?
- How are cortisone injections of a joint given?
- "I've always heard that cortisone injections are painful? Are they?"
- Corticosteroid (Cortisone) Injection of Joints & Soft Tissue At A Glance
- Patient Discussions: Cortisone Injection - Knee And Hip
- Patient Discussions: Cortisone Injection - Describe Your Experience
- Patient Discussions: Cortisone Injection - Side effects
What are corticosteroids?
Corticosteroids are a class of medications that are related to cortisone. Medications of this class reduce inflammation powerfully. They are used to reduce inflammation caused by a variety of diseases. Cortisone is one type of corticosteroid. For the purpose of this review, "cortisone" is used interchangeably with "corticosteroid."
Corticosteroids can be taken by mouth, inhaled, applied to the skin, given intravenously (into a vein), or injected into the tissues of the body. Examples of corticosteroids include prednisone and prednisolone (given by mouth), Solu-Medrol (given intravenously), as well as triamcinolone, Kenalog, Celestone, Depo-Medrol, and others (given by injection into body tissues). This article describes the role of cortisone injections into the soft tissues and joints.
Learn more about: Celestone
Is a cortisone injection merely a pain reliever or temporary remedy?
Corticosteroids are not pain relievers. They reduce inflammation. When corticosteroids relieve pain, it is because they have reduced inflammation.
While the inflammation for which corticosteroids are given can recur, corticosteroid injections can provide months to years of relief when used properly. These injections also can cure diseases (permanently resolve them) when the problem is tissue inflammation localized to a small area, such as bursitis and tendonitis.
For what conditions are cortisone injections used?
Cortisone injections can be used to treat the inflammation of small areas of the body (local injections), or they can be used to treat inflammation that is widespread throughout the body (systemic injections). Examples of conditions for which local cortisone injections are used include inflammation of a bursa (bursitis), a tendon (tendonitis), and a joint (arthritis). Knee arthritis, hip bursitis, painful foot conditions such as plantar fasciitis, rotator cuff tendinitis and many other conditions may be treated with cortisone injections. Epidural injections in the lumbar spine are cortisone injections inserted into a specific location in the spinal canal by a specialist under X-ray guidance (fluoroscopy). Systemic corticosteroid injections are used for conditions affecting many joints, such as allergic reactions, asthma, and rheumatoid arthritis.
What are the advantages of cortisone injections?
When a joint is swollen, sometimes joint fluid is removed before cortisone is injected. If fluid is removed, it can be analyzed to determine what caused the joint to swell. This is a big advantage as it is a powerful and accurate diagnostic test.
A distinct benefit of a corticosteroid injection is that the relief of localized inflammation in a particular body area is more rapid and powerful than with traditional anti-inflammatory medications given by mouth such as aspirin. A single injection also can avoid certain side effects, notably irritation of the stomach, that can accompany many oral anti-inflammatory medications. Cortisone injections can be administered easily in the doctor's office. Other advantages include the rapid onset of the medication's action, dependability, and minimal side effects.
Learn more about: aspirin
What are the disadvantages and side effects of cortisone injections?
Disadvantages of cortisone injections are the necessity of piercing the skin with a needle as well as potential short- and long-term side effects. It should be emphasized that though each of these side effects is possible, they usually do not occur.
Short-term complications are uncommon but include shrinkage (atrophy) and lightening of the color (depigmentation) of the skin at the injection site, introduction of bacterial infection into the body, local bleeding from broken blood vessels in the skin or muscle, soreness at the injection site, and aggravation of inflammation in the area injected because of reactions to the corticosteroid medication (postinjection flare). Increased pain after the injection is typically due to a postinjection flare as a true allergic reaction to cortisone is very rare. Tendons can be weakened by corticosteroid injections in or near tendons. Tendon ruptures as a result have been reported. Facial flushing may occur in up to 40% of cases but lasts only briefly. Sweating and insomnia are uncommon.
In people who have diabetes, cortisone injections can elevate the blood sugar. In patients with underlying infections, cortisone injections can suppress somewhat the body's ability to fight the infection and possibly worsen the infection or may mask the infection by suppressing the symptoms and signs of inflammation. Generally, cortisone injections are used with caution in people with diabetes and avoided in people with active infections. Cortisone injections are used cautiously in people with a bleeding disorder.
Long-term risks of corticosteroid injections depend on the dose and frequency of the injections. With higher doses and frequent administration, potential side effects include thinning of the skin, easy bruising, weight gain, puffiness of the face, elevation of blood pressure, cataract formation, thinning of the bones (osteoporosis), and a rare but serious damage to the bones of the large joints (avascular necrosis)
Are there special advantages in using cortisone injections for joint inflammation (arthritis)?
Cortisone injections into a joint can be beneficial in rapidly reducing joint pain while restoring function to a body part immobilized by inflammation, such as an arthritic knee or elbow. This might be particularly important in certain circumstances, such as the gainful employment of a family breadwinner or someone who lives alone. Despite potential and infrequently reported adverse reactions as described above, it is generally felt that low, intermittent doses of corticosteroids pose little risk of significant side effects.
Cortisone injections into a joint also can decrease the inflammation in diseased joints throughout the body when the corticosteroids are absorbed from the joint into the circulation.
Are there special side effects that can occur with cortisone joint injections?
Cortisone injections into a joint may have side effects in addition to those described above. Unique side effects of joint injections involve injury to the joint tissues, particularly with repeated injections. These injuries include thinning of the joint cartilage, weakening of the ligaments of the joint, increased inflammation in the joint (arthritis) due to a reaction to a corticosteroid that has crystallized, and introduction of infection into the joint.
How are cortisone injections of soft tissues given?
The medical professional administering the injection draws up the corticosteroid into a syringe. A local anesthetic (such as lidocaine) may simultaneously be drawn into the syringe. Next, the area to be injected is selected. Typically, the skin over the area to be injected is sterilized with a liquid solution, either alcohol or Betadine.
Sometimes, the area is topically anesthetized by rapid cooling using a spray such as ethyl chloride. The needle of the syringe then is inserted into the tissue to be injected and the solution is ejected from the syringe into the area of inflammation. The needle then is withdrawn, and a sterile bandage is applied to the injection site.
How are cortisone injections of a joint given?
The method of administering a cortisone injection to a joint is similar to that of soft-tissue injections. Betadine, however, is more commonly used for sterilization of the skin over the joint. Furthermore, if there is an excessive amount of fluid within the joint, it often is removed first with a separate syringe and needle prior to injection of the cortisone. Removal of this joint fluid allows the doctor to examine the fluid and submit a sample to the laboratory for diagnosis. Removal also rapidly relieves pain by reducing the pressure of the fluid within the joint. Finally, removal of fluid may allow the joint to heal more quickly.
"I've always heard that cortisone injections are painful? Are they?"
In an expert's hands, the opposite is more often the case. That is, minimal pain from the procedure is noted while relief from the pain of the inflammation occurs rapidly. Occasionally, cortisone injections of joints that have degenerated (become damaged) or that are particularly small (such as finger joints) can be associated with temporary, minor pain at the time of the injection. This is not generally expected. Less frequently, nerves can be irritated, either directly by the needle during the injection or by the corticosteroid medication. Again, this is not common or anticipated.
Corticosteroid (Cortisone) Injection of Joints & Soft Tissue At A Glance
- Corticosteroids are powerful anti-inflammatory medications.
- Cortisone injections can offer fast-acting relief of inflamed joints, tendons, and bursa.
- Complications are rare but may include infection and bleeding.
- When administered by an expert, cortisone injections offer significant pain relief with only minimal discomfort.
Ruddy, S., Harris, E.D., Sledge, C.B., Kelley, W.N., eds. Kelley's Textbook of Rheumatology. 7th ed. Philadelphia: WB Saunders, 2005.
Last Editorial Review: 7/15/2010
- What is diphtheria?
- What is the history of diphtheria?
- What causes diphtheria?
- How is diphtheria transmitted?
- What are the signs and symptoms of diphtheria?
- How is diphtheria diagnosed?
- What is the treatment for diphtheria?
- What are the complications of diphtheria?
- How is diphtheria prevented?
- Diphtheria At A Glance
What is diphtheria?
Diphtheria is an infectious disease caused by the bacterium Corynebacterium diphtheriae. This disease primarily affects the mucous membranes of the respiratory tract (respiratory diphtheria), although it may also affect the skin (cutaneous diphtheria) and lining tissues in the ear, eye, and the genital areas.
What is the history of diphtheria?
Throughout history, diphtheria was a leading cause of death among children, and it was once referred to as the "strangling angel of children." Through the ages, several epidemics struck Europe, and even the American colonies were affected by an outbreak in the 18th century. Most recently, in the 1990s, large outbreaks of diphtheria occurred in Russia and in the former independent states of the Soviet Union.
The diphtheria bacterium was first identified in the 1880s. In the 1890s, the antitoxin against diphtheria was developed, with the first vaccine being developed in the 1920s. With the development and administration of the diphtheria vaccine, the incidence of diphtheria has decreased significantly. Though it is still endemic in many parts of the world, respiratory diphtheria has now became a rare disease in the United States (with up to five cases per year). Furthermore, whereas diphtheria primarily affected younger children in the prevaccination era, an increasing proportion of cases today occur in unvaccinated or inadequately immunized adolescents and adults.
What causes diphtheria?
Diphtheria is caused by toxin-producing strains of the gram-positive bacillus Corynebacterium diphtheriae. There are four biotypes of the bacterium (gravis, mitis, intermedius, and belfanti), and each differs in the severity of disease it produces. Nontoxigenic strains are usually responsible for less severe cutaneous diphtheria.
The signs and symptoms of respiratory diphtheria are caused by the bacterium's ability to cause a localized inflammatory reaction of the cells lining the upper respiratory tract. In certain cases, the disease can become more severe and widespread, and it can involve other organs of the body as well.
How is diphtheria transmitted?
Diphtheria is transmitted to close contacts via airborne respiratory droplets or by direct contact with nasopharyngeal secretions or skin lesions. Rarely, it can be spread by objects contaminated by an infected person. Overcrowding and poor living conditions can further contribute to the spread of diphtheria.
Humans are the only known reservoir of Corynebacterium diphtheriae. Infected individuals may develop symptoms of diphtheria, or they may become carriers of the bacteria with no symptoms (asymptomatic carriers). These asymptomatic carriers can serve as reservoirs for active infection and may transmit the disease to other individuals.
What are the signs and symptoms of diphtheria?
The symptoms of respiratory diphtheria usually begin after a two- to five-day incubation period. Symptoms of respiratory diphtheria may include the following:
- sore throat,
- difficulty swallowing, or
- difficulty breathing.
With the progression of respiratory diphtheria, the infected individual may also develop an adherent gray membrane (pseudomembrane) forming over the lining tissues of the tonsils and/or nasopharynx. Individuals with severe disease may also develop neck swelling and enlarged neck lymph nodes, leading to a "bull-neck" appearance. Extension of the pseudomembrane into the larynx and trachea can lead to obstruction of the airway with subsequent suffocation and death.
The dissemination of diphtheria toxin can also lead to systemic disease, causing complications such as inflammation of the heart (myocarditis) and neurologic problems such as paralysis of the soft palate, vision problems, and muscle weakness.
Cutaneous diphtheria is characterized by a non-healing skin ulcer covered by a gray-brown membrane. It is typically a localized infection that is rarely associated with systemic complications.
How is diphtheria diagnosed?
The diagnosis of diphtheria is confirmed by isolation of the bacterium Corynebacterium diphtheriae. Diagnostic tests to isolate the bacterium involve obtaining cultures from the nose and throat in any individual suspected of having diphtheria, as well as their close contacts.
It is also important to determine whether or not the isolate is capable of producing diphtheria toxin, and this can be accomplished by testing in specialized laboratories. Finally, determining the patient's antibody levels to diphtheria toxin can also be helpful for evaluating the probability of the diagnosis of diphtheria and the potential for severe illness.
Other tests, such as ECG, imaging studies, and blood work can also help assess the extent of involvement of the disease.
What is the treatment for diphtheria?
If diphtheria is suspected in a patient, prompt treatment should be undertaken even before confirmatory lab results are available.
Diphtheria antitoxin is the mainstay of therapy. It neutralizes circulating diphtheria toxin and reduces the progression of the disease. The effectiveness of diphtheria antitoxin is greatest if it is administered early in the course of the disease. The U.S. Centers for Disease Control and Prevention (CDC) can assist in obtaining the diphtheria antitoxin. Antitoxin is not recommended for asymptomatic carriers and it is usually of no value in localized cutaneous diphtheria.
Antibiotics should also be administered as soon as possible to patients with suspected diphtheria. Antibiotics help eradicate the bacteria, thereby stopping toxin production, and they also help to prevent transmission of diphtheria to close contacts. Penicillin and erythromycin are the recommended antibiotics. Asymptomatic carriers, as well as all close contacts potentially exposed to diphtheria, also require antibiotic treatment.
Supportive measures, such as inserting a breathing tube (intubation), may be necessary if the patient cannot breathe on their own or if there is the potential for airway obstruction. Potential cardiac and neurologic complications also need to be closely followed and addressed in consultation with the proper specialist.
What are the complications of diphtheria?
The potential complications of diphtheria may include the following:
- cardiac (inflammation of the heart, heart valve infection, heart rhythm disturbances, and congestive heart failure),
- neurologic (muscle paralysis, muscle weakness, and vision problems),
- infectious (lung infection, blood infection, and bone infection), and
For respiratory diphtheria, the fatality rate is 10%-15%, although it may be higher in patients less than 5 years of age and older than 40 years of age. Airway obstruction and cardiac complications are the most common causes of death.
How is diphtheria prevented?
The prevention of diphtheria is best achieved through universal immunization with diphtheria toxoid-containing vaccines. Immunization for infants and children consists of five DTaP vaccinations generally given at ages 2, 4, and 6 months, with the fourth dose being administered between 15-18 months, and the fifth dose at ages 4-6 years. At age 11-12 years, children should receive a single Tdap vaccination if they have completed the recommended childhood vaccination schedule. Because immunity wanes over time, subsequent booster immunization is required every 10 years thereafter to maintain protective antibody levels.
Travelers to areas where diphtheria is endemic should review and update their vaccinations as necessary.
Diphtheria At A Glance
- Diphtheria is an infectious disease caused by the bacterium Corynebacterium diphtheriae.
- Diphtheria is primarily transmitted via airborne respiratory droplets or by direct contact with secretions from infected people.
- The symptoms of diphtheria include sore throat, fever, malaise, difficulty swallowing, and difficulty breathing.
- Diphtheria is treated with both antitoxin and antibiotics.
- Diphtheria can lead to cardiac and neurologic complications, as well as death.
- Immunization is the best prevention against diphtheria.
Last Editorial Review: 6/27/2008
Allergies and Cosmetics
- Introduction to cosmetic allergies
- What are the symptoms of a cosmetic reaction?
- What causes cosmetic reactions?
- How common are reactions to cosmetics?
- What should I do if I have an allergic reaction?
- How are allergic reactions diagnosed?
- How are cosmetic reactions treated?
- What can I do to prevent cosmetic reactions?
- Making sense of product labels
- More safety tips
- Find a local Dermatologist in your town
Products such as moisturizers, shampoos, deodorants, make-up, colognes, and other cosmetics have become part of our daily grooming habits. The American Academy of Dermatology reports the average adult uses at least seven different cosmetic products each day. Although cosmetics can help us feel more beautiful, they can cause skin irritation or allergic reactions. Certain ingredients used in cosmetics, such as fragrances and preservatives, can act as antigens, substances that trigger an allergic reaction.
What are the symptoms of a cosmetic reaction?
There are two reactions that might occur following exposure to cosmetics: irritant contact dermatitis and allergic contact dermatitis. Contact dermatitis is a condition marked by areas of inflammation (redness, itching and swelling) that form after a substance comes into contact with your skin.
Irritant contact dermatitis: This is more common than allergic contact dermatitis and can occur in anyone. It develops when an irritating or harsh substance actually damages the skin. Irritant contact dermatitis usually begins as patches of itchy, scaly skin or a red rash, but can develop into blisters that ooze, especially if the skin is further irritated from scratching. It generally occurs at the site of contact with the irritating substance. Areas where the outermost layer of skin is thin, such as the eyelids, or where the skin is dry and cracked are more susceptible to irritant contact dermatitis.
Allergic contact dermatitis: This occurs in people who are allergic to a specific ingredient or ingredients in a product. Symptoms include redness, swelling, itching, and hive-like breakouts. In some cases, the skin becomes red and raw. The face, lips, eyes, ears, and neck are the most common sites for cosmetic allergies, although reactions may appear anywhere on the body.
The time it takes for symptoms of irritant contact dermatitis to appear varies. For stronger irritants, such as perfumes, a reaction may occur within minutes or hours of exposure. However, it may take days or weeks of continued exposure to a weaker irritant, such as soap, before symptoms appear. In some cases, a person can develop an allergic sensitivity to a product after years of use.
What causes cosmetic reactions?
With irritant contact dermatitis, the skin breaks down when it comes into contact with harsh substances, most often chemicals that directly injure the outer layer of the skin, resulting in symptoms.
Allergic contact dermatitis occurs because the body's immune system is reacting against a specific substance (the allergen) that it considers foreign and harmful.
How common are reactions to cosmetics?
Serious allergic reactions associated with cosmetics are rare. However, it is not uncommon for a person to have a mild reaction or irritation to an ingredient in a cosmetic product. Studies suggest that up to 10% of the population will have some type of reaction to a cosmetic over the course of a lifetime. Reactions to cosmetics occur more often in women, most likely because women tend to use more cosmetic products than do men.
What should I do if I have a reaction?
If you have a reaction, stop using all cosmetics. When your symptoms are gone, start using them again, one product at a time. This may help you determine which product or products are responsible for the reaction. If you cannot identify the source of the reaction or if your symptoms do not go away after you stop using the cosmetics, consult your healthcare provider.
How are allergic reactions diagnosed?
Reactions are diagnosed by the appearance of symptoms and your history of exposure to various cosmetic products. Because most adults use many cosmetic products, identifying the product responsible for the reaction may be difficult. If your doctor suspects allergic contact dermatitis, he or she may use a patch skin test to identify the substances to which you are allergic.
How are cosmetic reactions treated?
Treatment generally involves avoiding the products causing the symptoms. Over-the-counter creams and ointments that contain cortisone, such as hydrocortisone (Cortisone 10) and hydrocortisone acetate (Cort-aid), may be used to help control itching, swelling, and redness. In more severe cases, a prescription-strength medication may be needed to relieve symptoms. If blistered skin becomes infected, an antibiotic medication may also be needed.
What can I do to prevent cosmetic reactions?
There are several steps you can take to try and avoid cosmetic allergy reactions, including:
- Read the list of ingredients on all cosmetic products. If you find an ingredient that has caused a reaction in the past, don't use that product. Keep track of ingredients that have caused reactions, and look for products that do not contain those ingredients.
- When considering a new product, do a "mini-patch test" first to see if it causes a reaction. Put a sample of the product on your inner wrist or elbow and wait 24 hours to see if a reaction occurs.
- Keep it simple. Choose products with simple formulas. More ingredients mean more potential allergens. With fewer ingredients, it's also easier to pinpoint the source if you do have a reaction.
- Apply perfume to your clothes rather than your skin, and allow the perfume to dry before putting on the clothes.
- Be especially careful with makeup because it stays in contact with the skin for a long time. Look for products that are hypoallergenic, fragrance free, and non-comedogenic, although products with these labels may still cause reactions.
Making sense of product labels
To get the best benefit from cosmetics and skin care products, it's important to be aware of each product's ingredients and to look for and avoid ingredients that are known allergens for you. To make this easier, the FDA requires cosmetic manufacturers to list the ingredients on the product label. Ingredients are listed in descending order of amount. Keep in mind, however, that trade secrets (including certain fragrances) do not have to be specifically listed.
Also, keep in mind that products labeled "unscented" or "fragrance free" may still contain small amounts of fragrances needed to cover the odor of other chemical ingredients. "Natural" generally means that the product includes ingredients extracted from plants or animal products rather than ingredients produced chemically. Products labeled "non-comedogenic" do not contain ingredients that commonly clog pores, which can lead to acne.
Labeling of cosmetics can be helpful when looking for specific ingredients, but be wary of certain product claims. For example, many products use the term "hypoallergenic," although there are no regulations or standards for use of this term. "Hypoallergenic" suggests that a product is less likely than another, similar product to cause an allergic reaction, but manufacturers are not required to prove this claim. In addition, products labeled "organic" are not less likely to cause an allergic reaction. Just remember: There is no cosmetic product that can guarantee never to produce an allergic reaction.
More safety tips:
- Always use good personal hygiene. Be sure to clean your hands and face before applying make-up.
- Never share make-up.
- If you want to test a product in the store, ask for a new, unused applicator, and ask the salesperson to wipe the opening of the tester with alcohol.
- Keep cosmetic containers tightly closed, except when being used. Keep containers free of dust and dirt.
- Keep cosmetics away from heat and out of direct sunlight.
- Do not use eye make-up if you have an eye infection, such as conjunctivitis. Discard those products and use new ones when your infection is gone.
- Discard products if the color changes or they develop an odor. This may mean the preservatives in the products are no longer able to fight bacteria.
- If the consistency of a product changes, do not add water. Discard the product.
- Clean cosmetic brushes and applicators frequently.
Reviewed by the doctors at The Cleveland Clinic Department of Pulmonary, Allergy and Critical Care Medicine.
Edited by Michael W. Smith, MD, November 1, 2006.
Portions of this page © The Cleveland Clinic 2000-2004
Fighting the effects of aging-on the outside. Your guide to the risks of cosmetic surgical and non-surgical procedures
Trying to fight the effects of aging? Below is a basic guide to the risks involved in both surgical and non-surgical cosmetic procedures. For more information on each procedure, click on the highlighted links of the procedure.
Cosmetic Procedures: Surgical
Breast Augmentation - Breasts are enlarged by placing an implant behind each breast.
- implants can rupture, leak, and deflate
- hardening of scar tissue around implant, causing breast firmness, pain, distorted shape, or implant movement
- nipples may get more or less sensitive
- numbness near incision blood collection around implant/incision
- calcium deposits around implant
- harder to find breast lumps
- Find a local Plastic Surgeon in your town
Breast Lift - Extra skin is removed from the breast to raise and reshape breast.
- skin loss
- infection loss of feeling in nipples or breast
- nipples put in the wrong place
- breasts not symmetrical
Breast Reduction - Fat, tissue, and skin is removed from breast.
- if nipples and areola are detached, may lose sensation and decreased ability to breastfeed
- harder to find breast lumps
- poor shape, size, or position of nipples or breasts
Eyelid Surgery: Extra fat, skin, and muscle in the upper and/or lower eyelid is removed to correct "droopy" eyelids.
- blurred or double vision
- bleeding under the skin
- dry eyes
- can't close eye completely
- pulling of lower lids
Facelift - Extra fat is removed, muscles are tightened, and skin is rewrapped around the face and neck to improve sagging facial skin, jowls, and loose neck skin.
- bleeding under skin
- irregular earlobes
- nerve damage causing numbness or inability to move your face
- hair loss
- skin damage
Facial Implant - infection feeling of tightness or scarring around implant shifting of implant
- feeling of tightness or scarring around implant
- shifting of implant
Forehead Lift: Extra skin and muscles that cause wrinkles are removed, eyebrows are lifted, and forehead skin is tightened.
- bleeding under skin
- eye dryness or irritation
- impaired eyelid function
- loss of feeling in eyelid skin
- injury to facial nerve causing loss of motion or muscle weakness
Lip Augmentation: Material is injected or implanted into the lips to create fuller lips and reduce wrinkles around the mouth.
- lip asymmetry
Liposuction: Excess fat from a targeted area is removed with a vacuum to shape the body.
- baggy skin
- skin may change color and fall off
- fluid retention
- fat clots in the lungs
- damage to organs if punctured
- numbness at the surgery site
- heart problems
- kidney problems
Nose Surgery: Nose is reshaped by resculpting the bone and cartilage in the nose.
- bursting blood vessels
- red spots
- bleeding under the skin
Tummy Tuck: Extra fat and skin in the abdomen is removed, and muscles are tightened to flatten tummy.
- blood clots
- fluid accumulation under the skin
Cosmetic Procedures: Non-Surgical
Botox Injection: Botox is injected into a facial muscle to paralyze it, so lines don't form when a person frowns or squints.
- face pain
- muscle weakness
- flu-like symptoms
- loss of facial expression
- droopy eyelids
- asymmetric smile
Collagen/fat Injection: Collagen from a cow or fat from your thigh or abdomen is injected into facial wrinkles, pits, or scars.
- trigger an autoimmune disease
- contour problems
- flu-like symptoms
Dermabrasion: A small, spinning wheel or brush with a roughened surface removes the upper layers of facial skin. A new layer of skin appears during healing, giving the face a smoother appearance. Used to treat facial scars, heavy wrinkles, and problems like rosacea.
- abnormal color changes
- allergic reaction
- fever blisters
- cold sores
- thickened skin
Hyaluronic acid injection: This gel is injected into your face to smooth lines, wrinkles, and scars on the skin.
- tissue hardening
- risks unknown if used in combination with collagen
Laser hair removal: Laser light is passed over the skin to remove hair.
- hair regrowth
- change in skin color
Laser skin resurfacing: Laser light is used to remove wrinkles, lines, age spots, scars, moles, tattoos, and warts from the surface of the skin.
- change in skin color
- herpes flare-up (fever, facial pain, and flu-like symptoms)
Sclerotherapy: A solution is injected into spider and varicose leg veins (small purple and red blood vessels) to remove the veins.
- blood clots
- color changes in the skin
- vein removal may not be permanent
Chemical Peel: A solution is put onto the face (or parts of the face) that causes the skin to blister and peel off. It is replaced with new skin.
- raised scarring
- allergic reaction
- cold sores
- color changes or blotchiness
- heart problems
Tooth Whiteners (peroxide agents): Depending on the product, either you or the dentist applies peroxide using strips; a mouth guard with gel; or a tray inside your mouth around your teeth
- If not customized for you by a dentist or dental hygienist, there may be unknown ingredients and unknown results
Source: The National Women's Health Information Center
- What is facelift surgery?
- How is facelift surgery performed?
- What are complications of facelift surgery?
- Facelift Surgery At A Glance
- Find a local Plastic Surgeon in your town
What is facelift surgery
A facelift is a surgical method that removes excess facial skin to make the face appear younger. However, the aging face not only loses skin elasticity and develops looser droopy skin, but also loses fat and muscle tone. Additional procedures which may be necessary to achieve the best results include: necklift, blepharoplasty (eyelid surgery), liposuction, autologous fat injection, removal of buccal (cheek) fat pad, forehead lift, browlift, chemical or laser peel, and malar (cheek), submalar or chin implants.
How is facelift surgery performed?
The traditional facelift procedure is performed through an incision starting in the hair or hairline above and in front of the ear (the temporal region). The incision is extended downward in front of the ear, comes under the ear and then upward behind the ear ending in the hair or hairline behind the ear. The skin and fatty tissues are then lifted off the underlying muscle and fascia (connective tissue) as far forward as is necessary to correct the loose skin problem. The underlying muscle and fascia can be tightened with sutures if the surgeon feels it is necessary. The skin is pulled back and upward and the excess skin removed. The wound is then closed with sutures and skin staples. Some surgeons leave a drain in the wounds to remove excess blood. Bandages are then applied. There are surgical techniques which go into deeper tissues rather than under the skin and fat. The results are similar.
What are complications of facelift surgery?
Although infrequent, the risks and complications of facelift surgery include:
- Bleeding, hematoma, bruising
- Neurological dysfunction (loss of muscle function or sensation), which is usually temporary
- Widened or thickened scar
- Loss of hair (around the incision site)
- Asymmetry (unevenness between two sides)
- Skin necrosis (loss of skin from tissue death)
Facelift is very satisfying to most patients. It achieves a youthful appearance which lasts approximately 10 years. The surgery is performed in an outpatient setting. This can be done in the outpatient surgi-center or even in a well-equipped physician's office. Pain and discomfort after surgery are minimal. Once the dressings are removed after approximately 3-5 days, the patient can resume social activities using makeup to cover bruising and hair over the ears to hide the sutures.
Face Lift At A Glance
- Facelift surgery helps to make the face appear younger.
- Results last approximately ten years.
- Recovery time is usually one week but activities can begin the day after surgery.
- Pain and discomfort are usually minimal.
- Additional procedures to supplement the facelift may be necessary for the best results.
- Why Have the Procedure?
- How Does Lipoplasty Differ From Other Liposuction Techniques?
- What Are the Benefits of Lipoplasty?
- What Happens During Ultrasonic-Assisted Lipoplasty?
- What Happens After Ultrasonic-Assisted Lipoplasty?
- Are The Results of Ultrasonic-Assisted Lipoplasty Permanent?
- Who Is a Good Candidate for Ultrasonic-Assisted Lipoplasty?
- Who Can Perform Ultrasonic-Assisted Lipoplasty?
- Are There Risks Involved With Ultrasonic-Assisted Lipoplasty?
- How Much Does Ultrasonic-Assisted Lipoplasty Cost?
- Find a local Plastic Surgeon in your town
Why Have the Procedure?
Some people have stubborn areas of fat cells that will not shrink no matter how much they diet or exercise. The common areas for these fat pockets include the chin, neck, hips, abdomen, thighs, buttocks and even calves and ankles.
A newer technique called ultrasonic-assisted lipoplasty (UAL) may help you address that unwanted fat. UAL is an enhancement to the currently used tumescent liposuction method. To keep your new shape and new weight after this lipoplasty, you will need to follow a proper diet and exercise plan.
How Does Lipoplasty Differ From Other Liposuction Techniques?
UAL uses high-frequency sound waves to liquefy fat beneath the skin's surface before removing it with gentle suction. Tumescent liposuction and traditional liposuction cannot liquefy fat cells, and this makes the fat more difficult to remove.
What Are the Benefits of Lipoplasty?
Early results by a select group of plastic surgeons internationally have been encouraging. However, further study is needed to determine if lipoplasty will replace existing liposuction techniques.
UAL allows physicians to remove significant amounts of fat in a single session because the fat is liquefied by sound waves. It can be especially useful in areas of dense fat such as the back. The use of sound waves prevents surrounding blood vessels and connective tissue from being damaged because fat cells are selectively destroyed and removed.
What Happens During Ultrasonic-Assisted Lipoplasty?
Several steps are involved. Similar to traditional liposuction, the skin is marked to indicate the precise area from which the fat will be removed. Next, a large amount of very dilute anesthetic solution is injected into the body site to numb and swell the fatty area (tumescent technique).
Then, in a step unique to lipoplasty, a thin tube-like instrument called an ultrasonic probe is inserted beneath the skin through a small incision. The probe is maneuvered in a crisscross pattern while sound waves generate negative pressure, causing the fat cells to implode, or collapse, and liquefy. The liquefied fat and anesthetic fluid are removed using gentle suction.
What Happens After Ultrasonic-Assisted Lipoplasty?
Patients are instructed to wear a tight-fitting garment, such as a girdle or thick support hose for up to six weeks after the procedure. Sometimes, postoperative pain medication is not needed because the injected anesthetic solution keeps the area numb for 12 hours or more.
Every person's outcome will vary somewhat based on factors such as volume of fat cells removed and area of removal. Your doctor will discuss what results you can expect to achieve, and how to best maintain your new body shape.
Are The Results of Ultrasonic-Assisted Lipoplasty Permanent?
The fat cells are removed permanently, so if you gain weight after the procedure, it will usually not concentrate in the treated area. This is because you now have less cells in the treated area in which fat can be deposited. However, ultrasonic-assisted lipoplasty will not prevent you from regaining weight.
Who Is a Good Candidate for Ultrasonic-Assisted Lipoplasty?
A thorough evaluation by a board-certified plastic surgeon experienced in lipoplasty will determine if you are a good candidate. But in general, a good candidate for lipoplasty (as well as other liposuction techniques) is a person of average or slightly above average weight, in good health, with a localized area of fat that does not respond well to diet and exercise.
Who Can Perform Ultrasonic-Assisted Lipoplasty?
Board-certified plastic surgeons who have undergone specialized training required by the Ultrasonic Liposuction Task Force can perform lipoplasty. This task force was established by three major plastic surgery societies: The American Society of Plastic and Reconstructive Surgeons, The Aesthetic Society and The Lipoplasty Society. Its mission is to set safety standards for the performance of UAL. Do not hesitate to ask your doctor about credentials and training and how many lipoplasty procedures he or she has performed.
Are There Risks Involved With Ultrasonic-Assisted Lipoplasty?
UAL has a good safety record to date, but carries the same risks as all liposuction surgery, such as rare occurrence of infection, blood or fat clots; or cosmetic risks like a change in skin pigmentation, or skin texture. Post-operative fluid collections, known as seromas may also form. However these can be drained with a needle and a syringe.
Unique to UAL is the risk of burns caused by heat from the ultrasonic probe. This risk is minimized when performed by a surgeon skilled in lipoplasty. Some patients may have an adverse reaction to the anesthetic, and may develop redness or other pigment changes.
How Much Does Ultrasonic-Assisted Lipoplasty Cost?
Ask to talk with a representative who can explain the costs of the procedure and payment options. Like other elective cosmetic procedures, UAL is not covered by health insurance plans.
Reviewed by the doctors at The Cleveland Clinic, Department of Plastic Surgery.
Edited by Charlotte E. Grayson , MD, Sept. 2003.
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