NEUROLOGY / PSYCHIATRY
Schizophrenia is a chronic and severe mental disorder that affects how a person thinks, feels, and behaves. People with schizophrenia may seem like they have lost touch with reality. Although schizophrenia is not as common as other mental disorders, the symptoms can be very disabling.
Signs and Symptoms
Symptoms of schizophrenia usually start between ages 16 and 30. In rare cases, children have schizophrenia too. The symptoms of schizophrenia fall into three categories: positive, negative, and cognitive.
Positive symptoms: “Positive” symptoms are psychotic behaviors not generally seen in healthy people. People with positive symptoms may “lose touch” with some aspects of reality. Symptoms include:
Thought disorders (unusual or dysfunctional ways of thinking)
Movement disorders (agitated body movements)
Negative symptoms: “Negative” symptoms are associated with disruptions to normal emotions and behaviors. Symptoms include:
“Flat affect” (reduced expression of emotions via facial expression or voice tone)
Reduced feelings of pleasure in everyday life
Difficulty beginning and sustaining activities
Cognitive symptoms: For some patients, the cognitive symptoms of schizophrenia are subtle, but for others, they are more severe and patients may notice changes in their memory or other aspects of thinking.
Poor “executive functioning” (the ability to understand information and use it to make decisions)
Trouble focusing or paying attention
Problems with “working memory” (the ability to use information immediately after learning it)
There are several factors that contribute to the risk of developing schizophrenia.
Genes and environment: Scientists have long known that schizophrenia sometimes runs in families. However, there are many people who have schizophrenia who don’t have a family member with the disorder and conversely, many people with one or more family members with the disorder who do not develop it themselves.
Scientists believe that many different genes may increase the risk of schizophrenia, but that no single gene causes the disorder by itself. It is not yet possible to use genetic information to predict who will develop schizophrenia.
Scientists also think that interactions between genes and aspects of the individual’s environment are necessary for schizophrenia to develop. Environmental factors may involve:
Exposure to viruses
Malnutrition before birth
Problems during birth
Different brain chemistry and structure: Scientists think that an imbalance in the complex, interrelated chemical reactions of the brain involving the neurotransmitters (substances that brain cells use to communicate with each other) dopamine and glutamate, and possibly others, plays a role in schizophrenia.
Some experts also think problems during brain development before birth may lead to faulty connections. The brain also undergoes major changes during puberty, and these changes could trigger psychotic symptoms in people who are vulnerable due to genetics or brain differences.
The diagnosis of schizophrenia is often not easy to make. It is not possible to make the diagnosis in one meeting. Even if the person has psychotic symptoms, that does not mean he or she has schizophrenia. It may take months or even years to see if the pattern of illness fits the description of schizophrenia.
Just as there are many causes of fever, there are many causes of psychosis. Part of an evaluation is to check for some of these other causes, for example, a mood disorder, a medical problem or a toxic substance.
Experts know that brain function is impaired in schizophrenia, but tests that examine the brain directly cannot yet be used to make a diagnosis. Brain imaging, such as computed tomography (CT), magnetic resonance imaging (MRI) or an electroencephalogram (EEG), is not diagnostic for schizophrenia. Such exams, however, can help to rule out other possible causes of symptoms, such as a tumor or a seizure disorder.
Treatments and Therapies
Schizophrenia requires lifelong treatment, even when symptoms have subsided. Treatment with medications and psychosocial therapy can help manage the condition. In some cases, hospitalization may be needed.
A psychiatrist experienced in treating schizophrenia usually guides treatment. The treatment team also may include a psychologist, social worker, psychiatric nurse and possibly a case manager to coordinate care. The full-team approach may be available in clinics with expertise in schizophrenia treatment.
Antipsychotic medications are usually taken daily in pill or liquid form. Some antipsychotics are injections that are given once or twice a month. Some people have side effects when they start taking medications, but most side effects go away after a few days. Doctors and patients can work together to find the best medication or medication combination, and the right dose.
These first-generation antipsychotics have frequent and potentially significant neurological side effects, including the possibility of developing a movement disorder (tardive dyskinesia) that may or may not be reversible. First-generation antipsychotics include:
These antipsychotics are often cheaper than second-generation antipsychotics, especially the generic versions, which can be an important consideration when long-term treatment is necessary.
These newer, second-generation medications are generally preferred because they pose a lower risk of serious side effects than do first-generation antipsychotics. Second-generation antipsychotics include:
These treatments are helpful after patients and their doctor find a medication that works. Learning and using coping skills to address the everyday challenges of schizophrenia helps people to pursue their life goals, such as attending school or work. Individuals who participate in regular psychosocial treatment are less likely to have relapses or be hospitalized.
Coordinated specialty care (CSC)
This treatment model integrates medication, psychosocial therapies, case management, family involvement, and supported education and employment services, all aimed at reducing symptoms and improving quality of life. The NIMH Recovery After an Initial Schizophrenia Episode (RAISE) research project seeks to fundamentally change the trajectory and prognosis of schizophrenia through coordinated specialty care treatment in the earliest stages of the disorder. RAISE is designed to reduce the likelihood of long-term disability that people with schizophrenia often experience and help them lead productive, independent lives.
Bipolar disorder, also known as manic-depressive illness, is a brain disorder that causes unusual shifts in mood, energy, activity levels, and the ability to carry out day-to-day tasks.
There are four basic types of bipolar disorder; all of them involve clear changes in mood, energy, and activity levels. These moods range from periods of extremely “up,” elated, and energized behavior (known as manic episodes) to very sad, “down,” or hopeless periods (known as depressive episodes). Less severe manic periods are known as hypomanic episodes.
Bipolar I Disorder— defined by manic episodes that last at least 7 days, or by manic symptoms that are so severe that the person needs immediate hospital care. Usually, depressive episodes occur as well, typically lasting at least 2 weeks. Episodes of depression with mixed features (having depression and manic symptoms at the same time) are also possible.
Bipolar II Disorder— defined by a pattern of depressive episodes and hypomanic episodes, but not the full-blown manic episodes described above.
Cyclothymic Disorder (also called cyclothymia)— defined by numerous periods of hypomanic symptoms as well numerous periods of depressive symptoms lasting for at least 2 years (1 year in children and adolescents). However, the symptoms do not meet the diagnostic requirements for a hypomanic episode and a depressive episode.
Other Specified and Unspecified Bipolar and Related Disorders— defined by bipolar disorder symptoms that do not match the three categories listed above.
Signs and Symptoms
People with bipolar disorder experience periods of unusually intense emotion, changes in sleep patterns and activity levels, and unusual behaviors. These distinct periods are called “mood episodes.” Mood episodes are drastically different from the moods and behaviors that are typical for the person. Extreme changes in energy, activity, and sleep go along with mood episodes.
Sometimes a mood episode includes symptoms of both manic and depressive symptoms. This is called an episode with mixed features. People experiencing an episode with mixed features may feel very sad, empty, or hopeless, while at the same time feeling extremely energized.
Bipolar disorder can be present even when mood swings are less extreme. For example, some people with bipolar disorder experience hypomania, a less severe form of mania. During a hypomanic episode, an individual may feel very good, be highly productive, and function well. The person may not feel that anything is wrong, but family and friends may recognize the mood swings and/or changes in activity levels as possible bipolar disorder. Without proper treatment, people with hypomania may develop severe mania or depression.
Proper diagnosis and treatment help people with bipolar disorder lead healthy and productive lives. Talking with a doctor or other licensed mental health professional is the first step for anyone who thinks he or she may have bipolar disorder. The doctor can complete a physical exam to rule out other conditions. If the problems are not caused by other illnesses, the doctor may conduct a mental health evaluation or provide a referral to a trained mental health professional, such as a psychiatrist, who is experienced in diagnosing and treating bipolar disorder.
People with bipolar disorder are more likely to seek help when they are depressed than when experiencing mania or hypomania. Therefore, a careful medical history is needed to ensure that bipolar disorder is not mistakenly diagnosed as major depression. Unlike people with bipolar disorder, people who have depression only (also called unipolar depression) do not experience mania. They may, however, experience some manic symptoms at the same time, which is also known as major depressive disorder with mixed features.
Bipolar Disorder and Other Illnesses
Some bipolar disorder symptoms are similar to other illnesses, which can make it hard for a doctor to make a diagnosis. In addition, many people have bipolar disorder along with another illness such as anxiety disorder, substance abuse, or an eating disorder. People with bipolar disorder are also at higher risk for thyroid disease, migraine headaches, heart disease, diabetes, obesity, and other physical illnesses.
Psychosis: Sometimes, a person with severe episodes of mania or depression also has psychotic symptoms, such as hallucinations or delusions. The psychotic symptoms tend to match the person’s extreme mood.
Anxiety and ADHD: Anxiety disorders and attention-deficit hyperactivity disorder (ADHD) are often diagnosed among people with bipolar disorder.
Brain Structure and Functioning: Some studies show how the brains of people with bipolar disorder may differ from the brains of healthy people or people with other mental disorders. Learning more about these differences, along with new information from genetic studies, helps scientists better understand bipolar disorder and predict which types of treatment will work most effectively.
Genetics: Some research suggests that people with certain genes are more likely to develop bipolar disorder than others. But genes are not the only risk factor for bipolar disorder. Studies of identical twins have shown that even if one twin develops bipolar disorder, the other twin does not always develop the disorder, despite the fact that identical twins share all of the same genes.
Family History: Bipolar disorder tends to run in families. Children with a parent or sibling who has bipolar disorder are much more likely to develop the illness, compared with children who do not have a family history of the disorder. However, it is important to note that most people with a family history of bipolar disorder will not develop the illness.
Treatments and Therapies
Treatment helps many people—even those with the most severe forms of bipolar disorder—gain better control of their mood swings and other bipolar symptoms. An effective treatment plan usually includes a combination of medication and psychotherapy (also called “talk therapy”). Bipolar disorder is a lifelong illness. Episodes of mania and depression typically come back over time. Between episodes, many people with bipolar disorder are free of mood changes, but some people may have lingering symptoms. Long-term, continuous treatment helps to control these symptoms.
Different types of medications can help control symptoms of bipolar disorder. An individual may need to try several different medications before finding ones that work best.
Medications generally used to treat bipolar disorder include: mood stabilizers, atypical antipsychotics, and antidepressants.
To Treat Mania
To Prevent Mania
Atypical: Olanzapine, Risperidone, Quetiapine
Typical: Chlorpromazine, Haloperidol
Usually used together with a mood stabilizer, not usually on their own
Lithium: Lithium has for 40 years been the most commonly used drug to prevent relapse.
When done in combination with medication, psychotherapy (also called “talk therapy”) can be an effective treatment for bipolar disorder. It can provide support, education, and guidance to people with bipolar disorder and their families. Some psychotherapy treatments used to treat bipolar disorder include:
Cognitive behavioral therapy (CBT)
Interpersonal and social rhythm therapy
Other Treatment Options
Electroconvulsive Therapy (ECT): ECT can provide relief for people with severe bipolar disorder who have not been able to recover with other treatments. Sometimes ECT is used for bipolar symptoms when other medical conditions, including pregnancy, make taking medications too risky. ECT may cause some short-term side effects, including confusion, disorientation, and memory loss. People with bipolar disorder should discuss possible benefits and risks of ECT with a qualified health professional.
Alzheimer’s disease is an irreversible, progressive brain disorder that slowly destroys memory and thinking skills, and eventually the ability to carry out the simplest tasks. In most people with Alzheimer’s, symptoms first appear in their mid-60s. Alzheimer’s disease is currently ranked as the sixth leading cause of death in the United States, but recent estimates indicate that the disorder may rank third, just behind heart disease and cancer, as a cause of death for older people.
Alzheimer’s is the most common cause of dementia among older adults. Dementia is the loss of cognitive functioning—thinking, remembering, and reasoning—and behavioral abilities to such an extent that it interferes with a person’s daily life and activities. Dementia ranges in severity from the mildest stage, when it is just beginning to affect a person’s functioning, to the most severe stage, when the person must depend completely on others for basic activities of daily living.
The causes of dementia can vary, depending on the types of brain changes that may be taking place. Other dementias include Lewy body dementia, frontotemporal disorders, and vascular dementia. It is common for people to have mixed dementia—a combination of two or more disorders, at least one of which is dementia. For example, some people have both Alzheimer’s disease and vascular dementia.
Changes in the Brain
Scientists continue to unravel the complex brain changes involved in the onset and progression of Alzheimer’s disease. It seems likely that damage to the brain starts a decade or more before memory and other cognitive problems appear. During this preclinical stage of Alzheimer’s disease, people seem to be symptom-free, but toxic changes are taking place in the brain. Abnormal deposits of proteins form amyloid plaques and tau tangles throughout the brain, and once-healthy neurons stop functioning, lose connections with other neurons, and die.
The damage initially appears to take place in the hippocampus, the part of the brain essential in forming memories. As more neurons die, additional parts of the brain are affected, and they begin to shrink. By the final stage of Alzheimer’s, damage is widespread, and brain tissue has shrunk significantly.
Signs and Symptoms
Memory problems are typically one of the first signs of cognitive impairment related to Alzheimer’s disease. Some people with memory problems have a condition called mild cognitive impairment (MCI). In MCI, people have more memory problems than normal for their age, but their symptoms do not interfere with their everyday lives. Movement difficulties and problems with the sense of smell have also been linked to MCI. Older people with MCI are at greater risk for developing Alzheimer’s, but not all of them do. Some may even go back to normal cognition.
The first symptoms of Alzheimer’s vary from person to person. For many, decline in non-memory aspects of cognition, such as word-finding, vision/spatial issues, and impaired reasoning or judgment, may signal the very early stages of Alzheimer’s disease. Researchers are studying biomarkers (biological signs of disease found in brain images, cerebrospinal fluid, and blood) to see if they can detect early changes in the brains of people with MCI and in cognitively normal people who may be at greater risk for Alzheimer’s. Studies indicate that such early detection may be possible, but more research is needed before these techniques can be relied upon to diagnose Alzheimer’s disease in everyday medical practice.
As Alzheimer’s disease progresses, people experience greater memory loss and other cognitive difficulties. Problems can include wandering and getting lost, trouble handling money and paying bills, repeating questions, taking longer to complete normal daily tasks, and personality and behavior changes. People are often diagnosed in this stage.
In this stage, damage occurs in areas of the brain that control language, reasoning, sensory processing, and conscious thought. Memory loss and confusion grow worse, and people begin to have problems recognizing family and friends. They may be unable to learn new things, carry out multistep tasks such as getting dressed, or cope with new situations. In addition, people at this stage may have hallucinations, delusions, and paranoia and may behave impulsively.
Ultimately, plaques and tangles spread throughout the brain, and brain tissue shrinks significantly. People with severe Alzheimer’s cannot communicate and are completely dependent on others for their care. Near the end, the person may be in bed most or all of the time as the body shuts down.
Scientists don’t yet fully understand what causes Alzheimer’s disease in most people. There is a genetic component to some cases of early-onset Alzheimer’s disease. Late-onset Alzheimer’s arises from a complex series of brain changes that occur over decades. The causes probably include a combination of genetic, environmental, and lifestyle factors. The importance of any one of these factors in increasing or decreasing the risk of developing Alzheimer’s may differ from person to person.
The Basics of Alzheimer’s
Scientists are conducting studies to learn more about plaques, tangles, and other biological features of Alzheimer’s disease. Advances in brain imaging techniques allow researchers to see the development and spread of abnormal amyloid and tau proteins in the living brain, as well as changes in brain structure and function. Scientists are also exploring the very earliest steps in the disease process by studying changes in the brain and body fluids that can be detected years before Alzheimer’s symptoms appear. Findings from these studies will help in understanding the causes of Alzheimer’s and make diagnosis easier.
One of the great mysteries of Alzheimer’s disease is why it largely strikes older adults. Research on normal brain aging is shedding light on this question. For example, scientists are learning how age-related changes in the brain may harm neurons and contribute to Alzheimer’s damage. These age-related changes include atrophy (shrinking) of certain parts of the brain, inflammation, production of unstable molecules called free radicals, and mitochondrial dysfunction (a breakdown of energy production within a cell).
Most people with Alzheimer’s have the late-onset form of the disease, in which symptoms become apparent in their mid-60s. The apolipoprotein E (APOE) gene is involved in late-onset Alzheimer’s. This gene has several forms. One of them, APOE-ε4, increases a person’s risk of developing the disease and is also associated with an earlier age of disease onset. However, carrying the APOE-ε4 form of the gene does not mean that a person will definitely develop Alzheimer’s disease, and some people with no APOE-ε4 may also develop the disease.
Also, scientists have identified a number of regions of interest in the genome (an organism’s complete set of DNA) that may increase a person’s risk for late-onset Alzheimer’s to varying degrees.
Early-onset Alzheimer’s disease occurs between a person’s 30s to mid-60s and represents less than 10 percent of all people with Alzheimer’s. Some cases are caused by an inherited change in one of three genes, resulting in a type known as early-onset familial Alzheimer’s disease, or FAD. For other cases of early-onset Alzheimer’s, research suggests there may be a genetic component related to factors other than these three genes.
Health, Environmental, and Lifestyle Factors
Research suggests that a host of factors beyond genetics may play a role in the development and course of Alzheimer’s disease. There is a great deal of interest, for example, in the relationship between cognitive decline and vascular conditions such as heart disease, stroke, and high blood pressure, as well as metabolic conditions such as diabetes and obesity. Ongoing research will help us understand whether and how reducing risk factors for these conditions may also reduce the risk of Alzheimer’s.
A nutritious diet, physical activity, social engagement, and mentally stimulating pursuits have all been associated with helping people stay healthy as they age. These factors might also help reduce the risk of cognitive decline and Alzheimer’s disease. Clinical trials are testing some of these possibilities.
Diagnosis of Alzheimer’s Disease
Doctors use several methods and tools to help determine whether a person who is having memory problems has “possible Alzheimer’s dementia” (dementia may be due to another cause) or “probable Alzheimer’s dementia” (no other cause for dementia can be found).
To diagnose Alzheimer’s, doctors may:
Ask the person and a family member or friend questions about overall health, past medical problems, ability to carry out daily activities, and changes in behavior and personality
Conduct tests of memory, problem solving, attention, counting, and language
Carry out standard medical tests, such as blood and urine tests, to identify other possible causes of the problem
Perform brain scans, such as computed tomography (CT), magnetic resonance imaging (MRI), or positron emission tomography (PET), to rule out other possible causes for symptoms.
These tests may be repeated to give doctors information about how the person’s memory and other cognitive functions are changing over time.
Alzheimer’s disease can be definitely diagnosed only after death, by linking clinical measures with an examination of brain tissue in an autopsy.
Maintaining Mental Function
Several medications are approved by the U.S. Food and Drug Administration (FDA) to treat symptoms of Alzheimer’s. Donepezil (Aricept®), rivastigmine (Exelon®), and galantamine (Razadyne®) are used to treat mild to moderate Alzheimer’s (donepezil can be used for severe Alzheimer’s as well). Memantine (Namenda®) is used to treat moderate to severe Alzheimer’s. These drugs work by regulating neurotransmitters, the chemicals that transmit messages between neurons. They may help reduce symptoms and help with certain behavioral problems. However, these drugs don’t change the underlying disease process. They are effective for some but not all people, and may help only for a limited time. The FDA has also approved Aricept® and Namzaric®, a combination of Namenda® and Aricept®, for the treatment of moderate to severe Alzheimer’s disease.
Common behavioral symptoms of Alzheimer’s include sleeplessness, wandering, agitation, anxiety, and aggression. Scientists are learning why these symptoms occur and are studying new treatments—drug and non-drug—to manage them. Research has shown that treating behavioral symptoms can make people with Alzheimer’s more comfortable and makes things easier for caregivers.
Looking for New Treatments
Alzheimer’s disease research has developed to a point where scientists can look beyond treating symptoms to think about addressing underlying disease processes. In ongoing clinical trials, scientists are developing and testing several possible interventions, including immunization therapy, drug therapies, cognitive training, physical activity, and treatments used for cardiovascular disease and diabetes.
Parkinson’s disease (PD) is a type of movement disorder. It happens when nerve cells in the brain don’t produce enough of a brain chemical called dopamine. Sometimes it is genetic, but most cases do not seem to run in families. Exposure to chemicals in the environment might play a role.
Tremor: Most people with Parkinson’s disease develop a tremor that is most prominent in the hands and fingers. It tends to occur when the limb is relaxed (a resting tremor), disappearing when performing tasks such as drinking or eating. Some people with Parkinson’s disease never develop a tremor.
Stiffness: Stiffness or rigidity is a common early sign of Parkinson’s disease and is most obvious in the arms, shoulder or neck, although it can occur in all muscle groups. People may have difficulty getting out of a chair, turning or rolling over in bed, or walking. Fine finger movements such as doing up a button or tying a shoelace may also be difficult. Pain or a deep aching sensation in the muscles may also be felt.
Bradykinesia: People have difficulty initiating movement and movement may be slow. There may also be a lack of coordination when moving and normal activities can prove difficult. Activities once performed quickly and comfortably, such as washing or dressing, may take several hours if not assisted.
Loss of Balance: This is a symptom that tends to develop later in Parkinson’s disease. Because of impaired balance and co-ordination (postural instability) a person with Parkinson’s disease can develop a forward or backward lean. They may start to walk with small steps as if hurrying forward to keep balance (festinations). Frequent falls are also common.
Parkinson’s disease occurs as the result of insufficient quantities of the neurotransmitter dopamine in a part of the brain called the substantia nigra. The substantia nigra helps in the planning and programming of movement. A neurotransmitter is a chemical substance that is released from the ends of neurones (nerve cells) to communicate with one or several other neurones. Dopamine levels are reduced as the neurones that produce dopamine die. As a result, messages concerning the planning and programming of movement are interrupted.
Genetic factors: Specific gene mutations that can cause Parkinson’s disease have been identified but these are uncommon, except in rare cases with many family members affected by Parkinson’s disease.
Environmental toxins: Despite no conclusive evidence that this is a cause, some scientists believe that an internal or external toxin affects the body’s ability to produce dopamine.
Accelerated ageing: One theory is that in some individuals, for some unknown reason, the normal, age-related death of the neurones that produce dopamine is accelerated.
Free Radicals: Some researchers believe that the neurones that produce dopamine die due to the activity of free radicals. Free radicals are potentially damaging molecules produced in the body during normal chemical reactions.
Lewy bodies: Many changes occur in the brains of people with Parkinson’s disease. One of these changes is the presence of Lewy bodies, which are abnormal clumps of protein within brain cells. Lewy bodies are believed to hold an important role to the cause of Parkinson’s disease.
There is no lab test for PD, so it can be difficult to diagnose. A diagnosis is based on:
• A person’s medical history
• Observing symptoms
• A neurological and physical examination – this may involve the use of imaging techniques such as computerized tomography (CT) or magnetic resonance imaging (MRI) to rule out other conditions.
• A trial does of carbidopa-levodopa, a Parkinson’s disease medication, may be given. A significant improvement in symptoms with this medication will often confirm a diagnosis of Parkinson’s disease.
PD usually begins around age 60, but it can start earlier. It is more common in men than in women. There is no cure for PD. A variety of medicines sometimes help symptoms dramatically. Surgery and deep brain stimulation (DBS) can help severe cases. With DBS, electrodes are surgically implanted in the brain. They send electrical pulses to stimulate the parts of the brain that control movement.
Medications can provide dramatic results and there are a number that can be prescribed. The two mediations most commonly used to help control symptoms are:
Carbidopa-levodopa: Levodopa has proven to be an effective treatment for many people. Levodopa is converted to dopamine within the brain, reducing many of the disabling symptoms of Parkinson’s disease. Over time the effect of levodopa can decrease and it can also cause unwanted side effects such as nausea and involuntary movements (dyskinesias). For this reason, it may be avoided in the early stages of the condition. Levodopa is combined with carbidopa to protect against premature conversion of the levodopa to dopamine outside of the brain, which prevents or lessens side effects.
Dopamine agonists: Whereas levodopa artificially replaces dopamine in the brain, dopamine agonists mimic the effects of the lost dopamine. They can be used alone or in combination with levodopa. Dopamine agonists can remain effective for several years and avoid some of the unwanted side-effects of levodopa.
Catechol-O-methyltransferase (COMT) inhibitors: this class of medication (eg: entacapone) mildly prolongs the effect of levodopa therapy by blocking an enzyme that breaks down dopamine.
Amantadine: this drug may be prescribed alone to provide short-term relief of symptoms of mild, early-stage Parkinson’s disease. It may also be given with carbidopa-levodopa during the later stages of Parkinson’s disease to control involuntary movements caused by levodopa.
Mobility, co-ordination, range of motion and muscle tone can all be improved with physiotherapy. Increasing muscle strength and improving gait and balance also helps prevent falls allowing the person with Parkinson’s disease to feel more confident and capable.
Surgery, while not commonly performed, may be appropriate in cases of very severe tremor or involuntary movements that cannot be adequately controlled with medication. This is done by a specialist neurosurgeon. In recent years, deep brain stimulation (DBS) has become the main surgical option for Parkinson’s disease. It involves implanting a small electrode into a specific area of the brain. The implanted electrode, controlled by a pacemaker-like device implanted under the skin below the collar bone, generates electrical currents that disrupt signals from the brain that cause tremors. DBS is not a cure and the criteria for selection of patients appropriate for the surgery are very strict.
Epilepsy is a neurological disease that causes people to have recurrent seizures. A seizure is a brief disruption of electrical activity in the brain.
• Epilepsy is not contagious.
• Epilepsy is not a mental illness.
• Epilepsy is not a developmental disability.
More than half the time, the cause is unknown. When a cause can be found, it is most often one of these:
• Head injury
• Infection of the brain
• Brain tumor
• Alzheimer’s disease
• Malformation of an area of the brain
• Genetic factors
Medical history, neurological examination, blood work, and other tests are important in diagnosing epilepsy. Eyewitness accounts of a person’s seizures are very important in helping determine the type of seizure(s) a person has. An electroencephalograph (EEG) is a commonly used test to help diagnose seizures. An EEG records the brain’s electrical activity during the test. Some patterns of activity are unique to particular types of seizures. In some situations, CT scans, MRIs, and PET scans may be used to look at the internal structure and function of the brain. These tests may help pinpoint causes of seizures and epilepsy.
Medication – Drugs used to treat epilepsy are called anti-seizure medication. More than 30 anti-seizure medications are currently approved to treat epilepsy. About 7 in 10 people achieve good seizure control on one or more of these medications. Other treatments are available if medicines don’t work.
Surgery – Certain types of surgery may be used for people whose seizures do not respond to medication. Surgery may be recommended when a seizure focus can be determined and removal of all or part of the affected area can be performed without hurting vital functions like speech or movement.
Vagus Nerve Stimulation (VNS) – A small device is implanted under the skin in the left side of the chest. A lead (small thin wire or electrode) goes from the device under the skin and attaches to the vagus nerve in the left side of the neck. The benefits of the VNS appear to improve over time. For example, after one or two years, up to 4 or 5 out of 10 people who have the VNS may see their seizures decrease by 50% or more.
Responsive Neurostimulation (RNS) – A small device for the RNS is placed under the scalp in a small area of the skull or bone surrounding the brain. One or two wires from the device are placed under or on the surface of the brain where seizures start. The device is able to sense a seizure and sends small pulses of electrical current through the wires to help stop or lessen seizure activity. Like the VNS, the RNS does not cure epilepsy and it may not work right away. Yet it can help stop or lessen the number of seizures a person has by 40% to 60% after one to three years.
Peripheral Neuropathy is a condition that develops as a result of damage to the peripheral nervous system — the vast communications network that transmits information between the central nervous system (the brain and spinal cord) and every other part of the body.
Symptoms can range from numbness or tingling, to pricking sensations (paresthesia), or muscle weakness. Areas of the body may become abnormally sensitive leading to an exaggeratedly intense or distorted experience of touch (allodynia). In such cases, pain may occur in response to a stimulus that does not normally provoke pain. Severe symptoms may include burning pain (especially at night), muscle wasting, paralysis, or organ or gland dysfunction. Damage to nerves that supply internal organs may impair digestion, sweating, sexual function, and urination. In the most extreme cases, breathing may become difficult, or organ failure may occur.
Peripheral nerves send sensory information back to the brain and spinal cord, such as a message that the feet are cold. Peripheral nerves also carry signals from the brain and spinal cord to the muscles to generate movement. Damage to the peripheral nervous system interferes with these vital connections. Like static on a telephone line, peripheral neuropathy distorts and sometimes interrupts messages between the brain and spinal cord and the rest of the body.
Peripheral neuropathies can present in a variety of forms and follow different patterns. Symptoms may be experienced over a period of days, weeks, or years. They can be acute or chronic. In acute neuropathies such as Guillain-Barré syndrome (in which the body’s immune system attacks part of the peripheral nervous system and impairs sending and receiving nerve signals), symptoms appear suddenly, progress rapidly, and resolve slowly as damaged nerves heal. In chronic forms, symptoms begin subtly and progress slowly. Some people may have periods of relief followed by relapse. Others may reach a plateau stage where symptoms stay the same for many months or years. Many chronic neuropathies worsen over time. Although neuropathy may be painful and potentially debilitating, very few forms are fatal.
In diabetic neuropathy, one of the most common forms of peripheral neuropathy, nerve damage occurs in an ascending pattern. The first nerve fibers to malfunction are the ones that travel the furthest from the brain and the spinal cord. Pain and numbness often are felt symmetrically in both feet followed by a gradual progression up both legs. Later, the fingers, hands, and arms may become affected.
Motor nerve damage is most commonly associated with muscle weakness. Other symptoms may include painful cramps and fasciculations (uncontrolled muscle twitching visible under the skin), muscle atrophy (severe shrinkage of muscle size), and decreased reflexes.
Sensory nerve damage causes a variety of symptoms because sensory nerves have a broad range of functions. Larger sensory fibers enclosed in myelin register vibration, light touch, and position sense. Damage to large sensory fibers impairs touch, resulting in a general decrease in sensation. Since this is felt most in the hands and feet, people may feel as if they are wearing gloves and stockings even when they are not. This damage to larger sensory fibers may contribute to the loss of reflexes. Loss of position sense often makes people unable to coordinate complex movements like walking or fastening buttons, or to maintain their balance when their eyes are shut.
Autonomic nerve damage symptoms are diverse since the parasympathetic and sympathetic nerves of the peripheral nervous system control nearly every organ in the body. Common symptoms of autonomic nerve damage include an inability to sweat normally, which may lead to heat intolerance; a loss of bladder control; and an inability to control muscles that expand or contract blood vessels to regulate blood pressure.
Physical injury (trauma) is the most common cause of acquired nerve injury.
Injury or sudden trauma, such as from automobile accidents, falls, sports-related activities, and surgical procedures can cause nerves to be partially or completely severed, crushed, compressed, or stretched, sometimes so forcefully that they are partially or completely detached from the spinal cord.
Repetitive stress frequently leads to entrapment neuropathies, a form of compression injury. Cumulative damage can result from repetitive, awkward, and/or forceful activities that require movement of any group of joints for prolonged periods.
Diseases or disorders and their related processes (such as inflammation) can be associated with peripheral neuropathy.
Metabolic and endocrine disorders impair the body’s ability to transform nutrients into energy and process waste products, and this can lead to nerve damage. Endocrine disorders that lead to hormonal imbalances can disturb normal metabolic processes and cause neuropathies.
Autoimmune diseases, in which the immune system attacks the body’s own tissues, can lead to nerve damage. Sjogren’s syndrome, lupus, and rheumatoid arthritis are among the autoimmune diseases that can be associated with peripheral neuropathy.
Kidney disorders may cause neuropathies. Kidney dysfunction can lead to abnormally high amounts of toxic substances in the blood that can damage nerve tissue. A majority of indviduals who require dialysis because of kidney failure develop polyneuropathy.
Cancers can infiltrate nerve fibers or exert damaging compression forces on nerve fibers. Tumors also can arise directly from nerve tissue cells. Paraneoplastic syndromes, a group of rare degenerative disorders that are triggered by a person’s immune system response to a cancerous tumor, also can indirectly cause widespread nerve damage.
Infections can cause peripheral neuropathy. Viruses and bacteria that can attack nerve tissues include herpes varicella zoster (shingles), Epstein-Barr virus, West Nile virus, cytomegalovirus, and herpes simplex members of the large family of human herpes viruses. These viruses can severely damage sensory nerves, causing attacks of sharp, lightning-like pain.
A physical examination and various tests may reveal the presence of a systemic disease causing the nerve damage. Tests of muscle strength, as well as evidence of cramps or fasciculations, indicate motor fiber involvement. Evaluation of the person’s ability to sense vibration, light touch, body position, temperature, and pain reveals any sensory nerve damage and may indicate whether small or large sensory nerve fibers are affected.
Blood tests can detect diabetes, vitamin deficiencies, liver or kidney dysfunction, other metabolic disorders, and signs of abnormal immune system activity. An examination of cerebrospinal fluid that surrounds the brain and spinal cord can reveal abnormal antibodies associated with some immune-mediated neuropathies. More specialized tests may reveal other blood or cardiovascular diseases, connective tissue disorders, or malignancies. Genetic tests are becoming available for a number of the inherited neuropathies.
Based on the results of the neurological exam, physical exam, patient history, and any previous screening or testing, the following additional tests may be ordered to help determine the nature and extent of the neuropathy:
Nerve conduction velocity (NCV)
Magnetic resonance imaging (MRI)
Besides medications used to treat conditions associated with peripheral neuropathy, medications used to relieve peripheral neuropathy signs and symptoms include:
Pain relievers. Over-the-counter pain medications, such as nonsteroidal anti-inflammatory drugs, can relieve mild symptoms. For more-severe symptoms, your doctor might prescribe painkillers. Medications containing opioids, such as tramadol (Conzip, Ultram) or oxycodone (Oxycontin, Roxicodone, others), can lead to dependence and addiction, so these drugs generally are prescribed only when other treatments fail.
Anti-seizure medications. Medications such as gabapentin (Gralise, Neurontin) and pregabalin (Lyrica), developed to treat epilepsy, may relieve nerve pain. Side effects can include drowsiness and dizziness.
Topical treatments. Capsaicin cream, which contains a substance found in hot peppers, can cause modest improvements in peripheral neuropathy symptoms. Lidocaine patches are another treatment you apply to your skin that might offer pain relief. Side effects can include drowsiness, dizziness and numbness at the site of the patch.
Antidepressants. Certain tricyclic antidepressants, such as amitriptyline, doxepin and nortriptyline (Pamelor), have been found to help relieve pain by interfering with chemical processes in your brain and spinal cord that cause you to feel pain. The serotonin and norepinephrine reuptake inhibitor duloxetine (Cymbalta) and the extended-release antidepressant venlafaxine (Effexor XR) also might ease the pain of peripheral neuropathy caused by diabetes. Side effects may include dry mouth, nausea, drowsiness, dizziness, decreased appetite and constipation.
Various therapies and procedures might help ease the signs and symptoms of peripheral neuropathy.
Transcutaneous electrical nerve stimulation (TENS). Electrodes placed on the skin deliver a gentle electric current at varying frequencies. TENS should be applied for 30 minutes daily for about a month.
Plasma exchange and intravenous immune globulin. These procedures, which help suppress immune system activity, might benefit people with certain inflammatory conditions.
Physical therapy. If you have muscle weakness, physical therapy can help improve your movements. You may also need hand or foot braces, a cane, a walker, or a wheelchair.
Surgery. If you have neuropathies caused by pressure on nerves, such as pressure from tumors, you might need surgery to reduce the pressure.
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