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Tremor is an unintentional, somewhat rhythmic, muscle movement involving to-and-fro movements (oscillations) of one or more parts of the body. It is the most common of all involuntary movements and can affect the hands, arms, head, face, vocal cords, trunk, and legs. Most tremors occur in the hands. In some people, tremor is a symptom of another neurological disorder. The most common form of tremor, however, occurs in otherwise healthy people. Although tremor is not life-threatening, it can be embarrassing to some people and make it harder to perform daily tasks.
Tremor is most commonly classified by clinical features and cause or origin. Some of the better known forms of tremor, with their symptoms, include the following: Essential tremor (sometimes called benign essential tremor) is the most common of the more than 20 types of tremor. Although the tremor may be mild and nonprogressive in some people, in others, the tremor is slowly progressive, starting on one side of the body but affecting both sides within 3 years. The hands are most often affected but the head, voice, tongue, legs, and trunk may also be involved. Head tremor may be seen as a "yes-yes" or "no-no" motion. Essential tremor may be accompanied by mild gait disturbance. Tremor frequency may decrease as the person ages, but the severity may increase, affecting the person's ability to perform certain tasks or activities of daily living. Heightened emotion, stress, fever, physical exhaustion, or low blood sugar may trigger tremors and/or increase their severity. Onset is most common after age 40, although symptoms can appear at any age. It may occur in more than one family member. Children of a parent who has essential tremor have a 50 percent chance of inheriting the condition. Essential tremor is not associated with any known pathology. Parkinsonian tremor is caused by damage to structures within the brain that control movement. This resting tremor, which can occur as an isolated symptom or be seen in other disorders, is often a precursor to Parkinson's disease (more than 25 percent of patients with Parkinson's disease have an associated action tremor). The tremor, which is classically seen as a "pill-rolling" action of the hands that may also affect the chin, lips, legs, and trunk, can be markedly increased by stress or emotions. Onset of parkinsonian tremor is generally after age 60. Movement starts in one limb or on one side of the body and usually progresses to include the other side. Dystonic tremor occurs in individuals of all ages who are affected by dystonia, a movement disorder in which sustained involuntary muscle contractions cause twisting and repetitive motions and/or painful and abnormal postures or positions. Dystonic tremor may affect any muscle in the body and is seen most often when the patient is in a certain position or moves a certain way. The pattern of dystonic tremor may differ from essential tremor. Dystonic tremors occur irregularly and often can be relieved by complete rest. Touching the affected body part or muscle may reduce tremor severity. The tremor may be the initial sign of dystonia localized to a particular part of the body. Cerebellar tremor is a slow, broad tremor of the extremities that occurs at the end of a purposeful movement, such as trying to press a button or touching a finger to the tip of one's nose. Cerebellar tremor is caused by lesions in or damage to the cerebellum resulting from stroke, tumor, or disease such as multiple sclerosis or some inherited degenerative disorder. It can also result from chronic alcoholism or overuse of some medicines. In classic cerebellar tremor, a lesion on one side of the brain produces a tremor in that same side of the body that worsens with directed movement. Cerebellar damage can also produce a "wing-beating" type of tremor called rubral or Holmes' tremor - a combination of rest, action, and postural tremors. The tremor is often most prominent when the affected person is active or is maintaining a particular posture. Cerebellar tremor may be accompanied by dysarthria (speech problems), nystagmus (rapid, involuntary rolling of the eyes), gait problems, and postural tremor of the trunk and neck.
Psychogenic tremor (also called hysterical tremor) can occur at rest or during postural or kinetic movement. The characteristics of this kind of tremor may vary but generally include sudden onset and remission, increased incidence with stress, change in tremor direction and/or body part affected, and greatly decreased or disappearing tremor activity when the patient is distracted. Many patients with psychogenic tremor have a conversion disorder (defined as a psychological disorder that produces physical symptoms) or another psychiatric disease. Orthostatic tremor is characterized by rhythmic muscle contractions that occur in the legs and trunk immediately after standing. Cramps are felt in the thighs and legs and the patient shakes uncontrollably when asked to stand in one spot. No other clinical signs or symptoms are present and the shaking ceases when the patient sits or is lifted off the ground. Orthostatic tremor may also occur in patients who have essential tremor. Physiologic tremor occurs in every normal individual and has no clinical significance. It is rarely visible to the eye and may be heightened by strong emotion (such as anxiety or fear), physical exhaustion, hypoglycemia, hyperthyroidism, heavy metal poisoning, stimulants, alcohol withdrawal, or fever. It can be seen in all voluntary muscle groups and can be detected by extending the arms and placing a piece of paper on of the hands. Enhanced physiologic tremor is a strengthening of physiologic tremor to more visible levels. It is generally not caused by a neurological disease but by reaction to certain drugs, alcohol withdrawal, or medical conditions including an overactive thyroid and hypoglycemia. It is usually reversible once the cause is corrected. Tremor can result from other conditions as well. Alcoholism, excessive alcohol consumption, or alcohol withdrawal can kill certain nerve cells, resulting in tremor, especially in the hand. (Conversely, small amounts of alcohol may help to decrease familial and essential tremor, but the mechanism behind this is unknown. Doctors may use small amounts of alcohol to aid in the diagnosis of certain forms of tremor but not as a regular treatment for the condition.) Tremor in peripheral neuropathy may occur when the nerves that supply the body's muscles are traumatized by injury, disease, abnormality in the central nervous system, or as the result of systemic illnesses. Peripheral neuropathy can affect the whole body or certain areas, such as the hands, and may be progressive. Resulting sensory loss may be seen as a tremor or ataxia (inability to coordinate voluntary muscle movement) of the affected limbs and problems with gait and balance. Clinical characteristics may be similar to those seen in patients with essential tremor.
The doctor will perform a neurological exam to assess nerve function and motor and sensory skills. The tests are designed to determine any functional limitations, such as difficulty with handwriting or the ability to hold a utensil or cup. The patient may be asked to place a finger on the tip of her or his nose, draw a spiral, or perform other tasks or exercises. The doctor may order an electromyogram to diagnose muscle or nerve problems. This test measures involuntary muscle activity and muscle response to nerve stimulation.
recommend the use of weights, splints, other adaptive equipment, and special plates and utensils for eating. Surgical intervention such as thalamotomy and deep brain stimulation may ease certain tremors. These surgeries are usually performed only when the tremor is severe and does not respond to drugs. Thalamotomy, involving the creation of lesions in the brain region called the thalamus, is quite effective in treating patients with essential, cerebellar, or parkinsonian tremor. This in-hospital procedure is performed under local anesthesia, with the patient awake. After the patient's head is secured in a metal frame, the surgeon maps the patient's brain to locate the thalamus. A small hole is drilled through the skull and a temperature-controlled electrode is inserted into the thalamus. A low-frequency current is passed through the electrode to activate the tremor and to confirm proper placement. Once the site has been confirmed, the electrode is heated to create a temporary lesion. Testing is done to examine speech, language, coordination, and tremor activation, if any. If no problems occur, the probe is again heated to create a 3-mm permanent lesion. The probe, when cooled to body temperature, is withdrawn and the skull hole is covered. The lesion causes the tremor to permanently disappear without disrupting sensory or motor control. Deep brain stimulation (DBS) uses implantable electrodes to send high-frequency electrical signals to the thalamus. The electrodes are implanted as described above. The patient uses a hand-held magnet to turn on and turn off a pulse generator that is surgically implanted under the skin. The electrical stimulation temporarily disables the tremor and can be "reversed," if necessary, by turning off the implanted electrode. Batteries in the generator last about 5 years and can be replaced surgically. DBS is currently used to treat parkinsonian tremor and essential tremor. The most common side effects of tremor surgery include dysarthria (problems with motor control of speech), temporary or permanent cognitive impairment (including visual and learning difficulties), and problems with balance.
An additional NINDS study will examine how dextromethorphan, a drug that alters reflexes of the larynx (voice box), might reduce voice symptoms in people with voice disorders, including vocal tremor. This study will compare the effects of dextromethorphan, lorazepam (a tranquilizer), and a placebo in patients with four types of voice disorders.
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and stress can all contribute to cell damage. In addition, abnormal clumps called Lewy bodies, which contain the protein alpha-synuclein, are found in many brain cells of individuals with Parkinson's disease. The function of these clumps in regards to Parkinson's disease is not understood. In general, scientists suspect that dopamine loss is due to a combination of genetic and environmental factors.
What is Parkinson's disease? What causes Parkinson's disease? What genes are linked to Parkinson's disease? Who is at risk for Parkinson's disease? What are the symptoms of Parkinson's disease? What other conditions resemble Parkinson's disease? How is Parkinson's disease diagnosed? What is the treatment for Parkinson's disease? How can people learn to cope with Parkinson's disease? Can Parkinson's disease be prevented? What is the prognosis for Parkinson's disease? Parkinson's Disease At A Glance Parkinson's Disease Glossary Parkinson's Disease Index Find a local Neurologist in your town
3. PARK7 (Parkinson's disease autosomal recessive, early onset 7): PARK7 mutations are found in early-onset Parkinson's disease. The PARK7 gene makes the DJ-1 protein, which may protect cells from oxidative stress. 4. PINK1 (PTEN-induced putative kinase 1): Mutations of this gene are found in early-onset Parkinson's disease. The exact function of the protein made by PINK1 is not known, but it may protect structures within the cell called mitochondria from stress. 5. LRRK2 (leucine-rich repeat kinase 2): LRRK2 makes the protein dardarin. Mutations in the LRRK2 gene have been linked to late-onset Parkinson's disease.
Several other chromosome regions and the genes GBA (glucosidase beta acid), SNCAIP (synuclein alpha interacting protein), and UCHL1 (ubiquitin carboxyl-terminal esterase L1) may also be linked to Parkinson's disease.
Age is the largest risk factor for the development and progression of Parkinson's disease. Most people who develop Parkinson's disease are older than 60 years years of age. Men are affected about 1.5 to 2 times more often than women. A small number of individuals are at increased risk because of a family history of the disorder. Head trauma, illness, or exposure to environmental toxins such as pesticides and herbicides may be a risk factor.
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What is Parkinson's disease? What causes Parkinson's disease? What genes are linked to Parkinson's disease? Who is at risk for Parkinson's disease? What are the symptoms of Parkinson's disease? What other conditions resemble Parkinson's disease? How is Parkinson's disease diagnosed? What is the treatment for Parkinson's disease? How can people learn to cope with Parkinson's disease? Can Parkinson's disease be prevented? What is the prognosis for Parkinson's disease? Parkinson's Disease At A Glance Parkinson's Disease Glossary Parkinson's Disease Index Find a local Neurologist in your town
Tremors: Trembling in fingers, hands, arms, feet, legs, jaw, or head. Tremors most often occur while the individual is resting, but not while involved in a task. Tremors may worsen when an individual is excited, tired, or stressed. Rigidity: Stiffness of the limbs and trunk, which may increase during movement. Rigidity may produce muscle aches and pain. Loss of fine hand movements can lead to cramped handwriting (micrographia) and may make eating difficult. Bradykinesia: Slowness of voluntary movement. Over time, it may become difficult to initiate movement and to complete movement. Bradykinesia together with stiffness can also affect the facial muscles and result in an expressionless, "mask-like" appearance. Postural instability: Impaired or lost reflexes can make it difficult to adjust posture to maintain balance. Postural instability may lead to falls. Parkinsonian gait: Individuals with more progressive Parkinson's disease develop a distinctive shuffling walk with a stooped position and a diminished or absent arm swing. It may become difficult to start walking and to make turns. Individuals may freeze in mid-stride and appear to fall forward while walking.
Secondary symptoms of Parkinson's disease While the main symptoms of Parkinson's disease are movement-related, progressive loss of muscle control and continued damage to the brain can lead to secondary symptoms. These vary in severity, and not every individual will experience all of them. Some of the secondary symptoms include:
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anxiety, insecurity, and stress confusion, memory loss, and dementia (more common in elderly individuals) constipation depression difficulty swallowing and excessive salivation diminished sense of smell
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increased sweating male erectile dysfunction skin problems slowed, quieter speech, and monotone voice urinary frequency/urgency
What is Parkinson's disease? What causes Parkinson's disease? What genes are linked to Parkinson's disease? Who is at risk for Parkinson's disease? What are the symptoms of Parkinson's disease? What other conditions resemble Parkinson's disease? How is Parkinson's disease diagnosed? What is the treatment for Parkinson's disease? How can people learn to cope with Parkinson's disease? Can Parkinson's disease be prevented? What is the prognosis for Parkinson's disease? Parkinson's Disease At A Glance Parkinson's Disease Glossary Parkinson's Disease Index Find a local Neurologist in your town
similarities to related movement disorders and other conditions with Parkinson-like symptoms. Individuals may sometimes be misdiagnosed as having another disorder, and sometimes individuals with Parkinson-like symptoms may be inaccurately diagnosed as having Parkinson's disease. It is therefore important to re-evaluate individuals in the early phase on a regular basis to rule out other conditions that may be responsible for the symptoms. A neurologist who specializes in movement disorders will be able to make the most accurate diagnosis. An initial assessment is made based on medical history, a neurological exam, and the symptoms present. For the medical history, it is important to know whether other family members have Parkinson's disease, what types of medication have been or are being taken, and whether there was exposure to toxins or repeated head trauma in the past. A neurological exam may include an evaluation of coordination, walking, and fine motor tasks involving the hands. Several guidelines have been published to assist in the diagnosis of Parkinson's disease. These include the Hoehn and Yahr scale and the Unified Parkinson's Disease Rating Scale. Tests are used to measure mental capacity, behavior, mood, daily living activities, and motor function. They can be very helpful in the initial diagnosis, to rule out other disorders, as well as in monitoring the progression of the disease to make therapeutic adjustments. Brain scans and other laboratory tests are also sometimes carried out, mostly to detect other disorders resembling Parkinson's disease. The diagnosis of Parkinson's disease is more likely if:
1. at least two of the three major symptoms are present (tremor at rest, muscle rigidity, and slowness); 2. the onset of symptoms started on one side of the body; 3. symptoms are not due to secondary causes such as medication or strokes in the area controlling movement; and 4. symptoms are significantly improved with levodopa (see below).
broken down before it reaches the brain. Co-treatment with carbidopa allows for a lower levodopa dose, thereby reducing side effects. In earlier stages of Parkinson's disease, substances that mimic the action of dopamine (dopamine agonists), and substances that reduce the breakdown of dopamine (monoamine oxidase type B (MAO-B) inhibitors) can be very efficacious in relieving motor symptoms. Unpleasant side effects of these preparations are quite common, including swelling caused by fluid accumulation in body tissues, drowsiness, constipation, dizziness, hallucinations, and nausea. For some individuals with advanced, virtually unmanageable motor symptoms, surgery may be an option. In deep brain stimulation (DBS), the surgeon implants electrodes to stimulate areas of the brain involved in movement. In another type of surgery, specific areas in the brain that cause Parkinson's symptoms are destroyed. An alternative approach currently being explored is the use of dopamine-producing cells derived from stem cells. While stem cell therapy has great potential, more research is required before such cells can become of therapeutic value in the treatment of Parkinson's disease. In addition to medication and surgery, general lifestyle changes (rest and exercise), physical therapy, occupational therapy, and speech therapy may be beneficial.
Parkinson's disease is a neurodegenerative disorder which leads to progressive deterioration of motor function due to loss of dopamine-producing brain cells. Primary symptoms include tremor, stiffness, slowness, impaired balance, and later on a shuffling gait. Some secondary symptoms include anxiety, depression, and dementia. Most individuals with Parkinson's disease are diagnosed when they are 60 years old or older, but early-onset Parkinson's disease also occurs. With proper treatment, most individuals with Parkinson's disease can lead long, productive lives for many years after diagnosis.
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REFERENCES: Arenas, E. Towards stem cell replacement therapies for Parkinson's disease. Biochemical and Biophysical Research Communications, 2010; vol 396: pp 152-156. Chen, J.C. Parkinson's Disease: Health-Related Quality of Life, Economic Cost, and Implications of Early Treatment American Journal of Managing Care, 2010; vol 16: pp S87S93. Fricker-Gates, R.A. and Gates, M.A. Stem cell-derived dopamine neurons for repair in Parkinson's disease. Regenerative Medicine, March 2010; vol 5(2): pp267-78. Hauser, R.A., Early Pharmacologic Treatment in Parkinson's Disease. American Journal of Managing Care, 2010; vol 16: pp S100-S107. Pahwa, R. and Lyons, K.E. diagnosis of Parkinson's disease: recommendations from diagnostic clinical guidelines. American Journal of Managing Care, 2010; vol 16: pp S194-S99.