Movement disorders

Definition

Movement disorders are a group of neurological diseases and syndromes that involve the motor and movement systems' ability to produce and control movement.

Description

Though it seems simple and effortless, normal movement actually requires an astonishingly complex system of control. Disruption of any portion of this system can cause a person to produce movements that are too weak, too forceful, too uncoordinated, or too poorly controlled for the task at hand. Unwanted movements may occur at rest. Intentional movement may become impossible. These conditions are examples of movement disorders.

Abnormal movements themselves are symptoms of underlying disorders. In some cases, the abnormal movements are the only symptoms. The more common diseases causing motor disorders include:

• spinal cord injury (SCI)
• stroke
• multiple sclerosis (MS)
• muscular dystrophy (MD)
• huntington's chorea (HC)
• cerebral palsy (CP)
• dystonias
• tremor
• myasthenia gravis (MG)
• parkinsonism (PD)
• Tourette syndrome

Other causes of motor disorders are Wilson's disease (WD), inherited ataxias (Friedreich's ataxia, Machado-Joseph disease, and spinocerebellar ataxias), and encephalopathies.

Causes and symptoms

Causes

Movement is produced and coordinated by several interacting brain centers, including the motor cortex, the cerebellum, and a group of structures in the inner potions of the brain called the basal ganglia. Sensory information provides critical input on the current position and velocity of body parts, and spinal nerve cells (neurons ) help prevent opposing muscle groups from contracting simultaneously.

To understand how movement disorders occur, it is helpful to consider a normal volunteer movements, such as reaching to touch a nearby object with the right index finger. To accomplish the desired movement, the arm must be lifted and extended. The hand must be held out to align with the forearm, and the forefinger must be extended while the other fingers remain flexed.

THE MOTOR CORTEX. Voluntary motor commands begin in the motor cortex located on the outer, wrinkled surface of the brain. Movement of the right arm is begun by the left motor cortex, which generates a large volley of signals to the involved muscles. These electrical signals pass along upper motor neurons, through the midbrain, to the spinal cord (SC). Within the SC, these signals connect to lower motor neurons, which convey the signals from the SC to the surface of the muscles involved. Neural activation of the muscles causes contraction, and the force of contraction pulling on the skeleton causes movement of the arm, hand, and fingers.

Damage to, or death of any of the neurons along this path, can cause weakness or paralysis of the affected muscles.

THE CEREBELLUM. Once the movement of the arm is initiated, sensory information is needed to guide the finger to its precise destination. In addition to sight, the most important source of information comes from the "position sense," provided by the many sensory receptors located within the limbs (proprioception). Proprioception allows a person to touch his or her nose with a finger even with the eyes closed. The balance organs in the ears provide important information about posture. Both postural and proprioceptive information are processed by a structure at the rear of the brain, called the cerebellum. The cerebellum sends out electrical signals to modify movements as they progress, "sculpting" the barrage of voluntary commands into a tightly controlled, constantly evolving pattern. Cerebellar disorders cause inability to control the force, fine positioning, and speed of movements (ataxia). Disorders of the cerebellum may also impair the ability to judge distance, so that a person under- or overreaches the target (dysmetria). Tremor during voluntary movements can also result from cerebellar damage.

THE BASAL GANGLIA. Both the cerebellum and the motor cortex send information to a set of structures deep within the brain that helps control involuntary components of movement (basal ganglia). The basal ganglia send output messages to the motor cortex, helping to initiate movements, regulate repetitive or patterned movements, and control muscle tone.

Circuits within the basal ganglia are complex. Within this structure, some groups of cells begin the action of other basal ganglia components, and some groups of cells block the action. These complicated feedback circuits are not entirely understood. Disruptions of these circuits are known to cause several distinct movement disorders. A portion of the basal ganglia, called the substantia nigra, sends electrical signals that block output from another structure, the subthalamic nucleus. The subthalamic nucleus sends signals to the globus pallidus, which in turn blocks the thalamic nuclei. Finally, the thalamic nuclei send signals to the motor cortex. The substantia nigra, then begins movement, and the globus pallidus blocks it.

This complicated circuit can be disrupted at several points. Loss of substantia nigra, cells increases blocking of the thalamic nuclei and prevents them from sending signals to the motor cortex. Degeneration of these nerve cells, as in PD, results in lower production of dopamine and fewer connections with other nerve cells and muscles, leading to a loss of movement (motor activity).

In contrast, cell loss in early HD decreases the blocking of signals from the thalamic nuclei, causing more cortex stimulation and stronger, but uncontrolled, movements.

Disruptions in other portions of the basal ganglia are thought to cause tics, tremors, dystonia, and a variety of other movement disorders, although the exact mechanisms are not well understood.

Some movement disorders, including HD, are caused by inherited genetic defects and inherited ataxias. Some diseases that cause sustained muscle contraction limited to a particular muscle group (focal dystonia) are inherited, but others are caused by trauma. The cause of most cases of PD is unknown, although genes have been identified for some familial forms.

ANTAGONISTIC MUSCLE PAIRS. This picture of movement, however, is too simple. One important refinement to it comes from considering the role of opposing, or antagonistic, muscle pairs. Contraction of the bicep muscle, located on the top of the upper arm, pulls on the forearm to flex the elbow and bend the arm. Contraction of the triceps, located on the opposite side, extends the elbow and straightens the arm. Within the spine, these muscles are normally wired so that willed (voluntary) contraction of one is automatically accompanied by blocking of the other. In other words, the command to contract the biceps provokes another command within the spine to prevent contraction of the triceps. In this way, these antagonist muscles are kept from resisting one another. Spinal cord or brain injury, can damage this control system and cause involuntary simultaneous contraction and spasticity, an increase in resistance to movement during motion.

While the peripheral mechanism, antagonistic muscle pairs, is certainly important, it is not the only one of concern with regard to movement disorders. Central pattern generators (CPGs) in the spinal cord are especially relevant because of their role in sensory processing. Filtration and processing of sensory input is accomplished locally, where the response of spinal pattern generator circuitry fits into continual movement, as necessary. Thus, although the brain receives much of the sensory input, the responses to spinal inputs are first the responsibility of the local spinal circuitry. Multi-segmental reflexes and anticipatory postural adjustments are as critical in the etiology of these syndromes.

Common conditions causing motor disorders

SPINAL CORD INJURY (SCI). Spinal cord injury (SCI) is very complex and can be very serious. An injury can affect the body in a multitude of ways depending on where the spinal cord (SC) is damaged. It is the largest nerve in the body and is composed of nerve fibers. These nerve fibers that manage the body's communication systems are responsible for its motor, sensory, and autonomic functions. They act as messenger between the brain and the rest of the body. The vertebral column—protective bone segments—surrounds the SC, perhaps because of its important in the nervous system. Approximately 18 inches (39 cm) long, the SC runs from the base of the brain, down the middle of the back, to the waist. Nerve fibers in the upper SC are upper motor neurons (UMNs). Spinal nerves branching off the SC that run up and down the neck and back are lower motor neurons (LMNs), and branch off between each vertebrae and go out to all parts of the body. The lower spinal nerve fibers continue down through the spinal canal to the sacram (tailbone) at the end of the SC.

Divided into four sections at the top of the spinal column is the cervical spine. It is composed of eight cervical nerves and seven cervical vertebrae. Further down is the thoracic sine, which includes the chest and twelve thoracic vertebrae. The lumbar spine is below that, and comprises five lumbar vertebrae. The bottom section is the sacral area, and there the bones fuse together into one bone.

When the SC is damaged by either a traumatic injury or from a disease, all nerves above the injury level still function normally. Those from the point of injury and below, however, are damaged, and messages between the brain and parts of the body that could once be sent are no longer are no longer possible. The patient must undergo physical examination by the doctor to earn the exact location of injury to the spinal cord. Frequently, the physician will use a "pin-prick" test," which evaluates the patient's level of feeling (sensory level). X rays are also frequently used to image the affected vertebrae. The patient's input is critical; he or she will be asked what parts of the body can be moved, and all major muscle groups will be tested (motor level) for strength. All of these tests are important, as they reveal what nerves and muscles are functioning. Each SCI is unique, and is defined by its type and level. Its level will be judged by the lowest level on the SC after which there is absence of feeling and/or movement (motor level).

Loss of feeling and/or movement in the head, neck, shoulder, arms, and/or upper chest is termed "tetraplegia," and is injury at level C1 to T1. The cervical spine is the highest part of the spinal cord and is designated by the letter "C." The thoracic spine is next to the highest, and is designated by the letter "T." T2 to S5 is paraplegia. The higher on the vertebral column , the closer the SCI is to the brain. Therefore, someone with a T-8 (thoracic spine; eight of 12 thoracic vertebrae) level injury would have more feeling and movement than someone with a C-5 (cervical spine; five of seven cervical vertebrae) level of injury.

STROKE. During a stroke, brain tissue is destroyed. This is cause by some malfunction of the brain's blood vessels . There are two major classifications of stroke: hemorrhagic and ischemic. The most common type of stroke is ischemic, caused by the same kind of vascular disease as heart attack. By "ischemic" it is meant that the blood flow to an area is insufficient; there is not enough oxygen to support the cells. The brain cells will cease to function if blood circulation is not restored quickly enough after a stroke. Cell death by lack of oxygen is termed "infarction." To be more specific, physicians often refer to this type of infarction as "cerebral." As of 2001, stroke is the third leading cause of disability and the fifth leading cause of death in the United States. Annually, 500,000 people suffer strokes; 150,000 die of them.

A hemorrhagic stroke happens with the rupture of a blood vessel. Bleeding occurs inside the skull . Usually, the cause is hypertension , or high blood pressure—but it can also be caused by trauma. An aneurysm (a sac formed by localized dilatation of the wall of an artery, a vein or the heart) may also cause a hemorrhagic stroke. Whatever the origin of the stroke, bleeding can rip through the tender connections within the brain, and ultimately compress brain cells until they die.

The extent of damage due to stroke depends on the severity of the stroke and where in the brain the blood supply was suspended. Each area of the brain is served by specific blood vessels; if a blood vessel in the area that controls muscle movements became blocked, those muscles will be weak, or paralyzed. The loss of function is greatest immediately after a stroke, but some usually some function is regained. Some brain cells do die, while some injured cells may recover. Bleeding on the brain, such as from a head injury or brain aneurysm, can also cause brain cell death from lack of oxygen. Symptoms may resemble those of a stroke. The best prevention for a stroke is for the patient to discuss risk factors with a physician.

MULTIPLE SCLEROSIS (MS). Multiple sclerosis (MS) is a demyelinating disease that is related to the inflammatory process. One feature of MS is multiple, separate, and harmful neurologic episodes caused by central nervous system (CNS) lesions. The result is multiple, clearly defined areas (plaque) of myelin (the protective sheath around nerves) in the brain's white matter SC known as perivenous distribution (i.e., not in the peripheral nervous system).

MS occurs early in the inflammatory phase, and disrupts the messages that are being transmitted within the body. The disease is called MS because the scar tissue (sclerosis) forms at various locations. Some of the diseased areas of the myelin may cause no obvious symptoms, while other areas may interfere with functions or sensations controlled by the brain or SC. For this reason, the symptoms and the severity of the disability varies greatly among persons with MS.

The cause of MS remains unknown, but many think that it may be an autoimmune disease. Normally, the immune system works by recognizing foreign invaders and producing its own cells to counteract or defend against attacks. In MS, the immune system is disrupted as the body incorrectly identifies itself as an invader and begins to attack its own cells. The body no longer recognizes myelin as its own and declares war on this nerve tissue. Further, linkage studies have noted significant genetic factors. A common first symptom is visual impairment, due to optic neuritis (inflammation of the optic nerve).

MUSCULAR DYSTOPHY (MD). The name "muscular dystrophy" (MD) encompasses a number of progressive hereditary diseases that makes muscles weaken and degenerate. Not a contagious disease, there are a multitude of variations. Each type has its own pattern of heredity, onset age, and speed with which muscle is lost. Alterations in specific genes causes different types of disease. There was no prevention or cure for MD as of 2001. However, because of research being done at this time, there is reason for hope for a cure.

HUNTINGTON'S CHOREA (HC). A genetically inherited disease, Huntington's chorea (HC) has neurological and psychotic characteristics. The forties or fifties are the usual ages of onset, but early and late onset are also possible. Either neurological or psychotic changes can mark the beginning of the disease. Symptoms of neurological changes may vary, but can begin with chorea—a series of movements that resemble dancing, with jerkiness and one part of the body moving to another. One might display clumsiness, jumpiness, and become fidgety. There may be movement in the face, particularly around the jaw, and walking may become difficult. It may be difficult to maintain posture. Paranoia, personality changes, and confusion may present, as well. It is also possible for dementia to occur.

Diagnosis of HC is dependent upon clinical symtomatology and MRI (magnetic brain imaging), as well as discovering family history of the disease. An MRI that reveals atrophy (shrinkage) of part of the basal ganglia, which is involved in movement and known as the caudate nucleus, is characteristic of HC.

CEREBRAL PALSY. In cerebral palsy (CP), abnormal development of or damage to motor areas in the brain disrupts the brain's ability to control movement and posture. The term CP is a term used to describe a group of chronic disorders impairing control of movement that appear in the first few years of life and generally do not worsen over time. Symptoms differ from person to person, and may change over time. Individuals with the disease may have difficulty with fine motor tasks (e.g., writing), and balance or walking. They may have involuntary movements. Cerebral palsy, which may be congenital (present at birth) or acquired after birth, results from brain injury that does not worsen over time. Possible causes of CP include developmental abnormalities of the brain, brain injury caused by low oxygen levels (asphyxia) or poor circulation, infection , and trauma to the fetus or newborn. Doctors encourage pregnant women to follow a program of regular prenatal care beginning early in pregnancy to help prevent CP.

DYSTONIAS. Dystonias are sustained muscle contractions that often cause twisting or repetitive movements and abnormal postures. Dystonias may be limited to one area (focal) or may affect the entire body (general). Focal dystonias may affect the neck (cervical dystonia or torticollis), the face (one-sided, or hemifacial spasm), contraction of the eyelid (blepharospasm), contraction of the mouth and jaw (oromandibular dystonia), simultaneous spasm of the chin and eyelid (Meige syndrome), the vocal cords (laryngeal dystonia), or the arms and legs (writer's and occupational cramps). Dystonia may be painful and incapacitating.

TREMORS. Uncontrollable (involuntary) shaking of body parts are known as tremors. Tremors may occur only when muscles are relaxed, during actions, or when holding active postures.

MYASTHENIA GRAVIS (MG). Myasthenia gravis (MG), a chronic autoimmune disease, is characterized by fluctuating degrees of weakness of the skeletal, or voluntary muscles. Muscle weakness of increasing severity is the key symptom of this disorder; it worsens with activity, and improves after periods of rest. It does not always include muscles that control facial expression, such as muscles of the eyes, talking, chewing, and swallowing, but can affect the muscles involved with breathing, the neck, and limb movements. A defect in the transmission of nerve impulses to muscles is responsible for MG. The symptoms of MG range in type and degree. It is not directly genetic, and it is not infectious. It can be controlled through medications that improve neuromuscular transmission, thereby improving muscle strength, or through medications that suppress the manufacture by the body of abnormal antibodies. Because of unpleasant, major side effects, these drugs must be used with caution and monitored carefully. Myasthenia gravis is caused by an autoimmune response attack on acetylcholine (neurotransmitter) receptors at muscular junctions.

PARKINSON'S DISEASE (PD). The possibility of developing Parkinson's disease , or parkinsonism, increases with age, with age of onset usually not less than 40 years of age. Approximately 500,000 people in the United States suffer from the disease, which affects both sexes equally. The cause of its most common form, PD (as well as related disorders) is not known—though genetic risk has been identified as a probable factor by the National Institutes of Health. Interestingly, the disorder is observed at the same rate in almost part of the globe, and is as common today as it was in late 1800s.

The two terms, Parkinson's disease (PD) and parkinsonism, are used interchangeably, as they both describe patients with the same symptoms. The four primary symptoms of PD are tremor or trembling, rigidity or stiffness of the limbs and trunk, bradykinesia (slowness of movement), and impaired balance and coordination.

There are a number of causes of parkinsonism, including degenerative neurologic disease, metabolic conditions, toxins, drugs, viral encephalitis (von Economo's disease), and related disorders result from the loss of dopamine, a chemical messenger responsible for transmitting signals within the brain. When certain nerve cells (neurons) that produce dopamine die or become impaired, dopamine is depleted. The result is nerve cells that fire out of control. Individuals with PD are then unable to direct or control their movements in a normal manner. The disease, which is usually not inherited, is both chronic and progressive, with subtle early symptoms and gradual progression.

Management of a movement disorder begins with determining its cause. Physical and occupational therapy may help to compensate for lost control and strength. Pharmacologic therapy can help to compensate for some imbalances of the basal ganglionic circuit. For instance, levodopa (L-dopa), or related compounds, can substitute for the loss of dopamine-producing cells in PD. Conversely, blocking normal dopamine action may be used to treat some hyperkinetic disorders, including tics. Oral medications can also help to reduce overall muscle tone. Local injections of botulinum toxin (BOTOX) can selectively weaken overactive muscles in dystonia and spasticity. Destruction of peripheral nerves through injection of phenol can reduce spasticity. It should be noted, however, that all of these treatments have some side effects.

Other movement disorders

Tic disorders are very quick, involuntary, rapid, non-rhythmic, and short-lived movements or sounds; tics can sometimes be controlled briefly. Tics are usually repeated movements. They commonly involve the motor systems and often involve the facial muscles, such as the eyelids or eyebrows. The most well-known tic disorder is Tourette syndrome. Tourette syndrome (TS) is an abnormal condition that causes uncontrollable facial grimaces and tics, and arm and shoulder movements. Tourette syndrome is best known, perhaps, for uncontrollable vocal tics that include grunts, shouts, and use of obscene language (coprolalia). It is also known as Gilles de la Tourette syndrome. Tics are more common among males than females. As with Tourette syndrome, tics may be associated with head injury, stroke, carbon monoxide poisoning , and mental retardation.

Myoclonus is a sudden, shock-like muscle contraction. Myoclonic jerks may occur singly or repetitively. Unlike tics, myoclonus cannot be controlled even briefly.

Postural instability is the loss of ability to maintain upright posture, caused by slow or absent righting reflexes (those that help to maintain balance).

Spasticity is a condition in which certain muscles are continuously contracted, causing stiffness or tightness of the muscles.

Flaccid paralysis is the loss of muscle tone of the paralyzed part and an accompanying absence of reflexes.

Diagnosis

A complete and thorough clinical examination should be performed. Diagnosis of movement disorders requires a careful medical history and a thorough physical and neurological examination. A thorough orthopedic exam may be important because patients with increased muscle tone may develop curvature of the spine (scoliosis ), hip dislocation, and tendon shortening. During the neurologic exam, the doctor will observe the individual's posture, tone, symmetry, and reflexes.

Certain symptoms may indicate a movement disorder disease. Doctors will pay special attention to the rate of development of children with CP, particularly with

KEY TERMS

Botulinum toxin (botox) —Any of a group of potent bacterial toxins or poisons produced by different strains of the bacterium Clostridium botulinum. The toxins cause muscle paralysis, and thus force the relaxation of a muscle in spasm.

Cerebral palsy (CJP) —A movement disorder caused by a permanent brain defect or an injury present at birth, or shortly after. It is frequently associated with premature birth. Cerebral palsy is not progressive.

Computed tomography (CT) —An imaging technique in which cross-sectional x rays of the body are compiled to create a three-dimensional image of the body's internal structures.

Encephalopathy —An abnormality in the structure or function of tissues of the brain.

Fetal tissue transplantation (FTT) —A method of treating PD and other neurological diseases by grafting brain cells from human fetuses onto the basal ganglia. Human adults cannot grow new brain cells, but developing fetuses can. Grafting fetal tissue stimulates the growth of new brain cells in affected adult brains.

Huntington's chorea (HC) disease (HD) —A rare, genetically inherited condition with both neurological and psychiatric manifestations that begins with either type of change. The chorea is progressive, and presents as jerky muscle movements and mental deterioration that ends in dementia. The symptoms of HC usually appear in patients in their 40s or 50s; however, early- or late-onset is possible. Huntington's chorea may also cause clumsiness, jumpiness, and fidgetiness, and facial movements—particularly around the jaw—may occur. It may become difficult to walk, and can affect posture. Paranoia, confusion, or personality changes may noted. A significant dementia develops as the disease progresses. There is no cure or effective treatment for the condition.

Levodopa (L-dopa) —A substance used in the treatment of PD. Levodopa can cross the blood-brain barrier that protects the brain. Once in the brain, it is converted to dopamine, and thus can replace the dopamine lost in PD.

Magnetic resonance imaging (MRI) —An imaging technique that uses a large circular magnet and radio waves to generate signals from atoms in the body. These signals are used to construct images of internal structures.

Paraplegia —Paralysis of the lower half of the body involving both legs and usually due to disease or injury to the spinal cord.

Parkinson's disease (PD) —A slowly progressive disease that destroys nerve cells in the basal ganglia and thus causes loss of dopamine, a chemical that aids in transmission of nerve signals (neurotransmitter). Parkinsonism is characterized by shaking in resting muscles, a stooping posture, slurred speech, muscular stiffness, and weakness.

Positron emission tomography (PET) —A diagnostic technique in which computer-assisted x rays are used to track a radioactive substance inside a patient's body. Biochemical activity of the brain can be studied using PET.

Progressive supranuclear palsy —A rare disease that shows some of the same features of PD, but differs in several ways. They usually do not develop tremors, but they have rigidity, bradykniesia (slow movements), and falls. The disorder gradually destroys nerve cells in the parts of the brain that control eye movements, breathing, and muscle coordination. The loss of nerve cells causes palsy (paralysis) that slowly gets worse as the disease progresses. The palsy affects the ability to move the eyes vertically (up and down) at first. Their eye movements then become even more restrictive (ophthalmoplegia). The ability to relax the muscles is lost, as is control over balance.

Tourette syndrome (TS) —An abnormal condition that causes uncontrollable facial grimaces and tics, and arm and shoulder movements. Tourette syndrome is best known, perhaps, for uncontrollable vocal tics that include grunts, shouts, and use of obscene language (coprolalia). Also known as Gilles de la Tourette syndrome.

Wilson's disease (WD) —An inborn defect of copper metabolism in which free copper may be deposited in a variety of areas of the body. Deposits in the brain can cause tremor and other symptoms of PD.

regard to head size and head growth, since abnormalities in these areas may point to a brain problem. Eye problems, such as blurred or double vision , red-green color distortion, or blindness in one eye, may occur. When combined with muscle weakness in extremities and paresthesias (transitory abnormal sensory feeling such as numbness or prickling), MS may be suspected.

Diagnostic tests should be conducted. These include brain imaging studies, such as computed tomography (CT) scan, positron emission tomography (PET ), or magnetic resonance imaging (MRI) scans. Routine blood and urine analyses are performed. A lumbar puncture (spinal tap) may be necessary. Video recording of the abnormal movement is often used to analyze movement patterns and to track progress of the disorder and its management. Genetic testing is available for some forms of movement disorders. If MS is suspected, physicians may study the patient's cerebrospinal fluid and the antibody, immunoglobulin G.

Treatment

Ongoing clinical studies indicate that estrogen may have beneficial effects on controlling movement disorders, such as PD, chorea, dystonia, tics, and myoclonus.

Deep brain stimulation, which inactivates the thalamus or globus pallidus through electrical shocks, may be useful to ease tremor of the arm in individuals with ET and tremor due to MS. In PD, the procedure may improve arm speed and dexterity, reduce tremor, and block the involuntary movements (dyskinesia) associated with the medications used to treat the disease.

Surgical destruction, or inactivation of basal ganglionic circuits, has proven effective for PD, and as of 2001 is being tested for other movement disorders. Transplantation of fetal cells into the basal ganglia has produced mixed results in PD.

Health care team roles

Nursing and allied health professionals play a key role in educating individuals with movement disorders about their conditions and appropriate treatment options. Physical, speech, and occupational therapy are often essential to the rehabilitation of individuals with movement disorders. Psychological counseling may be helpful to the individual and to family members and close friends.

The patient who has had a stroke may be treated by doctors, therapists, and nurses who work to keep the patient's muscles strong, prevent muscular contractions, avoid the bedsores that can result from being in one position for too long, and teach the patient to walk and talk again. With SCI, expert nursing care is important to prevent complications from weakness and paralysis, including bedsores. Physical and occupational therapy help to preserve muscle function and teach techniques to help the patient function despite lost functionality.

Prognosis

The prognosis for a patient with a movement disorder depends on the nature of the disorder. The age of onset has major implications in prognosis.

Prevention

Prevention depends on the specific disorder. With some diseases, certain preventive strategies can be particularly helpful. In the case of MS and stroke, for example, smoking cessation would drastically reduce the number of cases. Longtime smokers may face a much higher risk of both MS and stroke, according to researchers at Harvard University. In the case of MS, women who smoked at least one pack per day for at least 25 years had a greater chance of developing the disorder than nonsmokers.

A number of permanent cases of parkinsonism that presented in the early 1980s were caused by a contaminant found in some illicit street drugs. For the most part, cases of the disease induced by legal, prescribed drugs were only temporary: when the drug was stopped, the symptoms stopped, too. Permanent parkinsonism had only been the result of the contaminant found in the street drug.

In 1996, clinicians at the University of Hawaii found that patients with high blood levels of uric acid, a natural antioxidant, have a lower chance of developing Parkinsonism and gout (acute inflammatory arthritis) than people with lower levels. The study concluded that people with high levels of the antioxidant, uric acid, may be more resistant to developing parkinsonism. This was also shown in a pilot student in 1991, when investigator Stanley Fahn of Columbia University found that parkinsonism patients who were administered large doses of oral vitamin C and synthetic vitamin E supplements (3000 mg and 3200 iu daily, respectively) delayed the progression of the disease. He concluded that it was likely that it was the vitamin C alone, or in combination with vitamin E that actively worked.

• Parkinsonism (PD). Deprenyl (selegiline), administered early in the onset of the disorder, can slow progression of the disease. Antioxidants such as vitamin E and selenium may be of some benefit, as well.
• Spinal cord injury (SCI). Attention to following safety precautions may help to reduce the risk of SCI. The most frequent causes of SCI are motor vehicle crashes, falls , violence, and sports and recreation, especially diving. Proper protective equipment should be used if an injury is possible, and appropriate safety measures should be practiced. Depth of water should be checked and obstructions should be noted before diving. When in an automobile, seat belts should always be used.
• Stroke. Major risk factors include high blood pressure , high cholesterol level, smoking, and diabetes. Drugs, such as aspirin (half of an adult tablet or one children's tablet daily), can be taken to reduce the tendency of blood platelets (responsible for the clotting of blood) to form dangerous blood clots, a major cause of stroke. When stronger drugs are needed, a doctor may prescribe anticoagulants, such as heparin or warfarin (Coumadin). Research in the year 2001 suggests that paralysis and other symptoms may be prevented or reversed if certain drugs that break up clots are given within three hours of the onset of a stroke.

Resources

BOOKS

Adler, Charles H. and J. Eric Ahlskog, eds. Parkinson's Disease and Movement Disorders: Diagnosis and Treatment Guidelines for the Practicing Physician. Totowa, N.J.: Humana Press, 2000.

Cicala MD, Roger S. Brain Disorders Sourcebook. Lincolnwood, IL: Lowell House; NTC/Contemporary Publishing Group, Inc., 1999.

Floyd, R.T. and Clem W. Thompton. Manual of Structural Kinesiology. Dubuque, IA: McGraw-Hill, 2001.

Jankovic, Joseph and Eduardo Tolosa, ed. Parkinson's Disease and Movement Disorders. Baltimore: Williams & Wilkins, 1998.

Sawle, Guy, ed. Movement Disorders in Clinical Practice. Oxford: Isis Medical Media, 1999.

Vander, Arthur, James Sherman, and Dorothy Luciano. Human Physiology: The Mechanisms of Body Function. Boston: McGraw-Hill, 2001.

ORGANIZATIONS

American Association of Neuroscience Nurses, 4700 W. Lake Avenue, Glenview, IL 60025. (888) 557-2266. <http://www.aann.org>.

American Spinal Injury Association. 345 E. Superior Street, Chicago, IL 60611. (312)238-1242. <http:/www.asiaspinalinjury.org>.

Muscular Dystophy Association, 3300 East Sunrise Drive, Tucson, AZ 85718-3208, (520) 529-2000 or (800) 572-1717. <http://www.mdausa.org/>.

Myasthenia Gravis Foundation of America, Inc., 5841 Cedar Lake Road, Suite 204, Minneapolis, MN 55416, (952) 545-9438 or (800)541-5454. <http://www.myasthenia.org>.

National Institute of Neurological Disorders and Stroke. P.O. Box 5801, Bethesda, MD 20824, (800) 352-9424. <http://www.ninds.nih.gov>.

National Spinal Cord Injury Association, The Zalco Building, 8701 Georgia Avenue, Suite 500, 8701 Georgia Avenue, Silver Springs, MD 20910, (800) 962-9629 or (301) 588-6959. <http://www.spinalcord.org>.

National Spinal Cord Injury Statistical Center, UAB-Spain Rehabilitation Center, Rm 544, 619 19th Street South, SRC 544, Birmingham, AL 35249-7330, (205) 934-5359.

Paralyzed Veterans of America. 801 18th Street NW, Washington, DC 20006, (800) 424-8288 or [email protected], <http://www.pva.org>.

The Movement Disorder Society. 611 East Wells Street, Milwaukee, WI 53202, (414) 276-2145. <http://www.movementdisorders.org>.

WE MOVE. 204 West 84th Street, New York, NY 10024. (800) 437-MOV2 or (212) 875-8389. <http://www.wemove.org>.

OTHER

"Smoking Risk Factor for Multiple Sclerosis: Study." National Library of Medicine. National Institutes of Health. Medline Plus. <http://www.nlm.nih.gov/medlineplus/news/fullstory_2440.html>.

"Spinal Cord Injury Information Network: Understanding Spinal Cord Injury and Functional Goals." University of Alabama at Birmingham. <http://www.spinalcord.uab.edu>.

Randi B. Jenkins