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Motor neurone disease

 
Neurological Disorder:

Motor neuron diseases

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Definition

Motor neuron diseases are a group of progressive disorders involving the nerve cells responsible for carrying impulses that instruct the muscles in the upper and lower body to move. Motor neuron diseases are varied and destructive in their effect. They commonly have distinctive differences in their origin and causation, but a similar result in their outcome for the patient: severe muscle weakness. Amyotrophic lateral sclerosis (ALS), spinal muscular atrophy, poliomyelitis, and primary lateral sclerosis are all examples of motor neuron diseases.

Description

A motor neuron is one of the largest cells in the body. It has a large cell body with many extensions reaching out in 360° from the cell body (soma). These extensions are called dendrites and are chemically able to receive instructions from adjacent neurons. These instructions are received in the form of an impulse stimulation of a particular protein channel on the dendrite by a neurotransmitter termed acetycholine (ACh). Extending from the soma of the motor neuron is a long portion of the cell called the axon. When conditions are favorable, an electrical signal passes down the axon to a region of the cell identified as the axon terminals. These terminals also branch in many directions and have, at their tips, a region called the synaptic end bulb. This region releases ACh that crosses a small gap until it reaches a protein on another dendrite.

When motor neurons line up in a tract, they allow an electrical signal to spread from the brain to the intended muscle. There are a tremendous number of nerve tracts that extend to all the muscles of the body that are responsible for contraction and relaxation of all types of muscles, including smooth and cardiac, as well as skeletal muscle. When the motor neuron is affected or damaged and it cannot perform at peak performance, the muscles of the body are affected. Often, a disorder of the motor neurons results in progressive muscle atrophy (shrinking and wasting) of some, if not all, the muscles of the body. Muscle twitching (fasciculation) is common among these disorders. Motor neuron diseases are difficult to treat, debilitating to movement and, in some cases, fatal.

Amyotrophic lateral sclerosis (ALS) is a disorder that generally involves either the lower or upper motor systems of the body. In advanced stages, both regions of the body are affected. This disease is commonly known as Lou Gehrig's disease after the famous baseball player who died from the condition. It is caused by sclerosis (a hardening of the surrounding fibrous tissues) in the corticospinal tracts. Associated with the sclerosis is a loss of the tissue of the anterior horns (gray matter) in the spinal cord, including the brainstem. Lou Gehrig's disease is characterized by a wasting of the muscles that, in turn, produces weakness. The bulbar, or facial/mouth muscles can initially become involved, which may lead to slurring of speech and drooling. The significance of this involvement is that, with rapid progression, the patient may not be able to swallow properly. This may lead to the risk of choking and other difficulties with obtaining nutrition and proper respiration. Death from complications of ALS is common within five years.

Spinal muscular atrophies (SMAs) are a wide group of genetic disorders characterized by primary degeneration of the anterior horn cells of the spinal cord, resulting in progressive muscle weakness. Spinal muscular atrophies affect only lower motor neurons. In babies and children, many SMAs are rapidly progressive with paralysis of the legs, trunk, and eventually, the respiratory muscles. In teenagers and adults, SMAs are usually slowly progressive. Kennedy's disease, an X-linked (carried by women and passed on to male offspring) SMA, features similar wasting of facial muscles as seen in ALS, with characteristic difficulty speaking and swallowing.

Primary lateral sclerosis (PLS) is a rare motor neuron disease that resembles ALS. Primary lateral sclerosis often begins after age 50, and results in slowly progressive weakness and stiffness in the leg muscles, clumsiness, and difficulty maintaining balance. Symptoms worsen over a period of years. Muscle spasms in the legs may also occur, but in PLS, there is no evidence of the degeneration of spinal motor neurons or muscle wasting (amyotrophy) that occurs in ALS.

Unlike most motor neuron diseases, poliomyelitis results from infection with a virus. Contamination occurs through fecal or oral exposure. Once inside the body, the virus uses the cells of the gastrointestinal tract to enter the bloodstream and move throughout the body. Eventually, the poliovirus invades the nerve cells of the spinal cord and kills the motor neurons. When the motor neurons are destroyed, the muscles they connect to become damaged and weaken. The result is varying degrees of paralysis, including difficulty swallowing, walking, breathing, and control of speech.

Demographics

Motor neuron diseases are uncommon, as about one person in 50,000 is diagnosed with a motor neuron disease in the United States each year. In total, about 5,500 people in the United States each year receive a diagnosis of a motor neuron disease.

About 20,000 Americans are living with ALS and nearly 4,500 new cases are reported annually. The peak age for onset is around 55 years of age, but younger patients have been observed. Spinal muscular atrophies and primary lateral sclerosis are rare diseases.

The occurrence of poliomyelitis is seen in records of epidemics that were intricately documented in the last 100 years. A description of an epidemic in recent times in the United States discussed a low of 4,197 cases in the early 1940s to a high of 42,033 in 1949. By 1952, the number of case had reached over 58,000. In 1955, a vaccine was developed that used weakened forms of the virus. This vaccine and the subsequent Sabin vaccine nearly wiped out polio in the world. The Americas were declared free of polio in the 1990s. In 2002, there were less than 500 cases worldwide, and in 2003, that number decreased to less than 100 cases. It is expected that by the end of the year 2005, the disease will be eradicated. Although new cases have begun to appear in regions of Africa and India, the World Health Organization (WHO) is keeping track of the outbreaks, and scientists are hopeful that poliomyelitis will soon disappear from the list of motor neuron diseases.

Causes and symptoms

Causes of many motor neuron diseases are unknown, and others have varying causes according to the specific motor neuron disease. Most cases of ALS occur sporadically for an unknown reason, however, up to 10% of ALS cases are inherited. Most spinal muscular atrophies are inherited. A virus causes poliomyelitis. Additionally, environmental factors and toxins are under study as causes or triggers for motor neuron diseases.

Muscle weakness is the symptom common to all motor neuron diseases. Muscles of the legs are most often affected, leading to clumsiness, unstable gait, or lower limb paralysis. Muscle cramps and fasciculations (twitching) occur with most motor neuron diseases. Facial muscles may also be affected, leading to difficulty with speech (dysarthria). Later in the course of some motor neuron diseases, the muscles involved with swallowing and breathing may be impaired (dysphagia).

Diagnosis

Diagnosis of motor neuron disease is often based upon symptoms and exclusion of other neurological diseases. Nerve conduction studies can help distinguish some forms of peripheral neuropathy from motor neuron disease. Electromyelogram (EMG), a test measuring the electrical activity in muscles, can support the diagnosis of ALS and some other motor neuron diseases. Although computed tomography (CT) scans and magnetic resonance imaging (MRI) scans are often normal in persons with motor neuron disease, they may help exclude spinal malformations or tumors that could be responsible for similar symptoms. A muscle biopsy can exclude myopathies. Diagnosis of primary lateral sclerosis is especially difficult and often delayed, as it is frequently misdiagnosed as ALS. Polio may be diagnosed by recovering the virus from a stool or throat culture, examining antibodies in the blood or, rarely, by spinal fluid analysis. Finally, molecular genetic studies can aid in the diagnosis of spinal muscular trophies and the small percentage of inherited ALS cases.

Treatment team

Caring for a person with a motor neuron disease requires a network of health professionals, community resources, and friends or family members. A neurologist usually makes the diagnosis, and the neurologist and primary physician coordinate ongoing treatment and symptom relief. Physical, occupational, and respiratory therapists provide specialized care, as do nurses. Social service and mental health consultants organize support services.

Treatment

There are few specific treatments for motor neuron diseases, and efforts focus on reducing the symptoms of muscle spasm and pain while maintaining the highest practical level of overall health. Riluzole, the first drug approved by the U.S. Food and Drug Administration for the treatment of ALS, has extended the life of ALS patients by several months and also extended the time a person with ALS can effectively use his or her own muscles to breathe.

Other medications used to treat persons with motor neuron disease are designed to relieve symptoms and improve the quality of life for patients. These include medicines to help with depression, excess saliva production, sleep disturbances, and constipation.

Recovery and rehabilitation

Recovery from motor neuron diseases depends on the type of disease and the amount of muscle degeneration present. In diseases such as ALS, the emphasis is placed upon maintaining mobility and function for as long as possible, rather than recovery. With all motor neuron diseases, physical therapy can teach exercises to help with range of motion and prevent contractures (stiff muscles at the joints). Occupational therapy provides assistive devices for mobility such as wheelchairs, positioning devices, braces, and other orthotics for performing daily activities such as reaching and dressing. Respiratory therapists and speech therapists help prevent pneumonia by maintaining lung function and promoting safe eating strategies. Speech therapists also help with alternate forms of communication if facial muscles are involved.

Recovery from polio may be complete or only partial, depending on the degree of lower motor neuron damage. Years or decades after recovering from polio, persons may again experience muscle weakness and pain. This is known as postpolio syndrome. Vigorous exercise has been shown to cause additional weakness in postpolio syndrome, and physicians recommend energy conservation and lifestyle changes for these patients.

Clinical trials

The National Institutes of Health (NIH) has more than 20 clinical trials scheduled for 2004–05 for the study of motor neuron diseases, including one trial designed to evaluate a new drug, Minocycline, in the treatment of ALS. Details and up-to-date information about patient recruiting can be found at the NIH Website for clinical trails at .

Prognosis

The prognosis of persons with motor neuron diseases depends on the type of the disease and the amount and progression of muscle degeneration. Most persons with ALS die from complications of respiratory failure within five years of developing symptoms. About one out of 10 persons with ALS live a decade or longer with the disease. The prognosis for a person with spinal muscular atrophy varies greatly, according to the severity of the disease. Some forms result in immobility and death within a few years, while others impede movement, but do not affect a normal lifespan.

Special concerns

It is important to remember that even in the most severe motor neuron diseases, a person's personality, intelligence, reasoning ability, or memory are not impaired. The person with motor neuron disease also retains the senses of sight, smell, hearing, taste, and in the unaffected areas, touch.

Resources

BOOKS

Kunci, Ralph W. Motor Neuron Disease. Philadelphia: W.B. Saunders, 2002.

Oliver, David. Motor Neuron Disease: A Family Affair. London: Sheldon Press, 1995.

Silver, Julie. Postpolio Syndrome. Philadelphia: Hanley & Belfus, 2003.

Wade, Mary Dodson. ALS—Lou Gehrig's Disease. Berkeley Heights, NJ: Enslow Publishers, 2001.

OTHER

"NINDS Motor Neuron Diseases Information Page." National Institute of Neurological Disorders and Stroke. May 15, 2004 (June 1, 2004). http://www.ninds.nih.gov/health_and_medical/disorders/motor_neuron_diseases.htm.

ORGANIZATIONS

ALS Association (ALSA). 27001 Agoura Road, Suite 150, Calabasas Hills, CA 91301-5104. (818) 880-9007 or (800) 782-4747; Fax: (818) 880-9006. info@alsanational.org. http://www.alsa.org.

Families of SMA. PO Box 196, Libertyville, IL 60048-0196. (800) 886-1762; Fax: (847) 367-7623. sma@fsma.org. http://www.fsma.org.

Primary Lateral Sclerosis Newsletter. 101 Pinta Court, Los Gatos, CA 95032. (408) 356-8227; Fax: (408) 356-8227. 73112.611@compuserve.com.


Brook Ellen Hall, PhD


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Dental Dictionary: motor neuron disease
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Home > Library > Health > Dental Dictionary

n

A progressive disease that tends to affect middleage men with degeneration of anterior horn cells, motor cranial nerve nuclei, and pyramidal tracts. Amyotrophic lateral sclerosis is a motor neuron disease.

Medical Dictionary: motor neuron disease
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Home > Library > Health > Medical Dictionary

n.

Any of various diseases of motor neurons, such as progressive muscular atrophy, amyotrophic lateral sclerosis, progressive bulbar paralysis, and primary lateral sclerosis.

Wikipedia: Motor neurone disease
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Contents
Motor neurone disease
Classification and external resources

spinal diagram
ICD-10 G12.2
ICD-9 335.2
DiseasesDB 8358
MeSH D016472

The motor neurone diseases (or motor neuron diseases) (MND) are a group of neurological disorders that selectively affect motor neurones,[1] the cells that control voluntary muscle activity including speaking, walking, breathing, swallowing and general movement of the body.

Terminology

In this article, MND refers to a group of diseases that affect motor neurones. In the United States, MND is more commonly called Amyotrophic lateral sclerosis (ALS), or Lou Gehrig's disease, after the baseball player.[1] In France the disease is sometimes known as Maladie de Charcot (Charcot's disease), although it may also be referred to by the direct translation of ALS, Sclerose Laterale Amyotrophique (SLA). To avoid confusion, the annual scientific research conference dedicated to the study of MND is called the International ALS/MND Symposium.

History

Although other 19th century neurologists previously described the disease, a French neurologist, Jean-Martin Charcot, first suggested grouping together disparate conditions that affect the lateral horn of the spinal cord in 1869.

Classification

Forms of motor neurone disease include:

Spinal muscular atrophy (SMA) is classified under MND by MeSH, but not by ICD-10.

Causes

About 90% of cases of MND are "sporadic", meaning that the patient has no family history of ALS and the case appears to have occurred with no known cause. Genetic factors are suspected to be important in determining an individual's susceptibility to disease, and there is some weak evidence to suggest that onset can be "triggered" by as yet unknown environmental factors (see 'Epidemiology' below).

Approximately 10% of cases are "familial MND", defined either by a family history of MND or by testing positive for a known genetic mutation associated with the disease. The following genes are known to be linked to ALS: Cu/Zn superoxide dismutase SOD1, ALS2, NEFH (a small number of cases), senataxin (SETX) and vesicle associated protein B (VAPB).

Of these, SOD1 mutations account for some 20% of familial MND cases. The SOD1 gene codes for the enzyme superoxide dismutase, a free radical scavenger that reduces the oxidative stress of cells throughout the body. So far over 100 different mutations in the SOD1 gene have been found, all of which cause some form of ALS(ALSOD database). In North America, the most commonly occurring mutation is known as A4V and occurs in up to 50% of SOD1 cases. In people of Scandinavian extraction there is a relatively benign mutation called D90A which is associated with a slow progression. In Japan, the H46R mutation is most common. G93A, the mutation used to generate the first animal model (and by far the most widely studied), is present only in a few families worldwide. Future research is concentrating on identifying new genetic mutations and the clinical syndrome associated with them. Familial MND may also confer a higher risk of developing cognitive changes such as frontotemporal dementia or executive dysfunction (see 'extra-motor change in MND' below).

It is thought that SOD1 mutations confer a toxic gain, rather than a loss, of function to the enzyme. SOD1 mutations may increase the propensity for the enzyme to form protein aggregates which are toxic to nerve cells.

Pathophysiology

Skeletal muscles are innervated by a group of neurones (lower motor neurones) located in the ventral horns of the spinal cord which project out the ventral roots to the muscle cells. These nerve cells are themselves innervated by the corticospinal tract or upper motor neurones that project from the motor cortex of the brain. On macroscopic pathology, there is a degeneration of the ventral horns of the spinal cord, as well as atrophy of the ventral roots. In the brain, atrophy may be present in the frontal and temporal lobes. On microscopic examination, neurones may show spongiosis, the presence of astrocytes, and a number of inclusions including characteristic "skein-like" inclusions, bunina bodies, and vacuolisation.

The availability of mouse models has led to extensive research into the causes of SOD1-mutant linked familial ALS. The most commonly used mouse model is G93A [3], although many others have since been generated. At the gross physiological level, the mouse models faithfully recapitulate the features of human ALS (motorneuron death, muscle atrophy, respiratory failure).

Although there is no consensus as to the exact mechanism by which mutated SOD1 causes the disease (in either mice or patients), studies based largely on mouse models suggest a role for excitotoxicity and more controversially, oxidative stress, presumably secondary to mitochondrial dysfunction. Death by apoptosis has also been suggested.

Signs and symptoms

Symptoms usually present themselves between the ages of 50-70, and include progressive weakness, muscle wasting, and muscle fasciculations, spasticity or stiffness in the arms and legs, and overactive tendon reflexes. Patients may present with symptoms as diverse as a dragging foot, unilateral muscle wasting in the hands, or slurred speech.

Neurological examination presents specific signs associated with upper and lower motor neurone degeneration. Signs of upper motor neurone damage include spasticity, brisk reflexes and the Babinski sign. Signs of lower motor neurone damage include weakness and muscle atrophy.

Note that every muscle group in the body requires both upper and lower motor neurones to function. The signs described above can occur in any muscle group, including the arms, legs, torso, and bulbar region.

The symptoms described above may resemble a number of other rare diseases, known as "MND Mimic Disorders". These include, but are not limited to, multifocal motor neuropathy, Kennedy's disease, hereditary spastic paraplegia, spinal muscular atrophy and monomelic amyotrophy. A small subset of familial MND cases occur in children, such as "juvenile ALS", Madras syndrome, and individuals who have inherited the ALS2 gene. However, these are not typically referred to as MND, but by their specific names.

Diagnosis

The diagnosis of MND is a clinical one, established by a neurologist on the basis of history and neurological examination. There is no diagnostic test for MND. Investigations such as blood tests, electromyography (EMG), magnetic resonance imaging (MRI), and sometimes genetic testing are useful to rule out other disorders that may mimic MND. However, the diagnosis of MND remains a clinical one. Having excluded other diseases, a relatively rapid progression of symptoms is a strong diagnostic factor. Although an individual's progression may sometimes "plateau", it will not improve.

A set of diagnostic criteria called the El Escorial criteria[4][5] have been defined by the World Federation of Neurologists for use in research, particularly as inclusion/exclusion criteria for clinical trials. Owing to a lack of clinical diagnostic criteria, some neurologists use the El Escorial criteria during the diagnostic process, although strictly speaking this is functionality creep, and some have questioned the appropriateness of the criteria in a clinical setting.[6]

Type UMN degeneration LMN degeneration
ALS yes yes
PLS yes no
PMA no yes
Progressive bulbar palsy no yes - bulbar region
Pseudobulbar palsy yes - bulbar region no

The "bulbar region" in the table above refers to the mouth, face, and throat.

It is possible that Transcranial magnetic stimulation can be used to diagnose MND.[7]

Treatment

Currently there is no cure for ALS. The only drug that affects the course of the disease is riluzole. The drug functions by blocking the effects of the neurotransmitter glutamate, and is thought to extend the lifespan of an ALS patient by only a few months.

The lack of effective medications to slow the progression of ALS does not mean that patients with ALS cannot be medically cared for. Instead, treatment of patients with ALS focuses on the relief of symptoms associated with the disease. This involves a variety of health professionals including neurologists, speech-language pathologists, physical therapists, occupational therapists, dieticians, respiratory therapists, social workers, palliative care specialists, specialist nurses and psychologists.

Prognosis

Most cases of MND progress quite quickly, with noticeable decline occurring over the course of months. Although symptoms may present in one region, they will typically spread. If restricted to one side of the body they are more likely to progress to the same region on the other side of the body before progressing to a new region. After several years, most patients require help to carry out activities of daily living such as self care, feeding, and transportation.

MND is typically fatal within 2–5 years. Around 50% die within 14 months of diagnosis. The remaining 50% will not necessarily die within the next 14 months as the distribution is significantly skewed. As a rough estimate, 1 in 5 patients survive for 5 years, and 1 in 10 patients survive 10 years.[citation needed] Professor Stephen Hawking is a well-known example of a person with MND, and has lived for more than 40 years with the disease.

Mortality normally results when control of the diaphragm is impaired and the ability to breathe is lost. One exception is PLS, which may last for upwards of 25 years. Given the typical age of onset, this effectively leaves most PLS patients with a normal life span. PLS can progress to ALS, decades later.

Complications

Emotional lability

Main article: labile affect

Around a third of all MND patients experience labile affect, also known as emotional lability, pseudobulbar affect, or pathological laughter and crying. Patients with pseudobulbar palsy are particularly likely to be affected, as are patients with PLS.

Extra-motor change

Cognitive change occurs in between 33–50% of patients. A small proportion exhibit a form of frontotemporal dementia characterised by behavioural abnormalities such as disinhibition, apathy, and personality changes. A small proportion of patients may also suffer from an aphasia, which causes difficulty in naming specific objects. A larger proportion (up to 50%) suffer from a milder version of cognitive change which primarily affects what is known as executive function. Briefly, this is the ability of an individual to initiate, inhibit, sustain, and switch attention and is involved in the organisation of complex tasks down to smaller components. Often patients with such changes find themselves unable to do the family finances or drive a car. Depression is surprisingly rare in MND (around 5–20%) relative to the frequency with which it is found in other, less severe, neurological disorders e.g. ~50% in multiple sclerosis and Parkinson's disease, ~20% in Epilepsy. Depression does not necessarily increase as the symptoms progress, and in fact many patients report being happy with their quality of life despite profound disability. This may reflect the use of coping strategies such as reevaluating what is important in life.

Although traditionally thought only to affect the motor system, sensory abnormalities are not necessarily absent, with some patients finding altered sensation to touch and heat, found in around 10% of patients. Patients with a predominantly upper motor neurone syndrome, and particularly PLS, often report an enhanced startle reflex to loud noises.

Neuroimaging and neuropathology has demonstrated extra-motor changes in the frontal lobes including the inferior frontal gyrus, superior frontal gyrus, anterior cingulate cortex, and superior temporal gyrus. The degree of pathology in these areas has been directly related to the degree of cognitive change experienced by the patient, if any. Patients with MND and dementia have been shown to exhibit marked frontotemporal lobe atrophy as revealed by MRI or SPECT neuroimaging.

Epidemiology

The incidence of MND is approximately 1–5 out of 100,000 people. Men have a slightly higher incidence rate than women. Approximately 5,600 cases are diagnosed in the U.S. every year. By far the greatest risk factor is age, with symptoms typically presenting between the ages of 50-70. Cases under the age of 50 years are called "young onset MND", whilst incidence rates appear to tail off after the age of 85.

Tentative environmental risk factors identified so far include: exposure to severe electrical shock leading to coma, having served in the first Gulf War, and playing Association football (soccer). However, these findings have not been firmly identified and more research is needed.

There are three "hot spots" of MND in the world. One is in the Kii peninsula of Japan, one amongst a tribal population in Papua New Guinea. Chamorro inhabitants from the island of Guam in the Pacific Ocean have an increased risk of developing a form of MND known as Guamanian ALS-PD-dementia complex or "lytico bodig", although the incidence rate has declined over the last 50 years and the average age of onset has increased.[8] Putative theories involve neurotoxins in the traditional diet including cycad nut flour and bats that have eaten cycad nuts.[9][10]

Research efforts

The search for a drug that will slow MND progression is under way. Agents that are currently in trials include ceftriaxone, arimoclomol, IGF-1, lithium [11] and coenzyme Q10 to name but a few.

Etymology

Terminology around the motor neurone diseases can be confusing; in the UK "motor neurone disease" refers to both ALS specifically (the most common form of disease) and to the broader spectrum of motor neurone diseases including progressive muscular atrophy, primary lateral sclerosis, and progressive bulbar palsy. In the United States the most common terms used are ALS (both specifically for ALS and as a blanket term) or "Lou Gehrig's disease".

Amyotrophic comes from the Greek language: A- means "no", myo refers to "muscle", and trophic means "nourishment"; amyotrophic therefore means "no muscle nourishment," which describes the characteristic atrophication of the sufferer's disused muscle tissue. Lateral identifies the areas in a person's spinal cord where portions of the nerve cells that are affected are located. As this area degenerates it leads to scarring or hardening ("sclerosis") in the region.

See also

References

  1. ^ motor neuron disease at Dorland's Medical Dictionary
  2. ^ Types of MND at GPnotebook
  3. ^ Motor neuron degeneration in mice that express a human Cu,Zn superoxide dismutase mutation. Science, 1994. 264(5166): p. 1772-5.
  4. ^ Brooks BR (1994). "El Escorial World Federation of Neurology criteria for the diagnosis of amyotrophic lateral sclerosis. Subcommittee on Motor Neuron Diseases/Amyotrophic Lateral Sclerosis of the World Federation of Neurology Research Group on Neuromuscular Diseases and the El Escorial "Clinical limits of amyotrophic lateral sclerosis" workshop contributors". J. Neurol. Sci. 124 Suppl: 96–107. PMID 7807156. 
  5. ^ "El Escorial Revisited: Revised Criteria for the Diagnosis of Amyotrophic Lateral Sclerosis - Requirements for Diagnosis". http://www.wfnals.org/guidelines/1998elescorial/elescorial1998criteria.htm. Retrieved 2007-06-06. 
  6. ^ Belsh JM (2000). "ALS diagnostic criteria of El Escorial Revisited: do they meet the needs of clinicians as well as researchers?". Amyotroph. Lateral Scler. Other Motor Neuron Disord. 1 Suppl 1: S57–60. doi:10.1080/14660820052415925. PMID 11464928. 
  7. ^ "A Twitch of Potential". Time. http://www.time.com/time/pacific/magazine/article/0,13673,503060501-1186615,00.html. Retrieved 2006-12-30. 
  8. ^ Waring, S.C et al. (2004). "Incidence of Amyotrophic Lateral Sclerosis and of the Parkinsonism-Dementia Complex of Guam, 1950-1989". Neuroepidemiology 23 (4): 192–199. doi:10.1159/000078505. 
  9. ^ "Flying fox linked to disease - The Boston Globe". http://www.boston.com/news/science/articles/2003/12/09/flying_fox_linked_to_disease/. Retrieved 2007-06-06. 
  10. ^ Miller G (2006). "Neurodegenerative disease. Guam's deadly stalker: on the loose worldwide?". Science 313 (5786): 428–31. doi:10.1126/science.313.5786.428. PMID 16873621. http://www.sciencemag.org/cgi/content/full/313/5786/428. 
  11. ^ http://www.guardian.co.uk/science/2008/nov/03/lithium-motor-neurone-disease-trial

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