eMedicine Specialties > Emergency Medicine > Neurology

Amyotrophic Lateral Sclerosis

Kathleen Clem, MD, FACEP, Chair, Department of Emergency Medicine, Loma Linda University Medical Center
Joel C Morgenlander, MD, Professor, Division of Neurology, Duke University School of Medicine; Consulting Staff, Electromyography Laboratory, Muscular Dystrophy Association Clinic, Duke University Medical Center

Updated: Sep 15, 2009

Introduction

Background

Amyotrophic lateral sclerosis (ALS) is a disease of unknown cause characterized by slowly progressive degeneration of upper motor neurons (UMNs) and lower motor neurons (LMNs). The UMN findings include hyperreflexia and spasticity. They result from degeneration of the lateral corticospinal tracts in the spinal cord. The LMN findings include weakness, atrophy, and fasciculations. They are a direct consequence of muscle denervation. ALS is eventually fatal because of respiratory muscle weakness. Aspiration pneumonia and medical complications of immobility contribute to morbidity.

Amyotrophic lateral sclerosis terminology is derived from the combination of the clinical examination findings of amyotrophy with the pathological finding of lateral sclerosis.

Because Charcot made the first clinical description in the 1860s, the disease is named for him in Europe. In the United States, the disease often is called Lou Gehrig disease after the baseball legend who died from ALS in 1941.

Pathophysiology

No single cause for amyotrophic lateral sclerosis (ALS) explains its entire pathology; indeed, there may be multiple causes resulting in phenotypic similarity. While ALS is ultimately a diffuse disease, onset is often focal and asymmetric. At onset, bulbar motor neurons can be involved, resulting in bulbar weakness (progressive bulbar palsy), or spinal cord anterior horn cells can be affected, resulting in limb weakness (spinal muscular atrophy). When upper motor neuron involvement of bulbar muscles occurs, a syndrome of pseudobulbar palsy results, causing spastic dysarthria, dysphagia, and emotional incontinence. Upper motor neuron involvement of spinal cord tracks results in spastic weakness of the limbs (primary lateral sclerosis). Later, spread to other motor areas produces the classic combination of upper and lower motor neuron dysfunction recognized as ALS.

Five to 10% of patients with ALS have a family history following an autosomal dominant pattern of inheritance. About 20% of these patients have a mutation of the superoxide dismutase 1 (SOD1) enzyme. This mutation is believed to make a defective protein that is toxic to motor nerve cells. The SOD1 mutation, however, accounts for only 1 or 2% of ALS cases, or 20% of the familial (inherited) cases. This enzyme functions as an antioxidant. Glutamate toxicity, mitochondrial dysfunction, and autoimmunity all may play a role in causation.

Frequency

United States

Approximately 5,600 people in the United States are diagnosed with ALS each year. The incidence of ALS (2-3 per 100,000 people) is 5 times higher than Huntington disease and about equal to multiple sclerosis. It is estimated that as many as 30,000 Americans may have the disease at any given time.

International

No ethnic or racial predisposition to ALS is apparent worldwide, and the incidence is believed to be the same as that in the United States.

Mortality/Morbidity

ALS is a fatal disease. Median survival is 3-5 years. However, longer survival is not rare. About 30% of patients with ALS live 5 years after diagnosis, and about 10-20% survive for greater than 10 years. Long-term survival is associated with a younger age at onset, being male, and limb rather than bulbar symptom onset. Rare reports of spontaneous remission exist.¹

Race

The incidence of ALS is higher in men than in women prior to the age of 65-70 years, but, thereafter, the gender incidence is equal.

Sex

Incidence is higher in men than in women, with a male-to-female ratio of 1.6:1.

Age

Onset of ALS usually occurs in patients aged 40-60 years. Mean age of onset of sporadic ALS is 56 years; mean age of onset of familial ALS is 46 years.

Clinical

History

The diagnosis of amyotrophic lateral sclerosis (ALS) is primarily clinical. Electrodiagnostic testing contributes to the diagnostic accuracy. ALS can be differentiated from stroke or trauma due to the subacute or chronic progression of symptoms. When focal limb weakness occurs, ALS is differentiated from a root or peripheral nerve lesion by the lack of pain or sensory symptoms. While ALS is a slowly progressive disease, a precipitous event may occur to bring the patient to the ED.

• Bulbar symptoms: The patient's family first notices slurring of words or choking during a meal. An aspiration event or acute respiratory symptoms of air hunger occur.
• Extremity weakness: The patient notices wrist drop interfering with his or her work performance. Or, the patient may find reduced finger dexterity, cramping, stiffness, and weakness or wasting of intrinsic hand muscles. Less frequently, the patient may develop foot drop resulting in a fall or sprain.
• Fasciculations may present early on the disease, particularly in the tongue.

Physical

Lower motor neuron signs include weakness, atrophy, fasciculations, and depressed reflexes. Fasciculations are observed with the muscle at rest.

Upper motor neuron signs include an upper motor neuron pattern of weakness (greatest in the extensors of the arm and flexors of the leg), spastic bulbar and limb muscles, hyperreflexia, and extensor plantar responses. A hyperreflexic jaw jerk helps to confirm upper motor neuron involvement causing dysarthria and dysphagia.

Tendon reflexes are paradoxically brisk.

In patients with pseudobulbar palsy, emotional incontinence may cause the patient to over-react to sad or funny things. The patient is aware of the lack of control. Cognitive impairment, if present, most often is observed in patients with bulbar involvement.

Muscle cramps are common for patients with lower motor neuron involvement, while patients with upper motor neuron dysfunction can have clonus or painful extensor spasms.

Ocular, sensory, or autonomic dysfunction occurs only very late in the disease course, usually in patients living with ventilatory support.

The key finding in an involved limb is the combination of lower and upper motor neuron dysfunction with a weak, atrophic, fasciculating muscle occurring in combination with increased tone and hyperreflexia. 

When ALS first clinically manifests in the lower extremities, foot drop is common. Patients may report a "slapping" gait. Proximal pelvic girdle onset is less common, but, when it occurs, patients complain that they have difficulty climbing stairs and/or moving from a chair to standing. Patients may present to the emergency department due to tripping and falling.

Bulbar symptoms manifest as dysarthria or dysphagia and are the next most common presentation (20%). The symptoms may become worse after extended use of the voice. Patients may have more trouble with swallowing of thin liquids then thick, and they may need to swallow multiple times to complete transport of liquids through the esophagus to the stomach.

Rarely, patients with ALS may present with respiratory muscle weakness, generalized weakness, and difficulty with head control. They may develop disturbed nocturnal sleep and exhibit excessive daytime sleepiness.

When patients have axial truncal weakness they have difficulty maintaining an erect posture when standing and may support their trunk by placing their hands in their thighs and "walking" them up their leg to assist in standing erect. Some patients feel more secure when pushing a heavy object on wheels such as a grocery cart.

A link exists between ALS and frontotemporal executive dysfunction that may precede or follow the onset of ALS, but most patients with ALS do not have overt dementia, and cognitive impairment is usually subtle. The proportion of patients with ALS who meet criteria for frontotemporal dementia is 15%. When ALS is associated with frontotemporal dementia, there is an associated shorter survival than with ALS alone.²

• Lower motor neuron signs include atrophy and fasciculations.
• Upper motor neuron (ie, corticospinal tract) signs include spasticity and hyperactive tendon reflexes and may include the Babinski sign.
• No loss of anal sphincter tone occurs. Cardiac and smooth muscle are not involved.
• The course is progressive, and initial symptoms primarily are those of weakness.
• Weakness often is asymmetric and begins in the legs, arms, or oropharyngeal muscles with approximately equal frequency. Masticatory weakness occurs late. Ultimately, weakness becomes symmetrical.
• Ocular musculature is not involved.
• Muscle atrophy and weight loss almost always are recognized by the time the patient seeks medical treatment.
• Fasciculations may be quite widespread and active. Surprisingly, the patient often ignores this symptom.
• Patients may have inappropriately active tendon reflexes and weak, wasted, twitching muscles.
• Muscle cramps are common.
• Dysarthria, exaggeration of motor expressions, and emotional lability (pseudobulbar affect) may occur when the disease process involves the corticobulbar projections to the brainstem.
• Decubitus ulcers are rare.
• Hypoxia or cardiac arrhythmias are the most common cause of death in patients with ALS. The primary cause of death among patients electing to use ventilatory support is pulmonary infection.

Causes

The specific cause of amyotrophic lateral sclerosis (ALS) is unknown. Recent evidence suggests the existence of clusters of cases.³ Further evaluation of clusters may provide epidemiologic data associated with causes.

Differential Diagnoses

Other Problems to Be Considered

For patients with a new focal presentation, the differential diagnoses by region include the following:

• Upper motor neuron bulbar signs - Brainstem lesions including syrinx, mass, stroke, and demyelination forms or other degenerative diseases
• Lower motor neuron bulbar signs - Cranial nerve palsies
• Limb upper motor neuron signs - Cervical myelopathy, cord tumor, hereditary spastic paraparesis, transverse myelopathy, HIV-related myelopathy, syrinx
• Limb lower motor neuron signs - Radiculopathy, plexopathy, neuropathy

• Upper motor neuron signs - Compressive myelopathy, syrinx
• Lower motor neuron signs -Chronic inflammatory demyelinating polyneuropathy (CIDP), multifocal motor, toxic, or metabolic neuropathies or myopathies such as inclusion body myositis or polymyositis

Workup

Laboratory Studies

• No specific laboratory test identifies amyotrophic lateral sclerosis (ALS).

Imaging Studies

• Magnetic resonance imaging of the brain and spinal cord is performed to exclude conditions that might stimulate this condition such as multiple sclerosis, brainstem strokes, and tumors.
• Magnetic resonance spectroscopy is also being used, but it has a high false-negative rate.

Other Tests

• ALS does not lend itself to a quick definitive diagnosis. Often, neurologists need many months to exclude all other possible diagnoses in a patient presenting with upper and lower motor neuron signs.
• Nerve conduction studies can assess conduction amplitude and velocity of sensory and motor neurons, but the utility of this test has not yet been determined definitively for ALS.
• Electromyography shows fibrillation and fasciculations. The motor units are polyphasic and have high amplitude and long duration.
• Other laboratory studies sometimes ordered in the evaluation of a patient with possible ALS include anti-GM1 antibodies, as these can be seen in patients with multifocal motor neuropathy with conduction block. Vitamin B-12 and folate, HIV testing, Lyme serology, and CPK determinations may also be performed. CPK level can be elevated in ALS, but it is obviously not diagnostic.
• ALS research has expanded, and some research is showing that ALS may share common biological mechanisms with Alzheimer disease, Parkinson disease, and other neurodegenerative diseases. Collaborative research is increasing.⁴

Treatment

Emergency Department Care

Emergency physicians should be familiar with amyotrophic lateral sclerosis (ALS) and should consider the diagnosis in patients with only motor syndromes.

• Patients initially are cared for symptomatically, and emotional support should be available to the patient and family. Discussion of a new diagnosis of ALS in the ED is inappropriate before further evaluation occurs.
• If a living will or a declaration for a natural death is in place, keep patients comfortable and do not intubate.
• Complications, such as infections, deep vein thrombosis, or respiratory insufficiency, should be managed appropriately.
• Further information on diagnosis and treatment for patients with ALS is available from the European Federation of Neurological Societies.⁵

Consultations

• Refer patients to a neurologist experienced in the diagnosis and treatment of neuromuscular diseases.
• Refer to a pulmonologist if respiratory failure is imminent and patient wishes allow.

Medication

Treatment of pneumonia or urosepsis initially involves empiric use of a relatively broad-spectrum antibiotic or antibiotics effective against probable pathogens, after appropriate cultures and specimens for laboratory evaluation have been obtained. These medications may include cephalosporins, fluoroquinolones, vancomycin, penicillins, and aminoglycosides.

Amyotrophic Lateral Sclerosis Agent

These agents may inhibit the release of neurotransmitters.

Riluzole (Rilutek)

Only current disease-specific medication approved by US Food and Drug Administration for use in patients with ALS. Should only be prescribed by physician familiar with inclusion/exclusion criteria and who will be monitoring patient. Should not be prescribed in ED acutely. Blocks glutamatergic neurotransmission in CNS. Actions appear to be indirect. May activate guanosine triphosphate-binding signal transduction proteins (G-proteins) with resultant inhibition of neurotransmitter release. Glutamic acid is major excitatory neurotransmitter in CNS. Accumulation at synapses triggers excessive stimulation of excitatory amino acid receptors on postsynaptic cell with subsequent neuronal death (postulated pathogenesis of ALS).

Dosing

Adult

50 mg PO q12h; no benefit can be expected from higher qd doses, but adverse events are increased

Pediatric

ALS not seen in pediatric patients

Interactions

Coadministration with drugs that inhibit CYP450 1A2 (eg, caffeine, theophylline, amitriptyline, quinolones) may decrease rate of elimination of riluzole, increasing toxicity; inducers of CYP450 1A2 (eg, phenytoin, rifampin, omeprazole, cigarette smoke) may decrease blood levels by increasing rate of elimination

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in abnormal liver function; monitor liver enzymes closely; worsening of asthenia may occur

Antispasticity agents

Treatment of spasticity is not specific for ALS.

Baclofen (Lioresal)

Treats spastic muscles. May induce hyperpolarization of afferent terminals and inhibit both monosynaptic and polysynaptic reflexes at the spinal level.

Dosing

Adult

5 mg PO tid initially, followed by gradual increase of 5 mg/d q4-7d to therapeutic level (0.08-0.4 mcg/mL); not to exceed 80 mg/d divided qid

Pediatric

ALS not seen in pediatric patients

Interactions

Opiate analgesics, benzodiazepines, alcohol, tricyclic antidepressants, guanabenz, MAOIs, clindamycin, and hypertensive agents may increase effects

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in patients with history of autonomic dysreflexia and when spasticity is used to obtain increased function; autonomic dysreflexia can result from withdrawal of this medication

Tizanidine (Zanaflex)

Treats spastic muscles. Centrally acting muscle relaxant. Possesses alpha2-adrenergic agonist properties. Metabolized in liver and excreted in urine and feces.

Dosing

Adult

4-8 mg PO q8h prn; not to exceed 36 mg/d

Pediatric

ALS not seen in pediatric patients

Interactions

May interact with alcohol (increasing somnolence, stupor) and PO contraceptives (which decrease clearance); can cause increased hypotensive effects when administered concurrently with diuretics

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in renal impairment

Cholinergic agents

For patients with ALS who may have secondarily impaired neuromuscular junction transmission.

Pyridostigmine (Mestinon, Regonol)

Acts in smooth muscle, CNS, and secretory glands, where it blocks action of acetylcholine at parasympathetic sites and facilitates transmission of impulses across myoneural junction.

Dosing

Adult

Initial: 60 mg PO tid followed by a maintenance dose of 60 mg/d to 1.5 g/d, or 2 mg IV/IM q2-3h (or 1/30th the PO dose)

Pediatric

ALS not seen in pediatric patients

Interactions

Increases effects of depolarizing neuromuscular blockers; increases toxicity of edrophonium

Contraindications

Documented hypersensitivity; GI or GU obstruction

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in bronchial asthma and those receiving a cardiac glycoside; overdose may cause cholinergic crisis, which may be fatal; atropine IV should be readily available for treatment of cholinergic reactions

Follow-up

Further Inpatient Care

• Physical and occupational therapy and speech pathology consultations assist the patient with amyotrophic lateral sclerosis (ALS) in maintaining strength, daily living activities, and communication skills.
• When forced vital capacity (FVC) reaches about 50% of predicted levels, supplemental respiratory support may be needed. (The first symptom may be disturbed sleep.) Use of noninvasive positive pressure ventilation improves quality of life; further respiratory deterioration may necessitate tracheostomy and ventilator support.
• Patients with progressive weight loss, symptomatic dysphagia, or aspiration should be considered for percutaneous gastrostomy placement. Risk of percutaneous endoscopic gastrostomy (PEG) placement increases with declining respiratory function. PEG is best placed before FVC falls to less than 50% of predicted levels.
• Advance directives should be addressed by the patient's neurologist early in the course and should be discussed at regular intervals. Hospice referral may be appropriate to aid in care during the terminal phase of the disease.

Further Outpatient Care

• Early in the treatment course of ALS, encourage patients to continue routine activities.
• Patients are best cared for in a designated ALS center. Many mechanical aids can help overcome disabilities.
• Patients' length of survival and quality of life are enhanced by night-time breathing assistance early in the course of the disease and by aggressive application of alternate feeding options to ensure good nutrition once swallowing becomes difficult.⁶

Inpatient & Outpatient Medications

• Medications are patient specific.

Complications

• Pneumonia
• Urosepsis
• Constipation
• Depression
• Muscle cramps
• Immobility-related problems

Prognosis

• ALS is a fatal disease. Younger patients may have a slower rate of progression. Patients with bulbar onset, particularly the lower motor neuron type, have a poorer prognosis.

Patient Education

• Patients with ALS are eligible for participation in a Muscular Dystrophy Association clinic.
• Informational web sites include the following:
  • Muscular Dystrophy Association
  • ALS Association of America
  • National Institute of Neurological Disorders and Stroke (NINDS)
• For excellent patient education resources, visit eMedicine's Brain and Nervous System Center. Also, see eMedicine's patient education articles Amyotrophic Lateral Sclerosis (Lou Gehrig Disease) and Advance Directives.

Miscellaneous

Medicolegal Pitfalls

• Refer patients to a neurologist. In a patient with an established diagnosis of ALS, follow advance directives.

Multimedia

Media file 1: Amyotrophic lateral sclerosis (ALS) patient using eye-gaze computer device to conduct business and communicate.

References

1. Kimura F, Fujimura C, Ishida S, et al. Progression rate of ALSFRS-R at time of diagnosis predicts survival time in ALS. Neurology. Jan 24 2006;66(2):265-7. [Medline].

2. Murphy J, Henry R, Lomen-Hoerth C. Establishing subtypes of the continuum of frontal lobe impairment in amyotrophic lateral sclerosis. Arch Neurol. Mar 2007;64(3):330-4. [Medline].

3. Sabel CE, Boyle PJ, Loytonen M, et al. Spatial clustering of amyotrophic lateral sclerosis in Finland at place of birth and place of death. Am J Epidemiol. May 15 2003;157(10):898-905. [Medline].

4. Hudson AJ. The motor neuron diseases and related disorders. In: Clinical Neurology. Vol. 4. 1996:11-14.

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Keywords

ALS, Lou Gehrig disease, Lou Gehrig's disease, amyotrophic lateral sclerosis, Charcot disease, Charcot's disease, motor neuron disease

Contributor Information and Disclosures

Author

Kathleen Clem, MD, FACEP, Chair, Department of Emergency Medicine, Loma Linda University Medical Center
Kathleen Clem, MD, FACEP is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

Joel C Morgenlander, MD, Professor, Division of Neurology, Duke University School of Medicine; Consulting Staff, Electromyography Laboratory, Muscular Dystrophy Association Clinic, Duke University Medical Center
Joel C Morgenlander, MD is a member of the following medical societies: American Academy of Neurology, American Stroke Association, and North Carolina Neurological Society
Disclosure: Nothing to disclose.

Medical Editor

Roy Alson, MD, PhD, FACEP, FAAEM, Associate Professor, Department of Emergency Medicine, Wake Forest University School of Medicine; Medical Director, Forsyth County EMS; Deputy Medical Advisor, North Carolina Office of EMS; Associate Medical Director, North Carolina Baptist AirCare
Roy Alson, MD, PhD, FACEP, FAAEM is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, National Association of EMS Physicians, North Carolina Medical Society, Society for Academic Emergency Medicine, and Wilderness Medical Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

J Stephen Huff, MD, Associate Professor, Emergency Medicine and Neurology, Department of Emergency Medicine, University of Virginia Health Sciences Center
J Stephen Huff, MD is a member of the following medical societies: American Academy of Emergency Medicine, American Academy of Neurology, American College of Emergency Physicians, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Rick Kulkarni, MD, Assistant Professor of Surgery, Section of Emergency Medicine, Yale-New Haven Hospital
Rick Kulkarni, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: WebMD Salary Employment

Clinical trials

Safety and Efficacy of TRO19622 as Add-on Therapy to Riluzole Versus Placebo in Treatment of Patients Suffering From Amyotrophic Lateral Sclerosis (ALS)

Olanzapine for the Treatment of Amyotrophic Lateral Sclerosis (ALS) Cachexia

Efficacy and Tolerability of Tauroursodeoxycholic Acid in Amyotrophic Lateral Sclerosis

Combination Therapy in Amyotrophic Lateral Sclerosis (ALS)

Pilot Placebo-Controlled Trial of Early Noninvasive Ventilation for ALS

A Long-Term Study in Patients With Amyotrophic Lateral Sclerosis (ALS)

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