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Motor neuron disease in adults generally commences between 30 and 60 years of age There is degeneration of the anterior horn cells in the spinal cord, the motor nuclei of the lower cranial nerves, and the corticospinal and corticobulbar pathways The disorder is usually sporadic, but familial cases may occur and several genetic mutations or loci have been identified

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Bulbar involvement predominates owing to disease processes affecting primarily the motor nuclei of the cranial nerves

Bulbar involvement predominates in this variety also, but it is due to bilateral corticobulbar disease and thus reflects upper motor neuron dysfunction

This is characterized primarily by a lower motor neuron deficit in the limbs due to degeneration of the anterior horn cells in the spinal cord

A mixed upper and lower motor neuron deficit is found in the limbs This disorder is sometimes associated with cognitive decline (in a pattern consistent with frontotemporal dementia) or parkinsonism

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Difficulty in swallowing, chewing, coughing, breathing, and talking (dysarthria) occur with bulbar involvement In progressive bulbar palsy, there is drooping of the palate; a depressed gag reflex; pooling of saliva in the pharynx; a weak cough; and a wasted, fasciculating tongue In pseudobulbar palsy, the tongue is contracted and spastic and cannot be moved rapidly from side to side Limb involvement is characterized by motor disturbances (weakness, stiffness, wasting, fasciculations) reflecting lower or upper motor neuron dysfunction; there are no objective changes on sensory examination, although there may be vague sensory complaints The sphincters are generally spared The disorder is progressive, and amyotrophic lateral sclerosis is usually fatal within 3 5 years; death usually results from pulmonary infections Patients with bulbar involvement generally have the poorest prognosis

Weakness No sensory loss or sphincter disturbance Progressive course No identifiable underlying cause other than genetic basis in familial cases

This group of degenerative disorders is characterized clinically by weakness and variable wasting of affected muscles, without accompanying sensory changes

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Electromyography may show changes of chronic partial denervation, with abnormal spontaneous activity in the resting

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Cudkowicz ME et al Trial of celecoxib in amyotrophic lateral sclerosis Ann Neurol 2006 Jul;60(1):22 31 [PMID: 16802291] McGeer EG et al Pharmacologic approaches to the treatment of amyotrophic lateral sclerosis BioDrugs 2005;19(1):31 7 [PMID: 15691215] Rippon GA et al An observational study of cognitive impairment in amyotrophic lateral sclerosis Arch Neurol 2006 Mar;63(3):345 52 [PMID: 16533961] Winhammar JM et al Assessment of disease progression in motor neuron disease Lancet Neurol 2005 Apr;4(4):229 38 [PMID: 15778102]

muscle and a reduction in the number of motor units under voluntary control In patients with suspected spinal muscular atrophy or amyotrophic lateral sclerosis, the diagnosis should not be made with confidence unless such changes are found in at least three spinal regions (cervical, thoracic, lumbosacral) or two spinal regions and the bulbar musculature Motor conduction velocity is usually normal but may be slightly reduced, and sensory conduction studies are also normal Biopsy of a wasted muscle shows the histologic changes of denervation The serum creatine kinase may be slightly elevated but never reaches the extremely high values seen in some of the muscular dystrophies The cerebrospinal fluid is normal A familial form of amyotrophic lateral sclerosis has been described with autosomal dominant inheritance, related to mutations in the copper-zinc superoxide dismutase gene on the long arm of chromosome 21 Other familial forms with dominant or recessive inheritance have also been identified and mapped to other genetic loci X-linked bulbospinal neuronopathy is associated with an expanded trinucleotide repeat sequence on the androgen receptor gene and carries a more benign prognosis than other forms of motor neuron disease There have been recent reports of juvenile spinal muscular atrophy due to hexosaminidase deficiency, with abnormal findings on rectal biopsy and reduced hexosaminidase A in serum and leukocytes Pure motor syndromes resembling motor neuron disease may also occur in association with monoclonal gammopathy or multifocal motor neuropathies with conduction block A motor neuronopathy may also develop in Hodgkin s disease and has a relatively benign prognosis Infective anterior horn cell diseases (polio virus or West Nile virus infection) can generally be distinguished by the acute onset and monophasic course of the illness, as discussed elsewhere in this book

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