Motor neuron disease and multiple sclerosis

Strictly speaking, motor neuron disease and multiple sclerosis are diseases of the nervous system, rather than the musculoskeletal system. However, although these conditions are relatively rare, they are included here because the consequences of them affect skeletal muscle function and because health care professionals are likely to be involved in the care of patients with these two conditions. 

Motor neuron disease is also known as amyotrophic lateral sclerosis. It is a condition in which there is loss of spinal motor neurons and neurons of descending motor pathways from pyramidal cells of the cerebral cortex. The disease results in rapidly progressing muscular weakness, muscle atrophy, fasciculations, spasticity, difficulty speaking. 

There is one drug that can be used to slow the progression of motor neuron disease and extend life or prolong the time to mechanical ventilation. Riluzole inhibits the release and postsynaptic action of glutamate in the motor pathways. It is said to be neuroprotective and slows deterioration of nerve function. This could be because excessive amounts of glutamate are released in motor neuron disease and this is toxic to neurons. Riluzole must be used under specialist supervision. 

Side effects of riluzole are nausea, vomiting, tachycardia, headache, dizziness and vertigo. 

The cause of multiple sclerosis is unknown and there is no cure. 

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Neurodegenerative diseases (NDDs) are those in which the irreversible deteriorization of neurons affects movement and/or memory. A number of these diseases have been associated with neurotoxic chemical exposures. These include Parkinson s disease, Alzheimer s disease, amyotrophic lateral sclerosis (also called motor neuron disease), and multiple sclerosis. NDDs and their associations with neurotoxic exposures are introduced here. Specific examples and case studies are discussed in the following sections. 

Motor neuron disease and multiple sclerosis are diseases of the nervous system that affect muscle function. Both these diseases are progressive and there are no cures for... 

Apoptosis has been implicated in delayed neuronal death associated with many neurodegenerative disorders such as Parkinson s disease, stroke, Huntington s disease, traumatic head injury, Alzheimer s disease, motor neuron degeneration, spinal cord injury, and multiple sclerosis. Since an extensive description of the role of apoptosis in each of these disorders is beyond the scope of the present text, we shall focus on anti-apoptotic strategies for stroke, Parkinson s disease, and multiple sclerosis. 

The development of new medicinal products for narrower indications in serious, and usually poorly understood, diseases such as multiple sclerosis and motor neurone disease has resulted in a closer approximation of study subjects selected for the controlled clinical trial to the patients encountered in clinical practice. Many of these products are biologically derived, and while efficacy in the two situations may be similar, longer and larger trials will be needed to fully appreciate adverse event profiles. 

Multiple sclerosis and motor neuron disease are diseases of the nervous system, but are included here because major effects of these diseases are on skeletal muscle function. 

The author would like to acknowledge his former colleagues David Edgar and Rupert Timpl for their support during his initiation into the laminin field. He is supported by the National Health and Medical Research Council of Australia, the Australian Research Council, the Multiple Sclerosis Society of Australia and the A.L.S.-Motor Neurone Disease Society of Australia. 

CNS trauma damage, stroke or CNS suppression by overdose of drugs such as opiates and anaesthetlos reduces stimulation of the respiratory musoles Pamage to nerves between the CNS respiratory centre and the respiratory muscles causes hypercapnia, e.g. spinal cord damage, Guillain-Barr syndrome, multiple sclerosis, motor neurone disease, poliomyelitis... 

Defecation starts with stimulation of the sensory nerve fibers of the rectum, leading to an involuntary spinal reflex that causes contraction of the rectum and the opening of the internal and external sphincters. The voluntary, somatic system completes the evacuation, after which the brain sends signals to the external sphincter to close and inhibit further elimination. Any damage to the CNS, such as a cerebrovascular accident, brain tumor, multiple sclerosis, or motor neuron diseases, can impair the bowel s volrmtary and involuntary responses. These CNS changes may result in inaccurate, involrmtaiy responses of the bowel, such as flaccidity of the rectum, expulsion of contents, or sphincter and rectal hyperactivity (3). 

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