Lower motor neurons

Thiopentone is contraindicated in the presence of porphyria where it may lead to circulatory collapse, alimentary crises, cutaneous rashes and lower motor neurone paralysis. 

Small ribonucleic acid (RNA) containing viruses. For example, polio viruses, which destroy the anterior horn cells leading to lower motor neuron paralysis, are of this type. 

The history and physical examinadon provide the founda-don for the diagnosis and should clemonsdate the combina-don of lower motor neuron (LMN) involvement, manifested by weakness and muscle adophy, and upper motor neuron (UMN) involvement, evidenced by increased tone and hyper-reflexia, in at least three areas, including the limbs, tongue, and back muscles. Needle EMG and nerve conduedon studies should be performed to confirm the diagnosis in all padents with suspected ALS. 

A clinical diagnosis of ALS requires the demonstration of lower motor neuron involvement in wliich three areas ... 

In ALS, abundant evidence points to the effects of per-oxynitrite in affected tissues. Significant increases in levels of NT moieties are detected on CSF proteins from ALS patients (Aoyama et al., 2000 Shaw and Williams, 2000), including Mn superoxide cUsmutase (Mn-SOD) which is only slightly increased in patients with AD and PD (Chou et al., 1996 Aoyama et al., 2000). Moreover, NT immunoreac tivity is associated with motor neurons of the spinal cord and axons (Calin-gasan et al., 2005), and co-locahzes to axonal conglomerates and spheroid neurofilament accumulations of upper and lower motor neurons (Chou et al., 1996) and with Ap-40 depositions within abnormal neurons (Calingasan et al., 2005). 

In established neurogenic weakness and wasting due to lower motor neuron damage the characteristic appearances are those of groups of atrophic fibers, lately supplied by the damaged neuron, lying beside healthy fibers with intact innervation. This is in full accord with the structure of the motor unit, described above. In peripheral nerve disease, clinical evidence of sensory involvement, such as paraesthesias, may be present as weU. 

The cause of the progressive destruction of upper and lower motor neurons is unknown. The only drug available, riluzole, may act by inhibiting accumulation of the neurotransmitter, glutamate. In 959 patients, riluzole prolonged median survival time from 13 to 16 months, with no effect on motor function. It may cause neutropenia. 

Decreased bladder activity or hypotonicity due to a lower motor neuron lesion or overdistension of the bladder or to both. 

Gardner MB, Henderson BE, Officer JE, Rongey RW, Parker JC, Oliver C, Estes ID, HuebnerRl (1973) A spontaneous lower motor neuron disease apparently caused by indigenous type-C RNA virus in wild mice. 1 Natl Cancer Inst 51 1243-1254. 

Amyotrophic lateral sclerosis is an inexorably progressive motor neuron disease, in which both the upper motor neurons and the lower motor neurons degenerate leading to muscle atrophy. Patients eventually experience respiratory failure, usually within three to five years from diagnosis. However, the onset of ALS may be subtle and early symptoms are frequently overlooked. As many as 20,(X)0 Americans have ALS, and an estimated 5,0(X) people in the United States are diagnosed with the disease each year. Onset is usually in the 5th through 7th decade of life. 

Beach TP, Stone WA, Hamelberg W. Circulatory collapse following succinylcholine report of a patient with diffuse lower motor neuron disease. Anesth Analg 1971 50(3) 431-7. 

Hogue CW Jr, Itani MS, Martyn JA. Resistance to d-tubo-curarine in lower motor neuron injury is related to increased acetylchohne receptors at the neuromuscular junction. Anesthesiology 1990 73(4) 703-9. 

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