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Denervation muscular atrophy. Studies on the soleus muscle of the albino rat (LM, TEM, immunofluorescence, image analysis).

In previous researches the Authors hypothesized that the loss of cytoskeletal proteins such as desmin and vinculin lead to degenerative ultrastructural changes which occur in muscular disuse atrophy. In order to support this hypothesis they carried out a morphometric, structural, ultrastructural and immunofluorescence study on the soleus muscle of albino rats after resection of the ischiatic nerve. It was demonstrated that a chronological sequence of the damage took place in particular three levels of damage. The last level of damage proved to be irreversible; the first level assured complete recovery in the case of rapid reinnervation, whereas the possible reversibility of the second level remained open to question. The disappearance of vinculin and desmin was observed in a period between 72 hours and 7 days, i.e. before the appearance of ultrastructural damage. On this ground the Authors explained the correlation between the loss of the proteins and degenerative changes. In conclusion the Authors correlated the gene expression of cytoskeletal and contractile proteins with the neuropeptides released by motor axon.

Animals↗
PubMed1994

Biochemical and immunocytochemical analysis in chronic proximal spinal muscular atrophy.

Immunocytochemical and biochemical analyses were carried out on patients affected by chronic SMA. Three groups of patients were identified. In group I, the muscle presented a fascicular atrophy; a high percentage of atrophic type II fibers; and fibers expressing fast, slow, embryonic, and fetal myosin isoforms. In group II, the muscle was characterized by atrophic fibers and normal/hypertrophic fibers expressing only slow myosin isoforms. In group III, the muscle was characterized by fiber type grouping and fibers coexpressing fast and slow myosin isoforms but never embryonic or fetal MHC isoforms. The muscles of groups I and III contained both fast and slow myosins whereas group II muscles were predominantly slow by immunocytochemical analysis or only slow by biochemical analysis. In view of these results, immunocytochemical and histochemical analyses could help to classify chronic SMA and help to understand the different pathogenic processes which seem to be related to the maturational stage of the muscle at the age of onset of the disease.

Adolescent↗
PubMed2000

Juvenile muscular atrophy of distal upper extremity (Hirayama disease): focal cervical ischemic poliomyelopathy.

Hirayama disease is characterized by an initially progressive muscular weakness and atrophy of the distal upper limb(s) in adolescence, occurring predominantly in males, followed by spontaneous arrest within several years. Although the disease could be separated from motor neuron disease, some authors considered the illness to be a variant of degenerative motor neuron disease until the first autopsy case was reported which showed focal ischemic changes in the anterior horn of the lower cervical cord. Since then, many in Japan have recognized the disease as cervical ischemic poliomyelopathy; however, several authors in foreign countries did not or do not appreciate the pathologic findings of the disease, and still consider the illness a degenerative motor neuron disease. The pathology of the disease prompted neuroradiologic investigations, which have revealed dynamic changes of the cervical dural sac and spinal cord induced by neck flexion. The cause of these dynamic changes is unknown. However, as the number of patients is exceedingly large in Japan, there may be an ethnic factor.

Adolescent↗
PubMed1997

A collaborative study on the natural history of childhood and juvenile onset proximal spinal muscular atrophy (type II and III SMA): 569 patients.

We analyzed clinical data of 569 patients in two combined series with childhood and juvenile proximal SMA. This cohort included only patients who had achieved the ability to sit unaided (type II and III SMA). The survival rate among 240 type II patients (who sat but never walked) was 98.5% at 5 years and 68.5% at 25 years. SMA III (n = 329) (those who walked and had symptoms before age 30 years) was subdivided into those with an onset before and after age 3 years (type IIIa, n = 195; SMA IIIb, n = 134). In patients with SMA III, life expectancy is not significantly less than a normal population. The probabilities of being able to walk at 10 years after onset was 70.3%, and at 40 years, 22.0% in SMA IIa. For SMA IIIb, 96.7% were walking 10 years after onset and 58.7% at 40 years. The subdivision of type III SMA was justified by the probability of being ambulatory depending on age at onset; the prognosis differed for those with onset before or after age 3 years. The data provide a reliable basis of the natural history of proximal SMA and support a classification system that is based primarily on age at onset and the achievement of motor milestones.

Adolescent↗