BackgroundNeedle EMG may be negative in mild or predominantly sensory lumbosacral radiculopathies. In such cases, an increase in the latency of the soleus H-reflex is a useful diagnostic criterion for establishing sensory fiber compromise at the S1 root level. However, if clinical signs of radicular involvement are lacking, the latency of the H-reflex is normal. We therefore studied the recruitment curve of the soleus H-reflex to investigate whether a change in the electrical threshold for eliciting the H-reflex might be a more sensitive criterion for detecting subclinical S1 root dysfunction.MethodsClinical and electrophysiological findings from 26 patients with chronic back pain and radiculopathy were compared with data obtained from 40 healthy subjects.ResultsAn increase in the mean H-reflex threshold was the only abnormal electrophysiological finding in patients with no clinical sign of root injury (58%). A decrease in the mean H-reflex amplitude and a prolongation of H-reflex latency was observed in patients with radicular signs (42%). In both patients groups, F-wave and needle EMG studies were normal. No radiological evidence of S1 root compression was found.ConclusionsThe study of the recruitment curve of the soleus H-reflex may be usefully associated to F-wave and needle EMG studies to detect possible S1 root dysfunction in mild lumbosacral radiculopathies. An increase in H-threshold may be the earliest abnormality in the absence of focal neurological signs.
Recently, a rare form of congenital muscular dystrophy has been shown to be associated with a deficiency of laminin alpha 2 chain, a tissue-specific component of the basal lamina. Besides muscular dystrophy, children affected with this disorder also show electrophysiological and magnetic resonance imaging evidence of white matter involvement in the central nervous system (CNS). We have studied the precise localization of laminin alpha 2 chain in normal human brain, using specific electron microscopic techniques including thin-section fracture labeling and cryoultramicrotomy, in parallel with immunohistochemical techniques. We found that this laminin chain was localized to the basal lamina of all cerebral blood vessels, whereas blood vessels of the choroid plexus did not show any reaction. No positive reaction was found in meningeal blood vessels either. We hypothesize that in normal brain, laminin alpha 2 may be important for the selective filtration capability of the blood-brain barrier. The lack of laminin alpha 2 in cerebral vessels of children with laminin alpha 2-deficient congenital muscular dystrophy may cause impaired selective filtration, leading to leakage of plasma components and damage to the CNS. Further studies should be performed on patients affected by congenital muscular dystrophy associated with laminin alpha 2 deficiency to test this hypothesis.
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