Biomedical subjects
Publications and source records attributed to D Raimondo.
A 33-year-old woman three weeks after a febrile illness presented with a syndrome of ophthalmoplegia, ataxia and areflexia (SOAA) that characterizes clinically both Bickerstaff and Miller Fisher syndromes. The normality of the electrophysiological tests performed, the CSF findings and the magnetic resonance images proved that the syndrome stemmed from brainstem pathology.
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There is evidence from several laboratories of an increased prevalence of circulating immuno-complexes (CIC) in diabetic patients. It has also been suggested that CIC are pathogenetically related to chronic diabetic complications. The aim of this study was to assess peripheral nerve function in children with Type 1 diabetes and to evaluate the relationship between the neurophysiological abnormalities and the possible presence of CIC. The investigation was carried out in 25 Type 1 diabetic patients ranging in age from 7-19 years and in 20 normal controls. Neurophysiological assessment was performed to evaluate motor and sensory conduction velocity on median and tibial nerves. IgG-CIC were detected by the solid-phase C1q-binding and anti-C3 enzyme immuno-assay. The results of this study showed a greater slowing of median motor and sensory and tibial sensory conduction velocities in patients with CIC with respect to the patients without CIC, suggesting a possible role of immunological factors in the pathogenesis of diabetic neuropathy.
In 50 ulnar nerves of healthy subjects, F-wave latency, duration, amplitude and persistence were determined at different frequencies of the antidromic impulse (0.2-0.5-1-2 Hz). The F amplitude and persistence were found significantly increased at higher stimulation rates, suggesting that the frequency of the antidromic impulse influences the motoneuron pool discharges. Individual cross-correlation values (r) obtained for latency and duration, latency and amplitude, amplitude and duration did not show any significant changes at different stimulation rates.
The F response can provide a measure of motoneurone excitability (MNE) and so it may be used to investigate upper motoneurone disorders. This report studies the F-wave configuration in patients with stroke to evaluate the changes of the central excitability of the motoneurones at different times after an acute cerebral insult. Various parameters of the F response, including amplitude (absolute and F%/M), duration, and persistence have been determined in 26 patients with unilateral hemiplegia and in 32 healthy subjects of both sexes in the same age range. The investigation was carried out applying a series of 20 supramaximal stimuli at 0.5 Hz on tibial and ulnar nerves bilaterally. In all patients a detailed clinical examination and a CT scan were performed. Our results indicate that an initial stage of reduced spinal motoneuron excitability evidenced by a decreased F amplitude and persistence was present in the early phases after a stroke, followed within 90 days by an enhanced MNE. Moreover, F-wave amplitude shows a positive correlation with weakness and increased tone.
Various parameters of the F-response (latencies, chronodispersion, amplitude, duration, shape, persistence) were investigated in ulnar and tibial nerves of 50 healthy subjects of both sexes, aged between 16 to 79 years. The observations were made bilaterally and the results revealed no significant differences in any of the F-parameters by comparing side to side. The relationships between each neurophysiological F-response data and limb length, age and sex of control subjects were determined. Correlations of high statistical significance were found between minimum F-latency and limb length as well as between absolute and F%/M-amplitude and age. Cross-correlation coefficients correlating mean individual values of latency-duration, latency-amplitude and amplitude-duration did not show any significant relationship between latency, amplitude and duration in normal subjects.
The role of metabolic abnormalities in the development of diabetic neuropathy is controversial. To investigate the peripheral nerve function and the influence of hyperglycemia on nerve conduction in insulin-dependent diabetes, a one-year neurophysiological study was carried out in 30 type 1 diabetic patients ranging in age from 2-16 years. During the 12-month follow-up period the glycosylated hemoglobin determination, motor conduction velocity of the peroneal nerve and the motor and sensory conduction of the tibial nerve were assessed 3 times, at the beginning of the study and every 6 months thereafter. The sensory latency was found significantly delayed in these patients as compared with the controls. The degree of sensory conduction slowing correlated well with the glycosylated hemoglobin concentrations and improved with the reduction in hyperglycemia.
We observed a patient with the hypereosinophilic syndrome that showed as a prominent clinical feature peripheral nerve dysfunction. The neuropathy evolved over 4 months and affected sensory and motor functions. Nerve conduction studies and EMG were compatible with axonal neuropathy. Nerve and muscle biopsies revealed severe axonal degeneration with neurogenic atrophy of muscle. Morphometry of peroneal nerve showed marked axonal loss, more prominent in large myelinated fibers. There was no evidence of vasculitis process. Neuropathy is produced by eosinophil-released substances exerting a neurotoxic effect through direct altered vascular endothelial permeability and local mast cell histamine release.
The ulnar and tibial nerve F response latencies were analyzed to study the proximal motor conduction velocity in 15 patients with liver disease. The results were compared with those obtained from 15 normal subjects. The tibial MNCV (P less than 0.01) and FWCV from spinal cord to elbow and knee for ulnar and tibial nerves (P less than 0.001) were significantly reduced in patients compared to the controls. Minimum, mean and maximum F latencies showed significant differences for ulnar (P less than 0.001) and tibial (P less than 0.01) nerves in patients with respect to the controls. The mean F determination compared to the minimum F and delta F did not improve disease identification. The conduction abnormality in hepatic patients appeared to be present only in the proximal segment of the ulnar nerve, whereas it was more uniformly distributed along the entire length of the tibial nerve. This demonstrates that the peripheral nerve involvement in hepatic disease is more diffusely present than can be determined by conventional conduction study only.
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