Nerve conduction studies and prediction of mortality in hemodialysis patients.

BACKGROUND: The electrophysiological aspects of uremic neuropathy have been studied extensively, but never for prediction of mortality. In order to assess the parameters of nerve conduction study (NCS) as predictors of mortality in hemodialysis patients, a post hoc analysis of a prospective observation study was made. METHODS: We examined conventional electrophysiological parameters (motor nerve conduction velocity [MCV], terminal latency [TL], and F wave latency of the peroneal nerve, as well as sensory nerve conduction velocity [SCV] of the sural nerve) in 75 nondiabetic patients. Hemodialysis modality (bicarbonate dialysis and biocompatible membranes), Kt/V, comorbidity (ischemic heart disease and congestive heart failure), and clinical and laboratory parameters were also evaluated. Survival was analyzed using the Cox proportional hazard model. RESULTS: SCV was significantly higher (t-test, p < 0.01) in the group of patients treated with polysulfone compared to those using cuprophane membranes. On the other hand, MCV significantly correlated with Kt/V (Pearson, r = 0.388; p < 0.01). Multivariate Cox regression revealed only MCV as a significant predictor of mortality in this group of hemodialysis patients (HR = 0.92; CI (0.86-0.99); p < 0.05). CONCLUSION: Only MCV was a significant mortality risk predictor among NCS parameters. This parameter correlates significantly with dialysis dose. SCV was related to the use of biocompatible membranes, indicating the complexity of polyneuropathy in dialysis patients.

[Myasthenia gravis--a disease with variable impact on working capability].

Myasthenia gravis (MG) is a heterogeneous disease composed of several entities with disturbed neuromuscular transmission. The most frequent and clinically most important form of MG is an acquired autoimmune MG which includes more than 90% of all patients with failure of neuromuscular transmission. The main clinical feature of MG is changeable pathologic fatigability and weakness of one or more skeletal muscles and variable distribution of affected muscles. The disease is characterized by relapses and remissions. In 15% of patients the symptoms are limited to extraocular muscles causing variable ptosis, squint and double vision (Ocular MG). In remaining 85% of patients, during the first three years, the disease involves the majority of the head, neck and extremity skeletal muscles (Generalized MG). The clinical diagnosis may be sufficiently established by typical history, present or induced neurological signs of changeable muscle weakness and positive pharmacological tests. The assessment of the severity of the disease as well as the assessment of working capability is performed according to the classification recommended by Myasthenia Gravis Foundation of America (MGFA). The standardized score of the disease severity is based on testing function and strength of 9 groups of skeletal muscles. At the onset of the disease, regardless of the clinical form, the patient is incapable of work and subjected to hospitalization, clinical investigation and treatment. The efficacy of anticholinesterase drugs, thymectomy and/or immunosuppression determines the working capability and is recommended to be assessed six months after the initiation of treatment procedure.

[Antibodies to ganglioside GM1 and Campylobacter jejuni in patients with Guillain-Barré syndrome].

Guillain-Barré syndrome (GBS) is an acute immune mediated neuropathy, polyradiculoneuritis, characterized by rapid onset of symmetric extremity muscle paralysis, areflexia and albuminocytological dissociation in the cerebrospinal fluid (CSF). Recently, the heterogeneity of GBS has been noticed with definition of several GBS variants. The axonal GBS associated with anti-GM1 antibodies is the most important variant with the specific role of Campylobacterjejuni (CJ) in the induction of the disease. The role of our study was to determine the frequency of antecedent infection with CJ in the population of our patients with GBS, the association with anti-GM1 antibodies and the distribution of these antibodies within clinical forms of the disease. The diagnosis of GBS has been established in 17 patients according to clinical, electrophysiological and laboratory (CSF) criteria. The serum antibodies to 63 kDa flagellar protein isolated from CJ serotype 0:19 were determined by ELISA and Western blot and serum anti-GM1 antibodies by ELISA. In relation to the disability score two patients were ambulatory, five were ambulatory with support, seven were bedridden and two patients needed respirator. Five (29%) patients had pure motor, while 12 (71%) had sensorimotor GBS. The cranial nerves were involved in 11 (65%) and 9 (53%) patients had autonomic dysfunction. Electromyoneurography showed primary axonal, predominantly motor neuropathy in 6 (35%) and demyelinating sensorimotor neuropathy in 11 (65%) patients. The CSF protein content ranged from 0.47 to 3.88 g/L. The antecedent infection with CJ was shown by serum antibodies to CJ flagellar protein in 12 (71%) patients. Fifteen (88%) patients had IgG anti-GM1 antibodies. Twelve (71%) patients had both antibodies. In relation to the clinical form, anti-CJ antibodies were found in 8 (73%) out of 11 patients with demyelinating GBS and in 4 (66.6%) out of 6 patients with axonal GBS. The high titer of anti-GM1 antibodies was found in all patients (100%) with axonal and in 9 (82%) out of 11 patients with demyelinating GBS. The association of IgG anti-CJ and IgG anti-GM1 antibodies was found in 4 (66.6%) out of 6 patients with axonal and in 8 (73%) out of 11 patients with demyelinating GBS. The main features of our patients with GBS were high frequency of antecedent infection with CJ, unusually frequent association with anti-GM1 antibodies, and equally frequent association of anti-CJ and anti-GM1 antibodies in both, axonal and demyelinating GBS.

[Acute sciatic neuropathy--"post-Saturday palsy"].

This is a case report of 25-year old, unemployed male, admitted to hospital due to acute onset of the left foot drop, subsequent walking difficulty and numbness of the left calf and foot. Symptoms began after prolonged sleep with previous heroin abuse by sniffing. During neurological examination, mild weakness of knee flexors, moderate weakness of plantar flexors and paralysis of foot dorsiflexors, together with hypesthesia of the left calf, foot and fingers, predominantly in the innervation area of common peroneal nerve on the same side, were observed. The electrophysiologic examination revealed predominant involvement of peroneal division within the sciatic nerve, together with recorded conduction block indicating the compression as possible mechanism of nerve injury. The patient was administered corticosteroid therapy during two months, what resulted in almost complete recovery. The peculiarity of this case report is in the presence of the sciatic nerve "Saturday night palsy" with possible effect of former heroin abuse.