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Suramin, a promising chemotherapeutic agent, causes a dose-limiting sensorimotor polyneuropathy. We undertook a phase 1 study of suramin that included serial neurologic and electrophysiologic examinations as part of the safety evaluation. We found that 6 of 41 (15%) patients developed suramin-induced demyelinating neuropathy which resembled Guillain-Barre syndrome clinically. There was 1 asymptomatic patient with electrophysiologic abnormalities suggestive of a demyelinating neuropathy. In addition, 1 patient with mild axonal neuropathy at baseline had deterioration of his symptoms during suramin treatment. Four asymptomatic patients developed electrophysiologic findings suggestive of a mild axonal neuropathy. We conclude that: (1) serial electrophysiologic monitoring is helpful for early detection of suramin-induced neuropathy; and (2) fixed dosing schedule of suramin without adaptive control does not lead to an increased incidence of demyelinating neuropathy when compared to adaptively controlled dosing schedules.

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A new method for estimating the number of motor units using a surface EMG triggered averaging technique is described. This method provides an estimation of mean motor unit potential (MUP) amplitude at different levels of contraction, which can be utilized to estimate the number of motor units in a given muscle. Motor unit count estimated in abductor pollicis brevis (APB) muscle of 11 normal healthy subjects ranged from 131 to 371 with a mean of 246 +/- 68. In our preliminary study of patients with lower motor neuron lesions, there was a significant reduction in the number of motor units. We believe our new noninvasive method of motor unit counting is a relatively simple and reproducible physiological technique.

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We report seven cases of "rotatory seizures" with patients rotating around their axis one or several times. Contralateral EEG foci were localized in frontal and temporal regions. Computed tomography scan of three patients showed no structural lesion.

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Experience with computed tomography (CT) in patients with epilepsy has drawn attention to specific type of cerebral lesions widely prevalent in this part of the world. The lesions disappear spontaneously while patients receive only anticonvulsant therapy. The exact nature of these lesions is not yet understood. One-hundred and twenty-two such patients (M 77; F 45) were studied. Their age ranged from 3 to 57 (mean 21.8 +/- 12.7) years. Seizures were partial motor in 86 (70.5%), generalised tonic clonic in 31 (25.4%), complex partial in 4 and atonic in one case. Postictal hemiparesis was seen in 6 patients who completely recovered within 5 min to 7 days. One hundred patients underwent EEG examination. It was abnormal in 84 cases; 40 patients showed localisation which correlated with CT findings. Plain CT showed low attenuation lesions in all cases. Morphology on contrast enhancement was ring lesion in 50 (40.9%), disc lesion in 47 (38.5%), target lesion in 3 (2.5%), mixed lesion in 2 (0.8%), no enhancement in 18 (14.8%) and a speck with oedema in 2 (0.8%) cases. All lesions were cerebral, present at cortical-subcortical junction. The first follow-up scan was performed in 78 (63.9%) patients within 6-12 weeks. It showed complete disappearance of the lesion in 47 (60.3%) cases. Reduction in size of the lesion and surrounding oedema was observed in 24 (30.8%) cases. The follow-up scans in these 24 cases revealed disappearance of lesion in 11 cases and almost complete resolution of the lesion with a remaining speck in 13 cases. Cerebrospinal fluid (CSF) was normal in 95 out of 100 cases in which it was performed.(ABSTRACT TRUNCATED AT 250 WORDS)

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Cerebrospinal fluid (CSF) samples were collected from 12 patients with pyogenic meningitis (PM), 19 with tuberculous meningitis (TBM), 20 with clinically suspected but not definitely proved cases of tuberculous meningitis (STBM) and 12 normal controls. C-reactive proteins, immunoglobulins G, A, M and mycobacterial antigens were estimated in the CSF samples. Seven out of 51 (13.7%) samples obtained from the patient groups were positive for CRP. Immunoglobulins M and A were significantly raised in the PM group. When the TBM and STBM groups were compared with the controls a highly significant increase was obtained for all immunoglobulins. Mycobacterial antigens/epitopes were identified in 36.8% samples with TBAGB1 and TB68-H monoclonals and in 26.3% with WTB72-A2. In case of patients with suspected TBM, 6.6% were positive with TBAGB1 and WTB72-A2 and 13.3% with TB68-H. However, non-tuberculous patients also reacted with WTB72-A2 (10.5%) and TB68-H (21.0%). This is, to the authors' knowledge, the first report on the presence of CRP in the CSF. Technique for immunoglobulins in CSF is also updated in this paper. We infer that the monoclonal antibody TBAGB1 and immunoglobulins G and A may be safely considered as diagnostic markers of TBM. Estimation of CRP in CSF samples may be made to give a preliminary or additional diagnosis of meningitis regardless of its aetiology.

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A patient presented with acute arsenic neuropathy with asymmetric bilateral phrenic nerve involvement. The clinical and roentgenographic observations of phrenic nerve dysfunction were confirmed by prolonged phrenic nerve conduction time. The patient made a significant recovery with d-penicillamine therapy.

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H-reflex was studied in 43 patients with low back pain (including 20 patients with neurological deficit corresponding to S1 radix and 23 patients without deficit) and 20 control subjects. Among patients with neurological deficit the abnormality consisted of absent H-reflex (7 patients), increased H-latency (3 patients), reduced H/M maximal amplitude ratio (5 patients) or a combination of the latter two (2 patients). The H/M ratio was significantly reduced in this group as compared to control subjects and between affected and unaffected sides. Abnormal H-reflex correlated well with ankle jerk hypo- or areflexia, S1 sensory deficit and lumbar myelographic/CT abnormality. In 23 patients without deficit, increased H-latency and/or reduced H/M ratio was observed in 4 cases. Enhanced H/M ratio was noted in only 2 patients of this group. Use of H/M ratio seems to increase the sensitivity of H-reflex in the diagnosis of S1 radiculopathy.

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Leprous mononeuropathy may present without demonstrable maculoanesthetical patches. A case is described in whom wasting of the right hand was initially attributed to C8 T1 entrapment radiculopathy caused by cervical perineurial cysts. On the basis of the benign nature of the perineurial cysts and questionable right ulnar nerve thickening, the patient was given a trial of anti-leprosy drugs. A follow-up clinico-electrophysiological evaluation favored the diagnosis of leprotic ulnar mononeuropathy.

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A young female patient sustained bilateral parieto-occipital infarcts and presented with Balint's syndrome following treatment of eclampsia and caesarean section. Altered cerebral blood flow autoregulation and raised intracranial pressure due to eclampsia probably resulted in impaired cerebral perfusion and borderzone cerebral ischaemia in this patient. Careful reduction of blood pressure in patients with eclampsia is emphasized.

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Phrenic nerve conduction was performed bilaterally in 22 multibacillary (BL-LL) and 18 paucibacillary (BT-TT) leprosy patients and 25 control subjects. Prolonged phrenic nerve conduction time and/or reduced amplitude of diaphragm muscle action potential beyond 2.5 standard deviations of control mean values was observed in 9 BL-LL patients (4 bilateral) and 6 BT-TT patients (all unilateral). Out of the nine BL-LL patients with phrenic nerve involvement, median motor and/or sensory nerve conduction was also abnormal in seven patients. On fluoroscopy, diaphragm movements were normal in all patients. The study documents subclinical phrenic nerve involvement in leprosy--a fact not previously recognized.

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Landau-Kleffner syndrome is characterized by long-lasting acquired aphasia associated with seizures and EEG abnormalities. Three new cases of this rare syndrome are reported from India.

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Two cases of cyclic esotropia with associated central nervous system lesions are presented. One had a 48-hour cycle and the other a 24-hour cycle. In the first child, the condition developed after a third ventricular astrocytoma removal and in the second with the advent of an epileptiform disorder. Both were non-accommodative, non-paralytic in nature, and not associated with fusion disrupting factors. These patterns persisted uninterruptedly in one child for 22 months and in the other for more than 8 months until lost for follow-up.

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The effect of protein calorie malnutrition (PCM) and, thereafter, nutritional rehabilitation on neuromuscular dysfunction was evaluated electromyographically, histopathologically and biochemically in 24 young, growing, healthy rhesus monkeys. There were 2 control and 2 PCM groups with 6 animals in each group. Animals of one control and one PCM group were killed at 10-12 weeks and those of the second PCM group were rehabilitated and killed together with the second control group at 20-22 weeks. The animals with PCM demonstrated irritability, muscular wasting, weight loss and reduced physical activity. The electromyographic findings showed a myopathic pattern revealed by significant reduction in motor unit potential duration and amplitude, and amplitude of interference pattern at maximum effort. The histopathological abnormalities were non-specific and consisted of rare obliterations of cross striations and streaming fibrillar appearance, mild increase in epimysial and perimysial tissue and 29-34% reduction in fibre size. A statistically significant reduction in motor nerve conduction velocity of median, ulnar, common peroneal and tibial nerves was found. The muscle Na and K were evaluated in all groups of animals. Muscle K content was reduced and Na concentration was augmented following PCM. The change in concentration of electrolytes within the fibres and reduction in the diameter of muscle fibres could be related to the observed functional alterations. These changes returned to normal in rehabilitated group.

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The ultrastructure of skeletal muscle and activity of some enzymes of energy metabolism were studied to assess the effect of a deficiency of dietary energy and subsequent nutritional rehabilitation in 24 young, growing, healthy rhesus monkeys. Electron microscopy of muscles on energy-deficient animals showed thinning of myofibrils with widening of interfibrillar space and enlargement and accumulation of mitochondria at subsarcolemmal level. There was an apparent significant reduction in the fiber size. Muscle samples from each animal were analyzed for enzymes representative of glycolysis (phosphofructokinase [PFK] and lactate dehydrogenase [LDH], citric-acid cycle (isocitric dehydrogenase [ICDH] and citrate synthase [CS] and regeneration of ATP (creatine kinase [CK]. PFK and LDH activities were significantly augmented in energy-deficient animals. The increase in LDH activity resulted from a large increase in MU (skeletal muscle) LDH subunit. The activities of CS and ICDH were reduced. No alteration of CK in muscle and serum was observed. The morphological structure and enzyme activities returned to normal after nutritional rehabilitation.

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Forty-three children (aged 7 to 62 months) with protein calorie malnutrition (PCM) were studied; 13 had mild to moderate PCM and 30 severe PCM. A reduction of motor nerve conduction velocity and abnormalities of sensory conduction were present in both groups. The abnormality of motor nerve conduction was directly related to the severity of PCM and the presence of hypotonia and/or hyporeflexia. Sural nerve biopsies from both groups were studied for myelinated fibre density, fibre size spectrum, relationship of internodal length with diameter and qualitative light microscopic changes. The biopsies from children with mild to moderate PCM were characterized by a normal developmental change in myelinated fibres with an increasing proportion of medium and large size fibres, a transition from a unimodal to a bimodal distribution and an appropriate relationship of internodal length to fibre diameter. Evidence of mild segmental demyelination was observed in only one patient of this group. In contrast, in the biopsies from children with severe PCM, the normal developmental pattern for myelinated fibre size distribution was impaired with a persistence of small myelinated fibres, and there was a failure of internodal segments on large fibres to elongate with increase in age and significant segmental demyelination in about 50 per cent of cases. Retarded myelination and segmental demyelination probably form the morphological basis for impaired peripheral nerve function in PCM. Short internodes on large diameter fibres may also contribute to this effect.

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Forty four cases of the neurological complications of acute haemorrhagic conjunctivitis (AHC) seen in India during 1981 epidemic are reported. The disease predominantly affected adult males. The preceding attack of AHC, a latent period, prodromal symptoms of fever, myalgia and root pains followed by acute onset of lower motor neurone paralysis of limbs and/or cranial nerves formed the classical picture of neurological involvement. The recovery was poor and nearly half of the patients remained severely handicapped. Electrophysiological studies showed early appearance of widespread fibrillations and fasciculations, large polyphasic potentials of increased amplitude and reduced interference pattern. Nerve conduction studies were normal in most of the cases. Cerebrospinal fluid (CSF) examination revealed lymphocytic pleocytosis and rise in protein content. Significant antibody titres against enterovirus type 70 (EV 70) were demonstrated in the serum and the CSF. HLA studies showed low occurrence of A2 and B15 HLA antigens. Muscle biopsies revealed neurogenic atrophy and sural nerve biopsies were histologically unremarkable. The similarities of this disease with poliomyelitis and its pathogenesis are discussed.

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Acute cerebellar ataxia as an isolated neurological manifestation of enteric fever is very rare. Three cases of acute cerebellar ataxia associated with enteric fever are reported. The diagnosis of enteric fever was confirmed by positive blood culture, strongly positive Widal test and rising antibody titres. The major clinical features were rapid development of gait ataxia, limb ataxia and dysarthria. None of the patients had altered sensorium. The cerebellar involvement was noticed on the second or third day of fever which progressed for one to two days. The symptoms remained static for one to two weeks and thereafter all the patients showed gradual recovery in a few weeks. Acute onset of cerebellar lesion, self limiting course and cerebrospinal fluid pleocytosis suggest par- or post-infectious demyelinating pathology in these patients, who were not related to each other.

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