S. Misra
Institute of Medical Sciences, Banaras Hindu University
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Acta Neurologica Scandinavica | 1987
N.K. Singh; A. K. Jaiswal; S. Misra; Pramod K. Srivastava
ABSTRACT— Twenty‐four patients with Guillain‐Barré syndrome were prospectively evaluated for evidence of autonomic dysfunction. It occurred in 16 (66.7%) patients, usually during the peak period of paralysis, in the form of either excess or inadequate activity of sympathetic and/or parasympathetic nervous systems. Its clinical manifestations comprised of sinus tachycardia (33.3%), bradycardia (8.3%), hypertension (33.3%), postural hypotension (35%), urinary sphincteric disturbances (20.8%) and anhydrosis of lower limbs (12.5%). Assessment of cardiovascular responses to autonomic function tests revealed impaired alterations in heart rate during deep breathing (31.6%), Valsalvas manoeuvre (28.6%), sustained handgrip (25%), cold‐pressor test (36.4%), postural change (35%) and atropine test (20%); and impaired rise in blood pressure during firm handgrip (25%) and cold‐pressor test (36.6%). ECG abnormalities were noticed in 8 (33.3%) patients. They comprised of depressed ST segment in 5, inverted T wave in 3, tall T wave in 2 and prolonged QTc in 2 patients. Two patients died of respiratory failure. Autonomic dysfunction in Guillain‐Barré syndrome did not appear to have any prognostic significance as there was no significant difference in autonomic dysfunction between good—and bad—outcome groups of patients.
Acta Neurologica Scandinavica | 2009
S. N. Rao; B. C. Katiyar; K. R. P. Nair; S. Misra
Twenty unselected patients with hypothyroidism were evaluated by clinical and electrophysiological techniques for neuromuscular dysfunction. On clinical examination, muscle weakness was observed in four, paraesthesia in 11, carpal tunnel syndrome in three, and peripheral neuropathy in two of the patients.
Seizure-european Journal of Epilepsy | 2001
Maneesh Kumar Singh; Ravindra Kumar Garg; Gopal Nath; D.N. Verma; S. Misra
This study was planned to observe the clinical and radiological course of single small enhancing CT lesions in Indian patients presenting with new-onset-seizures. In this study, 75 patients with new-onset seizures and a single enhancing CT lesion were prospectively followed up for 1 year. All patients fulfilled the criteria of cysticercus granuloma. The repeat CT scans were performed 2 months after the first CT scan. Antiepileptic drug therapy was the only form of treatment given. The majority of patients were below 20 years of age. Simple partial seizure, with or without secondary generalization, was the commonest type of seizure encountered in these patients. In follow-up CT scans 84% of patients showed either disappearance or regression in the size of lesion. The proportion of patients showing complete disappearance of CT lesions was 0.73 (95% CI, 0.61-0.80). In 11 (15%) patients the lesions were calcified. In nine patients, in whom the lesion had persisted or regressed, another follow-up CT scan (6 months after the second scan) revealed either complete disappearance or calcification of the lesions. The majority (86.6%) of patients remained seizure free for 1 year after starting antiepileptic drugs. Ten patients experienced seizure recurrences within the first month of therapy. The proportion of patients who remained seizure free was 0.86 (95% CI, 0.76-0.92). Four patients experienced seizure recurrence even after complete disappearance of CT lesions. In the majority of patients the lesions disappeared spontaneously and in a few the lesions calcified; hence these patients did not require anticysticercal therapy. Antiepileptic therapy was helpful in controlling further recurrences of seizures in most of the patients. A few patients experienced seizures even after disappearance of CT lesions.
Acta Neurologica Scandinavica | 2006
A. Verma; S. Misra
Objectives – The duration of antiepileptic drug (AED) therapy in cases of solitary cerebral cysticercus granuloma (SCCG) presents a major dilemma and the efficacy of short‐term (6 months) vs long‐term (2 years) AED therapy has been studied.
Acta Neurologica Scandinavica | 1986
A.K. Chauhan; B. C. Katiyar; S. Misra; A.K. Thacker; N.K. Singh
ABSTRACT Twenty‐eight consecutive male patients with primary and secondary hypogonadism (14 each) were evaluated clinically and electrophysiologically for muscle dysfunction. Although generalised muscle weakness was initially reported by only 9 patients, on direct questioning, it was recorded in 19. Objective weakness was found in 13 patients and it involved both the proximal and distal limb muscles. Quantitative electromyography showed evidence of myopathy in the proximal muscle in 25 patients, i.e., reduced MUP duration and amplitude with increased polyphasia in the deltoid and the gluteus maximus. There were no denervation potentials. None of the patients showed clinical neuropathy or NCV abnormalities. Thus, the profile of muscle involvement in hypogonadism closely simulates limb‐girdle muscular dystrophy and other endocrine myopathies. The incidence of muscle involvement was higher in secondary hypogonadism. Diminished androgens in primary hypogonadism and diminished growth hormone in the secondary hypogonadism are probably responsible for the myopathy.
Acta Neurologica Scandinavica | 1988
A.K. Thacker; S. Misra; B. C. Katiyar
ABSTRACT‐ Proximal conduction studies by F‐wave technique, with conventional distal motor and sensory conduction were performed along the ulnar nerves of 20 patients each with cervical spondylotic radiculopathy and/or myelopathy and with classical motor neurone disease (MND). Such F‐wave parameters as shortest F‐latency, F‐conduction velocity, conduction time and F‐ratio were calculated. Twenty‐five age‐ and sex‐matched healthy volunteers acted as controls. Proximal slowing associated with sensory conduction abnormalities and normal distal motor conduction favored cervical spondylosis (CS). Distal slowing with a normal proximal motor and sensory conduction was associated with motor neurone disease.
Neurology India | 1999
Garg Rk; Karak B; S. Misra
Epilepsy Research | 2000
Ravindra Kumar Garg; Manish Kumar Singh; S. Misra
Neurology India | 2000
Garg Rk; S. Misra; Verma R
Neurology India | 2003
Singh Nn; Verma R; Pankaj Bk; S. Misra