Circling movements in human viral encephalitis.
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Biomedical subjects
Publications and source records attributed to K Radhakrishnan.
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A 28-year-old man with von Recklinghausen's neurofibromatosis was first seen with a spastic-ataxic gait and epileptic seizures of recent onset. computerized tomographic scan established the diagnosis of aqueductal stenosis, rarely reported in patients with von Recklinghausen's disease. The value of computerized tomography in the etiological diagnosis of hydrocephalus in von Recklinghausen's disease is emphasized and the pathogenesis of aqueductal narrowing in neurofibromatosis is discussed.
The clinical profile and therapeutic response of 25 patients with migrainous headaches with interparoxysmal electroencephalographic (EEG) abnormalities in the form of sharp complexes are discussed. The clinical features of these patients consisted of male preponderance, early age of onset in males, long history of illness in females, very low incidence of aura and family history of migraine, frequent severe paroxysms, poor response to routine anti-migraine drugs and good response to anti-convulsant drugs. It is speculated that the EEG abnormalities in migraine may have a congenital basis which finds expression in vasomotor instability through hypothalamus and autonomic nervous system.
The clinical pharmacological, and neuroradiological observations in six patients with spontaneous blepharospasm-oromandibular dystonia (Meige's) syndrome are recorded. This group consisted of five males and one female, mean age at onset being 50.3 years. The duration of symptoms ranged from three months to 12 years, three patients having had symptoms for over four years. The dyskinesia was arrhythmic and asymmetrical in the orbicularis oculi and masseter muscles electrophysiologically. Pharmacological studies evinced no consistent response to parenteral physostigmine, no response to oral levodopa and no significant improvement in the dyskinesia following oral haloperidol. Lumbar air encephalogram was done in five patients, and showed frontal cortical atrophy without ventricular dilation in three. It is concluded that Meige's syndrome is a distinct nosological entity, and that physostigmine test is unlikely to be helpful in the differential diagnosis from neuroleptic-induced tardive dyskinesia. Neurotransmitter imbalance in the basal ganglia in this disorder remains to be established, and at present there is no satisfactory drug treatment for this progressively disabling movement disorder.
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The arteriographic pattern of left hand vessels was studied in 20 patients in leprosy by percutaneous brachial arteriography. Arteriographic abnormalities noted consisted of occlusion, narrowing, tortuosity, dilatation, irregularity and incomplete filling of the lumen by contrast medium. Such abnormal findings were seen in all the arteriograms studied and more than one vessel involvement was noted in over 50 percent cases. This study clearly demonstrated that arterial involvement in leprosy was frequent. No correlation was found between motor weakness and vascular abnormalities. There was no difference in arterial lesions between the patients with and without trophic changes. There was also no correlation between the severity of vascular changes and decline in motor nerve conduction. Degree of histopathological abnormalities in the sural nerve biopsy from these patients showed no features of micro angiopathic neuropathy. It is concluded that the observed vascular abnormalities do not contribute significantly in the genesis of neurological deficit in leprosy.
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Fifty-four patients, with multiple sclerosis from North-West India are described. This included two pathologically proven cases of multiple sclerosis. Five patients conformed to the definition of neuromyelitis optica (Devic's syndrome). This study is in agreement with the other series reported from Asia regarding the special clinical features of multiple sclerosis described from this part of the world. There is more common occurrence of visual impairment at onset, predominant involvement of optic nerves and spinal cord and higher incidence of classical neuromyelitis optica. There is no relationship of any or all cerebro spinal fluid abnormalities with the type of multiple sclerosis, duration of an attack and disability, except for the possible relation between the type of colloidal gold reaction pattern and the type of multiple sclerosis.
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An Ala322Asp mutation in the GABRA1 gene was recently reported to be responsible for causing the autosomal dominant (AD) form of juvenile myoclonic epilepsy (JME) in a French-Canadian family. To study if JME families from India exhibiting the AD mode of inheritance carry the Ala322Asp mutation, we examined 35 unrelated JME-affected individuals from such families for the Ala322Asp mutation in GABRA1. Ala322Asp mutation was not observed in any of these JME-affected individuals, suggesting that this mutation is unlikely to be a predominant mutation involved in causation of epilepsy. To evaluate the possibility of other mutation(s) in and around GABRA1 that may predispose to JME, we compared the allele frequencies at two marker loci, D5S2118 and D5S422, flanking GABRA1, in probands and 100 matched population controls. One of the allele frequencies at D5S422 shows a significant difference between the cases and controls (chi-square = 11.44, d.f. = 1, P = 0.0007), suggesting genetic association between JME and genes located in the proximity of the DNA marker.
In this retrospective study the clinical features in 16 children with spinal muscular atrophy (SMA) were reviewed and classified into three stages. The muscle biopsy specimen were routinely processed with liquid-nitrogen-isopentane and 8 micron thick frozen-sections were studied for histochemical changes. The clinical features in Type III SMA resembled with limb-girdle muscular dystrophy and the muscle biopsy was useful in distinguishing these two entities. It is being evaluated that prenatal diagnosis of SMA is possible with DNA technology developed recently in our country.
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