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Biomedical subjects

H V Sardesai

Publications and source records attributed to H V Sardesai.

14 recordsLinked to original sources
PubMed1987

Electrophysiological studies in acute organophosphate poisoning.

Electrophysiological studies in suicidal patients with organophosphate poisoning are reported. Patients often developed muscular weakness of variable severity owing to diplorisation block at nicotinic receptors. During such paralysis nerve conduction velocity and distal latencies were normal even in severely paralysed patients. The amplitude of the compound action potential was smaller than in controls and often showed a repetitive response. The amplitude tended to be lower in those more severely affected. On repetitive stimulation there was usually no decrement with three stimuli per second and only occasional decrement at 10 per second. At 30 Hz several cases showed a decrement even in the absence of paralysis. This response to repetitive stimuli is thus quite distinct from that seen in either myasthenia or Eaton Lambert syndrome. On three occasions after poisoning with dichlorovos there was first anticholinesterase insecticide poisoning and later delayed neurotoxicity as seen with triorthocresylphosphate. These cases showed all the features of a severe pure motor axonal degeneration neuropathy.

Action Potentials↗
PubMed1985

Cerebellar ataxia in enteric fever.

In a study of enteric fever, cerebellar ataxia was found to be the commonest neurological manifestation, second only to toxic delirium. Excluding toxic delirium (found in 25-30% of cases) neurologic deficit was noted in 5.0% of a series of 718 consecutive cases; 2.3% showed cerebellar ataxia, either as an isolated feature or in association with other lesions. The ataxia usually appeared in the second week, and lasted a mean of 9.4 days. In 90% of cases it had cleared completely within a month.

Cerebellar Ataxia↗
PubMed1976

An unusual family of benign "X" linked muscular dystrophy with cardiac involvement.

A family of benign X-linked muscular dystrophy is described. Two of the 3 affected members appear quite representative of Becker's dystrophy. A third shows no pseudohypertrophy, only gross atrophy, affecting proximal and distal muscles and also shows early onset contractures and electrocardiographic abnormalities and is in these ways much more representative of the variety described by Emery and Dreifuss (1966). Two of the cases have distinctly abnormal electrocardiograms with extensive and deep Q waves and abnormal R/S ratios and VI. Both these have shown progression of electrocardiographic abnormalities during a 2-year follow-up. The family is reported to document this very unusual occurrence.

Adolescent↗
PubMed1974

Neurological manifestations of organophosphorous insecticide poisoning.

Neurological findings are described in 200 consecutive cases of suicidal ingestion of organophosphorous insecticides. Miosis is almost universal. We found impairment of consciousness in 10%, fasciculations in 27%, convulsions in 1%, toxic delirium in 50%, and paralysis in 26%. Toxic delirium was attributed to treatment with atropine. Paralytic signs were divided into type 1 signs (present on admission) and type 2 signs (appearing later while on atropine treatment). Type 1 signs, chiefly impaired consciousness and bilateral pyramidal tract signs, respond to atropine. The most common type 2 signs are proximal limb weakness, areflexia, and cranial nerve palsies. EMG studies during type 2 paralysis show a myasthenic response in some cases. Of 36 cases with type 2 signs 15 died from respiratory paralysis after a variable period of artificial respiration. Twenty-one recovered and no residual neurological deficit has been noted. Atropine did not influence type 2 paralysis. It is claimed that type 2 signs differ significantly from those described before as `delayed neurotoxicity' and may represent an alternative mode of human toxicity with organophosphorous compounds.

Facial Paralysis↗