Methods for establishing a surveillance system for cardiovascular diseases in Indian industrial populations.

OBJECTIVE: To establish a surveillance network for cardiovascular diseases (CVD) risk factors in industrial settings and estimate the risk factor burden using standardized tools. METHODS: We conducted a baseline cross-sectional survey (as part of a CVD surveillance programme) of industrial populations from 10 companies across India, situated in close proximity to medical colleges that served as study centres. The study subjects were employees (selected by age and sex stratified random sampling) and their family members. Information on behavioural, clinical and biochemical determinants was obtained through standardized methods (questionnaires, clinical measurements and biochemical analysis). Data collation and analyses were done at the national coordinating centre. FINDINGS: We report the prevalence of CVD risk factors among individuals aged 20-69 years (n = 19 973 for the questionnaire survey, n = 10 442 for biochemical investigations); mean age was 40 years. The overall prevalence of most risk factors was high, with 50.9% of men and 51.9% of women being overweight, central obesity was observed among 30.9% of men and 32.8% of women, and 40.2% of men and 14.9% of women reported current tobacco use. Self-reported prevalence of diabetes (5.3%) and hypertension (10.9%) was lower than when measured clinically and biochemically (10.1% and 27.7%, respectively). There was marked heterogeneity in the prevalence of risk factors among the study centres. CONCLUSION: There is a high burden of CVD risk factors among industrial populations across India. The surveillance system can be used as a model for replication in India as well as other developing countries.

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.

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.

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.

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.