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Biomedical subjects

K Puvanendran

Publications and source records attributed to K Puvanendran.

27 records · Page 2Linked to original sources
PubMed1982

Basal ganglia calcification on computer tomographic scan. A clinical and radiological correlation.

Computerised tomography of the brain was used to demonstrate basal ganglia calcification which may be of an insufficient degree to be seen on skull X-ray. Cases referred for CT scan from hospitals in Singapore for various reasons over a period of 12 months were studied for basal ganglia calcification. There was a startlingly high incidence of 1.5%, as 47 cases (all except 2 were Chinese) showed such calcification. In 42 cases there was no evidence of basal ganglia calcification on skull X-ray. 16 cases showed neurological affection, fits being the commonest manifestation. An unexpected finding was that no case had abnormality of calcium metabolism or evidence of hypoparathyroidism or pseudohypoparathyroidism. The CT scan is very sensitive in demonstrating minimal basal ganglia calcification and our impression is that such calcification is common.

Adolescent↗
PubMed1981

Cerebral metastasis in bronchial carcinoma.

A prospective study of 61 consecutive cases of bronchial carcinoma was done to detect cerebral metastasis and study their clinical presentations. Computerised tomography (CT Scan) was utilised as a screening procedure in 36 cases along with electroencephalography to detect cerebral secondaries. Of the cases studied with CT Scan and autopsy, 55% had brain secondaries. 18% of these cases had silent cerebral secondaries. 30% of the 61 cases studied has signs and symptoms referable to brain secondaries. An interesting clinical presentation was a dysequilibrium which in many of them was an extreme truncal ataxia, confining them helplessly to bed and relieved to some extent by a shunt operation.

Aged↗
PubMed1979

Neuromuscular transmission in thyrotoxicosis.

The occurrence of thyrotoxicosis in myasthenia gravis is estimated as 5.3% (Osserman et al. 1967) but the incidence of myasthenia in the course of thyrotoxicosis is only 0.2% (Simpson 1968). The association between these two diseases is not a chance one and there are two possible basic mechanisms viz. the action of thyroid hormone on the neuromuscular junction or the existence of a cause common to both. The fatigability seen clinically in thyrotoxic myopathy could be partly attributed to myasthenia. With these possibilities in mind, a search for electromyographic stigmata of latent myasthenia was done on 48 consecutive cases of hyperthyroidism who also had chronic myopathy by performing repeated nerve stimulation. Eight cases had abnormal neuromuscular transmission as in myasthenia gravis and one of these cases later developed clinical myasthenia involving the ocular muscles. Three other cases showed abnormal facilitation as in the Eaton-Lambert syndrome.

Humans↗
PubMed1979

Thyrotoxic myopathy: a clinical and quantitative analytic electromyographic study.

The clinical entity of chronic thyrotoxic myopathy was considered rare by Waldenström in 1945. Forty eight consecutive patients with thyrotoxicosis were studied clinically and by electromyography for muscle involvement. Quantitative electromyographic techniques were used to analyse both the electromyographic activity of the muscle at a standard tension and also the single motor potential obtained in isolation at minimal effort. The interference pattern was described in simple numerical terms such as the number of potential changes/s and the mean amplitude. All cases that were thyrotoxic (both clinically and on thyroid function tests) showed the changes of myopathy on electromyography, though only 68% of the cases showed clinical myopathy consisting of muscle weakness and/or atrophy.

Adolescent↗
PubMed1978

Syndrome of Dejerine's Fourth Reich.

Dejerine's (1914) precise description of the human corticobulbar tracts is now doubted and forgotten for want of clinical significance. He described them as five bundles of aberrant pyramidal fibres which separate out as leashes from the corticospinal fibres at different levels and each had its territory of bulbar nuclei (like the Reich which is the territory of the German empire of which there were only three). Five cases are described who presented with uppermotor neurone lesion of the 7th, 10th and 12th cranial nerves without evidence of involveement of the pyramidal fibres to the limbs. It is postulated that this is caused by a lesion of the 4th Reich described by Dejerine.

Cranial Nerves↗
PubMed1977

Electromyographic (EMG) study in thyrotoxic periodic paralysis.

Thyrotoxic periodic paralysis (TPP) is produced by a different metabolic disorder than familial periodic paralysis. In the familial disorder, a myopathic cause is well known, but although electromyography can be used to demonstrate the site of the lesion in TPP, such studies are rare in the medical literature and the results are conflicting. In this report, EMG studies were carried out on eight Chinese patients with thyrotoxic periodic paralysis during the attack and the results compared with studies repeated during a remission. Most cases showed a myopathic pattern during an attack of paralysis which disappeared during remission. The myopathic changes noted were a decrease in duration of muscle action potentials, an increase in polyphasic potentials, a satisfactory interference pattern with reduced amplitude and a reduced amplitude of the evoked muscle action potential on nerve stimulation. Peripheral nerve function was normal in the cases studied. It is concluded that the weakness in TPP is myopathic and that the peripheral nerve function during paralysis is normal.

Action Potentials↗
PubMed1977

Delayed facial palsy after head injury.

Where facial palsy follows head injury after many days, the mechanism is not clear, and there has been no detailed study on this condition. In this prospective study, an attempt is made to estimate this complication of head injury, and to study its pathogenesis, natural history, prognosis, and sequelae which differ markedly from Bell's palsy. It has a much worse prognosis and so surgical decompression should be considered early in this condition.

Adolescent↗
PubMed1977

Electrodiagnostic study in delayed facial palsy after closed head injury.

The time course of electrical reactions in this condition varied much from that after section of the facial nerve or after Bell's palsy. It was at least a week before denervation could be suspected in the latter conditions by electrodiagnostic methods. In post-traumatic delayed facial palsy we have demonstrated electrical reactions showing denervation at the time of palsy or even a few days before, and this is probably related to its pathogenesis. Denervation occurred in 82% of cases which is about double the incidence in Bell's palsy.

Craniocerebral Trauma↗