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Biomedical subjects

S S Pandya

Publications and source records attributed to S S Pandya.

At least 19 recordsLinked to original sources
PubMed1998

Correlation of quantitative tests of nerve and target organ dysfunction with skin immunohistology in leprosy.

Loss of nociception and hypohidrosis in skin are hallmarks of leprosy, attributed to early invasion by Mycobacterium leprae of Schwann cells related to unmyelinated nerve fibres. We have studied skin lesions and contralateral clinically unaffected skin in 28 patients across the leprosy spectrum with a range of selective quantitative sensory and autonomic tests, prior to biopsy of both sites. Unaffected sites showed normal skin innervation, when antibodies to the pan-neuronal marker PGP (protein gene product) 9.5 were used, with the exception of intraepidermal fibres which were not detected in the majority of cases. Elevation of thermal thresholds and reduced sensory axon-reflex flare responses in affected skin correlated with decreased nerve fibres in the subepidermis, e.g. axon-reflex flux units (means+/-SEM) for no detectable innervation; decreased innervation; and clinically unaffected skin, were 23+/-3.1; 41.2+/-7.3; and 84.5+/-4.0, respectively. Reduced nicotine-induced axon-reflex sweating was correlated with decreased innervation of sweat glands. Where methacholine-induced direct activation of sweat glands was affected, there was inflammatory infiltrate and loss of sweat gland structure. This study demonstrates a correlation between selective nerve dysfunction on clinical tests and morphological changes in skin, irrespective of the type of leprosy, and is the first to show that loss of sweating in leprosy may result either from decreased innervation and/or involvement of the sweat glands. The findings have implications for the selection and monitoring of patients with leprosy in clinical trials which aim to restore cutaneous function.

Autonomic Nervous System↗
PubMed1994

Severe pan-sensory neuropathy in leprosy.

The sensory loss which occurs in leprosy is essentially cutaneous, resulting from centripetally ascending infection, the host cellular response and fibrosis, from dermal to certain mixed nerves. The hallmark is pain/temperature and touch/pressure loss. Muscle denervation is a byproduct of mixed nerve involvement. Leprous sensory and motor neuropathy presents a stereotyped picture, with preservation of position sense, noninvolvement of the large girdle muscles, and retained deep tendon reflexes. We report clinical and investigative details of 7 patients (3 males, 4 females) with mild-to-moderate polyneuritic leprosy who manifested severe proprioceptive loss in the upper per limbs; the lower limbs were similarly affected in 4 of them. Tendon reflexes were absent in the ataxic limbs. No other cause was found for the ataxia. Electrophysiological studies confirmed damage to large cutaneous and muscle afferents, and a normal EMG pattern in hip and shoulder muscles. Of great interest was the histology of a lumbar sensory ganglion biopsied in a severely disabled patient. There was extensive neuron loss and degeneration and reactive proliferation of capsular cells ("nodules of Nageotte"), an inflammatory focus of lymphocytes, and no bacilli. This suggests to us that the proprioceptive loss in these patients could well be the result of an unusual "leprous ganglionitis." Further clarification of the mechanism of ganglion degeneration and the frequency of inflammation could come from immunohistology of tissues from African green monkeys with experimental polyneuritic leprosy.

Adult↗
PubMed1990

Simplified technique for recording human cortical & spinal evoked muscle potentials.

Muscle responses evoked on transcranial stimulation of the motor cortex (corticomotor) and motor roots (spinal) were studied in 20 healthy volunteers using a simplification of Rossini's technique and conventional EMG equipment. Cortical motor responses were consistently obtained from the contralateral upper limb with tolerable stimuli. Lower limb motor responses were inconsistent and sometimes required uncomfortably high stimulus strengths. In the upper limbs, peripheral conduction time (PCT) was estimated by the latency of the response to spinal stimulation. A comparable measure of PCT was obtained for the abductor pollicis brevis (APB) from the F-responses. The difference between the latency of the corticomotor response and the PCT was considered to represent central motor conduction time (CMCT). Corticomotor latencies were: APB 18.51 +/- 1.1 msec, biceps 9.77 +/- 0.46 msec and tibialis anterior 26.5 +/- 2.9 msec. CMCT from cortex to C8/T1 segments (APB) was 4.68 +/- 0.6 msec and between cortex and C5/C6 (biceps) 4.24 +/- 0.42 msec.

Adult↗
PubMed1987

Dapsone neuropathy--report of three cases and pathologic features of a motor nerve.

We report the clinical features, electrophysiologic findings, and dapsone and isoniazid excretion studies in three young people who ingested excessive amounts (2-4 times the prescribed dose) of dapsone for hypopigmented macules and who developed, subacutely, progressive motor neuropathy a few months later. Pathologic studies on a biopsied motor nerve confirmed the electrophysiologic conclusion of distal motor axonopathy. All made a rapid recovery in a few months after dapsone was stopped, although electrical abnormalities persisted. One patient was a rapid acetylator of isoniazid.

Adolescent↗
PubMed1983

Surgery on the peripheral nerves in leprosy.

In a short review the operative possibilities of peripheral nerve involvement in leprosy concerning pain and paralysis are discussed. External, extraneural and funicular neurolysis, transposition, and treatment of nerve abscess proved to be the methods of choice.

Abscess↗
PubMed1983

An attempt to influence nerve degeneration and regeneration by using macrophage cell homogenate.

The effect of the contents of activated macrophages on the degenerative/regenerative process in the mouse sciatic nerve was investigated as a possible model for leprosy. The whole cellular homogenate or saline was injected every week around physically impaired (to bypass the perineurial barrier) and normal nerves. Recovery of the nerve function was monitored clinically and electromyographically. After 14 weeks animals were sacrificed and nerves were processed for histology. The data obtained from 134 experimental and control nerves were rated and analysed statistically. The course of the nerve regeneration in the physically impaired nerve with and without homogenate was found to be similar. One of the reasons for this could be insufficient concentration of the homogenate in the endoneurial space.

Animals↗
PubMed1981

Electrophysiologic and histologic studies in leprosy and some acrodystrophic neuropathies.

In vitro electrophysiologic and light microscopic studies were carried out on the sural nerve in six patients with non-leprous neuropathy with plantar ulceration and in six patients with various types of leprous neuropathy. In the non-leprous group (with congenital and acquired neuropathy) the abnormalities in the compound action potentials of the myelinated (large and small) fibers were usually more striking than those in the unmyelinated fibers potentials. In the leprous neuropathies, on the other hand, the three major fiber groups tended to be involved indiscriminately, the unmyelinated fiber potential being as liable to abnormality as the myelinated fiber potentials. Histologically the nerve fiber damage in the congenital neuropathies appeared to be moderate to gross involvement of the myelinated fibers without the prominent demyelination and degeneration/regeneration seen in leprosy and the other acquired neuropathies. Leprous neuropathy showed, besides fiber abnormalities, the simultaneous deleterious effects of inflammation and fibrosis. It is a matter for speculation whether disturbed conduction in the large myelinated touch-pressure mediating fibers contributes significantly to impaired pain perception (mediated by small fibers) and plantar ulceration in leprosy and other acrodystrophic neuropathies.

Action Potentials↗
PubMed1980

Quantitative electromyography using automatic analysis--diagnostic utility of turns per unit amplitude.

Quantitative electromyographic (QEMG) data from 3 muscles recorded with a 50-micronV threshold for the turns and amplitude measurements are presented. Using turns per unit amplitude as the index, consistent and comparable readings were recorded from abductor digiti minimi, biceps brachii and vastus medialis in normal subjects, namely 1.132 +/- 0.08 (31 subjects), 1.059 +/- 0.122 (31 subjects) and 1.007 +/- 0.088 (11 subjects), respectively. It is shown here that the diagnostic yield increases when all 3 values, namely, turns/s, average amplitude and turns/unit amplitude are considered in conjunction rather than considering the first 2 alone.

Adult↗