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Biomedical subjects

U Seneviratne

Publications and source records attributed to U Seneviratne.

7 recordsLinked to original sources

Acute small fibre sensory neuropathy: another variant of Guillain-Barré syndrome?

Six patients who presented with acute sensory neuropathy were studied. All patients underwent detailed clinical assessment along with electrophysiological tests and relevant laboratory investigations. All patients had acute onset numbness, reaching the peak deficit within 4 weeks. Four of them had associated burning dysaesthesia. An antecedent illness was reported in four; diarrhoea in three, and urinary tract infection in one. The neurological examination disclosed normal muscle strength, symmetric glove and stocking type sensory loss for pain and temperature, normal proprioception, and vibration senses with normal or brisk tendon reflexes. Analysis of CSF demonstrated albuminocytological dissociation in all. Routine motor and sensory nerve conduction studies were normal. Sympathetic skin responses were also normal except for the lower limbs in one patient. Stool cultures for Campylobacter jejuni were negative. The outcome was favourable. Burning dysaesthesia disappeared within 4 months. Numbness and objective sensory loss tended to persist longer. The clinical features and normal routine nerve conduction studies, which assess large diameter nerve fibre function, indicate small sensory fibre dysfunction in the group. Their presentation and CSF findings would fit into the diagnosis of sensory Guillain-Barré syndrome. The current study suggests that acute small fibre sensory neuropathy (ASFSN) is another clinical entity which could perhaps be included in the heterogeneous range of Guillain-Barré syndrome.

Acute Disease↗

Bathing epilepsy.

A patient who had complex partial seizures provoked by bathing is reported. All the attacks occurred during or immediately after bathing, irrespective of water temperature. The semiology was suggestive of a seizure focus in the mesial temporal lobe. Though there are some similarities with hot-water epilepsy, this case appears to be a distinct type of reflex epilepsy.

Adult↗

Guillain-Barré syndrome.

Guillain-Barré syndrome is an autoimmune disorder encompassing a heterogeneous group of pathological and clinical entities. Antecedent infections are thought to trigger an immune response, which subsequently cross reacts with nerves leading to demyelination or axonal degeneration. Both intravenous immunoglobulin treatment and plasma exchange have been found to be equally beneficial. Several factors are useful in predicting the outcome of these patients.

Guillain-Barre Syndrome↗

Lambert-Eaton myasthenic syndrome.

The Lambert-Eaton myasthenic syndrome is a neuromuscular disorder characterised by defective neurotransmitter release at autonomic neurones and presynaptic terminals of the neuromuscular junction. It is caused by an IgG autoantibody formed against especially the P/Q type of voltage-gated calcium channels (VGCC) which is an essential component of the mechanism of neurotransmitter release. Many patients have an associated small cell carcinoma of the lung which appears to provide the antigenic stimulus for antibody production, although there is another group with no underlying malignancy. Both groups show an association with immunological disorders. Assay of VGCC antibody titres and electrophysiological tests help to differentiate Lambert-Eaton myasthenic syndrome from other disorders of the neuromuscular junction. Several drugs and therapeutic interventions capable of producing significant clinical improvement are currently available. Patients should also be investigated for underlying tumours, the specific treatment of which can result in remission or amelioration of symptoms.

4-Aminopyridine↗

Neurological manifestations of snake bite in Sri Lanka.

BACKGROUND AND AIMS: Snake bite is an important cause of mortality and morbidity in certain parts of Sri Lanka. This study was designed to determine the offending snakes, neurological manifestations, disease course, and outcome in neurotoxic envenomation. METHODS AND MATERIAL: Fifty six consecutive patients admitted with neurological manifestations following snake bite were studied prospectively. Data were obtained regarding the offending snakes, neurological symptoms, time taken for onset of symptoms, neurological signs, and time taken for recovery. RESULTS: The offending snake was Russell's viper in 27(48.2%), common and Sri Lankan krait in 19(33.9%), cobra in 3(5.4%), and unidentified in 7(12.5%). Ptosis was the commonest neurological manifestation seen in 48(85.7%) followed by ophthalmoplegia (75%), limb weakness (26.8%), respiratory failure (17.9%), palatal weakness (10.7%), neck muscle weakness (7.1%), and delayed sensory neuropathy (1.8%). Neurological symptoms were experienced usually within 6 hours after the bite. Following administration of antivenom, the signs of recovery became evident within a few hours to several days. The duration for complete recovery ranged from four hours to two weeks. CONCLUSIONS: Complete recovery of neuromuscular weakness was observed in all patients except for one who died with intracerebral haemorrhage shortly after admission.

Adolescent↗