PubMed Health⌕ Search

Biomedical subjects

N Senanayake

Publications and source records attributed to N Senanayake.

At least 19 recordsLinked to original sources
PubMed1992

Does pralidoxime affect outcome of management in acute organophosphorus poisoning?

Acute organophosphorus (OP) poisoning is usually treated with atropine plus cholinesterase reactivators such as oximes, but controlled trials to assess the efficacy of oximes in OP poisoning have not been done. A period when the acetyl cholinesterase reactivator pralidoxime chloride was not available in Sri Lanka gave us the opportunity to compare atropine alone for treatment of moderate to severe OP poisoning (21 patients) with atropine plus pralixodime (24 patients). Outcome, as assessed clinically, was similar in the two groups. These results cast doubt on the necessity of cholinesterase reactivators for treatment of acute OP poisoning.

Adolescent↗
PubMed1992

Disorders of neuromuscular transmission due to natural environmental toxins.

A variety of natural toxins of animal, plant, and bacterial origin are capable of causing disorders of neuromuscular transmission. Animal toxins include venomous snakes and arthropods, venoms of certain marine creatures, skin secretions of dart-poison frogs, and poisonous fish, shellfish, and crabs. There are plant poisons such as curare, and bacterial poisons such as botulinum toxin. These act at single or multiple sites of the neuromuscular apparatus interfering with voltage-gated ion channels, acetylcholine release, depolarization of the postsynaptic membrane, or generation and spread of the muscle action potential. The specific actions of these toxins are being widely exploited in the study of neuromuscular physiology and pathology. Some toxins have proved to be valuable pharmaceutical agents. Poisoning by natural neurotoxins is an important public health hazard in many parts of the world, particularly in the tropics. Poisoning may occur by a bite or a sting of a venomous animal, or by the ingestion of poisonous fish, shellfish or other marine delicacies. Contaminated food is a vehicle for poisons such as botulinum toxin. Clinically, a cardinal feature in the symptomatology is muscle paralysis with a distribution characteristic of myasthenia gravis, affecting muscles innervated by cranial nerves, neck flexors, proximal limb muscles, and respiratory muscles. Respiratory paralysis may end fatally. This paper reviews from the clinical and pathophysiologic viewpoints, naturally occurring environmental neurotoxins acting at the neuromuscular junction.

Animals↗
PubMed1992

Neurological manifestations of malaria.

The involvement of the nervous system in malaria is reviewed in this paper. Cerebral malaria, the acute encephalopathy which complicates exclusively the infection by Plasmodium falciparum commonly affects children and adolescents in hyperendemic areas. Plugging of cerebral capillaries and venules by clumped, parasitized red cells causing sludging in the capillary circulation is one hypothesis to explain its pathogenesis. The other is a humoral hypothesis which proposes nonspecific, immune-mediated, inflammatory responses with release of vasoactive substances capable of producing endothelial damage and alterations of permeability. Cerebral malaria has a mortality rate up to 50%, and also a considerable longterm morbidity, particularly in children. Hypoglycemia, largely in patients treated with quinine, may complicate the cerebral symptomatology. Other central nervous manifestations of malaria include intracranial hemorrhage, cerebral arterial occlusion, and transient extrapyramidal and neuropsychiatric manifestations. A self-limiting, isolated cerebellar ataxia, presumably caused by immunological mechanisms, in patients recovering from falciparum malaria has been recognized in Sri Lanka. Malaria is a common cause of febrile seizures in the tropics, and it also contributes to the development of epilepsy in later life. Several reports of spinal cord and peripheral nerve involvement are also available. A transient muscle paralysis resembling periodic paralysis during febrile episodes of malaria has been described in some patients. The pathogenesis of these neurological manifestations remains unexplored, but offers excellent perspectives for research at a clinical as well as experimental level.

Adult↗
PubMed1992

Neurological complications of malaria.

This paper reviews the neurological complications of malaria. Cerebral malaria, the acute encephalopathy which complicates exclusively the infection by Plasmodium falciparum commonly affects children and adolescents in hyperendemic areas. Plugging of cerebral capillaries and venules by clumped, parasitized red blood cells causing blood sludging in the capillary circulation is one hypothesis to explain its pathogenesis. The other is a humoral hypothesis which proposes a nonspecific, immune-mediated, inflammatory response with release of vasoactive substances capable of producing endothelial damage and alterations of permeability. Cerebral malaria has a mortality rate up to 50%, and also a considerable longterm morbidity, particularly in children. Hypoglycemia, largely in patients treated with quinine, may complicate the cerebral symptomatology. Other central nervous manifestations of malaria include intracranial hemorrhage, cerebral arterial occlusion, and transient extrapyramidal and neuropsychiatric manifestations. A self-limiting, isolated cerebellar ataxia, presumably caused by immunological mechanisms, in patients recovering from falciparum malaria has been recognized in Sri Lanka. Malaria is a common cause of febrile seizures in the tropics, and it also contributes to the development of epilepsy in later life. Several reports of spinal cord and peripheral nerve involvement are also available. A transient muscle paralysis resembling periodic paralysis during febrile episodes of malaria has been described in some patients. The pathogenesis of these neurological manifestations in malaria remains unexplored, but offers excellent perspectives for research at clinical as well as experimental level.

Adolescent↗
PubMed1990

Familial eating epilepsy.

Eating-related seizures affecting 20 individuals among 59 siblings belonging to nine families are presented. The type of epilepsy was partial in all the affected individuals, and the seizures complex in 15 and simple in 5, secondarily generalized in the majority. The onset of epilepsy, in most cases, was in the second decade of life. A remarkable degree of intra-family consistency was observed with regard to age at onset, symptomatology of seizures and timing of eating seizures. The study demonstrates sibling clustering in a partial epilepsy, implicating for the first time genetic susceptibility in the aetiology of eating epilepsy.

Adolescent↗
PubMed1988

Acute organophosphorus insecticide poisoning in Sri Lanka.

Records of 92 cases of acute organophosphorus (OP) insecticide poisoning were analysed. Of the patients 91% were under 30 years of age and 86% were males. The common agents were Dimethoate, Methamidophos, Malathion, Monocrotophos and Fenthion. Poisoning was due to ingestion with suicidal intent in the majority. In addition to the acute cholinergic features, the other important manifestations were delayed onset respiratory paralysis and delayed polyneuropathy. The overall mortality was 18%.

Adolescent↗
PubMed1988

Pattern of acute poisoning in a medical unit in central Sri Lanka.

One hundred and seventy nine cases of acute poisoning constituting 1.1% of all admissions to the medical unit over 3 years were analysed. Eighty-three per cent of the patients were under 30 years of age and 72% were males. The common agents were: OP insecticides in 51%, kerosene oil in 12%, rat poison in 8% and drugs in 8%. Ingestion with suicidal intent was the common mode of poisoning. The overall mortality was 16%. The results from four other major centres in Sri Lanka are presented for comparison.

Acute Disease↗
PubMed1988

Acute organophosphorus insecticide poisoning during pregnancy.

Intoxication with organophosphorus insecticides following ingestion with suicidal intent in two patients who were in the second and third trimesters of pregnancy is reported. Successful management of the cholinergic and intermediate phases of poisoning enabled each pregnancy to proceed to term and end in normal vaginal delivery of a healthy baby.

Adult↗
PubMed1987

Delayed cerebellar ataxia: a new complication of falciparum malaria?

Twelve cases of an unusual phenomenon of ataxia were investigated in otherwise well, conscious patients recovering from a febrile attack of presumed falciparum malaria. The ataxia occurred as the fever was subsiding, usually after an afebrile period of two to four days. The delay between onset of fever and the ataxia was three to four weeks. Peripheral blood of all the patients contained gametocytes of Plasmodium falciparum, and in some cases ring stages. The ataxia was most noticeable in the legs and the clinical picture suggested selective impairment of the cerebellar system. Signs of improvement appeared in a few weeks but complete recovery took one to four months. The most likely pathogenic mechanism of the ataxia in these cases was an immune reaction triggered by the malaria parasite and affecting the cerebellum or its connections, or both.

Adolescent↗
PubMed1987

Neurotoxic effects of organophosphorus insecticides. An intermediate syndrome.

Acute neurotoxic effects during the cholinergic phase of organophosphorus insecticide poisoning and delayed neurotoxic effects appearing two to three weeks later are well recognized. We observed 10 patients who had paralysis of proximal limb muscles, neck flexors, motor cranial nerves, and respiratory muscles 24 to 96 hours after poisoning, after a well-defined cholinergic phase. The compounds involved were fenthion, monocrotophos, dimethoate, and methamidophos. Four patients urgently required ventilatory support. The paralytic symptoms lasted up to 18 days. A delayed polyneuropathy later developed in one patient. Three patients died. Electromyographic studies showed fade on tetanic stimulation, absence of fade on low-frequency stimulation, and absence of post-tetanic facilitation, suggestive of a postsynaptic defect. This neuromuscular junctional defect may have been the predominant cause of the paralytic symptoms, with neural and central components contributing to various degrees. Our patients appeared to have a distinct clinical entity (a so-called intermediate syndrome) that developed after the acute cholinergic crisis and before the expected onset of the delayed neuropathy.

Adult↗