MyMedR

Oliva vidua fulminans, a marine mollusc, responsible for five fatal cases of neurotoxic food poisoning in Sabah, Malaysia

Kan SK, Singh N, Chan MK

Trans R Soc Trop Med Hyg, 1986;80(1):64-5.

PMID: 3727000

This is the first report in which a marine mollusc, Oliva vidua fulminans (olives), generally not known to be poisonous, was responsible for death in five children after consuming boiled olives with tamarind. The onset of symptoms was rapid 10 to 20 min after consumption of the olives. Signs and symptoms included nausea, vomiting, abdominal pain, tingling sensation around the lips, numbness around the mouth, drowsiness, lethargy and generalized weakness with paraesthesia in the limbs. The five deaths occurred within 3 to 4 hours after eating the poisoned olives and resulted from respiratory failure. Left-over olives from the affected household and freshly collected live olives had a toxicity of 14,200 mouse units (M.U.) and 15,000 M.U. per 100 g meat respectively. No other common chemical poison and organophosphorus insecticides were detected. The neurotoxic agent was acid and heat stable and was toxic at pH less than 4. Its action was similar to that of paralytic shellfish poisoning which was caused by toxins from certain dinoflagellates.

Matched MeSH terms: Nervous System Diseases/chemically induced

Does long term supplementation of vitamin E cause detrimental effects on the central nervous system? Morphological and histological study in experimental male Wistar rats

Mohamad Fairuz Y, Azian A, Nursiati MT, Srijit D, Hamzaini AH, Wan Zurinah WN, et al.

Clin Ter, 2013;164(2):119-24.

PMID: 23698204 DOI: 10.7417/CT.2013.1529

Aging is attributed to neuronal loss associated with increased oxidative stress. Vitamin E, and in particular, tocotrienol are potent antioxidants, which have been shown to be neuroprotective. The main aim of the present study was to observe the effect of long term intake of vitamin E in the form of tocotrienol rich fraction (TRF) and refined, bleached, deodorized palm olein (RBDPO) on the brain of experimental rats.

Matched MeSH terms: Central Nervous System Diseases/chemically induced*

Fulltext Lithium neurotoxicity

Suraya Y, Yoong KY

Med J Malaysia, 2001 Sep;56(3):378-81.

PMID: 11732087

Inspite of the advent of newer antimanic drugs, lithium carbonate remains widely used in the treatment and prevention of manic-depressive illness. However care has to be exercised due to its low therapeutic index. The central nervous system and renal system are predominantly affected in acute lithium intoxication and is potentially lethal. The more common side effect involves the central nervous system. It occurs early and is preventable. We describe three cases of lithium toxicity admitted to Johor Bahru Hospital, with emphasis on its neurological preponderance.

Matched MeSH terms: Central Nervous System Diseases/chemically induced

Fulltext Delayed chronic polyneuropathy following organophosphate poisoning: a case report

Low ET, Loh TG

Med J Malaysia, 1987 Jun;42(2):113-4.

PMID: 2845234

A patient with organophosphate poisoning who survived the acute phase and subsequently developed delayed neuropathy is presented. The features of this form of delayed neuropathy are described and the implications in our local context discussed.

Matched MeSH terms: Peripheral Nervous System Diseases/chemically induced*

Fulltext Evaluation of difference in the neurotoxicity produced by dermal application of chlorpyrifos on the neonatal and adult mice

Mitra NK, Lee MS, Nadarajah VD

Trop Biomed, 2010 Apr;27(1):19-29.

PMID: 20562809

Dermal exposure to organophosphate pesticide is important because of its popular use. This study planned to compare the changes in serum acetylcholinesterase, paraoxonase and neuronal density of hippocampus and iso-cortex between two age groups of Swiss albino mice (18-day-old and 150-day-old) after dermal application of (1/2) LD50 of chlorpyrifos for 14 days. Statistically significant reduction was observed in serum acetylcholinesterase (Mann-Whitney test, p<0.05) and neuronal density (Independent samples t-test, p<0.05) in exposed groups compared to the control. The reduction in serum AChE and neuronal density was more pronounced in exposed adult mice than in exposed neonatal mice. The paraoxonase level was insignificant in control neonatal mice, whereas it was 890-fold more in exposed neonatal mice. Upregulated paraoxonase levels may be extrapolated to produce relatively lower reduction of cholinesterase and neuronal density in neonatal mice.

Matched MeSH terms: Central Nervous System Diseases/chemically induced*

Non-Hodgkin's lymphoma with left suprascapular neuropathy on magnetic resonance imaging

Faridah Y, Abdullah BJ

Hong Kong Med J, 2003 Apr;9(2):134-6.

PMID: 12668827

Magnetic resonance imaging is gaining importance in the diagnosis of nerve and muscular disorders. The ability of magnetic resonance imaging to delineate the different muscles and the nerve in any plane has made the differentiation between the changes of neuropathy, denervation, and nerve entrapment possible. Although findings on magnetic resonance imaging are non-specific, their use, coupled with clinical symptoms and electromyographic findings, allow an accurate diagnosis to be made without resorting to invasive biopsies.

Matched MeSH terms: Peripheral Nervous System Diseases/chemically induced*

Adverse effects of cytotoxics-platinum agents

Selvaratnam G, Philips RH, Mohamed AK, Radzi A

Adverse Drug React Toxicol Rev, 1997 Aug;16(3):171-97.

PMID: 9512763

Matched MeSH terms: Peripheral Nervous System Diseases/chemically induced

Vincristine-induced peripheral neuropathy in survivors of childhood acute lymphoblastic leukaemia

Tay CG, Lee VWM, Ong LC, Goh KJ, Ariffin H, Fong CY

Pediatr Blood Cancer, 2017 Aug;64(8).

PMID: 28139029 DOI: 10.1002/pbc.26471

BACKGROUND: Vincristine, an essential component of childhood acute lymphoblastic leukaemia (ALL) therapeutic protocols, is associated with dose-dependent neurotoxicity, but its long-term morbidity in treated children has not been clearly elucidated. The aim of this study is to determine the prevalence of vincristine-induced peripheral neuropathy (VIPN) among Malaysian childhood ALL survivors and its impact on motor function and quality of life.

PROCEDURE: Survivors of childhood ALL aged 4-18 years who had completed chemotherapy for 2 years or more were evaluated for VIPN using both the clinical Total Neuropathy Score (cTNS) and nerve conduction studies. Motor function and quality of life of the survivors were assessed via the Bruininks-Oseretsky Test of Motor Proficiency Brief Form, Second Edition (BOT-2 Brief Form) and the Paediatric Quality of Life version 4.0 Generic Core Scales (PedsQL4.0) questionnaire, respectively.

RESULTS: One hundred and one survivors with a duration of follow-up ranging from 2.0 to 10.3 years were recruited. Twenty-seven (26.7%) had abnormal cTNS scores and 69 (68.3%) had electrophysiological evidence of neuropathy. Of these, 16 (15.8%) had combined clinical and electrophysiological neuropathy (VIPN). Those previously treated on the intermediate- or high-risk treatment stratification arms had a higher risk of developing VIPN (67.3 vs. 32.7%; odds ratio [OR]: 9.06, 95% confidence interval [CI]: 1.14-71.86; P = 0.014). Survivors with VIPN had significantly lower quality of life scores in the physical (P = 0.024) and social domains (P = 0.039) compared with peers without VIPN, but no association with poorer motor function was observed.

CONCLUSIONS: Sixteen percent of ALL survivors had VIPN. VIPN should be increasingly recognised as a late effect of chemotherapy, as it significantly affects physical and social function quality of life.

Matched MeSH terms: Peripheral Nervous System Diseases/chemically induced*

Neurophysiological symptoms and aspartame: What is the connection?

Choudhary AK, Lee YY

Nutr Neurosci, 2018 Jun;21(5):306-316.

PMID: 28198207 DOI: 10.1080/1028415X.2017.1288340

Aspartame (α-aspartyl-l-phenylalanine-o-methyl ester), an artificial sweetener, has been linked to behavioral and cognitive problems. Possible neurophysiological symptoms include learning problems, headache, seizure, migraines, irritable moods, anxiety, depression, and insomnia. The consumption of aspartame, unlike dietary protein, can elevate the levels of phenylalanine and aspartic acid in the brain. These compounds can inhibit the synthesis and release of neurotransmitters, dopamine, norepinephrine, and serotonin, which are known regulators of neurophysiological activity. Aspartame acts as a chemical stressor by elevating plasma cortisol levels and causing the production of excess free radicals. High cortisol levels and excess free radicals may increase the brains vulnerability to oxidative stress which may have adverse effects on neurobehavioral health. We reviewed studies linking neurophysiological symptoms to aspartame usage and conclude that aspartame may be responsible for adverse neurobehavioral health outcomes. Aspartame consumption needs to be approached with caution due to the possible effects on neurobehavioral health. Whether aspartame and its metabolites are safe for general consumption is still debatable due to a lack of consistent data. More research evaluating the neurobehavioral effects of aspartame are required.

Matched MeSH terms: Nervous System Diseases/chemically induced*

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