Dystonic-Parkinsonian syndrome after cyanide poisoning: clinical and MRI findings.

Carella, F.; Grassi, Maria Pia; Savoiardo, M.; Contri, P.; Rapuzzi, Barbara; Mangoni, A

doi:10.1136/jnnp.51.10.1345

Cited by 75 publications

(30 citation statements)

References 9 publications

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“…Some sequelae of cyanide toxicity in humans have been associated with damage to the basal ganglia, including Parkinsonian symptoms (Finelli, 1981;Uitti et al, 1985;Carella et al, 1988;Rosemberg et al, 1989;Feldman and Feldman, 1990;Messing, 1991), phobic anxiety (Nicholson and Vincenti, 1994) and psychosis (El Ghawabi et al, 1975;Kales et al, 1997). Furthermore, cyanide intoxication has been linked to personality change in a man (Uitti et al, 1985).…”

Section: Discussionmentioning

confidence: 98%

Clinical and pathological effects of short-term cyanide repeated dosing to goats

Soto-Blanco¹,

Stegelmeier²,

Górniak³

2005

J. Appl. Toxicol.

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The purpose of this work is to determine and describe the effects of subacute cyanide toxicity to goats. Eight female goats were divided into two groups. The first group of five animals was treated with 8.0 mg KCN kg(-1) body weight day(-1) for seven consecutive days. The second group of three animals was treated with water as controls. Complete physical examination, including observation for behavior changes, was conducted before and after dosing. One treated animal was euthanized immediately after dosing. Later, two of the remaining treated animals and a control goat were euthanized after a 30-day recovery period. Euthanized animals were necropsied and tissues were collected and prepared for histologic studies. Clinical signs in treated goats were transient and included depression and lethargy, mild hyperpnea and hyperthermia, arrhythmias, abundant salivation, vocalizations, expiratory dyspnea, jerky movements and head pressing. Two goats developed convulsions after day 3 of treatment. One animal developed more permanent behavioral changes as she became less dominant and aggressive. Histologic changes included mild hepatocellular vacuolation and degeneration, mild vacuolation and swelling of the proximal convoluted tubules of the kidneys and spongiosis of the white matter (status spongiosis) of the cerebral white tracts, internal capsule, cerebellar peduncles, spinal cord and peripheral nerves. In summary, sub-lethal cyanide intoxication in goats resulted in behavioral changes, and during the treatment period animals showed delayed signs of toxicity. Significant histologic lesions in goats were observed and need to be characterized further.

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Section: Discussionmentioning

confidence: 98%

Clinical and pathological effects of short-term cyanide repeated dosing to goats

Soto-Blanco¹,

Stegelmeier²,

Górniak³

2005

J. Appl. Toxicol.

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“…While high acute intoxication leads to rapid death, sublethal acute intoxication can result in basal ganglion damage manifesting itself as parkinsonism [20]. Long-term low cyanide exposure can be associated with neurodegeneration involving the peripheral nerves, dorsal columns, pyramidal tract, and optic and cochlear nerves [1,2,3].…”

Section: Discussionmentioning

confidence: 99%

Clinical and Etiological Profile of Tropical Ataxic Neuropathy in Kerala, South India

et al. 2008

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Background/Aims: Very little is known about the occurrence of tropical ataxic neuropathy (TAN) from southern India. This study describes the clinical spectrum of TAN from Kerala, southern India, and explores its etiology. Methods: We reviewed the clinical and laboratory profile of 40 TAN cases diagnosed in a tertiary referral center in central Kerala. We enquired the consumption of cassava foods and estimated the thiocyanate levels in the serum, urine and sural nerve. Results: The notable demographic characteristics included female preponderance, peak age at onset in the thirties, rural residence and poor socioeconomic status. The diet in the majority comprised a large amount of tapioca, which is low in protein. In addition to sensory peripheral neuropathy, 90% had decreased hearing, 50% had decreased vision, and 25% had spasticity involving the lower extremities. None had signs of overt vitamin deficiencies or malabsorption syndrome. Compared to the controls, the serum, urine and sural nerve thiocyanate levels were significantly elevated in the patients. With cessation of cassavaintake and better nutrition, improvement in the neurological disability occurred in the majority. Conclusions: This study, for the first time, provides evidence for the occurrence of TAN in south India and the possible etiological role of cassava intake.

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“…Cyanide can be released into the environment during the course of industrial usage, from smoke or vehicles exhaust containing the incomplete combustion products of nitrogen-containing organic polymers. Also, several plants contain cyanogen glycosides that can release hydrogen cyanide upon biodegradation or digestion [6].…”

Section: Introductionmentioning

confidence: 99%

Neuromodulatory effect of solvent fractions of Africa eggplant (Solanium dadyphyllum) against KCN-induced mitochondria damage, viz. NADH-succinate dehydrogenase, NADH- cytochrome c reductase, and succinate-cytochrome c reductase

et al. 2018

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Background: In the past few years, there has been a tremendous increase in the number of plant-based health supplements with respect to their safety and efficacy in diseases treatment and prevention. Solanum dasyphyllum, also known as Africa eggplant is ethnomedicinally used as an antivenom, pain reliever and anticonvulsant in various part of Nigeria, however, there is no scientific data to support some of these claims. Methods: This study evaluated the protective effect of solvent fractions of Solanum dasyphyllum, hexane fraction of S. dasyphyllum (HFSD), dichloromethane fraction of S. dasyphyllum (DFSD), ethylacetate fraction of S. dasyphyllum (EAFSD), methanolic fraction of S. dasyphyllum (MFSD) and crude fraction of S. dasyphyllum (CFSD) on cyanideinduced oxidative stress and neurotoxicity in vitro in the cerebral cortex. Neuroprotective activities were evaluated by assaying for markers of oxidative stress, neurotoxicity and electron transport system enzymes via evaluating lipid peroxidation (LPO), protein carbonyl (PC), reduced glutathione (GSH), acetylcholinesterase (AChE), NADH-succinate dehydrogenase (NSD), NADH-cytochrome c reductase (NCR), and succinate-cytochrome c reductase (SCR) in the homogenate of cerebral cortex.

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Dystonic-Parkinsonian syndrome after cyanide poisoning: clinical and MRI findings.

Cited by 75 publications

References 9 publications

Clinical and pathological effects of short-term cyanide repeated dosing to goats

Clinical and pathological effects of short-term cyanide repeated dosing to goats

Clinical and Etiological Profile of Tropical Ataxic Neuropathy in Kerala, South India

Neuromodulatory effect of solvent fractions of Africa eggplant (Solanium dadyphyllum) against KCN-induced mitochondria damage, viz. NADH-succinate dehydrogenase, NADH- cytochrome c reductase, and succinate-cytochrome c reductase

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