Disease relevance of Neurotoxicity Syndromes

• OBJECTIVES: This study determined whether performance in neurobehavioral tests deteriorates during subjectively annoying chemical challenge below known neurotoxic thresholds among persons with toxic encephalopathy with subjective hypersensitivity to chemicals [1].
• Asterixis and toxic encephalopathy induced by gabapentin [2].
• BACKGROUND: Solvent-induced chronic toxic encephalopathy (TE) is a slowly developing brain disorder associated with both a direct effect on the nervous system and as indirect experienced psychological distress [3].
• A 68-year-old woman with a history of mild hypertension developed a toxic encephalopathy following myelography with metrizamide [4].
• A toxic encephalopathy characterized by depressed level of consciousness, marked irritability, and ataxia developed in seven children, 5 years of age and younger, following administration of an antiemetic combination of pentobarbital and pyrilamine maleate [5].

Psychiatry related information on Neurotoxicity Syndromes

• Both clinical and epidemiological studies of the effects of exposure to toluene have shown that long-term exposure may result in chronic toxic encephalopathy, where one of the major symptoms is memory deficits [6].
• Psychological test performance during experimental challenge to toluene and n-butyl acetate in cases of solvent-induced toxic encephalopathy [1].

High impact information on Neurotoxicity Syndromes

• An outbreak of toxic encephalopathy caused by eating mussels contaminated with domoic acid [7].
• Two of these three patients had a severe neurotoxicity syndrome characterized by blindness, encephalopathy, and coma [8].
• Two epileptic patients developed an acute toxic encephalopathy consisting of altered behavior, deteriorating seizure control, and confusion while taking sodium valproate alone [9].
• Isoniazid-induced acute toxic encephalopathy [10].
• The value of routine 'one-off' measurements of valproate in clinical practice are further reduced by the absence of a clearly defined dose-related neurotoxicity syndrome [11].

Chemical compound and disease context of Neurotoxicity Syndromes

• Toxic encephalopathy induced by capecitabine [12].
• Toxic encephalopathy caused by topically applied diphenhydramine [13].
• Toxic encephalopathy is a rarely described side effect of 5-fluorouracil which usually presents with cerebellar, neuropsychiatric, and focal neurological symptoms [12].
• Toxic encephalopathy due to 1,1,1-trichloroethane exposure [14].
• Organo psycho syndrome (OPS) or chronic toxic encephalopathy (CTE) is a neurotoxic condition reported following long-term exposure to paints containing organic solvent and to other solvents [15].

Biological context of Neurotoxicity Syndromes

• Glutathione S-transferase M1 null genotype as a risk modifier for solvent-induced chronic toxic encephalopathy [16].
• We performed follow-up MRA (TOF 3D), MRI and transcranial doppler ultrasound (TCD) in the patients with isolated angiitis of the CNS (2/6), Crohn-disease-associated CV (1/6), and reversible arterial vasoconstriction (RAV) of the CNS (1 migraine, 1 eclampsia and 1 toxic encephalopathy) (3/6) [17].

Gene context of Neurotoxicity Syndromes

• We report the 1st case of capecitabine-induced toxic encephalopathy with epilepsy-like symptoms and diffuse white matter alterations on magnetic resonance imaging [12].
• The findings indicate that long-term exposure to CS2 involves a risk of developing toxic encephalopathy, demonstrable on both neurological and neuropsychological examination [18].
• Subjects with toxic encephalopathy of types 2A and 2B showed markedly lower P300 amplitudes than did controls in both paradigms [19].
• The sensitivity to an experimental toxic encephalopathy was evaluated using measures of EEG and the Buschke Memory Selective Reminding Test after the administration of scopolamine hydrobromide, 0.86 mg subcutaneously, to three healthy volunteers [20].
• The case illustrates the possibility of chronic toxic encephalopathy among patients with previous long-term exposure to CS2 [21].

References