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At least 19 recordsLinked to original sources

[Neurotoxic syndrome in infectious diseases in children].

On the material of 72 children with infectious toxicoses the authors describe the encephalic syndrome as a manifestation of the neurotoxic syndrome. The neurotoxic syndrome was studied clinically and morphologically. A marked syndrome was characterized by a considerable edema of the brain and its stem and not infrequently by the vedging of the cerebellum into the great occipital orifice. Hemispheric focal symptomatology was typically associated with intracranial hemorrhage which was considered as a manifestation of the DIC syndrome. The authors believe that the neurotoxic syndrome in infectious toxicoses should be considered as general cerebral disorders of noninflammatory nature manifested in non-specific morphofunctional and metabolic disturbances.

Brain↗

Neurotoxic syndrome associated with risperidone and fluvoxamine.

OBJECTIVE: To report a case of a neurotoxic syndrome in a patient undergoing concomitant treatment with risperidone and fluvoxamine. CASE REPORT: A 24-year-old African American woman hospitalized for psychosis was unresponsive to risperidone. Because of obsessive symptoms, low doses of fluvoxamine were added to her treatment regimen. Within 2 days, she developed confusion, diaphoresis, diarrhea, hyperreflexia, and myoclonus, which then progressed to rigidity, fever, and unresponsiveness, requiring endotracheal intubation. Symptoms resolved over 10 days with discontinuation of medication, hydration, and bromocriptine 5 mg 3 times daily. Ultimately, she was treated with olanzapine and fluvoxamine without adverse effects. DISCUSSION: This represents the first reported case of a neurotoxic syndrome secondary to treatment with risperidone and fluvoxamine. Differential diagnosis between neuroleptic malignant syndrome (NMS) and serotonin syndrome (SS) could not be accurately determined because of the overlap of signs and symptoms of both syndromes. NMS and SS may represent different aspects of a more generalized neurotoxic syndrome. This could be an important consideration in formulating treatment for neurotoxic syndromes. CONCLUSIONS: Clinicians should be aware of potentially serious adverse reactions that may occur during concomitant treatment with antipsychotics and selective serotonin-reuptake inhibitors.

Adult↗

Organophosphorus poisoning and intermediate neurotoxic syndrome.

Very few cases of the "intermediate neurotoxic syndrome", a type of neurotoxic effect or organophosphate compound have been reported in the literature. We are reporting a case that developed the clinical features of such type of neurotoxic effect after 55 hours of taking the organophosphorus compound.

Adult↗

Neurotoxic syndromes and occupational exposure to solvents.

Neurotoxic syndromes due to occupational solvent exposure present a worldwide health problem, the magnitude of which varies from country to country. Apart from the relatively clear-cut exposure-effect relationships in acute solvent intoxications, those caused by long-term, low-level occupational exposure to solvents are more difficult to detect. Controversial opinions and even debate are frequently encountered in literature on this matter. This is partly due to differences in neurobehavioral methods used, partly to difficulties in obtaining accurate information about exposure. These effects can be studied in humans using biochemical, clinical, and epidemiological methods. It is thus quite conceivable that direct comparison of the results obtained by different methods is not always possible. Moreover, exposure to a variable mixture of solvents is frequent in an occupational setting which is problematic from the toxicological point of view. The clinical pictures of "chronic" occupational solvent intoxications are, with few exceptions, quite nonspecific in nature and share several common features regardless of the underlying chemical exposure. The development of manifest disease is insidious and high interindividual variation of symptoms and signs exists. Some solvents cause primarily peripheral neuropathy. Deterioration in many psychological and neurophysiological functions can be seen. The most common subjective symptoms of solvent intoxication are headache, tiredness, memory disturbances, and dizziness. Clinical findings comprise signs of the central nervous system depression (psychoorganic syndrome, tiredness), dizziness, disturbances in coordination, and general neurasthenic signs. From the clinical point of view, it is important to define the criteria for a diagnosis. In different countries the diagnostic criteria for solvent intoxication may vary considerably, which provides additional difficulties in interpreting the results of studies in this field.

Central Nervous System↗

[Neurological syndromes linked with the intake of plants and fungi containing a toxic component (I). Neurotoxic syndromes caused by the ingestion of plants, seeds and fruits].

INTRODUCTION: A wide range of plants, seeds and fruits used for nutritional and medicinal purposes can give rise to neurotoxic symptoms. DEVELOPMENT: We review the neurological pathology associated with the acute or chronic consumption of plants, seeds and fruits in human beings and in animals. Of the plants that can trigger acute neurotoxic syndromes in humans, some of the most notable include Mandragora officinalis, Datura stramonium, Conium maculatum (hemlock), Coriaria myrtifolia (redoul), Ricinus communis, Gloriosa superba, Catharanthus roseus, Karwinskia humboldtiana and Podophyllum pelatum. We also survey different neurological syndromes linked with the ingestion of vegetable foodstuffs that are rich in cyanogenic glycosides, Jamaican vomiting sickness caused by Blighia sapida, Parkinson dementia ALS of Guam island and exposition to Cycas circinalis, Guadeloupean parkinsonism and exposition to Annonaceae, konzo caused by ingestion of wild manioc and neurolathyrism from ingestion of Lathyrus sativus, the last two being models of motor neurone disease. Locoism is a chronic disease that develops in livestock feeding on plants belonging to Astragalus and Oxytropis sp., Sida carpinifolia and Ipomea carnea, which are rich in swainsonine, a toxin that inhibits the enzyme alpha mannosidase and induces a cerebellar syndrome. CONCLUSIONS: The ingestion of neurotoxic seeds, fruits and plants included in the diet and acute poisoning by certain plants can give rise to different neurological syndromes, some of which are irreversible.

Administration, Oral↗

Pearls and pitfalls in the approach to patients with neurotoxic syndromes.

Neurotoxins are an important cause of neurologic disorders. A vast number of potentially neurotoxic compounds exist, including prescription drugs, illicit substances, and exposures through the workplace, residence, hobbies, and the environment. Effects of neurotoxins can mimic neurologic illnesses; therefore, it is important to consider neurotoxins in the differential diagnosis of any patient with neurological dysfunction. Paramount to the diagnosis of a possible neurotoxic syndrome is establishing causation. This can be done by a systematic approach utilizing principles in epidemiology and applying them to the individual patient. This approach is discussed in the following article in an attempt to bring structure to solving problems in a complex area of medicine.

Adult↗

[Characteristics of the neurotoxic syndrome in children with perinatal pathology of the nervous system].

Comprehensive examinations of 100 children aged under 1 year with perinatal pathology of the central nervous system have helped to detect clinical, biochemical, and immunologic features in the course of the neurotoxic syndrome that developed in the presence of vitamins A and E inadequate supply. The efficacy of parenteral aevit in correction of the detected disorders was studied.

Acute Disease↗

Neurotoxic syndrome produced in chickens by a cyclic phosphate metabolite of tri-o-cresyl phosphate--a clinical and pathological study.

A clinical and neuropathological comparison was made between chickens poisoned with tri-o-cresyl phosphate and those treated with the major cyclic phosphate metabolite of tri-o-cresyl phosphate. Ataxia was evident with both materials, and the degree of peripheral neuropathy increased with higher doses of these agents. Morphological changes were evident with the onset of symptoms and increased in number as the neurological signs progressed. Demyelination of the spinal cord following administration of the metabolite occurred at doses considerably below those necessary to effect peripheral nerve degeneration. Axon and myelin damage was prominent with both agents. The relationship between these effects and those produced by certain other organophosphates such as dyflos (diisopropyl fluorophosphonate) is discussed.

Animals↗

Neuropsychological toxicology: identification and assessment of neurotoxic syndromes.

Neuropsychological toxicology, or, more commonly, "neurobehavioral toxicology" is the study of how naturally or industrially produced nervous system poisons effect neuropsychological functioning. Research of this sort has been widely disseminated in European and Scandinavian medical literature during the past two decades but is only just beginning to enter neuropsychological literature of the United States. Neuropsychological sequelae of several representative human neurotoxins are briefly reviewed, including metallic lead, the solvent toluene, organophosphate pesticides and antihypertensive medication. These substances represent exemplars from some of the major classes of potentially neurotoxic substances; metals, solvents, pesticides, and prescription drugs. They are also examples of neurotoxins that have been examined with neuropsychological methods and for which neuropsychological symptoms or syndromes have been discovered. Testing procedures sensitive to neurotoxic exposure are also summarized. The role of the neuropsychologist as neurobehavioral toxicologist is explored. It is suggested that the neuropsychologist is in a unique position to perform research and clinical evaluations relating to neurotoxic exposure, and that the sub-clinical effects of neurotoxic exposure may be most sensitively discovered with these methods. Further, neurotoxic effects may be subject to misdiagnosis without knowledge of how to examine for these substances. The future expansion of neuropsychology into "neuropsychological toxicology" is advocated.

Journal Article↗

Angiostrongylus cantonensis: role of eosinophils in the neurotoxic syndrome (Gordon-like phenomenon).

The role of eosinophils in the pathophysiology of Angiostrongylus cantonensis infections was investigated in nonpermissive (guinea pig) and permissive (rat) hosts. Neurological symptoms similar to the Gordon phenomenon (ataxia, tremor, paralysis) together with a loss of Purkinje cells in the cerebellum were observed after intracraneal injection of human eosinophil extracts or after infection with A. cantonensis, only in guinea pigs and not in rats. Blood eosinophilia as well as eosinophil numbers present in the cerebellum and in the cerebrospinal fluid were higher in guinea pigs than in rats, at all times after infection with A. cantonensis. Increased levels of cytotoxicity toward L3 larvae in vitro were obtained in the presence of guinea pig eosinophils and IgE antibodies, rather than with the corresponding rat effector system. The detection of one eosinophil granule component, the eosinophil peroxidase, in the cerebrospinal fluid from infected guinea pigs but not from rats suggested that in nonpermissive hosts, neurological disorders, similar to the previously described Gordon phenomenon, might be due to eosinophil neurotoxins released after interaction of eosinophils with the parasites.

Angiostrongylus↗

p,p'-DDT-induced neurotoxic syndrome: experimental myoclonus.

p,p'-DDT (100 to 600 mg per kilogram orally) produced spontaneous and stimulus-sensitive myoclonus in mice and rats. Drugs that enhance brain serotonergic activity reduced p,p'-DDT-induced myoclonus, and serotonin antagonists invariably aggravated this syndrome. p,p'-DDT-treated rats had increased concentrations of 5-hydroxyindoleacetic acid (5-HIAA) in seven regional areas, but serotonin was increased only in the midbrain and cerebellum. We postulate that p,p'-DDT-induced myoclonus may be causally related to blockage of serotonin receptors or inhibition of serotonin release into the synapse, resulting in functional deficiency of this neurotransmiter at the receptor site.

5-Hydroxytryptophan↗