Neurological and neuropsychiatric

Table 4.1 Involvement and status of glutamate transporters in neurological and neuropsychiatric disorders... 

Wichmann T., DeLong M.R. Deep brain stimulation for neurologic and neuropsychiatric disorders. Neuron, 2006, 52,197— 204. 

Exposure to CO results in a wide variety of potential adverse effects, particularly in individuals who have pre-existing cardiac or lung disease. Infants, the elderly, and the developing fetus are particularly vulnerable since they have less capacity to tolerate cardiovascular compromise. An additional problem is the delayed neurological and neuropsychiatric effects that have been documented after some significant exposures. The incidence of delayed neurotoxicity is between 2% and 30%. 

In zooo, the prevalence of cerebral palsy in metropolitan Adanta was 3.1 per 1000 8-year-olds. Of 10-year-old children, 23 of every 10,000 had cerebral palsy. Eighty-one percent of these children had spastic cerebral palsy. Seventy-five percent had one or more other disabilities (epilepsy, mental retardation, hearing loss, or vision impairment).7 Like many neurological and neuropsychiatric disorders, a diagnosis of cerebral palsy is a description of symptoms, not an identification of causes. 

Folate deficiency may promote neurological and neuropsychiatric disorders. 

Delayed neurologic and psychiatric disorders following acute arsine exposures have been reported (Frank 1976). Exposure concentrations were not provided, but duration of exposure ranged from 10 to 90 min. Within hours after the exposures, characteristic signs of arsine poisoning (e.g., hemolysis and hematuria) were observed. Polyneuropathies and neuropsychiatric syndromes were detected at 1-36 mon after the acute exposures to arsine. 

Table 14-4 lists the psychiatric manifestations of CO poisoning. Survivors can experience chronic and progressive neurological and psychiatric deterioration (Roohi et al. 2001). Persons with severe poisoning may completely recover only to develop a neuropsychiatric syn-... 

In approximately two-thirds of patients infected with the TBE virus, only the early (viremic) phase is seen. In the remaining third, patients experience either the typical biphasic course of the disease or a clinical illness that begins with the second (neurologic) phase. The convalescent period can be long and the incidence of sequelae may vary between 30 and 60%, with long-term or even permanent neurologic symptoms. Neuropsychiatric sequelae have been repon in 10- 20% of patients. 

Neurological symptoms result from demyelination of the spinal cord and are potentially irreversible. The symptoms and signs characteristic of a vitamin B 2 deficiency include paresthesis of the hands and feet, decreased deep-tendon reflexes, unsteadiness, and potential psychiatric problems such as moodiness, hallucinations, delusions, and psychosis. Neuropsychiatric disorders sometimes develop independently of the anemia, particularly in elderly patients. Visual loss may develop as a result of optic atrophy. 

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