Neurobehavioral deficits

Kilbum KH. 1993. Case report Profound neurobehavioral deficits in an oil field worker overcome by hydrogen sulfide. Am J Med Sci 306 301-305. 

With disruption of this barrier, molecules such as albumin freely enter the brain and ions and water follow. Because the brain lacks a well-developed lymphatic system, clearance of plasma constituents is slow, edema occurs, and intracranial pressure rises. At lower levels of exposure, subtle dysfunction of the blood-brain barrier may contribute to neurobehavioral deficits in children (Bressler and Goldstein 1991 Goldstein 1993). The particular vulnerability of the fetus and infant to the neurotoxicity of lead may be due in part to immaturity of the blood-brain barrier and to the lack of the high-affinity leadbinding protein in astroglia, which is discussed later in this section. Results of measurements of transendothelial electrical resistance across the blood-brain barrier from mice of various ages showed that lead potentiates cytokines-induced increase in ion permeability of the blood-brain barrier (Dyatlov et al. 

The interaction between exposure intensity and duration of exposure in the development of neurobehavioral deficits is not understood, in part because of a lack of biomarkers of long-term lead exposure. The strongest evidence for health effects of low level lead exposures on neurodevelopmental deficits is based on relationships between measured health outcomes and PbB concentrations. Although these studies suggest that a significant amount of the variability in the health outcomes (e.g., neurobehavioral deficits) can be attributed to variability in PbB concentrations, a substantial amount of variability in the outcomes usually cannot be assigned to PbB, even after many known potential confounders have been considered (i.e., Needleman and Gatsonis 1990 Pocock et al. 1994 Schwartz 1994 Winneke 1996). 

Rothenberg SJ, Schnaas L, Cansino-Ortiz S, et al. 1989a. Neurobehavioral deficits after low level lead exposure in neonates The Mexico City pilot study. Neurotoxicol Teratol 11 85-93. 

Undoubtedly, there is growing evidence for an association between disturbed sleep and impaired adolescent functioning however, more attention needs to be directed toward identifying possible causal paths and possible strategies for intervention. Furthermore, clinicians need to become more aware of the potential role of sleep disorders when evaluating children with neurobehavioral deficits. 

Pavol MA, Meyers CA, Rexer JL, Valentine AD, Mattis PJ, Talpaz M. Pattern of neurobehavioral deficits associated with interferon alfa therapy for leukemia. Neurology 1995 45(5) 947-50. 

Abou-Donia et al, 2002). Intramuscular injection of 0.1 and 1.0 mg/kg for 7 days, followed by a 30-day observational period, resulted in sensorimotor deficits in rat behavior, differential levels of NO, and increased acetylcholinesterase activity in the cortex of animals dosed with 1 mg/kg, suggesting multiple exposures to low doses of uranyl acetate caused prolonged neurobehavioral deficits in rats after the initial exposure has ceased, similar to the exposures of Gulf War veterans (Abou-Donia et al, 2002). 

Generally, according to high-dose exposure studies, animals exposed to nerve agents that exhibit seizures that are not promptly controlled develop brain damage and subsequent neurobehavioral problems. Animals that do not develop seizures or those that are rapidly and effectively treated with drugs that stop the seizures suffer no brain lesion and display no long-term neurobehavioral deficits. 

RaIiiIL cl cl. 1906 hu 1 100 360 100 0 increased latency on a neunibehavioral task (not a biologically relevant neurobehavioral deficit)... 

Neurobehavioral deficits reflected as impaired performance on a spatial learning and memory task were seen in the progeny of monkeys fed 0.08 mg/kg/day Aroclor 1248 for 18 months and allowed to breed 32 months postexposure (Levin et al. 1988). The deficit did not appear to be due to memory impairment, but rather to impairment in associafional or attenfional processes. Aroclor 1016, tested at a dose level of 0.008 mg/kg/day, did not significantly alter performance on that task (Levin et al. 1988), but impaired the monkeys ability to learn a simple spatial discrimination problem at 0.03 mg/kg/day (Schantz et al. 1989). These long-term studies in monkeys showed that doses of 0.03 mg/kg/day of some PCBs can alter performance in neurobehavioral tests. 

Neurochemical effects of PCBs have been examined in rats, mice, and monkeys exposed to commercial PCB mixtures and to individual PCB congeners. Some studies have assessed both neurochemical and neurobehavioral effects of PCBs in an attempt to link a biochemical alteration to a particular neurobehavioral deficit. 

Crofton 1998). Rates of elimination of both hormones from serum were accelerated in the pups that had been exposed to Aroclor 1254, relative to controls. These observations suggest that the observed neurobehavioral deficits may have been attributable to deficits in thyroid hormone. The increased elimination of T4 and T3 from serum is consistent with an induction of UDP-GT or other elimination pathways for thyroid hormones (e.g., deiodination of T4 to T3). Reduction in T4 levels in pups also have been induced by maternal administration of the dioxin-like congeners 3,3, 4.4, 5-pentaPCB (PCB 126) (Rice 1999a) and 3,3, 4,4 -tetraPCB (PCB 77) (Darnerud et al. 1996a). 

Storzbach D, Rohlman DS, Anger WK, et al Neurobehavioral deficits in Persian Gulf veterans additional evidence from a population-based study. Environ Res 85 1-13,2001... 

---