Brain dysfunction

S100B Developmental brain dysfunction, learning and memory deficits... 

Conners, C.K. Psychological effects of stimulant drugs in children with minimal brain dysfunction. Pediatrics 49 702-708, 1972. 

Historically, the HRB NP test, the most widely used and well-validated of all NP test batteries, takes from 6 to 8 hours for complete administration. Reducing an established test battery to a 2- to 3-hour structured assessment procedure requires the use of selected subtests those most sensitive to PCP-induced brain dysfunction. The development and validation of briefer screening batteries, which represent a reduction in the total number of subtests used, professional time, and expense is an emergent trend (Hartlage and Mains 1982, Reynolds et al. 1983). Based on our literature review and results of a pilot sample study of 30 PCP and polydrug abusers, the following subtests are recommended for inclusion in a brief NP assessment battery. 

Compared to the Category Test, SSP and SRT results show a relatively mixed performance profile. This profile is indicative of temporal lobe impairment and may explain the idiosyncratic character of PCP-induced brain dysfunction. Other HRB subtest data suggest that parietal lobe-mediated functions are less influenced by PCP abuse, since approximately 30 percent of this sample had error-free performances on a test sensitive to finger agnosia. 

The net results of our pilot study suggest that PCP-induced brain dysfunction cannot be understood solely on the basis of the pharmacological characteristics of PCP itself. There appear to be as many individuals with histories of intermittent, light use as there are chronic, moderate to heavy abusers of PCP who show significant impairment on the NP tests. 

Michaelson A, Sauerhoff MW. 1974. An improved model of lead-induced brain dysfunction in the suckling rat. Toxicol Appl Pharmacol 28 88-96. 

R. C. Griggs (eds) Metabolic Brain Dysfunction in Systemic Disorders. Boston Little, Brown Co, 1992, pp 55-86. 

Walkley, S. U. Pathogenic cascades in brain dysfunction. In F. M. Platt and S. U. Walkley (eds), Lysosomal Disorders of the Brain. New York Oxford University Press, 2004, pp. 290-324. 

In liver phosphorylase deficiency (glycogenosis type VI, Hers disease Fig. 42-1) and in two genetic forms of phosphorylase kinase deficiency, one of which is X-linked recessive, the other of which is autosomal recessive, hypoglycemia is either absent or mild. Symptoms of brain dysfunction do not usually occur (type VIII, Fig. 42-1) [1],... 

Defects of complex IV. These disorders, also termed COX deficiency, have clinical phenotypes that fall into two main groups one in which myopathy is the predominant or exclusive manifestation and another in which brain dysfunction predominates (Fig. 42-3). In the first group, the most common disorder is fatal infantile myopathy, causing generalized weakness, respiratory insufficiency and death before age 1 year. There is lactic acidosis and renal dysfunction, with glycosuria, phosphaturia and aminoaciduria, also termed DeToni-Fanconi-Debre syndrome. The association of myopathy and cardiopathy in the same patient and myopathy and liver disease in the same family has also been described [14]. 

Your entire life is affected when one whiff of perfume, fabric softener or fresh paint can result in a throbbing headache, brain dysfunction, an asthma attack, a convulsion or a myriad of other symptoms. Work performance, relationships and community ties collapse when your olfactory system is so heightened that you become ill from the smell of laundry products on the clothes of someone sitting all the way across the room. Fear overcomes you when suddenly carpeting, photocopies, car exhaust and other products produce the same effects, and the only way to protect yourself is through isolation. 

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