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Deficit syndrome

Amphetamines (speed sulph, sulphate, uppers, wake-ups, billy whizz, whizz, whites, base) are synthetic stimulants which as medicines have been formed into a variety of tablets. Their current medical use is very limited and in fact only dexamphetamine sulphate, Dexedrine, is now available for use solely in the treatment of narcolepsy. The only other amphetamine available for medical use is methylphenidate (Ritalin) for the treatment of attention deficit syndrome in children. As a street drug, amphetamine usually comes as a white, grey, yellowish or pinky powder. The purity rate of street powders is less than 10%, the rest being made up of milder stimulants such as caffeine, other drugs such as paracetamol or substances like glucose, dried baby milk, flour or talcum powder. [Pg.512]

In view of these factors, it has been suggested that a deficiency of omega-3 fatty acid in the diet will decrease the concentration of these fatty acids available for synthesis of the required phospholipids in the body, including the brain. If this was a chronic deficiency it could increase the risk of development of some disorders, including depression, schizophrenia and attention deficit syndrome. There is some evidence that this is the case. [Pg.251]

Rosenheck R, Dunn L, Peszke M, et al. Impact of clozapine on negative symptoms and on the deficit syndrome in refractory schizophrenia. Department of Veterans Affairs Cooperative Study Group on Clozapine in Refractory Schizophrenia. Am J Psychiatry 1999 156 88-93. [Pg.94]

Specifically, the D2 receptors will also be blocked in the mesocortical DA pathway (Fig. 11-3), where DA may already be deficient in schizophrenia (see Figs. 10—10 and 10—11). When this happens, it can cause or worsen negative and cognitive symptoms. This is sometimes called the neuroleptic-induced deficit syndrome because it looks so much like the negative symptoms produced by schizophrenia itself and is reminiscent of neurolepsis in animals. [Pg.404]

Buchanan RW, Breier A, Kirkpatrick B, Ball P, Carpenter WT, Jr. (1998) Positive and negative symptom response to clozapine in schizophrenic patients with and without the deficit syndrome. Am J Psychiatry 155 751-760. [Pg.99]

In clinical studies, remoxipride has been shown to improve both positive and negative symptoms of schizophrenia and may have a place in the treatment of resistant schizophrenic patients. In addition such side effects as the neuroleptic-induced deficit syndrome, sedation and extrapyramidal side effects are apparently absent in patients treated with the drug. [Pg.272]

Putten, rediscovered drug-induced dysphoria, which was noted to be associated with neurological effects, especially akathisia2 (Van Putten 1974, 1975). This was later labelled as akinetic depression (Van Putten May 1978). In the 1990s the term neuroleptic-induced deficit syndrome was coined to describe affective and cognitive impairment (Lader 1994) and drug-induced dysphoria was revisited (Hollister 1992 King, Burke, Lucas 1995). [Pg.70]

Lader, M. 1994, Neuroleptic-induced deficit syndrome. Historical introduction, Acta Psychiatr.Scand.Suppl., vol. 380, pp. 6-7. [Pg.248]

Amphetamine a, P, CNS As CNS stimulant in treatment of children with attention deficit syndrome... [Pg.80]

In clinical discussions, the lobotomy effect is now sometimes subsumed under neuroleptic-induced deficit syndrome (NIDS). Malcolm Lader (1993), chairperson of an international symposium on the subject, wrote,... [Pg.36]

Lader, M. (1993). Neuroleptic-induced deficit syndrome. Journal of Clinical Psychiatry, 54, 493-500. [Pg.499]

MahadikSP, MukherjeeS, Scheffer R, CorrentiEE, Mahadik JS. 1998. Elevated plasma lipid peroxides at the onset of nonaffective psychosis. Biol Psychiatry 43 674-679. Malaspina D, Coleman E, Goetz RR, Harkavy-Friedman J, Corcoran C, et al. 2002. Odor identification, eye tracking and deficit syndrome schizophrenia. Biol Psychiatry 51 809-815. [Pg.308]

Tamminga CA, Thaker GK, Buchanan R, Kirkpatrick B, Alphs LD, et al. 1992. Limbic system abnormalities identified in schizophrenia using positron emission tomography with fluorodeoxyglucose and neocortical alterations with deficit syndrome. Arch Gen Psychiatry 49 522-530. [Pg.330]

Cimmer C, Szendi I, Csifcsak G, et al. 2006. Abnormal neurological signs, visual contrast sensitivity, and the deficit syndrome of schizophrenia. Prog Neuropsychopharmacol Biol Psychiatry 30 1225-1230. [Pg.348]

A Brief History of Negative Symptoms and the Deficit Syndrome. 508... [Pg.507]

List of Abbreviations Ach, acetylcholine AMPA, a-amino-3-hydroxy-5-methylisoxazole-4-propionic acid CNS, central nervous system COMT, catechol-O-methyltransferase DA, dopamine DRP-2, dihy-dropyrimidinase-related protein 2 DSM, diagnostic and statistical manual of mental disorders GNAS1, guanine nucleotide-binding protein (G-protein) alpha stimulating activity polypeptide 1 5-HIAA, 5-hydroxyindole acetic acid 5-FIT, serotonin (5-hydroxytryptamine) MAO, monoamine oxidase MHPG, 3-methoxy-4-hydroxyphenylglycol NE, norepinephrine NMDA, N-methyl-D-aspartate PCP, phencyclidine SSRI, selective serotonin reuptake inhibitor SDS, schedule for the deficit syndrome... [Pg.508]

This chapter will focus largely on the biology and neurochemistry of primary negative symptoms and the deficit syndrome. [Pg.511]

Brain metabolism patterns have also differentiated individuals with the deficit syndrome. In deficit patients, the thalamus and frontal/parietal cortices utilize less glucose at rest than in nondeficit patients and healthy controls (Buchanan et al., 1989 Tamminga et al., 1992). [Pg.511]

Studies of individuals with the deficit syndrome have noted problems with tasks of sensory integration, e.g., stereognosis, graphesthesia, and right-left confusion (Buchanan et al., 1990 Arango et al., 2000). Somatosensory information is received in the thalamus before being redirected to the parietal cortex. These findings are consistent with impairment in the thalamus and/or parietal cortex in the deficit syndrome. [Pg.512]

While this offers further support for prefrontal and inferior parietal dysfunction in the deficit syndrome, other areas of the brain have not been examined. However, it prompts interesting theories of the deficit syndrome being related to failure of normal neuronal migration. [Pg.512]


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