Cerebral chronic

Vinpocetine (2), another dmg initially categorized as a cerebral vasodilator, is a member of the vinca alkaloid family of agents (7). However, interest in this compound as a potential dmg for learning and memory deficits comes from its abiUty to act as a neuronal protectant. This compound was evaluated in 15 patients with AD over a one-year period and was ineffective in improving cognitive deficits or slowing the rate of decline (8). However, in studies of patients with chronic vascular senile cerebral dysfunction (9) and organic psycho syndrome (10), vinpocetine showed beneficial results. 

Beri-beri or clinically manifest thiamin deficiency exists in several subforms infantile beri-beri and adult beri-beri. Infantile beri-beri occurs in exclusively breastfed infants of thiamin-deficient mothers. Adults can develop different forms of the disease, depending on their constitution, environmental conditions, the relative contribution of other nutrients to the diet as well as the duration and severity of deficiency. First of all, there is a so called dry or atrophic (paralytic or nervous) form, including peripheral degenerative polyneuropathy, muscle weakness and paralysis. Second, a wet or exudative (cardiac) form exists. In this form, typical symptoms are lung and peripheral oedema as well as ascites. Finally, there is a cerebral form, that can occur as Wernicke encephalopathy or Korsakoff psychosis. Tli is latter form mostly affects chronic alcoholics with severe thiamin deficiency. 

Holman BL, Mendelson J, Garada B, er al Regional cerebral blood flow improves wirh treatment in chronic cocaine polydrug users. J Nucl Med 34 723—727, 1993... 

Kornetsky C Hyporesponsivity of chronic schizophrenic patients to dextroamphetamine. Arch Gen Psychiatry 33 1425—1428, 1976 Kosten TR Pharmacotherapy of cerebral ischemia in cocaine dependence. Drug Alcohol Depend 49 133-144, 1998... 

Kumar R, Orsoni S, Norman L, Verma AS, Tirado G, Giavedoni LD, Staprans S, Miller GM, Buch SJ, Kumar A (2006) Chronic morphine exposure causes pronounced virus replication in cerebral compartment and accelerated onset of AIDS in SIV/SHIV-infected Indian rhesus macaques. Virology 354 192-206... 

FurukawaM, Kashiwagi S, Matsunaga N, Suzuki M, Kishimoto K, Shirao S. Evaluation of cerebral perfusion parameters measured by perfusion CT in chronic cerebral ischemia comparison with xenon CT. J Comput Assist Tomogr 2002 26 272-278. 

Hart MN, Heistad DD, Brody Ml. Effect of chronic hypertension and sympathetic denervation on waMumen ratio of cerebral vessels. Hypertension 1980 2(4) 419 23. 

Ishimaru, M, Kurumaji, A and Toru, M (1994) Increases in strychnine-insensitive glycine binding sites in cerebral cortex of chronic schizophrenics evidence for glutamate hypothesis. Biol. Psychiat. 35 84-95. 

Though a recent facial impact injury may have caused additional diffuse cerebral damage, the total performance seemed more indicative of chronic PCP and alcohol abuse. Specifically, the NP profile was characteristic of deficits in frontal lobe-mediated adaptive abilities. While the severity of these deficits seemed slight as compared with the mental status of others of similar... 

There have been many sporadic reports that lipo-PGEj is effective in fulminant hepatitis, neuralgia associated with herpes zoster, multiple spinal canal stenosis, cerebral infarction, myocardial infarction, chronic renal failure, and bed sores as well as for its registered indications. 

Al Dhaheri AH, El-Sabban F, Fahim MA. 1995. Chronic lead treatment accelerates photochemically induced platelet aggregation in cerebral microvessels of mice, in vivo. Environ Res 69 51-58. 

Magata, Y., Kitano, H., Shiozaki, T. et al. Effect of chronic (-) nicotine treatment on rat cerebral benzodiazepine receptors. Nuclear Med. Biol. 27 57, 2000. 

Iyo, M., Namba, H., Yanagisawa, M. et al. Abnormal cerebral perfusion in chronic methamphetamine abusers a study using 99MTc-HMPAO and SPECT. Prog. Neuropsychopharmacol. Biol. Psychiatry. 21 789, 1997. 

Balestreri R, Fontana L and Astengo F (1987). A double-blind placebo controlled evaluation of the safety and efficacy of vinpocetine in the treatment of patients with chronic vascular senile cerebral dysfunction. Journal of the American Geriatrics Society, 35, 425—430. 

Co BT, Goodwin DW, Gado M, Mikhael M and Hill SY (1977). Absence of cerebral atrophy in chronic cannabis users. Journal of the American Medical Association, 237, 1229-1230. 

Johnstone EC, Crow TJ, Frith CD, Stevens J and Kreel L (1976). Cerebral ventricular size and cognitive impairment in chronic schizophrenia. Lancet, 1, 924-926. 

Kety SS (1956). Human cerebral blood flow and oxygen consumption as related to aging. Journal of Chronic Disease, 3, 478-486. 

R. Cespuglio, H. Faradji, Z. Hahn, and M. Jouvet, Voltammetric detection of brain 5-hydroxyindo-lamines by means of electrochemically treated carbon fiber electrodes chronic recordings for up to one month with movable cerebral electrodes in die sleeping or waking rat, in Measurements of Neurotransmitters Release in Vivo (C.A. Marsden, ed.), Wiley, Chichester (1984). 

Coli, S., Chang, H.-C., Mollner, S. et al. Chronic lithium regulates the expression of adenylate cyclase and Gia in rat cerebral cortex. Proc. Natl Acad. Sci. U.S.A. 88 10634-10637,1991. 

Ammonia concentrations in arterial blood of patients with liver failure rise to 0.5-1 mmol/1, in contrast to the normal range of 0.01-0.02 mmol/1. Using positron emission tomography (PET see Ch. 58), increases of the cerebral metabolic rate for ammonia (CMRA), i.e. the rate at which ammonia is taken up and metabolized by the brain, have been reported in chronic liver failure [9]. Increased CMRA in chronic liver failure is accompanied... 

Li+ was first found to interfere with inositol lipid metabolism when significantly decreased levels of myo-inositol were observed in the cerebral cortex of Li+-treated rats [89]. Subsequent work revealed a corresponding increase in the levels of Ins( 1 )P [90] and this behavior was shown to be the result of a Li+-induced inhibition of IMPase, the enzyme which dephosphorylates the monophosphates Ins(l)P, Ins(3)P, and Ins(4)P to produce free inositol [91]. These results stimulated much research in this field involving a wide variety of cell types, tissues, and animals where the Li+ inhibition of IMPase was found to be ubiquitous. However, it was found that, in vivo, this Li+-induced effect is predominantly limited to the brain, being observed in different regions of the brain to different extents, with similar results for both acute and chronic treatment with Li+. It is probable that those cells that are able to accumulate inositol, or which are exposed to and can rapidly import an extracellular supply of inositol, may be relatively insensitive to the effects of Li+. 

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