Neurology mechanisms

I want to reemphasize that drug-induced disturbances in mood or in behavior should be viewed as genuine neurological disorders rather than as vague mental illnesses. The capacity of speculative biochemical imbalances or genetic factors to cause or contribute to mania or depression remains unproven. Nor do we know the specific biochemical or neurological mechanisms whereby psychoactive substances cause mental disturbances. But the capacity for psychoactive substances to disrupt brain function and hence mental function is beyond dispute. Furthermore, a great deal of empirical data confirm their capacity to cause disinhibition, mania, depression, and other mental phenomena associated with violence toward oneself and others, as well as other destructive behaviors. 

Bauer M, Adli M, Baethge C, Berghofer A, Sasse J, Heinz A, Bschor J. Lithium augmentation therapy in refractory depression clinical evidence and neurological mechanisms. Can J Psychiatry 2003 48 440-8. 

At the start of my quest therefore, before I had worked out some of the cognitive and neurological mechanisms for the Habit Routine Model, I necessarily found myself toying with the concept of instinct. Believing that the influence of psychedelic drugs on proto-humans might have been a necessary catalyst for the rapid (4) transformation to culturally modern Homo sapiens, there seemed two possibilities to explore. Either the psychedelics might have... 

After three children were accidentally exposed to a large amount of mustard, two of them presented with abnormal muscular activity and the third alternated between coma and agitation. The first two children died 3- h after exposure, possibly from neurological mechanisms (Heully and Gmninger, 1956). It is unknown whether these CNS manifestations are from a cholinergic activity of mustard or from other mechanisms. 

Weinreb O, Mandel S, Amit T, Youdim MB (2004) Neurological mechanisms of green tea polyphenols in Alzheimer s and Parkinson s diseases. J Nutr Biochem 15(9) 506-516. doi 10.1016/j.jnutbio.2004.05.002, S0955286304001184 [pii]... 

Mechanism (if toxicologic damage is unimown for citrus oil extracts. Central and periph- eral vasodilatation may occur secondary to a neurologic mechanism. 

The WISC-R subtest analyses showed that eight out of 10 subtests administered were significantly associated with PbB. The overall pattern suggests that a wide range of abilities are influenced by lead, but it is difficult to draw firm conclusions about specific insults attributed to lead based on the WISC-R subtests profile (Kaufman, 1979). Moreover, it is not possible to speculate on the underlying neurological mechanisms by which lead affects brain function based on the data derived from this or similar studies. 

In addition to the role of chemokines/chemokine receptors in viral infection, transmission, and pathogenesis, chemokines also play important roles in cellular trafficking and survival pathways. The role of chemokines and their receptors are of particular importance in the development of neurologic complications of AIDS, involving mechanisms discussed in the following sections. 

Joseph EK, Chen X et al (2004) Novel mechanism of enhanced nociception in a model of AIDS therapy-induced painful peripheral neuropathy in the rat. Pain 107(1-2) 147-158 Jubelt B, Berger JR (2001) Does viral disease underlie ALS Lessons from the AIDS pandemic. Neurology 57(6) 945-946... 

With modest impairment of blood flow, this mechanism allows for preservation of oxidative metabolism without alteration in electrical function. However, when CPP and therefore CBF are sufficiently low, OEF reaches a maximum and cannot increase further. Brain tissue ceases to function electrically, resulting in a neurologic deficit. Microvascular collapse occurs, and CBV falls. If the oxygen supply falls low enough, the tissue dies. Of critical clinical importance is the observation that the amount of time it takes for tissue to suffer irreversible damage is inversely related to the severity of the ischemic insult. Tissue that is completely deprived of blood will die within a few minutes, but less severely hypoperfused tissue may survive for many hours, and may be saved by timely thrombolysis that restores perfusion, or perhaps by another therapeutic intervention. 

Electrolytes are involved in many metabolic and homeostatic functions, including enzymatic and biochemical reactions, maintenance of cell membrane structure and function, neurotransmission, hormone function, muscle contraction, cardiovascular function, bone composition, and fluid homeostasis. The causes of electrolyte abnormalities in patients receiving PN may be multifactorial, including altered absorption and distribution excessive or inadequate intake altered hormonal, neurologic, and homeostatic mechanisms altered excretion via gastrointestinal and renal losses changes in fluid status and fluid shifts and medications. 

Effect. No biomarkers have been identified to characterize the effects associated with exposure to diisopropyl methylphosphonate. Toxicity data for diisopropyl methylphosphonate are limited. No specific clinical signs or symptoms in humans have been positively linked to diisopropyl methylphosphonate exposure. Further research is needed to identify the mechanism of neurological effects and the clinical symptoms of diisopropyl methylphosphonate exposure. 

GSH-S deficiency is a more frequent cause of GSH deficiency (HI7), and more than 20 families with this enzyme deficiency have been reported since the first report by Oort et al. (05). There are two distinct types of GSH-S deficiency with different clinical pictures. In the red blood cell type, the enzyme defect is limited to red blood cells and the only clinical presentation is mild hemolysis. In the generalized type, the deficiency is also found in tissues other than red blood cells, and the patients show not only chronic hemolytic anemia but also metabolic acidosis with marked 5-oxoprolinuria and neurologic manifestations including mental retardation. The precise mechanism of these two different phenotypes remains to be elucidated, because the existence of tissue-specific isozymes is not clear. Seven mutations at the GSH-S locus on six alleles—four missense mutations, two deletions, and one splice site mutation—have been identified (S14). 

Effect. Potential biomarkers of the subclinical effects of hydrogen sulfide are decreases in the activities of the heme synthesis enzymes, ALA-S and Haem-S (Jappinen and Tenhunen 1990). These effects have nothing to do with the mechanism of toxicity, however. Neurological indices are also used as biomarkers of effect for hydrogen sulfide (Gaitonde et al. 1987 Kilbum 1993 Stine et al. 1976 Tvedt et al. 1991b). 

Target Organ Toxicity. This section focuses on mechanisms for sensitive health effects of major concern for lead—cardiovascular effects, hematological effects, and neurological effects, particularly in children. Bone is a major sink for lead, and there is some limited information regarding the effects of lead on bone and potential mechanisms of action. Renal effects occur at relatively high blood lead levels and evidence of renal carcinogenicity has been demonstrated only in animals mechanisms for these effects will be discussed briefly. 

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