Neurological effects stimulants

BHC produces a variety of neurological effects in insects and mammals. However, at both levels of the nervous system (peripheral and central), the mechanism of toxic action of BHC is poorly understood. Central nervous system stimulation appears to be due to blockade of the effects of y-aminobutyric acid. In vitro BHC isomers are reported to increase the calcium uptake of isolated rat brain synaptosomes. In addition, y-isomer of BHC has been shown to inhibit... 

Only one study was located regarding neurological effects in animals after dermal exposure to Stoddard solvent. Rats had a daily 3-hour exposure to white spirits for 6 weeks on a 12-cm area of the tail (Verkkala et al. 1984). The absorbed dose was calculated by the authors to be 210 mg, but they did not describe how the calculation was performed. Exposure had little effect on motor conduction velocity or motor amplitudes in response to stimulation. Histological analysis revealed axonal prenodal swellings. No other functional or behavioral tests were performed. 

Workers exposed to di- -butyl phthalate for 0.5-19 years at concentrations of 1.7-66 mg/m experienced neurological symptoms (pain, numbness, spasms, weakness) and exhibited reflex disturbances, elevated thresholds for pain sensitivity and olfactory stimulation, and depression of vestibular function (Milkov et al. 1973). The frequency and severity of these effects increased with increased duration of exposure. The workers were also exposed to other plasticizers, so these neurological effects may not have been caused by di- -butyl phthalate exposure. 

Sensitivity to Other Non-Social Exteroceptive Stimuli - Several studies indicate that PCPA increases various behavioral or neurological effects of electrical stimulation. Thresholds of current required to reinforce selfstimulation behavior are lowered by PCPA in rats,46 and PCPA has been reported to cause strong excitatory effects on intracranial self-stimulation rates in rats 3 days after treatment.47 5-HT-depleted animals have been reported to be more active than controls under conditions of extra environmental stimulation, particularly "novel" stimulation.18b,19c Cats "overreact to slight noises,"48 sensory thresholds are lowered,29 the responsiveness to a startle stimulus of rats with low basal responsiveness Is Increased,49 and habituation to an audltory-ellcited startle response, as measured by cortical electrical responses. Is reduced.50... 

Patients receiving monoamine oxidase inhibitors (MAOI) as antidepressant therapy have been especially subject to the hypertensive effects of vasoactive amines (52). These dietary amines have also been impHcated as causative agents ia migraine. Other aaturaHy occurring alkaloids (qv) have been recognized for centuries as possessing neurological stimulant and depressant properties. 

Oppenheimer SM, Gelb A, Girvin JP, Hachinski VC. Cardiovascular effects of human insular cortex stimulation. Neurology 1992 42(9) 1727-1732. 

Harmaline has also been found to have neurotoxic effects on Purkinje neurons (O Hearn and Molliver 1997). This likely results from excitotoxic consequences induced by prolonged stimulation of inferior olivary neurons. Whether this occurs in levels reached during human consumption has not been specifically addressed. Prolonged neurological symptoms have not been reported in those who consume the drug. 

Perhaps the most prominent and well-studied class of synthetic poisons are so-called cholinesterase inhibitors. Cholinesterases are important enzymes that act on compounds involved in nerve impulse transmission - the neurotransmitters (see the later section on neurotoxicity for more details). A compound called acetylcholine is one such neurotransmitter, and its concentration at certain junctions in the nervous system, and between the nervous system and the muscles, is controlled by the enzyme acetylcholinesterase the enzyme causes its conversion, by hydrolysis, to inactive products. Any chemical that can interact with acetylcholinesterase and inhibit its enzymatic activity can cause the level of acetylcholine at these critical junctions to increase, and lead to excessive neurological stimulation at these cholinergic junctions. Typical early symptoms of cholinergic poisoning are bradycardia (slowing of heart rate), diarrhea, excessive urination, lacrimation, and salivation (all symptoms of an effect on the parasympathetic nervous system). When overstimulation occurs at the so-called neuromuscular junctions the results are tremors and, at sufficiently high doses, paralysis and death. 

Erenberg, G., Cruse, R.P., and Rothner, A.D. (1985) Gilles de la Tourette s syndrome effects of stimulant drugs. Neurology 35 1346-1348. 

The effect of stimulants on child behavior was first reported in 1937. Charles Bradley, a physician working with children of normal intelligence who had neurological and behavioral disorders, prescribed Benzedrine to treat headaches in children who had undergone a spinal tap. Although the headaches did not disappear with the amphetamines, the children s level of activity decreased tremendously and their academic performance and compliance increased. 

For example, DFO treatment has been used to facilitate the removal of aluminum from bone and its entry into the blood where it can be removed by hemodialysis (Haddad and Winchester 1990). DFO is also used in dialyzed uremic patients for the treatment of neurological, hematopoietic, and skeletal toxicity. It should be noted that the clinical usefulness of DFO is limited by a variety of toxic effects including hypotension, skin rashes, stimulation of fungal growth, and possibly cataract formation. 

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