Overstimulation

Temporary mental paralysis The short lived incapacitation of the capability of making use of available information. Postulated as being due to the sudden switch from under- to overstimulation at times of crises... 

One of the chief adverse reactions associated with the amphetamines and anorexiants is overstimulation of the CNS, which may result in a variety of adverse reactions, including insomnia, tachycardia, nervousness, headache, anorexia, dizziness, and excitement. In some instances, die intensity of diese reactions is dose dependent, but some individuals may experience an intense degree of diese symptoms even widi low doses. Odier individuals experience few symptoms of CNS stimulation. 

Reviews possible adverse reactions, especially CNS overstimulation, with instructions to notify the health care provider immediately should any occur. 

Hyperstimulation of the uterus during labor may lead to uterine Many with marked impairment of the uteroplacental blood flow, uterine rupture, cervical rupture, amniotic fluid embolism, and trauma to the infant. Overstimulation of the uterus is dangerousto both the fetusand the mother and may occur even when the drug is administered properly in a uterus that is hypersensitive to oxytocin. 

Clinical signs and symptoms of toxicity are related to the overstimulation of muscarinic, nicotinic, and central nervous system receptors in the nervous system. Muscarinic receptors are those activated by the alkaloid drug muscarine. These receptors are under the control of the parasympathetic nervous system, and their hyperactivity results in respiratory and gastrointestinal dysfunction, incontinence, salivation, bradycardia, miosis, and sweating. Nicotinic receptors are those activated by nicotine. Hyperactivity of these receptors results in muscle fasciculations even greater stimulation results in blockade and muscle paralysis (Lefkowitz et al. 1996 Tafliri and Roberts 1987). Hyperactivity of central nervous system receptors results in the frank neurological signs of confusion, ataxia, dizziness, incoordination, and slurred speech, which are manifestations of acute intoxication. Muscarine and nicotine are not... 

Atropine acts as an antagonist of acetylcholine at muscarinic receptors, but not at nicotinic receptors. By acting as an antagonist, it can prevent overstimulation of muscarinic receptors by the excessive quantities of acetylcholine remaining in the synaptic cleft when AChE is inhibited. The dose of atropine needs to be carefully controlled because it is toxic. 

Acetylcholinesterase is a component of the postsynaptic membrane of cholinergic synapses of the nervous system in both vertebrates and invertebrates. Its structure and function has been described in Chapter 10, Section 10.2.4. Its essential role in the postsynaptic membrane is hydrolysis of the neurotransmitter acetylcholine in order to terminate the stimulation of nicotinic and muscarinic receptors (Figure 16.2). Thus, inhibitors of the enzyme cause a buildup of acetylcholine in the synaptic cleft and consequent overstimulation of the receptors, leading to depolarization of the postsynaptic membrane and synaptic block. 

False. Sniffing solvents is highly dangerous. There is a danger of sudden death caused by overstimulation of the heart or asphyxiation caused by swelling of the throat tissues or inhalation of vomit. Users also expose themselves to a high level of accident risk whilst intoxicated. 

N-Nitro-L-arginine methyl ester (L-NAME) is an inhibitor of NOS L-NAME reportedly reduces the volume of cortical and striatal infarct after middle cerebral artery occlusion in the rat. This protection can be reversed by co-injection of L-arginine. L-NAME also reduced the excitotoxic damage induced by NMDA injection. Finally, the authors showed that L-NAME reduced glutamate efflux produced by ischaemic injury in rats. The authors concluded that NOS induced by NMDA receptor overstimulation is a key event in the neuronal injury cascade (Buisson eta/., 1993). 

The relative eontribution of different mechanisms to stimulant-induced cardiac toxicities is not known. Currently, sympathetic overstimulation is thought to mediate many of these effects (Cregler and Mark 1986). 

Use of diethylpropion for a period longer than 3 months is associated with an increased risk for development of pulmonary hypertension. When used as directed, reported common central nervous system adverse effects included overstimulation, restlessness, dizziness, insomnia, euphoria, dysphoria, tremor, headache, jitteriness, anxiety, nervousness, depression, drowsiness, malaise, mydriasis, and blurred vision. In addition, diethylpropion can decrease seizure threshold, subsequently increasing a patient s risk for an epileptic event. Other organ systems also can adversely be affected, resulting in tachycardia, elevated blood pressure, palpitations, dry mouth, abdominal discomfort, constipation,... 

One factor in the differential cognitive results may be baseline or prestimulation arousal level. When baseline arousal is already elevated, highly arousing tasks, such as those that are complex or involve intense stimuli, can result in overstimulation. As Hasenfratz and Battig49 note, it may be such excessive levels of stimulation that account for the commis-... 

In addition to gender, task difficulty or complexity appears to be a substantial factor in arousal. Information processing tasks, particularly complex ones, have been shown to increase arousal levels in otherwise unstimulated subjects.60 The more complex the task, the higher the arousal level and the greater the chance that a given caffeine dosage would contribute to overstimulation. The additive nature of arousal sources — in this case caffeine and complexity — means that arousal is high when caffeine is present and complexity or difficulty level is substantial. The result is that caffeine impairs performance on complex tasks,50 51 particularly in female subjects. 

When I got stronger I moved back to my house and began doing volunteer work at a hospice. I continued to use my respirator and mask for three years, because my body was still quite sensitive. As I got stronger I allowed myself to eat more foods, a little bit at a time, in order to allow my body to slowly develop trust. I still lived reclu-sively because I felt overstimulated so easily. I needed that time alone to heal my nervous system. 

Nerve agent Chemical agent inhaled, absorbed through the skin, or ingested that causes interference with the neural synapses and overstimulation of the nervous system, which in turn leads to overreactivity in the muscles and malfunctioning of various organs. The primary agents are tabun, sarin, soman, and VX. 

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