Hyperactivity causes

Price SC, Ozalp S, Weaver R, et al. 1988b. Thyroid hyperactivity caused by hypolipodaemic compounds and polychlorinated biphenyls The effect of coadministration in the liver and thyroid. Arch Toxicol (Suppl 12) 85-92. 

Heffner TG, Seiden LS (1982) Possible involvement of serotonergic neurons in the reduction of locomotor hyperactivity caused by amphetamine in neonatal rats depleted of brain dopamine. Brain Res 244 81-90. 

Figure 72.5 The proposed pathogenesis of HTPP paralysis. Under the influence of This, insulin, cafecholamines and possibly androgen, fhe Na+/K+-ATPase pumps on skeletal tissue increase in number (not shown) and become hyperactive, causing a marked intracellular shift of K+ wifh subsequent hypokalemia and paralysis.

For many years, there has been concern by medical professionals and nutritionists over the effects of dietary sugar on human health. Sucrose has been imphcated as a cause of juvenile hyperactivity, tooth decay, diabetes meUitus, obesity, atherosclerosis, hypoglycemia, and nutrient deficiencies. 

Other studies indicate that sucrose does not cause hyperactivity. Carbohydrate ingestion increases levels of serotonin (5-hydroxytryptamine), a brain neurotransmitter that promotes relaxation and sleep. Dietary sucrose should theoretically have a calming effect and reduce activity, manifestations which have been observed in case studies (63). To date, clinical investigations have failed to show a significant connection between sucrose consumption and aggressive or dismptive behavior (66). 

Cessation of prolonged heavy alcohol abuse may be followed by alcohol withdrawal or life-threatening alcohol withdrawal delirium. Typical withdrawal symptoms are autonomic hyperactivity, increased hand tremor, insomnia and anxiety, and are treated with benzodizepines and thiamine. Alcoholism is the most common cause of thiamine deficiency and can lead in its extreme form to the Wernicke s syndrome that can be effectively treated by high doses of thiamine. 

Liddle s syndrome is an autosomal dominant disorder that is caused by persistent hyperactivity of the epithelial Na channel. Its symptoms mimic aldosterone excess, but plasma aldosterone levels are actually reduced (pseudoaldosteronism). The disease is characterized by early onset arterial hypertension, hypokalemia, and metabolic alkalosis. 

The dendrites of neurons adjacent to those which degenerate also show extensive growth and sprouting which could facilitate abnormal and disorganised synaptic transmission and cause hyperactivity. It is also known that the dendrites of cells around an alumina focus in monkeys, as well as in human epileptic brain, lose their spinous processes, which might contribute to the paroxysmal discharge by facilitating the spread of depolarisation to the neuron soma. Certainly an increase in the number of Na+ channels on the dendrites of spinal motoneurons, which would facilitate the occurrence of reactive dendritic Na+ spikes, has been seen after axotomy. 

Stimulation of 5-HT3 receptors triggers hypersensitivity and hyperactivity of the large intestine. Alosetron (Lotronex) is a selective 5-HT3 antagonist that blocks these receptors and is used to treat women with severe diarrhea-predominant IBS. Eligible patients should have frequent and severe abdominal pain, frequent bowel urgency or incontinence, and restricted daily activities. Alosetron has been shown to improve overall symptoms and quality of life. Alosetron can cause constipation in some patients. 

The exact cause of attention-deficit hyperactivity disorder is unknown, but dysfunction in neurotransmitters norepinephrine and dopamine has been implicated as a key component. 

A second theory of phantom pain suggests that second-order neurons in the dorsal horn of the spinal cord become hyperactive. Spontaneous firing of these neurons causes transmission of nerve impulses to the brain and the perception of pain. 

Reducing problematic behavior to biological causes calls for pharmaceutical solutions and here too powerful corporate interests foster such explanations. The redefinition of hyperactivity as Attention Deficit Disorder (ADD), for example, has significantly benefitted the pharmaceutical industry. The use of Ritalin as a treatment for ADD has doubled since 1995, and it is prescribed to over 4 million children in the US. Production of the drug is up 700 % since 1990, and 90 % of the production is consumed in the US where pharmaco-genomics is a burgeoning field. Europeans have been more cautious, and the International Narcotics Control Board of the UN has expressed concern about the growing tendency to redefine behavior as amenable to pharmaceutical modification. 

A second, more extensive experiment involved oral administration of three daily doses (100 mg/kg) of parachlorophenylalanine (PCPA). This tryptophan hydroxylase inhibitor (47), like reserpine, enhanced the behavioral effects of LSD (13) moreover, hypersensitivity occurred when 5-HT, but not other monoamine, concentrations were below normal in both forebrain and hindbrain (13). That is, effects were observed at 5 and 12 days (when 5-HT was depleted to 10-20% and 60-70% of normal) but not at 21 days (when 5-HT had returned to normal). Control experiments (13) indicated that (a) the interaction of PCPA, 5-HT, and LSD was probably not caused by generalized hyperactivity or hyperirritability sometimes seen after PCPA (73) (b) PCPA does not affect threshold doses of other psychoactive but nonserotonergic compounds, such as d-amphetamine (0.3 mg/kg) and (c) pretreatment with a-methylparatyrosine, a tyrosine hydroxylase inhibitor which depletes catecholamines rather than indoleamines, does not alter sensitivity to LSD. 

What has been difficult to determine is whether the neuropsychological problems are consequences of the abuse, or whether some of these cognitive problems may have preceded drug use. For example, many people who have drug problems also exhibit signs of hyperactivity or attention problems, but it is unclear whether these problems preceded the drug use or whether the drug use caused... 

Additionally, impulse-control and attention problems, hyperactivity, and even antisocial behavior could be caused by a prenatal exposure to psychoactive drugs that escaped detection. Research has linked these conditions with known prenatal toxicity, and the consequences of low levels of prenatal exposure to psychoactive substances can sometimes be missed. In these instances, the symptoms are more likely to be observed as behavioral and attributed to other causes (such as Attention-Deficit Disorder). Recent research also suggests that children of mothers who may have used substances during pregnancy also may be at risk for drug problems later in life (Baer, Sampson, Barr, Connor, Streissguth, 2003). 

In retrospect, Matthew s mother realizes that he was probably chemically sensitive at birth, but it was years before they understood the cause of his erratic, hyperactive, sometimes violent behavior. Because there seemed to be no rhyme or reason to his behaviors all that time, Matthew developed a poor self-image, impaired social skills, and a reputation for being difficult. 

FDC — Food, Drug and Cosmetic Act Causes hyperactivity in some children... 

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