Neurochemical Correlates of Sympathetic Activation during Severe Alcohol Withdrawal

Hawley, Rollin J.; Nemeroff, Charles B.; Bissette, Garth; Guidotti, Alessandro; Rawlings, Robert R.; Linnoila, Markku

doi:10.1111/j.1530-0277.1994.tb01429.x

Cited by 63 publications

(31 citation statements)

References 32 publications

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“…Patients with other psychiatric disorders, including mania (28), generalized anxiety disorder (28,51,52), panic disorder (28, 51, 52), somatization disorder (28), dementia without depression (28), and schizophrenia (19,53), have not been found to have a difference in CRF in comparison to control subjects. No studies have specifically examined CSF CRF in substance abuse, and the one study in alcoholics (which did find increased concentrations of CSF CRF) was conducted in individuals who were undergoing alcohol withdrawal (54). This finding was not applicable to our current group, since none of the patients was in alcohol withdrawal.…”

Section: Discussioncontrasting

confidence: 43%

Elevated CSF corticotropin-releasing factor concentrations in posttraumatic stress disorder

1997

AJP

603

122

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Objective: Corticotropin-releasing factor (CRF) C orticotropin-releasing factor (CRF) plays an important role in mediating the mammalian stress response (1). CRF released during stress (2) from nerve terminals originating in the paraventricular nucleus of the hypothalamus increases the secretion of adrenocorticotropin hormone (ACTH) from the anterior pituitary, which in turn stimulates release of cortisol from the adrenal (3). Cortisol has a number of effects that are beneficial to short-term survival, including suppression of reproductive and immune function, promotion of analgesia, activation of the peripheral autonomic system, suppression of gastric motility and gastric acid secretion, and increases in total oxygen consumption and glucose and glucagon concentrations in plasma (3). Chronic stress results in sustained increases in plasma glucocorticoid levels (4), with a potentiation of glucocorticoid responsiveness to subsequent stressors (5, 6) and neuronal "hypersecretion" of CRF.CRF neurons are distributed in a variety of locations outside of the hypothalamus, including the amygdala, bed nucleus of the stria terminalis, central gray area, locus ceruleus, parabrachial area, and dorsal vagus complex (7). Intraventricular administration of CRF to laboratory animals results in behavioral activation, as evidenced by 1) an increase in EEG activity (8); 2) increases in plasma norepinephrine and epinephrine concentrations (9, 10); 3) an increase in firing of the locus ceruleus, site of the majority of noradrenergic cell bodies in the brain, which results in a state of increased attention and arousal (11); 4) increased locomotor activity, grooming, and rearing (12); and 5) behaviors consistent with anxiety and fear, including a decrease in exploratory activity in an open field (13), decreased punished responding in the conflict test (14), and potentiation of acoustic startle (15,16). These studies support an important role for CRF in the promotion of anxiety and fear-related behaviors.

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Section: Discussioncontrasting

confidence: 43%

Elevated CSF corticotropin-releasing factor concentrations in posttraumatic stress disorder

1997

AJP

603

122

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“…Chronic alcohol abuse, alcohol intoxication, and withdrawal all induce activation of the hypothalamus-pituitary-adrenal (HPA) axis [11][12][13][14], and increased peripheral prolactin and catecholamine concentrations [13][14][15]. Thus, both alcohol intoxication and withdrawal may potentially alter immune function via neuroendocrine mechanisms, as acute and chronic activation of the HPA axis and sympathetic nervous system as well as elevations of other pituitary hormones produce marked changes in the distribution and function of immune cells [16].…”

mentioning

confidence: 99%

Concomitant Endocrine and Immune Alterations during Alcohol Intoxication and Acute Withdrawal in Alcohol-Dependent Subjects

Kutscher

Heise²,

Banger

et al. 2002

Neuropsychobiology

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Although both alcohol intoxication and withdrawal have been demonstrated to produce significant endocrine alterations, no data exist on the effects of acute withdrawal on immune functions. Therefore, the current study investigated the effect of alcohol intoxication and acute withdrawal on plasma cortisol, prolactin and catecholamines, and blood leukocyte subset distribution in alcohol-dependent subjects. Nine male alcoholics admitted to the university clinic for alcohol dependence and 9 age-matched controls participated in the study. Blood was drawn from the alcohol-dependent subjects at 10:30 a.m. on day 0 (chronic alcohol intoxication), at the same time during acute alcohol withdrawal (day 1) and following the resolution of acute withdrawal (day 7). Blood was drawn from age- and gender-matched healthy control subjects at the corresponding time points. Plasma was then analyzed for hormone concentrations and blood examined for leukocyte subsets by flow cytometry. Alcohol-dependent patients displayed significantly elevated plasma cortisol during intoxication and withdrawal, which decreased to control levels following resolution of acute withdrawal. Small elevations of plasma prolactin and catecholamines were also observed during intoxication. Furthermore, alcohol-dependent subjects showed reduced absolute numbers of CD4⁺ and CD8⁺ T cells and natural killer cells compared with healthy controls across all time points. In contrast, although monocyte numbers were lower in alcohol-dependent patients during intoxication, acute alcohol withdrawal increased the number of monocytes in patients. Thus, alcohol dependence produces a general suppression of leukocyte subset populations in blood. However, resolution of acute alcohol withdrawal is associated with a return of plasma cortisol to control levels, and a concomitant increase in peripheral blood monocyte numbers.

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“…The link between an increased function of hemodynamics and sympathetic activity in WS has been demonstrated earlier. The degree of hypertension and HR correlates with the severity of WS and 3-methoxy-4-hydroxyphenylglycol, a metabolite of noradrenaline concentrations (Hawley et al, 1985;Hawley et al, 1994;Kähkönen and Bondarenko, 2000).…”

Section: Discussionmentioning

confidence: 96%

Cardiovascular effects of propranolol in patients with alcohol dependence during withdrawal

Kähkönen

Бондаренко²,

Lipsanen

et al. 2007

International Journal of Psychophysiology

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Neurochemical Correlates of Sympathetic Activation during Severe Alcohol Withdrawal

Cited by 63 publications

References 32 publications

Elevated CSF corticotropin-releasing factor concentrations in posttraumatic stress disorder

Elevated CSF corticotropin-releasing factor concentrations in posttraumatic stress disorder

Concomitant Endocrine and Immune Alterations during Alcohol Intoxication and Acute Withdrawal in Alcohol-Dependent Subjects

Cardiovascular effects of propranolol in patients with alcohol dependence during withdrawal

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