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West Nile neuroinvasive disease (WNND) is a rare and severe manifestation of West Nile virus (WNV) infection that occurs in less than 1% of infected persons. It should be considered in patients who present with fever, neurological symptoms, and a history of recent outdoor activity where mosquitoes were active. This article highlights a case of a 55-year-old man whose history and symptoms of WNND were confounded with an alternate diagnosis, acute alcohol withdrawal. An overview of WNV infections, and important historical clues and objective findings characteristic of neuroinvasive disease, is discussed to increase readers' knowledge of WNV and awareness of when to consider WNND in the diagnostic differential.

Background Proton magnetic resonance spectroscopy (1 H-MRS) studies have demonstrated abnormal levels of a variety of neurometabolites in inpatients/outpatients with alcohol use disorder (AUD) following acute alcohol withdrawal relative to healthy controls. In contrast, few studies have compared neurometabolite levels between less severe, treatment-naive AUD individuals and light drinkers (LD) or related them to recent alcohol consumption. The present study compared neurometabolite levels between treatment-naive AUD and LD individuals. Methods Twenty treatment-naive individuals with AUD and 20 demographically matched LD completed an 1 H-MRS scan, approximately 2.5 days following their last reported drink. 1 H-MRS data were acquired in dorsal anterior cingulate (dACC) using a 2-dimensional J-resolved point-resolved spectroscopy sequence. dACC neurometabolite levels, with a focus on glutamate, glutamine, and GABA, were compared between AUD and LD participants. The associations between metabolite levels and recent drinking were explored. Results AUD participants had significantly lower concentrations of GABA (Cohen's d = 0.79, p = 0.017) and glutamine (Cohen's d = 1.12, p = 0.005), but not glutamate (Cohen's d = 0.05, p = 0.893), relative to LD. As previously reported, AUD participants' glutamate and N-acetylaspartate concentrations were inversely associated with their number of heavy drinking days. In contrast, neither number of drinking (mean p = 0.56) nor heavy drinking (mean p = 0.47) days were associated with metabolite concentrations in LD. Conclusions The present study demonstrated significantly lower levels of prefrontal γ-aminobutyric acid and glutamine in treatment-naive individuals with AUD relative to LD. Whether these findings reflect the neurotoxic consequence and/or neuroadaptive response of alcohol consumption versus a predrinking trait, and therefore a more durable neurochemical disturbance, awaits elucidation from longitudinal studies.

Objectives Although sleep disturbances are prominent during alcohol withdrawal, less is known about the specific components of sleep that are disturbed prior to and during acute detoxification. This study aimed to determine whether specific sleep components are affected prior to and during acute detoxification and their relationship to psychological distress. Methods Twenty-nine participants were recruited from a residential detoxification service in Melbourne, Australia, and completed both subjective methods of sleep and distress, in addition to wearing an actigraphy device. Results Daytime dysfunction, sleep quality, and sleep disturbances were the components that were most disturbed in the month prior to admission, and poor sleep efficiency was detected during acute withdrawal using actigraphy. A significant association was found between sleep and psychological distress in this group. Conclusions Specific disturbances in sleep are experienced prior to and during acute alcohol withdrawal, suggesting that tailored interventions may be effective in the treatment of sleep deficits during these periods.

This article describes a case of koro-like symptoms from Oman associated with alcohol withdrawal and illustrates how the socio-cultural practices of Ramadan-fasting affected the patterning and timing of presentation of severe alcohol withdrawal symptoms. The patient was severely distressed by the delusion that his penis had been amputated. The acute anxiety involving this delusion appears to be conceptually and phenomenologically similar to koro.

Background: Previous data in both rat and mouse genetic models suggest that there is a genetic relationship between acute alcohol withdrawal responses and innate alcohol drinking behavior. The purpose of the present study was to examine whether acute alcohol withdrawal responses, as measured by acoustic startle and prepulse inhibition (PPI) of acoustic startle, may be genetically related to innate differences in alcohol preference in 2 mouse lines selectively bred for high (HAP1 and HAP2) or low (LAP1 and LAP2) alcohol preference. Line differences in startle responses at baseline, prior to alcohol or saline treatment, were also measured. Methods: Alcohol-naive, male and female HAP1 (n = 35) and LAP1 (n = 32) and HAP2 (n = 43) and LAP2 (n = 40) mice were tested under baseline conditions and during withdrawal from a single injection of 4.0 g/kg alcohol or equal volume of saline at 4, 8, and 12 hours post-injection. Results: On most trial types, baseline startle responses and PPI were greater in both HAP lines than in both LAP lines, and startle responses were greater in males than in females. During acute alcohol withdrawal, both male LAP lines, and LAP1 females, showed reduced startle responses at the 4-hour time point during acute alcohol withdrawal. In contrast, both HAP1 males and females showed a trend toward enhanced startle at 4 hours in withdrawal. No clear differences in PPI during withdrawal were evident. Conclusions: These findings indicate good evidence for a genetic relationship between greater baseline acoustic startle responses and PPI and high alcohol preference. Modest support for a genetic correlation between low alcohol preference and reduced startle responses at 4 hours in withdrawal was found in male mice. The suppression in acoustic startle during acute alcohol withdrawal in male LAP lines but not in male HAP lines suggests that a genetic propensity toward low alcohol preference may be related to greater sensitivity to alcohol as measured by acoustic startle responses during acute alcohol withdrawal.

Negative affect promotes dysregulated alcohol consumption in non-dependent and alcohol-dependent animals, and cues associated with negative affective states induce withdrawal-like symptoms in rats. This study was designed to test the hypotheses that: (1) the kappa-opioid receptor (KOR) system mediates phenotypes related to alcohol withdrawal and withdrawal-like negative affective states and (2) cues associated with negative affective states would result in dysregulated alcohol consumption when subsequently presented alone. To accomplish these goals, intracerebroventricular infusion of the KOR antagonist nor-binaltorphimine (nor-BNI) was assessed for the ability to attenuate the increase in 22-kHz ultrasonic vocalizations (USVs) associated with alcohol withdrawal and KOR activation in adult male wistar rats. Furthermore, cues associated with a KOR agonist-induced negative affective state were assessed for the ability to dysregulate alcohol consumption and the efficacy of intracerebroventricular KOR antagonism to reduce such dysregulation was evaluated. KOR antagonism blocked the increased number of 22-kHz USVs observed during acute alcohol withdrawal and a KOR agonist (U50,488) resulted in a nor-BNI reversible increase in 22-kHz USVs (mimicking an alcohol-dependent state). Additionally, cues associated with negative affective states resulted in escalated alcohol self-administration, an effect that was nor-BNI sensitive. Taken together, this study implicates negative affective states induced by both alcohol withdrawal and conditioned stimuli as being produced, in part, by activity of the DYN/KOR system.

Background Mice selectively bred for high or low withdrawal to acute alcohol differ on a number of traits, including consumption of alcohol, conditioned place preference for alcohol, and sensitivity to alcohol-induced locomotor activity. One trait that has not been examined in these mice is behavioral inhibition. Methods High and low alcohol withdrawal mice (second replicate: high and low acute alcohol withdrawal [HAW-2/LAW-2]) were trained and tested in a Go/No-go task. Mice were administered 0.0, 0.5, 1.0, and 1.5 g/kg ethanol (EtOH) on 3 occasions according to an incomplete Latin Square. A separate cohort of C57BL/6J (B6) and DBA/2J (D2) mice (the progenitor strains for HAW-2/LAW-2 mice) underwent the same protocol, using the same EtOH doses. Results HAW-2 and LAW-2 mice did not differ in behavioral inhibition at baseline, although LAW-2 mice did have higher overall levels of responding in the task. EtOH did not alter behavioral inhibition in these mice. However, it did decrease responses to the Go cue, and this effect was greater in HAW-2 mice than in LAW-2 mice. D2 mice had lower behavioral inhibition than B6 mice at baseline, and EtOH slightly decreased behavioral inhibition in both strains. Conclusions The findings with D2 and B6 mice generally fit with the existing literature. However, the lack of a difference in behavioral inhibition between HAW-2 and LAW-2 mice was unexpected, as well as the absence of any effect of these doses of EtOH on behavioral inhibition in these mice. Nonetheless, the findings do suggest that selectively breeding for high or low withdrawal to acute alcohol can lead to differences in operant behavior in the Go/No-go task.

Scenario: A 53-year-old male arrived at the mentally ill/chemically addicted unit with acute alcohol withdrawal. His electrocardiogram (ECG) showed the cardiac rhythm below. The patient was a recovering alcoholic but a week earlier had left his family and checked into a motel to drink alcohol. He had stopped eating and had been drinking continuously when he noticed chest palpitations and shortness of breath the day before Thanksgiving. However, he delayed going to the hospital until after Thanksgiving because he wanted to watch the football games. Before the diagnosis of alcoholism 2 years earlier, the business executive had no medical issues; in fact, he had been very healthy and had run marathons. A regular feature of the American Journal of Critical Care, the ECG Puzzler addresses electrocardiogram (ECG) interpretation for clinical practice. To send an eLetter or to contribute to an online discussion about this article, visit www.ajcconline.org and click “Respond to This Article” on either the full-text or PDF view of the article. We welcome letters regarding this feature.

We have previously hypothesized that increased sensitivity to the dysphoric-like or aversive effects of alcohol withdrawal following an initial exposure to alcohol might be associated with a genetic propensity to avoid alcohol. A decrease in brain reward function, as measured by an elevation in intracranial self-stimulation (ICSS) reward threshold, is one of the few methods available to model dysphoric-like or aversive effects of drug withdrawal in rats. We compared brain reward function during withdrawal following an initial exposure to alcohol in alcohol-naive rats selectively bred for high (HAD1 line) versus low (LAD1 line) voluntary alcohol consumption. Male HAD1 (n = 5) and LAD1 (n = 6) rats were implanted with unilateral electrodes in the medial forebrain bundle and trained to bar press for delivery of a 100 μA current that varied in frequency from 45 to 200 Hz. Responding for ICSS was generally stable within subjects across multiple experimental sessions on a given day and across several consecutive days prior to alcohol or water administration. ICSS responding was assessed in both rat lines prior to and at 12, 14, 16, 18, 20, and 24 h following a single intragastric infusion of alcohol (4.0 g/kg body weight) or water. Rats of the LAD1 line, but not those of the HAD1 line, exhibited a decrease in brain reward function as evidenced by a decrease in bar-press responding for ICSS and an increase in ICSS stimulation threshold during alcohol withdrawal. The results suggest that rats selectively bred for low alcohol drinking may experience dysphoric-like effects during withdrawal from an initial exposure to alcohol, while rats selectively bred for high alcohol drinking may not.

Background: We have previously reported an association between greater alcohol withdrawal magnitude after a single alcohol exposure and a genetic predisposition toward low alcohol drinking in rats selectively bred for differences in alcohol intake when acoustic startle reactivity to a tone stimulus was used to index acute alcohol withdrawal. The purpose of this study was to examine whether the quality of the acoustic startle stimulus (noise versus tone) is important for detecting a genetic relationship between alcohol withdrawal magnitude and alcohol drinking behavior. Methods: Alcohol-naive male rats selectively bred for high alcohol intake [alcohol-preferring (P), high-alcohol-drinking (HAD)1, and HAD2] or low alcohol intake [alcohol-nonpreferring (NP), low-alcohol-drinking (LAD)1, and LAD2] received a single intragastric infusion of water or alcohol (4.0 g/20.3 ml/kg; 25% v/v), and acoustic startle test sessions were given at 14, 16, 18, 20, and 24 hr after infusion. Each test session consisted of a 5-min acclimation period followed by random presentation of various white noise stimuli (90, 100, 110, and 120 dB.) Results: Line differences in acoustic startle magnitude under control conditions were present in all three pairs of selectively bred lines; P rats showed a greater startle magnitude relative to NP rats, whereas both LAD lines showed a greater startle magnitude relative to both HAD lines. During alcohol withdrawal, the P, HAD1, and HAD2 lines showed enhanced startle magnitude compared with their water-treated controls. No change in startle magnitude during alcohol withdrawal was found in the NP, LAD1, or LAD2 lines. Conclusions: In contrast to our prior findings, these results showed a genetic association between high alcohol drinking and a greater startle response magnitude to a noise stimulus during alcohol withdrawal. It seems that the genetic association between alcohol drinking and alcohol withdrawal, as assessed by the acoustic startle response, depends on the quality of the acoustic startle stimulus.

Studies on the neuropsychological performance in detoxified alcoholic patients often begin by acknowledging that there is a cognitive impairment to be found. Only little attention has been paid to date to the question as to how acute alcohol withdrawal might affect cognitive functions. Twenty-nine alcohol-dependent inpatients, nine in moderate alcohol withdrawal, treated with carbamazepine (group 1), 10 in mild alcohol withdrawal without pharmacological treatment (group 2), 10 in mild alcohol withdrawal with carbamazepine treatment (group 3) and 31 healthy subjects as controls (group 4) underwent repeated investigations using memory tests. The tests were performed on the first, third, seventh and fourteenth days of withdrawal. Immediate free recall of a word-list was impaired in the three patient groups in comparison with the control group on the 1st day. Thereafter no significant differences could be revealed between patients and controls. In a word-list recognition test the memory functions were not impaired in group 1 and group 2 in comparison with the control subjects. However, patients in group 3 showed impairment in this recognition test in comparison with the healthy subjects on the first and third days. The present study suggests that acute alcohol withdrawal impairs memory functions, especially free recall. This should be considered in treatment interventions in the early days of withdrawal.

Aims: The brain volume of chronic drinkers is known to partially recover with abstinence from alcohol. To investigate the relative contribution of grey and white brain matter to this process, magnetic resonance imaging and brain tissue segmentation was used to study brain tissue in acute alcohol withdrawal and abstinence in seven alcohol-dependent men. Methods: The patients were studied on three occasions; within 48 h after the last drink and approximately one month and two and a half months later. Total brain tissue class volumes (grey matter (GM) and white matter (WM) and cerebrospinal fluid (CSF)) were measured. Eleven healthy volunteers were scanned twice to serve as a control group. The alcohol-dependent patients were investigated with regard to drinking variables, neuropsychological performance and blood biochemistry. Results: In the alcohol-dependent patients, intracranial volume and total GM volume did not change between scan occasions, except in a single patient who demonstrated a GM increase of 4.8% (4.2% relative volume) between scans 2 and 3. For all patients, the increase in total WM volume ranged between 1.9 and 22.4% (absolute volumes) and 2.1 and 21.2% (relative volumes). Between scans 2 and 3, the increase in total WM volume ranged between 0.3 and 13.2% (absolute volumes), and between 1.5 and 14.0% (relative volumes). One patient resumed drinking and was investigated a second time during acute withdrawal. In this patient, the measured decrease of 8.1 and 8.5% of absolute and relative WM volumes corresponded to the size of the volume increase between scans 1 and 2. CSF, GM and WM volumes in the healthy subjects were constant over time. Conclusions: The results demonstrate that changes in brain volume during short-term abstinence in chronic alcohol-dependent patients are confined to the WM. The time limit of WM volume restitution is variable and continues longer than 3 weeks after withdrawal.

The present investigation studied Jian Bu Wan's effect on «hangover», induced by acute alcohol withdrawal symptoms after a light alcohol intoxication. We found no difference between placebo of Jian Bu Wan's treatment in the effects on «hangover» symptoms

A 36-year-old patient with normal-appearing coronary arteries suffered an acute Q-wave myocardial infarction during acute alcohol withdrawal and delirium tremens. Sympathetic hyperactivity with coronary spasm and increased platelet reactivity are probably the underlying mechanisms.

Summary Platelet function was assessed before and one week after acute alcohol withdrawal in eighteen male alcoholics. Compared to normal male controls, the platelets of the alcoholics were slightly hypoaggregable on admission but became hyperaggregable one week after commencement of alcohol withdrawal therapy. The changes were most noticeable in those patients who were alcoholaemic on admission and when using ADP or adrenaline as aggregating agents. There was no consistent change in platelet counts or in platelet adenine nucleotide levels, both of which were normal.

Cerebrospinal fluid norepinephrine (NE) levels were determined by radioenzymatic assay in 21 patients with a variety of neurological diseases and 49 patients in acute alcohol withdrawal. A second determination was made in 19 patients who had recovered from the alcohol withdrawal syndrome. Cerebrospinal fluid NE concentration was higher in the patients during alcohol withdrawal (192.3 plus or minus 22.3 pg/mL) and decreased during recovery to 137.8 plus or minus 15.9 pg/mL. The CSF NE level was higher in both groups than in patients with other neurological disorders. This may help explain the adrenergic signs observed during alcohol withdrawal.

In a group of 20 patients with heavy alcohol intake a relation was found between withdrawal symptoms and fall in serum potassium. Total body potassium (TBK) was measured in all subjects and was lower in the group of subjects who displayed symptoms than in the group who did not. The subgroup of the four most severe reactors had a mean TBK value significantly less than the ‘non-reactor’ group. The minimum serum potassium levels observed for all subjects in the four day period following alcohol withdrawal correlated with their TBK values. We suggest that the mechanism for the serum potassium fall might be overactivity of the Na-K pump caused by ethanol consumption. There was also an association between withdrawal reaction and abnormal liver function and a transient rise in serum phosphate in the more severely reacting subjects.

A double-blind, randomized trial is described which was designed to compare the clinical effect of 600 mg daily of carbamazepine (Tegretol®) and of tiapride (Sereprile®) in hospitalized patients with pre-delirium tremens. Physicians' assessment of patients' progress was made following 2, 4 and 7 days of treatment. Of the sixty patients admitted to the study, five dropped out for various reasons, leaving fifty-five patients who completed the study. Both drugs were effective in the treatment of alcohol withdrawal symptoms; no significant difference was found between the two treatments with respect to total symptoms' score and visual analogue scale assessment. Carbamazepine gave faster relief of symptoms and demonstrated a preferential action on symptoms like fear and hallucinations. No case of delirium tremens was observed in those patients who completed the trial.

Severe alcohol withdrawal developed in an abstinent chronic alcoholic man. Massive doses of benzodiazepines (2,335 mg of diazepam intravenously, 21,225 mg of oxazepam orally) achieved only marginal control of delirium and agitation. Analysis of multiple blood samples drawn during and after the withdrawal episode indicated, as expected, very high concentrations of diazepam and metabolites and of oxazepam. There was no evidence of an abnormal pharmacokinetic profile. Benzodiazepine resistance in withdrawing alcoholics probably reflects a receptor-site phenomenon rather than an abnormal drug disposition.

A case of severe alcohol withdrawal complicated by seizures, hallucinosis, hypertension, and supraventricular tachycardia is presented. When the patient showed no response to intravenous diazepam (total, 70 mg over 30 minutes) three 0.5-mg increments of propranolol were administered intravenously, resulting in immediate conversion to sinus rhythm and reduction of blood pressure from 210/130 mm Hg to 130/80 mm Hg. The use of intravenous propranolol as an adjunct to standard therapy in the alcohol withdrawal syndrome is discussed.

Cardiac function was evaluated by noninvasive techniques in 50 patients hospitalized during acute alcohol withdrawal treatment. All patients had ingested large amounts of alcohol for at least five years, hut discontinued alcohol intake 24 to 72 hours prior to admission. There was no clinical history of heart disease in any of the patients. Our study employed 12-lead electrocardiograms (daily) and 24-hour Holter monitoring. M-mode echocardiography and systolic time intervals were evaluated in 24 patients. The results indicate that marked electrical irritability of a depressed myocardium during the acute phase of alcohol withdrawal indicates the need for close cardiac observation of such patients in order to avoid potential life-threatening arrhythmias.

We present a randomized double-blind study on the efficacy of caroverine in the treatment of alcohol withdrawal symptoms. The group B Ca2+ channel blocking agent caroverine was tested against meprobamate in inpatient treatment of alcohol withdrawal. Patients of both groups were similar in age, weight, duration of drinking, ingested quantities of alcohol and intensity of withdrawal symptoms in both groups. The symptoms were quantified daily by Syndromkurztest (SKT), Nurses' Observation Scale for Inpatient Evaluation (NOSIE), NGI; the Webster scale was applied to rate tremor, speech and coping. Duration of study was scheduled for 5 days after which other medication, e.g., levopromazine was applied if needed. As caroverine is registered and used as a spasmolytic drug in Austria, patients' verbal consent was sufficient. In both compounds we registered no difference of clinical efficacy, though caroverine presented less sedative side effects. This may be an important factor in the treatment and management of alcohol withdrawal symptoms. Dose ranges were 120 mg/day vs. 2,400 mg/day of caroverine and meprobamate, respectively. Thus, drug loading and metabolism can be thoroughly reduced by the application of caroverine--another important point in treatment of alcoholism. In 4 cases of manifest delirium tremens the infusional application of caroverine was openly tested with dose ranges of 2.5-5.0 mg/kg (24 h). Clinical effects were estimated to be similar with oral application as was therapeutic efficacy. This novel indication of a group-B Ca2+ channel blocker presents an interesting feature, which seems to warrant further investigation.

We compared the baseline cortisol secretory pattern and ACTH and cortisol responses to hCRH (100 μg) in eight patients acutely withdrawn from ethanol and 12 patients who abstained from ethanol for two to six weeks. Acute withdrawal from ethanol was characterized by elevated baseline cortisol and blunted ACTH release after hCRH, while medium-term abstention was associated with normalized cortisol secretion but persistence of decreased ACTH output following stimulation. These findings support an altered corticotrophic CRH receptor function in detoxified sober alcoholics. The pathophysiology underlying the blunted ACTH response to hCRH in medium-term ethanol abstention appears to be different from that in acute alcohol withdrawal and hypercortisolemic depression.

Gamma-aminobutyric acid (GABA) and cyclic adenosine monophosphate (AMP) and guanosine monophosphate (GMP) were compared in the cerebrospinal fluid (CSF) of 13 patients suffering from acute alcohol withdrawal, and the same patients during convalescence. No significant changes were found, but CSF norepinephrine (NE) levels were elevated in acute alcohol withdrawal and decreased toward normal during convalescence.

Interactions between ethanol, prostaglandins, and essential fatty acids (EFA) have led to the hypothesis that acute alcohol withdrawal and the sequelae of chronic alcoholism may be related to an EFA/prostaglandin deficiency. To test this hypothesis, EFA profiles in blood-lipid fractions, serum liver enzymes, cognitive function, and alcohol craving were measured in 27 acutely abstinent alcoholics before and after a 3-week double-blind trial of EFA supplementation. Upon entry into the study, alcoholics had significant differences in EFA levels as compared to normal controls, and serum levels of liver enzymes tended to correlate with these EFA levels. After 21 days, cognitive function, alcohol craving, and liver enzymes all improved in both the EFA and placebo groups; most EFA levels also approached normal values. There were no treatment effects of EFA supplementation at the dose used.

An open study was carried out in 21 chronic alcoholics with severe withdrawal symptoms and incipient delirium tremens to evaluate the efficacy of adjuvant treatment with intramuscular lorazepam (5mg). All symptoms subsided within 2 hours after a single injection and remained under control with oral lorazepam (mean daily dose 7 mg). No adverse reactions attributable to lorazepam were observed.

We performed a within-subject comparison of the kinetics of diazepam given to 7 alcoholic subjects during acute alcohol withdrawal and again after detoxification. The initial rapid exponential decline of plasma diazepam concentrations (t1/2 alpha) was more rapid during (0.21 +/- 0.03 hr) than after withdrawal (0.44 +/- 0.14 hr, p less than 0.05). Terminal t1/2, clearance, and volumes of distribution changed in individual patients, but mean values did not change. Protein binding was less in patients (93.4 +/- 2.4%) than in healthy controls (97.0 +/- 1.0, p less than 0.05). The effects of alcohol withdrawal on diazepam disposition do not explain the high doses of diazepam commonly required to treat the withdrawal.

The Jlexamethasone Suppression Test (DST) has received considerable attention as a possible biological marker of endogenous depression, yet it has been associated with other factors, such as medications and illness (Carroll et al. 1981), age (Feinberg and Carroll 1984; Nelson et al. 1984; Halbreich et al. 1985), serum sodium levels (Tollefson et al. 1986), weight loss (Edelstein et al. 1983: Targum 1983; Feinberg and Carroll 1984; Berger et al. 1985), and acute alcohol withdrawal (Abou-Saleh et al. 1984; Dackis et al. 1984). In the course of evaluating the DST as a diagnostic tool, we observed an apparent relationship between positive DST results and electroencephalogram (EEG) abnormalities, which, to our knowledge, has not been previously described.

A review of 260 consecutive admissions for alcoholic withdrawal to the Alcohol Detoxification Service of the Los Angeles County--University of Southern California Medical Center shows that 98% of the patients fulfill the criteria for alcoholism as stated by the National Council of Alcoholism Criteria Committee. Previous alcoholic history, current symptoms, physical findings, and laboratory tests indicate frequent multiple organ dysfunction in acute alcohol withdrawal. Hallucinations occurrred in more than 46% of patients with a blood alcohol over 100 mg%. More than 90% of the patients had one or more abnormal laboratory values, and the serum gamma glutamyl transpeptidase was the most commonly elevated laboratory test.

The relationship between maxillofacial trauma and alcohol abuse has been well documented. The onset of acute alcohol withdrawal following the injury can seriously complicate and compromise the treatment of the maxillofacial injuries as be potentially lethal for the patient. A clear understanding of the biochemistry, development, signs and symptoms, and management of acute alcohol withdrawal is necessary for the oral and maxillofacial surgeon.

Summary An intensive study was undertaken based upon the chart review of a large number of consecutive male admissions for acute alcohol withdrawal syndromes to a university psychiatric service. Basic psychosocial characteristics were examined along with the characteristics of the presenting picture and the clinical coarse. The patients had been treated with paraldehyde along principles described elsewhere3 The analysis of this data would document an extensive experience gained in a circumscribed zone of time and space. It was expected that it would contribute to a better understanding of the natural history of this group of related withdrawal syndromes by yielding, information about etiologic and prognostic factors. It would also summarize and make possible the evaluation of the treatment program. It would also serve to make a large body of data available for subsequent cross-cultural, cross-temporal and cross-therapeutic comparisons.

Lorazepam, a new minor benzodiazepine tranquillizer, was given intramuscularly to 19 patients suffering from acute alcohol withdrawal. The severity of their symptoms decreased rapidly. Lorazepam appears to be useful in the management of withdrawal symptoms, and more extensive trials are recommended.

RECENT evidence suggests a relationship in humans between reduction of stage-4 sleep (viz, high voltage, slow waves) and varying degrees of thought disturbance. Notable are the reports of marked decrease in stage-4 patterning in chronic schizophrenic patients 1-6 and patients with depression and manic-depressive illness, depressed phase. 7-10 Moreover, Feinberg and Carlson 11 observed stage-4 sleep to be a hyperbolic function of age, with verbal performance IQ a parabolic function showing maximum decline at periods of minimum stage-4 sleep. Hallucinations accompanying the symptoms of acute alcohol withdrawal were found to be inversely related to amount of stage-4 sleep. 12 The present investigation studied the allnight sleep electroencephalograms and power-density configurations for a group of psychotic and normal prepuberal children. Particular attention was focused on whether stage-4 sleep was affected in the psychotic population who were clearly manifesting thought disorders. Methods Subjects.—This study included 12 boys and seven