History Of Chronic Alcohol Abuse Research Articles

Hippocampal granule cell loss in human chronic alcohol abusers

Chronic alcohol abuse causes cognitive impairments associated with neurodegeneration and volume loss in the human hippocampus. Here, we hypothesize that alcohol reduces the number of granule cells in the human dentate gyrus and consequently contribute to the observed volume loss. Hippocampal samples were isolated from deceased donors with a history of chronic alcohol abuse and from controls with no alcohol overconsumption. From each case, a sample from the mid-portion of hippocampus was sectioned, immunostained for the neuronal nuclear marker NeuN, and counter stained with hematoxylin. Granule cell number and volume of granular cell layer in the dentate gyrus were estimated using stereology. We found a substantial reduction in granule cell number and also a significantly reduced volume of the granular cell layer of chronic alcohol abusers as compared to controls. In controls there was a slight age-related decline in the number of granule cells and volume of granular cell layer in line with previous studies. This was not observed among the alcoholics, possibly due to a larger impact of alcohol abuse than age on the degenerative changes in the dentate gyrus. Loss of neurons in the alcoholic group could either be explained by an increase of cell death or a reduced number of new cells added to the granular cell layer. However, there is no firm evidence for an increased neuronal death by chronic alcohol exposure, whereas a growing body of experimental data indicates that neurogenesis is impaired by alcohol. In a recent study, we reported that alcoholics show a reduced number of stem/progenitor cells and immature neurons in the dentate gyrus, hence that alcohol negatively affects hippocampal neurogenesis. The present results further suggest that such impairment of neurogenesis by chronic alcohol abuse also results in a net loss of granule cells in the dentate gyrus of hippocampus.

Wernicke’s Encephalopathy in a Patient Without Chronic Alcohol Abuse

Wernicke’s encephalopathy (WE) is traditionally seen in the emergency department in patients with chronic alcohol abuse. WE can result in significant morbidity and mortality if untreated, making early diagnosis and intervention paramount. We discuss a case of WE in a 63-year-old female with no history of chronic alcohol abuse, who presented with bilateral opthalmoplegia that resolved after intravenous thiamine administration. This case report highlights the varied clinical settings other than chronic alcohol abuse in which the diagnosis of WE should be considered.

Alcoholism and sexual dimorphism in the middle longitudinal fascicle: a pilot study.

Alcoholism can lead to a complex mixture of cognitive and emotional deficits associated with abnormalities in fronto-cortico-striatal-limbic brain circuitries. Given the broad variety of neurobehavioral symptoms, one would also expect alterations of postrolandic neocortical systems. Thus, we used diffusion tensor imaging (DTI) to study the integrity of the middle longitudinal fascicle (MdLF), a major postrolandic association white matter tract that extends from the superior temporal gyrus to the parietal and occipital lobes, in individuals with a history of chronic alcohol abuse. DTI data were acquired on a 3 Tesla scanner in 30 abstinent alcoholics (AL; 9 men) and 25 nonalcoholic controls (NC; 8 men). The MdLF was determined using DTI-based tractography. Volume of the tract, fractional anisotropy (FA), radial (RD), and axial (AD) diffusivity, were compared between AL and NC, with sex and hemispheric laterality as independent variables. The association of DTI measures with neuropsychological performance was evaluated. Men showed bilateral reduction of MdLF volume and abnormal diffusion measurements of the left MdLF. Analyses also indicated that the left MdLF diffusion measurements in AL men were negatively associated with Verbal IQ and verbal fluency test scores. Abstinent alcoholic men display macrostructural abnormalities in the MdLF bilaterally, indicating an overall white matter deficit. Additionally, microstructural deficits of the left MdLF suggest more specific alterations associated with verbal skills in men.

A case of marchiafava bignami disease with frontal cortex involvement and late onset, long-lasting psychiatric symptoms

AimsTo describe the case and management of a patient with marchiafava bignami disease (MBD) with frontal cortical lesions, no specific symptoms at first referral to the emergency room, and late onset of atypical psychiatric symptoms.MethodsWe report the case of a 44-year-old patient with a history of chronic alcohol abuse, eventually diagnosed with MBD.ResultsMagnetic resonance showed lesions in the splenium and in the body of corpus callosum and bilateral lesions of the frontal cortex. The patient showed late-onset atypical psychiatric symptoms, which were drug resistant.ConclusionsThe case we describe seems to support the existing few ones describing cortical involvement in MBD, which suggest that this is associated with a poorer prognosis. Psychiatric symptoms may be challenging to treat because of drug resistance. The involvement of psychiatrists together with neurologists and radiologists, with a consultation–liaison approach has proved important for the achievement of diagnosis and of the most appropriate management and treatment for this patient.Disclosure of interestThe authors have not supplied their declaration of competing interest.

Akut Marchiafava-Bignami Hastalığı Olan Bir Hastada Manyetik Rezonans Görüntüleme Bulguları

Marchiafava-Bignami disease or syndrome (MBD) is a rare disorder that all cases had a history of chronic alcohol abuse. It is thought to be due to vitamin B complex deficiency. All cases had a symmetrical lesions in the corpus callosum and causes progressive demyelination and necrosis. It can spread to white matter of the neighboring tissues and rarely to the subcortical areas. Clinical symptoms include not only dysarthria, ataxia, tetraparesis, disphagia, dementia as a clinical outcome, cognitive deficits but also disturbed consciousness, seizure and coma. Some of them show asymmetrical hypointense areas in multiple regions on susceptibility-weighted imaging. Here, we report a 25-year-old man had progressive ataxia, dysarthria, and disphagia. This is a case of MBD that was diagnosed by magnetic resonance imaging (MRI).

Marchiafava-Bignami disease with asymmetric extracallosal lesions.

Marchiafava-Bignami disease (MBD) is a rare disease in patients with chronic alcoholism and is characterized by symmetric demyelination and necrosis of the corpus callosum. Clinical features include neuropsychiatric disorders, dysarthria, tetraparesis, astasia-abasia, impaired consciousness and symptoms of interhemispheric disconnection. The lesions in MBD are not restricted to the corpus callosum, but also occur in extracallosal regions. However, no case of MBD with extracallosal lesions confined to one side of the brain has been reported. We present a patient with MBD showing asymmetric extracallosal lesions and complete resolution of magnetic resonance imaging (MRI) abnormalities.

Covering the Cover

Covering the Cover

Fomepizole in the treatment of acute methanol poisonings: experience from the Czech mass methanol outbreak 2012-2013.

During an outbreak of mass methanol poisonings in the Czech Republic in 2012-2013, fomepizole was applied as an alternative antidote to ethanol. We present the laboratory data, clinical features, adverse reactions, and treatment outcomes in all patients treated with fomepizole. Combined retrospective and prospective case series study in 25 patients, median age 50 (16-73) years, 18 males and 7 females. There were 24% fatalities, 36% survivors without health impairment, and 40% survivors with sequelae. All the patients who died were comatose on admission; the mortality was 50% among patients in a coma. The median intensive care unit length of stay was six (2-22) days. The median total dose of fomepizole was 2 (1-9) g. Complications were observed in 7/25 cases: aspiration pneumonia (4), sepsis (2), bleeding (2), malignant arrhythmia (1), delirium tremens (1), and rebound of acidosis (1). The patients who survived without impairment were less acidotic than those who died or survived with sequelae (P<0.01). No difference in serum methanol and formate was found between the three groups. There is no evidence whether fomepizole is a more efficient antidote than ethanol with regards to the hospital mortality. The possibility of delirium tremens in the patients with a history of chronic alcohol abuse has to be taken in consideration. The benefits of fomepizole were indirect: no need to monitor serum ethanol's level during the hemodialysis in severely poisoned patients and less working overload on ICU doctors treating several poisoned patients simultaneously.

Subacute encephalopathy with seizures in alcoholics (SESA syndrome) revisited

PurposeThe aim of this paper is to describe two additional cases of subacute encephalopathy with seizures in alcoholics (SESA syndrome), and to propose that this entity now should be considered as a subtype of nonconvulsive status epilepticus (NCSE). MethodsWe retrospectively analyzed the clinical characteristics, electroencephalography (EEG), neuroimaging data, and prognosis of these two further cases of SESA syndrome. In addition, we compare our findings with the cases previously described in the English literature in order to propose new diagnostic criteria. ResultsTwo adults with history of chronic alcohol abuse were admitted because of confusion and seizures. A routine EEG showed frequent periodic lateralized epileptiform discharges (PLEDs) localized over the right temporal regions. In one case, we captured two complex partial seizures (CPSs) arising from the right hemisphere. Neuroimaging studies revealed subjacent chronic vascular pathology. Following transfer to the intensive care unit (ICU), both improved to antiepileptic treatment and were discharged with full recovery. ConclusionOn the basis of our findings and a review of the literature, we suggest that SESA syndrome represents a subtype of partial or localization-related NCSE given its particular clinical, electroencephalographic, neuroimaging and prognostic characteristics.

Empiema necessitatis por &lt;i&gt;Staphylococcus aureus&lt;/i&gt;

Empyema necessitatis is a collection of exudative fl uid in the pleural space extending across the parietal pleura into the sur- rounding tissue forming a fi stulous tract. The most common etiologic agents are: Mycobacterium tuberculosis, Actinomyces israelii, Strepto- coccus pneumoniae, Escherichia coli, Pseudomonas aeruginosa, Aspergillus sp, anaerobes and less frequently by Staphylococcus aureus. The cases of empyema necessitatis are reported more frequently in immunosuppressed patients with risk factors such as type 2 diabetes, chronic alcoholism, poor dental health, chronic obstructive pulmonary disease, smoking, cachexia and bronchiectasis. We report the case of 54 years old male with a history of chronic alcohol abuse and poorly controlled type 2 diabetes, with history of 2 weeks of fever, progressive dyspnea, chest pain and erythema, hyperthermia and swelling in the right subclavian region. Clinically with pleural effusion syndrome. With tomographic evidence of fi stulous tract and bacterial isolation the diagnosis was made. The patient had a severe infectious condition requiring antibiotic treatment and surgical resolution with excellent evolution.

Histomorphological features of pancreas and liver in chronic alcoholics--an analytical study in 390 autopsy cases.

Chronic pancreatitis and liver disease are two conditions that commonly co-exist in chronic alcoholics with variable incidences. To evaluate frequency pancreatitis in patients with a history of chronic alcohol abuse. A total of 390 autopsies over 11 year's period were included in the study. Gross and microscopic assessment of liver and pancreas were performed. Available clinical and laboratory parameters were recorded. Age ranged from 22 to 65 years with a mean age of 45.32 years. All 390 consecutive patients included in the study were males. Majority of the patients had primarily presented with alcohol related liver diseases whereas few had presented with features of pancreatitis. Micronodular cirrhosis was present in 292 cases. Features of chronic pancreatitis were observed in 42 cases and 8 of these cases had associated changes of acute hemorrhagic pancreatitis. Prevalence of pancreatitis was more in cirrhotics as compared to non-cirrhotics, and acute pancreatitis was mostly seen in non-cirrhotics. Dominant pattern of fibrosis was perilobular followed by periductal, intralobular and diffuse. Chronic pancreatitis as evidence by the presence of parenchymal fibrosis was more frequently observed in alcoholic cirrhosis cases than that in non-cirrhotic alcoholic liver disease, thereby suggesting common underlying pathobiology in the development of fibrosis in liver as well as in pancreas.

Letter to the Editor Madelung’s disease in a patient with chronic alcohol abuse

A 47-year-old man with a history of chronic alcohol abuse was admitted to our hospital because of symmetrical face soft tissue enlargement for differential diagnosis. The lesions had appeared 4 years earlier and had been asymptomatic. Physical examination revealed painless, elastic tumors of the subcutaneous tissue in the mandibular angle region, with no clear relation to lymph nodes or salivary glands (Figure 1A). The laboratory tests showed elevated aspartate aminotransferase (ALT), 127 U/l; elevated alanine aminotransferase (ALT), 91 U/l, elevated γ-glutamyl transpeptidase (GGT), 643 U/l, and elevated lactate dehydrogenase (LDH) activity, 342 U/l. Test for antinuclear antibodies (ANA) was negative. HIV and HCV infections were excluded. Lipid profile results were within the normal range. An abdominal ultrasound revealed a fatty liver, but no other abnormality was noted. Ultrasonography of the parotid, submandibular and cervical region confirmed the correct size and structure of the salivary and thyroid glands and slight enlargement of the lymph nodes in both submandibular regions. In the place of visible symmetric thickening there was a tissue described as lipofibroma, 49 mm × 24 mm on the right side and 44 mm × 23 mm in size on the left side. Fine-needle biopsy revealed lipomatous tissue. A diagnosis of Madelung's disease was made. Figure 1 A – Frontal view of the patient at time of first hospitalization with visible symmetrical fatty masses. B, C – Frontal and lateral view of the patient at follow-up visit after 1 year; increase in the primary fatty deposit At the follow-up visit after 1 year, the patient had a computed tomography (CT) scan performed, which showed a slight increase in the primary fatty deposit and the appearance of another in the neck area (Figure 2A–C). Six months later the patient was disqualified from surgical treatment. The decision was motivated by the non-life-threatening condition and asymptomatic nature of the masses. Figure 2A–C Head and neck CT showing the symmetrical enhancement of the lipomatous tissue Madelung's disease (also known as benign symmetric lipomatosis or Launois-Bensaude syndrome) is a rare metabolic disorder of unknown etiology [1]. This disease usually affects men at the age of 30 to 60 years from the Mediterranean area. In reported cases, almost 90% of patients had a history of long-term alcohol abuse [2]. The disease is characterized by the presence of prominent, symmetrical deposits of non-encapsulated adipose tissue in the region of head, neck, nape and upper parts of the trunk [2, 3]. In contrast to other cases described in the literature, in our patient, the primary subcutaneous fat masses appeared in the parotid region, while the most common initial location is the neck. Although benign in nature, sometimes the fatty masses can reach very large sizes causing dyspnea, dysphagia, fatigue, and reduced neck movement ability [4]. The differential diagnosis includes familial multiple lipomatosis, simple obesity, Cushing's syndrome, angiolipoma, neurofibroma and liposarcoma [2, 4, 5]. The most effective treatment is surgery, especially in patients with esthetic deformity or compression of the aerodigestive tract [1, 3].

Paucisymptomatic Marchiafava–Bignami disease with relevant diffusion-weighted MRI lesions

Marchiafava–Bignami disease (MBD) is a rare alcohol-associated disorder characterized by demyelization and necrosis of the corpus callosum. Diffusion-weighted (DW) MRI may reveal the lesions in patients showing serious clinical manifestations, high mortality rate and severe cognitive sequelae, though some cases with good outcome have been reported. We describe a case of a man with a history of chronic alcohol abuse associated with malabsorption; the man presented mild clinical signs on the first neurological exam, despite the presence of DW-MRI lesions, bilaterally involving entire corpus callosum, that are compatible with MBD diagnosis.

DNA Methylation/Demethylation Network Expression in Psychotic Patients with a History of Alcohol Abuse

Recent studies suggest that protracted and excessive alcohol use induces an epigenetic dysregulation in human and rodent brains. We recently reported that DNA methylation dynamics are altered in brains of psychotic (PS) patients, including schizophrenia and bipolar disorder patients. Because PS patients are often comorbid with chronic alcohol abuse, we examined whether the altered expression of multiple members of the DNA methylation/demethylation network observed in postmortem brains of PS patients was modified in PS patients with a history of chronic alcohol abuse. DNA-methyltransferase-1 (DNMT1) mRNA-positive neurons were counted in situ in prefrontal cortex samples obtained from the Harvard Brain Tissue Resource Center, Belmont, MA. 10-11-translocation (TETs 1, 2, 3), apolipoprotein B editing complex enzyme (APOBEC-3C), growth and DNA-damage-inducible protein 45β (GADD45β), and methyl-binding domain protein-4 (MBD4) mRNAs were measured by quantitative real-time polymerase chain reaction in inferior parietal cortical lobule samples obtained from the Stanley Foundation Neuropathology Consortium, Bethesda, MD. We observed an increase in DNMT1 mRNA-positive neurons in PS patients compared with non-PS subjects. In addition, there was a pronounced decrease in APOBEC-3C and a pronounced increase in GADD45β and TET1 mRNAs in PS patients with no history of alcohol abuse. In PS patients with a history of chronic alcohol abuse, the numbers of DNMT1-positive neurons were not increased significantly. Furthermore, the decrease in APOBEC-3C mRNA was less pronounced, while the increase in TET1 mRNA had a tendency to be potentiated in those PS patients that were chronic alcohol abusers. GADD45β and MBD4 mRNAs were not influenced by alcohol abuse. The effect of chronic alcohol abuse on DNA methylation/demethylation network enzymes cannot be attributed to confounding demographic variables or to the type and dose of medication used. Based on these results, we hypothesize that PS patients may abuse alcohol as a potential attempt at self-medication to normalize altered DNA methylation/demethylation network pathways. However, before accepting this conclusion, we need to study alterations in the DNA methylation/demethylation pathways and the DNA methylation dynamics in a substantial number of alcoholic PS and non-PS patients. Additional investigation may also be necessary to determine whether the altered DNA methylation dynamics are direct or the consequence of an indirect interaction of alcohol with the neuropathogenetic mechanisms underlying psychosis.

Cerebral microhemorrhage in Marchiafava–Bignami disease detected by susceptibility-weighted imaging

Marchiafava-Bignami disease (MBD) is a rare alcohol-associated disorder. Clinical features include not only disturbed consciousness, dysarthria, tetraparesis, astasia-abasia, and symptoms of interhemispheric disconnection as initial symptoms but also cognitive deficits as clinical outcomes. The clinical significance of cerebral microhemorrhage (CMH) has been recognized in patients with cognitive deficits; however, the presence of CMH in patients with MBD has not been emphasized. The aim of the present study was to clarify the relationship between CMH and MBD. For this purpose, we report four patients with MBD, who showed asymmetrical hypointense areas in multiple cortico-subcortical regions on susceptibility-weighted imaging (SWI). All cases had a history of chronic alcohol abuse and symmetrical lesions in the entire corpus callosum. These patients' clinical symptoms included not only coma, dysarthria, and astasia-abasia as initial symptoms but also dementia as a clinical outcome. SWI showed asymmetrical hypointense areas in the multiple cortico-subcortical regions, indicating the presence of CMH. Compared with patients with normal cognitive function, demented patients showed higher severity of CMH. Our report would indicate that CMH is an important factor indicating the severity of dementia in patients with MBD.

Multiple Symmetric Lipomatosis

Multiple symmetric lipomatosis (MSL) is a relatively uncommon entity of unknown etiology characterized by symmetrically subcutaneous accumulation of nonencapsulated adipose tissue. Approximately 200 to 300 cases have been published. The aims of this article are to report the case of a 58-year-old Brazilian patient with MSL and provide a comprehensive overview of the current concepts concerning this disease. Our search yielded 28 articles on MSL, including case reports and reviews of the literature. MSL predominantly affects Mediterranean males with a history of chronic alcohol abuse. It is usually asymptomatic and may be associated with diabetes mellitus, hyperlipidemia, hyperuricemia, macrocytic anemia, and oral cancer. Surgical resection is the best treatment option. The case reported is a classic presentation of MSL; however, it is particularly uncommon owing to the association with immune thrombocytopenic purpura. This association has been described only once in the medical literature.

Posterior reversible encephalopathy syndrome following disulfiram intoxication

A 43-year-old man with a history of chronic alcohol abuse (8 beers per day for the last 6 months) was prescribed 1.2 g disulfiram a day by his general practitioner 3 weeks before hospital admission. He continued drinking alcohol during this period, despite abundant vomiting. Soon after starting disulfiram, he developed behavioral disorder. He lost 10 kg. He was then admitted to the emergency room. The patient was apyretic, with a blood pressure of 150/100 mmHg. He was disoriented to place and time, had retrograde amnesia for the past few days, paranoid delirium, and visual hallucinations. Neurological examination disclosed paretic dysarthria, bilateral horizontal gaze-evoked nystagmus, ataxic gait, and limb dysmetria. Two days later, with improved collaboration, proximal paraparesis and areflexia were found. Over the next 10 days, the paresis progressed to the distal lower limbs, upper limbs, and oropharyngeal muscles, with apparition of facial diplegia, and dysphagia. The weakness was associated with sensitive loss prevailing at extremities with intense dysesthesias and burning pain. During the first 3 days, blood pressure values remained between 130/80 and 150/100 mmHg. Then blood pressure increased to a maximum of 180/120 mmHg, returning to initial values after a few days with treatment by perindopril. Biology showed macrocytosis (MCV: 105 10 m (N \ 99.2), slightly abnormal hepatic enzymes (GPT : 75 IU/l (N \ 45) and GOT : 36 IU/l (N \ 35))], normal chemistry, C-reactive protein, ammoniemia, ethanolemia, B12 vitamin, and folate. Vitamin B1 dosage and transketolase activity were not performed due to local constraints. Brain CT scan on admission was normal. Brain MRI revealed bilateral cortical and subcortical parieto-occipital hyperintensities on T2-weighted and fluid-attenuated inversion-recovery (FLAIR) images (Fig. 1a). Normal signals were observed on the diffusion-weighted images (DWI); no contrast enhancement was observed. EEG showed diffuse background slowing. CSF analysis was normal. Urinary excretion of porphobilinogen and deltaaminolevulinic acid was normal. Antigangliosides antibodies and HIV serology were negative. Nerve conduction studies at onset of paraparesia and 1 week later disclosed rapidly progressing axonal polyneuropathy. A Wernicke–Korsakoff’s syndrome was first considered in the emergency room. High doses of thiamine (1.5 g/day) were administrated for 5 days. The radiological pattern was compatible with posterior reversible encephalopathy syndrome (PRES). This unexpected discovery coupled with the progressive cranial nerve involvement and tetraparesis prompted us to reconsider our diagnosis. Finally, the diagnosis of PRES and acute polyradiculoneuropathy secondary to disulfiram intoxication was made. We could not rule out a potential contributing role from previous chronic alcoholism and the possibility of an associated vitamin B1 deficiency. Disulfiram was discontinued and neurological rehabilitation was proposed. Facial and oropharyngeal paresis rapidly improved followed by improvement in the upper limb paresis. Cognition returned to normal. A brain MRI 14 days after symptom onset showed almost complete disappearance of PRES lesions (Fig. 1b). Lower limb paresis improved only very slowly during the following months. S. Coppens (&) G. Naeije N. Mavroudakis Department of Neurology, Hopital Erasme, ULB, Route de Lennik 808, 1070 Brussels, Belgium e-mail: sacoppen@ulb.ac.be

VHM07: Combined Cholangioscopy and Confocal Endomicroscopy of An Indeterminant Biliary Stricture

48 year old male with a history of chronic alcohol abuse presented with painless jaundice. CT scan and EUS revealed biliary dilation without an associated mass lesion. Initial ERCP showed a CBD stricture, however cytology brushings were non-diagnostic. The patient was then then referred to our institution for ERCP with cholangioscopy for further management of this indeterminant biliary stricture.

Dexmedetomidine Controls Agitation and Facilitates Reliable, Serial Neurological Examinations in a Non-Intubated Patient with Traumatic Brain Injury

We report the effective use of dexmedetomidine in the treatment of a patient with a history of chronic alcohol abuse and an acute traumatic brain injury who developed agitation that was unresolved if from traumatic brain injury, or alcohol withdrawal or the combination of both. Treatment with benzodiazepines failed; lorazepam therapy obscured our ability to do reliable neurological testing to follow his brain injury and nearly resulted in intubation of the patient secondary to respiratory suppression. Upon admission to hospital, the patient was first treated with intermittent, prophylactic doses of lorazepam for potential alcohol withdrawal based upon our institution's standard of care. His neurological examinations including a motor score of 6 (obeying commands) on his Glasgow Coma Scale testing, laboratory studies, and repeat CT head imaging remained stable. For lack of published literature in diagnosing symptoms of patients with a history of both alcohol withdrawal and traumatic brain injury, a diagnosis of agitation secondary to presumed alcohol withdrawal was made when the patient developed acute onset of tachycardia, confusion, and extreme anxiety with tremor and attempts to climb out of bed requiring him to be restrained. Additional lorazepam doses were administered following a hospital-approved protocol for titration of benzodiazepine therapy for alcohol withdrawal. The patient's mental status and respiratory function deteriorated with the frequent lorazepam dosing needed to control his agitation. Dexmedetomidine IV infusion at a rate of 0.5 mcg/kg/h was then administered and was titrated ultimately to 1.5 mcg/kg/h. After 8 days of therapy with dexmedetomidine, the patient was transferred from the ICU to a step-down unit with an intact neurological examination and no evidence of alcohol withdrawal. Airway intubation was avoided during the patient's entire hospitalization. This case report highlights the intricate balance between the side effects of benzodiazepine sedation for treatment of agitation and the difficulties of monitoring the neurological status of non-intubated patients with traumatic brain injury. Given the large numbers of alcohol-dependent patients who suffer a traumatic brain injury and subsequently develop agitation and alcohol withdrawal in hospital, dexmedetomidine offers a novel strategy to facilitate sedation without neurological or respiratory depression. As this case report demonstrates, dexmedetomidine is an emerging treatment option for agitation in patients who require reliable, serial neurological testing to monitor the course of their traumatic brain injury.

68: Is History of Chronic Alcohol Abuse in a Donor a Contraindication for Heart Transplant?

68: Is History of Chronic Alcohol Abuse in a Donor a Contraindication for Heart Transplant?