Three-Dimensional Mapping of Local Cerebral Perfusion in Alcoholic Encephalopathy With and Without Wernicke-Korsakoff Syndrome

Size: px
Start display at page:

Download "Three-Dimensional Mapping of Local Cerebral Perfusion in Alcoholic Encephalopathy With and Without Wernicke-Korsakoff Syndrome"

Transcription

1 Journal o/ Cerebral Blood Flow and Metabolism 7: Raven Press, New York Three-Dimensional Mapping of Local Cerebral Perfusion in Alcoholic Encephalopathy With and Without Wernicke-Korsakoff Syndrome Takashi Rata, John Stirling Meyer, Norio Tanahashi, Yoshiki Ishikawa, Akira Imai, Tamotsu Shinohara, *Maria Velez, *William E. Fann, tprasab Kandula, and :j:fumihiko Sakai Cerebral Blood Flow Laboratory, Veterans Administration Medical Center, and the Departments of Neurology, *Psychiatry, and tradiology, Baylor College of Medicine, Houston, Texas, U,S,A., and :f:department of Internal Medicine, Kitasato University, School of Medicine, Sagamihara-City, Kanagawa, Japan. Summary: Seventeen severe chronic alcoholic patients with and without Wernicke-Korsakoff syndrome (WKS) were examined prospectively after being treated by withdrawal from alcohol. The WKS patients also received thiamine supplements. Three-dimensional measurements of local cerebral blood flow (LCBF) and local partition coefficients (LA) were made utilizing xenon contrast computed tomography (Xe CT-CBF). Results were displayed as color-coded brain maps before and after treatment and these were correlated with neurological and cognitive examinations. Before treatment chronic alcoholics without WKS (n = 10) showed diffuse reductions of LCBF values throughout all gray matter including hypothalamus, vicinity of nucleus basalis of Meynert, thalamus, and basal ganglia. Similar, but more severe, reduc- tions were seen in patients with WKS (n = 7), however, white matter perfusion was also reduced. In WKS, most prominent reductions of LCBF were also seen in hypothalamus and basal forebrain nuclei but thalamus, basal ganglia, and limbic systems were severely reduced. After treatment, both groups with alcoholic encephalopathy showed marked clinical improvement and cerebral perfusion was restored toward normal. Chronic alcohol abuse, in the absence of thiamine deficiency, reduces CBF by direct neurotoxic effects. If thiamine deficiency is also present, more severe and localized hemodynamic reductions are superimposed. Key Words: Alcohol-Cerebral blood flow-chronic alcoholism-nucleus basalis of Meynert-Wernicke-Korsakoff syndrome-xe CT CBF. The CNS is more sensitive to the deleterious effects of alcohol than other organs of the body. Ethanol (ethyl alcohol) affects the CNS as a metabolic and functional depressant, with certain systems being more sensitive to its cumulative effects than others. Ethanol rapidly passes the blood-brain barrier to depress neuronal activity. Electrophysiological studies in human subjects, as well as animal Received June 27, 1986; accepted September 24, Address correspondence and reprint requests to Dr. J. S. Meyer, Director, at Cerebral Blood Flow Laboratory, Veterans Administration Center, 2002 Holcombe Boulevard, Houston, TX 77211, U. S.A. Abbreviations used: ATPase, adenosine triphosphatase; CCS E, Cognitive Capacity Screening Examinations; CMR02, cerebral metabolic rate for oxygen; CT-CBF, computed tomography-cbf; LCBF, local CBF; LA, local partition coefficients; MABP, mean arterial blood pressure; PEC02, end-tidal CO2; PE02, end-tidal 02; PEXe', end-tidal stable xenon gas concentrations; WKS, Wernicke-Korsakoff syndrome; Xe, xenon. models, (Porjesz and Bergleiter, 1981; Walker et ai., 1981) show that brain stem, diencephalon and limbic systems are affected earlier than cerebral cortex. Chronic ethanol administration disorders conformations of membrane-bound lipids and proteins, altering Na + -K + adenosine triphosphatase (ATPase) activity of neuronal membranes (Lyon et ai., 1981), so that some investigators postulate that fluxes of calcium ions across neuronal membranes account for many of the neurological signs seen in chronic alcoholism (Durand and Carlen, 1984). It is generally agreed that chronic alcohol ingestion deranges the synthesis, release, uptake, and functioning of cerebral neurotransmitters and their receptors including acetylcholine, dopamine, norepinephrine, gamma-amino-butyric acid, and serotonin (Littleton, 1983; Martin et ai., 1984). For 22 years, cerebral blood flow (CBF) measurements have been used for functional assess- 35

2 36 T. HATA ET AL. ment in chronic ethanolism. Cerebral blood flow, and less frequently cerebral metabolic rate for oxygen (CMR02), values reported have been consistently reduced (Hedlund et ai., 1964; Simojyo et ai., 1967; Berglund and Ingvar, 1976; Heiss et ai., 1976; Kruger and Hoyer, 1979; Berglund et ai., 1980; Berglund, 1981; J6hannesson et ai., 1982; Meyer et ai., 1985; Ishikawa et ai., 1986) and reductions correlate directly with estimates of neurological and cognitive impairments as well as estimates of brain atrophy (Meyer et ai., 1985; Ishikawa et ai., 1986). No information is available among patients with chronic ethanolism concerning local cerebral blood flow (LCBF) measured in the deep cerebral structures, which are probably most vulnerable to the toxic effects of ethanol, as judged by neuropathological studies and experiments in animal models (Berglund, 1981; Walker et ai., 1981). The present study reports three-dimensional measurements of CBF among patients with chronic ethanolism with and without Wernicke-Korsakoff syndrome (WKS) obtained by the use of stable xenon inhalation as a contrast medium for computed tomography (CT CBF). These were undertaken to determine whether there are LCBF differences between patients with neurotoxic effects of chronic ethanolism alone and those combined with the clinical signs of WKS. In previous communications, we reported two-dimensional measurements of CBF utilizing the xenon- 133 method in patients with ethanolic encephalopathy with and without Wernicke-Korsakoff syndrome (Meyer et ai., 1985; Ishikawa et ai., 1986). Three-dimensional CBF measurements now reported were successfully achieved in many of these patients. MATERIALS AND METHODS Tables la and b display relevant demography among 17 patients with longstanding ethanol dependency satisfying the diagnostic criteria established by the National Council on Alcoholism (1972). They were referred from the alcohol detoxification and rehabilitation ward by the psychiatric service of the Veterans Administration Medical Center, Houston, Texas. After treatment, they were followed by this laboratory as outpatients. The duration of excessive ethanol consumption ranged from 5 to 45 years (mean ± SD, 23.7 ± 10.8 years). The daily consumption of ethanol exceeded 80 g and ranged from 80 to 500 g/day (mean ± SD, 250 ± 140 g/day). Seven patients (Cases 1-7) had signs and symptoms fulfilling the diagnostic criteria for WKS established by Victor et al. (1971). The other patients (Cases 8-17) were admitted with symptoms and signs of neurotoxicity, including withdrawal symptoms but without fixed neurological signs, except for mild distal sensory neuropathy. The 17 patients listed in Tables la and b were part of a larger series in which measurements were attempted but were not always successful-because of problems with head movement. Among Cases 1-4 and 8-14, it was possible to measure CT-CBF values before and after treatment, which resulted in good recovery. Measurements were repeated 2-28 weeks after completion of treatment in patients with WKS, and 2-6 weeks after treatment in patients with signs of neurotoxicity but without WKS. Patients were excluded if there was any history of severe head injury, abuse of psychotropic drugs, the use of TABLE la. Demography of patients with ethanolic encephalopathy with or without Wernicke-Korsakoff syndrome Abnormal neurological findings Peripheral Eye signs Ataxia neuropathy CCSE scores Treatment Case no. Age Gender compliance Before After Before After Before After Before After 1 65 M E + IMP + + IMP M P + IMP + IMP M E + IMP + + IMP M P M E + IMP + IMP M E + IMP + IMP + IMP M P Mean ± SO 52.7 ± ± ± M E M E M E M E M E M E M E M E M ONR NE NE NE 29 NE 59 M ONR NE NE NE 29 NE Mean ± SO 52.7 ± ± ± 1.7 E, excellent; P, poor; ONR, did not return; IMP, improved; NE, not examined; CCSE, Cognitive Capacity Screening Examination. J Cereb Blood Flow Metab, Vol. 7, No.1, 1987

3 XE CT-CBF IN ALCOHOLIC ENCEPHALOPATHY 37 anticonvulsants, a history of chronic psychosis, and age exceeding 70 years. Seventeen age-matched normal volunteers underwent similar CT-CBF measurements and provided normative data that was pooled for purposes of comparison. The ages of normal volunteers ranged from 33 to 72 years (mean ± SD, 52.4 ± 11.5 years). They had normal neurological and cognitive examinations and were free from risk factors for stroke, consumed zero or less than 10 g of ethanol daily, and had normal EEGs and EKGs. Tables la and b summarize their age, gender, degrees of compliance with treatment, presence or absence of extraoccular movement disorder, nystagmus, presence or absence of ataxic gait, presence or absence of peripheral neuropathy, test scores, results of Cognitive Capacity Screening Examinations (CCSE) (Jacobs et ai., 1977), median daily intake of alcohol, duration of alcohol abuse, CBF values measured by the two-dimensional xenon-133 inhalation method, time intervals between CT-CBF measurements, and test results of performance before and after treatment. All patients underwent physical, neurological, and cognitive examinations at the time of CT CBF measurements before and after treatment. Complete blood counts, blood chemistries, urinalysis, and liver function tests were evaluated in all patients and cases were excluded if there were severe metabolic or hepatic dysfunctions. Therapy included detoxification by withdrawal of alcohol under medical and psychiatric supervision for 2-8 weeks, psychotherapy, counseling, and provision of a nutritious diet. Patients with WKS (Cases 1-7) were also administered oral thiamine supplementation in doses of 100 mg 3 times daily. Referral to the Cerebral Blood Flow Laboratory for neurological and CBF evaluations was delayed for 6-10 days until there was recovery from withdrawal symptoms. This was to exclude any acute effects of alcohol withdrawal and/or administration of tranquilizing drugs on CBF measurements and test performances. All sedative medications were discontinued for 48 h prior to referral to the CBF laboratory. Delirium tremens, seizures, and hallucinations were not present at the time of the CBF measurements. Local CBF and LA values were measured by the CT CBF method (Meyer et ai., 1980, 1981; Amano et ai., 1982). Normative values and standard deviations for LCBF and LA values are given in these and other publications (Meyer et ai., 1984; Tachibana et ai., 1984). The method was modified for computer analysis so that LCBF and LA values were provided as color-coded brain maps. Patients underwent neurological and cognitive testing 4-6 hours prior to CT -CBF measurements carried out with an EMI 1010 scanner. To reduce anxiety and potential hyperventilation, patients received a trial inhalation by wearing a face mask 4-6 h prior to CT-CBF measurements (Obrist et ai., 1985). Body nitrogen was displaced by inhalation of 100% oxygen for min prior to xenon inhalation. Inhalation mixtures of % xenon gas in oxygen were gradually incremented in the alveolar air over 7-9 min. It has been shown previously that % mixtures of xenon gas in oxygen cause minimal or no subanesthetic side-effects and that CBF values are not altered beyond the ± 15% error of the method (Meyer et ai., 1986). Furthermore, in the present study, xenon-l33 inhalation CBF measurements made on the same day in the same patients were in good agreement with Xe CT-CBF results (Meyer et ai., 1985; Ishikawa et ai., 1986). Four control scans were performed during the interval of denitrogenation (100% oxygen inhalation) followed by 3 or 4 serial scans during inhalation of TABLE lb. Demography of patients with ethanolic encephalopathy with or without Wernicke-Korsakoff syndrome Daily ethanol Duration of consumption drinking Case no. (g/day) (yrs) Before Fg CBF values by 133Xe inhalation method After Before Fw After Time interval between CT-CBF measurements (wks) NE 10.5 NE NE NE Mean ± SD 240 ± ± ± ± ± NE 19.4 NE ± NE NE 16.8 ± Mean ± SD 263 ± ± ± ± ± ± ± Xe, xenon-133; CT-CBF, computed tomography-cerebral blood flow; NE, not examined. J Cereb Blood Flow Metab, Vol. 7, No.1, 1987

4 38 T. HATA ET AL % stable xenon gas. A semiclosed partial rebreathing system was utilized to administer the gas mixtures so that a gradual rise time of xenon in alveolar air was achieved. End-tidal stable 38 xenon gas concentrations (PEXeS) were recorded throughout each inhalation by means of a Gow-Mac thermoconductivity gas analyzer. End-tidal xenon gas concentrations, which are known to be in equilibrium with arterial blood, were quantitated by means of a proportionality constant determined empirically. By these means, changes for concentrations of xenon gas in arterial blood were calculated in Hounsfie1d units and were utilized for correction of recirculation. Blood pressure was measured after CT -CBF measurements and end-tidal CO2 (PEcoz), end-tidal Oz (PEoz), EKG and EEG were recorded by means of a polygraph. Two back-to-back CT scans were serially examined before and during xenon in oxygen inhalation under standard conditions, utilizing 8 mm collimation, settings at 32 rna, and utilizing the rapid 120 kvp 60 s scanning mode. The total irradiation exposure to the center of the brain was 7-8 rads and the cornea of the eye was avoided. Computed tomographic image data were transferred from magnetic tapes to floppy diskettes and reconstructed by utilizing a microcomputer system (160 x 160 matrix). Data for each of the images, two before and during xenon enhancement were treated by unweighted 3 x 3 smoothing (presmoothing) without data compression before calculating LCBF and LA values. Effective cell areas covered were 3 x 3 of the original pixels, each corresponding to 20 mm of the brain sections and each voxe1 used for the calculations corresponded to 160 mm3 of brain tissue since each of the two slices were 8 mm thick. Thus, using this computer program for Xe CT-CBF measurements, the resolution is 160 mm3 The Xe CT CBF method has been reported previously to be capable of discriminating differences in flow between adjacent volumes as small as 80 mm3 (Meyer et ai., 1984). Data from these smoothed images (160 x 160 matrix) were used for LCBF and LA calculations. Four precontrast control scans were averaged and reconstructed as the average base line scan, and data for each of the enhanced scans were subtracted from it. Changes in Hounsfield units for each voxel were expressed as functions of time. On the second post-treatment visit, the patient's head was placed for the same two levels of the CT scanner using spot-lights attached to the scanner to locate the orbitomeatal line and Scout films were taken until images of both slices were superimposable on the pretreatment slices. The plane setting was never altered. Arterial input function was approximated as a first step exponential function, that is Ca(t) = Camax (1- e-mt), where Camax is the arterial xenon concentration at infinity and m is the rate constant for arterial xenon gas saturation over time (t). The values of Camax and m were estimated by using nonlinear least square fitting (Marquardt, 1963). Time dependent buildups for xenon concentrations in brain tissue were estimated by unweighted nonlinear least square fitting utilizing the damping Newton-Gauss algorithm or the Marquardt algorithm (1963). Analytical solution of Kety's formula (1951) was used as the model for fitting: Cj(n = AikJ Ca(t)e-k;(T-t)dt, Fj = Aiki, where Cj(n is the concentration of xenon in the specified region of interest at the time T and kj is the flow rate constant for that region of interest, Fj represents the regional cerebral blood flow to be derived and Aj is the partition coefficient for that region of interest. The double integration method of Amano et al. (1982), was omitted to simplify computer solutions. Scanning time was represented as the midscanning time for each 60 s scan. Results for LCBF and LA derived from this initial data processing (LCBF and LA) were reconstructed to the matrix of 160 x 160 voxels and a second unweighted 3 x 3 or 5 x 5 smoothing (postsmoothing) was used to decrease bias derived from instabilities of the fitting model. Smoothed LCBF and LA values (160 x 160 matrix) were now displayed on the CRT display by color-coding in 13 steps (LCBF values: mvloo g brain/min, LA values: 0-2.4). Local CBF and LA values could then be processed for any special region of interest by cursoring the precontrast plain CT images displayed next to the LCBF and LA maps. Region of interest values reported in this communication varied between 30 voxels (e.g., for head of caudate nucleus) to 300 voxels (e.g., for frontal cortex) as illustrated in Fig. 1. All data were calculated as the mean values ± standard deviations. Values for LCBF, LA, as well as neurological and cognitive test results were analyzed and compared between the two groups of chronic ethanolic patients with and without WKS, as well as between the group of age-matched normal volunteers utilizing the Mann-Whitney U test. Between group comparisons were also made before and after treatment utilizing the Wilcoxon signed rank test. Statistical significances were set at p < The consent forms and protocols for serial measurements of CBF by the CT -CBF method have been approved by the Institutional Review Boards of Veterans Administration Medical Center and Baylor College of Medicine, Houston, Texas. Informed consent was signed by all patients and volunteers prior to each CT-CBF measurement. RESULTS As previously reported (Meyer et ai., 1985), after treatment all patients in the WKS group showed improvements in tests of cognitive performance and their neurological deficits. The CCSE scores after treatment (26. 7 ± 4. 1) increased significantly compared with scores before treatment (22. 1 ± 3.8; p < 0.05). Cases 2, 4, and 7 occasionally indulged in some ethanol after discharge; nevertheless, they ate well and took thiamine supplements. Cases 1 and 3 fully complied with treatment and recovered without any residual symptoms, signs, or cognitive impairments. Chronic ethanolic patients without WKS on admission to the study exhibited neurotoxic effects of ethanol without fixed neurological signs as reported previously (Ishikawa et ai., 1986) including tremor, confusion, and/or hallucinations and mild sensory peripheral neuropathy, which recovered after treatment in Case 8. Cognitive functions scored by CCSE were mildly impaired before treatment and their CCSE scores (n = 8) significantly improved (p < 0.05) after abstinence from alcohol. Table 2 compares LCBF and LA values in pa- J Cereb Blood Flow Metab. Vol. 7. No.1, 1987

5 XE CT-CBF IN ALCOHOLIC ENCEPHALOPATHY 39 FIG. 1. Brain map showing computed tomographic (CT) image and local cerebral blood flow (LCBF) values obtained in a 53-year-old, right-handed man suffering from neurotoxic effects of ethanol without Wernicke-Korsakoff syndrome (Case 13). The LCBF and local partition coefficient (LA.) values were calculated by cursoring any predetermined region of interest, in this instance the thalamus is cursored in purple on the CT image. This ensures correspondence of LCBF and LA. values to anatomical regions of interest. The number of pixels counted and the computed LCBF values and LA. values were averaged and printed out by computer. FIG. 2. Local cerebral blood flow (LCBF) and local partition coefficient (LA.) maps made in a 65-year-old, right-handed man (Case 1). Diffuse hypoperfusion is measured typical of the acute and severe ethanolic Wernicke-Korsakoff syndrome. In this case, LCBF values determined in two slices 8 mm apart were reduced in temporal cortex, thalamus, hypothalamus, vicinity of nucleus basalis of Meynert, cingulate gyrus, and white matter bilaterally. The LA. values remain normal except for the subcortical white matter of both frontal lobes which were reduced. PEC02 = MABP = mean arterial blood pressure. end-tidal CO2, FIG. 3. Local cerebral blood flow (LCBF) and local partition coefficient (LA.) maps printed out by computer in a 35-year-old, right-handed chronic ethanolic man, without Wernicke-Korsakoff syndrome (Case 14). End-tidal CO2 (PEco2) was 27.6 mm Hg and mean arterial blood pressure (MABP) was 83 mm Hg. There are diffuse reductions of cortical and basal ganglia CBF values, however, perfusion of left thalamus is higher than right. The LA. values shown in the map to the right are entirely normal except for a single low LA. area in the right internal capsule. FIG. 4. a: Local cerebral blood flow (LCBF) maps measured in a 65-year-old male patient (Case 1) with acute Wernicke-Korsakoff syndrome (WKS) (left) and after complete recovery with treatment (right). In the acute phases of WKS, his LCBF values measured in two slices 8 mm apart were severely reduced in both gray and white matter, including both temporal lobes, thalamus, hypothalamus, vicinity of nucleus basalis of Meynert, and cingulate gyrus. After treatment, CBF values were restored to normal. b: The LCBF maps measured in a 63-year-old, right-handed man (Case 12) who had neurotoxic effects of ethanol without WKS before (left) and after (right) withdrawal from ethanol. Before treatment, LCBF values are diffusely reduced but less severely so than among patients with WKS. Hypoperfusion is most evident in frontal, temporooccipital and thalamic regions. The LCBF values in white matter are within normal limits. After abstinence, LCBF values improved, including the thalamus and temporal lobes bilaterally.

6 40 T. HATA ET AL. TABLE 2. Local cerebral blood flow and partition coefficient values compared among patients exhibiting alcoholic encephalopathy with and without Wernicke-Korsakoff syndrome Age-matched Chronic alcoholics normal controls without WKS WKS Regions (n = 17) (n = 10) (n = 7) Gray matter LCBF D. LCBF D. LCBF D. Frontal cortex a a 1.10 ± 7.7 ± 0.03 ± 8.5 ± 0.16 ± 12.1 ± 0.25 Temporal cortex a a 1.00 ± 6.2 ± ± 10.8 ± 0.16 ± 8.0 ± 0.21 Occipital cortex a a 1.02 ± 7.0 ± 0.05 ± 12.0 ± 0.22 ± 6.1 ± 0.23 Cingulate gyrus a a,b 1.08 ± 4.4 ± ± ± 0.25 ± 3.4 ± 0.27 Hippocampal gyrus , c ± 9.3 ± 0.06 ± 7,9 ± 0.47 ± 10.3 ± 0.27 (n = 2) (n = 2) Caudate nucleus a a 1.04 ± 6.8 ± ± ± 0.19 ± 13.6 ± 0.33 Putamen a a 1.12 ± 7.0 ± 0.08 ± 13.1 ± 0.30 ± 19.3 ± 0.33 Thalamus a d 1.12 ± 5.6 ± 0,04 ± ± 0,32 ± 19.1 ± 0.31 Hypothalamus and nucleus basalis , lc 1.24 of Meynert region ± 7.6 ± ± 13.4 ± 0.54 ± 12.8 ± 0.39 (n = 2) (n 2) = p < White matter Internal capsule ± 3.8 ± 0,09 ± 7. 1 ± 0.42 ± 6.4 ± 0.43 Frontal lobe a 23.5a,b 1.05a ± 3,7 ± ± 7,2 ± 0.43 ± 1.8 ± 0.28 Occipital lobe 28, I l.13d a ± 3,5 ± 0,08 ± 6,2 ± 0.44 ± 2,6 ± 0,32 Age in years ± ,7 ± 8, ± 9.9 MABP in mm Hg 95,9 ± ± 10, ± 11.2 PEC02 in mm Hg 36,1 ± ± ± 5.7 WKS, Wernicke-Korsakoff syndrome; LCBF, local cerebral blood flow; LA, local partition coefficients; MABP, mean arterial blood pressure; PEC02, end-tidal carbon dioxide. a p < 0.01; b p < 0.01; cp < 0,05; dp < 0,05 (a,d-compared between alcoholic encephalopathy and normal controls; h,c-compared between patients with WKS and patients without WKS). tients showing neurotoxic effects of chronic ethanolism with and without WKS. The LCBF values for cortical gray matter of WKS patients were diffusely decreased by about - 35% compared with age-matched normal values (p < 0.01). Subcortical gray matter likewise showed marked hypoperfusion, particularly in the hypothalamus and the vicinity of the substantia innominata, which includes the nucleus basalis of Meynert in which values were decreased by - 60% compared with normative values. The LA. values of gray matter were slightly but not significantly higher than normative values. Local CBF and LA. values for white matter in patients with WKS were reduced compared to agematched normal volunteers. Perfusion was particularly reduced in frontal white matter and LA. values were reduced in frontooccipital white matter (p < 0.05). Typical CT-CBF maps measured in a 65- year-old man with WKS (Case 1) are illustrated in Fig. 2. Reductions of LCBF values in patients with WKS were significantly greater than in patients showing neurotoxic effects of chronic ethanolism without WKS. In WKS, LCBF reductions were most striking in the cingulate and hippocampal gyri, the hypothalamus, including adjacent nucleus basalis of Mey'nert, and frontal white matter where CBF reductions were greater than among patients without WKS (p < 0.05). There were no significant differences for LA. values between the two groups. Local CBF and LA. values in patients without WKS are also summarized in Table 2. The LCBF 'values of cortical gray matter were diffusely decreased compared with age-matched normal volunteers, but LA. values remained within normal limits. Local CBF values in subcortical gray matter were decreased diffusely, particularly in the hypothalamus and the vicinity of the nucleus basalis of J Cereb Blood Flow Metab, Vol. 7, No.1, 1987

7 XE CT-CBF IN ALCOHOLIC ENCEPHALOPATHY 41 Meynert where they were decreased by about - 50% compared with normative values. The L values in subcortical gray matter were slightly higher than the normative values, but these differences were not statistically significant. Local CBF values for white matter were normal but L values for frontal white matter, including adjacent parts of centrum semiovale and for occipital white matter, including the optic radiations, were reduced. Typical LCBF and L maps obtained from a 35-year-old man (Case 14) with neurotoxic effects of chronic ethanolism without WKS are illustrated in Fig. 3. All patients were right-handed, but there were no significant differences between dominant and nondominant hemispheres. Mean arterial blood pressures (MABP) and partial pressures for end-tidal carbon dioxide (PEco2), compared between groups of ethanolic patients with and without WKS and between normal volunteers, did not differ (Table 2). All 17 patients reported subjective experience of paresthesia during stable xenon inhalation and all patients developed respiratory irregularities, especially respiratory slowing after 5 min of inhalation (Obrist et ai., 1985). Heart rate of all patients compared before and during CT-CBF measurements, but there is no significant change of heart rate as per our previous report (Meyer et ai., 1981). Table 3 shows effects of treatment on cerebral perfusion among both groups of patients with chronic ethanolism. In those without WKS, LCBF values increased diffusely throughout the brain after abstinence from ethanol. In patients with WKS, LCBF values increased more prominently than in patients without WKS after abstinence and thiamine supplementation. Improvements of cerebral perfusion were most marked in the hypothalamus plus the vicinity of nucleus basalis of Meynert, cingulate gyrus, hippocampal gyrus, and basal ganglia, all of which exceeded + 40%. The hypothalamus and nucleus basalis of Meynert were increased by + 64%. Local CBF values in white matter also increased diffusely throughout the brain after treatment. After treatment, pooled values for both types of ethanolic encephalopathy showed significant increases for LCBF in the regions including the hippocampal gyrus, thalamus, hypothalamus and adjacent nucleus basalis of Meynert, and the white matter of occipital lobes increased about +20%. Diffuse increases of CBF correlated with improvements of cognitive performance for both groups. Significant relationships were not found between residual cognitive impairments that persisted in one case after treatment of WKS (Case 2). Increases of LCBF values after treatment for any particular region did not appear to correlate any better with cognitive improvements than the diffuse increases measured in diencephalon, nucleus basalis of Meynert, temporal cortex, and limbic systems. All patients with WKS showed marked improvements of brain perfusion as did all but two patients with neurotoxic effects of ethanol (Figs. 4a, b, 5). DISCUSSION In the present study, the xenon contrast CT-CBF method has been utilized for measurements of local TABLE 3. Effects of treatment (abstinence, thiamine) on regional cerebral perfusion Chronic alcoholics without WKS (n = 7) WKS (n = 4) Both groups pooled (n = II) Regions Before After Before After Before After Mean CBF of slices Frontal cortex Temporal cortex Occipital cortex Cingulate gyrus Hippocampal gyrus Caudate nucleus Putamen Thalamus Hypothalamus and nucleus basalis of Meynert region Internal capsule Frontal lobe Occipital lobe 51.5 ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± 9. 4a 51.7 ± ± ± ± ± ± ± ± ± ± 6.1a 49.5 ± ± ± ± ± ± 14.4a 49.0 ± ± 17.5a 29.7 ± ± ± ± ± ± 7.0a WKS, Wernicke-Korsakoff syndrome. a p < J Cereb Blood Flow Metab, Vol. 7, No.1, 1987

8 42 T. HATA ET AL. Mean CBF Cortical Gray Matter Subcortical Gray Matter White Matter 90 '" ".. > U::]. 60 "'8.:: o iii.c 50 ca g 0.c f::;::. a E 40.. g..j i+p< i+p< i+p<o.ol-1 I- N.S.--I I I I I I I I I Before After Before After Before After Before After I Mean ± S.D. FIG. 5. Graph to show improvement of local cerebral blood flow values before and after treatment in the two categories of chronic ethanolic encephalopathy. Pooled gray matter values for cortex include frontal, temporal, and occipital cortex plus cingulate gyrus, and hippocampus. Pooled subcortical gray matter values include caudate, putamen, thalamus, hypothalamus, and vicinity of nucleus basalis of Meynert. Before treatment, cases with Wernicke-Korsakoff syndrome (WKS) indicated by closed circles, were more severely reduced than cases without WKS (open circles). Abstinence Abstinence Abstinence Abstinence cerebral blood flow and local partition coefficients. This method has certain advantages for investigating the pathophysiology of alcoholic encephalopathy. It makes possible measurements of local CBF of the deep brain structures such as the hypothalamus, substantia innominata, and adjacent regions in which the basal nuclei of the forebrain are located, as well as thalamus and limbic systems, which judging from studies in animal models, should be primarily affected by ethanol (Walker et ai., 1981; Lishman, 1986). It is also possible to detect changes in lipid composition of cerebral tissues by measuring alterations of local partition coefficients (Radue and Kendall, 1978). Changes of the lipid composition of the brain have been reported at autopsy among patients dying with chronic alcoholism (Lesch et ai., 1972). The greatest disadvantage of utilizing the method among chronic ethanolic patients is head movement probably associated with mild confusion and/or agitation. As discussed by several investigators, the CT -CBF method has some theoretical limitations (Gur et ai., 1982). However, the computer program described here for calculating and mapping LCBF and L.\ allows optimal correlations of disordered cognitive function with measurements throughout different systems of the brain (by cursoring regions of interest on the CT image) and the use of single compartmental analysis permits studies of small volumes of brain, despite problems of time dependent noise when relatively slow scanners are used (Ip et ai., 1983). Present results indicate diffuse and significant reductions of gray matter LCBF values throughout the entire cerebral cortex and deeper brain struc- tures among chronic ethanolic patients suffering from neurotoxic effects without WKS. Several investigators have described acute toxic effects of administration of ethanol on CBF and metabolism (Battey et ai., 1953; Fazekas et ai., 1955), but there are relatively few reports of CBF measurements among chronic alcoholic patients without WKS (Berglund and Ingvar, 1976; Heiss et ai., 1976; Kruger and Hoyer, 1979; Berglund et ai., 1980; J6- hannesson et ai., 1982; Ishikawa et ai., 1986). In these reports, two-dimensional methods were used. These did not permit analysis of any possible changes in perfusion of the hypothalamus and adjacent regions of basal forebrain nuclei or limbic systems and thalamus. The CT-CBF measurements make possible correlation of LCBF changes in these structures with neurocognitive status. In the present study, patients with WKS showed more severely reduced LCBF values than in chronic ethanolics without WKS. This is to be expected since thiamine deficiency also reduces neuronal activity and disturbs neurotransmitter function (McEntee and Mair, 1978; Martin et ai., 1984). Local CBF reductions in white matter appear to be characteristic of WKS and were not observed in chronic ethanolism without WKS. Possibly LCBF reductions reflect effects of thiamine deficiency by reducing transketolase activity of the oligodendrocytes, an important enzyme for lipid and protein synthesis (Dreyfus, 1965; Noble and Tewari, 1973; Tewari et ai., 1978; Sharp et ai., 1982). Recently, Lishman has discussed different types of cognitive impairments in chronic alcoholics and difficulties in separating some from Alzheimer's disease. Impaired recent memory is a feature of J Cereb Blood Flow Metab, Vol. 7, No. 1, 1987

9 XE CT-CBF IN ALCOHOLIC ENCEPHALOPATHY 43 both types of dementia and was evident in the present series of WKS patients. Lishman (1986) offers a unifying hypothesis to account for the pathogenesis of both Alzheimer's disease and WKS, postulating that alcohol exerts toxic effects on the basal forebrain nuclei, causing diffuse cortical cholinergic deficiencies, similar to those known to Alzheimer's disease. This would then account for the loss of recent memory in alcoholic dementias. Neuropathological studies support this hypothesis (Arendt et ai., 1983). Present LCBF measurements also support the Lishman hypothesis. Diffuse cortical CBF reductions were accompanied by more severe hypoperfusion in hypothalamus and adjacent regions of the substantia innominata which has been reported to harbor the cells of nucleus basalis of Meynert (Saper and Chelim sky, 1984). Damage to these basal forebrain nuclei would impair their cholinergic projections resulting in diffuse reductions in cortical and subcortical blood flow similar to CBF changes in Alzheimer's disease reported from this laboratory (Amano et ai., 1982; Tachibana et ai., 1984). Assuming that chronic consumption of ethanol, with or without WKS, exerts neurotoxic effects on the nucleus basalis of Meynert and adjacent systems, diffuse cortical reductions of CBF would be expected to result with maximal hypoperfusion in the hypothalamus and substantia innominata harboring the basal nuclei of the forebrain. Furthermore, if this assumption is correct, the CBF reductions should be rapidly reversible after abstinence from ethanol. In fact, this is what was observed in both groups of chronic ethanolic patients with and without WKS. Acknowledgment: This work was supported by the Veterans Administration, Washington, DC and by grants from Mr. and Mrs. Harry K. Smith, Mr. Albert K. Smith, Tenneco, Inc., Entex, Inc., and J. S. Abercrombie Foundation, Houston, Texas. Mrs. Barbara Williams Clark processed the manuscript for publication. REFERENCES Amano T, Meyer JS, Okabe T, Shaw T, Mortel KF (1982) Stable xenon CT cerebral blood flow measurements computed by a single compartment-double integration model in normal aging and dementia. J Comput Assist Tomogr 6: Arendt J, Bigl V, Arendt A, Tennstedt A (1983) Loss of neurons in the nucleus basalis of Meynert in Alzheimer's disease, paralysis agitans and Korsakoff's disease. Acta Neuropathol (Ber!) 61: Battey LL, Heyman A, Patterson JL, Jr (1953) Effects of ethyl alcohol on cerebral blood flow and metabolism. JAMA 152:6-10 Berglund M (1981) Cerebral blood flow in chronic alcoholics. Alcoholism (NY) 5: Berglund M, Ingvar DH (1976) Cerebral blood flow and its regional distribution in alcoholism and in Korsakoff's psychosis. J Stud Alcohol 37: Berglund M, Bliding G, Bliding A, Risberg J (1980) Reversibility of cerebral dysfunction in alcoholism during the first seven weeks of abstinence-a regional cerebral blood flow study. Acta Psychiatr Scand 62(suppl 286): Dreyfus PM (1965) The regional distribution of transketolase in the normal and the thiamine deficient nervous system. J Neuropathol Exp NeuroI24: Durand D, Carlen PL (1984) Decreased neuronal inhibition in vitro after long-term administration of ethanol. Science 224: Fazekas JF, Albert SN, Alman RW (1955) Influence of chlorpromazine and alcohol on cerebral hemodynamics and metabolism. Am J Med Sci 230: Gur D, Wolfson SK, Jr, Yon as H, Good WF, Shabason L, Latchaw RE, Miller DM, Cook EE (1982) Progress in cerebrovascular disease: local cerebral blood flow by xenon enhanced CT. Stroke 13: Hedlund S, Kohler V, Nylin G, Olsson R, Regnstrom 0, Rothstrom E, Astrom KE (1964) Cerebral blood circulation in dementia. Acta Psychiatr Scand 40: Heiss WD, Kiifferle B, Demel I, Reisner T, Roszuczky A (1976) Cerebral blood flow and severity of mental dysfunction in chronic alcoholism. In: Cerebral Vascular Disease (Seventh International Salzburg Conference, 1974) (Meyer JS, Lechner H, Reivich M, eds), Stuttgart, Georg Thieme, pp Ip WR, Holden JE, Winkler SS (1983) A study of the image discrepancies due to object time-dependence in transmission and emission tomography. Phys Med Bioi 28: Ishikawa Y, Meyer JS, Tanahashi N, Hata T, Velez M, Fann WE, Kandula P, Mortel KF, Rogers RL (1986) Abstinence improves cerebral perfusion and brain volume in alcoholic neurotoxicity without Wernicke-Korsakoff syndrome. J Cereb Blood Flow Metab 6:86-94 Jacobs JW, Bernhard MR, Delgado A, Strain JJ (1977) Screening for organic mental syndromes in the medically ill. Ann Intern Med 86:40-46 J6hannesson G, Berglund M, Ingvar DH (1982) Reduction of blood flow in cerebral white matter in alcoholics related to hepatic function: a CBF and EEG study. Acta Neural Scand 65: Kety SS (1951) The theory and applications of the exchange of inert gas at the lungs and tissues. Pharmacol Rev 3:1-41 Kriiger G, Hoyer S (1979) Brain blood flow and metabolism related to psychiatric syndromes in alcoholism. Acta Neurol Scand 72(suppl 60): Lesch P, Schmidt E, Schmidt FW (1972) Effects of chronic alcohol abuse on the structural lipids in the human brain: hepatocerebral degeneration, 1. Z Klin Chem Klin Biochem 10: Lishman WA (1986) Alcoholic dementia: a hypothesis. Lancet 1: Littleton JM (1983) Tolerance and physical dependence on alcohol at the level of synaptic membranes: a review. J R Soc Med 76: Lyon RC, McComb JA, Schreurs J, Goldstein DB (1981) A relationship between alcohol intoxication and the disordering of brain membranes by a series of short-chain alcohols. J Pharmacol Exp Ther 218: Martin PR, Weingartner H, Gordon EK, Burns RS, Linnoila M, Kopin IJ, Ebert MH (1984) Central nervous system catacholamine metabolism in Korsakoff's psychosis. Ann NeuroI15: Marquardt DW (1963) An algorithm for least-squares estimation of nonlinear parameters. J Soc Indust Appl Math 11: McEntee WJ, Mair RG (1978) Memory impairment in Korsakoff's psychosis: a correlation with brain noradrenergic activity. Science 202: Meyer JS, Hayman LA, Yamamoto M, Sakai F, Nakajima S J Cereb Blood Flow Metab, Vol. 7, No. 1, 1987

10 44 T. HATA ET AL. (1980) Local cerebral blood flow measured by CT after stable xenon inhalation. AJNR 1 : Meyer JS, Hayman LA, Amano T, Nakajima S, Shaw T, Lauzon P, Derman S, Karacan I, Harati Y (1981) Mapping local blood flow of human brain by CT scanning during stable xenon inhalation. Stroke 12: Meyer JS, Okayasu H, Tachibana H, Okabe T (1984) Stable xenon CT-CBF measurements in prevalent cerebrovascular disorders (stroke). Stroke 15:80-90 Meyer JS, Tanahashi N, Ishikawa Y, Hata T, Velez M, Fann WE, Kandula P, Mortel KF, Rogers RL (1985) Cerebral atrophy and hypoperfusion improve during treatment of Wernicke-Korsakoff syndrome. J Cereb Blood Flow Metab 5: Meyer JS, Hata T, Imai A, Sakai F (1986) Xenon CT helps reveal blood flow disorders. Diagnostic Imaging 8:92-96 National Council on Alcoholism, The Criteria Committee (1972) Criteria for the diagnosis of alcoholism. Am J Psychiatry 129: Noble EP, Tewari S (1973) Protein and ribonucleic acid metabolism in brains of mice following chronic alcohol consumption. Ann NY Acad Sci 215: Obrist WD, Jaggi JL, Harel D, Smith DS (1985) Effect of stable xenon inhalation on human CBF. J Cereb Blood Flow Metab 5(suppl 1): Porjesz B, Begleiter H (1981) Human evoked brain potentials and alcohol. Alcoholism (NY) 5: Radue EW, Kendall BE (1978) Iodine and xenon enhancement of computed tomography (CT) in multiple sclerosis (MS). Neuroradiology 15: Saper CB, Chelimsky TC (1984) A cytoarchitectonic and histochemical study of nucleus basalis and associated cell groups in the normal human brain. Neuroscience 13: Sharp FR, Bolger E, Evans K (1982) Thiamine deficiency limits glucose utilization and glial proliferation in brain lesions of symptomatic rats. J Cereb Blood Flow Metab 2: Simojyo S, Scheinberg P, Reinmuth 0 (1967) Cerebral blood flow and metabolism in Wernicke-Korsakoff syndrome. J Clin Invest 46: Tachibana H, Meyer JS, Okayasu H, Shaw TO, Kandula P, Rogers RL (1984) Xenon contrast CT-CBF scanning of the brain differentiates normal age-related changes from multiinfarct dementia and senile dementia of Alzheimer type. J GerontoI39: Tewari S, Murray S, Noble EP (1978) Studies on the effects of chronic ethanol ingestion on the properties of rat brain ribosomes. J Neurosci Res 3: Victor M, Adams RD, Collins OH (1971) The clinical findings. In: The Wernicke-Korsakoff Syndrome: A Clinical and Pathological Study of 245 Patients, 82 With Post-mortem Examinations. Philadelphia, FA Davis, pp Walker DW, Hunter BE, Abraham WC (1981) Neuroanatomical and functional deficits subsequent to chronic ethanol administration in animals. Alcoholism (NY) 5: CerebBloodFlow Metab, Vol. 7, No. 1, 1987

Martin Jackson. August 2011

Martin Jackson. August 2011 Martin Jackson August 2011 Substance Related Brain Injury: Basic Research Findings All neurotoxic substances have an acute intoxicating effect (and withdrawal effect) that produces changes in cognition,

More information

Alcohol and Brain Damage

Alcohol and Brain Damage Alcohol and Brain Damage By: James L. Holly, MD O God, that men should put an enemy in their mouths to steal away their brains! That we should, with joy, pleasance, revel, and applause, transform ourselves

More information

Alcohol Withdrawal. Introduction. Blood Alcohol Concentration. DSM-IV Criteria/Alcohol Abuse. Pharmacologic Effects of Alcohol

Alcohol Withdrawal. Introduction. Blood Alcohol Concentration. DSM-IV Criteria/Alcohol Abuse. Pharmacologic Effects of Alcohol Pharmacologic Effects of Alcohol Alcohol Withdrawal Kristi Theobald, Pharm.D., BCPS Therapeutics III Fall 2003 Inhibits glutamate receptor function (NMDA receptor) Inhibits excitatory neurotransmission

More information

Effects of hypoglycemia on brain. Ji Hyun Kim Department of Neurology Korea University College of Medicine

Effects of hypoglycemia on brain. Ji Hyun Kim Department of Neurology Korea University College of Medicine Effects of hypoglycemia on brain Ji Hyun Kim Department of Neurology Korea University College of Medicine Glucose and brain The brain is dependent on glucose as its principal fuel Interruption of glucose

More information

Cholinesterase inhibitors and memantine use for Alzheimer s disease TOPIC REVIEW

Cholinesterase inhibitors and memantine use for Alzheimer s disease TOPIC REVIEW Cholinesterase inhibitors and memantine use for Alzheimer s disease TOPIC REVIEW Diagnosis of Dementia : DSM-IV criteria Loss of memory and one or more other cognitive abilities Aphasia Apraxia Agnosia

More information

Alcohol Withdrawal Syndrome & CIWA Assessment

Alcohol Withdrawal Syndrome & CIWA Assessment Alcohol Withdrawal Syndrome & CIWA Assessment Alcohol Withdrawal Syndrome is a set of symptoms that can occur when an individual reduces or stops alcoholic consumption after long periods of use. Prolonged

More information

Steps to getting a diagnosis: Finding out if it s Alzheimer s Disease.

Steps to getting a diagnosis: Finding out if it s Alzheimer s Disease. Steps to getting a diagnosis: Finding out if it s Alzheimer s Disease. Memory loss and changes in mood and behavior are some signs that you or a family member may have Alzheimer s disease. If you have

More information

SUBSTANCE USE DISORDER SOCIAL DETOXIFICATION SERVICES [ASAM LEVEL III.2-D]

SUBSTANCE USE DISORDER SOCIAL DETOXIFICATION SERVICES [ASAM LEVEL III.2-D] SUBSTANCE USE DISORDER SOCIAL DETOXIFICATION SERVICES [ASAM LEVEL III.2-D] I. Definitions: Detoxification is the process of interrupting the momentum of compulsive drug and/or alcohol use in an individual

More information

Management in the pre-hospital setting

Management in the pre-hospital setting Management in the pre-hospital setting Inflammation of the joints Two main types: Osteoarthritis - cartilage loss from wear and tear Rheumatoid arthritis - autoimmune disorder Affects all age groups,

More information

Multifamily Groups in the Treatment of Severe Psychiatric Disorders

Multifamily Groups in the Treatment of Severe Psychiatric Disorders Text from pages 7-12 of Multifamily Groups in the Treatment of Severe Psychiatric Disorders By William R. McFarlane (2002) ISBN 1-57230-743-9. Published by The guilford Press, 72 Spring Street, New York,

More information

Neurobiology of Depression in Relation to ECT. PJ Cowen Department of Psychiatry, University of Oxford

Neurobiology of Depression in Relation to ECT. PJ Cowen Department of Psychiatry, University of Oxford Neurobiology of Depression in Relation to ECT PJ Cowen Department of Psychiatry, University of Oxford Causes of Depression Genetic Childhood experience Life Events (particularly losses) Life Difficulties

More information

75-09.1-08-02. Program criteria. A social detoxi cation program must provide:

75-09.1-08-02. Program criteria. A social detoxi cation program must provide: CHAPTER 75-09.1-08 SOCIAL DETOXIFICATION ASAM LEVEL III.2-D Section 75-09.1-08-01 De nitions 75-09.1-08-02 Program Criteria 75-09.1-08-03 Provider Criteria 75-09.1-08-04 Admission and Continued Stay Criteria

More information

Rarer causes of dementia

Rarer causes of dementia PBO 930022142 NPO 049-191 Rarer causes of dementia Alzheimer s disease is the most common cause of dementia, but there are many rarer diseases and syndromes that can lead to dementia. This information

More information

GUIDELINES FOR COMMUNITY ALCOHOL DETOXIFICATION IN SHARED CARE

GUIDELINES FOR COMMUNITY ALCOHOL DETOXIFICATION IN SHARED CARE GUIDELINES FOR COMMUNITY ALCOHOL DETOXIFICATION IN SHARED CARE Dr Millicent Chikoore MBBS MRCPsych Dr O Lagundoye MBBS MRCPsych Community based alcohol detoxification is a safe and effective option for

More information

Supported Alcohol Withdrawal Treatment Information

Supported Alcohol Withdrawal Treatment Information Supported Alcohol Withdrawal Treatment Information Alcohol Liaison Service What is Alcohol Withdrawal Syndrome? If you are dependent on alcohol and suddenly stop drinking or you are admitted to hospital

More information

Attention, memory and learning and acquired brain injury. Vicki Anderson. Jamie M. Attention & learning: an information processing model

Attention, memory and learning and acquired brain injury. Vicki Anderson. Jamie M. Attention & learning: an information processing model Attention, memory and learning and acquired brain injury Vicki Anderson Jamie M. Childhood acquired amnesia Attention & learning: an information processing model MANAGEMENT Organising, problem solving

More information

Source: National Institute on Alcohol Abuse and Alcoholism. Bethesda, Md: NIAAA; 2004. NIH Publication No. 04-3769.

Source: National Institute on Alcohol Abuse and Alcoholism. Bethesda, Md: NIAAA; 2004. NIH Publication No. 04-3769. Diagnosis and Treatment of Alcohol Dependence Lon R. Hays, MD, MBA Professor and Chairman an Department of Psychiatry University of Kentucky Medical Center Defining the Standard Drink A standard drink

More information

Alcohol Liaison Service. Alcohol Withdrawal. Information

Alcohol Liaison Service. Alcohol Withdrawal. Information Alcohol Liaison Service Alcohol Withdrawal Information Alcohol withdrawal If you are dependent on alcohol and suddenly stop drinking, there are a series of symptoms that you may experience. These include:

More information

placebo-controlledcontrolled double-blind, blind,

placebo-controlledcontrolled double-blind, blind, Clinical Potential of Minocycline for Depression with Psychotic Features Tsuyoshi Miyaoka Department of Psychiatry Shimane University School of Medicine Minocycline 1. Second-generation tetracycline which

More information

Source: National Institute on Alcohol Abuse and Alcoholism. Bethesda, Md: NIAAA; 2004. NIH Publication No. 04-3769.

Source: National Institute on Alcohol Abuse and Alcoholism. Bethesda, Md: NIAAA; 2004. NIH Publication No. 04-3769. Diagnosis and Treatment of Alcohol Dependence Lon R. Hays, MD, MBA Professor and Chairman Department of Psychiatry University of Kentucky Medical Center Defining the Standard Drink A standard drink = 14

More information

Alcohol: The good, the bad and

Alcohol: The good, the bad and Alcohol: The good, the bad and the Clare Wilhelm, Ph.D. Portland VA Medical Center Oregon Health & Science University Supported by VA Career Development Grant (BX001294) Overview Alcohol statistics the

More information

1. According to recent US national estimates, which of the following substances is associated

1. According to recent US national estimates, which of the following substances is associated 1 Chapter 36. Substance-Related, Self-Assessment Questions 1. According to recent US national estimates, which of the following substances is associated with the highest incidence of new drug initiates

More information

Practice Guideline. Neuropsychological Evaluations

Practice Guideline. Neuropsychological Evaluations Practice Guideline Neuropsychological Evaluations Adapted from the practice guideline of the same name by the Arizona Department of Health Services Division of Behavioral Health Services Effective: 06/30/2006

More information

New York State Office of Alcoholism & Substance Abuse Services Addiction Services for Prevention, Treatment, Recovery

New York State Office of Alcoholism & Substance Abuse Services Addiction Services for Prevention, Treatment, Recovery New York State Office of Alcoholism & Substance Abuse Services Addiction Services for Prevention, Treatment, Recovery USING THE 48 HOUR OBSERVATION BED USING THE 48 HOUR OBSERVATION BED Detoxification

More information

Reversibility of Acute Demyelinating Lesions in relapsingremitting

Reversibility of Acute Demyelinating Lesions in relapsingremitting Reversibility of Acute Demyelinating Lesions in relapsingremitting Multiple Sclerosis Omar A. Khan ( Division of Neuroimmunology, Department of Neurology, Neurology and Research Services. Veterans Affairs

More information

Conjoint Professor Brian Draper

Conjoint Professor Brian Draper Chronic Serious Mental Illness and Dementia Optimising Quality Care Psychiatry Conjoint Professor Brian Draper Academic Dept. for Old Age Psychiatry, Prince of Wales Hospital, Randwick Cognitive Course

More information

Symptom-Triggered Alcohol Detoxification: A Guideline for use in the Clinical Decisions Unit of the Emergency Department.

Symptom-Triggered Alcohol Detoxification: A Guideline for use in the Clinical Decisions Unit of the Emergency Department. Symptom-Triggered Alcohol Detoxification: A Guideline for use in the Clinical Decisions Unit of the Emergency Department. Dr Eugene Cassidy, Liaison Psychiatry; Dr Io har O Sulliva, E erge cy Department,

More information

Slide 4: Forebrain Structures. Slide 5: 4 Lobes of the Cerebral Cortex. Slide 6: The Cerebral Hemispheres (L & R)

Slide 4: Forebrain Structures. Slide 5: 4 Lobes of the Cerebral Cortex. Slide 6: The Cerebral Hemispheres (L & R) Slide 1: [Film Clip: The Brain #2- Phineas Gage] Integrated Bodily Communications Within Brain (Hemispheres and structures) The remaining Nervous System Endocrine System (Hormonal communication) Our bodies-

More information

Motor dysfunction 2: Spinal cord injury and subcortical motor disorders ANATOMY REVIEW: Basal Ganglia

Motor dysfunction 2: Spinal cord injury and subcortical motor disorders ANATOMY REVIEW: Basal Ganglia Motor dysfunction 2: Spinal cord injury and subcortical motor disorders ANATOMY REVIEW: Basal Ganglia A group of subcortical nuclei caudate, putamen, globus pallidus Caudate & Putamen = Neostriatum caudate

More information

A developing service. Cheshire and Wirral Partnership NHS Foundation Trust Mersey Care NHS Trust University of Liverpool

A developing service. Cheshire and Wirral Partnership NHS Foundation Trust Mersey Care NHS Trust University of Liverpool A developing service Cheshire and Wirral Partnership NHS Foundation Trust Mersey Care NHS Trust University of Liverpool Vascular disease Trauma Subcortical frontal disorders ARD Brain injury KP Involuntary,

More information

GP Drug & Alcohol Supplement No.7 May 1997

GP Drug & Alcohol Supplement No.7 May 1997 GP Drug & Alcohol Supplement No.7 May 1997 This is the seventh of the monthly Drug and Alcohol Supplements prepared for Central Coast GPs. Detoxification from Alcohol Dr Tony Gill Introduction The management

More information

SUBSTANCE ABUSE SCREENING

SUBSTANCE ABUSE SCREENING OVERVIEW Substance abuse in the elderly is a common problem that is frequently under- diagnosed by primary care doctors and families. Alcohol abuse is present in 10% to 15% of elderly individuals who seek

More information

Treatments for Major Depression. Drug Treatments The two (2) classes of drugs that are typical antidepressants are:

Treatments for Major Depression. Drug Treatments The two (2) classes of drugs that are typical antidepressants are: Treatments for Major Depression Drug Treatments The two (2) classes of drugs that are typical antidepressants are: 1. 2. These 2 classes of drugs increase the amount of monoamine neurotransmitters through

More information

Alcohol and nicotine are widely abused substances and are often used together One study showed that 15% of patients visiting a primary care practice

Alcohol and nicotine are widely abused substances and are often used together One study showed that 15% of patients visiting a primary care practice Dr IM Joubert Alcohol and nicotine are widely abused substances and are often used together One study showed that 15% of patients visiting a primary care practice for any reason had either an at-risk pattern

More information

Unit 2 - Subcortical systems, neurochemistry and brain function

Unit 2 - Subcortical systems, neurochemistry and brain function Unit 2 - Subcortical systems, neurochemistry and brain function Subcortical anatomy: Most of the five major subdivisions of the brain are subcortical. I. Telencephalon (cortical - part of forebrain) -

More information

TCHP Behavioral Health Psychological/Neuropsychological Testing Child/Adolescent Guidelines

TCHP Behavioral Health Psychological/Neuropsychological Testing Child/Adolescent Guidelines TCHP Behavioral Health Psychological/Neuropsychological Testing Child/Adolescent Guidelines Psychological testing involves the culturally and linguistically competent administration and interpretation

More information

Behavioral Health Psychological/Neuropsychological Testing Guidelines

Behavioral Health Psychological/Neuropsychological Testing Guidelines Behavioral Health Psychological/Neuropsychological Testing Guidelines Psychological testing (procedural code 96101) and Neuropsychological Testing (procedural code 96118) involve the culturally and linguistically

More information

Version 2 This guideline describes how to manage patients who are showing signs and symptoms of alcohol withdrawal and Wernicke s Encephalopathy.

Version 2 This guideline describes how to manage patients who are showing signs and symptoms of alcohol withdrawal and Wernicke s Encephalopathy. Title of Guideline (must include the word Guideline (not protocol, policy, procedure etc) Contact Name and Job Title (author) Directorate & Speciality A Guideline for the Management of Acute Alcohol Withdrawal

More information

Alcohol Overuse and Abuse

Alcohol Overuse and Abuse Alcohol Overuse and Abuse ACLI Medical Section CME Meeting February 23, 2015 Daniel Z. Lieberman, MD Professor and Vice Chair Department of Psychiatry George Washington University Alcohol OVERVIEW Definitions

More information

Symptom Based Alcohol Withdrawal Treatment

Symptom Based Alcohol Withdrawal Treatment Symptom Based Alcohol Withdrawal Treatment -Small Rural Hospital- Presenter CDR Dwight Humpherys, DO dwight.humpherys@ihs.gov Idaho State University Baccalaureate Nursing Program Lake Erie College of Osteopathic

More information

Benzodiazepines: A Model for Central Nervous System (CNS) Depressants

Benzodiazepines: A Model for Central Nervous System (CNS) Depressants Benzodiazepines: A Model for Central Nervous System (CNS) Depressants Objectives Summarize the basic mechanism by which benzodiazepines work in the brain. Describe two strategies for reducing and/or eliminating

More information

CAMBRIDGE UNIVERSITY CENTRE FOR BRAIN REPAIR A layman's account of our scientific objectives What is Brain Damage? Many forms of trauma and disease affect the nervous system to produce permanent neurological

More information

Does a "moderate" alcohol intake damage the brain?

Does a moderate alcohol intake damage the brain? Journal of Neurology, Neurosurgery, and PsYchiatrY 1988,51:909-913 Does a "moderate" alcohol intake damage the brain? CLIVE HARPER,*t JILLIAN KRIL,* JOHN DALY: From the Department ofpathology,* The University

More information

Chapter 7: The Nervous System

Chapter 7: The Nervous System Chapter 7: The Nervous System Objectives Discuss the general organization of the nervous system Describe the structure & function of a nerve Draw and label the pathways involved in a withdraw reflex Define

More information

Anoxic Brain Injury and Neural Damage: Three Case Reports

Anoxic Brain Injury and Neural Damage: Three Case Reports Anoxic Brain Injury and Neural Damage: Three Case Reports Abstract Anoxic brain injury (ABI) is common and can occur in a wide variety of disorders. This neural injury is associated with significant and

More information

Head Injury. Dr Sally McCarthy Medical Director ECI

Head Injury. Dr Sally McCarthy Medical Director ECI Head Injury Dr Sally McCarthy Medical Director ECI Head injury in the emergency department A common presentation 80% Mild Head Injury = GCS 14 15 10% Moderate Head Injury = GCS 9 13 10% Severe Head Injury

More information

Electrohypersensitivity and multiple chemical sensitivity: two clinicbiological. disorder?

Electrohypersensitivity and multiple chemical sensitivity: two clinicbiological. disorder? 5 th Paris Appeal Congress, 18th of May, 2015 Royal Academy of Medicine, Belgium IDIOPATHIC ENVIRONMENTAL INTOLERANCE: WHAT ROLE FOR ELECTROMAGNETIC FIELDS AND CHEMICALS? Electrohypersensitivity and multiple

More information

Practice Protocol. Neuropsychological Evaluations

Practice Protocol. Neuropsychological Evaluations Practice Protocol Neuropsychological Evaluations Jointly Developed by the Arizona Department of Health Services/Division of Behavioral Health Services and AHCCCS/Health Plans Effective June 30, 2006 Revised

More information

Chapter 10. Summary & Future perspectives

Chapter 10. Summary & Future perspectives Summary & Future perspectives 123 Multiple sclerosis is a chronic disorder of the central nervous system, characterized by inflammation and axonal degeneration. All current therapies modulate the peripheral

More information

ADVANCED BEHAVIORAL HEALTH, INC. Clinical Level of Care Guidelines - 2015

ADVANCED BEHAVIORAL HEALTH, INC. Clinical Level of Care Guidelines - 2015 The Clinical Level of Care Guidelines contained on the following pages have been developed as a guide to assist care managers, physicians and providers in making medical necessity decisions about the least

More information

Philip Moore DO, Toxicology Fellow, PinnacleHealth Toxicology Center Joanne Konick-McMahan RN MSRN, Staff RN, PinnacleHealth

Philip Moore DO, Toxicology Fellow, PinnacleHealth Toxicology Center Joanne Konick-McMahan RN MSRN, Staff RN, PinnacleHealth Philip Moore DO, Toxicology Fellow, PinnacleHealth Toxicology Center Joanne Konick-McMahan RN MSRN, Staff RN, PinnacleHealth I. II. Background A. AWS can occur in anyone who consumes alcohol B. Risk correlates

More information

INTOXICATED PATIENTS AND DETOXIFICATION

INTOXICATED PATIENTS AND DETOXIFICATION VAMC Detoxification Decision Tree Updated May 2006 INTOXICATED PATIENTS AND DETOXIFICATION Patients often present for evaluation of substance use and possible detoxification. There are certain decisions

More information

Chapter 3 The Anatomy of the Nervous System

Chapter 3 The Anatomy of the Nervous System Chapter 3 The Anatomy of the Nervous System Systems, Structures, and Cells That Make Up Your Nervous System 1 General Layout of the Nervous System Central Nervous System (CNS) Brain (in the skull) Spinal

More information

What is PD? Dr Catherine Dotchin MD MRCP Consultant Geriatrician

What is PD? Dr Catherine Dotchin MD MRCP Consultant Geriatrician What is PD? Dr Catherine Dotchin MD MRCP Consultant Geriatrician Overview of presentation Case history Video example pre and post treatment Historical review PD in the UK Epidemiology and aetiology Making

More information

NEURO M203 & BIOMED M263 WINTER 2014

NEURO M203 & BIOMED M263 WINTER 2014 NEURO M203 & BIOMED M263 WINTER 2014 MRI Lab 1: Structural and Functional Anatomy During today s lab, you will work with and view the structural and functional imaging data collected from the scanning

More information

Documentation Requirements ADHD

Documentation Requirements ADHD Documentation Requirements ADHD Attention Deficit Hyperactivity Disorder (ADHD) is considered a neurobiological disability that interferes with a person s ability to sustain attention, focus on a task

More information

ALCOHOL RELATED DISORDERS Includes Alcohol Abuse and Alcohol Dependence; Does Not Include Alcohol Use Disorders

ALCOHOL RELATED DISORDERS Includes Alcohol Abuse and Alcohol Dependence; Does Not Include Alcohol Use Disorders 1 MH 12 ALCOHOL RELATED DISORDERS Includes Alcohol Abuse and Alcohol Dependence; Does Not Include Alcohol Use Disorders Background This case definition was developed by the Armed Forces Health Surveillance

More information

Overview. Geriatric Overview. Chapter 26. Geriatrics 9/11/2012

Overview. Geriatric Overview. Chapter 26. Geriatrics 9/11/2012 Chapter 26 Geriatrics Slide 1 Overview Trauma Common Medical Emergencies Special Considerations in the Elderly Medication Considerations Abuse and Neglect Expanding the Role of EMS Slide 2 Geriatric Overview

More information

ALCOHOL DETOXIFICATION (IN-PATIENTS) PRESCRIBING GUIDELINE

ALCOHOL DETOXIFICATION (IN-PATIENTS) PRESCRIBING GUIDELINE ALCOHOL DETOXIFICATION (IN-PATIENTS) PRESCRIBING GUIDELINE Authors Sponsor Responsible committee Ratified by Consultant Psychiatrist; Pharmacist Team Manager Medical Director Medicines Management Group

More information

J/601/2874. This unit must be assessed in accordance with Skills for Care and Development s QCF Assessment Principles.

J/601/2874. This unit must be assessed in accordance with Skills for Care and Development s QCF Assessment Principles. Unit 13: Dementia Awareness Unit code: DEM 201 Unit reference number: J/601/2874 QCF level: 2 Credit value: 2 Guided learning hours: 17 Unit summary The aim of the unit is to enable learners to gain knowledge

More information

Mental health issues in the elderly. January 28th 2008 Presented by Éric R. Thériault etheriau@lakeheadu.ca

Mental health issues in the elderly. January 28th 2008 Presented by Éric R. Thériault etheriau@lakeheadu.ca Mental health issues in the elderly January 28th 2008 Presented by Éric R. Thériault etheriau@lakeheadu.ca Cognitive Disorders Outline Dementia (294.xx) Dementia of the Alzheimer's Type (early and late

More information

WHAT SHOULD WE KNOW ABOUT MARIJUANA

WHAT SHOULD WE KNOW ABOUT MARIJUANA WHAT SHOULD WE KNOW ABOUT MARIJUANA Marijuana is the most commonly used illicit drug in the U.S. The use of marijuana can produce adverse physical, mental, emotional, and behavioral effects. What is marijuana?

More information

hepatolenticular degeneration (E83.0) human immunodeficiency virus [HIV] disease (B20) hypercalcemia (E83.52) hypothyroidism, acquired (E00-E03.

hepatolenticular degeneration (E83.0) human immunodeficiency virus [HIV] disease (B20) hypercalcemia (E83.52) hypothyroidism, acquired (E00-E03. ICD-10-CM Codes for Mental, Behavioral and Neurodevelopmental Disorders Chapter 5 Mental, Behavioral and Neurodevelopmental disorders (F01-F99) Includes: disorders of psychological development Excludes2:

More information

ALCOHOL RELATED DISORDERS Includes Alcohol Abuse and Alcohol Dependence; Does Not Include Alcohol Use Disorders

ALCOHOL RELATED DISORDERS Includes Alcohol Abuse and Alcohol Dependence; Does Not Include Alcohol Use Disorders 1 MH 12 ALCOHOL RELATED DISORDERS Includes Alcohol Abuse and Alcohol Dependence; Does Not Include Alcohol Use Disorders Background This case definition was developed by the Armed Forces Health Surveillance

More information

2.6.4 Medication for withdrawal syndrome

2.6.4 Medication for withdrawal syndrome .6.3 Self-medication Self-medication presents a risk during alcohol withdrawal, particularly when there is minimal supervision (low level and medium level 1 settings). Inform patients of the risk of selfmedication

More information

Surgery in Individuals Age 65+ Possible Risks. Possible Benefits. Potential Causes of POCD 11/24/2014. What is POCD?

Surgery in Individuals Age 65+ Possible Risks. Possible Benefits. Potential Causes of POCD 11/24/2014. What is POCD? Surgery in Individuals Age 65+ Postoperative Cognitive Dysfunction in Older Adults Ryan W. Schroeder, Psy.D., LP, ABPP-CN Neuropsychologist & Assistant Professor University of Kansas School of Medicine

More information

Alcohol withdrawal A challenge in caring for patients after heart surgery

Alcohol withdrawal A challenge in caring for patients after heart surgery Abteilung Praxisentwicklung Pflege Alcohol withdrawal A challenge in caring for patients after heart surgery Wolfgang Hasemann, RN, PhD Deborah Leuenberger, MScN.cand. June 2015 Content Alcohol consumption

More information

Brain Injury during Fetal-Neonatal Transition

Brain Injury during Fetal-Neonatal Transition Brain Injury during Fetal-Neonatal Transition Adre du Plessis, MBChB Fetal and Transitional Medicine Children s National Medical Center Washington, DC Brain injury during fetal-neonatal transition Injury

More information

Treatment of Opioid Dependence with Buprenorphine/Naloxone (Suboxone )

Treatment of Opioid Dependence with Buprenorphine/Naloxone (Suboxone ) Treatment of Opioid Dependence with Buprenorphine/Naloxone (Suboxone ) Elinore F. McCance-Katz, M.D., Ph.D. Professor and Chair, Addiction Psychiatry Virginia Commonwealth University Neurobiology of Opiate

More information

Treatment for substance abuse and dependence at HC Marbella

Treatment for substance abuse and dependence at HC Marbella Detox Unit Treatment for substance abuse and dependence at HC Marbella The disease Addiction is a disease that is becoming a common problem in our society today. In actual fact, addiction is a chemical

More information

Long-Term Effects of Drug Addiction

Long-Term Effects of Drug Addiction Long-Term Effects of Drug Addiction Part 1: Addiction is a chronic disease Drug addiction is considered a chronic brain disease because drugs cause long-lasting changes in brain structure and function.

More information

Brain Damage & Recovery: The Resilience of the Brain, Addiction Impact & Therapeutic Repair. Michael Fishman, MD Director of Young Adult Program

Brain Damage & Recovery: The Resilience of the Brain, Addiction Impact & Therapeutic Repair. Michael Fishman, MD Director of Young Adult Program Brain Damage & Recovery: The Resilience of the Brain, Addiction Impact & Therapeutic Repair Michael Fishman, MD Director of Young Adult Program How Addiction Takes Hold Large & rapid upsurges in dopamine

More information

Montreal Cognitive Assessment (MoCA) as Screening tool for cognitive impairment in mtbi.

Montreal Cognitive Assessment (MoCA) as Screening tool for cognitive impairment in mtbi. Montreal Cognitive Assessment (MoCA) as Screening tool for cognitive impairment in mtbi. Suresh Kumar, M.D. AUTHOR Director of: Neurology & Headaches Center Inc. Neurocognitve &TBI Rehabilitation Center

More information

Memory Development and Frontal Lobe Insult

Memory Development and Frontal Lobe Insult University Press Scholarship Online You are looking at 1-10 of 11 items for: keywords : traumatic brain injury Memory Development and Frontal Lobe Insult Gerri Hanten and Harvey S. Levin in Origins and

More information

Yorkshire and the Humber SCN Guidance on Neuro-imaging in Dementia

Yorkshire and the Humber SCN Guidance on Neuro-imaging in Dementia Yorkshire and the Humber SCN Guidance on Neuro-imaging in Dementia January 2015 (Review date January 2017) Introduction This guidance has been written by the Yorkshire and Humber Strategic Clinical Network

More information

Update on Treatment of the Dementias

Update on Treatment of the Dementias Update on Treatment of the Dementias Mark Pippenger, MD Behavioral Neurology Associate Clinical Professor of Neurology University of Arkansas for Medical Sciences Disclosures I will be discussing off-label

More information

Stuart B Black MD, FAAN Chief of Neurology Co-Medical Director: Neuroscience Center Baylor University Medical Center at Dallas

Stuart B Black MD, FAAN Chief of Neurology Co-Medical Director: Neuroscience Center Baylor University Medical Center at Dallas Billing and Coding in Neurology and Headache Stuart B Black MD, FAAN Chief of Neurology Co-Medical Director: Neuroscience Center Baylor University Medical Center at Dallas CPT Codes vs. ICD Codes Category

More information

Neuropsychological Testing

Neuropsychological Testing Last Review Date: March 17, 2015 Number: MG.MM.ME.18dC2 Medical Guideline Disclaimer Property of EmblemHealth. All rights reserved. The treating physician or primary care provider must submit to EmblemHealth

More information

Psychological and Neuropsychological Testing

Psychological and Neuropsychological Testing Psychological and Neuropsychological Testing I. Policy University Health Alliance (UHA) will reimburse for Psychological and Neuropsychological Testing (PT/NPT) when it is determined to be medically necessary

More information

The relationship between alcohol

The relationship between alcohol The Association Between Alcohol Use and Dementia in the Elderly The association between alcohol use and dementia is complex and not all that well understood. Studies indicate that moderate alcohol consumption

More information

J. David Kinzie, M.D., FAC Psych. Professor of Psychiatry Oregon Health & Science University

J. David Kinzie, M.D., FAC Psych. Professor of Psychiatry Oregon Health & Science University J. David Kinzie, M.D., FAC Psych. Professor of Psychiatry Oregon Health & Science University 65-year-old Oromo male In the U.S. five years Interviewed the first time April, 2011 Symptoms: Almost no sleep,

More information

CHAPTER- 6. Okadaic acid induced neurotoxicity leads to central cholinergic dysfunction in rats. 1. Introduction. 2. Methods

CHAPTER- 6. Okadaic acid induced neurotoxicity leads to central cholinergic dysfunction in rats. 1. Introduction. 2. Methods CHAPTER- 6 Okadaic acid induced neurotoxicity leads to central cholinergic dysfunction in rats 1. Introduction Neurodegenerative disorders, such as AD are often characterized by the degeneration of the

More information

Version 1 2015. Module guide. Preliminary document. International Master Program Cardiovascular Science University of Göttingen

Version 1 2015. Module guide. Preliminary document. International Master Program Cardiovascular Science University of Göttingen Version 1 2015 Module guide International Master Program Cardiovascular Science University of Göttingen Part 1 Theoretical modules Synopsis The Master program Cardiovascular Science contains four theoretical

More information

STROKE CARE NOW NETWORK CONFERENCE MAY 22, 2014

STROKE CARE NOW NETWORK CONFERENCE MAY 22, 2014 STROKE CARE NOW NETWORK CONFERENCE MAY 22, 2014 Rehabilitation Innovations in Post- Stroke Recovery Madhav Bhat, MD Fort Wayne Neurological Center DISCLOSURE Paid speaker for TEVA Neuroscience Program.

More information

Diabetes Expert Witness on: Diabetic Hypoglycemia in Nursing Homes

Diabetes Expert Witness on: Diabetic Hypoglycemia in Nursing Homes Diabetes Expert Witness on: Diabetic Hypoglycemia in Nursing Homes Nursing home patients with diabetes treated with insulin and certain oral diabetes medications (i.e. sulfonylureas and glitinides) are

More information

PSYC PSYCHOLOGY. 2011-2012 Calendar Proof

PSYC PSYCHOLOGY. 2011-2012 Calendar Proof PSYC PSYCHOLOGY PSYC1003 is a prerequisite for PSYC1004 and PSYC1004 is a prerequisite for all remaining Psychology courses. Note: See beginning of Section F for abbreviations, course numbers and coding.

More information

Introduction to Neurophysiological Psychology (PSY 451)

Introduction to Neurophysiological Psychology (PSY 451) Portland State University Physiological Psychology Page 1 Introduction to Neurophysiological Psychology (PSY 451) Bill Griesar, Ph.D., Adjunct Instructor, bgriesar@pacifier.com OFFICE HOURS: Mondays, 11:30

More information

Alcohol Use Dates Back 7,000 to 10,000 Years. Though Scientists Still Debate the Mechanisms of Hangovers. Proposed Causes of Hangovers

Alcohol Use Dates Back 7,000 to 10,000 Years. Though Scientists Still Debate the Mechanisms of Hangovers. Proposed Causes of Hangovers Alcohol Use Dates Back 7,000 to 10,000 Years Though Scientists Still Debate the Mechanisms of Hangovers Proposed Causes of Hangovers Acute ethanol withdrawal Ethanol can alleviate symptoms Acetaldehyde

More information

Outpatient Treatment of Alcohol Withdrawal. Daniel Duhigg, DO, MBA

Outpatient Treatment of Alcohol Withdrawal. Daniel Duhigg, DO, MBA Outpatient Treatment of Alcohol Withdrawal Daniel Duhigg, DO, MBA DSM V criteria for Alcohol Withdrawal A. Cessation or reduction of heavy/prolonged alcohol use B. 2 or more of the following in hours to

More information

THE BASICS. Community Based Medically Assisted Alcohol Withdrawal. World Health Organisation 2011. The Issues 5/18/2011. RCGP Conference May 2011

THE BASICS. Community Based Medically Assisted Alcohol Withdrawal. World Health Organisation 2011. The Issues 5/18/2011. RCGP Conference May 2011 RCGP Conference May 2011 Community Based Medically Assisted Alcohol Withdrawal THE BASICS An option for consideration World Health Organisation 2011 Alcohol is the world s third largest risk factor for

More information

THEORIES OF NEUROLOGICAL AGING AND DEMENTIA

THEORIES OF NEUROLOGICAL AGING AND DEMENTIA THEORIES OF NEUROLOGICAL AGING AND DEMENTIA Aging Overview The primary care physician must advise middle-age and older patients about ways to age successfully. Dementia is a common disabling illness that

More information

REHABILITATION MEDICINE by PROFESSOR ANTHONY WARD

REHABILITATION MEDICINE by PROFESSOR ANTHONY WARD REHABILITATION MEDICINE by PROFESSOR ANTHONY WARD What is Rehabilitation Medicine? Rehabilitation Medicine (RM) is the medical specialty with rehabilitation as its primary strategy. It provides services

More information

ALCOHOLISM, ALCOHOL DEPENDENCE AND THE EFFECTS ON YOUR HEALTH.

ALCOHOLISM, ALCOHOL DEPENDENCE AND THE EFFECTS ON YOUR HEALTH. ALCOHOLISM, ALCOHOL DEPENDENCE AND THE EFFECTS ON YOUR HEALTH. Alcoholism also known as alcohol dependence is a disabling ADDICTIVE DISORDER. It is characterized by compulsive and uncontrolled consumption

More information

Section 15 IMAGES OF ALCOHOL AND DRUG ABUSE Brain Pollution and the Real Reason You Shouldn t Use

Section 15 IMAGES OF ALCOHOL AND DRUG ABUSE Brain Pollution and the Real Reason You Shouldn t Use Section 15 IMAGES OF ALCOHOL AND DRUG ABUSE Brain Pollution and the Real Reason You Shouldn t Use Studying the effects of drugs and alcohol on the brain has clearly been one of the most informative and

More information

Long Term Care Formulary HCD - 09. Anti-Dementia Drugs (e.g. donepezil, galantamine, rivastigmine, memantine)

Long Term Care Formulary HCD - 09. Anti-Dementia Drugs (e.g. donepezil, galantamine, rivastigmine, memantine) 1 of 8 USE OF CHOLINESTERASE (AChE) INHIBITORS The cholinesterase inhibitor anti-dementia drugs are indicated for the symptomatic treatment of patients with mild to moderate dementia of the Alzheimer s

More information

Management of Diabetes in the Elderly. Sylvia Shamanna Internal Medicine (R1)

Management of Diabetes in the Elderly. Sylvia Shamanna Internal Medicine (R1) Management of Diabetes in the Elderly Sylvia Shamanna Internal Medicine (R1) Case 74 year old female with frontal temporal lobe dementia admitted for prolonged delirium and frequent falls (usually in the

More information

Traumatic Brain Injury and Incarceration. Objectives. Traumatic Brain Injury. Which came first, the injury or the behavior?

Traumatic Brain Injury and Incarceration. Objectives. Traumatic Brain Injury. Which came first, the injury or the behavior? Traumatic Brain Injury and Incarceration Which came first, the injury or the behavior? Barbara Burchell Curtis RN, MSN Objectives Upon completion of discussion, participants should be able to Describe

More information

Tricia Cox on 7/18/2012 at Oncology Center. Sarah Randolf. Female

Tricia Cox on 7/18/2012 at Oncology Center. Sarah Randolf. Female SAMPLE This Survivorship Care Plan will facilitate cancer care following active treatment. It may include important contact information, a treatment summary, recommendations for follow-up care testing,

More information

Brain Power. Counseling and Mental Health

Brain Power. Counseling and Mental Health Brain Power Counseling and Mental Health TEA COPYRIGHT Copyright Texas Education Agency, 2012. These Materials are copyrighted and trademarked as the property of the Texas Education Agency (TEA) and may

More information

AMPHETAMINE AND COCAINE MECHANISMS AND HAZARDS

AMPHETAMINE AND COCAINE MECHANISMS AND HAZARDS AMPHETAMINE AND COCAINE MECHANISMS AND HAZARDS BARRY J. EVERITT Department of Experimental Psychology, University of Cambridge Stimulant drugs, such as cocaine and amphetamine, interact directly with dopamine

More information