- Email: [email protected]
Thalamic hypofunction in alcohol hallucinosis: FDG PET findings
Psychiatry Research: Neuroimaging 139 (2005) 259 – 262 www.elsevier.com/locate/psychresns
Brief report
Thalamic hypofunction in alcohol hallucinosis: FDG PET findings Michael Soyka a,*, Walter Koch b, Klaus Tatsch b a Psychiatric Hospital, University of Munich, Nubbaumstrabe 7, D-80336 Munich, Germany Department of Nuclear Medicine, Clinic of the University of Munich-Grosshadern, Marchioninistr. 15, D-81377 Munich, Germany
b
Received 30 October 2004; received in revised form 25 April 2005; accepted 5 May 2005
Abstract We report findings obtained with positron emission tomography with fluorodeoxyglucose-F18 (FDG PET) as tracer in two patients with acute alcohol hallucinosis. In line with previous findings, both patients had a significant hypometabolism in the left relative to the right thalamus. When the second patient was retested after clinical recovery, FDG PET findings were normalized, suggesting the probable thalamic dysfunction to be a functional rather than a structural abnormality. D 2005 Elsevier Ireland Ltd. All rights reserved. Keywords: Alcoholism; Alcohol-induced psychotic disorder with hallucinatory features; Positron emission tomography
1. Introduction Alcohol hallucinosis is a rare complication of chronic alcoholism. Clear epidemiological data about this condition are lacking. Tsuang et al. (1994), in a cohort of 643 alcoholic patients, reported a prevalence rate of 7.4%. The essential feature of this syndrome is that of an organic hallucinosis with vivid auditory hallucinations following cessation of or reduction of alcohol intake that usually develops within 48 h of cessation of alcohol intake (Glass, 1989a). Symptoms of alcohol delirium
* Corresponding author. Tel.: +49 89 5160 2777; fax: +49 89 5160 5617. E-mail address: [email protected] (M. Soyka).
such as clouding of sensorium and disorientation are missing. The prognosis is usually good (Glass, 1989b), and there is no evidence for an increased genetic loading for schizophrenia in patients with alcohol hallucinosis (Cook and Winokur, 1985; Kendler, 1985; Schuckit and Winokur, 1971). In ICD-10 (World Health Organization, 1999) and DSM-IV (American Psychiatric Association, 1994), the term balcohol hallucinosisQ has been replaced by balcohol-induced psychotic disorder with hallucinatory features.Q According to ICD-10, the syndrome is characterized by (typically auditory) hallucinations, delusions, misidentification, psychomotor disturbances, and abnormal affect. The pathophysiology is basically unclear (Soyka, 1995; Soyka et al., 2000a,b). Functional neuroimaging techniques may be of special interest in this respect. Previously, we reported positron emission
0925-4927/$ - see front matter D 2005 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.pscychresns.2005.05.009
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M. Soyka et al. / Psychiatry Research: Neuroimaging 139 (2005) 259–262
tomography (PET) findings in two cases of alcohol hallucinosis, both indicating hypometabolism of the thalamus (Soyka et al., 2000a,b). Very recently we studied two other cases of alcohol hallucinosis using PET with fluorodeoxyglucose-F18 (FDG) as tracer. Findings further suggest a thalamic hypofunction in patients with alcohol hallucinosis that may be of relevance for the pathophysiology of the syndrome.
2. Methods The PET studies were performed with an ECAT EXACT HR+ PET scanner (Siemens/CTI) after injection of 120 MBq of FDG. The regional cerebral metabolic rate of glucose (rCMRglc) was calculated using the methods described by Phelps et al. (1979). For further evaluation, the PET data were processed using the BRASS software (Nuclear Diagnostics), which allows registration of a patient’s study to a three-dimensional reference template created from a normal database. Regional analysis determined the mean rCMRglc within three-dimensional regions; here we confined data presentation to the thalamus. For exclusion of structural brain defects, either magnetic resonance imaging or computed tomography was performed.
3. Case reports M.J. was a 34-year-patient with long-term alcoholism who had suffered from auditory hallucinations (threatening or insulting voices) for 6 years, predominantly upon cessation of alcohol intake. Neither schizophrenic symptoms such as thought disorder and psychotic disorder nor withdrawal symptoms were observed. After 1 week of abstinence, the unmedicated patient was studied. While computed tomography of the brain was basically normal, with discrete enlargement of the ventricles, FDG PET revealed a normal and homogenous cortical metabolism but a remarkable hypometabolism of the left thalamus ( 14.7%) relative to the right thalamus. P.K. was a 42-year-old patient with an alcohol history of at least 15 years who, especially during various abstinence phases, experienced auditory hallucinations that persisted for weeks or a few months. Again, no signs of other types of schizophrenic symptoms were present. While magnetic resonance tomography did not show any abnormalities, the FDG PET scan showed a marked right-to-left asymmetry in the thalamus. While metabolism was normal on the left side, there was a 12.9% reduction on the right side. Interestingly, a follow-up PET scan 4 weeks later, which was performed in the symptom-free abstinent
Fig. 1. Standardized reoriented FDG PET scans in patient P.K. (A) during presence of hallucinations and (B) follow-up after 4 weeks in a symptom-free abstinent status. While there was a marked thalamic asymmetry in the baseline scan (A), thalamic asymmetry markedly improved during symptom-free abstinence (B).
M. Soyka et al. / Psychiatry Research: Neuroimaging 139 (2005) 259–262
261
patient, indicated an improvement of the right thalamic metabolism, now presenting only with a slight difference (5.6%) from the left side, which could no longer be considered pathological (see Fig. 1).
thalamus may be state-related and that metabolic activity may normalize upon clinical improvement. Further longitudinal studies in larger samples of patients are necessary to elucidate this phenomenon.
4. Discussion
Acknowledgments
The thalamus is a very interesting key structure both in alcohol research and for the development of hallucinations (Pakkenberg, 1990; Silbersweig et al., 1995). Deficits in thalamic sensory filtering have been implicated in the development of psychotic symptoms, especially in schizophrenia (Buchsbaum et al., 1996). Other studies have shown the thalamus to be dysfunctional in chronic alcoholism (Neiman and Litton, 2000), especially in Wernicke–Korsakoff syndrome as indicated by histopathological (Belzunegui et al., 1995) and neuroimaging studies (Fellgiebel et al., 2003; Reed et al., 2003; George et al., 2004; Szabo et al., 2004). The volume of both the left and right thalami was found to be decreased in alcoholics (Sullivan et al., 2003). The thalamus may also be one of the key structures for the development of addiction; activation of the (anterior) thalamus is seen in alcoholics exposed to alcohol cues (George et al., 2001; Myrick et al., 2004). The functional relevance of the thalamus for the development of hallucinosis in alcohol dependence has not been studied. In two previous cases of never-medicated patients with chronic alcohol hallucinosis, we were able to demonstrate a significant decrease in the right thalamus that was associated with normal FDG PET findings in the striatum and frontal cortex (Soyka et al., 2000b) and the thalamus bilaterally and the frontal cortex (Soyka et al., 2000a).The two cases presented in this report also suggest that the thalamus is a key structure in the development of alcohol hallucinosis. Dysfunction in thalamic sensory filtering may be of relevance for other behavioural correlates of alcoholism such as aggression (George et al., 2004). Whether the thalamic dysfunction suggested by our PET findings reflects an underlying structural abnormality warrants further studies with special reference to possible differences in laterality. In the cases published to date, either the left or the right thalamus may be impaired. The second case suggests that the hypometabolism of the
This article was prepared in the context of the Addiction Research Network ASAT (Allocating Substance Abuse Treatments to Patient Heterogeneity). Contact information: email: [email protected] (www.asat-verbund.de). ASAT is sponsored by a federal grant of the German Federal Ministry of Education and Research (01 EB 0140 - 0142).
References American Psychiatric Association, 1994. DSM-IV: Diagnostic and Statistical Manual of Mental Disorders, fourth ed. APA, Washington, DC. Belzunegui, T., Insausti, R., Ibanez, J., Ponzalo, L.M., 1995. Effects of chronic alcoholism on neuronal nuclear size and neuronal population in the mammillary body and the anterior thalamic complex of man. Histology and Histopathology 10, 633 – 638. Buchsbaum, M.S., Someya, T., Teng, C.Y., Abel, L., Chin, S., Najafi, A., Haier, R.J., Wu, J., Bunney Jr., W.E., 1996. PET and MRI of the thalamus in never-medicated patients with schizophrenia. American Journal of Psychiatry 153, 191 – 199. Cook, B.L., Winokur, G., 1985. Separate heritability of alcoholism and psychotic symptoms. American Journal of Psychiatry 142, 360 – 361. Fellgiebel, A., Scheurich, A., Siessmeier, T., Schmidt, L.G., Bartenstein, P., 2003. Persistence of disturbed thalamic glucose metabolism in a case of Wernicke–Korsakoff syndrome. Psychiatry Research: Neuroimaging 124, 105 – 112. George, M.S., Anton, R.F., Bloomer, C., Teneback, C., Drobes, D.J., Lorberbaum, J.P., Nahas, Z., Vincent, D.J., 2001. Activation of prefrontal cortex and anterior thalamus in alcoholic subjects on exposure to alcohol-specific cues. Archives of General Psychiatry 58, 345 – 352. George, D.T., Rawlings, R.R., Williams, W.A., Phillips, M.J., Fong, G., Kerich, M., Momenan, R., Umhau, J.C., Hommer, D., 2004. A select group of perpetrators of domestic violence: evidence of decreased metabolism in the right hypothalamus and reduced relationships between cortical/subcortical brain structures in positron emission tomography. Psychiatry Research: Neuroimaging 130, 11 – 25. Glass, I.B., 1989a. Alcohol hallucinosis: a psychiatric enigma: 1. The development of an idea. British Journal of Addiction 84, 29 – 41. Glass, I.B., 1989b. Alcohol hallucinosis: a psychiatric enigma: 2. Follow-up studies. British Journal of Addiction 84, 151 – 164.
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M. Soyka et al. / Psychiatry Research: Neuroimaging 139 (2005) 259–262
Kendler, K.S., 1985. A twin study of individuals with both schizophrenia and alcoholism. British Journal of Psychiatry 147, 48 – 53. Myrick, H., Anton, R.F., Li, X., Henderson, S., Drobes, D., Voronin, K., George, M.S., 2004. Differential brain activity in alcoholics and social drinkers to alcohol cues: relationship to craving. Neuropsychopharmacology 29, 393 – 402. Neiman, J., Litton, J.E., 2000. Reduced [11C]flumazenil radioligand binding in the thalamus in alcoholics. Addiction Biology 5, 97 – 99. Pakkenberg, B., 1990. Pronounced reduction of total neuron number in mediodorsal thalamic nucleus and nucleus accumbens in schizophrenia. Archives of General Psychiatry 47, 1023 – 1028. Phelps, M.E., Huang, S.C., Hoffman, E.J., Selin, C., Sokoloff, L., Kuhl, D.E., 1979. Tomographic measurement of local cerebral glucose metabolic rate in human with (F-18)2fluoro-2-deoxy-d-glucose: validation of method. Annals of Neurology 6, 371 – 388. Reed, L.J., Lasserson, D., Mardsen, P., Stanhope, N., Stevens, T., Bello, F., Kingsley, D., Colchester, A., Kopelman, M.D., 2003. FDG–PET findings in the Wernicke–Korsakoff syndrome. Cortex 39, 1027 – 1045. Schuckit, M.A., Winokur, G., 1971. Alcoholic hallucinosis and schizophrenia: a negative study. British Journal of Psychiatry 119, 549 – 550. Silbersweig, D.A., Stern, E., Frith, C., Cahill, C., Holmes, A., Grootoonk, S., Seaward, J., McKenna, P., Chua, S.E., Schnorr, L., Jones, T., Frackowiak, R.S.J., 1995. A functional neuroanatomy of hallucinations in schizophrenia. Nature 378, 176 – 179.
Soyka, M., 1995. Pathophysiologic mechanisms possibly involved in the development of alcohol hallucinosis. Addiction 90, 289 – 290. Soyka, M., Dresel, S., Horak, M., Ruther, T., Tatsch, K., 2000a. PET and SPECT findings in alcohol hallucinosis: case report and super-brief review of the pathophysiology of this syndrome. World Journal of Biological Psychiatry 1, 215 – 218. Soyka, M., Zetzsche, T., Dresel, S., Tatsch, K., 2000b. FDG–PET and IBZM–SPECT suggest reduced thalamic activity but no dopaminergic dysfunction in chronic alcohol hallucinosis [Letter]. Journal of Neuropsychiatry and Clinical Neurosciences 12, 287 – 288. Sullivan, E.V., Rosenbloom, M.J., Serventi, K.L., Deshmukh, A., Pfefferbaum, A., 2003. Effects of alcohol dependence comorbidity and antipsychotic medication on volumes of the thalamus and pons in schizophrenia. American Journal of Psychiatry 160, 1110 – 1116. Szabo, Z., Owonikoko, T., Peyrot, M., Varga, J., Mathews, W.B., Ravert, H.T., Dannals, R.F., Wand, G., 2004. Positron emission tomography imaging of the serotonin transporter in subjects with a history of alcoholism. Biological Psychiatry 55, 766 – 771. Tsuang, J.W., Irwin, M.R., Smith, T.L., Schuckit, M.A., 1994. Characteristics of men with alcoholic hallucinosis. Addiction 89, 73 – 78. Weltgesundheitsorganisation [World Health Organization], 1991. In: Dilling, H., Mombour, W., Schmidt, M.H. (Eds.), Internationale Klassifikation Psychischer Sto¨rungen ICD-10 Kapitel V (F). Verlag Hans Huber, Bern-Go¨ttingen-Toronto.
Brief report
Thalamic hypofunction in alcohol hallucinosis: FDG PET findings Michael Soyka a,*, Walter Koch b, Klaus Tatsch b a Psychiatric Hospital, University of Munich, Nubbaumstrabe 7, D-80336 Munich, Germany Department of Nuclear Medicine, Clinic of the University of Munich-Grosshadern, Marchioninistr. 15, D-81377 Munich, Germany
b
Received 30 October 2004; received in revised form 25 April 2005; accepted 5 May 2005
Abstract We report findings obtained with positron emission tomography with fluorodeoxyglucose-F18 (FDG PET) as tracer in two patients with acute alcohol hallucinosis. In line with previous findings, both patients had a significant hypometabolism in the left relative to the right thalamus. When the second patient was retested after clinical recovery, FDG PET findings were normalized, suggesting the probable thalamic dysfunction to be a functional rather than a structural abnormality. D 2005 Elsevier Ireland Ltd. All rights reserved. Keywords: Alcoholism; Alcohol-induced psychotic disorder with hallucinatory features; Positron emission tomography
1. Introduction Alcohol hallucinosis is a rare complication of chronic alcoholism. Clear epidemiological data about this condition are lacking. Tsuang et al. (1994), in a cohort of 643 alcoholic patients, reported a prevalence rate of 7.4%. The essential feature of this syndrome is that of an organic hallucinosis with vivid auditory hallucinations following cessation of or reduction of alcohol intake that usually develops within 48 h of cessation of alcohol intake (Glass, 1989a). Symptoms of alcohol delirium
* Corresponding author. Tel.: +49 89 5160 2777; fax: +49 89 5160 5617. E-mail address: [email protected] (M. Soyka).
such as clouding of sensorium and disorientation are missing. The prognosis is usually good (Glass, 1989b), and there is no evidence for an increased genetic loading for schizophrenia in patients with alcohol hallucinosis (Cook and Winokur, 1985; Kendler, 1985; Schuckit and Winokur, 1971). In ICD-10 (World Health Organization, 1999) and DSM-IV (American Psychiatric Association, 1994), the term balcohol hallucinosisQ has been replaced by balcohol-induced psychotic disorder with hallucinatory features.Q According to ICD-10, the syndrome is characterized by (typically auditory) hallucinations, delusions, misidentification, psychomotor disturbances, and abnormal affect. The pathophysiology is basically unclear (Soyka, 1995; Soyka et al., 2000a,b). Functional neuroimaging techniques may be of special interest in this respect. Previously, we reported positron emission
0925-4927/$ - see front matter D 2005 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.pscychresns.2005.05.009
260
M. Soyka et al. / Psychiatry Research: Neuroimaging 139 (2005) 259–262
tomography (PET) findings in two cases of alcohol hallucinosis, both indicating hypometabolism of the thalamus (Soyka et al., 2000a,b). Very recently we studied two other cases of alcohol hallucinosis using PET with fluorodeoxyglucose-F18 (FDG) as tracer. Findings further suggest a thalamic hypofunction in patients with alcohol hallucinosis that may be of relevance for the pathophysiology of the syndrome.
2. Methods The PET studies were performed with an ECAT EXACT HR+ PET scanner (Siemens/CTI) after injection of 120 MBq of FDG. The regional cerebral metabolic rate of glucose (rCMRglc) was calculated using the methods described by Phelps et al. (1979). For further evaluation, the PET data were processed using the BRASS software (Nuclear Diagnostics), which allows registration of a patient’s study to a three-dimensional reference template created from a normal database. Regional analysis determined the mean rCMRglc within three-dimensional regions; here we confined data presentation to the thalamus. For exclusion of structural brain defects, either magnetic resonance imaging or computed tomography was performed.
3. Case reports M.J. was a 34-year-patient with long-term alcoholism who had suffered from auditory hallucinations (threatening or insulting voices) for 6 years, predominantly upon cessation of alcohol intake. Neither schizophrenic symptoms such as thought disorder and psychotic disorder nor withdrawal symptoms were observed. After 1 week of abstinence, the unmedicated patient was studied. While computed tomography of the brain was basically normal, with discrete enlargement of the ventricles, FDG PET revealed a normal and homogenous cortical metabolism but a remarkable hypometabolism of the left thalamus ( 14.7%) relative to the right thalamus. P.K. was a 42-year-old patient with an alcohol history of at least 15 years who, especially during various abstinence phases, experienced auditory hallucinations that persisted for weeks or a few months. Again, no signs of other types of schizophrenic symptoms were present. While magnetic resonance tomography did not show any abnormalities, the FDG PET scan showed a marked right-to-left asymmetry in the thalamus. While metabolism was normal on the left side, there was a 12.9% reduction on the right side. Interestingly, a follow-up PET scan 4 weeks later, which was performed in the symptom-free abstinent
Fig. 1. Standardized reoriented FDG PET scans in patient P.K. (A) during presence of hallucinations and (B) follow-up after 4 weeks in a symptom-free abstinent status. While there was a marked thalamic asymmetry in the baseline scan (A), thalamic asymmetry markedly improved during symptom-free abstinence (B).
M. Soyka et al. / Psychiatry Research: Neuroimaging 139 (2005) 259–262
261
patient, indicated an improvement of the right thalamic metabolism, now presenting only with a slight difference (5.6%) from the left side, which could no longer be considered pathological (see Fig. 1).
thalamus may be state-related and that metabolic activity may normalize upon clinical improvement. Further longitudinal studies in larger samples of patients are necessary to elucidate this phenomenon.
4. Discussion
Acknowledgments
The thalamus is a very interesting key structure both in alcohol research and for the development of hallucinations (Pakkenberg, 1990; Silbersweig et al., 1995). Deficits in thalamic sensory filtering have been implicated in the development of psychotic symptoms, especially in schizophrenia (Buchsbaum et al., 1996). Other studies have shown the thalamus to be dysfunctional in chronic alcoholism (Neiman and Litton, 2000), especially in Wernicke–Korsakoff syndrome as indicated by histopathological (Belzunegui et al., 1995) and neuroimaging studies (Fellgiebel et al., 2003; Reed et al., 2003; George et al., 2004; Szabo et al., 2004). The volume of both the left and right thalami was found to be decreased in alcoholics (Sullivan et al., 2003). The thalamus may also be one of the key structures for the development of addiction; activation of the (anterior) thalamus is seen in alcoholics exposed to alcohol cues (George et al., 2001; Myrick et al., 2004). The functional relevance of the thalamus for the development of hallucinosis in alcohol dependence has not been studied. In two previous cases of never-medicated patients with chronic alcohol hallucinosis, we were able to demonstrate a significant decrease in the right thalamus that was associated with normal FDG PET findings in the striatum and frontal cortex (Soyka et al., 2000b) and the thalamus bilaterally and the frontal cortex (Soyka et al., 2000a).The two cases presented in this report also suggest that the thalamus is a key structure in the development of alcohol hallucinosis. Dysfunction in thalamic sensory filtering may be of relevance for other behavioural correlates of alcoholism such as aggression (George et al., 2004). Whether the thalamic dysfunction suggested by our PET findings reflects an underlying structural abnormality warrants further studies with special reference to possible differences in laterality. In the cases published to date, either the left or the right thalamus may be impaired. The second case suggests that the hypometabolism of the
This article was prepared in the context of the Addiction Research Network ASAT (Allocating Substance Abuse Treatments to Patient Heterogeneity). Contact information: email: [email protected] (www.asat-verbund.de). ASAT is sponsored by a federal grant of the German Federal Ministry of Education and Research (01 EB 0140 - 0142).
References American Psychiatric Association, 1994. DSM-IV: Diagnostic and Statistical Manual of Mental Disorders, fourth ed. APA, Washington, DC. Belzunegui, T., Insausti, R., Ibanez, J., Ponzalo, L.M., 1995. Effects of chronic alcoholism on neuronal nuclear size and neuronal population in the mammillary body and the anterior thalamic complex of man. Histology and Histopathology 10, 633 – 638. Buchsbaum, M.S., Someya, T., Teng, C.Y., Abel, L., Chin, S., Najafi, A., Haier, R.J., Wu, J., Bunney Jr., W.E., 1996. PET and MRI of the thalamus in never-medicated patients with schizophrenia. American Journal of Psychiatry 153, 191 – 199. Cook, B.L., Winokur, G., 1985. Separate heritability of alcoholism and psychotic symptoms. American Journal of Psychiatry 142, 360 – 361. Fellgiebel, A., Scheurich, A., Siessmeier, T., Schmidt, L.G., Bartenstein, P., 2003. Persistence of disturbed thalamic glucose metabolism in a case of Wernicke–Korsakoff syndrome. Psychiatry Research: Neuroimaging 124, 105 – 112. George, M.S., Anton, R.F., Bloomer, C., Teneback, C., Drobes, D.J., Lorberbaum, J.P., Nahas, Z., Vincent, D.J., 2001. Activation of prefrontal cortex and anterior thalamus in alcoholic subjects on exposure to alcohol-specific cues. Archives of General Psychiatry 58, 345 – 352. George, D.T., Rawlings, R.R., Williams, W.A., Phillips, M.J., Fong, G., Kerich, M., Momenan, R., Umhau, J.C., Hommer, D., 2004. A select group of perpetrators of domestic violence: evidence of decreased metabolism in the right hypothalamus and reduced relationships between cortical/subcortical brain structures in positron emission tomography. Psychiatry Research: Neuroimaging 130, 11 – 25. Glass, I.B., 1989a. Alcohol hallucinosis: a psychiatric enigma: 1. The development of an idea. British Journal of Addiction 84, 29 – 41. Glass, I.B., 1989b. Alcohol hallucinosis: a psychiatric enigma: 2. Follow-up studies. British Journal of Addiction 84, 151 – 164.
262
M. Soyka et al. / Psychiatry Research: Neuroimaging 139 (2005) 259–262
Kendler, K.S., 1985. A twin study of individuals with both schizophrenia and alcoholism. British Journal of Psychiatry 147, 48 – 53. Myrick, H., Anton, R.F., Li, X., Henderson, S., Drobes, D., Voronin, K., George, M.S., 2004. Differential brain activity in alcoholics and social drinkers to alcohol cues: relationship to craving. Neuropsychopharmacology 29, 393 – 402. Neiman, J., Litton, J.E., 2000. Reduced [11C]flumazenil radioligand binding in the thalamus in alcoholics. Addiction Biology 5, 97 – 99. Pakkenberg, B., 1990. Pronounced reduction of total neuron number in mediodorsal thalamic nucleus and nucleus accumbens in schizophrenia. Archives of General Psychiatry 47, 1023 – 1028. Phelps, M.E., Huang, S.C., Hoffman, E.J., Selin, C., Sokoloff, L., Kuhl, D.E., 1979. Tomographic measurement of local cerebral glucose metabolic rate in human with (F-18)2fluoro-2-deoxy-d-glucose: validation of method. Annals of Neurology 6, 371 – 388. Reed, L.J., Lasserson, D., Mardsen, P., Stanhope, N., Stevens, T., Bello, F., Kingsley, D., Colchester, A., Kopelman, M.D., 2003. FDG–PET findings in the Wernicke–Korsakoff syndrome. Cortex 39, 1027 – 1045. Schuckit, M.A., Winokur, G., 1971. Alcoholic hallucinosis and schizophrenia: a negative study. British Journal of Psychiatry 119, 549 – 550. Silbersweig, D.A., Stern, E., Frith, C., Cahill, C., Holmes, A., Grootoonk, S., Seaward, J., McKenna, P., Chua, S.E., Schnorr, L., Jones, T., Frackowiak, R.S.J., 1995. A functional neuroanatomy of hallucinations in schizophrenia. Nature 378, 176 – 179.
Soyka, M., 1995. Pathophysiologic mechanisms possibly involved in the development of alcohol hallucinosis. Addiction 90, 289 – 290. Soyka, M., Dresel, S., Horak, M., Ruther, T., Tatsch, K., 2000a. PET and SPECT findings in alcohol hallucinosis: case report and super-brief review of the pathophysiology of this syndrome. World Journal of Biological Psychiatry 1, 215 – 218. Soyka, M., Zetzsche, T., Dresel, S., Tatsch, K., 2000b. FDG–PET and IBZM–SPECT suggest reduced thalamic activity but no dopaminergic dysfunction in chronic alcohol hallucinosis [Letter]. Journal of Neuropsychiatry and Clinical Neurosciences 12, 287 – 288. Sullivan, E.V., Rosenbloom, M.J., Serventi, K.L., Deshmukh, A., Pfefferbaum, A., 2003. Effects of alcohol dependence comorbidity and antipsychotic medication on volumes of the thalamus and pons in schizophrenia. American Journal of Psychiatry 160, 1110 – 1116. Szabo, Z., Owonikoko, T., Peyrot, M., Varga, J., Mathews, W.B., Ravert, H.T., Dannals, R.F., Wand, G., 2004. Positron emission tomography imaging of the serotonin transporter in subjects with a history of alcoholism. Biological Psychiatry 55, 766 – 771. Tsuang, J.W., Irwin, M.R., Smith, T.L., Schuckit, M.A., 1994. Characteristics of men with alcoholic hallucinosis. Addiction 89, 73 – 78. Weltgesundheitsorganisation [World Health Organization], 1991. In: Dilling, H., Mombour, W., Schmidt, M.H. (Eds.), Internationale Klassifikation Psychischer Sto¨rungen ICD-10 Kapitel V (F). Verlag Hans Huber, Bern-Go¨ttingen-Toronto.