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Letter   |    
FDG-PET and IBZM-SPECT Suggest Reduced Thalamic Activity but No Dopaminergic Dysfunction in Chronic Alcohol Hallucinosis
Michael Soyka, M.D.; Thomas Zetzsche, M.D.; Stefan Dresel, M.D.; Klaus Tatsch, M.D.
The Journal of Neuropsychiatry and Clinical Neurosciences 2000;12:287-288. doi:10.1176/appi.neuropsych.12.2.287
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PET StudiesSPECT StudiesAlcohol

SIR: Although up to one-fourth of alcoholics were reported to have experienced hallucinations in their lifetime, chronic alcohol hallucinosis1 is a rare condition closely resembling paranoid schizophrenia.2 The pathophysiological basis of alcohol hallucinosis is not yet totally understood.3 There is no evidence for greater prevalence of schizophrenia in relatives of patients with alcohol hallucinosis.3,4 The dysfunction of special areas in the brain in alcohol hallucinosis has not been demonstrated yet. Several studies point at an increase in central dopaminergic activity during alcohol withdrawal,3 but dopamine receptor subsensitivity in alcohol hallucinosis has not been shown.

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Case Report

Mrs. A., a 35-year-old housewife with a long-term alcohol history of at least a decade with an average alcohol consumption of 400 g of alcohol per day, suffered from vivid and continuing auditory and recurrent visual hallucinations, fear, sleep disturbances, and mild delusions of persecution for a year. There was no evidence for any schizophrenic thought disorder or blunted affect, psychotic ego disturbances, or disturbances of orientation or consciousness. Auditory hallucinations also persisted in phases of reduced alcohol consumption or abstinence. The patient had never received any psychotropic medication before admission. At admission the patient was found to have elevated liver enzymes (serum gamma-glutamyl transaminase 180 U/l) and showed mild withdrawal symptoms. Hallucinations persisted over a period of 6 weeks following abstinence, despite later treatment with neuroleptics (flupentixol 10 mg/day).

Neurologic examination did not show any abnormal finding. Magnetic resonance imaging revealed a generalized cortical brain atrophy without any evidence for focal gray or white matter lesions. CSF and chest X-ray were normal. [123I]iodobenzamide (IBZM) SPECT was performed after 2 weeks of abstinence in the drug-naive patient on a triple-head gamma camera (Picker Prism 3000 XP, equipped with high-resolution fan beam collimators) after iv administration of 185 MBq [123I]IBZM. Images were acquired 2 hours after administration and were reconstructed by use of filtered backprojection. Finally, images were postfiltered by using a low-pass filter and attenuation corrected according to Chang's first-order method. The reconstructed scans displayed a homogeneous binding of the ligand to the postsynaptic dopamine D2 receptors. There was no evidence of any asymmetries or reduction of binding. The semiquantitative evaluation revealed a normal specific binding ([striatum—background]/background) of 0.8.

The [18F]fluorodeoxyglucose (FDG) PET scan was conducted on a dedicated ring PET system (Siemens ECAT Exact HR+). Transmission scans for attenuation correction were acquired and followed by iv injection of 120 MBq [18F]FDG. A dynamic acquisition was performed, images in transverse, sagittal, and coronal slice orientation were reconstructed, and attenuation was corrected. Using the input function, regional glucose metabolism was expressed in μmol/min per 100 g brain tissue. The images displayed a homogeneous, symmetric cortical uptake of FDG. There was no evidence of increased or diminished uptake in the temporal lobes. The right thalamus demonstrated a visibly decreased FDG uptake, calculated to be 10% to 18% lower than in the left thalamus. Normal uptake was seen in the striatum and the cerebellum.

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Comment

In the above case, although impaired dopamine D2 receptor dysfunction is unlikely according to IBZM-SPECT findings, the FDG PET results point at a significant impairment of thalamic function in chronic alcohol hallucinosis. This finding may be of special relevance because similar findings have been reported in schizophrenia. Buchsbaum et al.,5 in a PET and MRI study on 20 never-medicated schizophrenic patients, reported a diminished metabolic rate in the right thalamus and a loss of the normal pattern of right-greater-than-left asymmetry. The thalamus has been identified as a key structure in the development of hallucinations.6 Neuropathological studies have shown neuronal alterations in the thalamus in schizophrenic patients.7 The reduced thalamic activity observed in this study is in accordance with the concept that deficits in thalamic sensory filtering may be of pathophysiological importance in psychotic disorders, possibly including alcohol hallucinosis. A reduced activity in the thalamic region has repeatedly been described in alcoholics,8 but its functional relevance is not entirely clear. The question of whether alcoholic thalamopathy is essential for the development of this syndrome should be addressed in future studies.

Tsuang JW, Irwin MR, Smith TL, et al: Characteristics of men with alcoholic hallucinosis. Addiction  1994; 89:73—78
[CrossRef] | [PubMed]
 
Soyka M: Pathophysiologic characteristics in alcohol hallucinosis and paranoid schizophrenia. Acta Psychiatr Scand  1990; 81:255—259
[CrossRef] | [PubMed]
 
Soyka M: Psychopathological mechanisms possibly involved in the development of alcohol hallucinosis. Addiction  1995; 90:289—290
[CrossRef] | [PubMed]
 
Glass IB: Alcohol hallucinosis: a psychiatric enigma, I: the development of an idea. Br J Addict  1989; 84:29—41
[CrossRef] | [PubMed]
 
Buchsbaum MS, Someya T, Teng CY, et al: PET and MRI of the thalamus in never-medicated patients with schizophrenia. Am J Psychiatry  1996; 153:191—199
[PubMed]
 
Silbersweig DA, Stern E, Frith C, et al: A functional neuroanatomy of hallucinations in schizophrenia. Nature  1995; 378:176—179
[CrossRef] | [PubMed]
 
Pakkenberg B: Pronounced reduction of total neuron number in mediodorsal thalamic nucleus and nucleus accumbens in schizophrenia. Arch Gen Psychiatry 1990; 47:1023—  1028
 
Neiman J, Litton J-E: Reduced [11C]flumazenil radioligand binding in the thalamus in alcoholics. Addiction Biology  2000; 5:97—99
[CrossRef] | [PubMed]
 
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References

Tsuang JW, Irwin MR, Smith TL, et al: Characteristics of men with alcoholic hallucinosis. Addiction  1994; 89:73—78
[CrossRef] | [PubMed]
 
Soyka M: Pathophysiologic characteristics in alcohol hallucinosis and paranoid schizophrenia. Acta Psychiatr Scand  1990; 81:255—259
[CrossRef] | [PubMed]
 
Soyka M: Psychopathological mechanisms possibly involved in the development of alcohol hallucinosis. Addiction  1995; 90:289—290
[CrossRef] | [PubMed]
 
Glass IB: Alcohol hallucinosis: a psychiatric enigma, I: the development of an idea. Br J Addict  1989; 84:29—41
[CrossRef] | [PubMed]
 
Buchsbaum MS, Someya T, Teng CY, et al: PET and MRI of the thalamus in never-medicated patients with schizophrenia. Am J Psychiatry  1996; 153:191—199
[PubMed]
 
Silbersweig DA, Stern E, Frith C, et al: A functional neuroanatomy of hallucinations in schizophrenia. Nature  1995; 378:176—179
[CrossRef] | [PubMed]
 
Pakkenberg B: Pronounced reduction of total neuron number in mediodorsal thalamic nucleus and nucleus accumbens in schizophrenia. Arch Gen Psychiatry 1990; 47:1023—  1028
 
Neiman J, Litton J-E: Reduced [11C]flumazenil radioligand binding in the thalamus in alcoholics. Addiction Biology  2000; 5:97—99
[CrossRef] | [PubMed]
 
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