Nuklearmedizin - NuclearMedicine, Table of Contents

Nuklearmedizin 1997; 36(06): 194-201
DOI: 10.1055/s-0038-1629739

Originalarbeiten — Original Articles

Schattauer GmbH

Altered Relationships Between rCBF in Different Brain Regions of Never-Treated Schizophrenics

Abnormale interregionale rCBF-Korrelationen bei noch nie behandelten, floride psychotischen, schizophrenen Patienten

O. Sabri

¹From the Departments of Nuclear Medicine and Aachen, Germany

,

R. Erkwoh

²Psychiatry, Aachen University of Technology, Aachen, Germany

,

M. Schreckenberger

¹From the Departments of Nuclear Medicine and Aachen, Germany

,

U. Cremerius

¹From the Departments of Nuclear Medicine and Aachen, Germany

,

A. Owega

²Psychiatry, Aachen University of Technology, Aachen, Germany

,

C. Diekmann

¹From the Departments of Nuclear Medicine and Aachen, Germany

,

G. Schulz

¹From the Departments of Nuclear Medicine and Aachen, Germany

,

M. Zimny

¹From the Departments of Nuclear Medicine and Aachen, Germany

,

H. Sass

²Psychiatry, Aachen University of Technology, Aachen, Germany

,

U. Buell

¹From the Departments of Nuclear Medicine and Aachen, Germany

› Author Affiliations

Summary

Aim of this study was to investigate the relations between regiona cerebral blood flow (rCBF) of different brain regions in acute schizophrenia and following neuroleptic treatment.

Methods: Twenty-two never-treated, acute schizophrenic patients were examined with HMPAO brain SPECT and assessed psychopathological-ly, and reexamined following neuroleptic treatment (over 96.8 days) and psychopathological remission. rCBF was determined by region/cerebel-lar count quotients obtained from 98 irregular regions of interest (ROIs), summed up to 11 ROIs on each hemisphere. In acute schizophrenics, interregional rCBF correlations of each ROI to every other ROI were compared to the interregional correlations following neuroleptic treatment and to those of controls.

Results: All significant correlations of rCBF ratios of different brain regions were exclusively positive in controls and patients. In controls, all ROIs of one hemisphere except the mesial temporal ROI correlated significantly to its contralateral ROI. Each hemisphere showed significant frontal-temporal correlations, as well as cortical-subcortical and some cortico-limbic. In contrast, in acute schizophrenics nearly every ROI correlated significantly with every other ROI, without a grouping or relation of the rCBF of certain ROIs as in controls. After neuroleptic treatment and clinical improvement, this diffuse pattern of correlations remained.

Conclusions: These results indicate differences in the neuronal interplay between regions in schizophrenic and healthy subjects. In never-treated schizophrenics, diffuse interregional rCBF correlations can be seen as a sign of change and dysfunction of the systems regulating specificity and diversity of the neuronal functions. Neuroleptic therapy and psychopathologic remission showed no normalizing effect on interregional correlations.

Zusammenfassung

Ziel der vorliegenden Studie war es, die Beziehungen zwischen den rCBF-Werten von verschiedenen Hirnregionen bei noch nie behandelten, floride psychotischen, schizophrenen Patienten vor und nach neuroleptischer Medikation mit denen von Kontrollen zu vergleichen.

Methode: Zweiundzwanzig erstmanifeste Patienten wurden drug-naiv und nach neuroleptischer Medikation (96,8 Tage) und klinischer Besserung mit HMPAO-SPECT sowie psychiatrisch untersucht. rCBF wurde durch 98 ROIs, die zu je 11 Summen-ROIs auf jeder Hemisphäre zusammengefaßt wurden, durch Normierung auf das Zerebellum ausgewertet. Die interregionalen rCBF-Korrelationen von jeder Summen-ROI zu allen anderen Summen-ROIs der floriden Schizophrenen wurden verglichen vor und nach Therapie sowie mit dem Kontrollkollektiv (n = 20).

Ergebnisse: Alle signifikanten rCBF-Korrelationen waren bei Patienten und Kontrollen positiv. Bei den Kontrollen korrelierte der rCBF jeder Summen-ROI einer Hemisphäre mit Ausnahme der mesial temporalen signifikant zur korrespondierenden kontralateralen ROI. Weiterhin zeigten sich signifikante rCBF-Korrelationen frontal-temporal, kortikal-subkortikal sowie auch einige kortiko-limbische innerhalb der jeweiligen Hemisphäre. Im Gegensatz dazu korrelierte bei floriden Schizophrenen der rCBF praktisch jeder Summen-ROI mit allen anderen. Eine Gruppierung des rCBF nur bestimmter Regionen wie bei den Kontrollen war nicht zu erkennen. Auch nach neuroleptischer Therapie und klinischer Besserung änderte sich dieses diffuse Korrelationsmuster nicht.

Schlußfolgernd zeigen diese Resultate Unterschiede im neuronalen Netzwerk verschiedener Hirnregionen zwischen Schizophrenen und Kontrollen, was als Dysfunktion der die Spezifität und Vielfalt der neuronalen Funktionen regulierenden Systeme gedeutet wird. Erstmalig wurde gezeigt, daß kein normalisierender Effekt einer neuroleptischen Behandlung und klinischen Besserung auf die diffusen Interkorrelationen besteht.

Keywords

Keywords

HMPAO brain SPECT - rCBF - never-treated schizophrenics - PANSS - neuroleptic treatment - interregional correlations

Schlüsselwörter

Schlüsselwörter

HMPAO-Hirn-SPECT - rCBF - drug-naive Schizophrene - PANSS - neuroleptische Behandlung - interregionale Korrelationen

REFERENCES
1 Brodie JD, Christman DR, Corona JF. et al. Patterns of metabolic activity in the treatment of schizophrenia. Ann Neurol 1984; 15: 166-9.
2 Buchsbaum MS, Ingvar DH, Kessler R. et al. Cerebral glucography with positron tomography. Use in normal subjects and in patients with schizophrenia. Arch Gen Psychiatry 1982; 39: 251-9.
3 Farkas T, Wolf AP, Jaeger J, Brodie JD, Christman DR, Fowler JS. et al. Regional brain glucose metabolism in chronic schizophrenia. A positron emission transaxial tomographic study. Arch Gen Psychiatry 1984; 41: 293-300.
4 Ingvar DH, Franzen G. Abnormalities of cerebral blood flow distribution in patients with chronic schizophrenia. Acta Psychiatr Scand 1974; 50: 425-62.
5 Lewis SW, Ford RA, Syed GM, Reveley AM, Toone BU. A controlled study of Tc-99m-HMPAO single-photon emission imaging in chronic schizophrenia. Psychol Med 1992; 22: 27-35.
6 Wolkin A, Jaeger J, Brodie JD. et al. Persistence of cerebral metabolic abnormalities in chronic schizophrenia as determined by positron emission tomography. Am J Psychiatry 1985; 142: 564-71.
7 Catafau AM, Parellada E, Lomena FJ. et al. Prefrontal and temporal blood flow in schizophrenia. J Nucl Med 1994; 35: 935-41.
8 Cleghorn JM, Garnett ES, Nahmias C. et al. Increased frontal and reduced parietal glucose metabolism in acute untreated schizophrenia. Psychiatry Res 1989; 28: 119-33.
9 Szechtman H, Nahmias C, Garnett ES. et al. Effect of neuroleptics on altered cerebral glucose metabolism in schizophrenia. Arch Gen Psychiatry 1988; 45: 523-32.
10 Volkow ND, Brodie JD, Wolf AP, Angrist B, Rüssel J, Cancro R. Brain metabolism in patients with schizophrenia before and after acute neuroleptic administration. J Neurol Neurosurg Psychiatry 1986; 49: 1199-202.
11 Wiesel FA, Wik G, Sjögren I, Blomqvist G, Greitz T, Stone-Elander S. Regional brain glucose metabolism in drug-free schizophrenic patients and clinical correlates. Acta Psychiatr Scand 1987; 76: 628-41.
12 Sheppard G, Manchanda R, Gruzelier J. et al. 15-Ö positron emission tomographic scanning in predominantly never-treated acute schizophrenic patients. Lancet 1983; 2: 1448-52.
13 Devous MD Sr, Paulman RG, Herman J. et al. Single-photon tomography studies with schizophrenic patients. J Clin Exp Neuropsy-chol 1988; 10: 321-2.
14 Paulman RG, Devous MD Sr, Gregory RR. et al. Hypofrontality and cognitive impairment in schizophrenia: dynamic single-photon tomography and neuropsychological assessment of schizophrenic brain function. Biol Psychiatry 1990; 27: 377-99.
15 Sabri O, Erkwoh R, Schreckenberger M. et al. Regional cerebral blood flow and negative/positive symptoms in drug-naive schizophrenics. J Nucl Med 1997; 38: 181-8.
16 American Psychiatric Association.. DSM-III-R. In: Diagnostic and Statistical Manual of Mental Disorders, 3rd edition-revised. Washington DC: American Psychiatric Press; 1987
17 Kay SR, Fiszbein A, Opler LA. The positive and negative syndrome scale (PANSS) for schizophrenia. Schizophr Bull 1987; 13 (Suppl. 02) 261-76.
18 Kaiser HJ, Sabri O, Wagenknecht G, Lege B, Hellwig D, Buell U. A method of correlating and merging cerebral morphology and function by a special headholder. Nuklearmedizin 1994; 33: 123-6.
19 Sabri O, Hellwig D, Kaiser HJ. et al. Effects of Morphological Changes on Perfusion and Metabolism in Cerebral Microangiopathy. Nuklearmedizin 1995; 34: 50-6.
20 Neirinckx RD, Burke JF, Harrison RC. et al. The retention of technetium-99m HMPAO: intracellular reaction with glutathione. J Cereb Blood Flow Metab 1988; (Suppl) 8: 4.
21 Costa DC, Ell PJ, Cullum ID. et al. The in vivo distribution of ^99mTc-HMPAO in normal man. Nucl Med Commun 1986; 7: 647-58.
22 Chang LT. A method for attenuation correction in radionuclide computed tomography. IEEE Trans Nucl Sei 1978; 25: 638-43.
23 Syed GMS, Barret JJ, Toone BK. What does rCBF SPECT offer in schizophrenia?. Nucl Med Commun 1992; 13: 879-84.
24 Syed GMS, Eagger S, Toone BK. et al. Quantification of regional cerebral blood flow (rCBF) using 99Tcm-HMPAO and SPECT: choice of the reference region. Nucl Med Commun 1992; 13: 811-6.
25 Talairach J, Szlika G. Atlas d’anatomie stéréotaxique du télencéphale. Paris: Masson; 1967
26 Kretschmann HJ, Weinrich W. Klinische Neuroanatomie und kranielle Bilddiagnostik, 2nd edition. Stuttgart, New York: Thieme; 1991
27 Kojima A, Matsumoto M, Takahashi M. et al. Effect of spatial resolution on SPECT quantification values. J Nucl Med 1989; 30: 508-14.
28 Bortz J. Partialkorrelation und Multiple Korrelation. In: Statistik für Sozialwissenschaftler, 4th edition. Bortz J. (ed). Berlin, Heidelberg, New York: Springer; 1993: 411-46.
29 Benes FM, Davidson J, Bird ED. Quantitative cyto-architectural studies of the cerebral cortex of schizophrenics. Arch Gen Psychiatry 1986; 43: 31-5.
30 Wiesel FA, Wik G, Sjögren I, Blomqvist G, Greitz T. Altered relationship between metabolic rates of glucose in brain regions of schizophrenic patients. Acta psychiatr Scand 1987; 76: 642-7.
31 Friston KJ, Frith CD, Passingham RE. et al. Entropy and cortical activity: information theory and PET findings. Cerebral Cortex 1992; 2: 259-67.
32 Nauta WJH. The problem of the frontal lobe: A reinterpretation. J Psychiatr Res 1971; 8: 167-87.
33 Selemon LD, Goldman-Rakic PS. Longitudinal topography and interdigita of corticostri-atal projections in the rhesus monkey. J Neuroscience 1985; 5: 776-94.
34 Gloor P. Role of the human limbic system in perception, memory, and affect: Lessons from temporal lobe epilepsy. In: The limbic system. Functional organization and clinical disorders. Doane BK, Livingston KE. (eds). New York: Raven Press; 1986: 159-69.
35 Ebmeier KP, Blackwood DHR, Murray C. et al. Single-Photon Emission Computed Tomography with ^99mTc-Exametazime in Unmedicated Schizophrenic Patients. Biol Psychiatry 1993; 33: 487-95.
36 Crow TJ. Temporal lobe asymmetries as the key to the etiology of schizophrenia. Schizophr Bull 1990; 16: 433-43.
37 Horwitz B, Duara R, Rapoport SI. Age ^v Differences in Intercorrelations between Regional Cerebral Metabolic Rates for Glucose. Ann Neurol 1986; 19: 60-7.
38 Sabri O, Erkwoh R, Schreckenberger M, Owega A, Sass H, Buell U. Correlation of positive symptoms exclusively to hyperper-fusion or hypoperfusion of cerebral cortex in never-treated schizophrenics. Lancet 1997; 349: 1735-9.