Stroke. 1998;29:1149-1154
(Stroke. 1998;29:1149-1154.)
© 1998 American Heart Association, Inc.
Cerebral Blood Flow Velocity in Acute Schizophrenic Patients
A Transcranial Doppler Ultrasonography Study
Ammar Owega, MD;
Jürgen Klingelhöfer, MD;
Osama Sabri, MD;
Hanns Jürgen Kunert, PhD;
Matthias Albers, MD;
Henning Saß, MD
From the Departments of Psychiatry and Psychotherapy (A.O., H.J.K., M.A.,
H.S.) and Nuclear Medicine (O.S.), University of Technology (RWTH), Aachen,
Germany, and the Department of Neurology (J.K.), Technical University, Munich,
Germany.
Correspondence to Ammar Owega, MD, Department of Psychiatry and Psychotherapy, University of Technology (RWTH), Pauwelsstrasse 30, D-52074 Aachen, Germany.
 |
Abstract
|
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Background and PurposeThe aim of
this study was to determine whether acutely psychotic first-episode
schizophrenics show an increased cerebral blood flow velocity and
whether this condition is reversible on psychopathological
improvement.
MethodsIn the first of two examinations,
transcranial Doppler ultrasonography and assessment
with the Positive and Negative Syndrome Scale (PANSS) were performed on
28 acutely psychotic, neuroleptically naive, first-episode
schizophrenics. In the second examination, the same patients were
assessed psychometrically (PANSS) as well as with Doppler
ultrasonography after psychopathological improvement.
ResultsAcutely psychotic first-episode schizophrenics showed a
significant increase of the mean velocity on both sides in the middle
and anterior cerebral arteries and in the right posterior cerebral
artery. Blood flow showed significant correlations with productive
psychotic symptoms. After psychopathological improvement there was a
bilateral normalization of the mean velocity in the middle, anterior,
and posterior cerebral arteries.
ConclusionsAcutely psychotic first-episode schizophrenics show a
significantly increased bilateral cerebral blood flow velocity, which
normalizes on psychopathological improvement. There were significant
correlations of cerebral blood flow velocity with psychopathology.
Key Words: blood flow velocity cerebral blood flow schizophrenia ultrasonography, Doppler
 |
Introduction
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Blood flow changes in
schizophrenia have been demonstrated with SPECT and PET but with
inconsistent findings.1 2 3 Most studies
deal mainly with chronic schizophrenia, and the essential finding is
hypoperfusion. Using 133Xe inhalation, Ingvar and
Franzén4 were the first to report
hypofrontality in schizophrenics. Some recent imaging studies on acute
schizophrenia5 describe hyperperfusion in the
supply areas of the MCA and the ACA, occasionally with a left-side
predominance. An investigation of brain activity in schizophrenics
depends on the profile of the particular target symptom and on how
strongly it is pronounced in the patient group.6
Hoyer and Österreich7 found that acutely
psychotic schizophrenics show an increase in global cerebral perfusion
of about twice the normal value, whereas in chronic schizophrenics this
parameter is significantly lower than in acute
schizophrenics or healthy control subjects, without a significant
difference between control subjects and patients with paranoia or
schizophrenia simplex. It should thus be possible to demonstrate a
correlation between psychotic state and CBFV.
TCD is a standard method in neurology and neurosurgery but is not
yet widely used in psychiatry, and no systematic neuropsychiatric
studies have used this method. CBFV measurements by TCD show a high
reliability8 9 10 11 and correlation with
rCBF.12 13 14 15 TCD can locate vessels and quantify
blood flow velocity with precision,16 thus
allowing an accurate identification of the vessel irrigating the brain
area in question. CBFV is the decisive Doppler
parameter since flow velocity varies directly with the
diameter of the small resistance vessels, whereas the diameter of the
basal cerebral arteries remains essentially
constant.17 18 Given that CBF equals CBFV times
vessel diameter, where vessel diameter equals
r2, then CBFV is a direct indicator of
CBF.19 There are no known changes in vessel
diameter in schizophrenia, since this condition in and of itself does
not affect the blood vessels, and first-episode acute schizophrenic
patients not suffering from other diseases will not, as a rule, show
pathomorphological vessel changes.
It was the aim of this study to determine by means of TCD whether
there is a difference in the CBFV of the basal cerebral arteries under
resting conditions in acute schizophrenic patients and normal control
subjects; whether this difference is reversible after
psychopathological improvement; and what correlations exist between
schizophrenic symptoms (assessed by PANSS) and blood flow velocity in
the ACA, MCA, and PCA.
 |
Subjects and Methods
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Subjects
Subjects were 28 acutely psychotic, neuroleptically naive,
first-episode schizophrenic patients, diagnosed according to the
Diagnostic and Statistical Manual of Mental
Disorders, Fourth Edition and the International
Classification of Diseases, Ninth Revision, and screened according
to the usual exclusion criteria, ie, schizoaffective, bipolar mood,
organic brain, or any general neurological or medical disorder; mental
retardation; a history of severe head trauma, vascular-associated
headache, substance abuse, or neuroleptic treatment; age <18 or >65
years; and pregnancy. Controls were 20 age-matched normal subjects. The
mean age of patients was 33±12 years (15 male, 13 female), and that of
control subjects (10 male, 10 female) was 32±10 years. Each patient
gave informed consent and had extracranial and transcranial Doppler
ultrasonography and a cranial CT scan done before inclusion into the
study to screen out individuals with pathological findings. All
patients and control subjects had normal blood pressure
(systolic <140 mm Hg, diastolic <90
mm Hg). The first examination was done in the acute psychotic state
and the second after neuroleptic treatment and psychopathological
improvement, defined as a decrease of
50% of positive sum scores on
PANSS. Choice of neuroleptic drugs and dosage depended exclusively on
the individual target syndrome, which aimed at psychopathological
remission. Patients were assessed psychometrically both times with
PANSS,20 a 33-item scale with 1 to 7 points
(normal to extremely abnormal) for each item and subscores for 7
positive, 7 negative, and 16 global psychopathological symptoms:
delusions, formal thought disorders, hallucinations, agitation,
grandiosity, suspiciousness/persecution, and hostility (P1 to P7);
blunted affect, emotional withdrawal, poor rapport, social passivity
and apathy, difficulty in abstract thinking, lack of spontaneity and
flow of conversation, and stereotyped thinking (N1 to N7); and health
concerns, anxiety, guilt, tension, mannerisms and posturing,
depression, motor retardation, uncooperative behavior, unusual thought
contents, disorientation, poor attention, lack of judgment and insight,
avolition, poor impulse control, self-centeredness, and active social
avoidance (G1 to G16).
Transcranial Doppler Ultrasonography
For each examination, simultaneous bilateral
insonation was done sequentially on the basal MCA, ACA, and PCA with a
2-MHz pulsed-wave transducer probe (Neurogard, Medasonics).
The test-retest reliability found for the ACA, MCA, and PCA in the 20
healthy control subjects was 0.90<r<0.95. After resting
for 5 minutes, patients and control subjects were insonated under
standard resting conditions (supine position, eyes closed, darkened
room). Arteries were insonated transtemporally above the
zygomatic arch, and CBFV was measured at a depth of 50 to 55 mm
(MCA) and 60 to 70 mm (ACA, P2 segment of the
PCA).9 16 Recording of mean blood flow
velocities was started when no change in either the velocities or the
heart rate was observed over 15 successive cardiac cycles. Mean
(Vmean), systolic
(Vsyst), and diastolic
(Vdiast) blood flow velocities were determined.
The PI was determined as follows21,22:
 |
Statistical Analysis
CBFV values between schizophrenics and control subjects were
compared with the use of t tests for independent samples;
comparisons between examinations for CBFV and PI were made with
t tests for paired samples. The relationship between CBFV
and single symptoms was analyzed with Pearson correlations. All
calculations were done with the use of SAS
6.12.23
 |
Results
|
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The Vmean in the MCA and the ACA showed a
bilaterally significant increase (0.001<P<0.05) during the
acute psychotic stage compared with that of age-matched normal control
subjects (Table 1
). Velocities in the PCA were
marginally increased; only the right side showed a significantly
changed Vmean, while the change in the left side
remained below the level of significance (P>0.05). During
the acute stage, the PI was lowered in all insonated vessels, but this
did not reach significance (P>0.05) (Table 1
).
The increases in the MCA and the ACA correlated positively with the
positive sum score (0.55
r
0.59,
0.001<P<0.05) (Table 2
).
Delusions showed a positive correlation with blood flow velocity in the
MCA and ACA (0.52
r
0.58, 0.001<P<0.005) and
the left PCA (r=0.58, P=0.001), and grandiosity
showed a positive correlation with blood flow velocity in the MCA
(r=0.54, P=0.003). There were negative
correlations for lack of spontaneity and flow of conversation (negative
symptom 6) with the left MCA (r=-0.51, P=0.006),
negative correlations for motor retardation (global psychopathology
symptom 7) bilaterally both with the MCAs (r=-0.58,
P=0.001) and with the ACAs (r=-0.51,
P=0.005), and a negative correlation with the left MCA
(r=-0.52, P=0.005). All other PANSS symptoms
showed no significant correlation with the ACA, the MCA, or the PCA on
either side.
After psychopathological improvement there was a significant
(0.001<P<0.05) bilateral reduction in the
Vmean (Figure
),
with decreases bilaterally in the MCA and
the ACA. The PCA showed slightly significant changes on the right side.
Flow velocities in all vessels examined (ACA, MCA, PCA) returned to
normal levels and no longer differed significantly from those of normal
subjects (Table 3
). The PI showed a
significant increase in the left MCA (+0.078); the other vessels showed
a slight increase just below the level of significance.
 |
Discussion
|
|---|
It is hypothesized that acute schizophrenics show a state of
increased brain activity24 and therefore an
increased metabolic rate. An increased
metabolic rate requires an increased blood supply and
therefore a greater flow volume. Blood flow velocity is directly
related to flow volume.15 An increased velocity
therefore implies a correspondingly greater blood volume, which in turn
indicates increased brain activity.25 26 27
It may be argued that the increased CBFV seen in acute schizophrenics
is due to vasoconstriction. However, vasoconstriction would
considerably decrease brain perfusion, which in turn would result in
lowered oxygenation and glucose supply; under such
conditions, however, sustained activity is hardly possible.
Furthermore, there is no pathomorphological evidence for
vasoconstriction in schizophrenia. Studies on first-episode and
unmedicated schizophrenics are few,28 and unlike
studies with chronic schizophrenics, which exhibit
hypoperfusion,29 most studies on acute
schizophrenics have found a hyperperfusion in the frontotemporal
region.5 This hyperperfusion correlates
positively with at least some acute schizophrenic symptoms and their
severity,30 as imaging studies have
shown.3 5 28 31
This study is the first to demonstrate locally increased CBFV in
first-episode acute schizophrenics against age-matched normal control
subjects with the use of TCD. Increases were most pronounced in the MCA
and the ACA on both sides. These vessels supply the frontal and the
temporal lobes, which are actively involved in schizophrenia, where
Catafau et al5 found a slightly higher flow on
the left side. However, when we compared absolute values, our results
show the same left-side tendency. The increased flow velocities
correlated positively with acute psychotic symptoms as measured by
PANSS. Positive correlations of acute psychotic symptoms and rCBF
measured with 99mTc-HMPAO SPECT were also
reported by Sabri et al28 and Silbersweig et
al.30 After neuroleptic therapy and
psychopathological improvement, brain activity returned to near-normal
levels. The CBFV, although it remained marginally higher, also returned
to within normal values. It would therefore seem that cerebral blood
flow is a state (rather than a trait) marker.
In addition to the frontotemporal region, acutely psychotic
schizophrenic patients show an increased blood flow in the posterior
region.32 In the schizophrenic patients examined
in this study, we also found marginally increased velocities in the
PCA, which even showed a positive correlation with delusions. This
would indicate that the occipital region is also actively involved in
acute schizophrenia,33 34 and in our study we
found that velocities in the PCA (which also irrigates the occipital
region) show a marginal to significant increase relative to normal
control subjects and a weakly significant decrease after
psychopathological improvement.
Furthermore, associations between local blood flow changes and
specific psychopathological syndromes indicate the areas of irrigation
affected. The negative correlations for lack of spontaneity and flow of
conversation to blood flow velocity in the left MCA could indicate an
effect of decreased perfusion in the speech center. Vessels that do not
supply this area showed no significant correlation. Motor retardation
showed negative correlations bilaterally with both MCAs and ACAs, which
supply the motor centers. Since the PCA does not irrigate this area, no
correlations were found. These two findings show a direct correlation
of changes in the activity of functions that have been mapped
neuroanatomically, such as the speech or motor functions, with changes
in the blood flow velocity of the artery supplying their brain
areas.
Mapping specific psychopathological symptoms to a particular brain
region has been difficult and not entirely free of controversy.
However, we think that the findings in this study may contribute toward
a clearer understanding of this approach. Delusions showed highly
significant positive correlations with blood flow changes in the right
MCA and ACA, and grandiosity showed highly significant positive
correlations with blood flow changes in the MCA. Using
99mTc-HMPAO SPECT, Catafau et
al5 described an increased rCBF in acutely
psychotic schizophrenics bilaterally in the frontotemporal region.
Sabri et al28 also found a bilateral rCBF
increase in the frontotemporal region in acutely psychotic patients. A
similar increase could be shown in ketamine- and
psilocybin-induced experimental psychoses.35
There was a weak negative correlation of negative symptoms (assessed by
PANSS) with the MCA. Thus, the more pronounced the negative symptoms,
the lower are the CBFV values in the corresponding areas. Since
negative symptoms in chronic schizophrenics correlate with
hypoperfusion, it is interesting that we have found negative symptoms
in acute schizophrenics to correlate with a lowered CBFV. It would be
interesting to reexamine acute schizophrenic patients after a few years
and then in the chronic stage of their illness to verify whether
hyperperfusion first normalizes and then progresses to
hypoperfusion.
Further studies are needed to clarify how TCD can be used in
follow-up monitoring to identify and distinguish therapy responders
from nonresponders and whether it can yield additional information on
the course of therapy and possibly even be used as a predictor
variable (warning signs). Since it relies only on physically
measurable physiological parameters
(unlike psychometric evaluation methods), TCD can contribute toward a
more objective diagnosis of schizophrenia. An increase in the
Vmean could thus indicate a first or renewed
exacerbation of illness. In high-risk individuals (first-degree
relatives), onset of illness could be detected early by means of such
an increase and so be treated while still in the early stages, thereby
improving prognosis and shortening the hospital stay. Further empirical
studies are needed, particularly to evaluate the critical cutoff points
(areas) to distinguish the various subgroups of schizophrenic patients
regarding responders versus nonresponders.
This study suggests that, in addition to purely clinical fields such as
neurosurgery and neurology, in which it has long been used, TCD also
holds great potential for psychiatry. Thus, a new range of applications
could open up for TCD, particularly in view of its high temporal
resolution, which could be essential for examinations requiring
real-time monitoring.
Conclusions
CBFV was shown to be a possible indicator of acute schizophrenia
when acutely psychotic schizophrenic patients were compared with
age-matched control subjects and schizophrenic patients after
psychopathological improvement. Since it is noninvasive, TCD also
allows practically unlimited repeated measurements for blood flow
velocity status reports and follow-up; it is also readily available and
requires little preparation. Furthermore, a combination of the high
temporal resolution of TCD and the high spatial resolution of imaging
procedures such as PET and SPECT may result in further understanding of
the pathophysiological processes of mental illness
and thus may contribute toward more effective therapy.
 |
Selected Abbreviations and Acronyms
|
|---|
| ACA |
= |
anterior cerebral artery |
| CBF, rCBF |
= |
cerebral blood flow, regional cerebral blood flow |
| CBFV |
= |
cerebral blood flow velocity |
| HMPAO |
= |
hexamethylpropyleneamine oxime |
| MCA |
= |
middle cerebral artery |
| PANSS |
= |
Positive and Negative Syndrome Scale |
| PCA |
= |
posterior cerebral artery |
| PET |
= |
positron emission tomography |
| PI |
= |
pulsatility index |
| SPECT |
= |
single-photon emission computed tomography |
| TCD |
= |
transcranial Doppler ultrasonography |
| Vmean |
= |
mean blood flow velocity |
|
 |
Acknowledgments
|
|---|
This study was supported by the Research Committee of the
University of Technology Aachen, Medilab Ltd (Estenfeld, Germany), and
Weinmann Ltd (Hamburg, Germany). Thanks are also due to A. Rodón
for translation and editing.
Received February 10, 1998;
revision received March 13, 1998;
accepted March 13, 1998.
 |
References
|
|---|
-
DeLisi LE, Holcomb HH, Cohen RM, Pickar D,
Carpenter WT, Morihisa JM, King AC, Kessler RM. Positron emission
tomography (PET) in schizophrenic patients on and off neuroleptic
medication. J Cereb Blood Flow Metab.. 1985;5:201206.[Medline]
[Order article via Infotrieve]
-
Gur RE, Resnick SM, Alavi A, Gur RC, Caroff S, Dann R,
Silver FR, Saykin AJ, Chawluk JB, Kushner M, Reivich M. Regional brain
function in schizophrenia, I: a positron emission tomography study.
Arch Gen Psychiatry.. 1987;44:119125.[Abstract]
-
Szechtman HJ, Nahmias C, Garnett ES, Firnau G, Brown
GM, Kaplan RD, Cleghorn JM. Effect of neuroleptics on altered cerebral
glucose metabolism in schizophrenia. Arch Gen
Psychiatry.. 1988;45:523532.[Abstract]
-
Ingvar DH, Franzén G. Distribution of cerebral
activity in chronic schizophrenia. Lancet.. 1974;2:14841486.[Medline]
[Order article via Infotrieve]
-
Catafau AM, Parellada E, Lomeña FJ, Bernardo M,
Pavía J, Ros D, Setoain J, Gonzalez-Monclús E. Prefrontal
and temporal blood flow in schizophrenia: resting and activation
technetium-99m-HMPAO-SPECT patterns in young
neuroleptic-naive patients with acute disease. J Nucl
Med.. 1994;35:935941.[Abstract/Free Full Text]
-
Dolan RJ, Bench CJ, Liddle PF, Friston KJ, Frith CD,
Grasby PM, Frackowiak RS. Dorsolateral prefrontal cortex dysfunction in
the major psychoses: symptom or disease specificity? J
Neurol Neurosurg Psychiatry.. 1993;56:12901294.[Abstract]
-
Hoyer S, Österreich K. Blood flow and oxidative
metabolism of the brain in patients with schizophrenia.
Psychiatria Clin.. 1975;8:304313.
-
Saunders C, Salles-Cunha S, Andros G.
Transcranial Doppler: reproducibility of velocity
measurements in the middle cerebral artery. J Vasc Technol.. 1990;14:3032.
-
Sorteberg W, Langmoen IA, Lindegaard K-F, Nornes H.
Side-to-side differences and day-to-day variations of
transcranial Doppler parameters in normal
subjects. J Ultrasound Med.. 1990;9:403409.[Abstract]
-
Larsen FS, Olsen KS, Hansen BA, Paulson OB, Knudsen GM.
Transcranial Doppler is valid for determination of the
lower limit of cerebral blood flow autoregulation. Stroke.. 1994;25:19851988.[Abstract]
-
Alexandrov AV, Brodie DS, McLean A, Hamilton P, Murphy
J, Burns PN. Correlation of peak systolic velocity and
angiographic measurement of carotid stenosis revisited.
Stroke.. 1997;28:339342.[Abstract/Free Full Text]
-
Bishop CCR, Powell S, Rutt D, Browse NL.
Transcranial Doppler measurements of middle cerebral
artery blood flow velocity: a validation study. Stroke.. 1986;17:913915.[Abstract/Free Full Text]
-
Dahl A, Lindegaard K-F, Russell D, Nyberg-Hansen R,
Rootwelt K, Sorteberg W, Nornes H. A comparison of
transcranial Doppler and cerebral blood flow studies to
assess cerebral vasoreactivity. Stroke.. 1992;23:1519.[Abstract/Free Full Text]
-
Kirkham FJ, Padayachee TS, Parson S, Seargeant LS,
House FR, Gosling RG. Transcranial measurement of blood
velocities in the basal cerebral arteries using pulsed Doppler
ultrasound: velocity as an index of flow. Ultrasound Med
Biol.. 1986;12:1521.[Medline]
[Order article via Infotrieve]
-
Newell DW, Aaslid R, Lam A, Mayberg TS, Winn HR.
Comparison of flow and velocity during dynamic autoregulation testing
in humans. Stroke.. 1994;25:793797.[Abstract]
-
Aaslid R, Markwalder T-M, Nornes H. Noninvasive
transcranial Doppler ultrasound recording of
flow velocity in basal cerebral arteries. J Neurosurg.. 1982;57:769774.[Medline]
[Order article via Infotrieve]
-
Huber P, Handa J. Effect of contrast material,
hypercapnia, hyperventilation, hypertonic glucose and papaverine on the
diameter of the cerebral arteries. Invest Radiol.. 1967;2:1732.[Medline]
[Order article via Infotrieve]
-
Newell DW, Aaslid R. Transcranial
Doppler: clinical and experimental uses. Cerebrovasc Brain
Metab Rev.. 1992;4:122143.[Medline]
[Order article via Infotrieve]
-
Diehl RR, Berlit P. Funktionelle
Dopplersonographie in der Neurologie. Heidelberg, Germany:
Springer; 1996.
-
Kay SR, Fiszbein A, Opler LA. The Positive and Negative
Syndrome Scale (PANSS) for schizophrenia. Schizophr Bull.. 1987;13:261276.
-
Gosling RG, King DH. Arterial assessment by
Doppler-shift ultrasound. Proc Roy Soc Med.. 1974;67:447449.[Medline]
[Order article via Infotrieve]
-
Gosling RG. Doppler ultrasound assessment of
occlusive arterial disease.
Practitioner.. 1978;220:599609.[Medline]
[Order article via Infotrieve]
-
SAS® Version 6.12: SAS/STAT Software: Changes
and Enhancements. Cary, NC: SAS Institute Inc; 1996.
-
Gur RE, Gur RC, Skolnick BE, Caroff S, Obrist WD,
Resnick S, Reivich M. Brain function in psychiatric disorders, III:
regional cerebral blood flow in unmedicated schizophrenics. Arch
Gen Psychiatry.. 1985;42:329334.[Abstract]
-
Silvestrini M, Cupini LM, Matteis M, Troisi E,
Caltagirone C. Bilateral simultaneous assessment of
cerebral flow velocity during mental activity. J Cereb Blood
Flow Metab.. 1994;14:643648.[Medline]
[Order article via Infotrieve]
-
Knecht S, Henningsen H, Deppe M, Huber T, Ebner A,
Ringelstein E-B. Successive adaptation of both cerebral hemispheres
during cued word generation. Neuroreport.. 1996;7:820824.[Medline]
[Order article via Infotrieve]
-
Klingelhöfer J, Sander D, Matzander G, Schwarze
J, Boecker H, Bischoff C. Assessment of functional hemispheric
asymmetry by bilateral simultaneous cerebral blood flow
velocity monitoring. J Cereb Blood Flow Metab.. 1997;17:577585.[Medline]
[Order article via Infotrieve]
-
Sabri O, Erkwoh R, Schreckenberger M, Owega A,
Saß H, Büll U. Correlations of positive symptoms
exclusively to hyperperfusion or hypoperfusion of cerebral cortex in
never-treated schizophrenics. Lancet.. 1997;349:17351739.[Medline]
[Order article via Infotrieve]
-
Andreasen NC, Rezai K, Alliger RJ, Swayze II VW, Flaum
M, Kirchner P, Cohen G, O'Leary DS. Hypofrontality in
neuroleptic-naive patients and in patients with chronic schizophrenia:
assessment with xenon 133 single-photon emission computed tomography
and the Tower of London. Arch Gen Psychiatry.. 1992;49:943958.[Abstract]
-
Silbersweig DA, Stern E, Frith C, Cahill C, Holmes A,
Grootoonk S, Seaward J, McKenna P, Chua SE, Schnorr L, Jones T,
Frackowiak RSJ. A functional neuroanatomy of hallucinations in
schizophrenia. Nature.. 1995;378:176179.[Medline]
[Order article via Infotrieve]
-
Cleghorn JM, Franco S, Szechtman B, Kaplan RD,
Szechtman H, Brown GM, Nahmias C, Garnett ES. Toward a brain map of
auditory hallucinations. Am J Psychiatry.. 1992;149:10621069.[Abstract/Free Full Text]
-
Schröder J. Subsyndrome der chronischen
Schizophrenie: Ein psychopathologisches Konzept im Spiegel bildgebender
Verfahren. Heidelberg, Germany: University of Heidelberg; 1994.
Thesis.
-
Freeman T, Karson CN. The neuropathology of
schizophrenia: a focus on the subcortex. Psychiatr Clin North
Am.. 1993;16:281293.[Medline]
[Order article via Infotrieve]
-
Frith CD, Friston J, Herold S, Silbersweig D, Fletcher
P, Cahill C, Dolan RJ, Frackowiak RSJ, Liddle PF. Regional brain
activity in chronic schizophrenic patients during the
performance of a verbal fluency task. Br J
Psychiatry.. 1995;167:343349.[Abstract/Free Full Text]
-
Vollenweider FX, Leenders KL, Scharfetter C, Antonini
A, Maguire P, Missimer J, Angst J. Metabolic
hyperfrontality and psychopathology in the ketamine model of
psychosis using positron emission tomography (PET) and
[18F]fluorodeoxyglucose (FDG). Eur Neuropsychopharmacol.. 1997;7:924.[Medline]
[Order article via Infotrieve]
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