Talking psychiatry...The neurology of schizophrenia

1. INDEX www.yassermetwally.com
 INTRODUCTION
INTRODUCTION
Recent research has demonstrated that brain abnormalities are present in first-episode schizophrenia
and obsessive-compulsive disorder. There are some pathophysiological similarities, such as deficit of the
frontostriatal circuit, between schizophrenia and obsessive-compulsive disorder, but more structural
abnormalities are involved in schizophrenia. Future studies, investigating the neurological abnormalities
in schizo-obsessive or early-phase psychosis with obsessive-compulsive symptoms, are needed.
Due to the frequent observation of the coexistence of obsessive-compulsive and schizophrenic symptoms
in the same patient, there is growing interest in the pathophysiological overlap between the two
disorders. In order to identify the similarities and disparities between schizophrenia and obsessive-
compulsive disorder, this review summarizes the recent findings from structural/functional

2. neuroimaging, neuropsychological and electrophysiological literature on first-episode schizophrenia and
obsessive-compulsive disorder.
Recent research has identified that structural, cognitive and electrophysiological abnormalities are
present in schizophrenia and obsessive-compulsive disorder. In particular, brain abnormalities are
present even in the early stage of schizophrenia. The deficits in the frontostriatal and frontotemporal
pathways seem to be the pathophysiology of schizophrenia, and frontostriatal deficit is also involved in
obsessive-compulsive disorder. Although the frontostriatal deficit is present both in schizophrenia and
obsessive-compulsive disorder, schizophrenic patients show more structural abnormalities and cognitive
deficits. A few studies directly comparing obsessive-compulsive disorder with schizophrenia have
reported interesting findings on the pathophysiological mechanisms of the same neural circuits with
functional dissociations.
Although schizophrenia and obsessive-compulsive disorder (OCD) are separate psychiatric disorders,
patients having comorbidity of the two disorders are frequently observed in clinical practice, which has
led to the introduction of a new term 'obsessive-compulsive schizophrenia'. Recently, growing interest in
the possible overlaps between schizophrenia and Obsessive-Compulsive Disorder have arisen from
attempts to explain the pathophysiology of the two disorders on the basis of the functional and structural
neuroimaging findings.
Much evidence has been accumulated that suggests abnormalities in brain structure and function are
involved in both schizophrenia and Obsessive-Compulsive Disorder. Abnormalities in the
frontotemporal and frontostriatal pathways have been considered as pathophysiologies of schizophrenia.
The neurological findings in schizophrenia have been criticized for such confounding factors as
medication and the chronicity of the illness. In Obsessive-Compulsive Disorder, deficit in the
frontostriatal circuit has been consistently implicated as a pathophysiology.
In order to identify the similarities and disparities between schizophrenia and Obsessive-Compulsive
Disorder, this review summarizes the findings of the latest studies (November 2002-present) which have
investigated brain abnormalities in patients with schizophrenia and Obsessive-Compulsive Disorder. For
the structural and functional abnormalities in schizophrenia, only studies that employed first-episode
schizophrenia are considered to reduce the effects of confounding factors, such as medication and the
chronicity of the illness. The reviewed studies have been grouped into those studying
structural/functional, neuropsychological and electrophysiological (event-related potentials)
abnormalities in patients with schizophrenia and Obsessive-Compulsive Disorder.
 Brain Abnormalities in Schizophrenia
Recent neuroimaging, neuropsychological and electrophysiological studies investigating the
pathophysiology of first-episode schizophrenia are reviewed.
 Structural Abnormalities in Schizophrenia
Recent studies employing first-episode schizophrenic patients have demonstrated that structural
abnormalities exist in schizophrenia even at the onset of illness. Three studies focused on the
abnormalities of the medial temporal structures. Joyal et al.[1] compared the volumes of amygdala in 18
first-episode, neuroleptic-naïve schizophrenic patients and 22 healthy controls, and found bilaterally
reduced amygdaloid volumes in the patients compared with the controls. Another study[2] demonstrated
the bilaterally enlarged hippocampal fissures in schizophrenic patients (n=33) relative to the healthy
controls (n=19). The authors suggested that the enlarged hippocampal fissures in schizophrenia results
from a failure of the two sides of hippocampal fissures to fuse, indicating a neurodevelopmental origin of
schizophrenia. Szeszko and associates[3] separately measured the volumes of the posterior, anterior
hippocampal formation and amygdala in schizophrenic patients (n=46) and healthy comparison controls

3. (n=34). The patients showed a bilaterally reduced volume of the total anterior hippocampal formation
relative to the controls, but no difference was found in the volumes of either the posterior hippocampal
formation or amygdala.
Four studies investigated the abnormalities of the superior temporal gyrus (STG). Kim et al.[4]
compared the volumes of the lateral STG in male neuroleptic naïve schizophrenic patients (n=25) and
healthy males (n=25). This study found a volume deficit in the posterior STG on the right side, an
inverse correlation between the psychotic symptoms and the left anterior region of the STG (the greater
the severity of the psychosis, the smaller the volume of the anterior region) and a positive correlation
between the negative symptoms and the right posterior segment of the STG (the greater the severity of
the negative symptoms, the larger the volume of the posterior region) in the patient group. Kasai and
colleagues[5] compared patients with first-episode schizophrenia (n=13), first-episode affective psychosis
(n=15) and healthy controls (n=14), in terms of the volumes of the left STG over the first 1.5 years after
initial hospitalization. The schizophrenic patients showed reduced left STG volumes relative to the
patients with affective disorder or the normal controls. Furthermore, patients with schizophrenia
showed significant decreases in the gray matter volume over time in the left STG compared with the
patients with affective psychosis or the healthy controls, and the progressive volumetric decrease was
more prominent in the posterior portions of the left STG than in the anterior portions.
This research group also found a progressive volume reduction in the left Heschl gyrus and left planum
temporale gray matter in patients with schizophrenia in contrast to patients with first-episode affective
psychosis and healthy controls.[6] A bilateral volume reduction in the insular cortex gray matter was
observed in first-episode schizophrenic patients compared with first-episode patients with affective
psychosis and normal controls.[7]
Two studies investigated the abnormalities of the corpus callosum in first-episode schizophrenia.
Diwadkar et al.[8] compared first-episode schizophrenic patients (n=29), patients with first-episode
nonschizophrenic psychosis (n=11) and healthy controls (n=62), in terms of the microstructural integrity
of the corpus callosum. The schizophrenic patients showed reduced signal intensities in all the callosal
subregions including the genu, body, isthmus and splenium, reflecting the interhemispheric
disconnectivity in schizophrenia. Another study[9] found a reduced total corpus callosum and five
subdivisions (genu, rostral body, midbody, isthmus and splenium) in schizophrenic patients (n=31)
compared with the normal controls (n=12).
The gray and white matter volumes in first-episode schizophrenic patients were measured. Bagary et al.
[10] used magnetization transfer imaging, and found a bilateral reduction of the magnetization transfer
ratio in the medial prefrontal cortex, insular, and white matter incorporating the fasciculus uncinatus in
the patients (n=30) relative to the normal controls (n=30). Another study[11] examined the global gray
matter volumes in schizophrenic patients (n=34) and healthy controls (n=36), both at inclusion and after
1 year. On the first scan only the third ventricle volume was significantly larger in the patients than in
the controls, but on the second scan the total brain and cerebral gray matter volumes were found to be
smaller in the patients compared with the controls. The third ventricle volumes remained significantly
larger in the patients on the second scan. Harris and colleagues[12] examined the differences in gyral
folding in schizophrenic patients (n=34) and healthy controls (n=36). The gyrification index values (the
ratio of inner and outer cortical surface contours) were significantly increased in the right temporal lobe
of schizophrenic patients relative to the controls.
One study[13] investigated the abnormalities of cerebellar volumes and the cerebellar asymmetry in
patients with schizophrenia (n=69) and healthy controls (n=49). The cerebellar asymmetry was
measured by bisecting the cerebellum into the anterior and posterior quadrants using a midline
hallmark. No difference was noted in the regional cerebellar volumes between the patients and healthy
controls. The male patients, however, demonstrated significantly reversed anterior and posterior
asymmetries compared with the healthy male controls. In another study[14] an enlargement of lateral

4. ventricles in schizophrenic patients (n=19) was observed compared with healthy controls (n=29).
 Neuropsychological Abnormalities in Schizophrenia
The deficits in a broad range of cognitive functions, such as attention, abstraction, executive function,
learning and memory, have been considered as core features of schizophrenia.
Six studies recently examined the neuropsychological functions in first-episode patients. Mohr et al.[15]
investigated the neurological soft signs and cognitive impairments in schizophrenic patients (n=61)
compared with healthy controls (n=87). The schizophrenic patients showed more neurological soft signs
than the controls. In addition, the patients showed impaired performances on the measures of verbal
intelligence, language, spatial organization, verbal memory, visual memory and short-term memory.
Furthermore, there were correlations between the neurological soft signs and some of the cognitive
functions, such as verbal memory, language, visual motor processing and attention. One study[16]
administered neuropsychological tests to 307 schizophrenic patients during their first episode of illness,
and found the patients showed mild to moderate impairments on all measures, including verbal memory,
nonverbal memory, attention, verbal fluency and executive function, with reference to age and education
norms. Cognitive impairments from the premorbid period until shortly after the onset of the first
episode within the same schizophrenic patients were examined.[17] Forty-four schizophrenic patients
were compared with 44 healthy controls. The neuropsychological tests were administered twice (during
the premorbid period and after the manifestation of the first psychotic episode) to both groups. The
patients performed significantly worse on the neuropsychological tests that measured verbal reasoning,
concept manipulation, abstract reasoning and verbal intelligence. Furthermore, both groups did not
show significant changes in any of the cognitive measures between the first and second assessments.
Stirling et al.[18] found an impaired executive function in schizophrenic patients (n=24) compared with
normative data. Another study[19] compared neuroleptive-naïve schizophrenic patients (n=62) and
healthy individuals (n=67), and found impaired performances on the measures of verbal learning, short-
term memory, long-term memory and immediate attention in schizophrenic patients relative to the
controls. Furthermore, the memory deficit observed in patients with schizophrenia was related to the
reduced use of organizational strategies to facilitate verbal encoding and retrieval, and not to the rapid
forgetting or susceptibility to interferences. Hill and associates[20] evaluated the neuropsychological
functions of neuroleptic-naïve, first-episode schizophrenic patients (n=45) and healthy controls (n=33).
The patients showed deficits across the cognitive domains, such as executive function, verbal memory,
visual memory, motor skills and visual perception at baseline, which persisted over the 2-year follow-up
period.
 Event-Related Potential Findings in Schizophrenia
P300, which is one of the event-related potential (ERP) components, has been regarded as a reliable
biological marker for schizophrenia. Previous studies have consistently demonstrated a reduced P300
amplitude in patients with schizophrenia.
Recently, two studies investigated the ERP in first-episode schizophrenic patients. One study[21]
measured the P300 in drug-free male schizophrenic patients (n=20) and healthy male controls (n=23)
using an oddball paradigm, and found significantly reduced P300 amplitude and prolonged P300 latency
in patients. Brown et al.[22] investigated the ERP in schizophrenic patients (n=40), chronic
schizophrenic patients (n=40) and normal controls (n=80) using an auditory oddball paradigm. The first
episode and chronic patients showed reduced amplitudes (N100, N200 and P300) and an increased P200
amplitude, both to targets and nontargets, compared with the controls.
 Brain Abnormalities in Obsessive-Compulsive Disorder
Recent neuroimaging, neuropsychological and electrophysiological studies investigating the

5. pathophysiology of Obsessive-Compulsive Disorder are reviewed.
 Structural/Functional Abnormalities in Obsessive-Compulsive Disorder
Deficit in the frontal-subcortical circuit has been consistently implicated in the pathophysiology of
Obsessive-Compulsive Disorder.
Recently, Choi et al.[23] found a volume reduction of the left anterior orbitofrontal cortex in Obsessive-
Compulsive Disorder patients (n=34) compared with normal controls (n=34), suggesting the region may
be related to impaired organizational strategies in Obsessive-Compulsive Disorder. Four studies focused
on the brain function in Obsessive-Compulsive Disorder patients. One study[24] administered functional
magnetic resonance imaging, while 11 Obsessive-Compulsive Disorder patients and 11 healthy controls
performed spatial working memory tasks with multiple levels of difficulty. The Obsessive-Compulsive
Disorder patients performed poorly on the spatial memory tasks at the highest level of difficulty, and
showed elevated activity in the anterior cingulate cortex compared with the controls. Lacerda and
associates[25] compared drug-free Obsessive-Compulsive Disorder patients (n=16) and healthy controls
(n=17) using single photon emission computed tomography. Significantly increased resting regional
cerebral blood flow was found in the superior/inferior portions of the frontal lobe and right/left
thalamus in Obsessive-Compulsive Disorder patients compared with the controls. Kwon et al.[26]
measured the cerebral glucose metabolic rates in Obsessive-Compulsive Disorder patients (n=14) and
normal controls (n=14) by positron emission tomography. The right orbitofrontal cortex and left
parietooccipital junction showed increased and decreased metabolic activity, respectively, in the
patients. The correlations between metabolic rates and neuropsychological test performance in the
prefrontal cortex and putamen occurred in the patients but not in the controls. One study[27] reported
the changes in the cerebral glucose metabolic rates after treatment in Obsessive-Compulsive Disorder
patients (n=10). The changes in the metabolic rates were observed in multiple areas, particularly
involving frontal-subcortical circuits and parietal-cerebral networks.
 Neuropsychological Abnormalities in Obsessive-Compulsive Disorder
Previous studies have reported several cognitive dysfunctions such as impairments in attention, response
inhibition, visual memory, visuospatial ability and spatial working memory in Obsessive-Compulsive
Disorder patients.
Three recent studies investigated the neuropsychological abnormalities in Obsessive-Compulsive
Disorder patients. Aycicegi and colleagues[28] administered a comprehensive neuropsychological test
battery to patients with Obsessive-Compulsive Disorder (n=16) and healthy controls (n=15), in order to
investigate whether the cognitive dysfunctions in Obsessive-Compulsive Disorder patients were
associated with comorbid conditions. The Obsessive-Compulsive Disorder patients showed significant
performance deficits in tests on delayed memory, alternation learning, visuoconstructive ability,
executive function and response inhibition. When coexistent depressive and schizotypal symptoms were
taken into account, however, the Obsessive-Compulsive Disorder patients exhibited no impaired
performance in tests on the executive function and verbal fluency compared with the controls. In one
study,[29] drug-free Obsessive-Compulsive Disorder patients (n=14) and healthy controls (n=14) were
assessed on neuropsychological tests, and the Obsessive-Compulsive Disorder patients showed decreased
performance on the Rey-Osterrieth Complex Figure Test (copy), the Verbal Fluency Test and the
Wisconsin Card Sorting Test (WCST) (perseverative errors). Contrary to the above two studies, another
study[30] found no significant neuropsychological deficits in the drug-free Obsessive-Compulsive
Disorder patients compared with the healthy controls.
 Event-Related Potential Findings in Obsessive-Compulsive Disorder
Previous studies have reported inconsistent ERP findings in Obsessive-Compulsive Disorder patients.

6. Some studies found reduced P300 amplitudes and prolonged latencies, but others observed greater P300
amplitude and shortened P300 latencies.
Four recent studies measured the ERP in Obsessive-Compulsive Disorder patients. Three focused on the
P300 abnormalities, using auditory oddball paradigms. Mavrogiorgou and colleagues[31] studied the
P300 in drug-free Obsessive-Compulsive Disorder patients (n=21) and healthy controls (n=21) and found
an enhanced P300b amplitude and a shortened P300b latency in Obsessive-Compulsive Disorder
patients relative to the controls. However, no difference between the Obsessive-Compulsive Disorder
patients and the controls was found in terms of P300a. Kivircik et al.[30] recorded the ERP in drug-free
Obsessive-Compulsive Disorder patients (n=31) and normal controls (n=30). The Obsessive-Compulsive
Disorder patients showed a shorter P300 latency compared with the controls. Herrmann et al.[32]
measured the global field power P300, while the Obsessive-Compulsive Disorder patients (n=12) and
healthy controls (n=12) performed a cued Go-NoGo task, and observed a shortened global field power
latency of P300 in Go and NoGo conditions in the Obsessive-Compulsive Disorder patients relative to the
controls. In addition, the Obsessive-Compulsive Disorder patients showed reduced frontal activity
compared with the controls.
One study[33] investigated the P600 elicited during a working memory test in 20 drug-free Obsessive-
Compulsive Disorder patients and 20 normal controls. The patients showed enhanced P600 amplitudes
at the right temporoparietal area and prolonged P600 latencies at the right parietal site compared with
the controls.
 Findings from Direct Comparison of Obsessive-Compulsive Disorder wth Schizophrenia
Despite the abundance of literature regarding the pathophysiology and possible shared mechanism of
the frontostriatal circuits in the two disorders, few studies have directly compared Obsessive-
Compulsive Disorder patients with schizophrenics. There are no studies that compared first-episode
schizophrenic patients and Obsessive-Compulsive Disorder patients directly.
Kim and colleagues[34] compared the volumes of the insula in Obsessive-Compulsive Disorder patients
(n=21), chronic schizophrenic patients (n=21) and normal controls (n=21), under the assumption that the
insular volume would be decreased in schizophrenia but increased in Obsessive-Compulsive Disorder.
They found the reduced insular volume only in the schizophrenic group. The authors, however,
discussed the insensitivity of the region of interest method and did not exclude the possible involvement
of a subregion of the insula in Obsessive-Compulsive Disorder. In another volumetric study, Kwon et al.
[35] measured the volumes of the hippocampus, amygdala and thalamus in Obsessive-Compulsive
Disorder patients (n=22), schizophrenic patients (n=22) and normal controls (n=22). The results showed
that the hippocampal volume was bilaterally reduced both in Obsessive-Compulsive Disorder and
schizophrenic patients compared with the controls, suggesting that the nonspecificity of these findings
may be linked to the clinical overlap between the two disorders. The left amygdala volume was enlarged
in the Obsessive-Compulsive Disorder patients but not in the patients with schizophrenia or the controls.
The three groups did not differ in terms of their thalamic volumes.
Two studies have compared the neuropsychological performances in Obsessive-Compulsive Disorder
and schizophrenic patients. Kim et al.[36] administered a comprehensive neuropsychological battery to
Obsessive-Compulsive Disorder patients (n=19), chronic schizophrenic patients (n=22) and healthy
controls (n=21), and measured their P300. The Obsessive-Compulsive Disorder patients showed
impaired performances on the Rey-Osterrieth Complex Figure Test and the Trail Making Test B form,
compared with the controls, while the patients with schizophrenia showed decreased performances on
almost all measures compared with the controls. The authors also found a reduced P300 amplitude in
the Obsessive-Compulsive Disorder and schizophrenia patients relative to the controls. The Obsessive-
Compulsive Disorder, schizophrenic and control groups showed no difference in terms of their P300
latencies. Cavallaro et al.[37] performed a double dissociation study between ventromedial and

7. dorsolateral prefrontal cortices in 110 chronic schizophrenia patients, 67 Obsessive-Compulsive
Disorder patients and 56 controls, using the WCST, the Gambling Task and the Tower of Hanoi. Both
patient groups showed decreased performance on the Tower of Hanoi compared with the controls. The
schizophrenic group, however, performed poorly on the WCST compared with the Obsessive-
Compulsive Disorder patients and controls, and the Obsessive-Compulsive Disorder patients performed
poorly on the Gambling Task compared with the schizophrenics and controls. Their findings added
evidence of involvement of different functional subsystems within the frontostriatal circuits in Obsessive-
Compulsive Disorder and schizophrenia.
SUMMARY
The findings of recent studies on brain abnormalities of first-episode schizophrenia and Obsessive-
Compulsive Disorder are consistent with previous results. Patients with schizophrenia showed
abnormalities in the brain structure, cognitive functions and electrophysiology, even in the early stage of
the illness. The frontostriatal and frontotemporal deficits seem to be the hallmark of the
pathophysiology of schizophrenia. In Obsessive-Compulsive Disorder, functional imaging studies have
reported relatively consistent findings of the hyperactivation in the frontostriatal circuits. Deficits in the
frontostriatal circuits are present both in schizophrenia and Obsessive-Compulsive Disorder, but more
structural abnormalities and generalized cognitive impairment are involved in schizophrenia relative to
Obsessive-Compulsive Disorder. However, there have only been a few studies directly comparing the
similarities and disparities between schizophrenia and Obsessive-Compulsive Disorder, in terms of their
psychophysiology.
The clinical phenomenology and the possible pathophysiological interaction of the overlap between
Obsessive-Compulsive Disorder and schizophrenia are still unclear. Obsessive-compulsive symptoms in
the prodromal or early phase of schizophrenia may express either a domain of schizophrenic symptoms,
or a protective defense against the schizophrenic process. Future studies, comparing schizo-obsessive
patients with schizophrenics without obsessive-compulsive symptoms, or to Obsessive-Compulsive
Disorder patients without psychotic symptoms, will elucidate the interactions in question. In particular,
studies designed to investigate the neurological abnormalities in patients with obsessive-compulsive
symptoms, in their prodromal or early phase of psychosis, including follow-up, will be greatly
influential.
The development of promising neuroimaging techniques, with better spatial and temporal resolutions,
will allow more accurate measurements of the neurological abnormalities in psychiatric disorders. In
addition, novel multimodal imaging techniques can be applied to overcome the limitations of each of the
present imaging modalities. For example, Park et al.[38] described a model mapping current densities of
superior time resolution ERP with improved anatomical localizations by combining individual magnetic
resonance imaging data in their analysis. The structural and functional brain abnormalities in
Obsessive-Compulsive Disorder and schizophrenia and their longitudinal changes will require further
investigations with these types of equipment, providing the answers to many controversial questions.
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The author: Professor Yasser Metwally
Professor of neurology, Ain Shams university school of medicine,Cairo, Egypt
http://yassermetwally.com
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