Talking psychiatry...The neurology of schizophrenia

2,607 views

Published on

Talking psychiatry...The neurology of schizophrenia

Published in: Education, Health & Medicine
0 Comments
1 Like
Statistics
Notes
  • Be the first to comment

No Downloads
Views
Total views
2,607
On SlideShare
0
From Embeds
0
Number of Embeds
14
Actions
Shares
0
Downloads
88
Comments
0
Likes
1
Embeds 0
No embeds

No notes for slide

Talking psychiatry...The neurology of schizophrenia

  1. 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. 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. 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. 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. 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. 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. 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. References 1. Joyal CC, Laakso MO, Tiihonen J, et al. The amygdala and schizophrenia: a volumetric magnetic resonance imaging study in first-episode neuroleptic-naïve patients. Biol Psychiatry 2003; 54:1302- 1304. 2. Smith GN, Lang DJ, Kopala LC, et al. Developmental abnormalities of the hippocampus in first- episode schizophrenia. Biol Psychiatry 2003; 53:555-561.
  8. 8. 3. Szeszko PR, Goldberg E, Gunduz-Bruce H, et al. Smaller anterior hippocampal formation volume in antipsychotic-naïve patients with first-episode schizophrenia. Am J Psychiatry 2003; 160:2190- 2197. 4. Kim JJ, Crespo-Facorro B, Andreasen NC, et al. Morphology of the lateral superior temporal gyrus in neuroleptic naïve patients with schizophrenia: relationship to symptoms. Schizophr Res 2003; 60:173-181. 5. Kasai K, Shenton ME, Salisbury DF, et al. Progressive decrease of left superior temporal gyrus gray matter volume in patients with first-episode schizophrenia. Am J Psychiatry 2003; 160:156- 164. 6. Kasai K, Shenton ME, Salisbury DF, et al. Progressive decease of left heschl gyrus and planum temporale gray matter volume in first-episode schizophrenia. Arch Gen Psychiatry 2003; 60:766- 775. 7. Kasai K, Shenton ME, Salisbury DF, et al. Differences and similarities in insular and temporal pole MRI gray matter volume abnormalities in first-episode schizophrenia and affective psychosis. Arch Gen Psychiatry 2003; 60:1069-1077. 8. Diwadkar VA, DeBellis MD, Sweeney JA, et al. Abnormalities in MRI-measured signal intensity in the corpus callosum in schizophrenia. Schizophr Res (in press). 9. Bachmann S, Pantel J, Flender A, et al. Corpus callosum in first-episode patients with schizophrenia: a magnetic resonance imaging study. Psychol Med 2003; 33:1019-1027. 10. Bagary MS, Symms MR, Barker GJ, et al. Gray and white matter brain abnormalities in first- episode schizophrenia inferred from magnetization transfer imaging. Arch Gen Psychiatry 2003; 60:779-788. 11. Cahn W, Hulshoff Pol HE, Lems EBTE, et al. Brain volume changes in first-episode schizophrenia. Arch Gen Psychiatry 2002; 59:1002-1010. 12. Harris JM, Yates S, Miller P, et al. Gyrification in first-episode schizophrenia: a morphometric study. Biol Psychiatry (in press). 13. Szeszko PR, Gunning-Dixon F, Ashtari M, et al. Reversed cerebellar asymmetry in men with first- episode schizophrenia. Biol Psychiatry 2003; 53:450-459. 14. Chua SE, Lam IWS, Tai KS, et al. Brain morphological abnormality in schizophrenia is independent of country of origin. Acta Psychiatr Scand 2003; 108:269-275. 15. Mohr F, Hubmann W, Albus M, et al. Neurological soft signs and neuropsychological performance in patients with first episode schizophrenia. Psychiatry Res 2003; 121:21-30. 16. Heydebrand G, Weiser M, Rabinowitz J, et al. Correlates of cognitive deficits in first episode schizophrenia. Schizophr Res (in press). 17. Caspi A, Reichenberg A, Weiser M, et al. Cognitive performance in schizophrenia patients assessed before and following the first psychotic episode. Schizophr Res 2003; 65:87-94. 18. Stirling J, White C, Lewis S, et al. Neurocognitive function and outcome in first-episode schizophrenia: a 10-year follow-up of an epidemiological cohort. Schizophr Res 2003; 65:75-86.
  9. 9. 19. Hill SK, Beers SR, Kmiec JA, et al. Impairment of verbal memory and learning in antipsychotic- naïve patients with first-episode schizophrenia. Schizophr Res (in press). 20. Hill SK, Schuepbach D, Herbener ES, et al. Pretreatment and longitudinal studies of neuropsychological deficits in antipsychotic-naïve patients with schizophrenia. Schizophr Res (in press). 21. Wang J, Hirayasu Y, Hiramatsu KI, et al. Increased rate of P300 latency prolongation with age in drug-naïve and first episode schizophrenia. Clin Neurophysiol 2003; 114:2029-2035. 22. Brown KJ, Gonsalvez CJ, Harris AWF, et al. Target and non-target ERP disturbances in first episode vs. chronic schizophrenia. Clin Neurophysiol 2002; 113:1754-1763. 23. Choi JS, Kang DH, Kim JJ, et al. Left anterior subregion of orbitofrontal cortex volume reduction and impaired organizational strategies in obsessive-compulsive disorder. J Psychiatr Res (in press). 24. van der Wee NJA, Ramsey NF, Jansma JM, et al. Spatial working memory deficits in obsessive- compulsive disorder are associated with excessive engagement of the medial frontal cortex. Neuroimage (in press). 25. Lacerda ALT, Dalgalarrondo P, Caetano D, et al. Elevated thalamic and prefrontal regional cerebral blood flow in obsessive-compulsive disorder: a SPECT study. Psychiatry Res 2003; 123:125-134. 26. Kwon JS, Kim JJ, Lee DW, et al. Neural correlates of clinical symptoms and cognitive dysfunctions in obsessive-compulsive disorder. Psychiatry Res 2003; 122:37-47. 27. Kang DH, Kwon JS, Kim JJ, et al. Brain glucose metabolic changes associated with neuropsychological improvements after 4 months of treatment in patient with obsessive- compulsive disorder. Acta Psychiatr Scand 2003; 107:291-297. 28. Aycicegi A, Dinn WM, Harris CL, Erkmen H. Neuropsychological function in obsessive- compulsive disorder: effects of comorbid conditions on task performance. Eur Psychiatry 2003; 18:241-248. 29. Lacerda ALT, Dalgalarrondo P, Caetano D, et al. Neuropsychological performance and regional cerebral blood flow in obsessive-compulsive disorder. Prog Neuropsychopharmacol Biol Psychiatry 2003; 27:657-665. 30. Kivircik BB, Yener GG, Alptekin Y, Aydin H. Event-related potentials and neuropsychological tests in obsessive-compulsive disorder. Prog Neuropsychopharmacol Biol Psychiatry 2003; 27:601- 606. 31. Mavrogiorgou P, Juckel G, Frodl T, et al. P300 subcomponents in obsessive-compulsive disorder. J Psychiatr Res 2002; 36:399-406. 32. Herrmann MJ, Jacob C, Unterecker S, Fallgatter AJ. Reduced response-inhibition in obsessive- compulsive disorder measured with topographic evoked potential mapping. Psychiatry Res 2003; 120:265-271. 33. Papageorgiou CC, Rabavilas AD. Abnormal P600 in obsessive-compulsive disorder: a comparison with healthy controls. Psychiatry Res 2003; 119:133-143.
  10. 10. 34. Kim JJ, Youn T, Lee JM, et al. Morphometric abnormality of insula in schizophrenia: a comparison with obsessive-compulsive disorder and normal control using MRI. Schizophr Res 2003; 60:191-198. 35. Kwon JS, Shin YW, Kim CW, et al. Similarity and disparity of obsessive-compulsive disorder and schizophrenia in MR volumetric abnormalities of the hippocampus-amygdala complex. J Neurol Neurosurg Psychiatry 2003; 74:962-964. 36. Kim MS, Kang SS, Youn T, et al. Neuropsychological correlates of P300 abnormalities in patients with schizophrenia and obsessive-compulsive disorder. Psychiatry Res 2003; 123:109-123. 37. Cavallaro R, Cavedini P, Mistretta P, et al. Basal-corticofrontal circuits in schizophrenia and obsessive-compulsive disorder: a controlled, double dissociation study. Biol Psychiatry 2003; 54:437-443. 38. Park HJ, Kwon JS, Youn T, et al. Statistical parametric mapping of LORETA using high density EEG and individual MRI: application to mismatch negativities in schizophrenia. Hum Brain Mapp 2002; 17:168-178. The author: Professor Yasser Metwally Professor of neurology, Ain Shams university school of medicine,Cairo, Egypt http://yassermetwally.com To access all issues in quot;talking psychiatryquot; section of quot;http://yassermetwally.netquot; follow the link : http://wordpress.com/tag/talking-psychiatry/ or click on it if it appears as a link in your PDF reader

×