Basal ganglia volumes in first-episode schizophrenia and healthy comparison subjects

Gündüz, Handan; Wu, Houwei; Ashtari, Manzar; Bogerts, Bernhard; Crandall, David T.; Robinson, Delbert G.; Alvir, J.; Lieberman, Jeffrey A.; Kane, John M.; Bilder, Robert M.

doi:10.1016/s0006-3223(01)01345-2

Cited by 82 publications

(49 citation statements)

References 41 publications

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“…Recent studies, however, have reported findings that the volume of the caudate nucleus in schizophrenia (Gunduz et al 2002) and in SPD subjects (Suzuki et al 2004) was not significantly different compared with normal control (NC) subjects, which contradicted our findings (Levitt et al 2002) and other prior studies (Corson et al 1999;Keshavan et al 1998). There are several possible reasons for this lack of agreement.…”

contrasting

confidence: 99%

“…Furthermore, studies of SPD in female subjects, alone, help to elucidate specific associations between caudate nucleus volume and psychopathology in women, which might or might not resemble the specific associations found in male subjects. Of further note, as previously reviewed in the Introduction, some studies of neuroleptic-naïve patients diagnosed with schizophrenia have not shown significant caudate volume reduction (Chakos et al 1994;Gunduz et al 2002;Gur et al 1998). Of these studies, Gunduz et al (2002) reported larger caudate nucleus volume in patients diagnosed with schizophrenia compared with control subjects, although this was not statistically significant.…”

Section: Discussionmentioning

confidence: 92%

“…Of note, however, even in studies with drug-naïve subjects, there are inconsistencies in the literature with regard to caudate nucleus volume in schizophrenia. For instance, there were no differences in caudate nucleus volume reported in neuroleptic-naïve, first-episode patients (Chakos et al 1994;Gunduz et al 2002;Gur et al 1998) compared with control subjects. Furthermore, the inconsistency in these studies might be due to the differences in their sampling, scanning, and measurement methods.…”

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confidence: 96%

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Reduction of Caudate Nucleus Volumes in Neuroleptic-Naïve Female Subjects with Schizotypal Personality Disorder

Koo

Levitt

McCarley

et al. 2006

Biological Psychiatry

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Background-The caudate nucleus might contribute to the psychopathological and cognitive deficits observed in schizotypal personality disorder (SPD), a schizophrenia spectrum disorder. Here we focused on female patients, because this group is underrepresented in studies of SPD and schizophrenia, and we might learn more about the caudate and clinical and cognitive impairments that are unique to female patients diagnosed with SPD.

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contrasting

confidence: 99%

Section: Discussionmentioning

confidence: 92%

mentioning

confidence: 96%

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Reduction of Caudate Nucleus Volumes in Neuroleptic-Naïve Female Subjects with Schizotypal Personality Disorder

Koo

Levitt

McCarley

et al. 2006

Biological Psychiatry

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“…A correlation between excess [ 123 I]IBZM binding in the left basal ganglia of schizophrenic patients was also demonstrated to correlate with stereotyped behavior (Pedro et al, 1994). However, with regard to the structure of the basal ganglia in untreated patients with schizophrenia, there are several reports showing either no change or decreases in volume, but studies demonstrating structural asymmetry in these structures are lacking (Corson et al, 1999;Gunduz et al, 2002;Keshavan et al, 1998;Shihabuddin et al, 1998Shihabuddin et al, , 2001). Interestingly, Scheepers et al found a reduction in left caudate nucleus volume in patients who responded to clozapine treatment, but not in nonresponders (Scheepers et al, 2001).…”

Section: Discussionmentioning

confidence: 99%

Subchronic Haloperidol Downregulates Dopamine Synthesis Capacity in the Brain of Schizophrenic Patients In Vivo

Gründer¹,

Vernaleken²,

Müller³

et al. 2002

Neuropsychopharmacol

103

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The antipsychotic effect of neuroleptics cannot be attributed entirely to acute blockade of postsynaptic D 2 -like dopamine (DA) receptors, but may arise in conjunction with the delayed depolarization block of the presynaptic neurons and reduced DA synthesis capacity. Whereas the phenomenon of depolarization block is well established in animals, it is unknown if a similar phenomenon occurs in humans treated with neuroleptics. We hypothesized that haloperidol treatment should result in decreased DA synthesis capacity. We used 6-[ 18 F]fluoro-L-dopa (FDOPA) and positron emission tomography (PET) in conjunction with compartmental modeling to measure the relative activity of DOPA decarboxylase (DDC) (k D 3 , min À1 ) in the brain of nine unmedicated patients with schizophrenia, first in the untreated condition and again after treatment with haloperidol. Patients were administered psychometric rating scales at baseline and after treatment. Consistent with our hypothesis, there was a 25% decrease in the magnitude of k D 3 in both caudate and putamen following 5 weeks of haloperidol therapy. In addition, the magnitudes of k D 3 in cerebral cortex and thalamus were also decreased. Psychopathology as measured with standard rating scales improved significantly in all patients. The decrease of k D 3 in the thalamus was highly significantly correlated with the improvement of negative symptoms. Subchronic treatment with haloperidol decreased the activity of DDC in the brain of patients with schizophrenia. This observation is consistent with the hypothesis that the antipsychotic effect of chronic neuroleptic treatment is associated with a decrease in DA synthesis, reflecting a depolarization block of presynaptic DA neurons. We link an alteration in cerebral catecholamine metabolism in human brain with the therapeutic action of neuroleptic medication.

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“…For example, lesions involving the caudate nucleus, putamen, globus pallidus, subthalamic nucleus, thalamus, and cerebellum have been associated with particular spontaneous dyskinesias in several studies using a variety of methodological techniques (e.g., Antonini et al, 1998;Dooling & Adams, 1975;Kim et al, 2002;Krystkowiak et al, 2000;Krystkowiak et al, 1998;LeDoux & Brady, 2003;Lehericy et al, 1996;Lenz et al, 2002;Lozza et al, 2002;Naumann et al, 1996;Perlmutter et al, 1997). Moreover, an array of structural and functional abnormalities have been observed in several of these regions in individuals with schizophrenia, although substantial variation in findings exists (e.g., Danos et al, 2002;Gunduz et al, 2002;Jernigan et al, 1991;Keshavan et al, 1998;Lang et al, 2001;Marcelis et al, 2003;McCreadie et al, 2002;Menon et al, 2001;Muller et al, 2002;Sigmundsson et al, 2001;Staal et al, 2000;Staal et al, 2001;Young et al, 2000). Thus, to the extent that it has been demonstrated in individuals with spontaneous dyskinesia and in individuals with schizophrenia, the presence of pathology in brain regions integral to normal movement control is consistent with a connection between movement abnormalities and schizophrenia.…”

Section: Introductionmentioning

confidence: 99%

Spontaneous dyskinesia and familial liability to schizophrenia

Tarbox¹,

Pogue-Geile²

2006

Schizophrenia Research

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Several factors suggest that spontaneous dyskinesia may be a useful non-diagnosis phenotype for further elucidating the specific nature of the genetic contribution to schizophrenia. For example, involuntary movement abnormalities have been observed in both medicated and unmedicated schizophrenia patients, in individuals with schizotypal personality disorder, and sometimes in siblings of schizophrenia patients. However, there are many inconsistencies present in the literature to date. The current study thus sought to investigate the existence of spontaneous dyskinesia in schizophrenia patient probands, their non-psychotic siblings, and healthy controls in order to clarify its potential value as an "endophenotypes" in genetic studies of schizophrenia.Videotaped interviews were coded for the presence of spontaneous, involuntary movement abnormalities by a trained and reliable rater who was blind to group and family status. The results of this study indicated that siblings of schizophrenia patients did not display significantly more involuntary movements compared to controls, although tremor was observed in a few siblings. In contrast, schizophrenia patients did display significantly more involuntary movements compared to controls as well as their non-psychotic siblings. The lack of significant differences between siblings and controls argues against a strong association between spontaneous dyskinesia and an underlying genetic liability to schizophrenia. Thus, it appears that involuntary movement abnormalities may be limited in their utility as endophenotypes in genetic studies of schizophrenia, despite being associated with schizophrenia itself.ii

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Basal ganglia volumes in first-episode schizophrenia and healthy comparison subjects

Cited by 82 publications

References 41 publications

Reduction of Caudate Nucleus Volumes in Neuroleptic-Naïve Female Subjects with Schizotypal Personality Disorder

Reduction of Caudate Nucleus Volumes in Neuroleptic-Naïve Female Subjects with Schizotypal Personality Disorder

Subchronic Haloperidol Downregulates Dopamine Synthesis Capacity in the Brain of Schizophrenic Patients In Vivo

Spontaneous dyskinesia and familial liability to schizophrenia

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