Study Results
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Basic Information
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COMPLETED
45 participants
OBSERVATIONAL
2017-09-22
2018-09-11
Brief Summary
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Detailed Description
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Neuro-anatomic model of mood regulation :
The prefrontal cortex has extensive connectivity to cortical and subcortical circuits that may underlie its importance in cognitive functions and modulation of limbic activity .The main subcortical structures participating in these circuits are the basal ganglia, thalamus, hypothalamus, brainstem, and the white matter tracts that connect these structures among themselves and to the cerebral cortex . A limbic-thalamic-cortical circuit consisting of the amygdala, the medio-dorsal nucleus of the thalamus, and the medial and ventro-lateral prefrontal cortex, and a limbic-striato-pallidal-thalamic circuit comprising the striatum, the ventral pallidum, and the components of the other circuit are the main neuro-anatomic circuits that have been proposed to participate in the pathophysiology of mood disorders.
The basal ganglia connect with cortical and limbic regions through circuits that, despite functioning segregated, are organized in parallel , in such a way that lesions in different parts of these circuits could result in malfunction. Additionally, the cerebellum, through connections with the brainstem and limbic structures, may also be involved in mood regulation.
Both primary and secondary mood disorders may involve abnormalities in specific fronto-subcortical neuro-anatomic circuits. Abnormalities in these brain regions or in contiguous areas that can affect the connections between these regions could reflect malfunction of these circuits, associated with development of mood disorders. Alternatively, abnormalities in these circuits could confer vulnerability to mood disorders, and its onset could be determined by interactions with environmental and genetic factors. Deficits during brain development due to these factors could result in under-development of particular brain areas, which could be related subsequently with mood disorders. The aging process or pathology such as vascular brain disease could result in atrophy of some of these regions. Thus, the influence of genetic, environmental, developmental, and degenerative factors during the development of these brain structures may determine the onset of mood disorders .
Although structural brain abnormalities in Bipolar Disorder have been reported, the pattern of structural brain abnormalities based on magnetic resonance imaging is still not clearly defined.
Aim of the study :
To study the morphometric criteria of different brain structures in patients with Bipolar Disorder type I mania in comparison to healthy subjects.
Subjects and Methods:
Patients :
Inclusion criteria:
Patients diagnosed to have mood disorder Bipolar I mania with or without psychotic features according to criteria of Diagnostic and statistical Manual of Mental disorder-IV (American Psychiatric Association 1994) by psychiatric sheath of psychiatric unit at Assiut University hospital .
The patients will be arranged in Two subgroups:
first group: twenty five patients in more than one episode second group: twenty age and sex-matched healthy subjects will be enrolled in the study
.
Exclusion Criteria:
first and second degree relatives of psychiatric patients will be excluded from the healthy controls.
Persons with any neurological disorder or other psychiatric illness will be excluded from controls Patients with proven major structural abnormality as detected during Magnetic resonance Imaging Examination will be excluded from patients or healthy controls.
Conditions
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Study Design
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CASE_CONTROL
PROSPECTIVE
Study Groups
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first group
patients with more than one episodes of mania
Magnetic resonance imaging
A full Magnetic Resonance Imaging examination of the brain will be done for each of the subjects included in the study. The protocol of the study will include a high-resolution thin-cuts three Dimensions-T1 weighted gradient echo sequence to be used for the morphometric study.
The obtained images will be analyzed for any gross structural abnormalities. by using fully-automated computational voxel-based volumetric software that calculates the volume of different structures of the brain. The obtained data will be analyzed statistically using linear regression tests to determine the differences between Bipolar Disorder type I mania patients and the healthy controls
second group
sex-matched and age- matched healthy controls
Magnetic resonance imaging
A full Magnetic Resonance Imaging examination of the brain will be done for each of the subjects included in the study. The protocol of the study will include a high-resolution thin-cuts three Dimensions-T1 weighted gradient echo sequence to be used for the morphometric study.
The obtained images will be analyzed for any gross structural abnormalities. by using fully-automated computational voxel-based volumetric software that calculates the volume of different structures of the brain. The obtained data will be analyzed statistically using linear regression tests to determine the differences between Bipolar Disorder type I mania patients and the healthy controls
Interventions
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Magnetic resonance imaging
A full Magnetic Resonance Imaging examination of the brain will be done for each of the subjects included in the study. The protocol of the study will include a high-resolution thin-cuts three Dimensions-T1 weighted gradient echo sequence to be used for the morphometric study.
The obtained images will be analyzed for any gross structural abnormalities. by using fully-automated computational voxel-based volumetric software that calculates the volume of different structures of the brain. The obtained data will be analyzed statistically using linear regression tests to determine the differences between Bipolar Disorder type I mania patients and the healthy controls
Eligibility Criteria
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Inclusion Criteria
Exclusion Criteria
2. Persons with any neurological disorder or other psychiatric illness will be excluded from controls
3. Patients with proven major structural abnormality as detected during Magnetic Resonance Imaging examination will be excluded from patients or healthy controls.
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ALL
Yes
Sponsors
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Assiut University
OTHER
Responsible Party
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Shaza Ragab
principal investigator
Locations
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Assiut University Hospital
Asyut, , Egypt
Countries
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References
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Hibar DP, Westlye LT, van Erp TG, Rasmussen J, Leonardo CD, Faskowitz J, Haukvik UK, Hartberg CB, Doan NT, Agartz I, Dale AM, Gruber O, Kramer B, Trost S, Liberg B, Abe C, Ekman CJ, Ingvar M, Landen M, Fears SC, Freimer NB, Bearden CE; Costa Rica/Colombia Consortium for Genetic Investigation of Bipolar Endophenotypes; Sprooten E, Glahn DC, Pearlson GD, Emsell L, Kenney J, Scanlon C, McDonald C, Cannon DM, Almeida J, Versace A, Caseras X, Lawrence NS, Phillips ML, Dima D, Delvecchio G, Frangou S, Satterthwaite TD, Wolf D, Houenou J, Henry C, Malt UF, Boen E, Elvsashagen T, Young AH, Lloyd AJ, Goodwin GM, Mackay CE, Bourne C, Bilderbeck A, Abramovic L, Boks MP, van Haren NE, Ophoff RA, Kahn RS, Bauer M, Pfennig A, Alda M, Hajek T, Mwangi B, Soares JC, Nickson T, Dimitrova R, Sussmann JE, Hagenaars S, Whalley HC, McIntosh AM, Thompson PM, Andreassen OA. Subcortical volumetric abnormalities in bipolar disorder. Mol Psychiatry. 2016 Dec;21(12):1710-1716. doi: 10.1038/mp.2015.227. Epub 2016 Feb 9.
Angst F, Stassen HH, Clayton PJ, Angst J. Mortality of patients with mood disorders: follow-up over 34-38 years. J Affect Disord. 2002 Apr;68(2-3):167-81. doi: 10.1016/s0165-0327(01)00377-9.
Tondo L, Isacsson G, Baldessarini R. Suicidal behaviour in bipolar disorder: risk and prevention. CNS Drugs. 2003;17(7):491-511. doi: 10.2165/00023210-200317070-00003.
Rocha-Rego V, Jogia J, Marquand AF, Mourao-Miranda J, Simmons A, Frangou S. Examination of the predictive value of structural magnetic resonance scans in bipolar disorder: a pattern classification approach. Psychol Med. 2014 Feb;44(3):519-32. doi: 10.1017/S0033291713001013. Epub 2013 Jun 5.
Soares JC, Mann JJ. The anatomy of mood disorders--review of structural neuroimaging studies. Biol Psychiatry. 1997 Jan 1;41(1):86-106. doi: 10.1016/s0006-3223(96)00006-6.
Lipska BK, Jaskiw GE, Weinberger DR. Postpubertal emergence of hyperresponsiveness to stress and to amphetamine after neonatal excitotoxic hippocampal damage: a potential animal model of schizophrenia. Neuropsychopharmacology. 1993 Aug;9(1):67-75. doi: 10.1038/npp.1993.44.
Alexander GE, Crutcher MD. Functional architecture of basal ganglia circuits: neural substrates of parallel processing. Trends Neurosci. 1990 Jul;13(7):266-71. doi: 10.1016/0166-2236(90)90107-l.
Other Identifiers
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VBM MANIA
Identifier Type: -
Identifier Source: org_study_id
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