Alteration of cerebral perfusion and cortical thickness in depression episodes: a comparative MRI study

Yıl 2022, , 38 - 44, 17.01.2022

Özkan Kılınç Mustafa Hızal , Özden Arısoy Nur Özgedik Oya Kalaycıoğlu

https://doi.org/10.32322/jhsm.993848

Öz

Aim: We aimed to determine the difference between cerebral perfusion and cortical thickness between first attack and recurrent in major depression patients.
Material and Method: Our study was conducted prospectively between 01.03.2017-03.03.2018 in Izzet Baysal University Psychiatry department. 40 patients (21 first episodes and 19 recurrent episodes) diagnosed with depression according to DSM 5 by the American Psychiatric Association and a control group of 16 healthy individuals were evaluated for cerebral blood flow and cortical thickness with Perfusion MRI. Patients were also evaluated by Hamilton depression rating scale.
Findings: The cortical thickness was significantly decreased in recurrent attacks.There was no significant difference of CBF in first episode and recurrent episodes, except cingulate cortex, which showed significantly reduced CBF values in recurrent group. In patients with higher Hamilton depression scale points, the CBF values of insular cortex were decreased.
Conclusion: These findings suggests that cortical atrophy and activation of default mode network in recurrent episodes which leads to decreased response to treatment.

Anahtar Kelimeler

Depression, Cerebral perfusion, Cortical thickness, MRI

Kaynakça

• Fava M, Kendler KS. Major depressive disorder. Neuron 2000; 28: 335–41.
• Frank E, Thase ME. Natural history and preventative treatment of recurrent mood disorders. Annu Rev Med 1999; 50: 453–68.
• Chen XL, Xie JX, Han HB, Cui YH, Zhang BQ. MR perfusion weighted imaging and quantitative analysis of cerebral hemodynamics with symptom provocation in unmedicated patients with obsessive-compulsive disorder. Neurosci Lett 2004; 370: 206-11.
• Chen MH, Li CT, Lin WC, et al. Persistent antidepressant effect of low-dose ketamine and activation in the supplementary motor area and anterior cingulate cortex in treatment-resistant depression: A randomized control study. J Affect Disord 2018; 225: 709-14.
• Clark CP, Brown GG, Archibald SL, et al. Does amygdalar perfusion correlate with antidepressant response to partial sleep deprivation in major depression? Psychiatry Res 2006; 146: 43-51.
• Greenberg PE, Fournier AA, Sisitsky T, Pike CT, Kessler RC. The economic burden of adults with major depressive disorder in the United States. J Clin Psychiatry 2015; 76: 155-62.
• Andrade L, Caraveo-Anduaga JJ, Berglund P, et al. The epidemiology of major depressive episodes: results from the International Consortium of Psychiatric Epidemiology (ICPE) Surveys. Int J Methods Psychiatr Res 2003; 12: 3-21.
• Sheline YI, Sanghavi M, Mintun MA, Gado MH. Depression duration but not age predicts hippocampal volume loss in medically healthy women with recurrent major depression. J Neurosci 1999; 19: 5034-43.
• Coffey CE, Wilkinson WE, Weiner RD, et al. Quantitative cerebral anatomy in depression: a controlled magnetic resonance imaging study. Arch Gen Psychiatry 1993; 50: 7-16.
• Posener JA, Wang L, Price JL, et al. High-dimensional mapping of the hippocampus in depression. Am J Psychiatry 2003; 160: 83-9.
• MacQueen GM, Campbell S, McEwen BS, et al. Course of illness, hippocampal function, and hippocampal volume in major depression. Proc Natl Acad Sci USA 2003; 100: 1387-92.
• Frodl TS, Koutsouleris N, Bottlender R, et. al. Depression-related variation in brain morphology over 3 years: effects of stress. Arch Gen Psychiatry 2008; 65: 1156-65.
• Hasler G, Van der Veen JW, Tumonis T, Meyers N, Shen J, Drevets WC. Reduced prefrontal glutamate/glutamine and γ-aminobutyric acid levels in major depression determined using proton magnetic resonance spectroscopy. Arch Gen Psychiatry 2007; 64: 193-200.
• Lui S, Parkes LM, Huang X, et al. Depressive disorders: focally altered cerebral perfusion measured with arterial spin-labeling MR imaging. Radiology 2009; 25: 476-84.
• Compton WM, Conway KP, Stinson FS, Grant BF. Changes in the prevalence of major depression and comorbid substance use disorders in the United States between 1991-1992 and 2001-2002. Am J Psychiatry 2006; 163: 2141-7.
• Koolschijn P, Van Haren NE, Pol HEH, Kahn RS. Hypothalamus volume in twin pairs discordant for schizophrenia. Eur Neuropsychopharmacol 2008; 18: 312-5.
• Koolschijn P, Van Haren NE, Lensvelt‐Mulders GJ, Pol HEH, Hilleke E, Kahn RS. Brain volume abnormalities in major depressive disorder: A meta‐analysis of magnetic resonance imaging studies. Hum Brain Mapp 2009; 30: 3719-35.
• Aan het Rot M, Mathew SJ, Charney DS. Neurobiological mechanisms in major depressive disorder. CMAJ 2009; 180: 305-13
• Schatzberg AF. Major depression: causes or effects? Am J Psychiatry 2002; 159: 1077-9.
• Peterson BS, Warner V, Bansal R, et al. Cortical thinning in persons at increased familial risk for major depression. Proc Natl Acad Sci USA 2009; 106: 6273-8.
• Fountoulakis KN, Iacovides A, Gerasimou G, et al. The relationship of regional cerebral blood flow with subtypes of major depression. Prog Neuropsychopharmacol Biol Psychiatry 2004; 28: 537-46.
• Gold SM, Dziobek I, Rogers K, Bayoumy A, McHugh PF, Convit A. Hypertension and hypothalamo-pituitary-adrenal axis hyperactivity affect frontal lobe integrity. J Clin Endocrinol Metab 2005; 90: 3262-7.
• Sargent PA, Kjaer KH, Bench CJ, et al. Brain serotonin1A receptor binding measured by positron emission tomography with [11C] WAY-100635: effects of depression and antidepressant treatment. Arch Gen Psychiatry 2000; 57: 174-80.
• Pan W, Banks WA, Fasold MB, Blunth J, Kasten AJ. Transport of brain-derived neurotrophic factor across the blood–brain barrier. Neuropharmacology 1998; 37: 1553-61.
• Cotter D, Mackay D, Chana G, Beasley C, Landau S, Everall IP. Reduced neuronal size and glial cell density in area 9 of the dorsolateral prefrontal cortex in subjects with major depressive disorder. Cereb Cortex 2002; 12: 386-94.
• Matsuo K, Onodera Y, Hamamoto T, Muraki K, Kato N, Kato T. Hypofrontality and microvascular dysregulation in remitted late-onset depression assessed by functional near-infrared spectroscopy. Neuroimage 2005; 26: 234-42.
• Fregni F, Ono C, Santos C, et al. Effects of antidepressant treatment with rTMS and fluoxetine on brain perfusion in PD. Neurology 2006; 66: 1629-37.
• Teneback CC, Nahas Z, Speer AM, et al. Changes in prefrontal cortex and paralimbic activity in depression following two weeks of daily left prefrontal TMS. J Neuropsychiatry Clin Neurosci 1999; 11: 426-435.
• Bench CJ, Friston KJ, Brown RG, Scott LC, Frackowiak RS, Dolan RJ. The anatomy of melancholia–focal abnormalities of cerebral blood flow in major depression. Psychol Med 1992; 22: 607-15.
• Direk N, Koudstaal PJ, Hofman A, Ikram MA, Hoogendijk WJ, Tiemeier H. Cerebral hemodynamics and incident depression: the Rotterdam Study. Biol Psychiatry 2012; 72: 318-23.
• Drevets WC, Price JL, Furey ML. Brain structural and functional abnormalities in mood disorders: implications for neurocircuitry models of depression. Brain Struct Funct 2008; 213: 93-118.
• Narushima K, Kosier J, Robinson RG. A reappraisal of poststroke depression, intra-and inter-hemispheric lesion location using meta-analysis. J Neuropsychiatry Clin Neurosci 2003; 15: 422-30.
• Smith K, Morris J, Friston K, Cowen PJ, Dolan RJ. Brain mechanisms associated with depressive relapse and associated cognitive impairment following acute tryptophan depletion. Br J Psychiatry 1999; 174: 525-9.
• Killgore WDS, Gruber SA, Yurgelun-Todd DA. Depressed mood and lateralized prefrontal activity during a Stroop task in adolescent children. Neurosci Lett 2007; 416: 43-8.
• Chand GB, Wu J, Hajjar I, Qiu D. Interactions of Insula Subdivisions Based Networks with Default-Mode and Central-Executive Networks in Mild Cognitive Impairment. Front Aging Neurosci 2017; 9: 367.
• Menon V, Uddin LQ. Saliency, switching, attention and control: a network model of insula function. Brain Struct Funct 2010; 214: 655-67