Home | About IPJ | Editorial board | Ahead of print | Current Issue | Archives | Instructions | Contact us |   Login 
Industrial Psychiatry Journal
Search Articles   
    
Advanced search   
 


 
REVIEW ARTICLE
Year : 2010  |  Volume : 19  |  Issue : 2  |  Page : 82-89  Table of Contents     

Neuropsychophysiological correlates of depression


1 Department of Psychiatry, Armed Forces Medical College, Pune, Maharashtra, India
2 Graded Specialist Psychiatry Military Hospital, Danapur, India

Date of Web Publication28-Nov-2011

Correspondence Address:
Kalpana Srivastava
Department of Psychiatry, Scientist 'F', Armed Forces Medical College, Pune, Maharashtra
India
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0972-6748.90336

Rights and Permissions
   Abstract 

The neuropsychiatric and cognitive deficits have been shown to exist in various psychiatric disorders. An attempt has been made by authors to evaluate the evidence pertaining to electrophysiological, structural and neuropsychological domains in depression. Renewal of interest in testing patients with depression on a broad range of neuropsychological tasks has revealed distinct pattern of cognitive impairment in cases with depression. The review focuses on structural and neuropsychological evidence of deficit in cases of depression.

Keywords: Depression, electroencephalographic, neuropsychophysiology


How to cite this article:
Srivastava K, Ryali V, Prakash J, Bhat P S, Shashikumar R, Khan S. Neuropsychophysiological correlates of depression. Ind Psychiatry J 2010;19:82-9

How to cite this URL:
Srivastava K, Ryali V, Prakash J, Bhat P S, Shashikumar R, Khan S. Neuropsychophysiological correlates of depression. Ind Psychiatry J [serial online] 2010 [cited 2019 Sep 21];19:82-9. Available from: http://www.industrialpsychiatry.org/text.asp?2010/19/2/82/90336

Global burden of disease lists depression as the fourth leading cause of disability in terms of its physical, social and mental impact. The world health organization predicts it to be the second only cause of morbidity worldwide by the year 2020 and the leading disorder in females. [1] Surveys suggest that most cases of depression are either unrecognized or inappropriately treated, and this leads to a social burden on the family, functional decline and increased mortality with a lifetime prevalence of 10-20%. [2] In primary health care services in India, the estimated prevalence of depression was noted to be 20%. The prevalence of depressive disorder in Psychiatric departments of general hospital has ranged from 6 [3] to 34.7%. [4] In India, a metaanalysis of epidemiological studies performed in rural and urban areas since 1960 reported a median prevalence of 3.4% for mood disorders. [5]

There has been extensive research exploring the biopsychosocial model of depression over the years. Galen ascribed depression to the various humors, which was a departure from the approaches of early researchers, who looked into the domains of unresolved conflicts, faulty parenting and other psychological and social causation. In the post-1950 era, the concept of depression as a biological disorder emerged. Although a large range of existing neuropsychological, neuropsychiatric and, lately, neuroimaging investigations throw some light toward neurobiology of this malady, a consistent picture is yet to emerge, and the issue is far from settled. [6]


   Neurobiological Correlates Top


Biological research in affective disorders has focused primarily on the neurochemical basis of the disorder. Recently, there has been interest in the neuroanatomical basis of these disorders. [7] Radiological techniques that allow investigation of the living brain in health and disease have become widely available. Structural abnormalities in affective disorders were initially investigated with computerized tomographic scans. Later, the more precise methodology of magnetic resonance imaging (MRI) was applied with the ultimate aim of describing the structural and functional neuroanatomy in mood disorder. [8],[9],[10] Although still controversial, convergence of MRI and other findings from studies utilizing post-stroke depression and patients with primary mood disorder have led to attempts at detailed exploration of the neuroanatomical basis of mood disorders. [11] Studies using high-resolution MRI are now available to examine smaller brain structures with precision, and they have reported brain changes associated with major depression in the hippocampus (HC), amygdala, caudate nucleus, putamen and frontal cortex. [12]

Interestingly, neurobiological substrate for this disorder has not reached finality. The circuitry underlying the representation and regulation of normal emotion and mood involves the prefrontal cortex, anterior cingulate, HC and amygdala. The abnormalities in the structure and function of these different regions are implicated in depression. [13] The clinical manifestations of depressive disorder are considered to be mediated through changes in brain neurochemistry and structural/functional connectivity, irrespective of the etiology.


   Electroencephalographic Correlates of Depression Top


Apart from the newer modalities of research like MRI, evidence from electroencephalographic (EEG) as well has unequivocally established that "mental disorder" has definite correlates with brain dysfunction. Pathophysiological concomitants of psychiatric and developmental disorders have been provided by EEG and quantitative electroencephalography (QEEG). [14] The exclusion of neurological conditions for confirmation of psychiatric disorder has led to the application of EEG and QEEG investigation. [15] The percentage is as high as 64-68% of EEGs in psychiatric patients providing evidence of pathophysiology, and these results have additional utility beyond simply ruling out organic brain lesions. [16],[17] Such EEG studies may also aid in differential diagnosis, treatment patient selection and evaluation.


   Conventional Versus Quantitative Eeg in Depression Top


A voluminous literature attests to the robustness of conventional EEG studies and their clinical utility in disorders of brain function, which includes depressive disorders. [18],[19] The conventional EEG has contributed valuable information for the psychiatrist; however, this method is essentially based on visual pattern recognition. QEEG is now being increasingly used to decipher the neurobiological correlates in mood disorder. [20],[21]

These two EEG approaches complement each other. While conventional EEG provides reliable diagnostic information especially sensitive to "organic" or neurological disorders, detecting features of wave shapes, frequency relationships and transitions of state seldom encountered in the healthy individual, QEEG, in addition, enables precise comparison of the individual patient's record with normative and psychopathologic patient databases. Across both EEG and QEEG studies, a broad consensus exists on the high proportion of abnormalities found in different psychiatric disorders and often on their electrophysiological profiles. However, the generalization of these findings and application in clinical practice is limited by the non-specific nature of the detected abnormalities found in psychiatric patients. Also, there has been considerable controversy about the clinical utility of QEEG in psychiatric practice. [22],[23]

The incidence of abnormal conventional EEG findings in mood disorders appears to be substantial, ranging from 20% to 40%. [24],[25] Specific patterns noted in mood disorder patients include the controversial small sharp spikes (SSS), 6/s spike and wave complexes, and positive spikes, seen especially in patients with suicidal ideation. [26],[27] Evidence that the EEG is abnormal in depression has been coming of late from QEEG studies, and these have been in the form of increased alfa and/or theta power in a high percentage of depressed patients. [28] Interhemispheric asymmetry, especially in anterior regions, has been reported repeatedly. [29] Hence, both EEG and QEEG studies report that a high proportion of patients with mood disorders display abnormal brain electrical activity. EEG studies report that SSS and paroxysmal events are often found, especially on the right hemisphere, and that abnormal sleep studies are common.

EEG findings in studies of genetic unipolar depressives show that depressed persons display a disorganized atypical sleep pattern that skips a "level" of deep sleep and prominent delta and theta waves (which are sleep waves) in the waking state. [29] Therefore, we may conclude that the depressed person's brainwave activity in sleep is invaded by "waking" waves, and the reverse in the waking state.


   Neuroimaging in Depression Top


Although biochemical, pharmacologic and brain imaging techniques have all been used to shed light on the neurobiology of mood disorders, knowledge of the underlying pathobiology remains sketchy. Overall, brain imaging changes in mood disorders exhibit some putatively specific findings. [30] Studies using high-resolution MRI have reported brain changes associated with major depression in the HC, amygdala, caudate nucleus, putamen and frontal region, [31] structures that are extensively interconnected and comprise a neuroanatomic circuit that has been termed the limbic-cortical-striatal-pallidal-thalamic tract .

Using MRI, Schaefer demonstrated gray matter volume differences in the dorsolateral prefrontal cortex, a region consistently implicated in functional neuroimaging studies of affective disorders. [32] Volume reductions has been seen in the frontal cortex ranging from 7% overall reduction in the frontal lobe volume to 48% in the subgenual prefrontal cortex. [9],[33] In some ways, the most provocative data linking the HC to major depressive disorder (MDD) have been from MRI studies of the volume of the HC in patients with MDD. Volume loss in the HC is the most robust finding and the only change consistently observed to persist past the resolution of the depression. The importance of the HC in the pathophysiology of MDD has also been supported by a substantial body of evidence from basic and clinical studies. [34] Post-mortem studies have shown moderate apoptosis in the dentate gyrus and the CA1 and CA4 regions of the HC of patients with MDD. [35] In most of the studies that assessed depression in unipolar subjects and used high-resolution MRI techniques, depression was associated with hippocampal volume loss, ranging from 8 to 19%. [36]

Sheline and colleagues reported bilateral HC volume reductions in women with MDD. [37] Other studies have reported that patients with depression have smaller left HC volumes than control subjects. [38] At the same time, at least one research also found reduction of right HC volume in depression as compared with controls [39] [Table 1]. Hippocampal volume in depressed subjects appears to be predicted by the length of the illness and other variables associated with past burden of illness. Investigations of patients with recurrent episodes have consistently indicated that there are structural changes in the hippocampal formation. [35] Moreover, Sheline et al., [37] in a study of middle-aged depressed women, found that hippocampal volume reduction was related to total lifetime duration of depression. This finding was recently replicated in a larger sample of patients, where they reported that past illness predicted HC volume reduction; others reported that volumetric reductions were greatest in patients with a chronic course and large number of weeks ill than in those who recovered fully with shorter overall illness duration. [40] In one study, hippocampal atrophy was found in patients with chronic depression but not in patients with remitted depression. [41] Studies analyzed in the comprehensive review [42] have yielded conflicting evidence. Some studies have reported no changes when depressed patients are compared with healthy controls. [43],[44],[45],[46],[47] Predominantly, evidence is suggestive of bilateral reduction in HC volume, [48],[49],[50],[51],[52],[53] and it is negatively correlated with duration of depression [Table 1].
Table 1: Hippocampal complex in MDD

Click here to view



   Mechanism of Hippocampal Atrophy in Depression Top


In the studies of depression in which hippocampal atrophy has been found, the implication is that excessively high levels of cortisol associated with the stress-related disorder cause hippocampal cell death and result in the hippocampal atrophy seen on MRI. Cellular studies of the HC in depression have revealed that volume reductions of the HC might be the result of remodeling of key cellular elements, involving retraction of dendrites, decreased neurogenesis in the dentate gyrus and loss of glial cells. [54],[55] This dysregulation of glucocorticoid secretion with increased activity of excitatory amino acid neurotransmitters could result in both potentially reversible remodelling and irreversible cell death in the HC of patients with MDD. [56]

It has, therefore, been proposed that raised cortisol levels during depression might be associated with cognitive impairments, [57] especially in functions subserved by medial temporal lobe structures. [58] A large body of evidence has also established a link between stressful life events and development or exacerbation of depression. At the cellular level, evidence has emerged indicating neuronal atrophy and cell loss in response to stress and in depression. At the molecular level, it has been suggested that these cellular deficiencies, mostly detected in the HC, result from a decrease in the expression of brain-derived neurotrophic factor associated with elevation of glucocorticoids. [59]


   Cognitive Dysfunction in Depression Top


Cognitive deficits in mood disorders have been addressed in different function domains, some of them being attention, executive function (EF) and memory. It is interesting to observe that cognitive deficits are noted even during the euthymic/remitted states, which indicates that certain cognitive deficits may be associated with trait characteristics. Impairment of working memory (WM), sustained attention, abstract reasoning and visuomotor skills, [60],[61] verbal memory, [62] verbal fluency [63] and visuospatial ability [64] have all been reported, even in the euthymic phase of the illness. The deficits have been shown to correlate with both the number of affective episodes and the overall duration of illness. [65]

EF is commonly seen in major depression. [66] The types of executive deficits seen in depression include problems with planning, completing goal-directed activities, organizing, initiating, sequencing, shifting, information processing speed, inhibiting context-inappropriate responses and maintaining information in the working memory. [67],[68],[69] The presence of EF in depression is associated with vocational disability and possibly poorer treatment response. Studies have documented EF in depression using the wisconsin card sorting test (WCST) as well as other such tests of cognitive dysfunction. [70]

Lesion studies in animals and neuropathological reports in humans have shown that defects in the medial temporal lobe region, including the hippocampal formation, are associated with a severe and global amnesia. Aside from its well-documented contribution to learning and memory, the hippocampal formation plays a critical role in the regulation of motivation and emotion. [71] This contribution of the HC to emotion and affective style has only recently begun to be gleaned from the available corpus of animal studies on its role in context-dependent memory. [72] Other studies have attempted novel emotional modification of the Wisconsin Card Sorting Test [73] and brought out a possible role of HC in context-dependant memory. The WCST may actually check this context-dependant memory, with its substrate in the medial temporal lobe, and show the impairments in depression. The causes and associations of impaired cognitive function during depression remain uncertain. Some authors have proposed that hypercortisolemia during depression may be important. Studies in animals and humans, involving both exogenous steroid administration and conditions such as Cushing's syndrome and stress, which raise endogenous levels, have shown a relationship between raised cortisol levels and neuropsychological dysfunction, especially memory impairment. [74] Both glucocorticoid and mineralocorticoid steroid receptors are present in high concentrations in the HC, and prolonged and raised cortisol levels can produce neuronal dysfunction. [75] It has been proposed that raised cortisol levels during depression might be associated with cognitive impairments, especially in functions subserved by medial temporal lobe structures, and that persisting hypercortisolemia might cause hippocampal damage, explaining why impairments persist in depressed subjects, even when affective symptoms have resolved. [76]


   Relationship of Cognitive Dysfunction with Severity of Illness Top


Although executive deficits have been reported in more severely depressed subjects with melancholic or psychotic features, scores may be affected even with relatively mild depression and EF may vary as a function of the severity of depression. significant association between depressive symptoms and magnitude of Wisconsin Card Sorting Test deficits in major depression have been seen. A few studies have shown higher cognitive impairment in psychotic depression. [77]

Merriam et al. [78] studied Wisconsin Card Sorting performance in a large group of patients with major depression who had been without medication for at least 28 days. They found significant deficits on various indices of the Wisconsin Card Sorting task in these patients in comparison with controls. [79] In patients with major depression, Hamilton depression scale scores were moderately correlated with the number of categories achieved, number of perseverative errors, number of perseverative responses and the percentage of conceptual-level responses. Patients with major depression made more perseverative and non-perseverative errors, took longer to reach the first category, completed fewer categories overall and had fewer conceptual-level responses and lower learning-to-learn scores than healthy subjects. Moreover, patients with more severe depression performed more poorly. Other authors have also described a positive correlation with duration of illness as well as with recurrent episodes of depression. The investigation in patients with euthymic status have also revealed impairment in cognitive domain. [80] The speed of information processing and response latency is another area of concern in patients of depression. [81] A study done by Taj [82] on patients of bipolar disorder in remission noted significant impairments in attention, executive function and memory in the study group compared with a matched control group of normal subjects. In fact, memory deficit pattern also did not differ in both unipolar and bipolar cases of depression [83]

[Table 2]. However, cognitive deficits did present in both types of depression. [84],[85] Interestingly, severity of depression was not associated with cognitive deficits. [86] Further patients with somatic syndrome had slower psychomotor speed and less mental flexibility compared with the non-somatic syndrome group. [87] There appears to be internal consistency in the findings in the domain of cognition and depression. Patients with depression are noted to be having various types of cognitive deficits; primarily, the affected area may be executive functioning and memory.
Table 2: Cognitive deficits and depression

Click here to view



   Conclusion Top


Major depression is a mood disorder that is often accompanied by the impairment of cognitive function. The severity of illness, duration of illness and other structural changes appear to be natural concomitants influencing the outcome of depression. The large range of existing neuropsychological, electrophysiological and, lately, neuroimaging investigations have provided evidence of structural changes and cognitive deficits in cases of depression. The severity and type of depression in respect of cognitive changes and anatomical substrate have not yielded very consistent findings. The evidence is suggestive of common tenet of derangement of cognitive functions in depression irrespective of the type of depression. Similarly, reduction in hippocampal volume is another indication. However, much more exhaustive, explicit and specific data analysis is required to yield a definite conclusion on structural changes leading to cognitive deficits in the cases of depression.

 
   References Top

1.The WHO World Mental Health Survey Consortium. Prevalence, severity and unmet need for treatment of mental disorders in the world health organization world mental health surveys. JAMA 2004;291:2581-90.  Back to cited text no. 1
    
2.Kessler RC, Demler O, Frank RG, Olfson M, Pincus HA, Walters EE, et al. Prevalence and treatment of mental disorders, 1990 to 2003. N Engl J Med 2005;352:2515-23.  Back to cited text no. 2
[PUBMED]  [FULLTEXT]  
3.Rao V. Depressive illness in India. Indian J Psychiatry 1984;26:301-11.  Back to cited text no. 3
[PUBMED]  Medknow Journal  
4.Sen B, Williams P. The extent and nature of depressive phenomenon in primary health care: A study in Calcutta, India. Br J Psychiatry 1987;151:486-93.  Back to cited text no. 4
[PUBMED]    
5.Ganguly HC. Epidemiological findings on prevalence of mental disorders in India. Indian J Psychiatry 2000;42:14-20.  Back to cited text no. 5
    
6.Ravnkilde B, Videbech P, Clemmensen K, Egander A, Rasmussen NA, Rosenberg R. Cognitive deficits in major depression. Scand J Psychol 2002;43:239-51.  Back to cited text no. 6
[PUBMED]  [FULLTEXT]  
7.Campbell S, Marriott M, Nahmias C, MacQueen GM. Lower hippocampal volume in patients suffering from depression: A meta-analysis. Am J Psychiatry 2004;161:598-607.  Back to cited text no. 7
[PUBMED]  [FULLTEXT]  
8.Videbech P, Ravnkilde B. Hippocampal volume and depression: A meta-analysis of MRI studies. Am J Psychiatry 2004;161:1957-66.  Back to cited text no. 8
[PUBMED]  [FULLTEXT]  
9.Coffey CE, Wilkinson WE, Weiner RD, Parashos IA, Djang WT, Webb MC, et al. Quantitative cerebral anatomy in depression: A controlled magnetic resonance imaging study. Arch Gen Psychiatry 1993;50:7-16.  Back to cited text no. 9
[PUBMED]  [FULLTEXT]  
10.Drevets WC. Functional anatomical abnormalities in limbic and prefrontal cortical structures in major depression. Prog Brain Res 2000;126:413-31.  Back to cited text no. 10
[PUBMED]  [FULLTEXT]  
11.Newberg AR, Davydow DS, Lee HB. Cerebrovascular disease basis of Depression. Int Rev Psychiatry 2006;18:433-41.  Back to cited text no. 11
[PUBMED]  [FULLTEXT]  
12.Campbell S, MacQueen G. An update on regional brain volume differences associated with mood disorders. Curr Opin Psychiatry 2006;19:25-33.  Back to cited text no. 12
[PUBMED]  [FULLTEXT]  
13.Davidson RJ, Pizzagalli D, Nitschke JB, Putnam K. ­Depression: Perspectives from affective neuroscience. Annu Rev Psychol 2002;53:545-74.  Back to cited text no. 13
[PUBMED]  [FULLTEXT]  
14.Hughes JR, John ER. Conventional and quantitative electroencephalography in psychiatry. J Neuropsychiatry Clin Neurosci 1999;11:190-208.  Back to cited text no. 14
[PUBMED]  [FULLTEXT]  
15.Boutros NN. A review of indications of routine EEG in clinical psychiatry. Hosp Community Psychiatry 1992;43:716-9.  Back to cited text no. 15
[PUBMED]  [FULLTEXT]  
16.Small JG. Psychiatric disorders and EEG. In: Niedermeyer E, Lopes da Silva F, editors. Electroencephalography: Basic principles, clinical applications, and related fields. Baltimore: Williams and Wilkins; 1993. p. 581-96.  Back to cited text no. 16
    
17.Hughes JR. The EEG in psychiatry: An outline with summarized points and references. Clin Electroencephalogr 1995;26:92-101.  Back to cited text no. 17
[PUBMED]    
18.Small JG, Small IF, Milstein V, Moore DF. Familial associations with EEG variants in manic-depressive disease. Arch Gen Psychiatry 1975;32:43-8.  Back to cited text no. 18
[PUBMED]  [FULLTEXT]  
19.Monakhov K, Perris C. Neurophysiological correlates of depressive symptomatology. Neuropsychobiology 1980;6:268-79.  Back to cited text no. 19
[PUBMED]    
20.Nystrom C, Matousek M, Hallstrom T. Relationships between EEG and clinical characteristics in major depressive disorder. Acta Psychiatr Scand 1986;73:390-4.  Back to cited text no. 20
    
21.Knott VJ, Lapierre YD. Computerized EEG correlates of depression and antidepressant treatment. Prog Neuropsychopharmacol Biol Psychiatry 1987;11:213-21.  Back to cited text no. 21
[PUBMED]    
22.American Electroencephalographic Society. Statement on clinical use of quantitative EEG. J Clin Neurophysiol 1987;4:75.  Back to cited text no. 22
    
23.Nuwer M. Assessment of digital EEG, quantitative EEG and EEG brain mapping: Report of the American Academy of Neurology and the American Clinical Neurophysiology Society. Neurology 1997;49:277-92.  Back to cited text no. 23
[PUBMED]    
24.Pollock VE, Schneider LS. Quantitative, waking EEG research on depression. Biol Psychiatry 1990;27:757-80.  Back to cited text no. 24
[PUBMED]  [FULLTEXT]  
25.Nystrom C, Matousek M, Hallstrom T. Relationships between EEG and clinical characteristics in major depressive disorder. Acta Psychiatr Scand 1986;73:390-4.  Back to cited text no. 25
    
26.Nieber D, Schlegel S. Relationships between psychomotor retardation and EEG power spectrum in major depression. Biol Psychiatry 1992;25:20-3.  Back to cited text no. 26
    
27.Knott VJ, Lapierre YD. Computerized EEG correlates of depression and antidepressant treatment. Prog Neuropsychopharmacol Biol Psychiatry 1987;11:213-21.  Back to cited text no. 27
[PUBMED]    
28.Gale A, Edwards J. The EEG and human behavior. In: Gale A, Edwards J, editors. Physiological Correlates of Human Behavior. Vol. 2. New York: Academic Press; 1983. p. 99-127.  Back to cited text no. 28
    
29.Robbins J. A symphony in the brain. New York: Atlantic Monthly Press; 2000.  Back to cited text no. 29
    
30.Mervaala E, Fohr J, Kononen M, Valkonen-Korhonen M, Vainio P, Partanen K, et al. Quantitative MRI of the hippocampus and amygdala in severe depression. Psychol Med 2000;30:117-25.  Back to cited text no. 30
    
31.Campbell S, MacQueen G. An update on regional brain volume differences associated with mood disorders. Curr Opin Psychiatry 2006;19:25-33.  Back to cited text no. 31
[PUBMED]  [FULLTEXT]  
32.Schlaepfer TE, Harris GJ, Tien AY, Peng L, Lee S, Pearlson GD. Structural differences in the cerebral cortex of healthy female and male subjects: A magnetic resonance imaging study. Psychiatry Res 1995;61:129-35.  Back to cited text no. 32
[PUBMED]    
33.Drevets WC, Videen TO, Price JL, Preskorn SH, Carmichael ST, Raichle ME. A functional anatomical study of unipolar depression. J Neurosci 1992;12:3628-41.  Back to cited text no. 33
[PUBMED]  [FULLTEXT]  
34.Campbell S, MacQueen G. Role of the hippocampus in the pathophysiology of major depression. J Psychiatry Neurosci 2004;29:417-26.  Back to cited text no. 34
[PUBMED]  [FULLTEXT]  
35.Krishnan KR, Doraiswamy PM, Figiel GS, Husain MM, Shah SA, Na C, et al. Hippocampal abnormalities in depression. J Neuropsychiatry Clin Neurosci 1991;3:387-91.  Back to cited text no. 35
[PUBMED]  [FULLTEXT]  
36.MacMaster FP, Kusumaka V. Hippocampal volume in early onset depression. BMC Med 2004;2:2.  Back to cited text no. 36
    
37.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.  Back to cited text no. 37
[PUBMED]  [FULLTEXT]  
38.Bremner JD, Narayan M, Anderson ER, Staib LH, Miller HL, Charney DS. Hippocampal volume reduction in major depression. Am J Psychiatry 2000;157:115-7.  Back to cited text no. 38
[PUBMED]  [FULLTEXT]  
39.Steffens DC, Byrum CE, McQuoid DR, Greenberg DL, Payne ME, Blitchington TF, et al. Hippocampal volume in geriatric depression. Biol Psychiatry 2000;48:301-9.  Back to cited text no. 39
[PUBMED]  [FULLTEXT]  
40.Shah PJ, Ebmeier KP, Glabus MF, Goodwin GM. Cortical grey matter reductions associated with treatment-resistant chronic unipolar depression. Controlled magnetic resonance imaging study. Br J Psychiatry 1998; 172 :527-32.  Back to cited text no. 40
[PUBMED]    
41.Starkman MN, Giordani B, Gebarski SS, Berent S, Schork MA, Schteingart DE. Decrease in cortisol reverses human hippocampal atrophy following treatment of Cushing's disease. Biol Psychiatry 1999;46:1595-602.  Back to cited text no. 41
[PUBMED]  [FULLTEXT]  
42.Savitz J, Drevets WC. Bipolar and major depressive disorder: Neuroimaging the developmental-degenerative divide. Neurosci Biobehav Rev 2009;33:699-771.  Back to cited text no. 42
[PUBMED]  [FULLTEXT]  
43.Vakili K, Pillay SS, Lafer B, Fava M, Renshaw PF, Bonello-Cintron CM, et al. Hippocampal volume in primary unipolar major depression: A magnetic resonance imaging study. Biol Psychiatry 2000;47:1087-90.  Back to cited text no. 43
[PUBMED]  [FULLTEXT]  
44.Rusch BD, Abercrombie HC, Oakes TR, Schaefer SM, Davidson RJ. Hippocampal morphometry in depressed patients and control subjects: Relations to anxiety symptoms. Biol Psychiatry 2001;50:960-4.   Back to cited text no. 44
[PUBMED]  [FULLTEXT]  
45.Posener JA, Wang L, Price JL, Gado MH, Province MA, Miller MI, et al. High-dimensional mapping of the hippocampus in depression. Am J Psychiatry 2003;160:83-9.  Back to cited text no. 45
[PUBMED]  [FULLTEXT]  
46.Janssen J, Hulshoff Pol HE, Lampe IK, Schnack HG, de Leeuw FE, Kahn RS, et al. Hippocampal changes and white matter lesions in early-onset depression. Biol Psychiatry 2004;56:825-31.  Back to cited text no. 46
[PUBMED]  [FULLTEXT]  
47.Rydmark I, Wahlberg K, Ghatan PH, Modell S, Nygren A, Ingvar M, et al. Neuroendocrine, cognitive and structural imaging characteristics of women on longterm sickleave with job stress-induced depression. Biol Psychiatry 2006;60:867-73.   Back to cited text no. 47
[PUBMED]  [FULLTEXT]  
48.Lloyd AJ, Ferrier IN, Barber R, Gholkar A, Young AH, O'Brien JT. Hippocampal volume change in depression: Late- and early-onset illness compared. Br J Psychiatry 2004;184:488-95.   Back to cited text no. 48
[PUBMED]  [FULLTEXT]  
49.O'Brien JT, Lloyd A, McKeith I, Gholkar A, Ferrier N. A longitudinal study of hippocampal volume, cortisol levels, and cognition in older depressed subjects. Am J Psychiatry 2004;161:2081-90.  Back to cited text no. 49
[PUBMED]  [FULLTEXT]  
50.Frodl T, Schaub A, Banac S, Charypar M, Jager M, Kummler P, et al. Reduced hippocampal volume correlates with executive dysfunctioning in major depression. J Psychiatry Neurosci 2006;31:316-23.  Back to cited text no. 50
    
51.Hickie I, Naismith S, Ward PB, Turner K, Scott E, Mitchell P, et al. Reduced hippocampal volumes and memory loss in patients with early- and late-onset depression. Br J Psychiatry 2005;186:197-202.  Back to cited text no. 51
[PUBMED]  [FULLTEXT]  
52.Macmaster FP, Mirza Y, Szeszko PR, Kmiecik LE, Easter PC, Taormina SP, et al. Amygdala and hippocampal volumes in familial early onset major depressive disorder. Biol Psychiatry 2008;63:385-90.  Back to cited text no. 52
[PUBMED]  [FULLTEXT]  
53.Tae WS, Kim SS, Lee KU, Nam EC, Kim KW. Validation of hippocampal volumes measured using a manual method and two automated methods in chronic major depressive disorder. Neuroradiology 2008;50:569-81.   Back to cited text no. 53
    
54.Magarinos AM, Deslandes A, McEwen BS. Effects of antidepressants and benzodiazepine treatments on the dendritic structure of CA3 pyramidal neurons after chronic stress. Eur J Pharmacol 1999;371:113-22.  Back to cited text no. 54
[PUBMED]    
55.Malberg JE, Eisch AJ, Nestler EJ, Duman RS. Chronic antidepressant treatment increases neurogenesis in adult rat hippocampus. J Neurosci 2000;20:9104-10.  Back to cited text no. 55
[PUBMED]  [FULLTEXT]  
56.Rajkowska G. Postmortem studies in mood disorders indicate altered numbers of neurons and glial cells. Biol Psychiatry 2000;48:766-77.  Back to cited text no. 56
[PUBMED]  [FULLTEXT]  
57.Sapolsky RM. Glucocorticoids and hippocampal atrophy in neuropsychiatric disorders. Arch Gen Psychiatry 2000;57:925-35.  Back to cited text no. 57
[PUBMED]  [FULLTEXT]  
58.Fossati P, Ergis AM, Allilaire JF. Executive functioning in unipolar depression: A review. Encephale 2002;28:97-107.  Back to cited text no. 58
[PUBMED]    
59.McEwen BS. Stress and hippocampal plasticity. Annu Rev Neurosci 1999;22:105-22.  Back to cited text no. 59
[PUBMED]  [FULLTEXT]  
60.Ferrier IN, Stanton BR, Kelly TP, Scott J. Neuropsychological function in euthymic patients with bipolar disorder. Br J Psychiatry 1999;175:246-51.  Back to cited text no. 60
[PUBMED]    
61.Clark LD, Iversen SD, Goodwin G. Sustained attention deficit in bipolar disorder. Br J Psychiatry 2002;180:313-9.  Back to cited text no. 61
    
62.Van Gorp WG, Altshuler L, Theberge DC, Mintz J. Declarative and procedural memory in bipolar disorder. Biol Psychiatry 1999;46:525-31.  Back to cited text no. 62
[PUBMED]  [FULLTEXT]  
63.El-Badri SM, Ashton CH, Moore PB, Marsh VR, Ferrier IN. Electrophysiological and cognitive function in young euthymic patients with bipolar affective disorder. Bipolar Disord 2001;3:79-87.  Back to cited text no. 63
[PUBMED]  [FULLTEXT]  
64.Denicoff KD, Ali SO, Mirsky AF, Smith-Jackson EE, Leverich GS, Duncan CC, et al. Relationship between prior course of illness and neuropsychological functioning in patients with bipolar disorder. J Affect Disord 1999;56:67-73.  Back to cited text no. 64
    
65.Stordal KI, Lundervold AJ, Egeland J. Impairment across executive functions in recurrent major depression. Nord J Psychiatry 2004;58:41-7.  Back to cited text no. 65
    
66.Channon S. Executive dysfunction in depression: The Wisconsin Card Sorting Test. J Affect Disord 1996;39:107-14.  Back to cited text no. 66
[PUBMED]  [FULLTEXT]  
67.Chen AC, Shirayama Y, Shin KH, Neve RL, Duman RS. Expression of the cAMP response element binding protein (CREB) in hippocampus produces an antidepressant effect. Biol Psychiatry 2001;49:753-62.  Back to cited text no. 67
[PUBMED]  [FULLTEXT]  
68.Pardo JV, Pardo PJ, Humes SW, I Posner M. Neurocognitive dysfunction in antidepressant-free, non-elderly patients with unipolar depression: Alerting and covert orienting of visuospatial attention. J Affect Disord 2006;92:71-8.  Back to cited text no. 68
[PUBMED]  [FULLTEXT]  
69.Nebes RD, Butters MA, Mulsant BH, Pollack BG, Zmuda MD, Houck PR, et al. Decreased working memory and processing speed mediate cognitive impairment in geriatric depression. Psychol Med 2000;30:679-91.  Back to cited text no. 69
    
70.Must A, Szabo Z, Bodi N, Szasz A, Janka Z, Keri S. Neuropsychological assessment of the prefrontal cortex in major depressive disorder. Psychiatr Hung 2005;20:412-6.  Back to cited text no. 70
    
71.Zola SM, Squire LR. The medial temporal lobe and the hippocampus. In: Tulving E, Craig FI, editors. The Oxford Handbook of Memory. New York: Oxford University Press; 2000. p. 485-500.  Back to cited text no. 71
    
72.Faneslow MS. Contextual fear, gestalt memories, and the hippocampus. Behav Brain Res 2000;110:73-81.  Back to cited text no. 72
    
73.Kurtz MM, Wexler BE. Differences in performance and learning proficiency on the Wisconsin Card Sorting Test in schizophrenia: Do they reflect distinct neurocognitive subtypes with distinct functional profiles? Schizophr Res 2006;81:167-71.   Back to cited text no. 73
[PUBMED]  [FULLTEXT]  
74.Starkman MN, Giordani B, Berent S, Schork MA, Schteingart DE. Elevated cortisol levels in Cushing's disease are associated with cognitive decrements. Psychosom Med 2001;63:985-93.  Back to cited text no. 74
[PUBMED]  [FULLTEXT]  
75.Newcomer JW, Selke G, Melson AK, Hershey T, Craft S, Richards K, et al. Decreased memory performance in healthy humans induced by stress-level cortisol treatment. Arch Gen Psychiatry 1999;56:527-33.  Back to cited text no. 75
[PUBMED]  [FULLTEXT]  
76.Coville WB, Millner B. Loss of recent memory after bilateral hippocampal lesions. J Neurol Neurosurg Psychiatry 1957;20:11-21.  Back to cited text no. 76
    
77.Schatzberg AF, Posener JA, DeBattista C, Kalehzan BM, Rothschild AJ, Shear PK. Neuropsychological deficits in psychotic versus nonpsychotic major depression and no mental illness. Am J Psychiatry 2000;157:1095-100.  Back to cited text no. 77
[PUBMED]  [FULLTEXT]  
78.Merriam EP, Thase ME, Haas GL, Keshavan MS, Sweeney JA. Prefrontal cortical dysfunction in depression determined by Wisconsin Card Sorting test performance. Am J Psychiatry 1999;156:780-2.  Back to cited text no. 78
[PUBMED]  [FULLTEXT]  
79.Nagahama Y, Okina T, Suzuki N, Nabatame H, Matsuda M. The cerebral correlates of different types of perseveration in the Wisconsin Card Sorting Test. J Neurol Neurosurg Psychiatry 2005;76:169-75.  Back to cited text no. 79
[PUBMED]  [FULLTEXT]  
80.Tandon R, Singh AP, Sinha PK, Trivedi JK. Executive functions in depression: A clinical report. Indian J Psychiatry 2002;44:343-7.   Back to cited text no. 80
[PUBMED]  Medknow Journal  
81.Purcell R, Maruff P, Kyrios M, Pantelis C. Neuropsychological function in young patients with unipolar major depression. Psychol Med 1997;27:1277-85.  Back to cited text no. 81
[PUBMED]    
82.Taj M, Padmavati R. Neuropsychological impairment in bipolar affective disorder. Indian J Psychiatry 2005;47:48-50.  Back to cited text no. 82
  Medknow Journal  
83.Bearden CE, Glahn DC, Monkul ES, Barrett J, Najt P, Villarreal V, et al. Patterns of memory impairment in bipolar disorder and unipolar major depression. Psychiatry Res 2006;142:139-50.  Back to cited text no. 83
[PUBMED]  [FULLTEXT]  
84.Mondal S, Sharma VK, Das S, Goswami U, Gandhi A. Neuro-cognitive functions in patients of Major depression. Indian J Physiol Pharmacol 2007;51:69-75.  Back to cited text no. 84
[PUBMED]    
85.Stoddart SD, Craddock NJ, Jones LA. Differentiation of executive and attention impairments in affective illness. Psychol Med 2007;37:1613-23.  Back to cited text no. 85
[PUBMED]  [FULLTEXT]  
86.McClintock SM, Cullum M, Husain MM, Rush AJ, Knapp RG, Mueller M, et al. Evaluation of the effects of severe depression on global cognitive function and memory. CNS Spectr 2010;15:304-13.  Back to cited text no. 86
[PUBMED]    
87.Mahajan R, Mahajan NS, Kaur D. Cognitive functions in depressed young adults with or without somatic syndrome. J Mental Health Hum Behav 2011;16:33-36.  Back to cited text no. 87
    



 
 
    Tables

  [Table 1], [Table 2]

This article has been cited by
1 Diagnosing and treating depression in epilepsy
Christian E. Elger,Samantha A. Johnston,Christian Hoppe
Seizure. 2016;
[Pubmed] | [DOI]



 

Top
  
 
  Search
 
  
    Access Statistics
    Email Alert *
    Add to My List *
* Registration required (free)  

 
  In this article
    Abstract
    Neurobiological ...
    Electroencephalo...
    Conventional Ver...
    Neuroimaging in ...
    Mechanism of Hip...
    Cognitive Dysfun...
    Relationship of ...
   Conclusion
    References
    Article Tables

 Article Access Statistics
    Viewed2902    
    Printed316    
    Emailed0    
    PDF Downloaded95    
    Comments [Add]    
    Cited by others 1    

Recommend this journal