Regional Brain Abnormalities

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a. Cortical Changes Studies of frontal lobe abnormalities among patients with mood disorders have reported findings such as smaller mean frontal area or higher T1 values on MRI scan in the frontal lobe in patients with UP depressive disorder but not in patients with BP disorder. However, additional studies of prefrontal cortical gray matter volume with better definition of what constitutes medial, dorsal, lateral, and orbital frontal cortex are needed to determine whether structural frontal abnormalities are associated with primary mood disorder. Based on consistent findings using functional imaging techniques of abnormal function in prefrontal cortex, it seems likely that structural abnormalities of prefrontal cortex may be identified in the future.

Studies of temporal lobe structure have reported decreased temporal lobe area in patients with mood disorders. These findings, however, have been inconsistent; in fact, one study reported an increase in left temporal volume in BP patients compared to controls. Studies of temporal lobe asymmetries have reported smaller left compared to right temporal lobe volumes in BP patients compared to controls, but one study found the reversed pattern. Overall, there is lack of agreement as to whether structural temporal abnormalities occur in either BP patients or UP patients. Further studies need to be conducted using better definitions of temporal structures and including subregions within the temporal lobe.

b. Subcortical Changes Examinations of subcortical structures have found conflicting evidence about abnormalities of the thalamus. A recent study reported increased thalamic volume in patients with BP disorder compared to controls and decreased thalamic volume in unipolars compared to controls. Since the thalamus constitutes part of the cortical-striatal-thalamic loops that have been proposed in numerous studies to constitute the anatomical substrate of mood disorders (Fig. 1), additional studies of thalamic structures including examination of specific nuclei need to be conducted.

Several studies have examined the amygdala and hippocampus. However, there is a lack of consistent evidence demonstrating structural abnormalities in the amygdala or hippocampus in patients with mood disorders. Although the amygdala-hippocampal complex volume was reported in one study to be not significantly different than that of controls, another study reported increased hippocampal volume in bipolars, with the left hippocampus being significantly larger than the right compared with controls.

The largest number of subcortical structural studies have examined abnormalities of the basal ganglia. Several studies have reported significantly smaller putamen and caudate volumes in patients with UP disorder compared to controls. A few studies of patients with BP disorder have reported larger caudate volumes bilaterally in males compared to females.

Studies of subcortical hyperintensities on MRI scan have generally reported that the presence of basal ganglia lesions is strongly associated with mood disorder. These focal hyperintensities (thought to be predominantly vascular lesions) have been the most consistent structural abnormality found in patients

Figure 1 Schematic drawing of the relationship and direction of axonal projections for structures of the ventral-lateral limbic circuit. These interrelationships may explain why both acute lateral frontal (prefrontal) and basal ganglia (caudate) dysfunction could be associated with depression. These circuits may also explain why both metabolic and serotonin S2 receptor changes in the temporal cortex (basal polar) may also be associated with depression.

Figure 1 Schematic drawing of the relationship and direction of axonal projections for structures of the ventral-lateral limbic circuit. These interrelationships may explain why both acute lateral frontal (prefrontal) and basal ganglia (caudate) dysfunction could be associated with depression. These circuits may also explain why both metabolic and serotonin S2 receptor changes in the temporal cortex (basal polar) may also be associated with depression.

Figure 2 The percentage of patients with major or minor depression based on the localization of their subcortical lesions. Patients with left basal ganglia lesions had a significantly higher frequency of major depression than those with lesions at any other location. BG, basal ganglia; TH, thalamus (data from Starkstein et al., 1989, with the permission of Cambridge University Press).

Figure 2 The percentage of patients with major or minor depression based on the localization of their subcortical lesions. Patients with left basal ganglia lesions had a significantly higher frequency of major depression than those with lesions at any other location. BG, basal ganglia; TH, thalamus (data from Starkstein et al., 1989, with the permission of Cambridge University Press).

with primary mood disorders. However, this appears to be predominantly a phenomenon of the elderly since the majority of studies reporting hyperintensity have been conducted in this population. Only one or two studies of nonelderly depressives found these ischemic abnormalities.

Another new area of investigation in the structural brain imaging of patients with mood disorder has been the identification of silent brain infarctions. Two studies have reported an increased frequency of silent ischemic infarctions as imaged by MRI in patients with senile-onset major depression compared with prese-nile-onset depression. Silent cerebral infarction was found in 100% of patients with onset of depression after age 65 compared to 53.6% with onset of depression between ages 50 and 65 and 20% with onset of depression prior to age 50.

Among patients with secondary depressions, three studies have examined the role of basal ganglia lesions in depressive disorder. They have all reported a significant association between infarction in the basal ganglia and poststroke depressive disorder. In contrast, lesions of the thalamus have not been significantly associated with poststroke mood disorder (Fig. 2).

Laterality has also been examined with regard to the structural basis of mood disorders. Although studies of primary mood disorders have not identified lateralized structural asymmetries associated with mood disorder, functional imaging studies in patients with primary mood disorders have frequently reported brain asymmetries. In addition, studies of secondary depressive disorder have frequently reported an association between laterality of brain injury and frequency of mood disorders. Five independent studies have reported that major depression was significantly more frequent among patients with acute or subacute left frontal or left basal ganglia lesions compared to those with lesions in other locations (Fig. 2). However, the association of left frontal and left basal ganglia lesions with major depressive disorder appears to be a phenomenon influenced by time since injury. Patients who are studied within the first few months following stroke show the most prominent association between the hemispheric side of the lesion and the frequency of major poststroke depression (Fig. 3). The studies that have failed to show a lateralized effect of brain lesions on depression have generally examined patients who are several months to several years poststroke.

Additional support for the suggestion that lateralized brain mechanisms may be involved in the production of mood disorders is provided by two controlled case studies and numerous anecdotal case reports of mania associated with injury to the right hemisphere. Thus, left frontal and left basal ganglia lesions have been associated with major depression, whereas right orbital frontal, basotemporal, basal ganglia, and thalamic lesions have been associated with mania.

Figure 3 The frequency of major and minor depression defined by DSM-IV criteria associated with single lesions of the right (R) or left (L) hemisphere during the acute stroke period and at follow-up. The lateralized effect of left hemisphere lesions on both major and minor depression was found only during the acute stroke period. At short-and long-term follow-up, there were no hemispheric lesion effects on the frequency of depression. From Robinson (1998); reprinted with the permission of Cambridge University Press.

Figure 3 The frequency of major and minor depression defined by DSM-IV criteria associated with single lesions of the right (R) or left (L) hemisphere during the acute stroke period and at follow-up. The lateralized effect of left hemisphere lesions on both major and minor depression was found only during the acute stroke period. At short-and long-term follow-up, there were no hemispheric lesion effects on the frequency of depression. From Robinson (1998); reprinted with the permission of Cambridge University Press.

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