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Stroke as a model of affective disorder
BIOL PSYCHIATRY 1992;31:61A-252A
76A
Neurological Diseases and Psych,~atric Illness
Personality Questionnaire (TPQ) to study PD patients and matched medical controls. Two of these studies found novelty seeking (NS), which is thought to be dopamine dependent, to be significantly lower (p < 0.03, p < 0.05) in PD patients than in medical controls. There were no differences in either study between groups in traits thought to be dependent on serotonin or norepinephrine. Further data supporting this hypothesis that personality traits in PD are related to dopaminergic tone comes from preliminary data on the effect of L-deprenyl, an MAO-B inhibitor metabolized to amphetamine, on NS in PD. PD patients on deprCnyl were found to have significantly higher NS than those not on deprenyl.
33
ADRENOLEUKODYSTROPHY Hugo W. Moser Kennedy Institute, Baltimore, MD 21205. Adrenoleukodystrophy (ALD) is an X-linked recessive disorder that affects mainly the nervous system white matter, the adrenal cortex, and the Leydig cells in the testis. It is associated with the abnormal accumulation of saturated, very long chain fatty acids (VLCFA) due to the impaired capacity to degrade these substances, a reaction that normally takes place in the peroxisome. The disorder has been mapped to Xq28. Clinical manifestations vary markedly, from a rapidly progressive childhood cerebral form, to an adult form called adrenomyeloneuropathy (AMN) that progresses slowly over decades to a form that manifests as Addison's disease without neurological involvement. "l:he various phenotypes occur frequently within the same family and even sibships, and segregation analysis suggests the existence of a modifier gene. ALD presents commonly as a psychiatric disorder. Therapeutic interventions include a promising dietary approach and bone marrow transplantation.
34
STROKE AS A MODEL OF AFFECTIVE DISORDER Robert G. Robinson University of Iowa, College of Medicine, Iowa City, IA 52242. A major problem h~ studying the mechanism of affective disorder is uncertainty about the nature and location of neuropathology that underlies this mental disorder. We have used patients with stroke as a way of investigating important brain regions involved in affective disorder, in a study of 103 consecutive patients, major depression occurred in approximately 25% of patients with acute stroke and in 60% of the 16 patients with left dorsolateral frontal cortex and 80% of 8 patients with left basal ganglia lesions (p < 0,01 compared with 20 patients with right lesions or 12 with left tJosterior lesions). Variations in clinical presentation may also be related to differences in lesion location. For example, in a study of 98 patients with acute stroke, major depression with generalized anxiety disorder occurred in 16 of 19 patients with left frontal cortical brain injury compared with 7 of 15 with major depression alone or 13 of 27 with no mood disturbance group (p < 0.02). The hypothesis that this may be a model for studying the mechanisms of affective disorder is supported by the findings that clinical symptomatology and natural course of poststroke major depression and affective disorder are similar. In addition, PET studies by other investigators, as well as our group, have demonstrated the importance of left prefrontal cortex, left basal ganglia, and left temporal cortex in both affective disorder and poststroke model disorder.
76A
Neurological Diseases and Psych,~atric Illness
Personality Questionnaire (TPQ) to study PD patients and matched medical controls. Two of these studies found novelty seeking (NS), which is thought to be dopamine dependent, to be significantly lower (p < 0.03, p < 0.05) in PD patients than in medical controls. There were no differences in either study between groups in traits thought to be dependent on serotonin or norepinephrine. Further data supporting this hypothesis that personality traits in PD are related to dopaminergic tone comes from preliminary data on the effect of L-deprenyl, an MAO-B inhibitor metabolized to amphetamine, on NS in PD. PD patients on deprCnyl were found to have significantly higher NS than those not on deprenyl.
33
ADRENOLEUKODYSTROPHY Hugo W. Moser Kennedy Institute, Baltimore, MD 21205. Adrenoleukodystrophy (ALD) is an X-linked recessive disorder that affects mainly the nervous system white matter, the adrenal cortex, and the Leydig cells in the testis. It is associated with the abnormal accumulation of saturated, very long chain fatty acids (VLCFA) due to the impaired capacity to degrade these substances, a reaction that normally takes place in the peroxisome. The disorder has been mapped to Xq28. Clinical manifestations vary markedly, from a rapidly progressive childhood cerebral form, to an adult form called adrenomyeloneuropathy (AMN) that progresses slowly over decades to a form that manifests as Addison's disease without neurological involvement. "l:he various phenotypes occur frequently within the same family and even sibships, and segregation analysis suggests the existence of a modifier gene. ALD presents commonly as a psychiatric disorder. Therapeutic interventions include a promising dietary approach and bone marrow transplantation.
34
STROKE AS A MODEL OF AFFECTIVE DISORDER Robert G. Robinson University of Iowa, College of Medicine, Iowa City, IA 52242. A major problem h~ studying the mechanism of affective disorder is uncertainty about the nature and location of neuropathology that underlies this mental disorder. We have used patients with stroke as a way of investigating important brain regions involved in affective disorder, in a study of 103 consecutive patients, major depression occurred in approximately 25% of patients with acute stroke and in 60% of the 16 patients with left dorsolateral frontal cortex and 80% of 8 patients with left basal ganglia lesions (p < 0,01 compared with 20 patients with right lesions or 12 with left tJosterior lesions). Variations in clinical presentation may also be related to differences in lesion location. For example, in a study of 98 patients with acute stroke, major depression with generalized anxiety disorder occurred in 16 of 19 patients with left frontal cortical brain injury compared with 7 of 15 with major depression alone or 13 of 27 with no mood disturbance group (p < 0.02). The hypothesis that this may be a model for studying the mechanisms of affective disorder is supported by the findings that clinical symptomatology and natural course of poststroke major depression and affective disorder are similar. In addition, PET studies by other investigators, as well as our group, have demonstrated the importance of left prefrontal cortex, left basal ganglia, and left temporal cortex in both affective disorder and poststroke model disorder.