Treatment resistant depression in a case of minor head injury: an electrophysiological hypothesis.
A relatively small but highly concordant literature suggests that manic depressive psychoses may include familial as well as nonfamilial subtypes. The latter, which appears to be an acquired form, follows brain injury of various etiology, displays EEG abnormalities and tends to respond well to anticonvulsant therapy. In this study we postulate an extension of this dichotomy to a larger spectrum of affective disorder, including milder but "treatment resistant" forms often associated with a high degree of dysfunction. Central to this hypothesis is information gathered from the longitudinal study of a well defined case in which precise clinical and electrophysiological data have been obtained at critical junctures. This data also leads us to suggest the existence of a latent vulnerability to psychosocial stressors in a subgroup of minor head injured patients. Once triggered, the resulting psychopathological state may be clinically indistinguishable from similar but etiologically distinct conditions. However, they respond poorly, if at all, to the treatments usually effective for mood disorders, often causing puzzlement and frustration among clinicians as well as mounting hopelessness in patients. This organic mood disorder subtype, which can be described as "neuro-sensitization mood disorder," may be identified by combining a thorough history, including perinatal events and putative brain injury, with electrophysiological data consisting of quantitative EEG (QEEG) in association with evoked potentials. In cases with positive findings, anticonvulsants such as carbamazepine, clonazepam and valproic acid can be a treatment of choice.
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Brain Research Laboratories, New York University Medical Center, NY 10016.
Prichep
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Alper
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D000328:Adult; D000928:Antidepressive Agents / Q000627:therapeutic use*; D001714:Bipolar Disorder / Q000188:drug therapy / Q000503:physiopathology / Q000523:psychology; D002220:Carbamazepine / Q000627:therapeutic use*; D002540:Cerebral Cortex / Q000187:drug effects / Q000503:physiopathology; D003866:Depressive Disorder / Q000188:drug therapy / Q000503:physiopathology* / Q000523:psychology; D004569:Electroencephalography / Q000187:drug effects; D005071:Evoked Potentials / Q000187:drug effects / Q000502:physiology; D005260:Female; D006117:Grief; D016489:Head Injuries, Closed / Q000188:drug therapy / Q000503:physiopathology* / Q000523:psychology; D006801:Humans; D019965:Neurocognitive Disorders / Q000188:drug therapy / Q000503:physiopathology* / Q000523:psychology
D000928:Antidepressive Agents; D002220:Carbamazepine