Secondary Hypomania Following Left Temporopolar and Bilateral Orbitofrontal Damage
2
조회
0
다운로드
0
인용
0
참고문헌
키워드
초록
We present the case of a 49-year-old man with secondary hypomania and subtle cognitive and emotional deficits subsequent to a traumatic brain injury. Hypomanic symptoms followed by a depressive episode were observed 3 weeks after the traumatic injury. Neuroradiological examinations revealed a circumscribed lesion in the left temporal pole and bilateral orbitofrontal cortices. The hypomanic episode was successfully treated with quetiapine. However, subtle cognitive and emotional deficits, including inappropriate laughing in the absence of humorous or pleasurable content, nonspontaneous speech, and irrelevant speech during verbal communication, have persisted. The present case study supports the idea that both the left temporopolar and bilateral orbitofrontal dysfunctions are candidates for the neurobiological basis of bipolar disorder and that subtle cognitive and emotional deficits leading to functional impairments may remain after resolving secondary hypomania.
Abstract
We present the case of a 49-year-old man with secondary hypomania and subtle cognitive and emotional deficits subsequent to a traumatic brain injury. Hypomanic symptoms followed by a depressive episode were observed 3 weeks after the traumatic injury. Neuroradiological examinations revealed a circumscribed lesion in the left temporal pole and bilateral orbitofrontal cortices. The hypomanic episode was successfully treated with quetiapine. However, subtle cognitive and emotional deficits, including inappropriate laughing in the absence of humorous or pleasurable content, nonspontaneous speech, and irrelevant speech during verbal communication, have persisted. The present case study supports the idea that both the left temporopolar and bilateral orbitofrontal dysfunctions are candidates for the neurobiological basis of bipolar disorder and that subtle cognitive and emotional deficits leading to functional impairments may remain after resolving secondary hypomania.
참고문헌 (17)
- Robinson RG, "Price TR. Compari-son of mania and depresion after brain injury", pp.198 172~178
- Starkstein SE, "Robinson RG. Mechanisms of mania after brain injury. 12 case reports and review of the literature. J Nerv Ment Dis 1988", pp.87~100
- "Khosla N. Meningeal cryptococcosis misdiagno-sed as a manic episode. Am J Psychiatry 1984", pp.1459~1460
- Benoit N, "Lher-mitte F. Manic-like state after bilateral orbitofrontal and right temporoparietal injury efficacy of clonidine. Neurology 1989", pp.777~781
- Starkstein SE, "Mechanism of disinhibition after brain lesions", 185, pp.108~14 (1997)
- Fenn D, "Post-stroke mania late in life involving the left hemisphere", 33, pp.598~600 (1999)
- Brooks JO, "Hoblyn JC. Secondary mania in older adults. Am J Psychiatry 205", pp.2033~2038
- "Porto JAD. Bipolar disorder following a left basal-ganglia stroke. Br J Psychiatry 1993", pp.690~
- "Robinson RG. Mood Disorders Secondary to Stroke. Semin Clin Neuropsychiatry 197", pp.244~251
- Gafoor R, "Three case reports of secondary mania: evidence supporting a right frontotemporal locus", 18, pp.32~33 (2003)
- Shulman KI, "Disinhibition syndromes, secondary mania and bi-polar disorder in old age", 46, pp.175~182 (1997)
- Mendez MF, "Mania in neurologic disorders", 2, pp.440~445 (2000)
- Shenton ME, "et al. Differences and similarities in insular and temporal pole MRI gray matter volume abnormalities in first-episode schizophrenia and affective psychosis. Arch Gen Psychiatry 203", pp.1069~107
- Blair RJ, "Disocia-ble neural responses to facial expressions of sadness and anger", 122(5), pp.883~893 (1999)
- Arnold SE, "Hoesen GWV. Neuropathologic changes of the temporal pole in Alzheimers disease and Picks disease. Arch Neurol 194", pp.145~150
- asso-ciation areas, "Mesulam MM. Patterns in behavioural neuroanatomy Principles of Behavioral Neurology. Philadelphia" (1985)
- Murai T, "Rapid cycling bipolar disorder after left temporal polar damage", 17, pp.355~358 (2003)