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A Case of Traumatic Brain Injury Developing Frontal Lobe Syndrome after a Long Incubation Period
Author(s) -
Nagasawa Junya,
Amano Naoji,
Takahashi Miho,
Kaneko Tomoki
Publication year - 2001
Publication title -
psychogeriatrics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.647
H-Index - 32
eISSN - 1479-8301
pISSN - 1346-3500
DOI - 10.1111/j.1479-8301.2001.tb00011.x
Subject(s) - frontal lobe , medicine , atrophy , lesion , lateral ventricles , cerebral atrophy , temporal lobe , brain damage , magnetic resonance imaging , cardiology , anatomy , pathology , radiology , epilepsy , psychiatry
Abstract : A 55‐year‐old man, who was a heavy drinker for about 30 years, had experienced a heavy blow on the right posterior temporal region on account of a traffic accident at the age of 16. He recovered without any sequelae. However, he began to make mistakes and had trouble with his job about 40 years after the accident. His symptoms and neuropsychological examination suggested frontal lobe syndrome. Cranial magnetic resonance imaging (MRI) showed that the frontal and temporal lobes seemed to be predominantly atrophic and that there was great enlargement of the lateral and third ventricles, and a post‐contusion lesion in the left frontal lobe. Brain single photon emission computer tomography (SPECT) demonstrated diffuse cerebral hypoperfusion. Cranial MRI suggested that the contusion was proportionate to contre coup injury resulting from the accident. We supposed that the extensive brain damage induced edema and ischemia soon after the accident. Consequently, the circulatory disturbance might have caused cerebral atrophy and enlargement of the ventricles. Since he was relatively young at the time of the accident, the plasticity of his brain compensated for the injury intensively, and obvious symptoms suggesting frontal lobe syndrome were latent for about 40 years after the accident. Continuous drinking may have induced recent dysfunction of the compensated brain. However, such severe atrophy and focal damaged lesion could not be solely accounted for by heavy alcohol consumption. On the other hand, organic changes due to aging and brain circulatory insufficiency caused by hypertension or hyperlipidemia may also disclose the cerebral dysfunction. His cranial MRI and SPECT seemed not to be consistent with frontotemporal dementia. Furthermore, we considered that his case was also different from Alzheimer's disease and normal pressure hydrocephalus. However, it is necessary to follow up neuro‐imaging. Conclusively, he developed frontal lobe syndrome based on traumatic brain injury and induced by continuous drinking, aging, and brain circulatory insufficiency.