A Case of Traumatic Brain Injury Developing Frontal Lobe Syndrome after a Long Incubation Period
Autor: | Tomoki Kaneko, Junya Nagasawa, Miho Takahashi, Naoji Amano |
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Rok vydání: | 2001 |
Předmět: |
Cerebral atrophy
medicine.medical_specialty Traumatic brain injury Ischemia Brain damage medicine.disease Lesion Psychiatry and Mental health Atrophy Frontal lobe Normal pressure hydrocephalus Anesthesia Internal medicine medicine Cardiology Geriatrics and Gerontology medicine.symptom Psychology Gerontology |
Zdroj: | Psychogeriatrics. 1:147-150 |
ISSN: | 1479-8301 1346-3500 |
DOI: | 10.1111/j.1479-8301.2001.tb00011.x |
Popis: | 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 ac- count 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 atro- phic 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 emis- sion computer tornography (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. Conse- quently, 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 dys- function of the compensated brain. However, such severe atrophy and focal damaged lesion could not be solely accounted for by heavy alcohol consump- tion. 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 devel- oped frontal lobe syndrome based on traumatic brain injury and induced by continuous drinking, aging, and brain circulatory insufficiency. |
Databáze: | OpenAIRE |
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