A 67-year-old man presented with limbic encephalitis diagnosed from clinical symptoms and abnormal findings on brain magnetic resonance imaging. No abnormalities in laboratory measures of systemic inflammation were observed on admission. Fluorodeoxyglucose-positron emission tomography/computed tomography showed mild uptake in the right auricle. Histological examination of biopsy specimens showed abnormalities consistent with relapsing polychondritis. Subsequently, the patient developed bilateral auricular erythema, an elevated erythrocyte sedimentation rate and a raised serum C-reactive protein level. The early diagnosis of relapsing polychondritis in the present case was clinically challenging, as limbic encephalitis preceded the development of elevated systemic inflammation parameters and typical symptoms of relapsing polychondritis. Fluorodeoxyglucose-positron emission tomography/computed tomography has utility in the systemic evaluation of limbic encephalitis when the underlying cause is unknown.
Patient: Male, 42-year-old
Final Diagnosis: Traumatic posterior cerebral artery aneurysm
Symptoms: Deterioration of mental status and disorientation
Medication: —
Clinical Procedure: Parent artery occlusion by endovascular approach
Specialty: Neurosurgery
Objective:
Unusual clinical course
Background:
Subdural hematoma (SDH) caused by traumatic intracranial aneurysm (TICA) is rare. TICAs are known to rupture easily, resulting in a high morbidity and mortality rate. Therefore, accurate diagnosis and treatment are crucial for preserving life. We describe a case of delayed SDH in the setting of posterior cerebral artery (PCA) aneurysm.
Case Report:
A 42-year-old man presented with sustained head injury from a traffic accident, and was being followed-up conservatively for traumatic SDH and subarachnoid hemorrhage. Three weeks after the head trauma, the patient developed a sudden deterioration of mental status and disorientation. Computed tomography revealed de novo SDH at the cerebellar tentorium. Computed tomography angiography and magnetic resonance imaging demonstrated TICA in the PCA. The patient was diagnosed with SDH due to a ruptured PCA aneurysm at the quadrigeminal segment. To avoid SDH growth due to re-rupture of the aneurysm, parent artery occlusion was subsequently performed with no complications. The patient was discharged home 2 months after endovascular treatment, with moderate disability. Follow-up angiography 2 years after the operation showed no recanalization, and the patient had returned to work.
Conclusions:
TICA in the PCA can cause tentorial SDH with or without the presence of subarachnoid hemorrhage. Routine cerebrovascular assessment is crucial for head trauma with hematoma adjacent to the cerebellar tentorium. Parent artery occlusion via an endovascular procedure is an alternative treatment for TICA in the PCA that is less invasive than other approaches.
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