RESUMO
OBJECTIVE: To describe a case of a fusiform aneurysm of the basilar artery presented as a pontine infarct and 2 days later as a subarachnoid hemorrhage caused by the rupture of the same aneurysm. DESIGN: Case report. SETTING: Tertiary-care hospital. BACKGROUND: Fusiform aneurysm of cerebral vessels is a rare pathology that presents with ischemic stroke, subarachnoid hemorrhage, or mass effect. Ischemia and subarachnoid hemorrhage in the same patient 2 days apart, to our knowledge, was not reported before. SUBJECT: A 55-year-old Hispanic man with history of untreated hypertension and alcohol abuse presented with acute onset of right hemiparesis and dysarthria. On day 2 of his hospital admission, he developed arrhythmia and loss of consciousness. The patient expired from cardiac arrest on day 4 of his hospitalization. Initial head computed tomography scan showed dolichoectatic basilar artery and marked calcification of internal carotid arteries (ICA) and middle cerebral arteries (MCA). Brain magnetic resonance imaging showed left upper pons infarct 2 cm in diameter. Magnetic resonance angiography confirmed presence of a fusiform aneurysm of the basilar artery. Head computed tomography scan at the time of clinical deterioration on day 2 of hospital admission showed subarachnoid bleeding and significant brain edema. Autopsy revealed a ruptured basilar artery aneurysm with thrombus in the lumen and left pontine infarct. Microscopic examination of fusiform aneurysm showed atherosclerosis of the aneurysmal wall and attenuation and inflammation at the rupture site. CONCLUSIONS: We hypothesize that in our case, pontine infarct had developed because of occlusion of pontine perforators by a thrombus within an aneurysm, and subarachnoid hemorrhage had developed secondary to a rupture of weakened by inflammatory changes aneurysmal wall. We also hypothesize that in our case, ischemic stroke and subsequent subarachnoid hemorrhage may represent different stages of the same process of atherosclerosis and inflammation in an aneurysmal wall confirmed by autopsy. Origin as well as management of fusiform cerebral aneurysms are unclear. Antiplatelet agents and anticoagulation are recommended by some for stroke prophylaxis in patients with unruptured fusiform cerebral aneurysms. Our case shows that caution should be exercised in prescribing anticoagulants or even antiplatelet agents to a patient with fusiform aneurysm of cerebral arteries due to a possibility of rupture of an aneurysm. Randomized prospective study may be necessary to clarify this issue.
RESUMO
OBJECTIVE: To report an unusual presentation of mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS) manifested in late life with a clinical picture of herpes simplex encephalitis. DESIGN: Case report. SETTING: Clinical neurology department in a tertiary care hospital. CASE DESCRIPTION: A 55-year-old woman developed aphasia and delirium during ophthalmic herpes zoster infection treated with oral prednisone and ophthalmic steroids, which was followed by progressive cognitive decline without acute neurologic events for 5 years. At age 60, the patient presented with new onset of seizures, hemiparesis, and hemianopsia. Subsequently she developed cortical blindness, multiple traumatic soft tissue injuries from falls, acute psychosis, and severe dementia with periods of agitation. She died in a nursing home in March 1997, 6 years after initial presentation. RESULTS: Magnetic resonance imaging scan of the brain showed hyperintensity on T2-weighted images involving temporal, parietal, and occipital lobes bilaterally as well as mild atrophy of brainstem and cerebellum. Single photon emission computed tomographic imaging showed hypoperfusion of temporal, parietal, and occipital lobes. Results of video electroencephalographic monitoring showed periodic lateralizing epileptiform discharges in temporal and occipital areas. The serum lactate level was normal in May 1996 and elevated in October 1996. The creatine kinase level was elevated with a 100% MM fraction in August 1991 and normal in March 1996. Results of repeated cerebrospinal fluid analyses indicated elevated protein levels. Analysis of DNA was diagnostic of MELAS by mitochondrial DNA point mutation at position 3243. The results of autopsy showed moderate cerebral, cerebellar, and brainstem atrophy with signs of infarction in temporal and parietal lobes bilaterally. CONCLUSIONS: The clinical presentation as well as age at onset of MELAS are highly variable. Onset of mitochondrial disorders can be provoked by febrile illness when there is mismatch between energy requirements and availability. In the differential diagnosis of herpes encephalitides, MELAS syndrome should be considered.
