Vignette 1. A 33-year-old man had acute onset of right-sided numbness and weakness with associated speech disturbance. He had been complaining of a pressure-type headache behind the left eye and neck discomfort for the past 10 days following a strenuous football practice. He was otherwise healthy with an unremarkable personal history. He did not use tobacco or illicit drugs and occasionally drank alcohol.
Neurologic examination revealed word-finding difficulties, left Horner syndrome, mild right central facial weakness, right hemiparesis, decreased sensation over the right hemibody, and an upgoing toe on the right.
Blood count, electrolytes, coagulation profile, and metabolic panel were within normal limits. Urine toxicology screen was negative. Initial cranial CT was negative. Echocardiogram was normal. MRI of the head showed an area of restricted diffusion in the left subcortical frontal lobe. MRA of the head was normal; MRA of the neck showed a cervical left internal carotid artery dissection extending 1.5 cm rostrally with significant luminal narrowing. He was anticoagulated with intravenous unfractionated heparin and was subsequently switched to warfarin therapy. A 3-month follow-up MRA showed recanalization of the left internal carotid artery. He was then switched to aspirin 325 mg daily. He remains asymptomatic.
Vignette 2. A 39-year-old woman with migraine without aura on oral contraceptives presented with a sudden-onset “worst headache of her life” with presyncopal episodes and right hemibody numbness and hemiparesis. She had 2 generalized tonic-clonic seizures on the date of admission and was loaded with intravenous valproic acid. Neurologic examination revealed right upper extremity pronator drift and mild right upper extremity weakness. Head CT without contrast demonstrated mild Sylvian fissure/temporo-occipital and left frontal convexity subarachnoid hemorrhage. There was hyperdensity in the superior sagittal sinus. CT angiography revealed absence of contrast enhancement in nearly the entire superior sagittal sinus, right transverse and sigmoid sinuses, and right internal jugular vein. No perfusion deficits were noted, although there was mild vasospasm of the M2 segment of the right MCA. Angiography demonstrated filling defects in the above vessels and in numerous bilateral paramedian frontoparietal cortical veins.
Lupus-sensitive activated partial thromboplastin time (aPTT) was mildly prolonged. There was no evidence of lupus anticoagulant or antiphospholipid antibody, however. Protein C & S levels, antithrombin, factor V Leiden mutation, activated protein C resistance, and prothrombin 20210A gene mutation were unremarkable. C-reactive protein was elevated (33.56 mg/L), and erythrocyte sedimentation rate was mildly elevated (21 mm/hr). Homocysteine was low (2.2 mcmol/L). Pregnancy screen and human immunodeficiency virus test were negative. Fasting lipids, complete blood count, antineuronal nuclear antibody, and rheumatoid factor were normal.
She was anticoagulated with heparin and started on Lovenox as a bridge to warfarin therapy. Mild right upper extremity pronator drift persisted at discharge. She was placed on levetiracetam and had no further seizures. A plan was made to repeat the lupus anticoagulant and antiphospholipid antibodies at 12 weeks.
Vignette 3. A right-handed, 16-year-old Hispanic woman living in a coastal rural community was admitted to the hospital 5 days after the sudden onset of an excruciating, throbbing left occipital headache, nausea, vomiting, and reduced level of consciousness. Five months before, she had been diagnosed with a molar pregnancy at 12 weeks of gestation, requiring dilatation and evacuation. She had no history of alcohol abuse, illicit drugs use, cranial trauma, or hematological disease; she was given no follow-up procedure after the early termination of this first pregnancy.
At hospital admission, her systemic examination was unremarkable. The neurologic examination showed an agitated and confused patient whose pupils were symmetric and responsive to light. Direct funduscopic examination was normal. No motor deficit was noted, and meningeal signs were present.
Coagulation screening was normal. Serum human chorionic gonadotropin levels were over 10,000 UI/ml. An initial noncontrast cranial CT showed a large left parietal hematoma involving the grey and white matter surrounded by a severe perilesional edema and ipsilateral intraventricular extension. Pelvic and pulmonary metastases were detected by pelvic ultrasonography and CT of the thorax, respectively. A brain MRI with and without contrast disclosed a large left parietal hematoma with intraventricular extension and severe perilesional edema. A small, ill-defined hyperintense lesion was also observed on the contralateral parietal lobe.
A diagnosis of intracranial bleeding due to metastatic choriocarcinoma was established, and the oncology department planned to start intravenous chemotherapy. Nevertheless, her condition deteriorated over the course of the next 3 days. A second noncontrast CT scan showed a large bilateral hematoma in both parietal lobes. She was progressively unresponsive and then died. An autopsy was not performed.