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A 24-year-old man presented with a persistent headache of 5 day’s duration. It had increased in severity several hours before coming to the ED. The headache was relatively constant and had intermittent exacerbations. It was bitemporal, but worse on the right than left. At the time of his initial evaluation, the pain was rated 5/10 in severity. He had taken 800 mg of ibuprofen with partial relief.

There was no associated fever, sinus congestion, neck stiffness, or visual or focal neurological symptoms. There was no family history of migraine or other headache disorder. The patient had begun his third year of law school 3 weeks earlier.

He had no significant past medical history. He had not recently traveled outside of New York City and had no history of head trauma.

His physical examination was essentially normal, including vital signs, head, neck, and neurological examinations. There was no nuchal rigidity.

A head CT was obtained (Figure 1).

  • Are there any abnormalities?

(Had an LP been performed, the CSF cell count and chemistries would have been normal.)

Examination of a head CT in a patient with headache begins by looking for symmetry and midline shift. Next, the basilar cisterns are examined for evidence of SAH. Ventricular size and shape are assessed; ventricular enlargement may be a sign of hydrocephalus. Finally, several serious disorders can produce other, sometimes subtle, CT findings should be sought.

On this patient’s head CT, there is no midline shift, mass effect, or asymmetry. The basilar cisterns and ventricles are normal. On image 7 (Figure 2A), there is a small hyperattenuating region (white) in the posterior midline. This represents clotted blood. However, rather than being an extra-axial hematoma, it represents clotted blood within a cerebral venous sinus. It is located at the confluence of the superior sagittal sinus and transverse sinuses (the torcula) (Figure 3). On image 8 (Figure 2B), there is diffuse hyperattenuation in the region of the transverse sinuses. These findings are due to cerebral venous sinus thrombosis.

Figure 2

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