Sudden Headache and Vomiting in a 33-Year-Old Woman

Roshen Mathew, MBBS; Mathew Abraham, MD, DM

Disclosures

September 12, 2016

Discussion

This patient had an MRV that showed a superior sagittal sinus thrombosis. Lack of signal from the distal portion of the superior sagittal sinus was consistent with cerebral venous thrombosis (Figures 2 and 3), as was the patient's clinical presentation. Workup for a hypercoagulable state was negative.

Figure 2.

Figure 3.

CVT should be considered in any patient presenting with severe headache and vomiting when no other cause is identified, especially when papilledema is identified on ophthalmoscopy. Risk factors for CVT include:

However, no risk factors are identified in 14% of patients diagnosed with CVT.[1,2,3]

The typical pathophysiology in CVT is partial or complete occlusion of a cerebral venous sinus, which causes increased intracranial pressure and papilledema. The most frequently involved venous sinuses are the superior sagittal sinus or either of the paired transverse sinuses. If a thrombus extends into the cortical veins, dilatation of veins and capillary beds can occur, which then can lead to venous infarction, cerebral edema, and intraparenchymal hematoma formation. Seizures or cerebral herniation are potentially fatal complications.[2]

The clinical presentation of CVT is usually a severe headache that is aggravated by head movements, sneezing, or coughing. The headache is typically subacute and gradual in onset, although thunderclap headache occurs in 2%-10% of cases (as in this patient). Nausea and vomiting are often present, and severe cases are marked by a decreasing level of consciousness that may result from either a postictal state due to seizures or from cerebral swelling with or without herniation. Focal neurologic findings, including hemiparesis or isolated unilateral lower-extremity weakness, can be seen when a thrombus extends into the cortical veins. This is especially common in CVT of the superior sagittal sinus.

If the cavernous sinus is involved (which is associated almost exclusively with infection of the paranasal sinuses), proptosis and chemosis with ipsilateral periorbital edema, retinal hemorrhages, papilledema, extraocular movement abnormalities, and sensory loss in the V1 or V2 distribution of the trigeminal nerve may be seen. Isolated or multiple cranial nerve palsies (III, VII, VIII) have been reported in patients with unilateral occlusion of the transverse or sigmoid sinuses. This unusual presentation has been explained by venous congestion of the ventral pontine and lateral medullary veins. If the thrombus extends into the jugular bulb, a jugular foramen syndrome, with involvement of cranial nerves IX, X and XI, may be seen.

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