Cerebral Venous Thrombosis

may be on a continuum with IIH (pseudotumor cerebrii)

do not diagnose IIH without MRI/MRV to rule out CVT

OCPS may be a risk b/c hypercoag state

any hypercoag can lead to CVT

CVT may present with a sudden-onset headache, often associated with nausea and vomiting, clinically mimicking SAH.

CTs may be misinterpreted, and the failure to measure cerebrospinal fluid (CSF) pressure when performing an LP (which should be high in CVT) may add to the diagnostic lag.

CVT is an especially feared complication of pregnancy and the postpartum period

Treatment modalities for CVT include anticoagulation, thrombolytics, and careful observation. Antibiotics may be given if an infectious triggering event is suspected. Although anticoagulation may prevent further thrombus formation, it could theoretically cause further intracerebral hemorrhage, leading some to advocate heparin only when patients deteriorate despite symptomatic treatment.³⁷ However, several trials support the safety and efficacy of IV heparin, even in patients with preexisting hemorrhage.^180-183 The use of low molecular weight heparin results in a slightly more favorable outcome than unfractionated heparin.

The symptoms associated with CVT are quite varied. This variability stems from differences in thrombus location and acuity of thrombus formation. Headache is the primary feature of CVT in 74% to 90% of affected patients. Papilledema is noted in 45% of cases. Lethargy, decreased level of consciousness, or mental status changes may be seen. Seizures are seen in 50% of patients in the acute phase.

CT is ok for screening but need MRI/MRV for true diagnosis

Heparinize and admit

Clinical manifestations consist of headache, vomiting, focal or generalized seizure, confusion, blurred vision, focal neurologic deficits, and altered consciousness. The headache frequently precedes other symptoms, is diffuse, and often severe. The severity of symptoms correlates with the degree of thrombosis and the vessel involved. The diagnosis is confirmed by magnetic resonance imaging.

Treatment, which is started as soon as the diagnosis is confirmed, consists of reversing the underlying cause when known, control of seizures and intracranial hypertension, and the use of anticoagulants [ 13]. Local thrombolysis may be indicated in rare cases unresponsive to adequate anticoagulation.

Pregnancy related neuro emergencies:
Seizures, ischemic stroke, cerebral vasospasm, intracranial hemorrhage, cerebral venous thrombosis, hypertensive encephalopathy, pituitary apoplexy

Cerebral venous thrombosis — Cerebral venous thrombosis (CVT) is an uncommon but serious disorder. Headache is the most common clinical manifestation, occurring in 80 to 88 percent [ 79,80]. The headache frequently precedes other symptoms, is typically diffuse, and often severe. Headache onset may be "thunderclap," acute, or progressive [ 81]. Rarely, headache may be the only symptom of CVT.

Other clinical manifestations can include papilledema, visual loss, focal or generalized seizures, focal neurologic deficits, confusion, altered consciousness, and coma [ 80]. The severity of symptoms correlates with the degree of thrombosis and the vessel involved. The diagnosis is confirmed by CT venography, MRI combined with MR venography, conventional angiography, surgery, or autopsy.

Many cases have been linked to inherited and acquired thrombophilias, pregnancy, puerperium, infection, and malignancy [ 80].

Treatment, which is started as soon as the diagnosis is confirmed, consists of reversing the underlying cause when known, control of seizures and intracranial hypertension, and anticoagulation. Local thrombolysis may be indicated in rare cases unresponsive to adequate anticoagulation
(UpToDate)
pregnant-headache seizures consider CVT

Empty Delta Sign

chemosis, proptosis, opthalmoplegia.

Usually c CN III, IV, V, and V defects

Can be caused by tumor, fungal or bacterial infection, or vascular malformations

dural sinus in pregnant and postpartum (up to 3 months)

screen with ct, confirm with MRI.

Although somewhat controversial in efficacy given mixed results from two prospective randomised trials,^12,13 heparin is considered first line treatment in the initial management of DST

triad of dural sinus thrombosis? is headache, papilledema, and high CSF opening pressure. MRI with magnetic resonance venography is considered the gold standard for diagnosis (Am J EM, 2/07, pg. 218).

(From Neurocrit Care Volume 11, Number 3 / December, 2009, 330-337)

Presentation

The most common presenting symptom was headache, which was noted in 50/61 (82%) (Fig. 1). Headache generally progressed over days to weeks, but sudden, severe “thunderclap” headaches were noted in 4/61 patients (7%). Sudden severe headache did not appear to correlate with SAH, as only 1/4 of the patients with thunderclap headache had SAH. Nausea and vomiting occurred in 22/61 (36%). Neurologic deficits included focal motor or sensory deficits in 32/61 (52%), visual deficits in 17/61 (28%), and aphasia in 13/61 (21%). Overall, focal neurologic deficits were found in 44/61 (72%). Seizures occurred in 19/61 (31%), including 2/61 (3%) presenting with status epilepticus. On admission to our hospital, altered mental status was identified in 21/61 (34%), consisting of confusion in 17/61 (28%) and somnolence or coma in 4/61 (7%). Pulsatile tinnitus, a common symptom of DAVF, was a presenting symptom in only 6/61 (10%).

Fig. 1 Presenting CVT symptoms/signs with and without associated ICH. Bar graph shows the number of CVT patients presenting with specific neurological symptoms and signs

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Cerebral venous thrombosis patients with IPH had more severe neurological deficits on presentation than those without IPH (Fig. 1). In particular, patients with associated IPH were more likely to have depressed mental status (56% vs. 15%, P = 0.001), aphasia (41% vs. 6%, P = 0.001), seizures (44% vs. 21%, P = 0.046), and focal neurological deficits (67% vs. 41%, P = 0.048). Overall, an unfavorable admission mRS (3–6) was found in 88% of patients presenting with CVT and IPH, but in only 34% of patients presenting with CVT and no IPH (Fig. 3).

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