Diagnosis and treatment of deep cerebral vein thrombosis

Erbguth, Frank; Brenner, Peter J.; Schuierer, Gerhard; Druschky, K.-F.; Neundörfer, B.

doi:10.1007/bf00313042

Cited by 35 publications

(26 citation statements)

References 21 publications

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“…In most cases, a CT will show bithalamic hypoattenuation. At times the basal ganglia and the white matter will be also involved [11,12,17] . The thrombosed veins will be hyperattenuated.…”

Section: Discussionmentioning

confidence: 99%

“…The course of the ICV and its relatively narrow diameter make it prone to injury, largely from neurosurgical approaches to the lateral and the third ventricles, as well as to the thalamus and pineal region. Occlusion of the deep cerebral venous system can lead to a variety of clinical symptoms and signs including headache, vomiting, lethargy, pyrexia, hemiparesis, behavioral anomalies, decreased level of consciousness, coma, and death [2,3,[10][11][12][13] . However, deep cerebral venous system thrombosis is usually associated with thrombosis of the superficial veins and sinuses [1,3,11] and can be caused by the use of birth control pills, malignancies, and chronic illness [3] .…”

Section: Discussionmentioning

confidence: 99%

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Unilateral Postoperative Deep Cerebral Venous Thrombosis with Complete Recovery: A Report of 2 Cases

Benifla

Laughlin²,

Tovar-Spinoza³

et al. 2017

Pediatr Neurosurg

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Postsurgical deep brain venous thrombosis has not been well described in children before. When approaching thalamic or intraventricular lesions, extra care should be taken to prevent injury to the internal cerebral veins (ICVs) and the vein of Galen. However, even when they are well preserved during surgery, postoperative hemodynamic changes, mainly in the first 24 h, or surgical manipulation can cause thrombosis of these veins. We report 2 children with unilateral postoperative ICV thrombosis; in 1 of the patients the vein of Galen was also thrombosed. Although both patients had altered sensorium initially, no anticoagulation therapy was given, and they both recovered well. When approaching thalamic or intraventricular lesions, extra care should be taken to prevent injury to the ICV and the vein of Galen. The surgeon should respect the deep brain venous system when approaching midline structures. Both the neurosurgeon and the neuroradiologist should be aware of this possible complication in order to make a prompt diagnosis and to offer proper treatment if needed.

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“…In most cases, a CT will show bithalamic hypoattenuation. At times the basal ganglia and the white matter will be also involved [11,12,17] . The thrombosed veins will be hyperattenuated.…”

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Unilateral Postoperative Deep Cerebral Venous Thrombosis with Complete Recovery: A Report of 2 Cases

Benifla

Laughlin²,

Tovar-Spinoza³

et al. 2017

Pediatr Neurosurg

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“…The prognosis in cases with combined convexity and deep venous system thrombosis is generally poorer. 8,14,25,26,32,33 Treatment of such cases will be technically more problematic than treatment of convexity sinus thrombosis alone.…”

Section: Discussionmentioning

confidence: 99%

“…Eligibility for treatment was the same as for intravenous heparin alone. Presenting manifestations occurred over 1 to 40 days (average, 10 days) and included headache, 12 focal neurological deficits, 9 somnolence, 8 seizures, 5 and nausea and vomiting 4 (Table1).…”

Section: Methodsmentioning

confidence: 99%

Cerebral Venous Thrombosis

Frey

Muro

McDougall

et al. 1999

Stroke

200

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Background and Purpose —We chose to evaluate the safety and efficacy of combined intrathrombus rtPA and intravenous heparin in cerebral venous thrombosis (CVT). Methods —We treated 12 patients with symptoms of 1 to 40 days’ duration (eg, headache, somnolence, focal deficits, seizures, and nausea and vomiting). Pretreatment MRI disclosed subtle hemorrhagic venous infarction in 4 patients, obvious hemorrhagic infarction in 2, small parenchymal hemorrhage from recent pallidotomy in 1, and no focal lesion in 5. Magnetic resonance venography and contrast venography identified thrombi in the superior sagittal sinus (SSS) in 3 patients; transverse/sigmoid sinus (TS/SS) in 2; SSS and both TS/SS in 1; SSS and 1 TS/SS in 5; and SSS, 1 TS/SS, and straight sinus in 1 patient. A loading dose of rtPA was instilled throughout the clot at 1 mg/cm, followed by continuous intrathrombus infusion at 1 to 2 mg/h. Intravenous heparin was infused concomitantly. Results —Flow was restored completely in 6 patients and partially in 3, with a mean rtPA dose of 46 mg (range, 23 to 128 mg) at a mean time of 29 hours (range, 13 to 77 hours). Symptoms improved in these 9 patients concomitantly with flow restoration. Flow could not be restored in 3 patients. In 1 of them, treatment was stopped when little progress had been made, and fibrinogen level dropped to 118 mg/dL. In the other 2 patients, hemorrhagic worsening occurred, and treatment was abbreviated after initial rtPA dosing. In 1 of these, the hematoma was evacuated. Conclusions —Our experience with intrathrombus rtPA in conjunction with intravenous heparin in patients with CVT is encouraging. This therapy should probably be regarded as unsafe in patients with obvious hemorrhage. Time to restore flow may be faster than with urokinase (an average of 71 hours has been reported for 29 documented patients). Further evaluation of rtPA with heparin in CVT is warranted.

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“…Deep cerebral vein thrombosis (DCVT) should be suspected from computed tomography (CT) or magnetic resonance imaging (MRI), if bilateral parenchymal edema in the basal ganglia and the thalamus are present [1,4,5,7,11,14]. Additional neuroimaging findings are hydrocephalus, a hyperdense thrombus in the internal veins ("dense vein sign"), and rapid evolution with haemorrhagic venous infarction.…”

mentioning

confidence: 99%