The case of a 28 years old woman presenting with headache, drowsiness and vomiting of a short duration, is presented. She was diagnosed as deep cerebral venous thrombosis on the basis of MRI findings. Treatment with heparin gave completed recovery

Ahmad, Muhammad Nadeem

Ashraf, Kashif

Bari, Vaqar

Rafique, Muhammad Zafar

English

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eCommons@AKUDepartment of Radiology Medical College, PakistanSeptember 2005Cerebral deep venous thrombosis: case report andliterature reviewMuhammad Zafar RafiqueVaqar Barivaqar.bari@aku.eduKashif AshrafMuhammad Nadeem AhmadFollow this and additional works at: https://ecommons.aku.edu/pakistan_fhs_mc_radiolPart of the Radiology CommonsRecommended CitationRafique, M. Z., Bari, V., Ashraf, K., Ahmad, M. N. (2005). Cerebral deep venous thrombosis: case report and literature review. Journalof Pakistan Medical Association, 55(9), 399-400.Available at: https://ecommons.aku.edu/pakistan_fhs_mc_radiol/158399 J Pak Med AssocCase ReportCerebral Deep Venous Thrombosis: Case Report and Literature ReviewMuhammad Zafar Rafique, Vaqar Bari, Kashif Ashraf, Muhammad Nadeem AhmadRadiology Department, Aga Khan University Hospital, Karachi.AbstractThe case of a 28 years old woman presenting withheadache, drowsiness and vomiting of a short duration, ispresented. She was diagnosed as deep cerebral venousthrombosis on the basis of MRI findings. Treatment withheparin gave completed recovery. IntroductionAcute cerebral deep venous thrombosis (CDVT) ofinternal cerebral veins, vein of Galen and straight sinus withoutassociated sagittal sinus thrombosis is a very rare disorder andcan be associated with poor outcome.1 It causes infarction ofthalami which can be hemorrhagic. The diagnosis of CDVTbased on clinical symptoms is difficult but modern technologyof MRI is very useful for its diagnosis. Once CDVT is detected,immediate therapy should be started to avoid a devastating out-come.2 Prognosis can be favorable with prompt treatment. Case ReportA 28 years old female presented with complaints ofheadache for two days and drowsiness and vomiting for oneday. Patient delivered a baby two weeks ago and had post par-tum hemorrhage. Significant past history was hypertension forseven years. Neurological examination was non focal. EEGshowed generalized delta waves suggestive of encephalitis.MRI, including sagittal, axial and coronalT1WI, axial T2WI,coronal FLAIR images was performed. MRI showed hyperin-tense signals on T2 weighted images (figure 1) in the thalamibilaterally. Venous infarction was suspected and immediatelygadolinium enhanced MR Venography was performed. Thisshowed non visualization of internal cerebral veins, vein ofGalen and straight sinus (figure 2). These findings were con-sistent with deep cerebral venous thrombosis. Patient wastreated with heparin and recovered from her symptoms. Shewas discharged from the hospital after a few days. At the timeof discharge she had fully recovered without any neurologicaldeficits.DiscussionClinical findings of acute deep cerebral venous throm-bosis can be non specific and include, vomiting, change inmental status, alteration of consciousness and coma.3 Venousinfarction of thalami and some times basal ganglia infarctsoccur in this condition. Bilateral involvement is typical butunilateral involvement can also be seen.4 Bithalamic infarctsare usually attributed to thromboembolism of the top of thebasilar artery. Apart from the top of the basilar artery syn-drome, deep cerebral venous thrombosis should also be con-sidered as a cause of bithalamic infarcts.5Cerebral venous thrombosis may be associated withwide variety of causes.1 These include use of oral contra-ceptives,  pregnancy,  puerperium,  dehydration,Figure 1. Axial T2 weighted images show abnormal, hyperintense signal involving the thalamibilaterally. There is slightly more marked involvement of left thalamus.Figure 2. Post gadolinium MR Venograpy demonstrates non visualization of internal cerebral veins,vein of Galen and straight sinus. These findings are consistent with deep cerebral venous thrombosis.Vol. 55, No. 9, September 2005 400hypercoagulable states and infection specially mastoiditis.The Radiological diagnosis of deep cerebral venousthrombosis may be difficult because characteristic delta signof superior sagittal sinus thrombosis on contrast enhancedCT scan is not present.1 Flow related signals in straightsinus on MRI can normally be variable. Hyperdense throm-bus can be seen in deep veins on CT scan, which is sugges-tive of the diagnosis.1 Magnetic resonance imaging and MRvenography are confirmatory.6 Angiography may still benecessary when diagnosis is not clear. Diffusion and Perfusion weighted imaging have a rolein the diagnosis and assessment of prognosis.7 Venous obstruc-tion causes venous congestion and disruption of blood brainbarrier. Capillary filtration increases leading to cerebral edema.Vasogenic edema was thought to be the type of edema invenous stroke instead of cytotoxic edema as seen in arterialstroke. This concept is reinforced by Diffusion weighted imag-ing of a patient with venous stroke.8 In the acute phase value ofApparent Diffusion Coefficient (ADC) is increased. Previousstudies of CVT have shown cerebral blood flow reduction wellbelow the threshold of cytotoxic edema formation anddecreased ADC within the range of ADC values of pure arteri-al stroke.9 In venous thrombosis perfusion of affected brain tis-sue may still be possible at low flow rates if blood is drainedthrough the collateral pathways. Thus patient still may recovereven with significantly decreased ADC value.Anticoagulation with heparin is the mainstay of treat-ment even in the presence of hemorrhage.10 Direct thrombolysiswith Urokinase is also useful and lyses of thrombus with persist-ent recanalization of deep veins can be achieved.1In conclusion early diagnosis of deep venous throm-bosis is vital for prompt treatment. When edema or infarctswhich may be hemorrhagic, are present in thalami or basalganglia, one should suspect CDVT. It should also be sus-pected with non specific symptoms in patients with knownrisk factors. If detected immediate therapy should be startedto avoid a devastating outcome. With prompt treatmentprognosis can be favorable as in our case.References1. Spearman MP, Jungreis CA, Wehner JJ, Welch WC, Gerszten PC.Endovascular thrombolysis in deep cerebral venous thrombosis. AJNR1997;18:502-6.2. Honda M, Kaminogo M, Nagata I, Morikawa M. Deep cerebral venous throm-bosis: a report of three cases and review of the literature. No To Shinlei2004;56:689-94. 3. Lacour JC, Ducrocq X, Anxionnat R, Taillandier L, Augue J, Weber M.Thrombosis of deep cerebral veins in adults: clinical features and diagnosticapproach. Rev Neurol 2000;156:851-7.4. Kuker W, Schmidt F, Friese S, Block F, Weller M. Unilateral thalamic edemain internal cerebral venous thrombosis: is it mostly left? Cerebrovasc Dis2001;12:341-45.5. Ameridou I, Spilioti M, Amoiridis G. Bithalamic infarcts: embolism of the topof basilar artery or deep cerebral venous thrombosis? Clin Neurol Neurosurg2004;106:345-7.6. Crawford SC, Digre KB, Palmer CA, Bell DA, Osborn AG. Thrombosis of thedeep venous drainage of brain in adults. Analysis of seven cases with reviewof literature. Arch Neurol 1995;52:1101-8.7. Ducreux D, Oppenham C, Vandamme X, Dormonl D, Samson Y, Rancurel G,et al. Diffusion-weighted imaging patterns of Brain damage associated withcerebral venous thrombosis. AJNR 2001;22:261-8.8. Ewald K, Sebastian F, Horst U, Hans S. Schild. Diffusion and perfusion-weighted magnetic resonance imaging in deep cerebral venous thrombosis.Stroke 1999;30:1144-46.9. Gotoh M, Ohmoto T, Kuyama H. Experimental study of venous circulatorydisturbance by dural sinus occlusion. Acta Neurochir 1993;124:120-26.10. Fink JN, McAuly DL. Cerebral venous sinus thrombosis: a diagnostic chal-lenge. Intern Med J 2001;31:384-90.

Cerebral deep venous thrombosis: case report and literature review

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Cerebral deep venous thrombosis: case report and literature review

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