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CASE REPORT
Year : 2014  |  Volume : 3  |  Issue : 4  |  Page : 259-262

A case of unilateral thalamic venous hemorrhagic infarct in deep venous system thrombosis


1 Department of Neurology, Kasturba Medical College, Manipal, Karnataka, India
2 Department of Ophthalmology, JJMM College, Davanagere, Karnataka, India

Date of Web Publication10-Dec-2014

Correspondence Address:
Anirudda Deshpande
Department of Neurology, Kasturba Medical College, Manipal - 576 102, Karnataka
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2277-8632.146634

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  Abstract 

Cortical venous thrombosis (CVT) is a common and frequently unrecognized type of stroke that affects approximately five people per million annually and accounts for 0.5-1% of all strokes. Exact incidence in India is yet to be documented. Puerperal CVT may account for the majority of CVT cases in India. Cerebral venous sinus thrombosis (CVST) usually affects young to middle aged groups. Outcome of CVST patients may vary from complete recovery to permanent neurological deficits, with varying presentation of the natural course of the disease. Factors related to poor outcome were papilledema, altered consciousness, coma, age older than 33 years, diagnostic delay >10 days, intracerebral hemorrhage, and involvement of the straight sinus. This case report is of thrombosis in the deep venous system of brain causing venous infarction of unilateral thalamus. There are very few cases reported all over the world with unilateral thalamic venous infarct. Prognosis of unilateral deep cerebral vein thrombosis is said to be better than that of bilateral thrombosis, if detected early and timely treated. Patient with a unilateral thrombosis may show complete recovery from his neurologic symptoms. Reports of reversible edema of the thalamus are well documented. In this case, patient is overall well preserved except that he continues to have recent memory impairment even after 4 weeks of discharge from hospital.

Keywords: Deep venous system thrombosis, unilateral thalamic venous hemorrhagic infarct, cerebral venous sinus thrombosis, papilledema


How to cite this article:
Deshpande A, Shetty A, Sitaram A, Khardenavis S. A case of unilateral thalamic venous hemorrhagic infarct in deep venous system thrombosis. J NTR Univ Health Sci 2014;3:259-62

How to cite this URL:
Deshpande A, Shetty A, Sitaram A, Khardenavis S. A case of unilateral thalamic venous hemorrhagic infarct in deep venous system thrombosis. J NTR Univ Health Sci [serial online] 2014 [cited 2019 Sep 20];3:259-62. Available from: http://www.jdrntruhs.org/text.asp?2014/3/4/259/146634


  Introduction Top


Cortical venous thrombosis (CVT) is a common cause of stroke and more so deep internal cerebral vein thrombosis is less commonly seen. Most cases of deep CVT cause bilateral involvement of thalamus and basal ganglia. To best of our knowledge, there are very few reported cases (<5) of unilateral involvement of thalamus in deep internal cerebral vein thrombosis. We wish to emphasize timely treatability of this condition could be a lifesaving measure.


  Case report Top


A 31-year-old male patient with no significant pre morbidities, addictions or family history of hypercoagulable diseases presented with a history of new onset holocranial, throbbing headache, associated with nausea and vomiting. Headache was not associated with any neurological deficits or visual symptoms. On the 4 th day morning, after onset of headache, patient presented with status epilepticus - recurrent generalized tonic clonic seizures. After aborting the status with injection lorazepam, loading of phenytoin sodium was given, airway was secured by intubating the patient, emergency computerized tomography scan brain (plain) on admission showed right thalamic hyperdensity, thought of as intracerebral bleed. Since patient was a nonhypertensive and presented with status epilepticus, cause of which was uncertain. Electroencephalography showed sharp slow wave discharges in right cerebral hemisphere, predominantlt fronto-temporal leads (F4-T4). Magnetic resonance imaging (MRI) brain with contrast, magnetic resonance venography (MRV) was done. MRI with MRV showed unilateral right thalamic venous infarct with venous thrombosis of the deep system of veins including straight sinus, vein of galen, internal patient had to be given three antiepileptics (phenytoin, levetirecetam, and valproate) to achieve complete seizure control [Figure 1], [Figure 2], [Figure 3] and [Figure 4].
Figure 1: T1-weighted magnetic resonance imaging brain sagittal view showing hyperintensity in straight sinus, vein of galen, bilateral internal cerebral veins suggestive of thrombosis of deep venous system

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Figure 2: Susceptibility weighted imaging axial sequence of magnetic resonance imaging of brain suggestive of bloom in right thalamus, deep system of veins suggestive of venous hemorrhagic infarct of right thalamus and thrombosis of deep venous system

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Figure 3: Fluid attenuated inversion recovery magnetic resonance imaging brain axial view showing hyperintensity in straight sinus, vein of galen, bilateral internal cerebral veins suggestive of thrombosis of deep venous system

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Figure 4: Magnetic resonance venography of brain suggestive of thrombosis of deep system of veins

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Patient was subsequently extubated 36 h later. Neurological examination of the patient revealed mild left pronator drift and short-term memory impairment. Fundoscopy revealed bilateral papilledema. Rest of the neurological examination was unremarkable.

In addition to antiepileptic medications, he was started on low molecular weight heparin with overlap of oral anticoagulation in form of warfarin. International normalized ratio (INR) was titrated to values between 2 and 3 subsequently. His investigations including antinuclear antibody, antineutrophil cytoplasmic antibody, antiphospholipid antibody, vitamin B12, iron studies, folic acid, and homocysteine were found to be within normal limits. The etiology for his CVT could however not be found out (protein C, S, factor V Leiden deficiency, and antithrombin III was not done because of financial constraints of the patient). Cerebrospinal fluid (CSF) examination was not carried out in view of bilateral papilledema, signs of raised intracranial pressure and with the fear of central herniation. Patient was discharged after 18 days of rehabilitation and INR monitoring. Patient is overall well preserved except that he continues to have recent memory impairment even after 4 weeks of discharge from hospital.


  Discussion Top


Of the various disease entities affecting the deep gray matter region, the basal ganglia and thalamus are of special interest. These being paired structures are symmetrically affected most often as seen in various conditions such as toxic poisoning, metabolic abnormalities, and neurodegeneration.

To arrive at a correct diagnosis one must pay careful attention to the triad of clinical examination, laboratory findings, and imaging studies. [1],[2]

Neuroimaging diagnosis specifically is guided by:

  1. Carefully observing the changes/abnormalities in the cerebral cortex, white matter and brainstem.
  2. Identifying specific features and patterns on magnetic resonance (MR) such as hemorrhage presence and restricted diffusion.
  3. By deciding on case specific use of highly specific investigations such as diffusion weighted imaging (DWI), magnetic resonance angiography, MRV and MR spectroscopy, and unilateral thalamic lesions is a rare entity. Certain vascular conditions and tumors which present similarly. Thalamic arterial infarctions and tumors like germinomas and gliomas and cavernous hemangiomas, neurocytomas are commonly implicated.


diagnose this rare condition, one has to carefully study T1-weighted and T2-weighted images. Arterial, venous infarction both can present with hypo- and hyper-intensity on T1- and T2-weighted images respectively, however DWI and fluid-attenuated inversion recovery (FLAIR) sequences can differentiate the two. [3]

Arterial infarction is seen to have restricted diffusion, while in venous infarction there is enhanced diffusion, and cytotoxic edema along with vasogenic edema which in turn adds to the patchy areas of restricted and enhanced diffusion. Hence, in an arterial infarct early changes will be seen in DWI, but not in FLAIR.

Diffusion-weighted imaging may show very minimal or may be normal while early abnormalities in FLAIR in venous infarct suggesting that the underlying pathology in venous infarct is vasogenic edema rather than cytotoxic injury as seen in arterial infarcts.

Cavernomas are usually easily identified by a typical hypo-intense ring on T2- and T2*-weighted images. Gliomas, [4],[5] germinomas, [6] and neurocytomas [7] usually present with adjacent structure compression. Cavernomas usually have hypo-intense ring on T1- and T2-weighted images. However these changes are not specific.

Germinomas may show an elevated level of human chorionic gonadotropin in serum and CSF and enhance on MRI. Neurocytomas may show calcification on MRI.

Gliomas show choline peak. [8],[9],[10],[11] Perfusion imaging studies can help to differentiate between high and low grade gliomas by studying regional cerebral blood volume and mean transit time. [12],[13]

The mechanism of status epilepticus in hemorrhagic lesion in CVT is not well understood. Hemosiderin may cause focal cerebral irritation leading to the seizure as reported in traumatic brain injury and animal experiment. One of the possible mechanisms hypothesized is "thalamo-cortical facilitation." [14],[15]

Venous ischemia has specific characteristics, such as an early blood brain barrier disruption and an increase of the net capillary filtration that may result in early vasogenic edema. In our patient, the contrast between normal DWI studies and marked FLAIR abnormalities may reflect prominent and early vasogenic edema associated with mild cytotoxic features. This contrast may well explain the excellent and rapid recovery of neurological deficit of most cases of the venous stroke that is treated early. [16],[17],[18],[19],[20],[21],[22]

 
  References Top

1.
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2.
van den Bergh WM, van der Schaaf I, van Gijn J. The spectrum of presentations of venous infarction caused by deep cerebral vein thrombosis. Neurology 2005;65:192-6.  Back to cited text no. 2
    
3.
Crombé D, Haven F, Gille M. Isolated deep cerebral venous thrombosis diagnosed on CT and MR imaging. A case study and literature review. JBR-BTR 2003;86:257-61.  Back to cited text no. 3
    
4.
Kobayashi T, Kageyama N, Kida Y, Yoshida J, Shibuya N, Okamura K. Unilateral germinomas involving the basal ganglia and thalamus. J Neurosurg 1981;55:55-62.  Back to cited text no. 4
    
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Wong GJ, Hung KL, Huang JS, Chen TY. Unilateral thalamic tumor with atrophy of ipsilateral cortical cortex: report of a case. J Formos Med Assoc 1991;90:609-11, 587.  Back to cited text no. 5
    
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Kim DI, Yoon PH, Ryu YH, Jeon P, Hwang GJ. MRI of germinomas arising from the basal ganglia and thalamus. Neuroradiology 1998;40:507-11.  Back to cited text no. 6
    
7.
Nishio S, Morioka T, Suzuki S, Takeshita I, Fukui M. Thalamic gliomas: A clinicopathologic analysis of 20 cases with reference to patient age. Acta Neurochir (Wien) 1997;139:336-42.  Back to cited text no. 7
    
8.
Cheung YK. Central neurocytoma occurring in the thalamus: CT and MRI findings. Australas Radiol 1996;40:182-4.  Back to cited text no. 8
    
9.
Lazzarino LG, Nicolai A, Toppani D. Unilateral cavernous angioma of the thalamus disclosed by transitional disorders in the upward gaze. Minerva Med 1990;81:731-3.  Back to cited text no. 9
    
10.
Rapacki TF, Brantley MJ, Furlow TW Jr, Geyer CA, Toro VE, George ED. Heterogeneity of cerebral cavernous hemangiomas diagnosed by MR imaging. J Comput Assist Tomogr 1990;14:18-25.  Back to cited text no. 10
    
11.
Lövblad KO, Bassetti C, Schneider J, Ozdoba C, Remonda L, Schroth G. Diffusion-weighted MRI suggests the coexistence of cytotoxic and vasogenic oedema in a case of deep cerebral venous thrombosis. Neuroradiology 2000;42:728-31.  Back to cited text no. 11
    
12.
Fulham MJ, Bizzi A, Dietz MJ, Shih HH, Raman R, Sobering GS, et al. Mapping of brain tumor metabolites with proton MR spectroscopic imaging: Clinical relevance. Radiology 1992;185:675-86.  Back to cited text no. 12
    
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Yang D, Korogi Y, Sugahara T, Kitajima M, Shigematsu Y, Liang L, et al. Cerebral gliomas: Prospective comparison of multivoxel 2D chemical-shift imaging proton MR spectroscopy, echoplanar perfusion and diffusion-weighted MRI. Neuroradiology 2002;44:656-66.  Back to cited text no. 13
    
14.
Küçükkaya B, Aker R, Yüksel M, Onat F, Yalçin AS. Low dose MK-801 protects against iron-induced oxidative changes in a rat model of focal epilepsy. Brain Res 1998;788:133-6.  Back to cited text no. 14
    
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Willmore LJ. Post-traumatic seizures. Neurol Clin 1993;11:823-34.  Back to cited text no. 15
    
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Law M, Cha S, Knopp EA, Johnson G, Arnett J, Litt AW. High-grade gliomas and solitary metastases: Differentiation by using perfusion and proton spectroscopic MR imaging. Radiology 2002;222:715-21.  Back to cited text no. 16
    
17.
Villringer A, Mehraein S, Einhäupl KM. Pathophysiological aspects of cerebral sinus venous thrombosis (SVT). J Neuroradiol 1994;21:72-80.  Back to cited text no. 17
    
18.
Röther J, Waggie K, van Bruggen N, de Crespigny AJ, Moseley ME. Experimental cerebral venous thrombosis: Evaluation using magnetic resonance imaging. J Cereb Blood Flow Metab 1996;16:1353-61.  Back to cited text no. 18
    
19.
Gotoh M, Ohmoto T, Kuyama H. Experimental study of venous circulatory disturbance by dural sinus occlusion. Acta Neurochir (Wien) 1993;124:120-6.  Back to cited text no. 19
    
20.
Ungersböck K, Heimann A, Kempski O. Cerebral blood flow alterations in a rat model of cerebral sinus thrombosis. Stroke 1993;24:563-9.  Back to cited text no. 20
    
21.
Einhäupl KM, Villringer A, Meister W, Mehraein S, Garner C, Pellkofer M, et al. Heparin treatment in sinus venous thrombosis. Lancet 1991;338:597-600.  Back to cited text no. 21
    
22.
Moon WK, Chang KH, Kim IO, Han MH, Choi CG, Suh DC, et al. Germinomas of the basal ganglia and thalamus: MR findings and a comparison between MR and CT. AJR Am J Roentgenol 1994;162:1413-7.  Back to cited text no. 22
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4]



 

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