|Year : 2014 | Volume
| Issue : 4 | Page : 259-262
A case of unilateral thalamic venous hemorrhagic infarct in deep venous system thrombosis
Anirudda Deshpande1, Aakash Shetty1, Amith Sitaram1, Supriya Khardenavis2
1 Department of Neurology, Kasturba Medical College, Manipal, Karnataka, India
2 Department of Ophthalmology, JJMM College, Davanagere, Karnataka, India
|Date of Web Publication||10-Dec-2014|
Department of Neurology, Kasturba Medical College, Manipal - 576 102, Karnataka
Source of Support: None, Conflict of Interest: None
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 2020 Mar 28];3:259-62. Available from: http://www.jdrntruhs.org/text.asp?2014/3/4/259/146634
| Introduction|| |
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|| |
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|| |
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. ,
Neuroimaging diagnosis specifically is guided by:
- Carefully observing the changes/abnormalities in the cerebral cortex, white matter and brainstem.
- Identifying specific features and patterns on magnetic resonance (MR) such as hemorrhage presence and restricted diffusion.
- 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. 
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, , germinomas,  and neurocytomas  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. ,,, Perfusion imaging studies can help to differentiate between high and low grade gliomas by studying regional cerebral blood volume and mean transit time. ,
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." ,
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. ,,,,,,
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[Figure 1], [Figure 2], [Figure 3], [Figure 4]