|Year : 2022 | Volume
| Issue : 3 | Page : 146-147
A rare case of right-sided unilateral thalamic edema due to internal cerebral vein thrombosis
Nagesh Venkata Ivaturi1, Manoj Gopinath2
1 Department of Medicine, MH Amabala, Amabala, Haryana, India
2 Department of Radiodiagnosis, CH (EC) Kolkata, Kolkata, West Bengal, India
|Date of Submission||05-Dec-2021|
|Date of Decision||20-Dec-2021|
|Date of Acceptance||25-Dec-2021|
|Date of Web Publication||01-Jul-2022|
Dr. Nagesh Venkata Ivaturi
Department of Medicine, MH Amabala, Haryana
Source of Support: None, Conflict of Interest: None
32 yr old individual presented with headaches and detected to have cerebral venomous thrombosis. MRI revealed internal cerebral vein thrombosis with unilateral that edema. He was managed conservatively.
Keywords: Cerebral vein thrombosis, internal cerebral vein, unilateralthalamic edema
|How to cite this article:|
Ivaturi NV, Gopinath M. A rare case of right-sided unilateral thalamic edema due to internal cerebral vein thrombosis. J Mar Med Soc 2022;24, Suppl S1:146-7
| Introduction|| |
Acute cerebral deep venous thrombosis of internal cerebral veins, vein of Galen, and straight sinus without the involvement of sagittal sinus is very rare. Bilateral thalamic edema associated with venous thrombosis of internal cerebral veins is commonly described in the literature. However unilateral thalamic edema is very rare. We report a case of reversible unilateral thalamic edema with internal cerebral vein thrombosis.
| Case Report|| |
A 32-year-old male, staying at a high altitude area (12,000ft) for more than 6 months presented with complaints of the headache of 6 weeks duration. There was no history of vomiting, loss of consciousness, convulsions, fever, weakness of limbs, or sensory symptoms. The headache was continuous and persisting for most of the day and increased intensity while waking up from bed. Clinical examination revealed a heart rate of 86/min, blood pressure 136/86 mm of Hg, respiratory rate of 20/min. Systemic examination was normal. Visual acuity and fundoscopic examination were normal. Investigations revealed normal hematological and coagulation parameters. Electrocardiogram, chest radiograph, and 2D echocardiography, were normal. The findings of computerized tomographic and magnetic resonance imaging of the brain revealed unilateral thalamic edema (Rt) with Internal cerebral vein thrombosis as depicted in [Figure 1].
|Figure 1: (a) NCCT Axial, (b) T1 SPGR Axial, (c) T2 Axial, (d) FLAIR (Fluid Attenuated Inversion Recovery) Axial, (e) MIP (Maximum Intensity Projection) of 2D Time of Flight MR Venography|
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He was managed injection low-molecular-weight heparin enoxaparin 60 mg S/C bd. The headache was subsided after 7 days.
| Discussion|| |
Thrombosis of dural sinuses and/or cerebral veins is an uncommon form of stroke, constituting 0.5%–1% of all strokes. Deep cerebral vein thrombosis that affects only single thalamus is a rare entity. The incidence of thrombosis of the deep cerebral system constitutes 11% of all cerebral venous thrombosis. The deep venous system consists only of the internal cerebral veins, the basilar veins (vein of Rosenthal), the vein of Galen, and their tributaries. Both thalami drain into the vein of Galen and straight sinus, hence bilateral thalamic edema is commonly encountered with internal cerebral vein thrombosis. Unilateral thalamic edema may be due to collateral drainage of the thalamus. Thrombosis of the deep venous system, the straight sinus, and its branches causes centrally located often bilateral thalamic lesions but in this case, the lesions are unilateral which is very rare. Most of the reported cases in the literature, the infarction has been on the left side, but in our case, the thalamic edema was on the right side. It may be due to anatomic variant predisposing to the left-sided system, especially the left internal cerebral vein with insufficient collateral venous drainage of the thalamus.
The risk factors for venous thrombosis are linked classically to Virchow's triad of, stasis of blood, changes in the vessel wall and changes in components of blood.
The pathophysiology of symptoms in cerebral venous thrombosis can be explained by two mechanisms. In the case of occlusion of deep cerebral veins as it happened in this case, causes localized edema (either due to cytotoxic or vasogenic), and second is the development of raised intracranial hypertension as a result of occlusion of major sinuses.
Most of the symptoms of internal cerebral vein thrombosis are nonspecific. They can cover a wide range of symptoms from headache, nausea, and vomiting to focal neurologic deficits, hemiparesis, aphasia, seizures, coma, and death. This case concerns a benign form of deep cerebral venous thrombosis with isolated headaches and a normal clinical examination. The mainstay of treatment remains anticoagulation with heparins followed by oral anticoagulation for a minimum of 6 months. The use of these direct intra-sinus thrombolytic techniques and mechanical therapies is controversial and recommended only if clinical deterioration occurs despite the use of anticoagulation, or if the patient develops mass effect from a venous infarction or intracerebral hemorrhage that causes intracranial hypertension resistant to standard therapies.
The outcomes of deep cerebral vein thrombosis vary greatly and from complete recovery to death. Unilateral lesions carry a better prognosis than bilateral lesions.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
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Conflicts of interest
There are no conflicts of interest.
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