Asian Journal of Neurosurgery

LETTER TO EDITOR
Year
: 2019  |  Volume : 14  |  Issue : 3  |  Page : 1054--1055

Near complete resolution of bilateral thalamic venous infarct in the absence of superficial venous sinus thrombosis


Sachin Sampat Baldawa1, Sunil Hogade2,  
1 Department of Neurosurgery, Solapur Sahakari Rugnalaya, Solapur, Maharashtra, India
2 Department of Medicine, Solapur Sahakari Rugnalaya, Solapur, Maharashtra, India

Correspondence Address:
Sachin Sampat Baldawa
Department of Neurosurgery, Solapur Sahakari Rugnalaya, Solapur, Maharashtra
India




How to cite this article:
Baldawa SS, Hogade S. Near complete resolution of bilateral thalamic venous infarct in the absence of superficial venous sinus thrombosis.Asian J Neurosurg 2019;14:1054-1055


How to cite this URL:
Baldawa SS, Hogade S. Near complete resolution of bilateral thalamic venous infarct in the absence of superficial venous sinus thrombosis. Asian J Neurosurg [serial online] 2019 [cited 2020 Jul 5 ];14:1054-1055
Available from: http://www.asianjns.org/text.asp?2019/14/3/1054/231076


Full Text



 Case Description



A 45-year-old woman presented to the emergency department with a headache and progressive deterioration in sensorium since 2 days. On examination, her vitals were stable. Blood investigations were normal. Her Glasgow Coma Scale was 9/15. Bilateral plantar response was extensor. Magnetic resonance (MR) imaging of the brain demonstrated hypointense signals on T1 weighted images, hyperintense signals on T2 [[Figure 1]a white arrow], and fluid-attenuated inversion recovery (FLAIR) [[Figure 1]b white arrow] weighted images in bilateral thalamus. On diffusion weighted imaging (DWI), both the thalamus demonstrated isointense to hyperintense signals [[Figure 1]c white arrow] with corresponding hypointense signals on apparent diffusion coefficient imaging (ADC) [[Figure 1]d white arrow]. On susceptibility weighted imaging (SWI), blooming was evident in right thalamus [[Figure 1]e black arrow] and along the course of vein of Galen and straight sinus [[Figure 1]e white arrow]. On MR venogram, the vein of Galen and straight sinus was occluded [[Figure 1]f black arrow]. Superficial venous systems were patent. The imaging was consistent with the diagnosis of bilateral thalamic hemorrhagic venous infarct following occlusion of deep venous system. Her medical history was remarkable for multiple attacks of diarrhea before the onset of headache. On receiving anticoagulation, she showed gradual improvement in neurological status with near-complete recovery by 3 months. Investigations for coagulation disorder revealed normal protein C, protein S and antithrombin III levels. MR imaging (MRI) done at 3 months showed near complete reversal of signal changes in both the thalamic on T2 and FLAIR imaging [Figure 2]a and [Figure 2]b. Few discrete bilateral thalamic signal intensity changes were seen on T2 weighted, FLAIR, and SWI imaging [[Figure 2]a, [Figure 2]b, [Figure 2]c white arrow].{Figure 1}{Figure 2}

 Discussion



Isolated bilateral symmetrical infarction of the thalamus is an uncommon finding.[1] It can occur following occlusion of either the artery of Percheron or deep venous system.[2] Bilateral thalamic infarct following thrombosis of deep venous system in the absence of superficial venous sinus thrombosis is rarely reported.[2] Thrombosis of vein of Galen or straight sinus results in venous hypertension and hemorrhagic venous infarct in both the thalamus.[1] This leads to combination of both vasogenic and cytotoxic edema to a varying extent in both the thalami.[3] Vasogenic edema is evident by hyperintense signals on both T2, FLAIR and ADC sequences and isointense to hyperintense signals on DWI. Cytotoxic edema leads to high signal intensity on DWI and low signal intensity on ADC map.[3],[4] Advanced MRI sequences such as SWI and MR venogram demonstrates occlusion of the deep venous system thereby establishing correct diagnosis and optimizing early therapy to prevent permanent neurological deficit.[5] The degree of neurological deficit is directly proportional to extent of cytotoxic edema and varies inversely to degree of vasogenic edema.[3] Near complete reversal of signal changes in the present case on follow-up imaging is due to the resolution of vasogenic edema.

The overall neurological improvement following cerebral deep venous system occlusion depends on early diagnosis and extent of vasogenic edema on advanced MRI sequences and initiating early therapy.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

References

1Gossner J, Larsen J, Knauth M. Bilateral thalamic infarction - A rare manifestation of dural venous sinus thrombosis. Clin Imaging 2010;34:134-7.
2Hoitsma E, Wilmink JT, Lodder J. Bilateral thalamic infarction may result from venous rather than arterial obstruction. J Stroke Cerebrovasc Dis 2002;11:47-50.
3Herrmann KA, Sporer B, Yousry TA. Thrombosis of the internal cerebral vein associated with transient unilateral thalamic edema: A case report and review of the literature. AJNR Am J Neuroradiol 2004;25:1351-5.
4Bezerra DC, Michel P, Maulaz AB, Binaghi S, Bogousslavsky J. Resolution of bilateral thalamic lesions due to deep cerebral venous thrombosis. Arch Neurol 2005;62:1638-9.
5Jee RC, Lin SH. Teaching neuro images: Reversible bilateral thalamic lesions in vein of Galen thrombosis. Neurology 2009;73:e57.