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TOPIC OF THE ISSUE: CASE REPORT
Year : 2010  |  Volume : 58  |  Issue : 4  |  Page : 615-617

Susceptibility-weighted imaging in differentiating bilateral medial thalamic venous and arterial infarcts


Department of Imaging Sciences & Interventional Radiology, Sree Chitra Tirunal Institute for Medical Sciences & Technology, Trivandrum, Kerala-695 011, India

Date of Acceptance01-Feb-2010
Date of Web Publication24-Aug-2010

Correspondence Address:
Bejoy Thomas
Department of Imaging Sciences & Interventional Radiology, Sree Chitra Tirunal Institute for Medical Sciences & Technology, Trivandrum, Kerala-695 011
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0028-3886.68670

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 » Abstract 

Bilateral medial thalamic infarcts may be due to thrombosis of internal cerebral veins or occlusion of artery of Percheron. Conventional MR imaging is often not helpful in differentiating the two. We discuss two cases in whom susceptibility-weighted imaging, including phase images contributed in demonstrating the thrombosed or patent internal cerebral veins.


Keywords: Artery of percheron infarct, internal cerebral vein thrombosis, magnetic resonance imaging, susceptibility-weighted imaging


How to cite this article:
Chatterjee S, Thomas B, Kesavadas C, Kapilamoorthy TR. Susceptibility-weighted imaging in differentiating bilateral medial thalamic venous and arterial infarcts. Neurol India 2010;58:615-7

How to cite this URL:
Chatterjee S, Thomas B, Kesavadas C, Kapilamoorthy TR. Susceptibility-weighted imaging in differentiating bilateral medial thalamic venous and arterial infarcts. Neurol India [serial online] 2010 [cited 2022 Nov 27];58:615-7. Available from: https://www.neurologyindia.com/text.asp?2010/58/4/615/68670



 » Introduction Top


Venous drainage of thalami is through the internal cerebral veins and thrombosis of this vein results in thalamic infarcts with or without hemorrhage. The artery of Percheron is a solitary trunk representing an uncommon anatomic variant that provides bilateral arterial supply to the paramedian thalami and the rostral midbrain. Occlusion of this artery results in bilateral thalamic and mesencephalic infarctions. [1] In a clinical setting of stroke it is often difficult to differentiate between the two by conventional magnetic resonance imaging (MRI) sequences. MR venography may be helpful occasionally, however often it is difficult to visualize the small thrombosed internal cerebral veins. Susceptibility weighted image (SWI) with phase imaging can overcome this difficulty. We present two patients with bilateral medial thalamic infarcts, one due to internal cerebral vein thrombosis and the other presumably due to artery of Percheron thrombosis to demonstrate the usefulness of SWI in differentiating the two.


 » Case Reports Top


Case 1

A 27-year male presented with acute onset of headache of one week duration with history suggestive of acute left mastoiditis. He also complained of inability to read and write and one episode of seizure. On examination, he had agraphia and alexia, and could copy letters and figures but could not do so independently and had difficulty in identifying figures. MRI showed thrombosis of left distal transverse and sigmoid sinuses with hemorrhagic infarct in the left posterior temporal lobe and bilateral thalami. Careful analysis of susceptibility phase image showed replacement of normal hyper intense signal of internal cerebral veins on both sides by hypo intensity suggestive of phase changes due to internal cerebral vein thrombosis. This finding was confirmed on a dynamic contrast enhanced MR venography. Left vein of Labbe thrombosis was also detected on the phase images [Figure 1].
Figure 1 : FLAIR axial image (a) shows bilateral hypo intense thalamic lesions which on SWI (min IP) (b) shows significant blooming suggesting hemorrhage and on SWI (Phase image) (c), the internal cerebral veins show hypo intense signal (arrow), compared to straight sinus (double arrows), suggestive of luminal thrombosis. Contrast enhanced MRV (d) confirms lack of opacification of internal cerebral veins [(Reproduced from, Figure 6, Neuroradiology.2008;50(2):105-16. Clinical applications of susceptibility weighted MR imaging of the brain - a pictorial review.Thomas B, Somasundaram S, Thamburaj K et al- With kind permission of Springer Science+Business Media)]

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Case 2

A 66-year female presented with sudden onset of giddiness. The giddiness progressed over the next few hours and she became unresponsive. On examination, she was drowsy, irritable, but responding and obeying to simple commands. Bilateral ptosis, vertical gaze palsy and restriction of adduction of right eye were present. Right pupil was dilated and not reacting to light, the left pupil was normal. MRI showed T2-weighted and FLAIR hyper intensity with restricted diffusion on diffusion weighted imaging (DWI) involving bilateral medial thalami extending to ventral midbrain. Bilateral internal cerebral veins appeared patent with preserved hyper intense signal on phase images [Figure 2]. She was diagnosed to have an artery of Percheron infarct.
Figure 2: FLAIR axial image (a) shows bilateral hyper intense thalamic lesions and on DWI (b) and ADC (c) show restricted diffusion in the same region, SWI (min IP) (d) do not show any evidence of hemorrhage and SWI (Phase image) (e) shows patent internal cerebral veins (arrow)

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 » Discussion Top


Deep venous thrombosis involving the internal cerebral veins can result in thalamic infarcts. [2],[3],[4],[5] The most widely used techniques for MR angiography is time of flight (TOF) and phase contrast. However, these methods have limitations in terms of their ability to visualize slowly flowing blood in small vessels. One disadvantage with contrast-enhanced MR angiography is that meningeal enhancement obscures superficial vessels on 3D maximum intensity projection venous angiograms. Another drawback is that enhancement of thrombotic material makes reading of subsequent MR angiograms difficult. It is time consuming and patient may not cooperate for a lengthy examination. [6] In addition it needs contrast administration adding to the costs and risks of contrast. Pre imaging clinical suspicion of cerebral venous sinus thrombosis helps in including this sequence while evaluating these patients. Susceptibility-weighted imaging uses the paramagnetic deoxy-Hb as an intrinsic contrast agent. [7] Deoxyhemoglobin causes a reduction in T2* as well as a phase difference between the vessel and its surrounding parenchyma. [8],[9],[10] The T1 and T2 properties of blood are dependent on the oxygen saturation of the blood, hematocrit and the state of the red blood cells (RBCs). [11] At 1.5 T, arterial blood has a T2* of approximately 200 ms, while 70%saturated venous blood has T2* of 100 ms. Hence, long TEs will help in differentiating arteries from veins. SWI has been used for venous imaging in conditions like arteriovenous malformation, Sturge-  Weber syndrome More Details, and developmental venous anomalies. Susceptibility-weighted imaging with both phase and magnitude information facilitates the detection of cerebral venous thrombosis which are otherwise difficult to detect in conventional spin-echo T2 images. Lin et al. showed the differentiation of small patent venous structures originating from thrombosis using sequential pre- and post-contrast SWI and the phase pattern in SWI phase images. [12]

The thalami receive their arterial supply from both the anterior (internal carotid arteries) and posterior (vertebro-basilar system) circulation, and several variations in this supply are known to exist. [13],[14] Anterior circulation usually supplies the anteroinferior part of the thalami with thalamoperforator arteries from the posterior communicating arteries. The posterior circulation usually supplies the medial portion of the thalami and midbrain through perforating branches arising from P1 segments of the posterior cerebral arteries (PCAs). The lateral and superior regions of the thalami are supplied by branches from P2 segments of the PCAs. Percheron studied the variations of this arterial supply and its distribution and described three different types of supply originating from P1 segment. In the second type described by him, there is a common trunk arising from one of the P1 segments providing bilateral medial thalami. Occlusion of this trunk results in bilateral infarctions of the medial thalami. [15],[16],[17],[18],[19] The prevalence of artery of percheron infarct is not known. [20]

In the first patient, we could demonstrate the presence of thrombus in the internal cerebral veins by phase image of SWI. In our system, patent venous channels are hyper intense in phase image and thrombus show as hypo intense filling defect within the venous channels. The phase image reveals the venous occlusion as shown in our patient without the use of contrast agent, thus helping in differentiating artery of Percheron infarct from internal cerebral vein thrombosis in cases with bilateral thalamic stroke. In a given case clinical differentiation of the two entities may not be possible. In such cases SWI phase images may play an important role in the correct diagnosis. Thus without the use of contrast and without subjecting critically ill and uncooperative patient to long contrast MR venography sequence this important diagnostic information can be extracted from SWI sequence. The two patients described here differ in clinical presentation and areas involved, in one ventral midbrain lesion and in the other left posterior temporal lesion were present in addition to thalamic lesions. However, these two patients were presented to delineate the role of phase image in excluding internal cerebral vein thrombosis in cases with bilateral thalamic lesions.

 
 » References Top

1.Kostanian V, Cramer SC. Artery of percheron thrombolysis. AJNR Am J Neuroradiol 2007;28:870-1.  Back to cited text no. 1  [PUBMED]  [FULLTEXT]  
2.Bell DA, Wayne LD, Osborn AG, Harnsberger HR. Bithalamic hyper intensity on T2-weighted MR: vascular causes and evaluation with MR angiography. AJNR Am J Neuroradiol 1994;15:893-9.  Back to cited text no. 2      
3.Crawford SC, Digre KB, Palmer CA, Bell DA, Osborn AG. Thrombosis of the deep venous drainage of the brain in adults. Arch Neurol 1995;52:1101-8.  Back to cited text no. 3  [PUBMED]  [FULLTEXT]  
4.Crawford SC, Digre KB, Palmer CA, Bell DA, Osborn AG. Para-median thalamic and midbrain infarcts: clinical and neuro-pathological study. Ann Neurol 1981;10:127-48.  Back to cited text no. 4      
5.Guberman A, Stuss D. The syndrome of bilateral para-median thalamic infarction. Neurology 1983;33:540-546.  Back to cited text no. 5  [PUBMED]    
6.Kirchhof K, Welzel T, Jansen O, Sartor K. More reliable noninvasive visualization of the cerebral veins and dural sinuses: comparison of three MR angiographic techniques. Radiology 2002;224:804-10.  Back to cited text no. 6  [PUBMED]  [FULLTEXT]  
7.Reichenbach JR, Venkatesan R, Schillinger DJ, Kido DK, Haacke EM. Small vessels in the human brain. MR venography with deoxyhemoglobin as an intrinsic contrast agent. Radiology 1997;204:272-7.  Back to cited text no. 7  [PUBMED]  [FULLTEXT]  
8.Thulborn KR, Waterton JC, Matthews PM, Radda GK. Oxygenation dependence of the transverse relaxation time of water protons in whole blood at high field. Biochim Biophys Acta 1982;714:265-70.  Back to cited text no. 8  [PUBMED]  [FULLTEXT]  
9.Li D, Waight DJ, Wang Y. In vivo correlation between blood T2* and oxygen saturation. J Magn Reson Imaging 1998;8:1236-9.  Back to cited text no. 9  [PUBMED]    
10.Gomori JM, Grossman RI, Yu-Ip C, Asakura T. NMR relaxation times of blood: dependence on field strength, oxidation state, and cell integrity. J Comput Assist Tomogr 1987;11:684-90.  Back to cited text no. 10  [PUBMED]    
11.Reichenbach JR, Haacke EM. High-resolution BOLD venographic imaging: a window into brain function. NMR Biomed 2001;14:453-67.  Back to cited text no. 11  [PUBMED]  [FULLTEXT]  
12.Lin W, Mukherjee P, An H, Yu Y, Wang Y, Vo K, et al. Improving high resolution MR bold venographic imaging using a T1 reducing contrast agent. J Magn Reson Imaging 1999;10:118-23.  Back to cited text no. 12  [PUBMED]  [FULLTEXT]  
13.Percheron G. The anatomy of the arterial supply of the human thalamus and its use for the interpretation of the thalamic vascular pathology. Z Neurol 1973;205:1-13.  Back to cited text no. 13  [PUBMED]    
14.Lasjaunias P, Berenstein A, Brugge KG, editors. Surgical Neuroangiography. 2nd ed. Vol. 1. Berlin: Springer-Verlag; 2000. p. 526-62.   Back to cited text no. 14      
15.Roitberg BZ, Tuccar E, Alp MS. Bilateral paramedian thalamic infarct in the presence of an unpaired thalamic perforating artery. Acta Neurochir 2002;144:301-4.   Back to cited text no. 15      
16.Lepore FD, Gulli V, Miller DC. Neuro-ophthalmological findings with neuropathological correlation in bilateral thalamic-mesencephalic infarction. J Clin Neuroophthalmol 1985;5:224-8.   Back to cited text no. 16      
17.Kumral E, Evyapan D, Balkir K, Kutluhan S. Bilateral thalamic infarction, clinical etiological and MRI correlates. Acta Neurol Scand 2001;103:35-42.  Back to cited text no. 17  [PUBMED]  [FULLTEXT]  
18.Castaigne P, Lhermitte F, Buge A, Escourolle R, Hauw JJ, Lyon-Caen Paramedian thalamic and midbrain infarcts: clinical and neuropathological study. Ann Neurol 1981;10:127-48.   Back to cited text no. 18      
19.Biller J, Sand JJ, Corbett JJ, Adams HP Jr, Dunn V. Syndrome of the paramedian thalamic arteries: clinical and neuroimaging correlation. Clin Neuro-ophthalmol 1985;5:217-23.   Back to cited text no. 19      
20.Krampla W, Schmidbauer B, Hruby W. Ischaemic stroke of the artery of Percheron. Eur Radiol 2008;18:192-4.  Back to cited text no. 20  [PUBMED]  [FULLTEXT]  


    Figures

  [Figure 1], [Figure 2]

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