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Year : 2016  |  Volume : 19  |  Issue : 3  |  Page : 411-413

"Venous congestion" as a cause of subcortical white matter T2 hypointensity on magnetic resonance images

Department of Clinical neurosciences, Indo-American Hospital, Brain and Spine Centre, Vaikom, Kerala, India

Date of Submission01-Dec-2015
Date of Decision07-Jan-2016
Date of Acceptance17-Jan-2016
Date of Web Publication25-Jul-2016

Correspondence Address:
Jayaprakash Harsha Kamble
Department of Clinical neurosciences, Indo-American Hospital, Brain and Spine Centre, Chemmanakary, Vaikom - 686 143, Kerala
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0972-2327.179978

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Subcortical T2 hypointensity is an uncommon finding seen in very limited conditions such as multiple sclerosis, Sturge-Weber syndrome, and meningitis. Some of the conditions such as moyamoya disease, severe ischemic-anoxic insults, early cortical ischemia, and infarcts are of "arterial origin." We describe two conditions in which "venous congestion" plays a major role in T2 hypointensity - cerebral venous sinus thrombosis (CVST) and dural arteriovenous fistula (dAVF). The third case is a case of meningitis, showing T2 hypointensity as well, and can be explained by the "venous congestion" hypothesis. The same hypothesis can explain few of the other conditions causing subcortical T2 hypointensity.

Keywords: Cerebral venous sinus thrombosis (CVST), dural arteriovenous fistula (dAVF), magnetic resonance imaging (MRI), meningitis, venous congestion

How to cite this article:
Kamble JH, Parameswaran K. "Venous congestion" as a cause of subcortical white matter T2 hypointensity on magnetic resonance images. Ann Indian Acad Neurol 2016;19:411-3

How to cite this URL:
Kamble JH, Parameswaran K. "Venous congestion" as a cause of subcortical white matter T2 hypointensity on magnetic resonance images. Ann Indian Acad Neurol [serial online] 2016 [cited 2023 Jan 28];19:411-3. Available from:

   Introduction Top

Most cerebral pathologies cause T2 hyperintensity, while few conditions cause T2 hypointensity. In certain conditions such as nonketotic hyperglycinemia, [1] meningitis, encephalitis, leptomeningeal metastasis, the cause of subcortical hypointensity is not known. In some conditions such as moyamoya and infarcts, the T2 hypointensity is attributed to cerebral ischemia leading to accumulation of free radicals/nonheme iron. Our case series adds further to the list of etiologies of subcortical T2 hypointensity. We hypothesize "venous congestion" as a cause of some of these findings as well.

   Case Reports Top

Case 1

57-year-old male presented with one episode of a sudden transient loss of consciousness. Additionally, he gave a history of severe headache of a short duration and one episode of generalized tonic-clonic seizures. He underwent magnetic resonance imaging (MRI) that revealed right frontal sulcal subarachnoid hemorrhage (SAH) [Figure 1]a-c, with associated subcortical white matter T2/ fluid attenuated inversion recovery (FLAIR) hypointensity. Gradient recalled echo (GRE) imaging showed thrombosed superficial cortical veins [Figure 1]d and GRE blooming within the sulci corresponding to SAH [Figure 1]e. Magnetic resonance (MR) venogram showed occlusion of the anterior 1/3rd of the superior sagittal sinus [Figure 1]f. His blood investigations revealed polycythemia. He was treated with anticoagulants and venesection, after which he became symptom-free.
Figure 1: (a-c) Axial FLAIR MR image showing focal subcortical T2 hypointensity in the right frontal lobe, FLAIR hyperintensity in corresponding sulci (d and e) GRE images showing blooming in superficial cortical veins and within sulci (f) MR venogram showing occlusion of the anterior 1/3rd of the superficial sagittal sinus

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Case 2

40-year-old male gave a history of road traffic accident 2 years back, during which he sustained a head injury. He was managed conservatively at that time. After 15 days of accident, he had complaints of severe headache with vomiting, was diagnosed as right transverse sinus thrombosis, and was treated with anticoagulants for 6 months. He came to our hospital with a sudden onset of severe headache of a 10-day duration. He underwent repeat MRI that was suggestive of arteriovenous fistula with right transverse sinus occlusion. In addition, MRI showed T2/FLAIR hypointensity of right temporoparietal lobe white matter [Figure 2]a and b. The corresponding GRE blooming was seen in the GRE sequence. Few tortuous vessels were seen in the right temporoparietal lobe with slow flow within the sulci [Figure 2]a and b. He underwent digital subtraction angiography (DSA) that was suggestive of Cognard Type IIB dural arteriovenous fistula (dAVF) of right mid-transverse sinus [Figure 2]d-f, fed by the right occipital artery, ascending pharyngeal artery, middle meningeal artery, and the posterior meningeal artery. Proximal and distal portions of the right transverse sinus were occluded. There was significant cortical venous reflux into the right superficial middle cerebral vein that drains the brain territory corresponding to the region of MRI T2 hypointensity. Left transverse sinus was patent. Computed tomography (CT) scan showed few small foci of acute bleeding in the right temporoparietal lobe. Endovascular embolization was suggested.
Figure 2: (a and b) Axial FLAIR MR images showing subcortical white matter T2 hypointensity in right parietotemporal lobe (c) Corresponding GRE image shows subtle blooming (d and e) Right ECA angiogram showing right transverse dAVF with venous reflux into superficial middle cerebral vein (f) Right proximal and distal transverse sinus occluded. Left transverse sinus patent

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Case 3

A 22-year-old female presented with severe headache of 3-day duration and one episode of generalized tonic-clonic seizures. In view of clinical suspicion of meningitis, MRI was done that showed subcortical T2/FLAIR hypointensity in the right parietal lobe [Figure 3]a-d; in the corresponding region leptomeningeal contrast enhancement was seen [Figure 3]e and f, suggestive of meningitis. Her cerebrospinal fluid (CSF) study showed 84 cells with predominant neutrophils, protein −48 mg/dL, and sugar −60 mg/dL [corresponding random blood sugar (RBS) −159 mg/dL]. CSF was clear. CSF gram staining was negative for bacteria; tuberculosis polymerase chain reaction (TB PCR) was negative. Possible diagnosis of viral encephalitis was made.
Figure 3: (a-d) Axial T2 and FLAIR MR images showing focal subcortical T2 hypointensity in the right parietal lobe, with corresponding sulcal FLAIR hyperintensity (e and f) Corresponding region leptomeningeal contrast enhancement seen

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   Discussion Top

Subcortical white matter T2/FLAIR hypointensity is an uncommon finding of diverse etiology. The previously reported causes are Sturge-Weber syndrome, [2] moyamoya disease, [3] multiple sclerosis, [4] meningitis, [5] viral encephalitis, [5] and leptomeningeal metastasis. [5] Deep white matter T2 hypointensity along with deep gray matter nuclei is seen in arterial infarcts. [6],[7] Deep white matter T2 hypointensity is reported in young children with diffuse ischemic-anoxic cerebral injury as well. [8]

The few cases of T2 hypointensity secondary to ischemia reported previously are of arterial origin - Infarction, moyamoya disease, etc. However, we describe two cases, where "venous congestion" undoubtedly played a role in cerebral ischemia, causing subcortical white matter T2 hypointensity. Though previous observations by Hurst RW and Grossman RI [9] suggested the possible venous congestion as etiology of T2 hypointensity in spinal cord white matter, no cerebral cases have been reported till date. The underlying pathophysiology appears to be the same as arterial ischemia - accumulation of nonheme iron and/or free radicals in subcortical white matter. [10],[11],[12],[13],[14],[15] In the first case, acute onset of superficial cerebral vein thrombosis might have predisposed to increased accumulation of free radicals. While in the second case, chronic venous congestion due to dAVF associated with occlusion of proximal and distal portion of the transverse sinus lead to the interruption of axonal transport of iron and accumulation of nonheme iron. Such accumulation of paramagnetic substances in venous hypertensive myelopathy [9] are confirmed in a few studies; similar pathomechanism might be playing a role in subcortical T2 hypointensity as well, though further studies needed to substantiate the statement. The third case is a case of focal meningitis; contrast study showed abnormal leptomeningeal enhancement possibly contributing to venous congestion.

In addition, our findings hypothesize the possible cortical and subcortical venous congestion as an etiologic factor for T2 subcortical hypointensity in focal meningitis and encephalitis. [5] The "venous congestion" hypothesis can explain as well the reversal of T2 hypointensity after resolution of underlying etiology (meningitis/cerebral venous sinus thrombosis (CVST)/encephalitis/dAVF/leptomeningeal metastasis). The initial stage of T2 hypointensity could be a predisposing factor of later subcortical mineralization (as demonstrated by CT scans) in advanced cases of dAVF. [16] Possibly, similar pathomechanism might play a role in parenchymal mineralization of subcortical white matter in the vein of Galen malformation. [17] Additionally, in advanced cases of dAVF/vein of Galen malformation, dystrophic calcification might contribute to T2 hypointensity as well. Sturge-Weber syndrome is a disease due to primary venous dysplasia with resultant venous hypertension. [18] Again, "venous congestion" hypothesis can explain the excessive iron accumulation in subcortical white matter (as evidenced by T2 hypointensity/blooming in susceptibility weighted imaging). [19] Utility of perfusion studies in such cases may give more information about underlying pathophysiology, while histology/necropsy studies remains the gold standard for anatomical changes/mineral composition assessment.

However, the question raised by Lee et al., [5] remains valid to date as to why subcortical low intensity is seen in only few patients of various pathology, while not seen in others with the same pathology. There is a possibility of genetic factors, duration of illness, severity of illness playing a major role in answering these questions.

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Conflicts of interest

There are no conflicts of interest.

   References Top

Seo DW, Na DG, Na DL, Moon SY, Hong SB. Subcortical hypointensity in partial status epilepticus associated with nonketotic hyperglycemia. J Neuroimaging 2003;13:259-63.  Back to cited text no. 1
Jacoby CG, Yuh WT, Afifi AK, Bell WE, Schelper RL, Sato Y. Accelerated myelination in early Sturge-Weber syndrome demonstrated by MR imaging. J Comput Assist Tomogr 1987;11:226-31.  Back to cited text no. 2
Takanashi J, Sugita K, Tanabe Y, Ito C, Date H, Niimi H. T2 shortening in childhood moyamoya disease. Neuroradiology 1996;38(Suppl 1):S169-73.  Back to cited text no. 3
Russo C, Smoker WR, Kubal W. Cortical and subcortical T2 shortening in multiple sclerosis. AJNR Am J Neuroradiol 1997;18:124-6.  Back to cited text no. 4
Lee JH, Na DG, Choi KH, Kim KJ, Ryoo JW, Lee SY, et al. Subcortical low intensity on MR images of meningitis, viral encephalitis, and leptomeningeal metastasis. AJNR Am J Neuroradiol 2002;23:535-42.  Back to cited text no. 5
Cross PA, Atlas SW, Grossman RI. MR evaluation of brain iron in children with cerebral infarction. AJNR Am J Neuroradiol 1990;11:341-8.  Back to cited text no. 6
Ida M, Mizunuma K, Hata Y, Tada S. Subcortical low intensity in early cortical ischemia. AJNR Am J Neuroradiol 1994;15:1387-93.  Back to cited text no. 7
Dietrich RB, Bradley WG Jr. Iron accumulation in the basal ganglia following severe ischemic-anoxic insults in children. Radiology 1988;168:203-6.  Back to cited text no. 8
Hurst RW, Grossman RI. Peripheral spinal cord hypointensity on T2-weighted MR images: A reliable imaging sign of venous hypertensivemyelopathy. AJNR Am J Neuroradiol 2000;21:781-6.  Back to cited text no. 9
Kim SW, Kim RC, Choi BH, Gordon SK. Non-traumatic ischemic myelopathy: A review of 25 cases. Paraplegia 1988;26:262-72.  Back to cited text no. 10
Hurst RW, Kenyon LC, Lavi E, Raps EC, Marcotte P. Spinal dural arteriovenous fistula: The pathology of venous hypertensive myelopathy. Neurology 1995;45:1309-13.  Back to cited text no. 11
Adams J, Duchen L. Greenfield's Neuropathology. New York: Oxford University Press; 1992. p. 1107-10.  Back to cited text no. 12
Kim RC. Necrotizing myelopathy. AJNR Am J Neuroradiol 1991;12:1084-6.  Back to cited text no. 13
Jellinger K. Pathology of Spinal Vascular Malformations and Vascular Tumors. Berlin: Springer; 1978. p. 18-44.  Back to cited text no. 14
Hughes J. Disorders of the Spine and Spinal Cord. New York: Wiley; 1990. p. 799-806.  Back to cited text no. 15
Metoki T, Mugikura S, Higano S, Ezura M, Matsumoto Y, Hirayama K, et al. Subcortical calcification on CT in dural arteriovenous fistula with cortical venous reflux. AJNR Am J Neuroradiol 2006;27:1076-8.  Back to cited text no. 16
Lasjaunias PL, Chng SM, Sachet M, Alvarez H, Rodesch G, Garcia-Monaco R. The management of vein of Galen aneurysmal malformations. Neurosurgery 2006;59(Suppl 3):S184-94; discussion S3-13.  Back to cited text no. 17
Parsa CF. Sturge-Weber syndrome: A unified pathophysiologic mechanism. Curr Treat Options Neurol 2008;10:47-54.  Back to cited text no. 18
Jagtap S, Srinivas G, Harsha KJ, Radhakrishnan N, Radhakrishnan A. Sturge-Weber syndrome: Clinical spectrum, disease course, and outcome of 30 patients. J Child Neurol 2013;28:725-31.  Back to cited text no. 19


  [Figure 1], [Figure 2], [Figure 3]

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