Annals of Indian Academy of Neurology
LETTER TO THE EDITOR
Year
: 2015  |  Volume : 18  |  Issue : 1  |  Page : 121--123

Cerebral venous sinus thrombosis: Role of extra cranial collateral circulation


Chandramohan B Sharma, Jigar R Parekh, Dinesh Khandelwal, Bansi L Kumawat 
 Department of Neurology, Sawai Man Singh Medical College and Hospital, Jaipur, Rajasthan, India

Correspondence Address:
Jigar R Parekh
656, Adarsh Nagar, Near Krishna Mandir, Jaipur - 302 004, Rajasthan
India




How to cite this article:
Sharma CB, Parekh JR, Khandelwal D, Kumawat BL. Cerebral venous sinus thrombosis: Role of extra cranial collateral circulation.Ann Indian Acad Neurol 2015;18:121-123


How to cite this URL:
Sharma CB, Parekh JR, Khandelwal D, Kumawat BL. Cerebral venous sinus thrombosis: Role of extra cranial collateral circulation. Ann Indian Acad Neurol [serial online] 2015 [cited 2019 Nov 14 ];18:121-123
Available from: http://www.annalsofian.org/text.asp?2015/18/1/121/144280


Full Text

Sir,

A 30-year-old lady, on regular oral contraceptive (OC) drugs since three years, presented with three weeks history of headache, which was dull aching, bilateral fronto-parieto-occipital region with recurrent episodes of vomiting. She also had history of transient visual obscurations and diplopia on looking at distant gaze for one week. There was no history of limb weakness, numbness, seizures or altered mental status. There was no past history of any major medical illness.

On examination, pulse was 88/min and blood pressure was 124/ 80 mm Hg. Patient was conscious, oriented to time, place and person. Examination of cranial nerves showed bilateral papilledema and bilateral lateral rectus palsy. There was no motor weakness, deep tendon reflexes were normal with bilateral plantar flexor. There were no meningeal signs.

 Investigations



Hemoglobin level was 13.5 gm%, TLC - 8000/mm 3 , platelet count - 3.15 lakh/mm 3 . Erythrocyte sedimentation rate (ESR) was 15 at end of 1 st hour. Random blood sugar, renal function tests, liver function tests, thyroid function tests and serum electrolytes were normal. Anti-nuclear, anti-ds DNA and anti-phospholipid antibodies were within normal limits and serum homocystiene level was normal. Magnetic resonance imaging (MRI) brain revealed normal brain parenchyma with thrombus visualized in superior sagittal sinus, bilateral transverse sinuses and right sigmoid sinus. Computed tomography (CT) venogram showed filling defect in posterior half of superior sagittal sinus, bilateral transverse sinuses and right sigmoid sinus, with normal deep venous system. There were extensive collaterals in form of dilated superficial temporal veins, scalp veins, occipital vein, facial veins, vertebral venous plexus and pterygoid plexus.

 Treatment



Patient was managed with anti-coagulant therapy with low molecular weight heparin (LMWH) 1 mg/kg, twice daily followed by oral vitamin K antagonist to maintain prothrombin time-international normalized ratio (PT-INR) between two and three. Also, anti-edema treatment in form of acetazolamide 250 mg BD was started. Patient improved symptomatically during the hospital day over ten days of therapy. Patient was discharged in stable condition and was advised to follow-up in our department after two weeks.

In our patient, there was thrombosis of major cerebral venous sinuses including superior sagittal, bilateral transverse and right sigmoid sinuses as seen in MRI brain [Figure 1]. But the deep venous system was completely patent evident from the normal flow in inferior sagittal sinus, internal cerebral veins, basal veins, vein of Galen and straight sinus [Figure 2]. So, the venous drainage from the superficial venous system was established through the collateral route including:

Connections with deep venous system e.g. connection between superficial and deep middle cerebral vein within the sylvian fissure.From the cortical veins through anastomotic veins of trolard and labbe to the sylvian vein and subsequently through the spheno-parietal sinuses to the cavernous sinuses.Venous drainage via the parietal and occipital emissary veins to scalp veins and occipital veins. {Figure 1}{Figure 2}

The blood from the cavernous sinus drain through the petrosal sinuses into the transverse and sigmoid sinuses (intracranial) and via the emissary veins to the facial veins and the pterygoid and pharyngeal plexuses (extracranial) and subsequently to the systemic circulation [Figure 3]. The blood from the scalp veins (cork-screw shaped) and occipital veins drain to superficial temporal vein and vertebral venous plexus, respectively and subsequently to the systemic circulation [Figure 3]. Thus, these emissary veins play an important role in carrying the intracranial blood to extracranial circulation for subsequent systemic drainage.{Figure 3}

It can be presumed that chronic oral OC use may have led to gradual thrombosis of the major venous sinuses, which gave sufficient time for the extensive collateral circulation to be established. These collaterals paved the way for the required cerebral venous drainage and resultant sparing of the brain parenchyma.

In one study, the influence of venous hemodynamics on the outcomes in cerebral venous sinus thrombosis (CVST) patients was studied and it was shown that collateral circulation is very important in determining outcome. [1] Various types of collateral pathways were studied of which cavernous sinus pathway and deep venous drainage pathway are noteworthy. Accordingly, in our patient, both these pathways are important and the cavernous sinus pathway has both intracranial and extracranial routes. In addition, there is a third pathway through the scalp and occipital veins as mentioned above. Thus the extracranial collateral pathways through the facial veins, pharyngeal plexus, pterygoid plexus, superficial temporal vein, occipital vein and vertebral venous plexus are very important for drainage. These collateral pathways have a significant impact on the outcome as seen in our patient.

Cerebral venous sinus thrombosis is a common complication in OC pills users. [2] It can lead to gradual development of dural sinus thrombosis giving time for collateral circulation to establish and consequently present as isolated intracranial hypertension. Among the collateral circulation, the extracranial pathways through the emissary veins are also important routes of venous drainage.

References

1Stolz E, Gerriets T, Bodeker RH, Penzel MH, Kaps M. Intracranial venous hemodynamics is a factor related to favourable outcome in cerebral venous thrombosis. Stroke 2002;33:1645-50.
2Martinelli I, Taioli E, Palli D, Mannucci PM. Risk of cerebral vein thrombosis and oral contraceptives. Lancet 1998;352:326.