| Article Access Statistics|
| Viewed||4786 |
| Printed||103 |
| Emailed||7 |
| PDF Downloaded||111 |
| Comments ||[Add] |
| Cited by others ||3 |
Click on image for details.
|Year : 2000 | Volume
| Issue : 2 | Page : 195-6
Cortical sinovenous thrombosis following closed head injury.
Meena AK, Jayalaxmi SS, Murthy JM
|How to cite this article:|
Meena A K, Jayalaxmi S S, Murthy J M. Cortical sinovenous thrombosis following closed head injury. Neurol India 2000;48:195
LETTERS TO EDITOR
Cortical Sinovenous Thrombosis Following Closed Head Injury
Head injury rarely predisposes to development of cortical sinovenous thrombosis (CSVT).,,, We report a patient who developed CSVT following nonpenetrating head injury.
A 40 year male met a road traffic accident while travelling on a motorcycle. He denied any loss of consciousness or seizures at the time of accident. He was not an alcoholic. He had skin laceration over left frontotemporal region which was sutured. Two weeks later, he developed constant left frontotemporal dull ache and, in a single day, had five episodes of tonic clonic seizures involving right half of body with secondary generalisation. Each episode lasted 2 to 4 minutes. Neurological examination was essentially normal. EEG did not reveal any abnormalilty. As he was allergic to drugs, only plain CT scan of the brain was done which was essentially normal. He was put on phenytoin sodium 300 mg/day. Ten days later he had six episodes of numbness involving right upper and lower limbs, each episode lasting less than one minute. Next day he developed weakness of right upper and lower limb. On examination, he was conscious and ocular fundi showed bilateral papilloedema. He had right upper motor neuron type of facial weakness. Motor system examination showed mild decrease in tone on right side and power was graded at 4/5. Deep tendon reflexes were brisk on the right side and right plantar was extensor. Haemogram and blood biochemistry were normal. Platelet count was 2.2 lakhs/cumm. Prothrombin time and activated partial thromboplastin time were similar to control values. Protein C was 86% (70-130%), protein S 90% (65-140%), and antithrombin III 102% (96-112%). Repeat plain CT scan brain revealed a hyperdense lesions in the left parieto-occipital region near the straight sinus and the posterior part of the superior sagittal sinus. T1 and T2 weighted magnetic resonance images of brain showed hyperintense lesions in the posterior part of the superior sagittal sinus and in the straight sinus [Figure - 1]. The patient was given heparin infusion at the rate of 1000 units/hr for 7 days and was later switched over to acitrom. He showed significant improvement in headache and weakness during follow up. Neurological examination at 7 months follow up was essentially normal and acitrom was stopped.
Bagley gave the first description of superior sagittal sinus thrombosis following non penetrating head injury. Hesselbrock et al could find only 11 acceptable cases of post traumatic superior sagittal sinus thrombosis till 1985. Post traumatic CSVT can also involve other veins like vein of Galen and its tributary vessels. As a rule, CSVT following head trauma follows a subacute course. It may occur after few days to weeks following head injury as seen in our case.
The exact pathogenesis of CSVT following head injury is not clear. At times even trivial trauma can result in CSVT. In patients with depressed or compound fracture, non penetrating tangential injuries or blunt trauma, direct damage to the dural sinuses may be the factor responsible for sinus thrombosis. In patients with closed head injuries, endothelial damage and intramural haemorrhage secondary to rupture of the sinusoids at the site of entry of the draining veins may initiate the thrombotic process. Haemorrhage into the pacchionian corpuscules may be the other initiating event. The role of coagulopathy resulting from head trauma in the pathogenesis of CSVT is not clear. In our case, there was a definite temporal relation between head injury and development of CSVT. There was no pre-existing hypercoagulable state. In this case, probably damage to the endothelium of superior saggital sinus by rotational head and neck movements at the time of head injury might have been the initiating event for thrombosis.
|1.||Bagley C JR: Traumatic longitudinal sinus lesions. Report of two cases. Gynecol Obstet 1934; 58: 498-502. |
|2.||Hesselbrock R, Sawaya R, Tomsick T et al: Superior sagittal sinus thrombosis after closed head injury. Neurosurgery 1985; 16: 825-828 |
|3.||Yanez Bana RM, Rossi Lopez RE, Romero Lopez J et al: Deep venous thrombosis related to cranioencephalic injury (Spanish). Neurologia 1989; 4: 256-259. |
|4.||Kalbag RM, Woolf AL: Thrombosis and thrombophlebitis of cerebral veins and dural sinuses. In Vinken PJ, Bruyn GW (Eds) Handbook of Clinical Neurology, Vascular diseases of the nervous system, Part II, North Holland Publishing Company, Amsterdam 1972; 12: 422-446. |
|5.||Kalbag RM, Woolf AL: Cerebral venous thrombosis. London, Oxford University Press 1967. |
|6.||Schmidek HH, Auer LM, Kapp JP: The cerebral venous system. Neurosurgery 1985; 17: 663-678. |
|7.||Carrie AW, Jaffe' FA: Thrombosis of superior sagittal sinus caused by trauma without penetrating injury. J Neurosurg 1954; 11: 173-182. |