Neurol Med Chir (Tokyo) 40, 361 ~ 365, 2000 Sigmoid Sinus Thrombosis After Mild Closed Head Injury in an Infant: Diagnosis by Magnetic Resonance Imaging in the Acute Phase —Case Report— Hideki SATOH, Kiyoshi KUMANO, Ryo OGAMI, Tohru NISHI, Jun ONDA, Shigeru NISHIMURA, and Kaoru KURISU* Department of Neurosurgery, Kitakyushu General Hospital, Kitakyushu, Fukuoka; *Department of Neurosurgery, Hiroshima University School of Medicine, Hiroshima Abstract Intracranial sinus thrombosis following a mild closed head injury without a skull fracture or in- tracranial hematoma is extremely rare. A 23-month-old girl presented with vomiting and gait ataxia 1 day after occipital trauma. Computed tomography revealed a slightly increased density area in the region of the left sigmoid sinus. T,-weighted magnetic resonance (MR) imaging demonstrated an isointense area in the left sigmoid sinus and T,-weighted imaging showed a hyperintense area reflecting the characteristics of oxyhemoglobin. MR angiography and cerebral angiography indicated occlusion of the left sigmoid sinus. After 4 days of conservative treatment, her symptoms subsided completely. Follow-up MR angiography and cerebral angiography showed recanalization of the sigmoid sinus. The MR images and MR angiograms were useful for both early diagnosis and follow-up. Treatment should reflect the severity of individual cases, and early diagnosis will help achieve a good outcome. Key words: sinus thrombosis, sigmoid sinus, closed head injury, magnetic resonance imaging Introduction Intracranial sinus thrombosis is a relatively rare event associated with a poor prognosis, largely be- cause the diagnosis was difficult. Mild closed head injury without skull fractures or intracranial hema- tomas is an extremely rare cause, with only 11 reported cases.*°"?1522526 We treated an infant with sigmoid sinus thrombosis complicated by mild closed head injury. The thrombosis was identified in the acute phase by magnetic resonance (MR) imag- ing. Case Report A 23-month-old girl fell from a height of approxi- mately 1 m and struck her occiput on November 8, 1998. She suffered no loss of consciousness or vomiting and was able to walk. However, vomiting and gait disturbance appeared by the next morning. The patient was first taken to the pediatric depart- ment of a local hospital and then referred to our in- stitution for further evaluation. Her history included medical treatment for asthma for 3 months. Her family history was unremarkable. Neurological signs and symptoms on admission included moderate headache complaints, decreased muscle tone, and gait ataxia. There were no abnor- malities of the cranial nerves or motor or sensory disturbances in the extremities. Fundoscopy showed no evidence of a choked disc. No signs of dehydra- tion were present. Biochemical and hematologic screening tests disclosed no abnormal findings (hematocrit 34.6%, platelet count 25.8 x 10*/ul, white blood cell count 8.9 x 10°/ul, and C-reactive protein 0.1 mg/dl). All bleeding and coagulation test Received June 30,1999; Accepted March 14, 2000 Author’s present address: H. Satoh, M.D., Department of Neurosurgery, Hiroshima Prefectural Hospital, Hiroshima, Japan. 362 H. Satoh et al. Fig. 1 T,-weighted magnetic resonance (MR) image on admission demonstrating an isointense area in the left sigmoid sinus (left), and T,-weighted image demonstrating a hyperintense area (center). Phase-contrast MR angiogram (velocity encoding gradient = 15 cm/sec) showing occlusion of the left sigmoid sinus (right). There is no midline shift of the fourth ventricle. arrow: lateral wall of the sigmoid sinus, arrowhead: small extradural hematoma. Fig. 2 Cerebral angiogram performed on the sec- ond hospital day also demonstrating occlu- sion of the left sigmoid sinus. results were within the normal ranges (bleeding time 2 min, prothrombin activity 82% of control, activat- ed partial thromboplastin time 32.5 sec, fibrin degradation products 3.1 ug/ml). The control protein S activity was 102% and the control protein C ac- tivity was 123%, and the lupus anticoagulant was not detectable. The lumbar puncture opening pres- Fig. 3 T,-weighted magnetic resonance image 15 days after admission (left) and cerebral an- giogram on the following day (right) demon- strating that the left sigmoid sinus has recanalized. arrow: flow void phenomenon of the left sigmoid sinus. sure was 240 mmH.0O, and cell numbers and protein concentration in the cerebrospinal fluid were within the normal ranges. Computed tomography (CT) re- vealed a region of slightly increased density in the sigmoid sinus, which was enhanced by administra- tion of contrast medium. T;-weighted MR imaging obtained on the same day showed an isointense area, and T,-weighted imaging demonstrated a hyperintense area in the left sigmoid sinus (Fig. 1 left, center). MR angiography (phase-contrast Neurol Med Chir (Tokyo) 40, July, 2000 Sigmoid Sinus Thrombosis After Mild Closed Head Injury 363 method) demonstrated occlusion of the left sigmoid sinus (Fig. 1 right). Cerebral angiography confirmed occlusion of the left sigmoid sinus on November 10 (Fig. 2). Intravenous drip infusion of glycerol and steroid was administered to treat the increased intracranial pressure. Headache and vomiting resolved 3 days after admission, and the patient was able to walk 4 days after admission. MR imaging and MR an- giography 15 days after admission disclosed that the left sigmoid sinus had recanalized (Fig. 3 left). Con- ventional cerebral angiography on the following day showed the same finding (Fig. 3 right). The patient was discharged from the hospital 17 days after ad- mission with no neurological deficits. MR imaging and MR angiography 3 months after hospital dis- charge confirmed patency of the sigmoid sinus. Discussion Causes of sinus thrombosis include infection of the head and neck, pregnancy and delivery, oral con- traceptives, and dehydration. More recently, sinus thrombosis has resulted from hypercoagulable states caused by protein S deficiency, protein C deficien- cy, or antiphospholipid antibodies.” Sinus throm- bosis had been considered a very ominous event until recently, when mild cases have been resolved without residual neurological deficits because of technical advances.” Some cases of skull fracture or intracranial hematoma following head injury have caused thrombosis by direct compression of the sinus,” but thrombosis after mild closed head inju- ty without such complications is exceptionally rare. Symptoms of sinus thrombosis can be classified into two groups: manifestations of increased in- tracranial pressure such as headache, choked disc, and impaired consciousness”; and focal signs in- cluding convulsive seizures and hemiplegia caused by venous infarction, which is often hemorrhagic.” Cerebellar ataxia is not common, but gait ataxia oc- curred in all five cases with sigmoid sinus throm- bosis (including three with skull fractures), sug- gesting that gait ataxia is characteristic of sigmoid sinus involvement. The time interval between injury and symptom onset varies from moments after inju- ry to 8 months,” which is an obstacle to accurate diagnosis of traumatic sinus thrombosis. The severity of the manifestations of sinus throm- bosis depends on the extent of the thrombus, the anatomy of collateral veins, and the rate of progres- sion of thrombosis.” Sinus thrombosis following mild closed head injury in the 12 reported cases, including the present patient, originated in the su- perior sagittal sinus in five cases, the transverse si- Neurol Med Chir (Tokyo) 40, July, 2000 nus in five, the sigmoid sinus in four, and the straight sinus in one (multiple sinuses were involved in 2 cases). Condition on discharge was described in 11 patients. No deaths occurred, and neurological sequelae were noted in four patients, three of whom had superior sagittal sinus thrombosis. All three patients with sigmoid sinus thrombosis showed favorable outcomes on discharge. Proposed mechanisms of sinus thrombosis after mild closed head injury have involved endothelial damage within the venous sinus that causes throm- bosis by activating the coagulation system. The brain also contains an abundance of thromboplastin that is released after injury. Thromboplastin induces an abnormal hypercoagulable state like the destruc- tion of platelets and erythrocytes."'*?) However, fibrinolytic activity is higher in normal venous walls than in artery or capillary walls, and thrombi in the sinuses frequently recanalize with time due to fibrinolysis.”? This mechanism may account for the mild cases of sinus thrombosis. The characteristic CT findings of sinus thrombo- sis include the cord sign, dense vein sign, and empty-delta sign following the administration of contrast agents.*’°” Indirect evidence such as hemorrhagic infarcts, venous infarcts, extensive cerebral edema, and narrowing of the cerebral ven- tricles suggest sinus thrombosis in many cases.” Cerebral angiography, particularly digital subtrac- tion angiography, is the method of choice for diag- nosing sinus thrombosis. However, complete ab- sence of the transverse and sigmoid sinus may be a normal anatomic variation, so diagnosis of throm- bosis in these areas should proceed cautiously.” MR imaging findings in sinus thrombosis have also been reported.’”’? Four phases were identified based on sequential changes.’? In the first few hours, the thrombi appear as isointense to slightly hypointense on the T,-weighted images, and hyperintense on the T.-weighted images, reflecting the presence of oxy- hemoglobin.”” Several hours after thrombus forma- tion, the thrombus appears as hypointense on the T.-weighted images as deoxyhemoglobin becomes dominant. In the present case, the MR imaging findings were extremely valuable to establish the diagnosis during the acute phase, within several hours of thrombus formation, as confirmed by the signal intensities characteristic of oxyhemoglobin. Moreover, the phase-contrast MR angiography was used to depict veins selectively by appropriate flow-velocity settings.”"?? MR imaging was superior to CT or cerebral angiography in four ways: throm- bus in the sinus was visualized with no contrast medium; time elapsed since thrombosis could be estimated; the procedure was noninvasive and safe 364 for performance in a child; and sequential follow- up imaging was facilitated. No consensus has been reached for the treatment of sinus thrombosis, because the severity varies greatly from case to case. Hypertonic diuretics and steroids are useful to treat increased intracranial pressure, but severe cases may require barbiturate therapy and hypothermia. Anticoagulant therapy with heparin or warfarin is frequently administered to limit extension of the thrombus. Secondary ex- tension of the thrombus to cortical and deep veins has been found in autopsy cases, stressing the need to prevent extension.) Anticoagulant therapy for sinus thrombosis improves outcome, even in patients with hemorrhagic infarct, and does not in- crease the risk of exacerbation hemorrhagic com- ponents of infarcts.” However, since traumatic si- nus thrombosis can be accompanied by direct hemorrhagic injury, anticoagulant therapy should proceed carefully with adequate monitoring for complications such as new bleeding. Local throm- bolytic injections of urokinase or tissue plasminogen activator to facilitate recanalization may be given directly into the occluded sinus by intravascular techniques,’"*”® but evaluation of the therapeutic effects and complications including pulmonary em- bolism is required. The present case of sigmoid sinus thrombosis fol- lowing mild closed head injury in an infant was treated successfully as MR imaging allowed early diagnosis and observation of sequential changes. Treatment must be both prompt and appropriate for the individual patient to achieve a good outcome. References 1) Ameri A, Bousser MG: Cerebral venous thrombosis. Neurol Clin 10: 87-111, 1992 2) Bjérnebrink J, Liliequist B: Traumatic lateral sinus thrombosis. Angiology 27: 688-697, 1976 3) Bousser MG, Chiras J, Bories J, Castaigne P: Cerebral venous thrombosis. A review of 38 cases. Stroke 16: 199-213, 1985 4) Buoanno F, Moody D, Ball M, Cowan R, Laster W, Ball J: Computed cranial tomographic findings in cerebral sinovenous occlusion. J Comput Assist Tomogr 2: 281-290, 1978 : 5) Carrie AW, Jaffe FA: Thrombosis of superior sagittal sinus caused by trauma without penetrating injury. J Neurosurg 11: 173-182, 1954 6) Crimmins TJ, Rockswold GL, Yock DH Jr: Progres- sive posttraumatic superior sagittal sinus thrombosis complicated by pulmonary embolism. Case report. J Neurosurg 60: 179-182, 1984 7) D’Alise MD, Fichtel F, Horowitz M: Sagittal sinus thrombosis following minor head injury treated with 8) 9) 10) 11) 12) 13) 14) 15) 16) 17) 18) 19) 20) 21) 22) 23) 24) H. Satoh et al. continuous urokinase infusion. Surg Neurol 49: 430- 435, 1998 Einhaupl KM, Villringer A, Meister W, Mehraein S, Garner C, Pellkofer M, Haberl RL, Pfister HW, Schmiedek P: Heparin treatment in sinus venous thrombosis. Lancet 338: 597-600, 1991 Ferrera PC, Pauze DR, Chan L: Sagittal sinus throm- bosis after closed head injury. Am J Emerg Med 16: 382-385, 1998 Goldberg A, Rosenbaum A, Wang H, Kim W, Lewis V, Hanley D: Computed tomography of dural sinus thrombosis. J Comput Assist Tomogr 10: 16-20, 1986 Goodnight SH, Kenoyer G, Rapaport SI, Patch MJ, Lee JA, Kurze T: Defibrination after brain-tissue destruction. N Engl J Med 290: 1043-1047, 1974 Hesselbrock R, Sawaya R, Tomsick T, Wadhwa S: Superior sagittal sinus thrombosis after closed head injury. Neurosurgery 16: 825-828, 1985 Isensee C, Reul J, Thron A: Magnetic resonance im- aging of thrombosed dural sinuses. Stroke 25: 29-34, 1994 Kannuki S, Cervés-Navarro J, Matsumoto K: [Thrombus propagation and venous drainage distur- bance in cerebral sinus-vein thrombosis — 38 autop- sied cerebral sinus-vein thrombosis]. No To Shinkei 42: 781-787, 1990 (Jpn, with Eng abstract) Kinal ME: Traumatic thrombosis of dural venous sinuses in closed head injuries. J Neurosurg 27: 142- 145, 1967 Kuether TA, O’Neill O, Nesbit GM, Barnwell SL: Endovascular treatment of traumatic dural sinus thrombosis: case report. Neurosurgery 42: 1163- 1167, 1998 Macchi P, Grossman R, Gomori J, Goldberg H, Zimmerman R, Bilaniuk L: High field MR imaging of cerebral venous thrombosis. J Comput Assist Tomogr 10: 10-15, 1986 McLean BN: Dural sinus thrombosis. Br J Hosp Med 45: 226-231, 1991 McMurdo §, Brant-Zawadzki M, Bradley W, Chang G, Berrg B: Dural sinus thrombosis: study using in- termediate field strength MR imaging. Radiology 161: 83-86, 1986 Provenzale JM, Loganbill HA: Dural sinus throm- bosis and venous infarction associated with an- tiphospholipid antibodies: MR findings. J Comput Assist Tomogr 18: 719-723, 1994 Rippe D, Boyko O, Spritzer C, Meisler W, Dumoulin C, Souza S: Demonstration of dural sinus occlusion by the use of MR angiography. AJNR Am J Neu- roradiol 11: 199-201, 1990 Satoh H, Uozumi T, Kiya K, Arita K, Kurisu K, Sumida M, Ikawa F: [Venous thrombosis after closed head injury: A report of two cases presenting as in- tracranial hypertension]. No Shinkei Geka 21: 953- 957, 1993 (Jpn, with Eng abstract) Stringer WL, Peerless SJ: Superior sagittal sinus thrombosis after closed head injury. Neurosurgery 12: 95-97, 1983 Sueishi K: [Plasminogen activator], in Tanaka K (ed): Neurol Med Chir (Tokyo) 40, July, 2000 25) 26) Sigmoid Sinus Thrombosis After Mild Closed Head Injury 365 Thrombosis. Tokyo, Medicalview, 1989, pp 85-90 (pn, with Eng abstract) Suzuki M, Motohashi O, Nishio A, Shiina V, Mizoi K, Yoshimoto T, Kameyama M, Onuma T: Diphasic in- crease in thrombin-antithrombin III complex in blood from the internal jugular vein following severe head injury. Thromb Haemost 71: 155-157, 1994 (letter) Taha JM, Crone KR, Berger TS, Becket WW, Prenger EC: Sigmoid sinus thrombosis after closed head in- jury in children. Neurosurgery 32: 541-546, 1993 27) Thulborn KR, Waterton JC, Matthew PM, Radda GK: Oxygenation dependence of the transverse relaxa- tion time of water protons in whole blood at high field. Biochim Biophys Acta 714: 265-270, 1982 Neurol Med Chir (Tokyo) 40, July, 2000 28) Tsai FY, Higashida RT, Matovich V, Alfieri K: Acute thrombosis of the intracranial dural sinus: Direct thrombolytic treatment. AJNR Am J Neuroradiol 13: 1137-1141, 1992 29) Virapongse CV, Cazenave C, Quisling R, Sarwar M, Hunter S: The empty delta sign: Frequency and sig- nificance in 76 cases of dural sinus thrombosis. Radiology 162: 779-785, 1987 Address reprint requests to: H. Satoh, M.D., Department of Neurosurgery, Hiroshima Prefectural Hospital, 1-5- 54 Ujina-Kanda, Minami-ku, Hiroshima 734-8530, Japan.