- Email: [email protected]
Superior sagittal sinus thrombosis in a patient with postdural puncture headache
Case Reports
Superior Sagittal Sinus Thrombosis in a Patient With Postdural Puncture Headache Honorio T. Benzon, M.D., Muhammad Iqbal, M.D., Martin S. Tallman, M.D., Larry Boehlke, R.N., and Eric J. Russell, M.D. Background and Objective: The occurrence of concomitant intracranial pathology in a patient with postdural puncture headache (PDPH) is rare. We present a patient who had a superior sagittal sinus thrombosis in addition to his PDPH. The signs and symptoms of intracranial pathology in patients with dural puncture headache, in addition to their postural headache, are discussed. Case Report: A 32-year-old man with lymphoblastic lymphoma received treatment with daunorubicin, vincristine, and prednisone. He developed postural headache and severe nausea and vomiting after a diagnostic lumbar puncture. Magnetic resonance imaging (MRI) showed superior sagittal sinus (SSS) thrombosis and meningeal enhancement. An epidural blood patch was performed and enoxaparin was prescribed for 6 months. He has remained asymptomatic. Conclusions: Patients with PDPH have classic postural headache. The occurrence of additional signs and symptoms should alert the clinician to the presence of intracranial pathology. Patients with lymphoblastic lymphoma who had treatment with L-asparaginase and steroid are predisposed to the development of cortical venous thrombosis and may have this syndrome in addition to a dural puncture headache. Reg Anesth Pain Med 2003;28:64-67. Key Words:
Cephalalgia, Postural, Clot, Dural venous sinus.
H
eadache is a known sequela of dural puncture. The concomitant presence of intracranial pathology in patients with postdural puncture headache (PDPH) is rare. We describe a patient with lymphoma who had received chemotherapy, including prednisone. He developed postural headache and severe nausea and vomiting after a diagnostic dural puncture. Magnetic resonance imaging (MRI) showed superior sagittal sinus (SSS) thrombosis. His symptoms responded to an epidural blood patch.
Case Report A 32-year-old man who was diagnosed with Tcell lymphoblastic lymphoma received induction From the Departments of Anesthesiology (H.T.B., M.I.), Medicine (M.S.T., L.B.), and Radiology (E.J.R.), Feinberg School of Medicine, Northwestern University, Chicago, Illinois. Accepted for publication September 10, 2002. Reprint requests: Honorio T. Benzon, M.D., Department of Anesthesiology, Feinberg School of Medicine, Northwestern University, 251 E. Huron St, Feinberg Pavilion, Suite 5-704, Chicago, IL 60611. E-mail: [email protected] © 2003 by the American Society of Regional Anesthesia and Pain Medicine. 1098-7339/03/2801-0013$35.00/0 doi:10.1053/rapm.2003.50007
64
chemotherapy with daunorubicin, vincristine, and prednisone. Two weeks after chemotherapy, he underwent a diagnostic lumbar puncture for staging of his disease and for the administration of intrathecal methotrexate. The lumbar puncture was performed with a 20-gauge needle. Examination of the cerebrospinal fluid (CSF) showed a glucose level of 66 mg/dL (normal, 40 to 70 mg/dL), total protein concentration of 28 mg/dL (normal, 20 to 50 mg/dL), 1 leukocyte (normal, 0 to 5 cells), 12 red blood cells (RBC) (normal, 0 RBC), 80% lymphocytes (normal, 60% to 70%), and 20% monocytes (normal, 30% to 50%). One day after the lumbar puncture, he developed headache, severe nausea and vomiting, sweating, bilateral shoulder pain, and neck pressure when sitting up. His symptoms improved with the supine position. He had no fever, chills, neck stiffness, blurring of vision, and bowel or bladder disturbance. His symptoms did not respond to hydrocodone/acetaminophen and ondansetron. He was admitted to the hospital for further management. In the hospital, hydrocodone/acetaminophen, ondansetron, diflucan, bactrim, and allopurinol were prescribed. Despite these medications, the pa-
Regional Anesthesia and Pain Medicine, Vol 28, No 1 (January–February), 2003: pp 64 –67
Cortical Venous Thrombosis and Headache
•
Benzon et al.
65
hospital discharge, confirmed complete thrombosis of the superior sagittal sinus with extension of the thrombus into the proximal right transverse sinus and the straight sinus. Repeat MR venography 2 months after discharge showed complete resolution of the SSS thrombosis and patency of all the dural sinuses. The patient continued to be asymptomatic 6 months after the blood patch.
Discussion
Fig 1. Sagittal T1-weighted spin echo MR (TR 620, TE 14) showing SSS thrombosis. Note the lack of normal flow void; the hyperintense blood is outlined by arrows.
Headache after dural puncture has been attributed to leakage of CSF through a dural rent, resulting in low CSF pressure in the subarachnoid space.1 Decreased CSF pressure causes the brain to sag when the patient assumes the upright position resulting in traction on pain-sensitive vascular structures. There appears to be no direct relationship between the occurrence of headache and the volume of leaked CSF, or the cerebrospinal fluid pressure in the subarachnoid space.2,3 Marshall2 performed a second dural puncture in his patients and found no correlation between the opening subarachnoid pressure and the occurrence of head-
tient’s symptoms persisted, and he was not able to sit in the upright position for more than a minute. His MRI showed dural enhancement. PDPH was entertained, and the Pain Medicine Service was consulted for an epidural blood patch. Our neurologic examination, was essentially normal and consisted of evaluation of his mental status, sensory, motor, and reflex functions of his extremities. We performed an epidural blood patch on the fourth day after lumbar puncture with 20 mL of the patient’s blood. The patient was able to sit with very little headache 1 hour after the blood patch and was able to ambulate 3 hours later. His nausea and vomiting were completely resolved. The Radiology Department formally reviewed the MRI several hours after the blood patch, noting that the patient had SSS thrombosis in addition to the dural enhancement (Figs 1 and 2). Neurology and neurologic surgery services were consulted. Their neurologic examinations were normal, and no papilledema was noted. Coagulation profile studies showed prothrombin time of 15.4 seconds, international normalized ratio of 1.2, partial thromboplastin time (PTT) of 30.9 seconds, and normal concentrations of fibrinogen and D-Dimer. The patient was placed on enoxaparin, 80 mg twice daily 6 hours after the blood patch, to be continued for 6 months followed by an antiplatelet medication. The patient was discharged 2 days after the blood patch. MR venography of the head, performed a week after
Fig 2. Coronal T1-weighted postcontrast MR (TR 503, TE 14) showing SSS thrombosis. Note nonenhancing clot (arrowhead). Note also the meningeal enhancement (see arrows), presumably related to the intracranial hypotension.
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Regional Anesthesia and Pain Medicine Vol. 28 No. 1 January–February 2003
ache. The subarachnoid pressures of the 6 patients who developed headache ranged from 0 to 130 mm H2O, while the subarachnoid pressures of the 9 patients who did not have headache ranged from 0 to 50 mm H2O. In a more recent study, Iqbal et al.3 measured the amount of CSF leak after dural puncture. The volume of CSF leak was less than 10 mL in 2 patients, 10 to 110 mL in 1 patient, and ⬎ 110 mL in 1 patient. One patient in their study had continued CSF leak for 7 days, but never developed headache.3 The efficacy of the epidural blood patch has been attributed not only to the closure of the dural puncture by the injected blood, but also to the block of the adenosine receptors in the brain.4 The effect of caffeine on adenosine receptors, in addition to its cerebral vasoconstrictive effect, may explain its efficacy in relieving PDPH. The concomitant presence of intracranial pathology in a patient with PDPH is rare.5 The patients in these case reports had additional symptoms suggestive of an intracranial process. In one case report, the patient had significant nonpostural headache, in addition to her postural headache.6 In another case report, 2 patients reported a changing pattern of their headache.6 Their headache became constant, lost its postural component, and was associated with papilledema.6 Our patient’s headache was completely postural, and he had no abnormal neurologic findings. The only symptom that was unusual was the severity of his nausea and vomiting. In our experience, these symptoms are not prominent in patients with dural puncture headache. There have been several reports of postpartum cortical venous thrombosis.7-9 The thrombosis was thought to be secondary to damage of the venous sinuses from fluctuations in intracranial pressure during labor and delivery and to the hypercoagulable state during pregnancy.7,8 These patients had dural puncture, but their headache did not respond to epidural blood patch.7-9 In these reports, the headache, which was initially postural, became less postural7,9 or completely postural,8 throbbing in character,7 or accompanied by severe nausea or vomiting.7 Nausea and vomiting were ascribed to increased intracranial pressure from inadequate venous and CSF drainage. Some of the patients developed neurologic symptoms, including extremity weakness, sedation, and seizures.7-9 The cerebral veins empty into the dural venous sinuses, which are drained by the internal jugular veins. The superior sagittal sinus is commonly affected by thrombosis because of turbulent blood flow in this area.10 SSS thrombosis may be caused by infectious and noninfectious etiologies.10,11 Hereditary prothrombotic conditions, such as Factor V Leiden (causing increased resistance to activated
protein C) and deficiency of proteins C and S and antithrombin III account for 10% to 15% of cerebral venous sinus thrombosis.11 No underlying cause is found in 20% to 30% of these cases. SSS thrombosis has also been described in patients with acute lymphoblastic leukemia.10 The thrombosis has been ascribed to lymphoblastic infiltration of the superior sagittal sinus wall or to the chemotherapeutic agents used.10 L-asparaginase decreases plasma antithrombin, plasminogen, and fibrinogen concentrations,12 while prednisone may increase the levels of factor VIII.10 These hemostatic changes may predispose to thrombosis, especially in the setting of the turbulent flow in the superior sagittal sinus.10 The signs and symptoms of SSS thrombosis are variable. Headache is the presenting symptom in 80% of the cases.11 There may be an alteration of consciousness or cerebellar incoordination. Other neurologic signs include papilledema, focal deficits, or seizures. Papilledema may be associated with transient visual abnormalities, while seizures may be focal or generalized. Most deficits are motor and sensory, usually unilateral, and involve mostly the lower extremities.11 MRI is the imaging technique of choice in the immediate evaluation of cerebral venous thrombosis. Angiography, however, is the gold standard for the diagnosis of this syndrome. MR angiography has the advantage of being easily repeatable and noninvasive.11 The management of cerebral venous thrombosis is anticoagulant therapy, thrombolysis, and oral anticoagulants.13 The oral anticoagulant is continued for 3 to 6 months or longer when there is a known prothrombotic condition. Our patient had headache, nausea, and vomiting, but we attributed these symptoms to his previous dural puncture. His headache was postural in nature, characteristic of dural puncture headache, and all neurologic examinations were normal. While it is rare for a patient with cerebral venous thrombosis to be completely asymptomatic, this scenario has been described.14 We did not wait for the formal reading of the MRI because the initial reading showed dural enhancement, a classic MRI finding in low CSF pressure headache. Epidural blood patch would not have interfered with the treatment of his SSS thrombosis except for the timing of the enoxaparin administration. Our patient had enoxaparin 6 hours after the epidural, which is in accordance with the minimum 2-hour interval recommended by the American Society of Regional Anesthesia and Pain Medicine.15 We would have taken extra care in performing the epidural because a dural puncture and consequent CSF loss in patients with
Cortical Venous Thrombosis and Headache
elevated CSF pressures may lead to potentially fatal cerebellar or tentorial herniation.16 We routinely perform a neurologic examination in patients with PDPH before performing an epidural blood patch. While our neurologic examination does not include a fundoscopic examination, other investigators do.17 An abbreviated neurologic examination has been outlined by Martin and Hauser16 when there are no symptoms of “disturbed nervous system functioning.” This abbreviated examination includes evaluation of the pupils, ocular movements, optic fundi, facial movements, speech, strength of arm and leg muscles, tendon and patellar reflexes, pain and vibratory sensation in hands and feet, and gait.16 There have been several publications of intracranial pathology in patients with PDPH5-9 that an abbreviated neurologic examination should probably be performed. An MRI is not advisable in every patient who develops a headache after a dural puncture, but should be considered in patients in whom an intracranial pathology is suspected. This includes patients who exhibit additional neurologic signs and symptoms,5,6 patients who are predisposed to cortical venous thrombosis, including postpartum patients who do not respond to an epidural blood patch,7-9 and patients with leukemia who receive treatments with L-asparaginase and steroid. In summary, we describe a patient who had T-cell lymphoblastic lymphoma, SSS thrombosis, and PDPH. His headache was completely postural, he had no abnormal findings on neurologic examination, and he appropriately responded to an epidural blood patch. His only additional symptom was severe nausea and vomiting. The possibility of a dural venous thrombosis should be suspected in patients with lymphoblastic lymphoma who had treatment with L-asparaginase and prednisone. Patients with dural puncture headache and a concomitant intracranial pathology may not present with obvious neurologic signs and symptoms. Rather, they may exhibit the more subtle signs of intracranial pathology, such as significant nonpostural component of the headache, a changing pattern of their headache (postural headache becoming nonpostural in character), and severe nausea and vomiting.
References 1. Benzon HT, Wong C. Postdural puncture headache: Mechanisms, treatment, and prevention. Reg Anesth Pain Med 2001;26:293-295.
•
Benzon et al.
67
2. Marshall J. Lumbar puncture headache. Neurol Neursurg Psychiatr 1950;13:71-74. 3. Iqbal J, Davis LE, Orrison WW. An MRI study of lumbar puncture headaches. Headache 1995;35:420422. 4. Raskin NH: Lumbar puncture headache: A review. Headache 1990;30:197-200. 5. Benzon HT. Intracerebral hemorrhage after dural puncture and epidural blood patch: Non-postural and non-continuous headache (letter to the editor). Anesthesiology 1984;60:258-259. 6. Aidi S, Chaunu MP, Biousse V, Bousser MG. Changing pattern of headache pointing to cerebral venous thrombosis after lumbar puncture with intravenous high-dose corticoids. Headache 1999;39:559-564. 7. Gewirtz EC, Costin M, Marx GF. Cortical vein thrombosis may mimic dural postdural puncture headache. Reg Anesth Pain Med 1987;12:188-190. 8. Borun SE, Naul G, McLesky CH. Postpartum dural venous sinus thrombosis after postdural puncture headache and epidural blood patch. Anesthesiology 1997;86:487-490. 9. Stocks GM, Wooller DJA, Young JM, Fernando R. Postpartum headache after epidural blood patch: Investigation and diagnosis. Br J Anaesth 2000;84:407410. 10. Lockman LA, Mastri A, Priest JR, Nesbit M. Dural venous sinus thrombosis in acute lymphoblastic leukemia. Pediatrics 1980;66:943-947. 11. Allroggen H, Abbott RJ. Cerebral venous sinus thrombosis. Postgrad Med J 2000;76:12-15. 12. Priest JR, Ramsay NKC, Bennet AJ, Krivit W, Edson JR. The effect of L-asparaginase on antithrombin, plasminogen, and plasma coagulation during therapy for acute lymphoblastic leukemia. J Pediatr 1982;100: 990-995. 13. de Bruijn SF, Stam J. Randomized, placebo-controlled trial of anticoagulant treatment with low-molecular-weight heparin for cerebral sinus thrombosis. Stroke 1999;30:484-488. 14. Goldberg AL, Rosenbaum AE, Wang H, Kim WS, Lewis VL, Hanley DF. Computed tomography of dural sinus thrombosis. J Comput Assist Tomogr 1986;10: 16-20. 15. Horlocker TT, Wedel DJ. Neuraxial block and lowmolecular weight heparin: Balancing perioperative analgesia and thromboprophylaxis. Reg Anesth Pain Med 1998;23:167-177 (suppl 2). 16. Martin JB, Hauser SL. Approach to the patient with neurologic disease. In: Braunwald E, Fauci AS, Kasper DL, Hauser SL, Longo DL, Jameson JL, eds. Principles of Internal Medicine. 15th ed. New York, NY: McGraw-Hill; 2001:2328-2331. 17. Chisholm ME, Campbell DC. Postpartum postural headache due to superior sagittal sinus thrombosis mistaken for spontaneous intracranial hypotension. Can J Anaesth 2001;48:302-304.
Superior Sagittal Sinus Thrombosis in a Patient With Postdural Puncture Headache Honorio T. Benzon, M.D., Muhammad Iqbal, M.D., Martin S. Tallman, M.D., Larry Boehlke, R.N., and Eric J. Russell, M.D. Background and Objective: The occurrence of concomitant intracranial pathology in a patient with postdural puncture headache (PDPH) is rare. We present a patient who had a superior sagittal sinus thrombosis in addition to his PDPH. The signs and symptoms of intracranial pathology in patients with dural puncture headache, in addition to their postural headache, are discussed. Case Report: A 32-year-old man with lymphoblastic lymphoma received treatment with daunorubicin, vincristine, and prednisone. He developed postural headache and severe nausea and vomiting after a diagnostic lumbar puncture. Magnetic resonance imaging (MRI) showed superior sagittal sinus (SSS) thrombosis and meningeal enhancement. An epidural blood patch was performed and enoxaparin was prescribed for 6 months. He has remained asymptomatic. Conclusions: Patients with PDPH have classic postural headache. The occurrence of additional signs and symptoms should alert the clinician to the presence of intracranial pathology. Patients with lymphoblastic lymphoma who had treatment with L-asparaginase and steroid are predisposed to the development of cortical venous thrombosis and may have this syndrome in addition to a dural puncture headache. Reg Anesth Pain Med 2003;28:64-67. Key Words:
Cephalalgia, Postural, Clot, Dural venous sinus.
H
eadache is a known sequela of dural puncture. The concomitant presence of intracranial pathology in patients with postdural puncture headache (PDPH) is rare. We describe a patient with lymphoma who had received chemotherapy, including prednisone. He developed postural headache and severe nausea and vomiting after a diagnostic dural puncture. Magnetic resonance imaging (MRI) showed superior sagittal sinus (SSS) thrombosis. His symptoms responded to an epidural blood patch.
Case Report A 32-year-old man who was diagnosed with Tcell lymphoblastic lymphoma received induction From the Departments of Anesthesiology (H.T.B., M.I.), Medicine (M.S.T., L.B.), and Radiology (E.J.R.), Feinberg School of Medicine, Northwestern University, Chicago, Illinois. Accepted for publication September 10, 2002. Reprint requests: Honorio T. Benzon, M.D., Department of Anesthesiology, Feinberg School of Medicine, Northwestern University, 251 E. Huron St, Feinberg Pavilion, Suite 5-704, Chicago, IL 60611. E-mail: [email protected] © 2003 by the American Society of Regional Anesthesia and Pain Medicine. 1098-7339/03/2801-0013$35.00/0 doi:10.1053/rapm.2003.50007
64
chemotherapy with daunorubicin, vincristine, and prednisone. Two weeks after chemotherapy, he underwent a diagnostic lumbar puncture for staging of his disease and for the administration of intrathecal methotrexate. The lumbar puncture was performed with a 20-gauge needle. Examination of the cerebrospinal fluid (CSF) showed a glucose level of 66 mg/dL (normal, 40 to 70 mg/dL), total protein concentration of 28 mg/dL (normal, 20 to 50 mg/dL), 1 leukocyte (normal, 0 to 5 cells), 12 red blood cells (RBC) (normal, 0 RBC), 80% lymphocytes (normal, 60% to 70%), and 20% monocytes (normal, 30% to 50%). One day after the lumbar puncture, he developed headache, severe nausea and vomiting, sweating, bilateral shoulder pain, and neck pressure when sitting up. His symptoms improved with the supine position. He had no fever, chills, neck stiffness, blurring of vision, and bowel or bladder disturbance. His symptoms did not respond to hydrocodone/acetaminophen and ondansetron. He was admitted to the hospital for further management. In the hospital, hydrocodone/acetaminophen, ondansetron, diflucan, bactrim, and allopurinol were prescribed. Despite these medications, the pa-
Regional Anesthesia and Pain Medicine, Vol 28, No 1 (January–February), 2003: pp 64 –67
Cortical Venous Thrombosis and Headache
•
Benzon et al.
65
hospital discharge, confirmed complete thrombosis of the superior sagittal sinus with extension of the thrombus into the proximal right transverse sinus and the straight sinus. Repeat MR venography 2 months after discharge showed complete resolution of the SSS thrombosis and patency of all the dural sinuses. The patient continued to be asymptomatic 6 months after the blood patch.
Discussion
Fig 1. Sagittal T1-weighted spin echo MR (TR 620, TE 14) showing SSS thrombosis. Note the lack of normal flow void; the hyperintense blood is outlined by arrows.
Headache after dural puncture has been attributed to leakage of CSF through a dural rent, resulting in low CSF pressure in the subarachnoid space.1 Decreased CSF pressure causes the brain to sag when the patient assumes the upright position resulting in traction on pain-sensitive vascular structures. There appears to be no direct relationship between the occurrence of headache and the volume of leaked CSF, or the cerebrospinal fluid pressure in the subarachnoid space.2,3 Marshall2 performed a second dural puncture in his patients and found no correlation between the opening subarachnoid pressure and the occurrence of head-
tient’s symptoms persisted, and he was not able to sit in the upright position for more than a minute. His MRI showed dural enhancement. PDPH was entertained, and the Pain Medicine Service was consulted for an epidural blood patch. Our neurologic examination, was essentially normal and consisted of evaluation of his mental status, sensory, motor, and reflex functions of his extremities. We performed an epidural blood patch on the fourth day after lumbar puncture with 20 mL of the patient’s blood. The patient was able to sit with very little headache 1 hour after the blood patch and was able to ambulate 3 hours later. His nausea and vomiting were completely resolved. The Radiology Department formally reviewed the MRI several hours after the blood patch, noting that the patient had SSS thrombosis in addition to the dural enhancement (Figs 1 and 2). Neurology and neurologic surgery services were consulted. Their neurologic examinations were normal, and no papilledema was noted. Coagulation profile studies showed prothrombin time of 15.4 seconds, international normalized ratio of 1.2, partial thromboplastin time (PTT) of 30.9 seconds, and normal concentrations of fibrinogen and D-Dimer. The patient was placed on enoxaparin, 80 mg twice daily 6 hours after the blood patch, to be continued for 6 months followed by an antiplatelet medication. The patient was discharged 2 days after the blood patch. MR venography of the head, performed a week after
Fig 2. Coronal T1-weighted postcontrast MR (TR 503, TE 14) showing SSS thrombosis. Note nonenhancing clot (arrowhead). Note also the meningeal enhancement (see arrows), presumably related to the intracranial hypotension.
66
Regional Anesthesia and Pain Medicine Vol. 28 No. 1 January–February 2003
ache. The subarachnoid pressures of the 6 patients who developed headache ranged from 0 to 130 mm H2O, while the subarachnoid pressures of the 9 patients who did not have headache ranged from 0 to 50 mm H2O. In a more recent study, Iqbal et al.3 measured the amount of CSF leak after dural puncture. The volume of CSF leak was less than 10 mL in 2 patients, 10 to 110 mL in 1 patient, and ⬎ 110 mL in 1 patient. One patient in their study had continued CSF leak for 7 days, but never developed headache.3 The efficacy of the epidural blood patch has been attributed not only to the closure of the dural puncture by the injected blood, but also to the block of the adenosine receptors in the brain.4 The effect of caffeine on adenosine receptors, in addition to its cerebral vasoconstrictive effect, may explain its efficacy in relieving PDPH. The concomitant presence of intracranial pathology in a patient with PDPH is rare.5 The patients in these case reports had additional symptoms suggestive of an intracranial process. In one case report, the patient had significant nonpostural headache, in addition to her postural headache.6 In another case report, 2 patients reported a changing pattern of their headache.6 Their headache became constant, lost its postural component, and was associated with papilledema.6 Our patient’s headache was completely postural, and he had no abnormal neurologic findings. The only symptom that was unusual was the severity of his nausea and vomiting. In our experience, these symptoms are not prominent in patients with dural puncture headache. There have been several reports of postpartum cortical venous thrombosis.7-9 The thrombosis was thought to be secondary to damage of the venous sinuses from fluctuations in intracranial pressure during labor and delivery and to the hypercoagulable state during pregnancy.7,8 These patients had dural puncture, but their headache did not respond to epidural blood patch.7-9 In these reports, the headache, which was initially postural, became less postural7,9 or completely postural,8 throbbing in character,7 or accompanied by severe nausea or vomiting.7 Nausea and vomiting were ascribed to increased intracranial pressure from inadequate venous and CSF drainage. Some of the patients developed neurologic symptoms, including extremity weakness, sedation, and seizures.7-9 The cerebral veins empty into the dural venous sinuses, which are drained by the internal jugular veins. The superior sagittal sinus is commonly affected by thrombosis because of turbulent blood flow in this area.10 SSS thrombosis may be caused by infectious and noninfectious etiologies.10,11 Hereditary prothrombotic conditions, such as Factor V Leiden (causing increased resistance to activated
protein C) and deficiency of proteins C and S and antithrombin III account for 10% to 15% of cerebral venous sinus thrombosis.11 No underlying cause is found in 20% to 30% of these cases. SSS thrombosis has also been described in patients with acute lymphoblastic leukemia.10 The thrombosis has been ascribed to lymphoblastic infiltration of the superior sagittal sinus wall or to the chemotherapeutic agents used.10 L-asparaginase decreases plasma antithrombin, plasminogen, and fibrinogen concentrations,12 while prednisone may increase the levels of factor VIII.10 These hemostatic changes may predispose to thrombosis, especially in the setting of the turbulent flow in the superior sagittal sinus.10 The signs and symptoms of SSS thrombosis are variable. Headache is the presenting symptom in 80% of the cases.11 There may be an alteration of consciousness or cerebellar incoordination. Other neurologic signs include papilledema, focal deficits, or seizures. Papilledema may be associated with transient visual abnormalities, while seizures may be focal or generalized. Most deficits are motor and sensory, usually unilateral, and involve mostly the lower extremities.11 MRI is the imaging technique of choice in the immediate evaluation of cerebral venous thrombosis. Angiography, however, is the gold standard for the diagnosis of this syndrome. MR angiography has the advantage of being easily repeatable and noninvasive.11 The management of cerebral venous thrombosis is anticoagulant therapy, thrombolysis, and oral anticoagulants.13 The oral anticoagulant is continued for 3 to 6 months or longer when there is a known prothrombotic condition. Our patient had headache, nausea, and vomiting, but we attributed these symptoms to his previous dural puncture. His headache was postural in nature, characteristic of dural puncture headache, and all neurologic examinations were normal. While it is rare for a patient with cerebral venous thrombosis to be completely asymptomatic, this scenario has been described.14 We did not wait for the formal reading of the MRI because the initial reading showed dural enhancement, a classic MRI finding in low CSF pressure headache. Epidural blood patch would not have interfered with the treatment of his SSS thrombosis except for the timing of the enoxaparin administration. Our patient had enoxaparin 6 hours after the epidural, which is in accordance with the minimum 2-hour interval recommended by the American Society of Regional Anesthesia and Pain Medicine.15 We would have taken extra care in performing the epidural because a dural puncture and consequent CSF loss in patients with
Cortical Venous Thrombosis and Headache
elevated CSF pressures may lead to potentially fatal cerebellar or tentorial herniation.16 We routinely perform a neurologic examination in patients with PDPH before performing an epidural blood patch. While our neurologic examination does not include a fundoscopic examination, other investigators do.17 An abbreviated neurologic examination has been outlined by Martin and Hauser16 when there are no symptoms of “disturbed nervous system functioning.” This abbreviated examination includes evaluation of the pupils, ocular movements, optic fundi, facial movements, speech, strength of arm and leg muscles, tendon and patellar reflexes, pain and vibratory sensation in hands and feet, and gait.16 There have been several publications of intracranial pathology in patients with PDPH5-9 that an abbreviated neurologic examination should probably be performed. An MRI is not advisable in every patient who develops a headache after a dural puncture, but should be considered in patients in whom an intracranial pathology is suspected. This includes patients who exhibit additional neurologic signs and symptoms,5,6 patients who are predisposed to cortical venous thrombosis, including postpartum patients who do not respond to an epidural blood patch,7-9 and patients with leukemia who receive treatments with L-asparaginase and steroid. In summary, we describe a patient who had T-cell lymphoblastic lymphoma, SSS thrombosis, and PDPH. His headache was completely postural, he had no abnormal findings on neurologic examination, and he appropriately responded to an epidural blood patch. His only additional symptom was severe nausea and vomiting. The possibility of a dural venous thrombosis should be suspected in patients with lymphoblastic lymphoma who had treatment with L-asparaginase and prednisone. Patients with dural puncture headache and a concomitant intracranial pathology may not present with obvious neurologic signs and symptoms. Rather, they may exhibit the more subtle signs of intracranial pathology, such as significant nonpostural component of the headache, a changing pattern of their headache (postural headache becoming nonpostural in character), and severe nausea and vomiting.
References 1. Benzon HT, Wong C. Postdural puncture headache: Mechanisms, treatment, and prevention. Reg Anesth Pain Med 2001;26:293-295.
•
Benzon et al.
67
2. Marshall J. Lumbar puncture headache. Neurol Neursurg Psychiatr 1950;13:71-74. 3. Iqbal J, Davis LE, Orrison WW. An MRI study of lumbar puncture headaches. Headache 1995;35:420422. 4. Raskin NH: Lumbar puncture headache: A review. Headache 1990;30:197-200. 5. Benzon HT. Intracerebral hemorrhage after dural puncture and epidural blood patch: Non-postural and non-continuous headache (letter to the editor). Anesthesiology 1984;60:258-259. 6. Aidi S, Chaunu MP, Biousse V, Bousser MG. Changing pattern of headache pointing to cerebral venous thrombosis after lumbar puncture with intravenous high-dose corticoids. Headache 1999;39:559-564. 7. Gewirtz EC, Costin M, Marx GF. Cortical vein thrombosis may mimic dural postdural puncture headache. Reg Anesth Pain Med 1987;12:188-190. 8. Borun SE, Naul G, McLesky CH. Postpartum dural venous sinus thrombosis after postdural puncture headache and epidural blood patch. Anesthesiology 1997;86:487-490. 9. Stocks GM, Wooller DJA, Young JM, Fernando R. Postpartum headache after epidural blood patch: Investigation and diagnosis. Br J Anaesth 2000;84:407410. 10. Lockman LA, Mastri A, Priest JR, Nesbit M. Dural venous sinus thrombosis in acute lymphoblastic leukemia. Pediatrics 1980;66:943-947. 11. Allroggen H, Abbott RJ. Cerebral venous sinus thrombosis. Postgrad Med J 2000;76:12-15. 12. Priest JR, Ramsay NKC, Bennet AJ, Krivit W, Edson JR. The effect of L-asparaginase on antithrombin, plasminogen, and plasma coagulation during therapy for acute lymphoblastic leukemia. J Pediatr 1982;100: 990-995. 13. de Bruijn SF, Stam J. Randomized, placebo-controlled trial of anticoagulant treatment with low-molecular-weight heparin for cerebral sinus thrombosis. Stroke 1999;30:484-488. 14. Goldberg AL, Rosenbaum AE, Wang H, Kim WS, Lewis VL, Hanley DF. Computed tomography of dural sinus thrombosis. J Comput Assist Tomogr 1986;10: 16-20. 15. Horlocker TT, Wedel DJ. Neuraxial block and lowmolecular weight heparin: Balancing perioperative analgesia and thromboprophylaxis. Reg Anesth Pain Med 1998;23:167-177 (suppl 2). 16. Martin JB, Hauser SL. Approach to the patient with neurologic disease. In: Braunwald E, Fauci AS, Kasper DL, Hauser SL, Longo DL, Jameson JL, eds. Principles of Internal Medicine. 15th ed. New York, NY: McGraw-Hill; 2001:2328-2331. 17. Chisholm ME, Campbell DC. Postpartum postural headache due to superior sagittal sinus thrombosis mistaken for spontaneous intracranial hypotension. Can J Anaesth 2001;48:302-304.