Fall 2009
December 1, 2009 CONTACT AUTHOR

Contact Author

Please address all correspondence to:

Vikas Pathak
St. Barnabas Hospital
4422 (Mills building, 3rd floor)
183rd Street and 3rd Avenue
Bronx, NY 10457



Sagittal Sinus Thrombosis in a Young Migraineur

Vikas Pathak, MD1; Iliana Samara Hurtado Rendon, MD1; Lorenza Freddo, MD2; Mahesh Mani Dangal, MD1

  1. Resident, Department of Internal Medicine, St. Barnabas Hospital
  2. Neurologist and Head of the Department of Neurology, St. Barnabas Hospital

Keywords: cerebral venous thrombosis, sagittal sinus thrombosis


Cerebral venous thrombosis (venous sinus thrombosis) is an elusive diagnosis because of its nonspecific presentation and its numerous predisposing causes. The incidence of cerebral venous thrombosis (CVT) is difficult to determine. Generally, it is believed to be an uncommon cause of stroke. However, with the advent of newer imaging techniques, the reported incidence is likely to increase as less severe cases are found. In 1973, Towbin reported CVT in 9% of 182 autopsies.1 The ratio of venous to arterial strokes has been found to be 1:62.5. We present a case of a young female who presented with headache and was subsequently diagnosed with sagittal sinus thrombosis.


A 41 year old Hispanic female with a medical history of migraine and a history of using estrogen patch for the last five years presented to the emergency department with complaints of severe headache for one week. The headache, located on right fronto-temporal area, was throbbing in nature, with a 10/10 intensity. She also reported nausea and vertigo. The patient denied fever, neck pain or visual disturbances. She also denied any weakness or any numbness.

The patient’s migraine headaches had been well controlled medically in the past. She had no history of tobacco, alcohol, or drug use, and had no significant family history. Physical examination revealed normal vital signs. She was afebrile, alert, and oriented. Head, eyes, ears, nose, and throat examinations were unremarkable, with fundi having no papilledema. Cranial nerves were intact, and strength, sensation, reflexes, and results of gait testing were normal. There was no Babinski sign and no focal deficits were noted. Abstract thinking was intact and spontaneous language use while providing the history was fluent.

Laboratory testing showed blood chemistries and complete blood count to be normal. Prothrombin time and partial thromboplastin time were not increased. Computed tomography (CT) of the head was done. No subdural hematoma, acute hemorrhage, ischemia or midline shift were appreciated.

Image 1: CT of the head done in ER

After CT scan, lumbar puncture was performed, which showed completely normal CSF. Considering this as a migraine attack based on history, physical examination and investigation, the patient was discharged on analgesics and antiemetic. A week later, the patient went to her primary medical doctor complaining of persistent headache, and she was again sent to the ED for evaluation, at which time she was admitted with an impression of post- lumbar puncture headache: rule out intracranial mass. The patient was adequately hydrated, analgesics were given, and MRI of the brain was performed. The MRI showed superior sagittal sinus thrombosis. The patient was transferred to ICU for IV heparin drip and neurological monitoring.

Image 2: MRI of the brain: showing sagittal sinus and right lateral sinus thrombosis.

In the ICU, the patient was started on intravenous heparin drip. Coagulation profile was obtained every six hours, neurochecks were done hourly, morphine was given for pain management, and the contraceptive patch was stopped. During the ICU stay, the patient’s headache got better and was comfortable until fifth day of admission, when she complained of a tingling sensation in her left arm, left face, and left side of tongue, followed by throbbing pain in the right eye. MRI of the head was repeated, which showed substantial resolution of thrombus in sagittal sinus, but a new focus of subarachnoid blood was seen within one sulcus of the right parietal hemisphere. Heparin drip was immediately discontinued.

Image 3: MRI of the brain 5 days after anticoagulation: showing relative resolution of the thrombosis.

The patient had no neurological deficit at this time. In view of a new subarachnoid bleed in the face of anticoagulation, hematology recommended reversal of anticoagulation (patient’s INR was 1.9 at that time, PTT was 27.3) with four units of fresh frozen plasma and vitamin K. Hematologist also recommended hypercoagulable workup, which proved to be negative.

The remainder of the patient’s hospital stay was uneventful. A repeat MRI showed no interval change, and the patient was discharged home on long acting morphine.


Dural venous thrombosis is a rare phenomenon, most often seen secondary to either infection of adjoining structures or to a hypercoagulable state. Our patient had neither. Moreover, the diagnosis was made somewhat elusive given her history of migraine headaches, It does seem likely that the patient’s estrogen patch played a roll in her developing thromboembolic disease.

In conclusion, this patient’s case of CVT demonstrates physicians’ need to develop a broad differential diagnosis when evaluating patients with acute headache symptoms.


The International Study on Cerebral Vein Thrombosis (ISCVT) group identified most frequent predisposing conditions as follows: oral contraceptives (46%), prothrombotic conditions (27%), pregnancy/puerperium (17%), ear-nose-throat infections (8%), central nervous system (CNS) infections (5%), other infections (4%), CNS disorders (5%), cancer (8%), vasculitis/antiphospholipid antibodies (8%), and other systemic diseases (14%).

Thrombosis of the cerebral venous sinuses, particularly of the superior saggital or lateral sinus and the tributary cortical and deep veins, gives rise to a number of important neurologic syndromes. Clinical presentations of patients with CVT are different and variable from those with arterial stroke and other neurological conditions, making it a diagnostic challenge.2 Symptoms are sub acute and develop over several weeks.3 The associated neurologic dysfunction that is evident can be highly variable.4

A teenager who has had recent headaches after starting oral contraception, a woman who has had seizures after delivery in the obstetrical ward, and a comatose man with a dilated pupil in the emergency room all may have sinus thrombosis.5 The International Study on Cerebral Vein Thrombosis (ISCVT) reported that headache (89%), paresis (37%), generalized (30%) or focal (20%) seizures, papilledema (28%), and mental status disorders (22%) were the most frequent presenting symptoms and signs associated with the diagnosis of CVT.6

The suspected diagnosis of CVT necessitates demonstration of the thrombus by neuroimaging.

Intravenous heparin therapy in the acute phase is used for treatment, even in patients with intracerebral hemorrhage in the area of a venous infarction.3,4

Anticoagulation is continued for 6 months with Coumadin.


  1. Towbin A. The syndrome of latent cerebral venous thrombosis: its frequency and relation to age and congestive heart failure. Stroke 1973; 4:419-30.
  2. Fink JN, McAuley DL. Cerebral venous sinus thrombosis: a diagnostic challenge. Int Med J 2001; 31:384-90.
  3. Kimber J. Cerebral venous sinus thrombosis. Q J Med 2002; 95:137-42.
  4. Murry BJ, Llinas R, Caplan LR, Scammell T, Pascual-Leone A. Cerebral deep venous thrombosis presenting as acute micrographia and hypophonia. Neurology 2000; 54:751-3.
  5. Stam J. Thrombosis of the cerebral veins and sinuses: New Engl J Med 2005; 352:1791-1798.
  6. Ferro JM, Canhao P, Stam J, Bousser MG, Barinagarrementeria F. ISCVT Investigators; Prognosis of cerebral vein and dural sinus thrombosis: results of the International Study on Cerebral Vein and Dural Sinus Thrombosis (ISCVT): Stroke 2004; 35:664-70.