Cerebral Venous Sinus Thrombosis (CVST) is a subtype of venous thromboembolism, which occurs in the dural venous sinuses. The diagnosis of CVST is not easy because of variability of clinical symptoms and signs. Frequently superior sagittal sinus, transverse sinuses, sigmoid sinuses, cavernous sinus & sinus rectus are affected.1 CVST can be seen at any age but mostly young adults are affected. Prevalence is three times higher in women comparing to men.2     

Various risk factors for cerebral venous thrombosis include pregnancy, oral contraceptive pills, hyper-homocystenemia, cerebral nervous system

infections, autoimmune diseases, trauma, malignancy, infections, thrombophilia, dehydration and congenital or acquired abnormalities of the hemostatic system.3 A recent meta-analysis found a 7.59 times increase in incidence among women on Oral Contraceptive Pills.4 Present case is a case of a young woman who developed CVST with no apparent risk factors for the same; and was found to have been taking oral contraceptive pills since 2 months for abnormal uterine bleeding (AUB).

A 17 years 4 months, female was brought to ER with complaints of 3-4 episodes of GTCS, each episode lasting for 1-2 min and last episode lasting for 10 min since morning. Patient had post ictal drowsiness; headache associated with 3-4 episodes of vomiting’s/day since 4 days. History of usage of OCPs since 2-3 months for irregular menses. 

At admission, on general Examination, patient was drowsy, but arousable with deep stimulus, GCS (Glasgow Coma Scale) was E2 V1 M4. Bilateral Pupils were 3 mm reacting to light. Power could not be elicited Tone decreased in all 4 limbs. Plantars: B/L withdrawal. No meningeal signs. BP: 120/80mmHg, PR: 91/min, SPO2: 96% at room air.

Patient was evaluated with MRI brain and venogram showing left fronto parietal hemorrhagic infarct due to extensive cortical and deep venous thrombosis, diagnosed as a case of provoked CSVT secondary to OC pills with patient in status epilepticus and treated with antiepileptics as per protocol, anticoagulation along with neuro-protectives, fluid management and supportive intensive care. Gynecology opinion was taken in view of menstrual irregularities and was advised to avoid OC pills in future with further Gynaecology follow up. Patient gradually improved with conservative management and was discharged. At discharge

Patient was conscious, oriented, obeying commands. GCS (Glasgow Coma Scale): E4 VS M6, HMF: (N), CN (N). Motor system: Power was Right upper limb 4+/5, Left upper limb 5/5, Right Lower limb 5/5 & Left Lower limb 5/5. Tone: Normal; Plantars: B/L flexors. No meningeal signs. Sensory & cerebellum – Normal.

Cerebral venous sinus thrombosis is an uncommon but potentially fatal condition, especially in young women. CVST presents as severe headache (the most common symptom). Other features include nausea and vomiting, seizures, decreased level of consciousness to coma, and focal neurological deficits. Diagnosis is by neuroimaging the thrombosed vessel - the gold standard is the combination of MRI brain with venogram. The mainstay of therapy is anticoagulation and other procedures of recanalization.5,6 Common presenting features of CVST are symptoms of raised intracranial pressure, seizures, focal neurological deficits, and altered sensorium.5 Coutinho et al. documented complete recovery in 81% of women, dependency or death in 12%, and mortality in 6% of women with CVST. 6

Neuroimaging remains the cornerstone of CVT diagnosis. Non-contrast CT of the brain, although often the first imaging modality performed in suspected stroke cases, has low sensitivity for CVT, detecting direct signs (hyperdense cortical veins or sinus thrombosis) in only a subset of patients.7,8

The pathology for this increased incidence is multifactorial. The changes of the hemostatic system include stimulated procoagulation, inhibited anticoagulation and elevated fibrinolytic activity. The latter is caused by elevated plasminogen level and a higher tissue plasminogen activator (tPA) activity. The plasminogen activator inhibitor I (PAI – I) antigen and activity also decrease.9 The WHO recommends avoiding using OCPs in women who have thrombogenic mutations, smokers, those aged 35 years or more and 21 days post-partum to prevent thromboembolic complications.9 Progestin-only Preparations had no effect when used as contraceptives, but in the setting of primary menstrual disorders, they increased the risk for VTE.10 There are evidence that suggest that the probability of VTE is increased in the first months after the start of a new OCP, as seen in a study by Martinelli et al.,11 where it was found that the odds for developing VTE was 9.0 in short (<=1 year), 6.5 in long (>1 and < =5 years) and 5.9 in very long (>5 years) users.

The American College of Obstetrics and Gynecology's Committee on Gynecologic Practice acknowledges the increased risk associated with third-generation progestins but leaves the decision to use a desogestrel-containing formulation to the discretion of individual clinicians and patients, recognizing potential benefits for some individuals.12 Rajput R et al.,13 had documented a case of CVST in a young woman taking norethindrone acetate for menorrhagia who also had acquired hyperhomocysteinemia. Hitendra Singh et al.,14 had reported a case of norethisterone induced CVST presenting as subarachnoid haemorrhage in a patient of menorrhagia.

Uemura et al. described the clinical, postmortem 3T-MRI and autopsy features in a 20-year-old Japanese woman patient with CVST who died shortly after starting to use low-dose estrogen CHCs. An autopsy and histological examination revealed an organizing white thrombus occupying the lumen of the left sigmoid sinus while an acute, red thrombus was found in the left transverse, straight and tentorial sinuses, and the vein of Galen.

The prognosis of CVST varies and depends largely on a timely diagnosis along with the patients’ response to the anticoagulant heparin therapy and endovascular-based approach or neurosurgical decompression, whenever performed. The phenomenon is rare and easily escapes clinical diagnosis, particularly in the acute phase. However, with prompt recognition and treatment, the chances of survival, even without residual disability, are very high.

Present case illustrates vital lessons in the management of cerebral venous thrombosis (CVT) that should not be overlooked. Firstly, maintaining a high index of suspicion is crucial for early diagnosis—especially in young female patients exhibiting progressive headaches and neurological deficits. Secondly, rapid neuroimaging through magnetic resonance venography (MRV) or computed tomography venography (CTV) is indispensable for accurate and timely identification of this condition. Thirdly, initiating immediate anticoagulation is paramount to halt disease progression, even in cases where infarction is already present. Lastly, consistent long-term monitoring—including follow-up imaging and proactive risk factor management—is essential for achieving the best possible outcomes and preventing recurrence.

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