The pathogenesis of cerebral venous thrombosis during this period is linked to a physiological hypercoagulable state characterized by elevated coagulation factors, notably procoagulants (factors I, II, VII, VIII, IX, and XII), alongside a reduction in the anticoagulant system (markedly diminished protein S activity and resistance to activated protein C), as well as decreased fibrinolytic activity attributed to heightened placental PAI-2 expression ( Table 2). Elevated estrogen levels during pregnancy stimulate venous dilation and congestion. Venous stasis resulting from coagulation abnormalities exacerbates the risk of venous thrombosis in pregnancy. These physiological changes, while protective against hemorrhage during delivery, simultaneously elevate the risk of thromboembolic complications. ^{9– 13}

Pregnancy induces significant hematologic and hemodynamic changes, including a 60% increase in blood volume, elevated nitric oxide levels, enhanced venous capacitance, and increased arterial compliance—all of which contribute to venous stasis. ⁴ Additional factors such as dehydration, hyperemesis gravidarum, prolonged bed rest, hypertensive disorders of pregnancy, delivery trauma, and postpartum hemorrhage further exacerbate hypercoagulability. Other risk factors include anemia (Hb <9.9 g/dL), young maternal age, infections, and cesarean delivery. ^{4, 6, 7} The highest risk period for thrombotic events spans from the third trimester to the sixth postpartum week. ^{3, 6– 8}

Youth, postpartum status, and spinal anesthesia post-cesarean birth increase CVT risk. Insufficient hydration and mobility after delivery increase the risk of cerebral venous thrombosis in postpartum women. Few pregnant women have had cerebral venous thrombosis after spinal anesthesia ^{3, 14} and one after epidural analgesia. ⁷

CVT is often challenging to diagnose due to its nonspecific and overlapping symptoms with other neurological disorders. ¹⁵ Different thrombus sites cause different symptoms. Intracranial hypertension causes clinical symptoms and mass effect causes localized appearance. Intracranial hypertension is caused by sinus or cortical vein thrombus development, which raises venous pressure and reduces CSF absorption. It causes headaches, nausea, vomiting, and sudden symptomatic seizures due to high intracranial pressure. Thrombus-induced sinus occlusion increases blood flow into the venous system (venules and capillaries), raising local venous pressure. Reduced cerebral perfusion pressure (CPP) causes ischemia, cytotoxic edema, and blood-brain barrier breakdown, which may cause vasogenic edema. The structural variations between veins and arteries can increase capacitance and venous pressure, triggering venous wall rupture and intraparenchymal brain hemorrhage. Venous-capillary hypertension, cerebral edema, and brain parenchymal bleeding increase intracranial pressure (ICP) due to cerebral sinus thrombosis, which reduces cerebrospinal fluid absorption. ⁴ Venous thrombosis is most prevalent in the superior sagittal sinus (SSS, 72%), followed by the lateral, deep, and cortical sinuses. ^{3, 16}

In this case, recurrent focal seizures, decreased consciousness, and hemiparesis appeared rapidly during the puerperium. These are typical CVT symptoms, especially when the SSS and dominant hemisphere are affected. Symptoms may resemble preeclampsia or post-dural puncture headache (PDPH), presenting with headache, altered mental status, motor deficits, seizures, or visual disturbances. ^{6, 17} “Isolated cortical venous thrombosis” is characterized by headaches, convulsions, and focal neurological deficits. ¹ CVT-associated headaches are typically progressive and exacerbated by Valsalva maneuvers or changes in posture. In rare cases, acute onset may mimic subarachnoid hemorrhage with “thunderclap” headache and nuchal rigidity. ^{2, 4, 18}

Seizures are the second most frequent presenting symptom in CVT and a common reason for hospitalization. They occur more frequently than in arterial strokes and may be classified as acute symptomatic seizures (ASS, within 14 days of diagnosis; ~76%) or late-onset post-CVT epilepsy (>14 days; ~16%). ^{4, 19} Inflammation of cortical-subcortical parenchymal lesions or elevated ICP might cause seizures. Seizures are linked to superficial vein thrombosis (SSS), subcortical veins, and cortical veins, while deep venous thrombosis causes basal ganglia and thalamus edema, encephalopathy, mental impairment, lateralization, and coma. ¹⁸ In isolated intracranial hypertension (IIH), headache, nausea, vomiting, papilledema, visual abnormalities, and tinnitus are common. ² Sudden symptomatic seizures and consciousness changes may result from supratentorial injuries like hemorrhages, motor or sensory impairments, and thrombosis in the central nervous system (SSS). Status epilepticus, which may be refractory, can result from several supratentorial lesions with or without hemorrhages. A clinical presentation with thrombosis in the superior sagittal sinus (SSS) and deep venous system (DVS), bilateral parenchymal lesions, significant cerebral edema, and/or herniation includes poor consciousness, encephalopathy, bilateral or multifocal symptoms, seizures, and status epilepticus. ^{1, 2, 19} Early-onset seizures are associated with infarct hemorrhage, focal motor or sensory deficits, changed mental status, cerebral vein thrombosis, supratentorial edema/infarction, notably in the frontal lobe and superior sagittal sinus, and elevated D-dimer levels. ²⁰

Our patient presented with diffuse acute headache, positional worsening, bilateral motor deficits, and thrombosis in the SSS with bifrontal hemorrhagic infarction, edema, and subcortical damage—confirmed via CT and MRI-MRV ( Figure 4). Her symptoms, lasting over one month, reflect rare prolonged ICP elevation and venous congestion.

Diagnosing CVT is difficult due to nonspecific clinical and laboratory findings. D-dimer may support the diagnosis, showing ~94% sensitivity and ~90% specificity. ^{6, 18} In patients with a familial genetic background to thrombophilia, especially young ones, regardless of precipitating factors, it is recommended to test for congenital thrombophilia (including APC resistance, factor V Leiden mutation, factor III deficiency, protein S and C deficiencies, and prothrombin gene mutation) and systemic inflammatory markers associated with hypercoagulability. ¹⁸ Head imaging is needed to rule out preeclampsia and eclampsia. For optimal outcomes during pregnancy and postpartum, diagnostic modalities must be used sequentially to avoid radiation and intravenous contrast. MRI and MRV are best for detecting venous and sinus thrombosis. MRI can detect intraluminal thrombi and intraparenchymal abnormalities, including infarction and hemorrhage, while MRV can pinpoint blocked veins or sinuses by measuring flow rate. When MRI/MRV is absent, CT venography (CTV) can detect intraparenchymal abnormalities and deep (cortical) venous thrombosis, but it is less sensitive. ^{2, 4, 6} Digital subtraction angiography (DSA) can diagnose and remove thrombus clots. ⁴

Supportive treatment, intracranial pressure reduction, seizure and infection control, and thrombosis prevention are the goals of interdisciplinary CVT management. Even with cerebral hemorrhage, anticoagulants are first-line treatment, unlike arterial stroke. ²¹ Heparinization is the standard treatment for hyperacute CVT, although pregnant and postpartum women must consider fetal and labor risks. Enoxaparin Low molecular weight heparin (LMWH) reduces recurrent preeclampsia and eclampsia, is safe, has high absorption, a long plasma half-life, does not cross the placenta, and is not secreted in breast milk. Stop subcutaneous (SC) injection 24 hours before labor induction or cesarean section and resume 4-6 hours after normal birth or 6-12 hours after C-section. The recommended dose is 1 mg/kgBW/12 hours. Pregnant women should continue LMWH CVT for several weeks after birth. Activated partial thromboplastin time (APTT) determines the half-life and dose of unfractioned heparin (UFH), which can be antagonized with protamine sulfate but produce teratogenic consequences and fetal bleeding. Post-hyperacute oral vitamin K antagonists (DOACs) cross the placenta and harm fetal neural development and bleeding, making them unsafe during pregnancy. The best anticoagulant for pregnant, postpartum, or high-risk women with positive antiphospholipid test results for lupus, anticardiolipid, and anti-β2 glycoprotein antibodies is LMWH. ^{4, 6} LMWH was terminated due to coagulation difficulties and high fever, early infection symptoms. Sepsis and prothrombin time changes prevent anticoagulant medication, according to an Asian study. ⁶

Treatment aim to reduces intracranial pressure. Intracranial hypertension causes fatal ischemia and herniation. The Brain Trauma Foundation (BTF) suggests triple therapy for Intracranial Hypertension (HI): hyperosmolar therapy (mannitol 0.25-1 g/kg iv), sedation, analgesia, and CSF draining. Second-tier therapy includes hyperventilation to achieve 30–35 mmHg PaCO2 and muscle relaxants, and third-tier therapy includes decompressive craniectomy, hypothermia, and high-dose barbiturates. Acetazolamide, diuretics, and CSF shunting are contraindicated in CVT.

In cases of CVT with intraparenchymal hemorrhage and herniation, DC significantly reduces mortality. ^{4, 21– 23} Neurosurgery delayed decompressive craniectomy because the patient’s consciousness (GCS E3V5M6) was borderline, despite clinically progressive ICP elevation with extremity hemiparesis to hemiplegia, repeated seizures, decreased consciousness, and head CT results showing herniation. Only two cases (Gioti and Neelam) have reported successful DC during pregnancy/postpartum. ^{24, 25} These differ markedly from our case, as DC was planned after anticoagulant stabilization. DC may reduce ICP and prevent herniation, potentially improving prognosis—though long-term post-surgical complications remain a concern. ²⁶

The management of cerebral venous thrombosis (CVT) in postpartum patients remains a significant clinical challenge, particularly when patients develop signs of increased intracranial pressure (ICP) or transtentorial herniation. While decompressive craniectomy (DC) has been shown to improve survival in patients with malignant CVT accompanied by hemorrhagic infarction and herniation, ^{27, 28} the timing and criteria for surgical intervention in the postpartum context remain poorly defined. This uncertainty is compounded by the frequent clinical–radiological mismatch, where patients may exhibit borderline consciousness yet show radiological signs of impending herniation. Current recommendations such as those proposed by the European Stroke Organization (ESO) suggest considering DC in deteriorating CVT cases, but provide limited granularity regarding timing in obstetric populations. ²¹ Moreover, neurosurgical hesitation to operate in borderline Glasgow Coma Scale (GCS) patients and and concerns about ongoing anticoagulation may delay timely intervention, leading to missed surgical windows. ^{23, 29}

In our case, DC was deferred despite progressive neurological deterioration and imaging-confirmed herniation, highlighting a broader gap in decision-making frameworks for postpartum CVT. This issue is particularly acute in resource-limited settings, where delayed access to neurosurgical expertise and lack of standardized protocols may exacerbate poor outcomes. Our findings emphasize the urgent need for refined clinical criteria and prospective studies to define evidence-based thresholds for DC in high-risk postpartum patients with CVT.

As a final measure, the BTF’s third-tier intervention—thiopental coma—was initiated ( Figure 7). However, our center lacked burst suppression monitoring and hypothermia facilities. Ultimately, ischemia, infarction, and brain herniation led to brainstem death, confirmed by loss of reflexes and central temperature regulation ( Figure 4).