Cavernous sinus thrombosis (CST) is a rare but serious condition that can lead to significant morbidity and mortality if not diagnosed and treated early. The overlapping features with benign headache conditions, such as migraine headaches and the necessity of specialized imaging techniques often make this potentially fatal condition difficult to diagnose. CST most commonly arises from infections, particularly those involving the paranasal sinuses, or from hypercoagulable states, though it can also be seen in patients with a history of trauma, surgery, or malignancy [2] [3] . CST is characterized by the formation of thrombi within the cavernous sinus, which can lead to increased intracranial pressure, cranial nerve dysfunction, and even ischemic stroke if left untreated [2] [4] .

In patients with CST, the early symptoms often are nonspecific, however, the presence of atypical signs such as hearing loss, dizziness, or visual disturbances should raise suspicion for a more serious etiology [5] . In this case, a 31-year-old woman with a known history of migraines and iron deficiency anemia presented with headache, dizziness, and weakness. A comprehensive evaluation, including neuroimaging, revealed the presence of CST, which was later confirmed through MRI and MRV. This case highlights the importance of maintaining a high index of suspicion for CST in patients with persistent or atypical neurological symptoms, especially when they present with signs not traditionally associated with migraine or other benign causes [1] .

A 31-year-old female with a history of iron deficiency anemia and migraines presented to urgent care with a week-long left-sided headache, rated 8/10, and intermittent dizziness. Of note, the patient mentioned her legs became weak and gave out the day prior while walking a short distance, and reported having a similar occurrence the week before. The patient stated she was given a prescription for Naproxen 500 mg two days prior which did not resolve her symptoms. She denied symptoms of vision changes, chest pain, shortness of breath, mental status change, seizures, and change in bowel or bladder habits. The patient denied any past surgical history, tobacco, ethanol, recreational drug use, and home medication use. On exam, the vital signs were all within normal limits and the patient was able to walk, but only with the aid of her husband. The urgent care labs revealed a hemoglobin of 7.9 and blood glucose of 150, and the patient was sent to the nearby emergency department.

Upon obtaining history at the emergency department, the patient additionally admitted to symptoms of nausea and bilateral ear pain with decreased hearing. The patient described that the headache began on the left side of her head and radiated throughout the rest of her head. She denied known sick contacts, recent travel, cough, congestion, fever, sore throat, chills, dizziness, lightheadedness, numbness or tingling, focal weakness, chest pain, shortness of breath, dyspnea, abdominal pain, vomiting, diarrhea, neck pain, back pain, and rash. The patient’s vitals again were all within normal limits and on exam her external auricles were normal appearing bilaterally without postauricular erythema or edema, mastoid tenderness was not present, however tympanic membranes were bilaterally erythematous and slightly bulging. The patient was neurologically intact and her gait was normal. The differential diagnoses for the patient included subarachnoid hemorrhage, intracranial hemorrhage, ischemic stroke, temporal arteritis, venous sinus thrombosis, meningitis, encephalitis, intracranial mass and migraine headache. Labs were ordered and resulted. Complete blood count revealed microcytic anemia (hemoglobin of 7.6, hematocrit of 27.4, MCV of 60.1), increased red cell distribution width of 21.7, increased immature granulocyte count of 0.04, 1+ anisocytosis, 1+ ovalocytes, 1+ hypochromia, occasional macrocytosis, 1+ microcytosis, 1+ poikilocytosis, 1+ polychromasia, 1+ target cells, occasional teardrop cells, and occasional schistocytes. Complete metabolic panel revealed potassium of 3.4, chloride of 111, increased BUN/creatinine ratio of 25.9, increased total protein of 8.3, and increased globulin of 4.8. During the patient’s stay in the emergency department, she was given IV Toradol, Reglan, Benadryl, Decadron, and a fluid bolus. On re-evaluation, the patient was not in acute distress and stated that her headache had resolved. The patient was discharged with a diagnosis of headache and was told to return to the emergency department if her symptoms worsened.

Although the patient initially presented with a severe unilateral headache, intermittent dizziness, and reported leg weakness, her neurologic examination in the emergency department was unremarkable. Her symptoms improved significantly following administration of IV fluids, anti-inflammatory and anti-emetic medications, which are characteristic of a benign headache syndrome such as a migraine or tension headache. Additionally, her vital signs remained stable throughout the visit, and no acute abnormalities were identified in the lab work other than anemia. Given the absence of concerning features such as altered mental status, persistent focal deficits, fever, signs of increased intracranial pressure, or infectious source requiring urgent intervention, the clinical picture was most consistent with a primary headache disorder. Therefore, after symptom resolution and risk stratification, the diagnosis of headache was made, and the patient was deemed safe for discharge with close return precautions.

Three days later the patient returned to the emergency department with similar complaints of headache, dizziness, vomiting, and weakness. The patient stated that she was well until the night prior where she began vomiting, felt dizzy and weak, and fell to the ground. She denied loss of consciousness, head strike, fever, chills, vision changes, numbness, tingling, chest pain, shortness of breath, dyspnea, abdominal pain, and diarrhea. Vitals were taken and all were within normal limits. On physical examination, horizontal nystagmus was observed with 5/5 strength in upper and lower extremities, intact sensation, and finger-nose-finger without dysmetria. Laboratory workup was notable for a microcytic anemia with increased red cell distribution width, mild leukocytosis (WBC 11.18), and elevated absolute neutrophil count (7.45). Hemoglobin, hematocrit, and platelet levels were otherwise unremarkable. The remainder of the differential was non-contributory. Coagulation studies showed a mildly elevated prothrombin time (13.7), decreased partial thromboplastin time (21.3), and a normal international normalized ratio. A repeat complete metabolic panel did not reveal any significant differences from previous values.

Given the repeat occurrence of the patient’s symptoms, CT imaging was ordered with low suspicion for TIA, assuming migraine versus vertigo. The radiologist consulted the provider stating that the CT showed suspicion for a subfalcine subdural hematoma, seen in Figure 1 , and to consult neurosurgery for further plans. The neurosurgery team was consulted and after reviewing the head CT stated that there was concern for a sagittal sinus thrombosis, as seen in Figure 2 , and recommended an emergent MRI and MRV to be ordered. The MRV head without contrast showed extensive sagittal, straight, and transverse sinus thrombosis as seen in Figure 3 . The MRI brain without contrast showed restricted diffusion in the left frontal lobe, bilateral mastoid air cell effusions, and venous sinus thrombosis seen in Figure 4 . The neurosurgeon and radiologist recommended emergent transfer to a level I trauma center and STAT flight was activated. While preparing the patient for transfer, she received an IV heparin bolus and drip for anticoagulation as recommended by neurosurgery. The patient remained neurologically intact when the flight arrived.

Post transfer it was reported that an additional MRI brain with and without contrast and MRV showed extensive dural venous sinus thrombosis with extension into bilateral frontal cortical veins and into the proximal right parietal cortical vein with several foci of venous infarction in the left frontal lobe. The patient was noted to have no neurologic deficits and was converted from heparin to lovenox during admission. ENT, ophthalmology and hematology were consulted and the patient had a negative thrombotic workup. She was discharged home on therapeutic eliquis and was advised to follow up with her primary care physician and a hematologist.

Cavernous sinus thrombosis (CST) remains a challenging clinical entity, with its complex etiology, diverse presentation, and potential for rapid progression leading to significant morbidity and mortality. As outlined in the literature, the diagnosis and management of CST require a multi-faceted approach that incorporates an understanding of underlying risk factors, timely diagnostic imaging, and appropriate therapeutic interventions.

Cavernous sinus thrombosis is a rare but serious condition that demands a high level of clinical suspicion. The complexity of its etiology—ranging from infectious causes like sinusitis to thrombophilic disorders—requires a comprehensive diagnostic approach, including a detailed clinical history, imaging, and laboratory tests. The role of imaging is critical in confirming the diagnosis, with CT and MRI playing complementary roles in detecting the presence of thrombus and associated complications. Moreover, understanding the red flags associated with secondary headaches, such as fever and neurologic deficits, can help identify patients at risk for CST. Early diagnosis and intervention are essential to improve outcomes, highlighting the importance of a multidisciplinary approach to patient care.