A patient with traumatic head injury: Cause or consequence?

Diana Aguiar de Sousa and Lia Lucas Neto, from the Department of Neurosciences (Neurology) and the Department of Neuroradiology, Hospital de Santa Maria, University of Lisbon, Portugal

Case Report

A 39-year-old woman was admitted to our institution for evaluation after falling from the standing position. On admission, the patient was vomiting, had signs of minor head injury and could not explain why she fell. Her parents reported she was slightly confused when they found her. The neurological examination and head computer tomography (CT) scan were unremarkable. The patient was evaluated by the Neurosurgery team and discharged. A few hours later, the patient was admitted again in the emergency with seizures. Treatment with valproic acid was initiated and a repeated CT scan showed a right frontal hypodensity, which was considered to be traumatic. The patient reported headache (VAS 5/10) and no spontaneous retinal venous pulsations were seen in fundoscopy. The remaining neurological examination was unremarkable. When asked, the patient reported headache hours before the first fall. An MRI was requested, which confirmed thrombosis of the distal third of the superior sagittal sinus and cortical veins with associated venous infarction (Figure 1). Therapeutic anticoagulation was started and the patient was admitted in the Stroke Unit. At 3 months, she was asymptomatic. Repeated MRI showed venous recanalization (Figure 2) and regression of the brain lesion.


Headache, which is the most common symptom in cerebral venous thrombosis (CVT), is a very common complaint in the emergency setting. Although the typical pattern of headache includes worsening with effort, such as Valsava maneuver, and when recumbent, several types of headache have been reported in CVT, including thunderclap headache. Seizures are another common presenting sign, occurring in the acute phase in up to 40% of patients, which is a higher proportion comparing with other types of stroke. Importantly, in most of the cases they actually occur before the diagnosis has been established.

Parenchymal lesions are found in ~60% of patients with CVT and differ considerably from those that occur in arterial stroke, as they cross arterial boundaries and have a haemorrhagic component in almost two-thirds of cases. However, the CT scan often shows non-specific findings and is normal in up to 30% of cases. Therefore, a high index of suspicion for this sometimes elusive diagnosis is necessary, which should prompt investigation with magnetic resonance venography or CT venography.

In this case head trauma was probably already a consequence of an acute symptomatic seizure secondary to CVT. In these situations, when attention is focused on clinical and imaging changes related to head injury, the diagnosis can be easily overlooked. Importantly, CVT can be also a complication of traumatic head injury, especially in cases were skull fractures cross a venous sinus.  In those situations, symptoms of CVT, such as headache, can mimic or be masked by disturbances related with traumatic head injury.

So, do not forget that head trauma can be a cause or a consequence of neurological disease and consider CVT in the differential diagnosis when evaluating patients who were admitted with headache and seizures.

Figure 1. Cerebral venous thrombosis of the distal third of the superior sagittal sinus and cortical veins and right frontal venous infarction (A. FLAIR, B. GRE-T2*, C. T1 after GAD and venography).

Figure 2. Venous recanalization in the follow-up MRI at 3 months.