Delayed Onset Aphasia After Evacuation of Dominant Hemisphere Convexity Subdural Hematoma
A 76-year-old male was brought to the hospital following a ground-level fall. Despite an initial loss of consciousness, he was at his normal neurological baseline upon hospital admission. He has a prior history of atrial fibrillation, but due to previous GI hemorrhage was not on any form of anticoagulation.
A noncontrast head CT performed on arrival demonstrated a left frontal parietal subdural hematoma measuring 4 mm in thickness with 2 mm of midline shift (Figure). He was admitted to the ICU, and a repeat noncontrast head CT was performed 6 hours later. On repeat scans, the hematoma thickness increased to 9 mm, although he remained neurologically stable. He was managed conservatively.
Nearly 1 month later, he developed increasing confusion and headaches. A repeat head CT showed a left holohemispheric subdural hematoma measuring 13 mm in maximal thickness with 11 mm of midline shift.
He underwent a craniotomy for evacuation of the subdural hematoma with rapid improvement in his symptoms, and returned back to his normal baseline exam over the next 24 hours. However, on postoperative day 5, he developed new onset expressive aphasia without other focal neurological deficits.
A repeat head CT showed no new hemorrhage or infarct, and scalp electroencephalogram did not identify seizure activity. An MRI could not be obtained due to pacemaker implantation. After an extensive workup, no infectious or metabolic etiology could be ascertained; his symptoms spontaneously resolved approximately 1 week after onset.
Discussion. Chronic subdural hematomas are one of the most common neurosurgical issues with an incidence of 58 per 100,000 in persons age 70 years or older.1 Elderly patients are especially susceptible to developing subdural hematomas due to brain atrophy causing increased stretch of the bridging vessels.2 Management of chronic subdural hematomas is a well-established practice. However, postoperative morbidity following surgical evacuation of subdural hematomas can include repeat hemorrhage, infarct, seizures, infections, and electrolyte derangements.2 A less well-established cause for postoperative decline is cerebral vasospasm, which can cause new onset neurological deficits.
Vasospasm of vessels supplying the dominant hemisphere may contribute to clinical symptoms as described above, but the pathophysiology of vasospasm following trauma or surgical intervention is poorly understood. The incidence of traumatic vasospasm has been reported from 19% to 68%, although detailed vascular studies are not routinely performed.3 Only 4% to 17% of patients with radiographic vasospasm develop neurological deficits.3
Weber et al published one of the first prospective studies on cerebral vasospasm in trauma by measuring transcranial doppler (TCD) velocities in the middle cerebral and internal carotid arteries.4 This study found that increases in TCD velocities were first measured 48 hours after injury, and reached a peak between days 5 to 7. The velocities then returned to normal levels 2 to 3 weeks following injury.4
Unlike vasospasm resulting from subarachnoid hemorrhage, management of traumatic vasospasm with traditional hypertension, hypervolemia, and hemodilution is controversial, since these therapies can worsen cerebral edema.5 Calcium channel blockers are also used to treat vasospasm following aneurysmal hemorrhage by reducing calcium influx into vascular smooth muscle cells, thus preventing constriction.6
A meta-analysis of 6 separate trials involving 1862 patients studied the role of calcium channel blockers in traumatic brain injury, and a significant increase in hypotension in patients receiving calcium channel blockers was observed.7 Preemptive administration of calcium channel blockers in traumatic brain injury patients may therefore cause hypotension, hypoperfusion, and secondary brain injury.8 Thus, further studies are required to understand the etiology and treatment options for postoperative patients with delayed symptomatic onset.
Outcome of the case. This patient developed aphasia on post-operative day 5 following evacuation of a dominant hemisphere convexity subdural hematoma. Although etiology of the aphasia is unclear, delayed onset cerebral vasospasm may be a contributing factor. Both pathophysiology and treatment of vasospasm following aneurysm rupture have been studied, but less is known about vasospasm following trauma and subdural hemorrhage. Thus, a vascular study may be warranted if new neurological deficits develop in a trauma patient several days following injury.
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