What are the possible causes of dizziness in a patient following trauma, with a subgaleal hematoma, normal computed tomography (CT) scan, and taking anticoagulant or antiplatelet medication?

Causes of Dizziness Following Trauma in Patients with Subgaleal Hematoma, Normal CT, and Anticoagulation

In a patient with post-traumatic dizziness, subgaleal hematoma, normal CT scan, and anticoagulant/antiplatelet use, the most likely causes are peripheral vestibular disorders—particularly benign paroxysmal positional vertigo (BPPV), labyrinthine concussion, and otolith organ injury—rather than intracranial pathology, given the normal CT findings. 1, 2

Peripheral Vestibular Causes (Most Common)

Benign Paroxysmal Positional Vertigo (BPPV) is the most frequent vestibular disorder following head trauma and presents with brief episodes of vertigo triggered by head movements. 3, 1 This occurs when otoconia are dislodged from the utricle into the semicircular canals during trauma. 2 The Dix-Hallpike test can differentiate BPPV from more concerning central causes. 3

Labyrinthine concussion represents direct injury to the inner ear structures without temporal bone fracture, causing persistent dizziness, imbalance, and nystagmus. 1, 2 This diagnosis is made when vestibular symptoms persist beyond the acute period without identifiable structural damage on imaging. 2

Otolith organ damage (utricle and saccule) is increasingly recognized as more vulnerable to trauma than the semicircular canals, particularly in blast injuries and mTBI. 4 Patients may exhibit abnormal vestibular evoked myogenic potential (VEMP) testing despite normal horizontal canal function. 4

Perilymphatic fistula or labyrinthine dehiscence can occur from trauma causing abnormal communication between the inner ear and middle ear or intracranial space. 1, 2 These patients may report dizziness triggered by loud sounds (Tullio phenomenon) or changes in middle ear pressure. 1

Unilateral vestibular nerve injury may result from stretching or contusion of the vestibular nerve during trauma, presenting with acute vestibular syndrome (persistent vertigo, nausea, gait instability, and nystagmus). 3, 2

Central Vestibular Causes

Despite the normal CT scan, microstructural brain injury or diffuse axonal injury can cause central vestibular dysfunction that may not be visible on routine CT imaging. 1, 4 MRI with diffusion-weighted imaging is more sensitive for detecting these subtle injuries, though the diagnostic yield remains low (approximately 4%) in isolated dizziness. 3

White matter abnormalities from traumatic brain injury can disrupt central vestibular pathways, contributing to chronic dizziness even without visible hemorrhage. 4

Non-Vestibular Causes

Post-traumatic migraine-associated dizziness represents a complex interaction between migraine, anxiety, and the trauma itself. 2 This diagnosis should be considered when vestibular testing is normal but dizziness persists. 2

Cervicogenic dizziness from associated neck injury during trauma can present with dizziness related to neck movements and cervical muscle spasm. 1

Critical Considerations in Anticoagulated Patients

Delayed intracranial hemorrhage risk remains a concern despite the normal initial CT, though the absolute risk is low (0.6-6% for warfarin, 0.95% for DOACs). 5, 6 Patients on factor Xa inhibitors like apixaban have a 2.6% risk of intracranial hemorrhage versus 10.2% for warfarin. 5, 6

Subgaleal hematoma in anticoagulated patients can be massive even after mild trauma, as demonstrated in case reports of patients on apixaban. 7 The presence of subgaleal hematoma indicates significant scalp trauma that could have transmitted forces to the inner ear structures. 7

Temporal bone fracture must be excluded, though it would typically be visible on CT. 1 If clinical suspicion is high based on hemotympanum, Battle's sign, or CSF otorrhea, dedicated temporal bone CT should be obtained. 3

Diagnostic Algorithm

1. Perform bedside vestibular testing including Dix-Hallpike maneuver to identify BPPV, head impulse test to assess semicircular canal function, and test of skew to evaluate for central pathology. 3

2. Assess for neurologic symptoms beyond dizziness (diplopia, dysarthria, ataxia, focal weakness) that would increase concern for central pathology and warrant MRI. 3

3. Consider formal vestibular testing with videonystagmography (VNG) and VEMP testing if symptoms persist beyond 2-3 weeks, as these can identify peripheral vestibular dysfunction not apparent on clinical examination. 1, 4

4. Obtain MRI with diffusion-weighted imaging if symptoms persist, neurologic examination is abnormal, or there is concern for posterior fossa pathology, as CT has limited sensitivity for these findings. 3

5. Monitor for delayed hemorrhage with repeat CT only if neurologic deterioration occurs, as routine repeat imaging is not indicated in neurologically intact patients with negative initial CT. 5, 6

Common Pitfalls

Failing to identify and treat BPPV is the most common error, as this highly treatable condition accounts for a significant proportion of post-traumatic dizziness and responds well to canalith repositioning maneuvers. 1, 2

Attributing all symptoms to "post-concussive syndrome" without adequate vestibular evaluation delays diagnosis of treatable peripheral vestibular disorders. 1, 2

Premature discontinuation of anticoagulation without considering thromboembolic risk may cause more harm than the small risk of delayed hemorrhage in neurologically intact patients with normal CT. 5, 6

Over-reliance on CT imaging to exclude all causes of dizziness, when most post-traumatic vestibular disorders require clinical examination and specialized vestibular testing for diagnosis. 3, 1