Workup for New Nystagmus in a Patient with Severe TBI
A patient with severe traumatic brain injury (TBI) who develops new nystagmus requires urgent neuroimaging with brain MRI to evaluate for structural lesions, vascular injuries, or progression of TBI-related damage. 1
Initial Assessment
Immediate Evaluation
- Perform detailed neurological examination focusing on:
- Complete eye movement assessment (horizontal, vertical, rotatory movements)
- Characterization of nystagmus (direction, amplitude, frequency, triggers)
- Pupillary responses and fundoscopic examination
- Cranial nerve function, particularly CN III, IV, VI, and VIII
- Cerebellar function (coordination, ataxia)
- Level of consciousness (any deterioration from baseline)
Imaging Studies
Brain MRI with contrast (first-line imaging for new neurological findings with normal initial CT) 2
- T1, T2, FLAIR, DWI, and SWI sequences
- SWI is particularly sensitive for detecting microhemorrhages not visible on CT
- Focus on brainstem, cerebellum, and vestibular pathways
CT angiography of supra-aortic and intracranial vessels 2
- Indicated to evaluate for vascular injury, particularly with:
- Skull base fractures
- Cervical spine injuries
- Focal neurological deficits
- Indicated to evaluate for vascular injury, particularly with:
Repeat non-contrast head CT 2
- If MRI is not immediately available
- To evaluate for new hemorrhage, hydrocephalus, or mass effect
- Particularly important if neurological deterioration is present
Specialized Testing
Vestibular Assessment
- Transcranial Doppler (TCD) 2
- Evaluate cerebral blood flow velocities and pulsatility index
- Abnormal values: mean velocity <28 cm/s or diastolic velocity <20 cm/s with PI >1.4
Neurophysiological Testing
- Electrooculography (EOG) or video-oculography
- For quantitative measurement of eye movements
- Helps characterize nystagmus pattern (pendular vs. jerk)
Additional Considerations
- Visual and vestibular examination for all TBI patients 3
- Consider evaluation for benign paroxysmal positional vertigo (BPPV), which is common after head trauma 3
Differential Diagnosis
Central Causes (Higher Priority)
- Brainstem or cerebellar contusion/hemorrhage
- Post-traumatic hydrocephalus
- Vascular injury (dissection, stroke)
- Cerebellar edema
- Brainstem compression
- Medication effect (particularly sedatives, anticonvulsants)
Peripheral Causes
- Labyrinthine concussion
- Perilymphatic fistula
- Post-traumatic BPPV
- Vestibular nerve injury
Management Considerations
- Transfer to a specialized center with neurosurgical facilities if not already there 2
- Maintain adequate cerebral perfusion (systolic BP >110 mmHg, CPP ≥60 mmHg) 2
- Monitor for signs of increased intracranial pressure
- Consider neurosurgical consultation if structural abnormalities are identified
- Avoid medications that may worsen nystagmus or mask neurological deterioration
Red Flags Requiring Immediate Action
- Nystagmus accompanied by:
- Decreased level of consciousness
- New cranial nerve deficits
- Ataxia or strabismus (strongly associated with urgent conditions) 4
- Progressive headache
- Vomiting
- Papilledema
Follow-up
- Serial neurological examinations to monitor for progression
- Repeat imaging if symptoms worsen or fail to improve
- Consider neuro-ophthalmology or neuro-otology consultation for persistent nystagmus
The presence of new nystagmus in a patient with severe TBI represents a significant finding that warrants thorough investigation, as it may indicate progression of injury or new pathology requiring intervention to prevent further morbidity and mortality.