Bruns Nystagmus: Pathophysiology and Diagnosis
Bruns nystagmus is a distinctive ocular movement disorder characterized by a coarse, high-amplitude horizontal nystagmus when looking toward the lesion side and a fine, low-amplitude, high-frequency nystagmus when looking away from the lesion side, typically caused by large cerebellopontine angle tumors that compress the brainstem and cerebellum. 1
Pathophysiology
Bruns nystagmus occurs due to:
- Compression of the brainstem, particularly affecting the vestibular nuclei
- Distortion of the flocculus and/or vestibulocerebellum
- Disruption of neural pathways controlling horizontal eye movements
- Significant mass effect from large cerebellopontine angle lesions
The dual nature of this nystagmus results from different pathophysiological mechanisms:
- The coarse component (toward lesion side): Direct compression of ipsilateral vestibular structures
- The fine component (away from lesion side): Disruption of central compensatory mechanisms
Clinical Presentation
Key characteristics include:
- Asymmetric nystagmus that changes direction with gaze position
- Coarse, low-frequency nystagmus when looking toward the lesion
- Fine, high-frequency nystagmus when looking away from the lesion
- Often accompanied by other neurological symptoms due to mass effect
- May present with oscillopsia (visual disturbance with perception of objects oscillating)
- Can be associated with headache, nausea, and vomiting due to increased intracranial pressure
Diagnostic Approach
1. Clinical Examination
- Detailed ocular examination including assessment of visual acuity 2
- Careful documentation of nystagmus characteristics:
- Direction
- Amplitude
- Frequency
- Relationship to gaze position
- Effect of fixation
- Assessment of other neurological signs (cranial nerve deficits, cerebellar signs)
2. Neuroimaging
- MRI of the brain with and without contrast is the gold standard 2
- MRI should be performed urgently in cases of asymmetrical or unilateral nystagmus 2
- CT may be used if MRI is contraindicated but is less sensitive for posterior fossa lesions
3. Vestibular Testing
- Vestibular testing should not be ordered in patients who already meet clinical criteria for more common causes of positional nystagmus like BPPV 3
- However, comprehensive vestibular testing may be beneficial when:
- Clinical presentation is atypical
- Dix-Hallpike testing elicits equivocal findings
- Multiple concurrent peripheral vestibular disorders are suspected
- Additional symptoms beyond positional vertigo are present 3
Differential Diagnosis
Bruns nystagmus must be differentiated from:
Benign Paroxysmal Positional Vertigo (BPPV)
- Most common cause of positional nystagmus
- Typically fatigable and short-duration
- Responds to repositioning maneuvers
Central Positional Nystagmus
- May be apogeotropic (beating away from the ground)
- Can be an isolated finding in patients with cerebellar tumors
- Refractory to repositioning maneuvers 4
Other forms of nystagmus:
Red Flags Requiring Urgent Evaluation
- Asymmetrical or unilateral nystagmus 2
- Progressive symptoms
- Associated neurological deficits
- Nystagmus refractory to appropriate treatment for presumed peripheral causes
- Persistent headache, especially worse in the morning
- Papilledema suggesting increased intracranial pressure
Diagnostic Pitfalls
- Misdiagnosis as BPPV is common, especially with central positional nystagmus 4
- Failure to recognize the asymmetric nature of Bruns nystagmus
- Inadequate neuroimaging (CT instead of MRI) may miss posterior fossa lesions
- Focusing only on the nystagmus without evaluating for other neurological signs
- Repeated unsuccessful repositioning maneuvers for presumed BPPV should prompt consideration of central causes 4
Remember that Bruns nystagmus is a neurological red flag that requires prompt neuroimaging, as it typically indicates a significant space-occupying lesion in the posterior fossa that may require urgent neurosurgical intervention.