Is the fast phase of nystagmus directed opposite to the side of a brain‑stem or cerebellar infarct?

Nystagmus Direction in Cerebellar and Brainstem Infarction

In cerebellar and brainstem infarction, the fast phase of nystagmus typically beats TOWARD the side of the lesion, not opposite to it—this is the opposite pattern of peripheral vestibular lesions and is a critical distinguishing feature.

Key Distinguishing Pattern

Central vestibular lesions (cerebellar/brainstem infarcts) produce ipsilesional nystagmus, where the fast component beats toward the damaged side 1. This contrasts sharply with peripheral vestibular lesions, where nystagmus beats away from the affected ear.

Evidence from Cerebellar Infarction

• In superior cerebellar artery (SCA) territory infarcts, spontaneous nystagmus with a horizontal component always beat towards the lesion side in 80% of cases (8/10 patients) 1
• Damage to the rostral anterior cerebellum, including the ala of the central lobule and quadrangular lobule, was significantly associated with ipsilesional nystagmus (82% vs 37%, p=0.015) 1
• The proposed mechanism involves damage to the anterior cerebellar lobe, which disrupts vestibular output transmission to the fastigial nucleus 1

Complex Patterns in Medullary-Cerebellar Strokes

Direction-changing nystagmus can occur with concurrent brainstem and cerebellar involvement 2. In a documented case of left cerebellar-medullary PICA stroke:

• Right-beating nystagmus occurred in primary gaze and rightward gaze (contralesional) 2
• Left-beating nystagmus appeared with leftward gaze (ipsilesional) 2
• This complex phenotype results from simultaneous damage to vestibulo-ocular pathways (causing contralesional spontaneous nystagmus) and gaze-holding mechanisms in the nucleus prepositus hypoglossi/cerebellum (causing ipsilesional gaze-evoked nystagmus) 2

Critical Red Flags for Central Pathology

These nystagmus patterns mandate urgent neuroimaging 3, 4:

• Downbeat nystagmus without torsional component strongly suggests bilateral floccular lesion or cervicomedullary junction pathology 3, 4
• Direction-changing nystagmus that doesn't follow typical BPPV patterns (geotropic/apogeotropic) 4
• Baseline nystagmus present in primary position 4
• Associated cerebellar signs including ataxia, dysmetria, dysdiadochokinesia 4

Clinical Deterioration Monitoring

In cerebellar infarcts with swelling, monitor for brainstem compression signs 5:

• Pupillary changes: anisocoria, pinpoint pupils, loss of oculocephalic responses 5
• Altered level of consciousness (Glasgow Coma Scale <12 or decline ≥2 points) 5
• Irregular breathing patterns, bradycardia, sudden apnea 5

Diagnostic Algorithm

1. Assess nystagmus direction relative to suspected lesion side 1, 2
2. Check for downbeat component (suggests cervicomedullary/floccular pathology) 3, 4
3. Perform positional testing (Dix-Hallpike, supine roll) to distinguish from BPPV 4
4. Obtain urgent MRI (not CT) for posterior fossa evaluation when central features present 3, 4

Common Pitfall

The most dangerous error is misdiagnosing central positional nystagmus as benign BPPV 3, 4. BPPV produces torsional upbeating nystagmus in posterior canal disease 5, while central lesions produce downbeat or purely horizontal nystagmus without the characteristic torsional component 3, 4.