What is Central Positional Vertigo?
Central positional vertigo (also called central paroxysmal positional vertigo or CPPV) is positional vertigo caused by lesions in the brainstem or cerebellum—particularly near the fourth ventricle and vestibular nuclei—rather than by inner ear pathology. 1, 2
Pathophysiology and Location
Central positional vertigo arises from structural lesions affecting the central vestibular pathways, most commonly:
- Lesions dorsolateral to the fourth ventricle 3
- Dorsal vermis of the cerebellum 3
- Vestibular nuclei in the ponto-medullary brainstem 2
The mechanism involves vestibular tone imbalance caused by disinhibition of vestibular reflexes when head position changes relative to gravity 2. Unlike peripheral causes where debris moves in semicircular canals, central positional vertigo results from direct dysfunction of central vestibular processing centers 2, 3.
Key Distinguishing Features from Peripheral (BPPV)
Nystagmus Characteristics
Central positional vertigo produces nystagmus that is fundamentally different from benign paroxysmal positional vertigo (BPPV):
- Pure vertical nystagmus (upbeating or downbeating) without torsional component 1, 4
- Direction-changing nystagmus without changes in head position 1, 4
- Immediate onset without latency period (versus 5-20 second latency in BPPV) 4
- Persistent and does not fatigue with repeated testing 1, 4
- Not suppressed by visual fixation 1, 4
- Downbeating nystagmus on Dix-Hallpike maneuver, particularly without torsional component 1, 4
Clinical Presentation
- Severe postural instability with falling is characteristic of central causes, particularly vertebrobasilar insufficiency and cerebellar lesions 4
- Associated neurological symptoms including dysarthria, dysmetria, dysphagia, sensory or motor deficits, diplopia, or Horner's syndrome 1, 4
- Gaze-evoked nystagmus (nystagmus that beats in the direction of gaze) is typical of central lesions 4, 5
- Baseline nystagmus present without provocative maneuvers 1, 4
Response to Treatment
Central positional vertigo does not respond to canalith repositioning procedures (Epley maneuver) or vestibular rehabilitation that would typically resolve BPPV 1, 4. Failure to respond to appropriate peripheral vertigo treatments is itself a red flag for central pathology 1, 4.
Common Etiologies in Neurological Populations
In patients with neurological conditions, central positional vertigo may result from:
- Multiple sclerosis: Demyelinating lesions within vestibular nuclei or cranial nerve VIII root entry zone 6
- Posterior fossa tumors: Including cerebellar tumors, which may present with positional vertigo as the sole initial feature 7
- Brainstem or cerebellar stroke/TIA: Vertebrobasilar insufficiency can cause isolated transient vertigo that may precede stroke by weeks or months 4
- Obstructive hydrocephalus 7
- Vestibular migraine: Can mimic central positional vertigo with atypical nystagmus patterns 8
Critical Diagnostic Pitfalls
Approximately 10-20% of cases presenting as "positional vertigo" are actually due to central nervous system pathology rather than benign peripheral causes 3, 7. The term "benign" in BPPV specifically indicates absence of serious CNS pathology 7.
Red Flags Demanding Immediate Neuroimaging
- Downbeating nystagmus on Dix-Hallpike without torsional component 1, 4
- Any additional neurological symptoms (dysarthria, limb weakness, ataxia, diplopia) 1, 4
- Severe postural instability with falling 4
- New-onset severe headache with vertigo 4
- Nystagmus that does not fatigue and is not suppressed by gaze fixation 4
- Apogeotropic horizontal nystagmus on supine roll test 4
- Isolated positional downbeat nystagmus 4
- Failure to respond to appropriate peripheral vertigo treatments 1, 4
Diagnostic Approach
A diagnosis of BPPV can only be made if Dix-Hallpike or supine roll maneuver elicits nystagmus that is entirely consistent with peripheral BPPV 7. Any atypical features warrant investigation for central pathology 7.
When central positional vertigo is suspected:
- MRI with attention to posterior fossa is the imaging modality of choice 1
- Evaluate for specific nystagmus patterns: purely vertical without torsion, direction-changing, gaze-evoked 4, 5
- Assess for associated neurological deficits through comprehensive neurological examination 1, 4
- Consider vascular imaging (CTA or MRA) if vertebrobasilar insufficiency suspected 1
Common Misdiagnosis Risk
In patients with multiple sclerosis or other neurological conditions, BPPV can still occur and should not be automatically attributed to central pathology 6. However, empiric treatment with corticosteroids or vestibular suppressants should not be employed until careful bedside examination with diagnostic positional maneuvers is performed 6.