Central vertigo refers to dizziness and imbalance caused by pathology within the central nervous system — the brainstem, cerebellum, or their vascular supply — as opposed to the inner ear or vestibular nerve (peripheral vertigo). While peripheral causes (BPPV, vestibular neuritis, Menière's disease) account for the majority of vertigo presentations, central vertigo is disproportionately important because many of its causes are potentially life-threatening and time-critical: posterior fossa stroke (the most dangerous), TIA in the posterior circulation, cerebellar haemorrhage, and brainstem demyelination.
Central vertigo is dizziness and imbalance caused by pathology within the central nervous system — the brainstem, cerebellum, or their vascular supply — rather than the inner ear or vestibular nerve. While peripheral causes account for the majority of vertigo presentations, central vertigo is disproportionately important because many of its causes are time-critical emergencies: posterior fossa ischaemic stroke (PICA or AICA territory), cerebellar haemorrhage, brainstem haemorrhage, and posterior fossa TIA. The HINTS exam (Head Impulse + Nystagmus + Test of Skew) distinguishes central from peripheral vertigo at the bedside with sensitivity HIGHER than early MRI for posterior fossa stroke. Key central features: direction-changing or vertical nystagmus; NORMAL head impulse test in acute severe vertigo (the paradoxical danger sign); skew deviation; new headache with vertigo; focal neurological signs. PICA infarction (Wallenberg syndrome): crossed sensory loss (ipsilateral face + contralateral body) + ipsilateral Horner's + dysphagia + ataxia + vertigo — NO limb weakness. AICA infarction: Wallenberg-like features + ipsilateral hearing loss. Cerebellar haemorrhage: neurosurgical emergency.
| Fact | Details |
|---|---|
| Central vs peripheral | Central RED FLAGS: direction-changing or vertical nystagmus · NORMAL head impulse in acute severe vertigo · Skew deviation · Headache with vertigo · Focal neurological signs · Falls with eyes open toward same side |
| HINTS exam | Head Impulse: corrective saccade = peripheral (safe) · Normal impulse = central (DANGER) · Nystagmus: unidirectional horizontal = peripheral · Skew deviation = central · More sensitive than early MRI for posterior fossa stroke |
| PICA (Wallenberg) | Crossed sensory loss (ipsilateral face + contralateral body) · Horner's ipsilateral · Dysphagia + dysarthria · Ipsilateral ataxia · Vertigo · NO limb weakness |
| AICA | PICA-like features + ipsilateral sensorineural deafness (cochlea from internal auditory artery, AICA branch) · Ipsilateral facial palsy · Mimics labyrinthitis but central on HINTS |
| CT and MRI limitations | CT: bone artefact obscures posterior fossa, small infarcts invisible · MRI DWI: ~80% sensitivity in first 24h for posterior fossa stroke · Normal HINTS exam excludes posterior fossa stroke better than early imaging |
| Cerebellar haemorrhage | Neurosurgical emergency · Acute headache + vertigo + inability to walk + vomiting · CT for blood · Fourth ventricle compression · Tonsillar herniation risk · Immediate neurosurgical assessment |
| Emergency | 040-46324365 immediately for any vertigo with headache, focal neurological signs, or inability to stand even with eyes open |
Posterior fossa ischaemic stroke: PICA (posterior inferior cerebellar artery) · AICA (anterior inferior cerebellar artery) · Basilar artery · Cerebellar haemorrhage (mass effect, herniation risk) · Brainstem haemorrhage.
Vertebrobasilar TIA (preceding stroke risk) · MS/demyelination · Posterior fossa tumour (acoustic neuroma, metastases, ependymoma) · Chiari malformation · Vertebrobasilar migraine.
Lateral medullary infarction: crossed sensory loss (ipsilateral face + contralateral body) · Ipsilateral Horner's syndrome (ptosis, miosis, anhidrosis) · Dysphagia + dysarthria (nucleus ambiguus) · Ipsilateral ataxia · Vertigo and nystagmus · No limb weakness (corticospinal tract is spared).
Combines lateral pontine infarction features WITH hearing loss (internal auditory artery = branch of AICA supplies cochlea) · Ipsilateral facial palsy + ipsilateral deafness + vertigo = AICA syndrome · Mimics labyrinthitis (peripheral) but is central.
Direction-changing nystagmus · Vertical nystagmus (upbeat or downbeat) · NORMAL head impulse test in severe vertigo · Skew deviation · New headache with vertigo · Focal neurological signs · Falls TOWARD ipsilateral side in both eyes open AND closed (vs peripheral: falls in all directions).
Acute cerebellar haematoma: severe vertigo + headache + inability to walk (truncal ataxia) + vomiting · No focal limb weakness initially · Mass effect can cause obstructive hydrocephalus and brainstem compression · Surgical evacuation may be life-saving · Call 040-46324365 immediately.
Early DWI (first 24h) misses approximately 20% of posterior fossa ischaemic infarctions · Repeat MRI at 48–72h if clinical suspicion remains high despite initial normal MRI · HINTS exam is more sensitive than early MRI.
Vertebrobasilar disease is common in India: hypertension + diabetes + high prevalence in South Indian population · Basilar artery atherosclerosis: intracranial stenosis more common in Asians than Europeans · CT limitations must be explained to families.
Central vertigo refers to dizziness and imbalance caused by pathology within the central nervous system — the brainstem, cerebellum, or their vascular supply — as opposed to the inner ear or vestibular nerve (peripheral vertigo). While peripheral causes (BPPV, vestibular neuritis, Menière's disease) account for the majority of vertigo presentations, central vertigo is disproportionately important because many of its causes are potentially life-threatening and time-critical: posterior fossa stroke (the most dangerous), TIA in the posterior circulation, cerebellar haemorrhage, and brainstem demyelination.
The central challenge of acute vertigo medicine is that central and peripheral vertigo can look remarkably similar at first presentation — both cause intense vertigo, nausea, vomiting, and inability to walk steadily. The CT scan (which is the standard first test in most emergency departments) is insensitive for posterior fossa ischaemia. The HINTS exam — three specific bedside eye movement assessments — is the most accurate way to distinguish central from peripheral vertigo, outperforming early MRI in sensitivity for posterior fossa stroke. At KIMS, the HINTS exam is performed by a trained neurologist in all patients presenting with acute vertigo.
Emergency / Stroke Consultation
Speak directly with the KIMS emergency neurology and stroke teams — for acute posterior fossa stroke, vertebrobasilar TIA, suspected cerebellar haemorrhage, HINTS exam, and 24/7 MRI DWI with thrombolysis and mechanical thrombectomy where indicated.
040-44885000Stroke / posterior fossa emergency: 040-46324365Occlusion of the posterior inferior cerebellar artery (PICA) or the lateral medullary arteries that branch from the vertebral artery produces the lateral medullary (Wallenberg) syndrome — the most common brainstem infarction syndrome associated with vertigo. The lateral medulla contains the nucleus of the spinal trigeminal tract (ipsilateral facial pain and temperature), the spinothalamic decussation for the body (contralateral body pain and temperature), Horner's syndrome fibres (ipsilateral ptosis, miosis, anhidrosis), the nucleus ambiguus (causing ipsilateral dysphagia, dysarthria, and vocal cord paralysis), the vestibular nuclei (causing vertigo and nystagmus), and the inferior cerebellar peduncle (causing ipsilateral limb and gait ataxia). The characteristic crossed pattern — ipsilateral face + contralateral body sensory loss — is pathognomonic for a lateral medullary lesion. Notably, the corticospinal tract (which runs in the medial medulla, not the lateral medulla) is spared, so limb weakness is typically absent. PICA infarction can closely mimic vestibular neuritis — the HINTS exam is the critical bedside distinction.
Occlusion of the anterior inferior cerebellar artery (AICA) produces a lateral pontine infarction, often combined with cochlear infarction (because the internal auditory artery — the sole blood supply to the cochlea — is a branch of the AICA in approximately 80% of people). The result: sudden vertigo + ipsilateral hearing loss + ipsilateral facial palsy + ipsilateral cerebellar ataxia. The combination of acute vertigo WITH ipsilateral hearing loss is the key differentiator: in vestibular neuritis (peripheral), hearing is preserved; in AICA syndrome (central), hearing is lost. Any patient presenting with acute vertigo and ipsilateral hearing loss together should be considered to have AICA infarction until proven otherwise by MRI.
Acute cerebellar haematoma presents with sudden severe headache (in the occipital region or back of the neck), intense vertigo, vomiting, truncal ataxia (inability to sit or stand without support), and gaze deviation away from the side of the bleed. Unlike cortical haemorrhage, limb weakness is typically absent or minimal initially. The danger: the cerebellum is within the rigid posterior fossa, and a growing haematoma compresses the brainstem (at the level of the fourth ventricle), causing obstructive hydrocephalus, progressive coma, and respiratory failure. A haematoma larger than 3 cm, or any haematoma causing brainstem compression or hydrocephalus, requires emergency surgical evacuation at KIMS. CT brain without contrast detects acute haemorrhage with high sensitivity (>95%) — unlike ischaemic posterior fossa strokes, haemorrhage is reliably seen on CT.
Vertebrobasilar TIA presents as brief (minutes to hours) episodes of: vertigo · diplopia · dysarthria · dysphagia · facial numbness · perioral tingling · limb ataxia · drop attacks · bilateral visual disturbance · impaired consciousness. The critical feature: at least TWO of these symptoms occurring together (or recurrently) strongly suggests vertebrobasilar TIA rather than peripheral vestibular disease. Isolated vertigo as a TIA is possible but uncommon (and debated). After a vertebrobasilar TIA, the 48–90 day stroke risk is approximately 5–10% — making urgent evaluation and antiplatelet therapy + risk factor control the immediate priority.
Central vertigo is diagnosed at KIMS through a structured four-stage workflow that begins with the bedside HINTS exam (the most accurate test for distinguishing central from peripheral vertigo, outperforming early MRI), proceeds to mandatory MRI brain DWI when any central finding is identified, uses non-contrast CT brain only for acute triage and haemorrhage exclusion (CT is insensitive for acute posterior fossa ischaemia), and is followed by a full vascular risk factor assessment to identify the underlying aetiology and guide secondary prevention :
Head Impulse (positive/abnormal = peripheral = safe · Normal = central = danger) · Nystagmus direction (unidirectional horizontal = peripheral · Direction-changing or vertical = central) · Test of Skew (absent = peripheral · Present = central). Any single central finding = MRI brain DWI immediately. Performed by KIMS emergency neurologists in all acute vertigo presentations.
Standard MRI DWI protocol for posterior fossa stroke: axial DWI + ADC (restricted diffusion = acute ischaemia) · FLAIR (subacute infarction, white matter disease) · T2 · MRA (intracranial vessels — basilar stenosis, PICA/AICA occlusion) · TOF-MRA (vertebral arteries — dissection) · GRE/SWI (haemorrhage). Repeat MRI at 48–72 hours if initial study is negative but clinical suspicion remains high.
Non-contrast CT brain: detects posterior fossa haemorrhage with >95% sensitivity · Insensitive for acute ischaemic stroke in the posterior fossa (bone artefact) · CT angiography (CTA) of the posterior circulation if basilar artery occlusion is suspected (acute locked-in syndrome or basilar thrombosis).
Fasting lipid profile · HbA1c · 24-hour ambulatory BP monitoring · ECG + 24h Holter (for AF as source of embolism) · Echocardiogram (cardiac embolism) · Carotid + vertebral Doppler (proximal stenosis) · Hypercoagulable screen in young patients · Homocysteine.
Thrombolysis (IV tPA) — Acute Posterior Fossa Stroke: Within 4.5 hours of onset if eligible · Basilar artery occlusion: extended window with imaging confirmation of penumbra.
Mechanical thrombectomy — Acute Posterior Fossa Stroke: For large vessel occlusion (basilar artery, PICA/AICA origin) within 24 hours · Available at KIMS 24/7.
Antiplatelet therapy — Acute Posterior Fossa Stroke: Aspirin 300 mg immediately + clopidogrel 300 mg loading for non-haemorrhagic stroke · Dual antiplatelet for 21 days in minor stroke/TIA (POINT trial).
Cerebellar haemorrhage — Acute Posterior Fossa Stroke: Neurosurgical evacuation for haematoma >3 cm or with brainstem compression/hydrocephalus · ICP monitoring.
Antiplatelets — Secondary Prevention: Aspirin + dipyridamole or clopidogrel monotherapy for non-cardioembolic posterior circulation stroke.
Anticoagulation — Secondary Prevention: Warfarin or DOAC for cardioembolic source (AF, intracardiac thrombus).
Statin — Secondary Prevention: High-intensity statin · LDL <70 mg/dL.
Blood pressure — Secondary Prevention: Target <130/80 mmHg · Started after the acute phase (24–48 hours).
Vestibular Rehabilitation: Central vestibular rehabilitation after posterior fossa stroke targets the specific deficits: gaze stabilisation exercises for internuclear ophthalmoplegia · Balance retraining for cerebellar ataxia · Head movement tolerance exercises for persistent vestibular mismatch · Gait retraining and falls prevention.
Related Conditions
Central vertigo belongs to the family of vestibular and balance disorders evaluated and managed at KIMS Neuroscience. Explore related conditions
Vertigo with a headache. Double vision with the spinning. A HINTS exam that tells more than a CT scan ever could. When vertigo is central, every minute of the treatment window matters.
At KIMS Hyderabad, the emergency neurology team performs the HINTS exam, the MRI is available 24/7, and the stroke team activates immediately when a posterior fossa stroke is identified. Emergency: 040-46324365. Outpatient: 040-44885000.
International enquiries: info@kimsneurosciences.com