Functional & atypical syndromes

The neck is full of position sensors that help the brain know where the head is. After a neck injury such as whiplash, or with neck arthritis, those signals can become faulty and clash with the eyes and inner ear — producing imbalance brought on by neck movement.

Cervicogenic dizziness is attributed to abnormal cervical proprioceptive input reaching the vestibular nuclei, classically after whiplash or with spondylosis. Imbalance is provoked by neck movement or sustained posture, often with neck pain — and crucially without true vertigo or nystagmus.1 It is a clinical diagnosis of exclusion; response to cervical physiotherapy supports it.2

Cervicogenic dizziness remains contested precisely because no confirmatory test exists; diagnose only after excluding vestibular and central causes, and treat with manual therapy, postural training, and sensorimotor control exercises, particularly post-whiplash.2

Some people become dizzy in visually “busy” places — supermarket aisles, crowds, escalators, scrolling screens. Their balance system leans too heavily on vision, so a moving visual scene throws them off.

Visual vertigo arises when vision becomes the dominant balance reference — visual dependence — typically after vestibular hypofunction or with anxiety. Patients with vestibular loss sway more in moving visual environments, confirming the over-reliance on vision.3 Treatment is desensitisation: optokinetic stimulation, gaze-stabilisation, and simulator/VR-based rehabilitation.4

Distinguish visual vertigo (provoked by visual motion) from head-motion intolerance (provoked by head movement). Management retrains multisensory weighting through graded exposure; treat any anxiety comorbidity in parallel.4

After a cruise or long flight, most people briefly feel like they're “still moving.” In mal de débarquement, that rocking sensation doesn't fade — it can last weeks or months after the trip ends.

MdDS is a rare disorder of motion perception that begins afterprolonged passive motion stops — the opposite of motion sickness. Imaging and examination are normal; diagnosis is clinical.5 Connectivity studies implicate altered vestibular-cortex and default-mode networks, and there is a striking female predominance.6

There is no universal protocol; vestibular re-adaptation (optokinetic stimulation timed to head roll) shows benefit by realigning sensory integration, and SSRIs/benzodiazepines are used empirically.7

PPPD is the commonest chronic “functional” dizziness. After an initial trigger (often a vertigo attack), the brain stays stuck in a high-alert balance mode — leaving daily unsteadiness that is worse standing up and in busy places, long after the original problem has gone.

Formalised in the Bárány Society criteria (2017), PPPD is chronic non-vertiginous dizziness/unsteadiness ≥3 months, provoked by upright posture, motion, and complex visual environments.8 It typically follows an acute vestibular or psychological event; the brain fails to re-set its balance strategy and locks into high-vigilance, visually-dependent postural control.10

Imaging implicates hyperactivation of the anterior insula and cingulate — interoception and threat-vigilance hubs — consistent with a vestibular– anxiety amalgam.9 Treatment is multidisciplinary: vestibular rehabilitation, CBT, and SSRIs/SNRIs (effective even without overt mood disorder).10