Vestibular dysfunction, causing dizziness and imbalance, is a common yet poorly understood
feature in traumatic brain injury patients. Damage to the inner ear, nerve, brainstem, cerebellum
and cerebral hemispheres may all affect vestibular functioning, hence, a multi-level assessment
– from reflex to perception – is required. In a previous report, postural instability was the
commonest neurological feature in ambulating acute traumatic brain injury patients. We also
frequently observe, during ward assessment of acute traumatic brain injury patients with
common inner ear conditions and a related vigorous vestibular-ocular reflex nystagmus, a loss
of vertigo sensation, suggesting a “vestibular agnosia”. Vestibular agnosia patients were also
more unbalanced, however the link between vestibular agnosia and imbalance was confounded
by the presence of inner ear conditions. We investigated the brain mechanisms of imbalance in
acute traumatic brain injury, its link with vestibular agnosia, and potential clinical impact, by
prospective laboratory assessment of vestibular function, from reflex to perception, in patients
with preserved peripheral vestibular function. Assessment included vestibular-reflex function;
vestibular-perception by participants’ report of their passive yaw rotations in the dark;
objective balance via posturography; subjective symptoms via questionnaires; and structural
neuroimaging. We prospectively screened 918 acute admissions, assessed 146 and recruited
37. Compared to 37 matched controls, patients showed elevated vestibular-perceptual
thresholds (patients 12.92°/s vs. 3.87°/s) but normal vestibular-ocular reflex thresholds
(patients 2.52°/s vs. 1.78°/s). Patients with elevated vestibular-perceptual thresholds (3
standard deviations above controls’ average), were designated as having vestibular agnosia,
and displayed worse posturography than non-vestibular-agnosia patients, despite no difference
in vestibular symptom scores. Only in patients with impaired postural control (3 standard
deviations above controls’ mean), whole brain diffusion tensor voxel-wise analysis showed
elevated mean diffusivity (and trend lower fractional anisotropy) in the inferior longitudinal fasciculus in the right temporal lobe which correlated with vestibular agnosia severity. Thus,
impaired balance and vestibular agnosia are colocalised to the inferior longitudinal fasciculus
in the right temporal lobe. Finally, a clinical audit showed a sevenfold reduction in clinician
recognition of a common peripheral vestibular condition (benign paroxysmal positional
vertigo) in acute patients with clinically apparent vestibular agnosia. That vestibular agnosia
patients show worse balance, but without increased dizziness symptoms, explains why
clinicians may miss treatable vestibular diagnoses in these patients. In conclusion, vestibular
agnosia mediates imbalance in traumatic brain injury both directly via white matter tract
damage in the right temporal lobe, and indirectly via reduced clinical recognition of common,
treatable vestibular diagnoses.