The loss of balance of neurological origin is not limited to rotational vertigo or vague instability. Distinguishing a central impairment from a peripheral disorder during the first consultation determines the speed of management and, in some cases, the patient’s vital prognosis.
Oculomotor semiology: nystagmus as a rapid sorting tool
Nystagmus remains the most discriminating clinical sign to guide towards a central or peripheral origin. A unidirectional, horizontal-rotatory nystagmus, inhibited by fixation points to peripheral vestibular impairment. Conversely, a multidirectional, purely vertical or purely torsional nystagmus that persists despite visual fixation indicates a lesion of the brainstem or cerebellum.
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We frequently observe that non-specialized practitioners omit the head impulse test (Head Impulse Test). This test, which can be performed in consultation without equipment, detects a deficit in the vestibulo-ocular reflex. A normal test in a dizzy patient should raise concern: it points towards a central cause, as the vestibulo-ocular reflex is preserved when the lesion is located above the vestibular nucleus.
The combination of three maneuvers (HINTS: Head Impulse, Nystagmus, Test of Skew) surpasses early MRI in identifying a stroke in the vertebrobasilar territory in the context of acute vertigo. As detailed in Valbreon’s explanations, these neurological alarm signals justify rapid management when associated with sudden headache, diplopia, or unilateral weakness.
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PPPD and functional disorders: the gray area of balance diagnosis
Persistent perceptual postural dizziness (PPPD) is a clinical entity still underdiagnosed. It manifests as chronic instability without true rotational vertigo, worsened by prolonged standing, complex visual movements, and stimulus-rich environments.
This disorder often occurs after an acute vestibular episode (neuronitis, BPPV) or trauma. The vestibular system recovers, but the brain maintains an inappropriate postural compensation strategy. The patient becomes excessively visually dependent for postural control, at the expense of proprioception and vestibular inputs.
The diagnostic criteria for PPPD rely on three conditions:
- Symptoms of instability or non-rotatory movement sensation present on most days for at least three months
- Worsening with upright posture, active or passive movements, and exposure to complex visual stimuli
- Absence of another pathology that better explains the clinical picture, after vestibular, neurological, and imaging assessments
PPPD is distinguished from functional neurological disorder (FND) by the absence of positive functional signs (Hoover’s sign, entrainable tremors). We recommend not to confuse these two entities, as their management differs: vestibular rehabilitation and cognitive-behavioral therapy for PPPD, multidisciplinary neuropsychiatric approach for FND.
Common causes of balance loss and diagnostic hierarchy
Multimorbidity is the main risk factor in patients over 65 years old. Reducing balance loss to a single etiology leads to therapeutic dead ends. In the elderly, the intertwining of neurodegenerative pathologies, sensory deficits, and polypharmacy makes the etiological diagnosis complex.
The causes to systematically investigate, in order of clinical frequency:
- Peripheral vestibular impairment (BPPV, Meniere’s disease, neuronitis): rotational vertigo, typical nystagmus, paroxysmal episodes
- Peripheral neuropathy (diabetic, alcoholic, nutritional): proprioceptive deficit of the lower limbs, positive Romberg sign with slow oscillations
- Cerebellar syndrome: dysmetria, adiadocokinesis, staggering gait with widening of the base of support
- Vascular pathology of the brainstem: sudden onset, associated signs (diplopia, dysarthria, motor deficit)
- Medication-induced iatrogenesis: benzodiazepines, antiepileptics, antihypertensives, aminoglycosides
The clinical examination quickly distinguishes a gait disorder of proprioceptive origin (worsened with eyes closed) from cerebellar ataxia (present with eyes open as well as closed). This simple test avoids unnecessary additional examinations.
Walking and balance: when imaging becomes essential
Brain MRI is not systematic for every loss of balance. It becomes necessary when the clinical picture points towards a central neurological impairment: atypical nystagmus, focal neurological signs, progressive onset without identified peripheral cause, or resistance to treatment of a presumed vestibular pathology.
An MRI with diffusion sequences is the reference examination to exclude a posterior territory stroke. FLAIR sequences look for white matter lesions suggestive of multiple sclerosis, a condition that reveals balance disorders in a notable proportion of young patients.
Eletro-nystagmography (ENG) and video-nystagmography (VNG) complete the assessment by objectifying a vestibular deficit and quantifying its degree. The vestibular evoked myogenic potentials (VEMP) explore saccular and utricular function, useful when the clinical picture does not correspond to either BPPV or classic neuronitis.
The trap of apparent normality
A normal brain scan does not exclude a lesion in the posterior fossa. The sensitivity of the scan for strokes of the brainstem and cerebellum remains low in the early hours. An acute vertigo with HINTS examination suggestive of a central cause necessitates an MRI, even if the initial scan is reassuring.
The evaluation of balance loss remains primarily a clinical exercise. Maneuvers at the patient’s bedside, the semiology of nystagmus, and gait analysis guide the diagnosis more quickly than the multiplication of examinations. The challenge lies in the early identification of central pictures masked by benign-appearing symptoms, particularly in patients with vascular risk factors.