Acute Vestibular Deficit (AVD)
Acute vestibular deficit, also referred to as vestibular neuritis, is the sudden functional deficit or loss of one or both peripheral vestibular systems.
It can be considered an idiopathic clinical condition; however, a possible viral aetiology seems to play a role. Not infrequent are the detection of neurodegenerative lesions of the vestibular nerve and of the receptor neuroepithelium.
Many studies have shown the possible implication of Herpes Type 1 virus, with the identification of its DNA in the vestibular ganglia. For this reason, it is probable that the virus is latent in the vestibular ganglia, from where it can later become active following concomitant events, such as immune alterations due to acute pathological phenomena, or from concomitant chronic pathologies (e.g., diabetes, autoimmune diseases, rheumatological diseases).
Other viruses that could be implicated in the onset of AVD seem to be those belonging to the Torch complex, adenoviruses, and influenza viruses.
In the aetiology of AVD, however, there is space for the hypothesis of ischemic lesions, especially in the region supplied by the superior vestibular artery. This region corresponds to the utricle and lateral and anterior semicircular canals, which in turn are innervated by the superior vestibular nerve, which in turn is much more frequently affected by AVD than the inferior vestibular nerve.
The vascular cause is accompanied by predisposing or aggravating conditions, such as obesity, hypercholesterolemia, hyperhomocysteinemia, hypofolatemia, diabetes, arterial hypertension, autoimmune diseases, pre-existent central ischemic episodes.
Often AVD is preceded by flu or parainfluenza episodes, and not rare is the consequent positional vertigo due to BPPV overlap, referred to as Lindsay-Hemenway Syndrome, and therefore a lithiasis affecting the posterior semicircular canal, present in 10-20% of AVDs. Equally frequent is the onset as a complication of PPPD (Persistent Postural Perceptual Dizziness). AVD is to be considered as the third most frequent pathology of the vestibular area. There is no side or gender prevalence, with mean age of onset between 30 and 65 years.
The symptoms are characterized by:
- Acute / sudden onset of rotary vertigo accompanied by a perception of movement of the surrounding environment, which can be classified as oscillopsia
- Severe static and dynamic dizziness when the patient, especially during the initial 24 hours, is absolutely unable to walk and / or maintain an upright position
- The vertigo can disappear in a few days; however, a severe, persistent, and irreversible dizziness remains if not treated adequately both pharmacologically and in vestibular rehabilitation therapy.
The vestibular analysis is characterized by the presence of a violent horizontal-rotary nystagmus, and the presence of a torsional component in the acute phase, with a rapid phase directed towards the unaffected side. Moreover, the Halmagyi test is positive, with a compensatory saccade facing the healthy side, indicating a dynamic deficit of the VOR (Vestibulo ocular reflex).
Within about thirty days, the nystagmus can be reduced until it disappears completely. Later, however, a nystagmus beating towards the affected side may appear, which we refer to as RECOVERY NYSTAGMUS. When the spontaneous nystagmus disappears, it is very useful to carry out a Head Shaking Test, always under videonystagmoscopy observation, which leads to the onset of a rotary nystagmus towards the unaffected side.
Similarly, the mastoid vibration test also generally induces the onset of a rotary nystagmus directed towards the unaffected side. In AVD, VEMPS are absent or pathologically reduced in amplitude. The patient with AVD undergoing FHIT almost always shows a severe perceptual deficit on the pathological side, both in the darkened background test and in the rotary one, where the worsening of the clinical data is not uncommon. With VHIT there is generally a large de-structuring of the path due to the VOR deficit of the pathological side. Therefore, a deficit in the dynamic gain of the VOR is present.
In summary, the clinical and symptomatic characteristics of AVD are characterized by:
• Acute and sudden onset of vertiginous syndrome of severe intensity with the patient’s severe inability to maintain an upright position and posture in general, with the consequent walking impossibility.
• Intense autonomic symptoms with nausea, sweating, paleness, asthenia, sialorrhea, including the possible relaxation of the sphincter.
• Presence in videonystagmoscopy of intense horizontal rotary nystagmus with torsional component, beating towards the unaffected side, which can persist beyond 24 hours.
• Positive HIT towards the pathological side.
• Normal audio impedance measurement with no morphological or inflammatory lesions affecting the tympanic membrane and external auditory canal.
• Residual dizziness, even severe, following the acute phase, a condition which requires prompt rehabilitation / vestibular rehabilitation, instrumental and otherwise.
• After about 30 days, the previous nystagmus may have disappeared, and is often replaced by a less intense rotary and horizontal nystagmus, beating towards the pathological side.
• It is useful to perform a hyperventilation test in the patient under videonystagmoscopic observation which can induce the arrest of the spontaneous nystagmus and the possible appearance of a short-lasting nystagmus beating towards the pathological side.
• The patient with AVD generally has no concomitant neurological signs.
• The patient with AVD requires repeated and close checks, even and above all in the absence or with the attenuation of acute symptoms, up to the point of carrying out vestibular rehabilitation.
• PPPD is a frequent complication.
