ABSTRACT
Hyperventilation induces metabolic changes that can elicit nystagmus (hyperventilation-induced nystagmus, HVIN) in various vestibular disorders, revealing vestibular imbalance and bringing out central or peripheral asymmetries. In acute unilateral vestibulopathy (AUVP, namely vestibular neuritis), hyperventilation can induce different patterns of nystagmus (excitatory, inhibitory, or negative), disclosing or modifying existing static vestibular asymmetries through its ability to invalidate compensation or increase peripheral excitability. In this context, we followed the evolutionary stages of HVIN in AUVP across 35 consecutive patients, with the goal of assessing alterations in the oculomotor pattern caused by hyperventilation over time. In the acute phase, the incidence of the excitatory pattern (and the strongly excitatory one, consisting of a reversal nystagmus evoked by hyperventilation) was significantly higher compared to the inhibitory pattern; then, a progressive reduction in the incidence of the excitatory pattern and a concomitant gradual increase in the incidence of the inhibitory one were observed in the follow-up period. Assuming the role of the ephaptic effect and the transient loss of vestibular compensation as opposing mechanisms, i.e., excitatory and inhibitory, respectively, the oculomotor pattern evoked by hyperventilation is the result of the interaction of these two factors. The data obtained allowed us to hypothesize an interpretative model regarding the pathogenetic aspects of responses evoked by hyperventilation and the etiologies of the disease: according to our hypotheses, the excitatory pattern implies a neuritic (viral) form of AUVP; instead, the inhibitory (and negative) one can be an expression of both the neuritic (viral) and vascular forms of the disease.
ABSTRACT
Migraine pathogenic pathways may selectively target the cochlea. A qualitative and quantitative analysis of cochlear symptoms in migraine patients without vestibular migraine and/or Méniere's disease was conducted. We examined 60 consecutive patients with history of cochlear symptoms, including fullness, tinnitus, and hearing loss. Patients were divided into two groups based on migraine history: M (migraine) and nM (no migraine). The incidence of migraine was compared to a homogeneous control group with dysfunctional and inflammatory dysphonia without cochlear symptoms. The type, time of onset, recurrence, bilaterality of symptoms, and hearing threshold were analyzed. The incidence of migraine was significantly higher (p = 0.04) in patients with cochlear symptoms than in the control group. The onset of symptoms is significantly earlier (p < 0.05) in the presence of migraine. The fullness, recurrence, and bilaterality of symptoms are associated with migraine in a statistically significant way (p < 0.05). Pure tone audiometry shows a statistically significant increase in the hearing threshold (500-1000 Hz) in group M. Based on developing findings, cochlear migraine may be considered as a novel clinical entity, like vestibular migraine. It would be the expression, in the absence of vertiginous symptoms, of a selective suffering of the anterior labyrinth by known operating mechanisms of migraine.
ABSTRACT
Benign Paroxysmal Positional Vertigo (BPPV), Vestibular Migraine (VM), and Meniere Disease (MD) are among the most common episodic vestibulopathies. Persistent Postural Perceptual Dizziness (PPPD) is a chronic functional vestibular disorder that can arise in patients suffering from one or more of these conditions. We analyzed the role of these vestibular disorders as single or multiple associated comorbidities and as a precipitating condition for PPPD. A total of 376 patients suffering from dizziness with a known history of single or multiple vestibular disorders were preliminarily evaluated. We conducted a careful anamnesis to determine whether the reported dizziness could meet the diagnostic criteria for PPPD. PPPD was diagnosed in 24 cases; its incidence in patients with history of a single comorbidity or multiple vestibular comorbidities was 3.9% and 22.4%, respectively. BPPV, VM, and MD were identified as a precipitating condition in 2.34%, 16.45%, and 3.92%, respectively. BPPV constituted a precipitating condition mainly at the first episode. We observed that the presence of multiple vestibular comorbidities (BPPV, VM, and MD) in patients' clinical history increased the risk of PPPD. VM plays a significant role in representing a precipitating condition for PPPD, both when present individually or in association with the other vestibular disorders.
