Hearing loss stands as the most prevalent sensory deficit among humans, posing a significant global health challenge. Projections indicate that by 2050, approximately 10% of the world's population will grapple with disabling hearing impairment. While approximately half of congenital hearing loss cases have a genetic etiology, traditional interventions such as hearing aids and cochlear implants do not completely restore normal hearing. The absence of biological treatment has prompted significant efforts in recent years, with a strong focus on gene therapy to address hereditary hearing loss. Although several studies have exhibited promising recovery from common forms of genetic deafness in mouse models, existing challenges must be overcome to make gene therapy applicable in the near future. Herein, we summarize the primary gene therapy strategies employed over past years, provide an overview of the recent achievements in preclinical studies for genetic hearing loss, and outline the current key obstacles to cochlear gene therapy.
Objective: Persistent postural-perceptual dizziness (PPPD) is a syndrome described as secondary, when it is the consequence of an organic disorder (s-PPPD), or primary, when no somatic triggers can be identified. We evaluated a group of patients diagnosed as s-PPPD, with Benign Positional Paroxysmal Vertigo (BPPV) as the main somatic trigger, with the aim of identifying the predictive clinical elements of evolution towards PPPD.
Study design: Retrospective case review.
Setting: Tertiary referral center.
Patients: We evaluated 126 patients diagnosed with PPPD; 54 patients were classified as p-PPPD (43%) and 72 as s-PPPD (57%). Of these, 51 patients had BPPV as a somatic trigger of PPPD, and in this group, we evaluated the prevalence of some clinical features (age, sex, latency between the onset of BPPV and the final diagnosis, recurrence of BPPV and the presence of migraine headache) for comparison with a group of patients who suffered from BPPV without an evolution towards PPPD (control group).
Results: In the group with PPPD secondary to BPPV, we found a significantly higher mean age and a longer latency between the onset of BPPV and the final diagnosis compared to the control group. No difference between the two groups was found regarding sex, recurrence rate and the presence of migraine headache.
Conclusions: The parameters most involved as potential precipitants of PPPD after BPPV were the age of the patients and a long latency between the onset of BPPV and the final diagnosis; the mean age of the subjects who developed PPPD following BPPV was significantly higher. These findings lead us to emphasize the importance of the early identification and treatment of BPPV, especially in older patients.
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