Delayed sudden hearing recovery after treatment of a large vertebral artery aneurysm causing hearing loss and imbalance: a case report.

PURPOSE: Cerebral aneurysms that compress cranial nerve VIII can cause hearing loss and imbalance. Hearing function that does not recover after aneurysm occlusion can signal neurological damage with the potential for permanent deafness. CASE DESCRIPTION: A 72-year-old woman presented with gradually worsening left-sided hearing loss and imbalance over a period of 10 years. She was found to have a lesion of the cerebellopontine angle, which proved to be a large fusiform vertebral artery aneurysm with mass effect on cranial nerve VIII. The patient underwent surgical clip occlusion of the vertebral artery distal to the posterior inferior cerebellar artery and proximal to the aneurysm, which no longer filled on catheter angiography. Postoperatively, the patient experienced delayed complete loss of ipsilateral hearing on the third post-operative day. Otherwise, she made a good recovery with improvement in her balance issues. At that time, we suspected that delayed occlusion of a perforating vessel had probably caused irreversible hearing loss. Ten months later, the patient awoke with significant subjective recovery of her hearing. Audiometry confirmed substantial improvement in her hearing likely due to the aneurysm shrinking away from and decompressing the cranial nerve. CONCLUSION: This case highlights the continued usefulness of vascular occlusion in the management of selected cases of intracranial aneurysms and also that neurological function may recover suddenly, even in very delayed fashion, following treatment.

Enhancement of alcohol aversion by the nicotinic acetylcholine receptor drug sazetidine-A.

The prevalence of alcohol use disorders (AUDs) has steadily increased in the United States over the last 30 years. Alcohol acts on multiple receptor systems including the nicotinic acetylcholine receptors (nAChRs), which are known to mediate alcohol consumption and reward. We previously reported that the preclinical drug sazetidine-A, a nAChR agonist and desensitizer, reduces alcohol consumption without affecting nicotine consumption in C57BL/6J mice. Here, we found that sazetidine-A enhances the expression of alcohol aversion without affecting the expression or acquisition of conditioned alcohol reward in C57BL/6J mice. Microinjection of sazetidine-A into the ventral midbrain targeting the ventral tegmental area (VTA) reduced binge alcohol consumption, implicating this region in mediating the effects of sazetidine-A. Furthermore, the sazetidine-A-induced reduction in alcohol consumption was mediated by non-α4 containing nAChRs, as sazetidine-A reduced binge alcohol consumption in both α4 knock-out and wild-type mice. Finally, we found that in mice pretreated with sazetidine-A, alcohol induced Fos transcript in Th-, but not Gad2-expressing neurons in the VTA as measured by increased Fos transcript expression. In summary, we find that sazetidine-A enhances the expression of alcohol aversion, which may underlie the reduction in alcohol consumption induced by sazetidine-A. Elucidating the identity of non-α4 nAChRs in alcohol aversion mechanisms will provide a better understanding the complex role of nAChRs in alcohol addiction and potentially reveal novel drug targets to treat AUDs.

Unequal interactions between alcohol and nicotine co-consumption: suppression and enhancement of concurrent drug intake.

RATIONALE: Alcohol and nicotine addiction are prevalent conditions that co-occur. Despite the prevalence of co-use, factors that influence the suppression and enhancement of concurrent alcohol and nicotine intake are largely unknown. OBJECTIVES: Our goals were to assess how nicotine abstinence and availability influenced concurrent alcohol consumption and to determine the impact of quinine adulteration of alcohol on aversion-resistant alcohol consumption and concurrent nicotine consumption. METHODS: Male and female C57BL/6J mice voluntarily consumed unsweetened alcohol, nicotine, and water in a chronic 3-bottle choice procedure. In experiment 1, nicotine access was removed for 1 week and re-introduced the following week, while the alcohol and water bottles remained available at all times. In experiment 2, quinine (100-1000 µM) was added to the 20% alcohol bottle, while the nicotine and water bottles remained unaltered. RESULTS: In experiment 1, we found that alcohol consumption and preference were unaffected by the presence or absence of nicotine access in both male and female mice. In experiment 2a, we found that quinine temporarily suppressed alcohol intake and enhanced concurrent nicotine, but not water, preference in both male and female mice. In experiment 2b, chronic quinine suppression of alcohol intake increased nicotine consumption and preference in female mice without affecting water preference, whereas it increased water and nicotine preference in male mice. CONCLUSIONS: Quinine suppression of alcohol consumption enhanced the preference for concurrent nicotine preference in male and female mice, suggesting that mice compensate for the quinine adulteration of alcohol by increasing their nicotine preference.

Differential patterns of alcohol and nicotine intake: Combined alcohol and nicotine binge consumption behaviors in mice.

Late adolescence and young adulthood, corresponding to the high school and college years, are vulnerable periods for increased alcohol and nicotine use. The dramatic increase in the prevalence of electronic cigarette use is particularly concerning in these age groups. Late adolescents and young adults are more likely to engage in cycles of binge drug consumption, and alcohol and nicotine are frequently used together. However, there are few data examining the combination of alcohol and nicotine in binge models in animal models. In this study, our objectives were to determine how voluntary nicotine consumption beginning in late adolescence influenced subsequent binge alcohol consumption in young adulthood, how a combination of alcohol and nicotine binge consumption differed from alcohol-only binge consumption, and whether nicotine would be consumed when presented in a binge procedure. Male C57BL/6J mice voluntarily consumed unsweetened alcohol and nicotine in continuous-access bottle-choice procedures in combination with cycles of drinking-in-the-dark. Our results show that experience with voluntary nicotine consumption in late adolescence did not affect subsequent binge alcohol consumption in early adulthood. However, mice that consumed nicotine in adolescence showed an initial decrease in alcohol preference, and consequently increase in nicotine preference, on the first session of combined ethanol and nicotine binge consumption in adulthood compared with mice that drank only water during late adolescence. Lastly, we found that mice readily consumed unsweetened nicotine when presented in a binge procedure, and the level of consumption exceeded the nicotine consumption observed in the combination alcohol and nicotine binge. Our data show that expansion of the patterns of alcohol and nicotine co-consumption in a mouse models is possible, which will enable us to dissect relevant molecular targets underlying these consumption patterns and better inform drug development efforts.