Otoscopic examination revealed normal-appearing external auditory canals, intact tympanic membranes bilaterally, and normal middle ear anatomy. Audiogram at that time showed bilateral profound hearing loss with no responses to pure-tone or speech testing. Treatment
Auditory perception can improve with time. There seems to be a level of neuroplasticity that allows patients to recover the ability to perceive environmental and certain musical sounds. Patients presenting with cortical hearing loss and no other associated symptoms recover to a variable degree, depending on the size and type of the cerebral lesion. Patients whose symptoms include both motor deficits and aphasias often have larger lesions with an associated poorer prognosis in regard to functional status and recovery.Cochlear or auditory brainstem implantation could also be treatment options. Electrical stimulation of the peripheral auditory system may result in improved sound perception or cortical remapping in patients with cortical deafness. However, hearing aids are an inappropriate answer for cases like these. Any auditory signal, regardless if has been amplified to normal or high intensities, is useless to a system unable to complete its processing. Ideally, patients should be directed toward resources to aid them in lip-reading, learning American Sign Language, as well as speech and occupational therapy. Patients should follow-up regularly to evaluate for any long-term recovery. History
Early reports, published in the late 19th century, describe patients with acute onset of deafness after experiencing symptoms described as apoplexy. The only means of definitive diagnosis in these reports were postmortem dissections.
β1-selectivity
Bisoprolol β1-selectivity is especially important in comparison to other nonselective beta blockers. The effects of the drug are limited to areas containing β1 adrenoreceptors, which is mainly the heart and part of the kidney. Bisoprolol, whilst β1 adrenoceptor selective can help patients to avoid certain side-effects associated with non-selective beta-blocker activity at additional adrenoceptors (α1 and β2), it does not signify its superiority in treating beta-blocker indicated cardiac conditions such as heart failure but could prove beneficial to patients with specific comorbidities.Bisoprolol has a higher degree of β1-selectivity compared to atenolol, metoprolol and betaxolol. With a selectivity ranging from being 11-15 times more selective for β1over β2  However nebivolol is approximately 3.5 times more β1-selective. Renin-angiotensin system
Bisoprolol inhibits renin secretion by about 65% and tachycardia by about 30%. Pharmacokinetics
After ingestion, bisoprolol is absorbed and has a high bioavailability of approximately 90% with plasma half-life of 10-12 hours. When being eliminated, the body evenly distributes it (50–50) between kidney excretion and liver biotransformation (then excreted).Bisoprolol has both lipid- and water-soluble properties.The plasma protein binding of bisoprolol is approximately 35%, the volume of distribution is 3.5 L/kg and the total clearance is approximately 15 L/h. Bisoprolol is eliminated from the body in two ways - 50% of the substance is converted in the liver to inactive metabolites, which are then excreted in the kidneys. The remaining 50% is eliminated unchanged via the kidneys. Since elimination is equal in liver and kidney, no dose adjustment is required in patients with hepatic or renal impairment.