Sound waves reach the outer ear and are conducted down the ear canal to the eardrum, causing it to vibrate. The vibrations are transferred by the 3 tiny ear bones of the middle ear to the fluid in the inner ear. The fluid moves hair cells (stereocilia), and their movement generates nerve impulses which are then taken to the brain by the cochlear nerve. The auditory nerve takes the impulses to the brainstem, which sends the impulses to the midbrain. Finally, the signal goes to the auditory cortex of the temporal lobe to be interpreted as sound.
▶ For most inner ear problems, a sodium-restricted, caffeine-free diet is recommended. Caffeine is a central nervous system stimulant and its intake makes the symptoms of inner ear disorder (especially headache and dizziness) appear more pronounced. Hence, it is advisable to reduce the intake of caffeine as much as possible till the condition is completely treated. Excess sugar in the diet also triggers dizziness.
Shockwave therapy is the only current treatment on the horizon for ED that might offer a cure, which is the most desired outcome for men with ED. Shockwave therapy has also been suggested to improve the effect of pill therapy in nonresponders, reducing the need for more invasive treatments. Several single-arm trials have shown the benefit of shockwave therapy on patient-reported erectile function scores. Data from randomized trials appear to be conflicting, however, so questions remain to be answered before this therapy can routinely be offered to people.
TTTS was originally described by Dr I. Klockhoff (9-12), and has been proposed by Patuzzi, Milhinch and Doyle (13) and Patuzzi (7) as the neurophysiological mechanism causing most of the persistent ASD symptoms. TTTS is an involuntary condition where the centrally mediated reflex threshold for tensor tympani muscle activity becomes reduced as a result of anxiety and trauma, so it is continually and rhythmically contracting and relaxing, aggravated by intolerable sound exposure1. This appears to initiate a cascade of physiological reactions in and around the ear, which can include: tympanic membrane flutter; alterations in ventilation of the middle ear cavity leading to a sense of blockage or fullness, as well as muffled/echoey/distorted hearing; irritation of the trigeminal nerve innervating the tensor tympani muscle, leading to frequent neuralgic pain; and symptoms consistent with temporomandibular disorder (TMD).
Various theories about the pathophysiology of acoustic shock have been proposed.2–4,6,7 One popular theory is that the symptoms are caused by tonic tensor tympani syndrome2,3: the initial response after an acoustic incident is thought to be an exaggerated startle response with contraction of the tensor tympani muscle in addition to the normal acoustic protection provided by the stapedial reflex. Continued contraction of the tensor tympani muscle then generates many of the symptoms of acoustic shock including aural pain and fullness, tinnitus, vertigo and distortion of hearing. Although this model has many proponents there is as yet no robust scientific support. Cochlear damage has been suggested as a mechanism but the absence of sensorineural hearing loss in many cases militates against this theory.