Other noteworthy causes of pulsatile tinnitus are pseudotumor cerebri or raised intracranial pressure of any type, in which the noise is attributed to a pressure gradient between the cranial and cervical venous structures and the resulting venous turbulence; thyroid enlargement with increased venous blood flow. Other causes include intracranial aneurysm; aortic stenosis; and vascular tumors of the skull, such as histiocytosis X. In the case of a vascular tumor or a large arteriovenous malformation, the examiner may hear the bruit over the mastoid process. Obliteration of the sound by gentle compression of the jugular vein on the symptomatic side is a useful indicator of a venous origin. It has been suggested that diseases that raise the cardiac output markedly (such as severe anemia) may cause pulsatile tinnitus. A flow-related carotid bruit—originating from fibromuscular dysplasia, atherosclerotic stenosis, carotid dissection, and enhanced blood flow in a vessel contralateral to a carotid occlusion—has also been incriminated. However, carotid artery stenosis infrequently causes a self-audible bruit. The same holds for diseases of the vertebral artery. In 100 consecutive cases of pulsatile tinnitus collected by Sismanis and Smoker, the most common causes were intracranial hypertension, glomus tumors, and carotid disease. One must be cautious in overinterpreting this symptom, because normal persons can hear their pulse when lying with one ear on a pillow, and introspective individuals may become excessively worried about it. We have suggested that normal variations in the size and location of the jugular bulb may explain some benign cases (Adler and Ropper).
Another type of tinnitus is the rhythmic clicking of palatal myoclonus caused by intermittent contraction of the tensor tympani or stapedius muscles, termed middle ear myoclonus as discussed in Chap. 4 with other forms of tremor. This process has been treated with a variety of medications, including diazepam or, in extremely annoying cases, by section of the offending muscles (Badia et al). Clicking noises caused by palatal myoclonus have also been successfully treated by the injection of botulinum toxin into the soft palatal tissues (Jamieson et al).
In the unusual process of superior canal dehiscence (Llyod Minor syndrome) there are odd auditory experiences including enhanced sensitivity to one’s own voice (autophony) and heart sounds, and vertigo induced by sound (Tullio phenomenon). This condition is discussed further on.
This is the common persistent form of tinnitus that arises in the middle or inner ear and is associated in a proportion of patients with cochlear damage. For this reason, the first step in analysis after the clinical examination is an audiogram. Under ideal acoustic circumstances (in a soundproof room having an ambient noise level of 18 dB or less), slight tinnitus is present in 80 to 90 percent of adults (“physiologic tinnitus”). The ambient noise level in ordinary living conditions usually exceeds 35 dB and is of sufficient intensity to mask physiologic tinnitus. Tinnitus because of disease of the middle ear and auditory neural mechanisms may also be masked by environmental noise and hence becomes troublesome only in quiet surroundings—at night, in the country, etc.