FLEX January 2024

Review Clinical Review & Education

Diagnostic Approach to Pulsatile Tinnitus

Figure 1. Paraganglioma

Otoscopic view A

Axial CT image B

Coronal CT image C

Left-sided pulsatile tinnitus exacerbated by exercise. A, Otoscopy demonstrates a red retrotympanic mass (black arrowhead). B, Axial temporal bone computed tomographic (CT) scan demonstrates permeative lucency at the cochlear promontory (black arrowhead). Note that the carotid canal is intact. C, Coronal temporal bone CT reformat demonstrates retrotympanic mass (white arrowhead) at the cochlear promontory. D, Axial T1-weighted gradient-echo magnetic resonance imaging (MRI) demonstrates mild T1 signal (white arrowhead) at the expected location of complete signal loss owing to cortical bone. E, Axial T1-weighted gradient-echo MRI with fat saturation after contrast demonstrates an enhancing mass (white arrowhead).

Axial MRI T1-weighted gradient-echo with fat saturation before contrast D

Axial MRI T1-weighted gradient-echo with fat saturation after contrast E

medication can prevent progression prior to hearing loss. Vitamin toxic effects can also cause PT, with the most prominent in our prac tice being hypervitaminosis B6. Otoprotective medications are un der investigation for patients with chemotherapy-induced tinnitus. Pulsatile tinnitus can also result from spasm of 1 or both muscles in the middle ear, namely the tensor tympani (innervated by cranial nerve 5) or stapedius (innervated by cranial nerve 7) muscles, as well as the soft palate (innervated by cranial nerve 9), and this is typi cally described as pulse-asynchronous. Having patients tap out the rhythm of their PT on the table while the examiner measures the pulse is a simple method to determine pulse synchrony. Otoscopy can occasionally demonstrate rhythmic movement of the tym panic membrane, but impedance audiometry is often needed for di agnosis. This myoclonus can occur spontaneously or reflect neuro logic disease. Myoclonus of the palatal muscles that attach to the eustachian tube orifice can also result in clicking noises described as PT. Sometimes myoclonus is owing to a metabolic abnormality such as hypercalcemia. Palatal myoclonus more often reflects an un derlying neurologic disorder, such as multiple sclerosis, brainstem microvascular disease, or metabolic neuropathy. Retrotympanic botulinum toxin injections have been described for symptomatic relief. Systemic conditions like anemia or hyperthyroidism can also cause PT that tends to be high-pitched and related to increased car diac output. These can be diagnosed with blood tests of hemoglo bin levels and thyroid function with appropriate medical treatment depending on the results.

dehiscence often coexists with sigmoid sinus diverticula and intra cranial venous hypertension, often from underlying IIH, and the con tribution or dominance of these anatomic and physiologic abnor malities in causing PT should not be overlooked. We often evaluate patients with any dehiscence for underlying IIH as a cause, depend ing on their presenting symptoms, although 1 study has not dem onstrated an association between SSCD and IIH. 15 Other, less common structural causes of PT include endolym phatic sac tumors (sometimes seen in association with von Hippel Lindau disease), perilymph fistulas, meningoceles of the temporal bone, cholesterol granulomas, otospongiosis, meningiomas, facial nerve hemangiomas, or vascular metastases, particularly of the skull base. Metabolic Causes of PT Nonpulsatile tinnitus with pauses can sometimes masquerade as PT. Metabolic causes of nonpulsatile tinnitus are many; within this large category we sometimes find it difficult to pin down a single entity as the cause of an individual patient’s tinnitus. For example, tinni tus is often caused by ototoxic medications. A comprehensive list of ototoxic medications can be found with the American Tinnitus As sociation. The most common offending agents are antibiotics, such as oral aminoglycosides, and chemotherapeutic agents, such as cis platin. Other common ototoxic medications include ACE inhibi tors, loop diuretics, valproic acid, proton pump inhibitors, benzo diazepines, and antimalarial medications such as quinine and chloroquine. Tinnitus is often an early sign of ototoxicity prior to per manent sensorineural hearing loss; therefore, discontinuing the

(Reprinted) JAMA Otolaryngology–Head & Neck Surgery May 2022 Volume 148, Number 5 479

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