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Author: admin | 12.03.2015 | Category: Relieve Tinnitus

Glomus jugulare are benign tumors arising from neural crest progenitor crest cells (glomus bodies) located in and around the jugular foramen. Paragangliomas can present as multifocal lesions in up to 3-10% of sporadic cases and in 25-50% of familiar cases (a rarer form with autosomal dominant inheritance).
Meningiomas located at the cerebellopontine angle cistern can be a cause of pulsatile tinnitus.
Endolymphatic sac tumors are often initially confused with the much more common paragangliomas as their imaging characteristics are similar. The key to diagnosis is recognition of the epicenter of the lesion along the posterior petrous surface at the level of the vestibular aqueduct.
Certain anatomical vascular variants in the temporal bone are a frequent cause of pulsatile tinnitus and a vascular appearing tympanic membrane. Some anatomical variants or anomalies of the jugular bulb have been related to venous pulsatile tinnitus.
It remains unclear how or why these vascular anomalies cause sudden onset of pulsatile tinnitus. This condition is an uncommon anomaly due to failure of formation of the proximal ICA (C1 segment) in fetal life. Intracranial dural arteriovenous fistulas are recognized as an abnormal channel from the artery(s) to the vein within the dura mater. Arteriovenous fistula of the transverse and sigmoid sinus is most frequently involved in pulsatile tinnitus. On imaging the typical finding is a network of tiny ("crack-like") vessels in the wall of a thrombosed dural venous sinus (figure 11). This appear as an abnormal network of vessels showing arterial flow inside the hypoglossal canal (Figure 13).
The imaging of choice in this clinical setting should be cervical Doppler ultrasound (Figure 14). Some investigators believe that compression of cranial nerve VIII can cause pulsatile tinnitus. It has been postulated that vascular compression of the nerve in the internal auditory canal (Figure 16) results in pusatile tinnitus due to a resonance effect in the petrous bone transmitted to the cochlea. The anterior inferior cerebellar artery often makes a normal redundant loop within the IAC without disrupt the CN VIII. Intracraneal idiopathic hypertension comprises signs and symptoms of increased intracranial pressure without causative mass or hydrocephalus. Otosclerosis(or more appropriately known as otospongiosis) is an idiopathic slowly progressive primary disorder of the bony labirynth. Thin sliced petrous temporal bone CT scans demonstrate replacement of the normally dense middle layer of the bony labyrinth with areas of  “spongy” Haversian bone (Figure 18). Thin-section CT demonstrates the covering defect of the superior semicircular canal (Figure 19).
Tinnitus seems to be related to the intraosseous A-V shunting associated with the pagetic bone.
NPT is most frequently associated with functional injuries from exposure to environmental noise or the toxicity of certain medications. Vestibular schwannoma should be suspected in patients with unilateral persistent non-pulsatile tinnitus and progressive sensorineural hearing loss.
Them should be also aware thattinnitus may persist and even worsen after successful removal of the tumor. Solid component shows intense enhancement after intravenous contrast administration (Figure 21).
Myoclonic contractions of palatal muscles (Palatal myoclonus) may also cause objective tinnitus.
2 clicks for more privacy: On the first click the button will be activated and you can then share the poster with a second click. 8: The right ICA shows a more lateral position than usual, allowing protrusion into the middle ear cavity (arrow). 11: Coronal (A) and sagittal (B) FFE-T1 post Gad MRI nicely show multiple small vessels (arrows) that converge on the wall of the thrombosed right transverse sinus (neoangiogenesis). Coronal FLAIR (A) and axial T2W (B) shows signal voids reflecting anomalous arterial flow in the superior left ophthalmic vein (arrows). The pathologic arterio-venous communication is established between various arterial dural branches and venous vessels inside the left hypoglossal canal. Left hypoglossal canal (red arrow) appears enlarged in comparison, with abnormal flow voids inside. Axial T1WI (C) and postcontrast coronal T1WI (D) show T1 hyperintesity of the mass (*) due to hemorrhagic components and heterogeneous enhancement (arrow).
However, inspection of the analogous location on the left side demonstrates absence of the horizontal carotid canal or internal carotid artery.



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