Now rare postinfectious syndrome caused by the extension of a middle ear infection to the petrous apex with abducens palsy.

Guiseppe Conte Gradenigo, an Italian Otolaryngologist (1859-1926), described this syndrome in 1904.

Incidence has widely decreased since the development of antibiotics.

No genetic inheritance.

Caused by extension of an infection of the middle ear, mastoid sinus, or both to the petrous apex that occurs because of extensive pneumatization and the presence of bone marrow. The proximity of the venous sinuses to the petrous apex is the reason for the historically high incidence of venous sinus thrombosis associated with petrous apicitis. Petrous apicitis is believed to result when organisms, typically pseudomonas, become trapped within the complex air cell system of the petrous apex. Blockage of this air cell system may result from acute or chronic inflammation or from mechanical blockage by an obstructing lesion. The inflammation may extend into the Dorello canal, which contains cranial nerve (CN) VI and the Gasserian ganglion (CN V). Inflammation of the canal produces the triad of symptoms recognized by Gradenigo: lateral rectus (CN VI) palsy, retroorbital pain, and otorrhea.

Based on the clinical findings of a coexisting ear infection and ipsilateral paralysis of the abducens nerve and otorrhea. Severe pain in the area supplied by the ophthalmic branch of the trigeminal nerve is generally associated. The MRI can show focal enhancement of the meninges over the petrous apex and extension of the infection into Meckel cave (the cavity that harbors the trigeminal ganglion).

Pain is typically severe, centered within the ear, burning or throbbing, worse at night, aggravated by jaw movement, pressure over the tragus, and traction upon the auricle. Pain can be observed simultaneously in the frontal and parietal regions. In the largest series of patients with petrous apicitis, the most common presenting symptoms were hearing loss in 60% of patients, deep pain (50%), CN VIII involvement (50%), CN VI involvement and meningitis (25%), facial paralysis (25%), CN IX palsy (15%), and CN X palsy (15%). Other features include excessive lacrimation, fever, and reduced corneal sensitivity. Extension of the inflammatory process can involve palsy of CN II through X, Horner syndrome. Thrombosis of the venous sinuses, hemorrhage of the carotid artery, and meningoencephalitis are the most serious complications. Before the introduction of antibiotics, mortality rate was greater than 50%.

Evaluate neurologic function and review history (clinical, history, CT, MRI).

Avoid all intranasal probes because of infection. Since jaw movement may exacerbate pain, mouth opening may be limited in the awake state, but is expected to normalize once anesthesia has been induced.

Avoid nitrous oxide because of its effect on pneumatized spaces that may result in increased pain.

Chole RA, Donald ...

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