British Journal of Radiology (2005) 78, 948-951
© 2005 British Institute of Radiology
doi: 10.1259/bjr/71475327
CT, MRI and gallium SPECT in the diagnosis and treatment of petrous apicitis presenting as multiple cranial neuropathies
Y H Lee, MD1,
N J Lee, MD1,
J H Kim, MD1 and
J J Song, MD2
Department of 1 Radiology and 2 Otorhinolaryngology, Head and Neck Surgery, Korea University College of Medicine, Seoul, Korea
Correspondence: Nam Joon Lee, Departments of Radiology, Anam Hospital, Korea University College of Medicine, 126-1 Anamdong 5-Ga, Sungbuk-Gu, Seoul, 136-705, Republic of Korea
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Abstract
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We present a rare case of petrous apicitis initiated by middle ear inflammation in a diabetic patient with multiple cranial neuropathies for early diagnosis of this potentially life-threatening condition. The lesion appeared as opacification of middle ear, petrous apex with aggressive bony destruction on CT and diffuse petrosal T1 hypointensity with adjacent soft tissue propagation on MRI. Gallium-67 single-photon emission computed tomography (SPECT) scan also contributed to evaluate response to therapy.
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Introduction
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Petrous apicitis is defined as the spread of middle ear inflammation to the petrous apex of temporal bone, resulting in localized osteomyelitis and reactive meningitis. Its incidence has greatly decreased since the 1940s with the widespread use of antibiotics for the treatment of acute otitis media [1]. However, petrous apicitis continues to occur rarely, and is often recognized late owing to the subtlety of its sign and symptoms [2]. To our knowledge, although MRI and CT scans are considered more diagnostic than non-specific clinical findings of petrous apicitis, there are a few published cases that describe its CT and MRI findings [3–9]. We therefore present CT, MRI and gallium-67 scan findings as well as clinical features on the diagnosis and treatment of petrous apicitis.
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Case report
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A 62-year-old diabetic man presented with hoarseness, decreased sensation of right face and difficulty in swallowing following a 1 month history of headache, but no meningeal signs. He had undergone right mastoidectomy for chronic otomastoiditis 4 months before the onset of symptoms and Pseudomonas aeruginosa was isolated in the culture of a sample from the mastoidectomy. He did not have otorrhoea, otalgia or dizziness at admission. He had an intact grafted tympanic membrane. On examination, he was found to have palsies of the right vocal cord and soft palate with decreased right facial sensation. His ocular movement was normal. His temperature was 36.5°C. Laboratory tests showed his white blood cells count to be 19 190 mm–3 with 85% neutrophil. C-reactive protein was 44.9 mg l–1 and erythrocyte sedimentation rate (ESR) was 120 mm h–1. Lumbar puncture revealed no leukocytosis and no malignant cells in the cerebrospinal fluid. He underwent high-resolution temporal bone CT, MRI and gallium-67 SPECT.
Temporal bone CT scans revealed opacification of right temporal mastoid air cells and middle ear cavity (Figure 1
). Furthermore, the bony erosion was demonstrated along the cortical bone surrounding the petrosal pyramid and skull base in addition to complete destruction of the mandibular condyle. MRI of the head confirmed inflammatory change of the right petrous apex by T1 hypointense and T2 hyperintense marrow lesion replacing normal fatty marrow with enhancement when intravenous gadolinium was administered (Figure 2). They also extended beyond the confines of petrous bone to ipsilateral masticator space, skull base and temporomandibular joint. However, serious intracranial complications, such as cavernous or dural sinus thrombosis or meningoencephalitis, did not occur in this patient. Gallium-67 SPECT demonstrated intense focal uptake in the petrous ridge, indicating the presence of an inflammatory process (Figure 3a).
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Figure 1. (a) Axial, (b, c) coronal CT images (bone window) reveal opacification of air cells in right mastoid, middle ear cavity and petrous apex. Bony erosion was demonstrated along the cortex surrounding the petrosal pyramid (arrowheads) and occipital condyle (straight arrows) with widened petroclival fissure (asterisk). Note collapsed right mandibular condyle with destruction (curved arrow).
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Figure 2. (a, b) T1 weighted images, (c) T2 weighted image, (d) enhanced T1 weighted image. Serial MR images show T1 low and T2 high signal intensity lesions involving the right petrous (arrowheads), occipital clivus (small straight arrows), mandibular condyle (curved arrow) and masticator space (large straight arrows) with strong enhancement to opacified mastoid air cells.
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Figure 3. (a) Gallium-67 scan at admission, (b) follow-up scan: initial scan demonstrates intense uptake in right petrous ridge and mastoid, indicating acute inflammation. Decreased uptake is noted in follow-up scan after 3 months of antibiotic treatment.
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The diagnosis of petrous apicitis was suspected and the patient was treated with intravenous and oral antibiotics for 3 months and discharged from the hospital with prescribed antibiotics. Most of his symptoms had completely resolved after treatment and post-therapy gallium-67 SPECT demonstrated the decreased tracer uptake as compared with the initial scan (Figure 3b
).
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Discussion
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The petrous portion of the temporal bone is a truncated pyramid with a base formed by the mastoid and middle ear. Several longitudinally arranged air cells and venous channels within the petrous apex, which communicate with the middle ear cleft, have been considered to be a route for the spread of infection from the middle ear to the petrous apex leading to petrous apicitis and otogenic cavernous sinus thrombophlebitis [10, 11].
Petrous apicitis was a common life-threatening complication of middle ear infection until the 1940s, but became a rare disease with changes in the clinical presentation following the widespread use of antibiotics [2]. In 1907, Gradenigo [3] first described the classic syndrome consisting of abducens nerve paresis or paralysis, severe pain in the distribution of the trigeminal nerve and otorrhoea, which he attributed to petrous apicitis. The actual pathological mechanism of the symptom triad is considered local pachymeningitis secondary to the petrous apicitis because the trigeminal ganglion and abducens nerve lie close to the petrous apex, only separated by dura mater and easily engulfed by the inflammatory spread [3]. However, most cases do not present with the classic triad of Gradenigo's syndrome, probably due to extradural inflammation at the petrous tip because antibiotics usually stop the disease prior to the dural involvement. Patients may show other cranial nerve (II to X) involvement depending on the severity and extent of the infection within the petrous apex and its surrounding area, such as the skull base or cavernous sinus [2]. Certain groups of patients are more susceptible to developing this condition. They include: diabetics, those on high dose steroids and immunosuppresed patients with HIV infection. Therefore CT and MRI have been considered more diagnostic than the condition's subtle and non-specific presentations owing to widespread use of antibiotics [2].
Both CT and MRI scans have been recognized as the principal methods of investigation for the skull base and help to differentiate petrous apicitis from other non-infectious entities that involve the petrous apex [3–9]. While CT scans may demonstrate opacification of the air cells of the petrous apex with cortical bone erosion, MRI scans are very useful for assessing inflammatory soft tissue lesions around the petrous apex, especially the infratemporal fossa, on account of its superior soft tissue discrimination. Early marrow change of bone can be easily found on MRI prior to the destruction. They manifest as hypointense on T1 weighted and hyperintense/hypointense on T2 weighted images and are enhanced by Gd-DTPA. Our patient presented with headache, and multiple cranial neuropathies affecting the fifth, ninth and tenth cranial nerves and showed petrosal, clival and infratemporal fossa abnormalities on MR images, best appreciated on T1 weighted images.
Differential diagnostic possibilities include neoplastic process such as squamous cell carcinoma of head and neck with skull base extension, lymphoma or metastasis, but more focal destructive change with identifiable mass is usually observed in squamous cell carcinoma. Lymphoma or metastasis, however, can reveal similar appearances involving the bone marrow cavity with soft tissue extension, but elevation of ESR never occurs in the setting of neoplastic process. Several other processes, including inflammatory pseudotumour and other granulomatous diseases such as tuberculosis and sarcoidosis could occasionally show similar findings to petrous apicitis and must be included in differential diagnosis.
At times, gallium-67 scanning not only improves the sensitivity for detecting abnormalities in the skull base, but also allows a marker for disease activity and response to treatment [12]. Furthermore, it has been reported to be more useful for monitoring clinical resolution of successfully treated cranial osteomyelitis than bone scan, CT and MRI because abnormalities take several months to return to normal [13–15]. In our experience, serial gallium scans reflected the clinical disease activity with the degree of tracer uptake at initial diagnosis and after antibiotic treatment.
In conclusion, petrous apicitis must be considered in the setting of middle ear disease with headache, cranial neuropathy and an elevated ESR. Characteristic MR findings of petrous apicitis including petrosal marrow T1 hypointensity, soft tissue abnormalities with enhancement as well as obvious bone destruction on CT are essential in confirming this diagnosis and gallium scan provides a useful marker for disease activity and response to treatment.
Received for publication February 3, 2005.
Revision received April 6, 2005.
Accepted for publication April 15, 2005.
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Abstract
Introduction
