Extreme Hyperpneumatization of the Skull Base and C-Spine Associated with Meningitis: Mechanisms and Management

Introduction: Skull base pneumatization varies widely across populations, and patterns of air cell development are unique to each individual, originating from both sinonasal and temporal bone sources. “Hyperpneumatization” of the skull base is seen with some frequency in clinical practice, yet its precise incidence is not well known, perhaps due to lack of uniformity of definition. Specific causes of hyperpneumatization are also not known, but in published case reports and series, it has been theorized that hyperpneumatization of the temporal bone may occur as a result of increased pressures from the middle ear; it seems also likely that certain sinonasal conditions may similarly predispose to hyperpneumatization of the sinuses and anterior skull base. We present a rare case of a patient with “extreme hyperpneumatization” of the skull base, including the temporal bone, sphenoid bone, occipital bone and condyle, the majority of foramen magnum, and the C1 cervical vertebrae, who presented with clinical signs of meningitis. Mechanisms of hyperpneumatization and associated risk of meningitis will be discussed, along with literature review and recommendations for diagnosis and treatment. Implications for avoidance of long-term complications including future meningitis, CSF leakage, and fracture or instability of the craniocervical junction will also be presented.

Case: A 54-year-old female with a history of asthma, aspirin sensitivity, and chronic rhinosinusitis/nasal polyposis presented with nausea, diplopia, imbalance, and progressive somnolence over 7 to 10 days. She was confused, having difficulty finding her words, and slurring her speech. She had a history of two prior endoscopic sinus surgeries for extensive polyposis. She also reported a habit of frequent, vigorous, high-pressure nose blowing. Physical exam did not reveal photophobia or specific cranial neuropathy, but her cognition, memory and balance were severely disturbed. The clinical impression was that this patient likely had early meningitis. Imaging showed chronic inflammatory-polypoid changes throughout the paranasal sinuses, with absence of bone of the posterior sphenoid sinus and clivus. There was “extreme” hyperpneumatization of the clivus, temporal bone, occipital bone (including the condyle and much of the circumference of foramen magnum), and the right lateral C1 vertebra, notably with both intra- and extradural air at the craniocervical junction (See images). Initial management focused on medical therapy for the meningitis, and the patient responded to intravenous antibiotics, fully returning to her baseline mental, neurological, and functional status within a few days. She was discharged on day 6, and IV antibiotics were continued for 6 weeks. Surgical management 8 weeks later included revision bilateral maxillary, ethmoid, frontal and sphenoid sinusotomies, and placement of right tympanostomy tube. The patient has been clinically well since completing treatment, but we believe that there is clearly significant risk for future complications of this extreme hyperpneumatization. These risks include future meningitis and CSF leakage from dural exposure, and fracture or instability at the craniocervical junction due to fragile osseous structures. Strategies designed to limit these risks, and multidisciplinary evaluation and treatment options, will be discussed.

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No conflict of interest has been declared by the author(s).