Skull base syndromes are caused by malignancies or inflammatory conditions that affect the base of the skull and the cranial nerves exiting the skull. The location of the pathology can often be determined by characteristic features produced by nerve damage and other localizing space-occupying effects (e.g., pain, proptosis). Syndromes primarily involving the cranial nerves are discussed in a separate article (see ).
- Etiology: damage to the orbital fissure or the optic canal resulting from an inflammatory condition or space-occupying lesion
- Clinical features
- Swelling of the conjunctiva
Signs of CN palsy due to compression (CN III, IV, V-1, V-2, and VI pass through the cavernous sinus)
- Painful ophthalmoplegia: partial/complete paresis of oculomotor nerve (CN III), trochlear nerve (CN IV), and abducens nerve (CN VI)
- Absent corneal reflex: paresis of the ophthalmic branch of the trigeminal nerve (V1)
- Loss of upper facial and corneal sensation may occur due to damage to the trigeminal branches of V1 and V2 (see ““).
- Etiology: complication of otitis media and mastoiditis that spreads to the petrous apex of the temporal bone, can also be tumor growth in the same area
- Clinical features: typical triad
- Diagnostics: MRI to localize lesion, culture of middle ear effusion to determine pathogen
- Treatment: Broad spectrum IV antibiotics (eventually tailored to culture results); surgery for refractory or complicated cases despite medical therapy
- Etiology: inflammation or tumor growth at the base of the skull (e.g., nasopharyngeal cancer) which infiltrates the caudal cranial nerves (see “ “)
- Clinical features: unilateral paresis of the trigeminal (sensory and motor), facial, vestibulocochlear, glossopharyngeal, vagus, accessory, and hypoglossal nerves (see “ “)