Complete oculomotor nerve injury is characterized by ptosis and diplopia, a divergence of the globes with the affected eye resting in an abducted and slightly depressed position, loss of medial and most of the vertical movements of the eye, and a fixed, dilated pupil, as described in Chap. 12. The most common symptom is diplopia that is worse on looking down and compensatory tilting of the head indicating a trochlear nerve injury. In a series of 60 patients with head injury, Lepore confirmed that fourth-nerve palsy was the most common cause of diplopia, occurring unilaterally twice as often as bilaterally, followed in frequency by damage to one or both third nerves, then, least often, unilateral or bilateral sixth-nerve palsy. Five of his patients had palsies that reflected damage to more than one nerve and seven had supranuclear disorders of convergence. The long, circumferential subarachnoid course of the fourth nerve is usually given as the explanation for its frequent injury, but this mechanism has never been validated. These optic and ocular motor nerve disorders must be distinguished from those caused by displacement of the globe or entrapment of an extraocular muscle as a result of direct injury to the orbit.
Injury to the ophthalmic and maxillary divisions of the trigeminal nerve may be the result of either a basal fracture across the middle cranial fossa or a direct extracranial injury to the branches of the nerves. Numbness and paresthesia of the skin supplied by the nerve branch or chronic neuralgia can be troublesome sequelae of these injuries.
The facial nerve may be involved in one of two ways. In the first type of injury, associated with transverse fractures through the petrous bone, there is an immediate facial palsy, probably caused by contusion or transection of the nerve. Surgical anastomosis has sometimes been successful in restoring function in this circumstance. The second, more common type, is associated with longitudinal fractures of the petrous bone, the facial palsy then often being delayed for several days, a sequence that may be misinterpreted as progression of the intracranial traumatic lesion. This latter type is usually transitory, and its mechanism is not known.
Injury to the eighth cranial nerve because of petrous fractures results in a loss of hearing or in postural vertigo and nystagmus coming on immediately after the trauma. Deafness as a result of nerve injury must be distinguished from the high-tone hearing loss due to cochlear injury and from deafness caused by bleeding into the middle ear and disruption of the ossicular chain (conduction deafness). Also, vertigo must be distinguished from the very common symptom of posttraumatic dizziness discussed in a later section. The rare condition of fracture through the hypoglossal canal causes weakness of one side of the tongue. It should be kept in mind that blows to the upper neck may also cause lower cranial-nerve palsies, either by direct injury to their peripheral extensions or as a result of carotid artery dissection in the cervical segment of the artery.