Twelve pairs of cranial nerves (CNs) emerge from the brain and radiate from its surface. CN injuries occur before, during, or after passing through the skull from compression secondary to increased intracranial pressure, traction, transection, ischemic event, acceleration–deceleration injury, shearing, skull fracture, intracranial hemorrhage, vascular occlusion, or brainstem herniation ( Table 27.1 ). CN injuries are a relatively common complication of traumatic brain injury (TBI), but their incidence is difficult to estimate, and they have been shown to occur in mild to severe TBI. CN injury diagnosis is often based on physical examination, which may initially be complicated by the patient’s mental status. A complete CN examination is necessary to assess for CN injury during recovery from TBI. The CNs most susceptible to injury in TBI are CN I followed by CN VII and CN VIII. Trigeminal (CN V) and lower CN (CN IX–XII) injuries are rare.
| CN | Examination | Diagnostic Evaluation |
|---|---|---|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
| |
|
| |
|
|
|
Olfactory (CN I)
- •
Olfactory stimuli are detected by specialized chemoreceptors on bipolar primary sensory neurons of the olfactory nerve.
- •
Axons of these bipolar neurons travel via short olfactory nerves that traverse the cribriform plate of the ethmoid bone to synapse in the olfactory bulbs.
- •
From the olfactory bulbs, sensory information travels via olfactory tracts that communicate with the brain through the olfactory processing areas.
- •
Injury occurs from direct bony disruption, from olfactory bulb compression, or from a rapid shift in the position of the brain relative to the skull base, shearing the fixed olfactory receptor axons from the mobile olfactory bulb.
- •
Higher incidences of olfactory injury are associated with increased TBI severity, with anosmia in 25% to 30%, 15% to 19%, and 0% to 16% of patients with severe, moderate, and mild head injuries, respectively.
- •
Injury to the olfactory nerve is the only CN injury commonly associated with mild TBI.
- •
No treatments are available for CN I injury, and reversible confounding diagnoses—including nasal obstruction, polyps, injury to the nasal passages, rhinitis, sinusitis, medications, and seizures—should be identified and managed.
- •
Alterations in the sense of smell may also alter the sense of taste, which can result in anorexia.
- •
Inability to detect spoiled food and gas leakage are the two predominant adverse effects involving personal safety.
- •
Approximately one-third of patients may experience some degree of spontaneous recovery, which usually occurs within 6 to 12 months after injury.
Optic (CN II)
- •
The optic nerve provides the special sense of sight.
- •
It transmits visual information from the retina to the thalamus and then to the extrageniculate pathways.
- •
The reported incidence of optic nerve injury is 0.7% to 2.5%.
- •
Sphenoid bone fracture or optic nerve compression can result in unilateral blindness. Optic chiasm insults can lead to bitemporal hemianopsia.
- •
Treatment options include (1) systemic steroids, (2) surgical decompression of the optic canal, (3) combination of steroids and surgery, and (4) observation alone.
- •
A visual recovery rate of 40% to 60% has been reported, with baseline visual acuity being an important predictor of final outcome. Negative predictors of vision recovery include presence of blood in the posterior ethmoidal cells, age above 40 years, loss of consciousness, and absence of recovery after 48 hours of steroid treatment. ,
Oculomotor (CN III)
- •
The oculomotor nerve supplies somatic motor innervation to the levator palpebrae superior; superior, medial, and inferior rectus; and inferior oblique.
- •
CN III provides parasympathetic nerve fibers that innervate the sphincter muscle of the iris and the ciliary muscle, which controls the shape of the lens during accommodation.
- •
A complete oculomotor nerve palsy will result in exotropia with a characteristic down-and-out position in the affected eye, ptosis, and mydriasis ( Fig. 27.1 ).
• Fig. 27.1
Examination findings for isolated cranial nerve III, IV, and VI palsies.
- •
This nerve is often injured at the point of exit through the dura or from compression caused by uncal herniation related to increased intracranial pressure ( Fig. 27.2 ).
