1. Olfactory Nerve (Cranial Nerve I) - Anosmia (loss of the sense of smell), hyposmia (a decreased sense of smell), parosmia (a perversion of the sense of smell), or cacosmia (awareness of a disagreeable or offensive odor that does not exist) are common following TBI. Many of these patients are unaware of their deficits (Callahan & Hinkebein, 2002)
    • Causes
      • Injury to the neurofibrils
      • Compression of the olfactory bulbs by hemorrhage and edema or contusion and abrasion
      • Injury to the central pathways of olfaction
      • Injury to the nasal passages
      • Scarring or gliosis of the tissues of the cribriform plate, which can cause late cacosmia
      • Non-traumatic causes, such as upper respiratory infections, rhinitis sicca, allergic sinusitis, chronic polyposis, depression, and medications

    • Testing
      • Bedside testing with pure (nonirritant) odors should be performed during early recovery
      • Serial testing should be done in patients with anosmia
      • Quantification tests should be performed in patients at Rancho level V or higher
      • MR imaging frequently reveals abnormalities in the olfactory bulbs and tracts and in the inferior frontal lobes in patients with posttraumatic olfactory dysfunction (Yousem, et al 1996)
      • Olfactory event-related potentials (OERPs) may be useful as an objective tool for measuring sensory and cognitive loss after TBI (Geisler, 1999)
      • University of Pennsylvania Smell Identification Test (UPSIT) (Callahan & Hinkebein, 2002)

    • Recovery
      • Disorders due to olfactory neurofibril or central injury are resistant to treatment
      • Recovery during the first 4 -6 weeks may occur as edema or hematoma resolve, neurofibrils regrow (although scarring and gliosis can interfere with recovery) and there is central adaptation to perceived odor

  2. Optic Nerve (Cranial Nerve II) - Immediate monocular blindness (partial or complete), visual field deficits, blurring, scotomata, and monocular diplopia can occur following TBI
    • Causes
      • Immediate loss of vision is due to injury to the optic nerve due to ischemia or edema (which causes loss of blood supply to the nerve through the small arteries that feed the nerve) or shearing or contusion (which represent direct trauma to the nerve from movement of the contents of the orbit and cranium)
      • Delayed loss of vision is due to infarction of the optic nerve or, less frequently, by hematoma surrounding the nerve
      • Complete monocular blindness is usually due to functional (nonorganic) disorders
      • Blurring and scotomata are due to trauma to the cornea, vitreous tears, traumatically induced cataracts, retinal hemorrhage, retinal detachment, or intrabulbar hemorrhage (Torsion's syndrome)
      • Monocular diplopi is caused by injury to the cornea or contents of the anterior chamber
      • Visual impairment, including blindness, and associated secondary damage to the eye can be caused by intraocular (retinal or vitreous) hemorrhage, which may be related to acute elevation of ICP following TBI. (When associated with subarachnoid hemorrhage, intraocular hemorrhage is known as Terson's syndrome) (Medele, et al 1998)
      • Symptomatic convergence insufficiency following TBI may be due to a subdural hematoma (Spierer, et al 1995)

    • Testing
      • Patrial blindness should be documented immediately and followed closely for deterioration

    • Recovery/Treatment
      • Since axons of the optic nerve do not regenerate, there is no normal recovery from direct trauma. However, visual problems resulting from hemorrhage may improve as the hemorrhage resolves
      • Megadose steroids are of equal or greater benefit than surgical decompression in patients with no light perception and patients with a deterioration of partial visual function
      • Surgical decompression of the nerve may be of benefit in patients with light perception, but should be reserved for patients with:
        • Delayed visual loss who are unresponsive to 12 hours of megadose dexamethasone
        • A decrease in vision when megadose steroids are tapered or discontinued
      • Vitrectomy at 6 months or more postinjury is recommended for Terson's syndrome in cases where there is no tendency for blood resorption (Medele, et al 1998)
      • Surgical evacuation of a subdermal hematoma may result in complete resolution of secondary symptomatic convergence insufficiency (Spierer, et al 1995)
      • Special optics may improve visual field deficits in the affected field
      • Eyeglasses or surgery may improve blurring caused by corneal or lens problems

  3. Oculomotor Nerve (Cranial Nerve III) - Oculomotor nerve palsy, including isolated and bilateral oculomotor nerve palsies
    • Causes - injury to the oculomotor nerve, and possibly an oculomotor blowout

    • Signs
      • Outward and downward deviation of the eye
      • Ptosis of the eyelid
      • Dilation of the ipsilateral pupil in complete palsy

      (Parinaud syndrome - paralysis of upward gaze - is caused by injury to the dorsal midbrain, and not the peripheral oculomotor nerves)

    • Recovery - Return of function may begin within 2-3 months of injury

  4. Trochlear Nerve (Cranial Nerve IV) - Injury to the trochlear nerve can cause vertical diplopia on looking downward which improves with contralateral head tilt and worsens with ipsilateral head tilt

  5. Abducens Nerve (Cranial Nerve VI) - In a complete injury of the abducens nerve, the affected eye is turned medially. In an incomplete injury, the affected eye is seen at midline at rest, but the patient cannot deviate the eye laterally. Isolated sixth-nerve palsy, which can be either unilateral or bilateral, can resolve spontaneously, but the spontaneous recovery rate may be less than anticipated (Mutyala, et al 1996)

         Following TBI, combined injuries of the III, IV and/or V nerves are common and can result in the loss of depth perception and reading and visual scanning problems.  Treatment depends on the cause of the dysfunction and includes:

    • Eye patches or fresnel prisms for binocular diplopia
    • Botulinum toxin injection for neurogenic diplopia
    • Surgery for binocular diplopia - rare and should be delayed for 9-12 months to permit spontaneous recovery and accommodation

  6. Trigeminal Nerve (Cranial Nerve V) - Corneal drying, abrasions, and/or pain, decreased salivation, and, especially, anesthesia of the forehead, eyebrow, and/or nose can occur following TBI. Isolted trigeminal neuropathy following cranial trauma is exceptional (Ko and Chan, 1995)
    • Testing involves testing all three divisions of the nerve for light touch, pinprick, and vibratory and temperature sensations. Eyelid response to corneal testing with a cotton swab can distinguish trigeminal from facial nerve palsies:

      Ipsilateral Contralateral
      Normal response Closed Closed
      Trigeminal paresis Open Open
      Facial paresis Open Closed

    • Treatment
      • Copious eye irrigation with normal saline and lubricant gel and patching of the affected eye to treat corneal drying, abrasions, and/or pain
      • Lateral or complete tarsorrhapy if irritation continues to prevent corneal ulceration and opacities
      • Frequent consumption of water or use of sugarless gum for decreased salivation

  7. Facial Nerve (Cranial Nerve VII) - Complete or partial paralysis of the face, hyperacusis, and/or an unusual or impaired sense of taste can occur following TBI. The "disinhibition syndrome", in which there is an increase in cochlear amplifier gain, can occur susequent to head injury (Ceranic, et al 1998). Exposure keratitis secondary to inadequate lubrication can also occur, particularly in patients with damage to the facial nerve, and is prevented with an ophthalmic lubricant.
    • Causes
      • Cranial trauma - both longitudinal and transverse fractures of the temporal bone
        • Tears of the nerve or bony impingement result in immediate paralysis
        • Formation of edema or hematoma can cause delayed (> 4/6 days) paralysis
      • Dysfunction at any level of the auditory system may also cause tinnitus and the "disinhibition syndrome", in which a reduction in central efferent suppression of cochlear mechanics lead to an increase in cochlear amplifier gain (Ceranic, et al 1998)

    • Recovery/Treatment
      • Many facial nerve injuries resolve without surgery
      • Surgery is indicated:
        • If there is complete transection of the nerve. In this case, surgical revision and reanastomosis or cable nerve grafts may be necessary. Reanastomosis is also advisable for facial reanimation in patients with significant peripheral involvement of the cranial nerve
        • If there is delayed onset due to swelling and >90% loss of the evoked motor unit action potential. In this case, decompression of the nerve is usually sufficient
        • If there are problems with upper eyelid closure. In this case, gold weights may be surgically placed on the eyelid to minimize risk for corneal abrasion and exposure keratitis
      • If surgery is not indicated:
        • Liberal use of sterile eye drops and ointments helps maintain the integrity of the cornea
        • The affected eye can be taped closed at night
        • Lateral lid tarsorrhaphy can adequately protect the cornea in complete paralysis
        • Transcutaneous facial muscle stimulation can retard atrophy of the affected muscles until recovery occurs, in patients where the ipsilateral trigeminal nerve has been injured; this is not usually recommended for patients with complete and prolonged paralysis without surgery
        • Exercises in front of a mirror to strengthen muscles and their symmetrical use

  8. Vestibulocochlear Nerve (Cranial Nerve VIII) - Positional vertigo is the most common problem, although tinnitus, hearing loss, and deafness may also occur following TBI
    • Signs of positional vertigo - Positional vertigo occurs, usually for about 30 seconds, with sudden changes in position, usually from lying to sitting or from sitting to standing

    • Causes of hearing loss
      • Longitudinal fractures which disrupt the tympanic membrane
      • Transverse fractures which fracture the labyrinthine capsule
      • Cochlear concussion
      • Ossicular chain disruption
      • Perilymph fistula, which also causes dizziness and other unusual auditory sensations
      • Other abnormalities, which may be more prominent on single-photon-emission computed tomography (SPECT), than on MRI, CT or EEG (Sataloff, et al 1996)

    • Testing for hearing loss
      • Conscious patient
        • Tuning forks via the Weber and Rinne tests to test hearing
        • Brainstem auditory evoked responses (BAERs) to determine integrity of the auditory pathway and assess hearing acuity, vertigo and balance disturbances, nausea, dizziness, and tinnitus
        • Full audiologic testing to determine presence and extent of hearing loss
        • P50 evoked waveform response to paired auditory stimuli (Arciniegas, et al 2000)
      • Unconscious patient - obvious physical signs, such as otorrhea due to CSF, hemotympanum, or Battle's sign must be sought

    • Recovery/Therapy
      • Positional vertigo usually resolves with time
        • Positional exercises may facilitate the process; by overstimulating the vestibular response, these exercises may cause nausea at first
        • Medications should be carefully evaluated for efficacy and side effects and used in patients with extreme symptoms, such as travel-induced vertigo, only for short periods of time and if they are absolutely necessary
        • Meclizine, scopolamine patches, or other vestibular suppressants may be tried
      • Hearing aids for significant posttraumatic sensorineural deafness to understand verbal information and improve response in social interactions
      • Surgical repair of ossicular chain disruption for this type of hearing loss, although some patient recover this loss in time without treatment

  9. Glossopharyngeal Nerve (Cranial Nerve IX)
    Vagus Nerve (Cranial Nerve X)
    Spinal Accessory Nerve (Cranial Nerve XI)

    • Causes - Injury to any or all of these nerves causes usually weakness on the ipsilatteral side and other problems
      • Dysphagia and dysarthria are caused by injury to the nuclei of the glossopharyngeal and vagus nerves. Symptoms of neurogenic dysphagia include drooling, difficulty initiating swallowing, nasal regurgitation, difficulty managing secretions, choke/cough episodes while feeding, and food sticking in the throat (Buchholz, 1994)
      • Aphonia or weak/hoarse voice are caused by injury to the vagus nerve
      • Locked-in syndrome (severely decreased bowel sounds, intact response to suppository, and elevated but unchanging pulse) can result from injury to the nucleus of the vagus nerve and nerve tract (Haig, et al 1996)

    • Treatment - Treatment of glossopharyngeal and vagus nerve injuries is usually symptomatic, but:
      • Exercises of the palate and pharynx may improve dysarthria
      • Exercises for incomplete accessory nerve injury may improve strength and contraction speed of the trapezius
      • Surgery of the accessory nerve, after sectioning, may be done for cosmetic reasons

  10. Hypoglossal Nerve (Cranial Nerve XII) - Dysarthria and swallowing difficulties can occur following TBI
    • Testing - Testing shows weakness on the ipsilateral side and protusion of the tongue toward the side of the injury
    • Treatment includes:
      • Exercises of the palate and pharynx for dysarthria for injury due to blunt trauma
      • Learning and using compensatory strategies to ensure safe and efficient food intake
      • A multidisciplinary team approach when cognitive-communicative and behavioral impairments accompany dysphagia (Cherney and Halper, 1996)
      • Surgery for injury due to penetrating wounds

Based on information in Medical Rehabilitation of Traumatic Brain Injury, L.J. Horn and N.D. Zasler, eds. St. Louis, MO, Mosby, 1996, except for information where other papers are cited.