Cranial Nerve Palsies

Flora Hammond and Todd Masel

GENERAL PRINCIPLES

Epidemiology

True incidence of cranial nerve (CN) injuries in traumatic brain injury (TBI) is not certain, but it is thought to be common, and has been shown to occur even in mild TBI with a Glasgow Coma Scale (GCS) of 14 to 15 and no initial findings on computed tomography (CT) head [1].

• Most frequently injured—CN I, followed next by CN VII and CN VIII

• Less commonly injured—optic (CN II) and oculomotor (CN III) nerves

• Rarely injured—trigeminal (CN V) and lower CNs

Etiology

Etiology includes acceleration-deceleration, shearing, skull fracture, intracranial hemorrhage, intracranial mass lesion, uncal herniation, infarct, and vascular occlusion.

Mechanism of Injury

• Mechanisms include compression, traction, transection, and ischemia.

• Central (nuclear) CN injury occurs from brainstem damage; peripheral CN injury results from fracture or local injury.

• CNs are at particular risk for injury, because they traverse over bony protuberances and canals, or by direct injury from skull fracture.

Prognosis

• Olfactory (I)—Reported prognosis is: 33% recovery, 27% worsened, and 40% no change [2]. Recovery owing to olfactory nerve regeneration is usually noticed within the first 6 months and complete by 12 months post injury [3], with later recoveries (up to 5 years) reported [4]. Parosmia (sensation of smell in absence of stimulus) may be the first sign of return.

• Optic (II)—The optic nerve is a direct extension of the brain and does not regenerate.

• Oculomotor (III)—Recovery usually takes 6 to 12 months. Return of function is usually incomplete, with complete recovery in 40% [4].

• Facial (VII)—With delayed-onset palsy, CN VII is usually structurally intact and recovers in 8 weeks [3]. During nerve regeneration, aberrant reinnervation may occur, resulting in synkinesis (e.g., “crocodile tears,” in which tearing replaces salivation during eating).

DIAGNOSIS

Risk Factors

Risk factors include skull fractures due to close proximity to CN (especially CN: I, II, III, IV, V [first two branches], VII, and VIII); and increased intracranial pressure, causing compression (CN III).

Clinical Presentation

• Olfactory (I)—altered sense of smell.

• Optic (II)—altered visual acuity and/or visual fields.

• Oculomotor (III)—ptosis, lack of accommodation, dilated and fixed pupil, divergent strabismus, diplopia, and the eye only moving laterally. When looking straight ahead, the affected eye turns outward and slightly down. When looking inward, the affected eye can move only to the middle and cannot look up or down. Because the pupillary fibers of CN III are located at the periphery of the nerve whereas the fibers responsible for extraocular movements are located centrally, mechanical trauma or compression tend to cause pupillary abnormalities before causing extraocular movement abnormalities, while the converse is true for ischemic lesions to CN III.

• Trochlear (IV)—diplopia (especially when descending stairs); affected eye rotated out with inability to turn eye in and down, compensatory head tilt away from affected side.

• Trigeminal (V)—scleral injection caused by corneal abrasions and drying, decreased facial sensation and/or neurogenic pain, weakness with chewing.

• Abducens (VI)—impaired ability to turn affected eye outward, affected eye turns inward when looking straight ahead, diplopia with looking toward the affected side, esotropia (strabismus in which one or both eyes turn inward) worsened by lateral gaze, and head turned laterally toward paretic side.

• Facial (VII)—weakness of face and lid closure, and loss of taste sensation on anterior two-thirds of the tongue. Facial muscle weakness may affect mastication with impaired oropharyngeal swallowing phase.

• Vestibulocochlear (VIII)—hearing loss, vertigo, nystagmus, and/or impaired balance; commonly associated with temporal bone fracture, mastoid fracture, Battle’s sign, otorrhea, bleeding from the ear, and hemotympanum.

• Glossopharyngeal (IX)—loss of taste over posterior third of the tongue, deviation of the uvula contralaterally, decreased salivation, and slight dysphagia.

• Vagus (X)—palate paralysis with loss of the gag reflex, dysphagia, and aphonia or hypophonia due to unilateral paralysis of the vocal fold. Bilateral vagal disruption is fatal.

• Spinal (XI)—inability to turn the head to the opposite side, and ipsilateral shoulder drooping, which may result in shoulder dysfunction and pain.

• Hypoglossal (XII)—inability to protrude tongue on the affected side; may lead to dysphagia.

Physical Examination

Diagnosis is generally based on physical examination of CN functions. Examination may need to be repeated or completed as consciousness recovers.

• Olfactory (I)—Test detection of familiar, non-noxious smells with eyes closed. Giving the person choices may help overcome word-finding problems.

• Optic (II)—Assess visual acuity, visual fields, and pupillary reactivity, and perform ophthalmoscopic examination. Complete monocular blindness with preservation of normal pupillary reflexes is usually a sign of malingering or other types of functional (nonorganic) disorders.

• Oculomotor (III)—Assess tracking in the six cardinal positions, convergence on near targets, pursuit movements, saccades, pupillary reaction, and eyelid elevation. CN III palsy is indicated by difficulty moving the eye in, or up and down, with preserved outward movement, and may be associated with pupillary dilatation and ptosis. Doll’s eye maneuver and pupillary light reflex are used for assessment if unconscious. A fixed and dilated pupil signals herniation as the nerve runs medial to the temporal lobe at the tentorium edge.

• Trochlear (IV)—Assess adduction in conjunction with downward gaze of the involved eye. Individuals with CN IV palsy cannot look downward when the eye is adducted.

• Trigeminal (V)—Test facial sensation, corneal reflex, and motor function of the jaw. Differentiation between deficits of the three divisions of CN V may facilitate more precise localization of injury.

• Abducens (VI)—Look for deficiency in lateral gaze when testing movement of the eyes through the full extent of the horizontal plane.

• Facial (VII)—Test the five main functions: facial expression (smile, wrinkle forehead, puff cheeks, close eyes tightly), taste identification on anterior two-third of the tongue, external ear sensation, stapedius muscle function, and lacrimal and salivary gland function.

Upper motor neuron lesion—facial weakness contralateral to the lesion with sparing of forehead wrinkle because of the bilateral innervation of the frontalis muscle

Lower motor neuron lesion—ipsilateral facial weakness inclusive of flattened forehead wrinkle; inability to close eye

Pontine lesion (CN VII nucleus)—complete ipsilateral facial paralysis along with contralateral hemiparesis, and frequently accompanied by ipsilateral CN VI palsy

• Vestibulocochlear (VIII)—Examine tympanic membrane for tears, and test eye movement for nystagmus, postural responses, and hearing.

• Glossopharyngeal (IX)—Test sensation of posterior palate and gag reflex.

• Vagus (X)—Test palate elevation and gag reflex.

• Spinal (XI)—Test resisted head rotation to opposite side and ipsilateral shoulder shrug.

• Hypoglossal (XII)—Look for ipsilateral atrophy, tongue fasciculations, and deviation with tongue protrusion. The tongue deviates to the side of the weak tongue muscles because of the unopposed, contralateral muscles. In lesions at or below the level of the hypoglossal nucleus in the brainstem, this deviation is toward the side of the lesion. (In cortical lesions, the tongue deviation is away from the side of the lesion.)

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