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Problems in balance may follow trauma to which nerve

problems in balance may follow trauma to which nerve


  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
  • 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
  • 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
  • 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

  • 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
  • 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: problems in balance may follow trauma to which nerve
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    Category: Forex

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