Conductive hearing loss

Conductive hearing loss is disruption of the external and middle ear, including the ear canal, tympanic membrane, and ossicles. Causes include hemotympanum, tympanic membrane rupture, and ossicular disruption.

Sensorineural hearing loss

Sensorineural hearing loss is disruption of the inner ear or auditory nerve. Causes include temporal bone fracture, labyrinthine concussion, and brainstem contusion. This is the most common hearing deficit in TBI and is more prevalent in blast-related TBI because the ear is particularly susceptible to overpressurization during a blast.

Mixed hearing loss

Mixed hearing loss involves both conductive and sensorineural hearing loss.

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  Tests: Tuning fork to lateralize lesion, audiometry to assess frequency/type of hearing loss, auditory brainstem response (ABR) to diagnose auditory nerve or pathway disruption

  
  
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  Treatment: Hearing aids, frequency magnification (FM) devices, or cochlear implant for severe bilateral loss

Alignment deficits

Alignment deficits are a deviation of gaze and can be either tropia, a malalignment of one eye when both eyes are uncovered, or a phoria, a latent deviation when binocular vision is broken. Cranial nerve (CN) palsies are the most common cause of alignment deficits. More common in severe TBI. ^{, ,}

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  Pathophysiology: Damage along the efferent visual pathway. Neural problem is identified much more often in vertical phorias.

  
  
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  Horizontal

  
  
  
  
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    Eso: Eyes turn in

    
    
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    Exo: Eyes turn out

  
  
  
  
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  Vertical

  
  
  
  
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    Hyper: Eye alignment more superior in orbit (up)

    
    
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    Hypo: Eye alignment more inferior in orbit (down)

  
  
  
  
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  Symptoms: Diplopia, impaired depth perception, headaches

  
  
  
  
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    CN 3 (oculomotor): Ptosis, exotropia, lack of mydriasis, lack of accommodation, horizontal diplopia

    
    
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    CN 4 (trochlear): Compensatory head tilt, hyperphoria and hypertropia, vertical diplopia

    
    
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    CN 6 (abducens): Esotropia, horizontal diplopia

  
  
  
  
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  Tests:

  
  
  
  
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    Hirschberg: Measures alignment with eyes uncovered

    
    
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    Cover/crossed cover: Looking for deviation between being covered and uncovered

    
    
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    Maddox rod: Aids in determining deviations in vertical and horizontal planes

    
    
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    Treatment: Prism lenses: horizontal or vertical depending on deficit, vision therapy

  
  

Accommodation deficits

Accommodation deficits are an inability to maintain clear vision, sustain or change focus on an object. Accommodative insufficiency (most common), accommodative excess, dynamic accommodative infacility ^,

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  Pathophysiology: Crystalline lens changes through ciliary control to focus on an object through a complex pathway involving retinal cones, optic nerve, lateral geniculate nucleus (LGN), occipital lobe, posterior parietal lobe, frontal eye field, oculomotor nucleus, parasympathetic accessory oculomotor nucleus with contribution from the cerebellum

  
  
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  Symptom Blurred vision

  
  
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  Tests:

  
  
  
  
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    Accommodative amplitude test: Small accommodative target (20/20–20/30)—distance of the first sustained blur using either the pushup or the minus lens method

    
    
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    Amplitude facility with lens flippers: The patient should be able to clear these lenses monocularly within 11 cycles per minute without evidence of fatigue.

  
  
  
  
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  Treatment: Plus powered lenses (insufficiency), vision therapy

Vergence deficits

Vergence deficits are deficits in disjunctive eye movement—convergence insufficiency, convergence excess, divergence insufficiency. Convergence insufficiency is the most common oculomotor deficit after mild TBI. ^{, ,}

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  Symptoms: Diplopia, eyestrain, vision-related headaches, dizziness, exophoria, intermittent exotropia during near vision and fatigue

  
  
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  Tests:

  
  
  
  
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    Near-point convergence (NPC): Small target to measure the break in binocular vision or object doubles

    
    
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    Step vergence: Positive and negative fusional vergence amplitudes measured with a prism rod

  
  
  
  
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  Treatment: Oculomotor (vision) therapy, fusional prisms, patching—complete or partial ( Table 34.1 )

  
  
  
  

  TABLE 34.1

  
  

  Vergence Deficits

  
  

  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  

  Vergence Deficit	Primary Treatment	Secondary Treatment
  Convergence insufficiency	Oculomotor therapy	Prism lenses, surgery
  Convergence excess	Plus powered lenses	Oculomotor therapy
  Fusional vergence dysfunction	Oculomotor therapy
  Divergence insufficiency	Prism lenses	Oculomotor therapy

   
  
  

Versional deficits

Versional deficits are deficits in conjugate eye movement. Smooth pursuits are conjugate eye movements to smoothly and accurately track a slow-moving object. Saccades are rapid eye movements that allow quick and accurate scanning from one object to another. ^{, , ,}

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  Pathophysiology: Lesion along pathway from frontal eye fields, paramedian pontine reticular formation, rostral mesencephalon, parietal cortex, basal ganglia, superior colliculus, or cerebellum

  
  
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  Symptoms: Slow reading, loss of place when reading, misreading, floating text, and dizziness

  
  
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  Tests: Northeastern State University College of Optometry Oculomotor Test, Developmental Eye Movement Test, saccadic oculomotor testing, pursuit eye movement testing

  
  
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  Treatment: Large-print text, typoscope, vision therapy

Hemianopsia or quadrantanopsia

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  Symptoms: Ignoring one-half of an object, bumping into objects on one side, difficulty reading, slow rate of reading

  
  
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  Tests: Confrontation visual fields finger counting, Goldmann perimetry

  
  
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  Treatment: Compensatory, yoked prisms, half-Fresnel prisms, mirrors, visual scanning strategies

Other

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  Central scotoma: Central area of vision loss

  
  
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  Monocular vision: Complete loss of vision in one eye

Light sensitivity

Light sensitivity is ocular discomfort in the presence of light. ^,

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  Pathophysiology: Anomalous dark-light adaptation thresholds caused by disordered thalamic processing. Fluorescent light sensitivity is believed to be caused by anomalous critical flicker fusion frequency threshold.

  
  
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  Treatment: Tints 30% to 40% for indoors, 80% to 85% for outdoor, blue or gray for fluorescent, wear wide-brimmed hat

Color blindness

Color blindness is damage to the retina, optic nerve, parvocellular pathway of LGN, or visual area V4.

Posttrauma vision syndrome

Posttrauma vision syndrome is a constellation of binocular visual symptoms that can present after trauma caused by the disruption of visual processing at multiple levels from midbrain and cortex. Symptoms include diplopia (exotropia/esotropia), blurred near vision (accommodative insufficiency), movement of print when reading (convergence insufficiency), asthenopia (oculomotor dysfunction), headaches (increased myopia), and photophobia (low blink rate).

Visual midline shift syndrome

Visual midline shift syndrome is a shift in the perception of the visual midline that occurs with homonymous visual field deficits.

Visual vestibular deficits

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  Pathophysiology: Deficit along the vestibular ocular pathway from eye to inner ear

  
  
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  Symptoms: Dizziness, vertigo, nausea, photosensitivity to fluorescent lighting, sensitivity to visual motion, especially in visually stimulating environments

  
  
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  Treatment: Assess and treat any visual and vestibular deficits through coordinated oculomotor and vestibular therapy.

Visual processing dysfunction

Visual processing dysfunction include visual spatial, visual analysis, and visual motor integration deficits. Ocular exam and acuity are often normal.

Laboratory tests ^{, ,}

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  Visual evoked potential: Series of lights mount a recording measured by electrodes on the scalp

  
  
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  Electroretinogram: Measures retina pigment epithelium (activity of rod and cone cells) during photo stimulation by placing electrodes via contact lenses or foil tucked into the conjunctiva

  
  
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  Electrooculogram: Indirectly measures retina pigment epithelium by varying illumination during eye movement; recorded via electrodes on the canthi

Bedside tests ^,

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  Vestibular/oculomotor screening (VOMS): Assessment of severity of symptoms with visual and ocular provocative maneuvers

  
  
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  King-Devick Test: Timed test to read numbers on three test cards; tests oculomotor function

  
  
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  Subjective visual attention test: Search and cross out a letter or symbol; assess overall visual attention

Imaging

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  Computed tomography (CT): Detects structural damage—cranial fractures, hematomas

  
  
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  Magnetic resonance imaging (MRI): Detects brain damage in areas of the ocular pathway

Vision rehabilitation

Oculomotor therapy for accommodation and vergence includes three general phases. The first phase uses large targets with slow change. The second phase increases speed and decreases targets. Target training with monocular vision (patched) first and then progresses to binocular vision tasks. Accommodative flippers are also used in this phase. The third phase trains large jumps between stimuli presented (step vergence training). ^{, , ,}

Example of exercises:

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  Accommodation: Small copy of letters/numbers/objects handed to patient, same large copy on wall, and the patient moves between the two, reading line by line

  
  
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  Vergence: Stereograms, Brock string, step vergence amplitude training using prisms, step vergence facility training using prism flippers

  
  
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  Pursuit: Laser light follow, bouncing light, maze follow

  
  
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  Saccades: Identify differences in two pictures, read letters/numbers/objects spaced out on a page

Prisms

Prisms are applied to glasses to bend light to shift an object from its position. Prisms can be placed vertically or horizontally depending on the deficit correcting. They can be unilateral or bilateral. They are most effective in divergence insufficiency, esophoria, and vertical heterophoria.

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  Yoked prisms: Prism oriented in the same direction on both glasses, shifting visual perception

  
  
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  Homonymous hemianopsia/quadranopsia: Horizontal yoked prism oriented in the direction of visual loss displaces objects from the nonseeing into the seeing hemifield

  
  
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  Visual neglect: Yoked prisms may work but require larger magnitudes

  
  
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  Visual midline shift syndrome: Yoked prisms center the visual midline

  
  
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  Enhanced sector prisms: Bilateral prisms on portions of eyeglasses to improve awareness of the peripheral field; can be effective for homonymous hemianopsia/quadrantopsia, scotoma

  
  
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  Fresnel prisms: Stick-on prisms

Patching

Patching can be used to correct diplopia but renders the patient monocular impairing peripheral vision. Central occlusion patches can decrease diplopia while looking directly at an object but maintains peripheral vision.