Visual System/Eye Movements/Hearing and Balance

Question 1

Describe and be able to diagram the principle neurons that make up the retina, including the functional connections, specific neurons (rods, cones, interneurons and ganglion cells), and the direction of synaptic processing.

Answer 1

1. principle neurons that make up the retina

Question 2

Understand how information about “receptive fields” in the retina are relayed to the cortex.

Question 3

Diagram and describe the pathways used by the visual system to transmit the action potentials from the retina to the cortex, and brainstem nuclei involved in visual processing and control.

Question 4

Describe the anatomy/histology of the visual cortex and how it sorts the visual information, interprets specific subsets, and distributes this information to various other areas of the cortex.

Question 5

Be able to identify specific lesions associated with the visual system and correctly identify where in the visual pathway these various lesions occur.

Question 6

Conjugate eye movements-slow/pursuit

Answer 6

• Slow eye movements that keep images on the fovea (~100 degrees)

type a: smooth pursuit movements

• allows continuous feedback from vestibular and visual systems to regulate speed/duration
• Volitional, originates in the extrastriate cortex & uniquely requires cerebellum (flocculus) for its generation–attempts to “guess” where the target is going an move the fovea onto it as quickly as possible
• once the target is reached, smooth pursuit takes over and as long as the target is moving slowly, can keep the fovea on it and allows a sharp image
  
  • without a target, can only see fast saccadic eye movements
• smooth pursuit is a reflex and “automatic”

Question 7

Conjugate eye movements: Vestibulo-ocular reflex

Answer 7

• involves ascending MLF and PPRF
• clinically tested as part of the Doll’s eyes maneuver
• As the head rotates, VOR generates compensatory (same speed) eye movements in opposite direction from head movements, relies on vestibular input
  
  • without this reflec, image would appear smeared on retina
• Can be suppressed to allow head and eye movements to shift gaze
• want to keep an object on the fovea to maintain clarity

Once the head stops moving the eyes remain in that same direction of gaze

• “Stabilization” occurs through the nucleus prepositus hypoglossi
• Tonic activation maintains the activation/activity of the involved cranial nerve nuclei (the 3rd and 6th)

Question 8

Conjugate eye movements: vergence movements

Answer 8

• Accommodation signals are used to guide vergence eye movements (CN III, MR)
• Cerebellum involved but not essential for movements

Question 9

What are the two cortical centers for conjugate gaze?

Answer 9

1. frontal eye field
   
   1. moves eyes RIGHT
   2. brings and object onto the fovea
   3. initiates saccadic (blurry) eye movements
2. Occipital eye field
   
   1. moves eyes LEFT
   2. keeps an object on the fovea
   3. necessary for smooth pursuit

Question 10

Eye movement integration with vestibular system

Answer 10

Inputs:

• cortical inputs
• oculomotor inputs
• cerebellar inputs
• vestibular sensors (regular and irregular)
• neck proprioception

Outputs:

• estimation of self-motion
• gaze stabilization (VOR)
• posture and balance

Question 11

VOR: head right, eyes left

Answer 11

Head is rotating to the right—>

• The right horizontal canal is activated
• Right vestibular nucleus is “activated’
• The left 6th nucleus (via PPRF) is activated and the left lateral rectus muscle contracts
• The left PPRF “activates neurons in the right 3rd nucleus and the right medial rectus contracts

<—both eyes begin to move to the left

• The object of interest “stays” on the fovea

Question 12

Conjugate eye movements-saccadic

Answer 12

• Fast eye movements that move an image onto the fovea (~700 degrees); brainstem motor programs that are triggered by cerebral or cerebellar center.
• Ballistic eye movements place an image onto the fovea, same as fast phase of nystagmus
• Initiated from the contralateral frontal eye fields (middle frontal gyrus)
• Used in reading, scanning scenes & pictures, etc.
• Modulated by output from basal ganglia, inhibits frontal & supplementary eye fields, sc
• Modulated by the cerebellum (vermis), regulates timing of muscle contractions (dysmetric saccades)
• Rapid horizontal eye movements - generated from the paramedian pontine reticular formation (PPRF)
• Rapid vertical eye movements - generated from the reticular formation dorsomedial to the red nucleus (riMLF)

Question 13

Describe components/pathway for vergence eye movements

Question 14

Internuclear ophthalmoplegia

Answer 14

• MLF lesions=internuclear ophthalmoplegia
• internuclear=between CN nuclei, and is interfering with MLF
• MLF lesion is on the side of the eye that cant adduct on lateral gaze
• On testing convergence, both eyes can move in (adduct) and you confirm that the medial rectus of the eye that doesn’t adduct on lateral gaze is functional!
• Convergence involves the anterior portion of the MLF so. it “bypasses” the lesion in the inferior portion of the MLF where it is disrupted.

Question 15

Nystagmus

Answer 15

• Rhythmic back and forth movement of the eyes
• Usually the movement is slow in one direction (“smooth”) and fast (“saccadic”) in the other
• When you induce it by spinning yourself around….
  
  • The VOR is generating the slow phase which helps to keep an eye on a target
  • Once the eye approaches the maximum that it can turn, a saccade will then occur moving the eyes in an opposite direction and onto a new target (Optokinetic nystagmus or OKN)

Question 16

Rationale for why we experince dizziness

Answer 16

• Vestibular input without vision
  
  • While spinning in a chair with your eyes closed (the constant motion eventually results in the cupula membrane returning to its baseline) you suddenly open your eyes
• Sense of motion via the visual system, but without vestibular “confirmation”
  
  • Looking out a car window when an adjacent car moves away (false sense of motion)
• Sense of motion via the vestibular system, but without visual confirmation (“a disconnect”)
  
  • In the cabin of a boat during a storm (motion sickness)

Question 17

What are the three components of the basic bedside examination of the visual system?

Answer 17

1. measurement of visual acuity
2. evaluation of the visual fields
3. ophthalmoscopic examination/viewing of the optic disc and adjacent blood vessels and retina

Question 18

Examination of visual acuity (central vision)

Answer 18

• Snellen wall chart (or near card)
  
  • visual acuity=smallest row of numbers or letters a patient can accurately read=fxn of central vision involving the macula
  • each eye tested seperately
  • visual acuity is a fractional number which compares the pt’s vision with the nml population
  • 20/100 line means patient reads at 20 ft what a normal person sees at 100 ft
    
    • nml is 20/20
  • Can use pocket vision acuity chat but its problematic for older pts due to presbyopia, or age-related impairment of near vision
• Pinhole test
  
  • if vision improves looking through a pinhole (cheap corrective lens)=visual problem is ocular (refractive)
  • impaired visual acuity from a lesion of the optic nerve or macula, however, is not improved when looking though a pinjole, or by use of corrective lenses
    
    • if not improved, visual problem may be neurological

Question 19

Visual Field Examination

Answer 19

• mainly tests peripheral vision-“les sharp or acute” than central vision
• recorded on circular or polar graphs
• Perimetry=more quantitative method of visual field testing
  
  • computer randomly flashes “dots” of light on a tst screen, pt acknowledges by pushing a button
• Tested by “confrontation”:
  
  • pt and examiner facing and “focused on” eachother “eye-to’eye”, to se if a visual target perceived by the examiner’s visual field is likewise perceived in the pt’s
  • pt covers one eye at a time
• Pts with abnormally narrowed (or smaller) visual fields [=constricted/contracted visual fields] may have underlying glaucoma or a retinal degenerative disease
  
  • as examiner moves away from pt the constricted visual field should enlarge in cone-shaped fashion
  • tunnel vision=same narrow breadth of visual fields (both closer and further)
    
    • usually reflects a psychiatric rather than neuro problem

Question 20

Blind spots

Answer 20

• everyone normally has a physiological “blind spot” in the tepora visual field of each eye
  
  • Why? optic disc in the nasal retina has NO RODS or CONES
  • it abnormally enlarges in size in the presence of papilledema-where increased intracrnial pressure causes the optic nerve to appear swollen on ophthalmoscopic examination
• Scotomas-pathological, abnml blind spots ELSEWHERE in the visual field of one eye where vision is lost or decreased
  
  • Cause: lesions in the retina (infections or inflammation, macular degenration, or retinal detachments) or optic nerve (demyelination or ischemia)

Question 21

Normal visual system

Answer 21

• normally, a visual image is flipped L to R and inverted upside-down through the “camera” of the eye
• normally, images in the L visual fields are perceived by the right (side) retinas (nasal left retina, temporal right retina)
• beyond the decussation at the optic chiasm, images in the left visual fields are conveyed to the:
  
  • right optic tract
  • right lateral geniculate
  • right optic radiations
  • right visual cortex
• optic nerve lesion causes total, or complete L. SCOTOMA (monocular blindness)
• Hemianopsia: visual loss in half (nasal or temporal) of visual field in each eye.
  
  • Heteronymous = temporal/temporal, or nasal/nasal; hetero=left and right
  • homonymous = temporal/nasal; homo=LL or RR
  • bitemporal heteronymous hemianopsia from lesion in medial optic chiasm
  • L. homonymous hemianopsia is produced by lesions in the:
    
    • R. optic tract (or lateral geniculate)
    • R. optic radiations
    • –or– right visual cortex in occipital lobe
• Right nasal visual defect from lesion (due to aneurysm) compressing right outer optic chiasm
  
  • if bilat outer chiasm lesions were present, a hetero nasal hemianopsia would occur
• Left superior homonymous quadrantanopsia (quadrantic defect) from a lesion in the right temporal optic radiations.
• heteronymous hemianopsias-occur only at the chiasm
• homonymous hemianopsias are more incongruent with more anterior lesions, may show macular sparing with occipital lobe lesions

Question 22

Clinical syndromes of visual deficit/loss

Answer 22

• optic neuritis
  
  • often from MS
  • sudden visual loss in one eye (total blindness) or part (scotoma)
  • eye movement may be painful
  • optic disc in the involved eye often appears swollen, inflammed, with indistinct. blurry margins
    
    • *retrobulbar neuritis-in some pts inflamm is deeper or more posterior in the optic nerve, so the optic disc appears nml, despite visual impairment in that eye
• optic atrophy
  
  • weeks after optic nerve lesion, may have residual scotoma or loss of acuity
  • pale optic disc with sharp, distinct margins
  • due to destruction of retinal ganglion cell axons (does not occur with occipital lesions)
• Papilledema
  
  • increased intra cranial pressure (due to extensive brain tumor or intracranial mass), initially nml vision will be lost or impaired if untreated
  • bilateral swollen discs, may see flame hemorrhages around optic discs
  • blood vessels mound over blurred, indistinct disc margins
  • CP: HA, N/V, or impaired consciousness form the elevated intracranial pressure
• Pituitary tumor
  
  • common lesion affecting the optic chiasm
  • arises from the sella turcica and exerts pressure on the center of the chiasm from below
  • first affects: decussating, inferior, nasal retinal fibers=visual deficit in the superior temporal quadrants of the patient
  • total lesion of the center of the optic chiasm produces a BI-temporal HETEROnymous hemianopsia
  • would also, of course, have hormonal (endocrine) dysfunction, s&s
• Ischemic infarctions
  
  • also cause lesions in the optic radiations
  • inferior optic radiations bends anteriorly in the temporal lobe=Meyer’s loop
    
    • a lesion here causes contralateral superior homonymous quadrantanopsia (“pie in the sky”)
    • a lesion in the parietal lobe causes a contralateral inferior homonymous quadrantanopsia (“pie on the floor:
• cortical blindness:
  
  • severe visual loss form bilateral occipital lobe lesions
  • usually a stroke syndrome from thrombosis of the distal basilar artery or emboli down its PCA branches
    
    • pt is unable to see, BUT, pupillary light reflex is intact and the optic discs appear nml since the retinal ganglion cells are not involved

Question 23

Examination of auditory acuity

Answer 23

• Bedside testing (watch tick, finger rub, whispered word)
• Weber test (bedside)
  
  • if louder on one side-ipsilateral conductive deafness or contralateral nerve defect
• Rinne test (bedside)
  
  • compare air conduction (usually more efficient due to amplification syste) to bone conduction
  • vibrating fork on mastouc; if olouder here=conductive deafness
• Audiometry (audiogram)-most quantitative and precise id of deafness type, but need special equipment in a sound-proofed rm
  
  • Conductive deafness: low tone loss from impaired air conduction of sound stimuli
    
    • Causes: water or wax plugging up external ear canal, or fusion or disruption of the bony ossicles (ossicle lesion)
    • a problem BEFORE the hair cell receptors
    • low-tone hearing loss is typical
  • Nerve (sensorineural) deafness: high tone loss from degeneration of hair cells or auditory nerve
    
    • causes: drug toxicity, ischemia, trauma, or persistent exposure to loud noise
    • high-tone hearing loss is typical

Question 24

Vestibular System Examination

Answer 24

• dysfunction typically produces movement-induced dizziness or vertigo
• Electronystagmogram (ENG)
  
  • uses special equipment to record eye movements and assessment of nystagmus provoked by thermal stimuli (currents of warm or cool air entering the external ear canal)
  • determines whether the R or L vestibular system is impaired
  • this oculovestibular reflex is also assessed by the cold caloric or ice water caloric test in comatose pts (not tolerated in conscious pts)
• Nylen-Barany or Dix-Hallpike maneuver
  
  • the turned head is tilted 45 degrees below the plane of the exam table
  • if rotatory nystagmus is produced, the posterior semicircular canal on that tilted/lowered side is “overly sensitive” (positional vertigo)

Question 25

Clinial syndromes of Auditory and Vestibular deficit

Answer 25

• sudden, severe umilateral deafness may also be due to trauma, particularyl with petrous bone fractures; or from ischemia in the territory of the AICA
• Acute labyrinthitis
  
  • labyrinth of inner ear may be affected by a viral infection or inflammation causing severe vertigo–common
    
    • CP: N/V, hearing impairment, unsteadiness of gait
    • On examination: nystagmus, unilateral decreased hearing, gait atazia
    • prognosis: symptoms resolve within days to weeks
    • tx: benzodiazepine, anti-histamine, or antiemetic medication
• Ménière’s disease:
  
  • CP: recurrent episodes of vertigo, deafness and tinnitus
  • Path: membranous labyrinth swells and ruptures, allowing potassium-rich (K$) endolymph to leak into the surrounding perilymph, disrupting the ionic gradient required for nml hair cell function
  • symptoms and tx: same as acute laby
  • prognosis: repeated epsidoes of Ménière’s disease may lead to complete, permanent deafness
  • dietary salt restriction and diuretic medication may help reduce production of endolymph and lessen the risk of chronic deafness
• Benign positional vertigo
  
  • common problem for elderly patients
  • Path: degeneration of otoliths and displace calcium crystals an other debris can lodge around the cilia of semicircular canal hair cells, makes them “oversensitive” to minor movements of the head
  • CP: transient but annoying vertigo when standing up/getting out of bed/bending over or turning their heads
  • Diagnosis: Dix-Hallpike manuever
  • Tx: D-H similar head-turning exercises to disperse troublesome debris in the semicircular canals or help pt readapt to head movements
    
    • or benzodiazepines or anti-histamine meds