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					Dr. Ketcham                                                                              Ocular Pathology I
Notes by Jean Tass                                                                            Lecture #12
jean_tass@hotmail.com                                                                            11/29/05

Notes:
    The final is Monday, December 12 from 12:00-3:00. It will be approximately 50 multiple choice
       questions. We’ll do the third one-hour test before the final. There will be no percentage-type
       questions on the final.
    If you have any questions for Dr. Ketcham, please e-mail her.
    Make sure you know the signs & symptoms, pathophysiology, and treatments (especially those
       that are study-based) for the diseases.
    Example: A 55-year old woman complains of decreased vision when she reads more than at
       distance. She’s noticed this for 6 months. We’ll get a picture of the patient (her eyes aren’t red)
       and a picture of the crystalline lenses. There might be a couple different kinds of cataracts –
       which one would cause the decreased vision during reading more than at distance? (Posterior
       subcapsular)

                                Diabetic Retinopathy (Continued)
VIII) Treatments
     A) Medical management
         1) The most important tool for treating diabetes and its complications
         2) Tight blood sugar control
         3) Strict blood pressure control
         4) Hemoglobin A1c testing
         5) Routine eye exams every 12 months
            a) Type 2 diabetics should have their first eye exam at the time of diagnosis
            b) Type 1 diabetics should have their first eye exam no more than 5 years after diagnosis
            c) Get a good history from the patient
            d) Slit lamp exam
                 i) Cornea
                 ii) Iris (rubeosis)
                 iii) Glaucoma
            e) Stereo view of the posterior pole
            f) Fundus photography
            g) Know when to follow the patient and when to refer
            h) Communicate with the patient’s primary care provider and/or endocrinologist
     B) Fluorescein angiography (FA)
         1) Diagnostic tool for clinically significant macular edema (CSME)
            a) Also for severe or very severe non-proliferative diabetic retinopathy
         2) Reasons for FA
            a) Establish the cause of documented visual acuity loss
            b) Establish the extent of capillary non-perfusion (shows up as a lack of capillary flush)
            c) Identify subtle areas of neovascularization to define as occult and/or classic
     C) Laser
         1) The overall goal of any laser treatment is to reduce the rate of vision loss
         2) Treatment for CSME
         3) Focal photocoagulation
            a) Thermal damage (laser burns) directly applied to leaking areas (microaneurysms)
            b) 75% of patients stabilize or improve vision (by about 1 line)
            c) 25% of patients continue to lose vision
            d) The average patient needs 2-3 treatments over the course of the disease
         4) Grid photocoagulation
            a) Used when the leakage is diffuse in nature
            b) A grid pattern is applied over swollen areas of the retina



Ocular Pathology I                                                                                 Page 84
       5) Panretinal photocoagulation (PRP) or scatter
           a) Treatment does not improve vision, but it helps prevent blindness.
           b) Kill off the peripheral retina (trying to preserve the macula)
               i) This decreases the stimulus (vasoactive factors) that drives the neovascular process
           c) Laser burns are initially white or yellow and become darker over the course of a few
               months.
           d) Side effects include loss of peripheral vision, color vision defects, night vision problems,
               increased glare, reduced contrast, generalized blur
    D) Surgical
       1) Vitrectomy (done especially if there is a severe bleed)
       2) Main indications are persistent vitreous hemorrhage and tractional retinal detachment
           secondary to proliferative disease
       3) Should be considered in patients with rubeosis and vitreous hmeorrhages
       4) Side effects are severe vision loss, eye pain
       5) Major surgery
       6) Diabetic Retinopathy Vitrectomy Study (DRVS)
           a) Demonstrated that early vitrectomy for type 1 diabetics with severe vitreous hemorrhage
               was beneficial
           b) The same benefit was not demonstrated for type 2 diabetics
    E) Future drug treatments
       1) Protein kinase C inhibitors
           a) Oral (the first oral medication that has been attempted to help reduce DR)
           b) Eli Lilly is in clinical (safety) trials
           c) Inhibits protein kinase C pathways
       2) Intravitreous steroid (triamcinolone) injections
       3) Macugen (pegaptanib)
           a) AMD treatment
           b) Blocks vascular endothelial growth factor (VEGF), a protein that promotes vessel growth
       4) Benfotiamine
           a) Synthetic fat-soluble form of thiamine (vitamin B1)
           b) No large double-blind studies
           c) Reduces formation of advanced glycosylation end-products (AGEs) that cross-link body
               proteins like collagen, rendering them structurally and functionally ineffective
           d) Has been used in Europe for more than 10 years

                                         Visual Fields (VFs)
I) Overview
    A) Very powerful test
    B) Definition of the visual field
        1) Extent of object space that is visible while the eye is steadily fixating a target
        2) We have monocular and binocular visual fields
            a) Monocular VFs are usually tested
        3) Relative VFs
            a) 90° temporally
            b) 60° nasally and superiorly
            c) 70° inferiorly
            d) Binocular VF is 120°
                 i) This means that there is about 30° on each side that’s only seen by one eye
    C) Hill of vision
        1) 3-dimensional model of the VF
        2) X and Y axes determine the location
        3) Z axis determines the sensitivity at that location
        4) Traquair’s Hill of Vision
            a) An island of vision floating in a sea of blindness
        5) Slide 2-3 shows the scientific representation of the hill of vision


Ocular Pathology I                                                                                Page 85
              a) The most sensitive point (peak) is the fovea
              b) Blind spot (optic nerve)
          6) This is how every perimeter works
          7) The hill comes from the distribution of rods and cones (slide 3-1)
              a) The very center is just cones (fovea)
              b) As we move farther out, rods start to take over and sensitivity decreases a little, but it’s
                   easy to see movement
II) Types of perimetry
      A) Static perimetry
          1) Discrete points along the island of vision or VF are probed using a non-moving target.
          2) Either the brightness or the size of the target changes
          3) Allows us to quantify and qualify areas of vision loss (gives us absolute variations in a defect)
          4) Approaches the hill of vision from above (slide 4-2)
          5) Humphrey or Dicon VFs (automated)
          6) Terms used with static perimetry (slides 4-3, 5-1)
              a) Apostilbs are the measurement of light, but the numbers are very cumbersome
                   i) 10,000 apostilbs is the brightest
              b) Apostilbs are converted to decibels using a log scale
                   i) 10,000 apostilbs equals 0 decibels
                   ii) A spot with a reading of 0 decibels is very insensitive (like the physiologic blind spot)
              c) Goldmann comparison listed next to the scale
      B) Kinetic perimetry
          1) Moving target that goes from not-seeing to seeing
          2) The target approaches the hill of vision from the side
          3) The size of the target (once you see it) makes an isopter
              a) Isopters are different sized targets that have been moved in (slides 3-3, 4-1)
              b) They are the limits of retinal sensitivity to a specific test target and they determine the
                   circumference of the hill of vision
          4) Goldmann perimetry
III) Testing strategies
      A) Screening
          1) Make sure the patient has at least a “statistically normal” VF
          2) Very fast test used to detect a defect in the VF
          3) Usually no attempt is made to measure or quantify performance
          4) The patient’s age must be entered into the machine to compare with the normal population
              for their age group.
      B) Threshold
          1) The weakest stimulus that is seen 50% of the time
          2) Quantifies anything that it finds
          3) Used to characterize defects
          4) Frequency of seeing curve (slide 6-1)
              a) The probability of seeing a stimulus over a range of intensities
              b) 26 dB is seen 60% of the time
              c) 27 dB is seen 30% of the time
          5) Alters the stimulus intensity in 4 dB steps until the threshold is crossed (slide 6-2)
              a) Then it turns around and re-crosses the threshold in 2 dB steps
          6) Takes a long time
IV) Quantifying the severity of VF defects
      A) Absolute defect
          1) No stimulus perceived anywhere in the affected field
          2) The blind spot is a physiologic absolute defect
      B) Relative defect
          1) VF defect changes in size inversely with a change in the size and/or intensity of the stimulus
          2) Reduced sensitivity in an area
V) Monocular defects
      A) Scotomas (areas of depressed visual function surrounded by normal VF) (slides 7-2, 7-3)



Ocular Pathology I                                                                                     Page 86
        1)  Central – involves fixation
        2)  Cecocentral – fixation to the blind spot Central   Cecocentral    Paracentral   Pericentral
        3)  Paracentral – adjacent to fixation
        4)  Pericentral – surrounds fixation
        5)  Blind spot defects
            a) Enlargement of the blind spot
            b) Extension of the blind spot (Seidel’s scotoma)
    B) Sector defects                                            Enlargement      Extension
        1) Affect a section of the field and move the outer boundary inward (slide 8-1)
        2) Not surrounded by normal vision
        3) An example is a monocular retinal detachment
        4) Sector defects can be monocular, but are usually binocular
VI) Binocular defects
    A) Lesions are located from the optic chiasm all the way back into the brain
        1) Pre-chiasmal defects tend to respect the horizontal meridian
            a) Usually an ischemic event
        2) Post-chiasmal defects tend to respect the vertical meridian
            a) Usually a neurological event (e.g. stroke, tumor)
    B) Types of defects
        1) Sectoranopsia
        2) Quadrantanopsia
        3) Hemianopsia (slide 9-3)
            a) Complete
            b) Incomplete
        4) Altitudinal – superior or inferior
    C) Terms
        1) Congruity
            a) The relative similarity between the two eyes (how symmetrical the defects are)
            b) More similar = more congruous
            c) Lesions in the posterior visual pathway tend to be more congruous
            d) The top set in slide 9-3 is a complete congruous right hemianopsia. The bottom set in
                slide 9-3 is an incomplete incongruous left hemianopsia




              Complete congruous right hemianopsia            Incomplete incongruous left hemianopsia
        2) Homonymous
           a) Same side of visual space for each eye
           b) Both eyes have right or left visual field defects
           c) The lesion is posterior to the chiasm (usually in the optic tract)
           d) Slide 10-3 is a right complete congruous homonymous hemianopsia without macular
              sparing. Slide 11-1 is a left homonymous congruous hemianopsia with macular sparing.




                Without macular sparing              With macular sparing
                i) If macular sparing is present, the lesion is usually in the occipital lobe.
             e) Slide 11-2 is a left superior incongruous homonymous quadrantanopsia (pie in the sky)




        3) Heteronymous
           a) Opposite sides of visual space for each eye
           b) Bitemporal or binasal defects
           c) The lesion is usually at the optic chiasm.


Ocular Pathology I                                                                                Page 87
            d) Slide 10-2 shows a bitemporal hemianopsia due to pituitary compression that is
               heteronymous and congruous




VII) Determining the site of the lesion by the VF defect
     A) Know the anatomy of the visual pathway (slides 12-1, 13-2, 13-3)
        1) Sensory retina (pre-ganglion cells)
        2) Retinal NFL to the optic nerve
              a) The optic nerve rearranges twice (at the anterior and posterior portions of the NFL)
        3) Optic chiasm
        4) Post-chiasmal
     B) The visual pathway is distributed throughout much of the brain
        1) Frontal, medial, LGN, parietal, temporal, occipital
     C) Important anatomical territory
        1) Pre-chiasm
        2) Chiasm
        3) Post-chiasm
     D) General depression
        1) VF with an overall decrease in sensitivity
        2) Optical factors
              a) Uncorrected refractive error (slide 12-3 vs. slide 13-1)
                  i) If you see a ring scotoma (a ring around the entire VF), it might be due to a trial lens
              b) Greater effect centrally (at the fovea)
              c) Media opacities (e.g. cataracts, corneal scars, vitreal problems)
              d) No characteristic pattern
        3) Long-standing or advanced disease
VIII) Specific defects
     A) Sensory retina (pre-ganglion cells)
        1) The visual field defect is in a location that matches the lesion
        2) Does not respect the horizontal or vertical meridian
        3) The size of the defect doesn’t always correspond to the size of the lesion
              a) Due to concurrent damage to other retinal layers (usually the ganglion cell layer and NFL)
        4) If there is a disconnection of retinal elements (retinal detachment), the result is an absolute
              defect
        5) Slide 14-2 shows the effect of retinitis pigmentosa. The white spots in the right figure are the
              areas that remain of the visual field.
     B) NFL (slide 15-3)
        1) NFL organization
              a) Macula
                  i) Nasal and temporal post-ganglionic fibers enter the temporal portion of the optic disc
                      as the papillomacular bundle
                  ii) Cecocentral or paracentral scotomas
              b) Peripheral
                  i) Nasal post-ganglionic fibers enter the nasal portion of the optic disc
                      (1) A lesion here results in a wedge-shaped scotoma extending from the blind spot
                  ii) Temporal post-ganglionic fibers (except the macular fibers) enter the superior and
                      inferior poles of the optic disc
        2) NFL defects respect the nasal horizontal meridian
              a) This is due to the horizontal raphe (the superior and inferior fibers don’t cross it)




           Wedge (arcuate) defect                 Nasal step



Ocular Pathology I                                                                                  Page 88
      3) Visual field defects due to glaucoma start as a nasal step and progress to a wedge defect
      4) NFL drop-out (slide 16-3)
   C) Optic nerve
      1) A cut optic nerve results in a bind eye
      2) Anatomy (slide 17-2)
          a) Anterior optic nerve
              i) Maculopappilary bundle is located in the lateral portion of the nerve
              ii) Everything else is in the medial portion of the nerve
          b) Posterior optic nerve
              i) Posterior to the entrance of the central retinal artery
              ii) Macular fibers are located in the center of the nerve
              iii) Inferior nasal and superior nasal fibers located medially around the outside
              iv) Inferior temporal and superior temporal are located laterally around the outside
          c) We’re still dealing with just the right eye or the left eye
      3) Consequences of optic neuropathies
          a) Reduced acuities
          b) Light brightness diminished
          c) Reduced color vision perception
          d) (+) RAPD
      4) VF defects (slide 17-3)
          a) Sector defect
          b) Cecocentral defect
          c) Enlarged blind spot (Seidel)        Sector defect          Cecocentral defect  Enlarged blind spot
   D) Optic chiasm
      1) Anatomy
          a) Temporal fibers (nasal VF) pass directly through to the ipsilateral optic tract
          b) Nasal fibers (temporal VF) cross to the contralateral optic tract
              i) Superior nasal fibers (inferior temporal VF) decussate posteriorly
              ii) Inferior nasal fibers (superior temporal VF) cross anteriorly in the chiasm and course
                   anteriorly into the contralateral optic nerve
          c) The chiasm is the beginning of mixed fibers with a separation of the right and left VFs
      2) VF defects
          a) Respect the vertical meridian
          b) Originate from fixation
          c) Junctional scotoma
              i) Located at the anterior chiasm and posterior optic nerve
              ii) Knee of Wilbrand
                   (1) Inferior nasal fibers makes a little hook (#8 on slide 19-2)




          d) Bitemporal hemianopsia
               i) Superior
               ii) Inferior
               iii) Bitemporal
               iv) Usually caused by a pituitary adenoma
          e) Binasal hemianopsia (very rare)
          f) Homonymous hemianopsia
   E) Optic tract (slide 20-3)
      1) Incongruous homonymous hemianopsia without macular sparing




       2) Respect the vertical



Ocular Pathology I                                                                                   Page 89
      3) Corresponding retinal points from the two eyes image the same point in the VF, but they don’t
         run together in the optic tract
      4) Consequences of optic tract lesions
         a) Possibly decreased visual acuity
         b) Possible (+) RAPD
              i) The pupillomotor fibers leave the optic tract just before the LGN and synapse in the
                  pretectal nucleus
         c) “Bow tie” optic atrophy (if the problem is long-standing)
      5) The farther back the lesion is in the tract, the more congruous the defects are
   F) LGN (slide 21-2)
      1) Homonymous hemianopsia
      2) Keyhole or sectoral defects
         a) Usually without RAPD or reduced visual acuity




   G) Optic radiations in the temporal lobe (slides 22-2, 22-3)
      1) Inferior fibers (superior VF) course anteriorly around the lateral ventricle from the LGN into
          the temporal lobe, forming Meyer’s loop
      2) Incomplete homonymous hemianopsia or quantrantanopsia (pie in the sky)




   H) Optic radiations in the parietal lobe (slides 22-2, 22-3)
      1) Superior fibers (inferior VF) course directly into the parietal lobe
      2) Homonymous hemianopsia




        3) Abnormal OKN (optomotor pathway)
        4) No RAPD or decrease in visual acuity
   I)   Occipital cortex (slide 24-1)
        1) Anatomy (slide 23-2)
           a) The macular cortex is at the tip of the occipital lobe
           b) The visual cortex lies above and below the calcarine fissure
           c) Total length is 5 cm
        2) Congruous homonymous hemianopsia
        3) Obey the horizontal
        4) Macular sparing
           a) Due to the dual arterial supply to the macular cortex
                i) Posterior cerebral artery (basilar artery)
                ii) Middle cerebral artery (internal carotid artery)
           b) You can’t always rule out the occipital lobe if macular sparing is not present
           c) Notice that #22 (top left) doesn’t have macular sparing




Ocular Pathology I                                                                               Page 90
       5) Checkerboard field (slide 24-3)




   J) General overview (slide 25-1)
      1) Know this slide because we’ll probably see it again




Ocular Pathology I                                             Page 91

				
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