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ALZHEIMER'S AND EYE.pptx
- 1. OCULAR MANIFESTATIONS IN ALZHEIMER’S DISEASE ANUJA DHAKAL OPTOMETRIST
- 2. LAYOUT • Introduction • Pathophysiology • Ocular structural changes • Ocular functional visual changes
- 3. INTRODUCTION • Alzheimer’s disease (AD) is the most common form of dementia affecting the growing aging population today, with prevalence expected to rise over the next 35 years. • Clinically, patients exhibit a progressive decline in cognition, memory, and social functioning due to deposition of amyloid β (Aβ) protein and intracellular hyperphosphorylated tau protein. • AKA senile dementia of the Alzheimer’s type(SDAT).
- 4. • Presently, AD can only be diagnosed post-mortem on histo-pathological examination. Diagnostic investigations are limited, and physicians rely on clinical examination and exclusion of differential diagnoses that may cause cognitive impairment, such as Depression, Parkinson’s disease (PD), Hypothyroidism, Drug interactions, and Vitamin deficiencies . • Clinically, a diagnosis is made based on history, examination, and where available, accounts from relatives or carers.
- 6. PATHOPHYSIOLOGY Two signature lesions : 1)Neuritic plaques/ B – amyloid plaques Deposition of extracellular senile plaques, which is composed of amyloid β (Aβ) 2)Neurofibrillary tangles (NFT’S), build up inside the nerve cell Resulting from intracellular (intraneuronal) aggregates of hyperphosphorylated tau protein detected in the brain.
- 7. NEUROBIOLOGICAL MECHANISMS Mutations Environmental factors Amyloid precursor protein Amyloidogenic peptides Oligomers Amyloid plaques Tau pathology Neuronal death Amyloidogeneic proteolysis Aggregration Aggregration Synaptic Neurotransmitters Alterations
- 8. OCULAR ANATOMICAL CHANGES WITH ALZHEIMER’S 1. TEARFILM: Change in chemical barrier composition of tears 2. CORNEA: Reduced corneal sensitivity 3. AQUEOUS HUMOUR :Presence of β-amyloid peptides&chemokines 4. PUPIL: Atypical response to cholinergic antagonists Lower amplitude and latency to light reflex Pupillary mydriasis.
- 9. 5. LENS: Deposition of β-amyloid Predisposition to supranuclear cataract 6. RETINA : Decreased retinal blood flow RNFL thinning Ganglion cells degeneration & reduction in axons B-amyloid deposition in retina Deposition of : TAU, Aβ ,PTAU Reduced in retinal thickness Retrograde degeneration of cortical neurons Inflammation.
- 10. 7) CHOROID : Reduction/ Attenuation of choroidal thickness Choroidal vascular B-amyloid deposits. 8) OPTIC NERVE : Axonal degeneration Loss of optic nerve thickness Papillary paleness(increased pallor ) Increased Cup-Disc ratio Affect in Magnocellular pathway Optic disc atrophy in absence of Glaucoma.
- 11. VISUAL PATHWAY CHANGES 9. LATERAL GENICULATE NUCLEUS : Lipofuschin accumulation Resistance to tangle formation 10. SUPRACHIASMATIC NUCLEUS : Degeneration 11. VISUAL CORTEX : Myelin reduced in outer laminae Loss of pyramidal cells 12. B17 : Numerous cored senile plaques but few Tangles.
- 12. FUNCTIONAL VISUAL CHANGES 1. VISUAL ACUITY: Decreased in low luminance 2. VISUAL FIELD: Inferior hemi-field loss 3. STEREOPSIS: Reduced stereopsis, mean threshold >150” arc 4. COLOUR VISION: Poor colour discrimination Deficiency in tritan axis (blue-violet) Incomplete achromatopsia
- 13. 5. CONTRAST SENSITIVITY: Reduced contrast sensitivity in low luminance Reduced reading speed in low contrast. 6. MOTION PERCEPTION: Higher threshold for motion detection in all spatial frequencies 7. SACCADES: Abnormal hypometric saccades Abnormal saccadic initiation Delayed peak velocity 8. PURSUIT :Impaired with intrusion of saccades Increased latency
- 14. 9. VISUAL MASKING: Significantly affected by backward masking 10. FIXATION: Affected 11. EYE-HEAD CO-ORDINATION: Impaired 12. ERG: Reduction of wave amplitude in pattern ERG 13. CORTICAL VEP: Normal P100 latency & delayed flash P2 latency
- 15. 14. VISUOSPATIAL: Deficits observed in 40-50% 15. VISUAL HALLUCINATIONS: 20% of people experience it 16. CIRCADIAN RHYTHM: Alterations in circadian rhythm B-amyloid deposits around degenerative mRGCs
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