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HARVARD MEDICAL SCHOOLDEPARTMENT OF NEUROLOGY
MASSACHUSETTS GENERAL HOSPITAL
HARVARD MEDICAL SCHOOLDEPARTMENT OF NEUROLOGY
MASSACHUSETTS GENERAL HOSPITAL
HARVARD MEDICAL SCHOOLDEPARTMENT OF NEUROLOGY
MASSACHUSETTS GENERAL HOSPITAL
Parkinson’s Disease
Shirley H. Wray, M.D., Ph.D., Professor of Neurology, Harvard Medical School
Director, Unit for Neurovisual DisordersMassachusetts General Hospital
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Presenting Symptoms
Shuffling gait
Marked bradykinesia
Increasing rigidity
Diplopia reading
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Ocular Motor Performance
• Observe head position and posture
• Head movement + gaze
• Random eye movements
• Head tremor
• Eyelids blink rate (normal 25-30/min)
• Blepharospasm, clonus or apraxia
• Glabella hyperreflexia
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Ocular Motor Signs
Impaired convergence
Slow hypometric horizontal saccades
Normal vertical saccades
Saccadic substitution for smooth horizontal pursuit
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Convergence Insufficiency
Three factors:
Age
Parkinson’s disease
Medication (Sinemet)
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Ocular Motor Deficits in PD
The dopaminergic nigrostriatal pathways affected in PD control the latency, velocity and amplitude of saccades and the gain (ratio of smooth EM velocity to target velocity) of smooth pursuit.
Dysfunction of striatonigral-collicular circuits lead to abnormalities of normal programming of eye-head saccades.
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Saccadic EM in PD
Reflexive saccades to stimuli normalVolitional saccades impaired
Abnormal initiation and slow velocityRefixaiton saccades
Decreased amplitude, Hypometria, Increased saccadic latencies, Akinesia
Hypometria + Akinesia causes bradykinesiaAnti-saccades normal
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Potential nigro-colliculo-reticular sites which may disrupt saccadesFrontal eye field (FEF) + sup. colliculus (SC) lesion leads to slowed small saccadesFEFs project to corpus striatum, which has major outflow via substantia nigra pars reticulata (SNPR) to SCCells in SNPR which modulate with saccades and project through SC may be dysfunctionalSC activates pause cells in pontine RF
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PD: Eye Movements
Pursuit EMSlow and fast trackingAcceleration/de-acceleration
ConvergenceReflex EM Doll’s head and Bell’sTest for a phoria as cause of diplopiaAlternate eye cover, distance and near
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The severity of ocular motor impairment in PD correlates with the duration of the disease and the severity of bradykinesia and rigidity.
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Etiology of Slow Saccades
Spinocerebellar Ataxias (SCA), especially SCA2 (olivopontocerebellar atrophy)
Huntington’s DiseaseProgressive Supranuclear PalsyParkinson’s (advanced cases) and related
diseases. Lytico-BodigWhipple’s DiseaseWilson’s DiseaseAmyotropic Lateral Sclerosis (some cases)Drug intoxications: anticonvulsants,
benzodiazepines
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Courtesy of Mendez F. Cummengo JL. Dementia: A Clinical Approach. Third Edition. Butterworth Heinmann 2003.
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The following illustrations of
The brain MRI
Pathology of the midbrain
Lewy body
are taken from the case of an elderly
woman with Parkinson’s Disease
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Figure 1 Normal axial T2W1 through the midbrain shows the hypointense red nuclei and substantia nigra are separated by the pars compacta.
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Figure 2 In a patient with PD, the Axial T2W1 shows midbrain volume loss, especially the pars compacta, as shown by “touching” red nuclei and substantia nigra
Courtesy Anne Osborn, MD
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Figure 3 An autopsy in a patient with PD shows volume loss in the midbrain with pale-staining substantia nigra and decreased size of the pars compacta.
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Figure 4 Section of the brain showing cytoplasmic inclusion body within a surviving neuron with an eosinophilic core surrounded by a clear halo. The Lewy body is not entirely specific, but it is a highly sensitive marker for PD.
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Parkinson’s Disease
Due to dopaminergic cell death leading to dopamine deficiency
Defective gene for synuclein on Chr. 4q
Second locus on Chr. 2p
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ReferencesMendez MF and Cummings JL. Parkinsonian Disorders with Dementia. Ch. 7 Pg 235-290. Dementia a Clinical Approach, Third Edition, Butterworth-Heine, 2003.
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http://library.med.utah.edu/NOVEL/Wray/