The voluntary vertical saccades are typically affected in..
a. Cortico basal degeneration.
b. Drug induced parkinsonism.
c. Idiopathic parkinsonism.
d.Progressive supranuclear palsy.
Yes parin..
Here is the Harrison expantion of ur summary..
Progressive Supranuclear Palsy ..
This is a sporadic neurodegenerative disorder of unknown etiology associated with tau Pathology
. It presents in the sixth to seventh decades and progresses faster than PD1, with death in 5 to 10 years. Risk factors include head trauma, vascular disease, dietary exposure to benzyl-tetrahydroisoquinolines (TIQ, reticuline), and beta-carbolines (reports from the West Indies).
PSP21 is characterized by akinetic rigid parkinsonism, dizziness, unsteadiness, slowness, falls, and pseudobulbar dysarthria. Tremor is distinctly uncommon. Supranuclear eye movement abnormalities affecting downgaze occur first, followed by variable limitations of upward and horizontal eye movement. Because the vestibular ocular reflex ("doll's eyes" maneuver) and the Bell's reflex (elevation and abduction of eyes on attempted lid closure) are intact, these abnormalities are termed supranuclear. Neurologic examination often reveals prominent stare and furrowed brow, axial (especially nuchal) and proximal distal limb rigidity and dystonia, as well as upper motor neuron and occasional cerebellar signs. Virtually all patients develop frontal-type cognitive dysfunction (Chap. 350), and a significant number may develop dementia with distinct subcortical features (e.g., abulia, mental inflexibility, and defects in memory retrieval). Brain MRI22 reveals midbrain atrophy (superior colliculus), and PET23 studies show symmetric frontal and striatal hypometabolism. Although some response may occur to levodopa and other antiparkinson medications, especially early in the course, treatment is generally not highly effective. The diagnosis is made on clinical grounds.
Pathologically, PSP24 is characterized by deposition of neurofibrillary tangles histochemically positive for tau (mostly 4-repeat tau) and negative for amyloid or a-synuclein. The deposits are associated with varying degrees of degeneration in the brainstem, basal ganglia, and cerebellum. There is loss of dopamine and dopamine receptors due to intrinsic striatal damage. This is thought to account for the poor response to therapy.
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