Case Studies Flashcards
Parkinsons Disease: Basal ganglia
-basal ganglia in the diencephalon (near the thalamus) : caudate and putamen (striatum), globus pallidus, subthalamic, and substantia nigra nuclei
-basal ganglia receive synaptic input from motor cortex -> send output to thalamus -> cortex = motor loop
-planning and programming of voluntary movement
-direct pathway- excitatory input -> inhibit inhibitory output in internal globus pallidus -> excites
-indirect- excitatory input -> disinhibits inhibitory output of internal globus pallidus -> inhibits
Parkinson Dopamine
-dopamine release from pars compacta neurons in substantia nigra -> excites direct pathway
-excitation of the direction pathway -> inhibits inhibitory output -> excites
-dopamine also inhibits indirect pathway -> increases the inhibition of inhibitory output
-in parkinsons dopaminergic neurons lack -> allows greater inhibition of thalamic neurons and greater suppression of movements initiated in cortex -> hypokinetic signs/tremors
Night vision problems, blurry vision in peripheral fields, myopia. Visual acuity of 20/100 bilaterally with visual field deficits on right and left periphery.
-optic chiasm lesion -> affect peripheral vision of both eyes
-pituitary tumors are lesions of the optic chiasm
-optic nerve lesion- ipsilateral vision loss in that eye
-optic tract lesion- homonymous hemianopia
-pupil size and retinal changes reflect underlying medical conditions
fovea
-region of retina
-in line with visual axis through center of the lens
-specialized for high acuity vision
-highest acuity when light strikes fovea
saccades
-quick
-preprogrammed
-ballistic eye movements
-used for searching for visual targets
-to explore visual space
-smooth pursuit movements to keep a target image centered on the fovea
pupil dilation
-Intrinsic muscles of the eye are controlled by parasympathetic fibers (ciliary muscle,
which regulates accommodation by the lens, and pupillary constrictor muscles) and by
sympathetic fibers (pupillary dilation)
difficulty walking and coordination, acute change in gate, unclear speech, blurring of vision, tremor, loss of hand coordination, no headache or vertigo. Unstable gait, poor hand eye coordination, nystagmus, fine tremor when moving it. She started taking phenytoin after switching from valproic acid. -> cerebellar ataxia
-lack of voluntary movement
-flocculonodular lobe (vestibulocerebellum)- most primitive part -> connects to primary vestibular afferents and lateral vestibular nuclei -> control balance and eye movement
-spinocerebellum- modulate motor programs in posture, locomotion, and gaze
-cerebrocerebellum- motor control planning and assess errors in movement
-cerebellum include modulating intrinsic motor programs involved in posture, locomotion, gaze, motor planning, unconscious control of novel motor patterns acquired during motor learning
-lesions do NOT produce paralysis or sensory deficit
-lesions disturb balance or ataxia -> slurred speech, dysmetria, inability either to stop or alternate opposing movements rapidly
cerebellar cortex
-inhibitory loop
-purkinje cells and inhibitory interneurons release GABA
-GABA opens postsynaptic Cl- channels to hold postsynaptic potential close to resting potential
room is spinning, dizziness, decreased hearing, ringing in ear, fullness in both ears. episodically and increasing in frequency. ringing in ears is more prominent. low frequency hearing loss. -> Meiniere’s disease
-otolithic mass in saccule and utricle
-hair cells project into geltainous cap encrusted with dense calcium carbonate otoliths
-can detect linear acceleration in any direction
-inertia bends the hairs in semicanals
-bending towards kinocilium -> increase tension on tip ->opens cation channels -> K+ influx -> depolarization -> release glutamate -> depolarizes peripheral terminal of primary afferent neurons -> action potential along vestibular nerve -> brainstem
-when where bends away channels close -> reduce K+ influex -> hyperpolarization
