Exam III Flashcards
what pathway
perception of lines, shapes, colors, and texture.
ventral stream!
where pathway
perceptions of spacial orientation, location, movement, and spacial relations.
dorsal stream.
prosopagnosia
a.k.a inability to recognize faces.
result of lesion to ventral/what stream.
balint’s syndrome
result of lesion to dorsal/where stream (posterior parietal lobe).
characteristics of balint’s syndrome
OPTIC ataxia - deficit in reaching for objects (spacial orientation)
OCULAR apraxia - deficit in visual scanning
SIMULTANAGNOSIA - inability to perceive two things at once.
importance of faces in human interactions
communicates:
1) age, gender, personal identity (physical structures)
2) mood, emotional state (facial expression)
3) interest/attentional focus (direction of gaze)
Faces
as a category = highly homogenous (similar) - all share basic parts placed in a fixed configuration.
individually = highly different - vary in many different aspects
faces require 1) _______
1) higher specificty
* we need to recognize specific faces rather than a general, unfamiliar face.
face cells
respond to faces only! activates very little to other types of visual stimuli. these cells are highly specific, and are effected by “face blindness”
fusiform gyrus
home of face cells
human motor system
LMN = lower motor neurons UMN = upper motor neurons
LMN
in GM of spinal cord and brainstem.
- these send axons out of CNS that directly innervate skeletal muscle fibers.
*innervation ratio :
extraocular = 1:10, hand =
1:1000, gastrocemius in
knee = 1:2000gamme motor neuron
innervates intrafusal muscle fiber (proprioceptor)
alpha motor neuron
innervates extrafusal muscle fibers (skeletal movement)
local motor neurons
reflex coordination and rythmic coordination
joint flexion
closes joints
joint extension
opens joints
** antagonistic
lesion to LMN
- reduced muscle tone
- weak/absent stretch reflex
- muscle atrophy
- fibrillation, a.k.a loss of nerve supply to muscle fibers
polio
infectious viral RNA disease in which LMN are destroyed
UMN
neurons that supply input to LMN
lesion to UMN
common causes include infractions of primary motor cortex (M1) and premotor cortex
- weak/absent voluntary movement
- spasticity
primary motor cortex
voluntary movement
premotor cortex
planning movement
hierarchal control
1) cerebral cortex
2) brain stem
3) spinal cord
motor learning
result of communication between primary and premotor cortex in coordination and planning of complex sequences of movement.
cerebral cortex
includes primary and premotor cortex that project directly to spinal cord via corticospinal tract.
brainstem
includes reticular formation, vestibular nuclei (balance), and inferior olive (targets)
- the brainstem integrates visual and vestibular information with somatosensory input to modify movement initiated by the cortex.
spinal cord
muscle contractions and limb movement and receives sensory feedback from proprioceptors.
subcorical systems
act on cortex via THALAMUS
regulates information from subcortical systems toward cortex
cerebellum - receives input from spinal cord and projects to both the brainstem and the thalamus (and onto cortex)
- improves accuracy of movement by comparing descending information about resulting motor actions.
cerebellum
separated into anterior lobe, primary fissure, posterior lobe, and vermis.
1) vestibulocerebellum - involved in balance and eye movements. lesion to this results in the inability to utilize vestibular information to adjust movement.
2) spinocerebellum - modulates muscle tone and motor execution. lesion to this results in hypotonia.
3) cerebrocerebellum - involved in motor planning. lesion results in delayed intimation/termination of movement.
vestibulocerebellum
involved in balance and eye movements. lesion to this results in the inability to utilize vestibular information to adjust movement.
spinocerebellum
modulates muscle tone and motor execution. lesion to this results in hypotonia.
cerebrocerebellum
involved in motor planning. lesion results in delayed intimation/termination of movement.
