Lab 3/1 Flashcards
midbrain lesions lead to
affected gait, PLR, v-lat strabismus, globe rotation, altered state of consciousness
cerebellum fx
motor execution and error correction
coordination of movement
vestibular fx
cerebellar white matter
brainstem -> cortex
cerebellar nuclei -> cortex
brainstem -> cerebellar nuc
granule cell layer
deepest; small tightly packed neurons
purkinje cell layer
1 cell layer thick btwn granule cell layer and molecular cell layer
purkinje cell dendrites
into molecular layer; other axons come up perpendicular to those
molecular layer
mostly made of purkinje cell dendrites and axons projecting to purkinje cells
cerebellar input
sensory systems and motor programs
cerebellar output
purkinje cells -> cerebellar nuclei -> UMNs
purkinje cells ->
cerebellar nuclei -> UMNs
cerebellum lives in ____ bounded dorsally by ____
lives in cd cr fossa; bounded dorsally by tentorium cerebelli
cerebellar lesions will likley
also effect cd brainstem unless v small or vascular
vestibulocerebellum afferents
vestibular via ccp
vestibulocerebellum efferents
vestibular nuclei via ccp
vestibulocerebellum fx
- posture
- balance
- VOR
vestibulocerebellum incluse
floculonodular lobe -> vestibular nuclei -> vestibulocerebellum
spoinocerebellum major afferents
- spinocerebellar pathways (via CCP)
- cerebral cortex (UMNs and sensory via MCP)
spinocerebellum efferents
UMNs (via RCP)
spinocerebellum fx
- real time error correction
- posture
- balance
- tarted limb movements
- locomotion
- postural rxns
does cerebellum play a role in menace pathway
yes; its the step before synapse on facial nucleus
spinocerebellum includes
vermis and paravermis and fastigal and interposos nuclei
cerebrocerellum
planning and regulation of skilled movements
- less developed in domestic animals (lat hemisphere -> dentate nucleus -> motor cortex)
cerebellar cortical atrophy histo change
dispranized; granule cell layer = less tight and dense = more spread out purkinje cells over it there defining boundary between granular cell or molecular layers
general proprioceptive ataxia pathays
caused by lesion involving ascending proprioceptive pathways (spinocerebellar pathways, DCML pathways) in spinal cord or brainstem; can have lesion in forebrain but this is much less severe
GPA clinical signs
sloppy gait with long sloppy strides, scuffing, can’t predict where feet being placed; floating, delayed protraction
GPA ipsilateral if lesion in
- spinal cord
- medulla
- pons
GPA contralateral if lesion in
forebrain
vestibular ataxia seen with lesion in
vestibular apparatus, vestibular nerve, vestibular nuclei, flocularnodular lobe
vestibular ataxia clinical signs
wide based stance, short choppy strides, falling over (usually toward side of lesion)
cerebellar ataxia occurs with lesion in
cerebellum b/c loss of cerebellar circuits to regulate locomotion through rubrospinal and reticulospinal tracts/ pathways
cerebellar ataxia clinical signs
hypermetira, intention tremors, cerebellar lesion can also -> vestibular ataxia
wide based stance
can be seen with all 3 types of ataxia but is most pronounced with vestibular ataxia
decerebellate rigidity vs decerebrate rigidity
decerebellate rigidity will often have pelvic limbs flexed at hips and the big difference is that there is no mentation difference (ie the patient is wide awake and alert)
cerebellar cortical abiotrophy histo change
degeneration of prukinje cells
largest commissure connecting left and right side of telencephalon
corpus callous; shiny band of tissue deep within longitudinal fissure
what is ventral to corpus callous
fornix
fornix is associated with
hypocampal formation (archicortex)
lamina terminalis
rostral boundary of diencephalon; separates diencephalon from telencephalon
fibers between diencephalon and piriform lobe
fibers of internal capsule
optic tract path
moves cdly and dorsally until surrounds and synapses on LGN of thalamus
LGN
protrudes laterally from cd diencephalon
cd aspect of 3rd ventricle leads to
mesensephalic aquaduct