motor organization Flashcards
organization of motor systems
primary motor cortex (precentral)
secondary motor cortex (premotor)
teritary cortex (prefrontal division)
primary motor cortex
connects with cerebellum, basal ganglia, thalamus, secondary motor cortex
- lesions are area specific
secondary /supplemental motor area
secondary: integration of motor skills and learned motor programs
supplemental: arousal level, initiating responses
- face motor area: organization and patterning of speech
prefrontal areas
pathways to basal ganglia, thalamus, brainstem reticular formation
- attends, integrates, formulates and executes activity
damage - difficulties in voluntary action, movement initiiation and executive dysfunctions
spinal horn
dorsal (posterior) - sensory processing
ventral (anterior) - motor neurons
upper motor neuorns
carry motor system output from the cortex to lower motor neurons in the BS and spinal cord
lower motor neurons
synapse with upper motor nuerons in BS or spinal cord and project to peripheral muscles
lateral corticospinal tract
- motor pathway in NS
- controls movements in the extremities
- UMN originate in M1 and synapse on ventral horn of spinal cord
corticobulbar tract
projects from cortex to brain stem
anterior corticospinal tract
ipsilateral- information from the trunks
corticospinal fibers
85% decassation at pyramid (lateral)
15% remain ipsilateral (anterior)
babinskis sign
normal- toes flex down when scraped
extensor plantar response- toes fan up
- means cortex was affected
im/probable locations of unilateral face, arm and leg paralysis with no sensory deficits
improbable: cortex because sensory involvement would be present, spinal cord because face would not be involved, LMN because face arm and leg on same side
probable: corticospinal and corticobulbar tract fibers below cortex and above medulla
side: contralateral to paralysis because above pyrimidal decussation
im/probable locations of unilateral face, arm & leg paralysis with sensory deficits
imporable: spinal cord and medulla because face is involved, LMN because face is involved
probable: entire primary motor cortex or corticospinal tract fiber below cortex above medulla
side: contralateral to paralysis (above pyramidial decussation)
im/probable location unilateral arm & leg paralysis
improbable: LMN: arm and leg on same side of body required, CS b/w M1 and medula: face would be involved
probable: M1 if sensation is affected, CSC b/w medulla and c5 of cervical
side: if M1- contralateral because above decussation
if spinal cord- ipsilateral because below decussation
im/probable location of unilateral face and arm paralysis
probable: lower homonculus (assume sensory)
imporable: internal capsule would affect legs
corpus striatum
caudate nucleus + putamen
lenticular nucleus
globus pallidus + putamen
direct pathway
Glu from cortex excites striatum
+ DA (d1) inputs from SNc
Ach excites synapses with GABA in GPi
GABA inhibits GPi releasing it from inhibition of thalamus
thalamus can now excite cortex –> movement
(-1)(-1) = + 1
indirect pathway
Glu from cortex excites striatum
- DA (d2) inputs from SNc
Ach excites synapses with GABA, ENK in GPe
GPe is released from inhibiting STN
STN can then excite GPi which inhibits thalamus from stimulating cortex –> inhibition of movement
(-1)(-1)(+1)(-1) = (-1)
2 classes of disorders of basal ganglia
hypokinetic: less movement - parkinsons
hyperkinetic: excess movement - huntingtons
parkinsons disease characteristics
second most common neurogenarative disorder and most common motor disorder
- associated with mutations
symptoms: difficulty initiating movement, slowness, stiffness, shaking at rest
cause of parkinsons
degeneration and loss of dopamine producing neurons in STN
- formation of Lewy bodies
parkinsons basal ganglai effects
direct: loss of DA neurons:
- not as much excitation to GABA
GABA doesnt release inhibition of GPi enough
GPi inhibits thalamus –> inhibition of movement
indirect: loss of DA neurons
- striatum has too much excitation because it doesnt receive inhibition from DA
- results in too much excitation from thalamus to cortex and unwanted movements
huntingtons characteristics
hyper kinetic: excessive movement
- common CAG repeat on huntington gene genetic disorder (more repeats)
- if one parent has disorder than 50% of siblings will carry
onset around 35-50 years
symptoms of huntingtons disease
quick and jerkey involuntary movements, rigidity
mental: loss of ability to concentrate, decreased ability to perform daily tasks, deteroation of judgement and memory, depression, dementia
neuropathology of huntingtons
dysfunciton and death of neurons in striatumm, cortex, hypothalamus
huntingtons basal ganglia
direct: loss of GABAergic leads to overinhibition of the thalamus and less movement produced
indirect: loss of GABAergic neurons leads to overactivation of the thalamus and hyperkinesia
