Week 6: Descending Tracts, Reflexes, & Movement Flashcards
What is a UMN?
Starts & ends in the CNS
What is a LMN?
aka AMN; Synapses w/peripheral nerve
What is feed forward?
Anticipatory use of sensory info to prepare for movement (Used to create a motor program)
What is feedback?
Use of sensory info during/after movement to make corrections (Alters the motor program)
What is movement decomposition?
Segmented movement from a single jt rather than coordinated movement for multiple jt’s
What are 3 things that influence automatic movement routines?
Visual Input, Somatosensory Input, & Proprioceptive Input
Loss of visual, somatosensory, or proprioceptive input can cause what?
Some degree of movement decomposition
* Loss of accuracy * Timing issues * Loss of smoothness/efficiency * Can cause the need for conscious control
Other things that effect motor programs
- Intact NS/NS that needs to heal
- Skeletal muscle integrity & strength
- CV system
- Experience w/task
- Presence of well-learned movement patterns that need to be replaced
- Motivation (Conscious & unconscious)
Which tracts are for postural/gross movement tracts?
- Tectospinal
- Medial Reticulospinal
- Medial Corticospinal
- Medial Vestibulospinal
- Lateral Vestibulospinal
Where are the nuclei of postural/gross movement tracts located?
Medial spinal cord
What tracts are for fine movement & flexion?
- Lateral Corticospinal
- Lateral Reticulospinal
- Rubrospinal
Where are the nuclei of fine movement & flexion tracts located?
Lateral spinal cord
Examples of CPG’s
Walking, Running, Unicycling
CPG
Spinal cord circuitry that generates rhythmic, coordinated, & alternating movements w/minimal cortical input.
Results of UMN damage:
- Paresis/Paralysis
- Loss of fractionation
- Abn reflexes
- Velocity-dependent hypotonia
- Abn co-contractions–>Spastic CP
- Abn synergies
Results of LMN damage:
- Flaccid paralysis
- Atrophy
- Loss of reflexes
- Fibrillations
After a pt has a CVA, what side will they have motor & sensory loss?
Contralateral to the lesion
Sx’s of ALS
- Paresis
- Hyper-reflexia
- Babinski Sign
- Atrophy
- Fasciculations
- Difficulty swallowing, breathing, & speaking bc of CN involvement
Where does ALS cause destruction?
UMN’s, brainstem, & LMN’s
Brown-Sequard Syndrome
Injury to a hemisection of the SC
Sx’s of Brown-Sequard Syndrome
- Ipsilateral spastic paralysis below level of lesion
- Ipsilateral disruption of tactile, vibration, & position sense
- Contralateral destruction of pain & temp 1-2 levels below lesion
Sx’s of Brown-Sequard Syndrome
- Ipsilateral spastic paralysis below level of lesion
- Ipsilateral disruption of tactile, vibration, & position sense
- Contralateral destruction of pain & temp 1-2 levels below lesion
Explain crossed extension
Opposite side of the body doing opposite motions as a reflex
Explain reciprocal inhibition
Inhibitory neurons to an antagonist muscle
*Achieved by interneurons in the spinal cord linking LMN’s into fxnl groups
What is the fxn of the ventral anterior & lateral nuclei?
Motor planning & coordination
What is the fxn of the VPL?
Body sensation, pain, & temp
What is the fxn of the VPM?
Facial sensation, pain, temp, & taste
What is the fxn of the medial geniculate body?
Sound localization & perception
What is the fxn of the lateral geniculate body?
Coordination of visual signals