UMN and Spinal Cord Learning Objectives Flashcards
describe the meaning of GP and GSA
GP: general proprioception; the sensory system that detects the state of the position and the movement in muscles and joints
GSA: general somatic afferent: sensory for touch, temperature, and nociception
what do sensory nerves carry?
both GSA (general somatic afferent) and GP (general proprioceptive) information
what are the 2 components of proprioception? describe
unconscious transmission to the cerebellum: via sensory nerve input, the cerebellum knows where the limb/body is before you move it so that the cerebellum can modify that movement by influencing the UMN in the brain that will then generate gait
conscious: GP info goes to the cerebral cortex for conscious recognition of body movement (I moved my arm and I know I moved my arm)
define and describe GP ataxia
looks the same as UMN paresis! not knowing where your limbs are in space, crossing legs, scuffing
broadly define the course and components involved in postural reaction testing
- proprioceptors convey sensory information proximally along peripheral nerves
- this information ascends in the spinal cord to the cerebellum (unconscious) and the cerebrum (conscious)
- UMN from brain descend spinal cord to LMN to flip paw back over
need both normal proprioception and a functioning LMN unit for normal postural reactions!!
how do postural reactions in part assess the GP system?
need to be able to perceive that paw has been flipped over in order to know that you need to flip it back
is postural reaction testing specific for the assessment of the GP system or its components?
nope, also need a function LMN unit to be able to move limb or flip it back over!
what is needed for normal postural reactions?
normal function of UMN, LMN, and GP (tests everything!!)
what are the 4 major collections of UMN that project into the spinal cord? which are more important for gait generation? is the motor cortex of the cerebrum and corticospinal tracts necessary for gait development?
according to barber all we need to know about this right now is that the UMN cell bodies are located in the cerebrum an the brainstem and only the ones in the brainstem are important for gait generation!
how does UMN affect LMN?
UMN both facilitate AND inhibit the LM responsible for flexor muscles and the extensor muscles/tone
broadly describe the course of UMN from their origin (brain) through the spinal cord
UMN are found in various locations throughout the cerebrum and brainstem and descend from the brain mainly in lateral and ventral funiculus of the spinal cord
what does loss of UMN info result in?
UMN quality paresis
define UMN paresis/paralysis
inability to generate a gait;
1. paresis
2. spasticity
3. hyperreflexia
4. NO muscle atrophy
contrast LMN versus UMN gait quality
LMN is short and choppy, UMN is long and lopey/overreaching
in naturally occurring disease, can ascending GP and descending UMN be affected separately?
no they are bth affected and the resulting gait involves both GP ataxia and UMN paresis
describe reflexes, tone, and muscle size with a UMN lesion cranial to the intumescense
reflexes: normal to increased
tone: normal to increased
muscle size: normal/no atrophy
contrast UMN lesions with LMN lesions in assessment of reflexes, tone, and muscle size
LMN: decreased to absent reflexes, decreased/flaccid tone, decreased muscle size/atrophy
UMN: normal to increased reflexes, normal to increased tone, normal muscle size