TEST 3 TABLES

C5

elbow flexion

C6

wrist extension

C7

elbow extension

C8

flexion of tip of middle finger

T1

finger abduction

L2

hip flexion

L3

knee extension

L4

ankle dorsiflexion

L5

great toe extension

S1

ankle plantarflexion

postural tremors

occur when body part is maintained against gravity

intention tremor

occurs with voluntary movement

resting tremor

occurs in relaxed body part

resting tremor

caused by parkinson’s disease

intention tremor

tremor caused by cerebellar lesion

postural tremor

enhanced physiologic tremor

UMN dystonia

involuntary muscle contraction that contributes to spasticity.

UMN dystonia

produced by excess reticulospinal drive to LMNs

spasticity

velocity dependent hypertonia

spasticity

secondary to UMN lesion

paresis or paralysis

decreased or lost ability to generate the level of force required for a task

paresis or paralysis

occurs in all UMN lesions

myoplasticity

adaptive changes within muscle secondary to UMN lesion or prolonged positioning

myoplasticity

Ex: muscle atrophy, contracture and increased weak actin-myosin binding

muscle tone

amount of tension in resting muslce

muscle tone

is assessed passively

muscle tone

not an indicator of ability to move actively

muscle overactivity

muscle contraction that is excessive for the task

muscle overactivity

caused by excess neural input to the muscles

muscle overactivity

may be due to excess reticulospinal drive, excess vestibulospinal tract drive, pain, anxiety, or lack of skill in task performance

muscle contracture

adaptive shortening and stiffening of muscle caused by muscle remaining in shortened position for prolonged time

muscle contracture

decrease in length is caused by loss of sarcomeres

muscle contracture

increase in stiffness is caused by connective tissue thickening and loss of elatsticity

hyperreflexia

excessive reflex response to muscle stretch.

hyperreflexia

caused by reduced descending inhibition of LMNs and subsequent development of interneuron and LMN excessive excitability

hyperreflexia

contributes to movement disorders post spinal cord injury and in spastic cerebral pasly

hyperreflexia

rarely interferes with functional movement post stroke

pathologic cocontraction

temporal overlap of agonist and antagonist muscle contraction that interferes with achieving the movement goal.

pathologic cocontraction

prevalant in spastic cerebral palsy

abnormal synergy

abnormal coupling of movement due to stereotyped coactivation of muscles

abnormal synergy

shoulder abduction and external rotation combined with elbow flexion when someone tries to reach up

abnormal synergy

mechanism: loss of lateral corticospinal selective motor control plus voluntary activate if ipsilateral cortical drive to reticulospinal tracts

baclofen

can be oral or inarthecal (pump)

baclofen

interferes with excitatory transmission

dantrolene sodium

interferes with calcium release from skeletal muscle sarcomplasmic reticulum

dantrolene sodium

directly interferes with muscle contraction

botulinum toxin injection

preventing lower motor neurons from releasing ACh

C8

vertebral bodies: C6-C7

C8

bony spinous proces: C6

T1

vertebral bodies: C7-T1

T1

bony spinous process: C7

T10, T11

vertebral bodies: T9

T10, T11

bony spinous process: T8

L2-L5

vertebral bodies: T12

L2- L5

bony spinous process: T10

S1-S5

vertebral bodies: L1

S1-S5

bony spinous process: T12, L1

anterior cord syndrome

caused by disruption of blood flow in the anterior spinal artery

anterior cord syndrome

interferes with nociceptive and temperature sensation and with motor control

anterior cord syndrome

light touch and proprioception are spared

central cord syndrome

results from trauma

central cord syndrome

small loss of nociceptive and temperature info at level of lesion

central cord syndrome

larger lesions impair UE motor function, nocieceptive, temperature

brown-sequard syndrome

results from hemisection of spinal cord

brown-sequard syndrome

proprioception and light touch lost ipsilaterally: nociception and temperature lost contralateraly

cauda equina syndrome

causes my damage to lumbar and/or sacral spinal roots

cauda equina syndrome

causes flaccid paresis or paralysis or LE, bladder and bowls

cauda equina syndrome

spactisity and hyperflexia does not occur because of this because proper motor neurons intact

cauda equina syndrome

complete lesions are rare

tethered cord syndrome

vertebral cord elongates during development and spinal cord becomes stretched

C2, C3

Motor: facial muscles, upper trap

C2

sensory: posterior head, upper neck

C3

sensory: lower neck

C4

motor: diaphragm

C4

sensory: upper shoulder

C5

motor: elbow flexors

C5

sensory: lateral upper arm

C6

motor: wrist extensors

C6

sensory: lateral forearm, lateral hand

C7

motor: elbow extensors

C7

sensory: middle finger

C8

motor: finger flexors

C8

sensory: medial hand

T1

motor: finger abductors

T1

sensory: medial forearm

T2

sensory: medial upper arm

T3-T6

sensory: torso

T7,T8,T9,T10,T11,T12

motor: abdominals, lateral spine flexion

T7-T12

sensory: torso

T10

sensory: umbilicuslevel

L1

sensory: anterior upper thigh

L2

motor: hip flexors

L2

sensory: anterior thigh below L1

L3

motor: knee extensors

L3

sensory: anterior knee

L4

motor: ankle dorsiflexors

L4

sensory: medial leg

L5

motor: long toe extensors

L5

sensory: lateral leg, dorsum of foot

S1

motor: ankle plantar flexors