motor system, muscle tone, and UMN/LMN part 1

basal ganglia

input: cortex, output: cortex, pedunculopontine nucleus, reticular formation
regulate muscle force, sequencing

cerebellum

input: cortex/brainstem, SC, vestibular system
output: cortex, brainstem, vestibular system
coordinates movement and postural control, timing and error correction

postural control

orientation and balance, requires 3 systems of balance
head position: vestibular, cervical proprioception, visual
postural control: medial tracts

reach and grasp

requires vision and somatosensation
phases: fast approach (feedforward, prediction), slow (homing in, visual feedback), contact and fine adjustment (likely feedforward with error corrections)

reach and grasp descending control

med motor system: control prox muscle and move hand toward object
lat motor system: orient and preshape the hand (feedforward)

locomotion centers: cerebrum

motor, limbic, BG, visual pathways
adaptive control of walking - modulates skill, initiate volitional locomotion, if attention required

locomotion centers: MLR

mesencephalic locomotor region
stepping produced by stimulation here, increased stimulation amplitude increases gait speed

locomotion centers: MRF

medullary reticular formation
interlimb coordination

locomotion centers: spinal cord CPG

central pattern generator
basic stepping pattern generator

muscle tone/stiffness

amount of tension in a resting muscle/resistance to stretch
measured with PROM, should have little to no resistance

muscle tone/stiffness mechanism

mechanical: major contributor, viscoelastic properties of muscle, weak cross-bridge binding
neural: min to no contributor at rest, descending motor control and reflexes

hypotonia

abnormally low resistance to passive stretch
disorders: developmental, acute UMN injury (spinal shock), acute cerebellar disorders, LMN lesions or disease
mechanism: loss LMN input to muscle, decreased descending input

flaccidity

no resistance, complete loss of tone, severe loss of LMN to muscle

hypertonia

velocity-dependent increased resistance felt as joint is passively moved through ROM
associated disorders: chronic UMN disorders
mechanism: neuromuscular overactivity, myoplasticity

myoplastic hyperstiffness

changes due to UMN lesions
loss of sarcomeres, increase weak cross-bridging, atrophy (stroke: type II > I, SCI: type I > II)

hypertonia: stroke

primarily myoplastic: increase in weak cross-bridging and contracture, hyperreflexia not significant
cortical strokes: CS tract disruption (loss fractionation), spasticity (reticulospinal tracts more active), but less hyperreflexia

hypertonia: SCI

myoplastic and neural: increase in weak cross-bridging and contracture and hyperreflexia
limits joint ROM, interferes with function, can cause deformity
lose corticospinal and reticulospinal input so increased excitability leads to more resistance and hyperreflexia

medications for spasticity

work to reduce excitability
baclofen: interferes with NT release in spinal cord
botox: interferes with Ach release from alpha MN
dantrolene: interferes with release of Ca from SR
diazepam: facilitates inhibition of SC

abnormal cutaneous reflexes

with SCI muscle spasms may occur in response to cutaneous stimuli after recovery from spinal shock
most common: muscle stretch hyperreflexia, clonus, clasp-knife response

muscle stretch hyperreflexia

loss of inhibitory CS input, LMN and interneuron increased excitability results in excessive LMN response to afferent stretch input
excessive muscle contraction when spindles are stretched from excessive firing LMNs

tonic stretch reflex

only present in people with UMN lesions, continues as long as stretch is maintained
loss of presynaptic inhibition allows slow or sustained stretch of central spindle to elicit continual muscle contraction, feedback loop that maintains neurologic tone

excess reticulospinal tract drive

corticoreticular lesions diminish cortical control of reticulospinal tract, absence of contra CS control so ipsi CS tract increases drive to reticulospinal tract
causes UMN dystonia (spontaneous excess contraction even at rest), abnormal muscle synergy

abnormal muscle synergies

reticulospinal tract provides voluntary control of paretic limb post stroke, consists of abnormal synergies that mainly affect proximal joints
activation of muscle groups that are unable to achieve the desired result

clonus

involuntary, repeating, rhythmic muscle contractions
unsustained clonus fades after a few beats even with maintained muscle stretch
sustained clonus >5 beats always pathologic, produced when lack of UMN control allows activation of oscillating neural networks in SC

clasp-knife response

paretic muscle is slowly and passively stretched, resistance drops at specific point in ROM, change in resistance similar to opening pocketknife
type II and Ib afferents elicit
autogenic inhibition: GTO, with increased tendon stretch muscle becomes inhibited so resistance drops