DSA12 Shi Spinal Cord Physiology Flashcards
Type I muscle fibers
Oxidative, slow velocity of shortening
Type IIa muscle fibers
Fast-oxidative-glycolytic
Type IIb muscle fibers
Fast-glycolytic
Describe the symptoms of muscle denervation syndrome.
Atrophy, fasciculations and fibrillations.
Type Ia/II sensory fibers
In parallel with extrafusal fibers; sense changes in length/stretch
Type Ib sensory fibers
In series with extrafusal fibers (Golgi tendon organ); sense changes in force/tension.
stretch/myotatic reflex
Stretch receptors (type Ia/II) directly activate alpha motor neurons (monosynaptic). Also triggers reciprocal inhibition via interneurons.
skin receptors - reflex arc
Receptor sends signal to cell in dorsal horn which integrates signals and activates motor neurons in ventral horn to act on effectors. Reciprocal inhibition.
flexor reflex
Nociceptors enter the spinal gray and synapse on: ascending neurons (conscious perception), excitatory interneurons (flexors), and inhibitory interneurons (extensors).
crossed extension
Adding to the flexor reflex, nociceptors also activate interneurons that decussate and activate excitatory (extensors) and inhibitory (flexors) interneurons.
tendon organ reflex
Given excessive stretch, autogenic inhibition of the muscle will occur via the Golgi tendon organ neurons, which activate inhibitory (extensors) and excitatory (flexors) interneurons. Prevents the excessive action of the myotatic reflex.
rubrospinal tract
CARRIES: goal-directed motor movements
tectospinal tract
CARRIES: reflex head movement
Which is the only tract that decussates in the spinal cord?
Spinothalamic tract
plantar flexion reflex
Response to scratching surface of foot
Babinski sign
Dorsiflexion in response to scratching surface of foot. Indicates UMN damage.
abdominal reflex
Stroking skin below umbilicus produces contraction of abdominal muscles. Absent in UMN damage.
What are the signs of LMN damage?
Flaccid paralysis, decreased DTR, atrophy, fasciculations & fibrillations. No Babinski’s sign.
What are the signs of UMN damage?
Spastic paralysis, increased or unaffected DTR, Babinski’s sign. Atrophy can be present if due to long-term disuse. No fasciculations or fibrillations.
What tissue is affected in poliomyelitis?
Alpha motor neurons of spinal cord.
S/Sx of Tabes Dorsalis
Damage to dorsal columns and spinocerebellar tracts (due to neurosyphilis) leads to sensory ataxia (aka Friedreich ataxia or cerebellar ataxia); ROMBERG’S SIGN.
Romberg’s sign
The inability to maintatin steady posture with feet close together when eyes are closed because of loss of proprioceptive input. Demonstrative of degeneration of dorsal columns/spinocerebellar tracts, as in neurosyphilis/tabes dorsalis.
amyotrophic lateral sclerosis
Bilateral degeneration of both corticospinal tracts (UMNs) and motor neurons in cranial nuclei and ventral horns (LMNs), so patient has signs of both.
Brown-Sequard syndrome
Complete or partial hemisection; usually due to trauma.
syringomyelia
Progressive cavitation of central canal. Damages decussation of spinothalamic tract (thoracocervical area, so arms/hands/shoulders). Variable symptoms depending on the spread.
spinal shock
An initial reaction to interruption of cord reflexes immediately following SC transection (loss of tonic input throws reflexes off). Flaccid paralysis (may also have spastic paralysis), areflexia (resolves in 2 weeks-several months, but may be hyperexcitable; Babinski shows up), BP drop (resolves within a few days) and retention of urine & feces(usually return in a few weeks).
