Neuro II: Effects of SCI

what occurs with damage to descending motor tracts

UMN paralysis

what occurs with damage to the spinal nerves or cauda equina

LMN paralysis

UMN signs are due to

disruption of corticospinal connections (ascending or descending)

UMN signs

hyperreflexia, hypertonia (spasticity), flaciddity (early), discoordination, + babinski/clonus/other UMN signs

what must we differentiate UMN discoordination from

cerebellar discoordination (discoordination associated with UMN involvement is d/t motor impairment)

why might we see early flaccidity with UMN presentations?

spinal shock

T/F: we either see UMN or LMN presentation

F, can see widespread hypertonia but hypotonia locally at 1-2 levels

LMN signs

hyporeflexia, hypotonia, flaccidity

disruption of descending motor information traveling through the spinal cord impacts ___

gray matter at level of injury OR white matter traveling down the cord to other gray matter areas

how do motor system impairments present with SCIs

inability to contract/inefficient contraction of muscles w/ innervation below damaged area

what does increasing strength depend on?

completeness of injury, preservation of motor unit connections, propriospinal connection recovery and generation

what is usually disrupted in most SCIs? what does this lead to

sensation; dyscoordination, impaired awareness

sensory impairments are due to

disruption of ascending sensory information

where is light touch represented

spinothalamic, DCML

where is pain and temperature represented? where does it synapse?

spinothalamic; synapses and crosses in cord then travels up on contralat. side

what is represented in DCML? where does it cross?

proprioception, light touch, vibration; brain stem

what does sensory recovery depend on

repeated sensory input, restoration of connections, new connections through intact propriospinal networks

what is autonomic dysreflexia

pathological syndrome of massive imbalanced reflex sympathetic discharge causing hyperreflexia

who is autonomic dysreflexia unique to?

patients after SCI at/above T6 (above the sympathetic splanchic outflow)

what occurs with autonomic dysreflexia

massive reflex sympathetic surge from the thoracolumbar sympathetic nerves, causing widespread vasoconstriction and peripheral arterial hypertension

if not treated promptly, autonomic dysreflexia can lead to

stroke/death

signs/sx of autonomic dysreflexia

pounding headache, hypertension, bradycardia, sweating above lesion, goose bumps, flushing/blotching of skin above lesion, blurry vision

a bp of ___ mm Hg above baseline may be a sign of autonomic dysreflexia

20-40

acute management of autonomic dysreflexia

sit em up (drop BP), remove any binders/compression garments, search for the source

what are possible autonomic dysreflexia sources/stimuli

kinked catheter, full bladder, ingrown toenail, pressure irritation (restrictive clothes, binders, leg bag straps)

what occurs as a result of postural hypotension

dec cerebral blood flow and dec venous return to the heart

signs/sx of postural hypotension

dizziness, lightheadedness, ringing in ears, fainting

pt interventions for postural hypotension

graded progression to vertical, elevate HOB, recline WC with elevating leg rests, tilt table, compression stockings/binder

thermoregulation relies on

regulation of autonomic and somatic systems

why do we see thermoregulation difficulties with SCI? how does it present?

interruption of communication between hypothalamus and spinal cord; absence of thermoregulatory sweating below level of lesion (LOL), shivering below LOL`

what is the primary muscle of inspiration? what is its innervation

diaphragm; C3-5 (C4 primary)

what lesions results in inability to breathe without mechanical ventilation

above c4

external intercostals function and innervation

quiet inspiration by elevating ribs and increasing chest expansion; T1-12

what muscles are responsible for expiration? what is the result if they are lost?

abdominals (T5-12), internal intercostals; dec expiratory efficiency, dec cough effectiveness, dec secretion expulsion

during spinal shock, what occurs to muscles below LOL initially? what occurs as time passes?

areflexia; reflexes return and tone increases --> spasticity, clonus, inc DTRs

hypothesized reasons for changes in muscle tone

loss of inhibition from higher centers, loss of descending facilitation of afferents from GTOs, sprouting of new synaptic terminals within the cord CAUDAL to lesion, hypersensitivity of neurons CAUDAL to lesion

what is spasticity

velocity dependent resistance to passive stretch, resulting from hyper-excitability of the stretch reflex

when is spasticity most prevalent

higher lesions (cervical, upper thoracic), incomplete lesions (ASIA B, C)

advantages of altered muscle tone

circulation aided by muscle pumping, some tone can provide a functional assist, may dec extent of osteoporosis

disadvantages of altered muscle tone

dec ADL safety, masking of volitional movement, contractures, skin breakdown (shearing in WC), bowel/bladder dysfunction, pain

treatment strategies for muscle tone

stretching (helps temporarily, positioning out of spastic pattern, cryotherapy (temporary), e-stim, aquatic therapy (mixed evidence), EMG biofeedback

when might we see flaccid paralysis

caudal lesions d/t LMN paralysis, damage to anterior horn cell/nerve roots

what is required for voluntary control of urination/defecation

intact sacral cord communication with the brain

neurogenic bladder

detrusor stays relaxed, sphincter stays tight --> bladder continues to stretch and fill, cannot voluntarily void --> if overfilled can back up into kidneys and cause damage

what does neurogenic bladder require?

intermittent catheterization and bladder scans to keep volume under 500 mL

what must be regulated with neurogenic bladder

fluid intake (avoid excess alcohol, caffeine)

what are some of the issues with a folely

higher risk of recurrent infections, decreased bladder volume

what is LMN bladder

bladder muscle loses ability to contract and is easily stretched --> urine leaves the bladder when it is full and spills over into the urinary tract

how is LMN bladder managed

adult brief, condom catheter, maybe suprapubic catheter

what occurs with bowel management after SCI

messages from nerves in bowels aren't communicating with the brain --> patient does not know that their bowels are full

what occurs with bowel management after UMN

patient does not receive message that bowels are full and sphincter stays tight --> full bowels empty reflexively (involuntary)

what is neurogenic bowel

initial decrease in peristalsis and anal sphincter stays tight -> inability to volitionally contract/relax

management of neurogenic bowel

oral meds (to manage peristalsis), insertion of suppository, digital stimulation of bowel movement

considerations of bowel interventions

timed after meals to take advantage of gastro-colic reflex, consistent timing daily/every other day, good diet w/ insoluble fiber

what occurs with bowel management after LMN injury

message doesn't get to the spinal cord, therefore reflex doesn't work and anal muscles stay relaxed (flaccid bowel)

treatment for bowel issues after LMN injury

soluble fiber to bulk up stool and subsequent manual dis-impaction

what controls sexual function

controlled sacral nerves

what happens to male sexual function oftentimes after SCI

loss of genital sensation, degradation of sperm quality/motility

what is usually intact with sexual function after SCI

climax, erection in males

T/F: pregnancy is impossible after SCI

F, menstrual cycle may resume and pregnancy is still possible