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SNS thermoregulation
adrenal medulla increases metabolic rate, skin innervation controls blood vessel diameter, sweat gland secretion, and piloerection
SNS blood flow regulation
prevents pooling blood via vasoconstriction
SNS cardiac regulation
increased HR and contractility
SNS pulmonary regulation
bronchodilation
SNS GI regulation
decrease blood flow, peristalsis and digestion
SNS genitourinary regulation
stimulates orgasm, bladder and rectal wall relaxation/internal sphincter contraction
SNS head innervation
dilates pupil, elevates eyelid, innervates salivary glands
PNS CN
III, VII, IX, X
PNS head innervation
constrict pupil, widen lens, innervate lacrimal and salivary glands
PNS cardiac
decreased HR and decreased contractility
PNS pulmonary
bronchoconstriction
PNS GI
increased blood flow, peristalsis and digestion
Spinal nerves S2-4 GI
increased blood flow, peristalsis and digestion
Spinal nerves S2-4 Genitourinary
stimulates erection, bladder and rectal wall contraction/internal sphincter relaxation
acute ANS thermoregulation
hypothermia due to vasodilation
chronic ANS thermoregulation
hyperthermia due to loss of sweat gland innervation
OH Sx
decreased systolic >20mmHg or decreased diastolic >10mmHg, dizziness, nausea, lightheadedness, pallor, diaphoresis, LOC
preventative OH Tx
pharmaceuticals, ab binder, elastic stocking, tilt table protocol
treatment for symptomatic OH
recumbent position, elevate LE
autonomic dysreflexia
hypertension and bradycardia
autonomic dysreflexia most common in
T6 lesion and above
autonomic dysreflexia manifests (usually)
6 mo after injury as a result of maladaptive neuroplasticity
autonomic dysreflexia symptoms
pounding headache, flushing, profuse sweating, anxiety, nasal congestion, visual changes
autonomic dysreflexia preventative treatment
pharmaceuticals
autonomic dysreflexia symptomatic treatment
upright position /c dep LE, removal of noxious stimulus
injury above T6
interrupts descending modulation of thoracolumbar sympathetic neurons
thoracolumbar sympathetic neurons regulate
vasomotor tone in splanchnic vascular bed (organs)
splanchnic nerves arise from
T5-T12
splanchnic nerves? receive
25% of CO
AD can/cannot occur with an injury below T6
CAN (although uncommon, and HTN/HR changes more mild)
DVT common in
acute phase (72hrs to 2weeks)
underlying mechanism of DVT
peripheral vasodilation, decreased extremity function, immobility
Risk factors for DVT
M, flaccid paralysis, complete injury, paraplegia
S/S of DVT
edema, erythema, warmth
DVT prevention
anti-coagulants, compression devices, filters to minimize PE risk (sits in IVC)
80% of SCI pts have
neurogenic bowel dysfunction
enteric nervous system (ANS)
activated by rectal stretch, causes peristalsis and internal sphincter relaxation
ANS Bowel
parasympathetic division (spinal segments S2-4), works to augment intrinsic function
Without parasympathetic innervation there is
no defecation
Bowel cortex
stretch reflex ascends, volitional assist of evacuation/enhanced external sphincter functino
somatic motor neurons bowel
sacral spinal segments S2-4, volitional control of external spinchter and puborectalis
Arreflexive bowel
LMN lesion within/below conus medullar is affecting Parasympathetic and somatic cell bodies in S2-4, resulting in tonically active internal sphinchter and denervated external sphincter/puborectalis
in arreflexive bowel pt is at risk for
constipation/impaction and fecal incontinence
Reflexive bowel
UMN lesion above conus medullaris with preserved reflexive arc
bowel reflexive arc
afferent rectal stretch
triggers intrinsic and parasympathetic relaxation of internal sphincter
defecation
with reflexive bowl pt is at risk of
incontinence
Bowel recommendations
introduce consistent bowel routine
promote physical activity
abdominal massage
maintaining optimal stool consistency-diet and medication
reflexive bowel treatment
stool softeners, digital stimulation
arreflexive bowel treatment
bulkers for solid stool, manual evacuation, valsalva maneuver
bowel complications
ileus, GERD, ulcers, hemorrhoids, autonomic dysreflexia, pain
potential other bowel treatments
biofeedback, sacral nerve stimulation, sacral anterior root stimulation, epidural/non-invasive electrical simulation, surgical intervention (colostomy, ileostomy, MACE), transanal irrigation
parasympathetic bladder
S2-4, role in detrusor muscle contraction and internal sphincter relaxation
sympathetic bladder
T11-L2, role in detrusor m relaxation and internal sphincter contraction
brainstem bladder
pontine micturition center sends info via reticulospinal tract, resulting in inhibition of SNS and excitation of PNS
bladder somatic motor neurons
spinal segments S2-4, control of external urethral sphincter and pelvic floor musculature
cortex bladder
stretch signal to cortex, descending cortical inhibition for volitional urination/retention
arreflexive bladder
LMN within/below conus medullaris affecting parasympathetic and somatic cell bodies in S2-4, resulting in loss of parasympathetic input to bladder
pt with arreflexive bladder is at risk for
urinary retention and dribble incontinence
reflexive bladder
UMN lesion above conus medullaris with preserved reflexive arc
bladder reflexive arc
afferent urinary stretch
triggers parasympathetic contraction of detrusor m and relaxation of internal sphincter
urination
Pt with reflexive bladder is at risk for
incontinence and may develop dyssynergia
arreflexive bladder treatment
catheterization, manual pressure
reflexive bladder treatment
catheterization, reflex voiding
bladder dysfunction complications
UTI, urinary stones, renal damage, vesicoureteral reflux, AD
vesicoureteral reflux
pee goes up rather than down
reflexive erection
response to SA stimulus, PNS S2-4
psychogenic erection
response to whatever, origin in cortical centers, SNS T11-L2
Seminal emission is under control of
supra spinal centers and T10-T12 sympathetic spinal segments
ejaculation is mediated by
sacral reflexive activity
ejaculation reflex
semen in urethra, S2-4 sacral segments, somatic efferents
Erection in T11 lesion and above
reflexive arousal only
erection in sacral lesion
psychogenic arousal only
after SCI sexual dysfunction
most have erection capacity retained, infertility due to inability to ejaculate, decreased sperm count and motility
reflexive F arousal
response to SA stimulus, PNS segments S2-4
psychogenic F arousal
response to whatever, origin in cortical centers, SNS T11-L2
smooth m activation
uterine and fallopian tube activation
smooth m activation (sexual) under control of
supra spinal centers as well as T11-L2 sympathetic spinal segments
striated m contraction
mediated by sacral reflexive activity, continued afferent stimulation to S2-4 segments to SE
F arousal Complete T6 and above
only reflexive arousal
arousal sacral lesion (F)
only psychogenic arousal
striated m contract F SCI
more likely to achieve if reflexive arc is intact
F acute fertility
cessation of period for ~4mo /p injury
chronic fertility F
generally remains fertile
Risks of labor /c SCI
inability to feel contractions, AD
a pt in labor /c a SCI needs
an epidural or C section
neurological heterotrophic ossification
NHO or HO
NHO diagnosed by
radiograph
NHO/HO
formation of bone in soft tissue
NHO/HO may cause
skin breakdown, pain, ROM restriction
NHO/HO occurs in
10-50% of SCI, below NLI
NHO/HO frequently occurs
1-6 mo after injury
risk factors for NHO/HO
complete lesions, microtrauma, M, genetics, DVT, pressure ulcers, UTI, spasticity
osteoporosis in SCI develops
in extremities below lesion (more severe in LE)
etiology of osteoporosis
Poorly understood, likely reduced tensile forces from m, reduced WB, altered circulation, reduced innervation, endocrine/immune system changes
osteoporotic changes most rapid
first few months /p injury
increased likelihood of fractures after SCI
25-40%
fracture risk factors
motor complete (a/b), paraplegia, white, time since injury, advanced age, F, lower BMI
C1/2 VC
5-10% of baseline
C3-4 VC
24% of baseline
C5-8 VC
30% of baseline