3.19 Spinal Region 3 Flashcards
syndrome
collection of s/s that don’t indicate a specific cause
anterior cord syndrome interferes with
- pain sensation
- temp sensation
- motor control
central cord syndrome: small lesion
loss of pain and temp at lesion level
central cord syndrome: large lesion
UE motor function impaired
Brown-Séquard syndrome: ipsilateral
- voluntary motor
- conscious proprioception
- discriminative touch
Brown-Séquard syndrome: contralateral
pain and temperature sensation
cauda equina syndrome
- sensory impairment
- flaccid paresis or paralysis of LE muscles, bladder, and bowels
tethered cord syndrome causes:
- low back and LE pain
- difficulty walking
- excessive lordosis
- scoliosis
- bowel/bladder control issues
- foot deformities
spinal cord syndromes often caused by:
tumors
trauma
Damage by MVA, sports injuries, and falls usually have one or more of these effects on the SC
- crush
- hemorrhage
- edema
- infarction
What injury type results in severed neurons?
penetrating wounds
spinal shock
- immediately after traumatic injury to cord
- cord functions below lesion are depressed or lost
spinal shock due to
interruption of descending tracts that supply tonic facilitation to SC neurons
What is lost/impaired during spinal shock?
- somatic reflexes
- autonomic reflexes
- autonomic regulation
spinal shock: somatic reflexes lost include
- stretch reflexes
- withdrawal reflexes
- crossed extension reflexes
spinal shock: autonomic reflexes lost include
- smooth muscle tone
- reflexive emptying of bowel/bladder
spinal shock: result of loss in autonomic regulation of BP
hypotension
What happens several weeks post SCI? (spinal shock)
most get some recovery of SC function
» return of reflex activity below lesion
stretch reflex hyperreflexia
In some people, spina neurons become excessively excitable
Why does hyperreflexia develop?
neuroplasticity produces new synapses in the reflex pathway
chronic SCI
neurologic deficit is stable
abn interneuron activities in chronic SCI
- inhibitory interneuron responses to type Ia afferent activity is diminished
- transmission from cutaneous afferents to LMN is facilitated
What does inhibitory interneuron activity diminished in chronic SCI correlate with?
hyperreflexia
Why are LMNs facilitated in chronic SCI?
loss of descending inhibition
complete SCI
no sacral sparing
incomplete SCI
preservation and/or motor function in lowest sacral segment
Loss of descending sympathetic control with lesions above T6 results in 3 dysfunctions
- autonomic dysreflexia
- poor thermoregulation
- orthostatic hypotension
compensation for poor regulation
excessive sweating above lesion level
Why do people with complete lesions over T6 level avoid exposure to high temperatures?
risk of heat stroke
signs of heat stroke
- high body temp
- rapid pulse
- dry, flushed skin
signs of hypothermia
- irritability
- mental confusion
- hallucinations
- lethargy
- clumsiness
- slow respiration
- slow HR
orthostatic hypotension =
≥ 20 mmHg fall in systolic or ≥ 10 mmHg fall in diastolic BP going from lying down to upright
Why does orthostatic hypotension happen in SCI pts?
- no sympathetic vasoconstriction
- no muscle pumping action for blood return
barriers to regeneration following SCI
- oligodendrocytes
- glial scars
- decreased growth rate of mature neurons
functional losses not due to original trauma occur because of
- bleeding
- edema
- ischemia
- pain
- inflammation
typical complications after SCI
- UTI
- spasticity
- fever/chills
- pressure ulcers
- autonomic dysreflexia
- contractures
- pneumonia
- heterotopic ossification
What can protect against UTI and pneumonia?
upright posture
What can help prevent decubiti and contractures?
mobility
