Exam IV Flashcards
Concussion in association with SCI
temporary loss of function due to blow or violent shaking
Contusion in association with SCI
bleeding from local blood vessels due to bruising, causes compression from hemorrhages.
Laceration/maceration in association with SCI
more severe injury, may cause transection – from gunshot or knife wounds
Complete SCI
all functions below the injured area are lost, whether or not the spinal cord is severed. To be classified complete, there should be absence of all sensory and motor function in the lowest sacral segments supplied by S4-5 nerve roots.
Incomplete SCI
involves preservation of some motor and/or sensory function below the level of injury. For incomplete, needs some preservation of sensory or motor activity innervated by S4-S5, sacral sparing.
SCI Primary injury
In 1st 2 days – necrotic death secondary to direct trauma to tissue or blood vessels (causing hemorrhage and compression). Important to adequately stabilize injured spine to stop any additional damage.
SCI Secondary injury
In the following days/weeks/months - further progression of tissue injury due to biochemical mechanisms (excitotoxicity, inflammatory processes, oxidative damage, apoptosis, etc.)
Acute phase of secondary injury
Ischemia/hypoxia causing electrolyte imbalance, Excitotoxicity, Inflammation by immune cells, Edema, Oxidative damage
Subacute phase of secondary injury
Apoptosis, Demyelination, Wallerian degeneration, Evolution of glial scar
Chronic phase of secondary injury
Cystic cavity (Syringomyelia), progressive Wallerian degeneration, maturation of glial scar
Syringomyelia
Presence of fluid-filled cyst (syrinx) after SCI. Causes significant additional symptoms due to compression/destruction of the ascending/descending neural pathways and the autonomic nerves.
Syringomyelia symptoms
pain, loss of sensation, LMN signs (weakness, atrophy) due to damage to anterior horn cells, spasms, phantom sensations, autonomic signs (low BP with light-headedness, sweating, sexual dysfunction, loss of bladder/bowel control) due to damage to thoraco-lumbo-sacral autonomic nerves).
Most common site of syringomyelia – thoracic spine – signs distributed like cape over shoulders and back – progression from distal to proximal extremities
Anterior cord syndrome
Bilateral motor function loss
Bilateral loss of pain and temperature sensation
Preservation of proprioception, fine touch and vibration
Associated with flexion injuries
Posterior cord syndrome
Loss of proprioception, leading to severe gait and balance problems
Preservation of motor function, pain and temperature sense
Extremely rare
Central cord syndrome
Usually more severe deficits in UE than LE, due to sparing of peripheral regions of spinal cord
Function in lumbar and sacral regions can be spared or recovered sooner
Known as “suspended functional loss”
Brown-Sequard syndrome
Damage to one side of spinal cord
Loss of proprioception, fine touch, vibratory below ipsi side
Loss of pain and temperature some levels below contra side of lesion
UMN type lesion below ipsi side of lesion – spasticity, Babinski’s
Conus Medullaris and Cauda Equina syndromes
Perianal/Saddle anesthesia
bladder and bowel sphincter dysfunction – mostly flaccid
Lack of penile erection
Partial cord lesions
Spinothalamic tract lesion - loss of pain, temperature and touch below lesion on contralateral side
changes in muscle tone after SCI
Flaccidity, loss of reflexes (skeletal and autonomic) below level of lesion during spinal shock period, may persist for few hours, days or weeks. Spasticity then follows that can be exaggerated by noxious stimuli
Autonomic Dysreflexia
common above T6 lesions. Sudden rise in systolic (>20mmHg) and diastolic (>10mmHg) BP. Caused by unbalanced/unrestricted vasoconstriction by sympathetic nervous system below level of lesion
Autonomic Dysreflexia symptoms
HTN, slow pulse (bradycardia), pounding headache, sweating above level, nausea, blurred vision, restlessness/anxiety, nasal congestion
Triggered by noxious stimuli, problems with bladder/bowel emptying, clogged/kinked catheter, UTI, pressure ulcer, sexual activity, menstruation, etc.
Medical emergency
Pain associated with SCI
The number of pain sites increases with time, regardless of whether they are complete or incomplete. Depression is associated with worsening pain. Parathesia and musculoskeletal pain can come from faulty posture, overuse of UE due to dependency for ADLs – need to protect the shoulder joints from overuse injuries.
Fatigue associated with SCI
Due to ANS changes with lack of sweating, thermoregulation
Also due to deconditioning – lack of aerobic activity
Increased effort to accomplish basic ADL tasks
Respiratory complications after SCI
Occurs with cervical and thoracic lesions, Lesions above C4 cause diaphragm paralysis due to loss of phrenic nerve function – generally require artificial ventilation. Lesions from C5 through T12 – causes respiratory problems due to loss of intercostal and abdominal muscle innervations
Bladder/bowel control after SCI
Always affected regardless of level of injury, Lesions at conus medullaris/cauda equina cause flaccid bladder while lesions above conus medullaris causes spastic bladder.
Obstructive sleep apnea-hypopnea syndrome (OSAHS)
repeated O2 desaturation during sleep, risk high after cervical SCIs.
Signs of suspected OSAHS – frequent awakening during sleep, daytime sleepiness, obesity
Sensory grading for ASIA scale
0 = absent
1 = Altered, either decreased/impaired sensation or hypersensitivity
2 = Normal
NT = Not testable
Scale component (A)
Complete = No sensory or motor function is preserved in the sacral segments S4-5.
Scale component (B)
Motor Complete & Sensory Incomplete = No voluntary anal contraction AND no motor function (key or non-key muscles) more than three levels below the motor level on either side of the body, but some sensory sparing below the neurological level AND includes the sacral segments S4-5 (light touch OR pin prick at S4-5 OR deep anal pressure)
Motor Incomplete
Presence of voluntary anal contraction OR has some sparing of motor function (key or non-key muscles) more than three levels below the ipsilateral motor level on either side of the body, when the patient is sensory incomplete.
Motor Incomplete C
less than half of key muscle functions below the NLI have a muscle grade ≥ 3.
Motor Incomplete D
At least half (or more) of key muscle functions below the NLI have a muscle grade ≥ 3.
Scale component (E)
Normal = If sensation and motor function as tested with the ISNCSCI are graded as normal in all segments, and the patient had prior deficits, then the AIS grade is E. Someone without an initial
SCI does not receive an AIS grade.
Prognosis for SCI
In general, people with injuries to L1 or below will likely be able to walk at home or community with AD (HKAFO, KAFO, AFO), T1-T12 likely to walk around the house with AD (HKAFO, KAFO), and C7-C8 likely to live independently using manual w/c.
Alzheimer disease
An irreversible, neurodegenerative, slowly progressive brain disorder that gradually destroys memory and thinking abilities, and eventually the ability to carry out the simplest ADLs. Dementia is hallmark of Alzheimer.
Pick’s disease
uncommon, Pick bodies seen - clumps of misfolded Tau, neurons balloon in affected areas
Vascular dementia
vascular cause, associated with series of multiple minor strokes or watershed strokes, symptoms depend of area of stroke
PD dementia
dementia along with other motor problems of PD
Lewy body dementia
clinical findings and pathology overlap with AD and PD, has both Lewy bodies and plaques, pt unresponsive to PD meds with progressive cognitive decline
Frontotemporal dementia
affects frontal lobe mostly, drastic personality changes, overlaps with Pick’s disease
Stage 1 AD
No complains of cognitive decline, no deficit evident during interview
Stage 2 AD
Very mild cognitive decline (Age-associated memory impairment)
Subjective complaints of memory deficits – forgetting where one placed items, forgetting well known names
No objective memory deficit on clinical interview
No objective deficits in ADLs, job or social situations
Stage 3 AD
Mild cognitive decline (MCI)
Beginning of dementia stages, clear deficits in clinical interview
Short-term memory, judgement and attention deficits noted in clinical tests
Word and name finding difficulties more evident
Getting lost when travelling to unfamiliar locations, functional deficits at work or social situations
Stage 4 AD
Moderate cognitive decline (Mild dementia)
Clear-cut deficits during interview – decreased knowledge of current events, poor historian, concentration deficits
Decreased ability to travel, handle finances, perform complex tasks
No deficits with – face recognition, ability to travel to familiar locations, orientation to space and time
independent with basic ADLs, need supervision with IADLs, rigid with routine
Stage 5 AD
Moderately severe cognitive decline (Moderate dementia)
Unable to recall major close aspects of life
no assistance required with toileting and eating, but need assistance to bathe and change clothing (assistance with complex ADLs), can do routine tasks like laundry but needs structure
Motor skills – Tunnel vision, may feel cold, can sustain task for a few minutes, uses different grasps for different objects
Stage 6 AD
Severe cognitive decline (Moderately severe dementia)
Entirely dependent upon spouse/caregiver for survival
disoriented to time and place, loss of diurnal rhythm
require some assistance with all ADLs
fall risk, shuffling gait, posture and balance problems
agitated at times, depressed on other times, apathy, reserved from social life, wanders, psychotic behavior
Stage 7 AD
Very severe cognitive decline (Severe dementia)
All verbal abilities to communicate are lost, only unintelligible words, may express with grunting
ADLs – incontinent, dependent for all ADLs including feeding, dysphagia
Motor skills – unable to walk, may have trunk movement in bed, generalized rigidity, primitive reflexes may appear, risk for skin breakdown and contractures
Goal directed behavior
participates in evaluating the full context of potential actions and selects the appropriate action to take
Social Behavior
recognizes social cues, regulates self-control, and parses out relevant from irrelevant information
Emotional/Motivation behavior
is involved in predictions when the outcome is unknown
Hyperdirect Pathway
“Stop”
*Stops ongoing movement
Direct Pathway
“Go”
*Facilitates desired movement
Indirect Pathway
“No-Go”
*Suppresses unwanted movements
Postural Instability Gait Difficulty (PIGD)
Late Onset Parkinson’s Disease
Faster rate of cognitive decline and a higher incidence of dementia
Rapid disease progression is more common
Tremor Dominant PD
Young Onset Parkinson’s Disease
Good prognosis with slow progression
Often initially misdiagnosed as essential tremor, particularly if the patients have had a long-standing history of tremor
Cardinal signs for PD
Bradykinesia, Rigidity, Resting tremor (pill rolling), postural instability
