Neurological Dysfunction Flashcards
List of infectious neurological diseases
Meningitis
Encephalitis
Brain abscess
Acquired immunodeficiency syndrome (AIDS)
Meningitis
inflammation of the membranes of the SC or brain
Etiology: can be bacterial (more rapid) or viral
Treat infective organism with antibiotic therapy; maintain fluid and electrolyte balance
provide supportive symptomatic therapy: bed positioning, PROM, skin care; safety measures if confused
Encephalitis
severe infection and inflammation of the brain
Etiology: arboviruses, or a sequela in infleunza, chronic and recurrent sinusitis, otitis, or other infections; bacterial encephalitis, prion-caused disease (“mad cow”)
Treat infective organism
Provide supportive symptomatic therapy
Brain abscess
infectious process in which there is a collection of pyogenic material in the brain parenchyma
S&S: headaches, fever, brainstem compression, focal signs CN II & VI
can be extension of an infection (meningitis, otitis media, sinusitis, post TBI); typically frontal or temporal lobes or cerebellum
treat infective organism, surgical intervention
provide supportive symptomatic therapy
Acquired immunodeficiency syndrome (AIDS)
viral syndrome characterized by acquired and severe depression of cell-mediated immunity
Symptoms: wide ranging, 1/3 of patients exhibit CNS or PNS deficits
- AIDS dementia complex (ADC): symptoms range from confusion and memory loss to disorientation
- motor deficits: ataxia, weakness, tremor, loss of fine motor coordination
- peripheral neuropathy
treat with anti HIV drugs
Provide palliative and supportive care
Cerebrovascular Accident
CVA/Stroke
=sudden, focal neurological deficit resulting from ischemic or hemorrhagic lesions in the brain
*most common sites for lesions to occur are at the origin of the common carotid artery, at the main bifurcation of the MCA, and at the junction of the vertebral arteries with the basilar artery
Etiological categories for CVA
1- cerebral thrombosis: formation or development of a blood clot or thrombus within the cerebral arteries or their branches
2-cerebral embolism: traveling bits of matter (thrombi, tissue, fat, air, bacteria) that produce occlusion and infarction in the cerebral arteries
3- Cerebral hemorrhage: abnormal bleeding as a result of rupture of a blood vessel (extradural, subdural, subarachnoid, intracerebral)
risk factors for CVA
artherosclerosis
hypertension
cardiac disease: rheumatic valvular disease, endocarditis, arrhythmias, cardiac surgery
diabetes, metabolic syndrome
transient ischemic attacks: brief warning episodes of dysfunction (
Pathophysiology of CVA
cerebral anoxia: lack of oxygen supply to the brain (irreversible anoxic damage to the brain begins after 4-6 min)
cerebral infarction: irreversible cellular damage
cerebral edema: accumulation of fluids within brain; causes further dysfunction; elevates intracranial pressures, can result in herniation and death
CVA: Internal carotid syndrome (ICA)
ICA arises off the common carotid artery, gives off an ophthalmic branch and terminates in the anterior cerebral artery and middle cerebral artery
occlusions commonly produce S&S of MCA involvement with reduced levels of consciousness
lessions involving MCA and ACA distributions may produce massive edema, brain herniation and death
CVA: Anterior carotid artery syndrome
rarely involved
ACA supplies anterior 2/3 of the medial cerebral cortex
occlusions proximal to anterior communicating artery produce minimal deficits due to the circle of Willis
- *Symptoms:
- affects LE > UE
- contralateral hemiplegia and sensory loss
- can result in mental confusion, aphasia, and contralateral neglect if involvement is extensive on the dominant side
CVA: Middle cerebral artery syndrome
most commonly involved
MCA supplies lateral cerebral cortex, BG and large portions of the internal capsule
- *Symptoms:
- contralateral hemiplegia UE>LE involvement
- loss of sensation primarily in the arm and face
- homonymous hemianopsia is common
- Left infarction may produce aphasia and apraxia
- occlusion of the main stem of the MCA can cause global aphasia
CVA: Posterior cerebral artery syndrome
persistent pain syndrome or contralateral pain and temperature sensory loss can occur
homonymous hemianopsia, aphasia and thalamic pain syndrome also can result from occlusion of this artery
CVA: vertebralbasilar artery syndrome
2 vertebral arteries arise off the subclavian arteries and supply the ventral surface of the medulla and the posterior inferior aspect of the cerebellum before joining to form the basilar artery at the junction of the pons and medulla
-the basilar artery supplies the ventral portion of the pons and terminates in the PCA
often results in death from the edema associated with the infarct
if patient survives and the lesion affected the pons: the result could be quadriparxsis and bulbar palsy or a “locked in” state whereby the patient can communicate only by eye blinking
Other vertebral artery symptoms can include vertigo, coma, diplopia, nausea, dysphagia, and ataxia
CVA: Anterior inferior cerebellar
results in unilateral deafness, loss of pain and temperature on the contralateral side, paresis of lateral gaze, unilateral Horner’s syndrome (ptosis, constructed pupil, and loss of sweating), ataxia, vertigo, nystagmus
CVA: superior cerebellar
results in severe ataxia, dysarthria, dysmetria, and contralateral loss of pain and temperature
CVA: posterior inferior cerebellar
results in Wallenberg’s syndrome
“lateral medullary syndrome”
characterized by vertigo, nausea, hoarseness, dysphagia, ptosis, and decreased impairment of sensation in the ipsilateral face and contralateral torso and limbs
maybe Horner’s syndrome too
Horner’s syndrome
ptosis- drooped upper eyelid
pupillary constriction
absence of sweating
Sequential recovery stages of CVA
1: initial flaccidity, no voluntary movement
2: emergence of spasticity, hyperreflexia, synergies (mass patterns of movement)
3: voluntary movement possible, but only in synergies; spasticity strong
4: voluntary control in isolated joint movements emerging, corresponding decline of spasticity and synergies
5: increasing voluntary control out of synergy; coordination deficits present
6: control and coordination almost normal
Examining CVA
general signs of increased intracranial pressure
level of consciousness, cognitive function
Speech and communication
- aphasia (typically L CVA)
- perceptual deficits (typically R CVA)
Behaviors
Sensory deficits
- superficial, deep, cortical/combined
- hearing, vision
- CN function
Motor function
- tone and reflexes
- spasticity
- abnormal synergies
- paresis, incoordination, apraxia
- posture and balance
- gait
Outcome measures:
- fugl-meyer
- NIG stroke scale
- postural assessment scale for stroke
- stroke impact scale
- FIM
- functional assessment measure (FAM)
R vs. L CVA behaviors
L CVA: slow, cautious, hesitant, insecure
R CVA: impulsive, quick, poor judgement/safety, overestimate abilities
Typical gait deficits for CVA
Hip
- poor hip position (retracted, flexed
- Trendelenburg limp (weak abductors)
- scissoring (spastic adductors)
- insufficient pelvic rotation during swing
Weak hip flexors during swing may yield circumducted gait, ER with adduction, backward leaning of trunk or exaggerated flexion synergy
Knee:
- weak knee extensors (knee buckles in stance) - results in compensatory locking of knee in hyperextension
- spastic quads may also yield a hyperextended knee
Ankle:
- foot drop
- equinus gait - PF
- varus foot - weight is borne on lateral side of foot
- equinovarus position
unequal step lengths
decreased cadence, uneven timing
Synergies with stroke
primitive and stereotyped movement patterns associated with spasticity
- may be elicited reflexively, as associated reactions or as voluntary movement patterns
- flexion and extension synergies of each extremity
UE flexion synergy:
- scapular elevation and retraction
- shoulder abduction and ER
- elbow flexion (generally strongest component)
- forearm supination and wrist/finger flexion
LE flexion synergy :
- hip flexion (generally strongest component)
- hip abduction, ER
- knee flexion
- ankle DF and inversion
- toe DF
Extensor synergies are exactly the opposite except that wrist/finger flexion and ankle inversion are common to both
Hypotonicity:
tx?
floppy, low tone, flaccid
risk of dislocation of AA joint (SCI potential), hip, knee, elbow, shoulder, etc
hypoactive reflexes and shallow breathing patterns
Treatment:
- avoid joint hyperextension
- work for joint compression and facilitation to help normalize tone
- use resistance of functioning muscles and isometric holding to increase activation of inactive muscles
- facilitation techniques:
- –quick stretch
- –tapping of muscle belly/tendon
- –high frequency vibration
- –light touch, quick icing
- –fast spinning or rolling
- –Joint approximation facilitates co-contraction
Hypertonicity:
tx?
spastic, high tone with hyperactive reflexes and decreased thoracic mobility
- risk of contractures and deformity
- changes in body position can affect one
Treatment:
- work to inhibit reflex activity via postures, positions or techniques of relaxation training
- inhibition techniques
- –prolonged static muscle stretch
- –inhibiting postures
- –limb movements emphasizing rotation
- –slow stroking
- –neutral warmth
- –prolonged icing
- –deep pressure to tendons
- –Reciprocal inhibition: using facilitation techniques to the non spastic muscles will cause inhibition of the spastic muscles
Perceptual problems associated with stroke (R vs. L)
*depends on the side of the brain that is damaged
R CVA
- problems with spatial relationships and hand eye coordination
- irritability, short attention span
- can’t retain info, difficulty learning individual steps
- poor judgement affecting personal safety
- diminished body image with L sided neglect
- quick and impulsive
L CVA:
- apraxia
- difficulty starting and sequencing tasks
- perseveration
- easily frustrated with high levels of anxiety
- inability to communicate verbally
- cautious and slow
communication issues with stroke
receptive vs. expressive
1- receptive, Wenicke’s or fluent aphasia:
- speech may flow smoothly but auditory comprehension is impaired.
- following commands may be difficult
- use word repetition and manual cues during rehab
2- Expressive, Broca’s or nonfluent aphasia:
- syntax is impaired, speech may be slow, vocal is small.
- comprehension is good
- phrase questions in simple “yes” or “no” responses
3- Global aphasia:
- characterized by significant limitations in comprehension
- use of symbolic gestures may help
guidelines to promote learning with hemispheric differences (R vs. L CVA)
L CVA:
- develop an appropriate communication base: words, gestures, pantomime; assess level of understanding
- give frequent feedback and support
- don’t underestimate learning ability
R CVA:
- use VC; demos or gestures may confuse patients with visuospatial deficits
- give frequent feedback; focus on slowing and controlling movement
- focus on safety
- avoid environmental clutter
- don’t overestimate ability to learn
TBI
Etiology: MOI is contact forces to to skull and rotational acceleration forces, causing varying degrees of injury to the brain
various S&S associated with localized lesions of the cortex
Primary brain damage
Secondary brain damage
Concussion
primary brain injury:
diffuse axonal injury:
-disruption and tearing of axons and small blood vessels from shear-strain of angular acceleration; results in neuronal death and petechial hemorrhages
focal injury:
-contusions, lacerations, mass effect from hemorrhage and edema (hematoma)
coup-contracoup injury:
-injury at point of impact and opposite point of impact
closed or open injury (with fracture of skull)
secondary brain damage
hypoxic-ischemic injury:
-results from systemic problems (respiratory or cardiovascular) that compromise cerebral circulation
swelling/edema:
-can result in mass effect, with increased intracranial pressures, brain herniation (uncal, central or tonsillar) and death
electrolyte imbalance and mass release of damaging neurotransmitters
Concussion
loss of consciousness, either temporary or permanent, resulting from injury or blow to head, with impaired functioning of the brainstem reticular activating system
-may see changes in HR, RR, BP
Levels of brain injury:
Mild TBI:
- Loss of consciousness: 0-30 minutes
- alteration of consciousness: brief; >24 hours
- post-traumatic amnesia: 30 minutes, 24 hours
- post-traumatic amnesia: >1, 24 hours
- alteration of consciousness: >24 hours
- post-traumatic amnesia: >7 days
- Glascow coma scale:
Ranchos Los Amigos levels of cognitive functioning
delineates 8 general cognitive and behavioral levels
-descriptive scale of response to stimuli that is useful for communicating or documenting cognitive and/or behavioral status
I- no response to any stimuli
II- generalized response; reacts inconsistently and nonspecifically to stimuli
III- localized response; pt. reacts inconsistently but specifically to stimuli
IV- confused/agitated; heightened state of activity; behavior is bizarre and non purposeful relative to immediate environment; recall and attention span are poor
V- confused/inappropriate: pt. able to respond to simple commands but not to complex tasks; memory is impaired; verbalization is inappropriate
VI- confused-appropriate: pt. is dependent upon external input but can perform consistently; memory improved.
VII- automatic-appropriate: can perform automatically and appropriately in structured environments; judgement remains impaired
VIII- purposeful-appropriate: patient acts appropriately though not perfectly. may have some-problems in stressful or unusual circumstances
Glascow coma scale
an objective way to describe a patient’s level of consciousness
Each category is quantified:
- eye opening: spontaneous to none
- best motor response: follows commands to abnormal responses to no response
- verbal response: oriented to inappropriate to no response
mild TBI=13-15
moderate TBI=9-12
severe TBI=
arousal=
=the overall level of alertness or reaction to stimuli
low arousal associated with coma
high arousal may occur during agitated state following brain injury
-may require quiet environment and consistency in management (daily routine)
Recovery stages from diffuse axonal injury:
1: coma:
- state of unconsciousness in which there is neither arousal nor awareness; eyes remain closed, no sleep/wake cycle s
2- unresponsive vigilance/vegetative state:
- marked by the return of sleep/wake cycles and normalization of vegetative functions (respiration, digestion, BP control);
- persistent vegetative state= >1 year
3- mute responsiveness/minimally responsive:
-pt. is not vegetative and does show signs, even if intermittent, of fluctuating awareness
4- confusional state:
-mainly a disturbance of attention mechanisms; all cognitive operations are affected, patient is able to form new memories; may demo either hypoarousal or hyperarousal
5- emerging independence:
- confusion is clearing and some memory is possible
- significant cognitive problems and limited insight remain
- frequently inhibited social behaviors
6- Intellectual/social competence
-increasing independence, although cognitive difficulties (problem solving, reasoning) persist along with behavioral and social problems (mood swings)
*patient can plateau at any stage or regress under conditions of stress or repetitive brain injury
examining TBI
general signs of increased intracranial pressure
level of consciousness, cognitive function, learning disorders, memory and complex info processing
CN function
behavior changes
speech and communication
sensory deficits
motor function (cerebellar damage is common)
functional mobility
level of general de-conditioning following prolonged hospitalization
management for TBI based on decreased response levels (LOCF I-III)
maintain ROM, prevent contracture, positioning
maintain skin integrity
maintain respiratory status, prevent complications: postural drainage, percussion, vibration, suctioning to keep airway clear
provide sensory stimulation for arousal and to elicit movement: environmental and direct stimulation (auditory, visual, olfactory, gustatory, tactile stimuli)
promote early return of FMS: upright positioning for improved arousal, proper body alignment
management for TBI based on mid-level recovery (LOCF IV-VI)
provide structure, prevent overstimulation for confused, agitated patient: closed, reduced stimulus environment, daily schedules and memory logs, relaxation techniques
provide consistency: clear feedback, written contacts
engage patient in task-specific training; limit activities to familiar, well-liked ones; offer options; break down complex tasks into parts
provide verbal or physical assistance
control rate of instruction
emphasize safety, behavioral management techniques
model calm, focused behavior
management for TBI based on high level recovery (LOCF VII-VIII)
allow for increasing independence; wean patient from structure, involve patient in decision making
assist paitent in behavioral, cognitive, emotional reintegration: provide honest feedback, prepare for community reentry
promote independence in functional tasks: FMS, ADLs
improve postural control, symmetry and balance
encourage active lifestyle, improved cardiovascular endurance
common behavioral difficulties with TBI
depression dependent denial aggressive sexually inappropriate agitated poor judgement
Spinal cord injury (SCI)
etiology: partial or complete disruption of SC resulting in paralysis, sensory loss, altered autonomic and reflex activities
Paraplegia= only LEs are involved Tetraplegia/Quadriplegia= all 4 extremities are involved
Designation of spinal level:
- defined as the most caudal level of the SC that exhibits intact sensory and motor functioning
- muscles must have a grade of at least 3+/5 strength to demo intact innervation
- sensory areas are well demarcated and are innervated by a single SC segment
- complete lesions: total and permanent functional (sensory and motor) disruption of the SC >3 segments below the lesion
MOI:
- flexion- most common lumbar injury
- flexion-rotation- most common cervical injury
- compression
- hyperextension
- nontraumatic causes: disc prolapse, vascular insult, infections
Classification of SCI
1- level of injury: UMN injury
- lesion level indicates most distal uninvolved nerve root segment with normal function; muscles must have a grade of at least 3+/5 function
- tetraplegia/quadriplegia: injury occurs b/w C1 and C8, involves all 4 extremities and trunk
- Paraplegia: injury occurs b/w T1 and L1, involves both LEs and trunk (varying levels)
2- degree of injury
- complete: no motor or sensory function below level of lesion
- incomplete: preservation of sensory or motor function below level of injury; spotty sensation, some muscle function
- ASIA score
3- clinical syndromes
- central cord
- brown-sequard
- anterior cord
- posterior cord
- cauda equina
- sacral sparing
American spinal injury association (ASIA) impairment scale for SCI
A= complete, no motor or sensory function is preserved in the sacral segments S4-5
B= Incomplete: sensory but not motor function is preserved below the neurological level and includes the sacral segments S4-5
C= Incomplete: motor function is preserved below the neurological level, and most key muscles below the neurological level have a muscle grade of
Clinical syndromes of incomplete SCI
Brown sequard syndrome -UMN anterior cord -UMN central cord -UMN posterior cord -UMN cauda equina -LMN sacral sparing -
SCI: Central cord syndrome:
most commonly occurs with hyperextension injuries with minor trauma to the cervical region
results in damage to the central aspect of the SC affecting the UE sensation and motor functioning with normal LE functioning
- loss of spinothalamic tracts with bilateral loss of P&T
- loss of ventral horn with bilateral loss of motor function: primarily UE
- preservation of proprioception and discriminatory sensation
SCI: Anterior cord syndrome
results from trailer to the anterior cord or damage of the anterior spinal artery usually related to flexion injuries of the cervical region
characterized by loss of motor function and loss of pain and temperature below the level of lesion
- loss of lateral corticospinal tracts with bilateral loss of motor function, spastic paralysis below level of lesion
- loss of spinothalamic tracts with bilateral loss of P&T
- preservation of dorsal columns: proprioception, kinesthesia and vibration
SCI: Posterior cord syndrome
very rare with deficits of kinesthesia and proprioception
an ataxic gait with a wide base of support may result
- loss of dorsal columns bilaterally- loss of proprioception, vibration, and pressure sensations
- preservation of motor function, pain and light touch
SCI: Brown-Sequard syndrome
hemisection of the SC, usually from stab or gunshot
asymmetrical ipsilateral symptoms:
-weakness or motor paralysis, loss of proprioception, vibratory sense, and 2 point discrimination, decreased reflexes, clonus and spasticity
- ipsilateral loss of dorsal columns with loss of tactic discrimination, pressure, vibration and proprioception
- ipsilateral loss of corticospinal tracts with loss of motor function and spastic paralysis below level of lesion
- contralateral loss of spinothalamic tract with loss of P&T below level of lesion; at lesion level bilateral loss of P&T
SCI: cauda equina
injury below the L1 segment results in damage to lumbar and sacral roots of peripheral nerves (LMN)
sensory loss, paralysis and loss of bladder/bowel control can occur
because damage is to the peripheral nerve roots, regeneration may be possible
SCI: sacral sparing
sparing of tracts to centrally located sacral segments
perianal sensation, rectal spincter contraction, cutaneous innervation in the saddle area and active contraction of the scarily innervated toe flexors are intact
changes associated with recovery of SCI
spinal shock
- transient period of reflex depression and flaccidity
- may last several hours or up to 24 weeks
spasticity/spasms
autonomic dysreflexia (hyperreflexia)
heterotypic bone formation
DVT
autonomic dysreflexia
(hyperreflexia)
an emergency situation in which a noxious stimulus precipitates a pathological autonomic reflex with symptoms of:
- paroxysmal hypertension
- bradycardia
- headache
- diaphoresis (sweating)
- flushing
- diplopia
- convulsions
occurs in lesions above T6; more prevalent in first 3 years after SCI
examine for irritating stimuli
treat as medical emergency- elevate head, check and empty catheter first
most common cause: bladder distension
other stimuli: rectal dissension, pressure sores, urinary stones, bladder infections, noxious cutaneous stimuli, kidney malfunction and environmental temperature changes
bladder drainage system should be checked immediately and opened if necessary
if lying flat, bring patient to sitting position to lower BP
PT goals for SCI
monitor changes associated with recovery
- spinal shock
- spasticity/spasms
- autonomic dysreflexia
- heterotopic bone formation
- DVT
improve respiratory capacity
maintain ROM, prevent contractures, positioning
maintain skin integrity
improve strength
reorient pt. to vertical position (*orthostatic hypotension)
promote early return of FMS and ADLs
improve sitting tolerance, postural control, balance
appropriate wheelchair prescription and independence
gait training
cardiovascular endurance
Appropriate wheelchair prescriptions for SCI patients:
High cervical lesions (C1-4)
- require electric w/c with tilt in space seating
- microswitch or puff and sip controls
- portable respirator may be attached
Shoulder function, elbow flexion (C5)
- can use manual chair with propulsive aids (projections) for short distances on smooth surfaces
- may use electric w/c for distances and to conserve energy
Radial wrist extensors (C6)
-manual w/c with friction surface hand rims independently
Triceps (C7):
-same as C6 but with increased propulsion
Hand function (C8-T1 and below) -manual w/c, standard heigh rims
Gait training for SCI patients
Midthoracic lesions (T6-9):
- supervised ambulation for short distances
- requires bilateral KAFO and crutches
- swing-to gait pattern
- requires A
- may prefer standing devices/standing w/c
High lumbar lesions (T12-L3)
- can be independent in ambulation on all surfaces and stairs
- uses a swing through or 4 point gait and bilateral KAFOs and crutches
- may also use reciprocating gait orthoses with walker with or without FES system
- typically I household ambulators, w/c for community
Low lumbar lesions (L4-5)
-independent with bilateral AFOs and crutches or canes
Primary physical effects of SCI
Paralysis of voluntary motor control with damage to descending motor tracts, anterior horn cells or spinal nerves
Spasticity
- after spinal shock resolves, reflexes return and progressively become stronger, resulting in spasticity
- more prevalent with higher and incomplete lesions
Loss of sensation
-leads to discoordination of movements, impaired body awareness
Respiration dysfunction
Bowel and bladder incontinence
Genital function
Cardiovascular function
Thermoregulation
SCI effects on respiration
depending on the level of lesion, the diaphragm (innervated from C3-5) may not be active, affects patient’s ability to breathe (primarily inhalation)
-an artificial ventilator or phrenic nerve stimulator may be required to sustain life
disruption to the intercostals and abdominal muscles can impair respiration- primarily forced expiration and inhalation
following a SCI, tidal volume and vital capacity are reduced and secondary respiration muscles are utilized (scalene)
respiratory dysfunction
- most common cause of death in SCI
- inability to cough effectively allows secretions to build in the lungs and decreases forced expiration
- inadequate inhalation and exhalation can reduce ventilation of the lungs– lead to atelectasis, pneumonia and respiratory insufficiency
SCI effects on bowl and bladder continence
voluntary control of urination and defecation is lost after in injury to the sacral cord S2-4
following spinal shock, 2 types of bladder conditions will develop:
1- Reflex bladders (UMN):
-empty in response to a certain level of filling pressure
2-autonomous or nonreflex bladders (LMN):
-flaccid and can be emptied by increasing intraabdominal pressure or by manually compressing the lower abdomen
SCI effects on genital function
injury to the thoracolumbar and sacral regions of the SC alter the functioning of the genitals, disrupting sexual responses
female fertility is unchanged but men are likely infertile
SCI effects on cardiovascular function
when an injury to the SC blocks communication between the brainstem and the thoracolumbar cord, sympathetic input to the heart is lost and parasympathetic input remains
-results in bradycardia, peripheral vasodilation and hypotension
orthostatic hypotension occurs due to a drop in BP when the patient moves from horizontal to upright
problems are significant in people with lesions above T6 and often resolve within a few weeks
SCI effects on thermoregulation
cord injury that interrupts communication with the hypothalamus can cause hypothermia due to peripheral vasodilation
reflexive tone returns in the peripheral vasculature, resolving this problem
later, hyperthermia occurs due to a loss in sympathetic control of the sweat glands
below the level of the lesion sweating doesn’t occur
-to compensate, diaphoresis occurs above the lesion
possible complications of SCI
decubitus ulcers
respiratory dysfunction
- most common cause of death in SCI
- inability to cough effectively allows secretions to build in the lungs and decreases forced expiration
- inadequate inhalation and exhalation can reduce ventilation of the lungs– lead to atelectasis, pneumonia and respiratory insufficiency
contractures
osteoporosis
-loss of calcium from bones below lesion– ^risk of fractures
DVT
GI dysfunction
- stress ulcers
- bowel obstruction
- fecal impaction
- gastric dilation
autonomic dysreflexia
-occurs in lesions above T6
postural or orthostatic hypotension
heterotopic bone formation
orthostatic hypotension
a decrease in BP that occurs when a patient is moved from horizontal to vertical position
the lack of muscle tone and loss of sympathetic vasoconstriction causes venous pooling in the periphery
due to immobilization for 6-8 weeks
symptoms: dizziness and fitness or impending blackout
treatment: slow progression to vertical position while VS are monitored and use of compressive stockings and an abdominal binder to minimize hypotension effects
heterotopic bone formation
formation of new bone within muscles or other CT below the lesion
unknown etiology
different from myositis ossificans, which results from trauma to the muscle tissue and presents with bony deposits within muscle tissue
occurs in 16-53% of all patients with SCIs, usually appearing from 1-4 months after injury and can restrict joint ROM
Tx: combo of drug therapy and regular exercise during early stages of ectopic bone formation can be effective
Functional ability for SCI C1-C3
“tetraplegia”
capable of talking, mastication, sipping, blowing
key muscles: face and neck
dependent self-care
requires a portable ventilator or phrenic nerve stimulator,
requires a power tilt-in-space w/c with mouth control and a seatbelt for trunk control
SCI at C3 can attain w/c independence with power w/c on smooth level surfaces
Functional capabilities for SCI at C4
capable of respiration, scapular elevation
key muscles: diaphragm, trapezius
ventilator usually not needed
-glossopharyngeal breathing is used to cough
chin control to adjust w/c
limited feeding and ADLs amy be possible with use of mobile arm supports, environmental controls, adapted eating equipment head or mouth stick
