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
Functional capabilities for SCI at C5
capable of:
- elbow flexion and supination
- shoulder ER &abd to 90, and limited shoulder flexion
key muscles:
- biceps
- brachialis
- brachioradialis
- deltoid
- infraspinatus
- rhomboids
- supinator
mobile arm support assist UE ADL performance
mod to min A required for LE dressing and rolling
dependent for transfers with aid of a sliding board
power chair with hand controls (joystick) for community integration and manual w/c with rim projectors 200-300 ft indoors
driving is possible with van lift
may achieve ischial pressure relief with forward lean but usually dependent
needs assistance for manual cough technique
Functional capabilities of SCI at C6
capable of:
- shoulder flexion, extension, IR, adduction
- scapular abduction and upward rotation
- forearm pronation
- wrist extension
key muscles:
- ECR
- infraspinatus
- lats
- pec major
- serratus anterior
- teres minor
can become independent in half care with equipment- transfer with sliding board
independent in rolling and supported sitting can be LTG
use of a manual w/c with projections or friction hand rims for household mobility
- may require a power w/c for community
- locks on casters positioned sideways provide increased stability in transfers
uses manual cough technique independently
can live w/o A if well motivated
can drive automobile with hand controls
Functional capabilities of SCI at C7
capable of:
- elbow extension
- wrist flexion
- finger extension
key muscles:
- EPL, EPB
- extrinsic finger extensors
- FCR
- triceps
Independent in LE self ROM exercises
can use manual w/c with friction hand rims for community integration with some difficulty on rough terrain
button hook may be required for independent dressing
able to get w/c in and out of car
Functional capabilities for SCI at C8
capable of full use of all UE muscles except hand intrinsics
key muscles:
- extrinsic finger flexors
- FCU
- FPL and FPB
independent in living at home except for heavy work
may be able to independently go up/down curbs with manual w/c
may need tub seat, grab bars, et for full independence at home
able to work in a building free of architectural barriers
Functional capabilities for SCI T1-5
capable of:
- full use of UEs
- improved trunk control
- increased respiratory reserve
Key muscles:
- top half of intercostals
- long muscles of the back
- intrinsic finger flexors
independent in all areas including car transfers
standing table for physiologic standing
able to negotiate curbs using “wheelie” technique
participates in w/c sports
Functional capabilities for SCI T6-8
capable of:
- improved trunk control
- increased respiratory reserve
Key muscles:
-long muscles of the back including sarcrospinalis and semispinalis
independent in swing-to gait in parallel bars with bilateral KAFO for short distances
supervision with walker and KAFOs in home
will use w/c for community locomotion
Functional capabilities for SCI T9-12
capable of:
- increased endurance
- improved trunk control
Key muscles:
- lower abdominals
- all intercostals
independent swing-to or swing-through gait on level surfaces with bilateral KAFOs and a walker or forearm crutches
Independent floor to wheelchair and tub transfers
may be independent household ambulators
will usually use a w/c for outdoor locomotion and energy conservation
Functional capabilities for SCI T12-L3
capable of:
- hip flexion and adduction
- knee extension
Key muscles:
- gracilis
- iliopsoas
- quadratus lumborum
- rectus femoris
- sartorius
independent swing-to, swing-through or 4 point gain with bilateral KAFOs and forearm crutches on level surfaces and small elevations.
-Independent home ambulators
may use w/c for energy conservation in community
Functional capabilities for SCI L4-5
capable of:
- strong hip flexion and knee extension
- weak knee flexion
- improved trunk control
key muscles:
- low back muscles
- medial hamstring (weak)
- posterior tibialis
- quads
- anterior tibialis
independent home ambulators (can be community)
may use w/c for energy conservation
adaptive equipment for SCI
head or mouth stick:
- wooden/metal rod 12-18 inches long
- lesions C3-5
- holds utensils or types/turns pages
Mobile arm support:
- typically attached to w/c
- patients with weak proximal UE to improve function
- pts would have shoulder flexion, ER and elbow flexors between 1-3+
- helps with self-care and hand control in power chair
static wrist-hand orthosis:
- positional hand splint for pts w/o wrist extension (C1-5)
- maintains functional hand position- thumb abduction and palm support
- not functional
Wrist-driven orthosis (tenodesis splint)
- dynamic functional orthosis designed to assist with grasp
- transfers muscle force from wrist extension to provide finger flexion with C6-7 lesion
Wheelchair cushions
-regardless of cushion pressure relief should be performed 3-4x/hour
SCI effects on pulmonary function
Vital capacity
-depends on level of lesion and muscles innervated
Coughing
- T10 and below have functional cough
- manual cough- technique of abdominal compression to assist with clearing secretions in patients with weak or nonfunctional cough
- –pt. can perform themselves if lesion is C6 or below
glossopharyngeal breathing (frog breathing)
- technique used by high level quadriplegics
- -aggressive use of tongue, pharyngeal and laryngeal structures as a respiratory pump to help air and increase VC
Respiratory muscle innervations
the diaphragm is the primary muscle of inspiration
-innervated from C3-5
Intercostals (T1-12) assist in inspiration
Abdominals (T5-12) are utilized in forced expiration
Secondary muscles: assist in inspiration
- Trapezius (C1-4)
- SCM (C1-3)
- Scalenes (C3-5)
- Levator scapula (C3-5)
Multiple sclerosis (MS)
chronic, progressive, demyelinating disease of the CNS
mostly young adults
more prevalent in colder climates
demyelinating lesions (plaques) impair neural transmission, cause nerves to fatigue rapidly
variable symptoms:
- lesions scattered in time and place
- lesions common in pyramidal tract, dorsal columns and periventricular areas of cerebrum, cerebellar peduncles
Variable course with fluctuating periods
- exacerbations- worsening of symptoms
- remissions –> progressing to permanent dysfunction
precipitating or exacerbating factors: infections, trauma, pregnancy, stress
transient worsening of symptoms: adverse reactions to heat, hyperventilation, dehydration, fatigue
S&S of MS
sensory disturbances including tingling, numbness and pain
coordination problems and spasticity
fatigue (especially in the afternoon) ** #1 complaint
diplopia
bowel and bladder problems
-UTI
communication disorders
psychosocial problems including euphoria and/or depression
adverse reactions to heat
respiratory infection- common cause of death
Categories of MS
Relapse-remitting MS (RRMS):
- relapses with either full recovery or some remaining neurological S&S and residual deficit
- periods b/w relapse characterized by lack of disease progression
Primary-progressive MS (PPMS):
-disease progression from onset, w/out plateaus or remissions or with occasional plateaus and temporary minor improvements
Secondary-progressive MS (SPMS):
-initial relapsing-remitting course, followed by progression at a variable rate that may also include occasional relapses and minor remissions
Progressive-relapsing MS (PRMS):
- progressive disease from onset but w/out clear, acute relapses that may or may not have some recovery or remission
- commonly seen when onset >40 y/o
MS treatment
Medical Management:
- immunosuppressant drugs: treat acute flare ups and shorten duration
- interferon drugs: slow disease progression
- symptomatic management of spasticity
- symptomatic management of urinary problems: anticholinergic drugs
PT Tx:
- restorative following exacerbation
- functional maintenance: ROM, strength
- improve function
- prevent secondary problems
- breathing exercises
- PNF to tolerance
- skin integrity
- improve sensory awareness
- improve motor control/coordination
- postural control, symmetry
- gait or w/c training
- energy conservation
*preferably morning treatments
Parkinson’s disease
chronic, progressive disease of the CNS (basal ganglia) with degeneration of dopaminergic substantia nigra neurons and nigrostriatal pathways
-decrease in dopamine production and/or receptors in the brain
Etiology: infectious/postencephalic, atherosclerosis, idiopathic, toxic, drug induced
- deficiency of dopamine within the BG corpus striatum with degeneration of substantia nigra
- loss of inhibitory dopamine results in excessive excitatory output from cholinergic system (acetylcholine) of basal ganglia
S&S of Parkinson’s
resting tremor, rigidity and fatigue
-leadpipe or cogwheel rigidity
difficulty initiating or slowness of movement (bradykinesia)
abnormal gait (festinating or slow shuffling)
flexed posture
mask-like face
decreased postural reflexes
behavioral changes:
- memory loss
- apathy that leads to secondary problems: decubitus ulcers, muscle atrophy, contractures, decreased VC and falls
intellectual impairments/dementia in advanced stages
stages of Parkinson’s
I: minimal or absent disability
-unilateral symptoms
II: minimal bilateral or midline involvement
-no balance involvement
III: impaired balance, some restrictions in activity
IV: all symptoms present and severe
-stands and walks only with assistance
V: confinement to bed or wheelchair
Treatment for Parkinson’s
Medical management:
- Sinemet (levodopa/carbidopa): provides dopamine and decreases effects of disease
- –adverse effects: nausea, orthostatic hypotension, arrhythmias, dyskinesias, psychoses, abnormal behaviors
- dopamine agonist drugs
- anticholinergic drugs: control tremors
- amantadine: enhances dopamine release
selegiline: increases dopamine; used during early disease to slow progression - deep brain stimulation in thalamus
PT:
- monitor changes in disease progression and pharm interventions
- prevent secondary impairments
- compensator strategies for movement; repetitive stimulation
- improve strength
- PNF diagonals with rhythmic initiation to overcome bradykinesia
- gait training to increase stride width and length
- endurance
*best to treat in AM following dopamine agonist administration
Myasthenia gravis:
a neuromuscular junction disorder characterized by progressive muscular weakness and fatiguability on exertion
-muscular strength worse with continuing contraction, improved with rest
Etiology: autoimmunie antibody- mediated attack on acetylcholine receptors at neuromuscular junction
Generalized myasthenia: usually involves bulbar (extraocular, facial, and muscles of mastication) and proximal limb-girdle muscles
course varies: may progress from mild-severe, typically w/in 18 months
myasthenic crisis: respiratory failure, medical emergency
Epilepsy
symptoms?
Common causes?
disorder characterized by recurrent seizures (repetitive abnormal electrical discharges w/in the brain)
Symptoms:
- altered consciousness
- altered motor activity (convulsions): characterized by involuntary muscle contractions; tonic activity (stiffening/rigidity of muscles); clonic activity (rhythmic jerking)
- Sensory phenomena: somatosensory, visual, auditory, olfactory, gustatory and vertiginous sensations
- Autonomic phenomena: associated with sudden attack of anxiety, tachycardia, sweating, piloerection, abnormal sensation risking up in upper abdomen and chest
- Cognitive phenomena: sudden failure of comprehension, inability to communicate, illusions, hallucinations
Common causes of seizures:
- acquired brain disease or trauma: tumor, stroke
- degenerative brain diseases: Alzheimer’s dementia, amyloidosis
- developmental brain defects
- drug overdose
- drug withdrawal
- electrolyte disorders: hypo/hypernatremia, hypoglycemia, hypomagnesemia
- hyperthermia
- infections; brain abscess, meningitis, neurocysticercosis
- pregnancy complications: eclampsia
Classification of seizures
GENERALIZED SEIZURES:
1-Tonic-clonic (grand mal):
- dramatic loss of consciousness, with a cry, fall and tonic-clonic convulsions of all extremities; often with tongue biting and arrested breathing, urinary and fecal incontinence
- after 2-5 min, contractions subside, and consciousness is gradually regained
- patient is confused, drowsy and amnesiac about the event
- full recovery may take several hours; some attacks are preceded by brief aura
2-Absence seizures (petit mal):
- brief, almost imperceptible lapse of consciousness followed by immediate and full return to consciousness;
- posture is maintained, with no convulsive muscle contractions
- may occur as often as a hundred times a day
PARTIAL SEIZURES
1-Simple partial seizures: 2-Focal motor: 3- Focal motor with march (Jacksonian): 4- Temporal lobe seizure 5- Complex partial seizure
Secondarily generalized seizures: simple or complex partial seizures evolving to a generalized seizure
Status epilepticus: prolonged seizure or a series of seizures (lasting >30 min) with very little recovery between attacks
- may be life threatening
- medical emergency
Exam and treatment for epilepsy:
Exam/determine:
- time of onset, duration, type of seizure, sequence of events, frequency, duration
- patient activity at onset, presence of aura
- sensory elements, motor activity: type, degree and location of involvement
- presence of tongue biting, incontinence, respiratory distress
- behavioral elements, changes in mood
- patient responses after seizure
Medical management:
- antiepileptic meds: dilantin
- surgical intervention: lobe resection, hemmispherectomy
PT:
- protect patient form injury during seizure: remain with patient, remove potentially harmful nearby objects, loosen restrictive clothing and don’t restrain limbs
- establish airway, prevent aspiration: turn head to side or SL position; wait for tonic-clonic activity to subside before initiating artificial ventilation if needed
- promote regular routines for physical activity and emotional health
diseases of the cerebellum
hereditaty ataxia, Friedreich’s ataxia
neoplastic or metastatic tumors
infection
vascular: stroke
developmental: ataxic CP, Arnold-Chiari syndrome
Trauma: TBI
drugs, heavy metals
chronic alcoholism
lesions/impairments of the cerebellum
tend to produce ipsilateral S&S
Lesions of the archicerebellum
-vestibular symptoms
lesions of the paleo cerebellum
-hypotonia
lesions of the neocerebelum
-ataxic limb movements
asthenia: generalized weakness
hypotonia:
- especially in acute cerebellar lesions, difficulty with postural control of proximal muscles
motor learning impairments:
-decreased anticipatory control, feedback and learning delays
Cognition:
-deficits in information procession, attention deficits
emotional dysregulation: changes in emotional behaviors
Lesions of the archicerebellum:
Central vestibular symptoms:
- ocular dysmetria
- poor eye pursuit
- dysfunctional vestibular ocular reflex (VOR)
- impaired hand-eye coordination
Gait and trunk ataxia:
- poor postural control and orientation
- wide based gait
Little change in tone or dyssynergia of extremity movements
Lesions of the paleocerebellum
hypotonia
truncal ataxia:
-dysequilibrium, static postural tremor
-increased sway
wide BOS and high guard arm position
posture worse with eyes closed, narrow BOS (romberg)
-ataxic gait
-unsteady, increased falls, uneven/decreased step length, increased step width
Lesions of neocerebellum:
produces ataxic limb movements
intention tremor: irregular, oscillatory voluntary movements
dysdiadochokinesia: impaired rapid alternating movments
dysmetria:
- hypermetria: overshooting
- errors or force, direction, amplitude
- rebound phenomenon
Dyssynergia:
- abnormal timing (errors of velocity, onset and stop)
- movement decomposition of agonist/antagonist interactions
- impairments of multijoint coordination, movement sequences and complex motor tasks
errors in timing related to perceptual tasks
PT treatment for cerebellar disorders
Goals:
- improve accuracy of limb movements
- improve postural stability and dynamic postural control
- improve functional movement and safety
- stabilize VOR/vision
Eye-head coordination exercise: slow head movements with visual fixation; active eye and head movements
Stability exercises: use of WB postures, carefully graded resistance and approximation to promote steady holding. Use of theraband, weights, weighted waist belts and walkers to decrease ataxic movements
dynamic stability exercises: promote small range control, smooth reversals of movements, movement transitions, using carefully graded resistance
balance training
locomotor training
therapeutic pool: water provides graded resistance, decreases ataxic movement and postural instability
coordination exercises: proprioceptive neuromuscular facilitation (PNF) patterns, ball gymnastics to promote balance
stationary bike: assists timing of reciprocal movements
motor learning strategies: closed environment ideal; focus on practice and repetition; distributed practice
biofeedback
energy conservation
characteristics of vestibular disorders:
Dizziness: sensation of lightheadedness, giddiness, faintness
Vertigo: sensation of moving around in space or having objects move around; tends to come in attacks
-if severe: accompanied by nausea
Visual changes
- Nystagmus: involuntary, cyclical movement of the eyeball
- Blurred vision: gaze instability secondary to VOR dysfunction
Disequilibrium or postural instability: vestibular spinal reflex dysfunction; ataxia, gait disturbances; increased risk of falls
Anxiety, fear, depression
Indirect impairments: physical deconditioning, decreased cervical ROM
Unilateral vestibular disorders:
Trauma:
-vestibular symptoms seen in 30-65% of patients with TBI
Vestibular neuronitis, labyrinthitis
- acute infection with prolonged attack of symptoms, persisting for several days or weeks
- caused by viral or bacterial infection
Meniere’s disease
Benign paroxysmal positional vertigo
tumor
- acoustic neuroma
- gliomas/brainstem or cerebellar medulloblastoma
Meniere’s disease
recurrent and usually progressive vestibular disease
episodic attacks may last minutes to hours with severe symptoms:
- tinnitus
- deafness
- sensation of pressure/fullness within ear
etiology unknown
-edema of membranous labyrinth is a consistent finding
Benign paroxysmal positional vertigo
BPPV
brief attacks of vertigo and nystagmus that occur with certain head positions
-lying down, turning over in bed, tilting head back
may be related to degenerative processes, mechanical impairment of peripheral vestibular system
Tx techniques:
- canalith repositioning treatment: for horizontal SCC BPPV, posterior SCC BPPV
- liberatory maneuver: for posterior
- brandt-daroff exercises: for residual or mild vertigo
Hallpike Dix test
patient sits on table; clinician turns patient’s head horizontally 45 deg and quickly moves patient down to supine position with neck extended 30 deg below horizontal
check for symptoms - vertigo and nystagmus
return patient to sitting and test other side
+ for BPPV on side that produces symptoms
habituation training:
repetition of movements and positions that provoke dizziness and vertigo
gaze stability exercises
eye movements:
- side to side eyes on stationary target (X1 paradigm)
- side to side eyes on moving target (X2 paradigm)
head movements up and down, side to side while maintaining eyes focused on a visual target
- progressing slow to fast movements
- standing to walking
Peripheral nerve disease/injury
Pathological processes:
1-wallerian degeneration
2-segemental demyelination
3-axonal degeneration
Traumatic nerve injury classes:
Class I-neurapraxia
Class II-axonotmesis
Class III-neurotmesis
Wallerian degeneration:
transection (neurotmmesis) results in degeneration of the axon and myelin sheath distal to the site of axonal interruption
- chromatolysis and repair processes occurs in nerve cell body
- endoneuriusm (sheath) does not degenerate but forms a tube directing regeneration
Segmental demyelination:
axons are preserved (no wallerian degeneration)
-remyelination restores function
ex: Guillain-barre syndrome
Axonal degeneration
degeneration of axon cylinder and myelin, progressing from distal to proximal
“dying back” of nerves
ex: peripheral neuropathy
neurapraxia=
Class 1 traumatic nerve injury
injury to nerve that causes a brief loss of function (conduction block ischemia)
nerve dysfunction may be rapidly reversed or persist a few weeks (ex: compression)
axonotmesis=
Class 2 traumatic nerve injury
injury to nerve interrupting the axon and causing loss of function and wallerian degeneration distal to the lesion
with no disruption of the endoneurim regeneration is possible
ex: crush injury
neurotmesis=
Class 3 traumatic nerve injury
cutting of the nerve with severance of all structures and complete loss of function
re-innervation typically fails without surgical intervention because of aberrant regeneration (failure of regenerating axon to find its terminal end)
clinical symptoms of LMN syndrome
weakness/paresis of denervated muscle, hyporeflexia and hypotonia, (rapid atrophy, fatigue
sensory loss: corresponds to motor weakness; proprioceptive losses may yield sensory ataxia
autonomic dysfunction: vasodilation and loss of vasomotor tone (dryness, warm skin, edema, orthostatic hypotension)
hyper excitability of remaining nerve fibers
- sensory dysesthesias: hyperalgesia, pins and needles, numbness, tingling, burning
- motor: fasciculations, spasms
muscle pain (myalgia) with inflammatory myopathies -ex: post polio syndrome
neuropathy
any disease of nerves characterized by deteriorating neural function
polyneuropathy: bilateral symmetrical involvement of peripheral nerves, usually legs>arms, distal segments earlier and more involved than proximal
mononeuropathy: involvement of a single nerve
radiculopathy: involvement of nerve roots
trigeminal neuralgia (tic douloureux)
neuralgia of the trigeminal nerve (CN V)
Etiology: results from degeneration or compression
- mean age ~50
- abrupt onset
Characteristics:
- brief paroxysms of neurogenic pain (stabbing and/or shooting pain) recurring frequently
- occurs along unilateral distribution of the trigeminal nerve, mandibular and maxillary divisions (ophthalmic division is rare)
- autonomic instability: exacerbated by stress cold; relieved by relaxation
TENS can be effective for pain relief
Bell’s palsy
LMN lesion involving facial nerve (CN VII)
resulting in unilateral facial paralysis
Etiology: acute inflammatory process of unknown etiology– results in compression of the nerve w/in the temporal bone
Characteristics:
- weakened or paralyzed muscles of facial expression (wrinkling the forehead, closing the eye tightly, smiling)
- decrease taste sensation anterior 2/3 of tongue
- loss of control of salivation or lacrimation
- acute onset with max severity in a few hours or days
- commonly preceded by a day or 2 of pain behind the ear
- most fully recover in several weeks or months
- normal sensation
TX:
- protect corneas- artificial tears/patch
- E-stim to maintain tone, support facial muscles
- active facial muscle exercises
- functional retraining- foots, chewing
Bulbar palsy (bulbar paralysis)
refers to weakness or paralysis of the muscles innervated by the motor nuclei of the lower brainstem, affecting the muscles of the face, tongue, larynx and pharynx
Etiology: result of tumors, vascular or degenerative diseases of lower CN motor nuclei (ex: ALS)
Examine:
- glossopharyngeal and vagal paralysis: phonation, articulation, palatal action, gag reflex, swallowing
- changes in voice quality: dysphonia (hoarseness or nasal quality)
- bilateral involvement: severe airway restriction with dyspnea, difficulty with coughing
- possible complications: aspiration pneumonia
TX:
- suctioning, oral care
- maintenance of respiratory function, open airway
- elevated HOB
- dietary changes: soft foods, liquids
Guillian-Barre syndrome
a polyneuropathy resulting in symmetric motor paralysis and progressive muscular weakness that develops quickly
- probable immune-mediated viral origin
- usually occurs after recovery from an infectious illness (respiratory or GI)
Characteristics:
- involves acute demyelination of both cranial and peripheral nerves (LMN disease)
- sensory loss, paresthesias, pain (sensory loss typically less than motor loss) “stocking/glove” pattern
- motor paresis or paralysis: relative symmetrical distribution of weakness; progresses from LE to UE (ascending pattern) and from distal to proximal; may produce full tetraplegia with respiratory failure
- dysarthria, dysphagia, diplopia, and facial weakness may develop in severe cases
- progression evolves over a few days or weeks
- recovers slow (6 months -2 years) and usually complete (85%); some mild weakness persists; 3% mortality
Complications:
- respiratory impairment and failure
- autonomic instability: tachycardia, arrhythmias, BP fluctuations
- pain: myalgia
- risk of pneumonia
- prolonged hospitalizations and immobility
- relapse: if treatment inadequate
PT:
- ascending (disease progressing) phase: respiratory function, PROM, positioning, skin care
- when stabilized: prevent injury to denervated muscles, avoid overuse and fatigue, begin gentle stretching, and initiate moment in a controlled environment
- descending (recovery) phase: muscle re-ed with a mod exercise program, improve cardiovascular fitness and energy conservation
Amyotrophic lateral sclerosis (ALS)
degenerative disease affecting both UMN and LMN (degeneration of anterior horn cells and descending corticobulbar and corticospinal tracts)
-CN can be affected as well
Etiology: unknown; 5-10% genetic (autosomal dominant)
Characteristics:
- muscle weakness is progressive and can affect muscles of respiration
- weakness may appear in hands first progressing to whole body
- dysarthria, dysphagia, dysphonia
- muscle atrophy, cramping and fasciculations (LMN signs)
- spasticity and hyperreflexia (UMN signs)
- often no sensory changes
- typical sparing of bowel and bladder function
- normal cognition
- death typically in 2-5 years
stages of ALS
I: early disease
- mild focal weakness
- asymmetric distribution
- symptoms of hand cramping and fasciculations
II:
- moderate weakness in groups of muscles
- some atrophy of muscles
- modI with AD
III:
- severe weakness of specific muscles
- increasing fatigue
- mild-mod functional limitations
- ambulatory
IV:
- severe weakness and wasting of LEs
- mild weakness of UEs
- mod A and AD required
- w/c user
V:
- progressive weakness with deterioration of mobility and endurance
- increased fatigue
- mod-severe weakness of whole limbs and trunk
- spasticity, hyperreflexia
- loss of head control
- maxA
VI: bedridden
- dependent ADLs, FMS
- progressive respiratory distress
Post-polio syndrome
new, slowly progressive muscle weakness occurring in people with confirmed history of acute poliomyelitis
- follows a stable period of functioning
- new form of muscular dystrophy
- new denervation occurs with asymmetrical muscle weakness
S&S:
- myalgia
- joint pain
- variable asymmetrical muscle atrophy with decreased strength
- excessive fatigue and decreased endurance contribute to loss of function
- difficulty in concentration, memory, attention
- sleep disturbances
Tx:
- low intensity exercise never to the point of fatigue - stop exercise with pain or weakness
- use orthotic devices as needed to improve function
- endurance and energy conservation
nociceptive pain=
response to an immediate noxious stimulus signaling impending tissue damage
inflammatory pain occurs after tissue damage and increases sensitivity to pain
neurogenic pain
pain as a result of lesions in some part of the NS (central or peripheral)
usually accompanied by some degree of sensory deficit
1-central neurogenic pain: arises from injury or disease affecting CNS
- pain is often burning, acing or prickling
- hyperanalgeisa and allodynia (pain from normal stimulus)
2- peripheral neurogenic pain: arises from mechanical or chemical damage to peripheral nerves; may include symptoms of paresthesia, dysesthesia and pain
Central neurogenic pain
arises from injury or disease affecting CNS
- pain is often burning, acing or prickling
- hyperanalgeisa and allodynia (pain from normal stimulus)
1- central post-stroke (thalamic) pain:
- continuous, intense, central pain occurring on the contralateral hemiplegic side
- result of a store involving the ventral posterolateral thalamus
- autonomic and vasomotor dysfunction is common
2- TBI
3- fibromyalgia
Peripheral neurogenic pain:
arises from mechanical or chemical damage to peripheral nerves; may include symptoms of paresthesia, dysesthesia and pain
1- Complex regional pain syndrome I
-AKA reflex sympathetic dystrophy/causalgia
-a complex disorder or group of disorders that develop as a result of trauma affecting body parts and disuse
-CRPS I= tissue injury without nerve damage; CRPS II involves nerve injury
-“regional”= t/o limb, not in a peripheral nerve or distribution
reflex neurogenic inflammation affecting the SNS and pain disproportionate to injury
-pain maintained by the SNS, characterized by burning pain (causalgia)
-usually associated with traumatic injury
2- disorders of peripheral roots and nerves
- neuralgia: pain occurring along the branches of a nerve
- radiculalgia: neuralgia of nerve roots
- paresthesias
- allodynia
3- Herpes zoster (shingles)
- acute, painful mononeuropathy caused by varicella zoster virus
- characterized by vesicular eruption and marked inflammation of the posterior root ganglion of the affected spinal nerve or sensory ganglion of the CN
- ventral root involvement (motor weakness) in 5-10% of cases
- infection can last from 10 days to 5 weeks
- posthepetic neuralgia pain may persist for months or years
4- phantom limb pain
-folowing amputation
Complex regional pain syndrome I
-AKA reflex sympathetic dystrophy/causalgia
-a complex disorder or group of disorders that develop as a result of trauma affecting body parts and disuse
-CRPS I= tissue injury without nerve damage; CRPS II involves nerve injury
-“regional”= t/o limb, not in a peripheral nerve or distribution
reflex neurogenic inflammation affecting the SNS and pain disproportionate to injury
-pain maintained by the SNS, characterized by burning pain (causalgia)
-usually associated with traumatic injury
Herpes zoster
painful inflammation of the posterior root ganglion, caused by a virus resulting in the formation of vesicles (fluid filled sacs) along the course of a nerve (dermatome)
- acute, painful mononeuropathy caused by varicella zoster virus
- characterized by vesicular eruption and marked inflammation of the posterior root ganglion of the affected spinal nerve or sensory ganglion of the CN
- ventral root involvement (motor weakness) in 5-10% of cases
- infection can last from 10 days to 5 weeks
- posthepetic neuralgia pain may persist for months or years
musculoskeletal pain
1- fibromyalgia:
2- myofascial pain syndrome
3- postural stress syndrome
-postural malalignment produces chronic muscle lengthening and/or shortening and stress to soft tissues
4-movement adaptation syndrome
-habituated movement dysfunction leading to muscle strain and pain
fibromyalgia:
widespread pain accompanied by tenderness of muscles and adjacent soft tissues
a nonarticular rheumatic disease of unknown origin
myofascial pain syndrome
persistent, deep aching pains in muscle
nonarticular in origin
characterized by well defined, highly sensitive tender spots (trigger points)
psychosomatic pain
origin of pain experience is due to mental or emotional disorders
referred pain
pain arising from deep visceral tissues that is felt in a body region remote from site of pathology, resulting in tenderness and cutaneous hyperalgesia
ex:
- medial L arm and jaw pain with MI
- R subscapular pain from gallbladder attack
- thoracic or flank pain from kidney problems
- L upper quadrant and shoulder pain with spleen damage
- R upper quadrant pain with liver problems
SCI MOI
Non-traumatic:
- ~10%; most likely in ppl with narrowing spinal canals
- possible causes: disc prolapse, vascular insult, neoplasm, RA, radiation, spinal stenosis, surgery, cardiac arrest, AAA, infection
Traumatic:
- most result from from forces that create violent motions of the head/neck
- Cervical: *C5-7; flexion, vertical loading, and extension accompanied by rotation or lateral flexion are most likely
- Thoracic: less likely d/t rib cage and higher stability; *T12-L1 most common; flexion or vertical compression can cause wedge compression or burst fractures of vertebral bodies damaging the cord
- Lumbar: neuro damage from trauma is usually incomplete due to large vertebral canal and good vascular supply; most common L1-2; cauda equina less likely to sustain a complete injury
actual transection of the cord is rare
Mechanisms of secondary tissue destruction:
- ischemia
- edema
- demyelination and destruction
intrinsic vs. augmented feedback
intrinsic= sensory info self acquired during performance of task
augmented: externally presented feedback (VC)
knowledge of results vs. knowledge of performance
KR: augmented feedback about the outcome of a movement
KP: augmented feedback about the nature of the movement produced (characteristics)
forms of practice
Blocked: repetitive single skill
Variable: varied motor skills, rapid modifications
Random: skills in random order
Serial: group of skills in a predictable order
Massed: relatively continuous practice
Distributed: rest time is larger than practice
Mental: cognitive rehersal
strategies for effective learning:
feedback given after every trial improves performance
variable feedback improves learning and retention
early training should emphasize visual feedback (cognitive phase)
later training should focus on proprioceptive feedback (associative phase of learning)
early- closed environment –> open
supportive feedback (reinforcement) to shape behavior, motivate
stages of learning
1- cognitive – “what to do”
- develops understanding of task
- assess abilities
- develop overall understanding of the skill through trial and error
2- associated – “how to do”
- practices movements
- decreases errors
- refinement of the motor skill through continued practice
3-autonomous – “how to succeed”
- practices
- minimal level of cognitive monitoring
- largely error free
- after considerable practice the motor performance becomes largely automatic
Proprioceptive neuromuscular facilitation (PNF)
uses total patterns of movement and posture to promote motor learning in synergistic muscle patterns and prepare the body for advanced functional skills (gait)
utilizes proprioceptive elements: stretch resistance, overflow, manual contacts, approximation, traction
utilizes motor learning principles: VC, visual guidance of movement, repetition and practice
PNF diagonals:
D1 flexion for UE: “disco”
- starts with GH IR, abd and extension
- ends with ER, adduction and flexion
- D1 extension is the opposite
D2 flexion for UE: “seatbelt”
- starts with GH IR, adduction and extension
- ends with ER, abduction and flexion
- D2 extension is the opposite
D1 flexion of the LE
- starts with hip IR, abduction, and extension
- ends with ER, adduction, and flexion
- D1 extension is the opposite
D2 flexion of the LE
- starts with hip ER, adduction and extension
- ends with IR, abduction and flexion
- D2 extension is the opposite
PNF diagonal patterns of the head and neck
may be used to enhance breathing and movement patterns
supine or sitting chopping, upper trunk flexion with rotation and UE D1 extension facilitates rolling to prone position
supine lower trunk flexion with rotation to right or left; knees flexing
LE D1 flexion helps rolling in any direction
List of PNF techniques
agonist reversals
approximation
contract-relax
hold-relax
repeated contractions
rhythmic initiation
rhythmic stabilization
slow reversal
traction
Alzheimer’s disease
a chronic, progressive, widespread deterioration of the cerebrum
intellectual decline, loss of memory, confusion, anxiety, depression, loss of reasoning, possible motor impairment, and gait problems or contractures as the disease progresses
bipolar disorder
manic-depressive disorder
characterized by mood swings from depression to mania
conversion disorder
conversion reaction or hysterical paralysis
a response to severe emotional stress resulting in involuntary disturbance of physical functions
disturbances are often connected with the NS, resulting in problems with vision, sensation, hearing or motor disturbances (hemiplegia, paraplegia, quadriplegia, tics or tremors)
patient is frequently indifferent to the symptoms
antidepressants
Valium, Prozac, Elavil
require 3-4 weeks for mood-elevating effect
side effects:
- dry mouth
- blurred vision
- disturbed sleep
- increased anxiety
- disturbed balance
- postural hypotension
- increased HR
- weight gain
- blood glucose fluctuations
- orthostatic hypotension in elderly patients
schizophrenia
psychotic disorder
characterizted by loosening of association (fragmented thoughts, errors of logic, bizzarre ideas), autistic withdrawal, ambivalence to themselves and others, and inappropriateness of affect
Meds: Haldol, serouquel, risperdal
-probably block postsynaptic dopamine receptors
Side effects:
- sedation, drowsiness
- insomnia
- seizures
- headaches
- back pain
- tachycardia
- orthostatic hypotension
- dry mouth
- constipation
- weight gain
agnosia
inability to recognize familiar objects with one form of sensation (visual agnosia)
akinesia
inability to initiate movements
aphasia
disturbance to language that results in errors in word choice, comprehension or syntax (word order)
Expressive/Broca’s
- severe difficulty in verbal expression with impairment in object naming and writing abilities.
- mostly found in those with L CVA
Global
- most common and severe form of aphasia
- reduced speech AND comprehension
- reading and writing impaired also
Receptive/Wernicke’s
- severe disturbance in auditory comprehension
- reading, writing and word recognition also impaired
apraxia
inability to perform movements previously learned even though there is no loss of strength, coordination, sensation or comprehension
ideational apraxia: person no longer gets the “idea” of how to do a routine task
ideomotor apraxia: person can’t do a task on command but can spontaneously
asterognosis
inability to recognize objects by touch alone
asynergia
inability to move muscles together in a coordinated movement
ataxia
uncoordinated movement, especially gait
athetosis
slow involuntary, worm-like, twisting motions
usually seen in forms of CP
causalgia
painful burning sensations
often associated with CRPS I
Cheyne-stokes respiration
a common and bizarre breathing pattern
-period of apnea lasting 10-60 seconds followed by gradually increasing, then decreasing depth and frequency of respirations
accompanies depression of the frontal lobe and diencephalic dysfunction
postulated to be a result of an abnormality in the neurological respiration center
can occur with severe cases of TBI or CHF
chorea
rapid, involuntary, jerky movements
seen especially in Huntington’s disease
clonus
rhythmic oscillation of a muscle in response to sustained stretch in patients with UMN disease
decerebrate rigidity
contraction of the extensor muscles of both the UE and LE because of an injury at the brainstem
decorticate rigidity
contraction of the UE flexors and LE extensors
delirium
temporary confusion and loss of mental function
often as a result of illness, drug toxicity, or lack of oxygen
often reversible
dementia
loss of memory or intellectual functioning
may be reversible if caused by toxins, drugs, metabolic or psychiatric disorders
often slowly progressive and nonreversible if a result of alcoholism, Alzheimer’s, infarction, or Parkinson’s disease
dysmetria
inability to judge distances
seen in cerebellar dysfunctions
electromyography (EMG)
study of a graphic record of muscle contraction as a result of electrical stimulation
used to eval the voluntary electrical activity of muscle
glove and stocking anesthesia
can occur in generalized peripheral neuropathies in which the distal portions of the nerves degrease resulting in anesthesia of the distal extremities
seen in Guilin-barre
Morton’s neuroma
an excessive pronation during stance produces compression between the 3rd and 4th metatarsals
nerve can enlarge, forming a neuroma on the interdigital nerve resulting in metatarsalgia
nerve conduction velocity (NCV) test
determines speed of propagation of an action potential along a nerve or muscle fiber
if nerve is compressed or damaged, the velocity of AP will be slowed and the latency or time the potential takes to travel between two points will be increased
test utilized to determine the severity of nerve compression prior to surgery
nystagmus
rapid, usually back and forth movement of the eyeballs
reciprocal inhibition
inhibition of muscles antagonist to those being facilitated
essential for coordinated movement
somatagnosia
lack of awareness of the relationship of one’s own body parts or the body parts of others
visual field deficits
homonymous hemianopsia
- deficit of either the R or L halves of the visual field
- caused by damage to the contralateral optic tract
bitemporal hemianopsia
- deficit of the temporal or peripheral visual fields
- caused by injury at the optic chasm
- AKA tunnel vision
monocular blindness
- blindness in one eye
- result of damage to optic nerve
