neuro Flashcards
pusher syndrome
increased spasticity/tone neck and trunk muscles
pushes towards weak side
mobilize towards strong side
don’t use cane on strong side will push over
stand on posterior lateral weak side
brown sequard syndrome
ipsilateral motor/vibration loss
contralateral pain + temperature loss
stab/knife injury to half of spinal cord
anterior cord syndrome
damage to anterior spinal cord
cervical flexion injury
loss of motor function, pain/temp below level of lesion
central cord syndrome
damage to central portion of spinal cord
cervical hyperextension injury
motor loss > sensory
UE > LE
sacrum spared
posterior cord syndrome
posterior portion of spinal cord damaged
tumor/abscess
loss of proprioception, pressure sense, vibratory sense
no motor loss
sensory ataxia
cauda equina syndrome
flaccid paralysis LMN
areflexsive bowel and bladder, sacral anesthesia
autonomic dysreflexia
autonomic reflex to noxious stimulus causing sympathetic over-activity
LESION T6 OR ABOVE
widespread vasoconstriction, increased BP >20mmHg, increased HR then bradycardia, severe headache, profuse sweating, flushed skin
SIT PATIENT DOWN to lower BP - DO NOT LAY PATIENT DOWN!!
notify nurse, check for catheter, loosen clothing/source, document
C6 spinal cord lesion functioning abilities
limited self-care activities with tenodesis grasp (don’t stretch)
independent/min assist with slide board transfers
independent manual cough
wheelchair propulsion with projection rims (short distances)
power wheelchair community
drive car with adaptive controls
capable of living independently
NLI C5 and above resp. function
require ventilatory support using IPPV
deep breathing exercises
assisted cough capable
abdominal binder
respiratory muscle strengthening
repositioning in bed vs. in chair
in bed at least once every 2 hours
in chair - pressure relief maneuvers every 15 mins for 2+ mins
anterior cerebral artery syndrome (stroke)
medial aspect of frontal and parietal lobes
contralateral hemiparesis and hemi-sensory loss
LE > UE
urinary incontinence
absence of willpower/decision making (abulia)
akinetic mutism (reduced movement for speech)
difficulty with motor planning (apraxia)
broca’s aphasia (expressive)
middle cerebral artery syndrome (stroke)
lateral aspect of frontal, temporal and parietal lobes
contralateral hemiparesis and hemi-sensory loss face, UE, LE
UE > LE
contralateral homonymous hemianopia (vision = XO/XO)
wernicke’s aphasia (receptive speech)
broca’s aphasia
global aphasia
unilateral neglect, anognosia, apraxia, spatial disorganization/depth perception
internal carotid artery syndrome (stroke)
MCA + ACA (MCA > ACA)
significant edema
increased ICP - coma, pressure on brainstem (uncal herniation)
Posterior cerebral artery syndrome (stroke)
occipital lobe, medial and inferior temporal lobe, upper brainstem, posterior diencephalon
amnesia
homonymous hemianopia
visual agnosia
dyslexia
central post-stroke pain (thalamus)
sensory impairments
contralateral hemiplegia
oculomotor nerve palsy
vertebrobasilar artery syndrome (stroke)
supplies cerebellum and medulla, pons, internal ear
ipsilateral and contralateral symptoms
Ataxia (ipsilateral)
impaired sensation over face (ipsilateral)
impaired pain and thermal regulation (contralateral)
5 D’s, 3 N’s
Locked in syndrome
patient awake/aware but complete paralysis of voluntary muscles apart from eyes
preserved consciousness and sensation
lacunar syndrome
strongly associated with hypertension and diabetes
can be pure sensory
can be pure motor
higher cortical areas preserved - consciousness, language, visual fields
pseudobulbar affect
sudden outbursts of crying, laughing, other emotions not in context
left hemisphere lesion behaviours
slow, cautious, anxious, disorganized
hesitant to try new tasks - need encouragement, support, feedback
aware of deficits
difficulty communication/processing in sequential linear order
right hemisphere lesion behaviours
quick, impulsive, poor judgement
overestimate abilities
unaware of deficits
increased safety risk
difficulty with spatial-perceptual tasks and grasping whole idea
ideational apraxia
cant produce purposeful movement on command/automatically
no idea how to do the movement or plan
ideomotor apraxia
cant produce movement on command but may do it automatically
normal range ICP
5-20cm H2O
ICP > 20 - elevated
ICP > 25 - critical
signs of increased ICP
decreased consciousness - stupor/coma
altered vital signs
widened pulse pressure
cheyne-stokes breathing
vomiting
headache
non-reactive pupils (CN 3)
reduced motor function
seizures
cerebellar gait
ataxic gait
sensory ataxia with high stepping/stomping gait
intervention: add ankle weights, auditory cueing, proprioceptive feedback, slow movements, break down movements, give assistive device
spinal shock
transient period of areflexia immediately after SCI
lasts approx. 24 hours
impaired autonomic regulation - sweating, goosebumps, hypotension
24 hours - areflexia
1-3 days - gradual return of reflexes
1 to 4 weeks - increasing hyperreflexia
1-6 months - final hyperreflexia (UMN syndrome)
tetraplegia
loss of motor and/or sensory function all four limbs + trunk
lesions of cervical spinal cord (T1 and above)
paraplegia
loss of motor and/or sensory function all/part of trunk and lower extremities bilaterally
lesions of the thoracic or lumbar spinal cord, or cauda equina, T2 or below
neurological level of injury (NLI) definition
most caudal level of injury with intact motor + sensory function bilat.
lowest level!
ASIA scale
A = complete - no motor/sensory function preserved in sacrum S4 to S5
B = incomplete - sensory but no motor preservation below NLI and includes sacrum segments S4 to S5
C = incomplete - motor function preserved below NLI , and more than half of key muscles below NLI have grade LESS than 3
D = incomplete - motor function is preserved below NLI, and moe than half of key muscles below NLI have grade 3 or MORE
E = normal
MS description + aggravations
chronic inflammatory disease causing demyelination in the CNS
inflammation damages myelin sheath and myelin producing cells
damaged myelin is replaced by plaque/scar tissue
sclerotic plaque prevents nerve impulse transmission causing neuro signs
diagnosed by MRI + bloodwork to rule out other conditions
aggravated by:
viral infection
bacterial infection
disease of major systems - pancreatitis, heart/lung diseases
emotional and bodily stress
relapsing-remitting MS
relapses followed by recovery and disease stabilization
(steps with breaks)
relapse = new and recurrent symptoms for at least 24 hours
primary-progressive MS
steady disease progress
no distinct episodes or interruptions
(straight incline, no steps)
secondary-progressive MS
begins with relapse-remitting course followed by steady disease progression with no distinct periods of remission
(steps with breaks, then steady incline)
progressive-relapsing MS
progressive disease from onset with super imposed acute attacks or relapses that may or may not have recovery
(incline steps on steeper angle)
uhthoffs phenomenon (MS)
adverse reaction to heat (internal or external)
signs/symptoms MS
sensory changes - paresthesia, numbness
pain -trigeminal neuralgia, paroxysmal limb pain (++ at night), headaches
lhermittes sign - neck flexion causing electric shock down spine, msk pain
blurred vision, diplopia, optic neuritis, nystagmus
weakness, central fatigue (CNS), spasticity, impaired balance and coordination, impaired ambulation and mobility
dysarthria, dysphonia, dysphagia, increased risk aspiration pneumonia
cognitive impairments, depression, pseudobulbar effect
bowel/bladder dysfunction, sexual dysfunction
MS interventions - exercise considerations
exercise - take fatigue + heat into consideration
perform exercises in the morning (early hours) - higher energy levels, cooler body temp, cooler temps outside
keep hydrated, light, loose clothing with good ventilation
avoid hot baths/showers/thermal modalities
SUBMAX exercise intensities
more rest intervals (3 x 10 min bouts of cardio instead of 30 mins)
MS interventions - fatigue management
fatigue is most debilitating - sudden sleepiness/tiredness/weakness
diurnal - least in mornings, worst in afternoons
do not overwork or put into fatigue
parkinsons disease defintion
chronic progressive neurodegenerative disorder
loss of dopamine producing neurons in the substantia nigra
Parkinsons charactristics
T - tremor
R - rigidity
A - akinesia/bradykinesia
P - postural instability
tremor (resting!) - disappears with voluntary movement
“pill rolling” tremor of the hand
increases with emotional stress and fatigue
reduced when patient relaxed and disappears when sleeping
rigidity - increased resistance to movement (not velocity dependent)
“heaviness” or “stiffness”
AYMMETRICAL
PROXIMAL to DISTAL
cogwheel or leadpipe
akinesia - with voluntary movements
freezing gait
slowness in movement - reduced in speed, amplitude, range
postural instability - later in disease
abnormal posture synergies lead to reduced balance
flexed, stooped posture
increased weakness of trunk extensor muscles
kyphosis
increased falls - COG shifts forward
Parkinsons gait
festinating gait - shortened strides with progressively increasing speed
stooped posture
freezing episodes - exacerbated by obstacles, doorways, stress
anteropulsive (forward festinating) vs. retropulsive (backward festinating)
shuffling steps - reduced hip, knee, ankle flexion
reduced trunk rotation
reduced arm swing
difficulty with dual commands, or increased attentional demands
early signs/symptoms parkinsons
loss of smell
masked face (hypomimia)
dysphagia
dysphonia
micrographia
start hesitation gait
festinating gait
stooped posture
later signs/symptoms parkinsons
difficulty STS
cognitive changes/dementia
drooling
GI dysfunction
foot dystonia
Parkinsons interventions
medications to slow disease process/symptom management
levodopa - dopamine replacement
medications should not be discontinued suddenly - can be life threatening
side effects - dyskinesia, dystonia, motor fluctuations
PT management
exercise training
decline treadmill walking to reduce stooped posture
blocked training sessions with repetition instead of random practice
reduce cognitive competition demands
auditory cues - clapping, rhythmic music, metronome
visual cues - stepping over tape lines
tactile cues - tapping thigh, hip, leg
cognitive cues - imagery of stepping appropriate length (good for freezing)
ALS definition UMN/LMN affects
chronic degenerative disease of the motor neurons of the brain, brain stem and spinal cord
UMN degeneration in motor cortex and corticospinal tracts
cranial nerves 5 (trigeminal), 7 (facial), 9 (glossophyrangeal), 10 (vagus), 11 (hypoglossal)
LMN degeneration in anterior horns of the spinal cord
initially, sprouting of axons can preserve strength/function. As disease progresses, rate on reinnervation is overtaken by rate of degeneration causing rapid decline
areas spared in ALS
sensory system, spinocerebellar tracts
eye movements - cranial nerves 3 (oculomotor), 4 (trochlear), 6 (abducens)
anterior horn cells for S2 (pelvic floor)
ALS characteristics
UMN and LMN effects
asymmetrical distribution
DISTAL to PROXIMAL progression (trip over foot)
CAUDAL to ROSTRAL within spinal cord
ALS signs/symptoms
weakness - cardinal sign
focal and asymmetrical - may begin UE, LE, bulbar muscles (mouth/throat)
decreased ROM
contractures
deconditioning/fatigue and pain
atrophy
hyporeflexia
hypotonicity
bulbar ALS signs/symptoms
mixed palsy spasticity and flaccidity
dysphagia - risk of aspiration, weight loss
dysarthria - weakness tongue, lips, jaw, pharynx (bulbar muscles)
inability to project voice
drooling (sialorrhea) - absence of swallow to clear saliva
pseudobulbar affect
ALS cognitive impairments
frontotemporal dementia - cognitive decline, reduced executive functioning, difficulty with planning/organization, personality and behavioural changes
increased with bulbar-onset ALS
Guillain-barre syndrome (GBS) definition
auto-immune disorder causing acute inflammation and demyelination of the cranial and peripheral nerves myelin sheaths
involves schwann cells and causes impulse conduction slowing, dispersing or blocking
axonal damage if inflammation is severe
3 phases of GBS
1. progressive deterioration
2. plateau
3. recovery
- demyelination and axon damage lasting 1-4 weeks
- disease peaks, no further deterioration
- axonal regeneration and myelination 6 months - 2 years with complete recovery possible
strengthening not helpful stages 1-2
GBS characteristics
LMN syndrome
motor signs always present, sensory may not be
DISTAL to PROXIMAL
glove and stocking distribution
SYMMETRICAL
GBS signs/symptoms
distal lower extremity paresis/weakness
distal sensory disturbances (glove and stocking)
muscle aches and tenderness
high risk CRPS
LMN signs - atrophy, fatigue, hyporeflexia, hypotonia
deep, throbbing pain and aching - common low back/legs ++SLR
cranial nerve 7 - facial nerve
respiratory - phrenic nerve involvement (diaphragm)
GBS PT management
pulmonary rehab -prevent resp complications (DVT, pressure sores)
energy conservation techniques
maintain ROM and joint integrity
gentle stretching and positioning
Recovery phase:
improve resp function and CV fitness
inspiratory muscle strengthening
muscle strengthening
poliomyelitis definition / transmission
acute infectious viral disease caused by the poliovirus
fecal-oral route of transmission
poliomyelitis characteristics
LMN syndrome
wekaness/paralysis “patchy”
ASYMMETRICAL
LE > UE
partial or full recovery after up to 2 years
muscle hypertrophy and neuroplastic changes - sprouting terminal axons for neighboring motor units take over damaged ones causing hypertrophy
post-polio syndrome
poliomyelitis symptoms appearing 15+ years after polio
caused by neural fatigue
denervation > reinnervation
do not over fatigue patient!
post-polio characteristics
slow progression - periods of stability with new declines
NO SENSORY impairments
LMN syndrome
weakness/paralysis “patchy”
ASYMMETRICAL
LE > UE
post-polio signs/symptoms
fatigue!
muscle atrophy
weakness
pain
COLD intolerance
post-polio PT management
energy conservation techniques
weight loss
exercise therapy without over fatiguing
periods of rest and activity
hydrotherapy - warm water
