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physio > neuro > Flashcards

neuro Flashcards

1
Q

pusher syndrome

A

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

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2
Q

brown sequard syndrome

A

ipsilateral motor/vibration loss
contralateral pain + temperature loss
stab/knife injury to half of spinal cord

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3
Q

anterior cord syndrome

A

damage to anterior spinal cord
cervical flexion injury
loss of motor function, pain/temp below level of lesion

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4
Q

central cord syndrome

A

damage to central portion of spinal cord
cervical hyperextension injury
motor loss > sensory
UE > LE
sacrum spared

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5
Q

posterior cord syndrome

A

posterior portion of spinal cord damaged
tumor/abscess
loss of proprioception, pressure sense, vibratory sense
no motor loss
sensory ataxia

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6
Q

cauda equina syndrome

A

flaccid paralysis LMN
areflexsive bowel and bladder, sacral anesthesia

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7
Q

autonomic dysreflexia

A

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

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8
Q

C6 spinal cord lesion functioning abilities

A

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

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9
Q

NLI C5 and above resp. function

A

require ventilatory support using IPPV
deep breathing exercises
assisted cough capable
abdominal binder
respiratory muscle strengthening

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10
Q

repositioning in bed vs. in chair

A

in bed at least once every 2 hours
in chair - pressure relief maneuvers every 15 mins for 2+ mins

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11
Q

anterior cerebral artery syndrome (stroke)

A

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)

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12
Q

middle cerebral artery syndrome (stroke)

A

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

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13
Q

internal carotid artery syndrome (stroke)

A

MCA + ACA (MCA > ACA)
significant edema
increased ICP - coma, pressure on brainstem (uncal herniation)

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14
Q

Posterior cerebral artery syndrome (stroke)

A

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

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15
Q

vertebrobasilar artery syndrome (stroke)

A

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

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16
Q

Locked in syndrome

A

patient awake/aware but complete paralysis of voluntary muscles apart from eyes
preserved consciousness and sensation

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17
Q

lacunar syndrome

A

strongly associated with hypertension and diabetes
can be pure sensory
can be pure motor
higher cortical areas preserved - consciousness, language, visual fields

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18
Q

pseudobulbar affect

A

sudden outbursts of crying, laughing, other emotions not in context

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19
Q

left hemisphere lesion behaviours

A

slow, cautious, anxious, disorganized
hesitant to try new tasks - need encouragement, support, feedback
aware of deficits
difficulty communication/processing in sequential linear order

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20
Q

right hemisphere lesion behaviours

A

quick, impulsive, poor judgement
overestimate abilities
unaware of deficits
increased safety risk
difficulty with spatial-perceptual tasks and grasping whole idea

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21
Q

ideational apraxia

A

cant produce purposeful movement on command/automatically
no idea how to do the movement or plan

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22
Q

ideomotor apraxia

A

cant produce movement on command but may do it automatically

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23
Q

normal range ICP

A

5-20cm H2O
ICP > 20 - elevated
ICP > 25 - critical

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24
Q

signs of increased ICP

A

decreased consciousness - stupor/coma
altered vital signs
widened pulse pressure
cheyne-stokes breathing
vomiting
headache
non-reactive pupils (CN 3)
reduced motor function
seizures

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25
Q

cerebellar gait

A

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

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26
Q

spinal shock

A

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)

27
Q

tetraplegia

A

loss of motor and/or sensory function all four limbs + trunk
lesions of cervical spinal cord (T1 and above)

28
Q

paraplegia

A

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

29
Q

neurological level of injury (NLI) definition

A

most caudal level of injury with intact motor + sensory function bilat.
lowest level!

30
Q

ASIA scale

A

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

31
Q

MS description + aggravations

A

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

32
Q

relapsing-remitting MS

A

relapses followed by recovery and disease stabilization
(steps with breaks)

relapse = new and recurrent symptoms for at least 24 hours

33
Q

primary-progressive MS

A

steady disease progress
no distinct episodes or interruptions
(straight incline, no steps)

34
Q

secondary-progressive MS

A

begins with relapse-remitting course followed by steady disease progression with no distinct periods of remission
(steps with breaks, then steady incline)

35
Q

progressive-relapsing MS

A

progressive disease from onset with super imposed acute attacks or relapses that may or may not have recovery
(incline steps on steeper angle)

36
Q

uhthoffs phenomenon (MS)

A

adverse reaction to heat (internal or external)

37
Q

signs/symptoms MS

A

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

38
Q

MS interventions - exercise considerations

A

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)

39
Q

MS interventions - fatigue management

A

fatigue is most debilitating - sudden sleepiness/tiredness/weakness
diurnal - least in mornings, worst in afternoons
do not overwork or put into fatigue

40
Q

parkinsons disease defintion

A

chronic progressive neurodegenerative disorder
loss of dopamine producing neurons in the substantia nigra

41
Q

Parkinsons charactristics

A

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

42
Q

Parkinsons gait

A

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

43
Q

early signs/symptoms parkinsons

A

loss of smell
masked face (hypomimia)
dysphagia
dysphonia
micrographia
start hesitation gait
festinating gait
stooped posture

44
Q

later signs/symptoms parkinsons

A

difficulty STS
cognitive changes/dementia
drooling
GI dysfunction
foot dystonia

45
Q

Parkinsons interventions

A

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

46
Q

PT management

A

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)

47
Q

ALS definition UMN/LMN affects

A

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

48
Q

areas spared in ALS

A

sensory system, spinocerebellar tracts
eye movements - cranial nerves 3 (oculomotor), 4 (trochlear), 6 (abducens)
anterior horn cells for S2 (pelvic floor)

49
Q

ALS characteristics

A

UMN and LMN effects
asymmetrical distribution
DISTAL to PROXIMAL progression (trip over foot)
CAUDAL to ROSTRAL within spinal cord

50
Q

ALS signs/symptoms

A

weakness - cardinal sign
focal and asymmetrical - may begin UE, LE, bulbar muscles (mouth/throat)
decreased ROM
contractures
deconditioning/fatigue and pain
atrophy
hyporeflexia
hypotonicity

51
Q

bulbar ALS signs/symptoms

A

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

52
Q

ALS cognitive impairments

A

frontotemporal dementia - cognitive decline, reduced executive functioning, difficulty with planning/organization, personality and behavioural changes
increased with bulbar-onset ALS

53
Q

Guillain-barre syndrome (GBS) definition

A

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

54
Q

3 phases of GBS
1. progressive deterioration
2. plateau
3. recovery

A
  1. demyelination and axon damage lasting 1-4 weeks
  2. disease peaks, no further deterioration
  3. axonal regeneration and myelination 6 months - 2 years with complete recovery possible

strengthening not helpful stages 1-2

55
Q

GBS characteristics

A

LMN syndrome
motor signs always present, sensory may not be
DISTAL to PROXIMAL
glove and stocking distribution
SYMMETRICAL

56
Q

GBS signs/symptoms

A

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)

57
Q

GBS PT management

A

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

58
Q

poliomyelitis definition / transmission

A

acute infectious viral disease caused by the poliovirus
fecal-oral route of transmission

59
Q

poliomyelitis characteristics

A

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

60
Q

post-polio syndrome

A

poliomyelitis symptoms appearing 15+ years after polio
caused by neural fatigue
denervation > reinnervation
do not over fatigue patient!

61
Q

post-polio characteristics

A

slow progression - periods of stability with new declines
NO SENSORY impairments
LMN syndrome
weakness/paralysis “patchy”
ASYMMETRICAL
LE > UE

62
Q

post-polio signs/symptoms

A

fatigue!
muscle atrophy
weakness
pain
COLD intolerance

63
Q

post-polio PT management

A

energy conservation techniques
weight loss
exercise therapy without over fatiguing
periods of rest and activity
hydrotherapy - warm water

physio (9 decks)

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