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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
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
26
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)
27
tetraplegia
loss of motor and/or sensory function all four limbs + trunk lesions of cervical spinal cord (T1 and above)
28
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
29
neurological level of injury (NLI) definition
most caudal level of injury with intact motor + sensory function bilat. lowest level!
30
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
31
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
32
relapsing-remitting MS
relapses followed by recovery and disease stabilization (steps with breaks) relapse = new and recurrent symptoms for at least 24 hours
33
primary-progressive MS
steady disease progress no distinct episodes or interruptions (straight incline, no steps)
34
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)
35
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)
36
uhthoffs phenomenon (MS)
adverse reaction to heat (internal or external)
37
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
38
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)
39
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
40
parkinsons disease defintion
chronic progressive neurodegenerative disorder loss of dopamine producing neurons in the substantia nigra
41
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
42
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
43
early signs/symptoms parkinsons
loss of smell masked face (hypomimia) dysphagia dysphonia micrographia start hesitation gait festinating gait stooped posture
44
later signs/symptoms parkinsons
difficulty STS cognitive changes/dementia drooling GI dysfunction foot dystonia
45
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
46
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)
47
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
48
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)
49
ALS characteristics
UMN and LMN effects asymmetrical distribution DISTAL to PROXIMAL progression (trip over foot) CAUDAL to ROSTRAL within spinal cord
50
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
51
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
52
ALS cognitive impairments
frontotemporal dementia - cognitive decline, reduced executive functioning, difficulty with planning/organization, personality and behavioural changes increased with bulbar-onset ALS
53
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
54
3 phases of GBS 1. progressive deterioration 2. plateau 3. recovery
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
GBS characteristics
LMN syndrome motor signs always present, sensory may not be DISTAL to PROXIMAL glove and stocking distribution SYMMETRICAL
56
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)
57
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
58
poliomyelitis definition / transmission
acute infectious viral disease caused by the poliovirus fecal-oral route of transmission
59
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
60
post-polio syndrome
poliomyelitis symptoms appearing 15+ years after polio caused by neural fatigue denervation > reinnervation do not over fatigue patient!
61
post-polio characteristics
slow progression - periods of stability with new declines NO SENSORY impairments LMN syndrome weakness/paralysis "patchy" ASYMMETRICAL LE > UE
62
post-polio signs/symptoms
fatigue! muscle atrophy weakness pain COLD intolerance
63
post-polio PT management
energy conservation techniques weight loss exercise therapy without over fatiguing periods of rest and activity hydrotherapy - warm water

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