Study Guide Checklist for Exam Week

QUIZ 2 OSCE

Ascending Pathways

Sensory:

• Posterior (dorsal) columns 

• Spinothalamic tracts 

Motor:

• Pyramidal tract 

• Corticospinal tracts 

posterior / dorsal column 

sensory

fibers cross in brainstem

gracile fasciculus: positioned medial- carries fibers from lower body

cuneate fasciculus: positioned laterally- carries fibers from upper body

light touch and proprioception 

fibers cross in the brainstem 

spinothalamic tract

sensory

sit in dorsal horn of spinal tracts

cross near the level they enter the spinal cord

lateral: pain and temperature

anterior: crude touch

pyramidal tract

motor

voluntary control of muscle movements

corticospinal tracts

motor

UMN carry signals from primary motor cortex in brain, down spinal cord to trunk and limbs

~85% cross over to contralateral side in brainstem and travel in lateral tract

~15% cross within the spinal cord (at level they terminate) and are carried within anterior tract

autonomic dysreflexia- symptoms

sudden hypertension 

severe pounding headache 

bradycardia 

blotchy rash/flushing of skin above level 

sweating / goose bumps

SOB, anxiety 

nasal stuffiness, blurred vison 

autonomic dysreflexia - common causes

bladder and bowel

skin- burns, ingrown toenails, pressure injuries

other- fracture, kidney stones, menstrual cramps

common for injuries above T6

autonomic dysreflexia- treatment

medical emergency 

reduce BP

try and find cause

sit patient up, loosen tight clothing, find cause 

SCI- subjective assessment

respiration

• sob, talking, deep breath, cough, sputum, bronchospasm, nicotine use

neurological

• movement, sensation, spasms

pain

• neuropathic / msk

social history

• home, family, education, jobs, activities

SCI- objective

respiratory

circulation

skin

ROM

muscle bulk

spasm

sensation

muscle power

posture

SCI- medical chart review 

personal details

how did the injury occur 

what did they injure

• spinal cord, spinal column, soft tissue damage

other injuries

• fractures, contusions, respiratory 

orthopaedic management 

• surgical vs conservative 

medical history 

SCI- respiratory assessment

respiratory msk

breathing patterns, respiratory rate

effectiveness of cough, sputum

auscultation, palpation

x-ray, ABG’s

quality of voice

SCI- breathing patterns

epigastric rise

anterior / posterior movement

lateral flare

intercostal recession

upper chest movement

paradoxical (opposite)

ASIA - key parts 

sensation 

• light touch 

• pin prick 

motor

• 5 key muscles for UL 

• 5 key muscles for LL

ASIA- A

Complete

no sensory or motor function is preserved in the sacral segments S4/5

ASIA-B

sensory incomplete

sensory but no motor function preserved below the neurological level and includes the sacral segments S4/5

ASIA-C

motor incomplete 

motor function is preserved below the neurological level,

more than half the key muscles below the neurological level of injury have a muscle grade less than 3

ASIA- D

motor incomplete

motor function is preserved below the neurological level,

more than half of the key muscles below the neurological level of the injury have a muscle grade greater than or equal to 3

ASIA- E

normal sensory and motor function

ASIA sensory exam scale

0= absent

1= impaired

2= normal

NT= not testable

0*, 1*, NT*= non-SCI condition present

AISA- light touch

use face as reference point

“am i touching?”

see if there is accurate discrimination between touch and no touch

“does it feel the same?” = 2

“does it feel different?” = 1

can’t feel it= 0

AISA- sharp blunt

use face as reference point

“sharp or blunt?”

discrimination- same vs different

accurate sharp vs blunt, same as face = 2

accurate sharp vs blunt, different from face = 1

cannot accurate;y te;; the difference = 0

ASIA- motor exam

10 key muscles

palpate for flickers of muscle activity (grade 1)

AROM

active = passive (grade 2, 3, 4, 5)

grade 4-5 static muscle test

if less than 50% normal ROM = NT

if spasticity limits ROM= NT

AISA motor exam scale

0= total paralysis

1= palpable or visible contraction

2= active movement, full ROM with gravity eliminated

3= active movement, full ROM against gravity

4= active movement, full ROM against moderate resistance in a muscle specific position

5= (normal) active movement, full ROM against gravity and full resistance in a functional muscle specific position expected from an otherwise unimpaired person

NT= not testable (i.e. due to immobilisation, severe pain such that the patient cannot be graded, amputation of limb, or contracture of >50% of the normal ROM)

0*, 1*, 2*, 3*, 4*, NT* = non-SCI condition present

motor level

the lowest key muscle that has a grade of at least 3/5, providing the key muscle represented by segments above the are tested to be normal (grade 5)

what muscles are intact at different levels of injury?

C3-C5 = diaphragm

T1-T11= intercostals

T5-T2 = abdominals

physio: what to assess in your SCI patient

respiratory function

neurological- ASIA

motor strength - MMT/MLT

AROM, PROM

skin conditions

muscle tone and spasm

posture

balance

functional skills

mobility

assessment of equipment 

education 

discharge planning 

steps in classification of ASIA

1. determine sensory levels for right and left sides

2. determine motor levels for right and left sides (at least grade 3)

3. determine neurological level of injury (intact sensation and antigravity)

4. determine whether the injury is complete or incomplete

   1. voluntary anal contraction=no AND all S4-5 sensory scores= 0 AND deep anal pressure- no = complete

   2. otherwise = incomplete

5. determine ASIA - complete or incomplete

parkinson’s disease- pathophysiology 

loss of neurons in the midbrain of the substantia nigra which produce dopamine causing a lack of this transmitter leading to uncoordinated movements and an alteration of indirect and direct pathways of the basal ganglia

presence of Lewy bodies / clumps of protein called alpha-synuclein inside brain cells in midbrain, spinal cord, CNS/PNS- gut and olfactory system 

parkinson’s disease- etiology

environmental risk factors:

• pesticides and herbicides 

• illicit drug use 

• recurrent head trauma 

• medications (calcium channel blockers, NSAIDS) 

• oxidation and generation of free radicals damaging the thalamic nuclei 

  • genetics-if someone in the family has that disorder

parkinson’s signs and symptoms

resting tremor (usually unilateral) - disappears with use

bradykinesia

rigidity

gait disturbances

loss of postural reflexes

freezing of gait

flexed posture

postural instability

cardinal parkinson’s signs

bradykinesia, rigidity, resting tremor, postural instability

non-motor parkinson’s symptoms

olfactory dysfunction = hyposmia

Gi dysfunction

REM behaviour sleep disorders

insomnia

excessive daytime sleepiness

constipation

pain

depression 

hoegn and yahr scale 

1 = unilateral involvement- minimal or no functional disability 

1.5 = unilateral and axial involvement 

2 = bilateral or midline involvement without impairment of balance

2.5 = mild bilateral disease with recovery on pull test

3 = bilateral - mild-moderate disability with impaired postural reflexes; physical independent 

4 = severely disabling disease; still able to walk or stand unassisted 

5 = confinement to bed or wheelchair unless aided 

parkinson’s diagnosis

see presence of neurodegeneration

motor and non-motor symptoms present but clinical parkinson’s criteria are not met - cardinal features and hypsomia, constipation, RBD, low mood and fatigue

parkinson’s medications / surgical options

levodopa - dopamine agonist medication

• pt builds tolerance, substantia nigra generates more and dose must be increased to continue to reduce symptoms and cycle continues (window of opportunity starts large and as brain builds tolerance, gets smaller)

deep brain stimulation

• implanting electrodes in brain connected to a pulse generator to send electrical signals that help control movement symptoms

parkinson’s disease- physio early stages 

optimise 

increase and promote physical activity 

slow progression of disease

parkinson’s disease- physio middle stages 

continue promoting physical activity

falls prevention

task specific training and cueing strategies

amplitude training

dual task training

parkinson’s disease- physio late stages 

adapt

adaptive movement skills

avoid dual tasking

falls risk prevention

optimize and adapt environment

what areas of the brain are affected in each stage of parkinsons

Stage 1- peripheral nervous system, olfactory system and medulla

Stage 2- pons, spinal cord grey matter

Stage 3- pons, midbrain, basal forebrain, limbic system

Stage 4- limbic system, thalamus, temporal cortex

Stage 5/6- multiple cortical regions

What nuclei make up the basal ganglia?

Striatum (caudate and putament)

Subthalamic nucleus

Globus pallidis

Parkinson Gait 

Often have stooped posture 

Walk on a narrow base

Short, shuffling steps

Festination 

Patients tern en bloc 

Lack of arm swing 

Tremor of hands 

Freezing 

Slow gait speed 

Variability of stride  length (increases with a simultaneous cognitive task)

early symptoms seen in parkindon’s disease

reduced sense of smell

fatigue

shoulder pain

stiffness

reduced walking distance

tremor

small handwriting

trouble sleeping

soft voice

mask face

secondary impairments of parkinson’s disease

contractures

MSK pain as a result of disuse

muscle atrophy - decrease in overall strength 

decreased aerobic capacity 

decreased muscle length 

reduced physical activity 

respiratory dysfunction 

exercise benefits in parkinson’s disease

intensive exercise is recommended as potentially delaying the progression of the disease

increasing physical activity to 2.5h/week can slow the decline of QoL

best exercise: what the patient enjoys

recommendations for parkinsons

moderate high intensity exercise

resistance training 

balance exercise

external cueing 

community-based exercise

task-specific training 

integrated care

amplitude training 

dual-task training 

encouraging general pa- tai chi, yoga, stretching 

education on self management 

falls prevention 

peer/family support 

parkinson’s risk factors for falls

postural instability

axial rigidity

dyskinesia

festination

slow gait speed

freezing of gait

fear of falling

amplitude training for parkinsons

multiple repetitions

high intensity

increased complexity

potential to make and maintain significant functional gains (neuroplasticity)

extrinsics cues

facilitate attention

effect of visual environment

visual cues

auditory cues

somatosensory and vestibular cues

tactile cues

intrinsic cues 

attention 

emotional set

mental rehearsal- think about what you want to do

internal dialogue 

visualization 

FND

neurological symptoms that lack internal consistency and are unexplained by disease

FND symptoms

weakness

tremor

jerks

spasms

dystonic posture

altered gait patterns

6 abnormal circuits of FND- pathophysiology

attention

agency

predictive processing

interoception

emotional processing

perceptual interferences

pathophysiology theories of FND

psychological theory- explanations of FND including primary and secondary gains 

• primary gain- the conversion of psychological distress into physical symptoms 

• secondary gain- the benefit or material advantage (either coconscious or unconscious) of being “sick role”

learning theory- symptoms developed and maintained on a conscious level - FND patients learn abnormal movement patterns through practice or avoiding particular movement 

sociological theory- patient unconsciously motivated to seek legitmisation from doctor- “sick role”

FND subjective assessment

redisposing factors (potential causes to developing FND)

precipitating factors (things that trigger the symptoms)

perpetuating factors (things that keep the symptoms going)

• do you recognise an event that lead to these symptoms (Predisposing)

• triggers or warning signs (Precipitating)

• under what circumstances does the symptoms develop (Precipitating)

• what aggravates or eases or keeps it the symptoms (Perpetuating)

a list of symptoms, variability, severity and frequency

typical 24h routine

using adaptive aids and equipment

explore the patients understanding - ask what they have been told about the diagnosis

patient goals, experiences and therapy goals

FND objective assessment

neuro impairments assessment- muscle power, sensation/proprioception

assess in different positions (supine, sitting - compare

assess functional movements, transfers, mobility, balance

try to identify how movement / function can fluctuate or be inconsistent known as a ”positive sign”

FND 10 diagnostic tests

Hoover’s sign

Give way weakness / collapsing weakness

Hip abductor sign 

Hemifacial muscle overactivity 

Sternomastoid test 

Drift without pronation test 

Global weakness 

Tremor distractibility 

Dragging monoplegic gait 

Walking on ice gait 

FND treatment

goal oriented with responsibility to self-manage

limit “hands on treatment” when handling patient- facilitate rather than support

encourage weight bearing

promote good movement and posture re-training

avoid using equipment, mobility aids, splint and devices

recognize and challenge unhelpful thoughts and behaviors

psychological import and CBT

ATTENTION AND DISTRACTION

predictive processing (coding on information) - tap into expectation of movement

• set up an easy win

• change their expectation of movement

• positive experience in normal movement

• increase their awarness

FND- dissociative episodes

when the ‘nervous system’ becomes overwhelmed 

• detachment- separation from self and world 

• compartmentalization- is reversible loss of voluntary control of intact function 

Grounding:

• name 3 things you can see, hear, touch, smell

no formal diagnosis - what do you do?

feedback to MDT

encourage neurologist input

explain to MDT - evidence of positive diagnosis and improves prognosis

anxiety of no diagnosis will make symptoms worse

BPPV 

mechanical problem 

hardened otoconia (calcium carbonate) dislodge from utricle and “float” into semi-circular canals 

• canalithiasis - otoconia is freely mobile in the canal 

• cupulolithiasis- otoconia is adherent to the cupula 

recurrent attacks of positional vertigo / dizziness 

symptoms BBPV

vertigo

dizziness

unsteadiness

nausea, sweating, heart racing

vestibular neuritis

acute inflammation of vestibular nerve - CN8

can be preceded by viral infection- herpes, GI, URTI

vestibular neuritis symptoms

acute onset of prolonged rotary vertigo (symptoms last at least 24h)

symptoms exacerbated by head movement

acute stage- horizontal-rotary nystagmus beating away from affected ear

postural imbalance

nausea / vomiting

no hearing loss, tinnitus, or aural fullness

no central signs on exam

vestibular neuritis - clinical tests

clinical tests usually shows hyporesponsiveness or unresponsiveness of vestibular system ipsilesionally

deficit in VOR

head impulse test= corrective saccade

spontaneous nystagmus beating away from the affected side

vestibular neuritis - management

acute:

• initially rest and vestibular suppressants

• steroids (methylprednisolone)

• when patient able - ambulation

• encourage good visual inputs and gentle head movements

recovery:

• encourage neural compensation for loss of vestibular input on one side

• suppressants should be reduced as tolerated

vestibular labyrinthitis 

presentation identical to neuritis (acute onset, nausea, postural imbalances) along with additional symptom: hearing loss 

no tinnitus, no aural fullness

affects inner ear bony labyrinth 

assume AICA stroke until proven otherwise (can cause hearing loss) 

• refer to neurologist, ED 

polyneuropathies

GSB- AIDP

CIDP

diabetic neuropathy

critical care neuropathy

GBS- guillian-barr syndrome

umbrella term for inflammatory neuropathies

demyelinates axons - autoinflammatory - body attacks itself autoimmune disease

90% acute

patient gets infection that has a similar protein to myelin - body attacks infection but also normal myelin due to similar protein structure- becomes autoimmune

GBS- guillian-barr syndrome symptoms

weakness

decreased sensation

pain

respiratory muscle weakness

GBS- guillian-barr syndrome medical management

plasma exchange, intravenous immuno-globin, ICU-vent

CIDP- medical treatment

plasma exchange, intravenous immuno-globin, ICU-vent

plus corticosteroids

CIDP- secondary complications

atrophy

joint contractures

DVT

depression/anxiety

diabetes neuropathy

too much glucose in the blood = hyperglycemia 

decreases nerve signals peripherally as peripheral nerves do not like glucose 

diabetes neuropathy symptoms

pain

decreased sensation

burning sensation

weakness in peripheral (tib-ant) - foot drop

diabetes neuropathy management

medical: insulin, optimise blood sugar

physio: education, retraining gait, resistance training

critical care neuropathy 

ICU 

more risk factors- sepsis, bed rest, organ failure 

autoimmune- body attacking itself 

miener’s disease

• build up of endolymph fluid in the ear

hearing loss, tinnitus, aural fullness- episodic

symptoms last 20m-12h and must have 2x episodes for diagnosis to occur

unilateral vestibular hypofunction

lesion right horizontal canal = loss of right sided vestibular input (loss of “leftward push”

unopposed “rightward push” from the intact left horizontal canal creates a slow rightward drift of the eyes, this “slow phase” is eventually counteracted by a leftward “fast phase”

therefore hypofunction of the right horizontal canal creates left-beating nystagmus

vestibular: peripheral vs central issue 

central:

• vertical misalignment of the eyes

• nystagmus

  • pure vertical nystagmus

  • purely torsional

  • observed without eye or head movements

  • direction changing nystagmus

  • eyes move deconjugate

  • abnormal saccades

  • unable to cancel the VOR

  • saccadic pursuit

  • effect of gaze- does not change or reverses direction 

peripheral:

• direction of nystagmus fixed

• nystagmus decreases in normal room light (effect of fixation)

• usually mixed plane (horizontal/vertical and torsional)

• nystagmus increases with gaze toward direction of quick phase

tests of the VOR 

fast:

head impulse test - true test of VOR - gold standard 

head shaking nystagmus - VOR enhances asymmetry 

dynamic visual acuity (functional test) 

slow: 

VOR cancellation 

visually enhance VOR 

neurological symptoms or signs

any of the D’s

• diplopia

• dysarthria

• dysphagia

• dysphonia (hooarsness/hiccups)

• dysmetria

• dysesthesia (facial numbness)

• drop attacks

• down-is up distortions

response to fixation

peripheral nystagmus will become stronger when we take away fixation (ie. darkness) and reduce when fixation is present

ewalds 1st law 

the axis of nystagmus should match the anatomic axis of the semicircular canal that generated it 

a stimulation of the semicircular canal causes a movement of the eyes in the plane of the stimulated canal

in peripheral vestibular dysfunction, the axis of nystagmus will match the anatomic axis of the semicircular canal that generated it 

ewalds 2nd law

horizontal canals

endolymph flow towards ampulla = excitation 

ie. turn head left - L HSC excited - R HSC inhibited 

ewalds 3rd law

vertical canals

endolymph flow away from the ampulla (ampullofugal) = excitation

ie. right tilt back - R PSC excited - L ASC inhibited

ewalds law clinical meaning

a canal is excited by movement towards that canal, in the appropriate plane

responses to inputs that excite a canal are greater than those that inhibit a canal

unilateral vestibular loss

patients will avoid head motion toward the side of the lesion, as the inhibitory signal on the intact side is not adequate enough at high speeds

VOR

unblurred vision is made possible during the head movements 

2 components-

• angular - compensates for rotation gaze stabilisation - mediated by scc

• linear - compensates for translation - mediated by otolith organ

  • linear movement vertically - sensed by saccucle

  • linear movement horizontally - sensed by utricle

latency is 7-8 miliseconds

compensates for frequencies 0.5hz - 7hz (most effective over 2hz)

VOR gain

relationship of eye movement to head movement velocity

gain= output/input

gain x1- eye movement velocity = head movement velocity

gain x0.5- eye movement velocity is ½ of head movement velocity

vestibulospinal reflex

purpose of the VSR is to stabilise the body

uses otolith input to a greater extent than the VOR

peripheral apparatus = 5 sensory organs

3 semicircular canals

• anterior, horizontal, posterior

2 otolith organs

• utricle, saccule

vestibular labyrirnthitis management

acute

• bed rest and vestibular suppressants

• steroids or antibiotics

• O2 therapy via hyperbaric chamber

recovery:

• vestib, rehab to encourage neural compensation for loss of input on one side

meniere’s disease

disorder of inner ear function

onset more common- females, older, white, obese

accumulation of endolymph in the cochlear duct and vestibular organs

• endolymphatic hydrops

meniere’s disease- clinical features 

episodes of spontaneous vertigo 

fluctuating aural symptoms- episodic sensorineural hearing loss, tinnitus, aural fullness

typical attack = initial sensation of fullness of the ear, tinnitus, reduction in hearing, presence of rotary vertigo, imbalance, nystagmus and nausea 

attacks can last 20m - 12h - can occur multiple times a week or separated by weeks/months

meniere’s disease diagnosis 

diagnosis- 2x more attacks, hearing loss, fluctuating aural symptoms in affected ear, not better accounted for by another vestibular diagnosis 

meniere’s disease management

restricted salt intake

natural course- wait it out

pharma- betahistines

surgical

tests for BPPV

dix-hallpike - anterior and posterior canal

roll test - horizontal canal

what is multiple sclerosis

chronic progressive demyelinating disease; scars/plaques occur throughout the CNS

multiple sclerosis etiology 

genetic predisposition and risk factors:

• decreased vitamin d

• childhood obesity 

• smoking

• exposure to EPV 

  • exposure to chemical solvents