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PHYSIOTHERAPY YEAR 2 > Optimising Function - NEURO > Flashcards

Optimising Function - NEURO Flashcards

1
Q

Describe the stages of a motor examination for a neuro case.

A

Observation - tone, tremors and fascinations. Pronator drift
Tone - flexing, extending and rotating: spasticity, high tone, low tone, flacidity and rigidity.
MRC scale for strength - grade 5 (normal strength).

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2
Q

How should you test power in the upper limbs for the motor part of the assessment?

A

Shoulder abduction
Elbow flexion/extension
Wrist flexion/extension
Finger flexion/extension
Finger abduction
Thumb abduction

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3
Q

What nerve supplies shoulder abduction?

A

Auxiliary nerve: C5/6

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4
Q

What nerve supplies elbow flexion?

A

Musculocutaneous nerve: C5/6

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5
Q

What nerve supplies elbow extension?

A

Radial nerve: C6/7/8

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6
Q

What nerve supplies wrist extension?

A

Radial nerve: C6/7/8

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7
Q

What nerve supplies wrist flexion?

A

Median nerve: C6/7
Ulnar nerve: C7/8/T1

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8
Q

What nerve suppplies finger extension?

A

Radial nerve: C7/8

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9
Q

What nerve supplies finger flexion?

A

Median/ulnar nerve: C7/8

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10
Q

What nerve supplies finger abduction?

A

Ulnar nerve: C8/T1

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11
Q

What nerve supplies thumb abduction?

A

Median nerve: C8/T1

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12
Q

What is clonus?

A

Invulontary rhythmic muscle contractions and relaxations that occur in patients with UMN lesion.

  • test: quickly dorsiflex the foot.
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13
Q

What tests should you perform to assess power in the lower limbs as part of the motor assessment?

A

Hip flexion/extension
Hip abduction/adduction
Knee flexion/extension
Ankle dorsiflexion/plantarflexion
Ankle inversion/eversion

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14
Q

What nerves supply hip flexion?

A

Femoral nerve: L1/2/3

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15
Q

What nerves supply hip extension?

A

Inferior gluteal nerve: L4/5/S1

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16
Q

What nerves supply hip adduction?

A

Obturator nerve: L2/3/4

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17
Q

What nerve supplies hip abduction?

A

Superior gluteal nerve: L4/5/S1

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18
Q

What nerves supply knee flexion?

A

Sciatica nerve: L5/S1/S2

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19
Q

What nerves supply knee extension?

A

Femoral nerve: L3/4

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20
Q

What nerves supply ankle dorsiflexion?

A

Deep fibulas nerve: L4/5

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21
Q

What nerve supplies ankle inversion?

A

Tibial nerve: L4/5

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22
Q

What nerve supplies ankle eversion?

A

Superficial fibular nerve: L5/S1

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23
Q

What nerves supply ankle plantarflexion?

A

Tibial nerve: S1/2

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24
Q

What is the deep tendon reflex grading scale?

A

Grade 0 - no reflex
Grade 1 - diminished reflex (hyporeflexive)
Grade 2 - normal reflex
Grade 3 - brisk reflex (hyperreflexive)
Grade 4 - brisk reflex with clonus

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25
Q

What nerve does the biceps reflex test?

A

C5/6

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26
Q

What nerve does the triceps reflex test?

A

C6/7

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27
Q

What nerve does the patellar reflex test?

A

L2/3/4

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28
Q

What nerve does the Achilles reflex test?

A

S1/2

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29
Q

What is tested in the sensory part of the exam?

A

Temperature
Pain
Non-discriminative touch
Vibration
Proprioception

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30
Q

What parts of the sensory exam relate to the spinothalamic tract?

A

Non-discriminative touch
Temperature
Pain

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31
Q

What parts of the sensory exam relate to the posterior column medial meniscus tract?

A

Proprioception
Vibration

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32
Q

What may make a patient at risk of falls?

A

Falls in the past 3 months
Mobility problems and use of assistive devices
Gait problems, or use of a cane or walker
Medications - could cause sedation, confusion, impaired balance, blood pressure changes
Mental status - delirium, dementia or psychosis may be agitated or confused
Continence - urinary frequency, or frequent toiletting needs
IV pole
Orthostatic hypotension
Oxygen tubing
Clutter
Vision problems

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33
Q

What is tone?

A

Refers to the tension or resistance present in a muscle at rest. It is the natural state of muscle readiness for action even when not actively contracting.

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34
Q

What is spasticity?

A

A neurological condition characterised by an abnormal increase in muscle tone or stiffness. Typically caused by disruptions in the normal functioning of the nervous system, particularly the part that controls voluntary muscle movement.

Hypertonia.

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35
Q

What is rigidity?

A

Common muscle tone disorder in which there is resistance to passive movement irrespective of posture and velocity. Cardinal feature of Parkinson’s Disease and usually present in extrapyramidal disorders. Affects agonists and antagonists equally.

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36
Q

What is the systems model of balance control?

A

Postural Tasks - steady state, proactive, reactive
Individual - motor, sensory, cognitive
Environment - support surfaces, sensory context, cognitive load

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37
Q

What are various causes of falls?

A

Slippery or uneven surfaces
Loss of balance due to dizziness or fainting
Weakness or muscle imbalance
Medication side effects
Environmental hazards
Neurological conditions

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38
Q

What are the impacts of falls?

A

Physical injuries, fractures, bruising, wounds
Shear wounds and pressure injuries
Delayed rehab and time increase in hospital
Confidence/dignitity lack
Manual handling risks - constant repositioning
Expenses

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39
Q

What are some causes of falling?

A

Inadequate sitting assessment
Inadequate sitting equipment
Cognitive impairment
Level of consciousness/medication
Visual/sensory/proprioceptive problems
Muscle weakness
Joint restrictions - hip,knee,ankle and back
Medical problems/comorbidities
Neurological problems (new/old/progressive)

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40
Q

What are neurodegenerative disorders?

A

Caused due to loss of neurons, glial cells, neural networks in the brain and spinal cord.
Progressive in nature.

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41
Q

Describe the pathophysiology of NDDs?

A

Abnormal proteins aggregate and lodge in neural tissues - causing neuronal loss.

Altered degradation pathways
Mutations
Environmental influence
Unfolding
Transcriptional and translational errors.

Risk factors:
Genetic predisposition, environment, lifestyle

The site of origin of neuronal loss determines the primary clinical feature.

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42
Q

What is Parkinson’s?

A

Causes unintended or uncontrollable movements
Caused by a loss of nerve cells in the substantial nigra leading to a reduction in dopamine
Basal ganglia is unable to send a ‘good’ plan back to the cortex due to loss of neurones, affects the rest of the pathway.

Risk factors:
Familiar risk factors
Genetic
Environmental factors eg exposure to toxins

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43
Q

What are the clinical signs of Parkinson’s?

A

Rigidity, bradykinesia, tremors, fatigue, pain, postural instability.

44
Q

What is the Hoehn and Yahr scale for the stages of Parkinson’s disease?

A

Stage 1 - only one side of the body is affected
Stage 2 - symptoms affect both sides of the body
Stage 3 - balance and stability become affected
Stage 4 - symptoms increase, however are able to stand and walk
Stage 5 - assistance is required for everyday activities.

45
Q

What is the Pathophysiology of Alzheimer’s?

A

Abnormal proteins aggregating in the hippocampus, leading to neuronal death.

46
Q

What are the progressive stages of Alzheimer’s disease?

A

Preclinical: no symptoms, changes to the brain begin
MCI (mild cognitive impairment) stage: mild, memory lapses, changes in cognitive functions may be measurable
Mild: memory loss becomes noticeable, difficulty organising and expressing thoughts. Getting lost or misplacing belongings.
Moderate: greater memory loss and confusion, significant assistance for daily activities. Changes in sleep patterns, personality and behaviour.
Severe: nearly total memory loss, loss of ability to communicate, need for full time assistance.

47
Q

What are the clinical feature of Alzheimer’s?

A

Withdrawal from social activities
Confusion with time and location
Difficulty completing familiar tasks
Misplacing items
Difficulty solving problems
Memory loss
Difficulty with words
Trouble with images and spaces
Poor judgement
Unfounded emotions

48
Q

What is multiple sclerosis?

A

Autoimmune disease of the CNS, characterised by chronic inflammation, demylination, gliosis and neuronal loss.
Immune system starts killing the cells.
The immune system attacks and destroys myelin, which means communication between neurones breaks down.
Hard to predict symptoms due to myelin breakdown can occur anywhere.
Sensory, motor and cognitive problems.
Often diagnosed in 20s and 30s.

49
Q

What are some clinical features of MS? Broad symptoms?

A

Changes to vision
Muscle weakness and spasm
Numbness or pain
Loss of balance
Difficulty with cognitive function
Mood changes

50
Q

What are the classifications of MS?

A

Relapsing remitting
Secondary progressive
Primary progressive
Progressive relapsing

51
Q

What are some shared clinical features of NDDs?

A

Cognitive impairment
Neuropsychiatric impairments
Motor impairments
Age effects
Progressive phases
Caregiver/family stress

52
Q

What are some ways to prevent falls?

A

Understand medication side effects
Do strength and balance exercises
Get your vision and hearing checked regularly
Use night lights, grab bars and secured carpet
Stand up slowly to avoid dizziness
Use a cane or walker if you need more stability

53
Q

What are some exercises to help with balance?

A

Toe scrunches - grabbing a towel with your toes to work on fully extending your toes (toes help with balance)
Toe extensor stretch - so that toes can fully extend to make contact with the ground and improve balance

54
Q

What is the role of the motor cortex in the frontal lobe for postural stability?

A

Contralateral (opposite side to the brain) for motor control and voluntary movement via the corticospinal tract
Ipsilateral (same side) for stability

55
Q

What are some of the primary tracts for postural stabilisation? (Descending tracts)

A

Reticulospinal
Vestibuolospinal

56
Q

What part of the brain is the center for upright posture design?

A

Where the pons and the medulla meet: the pontomedullary reticular formation.
It inhibits flexion via descending spinal pathways.
Sitting in flexed posture on laptops is a deficit of the PMRF.

Also the house of the cranial nerves. Stimulation with sensory input at the PMRF (eg through the vestibule nerve) - which will inhibit the PMRF and have better upright stability.

The cranial nerves responsible for the vestibular system (the vestibular nuclei) are located in the PMRF, so when these are stimulated it stimulates postural stability.

57
Q

What might a cerebellum lesion look like?

A

Tremors as they are unable to hit their target.
Affects motor function.

It usually refines motor output.
Also communicates with the vestibular system, so is fundamental with postural neurology.

58
Q

How is the vestibular system linked to posture?

A

The vestibular nuclei live in the pontomedullary (PMRF), and so when these are stimulated it stimulates the PMRF, which inhibits flexion.
Equally, the vestibular system also stimulates upright postural extension.

Leads to upright postural design.

59
Q

What do differences in passive movements suggest about the area of the brain that is affected?

A

Floppy - cerebellum
Cogwheel rigidity - basal ganglia

60
Q

What is the decorticate posture?

A

Extended legs and flexed arms - physiological extensors

Decebrate posture - extended arms and supinated wrists

61
Q

What is the pull test?

A

Reactive postural control test
Examiner stands behind the subject, and the examiner gives a sudden brief backward pull to the shoulders.

0 = recovers independantly but may take 1 or 2 steps or an ankle reaction
4 = unable to stand without assistance

62
Q

What is the push and release test for reactive postural control?

A

Patient leans back onto practioner and then practioner lets go
0 = recovers independently, 1 step of normal length and width
4 = falls without attempting a step or unable to stand without assistance

63
Q

What is the wolf motor function test?

A

Assesses functional ability through a range of domains:
Forearm movement
Hand movement
Reaching
Lifting
Stacking
Flipping
Gripping
Turning
Folding
Lifting

64
Q

What are some grip types?

A

Power grip: Closing a hand with the thumb in opposition to all other fingers
Lumbrical grip
Spherical grip - eg holding a tennis ball
Hammer grip
Hook grip - eg handing from overhead bars

Pinch grip: the holding of an object between the thumb and fingers of a single hand
Tip pinch
Tripod pinch - eg holding a pencil
Lateral pinch - eg pinch to twist a key

65
Q

What are some ways you could rehab a patient with a low score on The Wolf Function Test?

A

PROM: maintain mobility, focussing on flexion and extension of the shoulder, elbow, wrist and fingers.
Active-Assissted Range: encourage partial voluntary movement
Functional electrical stimulation
Repetitive task specific training
Mirror therapy
Bilateral arm training: increases coordination
Strength training
Motor imagery and mental practice of movement

Key points: repetition, consistency, motivation and mental engagement.

66
Q

What are some ways you can assess visual field?

A

Confrontation visual field test: observing the examiner moving their fingers in the patients periphery vision. Detects large visual field deficits.

Amster grid: assessing central visual field defects . Patient looks at a grid to detect if any lines appear blurred or are missing.

67
Q

What are some ways you can assess reach and grasp?

A

Action Research Arm Test: 19 items assessed including: grasp, grip, pinch and gross movement

Wolf Motor Function Test

68
Q

What are some ways you can assess in-hand manipulation?

A

Nine Hole Peg Test: fine motor dexterity and finger coordination. Time taken to place 9 pegs into holes on a peg board.

69
Q

What are some ways you can assess bilateral coordination?

A

Cherokee Arm and Hand Ability Inventory (CAHAI): Evaluates 13 functional tasks: pouring water, opening a jar, use of a knife and fork, dressing tasks.

Nine-hole peg tests (performed bilaterally)

70
Q

What are some ways you can assess bilateral coordination?

A

Cherokee Arm and Hand Ability Inventory (CAHAI): Evaluates 13 functional tasks: pouring water, opening a jar, use of a knife and fork, dressing tasks.

Nine-hole peg tests (performed bilaterally)

71
Q

Some treatment to improve cognitive ability in post stroke patients?

A

Restorative therapy: re-building lost cognitive skills eg attention and memory
Compensatory strategies: use of tools like planners and reminders to compensate for cognitive deficits
Computer based cognitive training: eg Lumosity, Cognifit or BrainHQ
Cognitive Behavioural Therapy: managing frustration and anxiety
Cognitive Stimulation Therapy: discussions, puzzles, word games and reminiscence therapy.

72
Q

What is a traumatic brain injury?

A

Interncranial injury - injury to the brain caused by external force.
Can be classified based on mechanism (closed or penetrating head injury) or other features (occuring in specific locations or widespread areas)/

73
Q

What is concussion?

A

Mild traumatic brain injury
Symptoms: loss of conscioussness, headaches, thinking difficulty, lack of concentration, nausea, blurred vision, dizziness, sleep disturbances, mood changes.

Direct brain injury
Acceleration-decceleration injury (eg rotational forces)
Blast brain injury

The brain experiences forces, causing it to move backwards or forwards within the cranial vault.

Symptoms can be delayed by 1-2 days
Not unusual for symptoms to last 2 weeks in adults and 4 weeks in children

74
Q

What are some secondary injuries caused by concussion?

A

Cerebral blood flow - impaired autoregulation, brain odema, increased ICP
Oxygen - hypoxia, ischemia, impaired )2 regulation, impaired microcirculation
Energy flow - glucose utilisation, glucose availability, mitochondrial failure

75
Q

What is the neurometabolic cascade of concussion?

A

Kinetic impact
1. Neurones stretch/shear
2. Electrolytes (K, Na, Ca) move across gradients
3. Neurones ‘fire’ indiscrimintively via Ca — Glutamate release
4. Energy deficit results from restoring electrolyte gradient.

Simpler:
Potassium leaks out
Calcium rushes in
Glutamate (excitory) released (significant energy demands nerves become overexcited, swell and die).

Mitochondria gets impaired which prevents production of ATP
Brain must switch to anaerobic production of ATP, less efficient

Can last up to 30 days post concussion

76
Q

What are the four primary mechanisms of blood flow in the brain?

A

Cerebral autoregulation - autonomic system reacts to changes in systemic blood pressure
Cerebrovascular reactivity - changes in cerebral flow in response to changes in pp of CO2.
Neurovascular coupling - blood shunted to areas of the brain due to increased activity in this region
Neuroautonomic cardiovascular regulation - reflected in heart rate variability

77
Q

What us second impact syndrome?

A

When a concussed individual sustain a second impact upon their head before recovering form the first impact.
Symptoms:
loss of conscioussness
headache
vomitting
dilated pupils or vision loss
seizure

Common misdiagnosis: CV emergency, stroke, seizure

78
Q

What are the top 10 concussion symptoms?

A

Brain fog
Lack of focus
Headache
Memory difficulties
Fatigure
Iritability or nervoussness
Mood disruption
Light or sound sensitivity
Sleep problems
Change in quality of life

79
Q

What are common causes of concussion?

A

Fall
Collision
Struck by object
Struck by person
Assault
Unknown

80
Q

What are some effects of concussion on the brain?

A

Vestibular symptoms: balance, dizziness, nausea)
Ocular-motor symptoms: vision, movement, blurred vision, double vision, difficulty reading)
Headache
Cognitive symptoms: (decision making, processing information, brain fog, memory problems, concentration, word retrieval)
Mood related Symptoms (how you feel, anxiety, depression, irritation, feelings of overwhelm).

81
Q

What are the stages to recover from concussion?

A

No symptoms at rest
Light activity eg jogging
Light practice of sport
‘Yellow shirted’ - can participate but no contact
Full contact practice
Return to play

Any problems then must drop down to the level below

82
Q

What is SCAT5?

A

A standardised tool for evaluating suspected concussions. Includes the following section:
- red flags
- memory assessment - maddocks questions
- glasgow coma scale examination
- cervical spine assessment
- symptom evaluation
- cognitive screening
- neurological screening
- balance examination
- delayed recall

83
Q

What does ACVPU stand for?

A

Alert
Confusion
Voice
Pain
Unresponsive

84
Q
A
85
Q
A
86
Q

What are the stages of an assessment for concussion?

A

Smooth pursuit - clinician moves finger horizontally in front of patient 5 repetitions: looking for jerky eye movements or multiple beats of nystagmus

Horizontal and vertical saccades - look back and forth between two points for 20 repetitions: ask if symptomatic

Horizontal and vertical gaze stability - shake head looking at one spot for 20 repetitions: ask if symptomatic

Near point of convergence - bring pen towards eyes and stop when splits into two. 6cm or lower is normal

Left and right monocular accommodation: cover one eye and bring pen towards face until it blurs. Measure distance. 12cm or lower is normal.

Complex tandem gait - 5 steps forward and back (tightrope) eyes open and closed. Looking for errors and sway

87
Q

When should I test cranial nerves?

A
88
Q

When should I test cranial nerves?

A
89
Q

What are the sensory cranial nerves?

A

Offactory - smell
Optic - vision
Vestibulocochlear - hearing, balance/equillibirum

90
Q

What are the motor cranial nerves?

A

Occulomotor - eye movement, elevation of eyelid, pupil size, and reactivity to light
Trochlear - eye movement (vertical and aDduction)
Abducens - eye movement (abduction)
Accessory - head/neck/shoulder movement
Hypoglossal - tounge movement, speech

91
Q

What are the mixed cranial nerves?

A

Trigerminal - chewing/face/mouth sensation
Facial - facial expression, eyelid and lip closure, taste, corneal reflex
Glossopharyngeal - gagging, swallowing, taste
Vagus - gagging, swallowing, speech

92
Q

What is the Olfactory nerve?

A

SMELL
Sensory

Loss of smell - anosmia
Well-established sequels of head injury, can follow blunt traumas

Temporary anosmia due to inflammatory response

93
Q

What is the optic nerve?

A

VISION
Sensory
Optic neuritis - inflammation to the myelin sheath, may affect one or both eyes, common in MS
Glaucoma - high intra-ocular pressure causes cells to die. Atrophy of the optic nerve
Nutritional optic neuropathy - bilateral, symmetrical, and progressive impairment with loss of central vision acuity. Common due to widespread bariatric surgery and strict vegetarian diets.
Ischemic optic neuropathy - reduced blood flow to the optic nerve. May be linked to atherosclerosis or arteritis eg giant cell arteritis (headache presentation).

94
Q

What is the occulomotor nerve

A

EYE MOVEMENT
Motor
Disorders can impair ocular mobility, pupillary function, or both
Diplopia and ptosis (drooping of the upper eyelid).
Ask about double vision as may link to Horner’s syndrome.
Affected eye may deviate slightly out and down in a straight ahead gaze. Abduction is slow.

95
Q

What is the trochlear nerve?

A

EYE MOVEMENT
Motor
Palsy impairs superior oblique muscle, causing paresis of vertical gaze, mainly in aDduction
Patients report seeing double images, one above and slightly to the side of the other eyes do not abduct normally

Possible causes:
Closed head injury
Infarction due to small vessel disease eg diabetes
Can result from aneurisms or tumors

96
Q

What is the Trigeminal Nerve?

A

SOMATOSENSORY INFORMATION - touch, pain from the face and head
MOTOR - chewing
Motor and sensory

Mechanisms:
Manifests as severe facial pain and allodynia
Caused by compression of the nerve at its root by an adherent loop of an intracranial artery
Rarely, a venous loop may compress the 5th cranial nerve at its root entry into the brain stem
Less common causes include compression by tumour or MS

97
Q

What is the Abducens nerve?

A

EYE MOVEMENT
Motor
Mechanisms: affects lateral rectus muscle, impairing eye abduction and may cause severe headache
Eyes may be slightly aDducted when patient looks straight ahead
Causes impaired aDduction and horizontal diplopia
May be secondary to nerve infarction …..

98
Q

What is the facial nerve?

A

TASTE
SOMATOSENSORY information from the ear, controls muscles of facial expression
Mixed

Mechanisms:
Sudden onset, unilateral peripheral facial nerve palsy
Symptoms are hemispheres-facial peresis of the upper and lower face
Mechanism is thought to be swelling of the facial nerve due to an immune or viral disorder. Swollen nerve is maximally compressed as it passes through the labyrinthine portion of the facial cancel, resulting in ischemia and paresis.

Common viral causes: herpes simplex, herpes zoster. Cytomegalovirus, Epstein-Barr, mumps, rubella, influenza B.

99
Q

What is the Vestibulocochlear nerve?

A

HEARING AND BALANCE
Sensory
Nerve along which the sensory cells of the inner ear transmit information to the brain. This facilitates hearing and equllibrium.
Dysfunction of the nerve may cause hearing loss, vertigo, false sense of motion, loss of equilibrium, nystagmus, motion sickness or gaze-evoked tinnitus.

100
Q

What is the Glossopharyngeal nerve?

A

TASTE
Mixed
Somatosensory info from the tongue, tonsil, pharynx, control of some muscles used in swallowing
Episodic brief, excricusting pain occurring spnaaneously when chewing or swallowing, coughing, yawning or sneezing.

Usually. Begins in tonsil region and may radiate to the ear.

May be difficulty in swallowing.

101
Q

What is the Vagus nerve?

A

SENSORY, MOTOR and AUTONOMIC function
Mixed
Loss of reflex contraction of the palate or altered gag reflex, hoarseness of the voice

102
Q

What is the accessory nerve?

A

MOTOR FUNCTION - head/neck/shoulder

Dysfunction results in weakness of the sternocleidomastoid and upper portion of the trapezius
Diminished muscle mass, partial paralysis of trapezius muscle

103
Q

What is the Hypoglossal nerve?

A

MOTOR FUNCTION - tongue
Dysfunction is characterised by flaccid paralysis/weakness of ipsiliateral tongue musculature
Clinical feature may be muscle atrophy and tongue weakness

104
Q

What are some signs and symptoms that suggest you should test the cranial nerves?

A

Loss of smell
Alteration/loss of vision. Double vision/nystagmus
Drooping eyelid
Facial pain/allodynia
He I-facial paresis
Hearing loss
Vertigo/motion sickness
Gaze evoked tinnitus
Difficulty swallowing
Altered gag reflex
Hoarseness of the voice
Autonomic dysfunctions eg heart rate
Atrophy/partial paralysis of the sternocleidomastoid/trapezius muscles
Tongue function/weakness
Pain and headaches too …

105
Q

What are some linked conditions to cranial nerves?

A

Head injury
Road traffic collisions
Inflammation
Glaucoma
Atherosclerosis/Carotid aneurysm
Vasculitis/Giant cell arteritis
Nutritional neuropathy
Smalll vessel disease eg in diabetes
Herpes simplex
Demylinating disorders eg MS
Peritonsillar abscesses
Anatomical anomalies/space occupying lesions
Tomours/arterivenous malformation/aneurysm

106
Q

What is the H reflex?

A

A measure of motor neurone excitability

107
Q

What are ten basic procedures for proprioceptive neuromuscular facilitation? (Adler et al 2008)

A

Resistance
Irradiation and reinforcement
Manual contact
Body position and body mechanics
Verbal commands
Vision
Traction or approximation
Stretch
Timing
Patterns of movement

PHYSIOTHERAPY YEAR 2 (9 decks)

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