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Neuro - Physio > Neuro Pathologies > Flashcards

Neuro Pathologies Flashcards

1
Q

Pathophysiology of a Stroke

A

Central Nervous System pathology resulting from the sudden and focal death of brain cells, due to lack of oxygen when the blood flow to the brain is lost by blockage or rupture of an artery to the brain. 2 Types: Haemorrhagic = Ruptured blood vessel or build up of blood. and Ischaemic = Interruption to the blood supply (clot).

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2
Q

Non-Motor Impairments of a LCVA

A

Apraxias, agnosias, aphasias, Preservation

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3
Q

Non-Motor Impairments of a RCVA

A

Left hemi, pusher, inattention, neglect, and impersistance

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4
Q

7 Keys of Cerebellar Movement

A
  1. Stabilises oscillating outputs eg. control picking up a cup.
  2. Scaling of amplitude of movements. eg. decrease and increase movement.
  3. Crispness of movement.
  4. Distribution of appropriate commands across multiple joints eg. gait
    5.
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5
Q

7 Keys of Cerebellar Movement

A
  1. Stabilises oscillating outputs eg. control picking up a cup.
  2. Scaling of amplitude of movements. eg. decrease and increase movement.
  3. Crispness of movement.
  4. Distribution of appropriate commands across multiple joints eg. gait
  5. Redcues sensitivity to inward and outward inputs. eg. stopping the noise.
  6. Predicts system inputs and outputs. eg. picking up a water bottle and knowing its approximate weight.
  7. Ability to self correct eg. bottle is empty - adjust.
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6
Q

Special Considerations for Cerebellar treatment?

A

Allow some error. Want to constantly challenge the Cerebellar.
High dose, whole task practice is key.

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7
Q

Main Impairment in MND conditions

A

Loss of strength.

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8
Q

Pathophysiology TBI

A

TBI can impact on the cortex or cerebellum.

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9
Q

Special Considerations in TBI

A

Spasticity can be moderate - more than stroke - due to more widespread damage to the brain.

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10
Q

Outcome Measures for PD

A

10MWT, BESTtest

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11
Q

Outcome Measure for Cerebellar Problems

A

ICARS

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12
Q

Outcome Measures for Stroke

A

Fugal-Myer Assessment
MAS Scale

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13
Q

Non-Motor impairments for TBI

A

Possible behaviour impairments, especially if frontal lobe is affected. May have aggression, and disinhibition. Also will have the non-motor impairments of whatever side of the cortex is more impacted (if TBI has affected the cortex).

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14
Q

4 Types of Multiple Sclerosis

A

Relapsing Remitting MS, Primary Progressive MS, Secondary Progressive MS, Benign MS

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15
Q

Epidemiology of MS

A

Autoimmune system mediated, chronic inflammatory demyelinating disease of the CNS. Demyelination and plagues of white matter. White matter is anything myelinated in our CNS. Thus, any of this can be impacted by MS. Impairments are dependant on the location of the demyelination and plagues.

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16
Q

What happens with voluntary Movement for people with Parkinson’s Disease?

A

Dopaminergic neurons from the substantia nigra that usually project to the striatum, are dying off. So dopamine is no longer there, meaning you get signals of ‘start’, ‘stop’, start, stop. Which is why it is difficult for people with PD to initiate motor movement, and why they have a resting tremor (signal continues happening)

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17
Q

Roles of the Cerebellar

A
  1. Composition of movement–> Coordination and adaptation to error.
    Motor Learning –> Anticipatory Postural Control and movement consolidation
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18
Q

Dose for Cerebellar Issue

A

45-60mins 3X per week. 90mins for sub-acute cases.

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19
Q

Dose for PD

A

35-45mins 3X per week at an RPE of 6-8/10. Want it to be challenging

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20
Q

Dose for Stroke

A

100 reps per day

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21
Q

What is the Hemisphere of the Cerebellar responsible for?

A

Also known as Cerebrocerebellar tract. Fine tuning of movements. Adjusting for novel context. There is also a strong visual component here.

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22
Q

What is the Vermis and the Intermediate Zones of the Cerebellar responsible for?

A

Aka Spinocerebellar tract. Coordination. Responsible for head, neck and trunk control.
Affects gait and sitting balance. Imbalance, low tone, nystagmus, and ocular dysmetria.
Intermediate Zones: Initiating amplitude and timing of movement.

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23
Q

What is the Flocculonodular lobe of the Cerebellar responsible for?

A

Also known as vestibulocerebellar tract. Balance - Vestibular and ocular integration. Spatial and timing and position sense.

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24
Q

What are the perceptual impairments that can occur following ABI?

A

PIANO:
P: Pushing Behaviour
I: Inattention /extinction
A: Agnosias
N: Neglect (unilateral)
O: Other impairments of Visuospatial Awareness

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25
Q

Cerebellar Ataxia (from ABI)

A

5 D’s + I.
- Disturbance of speed, regularity and force of movement
- Decomposition of movement (movement occurs in a sequence of isolated steps rather than smooth)
- Decreased degrees of freedom (joint and limb stiffening)
- Dysmetria
- Dysdiadochokinesia
- Intenion Tremor

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26
Q

Dysdiadochokinesia and how to diagnose

A

Inability to perform movements of constant force and rhythm or impaired alternating movements.

Diagnose: Rapid pronation and supination

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27
Q

Dysmetria

A

Inaccuracy and impaired movement. Errors in direction amplitude, velocity and force of movement

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28
Q

Vestibular ataxia

A

Generally move slower. Minimal head and eye movement (reduces stimulation of vestibular system).
Less dysmetria more overall veering of movements, and reports dizziness, and jumpy or blurred vision.

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29
Q

Sensory Ataxia

A

Movements appear uncoordinated when visual feedback is decreased. eg. testing with eyes closed/darker environments.
Person will compensate by using their vision to provide feedback. Will avoid dual tasks, look at moving limb and turn on lights. Person will slow movement when visual feedback is limited.

CTSIB test.

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30
Q

Ataxia and symptoms

A

The loss of full control of bodily movements, usually from damage to the cerebellum (stroke, tumour, MS). Symptoms: Balance and coordination affected, wide based gait, difficulty with writing (dysgraphia) and eating, slow eye movement. dysphasia (slurring of speech)

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31
Q

Population of people who suffer with MS

A

W:M = 3:1
Average age onset is 20-50yo
Nearly normal life expectancy: 90-95% of average lifespan.
If people are born in winter months, they have higher rates of diagnosis.

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32
Q

Intention Tremor

A

Most pronounced at the end point of a movement

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33
Q

Pathophysiology of MS

A

Inflammatory processes cause oedema and the autoimmune response causes immune T-Cells to strip the axon of myelin. Disruption of transmission of information in the CNS - partial or full. Brain atrophy has been cited as possible predictor of disease progression in RRMS

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34
Q

Classification System of MS

A

Disease Steps:
0 = Normal
1 = Mild Disability
2 = Moderate Disability
3 = Early cane
4 = Late cane
5 = Bilateral support
6 = Confined to a wheelchair
U = unclassifiable

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35
Q

What is RRMS?

A

Relapsing Remitting MS. This is about 80%. Unpredictable attacks which may or may not leave permanent deficits followed by a period of remission

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36
Q

What is PPMS

A

Primary Progressive MS. About 10-20%. Steady increase in disability without attacks

37
Q

What is SPMS

A

Secondary Progressive MS. About 50% of RRMS. Initially RRMS that suddenly begins to have decline without periods of remission.

38
Q

Benign MS

A

About 10%. Distinguished by no residual disability after 10 years post dx and classification can only be made retrospectively.

39
Q

What are the clinical features/impairments of MS?

A

Weakness
Contracture (44% in the ankle)
Spasticity (can increase falls risk)
Fatigue

39
Q

Special Considerations when treating population with MS

A

Heat
Increased falls risk
Fatigue (80-90% MS).
Primary Fatigue = Directly related to the disease process.
Secondary Fatigue: Non-disease specific factors such as sleep disturbance, depressions, poor fitness etc.

39
Q

Objective Assessment for MS

A
  • Cardiorespiratory status.
  • Muscle strength, length, spasticity/contracture, tremors.
  • Sensation
  • Proprioception
  • Coordination (ataxia)
  • Vision
  • Vestibular / dynamic vision
  • Fatigue
  • Pain
39
Q

Physio Subjective assessment for people with MS

A
  • Good history including falls, pain, fatigue, heat sensitivity to guide functional assessment and objective impairment review.
    -Early symptoms can include: Tingling, numbness, loss of balance, weakness, blurred/double vision, sudden onset of paralysis, lack of coordination, cognitive difficulties - impacts on dual tasking
  • As disease progresses: Fatigue, spasticity, increase muscle weakness, bowel/bladder dysfunction, pain, cognitive problems, depressive/emotional changes, associated changes (contracture, reduced mobility, falls)
    -Long term view. View all ax with fatigue and heat related change in function in mind.
40
Q

List some of the drugs used for people with MS and the symptom they treat

A
  • Inferon-beta (IFN) = Ataxia.
  • Glatiramer acetate (GA) = Spasticity. Physio can treat with hydrotherapy, unloaded leg cycling, passing stretch, PNF eccentrics
  • Tysabri (Natalizumab) = bladder and bowel.
  • Cladribine = Pain
    Fingolimod (Gilenya) = Seisures
41
Q

Evidence for physio interventions in people with MS?

A

Multidisciplinary and exercise based rehab:
- Improves aerobic capacity and muscular strength. Improves walking/mobility. Improves fatigue and health-related QoL.

  • Progressive resistance/strength training:
  • Improves functional capacity and strength. Improves strength, fatigue, mood, QoL, function. Improves isometric strength, muscular endurance, max power, muscular hypertrophy of thighs and TUG. Improves arm strength, leg endurance, leg extensor power and fast walking speed.
  • Robot assisted gait training and Treadmill training +/- body weight support.
42
Q

How to address weakness as an impairment in people with MS

A

Strength training:
- 8 weeks minimum.
- 2x per week.
- Intensity: 10-15reps max, 2 sets, progressive resistance.
- Progress: 2-5% when able to complete 12-15 reps without loss of form.
- Broekmans et, al 2010 found that light to moderate intense resistance training improves muscle strength in people with MS.

43
Q

How to address Spasticity

A
  • Hydrotherapy
  • Unloaded leg cycling
  • PNF
    FES
  • Massage
  • Whole body vibration
  • Active and passive stretches + botox.
44
Q

How to consider heat when rehab someone with MS

A

Commence low to moderate levels of exercise with REGULAR REST periods. Minimise risk for deterioration - strenuous intensive training can be exhausting.

45
Q

How to consider fatigue when rehab someone with MS

A

Aerobic/endurance exercise improves function, strength, VO2 max, depression. Exercise therapy and strengthening exercises reduce fatigue.

46
Q

Address impairment of decreased aerobic endurance in people with MS

A
  • Duration: min 4 weeks to see improvement
  • Frequency: Safe progression to 30-40mins 3x/wk
  • Intensity: 55-85% of age predicted max heart rate, 60% VO2max
  • Type: Arm and leg ergometer and treadmill walking
  • Low to moderate intensity
47
Q

Address impairment of decreased balance/increased falls in people with MS

A

Cootes et al 2013 found:
- Duration: 10 weeks 2x/wk
- Resistance machines and balance exercise
- Group physio or 1on1
- Outcome measures: BBS, 6MWT, MSIS-29 accidental falls
- Significant improvement in all measures.

  • Appropriate intensity of practice of highly challenging balance activities is critical in maximising effectiveness
48
Q

Epidemiology of Parkinson’s Disease

A

Second most progressive neurodegen. disease after Alzheimer’s. Most common basal ganglia moto disorder.

1/1000 people 65+. 1/100 75+. 1/350 Aus living with PD. 1.5XM:F ratio. Dx age ~55-65yo.

49
Q

Pathophysiology of PD

A

Idiopathic - interaction between genetic and environmental factors.

It is a Hypokinetic movement disorder. = Dopamine-producing cells in the substantia nigra progressively degenerate.
Loss of dominergive neurons in the substania nigra, changes basal ganglia output. The role of substantia nigra in facilitating movement is lost and the action of the indirect pathway is more prominent, resulting in hypokinesia.

50
Q

Classification system of PD

A

(1) Postural Instability Gait Disorder (PIGD).
- 50% prevalence. Rigidity and hypokinesia. Problems maintaining balance, gait and freezing. More rapid course of PD. More problems with dementia and cognition.
(2) Tremor-dominant subtype.
- 40% prevalence. Poor response to medication. Lower risk of depression, dementia and slower disease progression.
(3) Mix-type.
- Combination of 1 and 2. 10% prevalence
(4) Young Onset PD (YOPD)
- <40yo. Slower disease progression. Increase rate of dystonia. Lower rate of dementia, and early onset of freezing.

51
Q

Prognosis/Stages of PD

A

Modifed Hoehn and Yahr Scale from 0-5.
Stages 1-2.5 characterise early stage of PD
Stages 2-4 represent mid stage where activities are affected and balance and falls are issue
Stage 3 is a marked reduction in quality of life.
Stage 4 is severe disability but still able to walk or stand unassisted.
Stage 5 is the last stage. Only 4% of people living with PD reach the late state. Wheelchair bound/bedridden unless assisted.

52
Q

Clinical features/impairments of PD

A

4 Cardinal Motor Symptoms:
- Hypokinesia/Bradykinesia
- Resting tremor
- Rigidity
- Postural Instability

Others:
- Akinesia (freezing).
- Respiratory disturbances
- Orofacial dysfunction (masked face)
- Speech dysfunction (dysarthria, dysphonia, dysphagia, drooling).
- Dystonia/Dyskinesia

Non-motor Symptoms:
- Autonomic changes -Blad/Bowel, sexual functional changes, postural hypotension
- Depression
- Dementia
- Emotional change
- Cognitive and memory deficits
- Personality changes

Impaired Execution of automatic movement!
- Difficulties switching from one movement to another
- Difficulties with grading amplitude and velocity

53
Q

Physio subjective ax for PD

A
  • Main problems
  • Goals
  • Expectations
  • Falls history/fear of falling
  • Freezing of gait
  • Physical activity level
  • Impact of non-motor symptoms
    Questionnaires:
  • ABC scale - measures confidence performing ADLs
  • Freezing of gait questionnaire
54
Q

Physio objective ax for PD

A

Important to assess on and off medication
Functional tasks:
- Sitting balance
- STS
- Standing balance
- Gait/turning
- Stairs
- UL reaching and manipulation
- Bed mobility

Impairments:
- MDS-UPDRS (impairment ax)
- Muscle strength
- Muscle length and joint ROM

Outcome Measures:
- Gait = 10MWT, TUG, 6MWT
- Standing balance = miniBEST, DGI, FGA, Marsden Test
- UL = 9 hole peg test
- Respiratory Function = FEV1 and FVC
- QoL = SF-36
PD = Modified Parkinson’s Activity Scale

55
Q

Outline the medical and physio mx for people with PD

A

Dopamine replacement therapy (levadope): Madopar and Sinemet (brands). This is GOLD standard for PD treatment.
Effective in treating motor symptoms esp early stages. Two major complications - fluctuations in motor performance and abnormal involuntary movements (dyskinesia).

  • Dopamine agonists
  • COMT inhibitors
  • MOA Type B inhibitors
  • Anticholinergic therapy

***PHYSIO Make sure correct dose of medication on time. Document time of ax and Rx and whether pt was in ‘on ‘ or ‘off’ stae.

56
Q

3 elements of Physio Mx in PD

A

3 elements: 1. Motor Strategies. 2. Mx of secondary adaptive changes and 3. promotion of physical activity, lifelong changes to behaviour.

57
Q

Define the 1. motor strategies in PD pts.

A

Bypass the defective BG circuitry and use prefrontal, frontal and parietal cortex and cerebellum to regular movement size or timing

58
Q

Describe the Evidence and Purpose of 1. motor strategies in PD pts.

A

Use visual (eg. tape, lined paper for writing, cones), auditory (music, metronome, verbal instruction) and somatosensory (strats to initiate mvt, eg, rocking knees in bed to roll over, or weight shift back-front to take step etc.) cues to initiate and maintain mvt. Breakdown complex mvt sequences into simple and logical in step parts.
Perform each part separately. Avoid simultaneous motor or cognitive tasks.

Purpose: To improve problem solving, reduce freezing, induce motor learning, improve qual of mvt, avoid de-conditioning.

Apply principles of neuroplasticity to training: Intensity, complexity, repetition, specificity etc.

59
Q

Describe the Evidence and Purpose of 2. management of secondary adaptive changes in PD pts.

A

Exercises to improve/maintain joint and muscle mobility

  • Dual task training (cognitive element). Auditory cues more effective than visual with dual tasking.

Inflexibility and stiffness = use large amplitude active movement and rotational activities (trunk).

Muscle deconditioning/CVF = Improve with strength training and aerobic exercises that encourage whole body movement (do during ‘on’ phase)

Rigidity, Dystonia, Dyskinesia and Tremor = Slow and rhythmical rotation of trunk combined with relaxed deep breathing. Slow sustained stretches (address dystonia), medication for dyskinesia, clasping hands behind back can help sometimes with tremor.

Balance retraining + LL strengthening to improve balance and reduce falls.

60
Q

Describe the Evidence and Purpose of 3. exercise and promoting physical activity in PD pts.

A

Exercise is needed in PD to maintain benefits. (neuroprotective role).

Dance: direct practice of walking in contexts that may involve freezing. Music can be external auditory cue. Improve gait and balance and mood.

Treadmill Training:
- With and without BWS
- Pt focus on big steps. Focus attention and provide augmented feedback. Consider adding a cognitive dual task while asking person to maintain stride length. Improves walking speed and stride length.

61
Q

Classification system for TBI

A

Closed Head Injury: Acceleration/deceleration injury or blow to the head and skull remains intact.

Open Head Injury:
Skull is fractured and brain covering (dura) are torn exposing the brain.

62
Q

2 types of TBI

A

Primary Damage:
Mechanical injuries - the direct result of damage and may be focal or diffuse.

Secondary Damage:
Due to the cerebral ischaemia and the resulting cascade biochemical changes occuring seconds, hours or days after trauma.

63
Q

Glasgow Coma Scale

A

Scale from 1-15. Lower score = worse.
8 or less = comatose patient. 3 or less = totally unresponsive

64
Q

What is Post Traumatic Amnesia (PTA)

A

Period of impaired consciousness that extends from initial injury until continuous memory for ongoing events is restored.

65
Q

Scales to measure PTA?

A

Modified Pxford PTA scale
GOAT (Galveston Orientation and Amnesia test.
Westmead PTA Scale

66
Q

Clinical course for TBI

A

Best outcomes are seen within 12 months, but recovery may continue for years. Intense rehab should start asap. People with TBIs at increased risk of falls, mental health issues, and over representation in criminal justice system.

67
Q

Prognosis for TBI

A

Depends on:
Lesion size and area. Time size lesion. Age. PTA. Severity of lesion/disability. Gender - male = lower outcomes.

68
Q

Define Spasticity

A

Velocity dependent increase in tonic stretch reflexes with exaggerated tendon jerks resulting from hyper excitability of the stretch reflex.

69
Q

Outline Physio Ax for people with TBI

A

-MMTs
-Muscle length (ROM)
-Spasticity ax (Tardieu scale)
-Coordination (higher level tasks as appropriate)
-Sensation (tactile and proprioception)
-Perceptual impairments (agnosia, unilateral neglect, body scheme disorders, ‘pusher syndrome’
-Vestibular dysfunction (Including BPPV)
-Fatigue
-Other msk eg. pain ax following whiplash or fracture

70
Q

What are some General Outcome Measure to measure mobility?

A

Functional Independence Scale (FIM)
Disability Rating Scale (DRS)
Modified Barthel Index (MBI)
Functional Assessment Measure (FAM)
Canadian Occupational Performance Measure (COPM)

71
Q

TBI Specific Outcome Measures?

A

Motor ax scale (MAS)
Clinical Outcome Variable Scale (COVS) *Functional motor ability - temporal or permanent need for wheelchair to ambulate, note a ceiling effect can occur with higher level pts.
High Level Mobility Ax Tool (HiMAT)
FIM
10MWT
6MWT
TUG +/- Dual task
Balance measures
Motor Fitness Tests

72
Q

Early Aims for Physio with pts with TBI

A
  • Optimise respiratory function and prevent complications
  • Check for DVT
  • Optimise MSK alignment and anticipate and minimise muscle length changes
  • Position pt SOOB to increase arousal levels
  • Retrain AROM ASAP
  • Work within pain limits and manage any source of pain
  • Work with family and carers to foster optimal plan for day
73
Q

Physiotherapy aims and mx strategies to address impairments for people with TBI

A

Increasing level of arousal: Position changes and environmental stimulation.

Head Control Problems: Practicing holding head in neutral with limited support –> Time trials holding head with no support –> Practice normal head movement

Eye Control Problems: Practice focal gaze –> Gaze stability (following moving object) –> focla gaze with head mvt –> focal gaze, stability in ranges of positions (supine, sitting etc.)

Rehabilitation of motor control: Treadmill training with partial BWS as adjunct to conventional therapy. –> Strength training to improve motor control in targeted muscle groups –> Gait re-education –> Exercise training to promote CRF.

Spasticity: Don’t treat specifically (no benefit shown). Treat as whole picture

Contracture: NO evidence for routine use of splinting and stretching. Active stretching at EOR, low load prolonged stretched and routine positioning. Serial casting - POP or fibreglass

CVF: Circuit class training

Balance: Reduce BOS –> Making controlled mvts of CoM –> Reduce UL use.

Focus on strengthening and practicing coordination

74
Q

What are the potential impairment in pts with TBI?

A

Lack of arousal
Head control problems
Eye control problems
Motor control problems
Spasticity
Contracture
CVF
Balance
Weakness/loss of coordination

75
Q

Physio subjective ax for people with TBI

A

Home environments
Support available
Usual function including occupation

76
Q

Physio objective ax for people with TBI

A
  • Mobility
  • Home access for iminent discharge/check stairs if needed
  • Dual task ability (TUG manual and cognitive)
  • Any Vestibular screening/education needed
  • Link to follow up as indicated with time frames
77
Q

Explain the Tardieu Scale

A

Measures muscle reaction and ROM achieved during joint movement at various speeds.
-Determines spasticity angle: V1 (slow) and V3 (fast).
- Large spasticity angle - large dynamic component of spasticity (minimal contracture)
- Small spasticity angle - small component of spasticity. Any limited range is more attributed to fixed contracture

78
Q

Explain the Goal Attainment Scale (GAS)

A

Method of achievement in set goals.

+2 = lot more than expected
+1 = Little more than expected
0 = Anticipated level of achievement
-1 = Baseline performance
-2 = Less than baseline

79
Q

Strategies for pts with behavioural or cognitive impairments

A
  • Keep info clear and brief
  • Avoid overstimulating environments
  • Keep training simple (whole task instead of part)
  • Maintain safe and secure environment
  • Liaise with other team members
  • Shorter sessions
  • Frequent task changes
  • Set limits around behaviours as able and appropriate
  • Set program time/routine
  • Communicate well as per SP
80
Q

What are the important components in Walking?

A

Stance Phase:
- Extension of the hip throughout
- Flexion of the knee (0-10deg) on heel strike, then extension through midstance and flexion prior to toe off
- DF of the ankle until end of stance then fast PF
- Lateral horizontal shift of the pelvis and trunk

Swing Phase:
- Flexion of the knee with hip in extension
- Hip flexion
- DF of the ankle throughout
- Slight lateral pelvic tilt downwards
- Rotation of the pelvis forward
- Extension of knee prior to heelstrike

81
Q

What are some common adaptive strategies used when walking?

A
  • Walking very slowly and increase time spent in DL support
  • Shorter step lengths
  • Trunk inclined forward during stance
  • Wide base of support
  • Elevation of the pelvis and abduction of the leg
  • Toes not clearing ground during swing
  • Trunk inclined backwards at end of seing
82
Q

Outline the clinical features in FND

A

Weakness, Tremor, Jerks, Dystonia, Gait abnormalities, Dyskinesia, Visual Disturbance, hearing issues, pain, fatigue, headaches, seizures, attention issues, pins and needles, numbness, speech issues

83
Q

Outline Physio ax for FND

A

-Gain detailed subjective overtime.
-Gauge pts understanding and confidence in dx
-Check if pt has developed successful strategies
-Over time build a holistic profile based on the biopsychosocial model. Reasons to improve vs reasons to not improve. Rapport building - get to know them (motivators/fears/values) and see the world from their eyes. Listen for language used (DIMS - danger) vs (SIMS - Safety). explain pain.
Set expectations of rx.
Perform Hoovers Sign and Entrainment test.

84
Q

Physio intervention for FND:

A

Education - normalise illness beliefs. Reinforce diagnosis.
Exercise - divert attention.
- Joint development of symptom formulation (individual biopsychosocial factors).
- Movement retraining with diverted attention
- Self-management strategies
- Goal setting

85
Q
A

Neuro - Physio (2 decks)

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