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נאורו של קליניק > MS > Flashcards

MS Flashcards

1
Q

who gets MS

A 
female, 
onset age 30-60
high risk US/europe/canada/new zealand australia (low risk africa/aisia)
genetics
stress trigger

Genetic + environment

most complain about ambulation and not getting PT

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2
Q

Relapse and Remitting

A

most common form

  • medication
  • worse (relapse) and improves (remission-degress of recovery to a degree but getting worse over tiem)

(not exacerbation which is an increase in disease activity, it is just a worsening of sx)

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3
Q

Relapse - progressive

A

varied relapse and then stabilize, relapse and stabilize (describe behavior not severity)

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4
Q

Chronic Progressive

A

(primary progressive)

no improvement: slowing of progression can happen but it progresses over time

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5
Q

Secondary progressive

A

start as more benign then becomes a straight slope of progressing

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6
Q

Benign

A

occasional sx without significant functional impairment

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7
Q

fulminant

A

rapid progressive

early severe disability and death

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8
Q

Dx MS

A

mcdonald

  1. attacks of:
    Spatial: 2 regions
    temporal: 6 months apart
  2. lab evidence of 2 or more distinct regions
  3. no other better explanation
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9
Q

what evoked potential slows

A

slow conduction velocity

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10
Q

his view on exacerbation

A

exacerbation is an acute demyelinating event

exercise doesnt cause this. fatigue, temperature, stress cause worsten of sx but not an exacerbation

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11
Q

EDSS

A

most used scale to measure severity of MS

disability scale measure 8 Functional systems: pyramidal (motor), cerebellar, brainstem, sensory B&B visual cerebral and other

only measure ambulation by distance and AD**

mild: 0-3.5
mod: 4-6.5
severe: 7-9.5

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12
Q

fatigue in MS

primary vs secondary

A

primary –lassitude/motor fatigue

secondary is treatable
-infection -tx the infection (drugs inhibit immune system so susceptible to infection which incr temp)

  • spasticity: E cost -tx baclophen
  • ataxia: high E cost
    weakness: sedentary cause disuse atrophy tx exercise
    depression: tx medicine

sleep deprivation (speascticity, B&B, polyuriam,)

Polypharmacy: too many medications

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13
Q

6MWT MS

A

each minute less distance covered than in the minute before

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14
Q

can exercise cause exacerbation

A

no

it can cause fatigue

will not cause more neuro damage or increase likelihood of relapse or exacerbation

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15
Q

some MS sx

12 primary

6 secondary

A

1-FATIGUE
2-SENSORY changes: anastehsia, Lhermitte sign (posterior cord)
3-TRIGEMINAL NEURALGIA (trig nerve inflammed)
4-WEAKNESS: plaque in pyramidal, disuse
5-OPTIC NEURITIS: abrupt lose vision 2-3 days, blur vision..usually transient
6-SPASTICITY: UMN involve, worse with time
7-HEAT SENSITIVITY: transient worse sx, (wont cause permanent damage, some pts benefit from cooling before exercise)
8. ATAXIA: cerebellar involve or posterior column
9. can disdiakokinsestia, tremor, vestibulopathy, dysmetria get vertigo(–BPPV is preipheral: more common in ms)
10) PSYCH
11) BLADDER
12) SPEECH/LANGUAGE

SECONDARY

1) musculoskeletal (bc innapropriate movement patterns)
2) weakness (not the primary of demylenation but resulting disuse)
3) change in respiration (primary death: lose muscle control of respiration or deconditioned)
4) posture (positionning)
5) osteoporosis (disuse/steroids)
infections (UTI)
6) balance loss (bc primary effeects of weak/spasticity, ataxia, sensory loss, loss motor control and vision ALSO secondary of weakness and contractures)

  • if fall rhomber eyes closed it bc visual dom in balance, train eyes closed
  • do better on balance when they not fatigued
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16
Q

nystagmus in CNS vs PNS

A 
Central: 
Nystagmus Direction changes
Rotary or linear nystagmus and not both
nystagmus can be seperate from vertigo
unable to suppress with fixation
Peripheral
unidirectional nystagmus
rotary AND linear components nystagmus
nystagmus matches with vertigo
suppresses with fixation
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17
Q

MS drugs

A

A) Disease modifying:
CRAB: copaxone, rebif, avonex, betaseron

  1. copaxone: limit inflammatory PROPERTY of cells that cross BBB
  2. beta interferon: PREVENT immune cells into BBB (avonex, bataseron, rebif)
  3. Tysabri: BLOCK inflammatory cells cross BBB
    - -can cause PML

Gilenya: prevent WBC leaving lymph nodes

B) Second order:
Mitoxantrone: sepress immmune

STEROIDS: limit inflammation process

C) Sx

Spasticity:
Baclophen: spasticity (specificity issue)

Zanaflex: Tizanidine: decr spasticity but lose tone elsewhere (specificity issue)

Dantrium: NMJ

Fatigue:
Ampyra: potasium channel blocker to improve nerve conduction

Provigil: act like missing myelin

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18
Q

Baclofen

Tizanidine

Dantrolene

A

Baclofen: spasticity of spinal origin (not as effective if cerebral origin)

i. Maximal dose effect: 80-100mg: after that patient gets drowsy and lethargic
ii. Past that amount get Drowsiness, lethargy
1. If not getting relief from spasticity at 80-100mg use a baclofen pump
iii. Act on level of CNS

Tizanidine, clonidine: (second order medication for spasticity, less effective but less drowsiness issue)

i. For Spasticity
ii. pain reducing effects
iii. Act on level of CNS

Dantrolene: (third order drug, works at PNS: NMJ, not at CNS)
–acts as the level of contractile unit, not the CNS
it works on the peripheral nervous system, the NMJ. If person has too much drowsiness with baclofen it is good to give them dantrolene.

The problem is it has a more global effect: reduce the tone in other muscles too (so get the spastic muscle to normal and get low tone in the other muscles): this happens to a greater extent than it does with the other medications

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19
Q

copaxone

A

: limit inflammatory PROPERTY of cells that cross BBB

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20
Q

beta interferon:

A

PREVENT immune cells into BBB (avonex, bataseron, rebif)

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21
Q

Tysabri

A

: BLOCK inflammatory cells cross BBB

–can cause PML

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22
Q

Gilenya

A

: prevent WBC leaving lymph nodes

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23
Q

Mitoxantrone

A

: sepress immmune

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24
Q

STEROIDS

A

: limit inflammation process

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25
Q

Ampyra

A

: potasium channel blocker to improve nerve conduction

against fatigue

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26
Q

Provigil

A

: act like missing myelin

against fatigue

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27
Q

if see exacerbation what may it be

A

UTI

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28
Q

MS BANDING

A

pain
feel like band pressing you around the middle

feel like being squeezed –but neuro cause

given neurontin / gabapentin

do TNES,

PT/OT: posture, gait, neiro affect ortho too , dont want compensations

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29
Q

does exercise help MS patients

A

yes
and not exacerbate

he found in his study that cooling helped them walk farther (before and during can cool them)

aquatic therapy good (study didnt show increased gait, did have strength increase)

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30
Q

how to exercise with MS

A

intermittent: we dont want the fatigue to come on but need amt for progress

**vital signs not always accurate indicator of fatigue

get more dose if more rest breaks: volume

MMT can be misleading, first few reps are strong then begin to deteriorate

strengthened with rest breaks and improved without fatigue

**THEY CAN EXERCISE (only pseudoexacerbations can occur): can get fatigue and thermosensitive so do cooling for more volume of exercise INTERMITTENT

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31
Q

is berg good for MS

A

no get fatigued later in day and fall;

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32
Q

a main cause of lack of fitness in MS

A

lack of training

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33
Q

Cerebellum

afferent
efferent

A

Afferent: from somatic, proprioceptors, visual, vestibular, auditory, motor and nonmotor cerebral cortex

Efferent: brainstem, midbrain, cerebral cortex

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34
Q

Paleocerebellum

A

input from spinocerebellar/cuneocerebellar/trigemninalcerebellar tracts with SOMATOSENSORY information from LIMBS and FACE

input from sensory and motor cortices

*unconscious proprioception

lesion of the spinocerebellum results in overshooting when reaching for something reach past object: abnormality in maintaining the muscle tone (ie in a rebound test)

abnormality in maintaining the muscle tone

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35
Q

Neocerebellum

A

input from: sensory, premotor, motor cortex

voluntary movement: planning and timing (skilled movements, more presice with practice)

**if lose hard to acquire lost skills in PT

(control of rapid movements, sudden movements (throw a ball and he quickly reacts to catch it) 
precise movement control
motor planning)
dysmetria
disdiadokinesia
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36
Q

Cerebellum in motor control

A

gets sensory input:

  • -somatic, vestibular, visual, auditory
  • -motor commands

defines body status : compare intent with actual movement *posture/equilibrium corrections for maintaining balance

MOTOR output to brainstem motor nuclei/motor /premotor cortex

37
Q

major role of cerebellum

A
  1. coordinates activity, fluid movement and postures
  2. comparison of motor activities to intend plan and modify it if not achieved (continual loop)
  3. modification of motor output based on sensory input and motor output: continuous loop
  4. compensation for motor tasks: predictive / anticipatory
    big role in predictive movement: feed forward, anticipatory *if cerebellar lesion hard time with anticipatory balance but less impaired with reactive balance
  5. major role in learning new motor programs because of its modifying function
38
Q

if cerebellum damaged

A

learning new motor programs is limited: challenge in PT because we depend on motor learning – here plasticity cannot occur

*if cerebellar lesion hard time with anticipatory balance but less impaired with reactive balance

depending on where lesion is in the cerebellum can change deficits

39
Q

Signs of Cerebellar Dysfunction

5 traits

A
  1. Dysmetria
  2. Asynergia/dysnergia
  3. Rebound phenomena
  4. Tremor
  5. Hypotonia
40
Q

vestibulocerebellum

A

posture and equilibrium

lesion: inability to maintain balance with rapid change of position

almost predominantly vestibulocerebellum

 receives feedback from vestibular system (semicircular canals, etc) to determine changes in direction of self motion

 almost instantaneously institutes corrections in postural motor signals necessary for maintain balance after these changes in positioning

 lesions in result in inability to maintain balance with rapid changes in position

41
Q

initiation of movement: do cerebellum do too early or too late?

A

late

42
Q

Friedreichs ataxia

A

 one of the most common hereditary disorders of CNS

 CNS & PNS

 sx begin at 8-15yo

 progressive ataxia, loss of DTR’s, impaired proprioception

 scoliosis & pes cavus

 abnormal eye movements

 cardiomyopathy

 ataxia due to loss of proprioception and tract involvement

o gait common first symptom

43
Q

Olivopnotoverebellar atrophy

A

 combined degeneration

 progressive ataxia with later onset

 initially pure cerebellar, w/ later pyramidal tract, BG and autonomic signs

44
Q

nutrition issues cerebellum

A

 thiamine deficiency

 alcoholism

 B12- deficiency

 E-deficiency

45
Q

neoplasms cerebellum

A

 primary tumors

 metastatic disease

 paraneoplastic syndrome

46
Q

Arnold Chiari Malformatios

A

most common developmental malformation of the posterior fossa

o herniation of cerebellusm, medulla & pons throught the foramen magnum

into upper c-spinal canal

47
Q

cerebellum vascular disorders

A

vascular disorders

 ischemia and hemorrhage

 mechanical trauma

 focal or multifocal

48
Q

Cerebellum tx

A

weighting
used to keep ataxic arms down but possibly just strengthening arm =>

if pt has too much movements for walker, this is good

 pool

dampens tremor while they are in pool
no functional overflow

 abdominal binders–quiets trunk

 vestibular rehab
only works if pure vestibular & central lesion (and unilateral)
3 sites: cortex, pons and cerebellar

 controlling degrees of freedom
using movement decomposition for compensation

 depends on etiology
single, focal, stable lesion => better chances
degenerative or multi- focal (MS) => poor chance

 plasticity?
not really because ‘skill producer’ is what is affected

 motor learning (small errors)
dependent on the learner detecting the errors and correcting them
pt is currently using ‘too large’ errors (large complex)
more forceful ataxia

 use single digit movements => limb

49
Q

Tonic clonic seizure = grand mal seizure

A

ENTIRE cerebral cortex

15-30 seconds of intermittnet contractions major muscle groups followed by jerking of extermities

followed by unconsious up to five minutes

dont hold them down, clear away furniture

**no aura

50
Q

absence (petite-mal) seizure

A

called this because many people wouldn’t even notice

 can see eye blinking (3/sec) or hand twitching

 short- term loss of awareness or consciousness

 can occur in clusters (someone can have 5-10 in 1 day)

 4-12 y.o most common age range

 no aura

51
Q

partial (focal) seizure

A

MOST COMMON

  • –usually caused by local (focal) brain involvement
  • stroke, AVN, head trauma, slow bleed post fall, tumor
---various presentations, twitching (from primary motor area), vision ‘abnormal sensation’ or hearing ‘abnormal sensation’ (not quite hallucination)--depends on where it is : 
auditory lobe
occipital obe
motor cortex 
etc
52
Q

Myoclonic seizure

A

brief, shock-like jerks of a muscle or a group of muscles

get a few contractions in one or 2 muscles

due to increased excitability of the motor system

53
Q

Multifocal Seizure

A

affect multiple areas of brain

presentation depend on where in brain

AUORA (only seizure he said had aura)

54
Q

cause of seizure

A

newborn or infant- due to something that occurred at birth (birth issue or anoxia) or a metabolic issue
-can occur with high fever and be benign

o up thru adolescence usually idiopathic

adults: trauma, tumors, aneurysm, drug toxicity, alcohol abuse/withdrawal,

arterial venous malformation (AVM)

55
Q

how do you know LOC and not seizure

A

another LOC after seizure isnt seizure, it is syncope ,

if it is syncope they will not clench teeth

56
Q

is brain pain innervated

A

no

57
Q

Primary Headaches

A
  1. Migraine
  2. Tension Headache
  3. Cluster Headache
58
Q

Migraine

A

multisystem,
at least 5 attacks to diagnose
4 hours-4 days
light and sound sensitive (also nausea and vomit)

unilateral, pulsating, mod-severe intensity, aggravated by exercise

genetic

NOT VASCULAR (maybe hypothalamus/upper brainstem issue)

Type 1: get aura : visual/ auditory/ sensory hallucination: if medicate here less sx
can affect c-spine

Without Aura: MORE COMMON : can be bilateral, can affect c-spine

59
Q

Tension Headaches

A

ACUTE type tension headache: due to posture/stress: muscular

muscle origin: traps, levator, c-spine muscle tension

can get from clenched teeth: TMJ induced

CHRONIC tension headache: neurotransmitter deficient causes ongoing chroninc (progress from acute, this one isnt muscular origin)

Chronic tension headache dx: 
15 headaches/month for at least 6 months 
\+ at least 2: 
1) pressing non pulsating pain
2) mild/mod intensity
3) bilateral location
4) not aggrevated by ADL

will have nausea or photosensitive or phonosenstiive

60
Q

Cluster Headaches

A

come in clusters
-alot in a period, go away, come back in a cluster

Men, trigger: alcohol, smoking, lack sleep

15 minutes - 3 hrs
unilateral near eye or frontal
eyes tears, nose run
can have ptosis of eyelid

Maybe ANS issue, medications affect bloodflow (some need vasoconstrict, others need dialate)

61
Q

Secondary Headaches

A
  1. Sinus headaches
  2. headache from lumbar puncture
  3. pathologies cause headaches:
    - –meningitis
    - –encephalitis
    - –AVM (incr pressure, especcially if develope glaucoma)
    - –aneurism
    - –glaucoma
    - –small hemorrhage

*headache from small hemorrhage or aneurism will be worst headache of their life

**RULEL OUT: TMJ

62
Q

Headache tx

A
  1. diary of food and environment and stuff
  2. biofeedback if tension headache
  3. relax, meditate, manage stress
  4. posture eval: alingment
  5. trigger point massage
  6. rapid cooling flourimethane spray and stretch
  7. constant coutnerstrain and muscle energy techniques
  8. mobilization of nervous system-tension testing of nerve, nerve flossing
  9. exercise for endorphins EXCEPT FOR MIGRAIGNe
63
Q

most demanding task in gait cycle

A 
weight acceptance (initial contact and loading) 
--shock absorb, initial limb stability, preservation of progression

hip extensors, quads, DF

64
Q

if tell elderly to walk faster wheat to they increase

A

increase hip power (but young will increase at all joints)

65
Q

is there a direct correlation between E cost and instability?

A

NO

66
Q

Facotors of elderly gait

A

high A/P and M/L limb acceleration, more medial to lateral COG displacement, lateral sway

Low A/P pushoff

increased hip flexion, knee flexion, ankle has decrease in plantarflexio, and has toe out angle

more land footflat downstairs

high falls and tripping , high heel contact skid velocity, late hamstring activation,

DIMINISHED LE ROM: hip extension and ankle DF

67
Q

implications elderly gait

A

diminished: limit of sway, control of narrow BOS,

limits of stable stance approached earlier

postural responses called in earlier

postural response may require less activation

elderly have increased sway when balance is challenged by removing a modality or rendering a modality unreliable

therefore diminished postural responses when need it

ELDERLY HAVE MULTIPLE CHANGES IN MOBILITY

STEREOTYPIC

LEADS TO DIMINISHED MOVEMENT, ACTIVITY, FALLS

PT INTERVENTIONS AVAILABLE

68
Q

Muscular Dystrophy

A

Muscle disease, not motor neuron

Dystrophin deficit, spontaneous degeneration of muscle

defect determines age and spread of progression

Type II fibers: fast phasic involved (Force)

*check blood for CPK bc proteins leak into blood from unstable muscle

PROXIMAL weakness and EXTENSOR weakness first

(if younger age onset, it progresses faster)

69
Q

Beckers Muscular Dystrophy

A

x linked

benign form of Muscular Dystrophy

PROXIMAL WEAKNESS
able to ambulate until mid teens

SLOWER PROGRESSION

*PT tx like DMD

70
Q

Fascioscapulohumeral Muscular Dystrophy

A

autosomal dominant

onset at any age, most have by age 20yrs

FACE, SCAPULA, HUMERAL

WINGING SCAPULA: scapula elevated,

weak face: obicularis oris, obicularis occuli (cannot close eyes, drink from straw, transverse smile, wrinkle forehead)

weak Upper arms: arm usually IR , pec atrophy, Lordosis

weak Shoulders *deltoid spared

weak ABDOMINALS

PT: clavicle strap, orthotic for LORDOSIS, eyedrops to keep moist, adaptive devices ADL independence, AFO if footdrop

71
Q

Limb Girdle Muscular Dystrophy

A

onset in 30s (autosomal recessive)

HIP and SHOULDER weakness (biceps, pecs)

  • popeye arm: proximal weakness and so distal arms look larger
  • antigravity muscles affected, ADL

SLOW PROGRESSION to all muscles 20 years after dx

PT: tx functional difficulties, raised toilet seat, elevated chair, elevate furniture, spring cushion

72
Q

Myotonic Muscular Dystrophy

A

autosomal dominant

combination of myotonia and dystrophy

1st sign: myotonia: cannot relax a muscle after a contraction or stimulation–more in cold weather

Progressive weakness to all muscle groups –dystrophy:
ptosis, bland expression, temporal atrophy, hands, feet, face, neck flexors, frontal balding

  • CRANIAL NERVE INVOLVED
  • BULBAR INVOLVED: swallow, chew, speech, weak

PT tx: functional sx,: AFO, ADL, AD, eval, home assess

73
Q

Duchennes Muscular Dystrophy

A

x linked

  • gowers sign, meryon sign (lift under axilla and not shoulder depress bv weak extensors)
  • LE weak (thigh and hip muscles 1st) –> then proximal shoulder and arm
  • enlarged calves

Wc by 10-12 yrs

POSTURE: to move wt line post hip, ant knee
Lumbar lordosis, hip abduction, hip flexion (weak extensors), knee flexion, equinovarus (hand on hip)–walk in abduction, PF + inversion

  • TIGHT: gastroc, TFL, illiopsoas*
    (contractures: sacromere shorten)

GIVE STEROIDS

Death: cardiac/pneumonia

PT tx: strengthen low intensity (3-5 reps/dont want disuse atrophy of the ones they dont use, not to fatigue), stretch, ADL, respiratory (weak resp muscles), keep mobility, scoliosis if iin wc, positioning (leg in extension), nightsplints,

  • orthotics when cannot climb stairs, LLB, tilt table
  • if surgery make them ambulatory the nxt day
74
Q

What is tight in Duchennes Muscular Dystrophy

A

TIGHT: gastroc, TFL, illiopsoas***

Age 2-3: illiopsoas
Age 3-4: heelcord
Age 4: TFL

75
Q

Duchennes Muscular Dystrophy tx

A

PT tx: strengthen low intensity (3-5 reps/dont want disuse atrophy of the ones they dont use, not to fatigue), stretch, ADL, respiratory (weak resp muscles), keep mobility, scoliosis if iin wc, positioning (leg in extension), nightsplints,

stretch: gastroc, TFL, illiopsoas***
Age 2-3: illiopsoas
Age 3-4: heelcord
Age 4: TFL

76
Q

which has enlarged calves

A

DMD

77
Q

which has popeye arm

A

Limb Girdle Muscular Dystrophy

78
Q

Scoliosis bracing

A

Boston low profile: clamshell
dynamic pad for counterpressure
cushion fabricated

Rigo cheneu orthotic: schroth: mult pts of pressure to leave open areas at CONCAVE side of curve so person can try to self correct in brace

75-90% ots with DMD

surgery vs conservative was same results by age 17

79
Q

Hoehna and Yard Stage 1

A

Mild UNILATERAL Disease:

1) impaired Diadochokinesis (rapid alternating: they have slow movements)
2) decreased FASCIAL EXPRESSION
3) decreased INITIATION of movements,
4) decreased speech VOLUME
5) loss of some EQUILIBRIUM REACTIONS
6) Slight RIGIDITY

Balance ok

Gait Ok

ADL ok

80
Q

Hoehn and Yahr Scale:

Stage 2:

A

STAGE 2: bilateral involvement

1) independent ADL
2) IMPAIRED POSTURE, postural changes,
3) BILATERAL RESTING TREMOR
4) BRADYKINESIA, DECREASED SPONTANEOUS movements
5) NO FACIALl expressions
6) SHUFFLING gait, difficulty TURNING
7) DEPRESSION

Postural changes (more flexed)

Gait Changes (shuffling gait, difficulty turning, less armswing, less trunk rotation)

FUNCTIONAL FOR ADL

81
Q

Hoehn and Yahr Scale:

Stage 3

A

BILATERAL INVOLVEMENT; MODERATE DIFFICULTY IN ADL

1) BALANCE IMPAIRED
2) loss of equilibrium reactions (no protective reactions)
3) Bradykinesia, akinesia

4) retropulsion: forward chasing of COG:
smaller more rapid steps with trunk flexed forward

5) FREEZING during gait (they know what they want to do but cant do it)
6) horrendous turning during gait
7) difficulty with dressing (initiation-not apraxia), ADL DIFFICULT

Impaired Balance

Impaired gait: retropulsion, freezing, bad turning

ADL: difficult

82
Q

Hoehn and Yahr Scale:

Stage 4:

A

SEVERE DISABILITY, MARKED GAIT DISTURBANCE

1) RIGIDITY increased
2) worse bradykinesia–>AKINESIA
3) bed mobility difficult (not weakness, a motor control issue)
4) “poor” balance
5) decreased dexterity
* ALL ADL DECREASED*

83
Q

Hoehn and Yahr Scale:

Stage 5:

A

CONFINED TO WC OR BED

1) non-ambulatory
2) severe rigidity
3) bradykinesia, akinetic: very few voluntary movements
4) Flexion posture
5) Drooling, dysphagia (eating difficult)
6) Decubeti (bed position, contractures and skin breakdown)
7) respiratory function decreased due to akinesia

AKINESIA: few voluntary movements

84
Q

PSP

progressive supranucleus palsy

A

cannot do up and down gaze

similar to PD

*face expression and back head tilt (to see up) key features

work on balance and eyes

the SCALE for psp only documents function, not for dx

85
Q

Dystonia

A

torticollis most common

also can be foot and hand

ABNORMAL INVOLUNTARY MOVEMENTS

sustained muscle contractions that produce twisting and repete motions and abnormal posturing

UKNOWN CAUSE
tx:

86
Q

Essential Tremor

A

happens when moving (unlike PD)

progresss slowly

87
Q

Huntingtons

A

CNS degeneration, choreaform movements –rapid, no purpose uncoordinated

high dopamine

weird gait

decrease mental function, ocular movements deteriorate, head and neck control too

cerebral and caudate nucleus issue

tx with adding Ach or getting rid of dopamine (opposite of PD)

***RESPIRATORY THERAPY

88
Q

Wilsons Disease

A

extrapyramidal (like PD) but under age 40

cannot metabolize COPPER and neurotoxic level: TREATABLE

medication to bind to copper to remove it

נאורו של קליניק (8 decks)

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