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Clin Med, Path, Pharm > Movement Disorders > Flashcards

Movement Disorders Flashcards

1
Q

What are the four cardinal manifestations of Parkinson’s disease?

A

Tremor, bradykinesia, rigidity, postural instability (gait disturbance)

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2
Q

Most common presenting symptom of PD

A

Tremor (pill rolling, resting tremor)

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3
Q

A pt complains of weakness, tiredness, and decreased manual dexterity of the fingers. What do we call this?

A

Bradykinesia

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4
Q

Ratchety pattern of resistance and relaxation as the examiner moves the limb through ROM

A

Cogwheel rigidity

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5
Q

What causes cogwheel rigidity?

A

In PD, from tremor superimposed on increased tone

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6
Q

Feeling of imbalance and tendency to fall

A

postural instability

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7
Q

Least responsive symptom of PD to dopaminergic therapies

A

Postural instability

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8
Q

difficulty initiating gait

A

freezing

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9
Q

short stepped gait

A

festination

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10
Q

A neurotransmitter that is responsible for motor control, motivation, and arousal

A

Dopamine

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11
Q

Enzymes that break down dopamine in the synapse

A

MAO and COMT

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12
Q

Where are dopamine neurons found?

A

Substantia nigra
Part of the basal ganglia
Part of the midbrain

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13
Q

The loss of dopamine _____ (increases, decreases) the excitatory drive in BG and disrupts voluntary motor control causing PD symptoms

A

increases

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14
Q

Abnormal proteins that develop inside the neurons of those with PD

A

Lewey Bodies

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15
Q

Characterized by visual hallucinations, fluctuating cognition, and parkinsonism

A

Dementia with Lewey Bodies

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16
Q

How do you distinguish corticobasal degeneration from PD?

A

Corticobasal degeneration:

  1. Does not have tremor
  2. Does not respond to levodopa
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17
Q

Presents with parkinsonism, dysautonomia, cerebellar involvement, and pyramidal signs.
No tremor, doesn’t respond to levodopa

A

Multiple System Atrophy

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18
Q

What meds are more likely to cause secondary parkinsonism?

A

Antipsychotics

Reglan

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19
Q

Most common form of secondary parkinsonism?

A

Drug-induced

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20
Q

What drugs cause tardive dyskinesia?

A

Antipsychotic drugs and metoclopramide (reglan)

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21
Q

What else can cause secondary parkinsonism besides meds?

A 
Toxins
Brain lesions
Trauma
Metabolic disorders
Infections
Cerebrovascular disease
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22
Q

How is PD diagnosed?

A

Gold standard is neuropathologic examination

No physiologic or blood tests exists

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23
Q

Most effective drug for symptomatic treatment of PD

A

Levodopa

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24
Q

What does the addition of carbidopa prevent when given in combination with levodopa?

A

N/V, orthostatic hypotension

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25
Q

What is Sinemet primarily effective for?

A

Bradykinesia

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26
Q

SE of Sinemet

A

Motor Complications (Dyskinesia, dystonia, freezing episodes)
dry mouth
mood changes
hallucination

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27
Q

Sinemet is C/I in who?

A

narrow angle glaucoma

Use of MAOIs within the last 2 weeks

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28
Q

Sinemet patient education

A

Take 30 minutes before meals
Don’t withdrawal rapidly–risk of neuroleptic malignant syndrome
Don’t take if you’ve taken MAOIs in the last 2 weeks

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29
Q

A pt presents with MS change, rigidity, fever, and dysautonomia. What are you worried about?

A

Neuroleptic malignant syndrome

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30
Q

What is the advantage of dopamine agonists over levodopa?

A

Longer duration of action

less motor fluctuations

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31
Q

SE of dopamine agonists

A

Impulse control disorder, peripheral edema

Can be avoided by initiating treatment in small doses

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32
Q

C/I of dopamine agonists

A

Breastfeeding

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33
Q

What are the dopamine agonists?

A

Ropinirole (Requip)
Pramipexole (Mirapex)
Bromocriptine (Cycloset)

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34
Q

A patient on dopamine agonists presents to you with anxiety, sweating, nausea, pain, and dizziness. What do you ask them?

A

Did you stop taking your DAs suddenly?

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35
Q

A 70 year old pt is put on a Sinemet for her PD. She shows no improvement. You decide to put her on a DA next. Is this okay?

A

No

DAs are ineffective in pts who have shown no response to levodopa

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36
Q

May be useful in pts with early PD

May be neuroprodective

A

MAOI
Rasagiline (Azilet)
Selegiline (Eldepryl)

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37
Q

-giline

A

MAOI

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38
Q

Patient education with rasagiline (Azilect)

A

C/I in liver disease

Avoid tyramine containing foods –> high BP

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39
Q

Patient education wiht selegiline (Eldepryl)

A

Can cause insomnia and confusion

Avoid with TCA or SSRIs

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40
Q

Antiviral that may reduce intensity of levodopa-induced dyskinesia and motor fluctuations

A

Amantadine (Symmetrel)

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41
Q

SE of Amantadine

A

Ankle edema, livedo reticularis, confusion, hallucinations

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42
Q

COMT inhibitor

A

Entacapone (Comtan)

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43
Q

Mostly used as an add on to treat patients iwth motor fluctuations who experience end of dose “wearing off”

A

Entacapone (Comtan)

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44
Q

Patient education for Comtan

A

Ineffective when given alone
Just a levodopa extender.
May cause dyskinesia

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45
Q

Non-Pharmocologic Tx for PD

A

Educations, therapy, nutrition, emotional support

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46
Q

Most frequently performed surgical procedure for the treatment of advanced PD

A

Deep brain stimulation

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47
Q

How long is DBS effective after treatment?

A

3-5 years after electrode implantation

48
Q

How does DBS work?

A

It blocks the abnormal nerve signals that cuase tremor and PD symptoms

49
Q

Seldom performed procedures except in regions where DBS is unavailable or not affordable. Uses liquid nitrogen to kill nbrain tissue

A

Thalamotomy and Pallidatomy

50
Q

Place dopamine producing cells in or near sites in the brain where dopamine production is lacking

A

Neural transplantation

51
Q

Alternating contractions of agonist and antagonist muscles in an oscillating, RHYTHMIC manner.

A

Tremor

52
Q

Type of tremor in PD

A

Resting tremor

53
Q

Type of tremor in essential tremor

A

Postural (ask pt to hold arms out forward, hands shake)

54
Q

Type of cerebellar tremor

A

Intentional or kinetic tremor (touch finger to nose)

55
Q

Most common movement disorder

A

Essential tremor

56
Q

High frequency tremor that predominantly affects the upper extremities. Manifests as postural or kinetic tremor.

A

Essential tremor

57
Q

Essential tremor is typically (bilateral/unilateral) and (symmetric, assymetric)

A

bilateral and symmetric

58
Q

Essential tremor most often involves what?

A

the head

59
Q

Tremor that is characteristically improved with alcohol and worse with stress

A

Essential tremor

60
Q

What is a difference between essential tremor and PD?

A

ET does not have cogwheel rigidity

61
Q

Treatment of mild cases of ET

A

reassurance

62
Q

Treatment of severe cases of ET that interfere with eating, writing, ADLs

A

beta blockers (propanolol) or mysoline (primidone)

63
Q

Vertigo, rash, agranulocytosis, and loss of appetite are side effects of what drug?

A

Mysoline (Primidone)

64
Q

What drug metabolizes to phenobarbital and raises the seizure threshold?

A

Mysoline (Primidone)

65
Q

What treatment might be helpful for limb or voice tremor?

A

Botox

66
Q

Which antiseizure meds may help with tremor?

A

Topiramate (Topamax) and Gabapentin (neurontin)

67
Q

Sustained or repetitive involuntary muscle contractions frequently associated with twisting or repetitive movements and abnormal posture

A

Dystonia

68
Q

How is dystonia classified?

A

Age of onset (childhood, vs adult)
Distribution (focal, multifocal, segmental, general)
Etiology (primary or secondary)

69
Q

Most common forms of dystonia

A

Facial dystonia.

Blepharospasm and Oromandibular dystonia

70
Q

Involuntary dystonic contractions of eyelids; blinking that can interfere with daily activities

A

blepharospasm

71
Q

Dystonic contractions of muscles of the lower face, lips, tongue, and jaw

A

Oromandibular dystonia

72
Q

Dystonic contractions of the vocal cords causing impaired speech (strained or whispering quality of speech)

A

Spasmodic dystonia

73
Q

Dystonic contractions of the neck muscles causing head to deviate to one side, forward, or backward

A

Cervical dystonia

74
Q

Writer’s cramp and musician’s cramp are examples of this

A

Limb dystonia

75
Q

Likely a source for some dystonias

A

Basal ganglia

76
Q

Dopaminergic therapy can (induce, treat) dystonia

A

both!

77
Q

Treatment of dystonia

A

Mostly symptomatic
Baclofen
Botox

78
Q

First line treatment for cervical dystonia

A

Botox

79
Q

What are the three characteristics of Hungtington’s disease?

A

Choreiform movements
Psychiatric problems
Dementia (can’t make decisions and multi-task)

80
Q

Rapid, jerky, nonrepetitive or ARRHTYMIC movements involving hte face, trunk, and limbs

A

Choreiform movements

81
Q

What might you see regarding the eye exam in a HD pt?

A

Delay in initiation of saccadic eye movements (pt can’t follow your finger right and left)

82
Q

Average age of death of HD

A

60

83
Q

Common symptom of HD that’s not in the main 3

A

Weight loss/cachexia

84
Q

What 3 categories are HD symptoms put in?

A

Neurologic (movements, reflexes, gait)
Psychiatric (mood, delusions)
Cognitive (thought, concentration, memory)

85
Q

Pathophys of HD

A

trinucleotide expansion of HTT gene which makes hte huntington protein toxic. Repeat numbers of the expanison >38 is diagnostic for HD

86
Q

Treatment of HD

A

No known cure
Symptomatic management. PT, OT, ST
(manage chorea, psychosis, and depression)

87
Q

FDA approved treatment for chorea in HD

A

Tetrabenazine (Xenozine)

Reduces dopamine transmission

88
Q

Used in HD patient wiht psychosis and chorea

A

Neuroleptics (Olanzapine, Risperidone, Quitiapine, Arpiprazole, Haldol)

89
Q

Last resort option for chorea in HD

A

Amantadine

RIluzole

90
Q

Characterized by multiple motor tics that are often accompanied by vocalizations (phonic tics)

A

Tourette’s

91
Q

Brief, rapid, recurrent and seemingly purposeless stereotyped motor contraction

A

Tic

92
Q

Blinking, jerking of the neck

A

Simple motor tic

93
Q

Jumping, sniffing, head banging

A

Complex motor tic

94
Q

Grunting

A

Simple vocal tic

95
Q

Repeating other people’s words

A

Echolalia

96
Q

Repeating one’s own words

A

Palilalia

97
Q

Expression of obscene words

A

Coprolalia

98
Q

Unpleasant focal sensations in the face, head, or neck

A

Sensory tics

99
Q

What age do tics occur? When do they stop?

A

between 2 and 15

stop in adulthood

100
Q

Associated problems with Tourettes

A

Anxiety, depression, ADHD, OCD, personality disorders, self destructive behaviors

101
Q

Pathophysiology of Tourettes

A

complex inheritance pattern

102
Q

Treatment of mild tourettes

A

education and counseling

103
Q

Treatment of tourettes with tics that are disabling/interfering with quality of life

A 
Clonidine
Guanfacine
Neuroleptics
Antipsychotics (if neuroleptics don't work)
Botox
(Giggles needs a bigger couch)
104
Q

Develops months to years after initiating neuroleptic treatment. Characterized by choreiform movements involving the mouth, lips, and tongue

A

Tardive dyskinesia

105
Q

Treatment of tardive dyskinesia

A

Stop the med. 1/3 have remission within 3 months, most improve over years

106
Q

Primary RLS vs Secondary RLS

A

Primary: genetic, idiopathic, onset at 27
Secondary: associated with pregnancy, anemia, renal failure, peripheral neuropathy

107
Q

What should you always check in someone with suspected restless leg syndrome?

A

Iron level

108
Q

How will the neuro exam be in someone with restless leg syndrome?

A

normal

109
Q

Four core symptoms for diagnosis of RLS

A
  1. Urge to move legs
  2. Sx begin/worsen with rest
  3. Relief with movement
  4. Worse during evening
110
Q

Treatment of RLS

A

Pramipexole (Mirapex) or Ropinirole (Requip)

^^Dopamine agonists

111
Q

Non-pharmacologic treatment of RLS

A

Mental alerting activities
Regular exercise
Leg massage
Heat

112
Q

Gnenetic abnormality inherited in an autosomal recessive manner that leads to impairment of cellular copper transport

A

Wilson’s disease

113
Q

Categories of clinical manifestations of Wilson’s disease

A

Psychiatric
Hepatic
Neurologic

114
Q

Pathophysiology of Wilson’s disease

A

Decreased level of ceruloplasmin (copper carrying protein in the blood)

115
Q

Where does copper accumulate in WIlson’s dz?

A

Liver, brain, and cornea

116
Q

What PE findings would you expect in someone with Wilson’s disease?

A 
Kayser-Fleischer rings (copper can be seen in eyes)
abdominal pain
Jaundice
Hepatomegaly and splenomegaly
Ascites
Upper GI bleeding
MS changes
117
Q

Brownish or gray-green rings that are due to fine pigmented granular deposits of copper in teh cornea.

A

Kayser-Fleischer rings

Clin Med, Path, Pharm (12 decks)

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