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Clin Med B 2 > Lecture 12: Movement Disorders > Flashcards

Lecture 12: Movement Disorders Flashcards

1
Q

What two parts of the brain are more associated with movement disorders?

A
  • Basal ganglia
  • Thalamus
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2
Q

What are the 3 NTs associated with movement disorders and what do they do?

A
  1. Dopamine: interneuronal communication and Inhibition of ACh
  2. GABA: Relaxes muscles and allows motor control
  3. ACh: NT at NMJ that increases neuronal excitability in CNS and Neuromodulator in PNS.
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3
Q

What is a tremor?

A

Impairment of regulation of voluntary motor activity

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4
Q

What is the most common movement disorder?

A

Tremor

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5
Q

What are the two causes of tremors?

A
  • Alternating antagonist muscle action
  • Synchronous antagonist muscle action
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6
Q

What are the types of tremors?

A
  1. Resting
  2. Action Postural: Attempting to maintain a specific posture (Think romberg)
  3. Action Kinetic: During voluntary movement
  4. Action Isometric: Muscle contraction against a stable object
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7
Q

What are the 3 types of action kinetic tremors?

A
  • Simple kinetic: non-target directed (pronation-supination)
  • Intentional: worsens approaching a target (eating)
  • Task-specific: think writing
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8
Q

What frequencies are considered fast and slow for tremor?

A
  • Slow: < 4 Hz
  • Fast: > 12 Hz
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9
Q

What are the descriptors for tremors?

A
  1. Frequency
  2. Amplitude
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10
Q

What is the MC type of action tremor and when is it present?

A

Enhanced physiologic tremor present only when sympathetic activation

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11
Q

What resolves an enhanced physiologic tremor?

A

Removal of precipitating cause

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12
Q

What i the most common adult onset movement disorder and when does it occur?

A

Essential tremor around 35-45

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13
Q

What is the underlying pathophysiology for an essential tremor and what is a common factor in a lot of patients with ETs?

A
  • Altered cellular activity in the ventral intermediate nucleus of the thalamus
  • Family history
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14
Q

How does an essential tremor present?

A
  • Bilaterally, hands and arms
  • Postural and kinetic properties
  • Most pronounced during drinking from a glass or F-N testing
  • Resolves with rest
  • Difficulty with fine motor activity
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15
Q

What exacerbates ETs?

A
  • Emotion
  • Hunger
  • Fatigue
  • Temperature extremes
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16
Q

What improves ETs?

A

Alcohol

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17
Q

What is the diagnostic criteria for ET?

A
  • Isolated tremor consisting of bilateral UE action without other motor abnormalities
  • 3y in duration
  • W or w/o tremors in other locations
  • Absence of other neurologic signs
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18
Q

How do you differentiate between enhanced physiological tremor and essential tremors?

A

Enhanced physiological tremors Worsen with caffeine and improve by removing the precipitating cause

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19
Q

When do we treat an ET?

A

Intermittent or persistent Disability

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20
Q

How do we treat intermittent ET?

A
  • 1st-line: Propranolol and Primidone (slower onset)
  • 2nd-line: xanax or klonopin
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21
Q

How do we manage persistent ET?

A
  • 1st-line: propanolol or primidone daily. or both! (combo)
  • 2nd-line: gabapentin, pregabalin, topiramate.
  • 2nd-line: Neurologist for botox A or surgical intervention via deep brain stim or thalamotomy
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22
Q

When is surgery indicated for ET? CI?

A
  • Indication: Failure of 2 oral regimens
  • CI: dementia, severe cognitive impairment, or uncontrolled anxiety/depression
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23
Q

What are the two neurosurgical procedures for treatment of ET?

A
  1. Thalamic ventralis intermedius (VIM) nucleus DBS
  2. MRI-guided focused US thalamotomy (opposite of affected arm)
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24
Q

What activity tests for intention/kinetic tremor?

A

F-N testing, which should reveal increasing severity as the movement becomes closer to the target

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25
Q

What is a holmes-stewart maneuver?

A

Inability to control rebound from a release of flexion against resistance

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26
Q

Damage to what may cause intention/kinetic tremor?

A
  • Midbrain
  • Thalamus
  • Cerebellum
  • Pons

Balance related

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27
Q

How do you manage an intention tremor?

A

Refer to neuro for surgery

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28
Q

What is dystonia?

A

Sustained or repetitive involuntary muscle contractions, frequently causing patterned, twisting movements, and/or abnormal posture

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29
Q

What worsens dystonia and improves it?

A
  • Worsening: Voluntary movement, stress & fatigue
  • Improving: Active relaxation and sensory tricks
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30
Q

What is the underlying physiology that causes dystonia?

A

Involuntary contraction of both agonist and antagonist muscles

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31
Q

What does generalized dystonia usually involve at minimum?

A

Torso and limbs

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32
Q

What is the MC form of focal dystonia?

A

Cervical dystonia/torticollis

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33
Q

When is the MC onset for torticollis?

A

30-50

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34
Q

What causes torticollis?

A

Abnormal contraction of neck muscles (SCM, traps, posterior cervical)

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35
Q

What triggers UE dystonias?

A

Repetitive activities and task-specific dystonias

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36
Q

What are the MC types of task-specific dystonias?

A
  • Writer’s cramp (MC)
  • Muscician’s
  • Putting in golf (yips)
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37
Q

When is the MC onset for UE dystonias?

A

10-50

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38
Q

What is involved with oromandibular dystonia? (OMD)

A

Masticatory, lingual, pharyngeal muscles

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39
Q

What two conditions are commonly associated with OMD?

A
  • Blepharospasm
  • Torticollis
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40
Q

How does blepharospasm usually present?

A
  • Bilateral
  • Synchronous
  • Symmetric
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41
Q

What is involved in spasmodic dysphonia?

A
  • Laryngeal muscles causing contraction of the vocal cords during speech
  • Characterized by irregular and involuntary voice breaks
  • pts often feel like they have to yell
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42
Q

How do we manage spasmodic dystonia?

A
  • Refer to movement disorder specialist
  • Botox (BoNT) injection
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43
Q

How do we treat generalized dystonia?

A

Trial of levodopa/carbidopa

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44
Q

What are the pharmacotherapies for generalized dystonia in adults?

A
  1. 1st-line: Clonazepam (GABA)
  2. Second-line: Baclofen (GABA agonist) or trihexyphenidyl (anticholinergic which increases dopamine release)
  3. Alternative second-line: VMAT2 inhibitor (-benazine and off-label use)
  4. Last resort: DBS
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45
Q

What are the pharmacotherapies for generalized dystonia in children?

A
  1. trihexyphenidyl
  2. Baclofen and BZDs
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46
Q

What is the MCC of infantile torticollis?

A

Damage or inflammation to SCM or traps.

R/o infectious etiology

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47
Q

How do you treat infantile torticollis?

A
  • NSAIDs
  • Soft cervical collar PT
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48
Q

Describe restless leg syndrome (RLS)

A

Idiopathic neurological movement disorder of limbs most associated with sleep complaint

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49
Q

What is the common demographic for RLS?

A
  • Middle aged and older
  • White women
  • Familial
  • Pregnancy
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50
Q

What nutrient deficiency is MC implicated in RLS?

A

Iron deficiency anemia

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51
Q

What are the risk factors for RLS?

A
  • Frequent blood donation
  • DM
  • Chronic alcohol use
  • Amyloidosis
  • Motor neuron disease
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52
Q

How does RLS present?

A
  • Not painful but bothersome
  • Irresistible urge to move the legs
  • Temporary relief after movement
  • Worse in the evenings or inactivity
  • Daytime fatigue
  • Insomnia
  • Involuntary, jerking limb movements
  • Anxiety or depressive symptoms related to chronic sleep deprivation
53
Q

What are the aggravating factors for RLS?

A
  • Caffeine
  • Sleep deprivation
  • Antihistamines, Dopamine antagonists (METOCLOPRAMIDE), antidepressants
54
Q

How do we work-up RLS?

A
  • Lots of labs
  • Iron studies
55
Q

Which iron lab is most indicative for actual iron levels in the body?

A

Ferritin < 75 mcg/L

56
Q

What medications are used to help treat RLS?

A
  • Alpha-2-delta calcium channel ligands: Gabapentin, Pregabalin, Gabapentin encarbil
  • Dopamine agonists: Pramipexole, ropinirole, rotigotine (patch)

Alpha-2: Risk of dependece and addiction
Dopamine agonists: oral forms have a risk of augmentation as well as impulse control disorder.

57
Q

How do you prevent augmentation of RLS due to dopamine agonists?

A

Holidays

58
Q

What does augmentation of RLS look like?

A
  • Earlier onset of symptoms
  • Increased intensity of symptoms
  • Shorter duration of drug action
59
Q

What is Tourette’s?

A

Neurological disorder characterized by chronic motor and vocal tics prior to adulthood

60
Q

What is the demographic for Tourette’s (TS)?

A
  • Males
  • 6-11 y/o
  • Potentially genetic
61
Q

What are the suggested risk factors for TS?

A
  • Smoking during pregnancy
  • Complications during pregnancy
  • Low birth weight
62
Q

What is the hypothesis behind TS pathophysiology?

A

Disorder of Neurotransmission in the mesolimbic circuit, disinhibiting the motor and limbic systems.

63
Q

What exacerbates TS?

A

Fear or anxiety

Can sometimes be voluntarily suppressed

64
Q

What are the tic types in TS?

A
  1. Motor (MC initial and in the face)
  2. Phonic tics
  3. Sensory tics
65
Q

Difference between echolalia and palilalia and coprolalia?

A
  • Echolalia: Repeating someone’s words
  • Palilalia: Repeating the same word
  • Coprolalia: Cussing uncontrollably
66
Q

What are psychiatric conditions is TS often associated with?

A
  • OCD/ADHD
  • Behavioral problems
  • Mood disorders
67
Q

What is the diagnostic criteria for TS?

A
  • Motor and vocal tics prior to 21.
  • Must occur multiple times per day, almost everyday for a year
  • Tics must change over time
  • Must affect daily functioning
  • Must be witnessed by a reliable examiner or recorded on video
68
Q

What are the indications for treating TS?

A
  • Affecting ADLs, and daily life in general.
  • Causes pain, discomfort, or injury
69
Q

What is the non-pharmcologic therapy for TS?

A
  • Habit reversal: Tic-awareness training or competing-response treatment
70
Q

What are the 1st-line drugs for TS? 2nd-line?

A
  1. FDA approved: Haldol, primozide, aripiprazole
  2. Non-FDA approved: VMAT2 inhibitor (tetrabenazine), clonidine, guanfacine

Clonidine cheaper
Guanfacine less SE

71
Q

What are the last resort options for TS?

A
  • Botox A
  • Bilateral high frequency brain stimulation
72
Q

What is Huntington’s disease? (HD)

A
  • Hereditary disorder
  • Gradual onset of chorea and dementia
73
Q

What is the pathophysiology of HD?

A
  • Autosomal dominant
  • Neuronal cell loss in cerebral cortex and corpus striatum

Any carrier will develop HD.

74
Q

What is chorea?

A
  • Brief, abrupt, involuntary, large movements
  • Loss of voluntary motor control
  • Hypotonia with hyperreflexia
  • Loss of voluntary eye control

Think of inflatable men at car dealerships

75
Q

What are the non-motor S/S of HD?

A
  • Wt loss and cachexia
  • Mental status changes, eventually ending in dementia
76
Q

How do you work-up HD?

A
  • Genetic testing for HTT gene
  • CT or MRI showing atrophy of cerebral cortex or caudate nucleus. (Not needed for dx)
77
Q

What medications may help with HD?

A
  • Motor: VMAT2 inhibitors (xenazine, deutetrabenazine, and valbenazine) & 2nd-gen antipsychotics (haldol, pimozide, aripiprazole)
  • Psychiatric: SSRIs
78
Q

If a patient has suspected HD or asks about testing, what should we do?

A

Recommend a genetic counselor to test it.

79
Q

What is parkinsonism?

A

Any conditions causing a combination of movement abnormalities.

  • Tremor
  • Slow movement
  • Impaired speech
  • Muscle stiffness
  • Loss of dopamine containing neurons
80
Q

What is Parkinson’s disease? (PD)

A
  • 2nd MC neurodegenerative disease (Alzheimer is MC)
  • Slowly progressing disease characterized by tremor, bradykinesia, rigidity, and postural instability
  • MC in men
  • MC form of parkinsonism
  • Onset after 60
81
Q

What factors reduce risk of PD?

A
  • Caffeine
  • Ibuprofen
  • Statins
  • Smoking
  • Moderate exercise
82
Q

What factors increase risk of PD?

A
  • Age
  • Family Hx
  • Pesticides/herbicides
83
Q

What is the pathophysiology of PD?

A
  • Degeneration of the dopamine-producing neurons in the substantia nigra
  • Imbalance between dopamine and ACh
  • Lewy bodies
  • Depletion of dopamine.

Low dopamine = slow voluntary motor control
High ACh = dyskinesia

84
Q

How does PD present?

A
  1. Tremor resting and fine (MC)
  2. Rigidity
  3. Bradykinesia
  4. Postural instability

Tremor is often described as pill-rolling

85
Q

What aggravates and alleviates the resting tremor in PD?

A
  • Aggravating: emotional stress or increase in mental activity
  • Alleviating: voluntary movement
  • Will spread up the body unilaterally.
86
Q

What are the rigidity types that may appear in PD?

A
  • Unilaterally initially on same side as tremor
  • Cogwheel (ratchety pattern)
  • Lead pipe (persistent)
87
Q

What is the major cause of disability in PD?

A

Bradykinesia

88
Q

What does bradykinesia look like in PD?

A
  • Loss of distal first
  • Loss of fine motor skills of fingers
  • Loss of normal arm swing during walking
  • Shuffling gait, Frequent falls
  • Mask-like face with infrequent blinking
  • Soft, poor quality voice
89
Q

What test and sign is associated with postural instability?

A
  • Pull test
  • Myerson sign: tapping over the bridge of the nose and produces sustained blink
90
Q

How do we diagnose PD?

A
  • Bradykinesia with rigidity or tremor
  • Must respond to a dopaminergic agent (if no response, prob not PD)
  • No muscle weakness or DTR changes
91
Q

How do we manage PD?

A
  • Neuro consult
  • PT/OT/ST
  • Pharm goal: increase dopamine while reducing ACh
92
Q

For minimal PD, what drugs are indicated?

A
  • Young patients with tremor: Anticholinergics such as benztropine and trihexyphenidyl to reduce ACh present in NMJ.
  • NMDA receptor antagonists: Amantadine to improve motor, making more dopamine
  • MAOI: selegiline, rasagiline, and safinamide to prevent early metabolism of dopamine, alleviating the minimal S/S of PD.
93
Q

For moderate PD, waht drugs are indicated?

A
  • Dopamine agonists in younger pts: pramiprexole, ropinirole, rotigotine (patch)
  • Carbidopa/levodopa for older pts.
94
Q

For severe PD, what is the main drug of choice?

A
  • Carbidopa/levodopa (Sinemet)
  • Prevents breakdown of levodopa prior to crossing the BBB.
  • take on empty stomach and avoid high protein diet
  • best for controlling bradykinesia
95
Q

What are COMT inhibitors used for and what are they?

A
  • Preventing the early breakdown of levodopa
  • Entacopone (5x a day) and tolcapone (3x a day, but associated with liver and hepatic necrosis)
  • Stalevo: entacopone + levodopa/carbidopa
96
Q

What are the more specialized therapies for PD?

A
  • Dementia: ACh inhibitors & memantine
  • Psychosis: atypical antipsychotic: quetiapine
97
Q

What are the invasive therapies for PD?

A
  • DBS: AVOID IN COGNITIVE DYSFUNCTION
  • Continuous levodopa-carbidopa intestinal gel (LCIG)
  • Convential vs MRI guided US: thalamotomy, subthalamotomy, pallidotomy
98
Q

What is ataxia?

A

Loss of full control of bodily movement

99
Q

What are the underyling anatomical lesions associated with ataxia?

A
  • Cerebellar hemispheres
  • Midline cerebellum (cerebellar vermis, spinocerebellum, and vestibulocerebellum)

Midline: Gait, balance, ocular
Hemispheres: Dysdiadochokinesias, dysmetria, limb ataxia, tremor, speech

100
Q

What are the 3 types of ataxia?

A
  • Motor/cerebellar ataxia
  • Sensory/proprioceptive ataxia
  • Vestibular ataxia
101
Q

What does motor/cerebellar ataxia look like?

A
  • Imbalance and coordination
  • Ataxic gait (drunk)
  • Unclear (scanning) speech
  • Nystagmus => visual blurring
  • Loss of hand coordination
  • Intention tremor
102
Q

What is the underlying pathophysiology behind sensory/proproceptive ataxia?

A
  • Inadequate transmission of positional info to the CNS.
  • Results from disorders of peripheral nerves, spinal cords, or cerebellar input tracts
103
Q

How does sensory/proprioceptive ataxia present?

A
  • Abnormal F-N with closed eyes
  • Abnormal vibratory sense
  • Positive romberg
  • Unsteady gait with closed eyes
  • Stomping gait
104
Q

What is the underyling pathophysiology behind vestibular ataxia?

A

Dysfunction of the inner ear

105
Q

How does vestibular ataxia present?

A
  • N/V
  • Vertigo/dizziness
  • Disequilibrium
  • Gravity dependent ataxia (incoordination during standing/walking) & deviation of gait to side of affected ear
  • Nystagmus Most pronounced when patients gazes away from affected ear
106
Q

Pramipexole/Mirapex MOA, indications, metabolism, special pharmacokinetics

A
  • MOA: Non-ergot dopamine agonist, working on D2 dopamine receptors
  • Indications: RLS, mild Parkinson’s
  • Metabolism: urinary
  • Special pharmacokinetics: extended in elderly patients (12 hrs)
107
Q

Pramipexole/Mirapex SEs

A
  • Nausea
  • Somnolence
  • Fatigue
  • HA
  • PD: orthostatic hypotension, constipation, dyskinesia, somnolence, dizziness, hallucinations, imsomnia, weird dreams
108
Q

Pramipexole/Mirapex DDI

A
  • Alcohol
  • Dopamine antagonists

It is an agonist

109
Q

Ropinirole/Requip MOA, Indications, Metabolism

A
  • MOA: Non-ergot dopamine agonist, D2 and D3 dopamine receptors
  • Indications: RLS, mild parkinson’s
  • Metabolism: Liver
110
Q

Ropinirole/Requip SEs

A
  • Syncope
  • Somnolence
  • Dizziness
  • Fatigue
  • N/V
  • Viral infection
  • Dyskinesias
111
Q

Ropinirole/Requip DDI

A
  • Alcohol
  • Dopamine antagonists
  • CNS depressants
  • Estrogens
  • Cipro
112
Q

Rotigotine/Neupro MOA, Indications, Pharmacokinetics, Metabolism

A
  • MOA: non-ergot dopamine agonist, D1, D2, D3 receptors
  • Indications: RLS, parkinson’s
  • Pharmacokinetics: patch form, lasts 5-7 hours post patch and 15-18 upon application
  • Metabolism: NONE
113
Q

Rotigotine/Neupro SEs

A
  • Site reaction
  • Hypotension
  • Nausea
  • Somnolence
  • Dizziness
  • Dyskinesia

The least SEs between pramipexole, ropinirole, and rotigotine.

114
Q

Rotigotine/Neupro DDIs

A
  • Alcohol
  • Dopamine antagonists
  • Anti-HTNs
115
Q

Tetrabenazine/Xenazine MOA, indication, metabolism

A
  • MOA: VMAT2 inhibitor, inhibiting release of dopamine, noradrenaline, and serotonin
  • Indication: Huntington’s
  • Metabolism: Liver
116
Q

What patients should NOT use tetrabenazine?

A
  • Active SI
  • Uncontrolled depression
  • Hepatic impairment
  • MAOi use in 14d
  • Reserpine use in past 20d
117
Q

What syndrome is associated with use of tetrabenazine?

A

Neuroleptic malignant syndrome (NMS)

118
Q

Amantadine MOA, indications, Metabolism

A
  • MOA: NMDA antagonist, inhibiting NMDA-glutamate and muscarinic receptors; **stimulates dopamine release **
  • Indications: Parkinsonism, Extrapyramidal symptoms, flu
  • Metabolism: liver

Extrapyramidal: Voluntary movements now being uncontrolled

119
Q

Amantadine DDIs

A
  • Alcohol: dizziness/circulation
  • Tramadol: Seizures
120
Q

Amantadine SEs

A
  • Restlessness
  • Confusion
  • Skin rashes
  • Edema
  • Disturbances of cardiac rhythm
121
Q

What are the MAOB inhibitors and their main indications and MOA?

A
  • Selegiline, Rasagiline, and safinamide
  • Indications: Monotherapy OR adjunct with levodopa for PD
  • MOA: Increases dopamine conc in striatum
122
Q

What are the risks associated with MAOB inhibitor use?

A
  • Orthostatic hypotension
  • Serotonin syndrome
  • Psychotic episode with concomitant use of st johns or DXM

DXM = dextromethorphan (cough syrup)

123
Q

What is levodopa and carbidopa?

A
  • Levodopa = precursor of dopamine
  • Carbidopa = inhibits the enzyme that breaks down levodopa in the peripheral circulation
124
Q

What is the main purpose of carbidopa and what is the main symptom that carbidopa/levodopa help with?

A
  • Carbidopa lowers the amount of levodopa needed.
  • Carbidopa/levodopa is primarily for bradykinesia in PD, and is First-line therapy for symptomatic PD
125
Q

What are the contraindications to carbidopa/levodopa?

A
  • MAOi use
  • Psychosis
  • Melanoma
  • Narrow angle glaucoma
126
Q

What kind of diet should you avoid when taking carbidopa/levodopa?

A

High protein diets

127
Q

What is entacapone used for?

A

It is a COMT inhibitor used to stabilize plasma levels of dopamine as adjunct therapy with levodopa.

128
Q

How is entacapone excreted?

A

Liver

Clin Med B 2 (44 decks)

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