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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
What is a holmes-stewart maneuver?
Inability to control rebound from a release of flexion against resistance
26
Damage to what may cause intention/kinetic tremor?
* Midbrain * Thalamus * Cerebellum * Pons | Balance related
27
How do you manage an intention tremor?
Refer to neuro for surgery
28
What is dystonia?
Sustained or repetitive involuntary muscle contractions, frequently causing patterned, twisting movements, and/or abnormal posture
29
What worsens dystonia and improves it?
* Worsening: Voluntary movement, stress & fatigue * **Improving: Active relaxation and sensory tricks**
30
What is the underlying physiology that causes dystonia?
Involuntary contraction of **both agonist and antagonist muscles**
31
What does generalized dystonia usually involve at minimum?
Torso and limbs
32
What is the MC form of focal dystonia?
Cervical dystonia/**torticollis**
33
When is the MC onset for torticollis?
30-50
34
What causes torticollis?
Abnormal contraction of neck muscles (**SCM, traps, posterior cervical**)
35
What triggers UE dystonias?
Repetitive activities and task-specific dystonias
36
What are the MC types of task-specific dystonias?
* **Writer's cramp (MC)** * Muscician's * Putting in golf (yips)
37
When is the MC onset for UE dystonias?
10-50
38
What is involved with oromandibular dystonia? (OMD)
Masticatory, lingual, pharyngeal muscles
39
What two conditions are commonly associated with OMD?
* Blepharospasm * Torticollis
40
How does blepharospasm usually present?
* Bilateral * Synchronous * Symmetric
41
What is involved in spasmodic dysphonia?
* **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**
42
How do we manage spasmodic dystonia?
* Refer to movement disorder specialist * Botox (BoNT) injection
43
How do we treat generalized dystonia?
Trial of levodopa/carbidopa
44
What are the pharmacotherapies for generalized dystonia in adults?
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
45
What are the pharmacotherapies for generalized dystonia in children?
1. trihexyphenidyl 2. Baclofen and BZDs
46
What is the MCC of infantile torticollis?
Damage or inflammation to SCM or traps. | R/o infectious etiology
47
How do you treat infantile torticollis?
* NSAIDs * Soft cervical collar PT
48
Describe restless leg syndrome (RLS)
Idiopathic neurological movement disorder of limbs most associated with **sleep complaint**
49
What is the common demographic for RLS?
* Middle aged and older * White women * Familial * Pregnancy
50
What nutrient deficiency is MC implicated in RLS?
Iron deficiency anemia
51
What are the risk factors for RLS?
* Frequent blood donation * DM * Chronic alcohol use * Amyloidosis * Motor neuron disease
52
How does RLS present?
* 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
What are the aggravating factors for RLS?
* Caffeine * Sleep deprivation * Antihistamines, Dopamine antagonists (**METOCLOPRAMIDE**), antidepressants
54
How do we work-up RLS?
* Lots of labs * **Iron studies**
55
Which iron lab is most indicative for actual iron levels in the body?
Ferritin < 75 mcg/L
56
What medications are used to help treat RLS?
* Alpha-2-delta calcium channel ligands: Gabapentin, Pregabalin, Gabapentin encarbil * Dopamine agonists: Pramipexole, ropinirole, rotigotine (patch) ## Footnote Alpha-2: **Risk of dependece and addiction** Dopamine agonists: oral forms have a **risk of augmentation** as well as impulse control disorder.
57
How do you prevent augmentation of RLS due to dopamine agonists?
Holidays
58
What does augmentation of RLS look like?
* Earlier onset of symptoms * Increased intensity of symptoms * Shorter duration of drug action
59
What is Tourette's?
Neurological disorder characterized by chronic motor and vocal tics **prior to adulthood**
60
What is the demographic for Tourette's (TS)?
* Males * 6-11 y/o * Potentially genetic
61
What are the suggested risk factors for TS?
* Smoking during pregnancy * Complications during pregnancy * Low birth weight
62
What is the hypothesis behind TS pathophysiology?
Disorder of **Neurotransmission in the mesolimbic circuit**, disinhibiting the motor and limbic systems.
63
What exacerbates TS?
Fear or anxiety | Can sometimes be **voluntarily suppressed**
64
What are the tic types in TS?
1. **Motor (MC initial and in the face)** 2. Phonic tics 3. Sensory tics
65
Difference between echolalia and palilalia and coprolalia?
* Echolalia: Repeating someone's words * Palilalia: Repeating the same word * Coprolalia: Cussing uncontrollably
66
What are psychiatric conditions is TS often associated with?
* OCD/ADHD * Behavioral problems * Mood disorders
67
What is the diagnostic criteria for TS?
* 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
What are the indications for treating TS?
* Affecting ADLs, and daily life in general. * Causes pain, discomfort, or injury
69
What is the non-pharmcologic therapy for TS?
* Habit reversal: Tic-awareness training or competing-response treatment
70
What are the 1st-line drugs for TS? 2nd-line?
1. FDA approved: Haldol, primozide, aripiprazole 2. Non-FDA approved: VMAT2 inhibitor (tetrabenazine), clonidine, guanfacine ## Footnote Clonidine cheaper Guanfacine less SE
71
What are the last resort options for TS?
* Botox A * Bilateral high frequency brain stimulation
72
What is Huntington's disease? (HD)
* **Hereditary disorder** * Gradual onset of **chorea and dementia**
73
What is the pathophysiology of HD?
* Autosomal dominant * Neuronal cell loss in cerebral cortex and corpus striatum | Any carrier will develop HD.
74
What is chorea?
* 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
What are the non-motor S/S of HD?
* Wt loss and cachexia * Mental status changes, eventually ending in dementia
76
How do you work-up HD?
* Genetic testing for HTT gene * CT or MRI showing atrophy of cerebral cortex or caudate nucleus. (Not needed for dx)
77
What medications may help with HD?
* Motor: VMAT2 inhibitors (xenazine, deutetrabenazine, and valbenazine) & 2nd-gen antipsychotics (haldol, pimozide, aripiprazole) * Psychiatric: SSRIs
78
If a patient has suspected HD or asks about testing, what should we do?
Recommend a genetic counselor to test it.
79
What is parkinsonism?
Any conditions causing a combination of movement abnormalities. * Tremor * Slow movement * Impaired speech * Muscle stiffness * Loss of dopamine containing neurons
80
What is Parkinson's disease? (PD)
* 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
What factors reduce risk of PD?
* Caffeine * Ibuprofen * Statins * Smoking * Moderate exercise
82
What factors increase risk of PD?
* Age * Family Hx * Pesticides/herbicides
83
What is the pathophysiology of PD?
* Degeneration of the dopamine-producing neurons in the substantia nigra * Imbalance between dopamine and ACh * Lewy bodies * Depletion of dopamine. ## Footnote Low dopamine = slow voluntary motor control High ACh = dyskinesia
84
How does PD present?
1. **Tremor resting and fine (MC)** 2. Rigidity 3. Bradykinesia 4. Postural instability ## Footnote Tremor is often described as **pill-rolling**
85
What aggravates and alleviates the resting tremor in PD?
* Aggravating: emotional stress or increase in mental activity * Alleviating: voluntary movement * Will spread up the body unilaterally.
86
What are the rigidity types that may appear in PD?
* Unilaterally initially on **same side as tremor** * Cogwheel (ratchety pattern) * Lead pipe (persistent)
87
What is the major cause of disability in PD?
Bradykinesia
88
What does bradykinesia look like in PD?
* 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
What test and sign is associated with postural instability?
* Pull test * **Myerson sign: tapping over the bridge of the nose and produces sustained blink**
90
How do we diagnose PD?
* Bradykinesia with rigidity or tremor * **Must respond to a dopaminergic agent (if no response, prob not PD)** * No muscle weakness or DTR changes
91
How do we manage PD?
* Neuro consult * PT/OT/ST * Pharm goal: increase dopamine while reducing ACh
92
For minimal PD, what drugs are indicated?
* **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
For moderate PD, waht drugs are indicated?
* Dopamine agonists in younger pts: pramiprexole, ropinirole, **rotigotine (patch)** * Carbidopa/levodopa for older pts.
94
For severe PD, what is the main drug of choice?
* 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
What are COMT inhibitors used for and what are they?
* 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
What are the more specialized therapies for PD?
* Dementia: ACh inhibitors & memantine * Psychosis: atypical antipsychotic: quetiapine
97
What are the invasive therapies for PD?
* DBS: **AVOID IN COGNITIVE DYSFUNCTION** * Continuous levodopa-carbidopa intestinal gel (LCIG) * Convential vs MRI guided US: thalamotomy, subthalamotomy, pallidotomy
98
What is ataxia?
Loss of full control of bodily movement
99
What are the underyling anatomical lesions associated with ataxia?
* Cerebellar hemispheres * Midline cerebellum (cerebellar vermis, spinocerebellum, and vestibulocerebellum) ## Footnote Midline: Gait, balance, ocular Hemispheres: Dysdiadochokinesias, dysmetria, limb ataxia, tremor, speech
100
What are the 3 types of ataxia?
* Motor/cerebellar ataxia * Sensory/proprioceptive ataxia * Vestibular ataxia
101
What does motor/cerebellar ataxia look like?
* Imbalance and coordination * Ataxic gait (drunk) * Unclear (scanning) speech * Nystagmus => visual blurring * Loss of hand coordination * Intention tremor
102
What is the underlying pathophysiology behind sensory/proproceptive ataxia?
* Inadequate transmission of positional info to the CNS. * Results from disorders of **peripheral nerves, spinal cords, or cerebellar input tracts**
103
How does sensory/proprioceptive ataxia present?
* Abnormal F-N **with closed eyes** * **Abnormal vibratory sense** * **Positive romberg** * Unsteady gait with **closed eyes** * **Stomping gait**
104
What is the underyling pathophysiology behind vestibular ataxia?
Dysfunction of the inner ear
105
How does vestibular ataxia present?
* 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
Pramipexole/Mirapex MOA, indications, metabolism, special pharmacokinetics
* 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
Pramipexole/Mirapex SEs
* Nausea * Somnolence * Fatigue * HA * PD: orthostatic hypotension, constipation, dyskinesia, somnolence, dizziness, hallucinations, imsomnia, weird dreams
108
Pramipexole/Mirapex DDI
* Alcohol * Dopamine antagonists | It is an agonist
109
Ropinirole/Requip MOA, Indications, Metabolism
* MOA: **Non-ergot dopamine agonist**, D2 **and** D3 dopamine receptors * Indications: RLS, mild parkinson's * Metabolism: **Liver**
110
Ropinirole/Requip SEs
* Syncope * Somnolence * Dizziness * Fatigue * N/V * **Viral infection** * Dyskinesias
111
Ropinirole/Requip DDI
* Alcohol * Dopamine antagonists * CNS depressants * Estrogens * Cipro
112
Rotigotine/Neupro MOA, Indications, Pharmacokinetics, Metabolism
* 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
Rotigotine/Neupro SEs
* Site reaction * Hypotension * Nausea * Somnolence * Dizziness * Dyskinesia | The least SEs between pramipexole, ropinirole, and rotigotine.
114
Rotigotine/Neupro DDIs
* Alcohol * Dopamine antagonists * Anti-HTNs
115
Tetrabenazine/Xenazine MOA, indication, metabolism
* MOA: **VMAT2 inhibitor**, inhibiting release of dopamine, noradrenaline, and serotonin * Indication: **Huntington's** * Metabolism: **Liver**
116
What patients should NOT use tetrabenazine?
* Active SI * Uncontrolled depression * Hepatic impairment * MAOi use in 14d * Reserpine use in past 20d
117
What syndrome is associated with use of tetrabenazine?
Neuroleptic malignant syndrome (NMS)
118
Amantadine MOA, indications, Metabolism
* MOA: **NMDA antagonist**, inhibiting NMDA-glutamate and muscarinic receptors; **stimulates dopamine release ** * Indications: Parkinsonism, Extrapyramidal symptoms, flu * Metabolism: **liver** ## Footnote Extrapyramidal: Voluntary movements now being uncontrolled
119
Amantadine DDIs
* Alcohol: dizziness/circulation * **Tramadol: Seizures**
120
Amantadine SEs
* Restlessness * Confusion * Skin rashes * Edema * Disturbances of cardiac rhythm
121
What are the MAOB inhibitors and their main indications and MOA?
* Selegiline, Rasagiline, and safinamide * Indications: Monotherapy OR **adjunct with levodopa for PD** * MOA: **Increases dopamine conc in striatum**
122
What are the risks associated with MAOB inhibitor use?
* Orthostatic hypotension * Serotonin syndrome * Psychotic episode with concomitant use of st johns or DXM ## Footnote DXM = dextromethorphan (cough syrup)
123
What is levodopa and carbidopa?
* Levodopa = precursor of dopamine * Carbidopa = inhibits the enzyme that breaks down levodopa in the peripheral circulation
124
What is the main purpose of carbidopa and what is the main symptom that carbidopa/levodopa help with?
* Carbidopa lowers the amount of levodopa needed. * Carbidopa/levodopa is primarily for **bradykinesia in PD**, and is **First-line therapy for symptomatic PD**
125
What are the contraindications to carbidopa/levodopa?
* MAOi use * Psychosis * **Melanoma** * **Narrow angle glaucoma**
126
What kind of diet should you avoid when taking carbidopa/levodopa?
High protein diets
127
What is entacapone used for?
It is a COMT inhibitor used to stabilize plasma levels of dopamine as **adjunct therapy with levodopa**.
128
How is entacapone excreted?
Liver

Clin Med B 2 (44 decks)

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