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Lecture 12: Movement Disorders Flashcards

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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 is 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: BZD
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21
Q

How do we manage persistent ET?

A
  • 1st-line: The same as intermittent but you give the drug daily!
  • 2nd-line: Anticonvulsants
  • 2nd-line: Neurologist for botox A or surgical intervention
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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 | Order switched in children between first and 2nd line
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 dependence and addiction** Dopamine agonists: oral forms have a **risk of augmentation**
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 (**echoing**) * Palilalia: Repeating the same word * **Coprolalia: Cussing** uncontrollably
66
What 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-pharmacologic 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) | Genetic testing is primary
77
What medications may help with HD?
* Motor: VMAT2 inhibitors (xenazine, deutetrabenazine, and valbenazine) & **2nd-gen antipsychotics (haldol, pimozide, aripiprazole)** * Psychiatric: SSRIs | 2nd gens are the same FDA approved tx for TS!!
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 (bradykinesia) * 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.** | Dopamine inhibits ACh as well ## 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 produces sustained blinks**
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 reducing ACh**
92
For minimal PD, what drugs are indicated?
* **Young patients with tremor**: Anticholinergics such as **benzatropine 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, what drugs are indicated?
* Dopamine agonists in younger pts: pramiprexole, ropinirole, **rotigotine (patch)** * Carbidopa/levodopa for older pts. | Same as RLS ## Footnote Prami and ropi have augmentation effects
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 | AKA coordination
99
What are the underlying 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 underlying 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) | gotta pee to use prami
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 | Hepatic clearance + Serotonin inhibitor
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** | Inhibition of ACh via dopamine release ## 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

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