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RRCCPA Clin Med Exam 2 > Movement Disorders > Flashcards

Movement Disorders Flashcards

1
Q

What is a tremor?

A

Rhythmic, involuntary movement of a body part. Caused by conrtaction of antagonistic muscles.

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2
Q

What are the four types of tremor?

A
  • Resting
  • Action
  • Postural
  • Kinetic
  • Isometric
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3
Q

What is a resting tremor?

A

When the body part is supported and at rest» better with movement, worse with observation/stress

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4
Q

What is an action tremor and what are three types?

A

An action tremor occurs during a voluntary movement.

  • Postural: seen with body part held against gravity
  • Kinetic: seen with voluntary movement of the limb (intention tremor)
  • Isometric: occur during muscle contraction against stationary objects
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5
Q

What is a benign essential tremor (AKA familiar tremor)?

A

Typically postural/action tremor (worse with movement)

“Familial tremor”/grandma tremor.

Affects: hands, forearms, head, voice…^ with age (gradual progression). Can be inherited (~ 50%).

Worse with emotional stress

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6
Q

What is the treatment for benign essential tremor?

A

If intermittent= intermittent tx (propranolol/alcohol),

persistent disability= persistent tx (Propranolol, Primidone) or deep brain stimulation/botox injections (if all other tx fails)

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7
Q

Ddx for essential tremor

A

Parkinson’s Disease, Cerebellar tremor, Drug-induced, Physiologic, Primary Writing Tremor

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8
Q

What is a physiologic tremor?

A

Tremor that everyone’s got (no neurologic disease).

Not ususally visible to eye b/c low amplitude. ^ (enhanced physiologic tremor) with fear/anxiety, hypoglycemia, exhaustion, caffeine, alcohol/withdrawal/fever.

Low amplitude, high frequency, at rest and action

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9
Q

What is a parkinsonian tremor?

A

Rest tremor. Improves with voluntary movment.
“Pill rolling”, typically unilateral.
Sx. Bradykineasia (arms are slow), rigidity.

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10
Q

What is a cerebellar tremor?

A

Intention tremor, worse when approaching target. Tested with Finger-to-nose/heel-to-shin. Common causes= MS, CVA, brain tumor.

Tx: Symptomatic tx for underlying cause, do brain imaging.

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11
Q

What is a drug-induced tremor?

A

Caused by drugs that stimulate autonomic NS.
Also psych drugs.
Common meds: Inhalers, steroids, Amiodarone, Amphetamines, B-andreergic agonists (ex: albuterol), Caffeine, Corticosteroids, Epinephrine, Floxetine (prozac),….etc

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12
Q

What is an orthostatic tremor?

A

In legs/trunk immediately s/p standing. Feels like “unsteadiness”. Not usually visible.

Tx: Clonazepam

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13
Q

What is a Psychogenic tremor?

A

“Functional tremor” a variable tremor that can look like any kind of tremor movement. Often sudden onset & remission (not present if not being observed). Changeable features/extinction with distraction/ increase with attention. ^ under stress.

Focus on one thing can cause the tremor to go away (FAKE)

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14
Q

What is a primary writing tremor?

A

Action tremor limited to the hand. Only when writing. No other neruo involvement.

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15
Q

What is restless leg syndrome?

A

Patients have uncomfortable urge to move their legs, especially when relaxed

Involuntary limb movement during sleep

sx: “I can’t sit still”, “I feel like I have to move my legs”, tingling/creeping/crawling sensation during periods of inactivity.

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16
Q

What are the risk factors of RLS?

A
  • Caucasian
  • Women > men
  • prevalence increases w/ age
  • DM, IDA (iron difficency anemia), ESRD on HD (end stage renal disease), RA (rheumatoid arthritis), PD (parkinson’s), neuropathy, myelopathy.
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17
Q

What is a major cause of RLS?

A

Iron deficiency anemia

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18
Q

What is the treatment of RLS?

A
  • Iron replacement
  • behavioral strategies (exercising, crossword puzzles)
  • avoid aggravating factors (sleep deprivation)
  • devices (relaxis pad).
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19
Q

Intermittent tx of RLS?

A
  • Levadopa “on-demand”

- Benzodiazapines

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20
Q

Tx for constant RLS?

A

Dopamine agonists

  • Requip
  • Mirapex
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21
Q

Chronic or persistent RLS tx?

A

Seizure meds

  • Gapabentin
  • Pregablin
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22
Q

What is the last treatment option for RLS when all other options are exhausted?

A

Opoids (for terminal dx)

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23
Q

What is Huntington’s disease?

A

Inherited, progressive neuro disorder characterized by chorea, psychiatric disturbances and dementia.

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24
Q

What people are at risk for Huntington’s disease?

A

Parent with disease (autosomal dominant with 100% penitrance).

Peak age 30-40s and can be from 2-70 y.o.

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25
What is the prognosis for Huntington's?
FATAL (avg. lifespan sp dx= 15yrs)
26
What are the symptoms of Huntington's?
Sx: Dance-like movements (chorea), weight-loss, dementia, impairment of attention & executive function, psych sx (depression, irritability, apathy (lack of interest), disrupted social relationships, SI)
27
Pathophysiology of Huntingtons?
- inherited autosomal dominant - short arm chromosome 4 has a trinucleotide repeat - Diffuse, marked caudate atrophy and atrophy of putamen
28
What is the tx for Huntington's?
Tx: No cure. Sx management and supportive tx. PT, OT, end of life discussions. Meds for slowing progression: Tetrabenazine (Xenazine)- dopamine depleting agent Psych meds: Olanzapine, risperidone (Risperdal), Haloperidol (haldol), Clozapine (clozaril)
29
What is Parkinson's Disease?
Progressive neurodegenerative disorder characterized by... - bradykinesia - tremor - rigidity - postural instability
30
What causes Parkinson's disease?
- sporatic/idiopathic (unknown cause) - older than 60yo - family hx
31
What are risk factors for parkinson's?
Depression, constipation, likely pesticide exposure
32
What are protective factors for parkinson's?
Smoking, coffee/caffeine consumption
33
What is the pathophysiology of Parkinson's?
- Degeneration of dopaminergic neurons in substantia nigra (manifests as bradykinesia & other signs of parkinsonism) - Imbalance of dopamine and acetylcholine (dopamine is decreased >> excess acetylcholine relative to dopamine)
34
What are the clinical presenting features of parkinson's?
- Resting tremor "Pill rolling" - Bradykinesia - Rigidity. Most noticeable at rest. Initally one side of the body, but eventually progresses to all limbs. Exacerbated with stressful situations.
35
What is bradykinesia?
Generalized slowness of voluntary movement (80% of pts with Parkinsons). Sx: Slow shuffling gait/festinating gait, Reduced blinking and masked facies (hypomimia).
36
What is rigidity?
Increased resistance to passive movement of a joint. Sx: Cogwheel rigidity (specific to PD), lead pipe rigidity, decreased arm swing while walking, stooped posture. Test: Passive movement of limbs
37
What is postural instability?
General feeling of imbalance w/ tendency to fall (due2 impairement of centrally-mediated postural reflexes). Occures later in disease course. Test: "pull test".
38
How to diagnose Parkinsons?
@min need Bradykinesia and tremor/rigidity. *Positive response to dopaminergic therapy (if no response then probably not parkinsons). No labs
39
What is the best short-term monotherapy for parkinsons?
Amantadine - good to use early in the disease. Anti-viral med that has mild antiparkinsonian activity - adverse effects: orthostatic hypertension, edema, confusion, GI distress
40
What medication would you use for Parkinson's if a patient had drooling or tremor?
Anticholinergic meds S/E: "Can't see, can't pee, can't sit, can't shit"
41
What is the best tx for Parkinson's?
Levodopa - Combined with carbidopa to decrease s/e of levadopa alone - S/E: orthostatic hypotension, dyskinesia, dizziness, hallucinations
42
When would you use a dopamine agonist for parkinson's?
When a patient doesn't respond to levadopa
43
What medication can help prolong Levadopa effect?
COMT inhibitors (reduce metabolism of levadopa) S/E: orange pee, ortho hypotension, others
44
What is tardive dyskinesia?
Hyperkinetic movment disorder with a delayed onset that appears after prolonged used of dopamine receptor blocking agents, mainly antipsychotis and antiemetics. Sx: Dyskinesia involving face/mouth, neck/trunk, respiratory sx. Frequentlly first appears after a dose reduction, discontinuation, or switch to a less potent antipsychotic
45
What are orofacial manifestations of tardive dyskinesia?
Protruding, twisting movements of the tongue. Smacking of the lips, retraction of the corners of the mouth, puffing out of the cheeks, chewing movements, puckering lips
46
What are limb manifestations of tardive dyskinesia?
Twisting finger movments, "Piano-playing" movements, finger spreading, tapping foot movments, extending the toes.
47
What are trunk/neck manifestations of tardive dyskinesia?
Retrocollis, shoulder shrugging, rocking or swaying movements, rotating hip movments, thrusting hip movments.
48
What is respiratory dyskinesia?
Tacypnea, Irregular breathing rhythms, Grunting noises, May be misinterpreted as a primary respiratory issue
49
How is tardive dyskinesia diagnosed?
Clinical diagnosis. Must have: Dyskinetic or dystonic involunary movments - at least 1 month hx of antiphychotic drug tx - excluded other causes of abnormal movements.
50
What is the tx for tardive dyskinesia?
Discontinue offending medication if possible. Switch from typical to atypical antipsychotic (Clozapine=1st choice, or Seroquel=2nd). Clozapine= bone-marrow supression (agranulocytosis= bone dosent produce RBC). Pt's need CBC weekly while on it. Other tx: Botox injections, benzodiazepine, tetravenazine, deep brain stimulation of globus pallidus. Prevention: avoid treatment with antipsychotics and metoclopramide (dont use metoclopamide for more thatn >12 weeks)
51
What is ALS?
Lou Gehirgs's disease. Progressive neruodegenerative disorder of motor neurons that causes muscle weakness, disability, and death. Sx in limbs: Combination of UMN and LMN LMN sx= spasticity, slowed rapid alternating movments UMN= hyperreflexia, spastic gait, stiffness/slowness, uncoordinated movment, poor balance. Weakness, muscle atrophy, fasicualations, foot drop. Most cases are sporadic and 10% are familial from mutation
52
What are bulbar clinical features of ALS?
Jaw spasticity, slow tongue movment, facial diparesis (weakness), dysphagia, dysarthria (difficulty forming words), Laryngospam, Peudobulbar affect. Progresses Faster.
53
What are axial clinical features of ALS?
No abdominal reflexes, difficulty holding up the head, difficulty maintaining an errect body posture, Lumbar lardosis, cramps.
54
What are respiratory clinical features of ALS?
Respiratory Clinical Features: Tachypnea, reduced vocal volume, accessary muscle use, dyspnea, weak cough, sleep disordered breathing, confusion.
55
What is the tx for ALS? What are the S/E?
Riluzole (Rilutek) is the only FDA-approved med known to extend tracheostomy-free survival. S/E: S/E: nausea, weakness, hepatic impairment, neuropenia, dizziness.
56
What is the prognosis for ALS?
Very poor >> relentlesly progressive. Mean survival= 3-5yrs Referral to neurologist experienced in ALS
57
What is myasthenia gravis?
Autoimmune disorder characterized by dysfunction at the neuromuscular junction, causing weakness and fatigability of skeletal muscles.
58
What is the pathophysiology of myasthenia gravis?
Autoantibodies against Ach recpetor in postsymaptic neuromuscular junction >> defective neuromuscular transmission >>weakness and fatiuge of muscles. -Breakdown in communication between nerves and muscles Usually in ppl w/ thymic abnormalities
59
What are the clinical features of myasthenia gravis?
Sx: mostly ocular sx (>50%) = weakness of eyelid/ptosis, extraocular muscles produce diplopia, pppils are always spared. Bulbar sx: Dysarthria, dysphagia, fatigable chewing, dropped head syndrome. "She lost her smile"- weakness of orbicularis muscle
60
How do you diagnose myasthenia gravis?
Clincally: Ice pack test, Edrophonium test (IV edrophonium or neostigmine given>> impove), Serum AChR antibodies in 85-90% (+ antibodies= have MG).
61
What is the tx for MG?
First line > Acetylcholinesterase inhibiters= Mestinon. Immunotherapy, Plasmapherisis, Thymectomy.
62
Medications to avoid for MG?
Quinolones (Cipor/Levaquin), Macrolides (Erythromycin/Azithromycin), Beta-blockers (Propanalol, atenolol, meroprolol), Anesthetics (Procaine, Xylocaine), Botox, Quinne and dervatives, magnesium
63
What is the prognosis for MG?
Much improved in recent decades. Variable disease cause.
64
What is tourette syndrome?
Neuro disorder manifested by multiple motor and phonic tics. Usually has onset in childhood (2-15yo M) Is an interaction between social and environmental factors and multiple genetic abnormalities (bilineal transmission)
65
What are the clinical features of tourette syndrome?
Motor and phonic tics
66
What are tics?
Tics: Sudden, brief intermittent movements or utterances. Considered involuntary, but can be suppressed at times
67
What are motor tics?
-Simple: blinking, grimacing, head thrusting, sniffing, shoulder shrugging. - Complex: gesturing, sequence of tics. - Most commonly involve the face, neck, shoulders. - Occur initially in 80% of patients. -Echopraxia: imitation of the movement of others. Some are self-mutilating: hair-pulling, biting lips/tongue, nail biting
68
What are phonic tics?
- Phonic tics: Grunts, hisses, coughing, verbal utterances, barks. - Coprolalia: Involuntary obscene speech. - Echolalia: Repetition of others’ speech. - Palilalia: Repetition of words or phrases. Apart from tics, exam will be normal
69
What are common comorbidities of tourettes?
ADHD, OCD, Learning disorder, Conduct disorder/ODD
70
What is the clinical diagnostic criteria for tourettes?
* Both multiple motor tics and ≥1 phonic tics must be present at some point during the illness * Tics must occur many times a day, nearly every day, or intermittently for at least 1 year * Onset of tics is before age 21 (DSM-5 says before age 18) * Anatomical location, number, frequency, type, complexity, or severity of tics must change over time •Can’t be better explained by another medical condition * Tics must be witnessed by a reliable examiner or recorded by videotape
71
What is the general treatment for tourettes?
Tx: Cognatie behavioral therapy (habit reversal training = HRT) Educaiton of all ppl who interact with the patient. Meds: Haldol (1st gen antipsychotic = suppresses dopamine) S/E: Dystonic rxn, ESP/TD, blurred vision, drowsiness, esophageal dismotility. Pimozide S/E: Sedation, akathisia, akninesia, xerostomia, impotence, visual disturbance. Tx with Alpha Adrenergic Agonists: Clonidine, Guanfacine. Tx for focal tics: Botulinum toxin. Tx for those with TS + OCD = behavioral therapy + SSRI. Tx for disabling tics= deep brain stimulation.

RRCCPA Clin Med Exam 2 (4 decks)

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