Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the four types of tremor?

A
  • Resting
  • Action
  • Postural
  • Kinetic
  • Isometric
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is a resting tremor?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Ddx for essential tremor

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is a parkinsonian tremor?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is an orthostatic tremor?

A

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

Tx: Clonazepam

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is a primary writing tremor?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is a major cause of RLS?

A

Iron deficiency anemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the treatment of RLS?

A
  • Iron replacement
  • behavioral strategies (exercising, crossword puzzles)
  • avoid aggravating factors (sleep deprivation)
  • devices (relaxis pad).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Intermittent tx of RLS?

A
  • Levadopa “on-demand”

- Benzodiazapines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Tx for constant RLS?

A

Dopamine agonists

  • Requip
  • Mirapex
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Chronic or persistent RLS tx?

A

Seizure meds

  • Gapabentin
  • Pregablin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

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

A

Opoids (for terminal dx)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is Huntington’s disease?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is the prognosis for Huntington’s?

A

FATAL (avg. lifespan sp dx= 15yrs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are the symptoms of Huntington’s?

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Pathophysiology of Huntingtons?

A
  • inherited autosomal dominant
  • short arm chromosome 4 has a trinucleotide repeat
  • Diffuse, marked caudate atrophy and atrophy of putamen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is the tx for Huntington’s?

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is Parkinson’s Disease?

A

Progressive neurodegenerative disorder characterized by…

  • bradykinesia
  • tremor
  • rigidity
  • postural instability
30
Q

What causes Parkinson’s disease?

A
  • sporatic/idiopathic (unknown cause)
  • older than 60yo
  • family hx
31
Q

What are risk factors for parkinson’s?

A

Depression, constipation, likely pesticide exposure

32
Q

What are protective factors for parkinson’s?

A

Smoking, coffee/caffeine consumption

33
Q

What is the pathophysiology of Parkinson’s?

A
  • Degeneration of dopaminergic neurons in substantia nigra (manifests as bradykinesia & other signs of parkinsonism)
  • Imbalance of dopamine and acetylcholine (dopamine is decreased&raquo_space; excess acetylcholine relative to dopamine)
34
Q

What are the clinical presenting features of parkinson’s?

A
  • 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
Q

What is bradykinesia?

A

Generalized slowness of voluntary movement (80% of pts with Parkinsons).

Sx: Slow shuffling gait/festinating gait, Reduced blinking and masked facies (hypomimia).

36
Q

What is rigidity?

A

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
Q

What is postural instability?

A

General feeling of imbalance w/ tendency to fall (due2 impairement of centrally-mediated postural reflexes). Occures later in disease course. Test: “pull test”.

38
Q

How to diagnose Parkinsons?

A

@min need Bradykinesia and tremor/rigidity.

*Positive response to dopaminergic therapy (if no response then probably not parkinsons).

No labs

39
Q

What is the best short-term monotherapy for parkinsons?

A

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
Q

What medication would you use for Parkinson’s if a patient had drooling or tremor?

A

Anticholinergic meds

S/E: “Can’t see, can’t pee, can’t sit, can’t shit”

41
Q

What is the best tx for Parkinson’s?

A

Levodopa

  • Combined with carbidopa to decrease s/e of levadopa alone
  • S/E: orthostatic hypotension, dyskinesia, dizziness, hallucinations
42
Q

When would you use a dopamine agonist for parkinson’s?

A

When a patient doesn’t respond to levadopa

43
Q

What medication can help prolong Levadopa effect?

A

COMT inhibitors (reduce metabolism of levadopa)

S/E: orange pee, ortho hypotension, others

44
Q

What is tardive dyskinesia?

A

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
Q

What are orofacial manifestations of tardive dyskinesia?

A

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
Q

What are limb manifestations of tardive dyskinesia?

A

Twisting finger movments, “Piano-playing” movements, finger spreading, tapping foot movments, extending the toes.

47
Q

What are trunk/neck manifestations of tardive dyskinesia?

A

Retrocollis, shoulder shrugging, rocking or swaying movements, rotating hip movments, thrusting hip movments.

48
Q

What is respiratory dyskinesia?

A

Tacypnea, Irregular breathing rhythms, Grunting noises, May be misinterpreted as a primary respiratory issue

49
Q

How is tardive dyskinesia diagnosed?

A

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
Q

What is the tx for tardive dyskinesia?

A

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
Q

What is ALS?

A

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
Q

What are bulbar clinical features of ALS?

A

Jaw spasticity, slow tongue movment, facial diparesis (weakness), dysphagia, dysarthria (difficulty forming words), Laryngospam, Peudobulbar affect. Progresses Faster.

53
Q

What are axial clinical features of ALS?

A

No abdominal reflexes, difficulty holding up the head, difficulty maintaining an errect body posture, Lumbar lardosis, cramps.

54
Q

What are respiratory clinical features of ALS?

A

Respiratory Clinical Features: Tachypnea, reduced vocal volume, accessary muscle use, dyspnea, weak cough, sleep disordered breathing, confusion.

55
Q

What is the tx for ALS? What are the S/E?

A

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
Q

What is the prognosis for ALS?

A

Very poor&raquo_space; relentlesly progressive. Mean survival= 3-5yrs

Referral to neurologist experienced in ALS

57
Q

What is myasthenia gravis?

A

Autoimmune disorder characterized by dysfunction at the neuromuscular junction, causing weakness and fatigability of skeletal muscles.

58
Q

What is the pathophysiology of myasthenia gravis?

A

Autoantibodies against Ach recpetor in postsymaptic neuromuscular junction&raquo_space; defective neuromuscular transmission&raquo_space;weakness and fatiuge of muscles.

-Breakdown in communication between nerves and muscles

Usually in ppl w/ thymic abnormalities

59
Q

What are the clinical features of myasthenia gravis?

A

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
Q

How do you diagnose myasthenia gravis?

A

Clincally: Ice pack test, Edrophonium test (IV edrophonium or neostigmine given» impove), Serum AChR antibodies in 85-90% (+ antibodies= have MG).

61
Q

What is the tx for MG?

A

First line > Acetylcholinesterase inhibiters= Mestinon. Immunotherapy, Plasmapherisis, Thymectomy.

62
Q

Medications to avoid for MG?

A

Quinolones (Cipor/Levaquin), Macrolides (Erythromycin/Azithromycin), Beta-blockers (Propanalol, atenolol, meroprolol), Anesthetics (Procaine, Xylocaine), Botox, Quinne and dervatives, magnesium

63
Q

What is the prognosis for MG?

A

Much improved in recent decades. Variable disease cause.

64
Q

What is tourette syndrome?

A

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
Q

What are the clinical features of tourette syndrome?

A

Motor and phonic tics

66
Q

What are tics?

A

Tics: Sudden, brief intermittent movements or utterances. Considered involuntary, but can be suppressed at times

67
Q

What are motor tics?

A

-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
Q

What are phonic tics?

A
  • 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
Q

What are common comorbidities of tourettes?

A

ADHD, OCD, Learning disorder, Conduct disorder/ODD

70
Q

What is the clinical diagnostic criteria for tourettes?

A
  • 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
Q

What is the general treatment for tourettes?

A

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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions