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Neuro Behavioral Med I > 10 - Movement Disorders > Flashcards

10 - Movement Disorders Flashcards

1
Q

What is a tremor?

A

Rhythmic, oscillating movement of body part; i.e. hand (but can be in the head)

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2
Q

What is ataxia?

A
  • Clumsiness, instability, imbalance, or lack of coordination with voluntary movements
  • Movements appear disjointed, unsteady gait, falls
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3
Q

What is dystonia?

A
  • Involuntary muscle spasms

- Can be generalized or focal (hand - Writer’s cramp, neck - torticollis)

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4
Q

What is dyskinesia?

A
  • Repetitive, purposeless, involuntary movements
  • Grimacing, lip-smacking, rapid arm/leg movements
  • Prolonged exposure to antipsychotics, neuroleptics
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5
Q

What is dysdiadochokinesia?

A
  • Impaired ability of rapid alternating movements
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6
Q

What is chorea?

A
  • Non-repetitive jerking movements of limbs, face or trunk
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7
Q

Describe the characteristics of an essential tremor

A
  • “Senile tremor”, “benign essential tremor”
  • Most common tremor disorder
  • Involuntary rhythmic, oscillatory movements (Alternating contraction of opposing muscles)
  • There is NO related neurologic disease or medication ***
  • It is just a tremor… It is essential
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8
Q

What are the two types of essential tremor?

A
  • Kinetic

- Postural

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9
Q

Describe a kinetic essential tremor

A

Kinetic – tremor with movement of body part (writing, etc)

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10
Q

Describe a postural essential tremor

A

Postural – tremor when body part held against gravity

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11
Q

Describe the epidemiology of essential tremors

A
  • Typical onset is in the mid 50s
  • Average age at first clinic visit = 71 years old
  • Slight male predominance (53%)
  • Estimated prevalence of about 4% in adults
  • Annual incidence of 0.6% for age > 65 years
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12
Q

What are some possible risk factors for an essential tremor?

A
  • Lead, beta-carboline alkaloids

- D3 dopamine receptor gene variant possibly associated with familial essential tremor

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13
Q

How do you diagnose an essential tremor?

A
  • Based on history and physical exam
  • Tremor usually 4-12 Hz (cycles/second)
  • Usually asymmetric, hands > lower extremities
  • Tremor of head may sole symptom or associated with extremity tremor
  • Need to rule out other disorders that may mimic essential tremor *** (main point)
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14
Q

What things do you need to check if you are trying to figure out whether or not something is an essential tremor?

A

Check thyroid function, ceruloplasmin (to exclude Wilson’s disease especially in a patient

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15
Q

What is on your differential diagnosis when investigating for an essential tremor?

A
  • Hyperthyroidism
  • Parkinson’s Disease
  • Enhanced physiologic tremor
  • Wilson’s Disease (dysfunction of copper in the body - liver and eye)
  • Medications
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16
Q

What types of medications can cause an essential tremor?

A

Amiodarone

  • Beta agonists
  • Lithium
  • Theophylline
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17
Q

What are the treatment options for an essential tremor?

A

Treatment is targeted at symptom management

  • Propranolol*
  • Primodone
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18
Q

Describe propranolol as a treatment for essential tremor

A
  • Beta blocker, non-selective
  • Long or short acting, 60-800 mg/dy for short acting
  • Improved clinical symptoms and reported severity

FIRST LINE ***
Give this unless they cannot tolerate this

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19
Q

Describe primidone as a treatment for essential tremor

A
  • Unclear mechanism, likely GABA effect, 50-250 mg/day

- May be more beneficial in the setting of kinetic or intention tremors

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20
Q

Describe the disease condition described in Alice in Wonderland

A
  • Todd’s syndrome

- Characterized by migraines predominantly in children that cause micropsia/macropsia (seeing small or large things)

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21
Q

Describe the pathophysiology of Parkinson’s disease

A
  • Loss of dopaminergic neurons in Substania Nigra
  • Neurons die and degenerate
  • Imbalance in DA : Ach in striatum = improper signalling pathway for cortical motor commands
  • Possibly related to alpha-synuclein; defective degradation leads to increased alpha-synuclein in nigrostriatal neurons

We currently believe that this build up of alpha-synuclein can cause the symptoms of Parkinson’s

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22
Q

Describe the epidemiology of Parkinson’s disease

A
  • Slight male predominance
  • Prevalence increases with age
  • 41 per 100,000 in age 40-49 years old
  • 1,903 per 100,000 in age >80 years old
  • Gets a lot more prevalent as you get older
23
Q

What are the possible risk factors associated with Parkinson’s disease?

A
  • Pesticides
  • Head injury
  • Family history
  • History of poliomyelitis (polio)
  • Genetic predisposition – 9 genes, several loci
  • Approximately 10-15% of PD patients have this genetic predisposition
  • PARK2 gene in 8.6% of early onset PD patients have this predisposition

None of which have been proven very well

24
Q

What are the two classifications of PD?

A
  • Primary

- Secondary

25
Q

Describe primary PD

A

Idiopathic Parkinson’s Disease

26
Q

Describe secondary PD

A

History of another condition which has contributed to the development of PD

  • Infectious (viral encephalitis)
  • Atheroslcerotic
  • Drug induced
  • Toxic agents (CO, manganese)
  • Head trauma, tumors
27
Q

What is MPTP?

A
  • Precursor to MPP+, a neurotoxin that destroys dopaminergic receptors in substania nigra
28
Q

Describe the unfortunate 1976 discovery of MPTP

A
  • Graduate chemistry student who synthesized MPPP (opioid drug, similar to morphine)
  • Injected into himself, along with MPTP impurity
  • Rapidly developed Parkinson’s like symptoms
  • He was treated with levodopa
  • Died almost 2 years later from cocaine overdose
  • Autopsy revealed destruction of dopaminergic neurons in SN

This has given us the idea that these patients may have some sort of a neurotoxin affecting them

29
Q

What are the 4 cardinal signs and symptoms of PD?

A
  • Resting tremor (4-6 Hz)
  • Cogwheel rigidity
  • Bradykinesia
  • Postural instability
30
Q

What are some other early motor findings associated with PD?

A

May occur before the big 4 cardinal signs will begin

  • Micrographia, decreaesd dexterity
  • Intermittent unilateral resting tremor
  • Hypophonia – softening of voice
  • Stooping posture
  • Masked face (look like no expression on their face - sad)
  • Shorter steps with unsteady gait
31
Q

How do you treat PD?

A
  • Treatment is targeted to symptom management
  • Treat the most bothersome symptoms first
  • Initiate treatment when patient begins having functional disability
  • Consider limiting levadopa therapy in younger patients or those with expected long-term treatment

If someone has a symptom that is not really bothering someone, you don’t have to treat them because the side effects are significant

32
Q

What are the three classes of treatment options for PD?

A
  • Dopaminergic agents
  • COMT inhibitors
  • Antiviral agents
33
Q

What dopamine agents will we talk about?

A
  • Levadopa/Carbidopa
  • Dopamine Agonists
  • MAO-B Inhibitor
  • Anticholinergic Agents
34
Q

Describe the levodopa/carbidopa combo drug

A

Levodopa – crosses the BBB to act as dopamine precursor

Carbidopa – inhibits the peripheral degradation of levodopa by inhibiting dopamine decarboxylation

Combination medication = Sinemet *****

35
Q

What are the advantages of levodopa/carbidopa therapy?

A

MOST EFFECTIVE TREATMENT FOR PD ***

  • Most efficacious PD medication
  • Nearly all patients respond
  • Symptomatic Improvement
  • Possible decreased mortality
36
Q

What are the disadvantages of levodopa/carbidopa therapy?

A
  • Does not stop progression
  • Motor fluctuations (wears off throughout the day - “on-off” phenomenon)
  • Most patients develop motor complications because there is overstimulation (Dyskinesia
    Choreoathetotic, Dystonic)
37
Q

Describe the details of levodopa/carbidopa complications

A
  • Motor fluctuations dependent on duration and dose
  • Majority of patients will have issues >15 yrs of treatment
  • Difficult management of symptoms
  • Does not stop: freezing, instability, autonomic dysfunction
  • Levodopa is absorbed by the gut via amino acid transporters
  • High protein diets can effect absorption
38
Q

What are the two types of dopamine agonists?

A
  • First generation

- Second generation

39
Q

What is the first generation dopamine agonist?

A

Bromocriptine (Parlodel)

Do NOT need to memorize this ***

40
Q

What are the second generation dopamine agonists?

A
  • Ropinirole (Requip)
  • Pramipexole (Mirapex)
  • Rotigotine (Neupro)

Do NOT need to memorize this ***

41
Q

What are the advantages of using these dopamine agonists?

A
  • Direct dopamine stimulation
  • Good monotherapy in early PD
  • No interference with dietary protein or amino acids
  • Longer duration
  • Less motor complications
  • Possible protective effect
42
Q

What are the disadvantages of dopamine agonists?

A
  • Not a long term monotherapy
  • Still some motor complications
  • Does not stop progression
  • Does not treat all aspects (freezing, instability, autonomic dysfunction)
43
Q

What are the two MAO-B inhibitors that you need to know?

A

B means Brain - they act in the brain

  • Selegiline
  • Rasaligine
44
Q

Describe the use of MAO-B inhibitors in PD patients

A
  • Monoamine oxidase inhibitors
  • Inhibit dopamine metabolism in the brain
  • May be initial treatment for patients with minimal functional disability
  • Some may have neuroprotective effects (rasaligine)

If they don’t have any dopamine being made (later on in the disease), it will not e effective - only works early on***

45
Q

What are the two anticholinergics that you need to know?

A

Anticholinergics

  • Trihexyphenidyl
  • Benztropine
46
Q

Describe the use of anticholinergics in PD patients

A
  • When dopamine decreases, cholinergic effects predominate
  • Treatment is intended to decrease cholinergic activity and balance the decreased dopamine effect
  • Predominantly used for tremor
  • ASE: dry mouth, urinary retention, altered mental status
47
Q

What are the COMT inhibitors that you need to know?

A

COMT inhibitors

  • Entacapone
  • Tolcapone
48
Q

Describe the use of COMT inhibitors in the treatment of PD patients

A
  • Increases duration of levodopa by inhibiting metabolism of levodopa by COMT
  • Adjunctive treatment with levodopa/carbidopa to decrease “wearing off” effect
  • NOT MONOTHERAPY ***
  • Monitor LFTs with Tolcapone due to possible hepatotoxicity
49
Q

What is the antiviral agent that you need to know?

A

Amantadine

Sometimes used as an anti-viral, used to treat the flu

50
Q

Describe the use of antiviral agents used to treat PD patients

A
  • Discovered to have antiparkinson activity
  • Unknown mechanism of action
  • Possibly useful early on, or as adjunct to levodopa therapy
51
Q

What is the use of surgical treatment of PD patients?

A
  • Intended for disabling PD despite optimal medical management
  • Poor candidates include those with high operative risk or significant cognitive decline
52
Q

What are the surgical options for treating PD patients?

A
  • Ablation – thalamotomy, pallidotomy
  • Deep Brain Stimulation – placed with stereotactic approach with MRI or CT
  • Restorative – fetal human/porcine nigral transplant
53
Q

Here are the things you need to know…

A
  • Big things – how do you diagnose essential tremor
  • How do you treat essential tremor or PD
  • What are the things you look for in patients with a tremor
  • Don’t need to know any dosing information
  • Do need to know which medications to use, when to use them and whether or not they are indicated

Neuro Behavioral Med I (15 decks)

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