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Neuro > Movement Disorders - Exam 4 > Flashcards

Movement Disorders - Exam 4 Flashcards

1
Q

What part of the brain do movement disorders effect? What is one important thing to note?

A

basal ganglia

usually subside while the pt is sleeping

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2
Q

What are the 3 functions of the basal ganglia?

A

motor control

executive decision making

reward, habits and addiction

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3
Q

_______ neurotransmitter that inhibits the release of acetylcholine at the nerve terminal to help produce smooth motor movements and control. What is one additional feature?

A

dopamine

also plays a role in reward and motivation pathways

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4
Q

______ inhibitory neurotransmitter that relaxes muscle and allows motor control

A

Gamma-aminobutyric acid (GABA)

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5
Q

________ neurotransmitter found at the neuromuscular junction and in autonomic ganglia. What is the the role in the peripheral? CNS?

A

Acetylcholine (Ach)

Excitatory in peripheral nerves

Neuromodulator in CNS

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6
Q

______ is the MC movement disorder. What is it caused by?

A

tremor in the HANDS -MC

Caused by alternating or synchronous contractions of antagonistic muscles

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7
Q

a “pill-rolling” tremor is associated with _________. An action tremor that occurs with voluntary movement indicates _________.

A

“Pill-rolling” tremor - Parkinson’s Disease

Cerebellar disease

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8
Q

Give an example of a physiologic postural tremor

A

fine tremor of outstretched hands

aka a tremor that occurs with sustained posture or position

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9
Q

How are tremors categorized?

A

rest or action

frequency: Hz per second (speed)

amplitude: amount of motion
- low: smaller movement
- high: larger movement

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10
Q

______ are rapid irregular muscle jerks. How are they classically described?

A

chorea

Classically involuntary and unpredictable

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11
Q

chorea usually have normal strength but _______. What are 3 different variations of chorea?

A

difficulty maintaining contraction

Milkmaid’s grasp - hand grip relaxes intermittently
Dancing gait - irregular, unsteady, dips and lurches
Irregular speech - erratic volume and tempo

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12
Q

_______ slow, writhing, sinuous movements. _______ excessive or inappropriate contraction
of muscles causing sustained abnormal posture. When are these movements usually worse? Better?

A

athetosis

dystonia

worse with stress and activity

improve with sleep

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13
Q

What PE findings are associated with Wilson’s disease? What is it?

A

athetosis, dystonia, dysarthria, chorea

excessive copper storage disease

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14
Q

______ sudden, recurrent, quick, coordinated, abnormal movements. What is important to note? Can they be suppressed?

A

COORDINATED!- can also be vocal

can be voluntarily suppressed for short periods

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15
Q

______ neurodevelopmental disorder causing people to develop multiple chronic motor and vocal tics

A

Tourette Syndrome

Eventually progress to combination of multiple types of tics
Remissions and relapses often seen

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16
Q

______ sudden, rapid, twitch-like contraction. What are the 5 different variations?

A

myoclonus

action
essential
physiologics
epileptic
secondary

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17
Q

_______ sudden jerky movement caused by interruption of normal muscle activity. What is the classic example? What are they often due to?

A

Asterixis: form of negative myoclonus seen when attempting to hold arms out and extend fingers and wrists (“flapping tremor”)

epilepsy, metabolic encephalopathy-> think alcoholic and liver failure

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18
Q

What is the difference between bradykinesia and hypokinesia?

A

Bradykinesia - slowed movement

Hypokinesia - decrease in amount of movement

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19
Q

What is freezing?

A

difficulty in starting or maintaining a rhythmic repetitive activity

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20
Q

What is an enhanced physiologic tremor? What is the underlying cause?

A

Very LOW-amplitude, HIGH-frequency (8-12 Hz) physiologic action tremor in the upper limbs

Occurs when there is increased sympathetic activation -> think stress, anxiety, caffeine, excitement, substance withdrawal, albuterol

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21
Q

What is the MC adult-onset movement disorder? What is the pathophys behind it? What is the mean age of presentation?

A

Essential Tremor

Altered cellular activity in the ventral intermediate nucleus of the thalamus, some genetic component

35-45 years old, usually manifests by 65

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22
Q

What is the MC mode of genetic transmission in movement disorders?

A

autosomal dominant

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23
Q

What 2 scenarios can an essential tremor present?

A

postural: when arms are postured against gravity

kinetic: present with goal directed movements

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24
Q

How will an essential tremor present?

A

typically affects bilateral HANDS and ARMS and pts will complain of trouble with fine motor activity

and progresses over time

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25
Q

Can an essential tremor just be isolated to the head/voice?

A

NO! not considered essential tremor unless it effects the arms/hands

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26
Q

What makes an essential tremor better? worse?

A

Aggravating factors - emotion, hunger, fatigue, temperature extremes
NOT worse with caffeine!

Alleviating factors - improves or resolves with alcohol

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27
Q

What are some PE findings consistent with essential tremor?

A

tremor is often mild or absent until target is reached

Other than tremor, neuro exam is usually benign

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28
Q

What labs should you order in essential tremor? Why?

A

CMP (electrolytes), thyroid, ceruloplasmin (Wilson disease)

to rule out secondary causes of tremor

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29
Q

What is the International Parkinson and Movement Disorder Society (IPMDS) Task Force diagnostic criteria for essential tremor?

A

Isolated tremor consisting of bilateral upper limb action (kinetic and postural) tremor, without other motor abnormalities

At least three years in duration

With or without tremor in other locations

Absence of other neurologic signs, such as dystonia, ataxia, or parkinsonism

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30
Q

What is first line intermittent treatment for essential tremor? 2nd line?

A

1st: Propranolol 30 minutes prior to activity/event

1st: Primidone nightly -> takes a few weeks to start seeing the effect

2nd: BZDs, topiramate, gabapentin

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31
Q

When is essential tremor tx CI?

A

CI in asthma or bradycardia

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32
Q

What are the SE of primidone? What is the rare major one?

A

Sedating, can cause ataxia and vertigo

rarely suppresses bone marrow -> need to check CBC

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33
Q

What is the continuous treatment for essential tremor?

A

1st line - Propranolol BID or Primidone daily (may consider combination of both drugs)

2nd line - topiramate, gabapentin

neurology referral, botox injections, sx (deep brain stimulation or thalamotomy)

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34
Q

When is surgical intervention indicated in essential tremor? When is it CI?

A

disabling tremor with failure of 2+ oral options

CI - dementia, severe cognitive impairment; uncontrolled anxiety/depression

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35
Q

How does the Thalamic ventralis intermedius (VIM) nucleus deep brain stimulation work?

A

Implantation of an electrode into the VIM nucleus connected to a pulse generator implanted in the chest wall below the clavicle which delivers unilateral high-frequency electrical stimulation when activated

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36
Q

How does MRI-guided focused ultrasound thalamotomy work?

A

Uses high-energy US beams to create a permanent lesion in the VIM nucleus of the thalamus - performed on the opposite side of the most severely affected arm

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37
Q

What is an intention tremor? What is the pathophys behind it? What is the highlighted disease associated with it?

A

Target-directed, coarse tremor that worsens when closest to the terminal target

Damage to the superior cerebellar peduncle or dentate nucleus (cerebellar disease)

MS

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38
Q

When is a intention tremor the most noticeable? What kind of oscillation is seen with it? What PE test will be abnormal? What frequency?

A

and is most active during the most demanding phases of a movement

Increases as action continues and fine adjustments are needed

Side-to-side oscillation

abnormal point-to-point testing (finger/nose)

3-4 Hz

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39
Q

What is Holmes-Stewart maneuver? What movement disorder?

A

inability to control rebound from a release of flexion against resistance

intention tremor

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40
Q

What is the tx for intention tremor?

A

no meds indicated

refer to neurology for DBS or thalamotomy as for essential tremor

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41
Q

What is restless leg syndrome? Who is the MC patient? What are some common associated findings with RLS?

A

Idiopathic movement disorder of the limbs characterized by a strong urge to move the legs and unpleasant sensations, often associated with a sleep complaint

middle age/older female symptoms tend to get worse with age

daytime fatigue and insomnia

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42
Q

What is Periodic limb movements of sleep (PLMS)?

A

involuntary, jerking movements of legs during sleep - usually forceful dorsiflexion, every 20-40 seconds

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43
Q

What is Periodic limb movement disorder (PLMD)?

A

sleep disturbance or impaired daytime functioning in the absence of RLS

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44
Q

What is the pathophys behind RLS?

A

abnormal iron levels, poor dopamine reuptake

some genetic component and inherited autosomal dominant

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45
Q

**What labs do you need to order in a pt with RLS? What do you need to do next?

A

**need to check a ferritin level, iron and transferrin saturation

**Recommended to give iron to any RLS patient with a ferritin <75

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46
Q

What are risk factors for RLS?

A

Frequent blood donation
Pregnancy
DM
Motor neuron disease
Chronic excessive alcohol use
Amyloidosis

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47
Q

How will a pt describe RLS? What will they NOT say?

A

“need to move,” “crawling,” “tingling,” “restless,” “cramping,” “pulling,” “creeping,” “electric,” “tension,” “discomfort”

NOT PAINFUL!!

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48
Q

What makes RLS worse? What makes it better?

A

evenings, periods of inactivity,
Caffeine or sleep deprivation, medications

temporary relief with movement (walking, stretching)

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49
Q

What medications make RLS worse?

A

Antihistamines-> Benadryl

Serotonergic antidepressants (TCAs, SSRIs, SNRIs)

Dopamine antagonists (antipsychotics, metoclopramide)

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50
Q

When should you tx a patient with RLS?

A

3+ nights a week

if fasting serum ferritin is below 75 mcg/L

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51
Q

What is the pt education for a pt on ferrous sulfate? when do you d/c? When should you repeat iron panel?

A

With vitamin C or a glass of orange juice

Discontinue iron when ferritin is >75 mcg/L and iron saturation >20%

repeat iron panel in 3-6 months

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52
Q

What are some non-pharm tx for RLS?

A

Keeping mind busy during times of rest
Avoid exacerbating factors (caffeine, medications)
Good sleep hygiene
Moderate regular exercise

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53
Q

What are the pharm options for RLS? What drug class?

A

pramipexole (Mirapex), ropinirole (Requip), rotigotine (Neupro) transdermal patch

Dopamine agonist

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54
Q

When should a pt take pramipexole (Mirapex)/ropinirole (Requip)? **What do these medications in the pt’s risk for?

A

oral therapy, 2 hours before bed and need to titrate meds

risk of worsening impulse control disorders (sex, gambling, eating, shopping, etc.)

risk of augmentation: overall increase in RLS symptom severity with increasing doses of oral dopamine agonists

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55
Q

Which dopamine agonist used to treat RLS coming in a transdermal patch?

A

rotigotine (Neupro) transdermal patch - 1 mg patch per day

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56
Q

What are s/s of augmentation associated with dopamine agonists of RLS medications? What happens if your pt starts exhibiting any of these symptoms?

A

earlier onset of symptoms during the day with increased intensity of symptoms

topographic spread of symptoms to other body parts, including the trunk and arms

shorter duration of drug action

switch to alpha-2-delta calcium channel ligand and/or refer to neurology

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57
Q

What are the drugs in alpha-2-delta calcium channel ligand class that are used for RLS? What are the SE?

A

gabapentin (IR) (Neurontin), pregabalin (IR) (Lyrica), gabapentin enacarbil (ER) (Horizant)

depression, mental fog, dizziness, weight gain, need lower dose in the pt is renal impaired

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58
Q

_______ sustained and repetitive involuntary muscle contractions. What induces it? What makes it worse? What makes it better?

A

Dystonia

voluntary movements

worse: stress and fatigue

improved: relaxation and sensory distraction

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59
Q

What is the pathophys behind dystonia?

A

unknown but found involuntary contraction of both agonistic and antagonistic muscles

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60
Q

What are the factors that dystonia classifications are based on?

A

age

body distribution

anatomical location

inherited or acquired

primary or secondary

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61
Q

What are the age categories associated with dystonia classifications?

A

Infancy: birth to 2 years
Childhood: 3 to 12 years
Adolescence: 13 to 20 years
Early adulthood: 21 to 40 years
Late adulthood: >40 years

62
Q

What is the difference between primary and secondary dystonia when talking about classifications?

A

Primary
no other neuro s/s

Secondary
due to underlying disease
other neuro s/s are noted

63
Q

What is the generalized dystonia? Can be ______ or _______

A

Generalized dystonia involves multiple areas of the body often including the torso and limbs

genetic: (childhood or adolescent onset) or acquired

64
Q

What are some causes of acquired generalized dystonia?

A

birth injury, exposure to certain drugs, head injury, infection

65
Q

What is focal dystonia? What is the MC form? Who is the MC pt population?

A

think slow/no movement in a smaller group of muslces

writer’s cramp: focal dystonia of the hand but pts DO NOT usually seek tx for it

women in 40-60s

66
Q

What are some focal dystonia subtypes?

A
67
Q

What type of focal dystonia? ________ contractions of the lower face, lips, tongue, and/or jaw, causing difficulty speaking and swallowing

A

Oromandibular Dystonia

68
Q

What type of focal dystonia? ________ blepharospasm + oromandibular dystonia

A

meige syndrome

69
Q

What type of focal dystonia? ________ vocal cord contractions during speech

A

Spasmodic Dysphonia

70
Q

________ - MC focal dystonia (50%) that pt’s seek tx for. What is the age of onset?

A

Cervical dystonia (aka. torticollis)

30-50 years old

71
Q

What is the tx for dystonia? give both focal and generalized tx options.

A

no cure; symptomatic only
Should refer to neurology / movement disorder specialist

focal: botox injections

generalized:
trial of levodopa/carbidopa (Sinemet) usually NOT helpful but can try it

72
Q

______ MOA blocks release of Ach at the neuromuscular junction

A

botox injections

73
Q

______ MOA dopamine inhibits release of Ach at axon terminals

A

levodopa/carbidopa (Sinemet)

74
Q

for levodopa/carbidopa (Sinemet), ______ is converted to dopamine; _______ reduces breakdown of _______ before it gets to the CNS

A

Levodopa

carbidopa

levodopa

levodopa is the med and carbidopa is the transporter

75
Q

What is the tx for generalized dystonia in adults who failed levodopa/carbidopa?

A

First-line: clonazepam (Klonopin)

Second-line: baclofen (GABA agonist)
Can be given orally or intrathecally)

Third-line: trihexyphenidyl (Artane)

76
Q

What is the tx for generalized dystonia in children who failed levodopa/carbidopa?

A

First-line: trihexyphenidyl

Second-line: baclofen, BZDs

77
Q

_____ MOA muscarinic receptor antagonist and increases striatal dopamine release and efflux

A

trihexyphenidyl (Artane)

78
Q

What is the tx for refractory generalized dystonia? What drug class?

A

tetrabenazine (Xenazine) and deutetrabenazine (Austedo)

VMAT2 inhibitors

79
Q

______ MOA depletes dopamine (and other monoamines) at the neuron synapse reducing the excitability of the neurons. What are the SE?

A

VMAT2 inhibitors

tetrabenazine (Xenazine) and deutetrabenazine (Austedo)

depression, anhedonia

80
Q

_______ is the last resort in dystonia patients who fail all other conservative therapies

A

Deep brain stimulation (DBS)

81
Q

What is the underlying cause of infanitle torticollis? What do you need to rule out?

A

Most often d/t damage or inflammation to the SCM or trapezius

rule out infectious etiologies

82
Q

What is the tx for infantile torticollis?

A

NSAIDS, soft cervical collar physical therapy

83
Q

What is Tourette’s Syndrome characterized by? What is the average age of onset?

A

Common genetic neurological disorder characterized by chronic motor and vocal tics beginning before adulthood

6 – 11 y/o and more common in males with a genetic inheritance (autosomal dominant)

84
Q

What are some risk factors for Tourette Syndrome?

A

Smoking during pregnancy
Complications during pregnancy
Low birth weight

85
Q

What is the thought processes of the pathophys behind Tourette Syndrome?

A

Thought to be caused by abnormal neurotransmission in the cortico-striatal- thalamic-cortical (mesolimbic) circuit which leads to disinhibition of the motor and limbic system

86
Q

What are the different types of tics? What makes it worse? Can they be suppressed?

A

involuntary complex neurologic functions

Motor - sudden, brief, intermittent movements

Vocal/Phonic - brief, involuntary utterances

Sensory - intermittent, unprovoked sensations

Exacerbated by fear or anxiety

Known to be involuntary, but CAN BE temporarily be voluntarily SUPPRESSED!

87
Q

What is simple Tourette Syndrome presentation?

A

Simple: Brief movements involving one muscle group that are characterized by simple sounds

motor tics are present in 80%

88
Q

What is complex Tourette Syndrome?

A

Complex:
More purposeful, orchestrated movements
Longer patterns of speech

89
Q

Where do motor tics in TS commonly present?

A

Most common in FACE; also common in head and shoulders

90
Q

What other conditions is Tourette Syndrome associated with?

A

OCD and/or ADHD in 50% of patients

Up to 80% of ASD patients have tics

Behavioral problems

Mood disorders

91
Q

What is the dx criteria for Tourette Syndrome?

A
92
Q

What is the management for Tourette Syndrome? When should you treat?

A

treatment is symptomatic, not curative. Refer to neurologist or psychiatrist trained in treating TS

when tics interfere with daily life (social interactions, school or job performance, ADLs), or causing subjective discomfort, pain, or injury

93
Q

What are the first line pharm txs in Tourette’s Syndrome? What do they help with?

A

1st: haloperidol (Haldol), pimozide (Orap), aripiprazole (Abilify)

Tics improved by up to 80% with treatment

94
Q

What are the 2nd line pharm tx for Tourette Syndrome? Are they FDA approved?

A

VMAT2 Inhibitor: Tetrabenazine (Xenazine)

Alpha-adrenergic agonists: clonidine and guanfacine (Intuniv)

NOT FDA approved

95
Q

_____ MOA stimulates function of the prefrontal cortex, increasing ability to control unwanted impulses

A

Alpha-adrenergic agonists: clonidine and guanfacine (Intuniv)

96
Q

What are the non-pharm tx for TS?

A

tic-awareness training

competing-response training

consider: Botox and Bilateral high frequency brain stimulation

97
Q

Huntington’s Disease is a hereditary disorder of the nervous system characterized by the gradual onset and subsequent progression of _____ and ______. What is the age of onset?

A

chorea and dementia

30-50 years old

98
Q

What gene is mutated in Huntington’s Disease?

A

Autosomal dominant disorder resulting in a mutation in the Huntington gene (HTT)

99
Q

Huntington’s Disease is a neuronal cell loss, particularly in the _____ and _______ which leads to ________

A

cerebral cortex and corpus striatum

neurotransmitter dysfunction which leads to reduced GABA and Ach as well as their associated enzymes

100
Q

How does HD present? specifically _____

A

May have either abnormal movements or intellectual changes first

Chorea: can be mild fidgetiness or severe uncontrollable flailing

101
Q

What does early mental status changes look like in HD? late?

A

early: irritability, moodiness, and antisocial behavior

late: dementia

often associated with weight loss and cachexia

102
Q

How do you make the dx of HD?

A

Genetic testing: mutation of the HTT gene

Can do CT/MRI which will demonstrate atrophy of the cerebral cortex and caudate nucleus but NOT necessary for the diagnosis

103
Q

What drug do you use in HD to help with the motor symptoms?

A

VMAT2 inhibitors:
tetrabenazine (Xenazine), deutetrabenazine (Austedo), valbenazine (Ingrezza - FDA approval 8/2023)

Second-gen antipsychotic:
haloperidol (Haldol), pimozide (Orap), and aripiprazole (Abilify)

overall no cure or tx, medications aimed at the s/s

average life span is 15 years after onset

104
Q

What are classic abnormalities seen with parkinsonism/ Parkinson’s Disease?

A

resting tremor
slow movement
impaired speech
muscle stiffness

105
Q

What is the 2nd MC neurodegenerative disease? What is the typical pt?

A

Parkinson’s Disease (PD) with Alzheimer’s being the first

over 60 year old man

106
Q

What is the underlying cause of PD?

A

combo of genetics and environment

107
Q

What reduces risk of PD?

A

Diet - caffeine, coffee
Meds - Ibuprofen, statins
Lifestyle - cigarette smoking, moderate exercise

108
Q

What increases the risk of PD?

A

Increased age
(+) fam hx
Repetitive head trauma
Toxins - herbicide/pesticide exposure, heavy metals, well wate

109
Q

What is the pathophys behind PD?

A

Degeneration of the dopamine-producing neurons in the substantia nigra

110
Q

What is the dopamine depletion seen in PD? _____ in the striatum normally helps balance the amount of ____

A

imbalance between dopamine and acetylcholine

Dopamine

Ach

111
Q

in PD, low ______ equals slow voluntary motor control. high ______ equals ______. What prevents the neurons from working properly?

A

low dopamine

high acetylcholine = dyskinesia

Lewy bodies prevent the neurons from working properly

112
Q

What are Lewy bodies?

A

(abnormal protein aggregations) can be seen within neurons

113
Q

What are the 4 cardinal features of PD?

A

Tremor

Rigidity

Bradykinesia

Postural instability

114
Q

The tremor that is classic in PD is most noticeable at ______. worse with ____ and improves with _____

A

most noticeable at rest

worse with stress

improve with activity and voluntary movement

classic: “pill rolling” tremor

115
Q

Describe the rigidity associated with PD?

A

Increase in resistance to passive movement of a joint that usually begins unilaterally on the same side of the tremor

“Cogwheel rigidity”

Causes flexed posture

116
Q

_______ a ratchety pattern of resistance and relaxation. _______ rigidity that persists throughout the entire movement

A

Cogwheel rigidity

Lead pipe rigidity

117
Q

How does the bradykinesia present in PD?

A

starts distal and moves proximally

loss fine motor skills
decreased extremity movements: shuffling steps
“mask-like” face with infrequent blinking
soft, poor quality voice

118
Q

How do you test postural instability in PD? describe each

A

pull test: stand behind pt and pull them backwards

myerson sign: tap the bridge of the nose and the pt with PD with start blinking

119
Q

What is the Glabellar reflex?

A

Tapping the bridge of the nose produces sustained blink

120
Q

**How do you make the dx of PD?

A

Must have bradykinesia with either rigidity and/or tremor

Must respond to a dopaminergic agent

No muscle weakness or changes in DTRs or plantar response

no labs/imaging are required

121
Q

What is the tx for MILD PD?

A

benztropine (Cogentin) , trihexyphenidyl (Artane)

Amantadine

selegiline (Eldepryl), rasagiline (Azilect), safinamide (Xadago)

122
Q

_______ and _____ are reserved for mild PD young patients with tremor

A

benztropine (Cogentin) , trihexyphenidyl (Artane)

123
Q

______ MOA increases endogenous production of dopamine. What drug class? What is important to remember?

A

Amantadine

N-Methyl-D-Aspartate (NMDA) receptor antagonists

improves all the motor features of parkinsonism

124
Q

_____ MOA prevents early metabolism of dopamine

A

Selective Monoamine Oxidase Inhibitors (MAOI): selegiline (Eldepryl), rasagiline (Azilect), safinamide (Xadago)

125
Q

What is the treatment for MODERATE PD? Which ones are preferred in younger pts?

A

dopamine agonist: -> preferred in younger patients

pramipexole (Mirapex)
ropinirole (Requip)
ropinirole (Requip XL)
rotigotine (Neupro)

Carbidopa/Levodopa (Sinemet)-> better than dopamine agonists for older patients

126
Q

What is the tx for severe PD? What is the associated pt education?

A

Carbidopa/Levodopa (Sinemet)

start low and titrate slowly, take on empty stomach, AVOID high protein diets

127
Q

What is the drug class adjuvant treatment for PD?

A

Catechol-O-methyltransferase (COMT) inhibitors:
entacapone (Comtan)
tolcapone (Tasmar)
Opicapone (Ogentys)

Acetylcholinesterase (Cholinesterase) inhibitors:
rivastigmine (Exelon)
donepezil (Aricept)

N-Methyl-D-Aspartate (NMDA) Receptor Antagonist:
memantine (Namenda)

add additional antipsychotics if needed: quetiapine (Seroquel)

deep brain stimulation

128
Q

__________ MOA increases dopamine levels and prevents early metabolism of levodopa by blocking COMT (dopaminergic enzyme)

A

Catechol-O-methyltransferase (COMT) inhibitors

129
Q

______ is loss of full control of body movement. It is NOT a ____ but a _____. What part of the brain?

A

ataxia

dx but a symptom

disease of the cerebellum or its pathways

130
Q

______ is the test for ataxia.

_______ is difficulty judging distance, speed, power (abnormal point-to-point)

______: ataxic dysarthria; words are broken into syllables

What part of the brain are all of these tests associated with?

A

cannot perform rapid alternating movements (Dysdiadochokinesis)

Dysmetria

Scanning speech

cerebellar hemisphere

131
Q

gait ataxia, imbalance, vertigo, head bobbing are all associated with ________ cerebellum disfunction

A

midline cerebellum

132
Q

what are the 3 major ataxia types?

A

motor: cerebellar disease

sensory: gets worse when the pt closes their eyes

vestibular: vertigo and dizziness alongside gait issues

133
Q

What will motor ataxia present like?

A

lack of balance and coordination

wide-based gait abnormalities, unclear scanning speech, visual blurriness due to nustagmus, tremor with movement

134
Q

What is sensory ataxia? What is the underlying cause? What will it present like?

A

Inadequate transmission of proprioception or position sense information to the CNS

Damage to peripheral nerves, spinal cord, or cerebellar input tracts

135
Q

What is vestibular ataxia? What will it present like?

A

Dysfunction of the inner ear

136
Q

What should be included in your work up of a pt with ataxia?

A

brain CT/MRI
CSF if concerned for CSF infection
Labs: normal ones plus Vit B12, Vit E, serum ceruloplasmin (copper) and 24 hour urine for copper, serum lactate and pyruvate for mitochondrial disorders

137
Q

rank the dopamine agonists for LEAST to MOST. What is important to note about each MOA? Which one comes in a patch?

A

LEAST: Pramipexole (Mirapex) -D2 receptor only
Ropinirole (Requip) -D2 and D3
MOST: Rotigotine (Neupro)- D1, D2 and D3- comes in patch

138
Q

What are the special instructions with regards to dopamine agonists? When are they used?

A

taper to discontinue; remove patch prior to MRI or cardioversion; watch for augmentation

RLS and Parkinson’s

139
Q

What is the DDI for all dopamine agonists?

A

alcohol

140
Q

orthostatic hypotension, constipation, dyskinesia, somnolence, dizziness, hallucinations, headache, insomnia, abnormal dreams

A

What are the SE of pramipexole at higher dose common seen in PD?

141
Q

_____ MOA blockade of NMDA-preferring glutamate and muscarinic cholinergic receptors and stimulation of dopamine release. What drug class?

A

Amantadine (Gocovri, Osmolex ER)

NMDA Antagonist

142
Q

______ MOA inhibits dopamine, noradrenaline and serotonin release. What drug class?

A

tetrabenazine (Xenazine)

VMAT2 inhibitors

143
Q

What are the 2 CI for tetrabenazine (Xenazine)?

A

liver impairment or use within 14 days of MAOIs

144
Q

**What is the BBW for tetrabenazine (Xenazine)?

A

Black Box Warning:
Worsening Suicidal Ideation/Depression

145
Q

______ MOA irreversible inhibitor of monoamine oxidase (MAO) causing an increase in extracellular levels of dopamine in the striatum. What drug class?

A

selegiline (Eldepryl), rasagiline (Azilect), safinamide (Xadago)

Selective Monoamine Oxidase (MAO B) inhibitors

146
Q

What is the DDI selegiline (Eldepryl), rasagiline (Azilect), safinamide (Xadago)?

A

risk of serotonin syndrome and psychotic episodes

147
Q

**What is the BBW for MAOIs B? Why is the patch CI in children?

A

Worsening Suicidal Ideation/Depression in children/teens

Patch CI in children due to HTN crisis risk

148
Q

_____ MOA Increases levels of dopamine in the CNS. What unique form can this medication be given in?

A

Levodopa / Carbidopa (Sinemet)

Can be given as GI solution (enteral suspension)

149
Q

What are the special instructions for Levodopa / Carbidopa (Sinemet)?

A

avoid abrupt withdrawal, preferred to take on empty stomach to improve absorption if nausea is tolerable, avoid diets high in protein as this will interfere with levodopa transport across the BBB

150
Q

______ MOA inhibit enzyme that breaks down levodopa. What do you need to monitor?

A

entacapone (Comtan), tolcapone (Tasmar), opicapone (Ogentys)

liver function tests with tolcapone due to hepatic necrosis

151
Q
A

Neuro (13 decks)

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