Movement Disorders - Exam 4 Flashcards
What part of the brain do movement disorders effect? What is one important thing to note?
basal ganglia
usually subside while the pt is sleeping
What are the 3 functions of the basal ganglia?
motor control
executive decision making
reward, habits and addiction
_______ neurotransmitter that inhibits the release of acetylcholine at the nerve terminal to help produce smooth motor movements and control. What is one additional feature?
dopamine
also plays a role in reward and motivation pathways
______ inhibitory neurotransmitter that relaxes muscle and allows motor control
Gamma-aminobutyric acid (GABA)
________ neurotransmitter found at the neuromuscular junction and in autonomic ganglia. What is the the role in the peripheral? CNS?
Acetylcholine (Ach)
Excitatory in peripheral nerves
Neuromodulator in CNS
______ is the MC movement disorder. What is it caused by?
tremor in the HANDS -MC
Caused by alternating or synchronous contractions of antagonistic muscles
a “pill-rolling” tremor is associated with _________. An action tremor that occurs with voluntary movement indicates _________.
“Pill-rolling” tremor - Parkinson’s Disease
Cerebellar disease
Give an example of a physiologic postural tremor
fine tremor of outstretched hands
aka a tremor that occurs with sustained posture or position
How are tremors categorized?
rest or action
frequency: Hz per second (speed)
amplitude: amount of motion
- low: smaller movement
- high: larger movement
______ are rapid irregular muscle jerks. How are they classically described?
chorea
Classically involuntary and unpredictable
chorea usually have normal strength but _______. What are 3 different variations of chorea?
difficulty maintaining contraction
Milkmaid’s grasp - hand grip relaxes intermittently
Dancing gait - irregular, unsteady, dips and lurches
Irregular speech - erratic volume and tempo
_______ slow, writhing, sinuous movements. _______ excessive or inappropriate contraction
of muscles causing sustained abnormal posture. When are these movements usually worse? Better?
athetosis
dystonia
worse with stress and activity
improve with sleep
What PE findings are associated with Wilson’s disease? What is it?
athetosis, dystonia, dysarthria, chorea
excessive copper storage disease
______ sudden, recurrent, quick, coordinated, abnormal movements. What is important to note? Can they be suppressed?
COORDINATED!- can also be vocal
can be voluntarily suppressed for short periods
______ neurodevelopmental disorder causing people to develop multiple chronic motor and vocal tics
Tourette Syndrome
Eventually progress to combination of multiple types of tics
Remissions and relapses often seen
______ sudden, rapid, twitch-like contraction. What are the 5 different variations?
myoclonus
action
essential
physiologics
epileptic
secondary
_______ sudden jerky movement caused by interruption of normal muscle activity. What is the classic example? What are they often due to?
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
What is the difference between bradykinesia and hypokinesia?
Bradykinesia - slowed movement
Hypokinesia - decrease in amount of movement
What is freezing?
difficulty in starting or maintaining a rhythmic repetitive activity
What is an enhanced physiologic tremor? What is the underlying cause?
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
What is the MC adult-onset movement disorder? What is the pathophys behind it? What is the mean age of presentation?
Essential Tremor
Altered cellular activity in the ventral intermediate nucleus of the thalamus, some genetic component
35-45 years old, usually manifests by 65
What is the MC mode of genetic transmission in movement disorders?
autosomal dominant
What 2 scenarios can an essential tremor present?
postural: when arms are postured against gravity
kinetic: present with goal directed movements
How will an essential tremor present?
typically affects bilateral HANDS and ARMS and pts will complain of trouble with fine motor activity
and progresses over time
Can an essential tremor just be isolated to the head/voice?
NO! not considered essential tremor unless it effects the arms/hands
What makes an essential tremor better? worse?
Aggravating factors - emotion, hunger, fatigue, temperature extremes
NOT worse with caffeine!
Alleviating factors - improves or resolves with alcohol
What are some PE findings consistent with essential tremor?
tremor is often mild or absent until target is reached
Other than tremor, neuro exam is usually benign
What labs should you order in essential tremor? Why?
CMP (electrolytes), thyroid, ceruloplasmin (Wilson disease)
to rule out secondary causes of tremor
What is the International Parkinson and Movement Disorder Society (IPMDS) Task Force diagnostic criteria for essential tremor?
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
What is first line intermittent treatment for essential tremor? 2nd line?
1st: Propranolol 30 minutes prior to activity/event
1st: Primidone nightly -> takes a few weeks to start seeing the effect
2nd: BZDs, topiramate, gabapentin
When is essential tremor tx CI?
CI in asthma or bradycardia
What are the SE of primidone? What is the rare major one?
Sedating, can cause ataxia and vertigo
rarely suppresses bone marrow -> need to check CBC
What is the continuous treatment for essential tremor?
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)
When is surgical intervention indicated in essential tremor? When is it CI?
disabling tremor with failure of 2+ oral options
CI - dementia, severe cognitive impairment; uncontrolled anxiety/depression
How does the Thalamic ventralis intermedius (VIM) nucleus deep brain stimulation work?
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
How does MRI-guided focused ultrasound thalamotomy work?
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
What is an intention tremor? What is the pathophys behind it? What is the highlighted disease associated with it?
Target-directed, coarse tremor that worsens when closest to the terminal target
Damage to the superior cerebellar peduncle or dentate nucleus (cerebellar disease)
MS
When is a intention tremor the most noticeable? What kind of oscillation is seen with it? What PE test will be abnormal? What frequency?
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
What is Holmes-Stewart maneuver? What movement disorder?
inability to control rebound from a release of flexion against resistance
intention tremor
What is the tx for intention tremor?
no meds indicated
refer to neurology for DBS or thalamotomy as for essential tremor
What is restless leg syndrome? Who is the MC patient? What are some common associated findings with RLS?
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
What is Periodic limb movements of sleep (PLMS)?
involuntary, jerking movements of legs during sleep - usually forceful dorsiflexion, every 20-40 seconds
What is Periodic limb movement disorder (PLMD)?
sleep disturbance or impaired daytime functioning in the absence of RLS
What is the pathophys behind RLS?
abnormal iron levels, poor dopamine reuptake
some genetic component and inherited autosomal dominant
**What labs do you need to order in a pt with RLS? What do you need to do next?
**need to check a ferritin level, iron and transferrin saturation
**Recommended to give iron to any RLS patient with a ferritin <75
What are risk factors for RLS?
Frequent blood donation
Pregnancy
DM
Motor neuron disease
Chronic excessive alcohol use
Amyloidosis
How will a pt describe RLS? What will they NOT say?
“need to move,” “crawling,” “tingling,” “restless,” “cramping,” “pulling,” “creeping,” “electric,” “tension,” “discomfort”
NOT PAINFUL!!
What makes RLS worse? What makes it better?
evenings, periods of inactivity,
Caffeine or sleep deprivation, medications
temporary relief with movement (walking, stretching)
What medications make RLS worse?
Antihistamines-> Benadryl
Serotonergic antidepressants (TCAs, SSRIs, SNRIs)
Dopamine antagonists (antipsychotics, metoclopramide)
When should you tx a patient with RLS?
3+ nights a week
if fasting serum ferritin is below 75 mcg/L
What is the pt education for a pt on ferrous sulfate? when do you d/c? When should you repeat iron panel?
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
What are some non-pharm tx for RLS?
Keeping mind busy during times of rest
Avoid exacerbating factors (caffeine, medications)
Good sleep hygiene
Moderate regular exercise
What are the pharm options for RLS? What drug class?
pramipexole (Mirapex), ropinirole (Requip), rotigotine (Neupro) transdermal patch
Dopamine agonist
When should a pt take pramipexole (Mirapex)/ropinirole (Requip)? **What do these medications in the pt’s risk for?
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
Which dopamine agonist used to treat RLS coming in a transdermal patch?
rotigotine (Neupro) transdermal patch - 1 mg patch per day
What are s/s of augmentation associated with dopamine agonists of RLS medications? What happens if your pt starts exhibiting any of these symptoms?
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
What are the drugs in alpha-2-delta calcium channel ligand class that are used for RLS? What are the SE?
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
_______ sustained and repetitive involuntary muscle contractions. What induces it? What makes it worse? What makes it better?
Dystonia
voluntary movements
worse: stress and fatigue
improved: relaxation and sensory distraction
What is the pathophys behind dystonia?
unknown but found involuntary contraction of both agonistic and antagonistic muscles
What are the factors that dystonia classifications are based on?
age
body distribution
anatomical location
inherited or acquired
primary or secondary
What are the age categories associated with dystonia classifications?
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
What is the difference between primary and secondary dystonia when talking about classifications?
Primary
no other neuro s/s
Secondary
due to underlying disease
other neuro s/s are noted
What is the generalized dystonia? Can be ______ or _______
Generalized dystonia involves multiple areas of the body often including the torso and limbs
genetic: (childhood or adolescent onset) or acquired
What are some causes of acquired generalized dystonia?
birth injury, exposure to certain drugs, head injury, infection
What is focal dystonia? What is the MC form? Who is the MC pt population?
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
What are some focal dystonia subtypes?
What type of focal dystonia? ________ contractions of the lower face, lips, tongue, and/or jaw, causing difficulty speaking and swallowing
Oromandibular Dystonia
What type of focal dystonia? ________ blepharospasm + oromandibular dystonia
meige syndrome
What type of focal dystonia? ________ vocal cord contractions during speech
Spasmodic Dysphonia
________ - MC focal dystonia (50%) that pt’s seek tx for. What is the age of onset?
Cervical dystonia (aka. torticollis)
30-50 years old
What is the tx for dystonia? give both focal and generalized tx options.
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
______ MOA blocks release of Ach at the neuromuscular junction
botox injections
______ MOA dopamine inhibits release of Ach at axon terminals
levodopa/carbidopa (Sinemet)
for levodopa/carbidopa (Sinemet), ______ is converted to dopamine; _______ reduces breakdown of _______ before it gets to the CNS
Levodopa
carbidopa
levodopa
levodopa is the med and carbidopa is the transporter
What is the tx for generalized dystonia in adults who failed levodopa/carbidopa?
First-line: clonazepam (Klonopin)
Second-line: baclofen (GABA agonist)
Can be given orally or intrathecally)
Third-line: trihexyphenidyl (Artane)
What is the tx for generalized dystonia in children who failed levodopa/carbidopa?
First-line: trihexyphenidyl
Second-line: baclofen, BZDs
_____ MOA muscarinic receptor antagonist and increases striatal dopamine release and efflux
trihexyphenidyl (Artane)
What is the tx for refractory generalized dystonia? What drug class?
tetrabenazine (Xenazine) and deutetrabenazine (Austedo)
VMAT2 inhibitors
______ MOA depletes dopamine (and other monoamines) at the neuron synapse reducing the excitability of the neurons. What are the SE?
VMAT2 inhibitors
tetrabenazine (Xenazine) and deutetrabenazine (Austedo)
depression, anhedonia
_______ is the last resort in dystonia patients who fail all other conservative therapies
Deep brain stimulation (DBS)
What is the underlying cause of infanitle torticollis? What do you need to rule out?
Most often d/t damage or inflammation to the SCM or trapezius
rule out infectious etiologies
What is the tx for infantile torticollis?
NSAIDS, soft cervical collar physical therapy
What is Tourette’s Syndrome characterized by? What is the average age of onset?
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)
What are some risk factors for Tourette Syndrome?
Smoking during pregnancy
Complications during pregnancy
Low birth weight
What is the thought processes of the pathophys behind Tourette Syndrome?
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
What are the different types of tics? What makes it worse? Can they be suppressed?
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!
What is simple Tourette Syndrome presentation?
Simple: Brief movements involving one muscle group that are characterized by simple sounds
motor tics are present in 80%
What is complex Tourette Syndrome?
Complex:
More purposeful, orchestrated movements
Longer patterns of speech
Where do motor tics in TS commonly present?
Most common in FACE; also common in head and shoulders
What other conditions is Tourette Syndrome associated with?
OCD and/or ADHD in 50% of patients
Up to 80% of ASD patients have tics
Behavioral problems
Mood disorders
What is the dx criteria for Tourette Syndrome?
What is the management for Tourette Syndrome? When should you treat?
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
What are the first line pharm txs in Tourette’s Syndrome? What do they help with?
1st: haloperidol (Haldol), pimozide (Orap), aripiprazole (Abilify)
Tics improved by up to 80% with treatment
What are the 2nd line pharm tx for Tourette Syndrome? Are they FDA approved?
VMAT2 Inhibitor: Tetrabenazine (Xenazine)
Alpha-adrenergic agonists: clonidine and guanfacine (Intuniv)
NOT FDA approved
_____ MOA stimulates function of the prefrontal cortex, increasing ability to control unwanted impulses
Alpha-adrenergic agonists: clonidine and guanfacine (Intuniv)
What are the non-pharm tx for TS?
tic-awareness training
competing-response training
consider: Botox and Bilateral high frequency brain stimulation
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?
chorea and dementia
30-50 years old
What gene is mutated in Huntington’s Disease?
Autosomal dominant disorder resulting in a mutation in the Huntington gene (HTT)
Huntington’s Disease is a neuronal cell loss, particularly in the _____ and _______ which leads to ________
cerebral cortex and corpus striatum
neurotransmitter dysfunction which leads to reduced GABA and Ach as well as their associated enzymes
How does HD present? specifically _____
May have either abnormal movements or intellectual changes first
Chorea: can be mild fidgetiness or severe uncontrollable flailing
What does early mental status changes look like in HD? late?
early: irritability, moodiness, and antisocial behavior
late: dementia
often associated with weight loss and cachexia
How do you make the dx of HD?
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
What drug do you use in HD to help with the motor symptoms?
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
What are classic abnormalities seen with parkinsonism/ Parkinson’s Disease?
resting tremor
slow movement
impaired speech
muscle stiffness
What is the 2nd MC neurodegenerative disease? What is the typical pt?
Parkinson’s Disease (PD) with Alzheimer’s being the first
over 60 year old man
What is the underlying cause of PD?
combo of genetics and environment
What reduces risk of PD?
Diet - caffeine, coffee
Meds - Ibuprofen, statins
Lifestyle - cigarette smoking, moderate exercise
What increases the risk of PD?
Increased age
(+) fam hx
Repetitive head trauma
Toxins - herbicide/pesticide exposure, heavy metals, well wate
What is the pathophys behind PD?
Degeneration of the dopamine-producing neurons in the substantia nigra
What is the dopamine depletion seen in PD? _____ in the striatum normally helps balance the amount of ____
imbalance between dopamine and acetylcholine
Dopamine
Ach
in PD, low ______ equals slow voluntary motor control. high ______ equals ______. What prevents the neurons from working properly?
low dopamine
high acetylcholine = dyskinesia
Lewy bodies prevent the neurons from working properly
What are Lewy bodies?
(abnormal protein aggregations) can be seen within neurons
What are the 4 cardinal features of PD?
Tremor
Rigidity
Bradykinesia
Postural instability
The tremor that is classic in PD is most noticeable at ______. worse with ____ and improves with _____
most noticeable at rest
worse with stress
improve with activity and voluntary movement
classic: “pill rolling” tremor
Describe the rigidity associated with PD?
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
_______ a ratchety pattern of resistance and relaxation. _______ rigidity that persists throughout the entire movement
Cogwheel rigidity
Lead pipe rigidity
How does the bradykinesia present in PD?
starts distal and moves proximally
loss fine motor skills
decreased extremity movements: shuffling steps
“mask-like” face with infrequent blinking
soft, poor quality voice
How do you test postural instability in PD? describe each
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
What is the Glabellar reflex?
Tapping the bridge of the nose produces sustained blink
**How do you make the dx of PD?
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
What is the tx for MILD PD?
benztropine (Cogentin) , trihexyphenidyl (Artane)
Amantadine
selegiline (Eldepryl), rasagiline (Azilect), safinamide (Xadago)
_______ and _____ are reserved for mild PD young patients with tremor
benztropine (Cogentin) , trihexyphenidyl (Artane)
______ MOA increases endogenous production of dopamine. What drug class? What is important to remember?
Amantadine
N-Methyl-D-Aspartate (NMDA) receptor antagonists
improves all the motor features of parkinsonism
_____ MOA prevents early metabolism of dopamine
Selective Monoamine Oxidase Inhibitors (MAOI): selegiline (Eldepryl), rasagiline (Azilect), safinamide (Xadago)
What is the treatment for MODERATE PD? Which ones are preferred in younger pts?
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
What is the tx for severe PD? What is the associated pt education?
Carbidopa/Levodopa (Sinemet)
start low and titrate slowly, take on empty stomach, AVOID high protein diets
What is the drug class adjuvant treatment for PD?
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
__________ MOA increases dopamine levels and prevents early metabolism of levodopa by blocking COMT (dopaminergic enzyme)
Catechol-O-methyltransferase (COMT) inhibitors
______ is loss of full control of body movement. It is NOT a ____ but a _____. What part of the brain?
ataxia
dx but a symptom
disease of the cerebellum or its pathways
______ 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?
cannot perform rapid alternating movements (Dysdiadochokinesis)
Dysmetria
Scanning speech
cerebellar hemisphere
gait ataxia, imbalance, vertigo, head bobbing are all associated with ________ cerebellum disfunction
midline cerebellum
what are the 3 major ataxia types?
motor: cerebellar disease
sensory: gets worse when the pt closes their eyes
vestibular: vertigo and dizziness alongside gait issues
What will motor ataxia present like?
lack of balance and coordination
wide-based gait abnormalities, unclear scanning speech, visual blurriness due to nustagmus, tremor with movement
What is sensory ataxia? What is the underlying cause? What will it present like?
Inadequate transmission of proprioception or position sense information to the CNS
Damage to peripheral nerves, spinal cord, or cerebellar input tracts
What is vestibular ataxia? What will it present like?
Dysfunction of the inner ear
What should be included in your work up of a pt with ataxia?
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
rank the dopamine agonists for LEAST to MOST. What is important to note about each MOA? Which one comes in a patch?
LEAST: Pramipexole (Mirapex) -D2 receptor only
Ropinirole (Requip) -D2 and D3
MOST: Rotigotine (Neupro)- D1, D2 and D3- comes in patch
What are the special instructions with regards to dopamine agonists? When are they used?
taper to discontinue; remove patch prior to MRI or cardioversion; watch for augmentation
RLS and Parkinson’s
What is the DDI for all dopamine agonists?
alcohol
orthostatic hypotension, constipation, dyskinesia, somnolence, dizziness, hallucinations, headache, insomnia, abnormal dreams
What are the SE of pramipexole at higher dose common seen in PD?
_____ MOA blockade of NMDA-preferring glutamate and muscarinic cholinergic receptors and stimulation of dopamine release. What drug class?
Amantadine (Gocovri, Osmolex ER)
NMDA Antagonist
______ MOA inhibits dopamine, noradrenaline and serotonin release. What drug class?
tetrabenazine (Xenazine)
VMAT2 inhibitors
What are the 2 CI for tetrabenazine (Xenazine)?
liver impairment or use within 14 days of MAOIs
**What is the BBW for tetrabenazine (Xenazine)?
Black Box Warning:
Worsening Suicidal Ideation/Depression
______ MOA irreversible inhibitor of monoamine oxidase (MAO) causing an increase in extracellular levels of dopamine in the striatum. What drug class?
selegiline (Eldepryl), rasagiline (Azilect), safinamide (Xadago)
Selective Monoamine Oxidase (MAO B) inhibitors
What is the DDI selegiline (Eldepryl), rasagiline (Azilect), safinamide (Xadago)?
risk of serotonin syndrome and psychotic episodes
**What is the BBW for MAOIs B? Why is the patch CI in children?
Worsening Suicidal Ideation/Depression in children/teens
Patch CI in children due to HTN crisis risk
_____ MOA Increases levels of dopamine in the CNS. What unique form can this medication be given in?
Levodopa / Carbidopa (Sinemet)
Can be given as GI solution (enteral suspension)
What are the special instructions for Levodopa / Carbidopa (Sinemet)?
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
______ MOA inhibit enzyme that breaks down levodopa. What do you need to monitor?
entacapone (Comtan), tolcapone (Tasmar), opicapone (Ogentys)
liver function tests with tolcapone due to hepatic necrosis
