movement Flashcards
resting tremor: etiology, key characteristics, dx, tx
Etiologies:
-Parkinson’s (esp Pill rolling tremor)
-Drug induced Parkinsonism’s (metoclopramide, neuroleptics)
-Supranuclear palsy
-Wilson’s disease
key characteristics:
-usually Asymmetric at low frequency with coarse movements
-Improved with target-direct movements + cognitive function (spell world backward)
-Worsens with stress
-Occurs when relaxed and supported against gravity
Clinical diagnosis
-Tx: Dopaminergic agents (carbidopa-levodopa)
essential tremor: clinical manifestations; what makes it better or worse
-MC movement disorder (5% worldwide)
-Autosomal dominant
-Teens and 60s (Young pt with anxiety - b/l), incidence increases with age
Action tremor:
-POSTURAL, bilateral, intentional tremor of the hands (90%), forearms, head (30%), neck or voice (15%)
-UE»_space;> LE
-Bilateral (symmetric compared to Parkinsons)
- improves with: Temporary relief with ETOH!!!**, body is supported, at rest
worse:
- -anxiety/stress/caffeine
- intentional/goal directed activity
- postural movements against gravity: hold arms out outstretched
essential tremor PE, workup, treatment
Exam:
-On finger-to-nose test -> tremor increases as it approaches the target -> but no dysmetria
- tremors decrease during cognitive function (spell world backward)
-No other neuro findings!!!!
Workup:
- Electrolytes, TFTs, family hx
-No brain imaging required
Tx not usually required
-PROPANOLOL!!! may help if severe or situational
- consider short acting BZD or primidone
-Resistant/treatment failure: gabapentin, topiramate, nimodipine
action tremor: intention tremor
Definition:
-zig zap tremor gets worse as you get close to target
-Coarse hand tremors
-Improved with rest
- aka CEREBELLAR tremor: dysmetria on finger to nose
Etiology:
-Cerebellar lesions! (stroke, tumor, trauma)
-Drug induced: alcohol abuse, lithium
-Multiple sclerosis
-Wilson’s disease
-Midbrain stroke/trauma
workup:
-CT/MRI assess for cerebellar lesions, multiple sclerosis
-Screen for alcohol abuse or lithium toxicity
Remember the other cerebellar signs:
-Dysmetria (FTN, HTS test)- finger to nose -> over/under shoot
-Dysdiadochokinesia (RAHM test)- rapid alternating
-Dysarthria, nystagmus, abnormal gait
- Cerebellar: double decussation -> ipsilateral sx
physiologic tremor
action tremor:
-We ALL have these
-Does NOT dictate an underlying disorder
Due to SNS stimulation:
-Stress, exercise, fatigue
-Intoxication: caffeine, alcohol
-Drug: valproate, lithium, SSRI, TCAs, B2 agonists, levothyroxine
-Withdrawal: Alcohol, benzodiazepines, barbituates, marijuana
-Medical: Hyperthyroidism, pheochromocytoma
-Other: Hypoglycemia
-Clear history = no diagnostic testing
what meds and substances exacerbate tremors
hyperkinesis vs hypokinesis sx
hyperkinesis: increased movement
- EPS sx, dyskinesia
- tremors
- dystonia: involuntary sustained muscle contractions
- chorea: dance like movement
- tics: sudden repetitive movements, vocalization
- myoclonus: involuntary muscle jerks
Hypokinesis:
- bradykinesia
- rigidity: velocity independent stiffness in muscle tone
- resting tremor
Hyperkinetic movements: tremors, dystonia, chorea
Tremors:
-Rhythmic oscillations usuallybrought onby action
-MC organic and functional movement disorder
Dystonia:
- Huntington ds and med ADR
-sustained, Patterned movements
-Sensory trick- do certain things to stop it like touch your face
-May be task-specific- worsens when you try to stop it
Chorea:
-Random movements, parakinesia (attempt to incorporate into their normal movements)
-DANCE like, rhythmic
-incorporate it into daily movements
-Motor impersistence: Cant listen to instructions - cant stay still
Tics:
-paroxysmal + stereotypes muscle contractions causing movements or vocalizations with premonitory urge
-similar patterns repeat
-temporarily suppressible
-Suggestible = talking about it may trigger it
Premonitory urge: before they tic, feel that they need to tic -> pressure goes away after tic
Myoclonus:
-Lightning-like movements
-Negative (loss of tone with compensatory contraction ->Asterixis)
-or positive (involuntary contraction
Hyperkinetic movements: tics and myoclonus
Tics:
-paroxysmal + stereotypes muscle contractions causing movements or vocalizations with premonitory urge
-similar patterns repeat
-temporarily suppressible
-Suggestible = talking about it may trigger it
Premonitory urge: before they tic, feel that they need to tic -> pressure goes away after tic
Myoclonus:
-Lightning-like movements
- sudden brief muscle jerks
-Negative (loss of tone with compensatory contraction ->Asterixis)
-or positive (involuntary contraction)
57 year oldmale
PMH: HTN (lisinopril) hypothyroidism (synthroid)
Right arm shaking x 2years
Initially in thumb, nowslowly progressed toentire hand
Mostly at rest, improves with movement
ROS: Mild decrease in smell
Otherwise no other neurologic symptomsincludingchanges in walking orbalance,sleep
Mild rest tremor noted in right hand
Trace rest tremor in left hand
Tremor re-emerges on posture holding
Slight slowness of left finger/toe taps
Decreased left arm swing
Pull test normal
PMH: HTN (lisinopril) hypothyroidism (synthroid)
Right arm shaking x 2years
Initially in thumb, nowslowly progressed toentire hand
Mostly at rest, improves with movement
ROS: Mild decrease in smell
Otherwise no other neurologic symptomsincludingchanges in walking orbalance,sleep
Mild rest tremor noted in right hand
Trace rest tremor in left hand
Tremor re-emerges on posture holding
Slight slowness of left finger/toe taps
Decreased left arm swing
Pull test normal
tremors
-bradykinesia
-no arm swing
-pull test normal -> not severe
-parkinsons
Parkinsonism 2/3
- Hypokinesia
- r/o parkinsons
parkinson’s disease definition and overview, risk factors
Def: Neurogenerative disease of the DOPAMINE producing neurons in substantia NIGRA of the basal ganglia
-2nd most common neurodegenerative disease after Alzheimer’s
-Age onset: 45-65 years
-1% of adults > 65 years old
-progressive and chronic with no cure
-motor symptoms first then dementia
Risk factors:
-Genetic: 10-15% are familial
-Diet/metabolism: Low Vit D, high iron, obesity, Wilsons disease (too much copper)
-Hx of TBI
-DoPAmine Down = PArkinsons Dz!
parkinson’s disease: etiology and what is the pathologic hallmark in histology
Normally: dopamine inhibits ACH in the substantia nigra of the basal ganglia
-In Parkinson’s, there is damage to the substantia nigra and dopaminergic neurons
-Less dopamine -> more ACH -> uncontrolled movement
Hallmark:
-Aggregates of misfolded α-Synuclein and other proteins = LEWY BODIES***
parkinsonism motor triad
-Bradykinesia, resting tremor, rigidity
Primary Parkinsonism
Parkinson’s disease:
-Idiopathic dopamine depletion!!!!!
-Possible genetic factors: α-Synuclein, LRRK2, PARK2 mutations
secondary parkinsonisms
-Drug induced = Typical antipsychotics (Haldol), antiemetics (metoclopramide, chlorpromazine), amiodarone, valproate, lithium
-Vascular = ischemic small vessel disease (lacunar) esp of the internal capsule
-Structural brain lesions = hydrocephalus, chronic SDH, tumors
-Recurrent TBI
-Metabolic disorders/toxins = chronic liver failure, rapid sodium shifts, copper or iron deposition diseases in basal ganglia, certain pesticides etc.
atypical parkinsonisms
-diagnosed by specialists
-dont need to know these
-Progressive supranuclear palsy (PSP)
-Corticobasal degeneration (CBD)
-Multiple system atrophy (MSA)
parkinson’s disease: non-motor symptoms
SOAP
Sleep disturbances:
-Insomnia
-REM sleep behavioral disorder
-Restless leg syndrome
-Excessive daytime sleepiness
Other:
-Fatigue
-Seborrheic dermatitis (20-60%)
-Anosmia
Autonomic symptoms:
-Drooling
- CONSTIPATION
-Sexual dysfunction
-Urine problems
-Dysphagia or speech impairment
-Orthostatic hypotension
Psychologic:
-ANXIETY/DEPRESSION/APATHY
-Psychosis (20-40%)
-Dementia develops in 50% of patient (late finding)
parkinson’s disease PE over time and tremors
Signs of Parkinson’s progress over time
-Unliteral at onset -> progress to bilateral
Tremors:
-Often: resting, distal UE, ASYMMETRIC
- resting tremor “pill-rolling”
-Hold arms out against gravity (postural tremor) -> Once they settle into their position -> resting tremor
-Finger to nose test: action/kinetic tremor
-Can involve: jaw, lips, tongue, legs
- Micrographia: handwriting becomes progressively smaller and cramped
parkinson vs huntington main differences: reflexes, onset, and cognitive decline onset
Deep tendon reflex:
- PD: normal or diminished -> rigidity, bradykinesia
- Huntington ds: hyperreflexia -> chorea
Onset:
- PD: 45-65
- Huntington ds: 30-50s
cognitive decline:
- PD: dementia and cognitive decline is late onset sx
- huntington: Early onset, often associated with psychiatric symptoms (depression, anxiety, aggression).
parkinsons disease: rigidity - most sensitive area to test?
Resistance to passive joint movement independent of speed
-Most sensitive area is the wrist!!!
-Froment maneuver can make it easier to detect subclinical rigidity -> make them do something with one wrist and observe the other
-Cogwheel rigidity = ratchet pattern of resistance/relaxation while moving the limb through full ROM, feels as if the limb is moving in small steps rather than smoothly.
-Lead-pipe rigidity= smooth and constant resistance in passive ROM
- Stooped posture, decreased arm swing, stiffness and pain
-Masked facies
parkinson’s disease exam: akinesia/bradykinesia sx
-Slowness of voluntary movement + decreased automatic movements described as “weakness, incoordination, tiredness”
-Decreased blinking
-Difficulty with rapid finger tapping, or, opening and closing a fist
-Wrist pronation-supination slower
-Toe or heel taps
- micrographia
parkinson’s disease exam: postural instability (coordination and gait) and how to test
-progressive: starts with difficulty out of chair -> shuffling, difficulty turning -> falls
-Imbalance and tendency to fall
Shuffling gait: short quick steps, decreased arm swing, and freezing
-!+Pull test = Unable to stop themselves from going forward (propulsion) or backward (retropulsion)
parkinson dx
-Clinical diagnosis
-CT/MRI brain: r/o secondary causes
-DaTSCAN: SPECT scan to evaluate levodopa uptake and conversion to dopamine within the substania nigra
early tx of parkinsons disease: drug names and MOA
No cure! Goal is to improve symptoms. Does not slow down progression
-pts can refuse until they need tx
Levodopa (L-Dopa), Levodopa-Carbidopa (Sinemet): #1 choice!!!
-Precursor to dopamine
- best drug for motor sx
Dopamine receptor agonists:
- Pramipexole*
- Ropinirole *
- Rotigotine
MAO-B inhibiters:
- Selegiline**
- Rasagiline, Safinamide
- MAO-B normally breaks down dopamine -> prevents dopamine breakdown
Levodopa (L-Dopa), Levodopa-Carbidopa (Sinemet): class, overview, indication, ADRs, important consideration
Dopamine precursor
Carbidopa - extends the half-life but still needs multiple times per day and need to take even more often once it gets worse
-Most effective tx for MOTOR SX and generally safe BUT is associated with time/dosage dependent dyskinesias + PSYCHOSIS/hallucinations
ADRs:
- N/V **
- orthostatic hypotension**
- dizziness, somnolence or insomnia
- tardive dyskinesia***
- impulse control
- behavioral abnormalities
- PSYCHOSIS + visual hallucinations
Cons:
- Multiple times per day dosing -> need to take it more and more as time goes on
-Do NOT abruptly stop -> Akinetic crisis -> neuroleptic malignant syndrome
Dopamine receptor agonists: drug names, indication, adrs
pramipexole*
ropinirole*
rotigotine
apomorphine
Indication:
-Less effective for motor sx than levopdopa
- less dyskinesia in YOUNGER pts: consider for initial tx in YOUNGER PD pts to delay use of levodopa
- once a day dosing!!!!!!
ADRs:
- n/v*
- orthostatic hypotension
- More frequent cognitive side effects than levodopa: confusion, impulse control, HALLUCINATION
-If pt is resistant to levodopa, will be resistant to dopamine agonists
MAO-B inhibiters: drug names, indication, consideration
drug names: SELEGLINE, Rasagiline, Safinamide
MOA:
-MAOB normally breaks down dopamine -> block dopamine breakdown
Indication:
- mild parkinsons ds sx with minimal impact on QOL
Considerations:
-Poorer efficacy
- less side effects
- more likely to cause serotonin syndrome: do NOT GIVE WITH TCAs and SSRIs)
- HTN crisis with tyramine food
MAO = SRS (SELEGLINE, Rasagiline, Safinamide)
- youre the devil srs..
- but you dont work that well and have minimal impact on QOL
- SRS: SSRI, SEs less, tyramine
major ADRs/cons of parkinson treatment drugs
Levodopa:
- N/V
- orthostatic hypotension
- time/dosage dependent dyskinesias
- PSYCHOSIS + HALLUCINATIONS
- stopping abruptly: AKINETIC CRISIS
Dopamine receptor agonist:
- more frequent cognitive side effects than levodopa
- if resistant to levodopa -> resistant to this class
MAO-B inhibitiors:
- poorer efficacy but less adrs
- more likely to cause SEROTONIN SYNDROME -> dont give with TCAs and SSRIs
Patient eventually started on LEVODOPA after discussion on side effects and efficacy
Fast forward 5 years:
States good control until recently
Levodopa only works for ~1 hr
He is slower, stiffer, and occasionally falls when the levodopa wears off
Also new hyperkinetic movements
Difficulty concentrating, multi-asking, and getting words out
Depressed and anxious
Acting out vivid dreams
Is this typical of Parkinsons?
Fast forward 5 years:
States good control until recently
Levodopa only works for ~1 hr
He is slower, stiffer, and occasionally falls when the levodopa wears off
Difficulty concentrating, multi-asking, and getting words out
Depressed and anxious
Is this typical of Parkinsons?
yes
-late stage parkinsons
progression of parkinsons
Prodromal parkinson:
- sleep problems, constipation, anosmia, depression
-early stage dx: bradykinesia, rigidity, tremor
- mid stage: urinary sx, dyskinesias, orthostatic hypotension (more autonomic)
-late- falls, dementia, psychosis/hallucinations
on-off phenomenon
-Progressive degeneration of nigrostriatal dopamine terminals limits the normal uptake/release of dopamine
-Reduces buffering of natural fluctuations of levodopa due to short half life
-mild stages of parkinsons- a lot of dopamine neurons available -> therapeutic window is larger
-troughs happen when you take levadopa -> peaks throughout day
-on time: when the meds are working
-off time: no levadopa in the system -> symptoms
-as you have less and less neurons as disease progresses -> therapeutic window becomes smaller and smaller -> delayed-on and wears off faster
-too much dopamine for the receptors -> dyskinesia
Benztropine: moa, indication, adrs
MOA: Anticholinergic
-Decreases acetylcholine concentration
Indication:
-monotherapy in young patients whose only symptoms are TREMORS***
- late tx for parkinsons ds
-Does not improve bradykinesia
ADRs:
-Cognitive side effects are severe: memory impairment, CNS toxicity
- anti-SLUDGE: dry mouth, dry eyes, constipation, urinary retention, impaired sweating, tachycardia
Deep brain stimulation:
late tx for parkinsons ds
-Implanted leads connect to an impulse generator in the chest under the skin, which stimulates the globus palladus or subthalamic nucleus for MOTOR CONTROL
- Safe, reversible
- good for rigidity and tremors in select pts
- Cons: hardware can fail, peri-op and post-op complications
COMT inhibitors: moa, indication, adr
Drug names: Entacapone, Opicapone, Tolcapone
MOA:
-Extends half life of levodopa by inhibiting the enzyme that breaks down levodopa
Indication:
-Treats “off” phase of levodopa: combats end of dose akinesia
-Can worsen some dyskinesias
- late tx for parkinsons ds
ADR
-Liver toxicity
late tx for parkinsons ds list of tx options
- Amantadine
- benztropine
- COMT inhibitors: Entacapone, Opicapone, Tolcapone
-Deep brain stimulation
NMDA Antagonist: Amantadine
MOA:
-Increases dopamine release, and decreased reuptake
indication:
- short term tx of mild sx
- levodopa-induced DYSKINESIA ***
- late tx for parkinsons ds
ADRs:
-Can worsen PSYCHOTIC SX: confusion, hallucinations, nightmares
- avoid in: renal failure and causes PROLONGED QT
Most important differential when considering Parkinson’s disease?
drug induced parkinsonisms!!!
-Drug induced = potentially reversible with cessation of agent
-Clinically indistinguishable from Parkinson’s (except maybe more bilateral?)
-Symptoms/signs can improve in ~80% of pts within 8 wks of discontinuation of offending agent
-haldols, antiemetics-metoclopramide
- Metoclopramide -> often give Benadryl to hide parkinsonism sx
A 72 year old woman with a history of Parkinson’s controlled with levodopa, presents because of seeing things that she knows are not there. Sometimes she sees a dog in her kitchen, or a stranger in her garden, which no one else sees. She reports quitting drinking alcohol three months ago. Reports no motivation to do daily tasks. Exam shows a mild resting tremor of the hands and bradykinesia. Her thought process is logical. Which of the following is the most likely cause of her symptoms?
B. Adverse effect of medication!!! -> levadopa can cause hallucinations
huntington’s disease def and cause and imaging results
-Inherited, progressive neurodegenerative disorder of nerve cells in cerebral cortex and caudate nucleus
-Autosomal dominant
-genetic cause: CAG trinucleotide repeat expansion in the HTT (Huntingtin) gene on chromosome 4p16.3. -> abnormally long huntingtin protein -> earlier and worse symptoms
labs/imaging:
-High dopamine levels, low ACH and GABA
-Causes neurotoxicity, cerebral and caudate nucleus atrophy -> ↓ ACH and GABA
-Male > Female
-Higher prevalence in western European
-Symptom onset ~30-40 years old
-fatal within 15-20y after onset
-5-10% of cases occur as juvenile HD
-becoming earlier and earlier bc more repeats of CAD
huntington ds hallmark sx
3 hallmarks: 3 Ms = Mood Movement and Memory
- mood: Psychiatric problems
- movement= chorea
- memory: dementia and cognitive impairment with executive dysfunction
MOOD:
- Marked behavioral, personality, psychiatric changes
- can occur years prior to onset of chorea or at any point
- MDD
- SCHIZOPHRENIC psychosis: paranoid, auditory hallucinations
-Aggression, apathy, anxiety
- suicidal ideation
MOVEMENT = CHOREA -> defining feature at dx in face, trunk, limbs
- worse with voluntary movements and stress
MEMORY = Dementia and cognitive impairment
- executive function, recall
- late: memory loss
huntington ds: how does wt change and what type of eye pathology?
wt loss and cachexia/muscle wasting despite caloric intake
- moa unknown
eye movement: delay in initiating volitional saccades -> bad at shifting gaze between points
huntington manifestations: chorea
Defining feature at dx – face, trunk, limbs
-Chorea (“dance-like gait”) = involuntary, sudden, irregular, non-repetitive, arrhythmic movements of the limbs, neck, head, and/or face
-May be unaware of movements or incorporate into purposeful actions (termed parakinesia)
-Hypotonia with hyperreflexia (early signs) +/- dystonia
-!!Progressive loss of voluntary motor control
-Becomes more florid, widespread, interfering with movement
-Late: affects diaphragm, pharynx, larynx -> dysarthria, dysphagia, involuntary vocalizations
-Motor impersistence: difficulty with sustained tongue protrusion
-CHOREA is common in early stages. Hypokinetic/akinetic symptoms may dominate in late stages.
huntingtons manifestations: psychiatric symptoms
-Can occur years prior to onset of chorea/at any point
- behavioral changes: Aggression, apathy, anxiety
-MDD
-Schizophrenic-like psychosis: Paranoid delusions, Auditory hallucinations
huntington manifestations: atypical features in adults vs kids
-Adults – can present with signs of parkinsonism without tremor
Juvenile - <20 y/o, can include myoclonus, seizures, behavioral Parkinsonism; absent chorea
huntington’s disease workup and testing
-Neuroimaging not needed but MRI/CT reveals CAUDATE nucleus atrophy
Genetic testing: PCR for CAG (autosomal dominant)
->36 repeats is confirmatory
-More repeats = earlier onset of sx
Genetic testing indicated in:
-Adults with motor signs suggestive of Huntington’s disease
-Children with fam hx of HD with signs of juvenile onset HD
-Not recommended in asymptomatic children/adults
huntington disease: treatment overview
-There is NO CURE, NO SLOWING, NO REVERSING (fatal within ~ 15 yrs)
Goals of care:
-Multi-disciplinary approach - Neurologist, psychiatric, psychologist, geneticist, SW, PT, OT, SPT, Hospice
Chorea sx relief:
- Tetrabenazine*** : dopamine-depleting agent -> decreases release of dopamine from presynaptic neurons
- 2nd gen antipsychotics: olanzapine, risperidone, aripiprazole,
- 1st gen antipsychotics: haloperidol, chlorpromazine
tetrabenzaine: indication, moa, ADRs
Indications: mild, mod, severe chorea, refractory to non-pharm measures
MOA:
-Dopamine-depleting agents: inhibit pre-synaptic vesicular monoamine transporter type 2 (VMAT2) -> depletes dopamine release
-Dosing: 12.5 mg QD x 1 week, then 12.5 mg BID, increase by 12.5 mg increments/week until chorea improves or AE occur
-Can be expensive, manufacturer assistance program
ADRs:
- depressed mood (rapid, severe onset), sedation, akathisia, parkinsonism, prolonged QTc
-BB: Increased risk of suicidality
-With SSRIs (CYP 2D6 inhibitor) – reduce dose by 50%
38 year old male presents for worsening mood and irritability that first began several months ago. His wife also notes that he has been having “shaky” movements in the limbs and trunk. No past medical history or medication use. Father died of suicide at age 45 years old. He speaks slowly and quietly. Recall is poor at 1/3 words. There are irregular movements of the arms and legs at rest. Muscle strength 5/5, reflexes 2+, sensation intact. Further evaluation might show which of the following?
D. Caudate nuclear atrophy on MRI!!!
Restless leg syndrome: AKA Willis-Ekbom Disease (WED): definition, worse with what and relieved with what, consequences and epidemiology
Definition: SLEEP related movement disorder
- involuntary jerking movements! of leg during sleep: called periodic limb movements of sleep (PLMS)
-Urge to move the legs- Associated with an unpleasant sensation in the legs
-Worsens with rest (sitting, lying down) thus worse at night!
- Worse w/ antihistamines, DAs, TCAs/SSRIs/SNRIs, Mirtazapine
-Relieved with movement (walking, stretching, rubbing/pressure)
- -Consequences:
-Sleep onset insomnia, nocturnal awakenings, depression/anxiety
Epidemiology:
-5-15% of adults; primarily Caucasian
-FH (+) in 40-60%
-Female > male
-Peak incidence: 30-40 years of age
restless leg syndrome primary vs secondary
Primary RLS: Idiopathic, familial in up to 77% of cases
Secondary RLS: Underlying condition or drug
-Iron deficiency
-Vitamin deficiency
-Peripheral neuropathy (esp DM)
-Kidney failure (uremia)
-Depression, anxiety
-Inflammatory: Celiac, rheumatoid, IBD
-Neuro: PARKINSONS disease, Multiple sclerosis, Polyneuropathies, spinal cord diseases
-Drugs: H1 antihistamines, antidepressants, dopamine antagonists, lithium, beta blockers
-Pregnancy
Not attributable to: myalgia, venous stasis, leg edema, arthritis, leg cramps, positional discomfort, habitual foot tapping
restless leg syndrome: dx and tx
dx:
-Clinical diagnosis
-Check for: CBC/Ferritin (Iron stores), BUN/Cr (Uremia)
Non pharmacologic therapy:
-Avoid alcohol / caffeine , certain medications (antidepressants, metoclopramide, Benadryl)
-Do mentally alerting activities while at rest
-Regular exercise
-Leg massage, soaking legs in warm bath, pneumatic compression devices.
Treat underlying cause in secondary!!!
-PO iron repletion therapy if serum ferritin ≤ 75 mg/dl
Gabapentinoids (Alpha-2-delta calcium channel ligands): Gabapentin, Pregabalin
-Comorbid pain, anxiety, insomnia
-First line tx for most patients unless contraindicated!!!!!
Dopamine Agonists: Pramipexole (Mirapex), Ropinirole (Requip)
-comorbid depression or obesity/metabolic syndrome
tic disorders overview
-1. tourettes syndrome
-2. persistent motor or vocal tic disorder
-3. provisional tic disorder
-Tics are considered a neuropsychiatric disorder
def: Quick, involuntary, intermittent, non-rhythmic movements or vocalizations
-Happen repetitively
-Not cause by other disorders (substance abuse, HD)
-Premonitory urge: Tics are often preceded by a feeling or urge to tic
-Diagnosed in 1% of children (motor and vocal tics)
-Male»_space;Female
-Associated with: ADHD!, OCD!, learning disabilities, sleep disorders, conduct disorders, mood/anxiety disorders, Family history of tics, or Tourette’s
-Most severe before puberty-> Worsens with stress, anxiety, exhaustion + 50% have symptom resolution by age 18
vocal and motor tics
tourettes syndrome criteria
-Onset before 18 (usually between 4-6)
-Tics persist ≥ 1 year
-≥ 2 motor tics
-≥ 1 vocal tic
-NOT explained by other medical conditions or substance use (cocaine)
tourette’s syndrome and tic disorders: management
Management:
-Cognitive behavior intervention for tics (CBIT)
-Habit reversal training (HRT)
-Anxiety and depression reducing strategies
Medication
-Dopamine blocking agents (Haloperidol, Risperidone. New: Tetrabenazine off-label) -> Side effects: tardive dyskinesia
-Botox injections minimize appearance of tics
-SSRI: if concomitant OCD
-Consider Alpha-adrenergics (!clonidine, guanfacine!) if concomitant ADHD
-If mild symptoms: watchful waiting
-Most persons have symptom improvement during adolescence
-50% have spontaneous resolution by 18yo
dystonias how does it compare to tics
-slower than tics
-involuntary muscle contractions
tardive dyskinesia
Definition: Medication induced movement disorder a/w dopamine blocking agents
-E.g. ANTIPSYCHOTICS (haloperidol), metoclopramide (antiemetic), prochlorperazine
-Dystonic (hyperkinetic) movements that persist at least 1 MONTH after discontinuation of causative medications
sx:
-Protruding and twisting movements of the tongue
-Pouting, puckering, smacking of the lips
-Blepharospasms
-“piano playing” finger movements
-Shoulder shrugging
Diagnosis
- med hx: at least 1 month of dopamine blocking agent
- exclusion of other abnormal movements
extrapyramidal symptoms
-EPS = movement disorders due to disruption of dominergic pathways in the basal ganglia causing bradykinesia, rigidity, dystonia, athetosis, chorea, ballismus, akathisia, tics, tremors
-Higher risk with first generation and high dose antipsychotics
-Metoclopramide and some antidepressants can also cause EPS
ADAPT:
- acute dystonia
- akathisia: restlessness
- parkinsonism
- tardive dyskinesia
dystonia due to med ADRs: hours to days vs days to week vs months to years
hours to days: acute dystonia
- toricolis -> oculogyric crisis, tongue protrusion
-give antihistamine, benzos
days to weeks: pseudoparkinsonism and akathisa (restlessness, cant sit still)
- give propanolol
months to years: tardive dyskinesia
- late finding from high dose antipsychotics
- not very reversible
- involves mouth and neck
- found in schizo
