NMS and EPS Flashcards by Alexander Nachlis

EPS definition and association

constellation of disorders relating to movement

associated with exposure to dopamine antagonists

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EPS acute manifestation

dystonia
akathisia
parkinsonism

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EPS chronic manifestation

Tardive Dyskinesia

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Acute EPS pathophysiology

Release of ACH is regulated by release of dopamine

Dopamine inhibits ACH

But when taking D2, the D2 receptors blocked and the ability to inhibit ACH blocked

So more ACH released which leads to the movement sx

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Dystonia definition, onset, course, sx

Prolonged and unintentional contractions of voluntary and or involuntary muscles

Can occur within hours of 1st dose of antipsych drug

Occasionally chronic presentation

Causes repetitive and twisting movements

Often affects the head and neck

Visuals

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Dystonia presentations and name

oculogyric crisis
trismus
torticollis
blepharospasm

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Dystonia tx prophylaxis

anticholinergic (benztropine) in higher risk pt

also if admin 1st dose high potency IM

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Dystonia tx acute/urgent

options:
Biperiden 5mg
benztropine 1-2mg
diphenhydramine 50mg IM or IV

also consider BZD in oculogyric crisis that doesnt respond to anticholinergic rx

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Akathisia definition, onset, risk factor

subjective and objective psychomotor restlessness

Patients often unable to remain still: “mounting tension” or irresistible urge to move around

Typically occurs early in treatment with antipsychotics

Risk appears to be higher in antipsychotic-naïve patients started on a new drug

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Akathisia tx

reduce dose or d/c

1st line tx propranolol 10mg and titrate to response

2nd line: 5HT2A antagonist (mirtazapine, cyproheptadine) and BZD

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Akathisia prevention

avoid polypharmacy and rapid dose inc with antipsychotics

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lower risk drug for akathisia

risperidone
olanzapein
ziprasidone
quetiapine

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parkinsonism sx, patient profile

Drug-induced Parkinsonism is associated with bradykinesia, postural instability, tremor, and rigidity

More common in elderly and female patients

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parkinsonism differentiation

Differentiating between idiopathic and drug-induced Parkinsonism:

Drug-induced presents as symmetrical akinetic rigidity

Follows the ingestion of an associated medication

Does not respond to anti-Parkinson’s drugs

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Parkinsonism tx

reduce dose
switch to agent with lower risk
Benztropine (caution in elderly)
Amantadine (useful in elderly r/t anticholinergic)

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Tardive Dyskinesia onset, sx, presentation, risk factor, prognosis

Onset: months to years and slow

Presents as involuntary movements of lower face, limbs, trunk
Ex: lip smacking/puckering, tongue movements, excessive blinking

May also present with sx similar to EPS, tremor, myoclonus, tourettism

Risk factor: early presence of EPS

Prognosis: may be irreversible

Tardive Dyskinesia pathophysiology

chronic blockade of D2 receptors leads them to up regulate

upregulation takes time hence why slow onset

now patient is hypersensitive to dopamine which causes involuntary movements

Tardive Dyskinesia tx

reduce or switch: Little benefit

VMAT2 inhibitor: Valbenazine, deutetrabenazine

modest evidence for clonazepam

Gingko biloba extract

AIMS scale

Applies to any EPS acute or chronic

Diagnosing EPS

Includes dental status cuz it looks like EPS

Important if they are going to be on antipsychotic therapy

antipsychotic AE profile chart

Neuroleptic Malignant Syndrome and sx

Acute side effect of neuroleptic medications

Characterized by:
fever
muscular rigidity
altered level of consciousness
autonomic instability

DSM criteria for NMS

hyperthermia >38 on 2 separate occasions

CPK >4x ULN

mental status change: delirium, ALOC

Autonomic activation:
tachy >25% inc
diaphoresis
BP inc >25%
BP fluctuation >20 dia or >25 syst
incontinence
pallor
tachypnea >50% inc

NMS DDX and key difference

NMS etiology

not well understood

Thinking is that a dopamine antagonist can lead to a hypothalamic dopamine blockade

this Can cause hyperthermia and autonomic dysfunction

That leads to cascade of other sx
1. Vasomotor sx
2. Issues with sympathetic nervous system
3. ALOC

Not many build on to each other
1. Hyperthermia leads to inc sweating which leads to dehydration which can lead to kidney complications

Supported by inc rate of NMS in those initiating antipsychotics

NMS risk factors modifiable

* High Temperature * Low Iron * Dehydration * Restraint * Medication with D2 antagonistic activity (IV or IM administration associated with greater risk)

NMS risk factors not modifiable

* Advanced Age * Personal or Family History of Catatonia * Concurrent Medical Conditions

NMS risk factor drugs: antipsychotics

Antipsychotic Drugs Atypical: * Clozapine, olanzapine, risperidone, quetiapine, aripiprazole, paliperidone, asenapine, ziprasidone Typical: * Haloperidol, fluphenazine, thioridazine, chlorpromazine, prochlorperazine, loxapine, periciazine, trifluoperazine, flupentixol, zuclopentixol, methotrimeprazine SGAs are more associated with EPS and NMS but SGAs implicated too Clozapine: may present differently (less rigidity/tremors)

NMS risk factor drugs: others

Other Drugs Mood Stabilizers * Lithium, carbamazepine Antidepressants * Paroxetine, sertraline, amitriptyline Antiemetics * Metoclopramide Evidence for the role of these drugs in NMS is limited

management of NMS: first

1st: D/c suspected agent dont wait for lab results

NMS staging based treatment

Basically it is 1-5 1 looks like typical EPS and you may be able to get away with switching the agent 3 looks like proper NMS and will need to d/c the agent

NMS mgmt supportive care

note there is an aspiration risk note that an antipyretic may not work

NMS mgmt pharmacotherapy: supportive

Agitation * Benzodiazepines can be used to control agitation Blood Pressure Control * NMS is associated with severe and labile HTN * Beta blockers such as labetalol and DHP calcium channel blockers such as amlodipine have been used VTE * Use heparin as necessary for VTE prophylaxis

NMS mgmt pharmacotherapy: treatment

Three main agents: 1. Dantrolene 2. Bromocriptine 3. Amantadine limited data

Dantrolene

Mechanism: peripheral skeletal muscle relaxant * Directly decreases rigidity and hyperthermia * Most useful in cases with severe hyperthermia and rigidity Dosing * 1-2.5mg/kg IV initially, followed by 1mg/kg every six hours Adverse effects * Anaphylaxis, hepatotoxicity, flushing, heart failure, tachycardia

Bromocriptine

Mechanism: Dopamine agonist * Displaces dopamine antagonist drugs from D2 receptors Dosing * 2.5mg every 8-12 hours via NG tube Adverse effects * Hypotension, GI ulcer, psychosis

Amantadine

Mechanism: Dopamine agonist * Displaces dopamine antagonist drugs from D2 receptors Dosing * 200-400mg daily in 2-3 divided doses Adverse effects * Orthostatic hypotension, agitation, UTI, nausea

Reinitiating antipsychotics after NMS

note future risk of NMS episodes --30% possibly wait 2 wks before resuming rx start low with rx that is low potency and titrate slowlyt

thermoregulation in schizophrenia

Dysregulation is common Different baseline Abn daily range Impaired compensation to heat but more effective compensation to cold May be cuz of dx or rx but don’t know Good to counsel patients 1. May have poor access to air conditioning