Drug Masterlist (God save us all)

What Drug Family/ Class: Procaine

• Esters

• Anesthetics

What Drug Family/ Class: Chloroprocaine

• Esters

• Anesthetics

What Drug Family/ Class: Tetracaine

• Esters

• Anesthetics

What Drug Family/ Class: benzocaine 

• Esters

• Anesthetics

What Drug Family/ Class: lidocaine

• Amides 

• Anesthetics

What Drug Family/ Class: mepivacaine

• Amides 

• Anesthetics

What Drug Family/ Class: bupivacaine

• Amides 

• Anesthetics

What Drug Family/ Class: Ropivacaine

• Amides 

• Anesthetics

What Drug Family/ Class: Prilocaine

• Amides 

• Anesthetics

What Drug Family/ Class: articaine 

• Amides 

• Anesthetics

COCAINE

• What is it?

• Clinical Uses:

• Metabolism:

• Adverse Effects:

• What is it?

  • ENT anesthetic + vasoconstrictor

• Clinical Uses:

  • Nasal/laryngeal procedures (↓ bleeding, ↓ secretions)

• Metabolism:

  • Via plasma esterases + liver; 

  • t½ ~1 hour

• Adverse Effects:

  • sympathomimetic vasoconstriction → arrhythmias + coronary vasospasm

  • High abuse/addiction potential

Drug class: clonidine

• A2 Agonist

Drug Class: dexmedetomidine

• A2 Agonist

Lidocaine

• Class

• Use Caution?

:

• Topical Anesthetics

• Use Caution:

  • Avoid overuse + large surface areas

  • High  absorption risk on broken skin / occlusion / kids

Benzocaine

• Class?

• Use Caution

• Topical Anesthetics

• Use Caution:

  • Avoid overuse + large surface areas

  • High  absorption risk on broken skin / occlusion / kids

  • Fast numbness

  • Watch for methemoglobinemia (cyanosis)

Bupivacaine

• Class

• Benefits

• AKA

• Why Dangerous?

• AKA?

  • The “cardiotoxic one”

• PERIPHERAL NERVE BLOCK

• Benefits:

  • Analgesia without “dead limb”

    • Creates loss of sensory over motor; when function matters (postop)

• Why is it Dangerous

  • Strong Na⁺ channel binding → slow dissociation → malignant ventricular arrhythmias

    • Highest risk w/  intravascular injection / high dose / high-vascular sites

  • LAST from bupivacaine can be harder to reverse

Ropivacaine

• Class

• Benefits

• PERIPHERAL NERVE BLOCK

• Benefits:

  • Analgesia without “dead limb”

    • Creates loss of sensory over motor; when function matters (postop)

  • tends to spare motor vs bupivacaine

Benzodiazepines 

• For?

• Avoids?

• For Seizures of LAST

• Avoid w/ muscle relaxtants

Succinylcholine (SCh)

• Type

• Onset

• Duration

• MOA

• AE

• What type is it?

  • Depolarizing NM blocker

• Onset

  • Very fast → ideal for rapid sequence intubation

• Duration

  • Short (rapid hydrolysis by plasma pseudocholinesterase)

• MOA

  • Nm agonist → channel opens → sustained depolarization → paralysis

---

ADVERSE EFFECTS

• Hyperkalemia risk

  • Avoid burns, crush/trauma, denervation/spinal cord injury, neuromuscular disease/immobility (↑ extrajunctional AChRs)

• Malignant hyperthermia trigger

  • w/ volatile anesthetics

• Bradycardia (esp. pediatrics or repeat dosing)

• ↑ IOP / ↑ intragastric pressure + myalgias (post- op muscle pain)

• Prolonged paralysis

  • Atypical pseudocholinesterase or inhibitors → slow breakdown → slow recovery

NOTE: Brief fasciculations → flaccid paralysis

Ro-curonium

• Class

• Family

• MOA

• Potency vs Onset

• Elimination

Ro-curonium

• Class: Non-Depolarizers

• Family: Aminosteroids

• MOA: 

  • Nm antagonists → blocks Ach from binding -> flaccid paralysis 

• Potency vs Onset: 

  • Less potent → faster onset

• Elimination

  • Cisatracurium/atracurium

    • Hofmann elimination ± ester hydrolysis → organ-independent (useful in liver/kidney dysfunction)

Ve-curonium

• Class:

• Family:

• MOA: 

• Potency vs Onset: 

• Elimination

Ve-curonium

• Class: Non-Depolarizers

• Family: Aminosteroids

• MOA: 

  • Nm antagonists → blocks Ach from binding -> flaccid paralysis 

• Potency vs Onset: 

  • Less potent → faster onset

• Elimination

  • Cisatracurium/atracurium

    • Hofmann elimination ± ester hydrolysis → organ-independent (useful in liver/kidney dysfunction)

Pan-curonium

• Class:

• Family:

• MOA: 

• Potency vs Onset: 

• Elimination

Pan-curonium

• Class: Non-Depolarizers

• Family: Aminosteroids

• MOA: 

  • Nm antagonists → blocks Ach from binding -> flaccid paralysis 

• Potency vs Onset: 

  • Less potent → faster onset

• Elimination

  • Cisatracurium/atracurium

    • Hofmann elimination ± ester hydrolysis → organ-independent (useful in liver/kidney dysfunction)

Cis-atra-curium

• Class:

• Family:

• MOA: 

• Potency vs Onset: 

• Elimination

Cis-atra-curium

• Class: Non-Depolarizers

• Family: Benzylisoquinoliniums

• MOA: 

  • Nm antagonists → blocks Ach from binding -> flaccid paralysis 

• Potency vs Onset: 

  • Less potent → faster onset

• Elimination

  • Cisatracurium/atracurium

    • Hofmann elimination ± ester hydrolysis → organ-independent (useful in liver/kidney dysfunction)

Atra-curium

• Class:

• Family:

• MOA: 

• Potency vs Onset: 

• Elimination

Atra-curium

• Class: Non-Depolarizers

• Family: Benzylisoquinoliniums

• MOA: 

  • Nm antagonists → blocks Ach from binding -> flaccid paralysis 

• Potency vs Onset: 

  • Less potent → faster onset

• Elimination

  • Cisatracurium/atracurium

    • Hofmann elimination ± ester hydrolysis → organ-independent (useful in liver/kidney dysfunction)

Miva-curium

• Class:

• Family:

• MOA: 

• Potency vs Onset: 

• Elimination

Miva-curium

• Class: Non-Depolarizers

• Family: Benzylisoquinoliniums

• MOA: 

  • Nm antagonists → blocks Ach from binding -> flaccid paralysis 

• Potency vs Onset: 

  • Less potent → faster onset

• Elimination

  • Cisatracurium/atracurium

    • Hofmann elimination ± ester hydrolysis → organ-independent (useful in liver/kidney dysfunction)

Mivacurium

• What is it?

• Clinical Use:

• Metabolism

• Adverse Effects:

Mivacurium

• What is it?

  • Short-acting nondepolarizing blocker

• Clinical Use:

  • For Brief paralysis / intubation

• Metabolism

  • Rapid plasma cholinesterase metabolism

• Adverse Effects:

  • Prolonged in pseudocholinesterase deficiency

  • Histamine release → 

    • flushing, hypotension, bronchospasm

Neostigmine

• Class:

• Family:

• MOA:

• Synergy?

Neostigmine

• Class: AChE INHIBITORS

• Family: Quaternary ammonium

• Intermediate acting

• MOA:

  • ↑ ACh to outcompete nondepolarizer at Nm

• Synergy?

  • Pair w/ antimuscarinic ->  prevents bradycardia + secretions

    • Glycopyrrolate (or atropine)

Pyridostigmine

• Class:

• Family:

• Usage

• MOA:

• Synergy?

Pyridostigmine

• Class: AChE INHIBITORS

• Family: Quaternary ammonium

• Usage:

  • Long-acting, MG maintenance

• MOA:

  • ↑ ACh to outcompete nondepolarizer at Nm

• Synergy?

  • Pair w/ antimuscarinic ->  prevents bradycardia + secretions

    • Glycopyrrolate (or atropine)

Physostigmine

• Class:

• Family:

• MOA:

• Synergy?

Physostigmine

• Class: AChE INHIBITORS

• Family: Tertiary amine

• Crosses CNS, not for NMJ reversal

• MOA:

  • ↑ ACh to outcompete nondepolarizer at Nm

• Synergy?

  • Pair w/ antimuscarinic ->  prevents bradycardia + secretions

    • Glycopyrrolate (or atropine)

Sugammadex

• What is it?

• MOA:

• Synergy?

• Adverse Effects?

Sugammadex

• What is it?

  • Selective relaxant binding agent 

  • (“molecular trap”)

• MOA:

  • Encapsulates rocuronium + vecuronium → pulls drug out of circulation → rapid reversal (even deep block)

• Synergy?

  • No antimuscarinic needed 

    • (not an AChE inhibitor)

• Adverse Effects?

  • can bind steroidal molecules & may lower exposure to estrogen/progestin contraceptives

Methocarbamol

• AKA:

• Class:

• What are they?

• Clinical Usage

• Adverse Effects:

Methocarbamol

• AKA: Metaxalone

• Class: Spasmolytics

• Sedation

• What are they?

  • Outpatient “muscle relaxants”

    • Acute spasm meds (not NMJ blockers)

• Clinical Usage

  • For Acute low back/neck spasm after strain

  • Short-term adjunct to NSAIDs/acetaminophen + early mobility

• Adverse Effects:

  • Sedation/dizziness

    • Caution with driving, alcohol, CNS depressants

Metaxalone

• AKA:

• Class:

• What are they?

• Clinical Usage

• Adverse Effects:

Metaxalone

• AKA: Methocarbamol

• Class: Spasmolytics

• Sedation

• What are they?

  • Outpatient “muscle relaxants”

    • Acute spasm meds (not NMJ blockers)

• Clinical Usage

  • For Acute low back/neck spasm after strain

  • Short-term adjunct to NSAIDs/acetaminophen + early mobility

• Adverse Effects:

  • Sedation/dizziness

    • Caution with driving, alcohol, CNS depressants

Carisoprodol

• Class:

• What are they?

• Clinical Usage

• Adverse Effects:

Carisoprodol

• Class: Spasmolytics

• Misuse/dependence risk

• What are they?

  • Outpatient “muscle relaxants”

    • Acute spasm meds (not NMJ blockers)

• Clinical Usage

  • For Acute low back/neck spasm after strain

  • Short-term adjunct to NSAIDs/acetaminophen + early mobility

• Adverse Effects:

  • Sedation/dizziness

    • Caution with driving, alcohol, CNS depressants

Chlorzoxazone

• Class:

• What are they?

• Clinical Usage

• Adverse Effects:

Chlorzoxazone

• Class: Spasmolytics

• What are they?

  • Outpatient “muscle relaxants”

    • Acute spasm meds (not NMJ blockers)

• Clinical Usage

  • For Acute low back/neck spasm after strain

  • Short-term adjunct to NSAIDs/acetaminophen + early mobility

• Adverse Effects:

  • Sedation/dizziness

    • Caution with driving, alcohol, CNS depressants

Dantrolene

• Class:

• Clinical Usage:

• Key Limitations:

• NOTE:

Dantrolene

• Class: Antispasticity drugs

• Direct skeletal muscle action

• Clinical Usage:

  • Chronic UMN spasticity

• Key Limitations:

  • sedation 

  • weakness

  • dizziness

  • falls

• NOTE:

  • Baclofen or tizanidine often first

  • Add/consider dantrolene or selected benzodiazepines

  • Use botulinum toxin for focal spasticity

Cyclobenzaprine

• Clinical Usage:

• MOA:

• Adverse Effects

• Synergy?

Cyclobenzaprine

• Clinical Usage:

  • Central muscle relaxant for acute spasm (short course)

• MOA:

  • Acts centrally in brainstem to reduce tonic somatic motor activity 

    • (likely via 5-HT/NE modulation)

• Adverse Effects

  • Sedation + anticholinergic 

    • (dry mouth, urinary retention, blurred vision, constipation) 

  • confusion/falls

• Synergy?

  • Avoid w/  MAOIs 

    • (risk of serious toxicity/serotonergic effects)

Baclofen 

• Class:

• MOA:

• Clinical Usage:

• Key Limitations:

• NOTE:

Baclofen 

• Class: Antispasticity drugs

• MOA:

  • GABAB agonist

• Clinical Usage:

  • Chronic UMN spasticity

• Key Limitations:

  • sedation 

  • weakness

  • dizziness

  • falls

• NOTE:

  • Baclofen or tizanidine often first

  • Add/consider dantrolene or selected benzodiazepines

  • Use botulinum toxin for focal spasticity

Tizanidine 

• Class:

• MOA:

• Clinical Usage:

• Key Limitations:

• NOTE:

Tizanidine 

• Class: Antispasticity drugs

• MOA:

  • α2 agonist

• Clinical Usage:

  • Chronic UMN spasticity

• Key Limitations:

  • sedation 

  • weakness

  • dizziness

  • falls

• NOTE:

  • Baclofen or tizanidine often first

  • Add/consider dantrolene or selected benzodiazepines

  • Use botulinum toxin for focal spasticity

Diazepam 

• Class:

• MOA

• Clinical Usage:

• Key Limitations:

• NOTE:

Diazepam 

• Class: Antispasticity drugs

• MOA:

  • enhances GABAA

• Clinical Usage:

  • Chronic UMN spasticity

• Key Limitations:

  • sedation 

  • weakness

  • dizziness

  • falls

• NOTE:

  • Baclofen or tizanidine often first

  • Add/consider dantrolene or selected benzodiazepines

  • Use botulinum toxin for focal spasticity

Botulinum toxin 

• Class:

• MOA

• Clinical Usage:

• Key Limitations:

• NOTE:

Botulinum toxin 

• Class: Antispasticity drugs

• MOA

  • Blocks ACh release

• Clinical Usage:

  • Chronic UMN spasticity

• Key Limitations:

  • sedation 

  • weakness

  • dizziness

  • falls

• NOTE:

  • Baclofen or tizanidine often first

  • Add/consider dantrolene or selected benzodiazepines

  • Use botulinum toxin for focal spasticity

Botulinum toxin 

• What is it?

• MOA:

• Uses:

• Adverse effects

Botulinum toxin 

• What is it?

  • presynaptic blocker

• MOA:

  • Blocks ACh release at NMJ via SNARE cleavage → focal weakness

• Uses:

  •  focal spasticity

  • dystonia

• Adverse effects

  • local weakness, 

  • rare spread effects

Tizanidine

• MOA

• Adverse Effects:

• How to stop?

Tizanidine

• MOA

  • Central α2-agonist → ↓ excitatory outflow to motor neurons → ↓ spasticity/spasm

• Adverse Effects:

  • Sedation + dizziness

  •  ↓ BP / bradycardia

    • (additive with other CNS depressants/antihypertensives)

  • Rare hepatotoxicity

    • Check LFTs

• How to stop?

  • Taper it

Baclofen

• MOA

• Adverse Effects:

• Abrupt Withdrawal?

Baclofen

• MOA

  • Spinal GABA(B) agonist -> 

    • ↓ excitatory transmitter release

    • Relieves muscle spasticity

• Adverse Effects:

  • sedation, weakness, dizziness

• Abrupt Withdrawal?

  • Dangerous

    • Withdrawal risk ↑ with intrathecal use

Benzodiazepines 

• MOA:

• Adverse Effects 

Benzodiazepines 

• MOA:

  • enhances GABAA -> inhibitory CNS signaling

    • Reduce spasticity

• Adverse Effects 

  • Sedation

  • Dependence

  • Respiratory depression risk 

    • w/ other depressants

Dantrolene

• What is it?

• MOA:

• Clinical Usage:

• Adverse effects 

Dantrolene

• What is it?

  • Peripheral muscle relaxant

• MOA:

  • Blocks RyR1 in skeletal muscle -> ↓ SR Ca²⁺ release

• Clinical Usage:

  • malignant hyperthermia (MH)

  • selected spasticity

• Adverse effects 

  • Weakness

  • hepatotoxicity

What drug for diagnosis of MG

For Diagnosis of MG

Tensilon test: 

• Inject edrophonium (AcHE inhibitor) -> improvement in ptosis/ ophthalmoparesis

Treatment of MG

• Crisis

• Ongoing Treatment

Treatment of MG

Crisis

• Plasma Exchange (1.5 total blood volume)

• IVIG

  • Efficacy equal but fewer side effects 

• IV Rituxan for refractory cases

  • More efficacious in Musk positive patients

Ongoing Treatment

• Pyridostigmine 

• Oral steroids

• Oral immunosuppressants

  • Azathioprine

  • Cellcept-Avoid in pregnancy

Soliris 

• AKA:

• Usage: 

• Uses besides MG

• MOA

• Req. to Prescribe:

• Costs:

Soliris 

• AKA:

  • Eculizumab

• Usage: 

  • MG

• Uses besides MG

  •  Paroxysmal Nocturnal Hemoglobinuria 

  • Typical Hemolytic Uremic Syndrome

• MOA

  • binds + inhibits cleavage of C5 

• Req. to Prescribe:

  • generalized MG

  • AChR-Ab POSITIVE

  • Failed other immunosuppressants

• Costs:

  •  $500,000 annually

Eculizumab 

• AKA:

• Usage: 

• Uses besides MG

• MOA

• Req. to Prescribe:

• Costs:

Eculizumab 

• AKA:

  • Soliris

• Usage: 

  • MG

• Uses besides MG

  •  Paroxysmal Nocturnal Hemoglobinuria 

  • Typical Hemolytic Uremic Syndrome

• MOA

  • binds + inhibits cleavage of C5 

• Req. to Prescribe:

  • generalized MG

  • AChR-Ab POSITIVE

  • Failed other immunosuppressants

• Costs:

  •  $500,000 annually

Ultomiris

• AKA:

• Usage: 

• MOA:

• Req. to Prescribe:

• Costs:

• Dose:

Ultomiris 

• AKA: 

  • ravulizumab-cwvz

• Usage: 

  • MG

• MOA:

  • Long acting C5 complement inhibitor

• Req. to prescribe:

  • AChR-Ab positive

• Cost:

  • $458,000 annually

• Dose:

  • Loading dose based on weight then Infusion every 8 weeks

Ravulizumab-cwvz 

• AKA:

• Usage: 

• MOA:

• Req. to Prescribe:

• Costs:

• Dose:

Ravulizumab-cwvz 

• AKA: 

  • Ultomiris

• Usage: 

  • MG

• MOA:

  • Long acting C5 complement inhibitor

• Req. to prescribe:

  • AChR-Ab positive

• Cost:

  • $458,000 annually

• Dose:

  • Loading dose based on weight then Infusion every 8 weeks

Vyvgart

• AKA:

• Usage: 

• MOA:

• Req. to Prescribe:

• Costs:

Vyvgart 

• AKA: 

  • Efgartigimod-alpha

• Usage: 

  • MG

• MOA:

  • IgG Abs to Fc of IgG auto Abs -> degradation

• Req. to Prescribe:

  • general MG patients who are AChR-Ab positive

• Cost: $225,000 annually

Efgartigimod-alpha 

• AKA:

• Usage: 

• MOA:

• Req. to Prescribe:

• Costs:

Efgartigimod-alpha 

• AKA: 

  • Vyvgart

• Usage: 

  • MG

• MOA:

  • IgG Abs to Fc of IgG auto Abs -> degradation

• Req. to Prescribe:

  • general MG patients who are AChR-Ab positive

• Cost: $225,000 annually

LEMS Treatments

LEMS Treatments

• Treat underlying malignancy

• Pyridostigmine

• 3,4-DAP (Di-Amino Pyridine) Trade name=Ampyra

Botulin Treatment

Botulin Treatment

• Anti-toxin

• Surgical removal of wound

Treatment for Isaacs’

Treatment for Isaacs’

• Immunosuppressive therapy 

  • Plasma exchange 

• Anticonvulsants

Treatment for ALS

• Treatment components:

• Symptomatic

Treatment for ALS

Treatment components:

• Patient education

• Disease-directed

• Adaptive/supportive care

  • Dysphagia

    • Percutaneous gastrostomy

• Respiratory support

  • Non-invasive ventilation

• Functional dependence

Symptomatic

• Limb spasticity

  • muscle relaxants

• Excessive salivation

  • anticholinergics, sympathomimetics, botulinum toxin

• Pseudobulbar Palsy

  • neudexta

• Pain 

  • Standard medication

• Fatigue

  • Standard medication

• Depression

  • Standard medication

Riluzole

• AKA:

• Usage:

• MOA:

• Different Forms:

Riluzole

• AKA:

  • Rilutek

• Usage:

  • ALS

• MOA:

  • Glutamate pathway antagonist

• Different Forms:

  • thickened liquid form [Tiglutik]

Rilutek

• AKA:

• Usage:

• MOA:

• Different Forms:

Rilutek

• AKA:

  • Riluzole

• Usage:

  • ALS

• MOA:

  • Glutamate pathway antagonist

• Different Forms:

  • thickened liquid form [Tiglutik]

Edaravone 

• AKA:

• Usage:

• MOA:

• Purpose:

• Forms:

Edaravone 

• AKA: 

  • Radicava

• Usage:

  • ALS

• MOA:

  • Free radical scavenger

• Purpose:

  • Slows decline in physical function

• Forms:

  • Oral formulation approved in 2022

Radicava 

• AKA:

• Usage:

• MOA:

• Purpose:

• Forms:

Radicava 

• AKA: 

  • Edaravone

• Usage:

  • ALS

• MOA:

  • Free radical scavenger

• Purpose:

  • Slows decline in physical function

• Forms:

  • Oral formulation approved in 2022

Qalsody 

• AKA:

• Usage:

• MOA:

Qalsody 

• AKA: 

  • Tofersen

• Usage:

  • ALS

• MOA:

  • treat ALS associated with a mutation in the superoxide dismutase I [SODI] gene.

Tofersen 

• AKA:

• Usage:

• MOA:

Tofersen 

• AKA: 

  • Qalsody

• Usage:

  • ALS

• MOA:

  • treat ALS associated with a mutation in the superoxide dismutase I [SODI] gene.

Relyvrio

• AKA:

• Usage:

• MOA:

Relyvrio

• AKA:

  • AMX0035

• Usage:

  • ALS

• MOA:

  • Combo of phenylbutyrate and tarursodiol -> prevent nerve cell death by blocking stress signals

AMX0035

• AKA:

• Usage:

• MOA:

AMX0035

• AKA:

  • Relyvrio

• Usage:

  • ALS

• MOA:

  • Combo of phenylbutyrate and tarursodiol -> prevent nerve cell death by blocking stress signals

Treatment for Diabetic Neuropathy

Treatment for Diabetic Neuropathy

• Optimize control of diabetes

• Symptomatic

  • Tricyclic antidepressants, SSRI/SNRI, anti-epileptic drugs, capsaicin, analgesics

Treatment for GBS

• Management for GBS

• Supportive care for GBS

• Immunization for GBS

Management for GBS

• Hospitalize patient due to risk of respiratory compromise

• Directed vs. immune system

  • Intravenous immunoglobulin (IVIG)

  • Plasma exchange

  • Note: Steroids are NOT effective

Supportive care for GBS

• Manage cardiovascular complications

• Bowel and bladder care

• Rehabilitation

• Pain management

Immunization for GBS

• Avoid revaccinating with immunization associated with GBS

  • Usually influenza

  • Warning with J&J Covid-19 vaccination

• May give other immunizations

• Do not give immunizations till a year after the GBS episode

Treatment for Bell's palsy

Treatment for Bell's palsy

• Anti-viral/Corticosteroids if < 3 days

• Protect the eye if unable to close

• CN V and VII transfer

Treatment for Carpal Tunnel

Treatment for Carpal Tunnel

• Splinting, steroid injection

• Surgery when severe, protracted 

Treatment for Meniere’s

Treatment for Meniere’s:

• Symptomatic

• Low salt diet + diuretics 

  • ( ie. Hydrochlorothiazide or triamterene or acetazolamide).

• Antiemetics 

  • (Meclizine or dimenhydrinate or prochlorperazine or promethazine).

• Surgery 

• remove bony/membranous labyrinth or vestibular neurectomy. 

• decompression or shunting of endolymphatic sac.

  • Nondestructive

Treatment of VESTIBULAR NEURITIS/LABYRINTHITIS

Treatment of VESTIBULAR NEURITIS/LABYRINTHITIS:

• Prednisone 

  • (corticosteroid therapy)

• Symptomatic treatment: 

  • antiemetics, antihistamines, anticholinergics, and benzodiazepines

• Vestibular rehabilitation

Treatment of Ramsay Hunt

Treatment of Ramsay Hunt

• corticosteroids 

• acyclovir

Treatment of Disembarkment syndrome

Treatment of Disembarkment syndrome

• Scopolamine

• Promethazine

• Anti-histamine

  • ( dimenhydrinate, Diphendryamine)

Treatment of Craniocervical junction disorders

Treatment of Craniocervical junction disorders

• surgical decompression

CARBIDOPA/LEVODOPA: SINEMET

• Clinical Importance:

• MOA:

• NOTE:

• Side effects:

• Motor Toxicity

CARBIDOPA/LEVODOPA: SINEMET

• Clinical Importance:

  • Most effective drug in the treatment of PD

    • Decreases morbidity and mortality

• MOA:

  • Levodopa: Precursor to dopamine

  • Carbidopa: Decarboxylase inhibitor

    • Prevents peripheral conversion

      •  levodopa -> dopamine

• NOTE:

  • Use the lowest dose that provides response

Side effects:

• Anorexia

• N/V

• Orthostatic hypotension

• Hallucinations, delusions

• Sleep disturbance, “sleep attacks”

• Sudden d/c may result in neuroleptic malignant syndrome

Motor Toxicity

• Motor fluctuations

  • Alt. btw “on” and “off”

  • long term use ->  Response duration gets shorter (4 hours)

• Dyskinesia

  • What is it?

    • Involuntary movements

  • STATs

    • 50-90% of patients on levodopa for 5-10 years

  • Generally not considered painful/bothersome

Bromocriptine 

• Class:

• AKA:

• Usage:

• MOA

• Benefits:

• Clinical Strategy:

• Side Effects

Bromocriptine 

• Class: Dopa Agonist

• AKA:

  • Parlodel

• Usage:

  • PD

• MOA

  • Directly stimulate dopamine receptors

• Benefits:

  • Can be monotherapy in early Parkinson

  • Similar Benefits to Carbidopa/Levodopa in the early stages

• Clinical Strategy:

  • To decrease risk of dyskinesias w/ higher doses of levodopa, a dopamine agonist can be combined with levodopa

  • Delay use of Carbidopa/Levodopa for early stages

• Side Effects

  • N/V

  • Postural hypotension

  • Psychiatric symptoms

    • Hallucinations, Psychosis

  • Compulsive behaviors

  • Somnolence

  • tolerance (days to weeks)

Parlodel 

• Class:

• AKA:

• Usage:

• MOA

• Benefits:

• Clinical Strategy:

• Side Effects

Parlodel 

• Class: Dopa Agonist

• AKA:

  • Bromocriptine

• Usage:

  • PD

• MOA

  • Directly stimulate dopamine receptors

• Benefits:

  • Can be monotherapy in early Parkinson

  • Similar Benefits to Carbidopa/Levodopa in the early stages

• Clinical Strategy:

  • To decrease risk of dyskinesias w/ higher doses of levodopa, a dopamine agonist can be combined with levodopa

  • Delay use of Carbidopa/Levodopa for early stages

• Side Effects

  • N/V

  • Postural hypotension

  • Psychiatric symptoms

    • Hallucinations, Psychosis

  • Compulsive behaviors

  • Somnolence

  • tolerance (days to weeks)

Pergolide

• Class:

• AKA:

• Usage:

• MOA

• Benefits:

• Clinical Strategy:

• Side Effects

Pergolide

• Class: Dopa Agonist

• AKA:

  • Permax

• Usage:

  • PD

• MOA

  • Directly stimulate dopamine receptors

• Benefits:

  • Can be monotherapy in early Parkinson

  • Similar Benefits to Carbidopa/Levodopa in the early stages

• Clinical Strategy:

  • To decrease risk of dyskinesias w/ higher doses of levodopa, a dopamine agonist can be combined with levodopa

  • Delay use of Carbidopa/Levodopa for early stages

• Side Effects

  • N/V

  • Postural hypotension

  • Psychiatric symptoms

    • Hallucinations, Psychosis

  • Compulsive behaviors

  • Somnolence

  • tolerance (days to weeks)

Permax

• Class:

• AKA:

• Usage:

• MOA

• Benefits:

• Clinical Strategy:

• Side Effects

Permax

• Class: Dopa Agonist

• AKA:

  • Pergolide

• Usage:

  • PD

• MOA

  • Directly stimulate dopamine receptors

• Benefits:

  • Can be monotherapy in early Parkinson

  • Similar Benefits to Carbidopa/Levodopa in the early stages

• Clinical Strategy:

  • To decrease risk of dyskinesias w/ higher doses of levodopa, a dopamine agonist can be combined with levodopa

  • Delay use of Carbidopa/Levodopa for early stages

• Side Effects

  • N/V

  • Postural hypotension

  • Psychiatric symptoms

    • Hallucinations, Psychosis

  • Compulsive behaviors

  • Somnolence

  • tolerance (days to weeks)

Ropinirole

• Class:

• AKA:

• Usage:

• MOA

• Benefits:

• Clinical Strategy:

• Side Effects

Ropinirole

• Class: Dopa Agonist

• AKA:

  • Requip

• Usage:

  • PD

• MOA

  • Directly stimulate dopamine receptors

• Benefits:

  • Can be monotherapy in early Parkinson

  • Similar Benefits to Carbidopa/Levodopa in the early stages

• Clinical Strategy:

  • To decrease risk of dyskinesias w/ higher doses of levodopa, a dopamine agonist can be combined with levodopa

  • Delay use of Carbidopa/Levodopa for early stages

• Side Effects

  • N/V

  • Postural hypotension

  • Psychiatric symptoms

    • Hallucinations, Psychosis

  • Compulsive behaviors

  • Somnolence

  • tolerance (days to weeks)

Requip

• Class:

• AKA:

• Usage:

• MOA

• Benefits:

• Clinical Strategy:

• Side Effects

Requip 

• Class: Dopa Agonist

• AKA:

  • Ropinirole

• Usage:

  • PD

• MOA

  • Directly stimulate dopamine receptors

• Benefits:

  • Can be monotherapy in early Parkinson

  • Similar Benefits to Carbidopa/Levodopa in the early stages

• Clinical Strategy:

  • To decrease risk of dyskinesias w/ higher doses of levodopa, a dopamine agonist can be combined with levodopa

  • Delay use of Carbidopa/Levodopa for early stages

• Side Effects

  • N/V

  • Postural hypotension

  • Psychiatric symptoms

    • Hallucinations, Psychosis

  • Compulsive behaviors

  • Somnolence

  • tolerance (days to weeks)

Pramipexole

• Class:

• AKA:

• Usage:

• MOA

• Benefits:

• Clinical Strategy:

• Side Effects

Pramipexole

• Class: Dopa Agonist

• AKA:

  • Mirapex

• Usage:

  • PD

• MOA

  • Directly stimulate dopamine receptors

• Benefits:

  • Can be monotherapy in early Parkinson

  • Similar Benefits to Carbidopa/Levodopa in the early stages

• Clinical Strategy:

  • To decrease risk of dyskinesias w/ higher doses of levodopa, a dopamine agonist can be combined with levodopa

  • Delay use of Carbidopa/Levodopa for early stages

• Side Effects

  • N/V

  • Postural hypotension

  • Psychiatric symptoms

    • Hallucinations, Psychosis

  • Compulsive behaviors

  • Somnolence

  • tolerance (days to weeks)

Mirapex

• Class:

• AKA:

• Usage:

• MOA

• Benefits:

• Clinical Strategy:

• Side Effects

Mirapex

• Class: Dopa Agonist

• AKA:

  • Pramipexole

• Usage:

  • PD

• MOA

  • Directly stimulate dopamine receptors

• Benefits:

  • Can be monotherapy in early Parkinson

  • Similar Benefits to Carbidopa/Levodopa in the early stages

• Clinical Strategy:

  • To decrease risk of dyskinesias w/ higher doses of levodopa, a dopamine agonist can be combined with levodopa

  • Delay use of Carbidopa/Levodopa for early stages

• Side Effects

  • N/V

  • Postural hypotension

  • Psychiatric symptoms

    • Hallucinations, Psychosis

  • Compulsive behaviors

  • Somnolence

  • tolerance (days to weeks)

Apomorphine

• Class:

• Usage:

• MOA

• Benefits:

• Clinical Strategy:

• Side Effects

Apomorphine

• Class: Dopa Agonist

• Usage:

  • PD

• MOA

  • Injectable – fast onset

  • Directly stimulate dopamine receptors

• Benefits:

  • Can be monotherapy in early Parkinson

  • Similar Benefits to Carbidopa/Levodopa in the early stages

• Clinical Strategy:

  • To decrease risk of dyskinesias w/ higher doses of levodopa, a dopamine agonist can be combined with levodopa

  • Delay use of Carbidopa/Levodopa for early stages

• Side Effects

  • N/V

  • Postural hypotension

  • Psychiatric symptoms

    • Hallucinations, Psychosis

  • Compulsive behaviors

  • Somnolence

  • tolerance (days to weeks)

Tolcapone

• Class:

• AKA:

• Usage

• Clinical Usage:

• Side Effects

• NOTE

Tolcapone

• Class: Catechol-O-methyltransferase (COMT) inhibitors

• AKA:

  • Tasmar

• Usage

  • PD

• Clinical Usage:

  • For smoother plasma levodopa levels and more continuous availability

  • decrease ‘on’ and ‘off’ time

  • Use only with levodopa

• Side Effects

  • Dyskinesia

    • If dopaminergic side effects occur, decrease levodopa not COMT inhibitor

  • Severe diarrhea

  • Liver toxicity

  • Discoloration of urine (harmless)

• NOTE

  • Reduce dose of levodopa by 15-30% when adding a COMT Inhibitor

Tasmar

• Class:

• AKA:

• Usage

• Clinical Usage:

• Side Effects

• NOTE

Tasmar

• Class: Catechol-O-methyltransferase (COMT) inhibitors

• AKA:

  • Tolcapone

• Usage

  • PD

• Clinical Usage:

  • For smoother plasma levodopa levels and more continuous availability

  • decrease ‘on’ and ‘off’ time

  • Use only with levodopa

• Side Effects

  • Dyskinesia

    • If dopaminergic side effects occur, decrease levodopa not COMT inhibitor

  • Severe diarrhea

  • Liver toxicity

  • Discoloration of urine (harmless)

• NOTE

  • Reduce dose of levodopa by 15-30% when adding a COMT Inhibitor

Entacapone

• Class:

• AKA:

• Usage

• Clinical Usage:

• Side Effects

• NOTE

Entacapone

• Class: Catechol-O-methyltransferase (COMT) inhibitors

• AKA:

  • Comtan

• Usage

  • PD

• Clinical Usage:

  • For smoother plasma levodopa levels and more continuous availability

  • decrease ‘on’ and ‘off’ time

  • Use only with levodopa

• Side Effects

  • Dyskinesia

    • If dopaminergic side effects occur, decrease levodopa not COMT inhibitor

  • Severe diarrhea

  • Liver toxicity

  • Discoloration of urine (harmless)

• NOTE

  • Reduce dose of levodopa by 15-30% when adding a COMT Inhibitor

Comtan

• Class:

• AKA:

• Usage

• Clinical Usage:

• Side Effects

• NOTE

Comtan

• Class: Catechol-O-methyltransferase (COMT) inhibitors

• AKA:

  • Entacapone

• Usage

  • PD

• Clinical Usage:

  • For smoother plasma levodopa levels and more continuous availability

  • decrease ‘on’ and ‘off’ time

  • Use only with levodopa

• Side Effects

  • Dyskinesia

    • If dopaminergic side effects occur, decrease levodopa not COMT inhibitor

  • Severe diarrhea

  • Liver toxicity

  • Discoloration of urine (harmless)

• NOTE

  • Reduce dose of levodopa by 15-30% when adding a COMT Inhibitor

Azilect

• Class:

• AKA:

• Usage

• MOA:

Azilect

• Class: Monoamine Oxidase-B (MAO-B) Inhibitors

• AKA:

  • Rasagiline

• Usage

  • PD

• Can use monotherapy

• MOA:

  • Blocks levodopa breakdown in brain

Rasagiline

• Class:

• AKA:

• Usage

• MOA:

Rasagiline

• Class: Monoamine Oxidase-B Inhibitors

• AKA:

  • Azilect

• Usage

  • PD

• Can use monotherapy

• MOA:

  • Blocks levodopa breakdown in brain

Eldepryl

• Class:

• AKA:

• Usage

• MOA:

Eldepryl

• Class: Monoamine Oxidase-B Inhibitors

• AKA:

  • Selegiline

• Usage

  • PD

• Only with Levodopa

• MOA:

  • Blocks levodopa breakdown in brain

Selegiline

• Class:

• AKA:

• Usage

• MOA:

Selegiline

• Class: Monoamine Oxidase-B Inhibitors

• AKA:

  • Eldepryl

• Usage

  • PD

• Only with Levodopa

• MOA:

  • Blocks levodopa breakdown in brain

Rihexyphenidyl

• Class:

• AKA:

• Usage

• Clinical Usage:

Rihexyphenidyl

• Class: Anticholinergics

• AKA:

  • Artane

• Usage

  • PD

• Clinical Usage:

  • tremors 

  • may ease dystonia 

    • associated w/ wearing-off or peak-dose effect

• Clinical Usage:

  • In pts < 60 w/

    • resting tremor + cognitive function preserved

  • Avoid in Elderly

Artane

• Class:

• AKA:

• Usage

• Clinical Usage:

Artane

• Class: Anticholinergics

• AKA:

  • Rihexyphenidyl

• Usage

  • PD

• Clinical Usage:

  • tremors 

  • may ease dystonia 

    • associated w/ wearing-off or peak-dose effect

• Clinical Usage:

  • In pts < 60 w/

    • resting tremor + cognitive function preserved

  • Avoid in Elderly

Benztropine mesylate

• Class:

• AKA:

• Usage

• Clinical Usage:

Benztropine mesylate

• Class: Anticholinergics

• AKA:

  • Cogentin

• Usage

  • PD

• Clinical Usage:

  • tremors 

  • may ease dystonia 

    • associated w/ wearing-off or peak-dose effect

• Clinical Usage:

  • In pts < 60 w/

    • resting tremor + cognitive function preserved

  • Avoid in Elderly

Cogentin

• Class:

• AKA:

• Usage

• Clinical Usage:

Cogentin

• Class: Anticholinergics

• AKA:

  • Benztropine mesylate

• Usage

  • PD

• Clinical Usage:

  • tremors 

  • may ease dystonia 

    • associated w/ wearing-off or peak-dose effect

• Clinical Usage:

  • In pts < 60 w/

    • resting tremor + cognitive function preserved

  • Avoid in Elderly

Managing confusion and psychosis in PD

Managing confusion and psychosis in PD

• Simplify PD medications 

• lower overall dose of dopaminergic medications

• Using Specific Drugs:

  • Clozapine and quetiapine 

    • fewer extrapyramidal side effects 

      • (than other antipsychotic agents)

  • Pimavanserin 

    • newer atypical antipsychotic

Treatment for Hunts

Treatment for Hunts

Treatment (symptomatic)

• Chorea may respond to 

  • tetrabenazine, 

  • amantadine, 

  • riluzole

Treatment for Hemibalism

Treatment for Hemibalism

• Dopamine blocker (haloperidol)

• Dopamine depleter (tetrabenazine)

• Neurosurgery for refractory, persistent symptoms

Causes of Dystonia

Causes of Dystonia

Acute generalized dystonia

• Antipsychotics

• Metoclopramide