High Yield NSGY Pharm

Drugs for LP

Try not to, but if you must you can use one of these on the floor without ICU team.

DRUG	DOSE AND ROUTE	USE FOR
Lido with epi	Subcutaneous	Needle-site pain, especially if anticipate you will try multiple levels as the bottle in LP kits has a very small volume adequate for only one level. Order this and ask nurse to get it ready on every single patient but don't open unless needed
Fentanyl	25 mg IV for normal sized adult can go up to 50 mg IV for large people (>100kg) If no access, same doses intranasally will work
Ativan (Lorazepam)	0.5mg-1mg PO or 0.5mg-1.0mg IV
Ketamine	0.3 mg/kg max of 35 mg over 15 minutes in an NS bag	only use if in the ICU; key is to push it slow to not cause laryngospasm! This rate is slow and likely will be ok on the floor.

Drugs for MRI

MRI will frequently page you that a patient is freaking out/ in too much pain to sit still for an MRI.

Return the call immediately and dose one of the following drugs.

Remember rules for conscious sedation at PUH only allow you to dose 1 at a time w/o ICU presence and certainly with just an MRI nurse (see below).

TIP: if you know a pt is likely to freak out or be in too much pain to stay still, order one of the drugs below PRN and specify in comments to use in MRI if needed (save yourself a page).

NOTE: when ordering any of these drugs which may depress respiration, there is no harm in playing it safe and just putting the patient on a cardiac monitor with pulse ox. This is something that can easily go into the scanner with the patient, no reason not to do it.

DRUG	DOSE AND ROUTE	USE FOR
Valium	5mg PO, 2.5mg IV	Anxiety / Agitation / claustrophobia
Dilaudid	0.2mg IV (0.5 if large / non-opioid ideally, naive only if "<65")	Pain
Ativan	0.5mg-1mg PO or 0.5mg-1.0mg IV	Anxiety / Agitation / claustrophobia
Zyprexa (olanzapine)	start w/ 2.5 P.O. if geriatric / small / TBI up 5.0mg ODT/IM if excessive agitation / large up to 10mg max	Agitation

Anticoagulants / Antiplatelets

Drug	MOA	Dosing	Reversal	Notes
Aspirin	COX1 inhibitor (irriversible)	ㅤ	Platelets	inhibits platelet function 8-10 days
Plavix (clopidogrel)	P2Y12 receptor antagonism	ㅤ	ㅤ	ㅤ
Brillinta (ticagrelor)	P2Y12 receptor antagonism	ㅤ	ㅤ	ㅤ
Effient (prasugrel)	P2Y12 receptor antagonism	ㅤ	ㅤ	ㅤ
Integrellin (eptifibatide)	Gp IIb/IIIa inhibition	ㅤ	ㅤ	ㅤ
Pradaxa (dabigatratan)	direct 2a inhibition	ㅤ	Idarucizumab	mAB fragment
Eliquis (apixaban)	direct reversible 10a inhibitors	ㅤ	Adnexa, PCC (Kcentra)	ㅤ
Xarelto (rivaroxaban)	ㅤ	ㅤ	ㅤ	ㅤ
Fondaparinux (Arixtra)	ㅤ	ㅤ	ㅤ	ㅤ
Unfractionated Heparin	ㅤ	ㅤ	ㅤ	ㅤ
Low Molecular Weight heparin (Enoxaparin = Lovenox)	ㅤ	ㅤ	ㅤ	ㅤ

Blood Products and Anticoagulant Reversal Agents

Reversal Agent	Contents / Mechanism	Drugs reversed	Labs affected	NOTES
Vitamin K
FFP		tPA (2nd line)		#2 option for tPA reversal
4 Factor PCC (K Centra)		Xarelto (rivaroxaban)
Cryoprecipitate	fibrinogen, vWF, fibronectin Factor 7, AT-III	tPA	Fibrinogen	tPA depletes fibrinogen (contained in cryo)
Protamine	binds heparin to form salt without AC properties	Heparin (full), Lovenox (partial)	Xa	Dosing: 1-mg to 100-U
TXA	reduces fibrinolysis	tPA (2nd line)		#2 option for tPA reversal
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Tranexamic acid

TXA protocol for cSDH medical management

TAX 650 mg PO BID for 14 days, 28 tabs

Atorvastatin 40 mg daily until follow up

ICP Controls

Drug	Dosing	Notes
Mannitol	0.5- to 1-g/kg bolus for ICP reduction	- can also act as a free radical scavenger and decrease blood viscosity resulting in a transient elevation of CBF.

Analgesics

Tylenol

Drug	Dosing	Notes
APAP	1g q6H	unless liver concerns or patient is also on Norco (which has tylenol), no reason to not max someone in pain out on standing 4g of tylenol daily

Narcotics / Narcotic Drips

Mechanism: opioid drugs are µ opiod agonists → inhibit cAMP

opioids: Inhibition of pre-synaptic gated calcium channels

Drug	Dosing	Notes
Oxy IR	5.0 for mod 4-6 pain 10 for severe 7-10 pain 2.5 is a baby dose sometimes effective	For discharge Rx: generally, ordering 5mg tabs x 28 will be the most painless for you, as more will require insurance authorization.
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Drips (ok for floor)

Drug	Dosing	Notes
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NSAIDs

Drug	Dosing	Notes
Ibuprofen	ㅤ	ㅤ
Naproxen	ㅤ	ㅤ
Aspirin	ㅤ	ㅤ

Muscle relaxers

Drug	Dosing	Notes
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Neuropathic pain

Drug	MOA	Dosing	Notes
Gabapentin	prevents delivery of Ca2+ channels to membrane → ↓ NT release	ㅤ	ㅤ
Lyrica (pregabalin)	inhibits Ca2+ channels → ↑L-glutamic acid decarboxylase to synthesize GABA	- start 50-75 mg BID - max dose 300-600 mg daily	- renal excretion - Avoid abrupt d/c, taper over ≥1 week. - analgesic effect within 1 week, full effect 2-4 weeks

Topical

Drug	Dosing	Notes
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Other

Drug	Dosing	Notes
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Antiseizure medicines (ASMs) / Antiepileptic Drugs (AEDs)

❗

AEDs are not harmless and should be thoughtfully prescribed. 2008 meta-analysis of 199 RCTs of 11 AEDs showed risk of suicidality 2x as high

https://www.nejm.org/doi/full/10.1056/NEJMoa0909801

Enzyme-inducing AEDs

Carbamazepine

Ketamine

inhibits NMDA receptor (an excitatory receptor)

Phenytoin

load 17 mg/kg slow IV over 1 hr

Maintenance 100q8

Primidone

Barbiturates

MOA: increase duration of open state in response to GABA presence

Phenobarbital (PHB)

MOA in trauma: decreased cerebral metabolic rate (less synaptic transmission), shunt blood from normal perfusion to reduced CBF, decreased nitrogen excretion, higher intracerebral glucose, glucagon energy stores

AEs:

hypo-kalemia

Non-enzyme-inducing AEDs

Keppra

does NOT have significant hepatic enzyme interaction

consider giving instead of fosphenytoin in < 80 year-olds if complex meds list

Enzyme-inhibiting AEDs

Valproic acid

Benzodiazepenes

MOA: increase frequency of open state that a chloride channel is activated

GABA A receptor activators → Cl- ion channel gets activated → anion influx and hyperpolarization → anxiolysis, amnesia, sedation, hypnosis, anticonvulsant

positive allosteric modulators of GABAA receptor (promote further binding of GABA) in the limbic system and hypothalamus

Drug	Dosing	Use
Alprazolam (Xanax)	ㅤ	ㅤ
Clonazepam (Klonopin)	ㅤ	ㅤ
Diazepam (Valium)	ㅤ	duration of AED effect: 15-30 min
Lorazepam (Ativan)	0.5 - 1.0 mg PO for anxiolysis 0.1 mg/kg (up to 2mg) for seizures	duration of AED effect: 12-24 hrs
Midazolam (Versed)	ㅤ	ㅤ

Spasticity

Baclofen

Mechanism: GABA B activation → muscle spasticity

inhibitory NT

blocks monosynaptic/polysynaptic reflexes

Anti-Pyschotic Drugs

Reviewed below are all antipsychotics with an emphasis on the common inpatient drugs you will prescribe in neurosurgery.

Neurosurgery-relevant antipsychotics

Drug	MOA	Dose
Zyprexa (olanzapine)	SGA D2 antagonist 5-HT2a antagonist H1 antagonist M1 antagonist alpha1 antagonist	- start w/ 2.5 P.O. if geriatric / small / TBI - up 5.0mg ODT/IM if excessive agitation / large - up to 10mg max
Haldol (haloperidol)	FGA potent, competitive antagonist at dopamine D₂ receptors in the mesolimbic and mesocortical pathways, producing antipsychotic and sedative effects	- 2–5 mg IM every 4–8 hours PRN (max 20 mg/day)

Complete Review

Drug Class	MOA	Drugs	Notes
Typical (First generation) antipsychotics	bind and inhibit D2	Haloperidol (Haldol), Fluphenazine, Trifluoperazine, Pimozide, Perphenazine, Loxapine, Chlorpromazine, Thioridazine	ㅤ
Atypical (Second generation) antipsychotics	bind and inhibit D2/5-HT2a receptors	Clozapine, Olanzapine, Quetiapine, Risperidone, Paliperidone, Ziprasidone, Lurasidone, Iloperidone, Aripiprazole, Brexpiprazole, Cariprazine, Asenapine, Lumateperone, Pimavanserin	- treat pos schizophrenia sx (D2) and neg sx (serotonin) - BPD, MDD - Less EPS sx

FGA Classification by Potency

Potency	Examples	Key Features
High-potency FGAs	Haloperidol, Fluphenazine, Trifluoperazine, Pimozide	Strong D₂ blockade → high EPS risk, less sedation, less anticholinergic
Mid-potency FGAs	Perphenazine, Loxapine	Intermediate EPS, sedation, and autonomic effects
Low-potency FGAs	Chlorpromazine, Thioridazine	Weaker D₂ blockade → less EPS, but more sedation, orthostatic hypotension, anticholinergic side effects

Side effects of FGAs

Mechanism	Effect
D₂ blockade (nigrostriatal)	Extrapyramidal symptoms (dystonia, parkinsonism, akathisia, tardive dyskinesia)
D₂ blockade (tuberoinfundibular)	↑ Prolactin → galactorrhea, gynecomastia, amenorrhea
H₁ blockade	Sedation, weight gain
α₁ blockade	Orthostatic hypotension
M₁ blockade	Dry mouth, constipation, urinary retention, blurred vision
Rare:	Neuroleptic Malignant Syndrome (NMS) — life-threatening rigidity, fever, ↑ CK

Potency	Representative Drugs	Main Side Effects
High	Haloperidol, Fluphenazine, Trifluoperazine	EPS, NMS
Medium	Perphenazine, Loxapine	Moderate EPS/sedation
Low	Chlorpromazine, Thioridazine	Sedation, hypotension, anticholinergic effects

Neurostimulation

Drug	MOA	Dosing	Notes
Amantadine	NMDA antagonist	50-100 bid to TID	ㅤ

Anti-hypertensives

Anti-emetics

Drug	MOA	Dosing	Notes
metoclopramide (Reglan)	D2 antagonist	ㅤ	Tardive dyskinesia: choreoathetoid movements in face/arms/legs

Anesthesia

Local Anesthetics

MOA: block voltage-gated sodium channels

Drug	Mechanism of Action	Onset / Duration	Pertinent Notes
Lidocaine (Xylocaine)	Reversibly blocks voltage-gated Na⁺ channels, preventing depolarization and nerve impulse conduction	Rapid onset (1–2 min) / Moderate duration (1–2 hr; up to 3 hr with epinephrine)	Widely used; safe and versatile; can cause CNS toxicity (tinnitus, seizures) or cardiac depression in overdose
Bupivacaine (Marcaine, Sensorcaine)	Same Na⁺ channel blockade	Slower onset (5–10 min) / Long duration (3–8 hr)	Excellent for long procedures or post-op analgesia; cardiotoxicity risk higher than others — use cautiously in obstetrics
Ropivacaine (Naropin)	Na⁺ channel blockade; slightly less lipid soluble than bupivacaine	Slower onset / Long duration (2–6 hr)	Less cardiotoxic than bupivacaine; preferred for continuous peripheral nerve blocks

To make lidocaine hemostatic, it is combined with epinephrine (adrenaline).

Preparation	Mechanism	Effect on Bleeding
Plain Lidocaine	Na⁺ channel blockade; mild vasodilation	May increase bleeding slightly
Lidocaine + Epinephrine (e.g., 1:100,000 or 1:200,000)	Epinephrine causes α₁-mediated vasoconstriction of arterioles	Significantly reduces bleeding at injection site

Formulation	Max mg/kg	Approx. Adult Max	Epinephrine Effect
Plain Lidocaine	4.5 mg/kg	300 mg	None
Lidocaine + Epinephrine	7 mg/kg	500 mg	Prolongs duration, reduces bleeding
Tumescent (very dilute, with epi)	35–55 mg/kg	Variable	Only under monitored conditions

Paralytics (neuromuscular blockade)

Drug	MOA	Notes
succinylcholine	depolarizing agent; nACh agonist without unbinding →depolarization unnaturally prolonged →desensitized receptor →flaccid paralysis	- rapid onset (30-60s) - short duration (5-10min)
rocuronium	non-depolarizing agent; nACh competitive antagonist → blocks ACh binding → prevents depolarization → flaccid paralysis	- onset: 60-90s - duration: 30-60min - reversed by neostigmine or sugammadex
Tubocurarine	competitive antagonist of nACh R	- first clinically used non-depolarizing NMBA - replaced by modern agents that provide faster onset, shorter duration, and fewer cardiovascular side effects.

Anesthetic Effects on Evoked Potentials

Quick Takeaways

Volatile anesthetics + N₂O = worst for both SSEPs and MEPs.

TIVA (Propofol + Opioid) = gold standard for reliable neuromonitoring.

MEPs are more sensitive than SSEPs — any suppression seen in SSEPs will be worse for MEPs.

Ketamine and Etomidate can enhance both signals.

Drug / Class	Effect on SSEPs	Effect on MEPs	Clinical Notes / Recommendations
Volatile agents(Isoflurane, Sevoflurane, Desflurane, Halothane)	⛔ ↓ Amplitude, ↑ Latency (dose-dependent)	⛔ Often abolish MEPs even at low MAC	Keep <0.5 MAC if absolutely needed; TIVA preferred
Nitrous Oxide (N₂O)	⛔ Major amplitude suppression	⛔ Abolishes MEPs	Avoid entirely
Barbiturates (Thiopental, Pentobarbital)	⛔ ↓ Amplitude, ↑ Latency	⛔ ↓ Cortical excitability; may abolish	Sometimes used intentionally for burst suppression
Benzodiazepines (Midazolam, Diazepam)	⚠️ Mild-moderate ↓ amplitude	⚠️ Mild-moderate ↓ amplitude	Avoid or minimize
Propofol (TIVA)	⚠️ Mild ↓ amplitude, slight ↑ latency	⚠️ Moderate ↓ amplitude at high doses	Safe if steady infusion (avoid boluses)
Opioids (Fentanyl, Remifentanil, Sufentanil, Morphine)	✅ Minimal effect	✅ Minimal effect	Excellent for TIVA; maintain stable plasma levels
Ketamine	✅ ↑ Amplitude, minimal latency change	✅ ↑ Amplitude (enhances corticospinal excitability)	Very useful adjunct, especially with weak signals
Etomidate	✅ ↑ Amplitude, minimal latency change	✅ ↑ Amplitude	Great for induction or poor signal quality
Dexmedetomidine	✅ Slight latency ↑, amplitude preserved	⚠️ Mild ↓ amplitude (usually acceptable)	Good adjunct; use low–moderate infusion rate
Neuromuscular blockers (Rocuronium, Vecuronium, etc.)	✅ No direct effect on sensory pathway	⛔ Abolish muscle response	Use only for intubation; avoid during MEP monitoring

Review of Neurobiology / Pharmacology

Neuropeptides and Neurotransmitters

Feature	Neurotransmitters	Neuropeptides
Location in neuron	Found only in axon terminals of the presynaptic neuron	Found throughout the neuron (cell body, dendrites, and axon)
Site of synthesis	Synthesized locally in axon terminals	Synthesized in the cell body and transported along the axon
Chemical nature	Usually small molecules (individual amino acids or derivatives)	Chains of 2–36 amino acids (short proteins)
Speed of action	Fast-acting	Slow-acting
Duration of effect	Short-term (milliseconds to seconds)	Prolonged (seconds to minutes or longer)
Typical function	Rapid synaptic transmission	Neuromodulation, long-lasting effects

Neurotransmitters and Neuropeptides

NT	Type	Function	Associated Drugs
GABA	AA	inhibitory effect on BRAIN	agonists: benzos/barbs/propofol
Glycine	AA	inhibitory effect on SPINE	ㅤ
Glutamate	AA	excitatory effect on CNS	ㅤ
Aspartate	AA	excitatory effect on CNS	ㅤ
ACh	AA	excitatory effect on CNS	ㅤ
Serotonin	mono-aminergic	varies	ㅤ
Dopamine	ㅤ	varies	ㅤ
NE	mono-aminergic	ㅤ	ㅤ
NMDA	ㅤ	ㅤ	ketamine: NMDA receptor blockade
Alpha 2	ㅤ	ㅤ	agonists: clonidine, dexmedetomidine
5-HT2A	ㅤ	ㅤ	LSD: activates 5-HT2A receptor
Hypocretin	neuro-peptide	ㅤ	critical in maintenance of awake state; deficiency associated with narcolepsy
Neuro-peptide Y	neuro-peptide	ㅤ	ㅤ
Substance P	neuro-peptide	activates neurokinin-1 receptors →transmits nociception	ㅤ

Essential amino acids: serotonin, histamine

Inhibitory effect on post-synaptic membrane: chloride influx → hypo-polarizes membrane

Excitatory effect on post-synaptic membrane: depolarizing

Severe Drug Reactions

Malignant Hyperthermia

caused by AD mutation in ryodine receptor gene

exposure to volatile anesthetics or succinylcholine → uncontrolled Ca2+ release →ATP depletion →O2 consumption, CO2 production

Feature	Description
Onset	Hours to days after starting or increasing a dopamine-blocking drug
Key findings	- Earliest sign: ↑ET CO2, tachycardia - Fever (>38.5°C) - Generalized “lead-pipe” rigidity - Altered mental status (agitation → stupor) - Autonomic instability: tachycardia, labile BP, diaphoresis
Lab findings	- ↑ CK (often >1000 U/L) - Leukocytosis - Metabolic acidosis, hyperkalemia, myoglobinuria → may cause renal failure
Treatment	- remove the offending anesthetic (volatile anesthetic / succinylcholine) - hyperventilation with 100% O2 - dantrolene (muscle relaxant - inhibits Ca2+ release from sarcoplasmic reticulum)