Nervous System Medicines: Emergency Drugs

Table of Contents

Nervous System Medicines: Classes, Emergency Uses and Safety

Why this topic matters in emergency medical care

Neurological medicines can rapidly change consciousness, airway tone, breathing, seizure activity, pain, behaviour, blood pressure and intracranial physiology. Emergency medical technicians must know which medicines are time-critical, which can depress respiration, which must not be stopped suddenly and which findings require immediate referral. This lesson connects nervous-system pharmacology to structured assessment, safe administration and emergency decision-making.

The content is designed for EMT and nursing learners. It supports supervised clinical practice and examinations; use current Uganda Ministry of Health guidance, facility protocols, prescriber orders and product information for patient care.

Learning outcomes

Describe the organisation of the central and peripheral nervous systems and the neurotransmitters targeted by medicines.
Classify analgesics, anaesthetics, sedatives, antiseizure medicines, antiparkinson medicines, psychotropic medicines, antimigraine drugs and emergency antidotes.
Recognise and initially manage convulsive status epilepticus, opioid toxicity, acute agitation, stroke symptoms, severe headache and raised intracranial pressure.
Explain onset, duration, routes, adverse effects, interactions and monitoring requirements for high-risk neurological medicines.
Apply safe principles for airway protection, dose verification, titration, reassessment, documentation and handover.
Use clinical scenarios and revision questions to integrate pharmacology with ABCDE assessment.

1. Nervous-system physiology and medicine targets

The central nervous system (CNS) consists of the brain and spinal cord. The peripheral nervous system includes cranial and spinal nerves, sensory pathways and motor pathways. The autonomic nervous system regulates involuntary function: sympathetic activity supports “fight or flight,” while parasympathetic activity supports rest, digestion and recovery. Medicines can alter ion channels, neurotransmitter release, receptor activity, cerebral blood flow, pain pathways or neuromuscular transmission.

Target or neurotransmitter	Major effects	Medicines that act here	Emergency relevance
GABA	Inhibitory neurotransmission; reduces neuronal firing	Benzodiazepines, barbiturates, some anaesthetics	Stops seizures and reduces agitation, but excessive effect causes respiratory depression.
Glutamate	Major excitatory neurotransmission and learning	Ketamine and several antiseizure medicines modify glutamate pathways	Excitotoxicity contributes to brain injury; dissociative medicines alter perception and airway reflexes.
Opioid receptors	Analgesia, sedation, cough suppression and respiratory drive	Morphine, fentanyl, tramadol, codeine, naloxone	Overdose causes respiratory depression; naloxone can reverse the opioid component.
Dopamine	Movement, reward, attention and endocrine regulation	Levodopa, dopamine agonists, antipsychotics, metoclopramide blockade	Dopamine loss causes parkinsonism; dopamine blockade may cause rigidity or neuroleptic malignant syndrome.
Serotonin	Mood, nausea, pain modulation, sleep and vascular tone	SSRIs, SNRIs, triptans, ondansetron	Excess can cause serotonin syndrome; serotonergic combinations need careful review.
Acetylcholine	Memory, autonomic function and neuromuscular transmission	Anticholinergics, cholinesterase inhibitors, some muscle relaxants	Anticholinergic toxicity causes delirium, hyperthermia and urinary retention; cholinergic excess causes secretions and bradycardia.
Voltage-gated sodium/calcium channels	Action-potential generation and neurotransmitter release	Phenytoin, carbamazepine, lidocaine, gabapentin, pregabalin	Channel blockade suppresses seizures or pain but may cause arrhythmia, ataxia or sedation.

2. Practical classification of nervous-system medicines

Medicine group	Representative examples	Main role	Major safety concern
Non-opioid analgesics	Paracetamol/acetaminophen, NSAIDs	Mild–moderate pain and fever	Liver toxicity from overdose; renal, gastrointestinal and bleeding risks with NSAIDs
Opioid analgesics	Morphine, fentanyl, codeine, tramadol	Moderate–severe pain, palliative symptoms	Respiratory depression, hypotension, sedation, constipation and dependence
Local anaesthetics	Lidocaine, bupivacaine	Regional or local anaesthesia; selected arrhythmia indications	Local-anaesthetic systemic toxicity with seizures or cardiovascular collapse
Sedatives/anaesthetics	Midazolam, diazepam, ketamine, propofol	Seizures, procedural sedation, induction or agitation	Airway loss, hypoventilation, hypotension and aspiration
Antiseizure medicines	Levetiracetam, phenytoin/fosphenytoin, valproate, phenobarbital, carbamazepine, lamotrigine	Acute seizure termination and long-term seizure prevention	Respiratory depression, arrhythmia, rash, liver injury, pregnancy risks and interactions
Antiparkinson medicines	Levodopa/carbidopa, dopamine agonists, amantadine, MAO-B inhibitors	Improve bradykinesia, rigidity and tremor	Do not omit scheduled levodopa; hypotension, hallucinations and dyskinesia may occur
Psychotropic medicines	Antidepressants, antipsychotics, mood stabilisers, anxiolytics	Depression, psychosis, bipolar disorder and anxiety	Suicide risk, QT prolongation, serotonin syndrome, lithium toxicity and neuroleptic malignant syndrome
Antimigraine medicines	Triptans, antiemetics, preventive anticonvulsants or beta-blockers	Acute or preventive migraine treatment	Vascular contraindications, medication-overuse headache and sedation
Antidotes	Naloxone, flumazenil, atropine, pralidoxime	Reverse selected toxic effects	Withdrawal, seizures, dysrhythmia or incomplete reversal; antidote never replaces ABCDE care

3. General principles of nervous pharmacology

Small dose changes can have large effects: the therapeutic window is narrow for opioids, sedatives, lithium, phenytoin and tricyclic antidepressants.
Airway and breathing come first: a medicine that improves agitation but removes airway protection may worsen the overall emergency.
Time and trend matter: document the pre-treatment neurological state and reassess after onset, peak and any repeat dose.
Never stop some medicines abruptly: sudden withdrawal of benzodiazepines, opioids, antiseizure medicines, levodopa or corticosteroids can trigger severe rebound effects.
Think of interactions: alcohol, opioids, sedatives, antihistamines and antipsychotics can combine to depress consciousness and ventilation.
Check the cause before labelling behaviour: hypoglycaemia, hypoxia, stroke, head injury, sepsis, intoxication and postictal confusion can all look like agitation or psychosis.

4. Analgesics and antipyretics

4.1 Paracetamol/acetaminophen

Paracetamol is useful for mild-to-moderate pain and fever and is often combined with another analgesic. Therapeutic dosing is generally well tolerated, but overdose saturates normal conjugation pathways and produces toxic metabolites that can cause delayed hepatic failure. Ask about all combination products because patients may unknowingly take paracetamol from several sources.

Check weight, liver disease, malnutrition, chronic alcohol use and the total dose taken in the previous 24 hours.
Do not rely on the patient appearing well after an overdose; early symptoms may be mild before liver injury develops.
Urgent referral is required for intentional overdose, an unknown amount, staggered ingestion or symptoms of hepatic injury.

4.2 Non-steroidal anti-inflammatory drugs (NSAIDs)

Effect	Benefit	Important adverse effect	Use caution or avoid in
COX inhibition	Reduces prostaglandin-mediated pain, fever and inflammation	Dyspepsia, ulceration, gastrointestinal bleeding	Peptic ulcer disease, anticoagulation or active bleeding
Renal prostaglandin reduction	Analgesic and anti-inflammatory effect	Acute kidney injury, sodium retention and hypertension	Dehydration, shock, chronic kidney disease or heart failure
Platelet effects (especially aspirin)	Antiplatelet action at low dose	Bleeding and bronchospasm in aspirin-sensitive asthma	Haemorrhage, severe allergy or suspected intracranial bleeding
Pregnancy effects	Short-term symptom relief when prescribed	Fetal and maternal risks vary by trimester	Pregnancy requires clinician-directed selection and dose.

4.3 Opioid analgesics

Opioids activate mu receptors and produce analgesia, euphoria, sedation, reduced cough and dose-dependent respiratory depression. Morphine may release histamine and lower blood pressure; fentanyl acts rapidly and may cause chest-wall rigidity with very rapid high doses. Tramadol also affects serotonin and noradrenaline pathways and can provoke seizures or serotonin syndrome.

Medicine	Useful feature	Major concern	EMT monitoring
Morphine	Strong analgesia; familiar emergency medicine	Hypoventilation, hypotension, nausea, histamine reaction	Respiratory rate, SpO2, work of breathing, BP, mental status and pain score
Fentanyl	Rapid, potent analgesia with less histamine release	Apnoea, chest-wall rigidity, bradycardia	Continuous respiratory observation; have airway and ventilation equipment ready
Codeine	Oral mild–moderate analgesia in selected patients	Variable metabolism, sedation, constipation and dependence	Assess other sedatives and respiratory disease
Tramadol	Dual analgesic mechanism	Seizures and serotonin syndrome, especially with antidepressants	Ask about SSRIs/SNRIs/MAOIs and seizure history

5. Sedatives, benzodiazepines and procedural medicines

5.1 Benzodiazepines

Midazolam, diazepam and lorazepam enhance GABA-A receptor activity. They reduce anxiety, induce sedation, relax skeletal muscle and terminate seizures. They are first-line medicines in many convulsive seizure protocols, but the same respiratory-depressant effect becomes dangerous when combined with opioids, alcohol or other sedatives.

Medicine	Common emergency role	Advantages	Risks and monitoring
Midazolam	Buccal, intranasal, IM or IV seizure rescue; procedural sedation	Rapid onset and non-IV routes	Apnoea, hypotension and paradoxical agitation; monitor airway, breathing and level of consciousness.
Lorazepam	IV seizure termination; selected severe agitation	Longer anticonvulsant effect than diazepam	Respiratory depression and prolonged sedation, especially in older adults or lung disease.
Diazepam	IV or rectal seizure rescue; muscle spasm	Rapid CNS penetration and available rectal route	Redistribution can cause seizure recurrence; respiratory depression and hypotension.

5.2 Ketamine and propofol

Ketamine: dissociative anaesthesia through NMDA receptor antagonism. It can provide analgesia and preserve spontaneous breathing better than many sedatives, but laryngospasm, hypersalivation, vomiting, emergence reactions, hypertension or tachycardia may occur. It still requires airway preparedness.
Propofol: rapid induction and short recovery, but dose-related hypotension, apnoea and loss of airway reflexes are common. It requires advanced airway skills and continuous monitoring.
Etomidate: rapid induction with comparatively limited cardiovascular depression in some settings, but myoclonus, adrenal suppression and injection discomfort are possible. Use only within the authorised advanced airway protocol.

6. Local anaesthetics and local-anaesthetic systemic toxicity

Lidocaine, bupivacaine and related agents block voltage-gated sodium channels. They prevent nerve conduction when injected locally. If too much enters the circulation, early neurological symptoms (perioral tingling, metallic taste, tinnitus, dizziness, agitation or seizures) may progress to bradycardia, wide-complex arrhythmia and cardiovascular collapse.

Stop injecting, call for advanced help and bring the lipid-emulsion rescue kit if available.
Support airway and ventilation; correct hypoxia and acidosis because they worsen toxicity.
Treat seizures with a benzodiazepine in a carefully titrated dose; avoid large doses of local anaesthetic or additional sodium-channel blockers.
Follow the local lipid-emulsion and resuscitation protocol for cardiovascular toxicity; standard cardiac arrest algorithms may need modification.

7. Antiseizure medicines

Antiseizure medicines reduce neuronal excitability through sodium-channel inactivation, calcium-channel modulation, GABA enhancement or multiple mechanisms. Choice depends on seizure type, age, pregnancy, comorbidity, interactions and availability. A person who is seizure-free on a regular medicine can deteriorate when doses are missed, vomiting prevents absorption or a drug interaction lowers levels.

Medicine	Principal action	Common use	Important adverse effects
Levetiracetam	Modulates synaptic vesicle protein SV2A	Focal and generalised seizures; IV loading in status epilepticus	Somnolence, dizziness, irritability or behavioural change; adjust in renal impairment.
Phenytoin/fosphenytoin	Use-dependent sodium-channel blockade	Established status epilepticus and long-term focal seizure control	Hypotension, arrhythmia with rapid IV use, nystagmus, ataxia, gingival hyperplasia and many interactions.
Valproate	Multiple effects on sodium channels and GABA	Generalised seizures, status epilepticus in selected patients, mood stabilisation	Hepatotoxicity, pancreatitis, thrombocytopenia, weight gain and major fetal risk; avoid in pregnancy unless specialist direction.
Phenobarbital	Enhances GABA-mediated inhibition	Established status epilepticus; selected neonatal or resource-limited protocols	Respiratory depression, hypotension, sedation and enzyme induction.
Carbamazepine	Sodium-channel blockade	Focal seizures and trigeminal neuralgia	Hyponatraemia, rash/Stevens–Johnson syndrome, blood dyscrasias and interactions.
Lamotrigine	Sodium-channel blockade and reduced glutamate release	Focal/generalised epilepsy and bipolar maintenance	Serious rash if titrated rapidly; do not restart at a full dose after a prolonged interruption without advice.
Gabapentin/pregabalin	Modulate alpha-2-delta calcium-channel subunit	Neuropathic pain and selected seizure disorders	Dizziness, ataxia, sedation and additive respiratory depression with opioids.

8. Convulsive seizures and status epilepticus

Status epilepticus is a medical emergency. A convulsive seizure lasting five minutes or more, or repeated seizures without recovery, should trigger a time-based emergency response. WHO and NICE guidance support immediate benzodiazepine treatment, with a second-line IV antiseizure medicine if seizures persist after two benzodiazepine doses and appropriate monitoring is available.

8.1 First five minutes: safety and ABCDE

Protect the patient from injury; remove nearby hazards and cushion the head. Do not restrain limbs or place anything in the mouth.
Note the exact start time, seizure pattern, focal signs, pregnancy status, diabetes, fever, trauma and known epilepsy.
Assess airway and breathing after convulsions; suction secretions, position laterally when safe and provide oxygen for hypoxaemia.
Check capillary glucose early and correct severe hypoglycaemia; consider thiamine before glucose in a severely malnourished alcohol-dependent patient when this does not delay glucose.
Obtain IV/IO access, monitor ECG and vital signs, and look for reversible causes: hypoglycaemia, eclampsia, infection, stroke, head injury, electrolyte abnormality or intoxication.

8.2 Time-based medicine sequence

Time/response	Action	Reasoning
Seizure ≥5 minutes	Give the authorised first-line benzodiazepine by the fastest safe route; prepare ventilation support.	Early treatment reduces progression to established status.
Still convulsing after 5–10 minutes	Repeat one benzodiazepine dose only if the protocol permits; reassess airway and breathing.	Repeated sedatives can cause apnoea; count total doses and time.
After two benzodiazepine doses	Escalate for IV levetiracetam, valproate, phenytoin/fosphenytoin or phenobarbital according to local protocol.	Established status needs a longer-acting antiseizure medicine and monitored care.
Refractory status	Advanced airway, ICU-level anaesthesia and continuous EEG may be required.	Ongoing electrical seizure activity may persist despite visible cessation.

Postictal care: do not assume persistent unconsciousness is “just postictal.” Recheck glucose, oxygenation, temperature, pupils, trauma, toxins and focal neurological signs. Non-convulsive status, stroke, hypoxia and intracranial bleeding can mimic a prolonged postictal state.

9. Stroke and cerebrovascular emergency medicines

Stroke is a time-critical neurological emergency. Medicines are selected only after brain imaging and specialist assessment have distinguished ischaemic from haemorrhagic stroke. The EMT’s contribution is rapid recognition, glucose check, last-known-well time, airway support, blood-pressure and rhythm assessment, and transport to a stroke-capable facility.

Medicine/intervention	Purpose	Important safety point
IV thrombolytic (alteplase or tenecteplase where authorised)	Reperfuses eligible acute ischaemic stroke by dissolving fibrin clot	Requires specialist eligibility, imaging, time window and bleeding-risk assessment; never give for an undifferentiated stroke in the field.
Antiplatelet therapy	Reduces recurrent platelet-mediated thrombosis after haemorrhage is excluded	Timing depends on imaging and thrombolysis status; avoid assuming aspirin is safe before the stroke type is known.
Anticoagulant reversal	Limits bleeding in intracranial haemorrhage associated with anticoagulants	Specific reversal depends on the drug and time of last dose; urgent hospital laboratory and specialist input are required.
Blood-pressure agents	Carefully lower dangerously high pressure or meet thrombolysis thresholds	Over-rapid reduction may worsen cerebral perfusion; treat according to stroke protocol.
Glucose treatment	Corrects hypoglycaemia that can mimic stroke	Reassess neurological deficits after glucose but do not delay stroke transfer if deficits persist.

9.1 Stroke assessment checklist

Use a validated screen such as FAST/BE-FAST and record the exact time last known well.
Check glucose, oxygen saturation, temperature, blood pressure, pulse and rhythm.
Ask about anticoagulants, antiplatelets, recent surgery, bleeding, seizures, migraine and previous disability.
Keep the patient nil by mouth until a swallow assessment; protect the airway and position safely.
Pre-alert the receiving stroke service and bring the medicine list or anticoagulant package.

10. Raised intracranial pressure and cerebral oedema

Raised intracranial pressure may follow traumatic brain injury, intracranial haemorrhage, tumour, infection, hydrocephalus or severe metabolic injury. Warning signs include worsening headache, vomiting, reduced consciousness, unequal pupils, new focal weakness, abnormal posturing, hypertension with bradycardia and irregular breathing.

Prioritise oxygenation and ventilation; avoid hypoxia and hypotension because both worsen secondary brain injury.
Keep the head midline with modest elevation when not contraindicated, avoid tight collars or tubes obstructing venous drainage and prevent fever.
Hypertonic saline or mannitol may be used in specialist protocols; these require serum sodium/osmolality, renal function, haemodynamic assessment and controlled administration.
Do not give routine hyperventilation as a prolonged treatment. Brief controlled ventilation may be a bridge for impending herniation under advanced guidance.
Urgent neurosurgical and critical-care transfer is required for deteriorating consciousness, pupillary change or herniation signs.

11. Opioid toxicity and naloxone

Opioid overdose classically produces reduced consciousness, slow or absent breathing, pinpoint pupils and reduced bowel sounds, but pupils can be normal and mixed overdoses are common. WHO identifies naloxone as a medicine that can prevent death when given in time. The priority remains ventilation and oxygenation; naloxone is a titrated reversal medicine, not a substitute for basic life support.

Ensure scene safety and use standard precautions; consider an unknown substance or co-ingestants.
Open the airway, provide rescue breaths or bag-mask ventilation and oxygen as indicated. Call for advanced help.
Give naloxone by the authorised route and concentration, titrating to adequate spontaneous breathing rather than complete arousal or severe withdrawal.
Reassess repeatedly. Naloxone may wear off before a long-acting opioid, so recurrent respiratory depression is possible.
Search for trauma, hypoglycaemia, stroke, sepsis or sedative co-ingestion; transport for observation even when the patient initially improves.

Target of naloxone: adequate ventilation and airway protection. A suddenly agitated, vomiting patient in acute withdrawal is not necessarily “fully treated”; continue monitoring and protect staff and patient.

12. Flumazenil and mixed sedative overdose

Flumazenil can antagonise benzodiazepine effects but is not a routine antidote for undifferentiated coma. It can precipitate seizures or acute withdrawal in chronic benzodiazepine users, mixed overdoses or patients with pro-convulsant co-ingestants such as tricyclic antidepressants. Supportive airway and ventilation care is usually safer while the toxicology plan is clarified.

13. Acute agitation, psychosis and behavioural emergencies

Agitation is a symptom, not a diagnosis. Hypoxia, hypoglycaemia, head injury, delirium, sepsis, stroke, intoxication, withdrawal, mania and psychosis require different treatment. Verbal de-escalation, a low-stimulation environment and a team safety plan come before medication whenever possible.

Medicine group	Examples	Useful role	Major risks
Benzodiazepine	Midazolam, lorazepam	Severe anxiety, stimulant intoxication, alcohol withdrawal or rapid sedation when indicated	Respiratory depression, paradoxical agitation and hypotension; avoid stacking with opioids without close monitoring.
Antipsychotic	Haloperidol, olanzapine, risperidone	Psychosis or severe agitation under a clinician-directed protocol	QT prolongation, dystonia, hypotension, aspiration and neuroleptic malignant syndrome.
Ketamine	Ketamine	Extreme excited delirium or dangerous agitation when rapid control is necessary	Airway complications, hypertension, tachycardia and emergence reactions; advanced monitoring is essential.

13.1 Neuroleptic malignant syndrome (NMS)

NMS is a life-threatening reaction to dopamine blockade or abrupt withdrawal of dopaminergic medicines. Fever, severe rigidity, altered mental status, autonomic instability and markedly raised creatine kinase are characteristic. Stop the causative medicine, begin cooling and ABCDE support, treat complications and arrange urgent critical-care review.

14. Antidepressants and serotonin safety

Class	Examples	Clinical role	Emergency cautions
SSRIs	Fluoxetine, sertraline, citalopram, escitalopram	Depression, anxiety and several trauma-related conditions	Delayed benefit; nausea, sexual effects, hyponatraemia, bleeding and serotonin syndrome. Citalopram/escitalopram may prolong QT.
SNRIs	Venlafaxine, duloxetine	Depression, anxiety and some neuropathic pain	Blood-pressure elevation, withdrawal symptoms and serotonin toxicity.
Tricyclic antidepressants	Amitriptyline, imipramine	Depression and neuropathic pain in selected patients	Overdose causes anticholinergic delirium, seizures, hypotension and wide-QRS arrhythmia.
MAO inhibitors	Phenelzine, tranylcypromine; selegiline in selected Parkinson care	Specialist treatment	Many food and drug interactions; serotonin syndrome or hypertensive crisis.
Mirtazapine	Mirtazapine	Depression with insomnia or poor appetite in selected patients	Sedation and weight gain; overdose still requires assessment.

14.1 Serotonin syndrome

Serotonin syndrome develops after serotonergic excess, often from combinations or overdose. Mental-status change, autonomic instability, hyperreflexia, clonus, tremor, sweating, diarrhoea and hyperthermia are clues. Stop serotonergic agents, provide supportive care, control agitation and temperature, and urgently escalate when rigidity, hyperthermia or organ failure develops.

15. Antipsychotics and mood stabilisers

Group	Examples	Important monitoring	Emergency warning
First-generation antipsychotics	Haloperidol, chlorpromazine	ECG/QT, movement symptoms, blood pressure, temperature	Acute dystonia, akathisia, NMS, torsades risk and sedation.
Second-generation antipsychotics	Risperidone, olanzapine, quetiapine, aripiprazole	Metabolic parameters, movement symptoms, ECG and sedation	Orthostatic hypotension, aspiration, NMS and increased stroke/mortality risk in some older adults with dementia.
Lithium	Lithium carbonate	Serum level, renal/thyroid function, sodium and hydration	Tremor, ataxia, vomiting, diarrhoea, confusion, coarse tremor and seizures indicate possible toxicity.
Valproate/carbamazepine/lamotrigine	Mood stabilisers also used as antiseizure medicines	Liver function, blood count, pregnancy risk and drug levels where indicated	Severe rash, liver failure, pancreatitis, blood dyscrasia or toxicity.

15.1 Lithium toxicity

Risk increases with dehydration, vomiting/diarrhoea, kidney impairment, low sodium and interacting medicines such as NSAIDs, ACE inhibitors or thiazide diuretics.
Do not induce vomiting. Protect the airway, stop further lithium, obtain urgent levels/electrolytes/renal function and transport.
Neurological signs may progress from coarse tremor and ataxia to confusion, seizures and coma; cardiac monitoring is important.

16. Parkinson medicines

Parkinson disease involves loss of dopamine-producing neurons, causing bradykinesia, rigidity, tremor and postural instability. NICE emphasises timely administration of levodopa in hospital because delayed or omitted doses can cause severe immobility, swallowing difficulty or an akinetic crisis.

Medicine/class	Action	Common concerns	Emergency teaching point
Levodopa + carbidopa/benserazide	Replaces dopamine precursor; peripheral decarboxylase inhibitor reduces nausea	Wearing-off, dyskinesia, hallucinations, orthostatic hypotension	Give at the patient’s individual times; do not substitute with a generic “three times daily” schedule.
Dopamine agonists	Stimulate dopamine receptors	Somnolence, hallucinations, impulse-control disorder, hypotension	Sudden withdrawal can cause severe rigidity or dopamine-agonist withdrawal syndrome.
MAO-B inhibitors	Reduce dopamine breakdown	Interactions with serotonergic or sympathomimetic medicines	Check the full medicine list before giving interacting analgesics or antidepressants.
Amantadine	Modulates dopamine and glutamate pathways	Confusion, hallucinations, ankle oedema and renal accumulation	Reduce risk by checking renal function and mental state.

17. Migraine and severe headache medicines

Before labelling a headache “migraine,” screen for thunderclap onset, fever/neck stiffness, new neurological deficit, papilloedema, pregnancy-related hypertension, head trauma, cancer, immunosuppression or a new headache in older age. These red flags require urgent assessment rather than repeated analgesia.

Medicine	Role	Safety points
Triptans (for example sumatriptan)	5-HT1 receptor agonists that constrict cranial vessels and reduce trigeminal signalling	Avoid in significant ischaemic heart disease, uncontrolled hypertension, some cerebrovascular disease and with certain interacting medicines.
Antiemetics (metoclopramide, prochlorperazine)	Treat nausea and may improve migraine symptoms	Dystonia, akathisia, sedation and QT effects; metoclopramide blocks dopamine.
NSAID or paracetamol	Analgesia for acute migraine when appropriate	Check renal, gastrointestinal, liver and bleeding risks; avoid medication overuse.
Preventive medicines	Beta-blockers, topiramate, valproate and others	Selection depends on pregnancy, asthma, cognition, mood and comorbidity; not an acute rescue dose.

18. High-risk interactions and special populations

Situation	Why risk increases	Practical action
Opioid + benzodiazepine/alcohol	Additive respiratory depression and loss of airway reflexes	Use the lowest authorised dose, monitor continuously and have ventilation equipment ready.
Valproate in pregnancy	Major fetal and neurodevelopmental risk	Do not stop suddenly; urgent specialist review and pregnancy-safe planning are required.
Antiseizure medicine + oral contraceptive	Enzyme induction can reduce contraceptive effectiveness	Ask about pregnancy possibility and counsel for specialist review.
SSRI/SNRI + tramadol/MAOI/triptan	Serotonin syndrome risk	Check for clonus, hyperreflexia, fever and autonomic instability.
Lithium + dehydration/NSAID/ACE inhibitor	Reduced renal clearance and toxicity	Stop further doses pending clinician review; check hydration and renal status.
Parkinson disease + dopamine-blocking antiemetic	Worsens rigidity and movement	Ask for a Parkinson-safe alternative and preserve levodopa timing.
Renal or hepatic failure	Accumulation changes sedative and antiseizure exposure	Use prescribed dose adjustments and longer monitoring; avoid casual repeat doses.

19. Medication administration and monitoring checklist

Indication: identify the problem being treated and exclude a reversible cause such as hypoglycaemia or hypoxia.
Patient: confirm two identifiers, allergies, age, weight, pregnancy status and baseline neurological state.
Medicine: verify name, concentration, expiry, route, prescribed dose and maximum repeat dose.
Interactions: ask specifically about opioids, alcohol, benzodiazepines, antidepressants, antiseizure medicines, anticoagulants and Parkinson medicines.
Preparation: prepare airway, oxygen, suction, bag-mask ventilation, monitoring and a second clinician before sedating or giving a seizure medicine.
Administration: give slowly or titrate when required; do not stack doses without counting time and effect.
Reassessment: record respiratory rate, oxygen saturation, pulse, blood pressure, GCS/AVPU, pupils, seizure activity, pain and adverse effects.
Handover: communicate the indication, exact time/dose/route, response, remaining risk and next monitoring requirement.

20. Clinical scenarios

Scenario 1: Convulsive status epilepticus

A patient has been convulsing continuously for seven minutes. Protect from injury, time the seizure, check glucose, support airway and breathing, and give the authorised benzodiazepine promptly. If still convulsing after two doses, escalate for a monitored second-line antiseizure medicine rather than repeatedly giving sedatives without airway support.

Scenario 2: Postictal confusion or stroke?

A patient remains aphasic and weak on one side 30 minutes after a witnessed seizure. Do not assume postictal paralysis without reassessment. Check glucose, document last known well, evaluate focal deficits and transport urgently for stroke and intracranial pathology assessment.

Scenario 3: Opioid overdose

A drowsy patient has a respiratory rate of six and shallow breaths. Begin ventilation and oxygen, call for advanced help and give titrated naloxone under protocol. Continue observation because a long-acting opioid may outlast naloxone.

Scenario 4: Severe agitation

An agitated patient is hot, confused and tachycardic. Before sedation, check glucose, oxygenation, temperature, trauma, intoxication and infection. Use de-escalation and a team safety plan; if medication is essential, choose a protocol-based option with airway and ECG monitoring.

Scenario 5: Lithium toxicity

A patient taking lithium has vomiting, coarse tremor and ataxia after several days of diarrhoea. Stop further doses pending medical review, protect the airway, check glucose and ECG, establish access and arrange urgent renal function and lithium-level testing.

Scenario 6: Parkinson medicine omission

An inpatient with Parkinson disease becomes rigid and unable to swallow after levodopa doses were omitted. Treat the missed timing as clinically important, seek the prescribed alternative route and avoid dopamine-blocking antiemetics unless specifically directed.

Scenario 7: Thunderclap headache

A patient reports the “worst headache of life” reaching maximum intensity within seconds. Do not repeatedly administer migraine medicines without investigation. Stabilise, assess for meningism and neurological deficit, record onset exactly and transport urgently.

21. Calculations and dose safety

For a weight-based medicine, dose required = ordered dose per kilogram × weight in kilograms. For a liquid, volume = dose required ÷ concentration. Write units at each step and independently recheck high-alert medicines. Never convert milligrams, micrograms, millilitres and units from memory during a moving emergency.

Calculation check	Question to ask	Common error
Weight	Is the weight current and in kilograms?	Using pounds as kilograms or an estimated adult dose in a child
Concentration	How many mg/mL, micrograms/mL or units/mL are in this ampoule?	Confusing different strengths or prefilled devices
Maximum dose	Has the patient already received a dose from another team or carer?	Duplicate dosing during handover failure
Infusion rate	What pump rate delivers the prescribed dose per hour?	Mixing up total volume per hour with drug dose per hour
Reassessment time	When will effect, peak or recurrence be checked?	Giving repeated sedative or naloxone doses too close together

22. Documentation and structured handover

Document baseline mental status, GCS/AVPU, pupils, seizure duration and pattern, airway interventions, oxygenation, glucose, pain score, medicine name/concentration, dose, route, exact time, response, adverse effects and repeat doses. Use an SBAR handover:

Situation: “Seven-minute convulsive seizure” or “opioid-associated respiratory depression.”
Background: known epilepsy, pregnancy, Parkinson disease, opioid prescription, anticoagulants, psychiatric medicines and allergies.
Assessment: airway, breathing, circulation, neurological signs, glucose, temperature, ECG and response to treatment.
Recommendation: required imaging, toxicology, ICU review, repeat observations and concern about recurrence.

23. Revision questions

Explain why benzodiazepines can stop seizures but also cause respiratory depression.
List the first priorities when a patient is convulsing for more than five minutes.
What is the difference between a postictal state and ongoing non-convulsive status?
Compare levetiracetam, phenytoin/fosphenytoin, valproate and phenobarbital in status epilepticus.
Why should glucose be checked early in any patient with altered consciousness?
Describe the classic opioid toxidrome and the correct target of naloxone therapy.
Why is flumazenil unsafe in some benzodiazepine overdoses?
List the red flags that make a headache an emergency rather than routine migraine.
Explain the pre-hospital contribution to acute stroke care before imaging.
What are the signs of local-anaesthetic systemic toxicity?
Why must levodopa be given at the patient’s prescribed time?
Compare serotonin syndrome and neuroleptic malignant syndrome.
List four causes of acute agitation that are not primary psychiatric illness.
Why is lithium toxicity more likely after dehydration or NSAID use?
What monitoring is required after giving an opioid or benzodiazepine?
Which antiseizure medicines have major pregnancy concerns?
What is the safest approach to suspected mixed sedative overdose?
How can antidepressants contribute to serotonin syndrome?
Why is repeated analgesia unsafe in thunderclap headache?
Write the essential elements of a neurological medicine handover.

24. Key takeaways

Neurological medicines can improve pain, seizures and behaviour while simultaneously threatening airway protection and breathing.
Status epilepticus is time-critical: protect, check glucose, give protocol-based benzodiazepine treatment and escalate after two doses.
Naloxone reverses opioid effects, but ventilation and continued observation remain essential.
Stroke medicines are selected only after urgent assessment and brain imaging; EMTs preserve the treatment window through rapid transport and accurate last-known-well documentation.
Do not omit scheduled levodopa, antiseizure medicines or other high-risk chronic medicines without clinical advice.
Serotonin syndrome, neuroleptic malignant syndrome, lithium toxicity and local-anaesthetic systemic toxicity require early recognition and urgent escalation.
Every sedative, opioid or seizure medicine dose needs airway preparation, monitoring, exact documentation and a planned reassessment.

25. Recommended references for further study

Clinical note: This page supports EMT learning and revision. It does not replace an authorised prescription, local emergency protocol, senior clinical supervision or individual toxicology/neurology advice. In a deteriorating patient, stabilise ABCDE, call for advanced help and transfer urgently.