NCLEX Neuro Review: Stroke, ICP, and Seizures

Neurological questions on the NCLEX live and die by priority recognition. A missed LOC change, a missed early ICP sign, or the wrong position for a stroke patient can change the outcome in minutes. This review covers stroke (ischemic and hemorrhagic), increased intracranial pressure, seizures, Parkinson, multiple sclerosis, and myasthenia gravis – the neuro content most heavily tested on the NCLEX-RN.

Key takeaways

• Stroke type drives everything: ischemic strokes may get IV alteplase within 4.5 hours of last-known-well, while hemorrhagic strokes must never receive tPA and need aggressive BP control plus anticoagulation reversal.
• A decreased level of consciousness is the earliest and most sensitive sign of rising ICP – it appears long before the late, ominous Cushing’s triad of bradycardia, widened pulse pressure, and irregular respirations.
• Seizure care is just two things: airway and safety. Turn the patient to the side, protect the head, never put anything in the mouth, never restrain, and stay with the patient.
• Status epilepticus (a seizure 5 or more minutes long, or repeated seizures without return to baseline) is an emergency – IV lorazepam is first-line.
• Wet vs dry distinguishes the MG crises: cholinergic crisis (overmedicated) brings wet SLUDGE findings, while myasthenic crisis (undermedicated) brings dry findings. Airway protection is the priority for both.
• Parkinson is a dopamine problem treated with dopamine (levodopa/carbidopa), and neuro patients need a focused assessment – GCS, pupils, motor strength – every shift, trending the change from baseline.

Stroke: ischemic vs hemorrhagic

Stroke is a leading cause of serious long-term disability in U.S. adults. The NCLEX will test whether you can recognize symptoms fast, know the treatment windows, and position the patient correctly based on stroke type.

The FAST screening

The American Heart Association uses FAST for public and nursing recognition.

• Face drooping – ask the patient to smile. Does one side droop?
• Arm weakness – ask the patient to raise both arms. Does one drift down?
• Speech difficulty – ask the patient to repeat a simple phrase. Is it slurred or garbled?
• Time – note exact time of symptom onset. This determines eligibility for reperfusion therapy.

A more complete tool is the NIH Stroke Scale (NIHSS), which the nurse should be able to administer or assist with. Memorize that “last known well” time is the single most critical piece of data you collect on a suspected stroke patient.

Ischemic stroke (87% of strokes)

A clot blocks cerebral blood flow. The goal is reperfusion before irreversible infarction. Two treatment options:

• IV thrombolytics – alteplase (tPA) or tenecteplase: Within 4.5 hours of last-known-well is the current standard for eligible patients. The 2026 AHA/ASA acute ischemic stroke guideline gives tenecteplase 0.25 mg/kg (max 25 mg) and alteplase 0.9 mg/kg equal Class 1 standing in that window; most NCLEX items still name alteplase (tPA). Every minute matters – “time is brain.”
• Mechanical thrombectomy: Catheter-based clot retrieval for large vessel occlusion. Window extends to 24 hours in selected patients with favorable imaging.

tPA contraindications (high-yield)

The NCLEX loves to ask which patient is not a candidate for tPA. Contraindications and cautions include:

• Active internal bleeding or recent hemorrhage
• History of intracranial hemorrhage
• Ischemic stroke in the past 3 months
• Major surgery in the past 14 days
• Recent head trauma
• Severe uncontrolled hypertension (greater than 185/110 despite treatment)
• Platelets less than 100,000
• INR greater than 1.7 on warfarin
• Current use of direct oral anticoagulants (DOACs) within last 48 hours
• Blood glucose less than 50 or greater than 400 mg/dL – correct the glucose first, since both extremes are stroke mimics; if deficits persist after normalization, thrombolysis may still be reasonable in an otherwise eligible patient

Nursing during and after tPA: strict BP control (less than 180/105 during and for 24 hours after), no NG tubes or urinary catheters for 24 hours, no arterial punctures, neuro checks every 15 minutes for 2 hours then every 30 minutes for 6 hours, hold antiplatelets and anticoagulants for 24 hours, then restart per protocol.

Hemorrhagic stroke

A vessel ruptures. Intracerebral hemorrhage (ICH) or subarachnoid hemorrhage (SAH, often from an aneurysm). Thunderclap headache (“worst headache of my life”) is classic for SAH.

• Do not give tPA – you will kill the patient
• BP management is aggressive – for ICH, lower SBP toward 140 mmHg (keep about 130-150, avoid below 130); for SAH before the aneurysm is secured, keep SBP below about 160 to reduce rebleeding (per protocol)
• Reverse anticoagulation (vitamin K plus 4-factor PCC for warfarin; 4-factor PCC for factor Xa inhibitors such as apixaban and rivaroxaban, since andexanet is no longer available in the U.S.; idarucizumab for dabigatran)
• Neurosurgical evaluation for surgical evacuation, aneurysm clipping, or coiling
• Monitor for vasospasm in SAH (days 3-14 after bleed, peak 7-10) – nimodipine is prophylactic, not a rescue drug: 60 mg enterally every 4 hours started early in all aneurysmal SAH patients and continued for 21 days to prevent delayed cerebral ischemia. Check BP before each dose and hold for hypotension

Positioning based on stroke type

This is a frequently tested NCLEX discriminator.

• Ischemic stroke: HOB at 30 degrees is most common. Some protocols use flat positioning initially to maximize cerebral perfusion until reperfusion is achieved. Follow the facility protocol and provider order.
• Hemorrhagic stroke: HOB 30 degrees to reduce intracranial pressure. Avoid flat positioning because it worsens ICP.
• Either stroke, post-op craniotomy for tumor or aneurysm: HOB elevation per surgical order (usually 30 degrees), head midline, avoid neck flexion

Increased intracranial pressure (ICP)

Normal ICP is less than 15 mmHg. Sustained elevation above 20 mmHg is treated aggressively because it reduces cerebral perfusion pressure (CPP = MAP – ICP) and causes ischemia. Sustained elevation causes herniation, which is rapidly fatal.

Early signs of increased ICP

These come first and they are subtle. This is where the NCLEX tests your assessment skills.

• Decreased level of consciousness is the earliest and most sensitive sign. Restlessness, confusion, lethargy, difficulty following commands
• Pupillary changes – sluggish light reaction or slight inequality on the side of the lesion (a fixed, dilated ‘blown’ pupil is a late sign of herniation)
• Headache that worsens with coughing, straining, or position changes
• Vomiting, often projectile and without preceding nausea
• Visual changes – blurring, diplopia

Late signs: Cushing’s triad

When you see Cushing’s triad, brainstem herniation is imminent. This is a late, ominous finding, not a routine observation.

1. Bradycardia (often in the 40s or 50s)
2. Widened pulse pressure (systolic rises, diastolic stable or falls)
3. Irregular respirations (Cheyne-Stokes, apneustic, or ataxic breathing)

If you see these on an NCLEX stem, the answer involves emergent provider notification and rapid intervention – mannitol, hypertonic saline, possibly intubation with hyperventilation to briefly reduce PaCO2, and neurosurgical consultation.

ICP nursing interventions

• HOB at 30 degrees, head midline, avoid neck flexion or rotation
• Avoid Valsalva maneuver: prevent straining at stool (stool softeners), avoid prolonged breath holding, suction only when necessary and for less than 10 seconds with hyperoxygenation
• Cluster nursing care to allow rest periods – each stimulus raises ICP
• Quiet environment: dim lights, limit visitors, reduce noise
• Maintain normothermia: fever increases cerebral metabolism and ICP
• Blood pressure: avoid hypotension (reduces CPP) and severe hypertension (worsens edema in hemorrhagic stroke)
• Oxygenation: maintain SpO2 greater than 94%. Hypoxia and hypercapnia both worsen ICP
• Osmotic therapy: mannitol 0.25-1 g/kg IV (monitor serum osmolality, avoid above 320 mOsm/kg; it causes osmotic diuresis so monitor I/O, electrolytes, and renal function) or 3% hypertonic saline

Never give hypotonic fluids (0.45% saline, D5W) to a patient with increased ICP – they worsen cerebral edema. Use normal saline or hypertonic saline.

Seizures: types and priorities

Seizure types in brief

• Focal (partial) seizures: Start in one area. Simple focal (awareness preserved) vs complex focal (awareness impaired).
• Generalized tonic-clonic: Loss of consciousness, tonic phase (stiffening), clonic phase (rhythmic jerking), postictal confusion.
• Absence: Brief staring spells, mostly in children, no postictal period.
• Myoclonic: Sudden muscle jerks.
• Atonic: Sudden loss of muscle tone, falls.

Nursing priorities during a seizure

The priority is safety and airway. That is it. Do not overthink this.

1. Stay with the patient – do not leave to get help; call out or use the call light
2. Protect the head and airway: lower the patient to the floor if standing, pad hard surfaces, turn to the side (lateral position) to prevent aspiration
3. Loosen restrictive clothing around the neck
4. Do not restrain the patient – you can cause fractures
5. Do not put anything in the mouth – no tongue blade, no bite block. The old teaching about the tongue is wrong and dangerous.
6. Time the seizure – document onset, type, progression, duration, postictal findings
7. Administer oxygen if available and suction the airway after the seizure ends
8. Assess postictally: LOC, neurological status, Todd’s paralysis (transient focal weakness), urinary or fecal incontinence, tongue biting, injury

Status epilepticus

A seizure lasting 5 or more minutes, or two or more seizures without return to baseline in between, is status epilepticus. This is a medical emergency with high mortality if untreated.

• IV lorazepam is first-line (0.1 mg/kg, max 4 mg per dose, may repeat). Diazepam or midazolam are alternatives.
• Second-line after benzodiazepines fail: levetiracetam, fosphenytoin, or valproate IV
• Third-line: continuous IV infusion (midazolam, propofol) with intubation
• Throughout: maintain airway (may require intubation), oxygen, IV access, check glucose (treat hypoglycemia with dextrose), rule out reversible causes

Discharge teaching for seizure patients

• Take antiepileptic medications at the same time every day. Do not stop abruptly – can trigger status epilepticus.
• Many antiepileptics cause enzyme induction – reduced effectiveness of oral contraceptives (use backup), warfarin interactions, drug-drug checks
• No driving until cleared by the provider (state-specific, commonly 3-12 months seizure-free, most often 6)
• No swimming alone, no baths (shower instead), caution with heights, ladders, machinery
• Medical alert bracelet
• Family teaching on seizure first aid
• Avoid triggers: alcohol, sleep deprivation, flashing lights (for photosensitive seizures), skipped meals

Parkinson disease

Progressive degeneration of dopaminergic neurons in the substantia nigra. Clinical tetrad: Tremor (resting, “pill rolling”), Rigidity (cogwheel), Akinesia/bradykinesia, Postural instability (TRAP mnemonic). Masked facial expression, shuffling gait, stooped posture, micrographia.

Medications

• Levodopa/carbidopa (Sinemet): First-line. Levodopa crosses the blood-brain barrier and converts to dopamine; carbidopa blocks peripheral conversion to reduce side effects. Take on an empty stomach or with low-protein snack – dietary protein competes with levodopa for absorption across the gut and the blood-brain barrier. If GI upset occurs, take with a small low-protein snack. Full meals high in protein blunt the drug’s effect.
• “On-off” phenomenon: symptoms fluctuate as drug level rises and falls. Dose timing and adjunct meds minimize this.
• Dyskinesia (involuntary movements) develops over years of use.
• Monitor for hypotension, hallucinations, impulse control disorders.
• Dopamine agonists (pramipexole, ropinirole): used alone in early disease or with levodopa later
• MAO-B inhibitors (selegiline, rasagiline): reduce dopamine breakdown. Avoid with tyramine-rich foods at high doses.
• COMT inhibitors (entacapone): extend levodopa action
• Anticholinergics (benztropine): help tremor, used cautiously in elderly (confusion, urinary retention)

Nursing care

• Fall risk is high – clear pathways, assistive devices, well-lit rooms
• Swallowing evaluation – aspiration risk increases with disease progression
• Small frequent meals with thickened liquids if dysphagia present
• Encourage exercise and active ROM to maintain mobility
• Speech therapy for hypophonia (quiet speech)
• Do not stop Parkinson medications abruptly – neuroleptic malignant syndrome-like reaction possible

Multiple sclerosis (MS)

Autoimmune demyelination of the CNS. Relapsing-remitting course is most common. Symptoms depend on plaque location but commonly include optic neuritis, sensory changes, weakness, ataxia, spasticity, bladder dysfunction, and fatigue.

• Heat worsens symptoms (Uhthoff’s phenomenon) – avoid hot baths, hot weather, fever
• Stress and infection can trigger relapses
• Disease-modifying therapies: interferon beta, glatiramer, natalizumab, ocrelizumab, fingolimod
• Acute relapse treatment: IV methylprednisolone 1 g daily for 3-5 days
• Symptomatic management: baclofen for spasticity, oxybutynin for bladder spasticity, amantadine or modafinil for fatigue
• Encourage cool environments, energy conservation, bladder schedule, fall prevention

Myasthenia gravis (MG)

Autoimmune destruction of acetylcholine receptors at the neuromuscular junction. Causes fluctuating weakness that worsens with use and improves with rest. Classic findings: ptosis, diplopia, dysphagia, dysarthria, proximal muscle weakness. Severe cases involve respiratory muscle weakness.

Diagnosis

• Acetylcholine receptor antibody assay
• Edrophonium (Tensilon) test: brief cholinesterase inhibitor; transient improvement suggests MG (less commonly used now due to risks)
• Electromyography with repetitive nerve stimulation

Treatment

• Pyridostigmine (Mestinon): cholinesterase inhibitor – increases acetylcholine at the synapse. Take 30-60 minutes before meals to improve chewing and swallowing strength.
• Immunosuppressants (prednisone, azathioprine, mycophenolate)
• Plasmapheresis or IVIG for acute exacerbation
• Thymectomy can produce long-term remission

Cholinergic crisis vs myasthenic crisis

Both look like severe weakness, including respiratory failure. Both can require intubation. The question is what caused it – too much medication (cholinergic) or too little / an exacerbation (myasthenic).

• Myasthenic crisis: undermedicated, often triggered by infection, surgery, or stress. Weakness without the muscarinic ‘wet’ SLUDGE findings (often tachycardia and hypertension) – but secretions may still pool because the patient is too weak to swallow or cough them up.
• Cholinergic crisis: overmedicated with pyridostigmine. Weakness plus wet findings – the SLUDGE response: Salivation, Lacrimation, Urination, Defecation, GI cramping, Emesis. Also miosis (small pupils), bradycardia, bronchospasm.
• The edrophonium (Tensilon) test distinguishes them: transient improvement in weakness suggests myasthenic crisis (more drug needed); transient worsening suggests cholinergic crisis (drug must be held). Atropine is the antidote for cholinergic crisis.
• Priority for both is airway protection. Intubation may be needed.

Neuro assessment essentials

Every neuro patient needs focused assessment every shift, and more often when unstable.

• Glasgow Coma Scale (GCS): Eye opening (1-4), Verbal response (1-5), Motor response (1-6). Score 15 is normal. 8 or less = intubate. Trend matters more than the number.
• Pupil check: PERRLA (pupils equal, round, reactive to light and accommodation). Unilateral dilation is worrisome for ICP.
• Motor strength: Graded 0-5 in all extremities. Compare right to left.
• Cranial nerves: Abbreviated exam at minimum – pupil reactivity (CN II, III), facial symmetry (CN VII), gag reflex (CN IX, X)
• Vital signs: Watch for Cushing’s triad. Trend the numbers.

For the acute neuro patient, a change in LOC from baseline is the earliest sign of deterioration. If your patient is more lethargic, confused, or harder to arouse than at the last check, escalate.

Bring it home

Neuro content rewards anatomic thinking. Stroke type determines treatment and positioning. ICP has a predictable cascade. Seizure care is airway and safety. Myasthenia and cholinergic crises are distinguished by wet vs dry findings. Parkinson is a dopamine problem treated with dopamine. Map the pathophysiology to the intervention and the questions get easier.

For the pharmacology that threads through all of this – tPA, mannitol, levodopa, pyridostigmine, antiepileptics – see our pharmacology review. For recognizing priority scenarios and ordering interventions, see the resources page. For NGN case study formats that combine neuro assessment with clinical judgment, see the NGN question types guide.

Frequently Asked Questions

How do you interpret a Glasgow Coma Scale score?

The Glasgow Coma Scale adds three components – eye opening (1-4), verbal response (1-5), and motor response (1-6) – for a total of 3 to 15. A score of 15 is normal, fully awake and oriented. A score of 8 or less generally indicates a comatose patient who needs the airway protected (intubation). The trend matters more than any single number, so a falling GCS from one check to the next signals deterioration and should be escalated. For the full breakdown of how each component is scored, see our Glasgow Coma Scale reference.

What is the difference between decorticate and decerebrate posturing?

Both are abnormal motor responses to a noxious stimulus that reflect serious brain injury and score low on the motor component of the GCS. Decorticate posturing means the arms flex inward toward the core (“toward the cord”) with the legs extended – think arms drawn up to the chest. Decerebrate posturing means the arms and legs both extend, with the arms adducted and internally rotated and the forearms pronated (palms turned down), which generally indicates a deeper, more caudal brainstem injury and is the more ominous of the two. A patient who progresses from decorticate to decerebrate posturing is worsening, and this change should be reported immediately.

What are the early versus late signs of increased intracranial pressure?

The earliest and most sensitive sign of rising ICP is a decreased level of consciousness – restlessness, confusion, lethargy, or difficulty following commands. Other early signs include a headache that worsens with coughing or straining, projectile vomiting without nausea, pupillary changes, and visual changes. The late signs make up Cushing’s triad: bradycardia, a widening pulse pressure, and irregular respirations. By the time you see Cushing’s triad, brainstem herniation is imminent, so you act on the subtle early LOC changes long before the triad appears. See our classic triads reference for more on Cushing’s triad.

Why should you never give tPA to a hemorrhagic stroke patient?

Alteplase (tPA) is a thrombolytic that dissolves clots, which is the goal in an ischemic stroke where a clot is blocking blood flow. In a hemorrhagic stroke a vessel has already ruptured and is bleeding into the brain, so giving a clot-busting drug would dramatically worsen the bleeding and can be fatal. That is why imaging to rule out hemorrhage is required before tPA, and why hemorrhagic stroke care focuses on aggressive blood pressure control and reversing any anticoagulation instead.

What is the priority during an active seizure?

The priority is airway and safety – nothing more complicated than that. Turn the patient onto their side to let secretions drain and prevent aspiration, protect the head, move nearby objects out of the way, loosen restrictive clothing, and stay with the patient. Never put anything in the mouth and never restrain the patient, since both can cause serious injury. Time the seizure, and remember that one lasting 5 or more minutes is status epilepticus, a medical emergency for which IV lorazepam is first-line.