Cerebrovascular Disorders and Increased Intracranial Pressure - Cheat Sheet
Your last-minute revision companion for rapid recall of stroke types, tPA criteria, ICP management, and emergency interventions. Focus on pathophysiology, nursing priorities, and exam-critical distinctions.
STROKE: ISCHEMIC vs HEMORRHAGIC
Common values
Value
Within 3 hours of symptom onset (extended to 4.5 hours in eligible patients)
Symbol
tPA window
Quantity
Time window for tPA (ischemic stroke only)
Value
Complete resolution within 24 hours (typically within 1 hour)
Symbol
24-hour rule
Quantity
TIA symptom resolution time
Value
80–85%
Symbol
Ischemic %
Quantity
Ischemic stroke percentage of all strokes
Value
15–20%
Symbol
Hemorrhagic %
Quantity
Hemorrhagic stroke percentage of all strokes
Important facts
- ISCHEMIC: caused by THROMBUS (in-situ clot) or EMBOLUS (traveling clot, often from A-fib).
- HEMORRHAGIC: caused by RUPTURE of cerebral vessel, often from uncontrolled HTN or cerebral aneurysm.
- Subarachnoid hemorrhage (SAH) from ruptured aneurysm = 'WORST HEADACHE OF MY LIFE' + neck stiffness + meningeal signs.
- FIRST DIAGNOSTIC STEP = non-contrast CT head to distinguish ischemic from hemorrhagic (rules out bleeding before tPA).
- Ischemic stroke deficits are OPPOSITE the lesion: LEFT brain lesion = RIGHT-sided weakness; RIGHT brain lesion = LEFT-sided weakness.
- LEFT-hemisphere stroke dominance: expressive aphasia, receptive aphasia, right hemiplegia, analytical deficits.
- RIGHT-hemisphere stroke: spatial-perceptual deficits, unilateral neglect, left hemiplegia, impulsiveness.
- TIA is a MAJOR WARNING SIGN — 10–15% progress to full stroke within 90 days; many within days.
- Dysphagia is a MAJOR ASPIRATION RISK in acute stroke; NPO until swallow assessment complete.
- Modifiable risk factors: HTN (single most important), A-fib, diabetes, dyslipidemia, smoking, obesity, carotid stenosis.
Key definitions
Ischemic Stroke
Example
Left middle cerebral artery thrombosis causes right hemiparesis and expressive aphasia.
Sudden loss of brain function from blocked cerebral blood flow due to thrombus or embolus; accounts for 80–85% of all strokes.
Hemorrhagic Stroke
Example
Hypertensive intracerebral hemorrhage in the basal ganglia with rapid deterioration.
Sudden brain dysfunction from rupture of a cerebral vessel, causing bleeding into brain tissue; accounts for 15–20% of strokes.
Penumbra
Example
Target tissue for tPA therapy within the critical 3-hour window.
Zone of at-risk, ischemic but not yet infarcted brain tissue surrounding the infarct core; salvageable with rapid reperfusion.
Transient Ischemic Attack (TIA)
Example
Expressive aphasia and right arm weakness that resolve completely in 45 minutes.
Brief episode of neurologic dysfunction from temporary cerebral ischemia, with complete symptom resolution within 24 hours and NO permanent infarction.
Diagrams to know
- FAST mnemonic: Face drooping, Arm weakness, Speech difficulty, Time to call EMS.
- Stroke-to-scan timeline: activate emergency response → STAT non-contrast CT → differentiate → treatment decision.
- Cerebral perfusion zones: MCA (most common), ACA, PCA; each produces characteristic deficits.
tPA (ALTEPLASE) THERAPY — CRITICAL FOR NLE
Formulas
Alteplase dose = 0.9 mg/kg body weight (maximum dose 90 mg)
Meaning
0.9 = standard dose per kilogram; max = 90 mg total; initial bolus = 10% of total dose IV push over 1 minute; remainder over 60 minutes
Watch out
MOST COMMON MISTAKE: giving the dose too slowly or over the wrong time interval. The BOLUS is 10% over 1 min, THEN the rest over 60 min. Total drug must be dosed by ACTUAL body weight, not estimated weight.
When to use
When administering IV thrombolytic for acute ischemic stroke within approved time window.
Common values
Value
0.9 mg/kg (max 90 mg total)
Symbol
Alteplase dose
Quantity
Standard tPA dose
Value
10% of total dose over 1 minute
Symbol
Bolus
Quantity
Initial IV bolus
Value
90% of total dose over 60 minutes
Symbol
Infusion
Quantity
Remaining infusion
Value
<185/110 mmHg
Symbol
BP limit
Quantity
BP threshold before tPA
Value
≤3 hours from symptom onset
Symbol
Standard window
Quantity
Time window standard
Value
≤4.5 hours (select patients)
Symbol
Extended window
Quantity
Extended time window
Important facts
- tPA is for ISCHEMIC STROKE ONLY. Contraindicated in hemorrhagic stroke (causes catastrophic bleed expansion).
- ABSOLUTE CONTRAINDICATIONS: active internal bleeding, recent ICH, head trauma or intracranial surgery within 3 months, history of ICH, uncontrolled severe HTN.
- Blood pressure MUST be lowered to <185/110 mmHg BEFORE tPA is given.
- If onset time is UNKNOWN (e.g., patient woke with symptoms), standard tPA window does not apply; selective imaging protocols may be used.
- MOST DANGEROUS COMPLICATION = intracranial hemorrhage from tPA; classic signs: sudden severe headache, vomiting, hypertension, worsening neuro deficit.
- During and after tPA: AVOID all invasive procedures (arterial punctures, IM injections, indwelling catheters, urinary catheter insertion if possible).
- NO aspirin or other antiplatelet agents within 24 hours after tPA completion.
- Monitor neuro status (NIHSS or similar) and vital signs frequently during infusion.
- If any sign of bleeding during/after infusion: STOP tPA immediately, notify provider, prepare for reversal (fresh frozen plasma, cryoprecipitate if needed).
- Endovascular mechanical thrombectomy extends treatment window for large-vessel occlusions in comprehensive stroke centers.
Key definitions
Tissue Plasminogen Activator (tPA / Alteplase)
Example
Given at 0.9 mg/kg for acute ischemic stroke within 3 hours to 'open up' the blocked artery.
Intravenous thrombolytic enzyme that binds to fibrin and activates plasminogen, dissolving the clot to restore cerebral perfusion.
Last Known Well (LKW)
Example
Patient woke with symptoms at 0700 but was normal at 0600 — LKW is 0600, so tPA window closes at 0900 (3 hours).
The exact time the patient was observed to be normal; critical for determining tPA eligibility.
Thrombolytic Window
Example
Standard window = within 3 hours of symptom onset; extended window = up to 4.5 hours in select patients without contraindications.
The timeframe during which thrombolytic therapy is safe and effective for dissolving acute blood clots.
Diagrams to know
- tPA dosing algorithm: weight calculation → 10% bolus (1 min IV) → 90% infusion (60 min).
- Decision tree: symptom onset known? → within 3 hours? → no contraindications? → YES to all = tPA eligible.
- Complication monitoring: neuro decline + severe headache + hypertension = STOP infusion immediately.
INCREASED INTRACRANIAL PRESSURE (ICP) — PATHOPHYSIOLOGY & SIGNS
Formulas
Cerebral Perfusion Pressure (CPP) = MAP − ICP
Meaning
MAP = mean arterial pressure; ICP = intracranial pressure; CPP must be maintained ≥60 mmHg to ensure adequate brain perfusion.
Watch out
COMMON MISTAKE: forgetting that ICP is SUBTRACTED from MAP. If ICP rises and MAP stays the same, CPP FALLS, reducing cerebral perfusion. Student nurses often confuse the direction of change.
When to use
Assessing whether cerebral blood flow is adequate in patients at risk for increased ICP (stroke, head trauma, tumor, hemorrhage).
Monro-Kellie Doctrine: Skull volume = Brain tissue + Blood + CSF (rigid, fixed space)
Meaning
The skull is a closed box; if one component increases, others must decrease or pressure rises catastrophically.
Watch out
Do not think of the skull as expandable; it is RIGID. Any increase in brain, blood, or CSF volume must be compensated by a decrease elsewhere, or ICP rises.
When to use
Understanding WHY increased ICP occurs and why interventions aim to reduce one component (e.g., osmotic diuretics reduce brain edema volume).
Common values
Value
5–15 mmHg
Symbol
Normal ICP
Quantity
Normal intracranial pressure
Value
>20 mmHg sustained
Symbol
Pathologic ICP
Quantity
ICP threshold requiring treatment
Value
60–70 mmHg
Symbol
CPP target
Quantity
Target cerebral perfusion pressure
Value
<60 mmHg
Symbol
CPP minimum
Quantity
Critical CPP threshold (brain ischemia risk)
Important facts
- Normal ICP = 5–15 mmHg; sustained ICP >20 mmHg requires treatment.
- EARLIEST and MOST IMPORTANT sign of increased ICP = DECREASING LEVEL OF CONSCIOUSNESS (not Cushing's triad, which is late).
- Cushing's triad is a LATE, OMINOUS sign of impending herniation (NOT early sign). Do not wait for it; act on LOC changes.
- Headache, projectile vomiting (without nausea), and papilledema are classic but develop AFTER LOC changes begin.
- Pupillary signs: unilateral FIXED DILATED pupil (from CN III compression) is a red flag for herniation.
- Abnormal posturing: decorticate (arms flexed, legs extended = midbrain) progresses to decerebrate (all limbs extended = brainstem), indicating worsening ICP.
- Causes of increased ICP: cerebral edema (stroke, trauma, hypoxia), hemorrhage (epidural, subdural, SAH, intracerebral), tumor, hydrocephalus, infection (meningitis, encephalitis).
- CPP target = 60–70 mmHg; if CPP drops below 60, cerebral ischemia worsens; if ICP unchecked, CPP falls to zero (brain death).
- Fever RAISES ICP by increasing cerebral metabolism; aggressive temperature management is critical.
- Hypoxia and hypercapnia (high CO2) are potent cerebral vasodilators; they INCREASE ICP; avoid these.
Key definitions
Increased Intracranial Pressure (ICP)
Example
Brain edema from ischemic stroke raises ICP; if untreated, causes herniation and death.
Elevated pressure within the cranial vault (normal 5–15 mmHg; pathologic >20 mmHg), compressing and shifting brain tissue.
Cerebral Edema
Example
Ischemic stroke causes cytotoxic edema (does NOT respond to corticosteroids); tumor causes vasogenic edema (responds to dexamethasone).
Accumulation of fluid in brain tissue; CYTOTOXIC (intracellular, from hypoxia/ischemia) or VASOGENIC (extracellular, from tumor/hemorrhage).
Herniation
Example
Uncal herniation from supratentorial mass compresses the ipsilateral CN III, causing fixed dilated pupil and contralateral hemiplegia.
Protrusion of brain tissue through a structural opening due to uncontrolled increased ICP; causes brainstem compression and death.
Cushing's Triad
Example
Severe head trauma with ICP >25 mmHg → BP 180/80, HR 40, irregular breathing = impending herniation, life-threatening emergency.
Three late, ominous signs of increased ICP: widened pulse pressure (rising systolic with falling diastolic), bradycardia, and irregular respirations.
Diagrams to know
- ICP waveform interpretation: normal (A waves < 5 mmHg), plateau waves (A waves, pathologic), sharp peaks indicate crises.
- Timeline of neurologic deterioration: LOC decline → headache/vomiting → pupil changes → Cushing's triad → herniation/death.
- Brainstem compression sequence: CN III compression (ipsilateral fixed pupil) → midbrain dysfunction → pontine damage → medullary failure.
ICP MANAGEMENT — NURSING INTERVENTIONS & PHARMACOLOGY
Common values
Value
30 degrees
Symbol
HOB angle
Quantity
Head of bed elevation
Value
10–15 seconds
Symbol
Suction time
Quantity
Suctioning duration maximum
Value
0.25–1 g/kg IV
Symbol
Mannitol dose
Quantity
Mannitol dose
Value
30–35 mmHg (brief use only)
Symbol
PaCO2 target
Quantity
Hyperventilation target PaCO2
Value
Keep <320 mOsm/kg
Symbol
Max osmolality
Quantity
Serum osmolality threshold (mannitol)
Important facts
- AIRWAY PATENCY & OXYGENATION = TOP PRIORITY. Hypoxia and hypercapnia dilate cerebral vessels and INCREASE ICP.
- Suctioning: ≤10–15 seconds maximum to avoid suctioning-induced ICP spike; pre-oxygenate, pause between suctioning passes.
- HOB 30°: standard position to promote venous return and reduce ICP. Reassess with any change in neurologic status.
- Head/neck MIDLINE and NEUTRAL: avoid extreme flexion/extension/rotation. Even 30–45° head turn can impair venous drainage.
- AVOID VALSALVA maneuvers: straining, coughing, pushing with bowel movements, breath-holding, bearing down. All INCREASE ICP.
- Stool softeners and gentle laxatives prevent straining; bowel regimen is standard for increased ICP patients.
- Cluster nursing care: group all activities (bathing, vitals, assessments) into one session, then allow 30–40 minutes of rest to prevent cumulative ICP elevation.
- Environment: quiet, calm, cool room (fever increases cerebral metabolism and ICP); minimal noxious stimuli.
- Pain and agitation INCREASE ICP; adequate analgesia and sedation are key (avoid oversedation that masks neurologic decline).
- Hyperthermia management: acetaminophen, cooling devices, tepid sponging for fevers >38.5°C.
- Monitor ICP continuously if catheter in place; record and report sustained elevations or plateau waves.
- Avoid hypotension: maintains CPP. Fluid management balanced to maintain euvolemia without pulmonary edema.
- Hyperventilation (target PaCO2 30–35 mmHg) briefly constricts cerebral vessels to reduce ICP in acute crises (NOT long-term management; causes rebound ICP rise).
- MANNITOL: osmotic diuretic, standard agent for acute ICP. Dose 0.25–1 g/kg IV through a FILTER; monitor serum osmolality, urine output, electrolytes.
- HYPERTONIC SALINE (3%): alternative osmotic agent; may be preferred in some settings.
- DEXAMETHASONE: reduces VASOGENIC edema (tumors, swelling around lesions), NOT cytotoxic edema (ischemic stroke, head trauma).
- ANTISEIZURE MEDICATIONS (levetiracetam, phenytoin): prophylaxis in high-risk situations (post-trauma, post-surgery, tumor).
- Sedation/analgesia reduce metabolic demand and prevent ICP spikes from agitation/pain.
Key definitions
Head of Bed (HOB) Elevation to 30°
Example
Patient with epidural hematoma: HOB 30°, head midline, neutral neck alignment; avoids ICP spike from poor positioning.
Positioning intervention that promotes venous drainage from the cranium, reducing ICP by gravity and improving CPP.
Midline Head Alignment
Example
Avoid turning head sharply; pillow under head, not under shoulders; neck not flexed or extended.
Positioning of the patient's head and neck in neutral position, straight on the midline, to prevent venous obstruction and ICP rise.
Osmotic Diuretic
Example
Mannitol 0.25–1 g/kg IV reduces cytotoxic and vasogenic edema in acute increased ICP.
Medication that increases serum osmolality, drawing fluid from brain tissue into the vasculature to reduce cerebral edema volume.
Diagrams to know
- ICP management hierarchy: airway/oxygenation → position (HOB 30°, midline) → avoid triggers (Valsalva, suctioning, hyperthermia) → medications → advanced measures (hyperventilation, osmotic diuretics, surgery).
- Mannitol administration: prepare in filter, push IV, monitor urine output (osmotic effect), check osmolality q6-8h, watch for rebound edema.
TRAUMATIC BRAIN INJURY & HEAD INJURY TYPES
Common values
Value
Acute (hours)
Symbol
Epidural timeline
Quantity
Epidural hematoma onset
Value
<72 hours
Symbol
Subacute onset
Quantity
Subdural acute onset
Value
3–20 days
Symbol
Subacute timeline
Quantity
Subdural subacute onset
Value
>20 days
Symbol
Chronic timeline
Quantity
Subdural chronic onset
Important facts
- EPIDURAL HEMATOMA: arterial bleed (middle meningeal artery most common), produces high-pressure bleed that strips dura from bone. CLASSIC = brief LOC, lucid interval, then rapid decline. SURGICAL EMERGENCY (craniotomy & evacuation).
- SUBDURAL HEMATOMA: venous bleed beneath dura, slower accumulation. Acute = symptoms within 72 hours; subacute = 3–20 days; chronic = >20 days (common in elderly, alcoholics, anticoagulated patients).
- BASILAR SKULL FRACTURE clinical signs: CSF rhinorrhea (nose drainage), CSF otorrhea (ear drainage), raccoon eyes (bilateral periorbital bruising), Battle's sign (mastoid region bruising).
- CSF identification: halo sign (CSF on dressing shows clear center surrounded by blood ring), glucose positive (CSF contains glucose, blood drainage does not).
- CONTRAINDICATIONS with basilar skull fracture: NEVER pack the nose or ears, NEVER insert nasogastric tube (risk of intracranial placement), NEVER insert nasal airway. Use oral airway instead.
- NO nasal suctioning or nasal procedures in suspected basilar skull fracture.
- Head injury complications: diffuse axonal injury (DAI) from rotational forces, epidural/subdural/intracerebral hemorrhage, increased ICP, cerebral contusion, post-traumatic seizures, post-concussive syndrome.
- Concussion: mild TBI with brief LOC or confusion, usually resolves without imaging, but repeated concussions carry cumulative risk.
- Management priorities: stabilize spine (C-spine immobilization until cleared), maintain airway/oxygenation, prevent secondary injury, ICP management, surgical consultation if indicated.
- Serial neuro checks detect deterioration early (worsening LOC, pupil changes, motor weakness).
Key definitions
Epidural Hematoma
Example
Temporal bone fracture lacerates middle meningeal artery → rapid epidural bleed → patient awake, alert, then deteriorates over hours.
Arterial bleeding between the skull and dura mater; classic presentation includes brief LOC, then LUCID INTERVAL, then rapid deterioration; surgical emergency.
Subdural Hematoma
Example
Fall in elderly patient on anticoagulation → slow venous bleed → weeks later, confusion, lethargy, then LOC loss.
Venous bleeding beneath the dura but outside brain tissue; can be acute (hours), subacute (days), or chronic (weeks); high mortality.
Basilar Skull Fracture
Example
Severe head trauma → watery drainage from nose ('halo sign' positive for CSF) + bruising around eyes = basilar skull fracture.
Fracture of the base of the skull, presenting with CSF leak from nose (rhinorrhea) or ears (otorrhea), raccoon eyes (periorbital ecchymosis), and Battle's sign (mastoid ecchymosis).
Lucid Interval
Example
Patient knocked unconscious briefly, then wakes and seems fine, then 2 hours later becomes unresponsive (subdural bleeding).
Brief period of consciousness between initial trauma and secondary deterioration; classic for epidural hematoma.
Diagrams to know
- Epidural vs subdural: epidural = arterial, acute onset, lucid interval, crescent moon shape on CT; subdural = venous, slower, concave/crescent, high risk in elderly.
- Basilar skull fracture red flags: CSF leak, raccoon eyes, Battle's sign → contraindicate nasal procedures.
- Head injury secondary prevention: avoid hypoxia, hypercapnia, hypotension, hyperthermia, elevated ICP.
BRAIN TUMORS & POST-CRANIOTOMY CARE
Common values
Value
4 mg q6h (post-op), tapered
Symbol
Dex dose
Quantity
Typical dexamethasone dose
Value
Every 1 hour
Symbol
Neuro check frequency
Quantity
Post-op neurologic check frequency (initial)
Important facts
- Brain tumors are dangerous even if benign because they RAISE ICP within the rigid skull.
- Manifestations: headache (often worse in morning from overnight CSF accumulation), seizures (30–40% of brain tumors), focal neurologic deficits (depend on location), personality/behavioral change, signs of increased ICP.
- Diagnosis: MRI with contrast (detects enhancing tumor and edema), biopsy for tissue diagnosis.
- Treatment: surgical resection (craniotomy), radiation therapy, chemotherapy; combination depends on tumor type and grade.
- DEXAMETHASONE reduces VASOGENIC edema around brain tumors; typical dose 4 mg q6h, tapered carefully post-surgery (abrupt withdrawal causes rebound edema).
- Post-craniotomy: strict neurologic checks q1h initially, then per protocol; monitor for signs of increased ICP, infection, hemorrhage.
- Post-op positioning: depends on surgical approach (supratentorial vs infratentorial, size of resection). Follow surgeon's orders strictly.
- Supratentorial (above tentorium) = HOB 30°; infratentorial (below tentorium, cerebellum) = flat or slight reverse to reduce brainstem strain.
- Avoid extreme positioning; frequent position changes unless contraindicated.
- Wound care: monitor incision for CSF leak, infection, dehiscence; aseptic dressing changes.
- ICP monitoring: if ventriculostomy (EVD) in place, monitor for obstruction, infection, overflow.
- Pain management: adequate analgesia without oversedation (masks neuro changes).
- DVT/PE prophylaxis: early mobility, compression stockings, pharmacologic prophylaxis per protocol.
- Seizure prophylaxis: antiseizure meds per protocol, especially first 7 days post-op.
- Discharge teaching: medication adherence (dexamethasone taper, antiseizure meds), activity restrictions, signs of increased ICP or infection, follow-up neuro checks, driving restrictions.
Key definitions
Primary Brain Tumor
Example
Glioblastoma (malignant astrocytoma), meningioma (benign, slow-growing).
Tumor originating in brain tissue (glioma, meningioma, astrocytoma); benign or malignant.
Metastatic Brain Tumor
Example
Lung cancer metastases to brain, causing multiple lesions and increased ICP.
Tumor that has spread to the brain from a primary cancer elsewhere (lung, breast, melanoma most common).
Peritumoral Edema
Example
Brain tumor surrounded by swollen tissue; dexamethasone reduces edema and symptoms.
Vasogenic edema surrounding a brain tumor; responsive to corticosteroids (dexamethasone) unlike cytotoxic edema of stroke.
Craniotomy
Example
Supratentorial craniotomy for frontal lobe tumor resection; postop position per surgical approach.
Surgical opening of the skull to access brain tissue for tumor resection, biopsy, or other procedures; requires specialized post-op care.
Diagrams to know
- Brain tumor location → symptoms: frontal = personality/judgment change; temporal = seizures/memory; parietal = sensory deficits; occipital = visual deficits; posterior fossa = ataxia/hydrocephalus.
- Dexamethasone dosing post-op: initiate pre-op or immediately post-op, taper slowly over days to weeks to prevent rebound ICP elevation.
CLINICAL PEARLS & EXAM TRAPS
Important facts
- EXAM TRAP #1: Students confuse Cushing's triad as an EARLY sign. It is LATE and ominous. Early sign is DECREASING LOC.
- EXAM TRAP #2: tPA is given to ISCHEMIC stroke ONLY. Hemorrhagic stroke = contraindication (causes bleed expansion and death).
- EXAM TRAP #3: Mannitol is an osmotic diuretic that REDUCES edema volume but does NOT treat the underlying cause (stroke, tumor, trauma). It buys time for definitive treatment.
- EXAM TRAP #4: Dexamethasone reduces edema AROUND TUMORS (vasogenic), not in ischemic stroke (cytotoxic edema). Students mix these up.
- EXAM TRAP #5: Suctioning raises ICP. Limit to ≤10–15 seconds, pre-oxygenate, allow rest between passes.
- EXAM TRAP #6: A patient with basilar skull fracture and CSF leak is at HIGH RISK for meningitis/encephalitis. Avoid packing/nasal procedures; prophylactic antibiotics per protocol.
- EXAM TRAP #7: Unilateral FIXED DILATED pupil (CN III palsy) is a sign of uncal herniation and brain death unless reversed immediately.
- EXAM TRAP #8: Left-hemisphere dominance means left frontal = expressive aphasia, left temporal = receptive aphasia. Right hemisphere = spatial neglect, impulsiveness, left-sided weakness.
- EXAM TRAP #9: TIA is NOT a stroke; symptoms resolve fully by definition. But it is a major warning sign — up to 15% progress to stroke.
- EXAM TRAP #10: Normal ICP is 5–15 mmHg; pathologic is >20 mmHg. CPP target is 60–70 mmHg (not ICP level). CPP = MAP − ICP.
Key definitions
FAST Screening
Example
Patient's smile uneven, right arm drifts downward, speech slurred = FAST positive, time to activate stroke code.
Rapid stroke assessment tool: Face (drooping), Arm (weakness), Speech (difficulty), Time (to call EMS). Present = stroke; activate emergency response.
Contralateral Deficit
Example
LEFT hemisphere stroke = RIGHT-sided hemiparesis; RIGHT hemisphere stroke = LEFT-sided hemiparesis.
Neurologic deficit on the opposite side of the body from the brain lesion (due to crossing of motor/sensory tracts).
Expressive Aphasia (Broca's Aphasia)
Example
Patient understands commands but struggles to speak; 'uh-uh' or single words only; knows what to say but cannot say it.
Difficulty producing speech while comprehension is relatively preserved; suggests LEFT frontal (Broca's area) involvement.
Receptive Aphasia (Wernicke's Aphasia)
Example
Patient speaks fluently but content is garbled nonsense; does not follow commands; seems unaware of error.
Difficulty understanding speech while producing fluent but meaningless speech; suggests LEFT temporal (Wernicke's area) involvement.
Diagrams to know
- Neuro decline red flag timeline: normal → LOC dropping (early) → headache/vomiting → pupil change → Cushing's (late) → herniation (death).
- Aphasia quick ID: Broca's (expressive, left frontal) vs Wernicke's (receptive, left temporal).
Must remember
- 1. EMERGENT NON-CONTRAST CT SCAN FIRST to distinguish ischemic from hemorrhagic stroke — treatment is opposite. tPA is only for ischemic; it is CONTRAINDICATED in hemorrhage.
- 2. tPA (ALTEPLASE) WINDOW: within 3 hours of symptom onset (extended to 4.5 hours in eligible patients). Dose = 0.9 mg/kg (max 90 mg): 10% bolus IV over 1 min, 90% over 60 min. Establish EXACT 'last known well' time.
- 3. ABSOLUTE tPA CONTRAINDICATIONS: any hemorrhage on CT, active internal bleeding, recent head trauma/intracranial surgery, history of ICH, uncontrolled HTN (must lower to <185/110 mmHg first).
- 4. MOST DANGEROUS tPA COMPLICATION = intracranial hemorrhage during/after infusion. Signs: sudden severe headache, vomiting, worsening neuro deficit, hypertension. If suspected: STOP infusion, notify provider immediately.
- 5. TIA = transient ischemia with COMPLETE symptom resolution within 24 hours and NO permanent infarction. It is a MAJOR WARNING SIGN — 10–15% progress to full stroke within 90 days; workup and secondary prevention urgent.
- 6. CUSHING'S TRIAD (rising SBP with widening pulse pressure + bradycardia + irregular respirations) is a LATE, OMINOUS sign of impending herniation, NOT an early sign. EARLIEST sign of increased ICP = DECREASING LEVEL OF CONSCIOUSNESS.
- 7. ICP MANAGEMENT PRIORITIES: (a) maintain patent airway & oxygenation (hypoxia/hypercapnia worsen ICP); (b) HOB 30°, head midline neutral alignment; (c) avoid Valsalva, straining, suctioning >10–15 sec; (d) quiet cool environment; (e) cluster care; (f) medications (mannitol, dexamethasone for tumors only, antiseizure prophylaxis).
- 8. MANNITOL dosing: 0.25–1 g/kg IV through a FILTER. Osmotic diuretic that reduces cerebral edema volume. Monitor serum osmolality (keep <320 mOsm/kg), urine output, electrolytes, and dehydration. Dexamethasone reduces edema AROUND TUMORS (vasogenic), NOT in ischemic stroke (cytotoxic).
- 9. EPIDURAL HEMATOMA = arterial bleed with CLASSIC 'LUCID INTERVAL' (brief LOC, then alert, then rapid decline). SURGICAL EMERGENCY. SUBDURAL = venous bleed; acute/subacute/chronic; high mortality. BASILAR SKULL FRACTURE = CSF leak (rhinorrhea/otorrhea), raccoon eyes, Battle's sign. CONTRAINDICATE nasal procedures, packing, NG tube; risk of meningitis.
- 10. STROKE DEFICITS ARE CONTRALATERAL: LEFT brain lesion = RIGHT-sided weakness, expressive/receptive aphasia; RIGHT brain lesion = LEFT-sided weakness, spatial neglect, impulsiveness. Use FAST (Face, Arm, Speech, Time) for rapid screening.
Last minute tips
- TIP #1 — DIAGNOSIS FIRST: Non-contrast CT is the gateway decision. If hemorrhage, tPA is out; if ischemic, clock is ticking. You cannot treat until you know the type. Always state this in any stroke scenario.
- TIP #2 — tPA BOLUS TIMING: Students memorize the dose but botch the timing. 10% over 1 MINUTE (bolus), THEN 90% over 60 MINUTES (infusion). Slow administration = ineffective. Get this right on exam questions.
- TIP #3 — ICP SIGN HIERARCHY: Never start with Cushing's triad as your first answer. Decreasing LOC is ALWAYS the earliest warning. Only mention Cushing's when answering 'late signs of increased ICP' or 'impending herniation.' This distinction wins points.
- TIP #4 — DEXAMETHASONE CONTEXT: If the question says 'brain tumor' or 'peritumoral edema,' dexamethasone is your answer. If it says 'ischemic stroke' or 'head trauma,' dexamethasone does NOTHING (cytotoxic edema). This is a favorite NLE trap — read carefully.
- TIP #5 — EXAM SCENARIO KEYWORDS: Watch for 'worst headache of my life' (SAH, ruptured aneurysm), 'lucid interval' (epidural hematoma), 'CSF leak from nose' (basilar skull fracture, contraindicate NG tube), 'blood pressure rising with slowing heart rate' (Cushing's, late sign). These keywords often signal the correct answer instantly.
Comparison tables
Ischemic vs Hemorrhagic Stroke — Critical Distinctions
| Feature | Ischemic Stroke | Hemorrhagic Stroke |
|---|---|---|
| Cause | Thrombus or embolus blocking blood flow | Rupture of cerebral vessel causing bleeding |
| Frequency | 80–85% of all strokes | 15–20% of all strokes |
| CT scan findings | No blood; area of hypodensity (infarct) appears later | HYPERDENSE (bright) blood visible immediately |
| tPA (alteplase) | INDICATED; restores perfusion within 3–4.5 hours | CONTRAINDICATED; worsens bleeding |
| Anticoagulation | Indicated (after thrombolytics or if not thrombolytic candidate) | Contraindicated; increases bleeding |
| First diagnostic step | Non-contrast CT to rule out hemorrhage | Non-contrast CT confirms bleeding |
| Mortality | Lower | Higher (30–50%) |
| Classic SAH presentation | N/A | Worst headache of my life + neck stiffness + meningeal signs |
TIA vs Ischemic Stroke — Key Difference for NLE
| Feature | TIA | Ischemic Stroke |
|---|---|---|
| Definition | Temporary ischemia; neurologic symptoms | Permanent ischemia; neurologic deficits with infarction |
| Symptom duration | Resolves completely within 24 hours (usually <1 hour) | Persists >24 hours |
| Brain imaging | No infarction on MRI; CT normal | Infarction visible on DWI-MRI; CT shows hypodensity later |
| Functional outcome | Complete resolution; no permanent deficit | May have permanent deficits depending on size/location |
| Clinical significance | Major warning sign; 10–15% progress to stroke within 90 days | Full stroke; requires urgent thrombolytic or thrombectomy |
| Secondary prevention | Urgent (antiplatelet, BP/lipid control, carotid workup) | Urgent (antiplatelet/anticoagulant, rehabilitation, risk factor control) |
Epidural vs Subdural Hematoma — Head Injury Comparison
| Feature | Epidural Hematoma | Subdural Hematoma |
|---|---|---|
| Location | Between skull and dura mater | Beneath dura, outside brain tissue |
| Bleeding source | Arterial (middle meningeal artery, usually) | Venous (cortical veins) |
| Onset of symptoms | Acute (hours); rapid deterioration | Acute (<72 h), subacute (3–20 d), or chronic (>20 d) |
| Classic presentation | Brief LOC → LUCID INTERVAL → rapid decline | May be subtle initially; slow accumulation; confusion/lethargy |
| CT appearance | Convex (crescent) shape between skull and brain | Concave (crescent) shape; follows brain contour |
| Risk factors | Temporal bone fracture, severe head trauma | Elderly, alcoholics, anticoagulation, falls |
| Treatment | URGENT surgery (craniotomy); evacuation | Surgery if >10 mm thickness or >5 mm midline shift; may observe small bleeds |
| Mortality | 20–30% with treatment | Up to 60% in severe acute cases |
Cerebral Edema Types — Pathophysiology & Treatment Response
| Feature | Cytotoxic Edema | Vasogenic Edema |
|---|---|---|
| Location | Intracellular (within brain cells) | Extracellular (between brain cells) |
| Cause | Hypoxia, ischemia, hypoglycemia; cell pump failure | BBB breakdown from inflammation, tumor, hemorrhage |
| Typical conditions | Ischemic stroke, head trauma, anoxia | Brain tumor, hemorrhage, infection, post-op |
| Dexamethasone response | NO benefit | YES; significant reduction |
| Osmotic diuretic response | Limited; affects extracellular space | YES; pulls fluid from extracellular space |
| Mannitol effectiveness | Moderate; buys time | YES; effective |
Left vs Right Hemisphere Stroke — Deficits & Personality
| Feature | Left Hemisphere (Dominant) | Right Hemisphere (Non-dominant) |
|---|---|---|
| Motor deficit side | RIGHT-sided hemiparesis/hemiplegia | LEFT-sided hemiparesis/hemiplegia |
| Language | Expressive or receptive aphasia (Broca's or Wernicke's) | Intact speech but may have dysprodia (odd rhythm) |
| Cognition | Analytical thinking affected; calculation difficulty | Spatial perception affected; left neglect common |
| Behavioral | Slow, cautious, aware of deficits; depression risk | Impulsive, judgment poor, unaware of deficits; denial |
| Visual deficit | RIGHT hemianopia (loss of right visual field) | LEFT hemianopia (loss of left visual field) |
| Recovery style | Slower, more aware; prone to depression | May overestimate recovery; less aware of deficits |
Diagrams
Acute Stroke Management Algorithm — From Symptom Onset to Treatment Decision
Complete flowchart from stroke recognition through diagnostic CT interpretation to treatment decision (tPA vs conservative management). Critical decision points include hemorrhage rule-out, time window, and tPA contraindications.
Increased ICP Pathophysiology & Clinical Progression
Mind map showing ICP causes (edema, hemorrhage, tumor), the Monro-Kellie doctrine, clinical progression from early (LOC drop) to late (Cushing's) to herniation, and management hierarchy (airway → position → pharmacology).
Stroke Deficits: Location Predicts Deficit — Contralateral Rule
Flowchart demonstrating the contralateral nature of stroke deficits: left hemisphere damage causes right-sided weakness and language deficits (aphasia); right hemisphere damage causes left-sided weakness and spatial neglect. Critical for neurologic localization.
Neurologic Deterioration Timeline: From Alert to Herniation
State diagram showing the progressive neurologic deterioration from alert baseline through drowsiness (earliest sign), posturing, Cushing's triad (late), and herniation. Emphasizes that Cushing's is NOT early, and immediate intervention is needed at the drowsiness stage.
tPA Administration Sequence: Timing is Critical
Sequence diagram showing the step-by-step process from patient assessment through tPA infusion, emphasizing timing (10% bolus in 1 min, 90% infusion in 60 min), weight-based dosing, and continuous monitoring for intracranial hemorrhage.