Neuro

• SECTION 1 — NORMAL BRAIN CONCEPTS

• Brain coverings: dura → arachnoid → pia mater

• Function: Cushioning, immune protection, CSF flow (in subarachnoid space)

From the outside → inward:

1. Dura Mater
   • The toughest, thickest outer layer
   • Sticks to the inside of the skull like a protective shield
   • Contains blood vessels
   • Purpose: defense against trauma

Easy memory: “Dura = Durable”

2. Arachnoid Mater
   • Middle layer
   • Looks like a spider web
   • Space beneath it holds cerebrospinal fluid (CSF)
   → This space is the subarachnoid space
   • CSF here cushions the brain and carries nutrients/waste

Memory trick: “Arachnoid = Arachnid = Spider Web”

3. Pia Mater
   • Thin, delicate inner layer
   • Directly attached to the brain surface
   • Follows every groove and curve of the brain
   • Has lots of blood vessels to feed brain tissue

Memory trick: “Pia = Pet (sits right on the brain)”

• Normal Brain Circulation - Arterial Supply (Blood Going Into Brain)

There are two main systems:

Quick memory:

• ICA = Intelligence (speech, movement)

• Vertebral = Vital (breathing, HR, coordination)

Circle of Willis (Backup System)

• Connects anterior + posterior circulation so blood can reroute if a blockage happens.

  • Helps prevent complete stroke, but not always perfect.

Venous Drainage (Blood Leaving Brain)

• Deoxygenated blood drains:

  • Veins → Superior sagittal & transverse sinuses → Internal jugular veins

    • If venous drainage is blocked → ICP ↑

Nursing MUST-KNOW

• To reduce ICP and help venous return:

  • HOB 30 degrees

  • Neck straight (not flexed or turned)

  • Avoid tight collar/ET ties

  • Prevent coughing/straining

Mnemonic:

“N.E.C.K.”

• Neutral neck

• Elevate head

• Collars loose

• Keep coughing down

ONE Patho Sentence to Remember ✅

Brain circulation must stay constant → if blood flow ↓ even slightly → brain cells die within minutes because they cannot store oxygen or glucose.

• Cerebral Perfusion Pressure (CPP):

• CPP = MAP − ICP

• Goal: 70–90 mmHg

• Rationale: Brain cannot store oxygen or glucose; requires constant perfusion to prevent ischemia.

• Monro-Kellie Doctrine:

The skull is a fixed vault containing brain tissue, blood, and CSF.

If one increases, others must decrease or ICP rises.

• SECTION 2 — PATHOPHYSIOLOGY AFTER BRAIN INJURY

• Primary injury: happens at time of trauma

• Secondary injury: cascades that worsen damage

  • Inflammation → cytokines → edema

  • Cortisol response → increased metabolic demand

  • Acute traumatic coagulopathy → worsened bleeding

• Hypoxic-Ischemic injury:

  • Lack of oxygen → cellular death → cerebral edema → further ICP increase.

• Normal Brain: Circulation

• Arterial supply to cerebrum and cerebellum originates from internal carotid arteries

  • → The carotids feed the Circle of Willis, supplying most higher brain functions (thinking, speech, movement).

  • → If a carotid is blocked → ischemic stroke, TIA, aphasia, contralateral motor weakness.

• Arterial supply to brainstem originates from vertebral arteries

  • → Vertebral arteries join to form the basilar artery → supplies vital life centers: respiratory drive, cardiac regulation.

  • → Vertebral/basilar occlusion = Worst neurological outcomes (loss of respiratory drive, locked-in syndrome).

• Venous return flows into superior sagittal and transverse sinuses and descends to internal jugular vein

  • → If venous drainage is blocked → increased intracranial pressure (ICP) → headache, papilledema, decreased LOC.

Critical Concept

• Brain is highly metabolic — uses 20% of body’s O2 → deprivation quickly leads to neuronal death.

• Brain Injury Physiology

• The HPA-axis stress response kicks in after TBI:

  • Immunologic responses

    • → Release of pro-inflammatory cytokines (TNF-α, IL-1, IL-6) → cause swelling, increased ICP.

  • Metabolic responses (cortisol-driven)

    • → Hyperglycemia is common (stress response).

    • → High glucose worsens outcomes → more oxidative damage.

    • → Tight glucose control = nursing intervention

  • Acute traumatic coagulopathy

  • → Due to tissue injury + shock + inflammation → increased bleeding risk

    • (Why TBI patients often get massive transfusion protocols)

• Nursing Alert

  • Avoid hypoxia + hypotension — they double mortality in TBI!

• Brain Injury Physiology: Cellular & Immune Response

• Neuronal death and tissue loss

  • → Cells die → release glutamate → excitotoxicity → more cell death (spreads injury)

• BBB breakdown and edema

  • → Leaky capillaries → fluid shifts into brain tissue → ↑ ICP

• Upregulation of inflammatory mediators

  • → Microglia activate → more cytokines → secondary injury peaks 24–72 hrs

• Gliosis and cell infiltration

  • → Scar-like tissue → disrupts normal pathways → long-term cognitive/motor deficits

Key Exam Tip

• Primary brain injury = at moment of impact

• Secondary brain injury = hours to days later → this is what we can treat

• Mechanism of Injury

• Forces causing injury to the brain (macro- and microscopically)

• Types:

  • Penetrating trauma – bullet, stab

    • → often focal + high infection risk

  • Hypoxic-ischemic – cardiac arrest, drowning

    • → global brain injury

  • Blunt trauma – falls, MVCs

    • → bruising + swelling

  • Acceleration-deceleration – brain moves inside skull

    • → DAI risk

  • Mass effect – something takes up space

    • → ↑ ICP + herniation risk

• Priority Nursing Goal

  • Prevent worsening secondary injury: maintain oxygenation + perfusion (MAP)

• Hypoxic-Ischemic Injury

• ↓ Perfusion → ↓ O2 + glucose → ↓ ATP

• → Pump failure → Na+ & Ca++ flood cells → cytotoxic edema

• → Swelling in a fixed space (skull)

• → ICP ↑ → Perfusion ↓ even more → vicious cycle

• Inflammation → delayed neuronal death hours later → Worsening neuro status over time = EMERGENCY

• 🧠 CPP (Cerebral Perfusion Pressure)

• CPP = MAP − ICP

• Goal: CPP > 60 mmHg to protect the brain

• Coup vs Coup-Contrecoup

• Coup: brain injury at impact site

• Coup-Contrecoup: brain hits one side → bounces → damages opposite side

  • Classic causes: falls, motor vehicle collisions

• Symptoms depend on lobes involved:

  • Frontal: personality changes

  • Occipital: vision problems

  • Temporal: memory + speech

• Pathology: Diffuse Axonal Injury (DAI)

• Rotational/shearing forces damage axons

  • → Signal transmission disrupted

• Often from high-speed deceleration

• Leads to widespread disconnection between brain regions

• 25% die

  • Survivors often have long-term severe disability

DAI: Clinical Manifestations

• Immediate loss of consciousness — hallmark sign

• Severe: persistent vegetative state

• Dysautonomia

• Tachycardia

• Tachypnea

• Posturing (decorticate/decerebrate)

  • Outcome: poor with limited recovery potential

• Nursing Priorities

  • Prevent hypoxia, control ICP, maintain MAP/CPP

  • Family support + long-term rehab planning

Diffuse Axonal Injury (DAI):

• Mechanism: shearing/stretching of axons at gray-white junction during rapid deceleration.

• Leads to: loss of signal transmission → immediate LOC → persistent vegetative state common.

• Outcome: Poor due to widespread disconnection of neural pathways.

• Mass Effect

• Monroe-Kellie Doctrine

  • The skull is a fixed space. If one component increases → others must decrease.

Normal brain space =

• 80% brain tissue

• 10% CSF

• 10% blood

If replaced by:

• Blood (hemorrhage)

• CSF (blocked reabsorption → hydrocephalus)

• Tumor/cyst

• Bone fragments from fractures

→ ICP increases → herniation risk

• Late sign of ↑ ICP = Cushing’s Triad

1⃣ ↑ SBP + widened pulse pressure

2⃣ ↓ HR

3⃣ Irregular respirations

This = impending brainstem herniation

• Intracranial Bleeding Types

• Epidural hemorrhage (EDH)

→ Arterial bleed (middle meningeal artery)

→ Lucid interval then rapid decline

→ Neurosurgical emergency

• Subdural hematoma (SDH)

→ Tearing of bridging veins

→ Slower onset (hours–days)

→ Elderly + alcoholics = high risk

• Subarachnoid hemorrhage (SAH)

→ Worst headache of their life

→ Caused by aneurysm rupture

→ Risk: vasospasm → ischemia

• Intracerebral/Intraparenchymal

→ Trauma or HTN strokes

→ Focal neuro deficits based on bleed location

• All bleeds:

  • Monitor LOC (earliest sign!), pupil changes, neuro checks q1h or more

Quick Nursing Mnemonics

ICP RED FLAG:

PUPILS

P — Pupils change

U — Unable to wake

P — Posturing

I — Increasing headache

L — Lower HR

S — Seizures

DAI = DAMN axons

D — Diffuse injury

A — Axonal shearing

M — Motor/posturing issues

N — Not waking up

• SECTION 3 — MASS EFFECT AND BLEEDS COMPARISONS

• Mass effect: Anything taking up space increases ICP.

• Comparison Chart

• Elderly have higher SDH risk due to brain atrophy stretching veins.

• SECTION 4 — INCREASED INTRACRANIAL PRESSURE

• Causes: edema, hemorrhage, CSF obstruction, CSF overproduction

Physiologic problem:

• ICP ↑ → CPP ↓ → ischemia worsens → more swelling → herniation risk

• Symptoms explained:

Cushing Reflex progression:

1. Tachycardia + hypertension (sympathetic surge)

2. Bradycardia + hypertension + altered respirations → impending herniation

• SECTION 5 — MANAGEMENT OF ICP

• Goals: prevent secondary injury, maintain CPP and brain oxygenation.

Intervention Table with Rationales

• High-risk nursing errors are testable:

• Never suction longer than 10 seconds.

• Cluster care only if patient remains stable.

• SECTION 6 — ICP MONITORING

Devices:

• Bolt: measures ICP but no drainage

• Ventriculostomy: measures and drains CSF (highest infection risk)

• Intraparenchymal fiberoptic catheter: no drainage

• Zero level is external auditory canal.

• Must clamp before patient repositioning to prevent over-drainage and herniation.

Nursing priorities:

• Monitor output color and amount

• Keep pressure system at ordered level

• Replace output only if ordered

• Aseptic technique for CSF sampling

• SECTION 7 — HERNIATION

• Herniation: brain tissue shifts due to extreme pressure differentials.

  • Occurs when pressure in one part of the brain is significantly greater than in another part → brain tissue is forced from a high-pressure area into a low-pressure area

    • This movement compresses structures that should never be compressed — especially blood vessels and the brainstem

• Descending transtentorial herniation compresses brainstem → death.

Patho You Must Know

• Herniation happens due to severe increased ICP

• As brain tissue shifts, blood flow is cut off → ischemia → even more swelling

• This becomes a rapid, life-threatening cycle

• Brainstem compression → respiratory arrest + loss of consciousness

Key

• Descending Transtentorial Herniation (also called central or uncal herniation)

• Brain pushes downward through the tentorial notch

• This compresses the brainstem

  • → Associated with brain death if not reversed quickly

Critical Nursing Recognition

• Earliest sign:

  • Change in level of consciousness (sudden worsening GCS)

Rapidly followed by:

• Blown pupil (ipsilateral fixed and dilated — CN III compressed)

• Cushing’s Triad (late and pre-terminal):

  • ↑ SBP with widened pulse pressure

  • ↓ HR

  • Irregular respirations

• Posturing (decorticate → decerebrate)

• Loss of brainstem reflexes (gag/corneal)

• Once brainstem reflexes are gone → brain death

Quick Exam Mnemonic

HERNIATE

H — Herniation emergency

E — Early: ↓ LOC

R — Respirations abnormal

N — Nerve III → blown pupil

I — Increased SBP, ↓ HR (Cushing’s)

A — Abnormal posturing

T — Tonsillar/Transtentorial types fatal

E — End of brain function if untreated

• SECTION 8 — BRAIN DEATH

Brain Death

• Cessation of all cerebral and brainstem function that is irreversible.

• Criteria:

  • Persistent coma (GCS of 3)

    • No eye opening

    • No verbal response

    • No motor response

      • Absence of brainstem reflexes shown by cranial nerve testing

      • Lack of ability to breathe independently

    • Confirmed by 10-minute apnea test

• Pathophysiology connection:

  • When intracranial pressure rises high enough to stop cerebral blood flow, oxygenation of neurons ceases, causing permanent loss of brain function.

• Statistics:

  • About 2% of hospital deaths are brain deaths (not cardiac arrest deaths)

  • Post-resuscitation patients: 8.9% progress to brain death due to anoxic ischemia

  • TBI patients: ~6% progress to brain death due to uncontrolled ICP → decreased CPP and poor oxygen delivery to neurons

• Importance for nurses:

  • Maintain perfusion and oxygen until diagnosis to avoid false determination and allow potential organ donation.

• Brain Death Evaluation

Evaluation occurs in a specific order to rule out reversible causes.

• Step 1: Pre-Exam Criteria

  • Must be met before testing:

    • Known cause of coma (TBI, hypoxia, stroke)

    • Temperature > 36.5°C

    • Hypothermia can suppress brain activity and mimic brain death

    • No drug effects that depress CNS

    • Narcotics, sedatives, alcohol, neuromuscular blockers

    • Wait 5 drug half-lives or check drug levels

      • Systolic BP > 100 mmHg

    • Brainstem perfusion must be adequate

    • Vasopressors can be used to reach target

  • Nursing role:

    • Warm patient, ensure normotension, review medications/tox screens, correct metabolic derangements.

• Step 2: Clinical Neurologic Exam

  • Includes GCS evaluation and cranial nerve testing.

Brainstem Reflex Testing

• Absent brainstem reflexes must be present on testing by trained evaluators.

• Step 3: Apnea Test

  • Performed only after cranial nerve testing confirms no brainstem reflexes.

  • Purpose:

    • To determine if respiratory drive is permanently absent.

  • Process:

    • Baseline ABG to confirm normal PaCO2 and adequate oxygenation

    • Patient given 100% FiO2 through the endotracheal tube

    • Ventilator disconnected while oxygen continues

    • Observe 10 minutes for any respiratory effort

    • ABG repeated: PaCO2 must rise to > 60 mmHg

  • Interpretation:

    • No breathing effort and PaCO2 > 60 → brain death confirmed

    • If respirations occur → not brain dead

  • Nursing considerations:

    • Maintain oxygenation

    • Monitor hemodynamics

    • Stop test if SpO2 < 85% or BP < 100 mmHg

• If Apnea Test Cannot Be Completed Safely

  • If unable to maintain:

  • • SpO2 > 85%

  • • Systolic BP > 100 mmHg

• Then ancillary testing is required.

  • Acceptable confirmatory tests:

    • Cerebral angiography: no blood flow in intracranial vessels

    • Transcranial ultrasound: no pulsatile intracranial flow

    • CT-angiography or MRA: absence of cerebral blood flow

    • Radionuclide brain imaging: absent uptake in brain tissue

• These tests prove that the brain has lost circulation and function permanently.

Key Differences: Brain Death vs Coma vs Vegetative State

Nursing Priorities in Brain Death Determination

• Maintain physiological stability: oxygenation, BP, normothermia

• Explain tests and findings compassionately to families

• Support decision-making (including organ donation conversations by trained staff)

• Prevent skin breakdown, infections while determination is underway

• Ensure accurate documentation and legal requirements

High-Yield NCLEX Points

• Brain death = legally dead in all US states

• The apnea test is essential unless contraindicated

• Must rule out drug intoxication and hypothermia first

• Pupils fixed and dilated = critical brainstem sign

• Pain response absent in brain death

• Diagnosis requires a known irreversible cause

NCLEX-STYLE PRIORITIZATION HIGHLIGHTS

• Most sensitive indicator of deteriorating neuro status:

• Change in mental status

• Most dangerous finding:

  • Cushing’s triad or unilateral fixed pupil → impending herniation

• Never:

  • Lay patient flat

  • Allow hyperthermia

  • Increase CO2 unnecessarily

  • Move a patient with ventriculostomy unclamped

MNEMONICS FOR NEURO INJURY AND ICP MANAGEMENT

1. EARLY SIGNS OF INCREASED ICP “HEADS”

• H = Headache

• E = Early changes in LOC (confusion, irritability)

• A = Alertness declines

• D = Double vision or pupil changes

• S = Seizures possible

  • Rationale: Cortical oxygen deprivation appears first as LOC changes.

2. CUSHING’S TRIAD “HI-BP”

• H = Hypertension

• I = Irregular respirations

• B = Bradycardia

• P = Poor prognosis (late sign pointing toward herniation)

  • Rationale: Brainstem compression causes reflexive hypertension and dysautonomia.

3. ICP NURSING POSITIONING “HIP 30”

• H = Head midline

• I = Immobile neck (no twisting)

• P = Prevent hip flexion

• 30 = HOB 30 degrees

  • Purpose: Improve venous drainage, prevent increased intrathoracic and abdominal pressure.

4. VENTRICULOSTOMY CARE “LEVEL, LOOK, LOCK”

• Level = Line transducer with tragus

• Look = Check drainage amount, color, clarity

• Lock = Clamp before movement to prevent over-drainage

  • Application: Protect the brain from rapid loss of CSF leading to herniation.

5. MASS EFFECT CAUSES “3 B’s”

• Brain swelling (edema)

• Blood (SAH, SDH, epidural, intraparenchymal)

• Blockage (CSF obstruction or tumor)

  • Ties directly back to Monro-Kellie doctrine.

6. DIFFUSE AXONAL INJURY “SHEDD”

• S = Shearing force

• H = High-speed deceleration

• E = Extensive unconsciousness (immediate LOC)

• D = Disruption of gray-white matter

• D = Disconnection = poor recovery

  • Key takeaway: This is not a focal bleed; it’s widespread axonal injury.

7. BRAIN DEATH CHECKS “NO BRAIN”

• N = No pupillary response

• O = Oculocephalic and cold caloric reflex absent

• B = Breathing absent during apnea test

• R = Reflexes in brainstem gone (corneal, gag, cough)

• A = ABG PaCO2 > 60 with no respiratory drive

• I = Identify and rule out reversible causes (drugs, hypothermia)

• N = Known neurological explanation for coma

  • Used in formal determination requirements.

8. HEMATOMA LOCATION DIFFERENCE “EDH is Emergency, SDH is Slow Developing”

• Epidural = artery = rapid decline → emergency

• Subdural = veins = slower progression

  • Clinical interpretation: watch for gradual neuro worsening in SDH.

SHORT MINI-MAPS FOR RAPID STUDY

• Differences in Bleeds — One-Liner Recall

• Epidural: Knocked out → up → crash

• Subdural: Slow sinus bleed → subtle confusion

• SAH: Sudden thunderclap → meningeal signs

• Intraparenchymal: Localized deficits → stroke-like

• Early Neuro Decline Prioritization

  • If LOC changes, act. Pupils change, run. Cushing’s triad, call now.