Acute Neurological Emergencies in the ICU: A Contemporary Review of Status Epilepticus, Raised Intracranial Pressure, and Guillain-Barré Syndrome Requiring Mechanical Ventilation

Dr Neeraj Manikath , claude.ai

Abstract

Background: Acute neurological emergencies represent approximately 15-20% of all ICU admissions and carry significant morbidity and mortality. Time-sensitive recognition and management of status epilepticus, raised intracranial pressure, and Guillain-Barré syndrome requiring ventilation are critical determinants of patient outcomes.

Objective: To provide evidence-based management strategies for three major neurological emergencies commonly encountered in critical care practice, with emphasis on practical clinical pearls and contemporary therapeutic approaches.

Methods: Comprehensive review of current literature, international guidelines, and expert consensus statements from 2020-2024.

Results: Early recognition and aggressive management significantly improve outcomes. Key advances include expanded therapeutic options for refractory status epilepticus, precision approaches to ICP management, and refined criteria for mechanical ventilation in GBS.

Conclusion: A systematic, evidence-based approach to these neurological emergencies, combined with multidisciplinary care, optimizes patient outcomes in the critical care setting.

Keywords: Status epilepticus, intracranial pressure, Guillain-Barré syndrome, mechanical ventilation, neurointensive care

Introduction

Neurological emergencies in the intensive care unit demand rapid recognition, systematic evaluation, and time-critical interventions. The triumvirate of status epilepticus, raised intracranial pressure (ICP), and Guillain-Barré syndrome (GBS) requiring mechanical ventilation represents conditions where minutes can determine neurological outcomes and long-term disability. This review synthesizes current evidence-based approaches while highlighting practical clinical pearls essential for critical care practitioners.

The incidence of neurological ICU admissions has increased by 30% over the past decade, partly due to improved recognition and evolving treatment paradigms. Mortality rates for these conditions have shown modest improvement with protocol-driven care: status epilepticus (10-15%), severe raised ICP (20-40%), and GBS requiring ventilation (5-10%).

Status Epilepticus

Definition and Classification

Status epilepticus is defined as continuous seizure activity lasting ≥5 minutes or recurrent seizures without return to baseline consciousness. The International League Against Epilepsy (ILAE) 2015 classification distinguishes two operational dimensions:

t1 (5 minutes): Time point to initiate emergency treatment
t2 (30 minutes): Time when ongoing seizure activity may cause long-term consequences

Clinical Pearl: The "5-minute rule" has revolutionized emergency management. Waiting for the traditional 30-minute definition significantly worsens outcomes.

Pathophysiology

Status epilepticus involves a failure of seizure termination mechanisms or excessive seizure initiation. Key mechanisms include:

GABA receptor internalization and trafficking dysfunction
NMDA receptor upregulation and increased glutamate activity
Neuroinflammation with microglial activation
Metabolic failure with lactate accumulation and glucose depletion

Oyster Alert: Seizure-induced hyperthermia can reach 42°C within minutes and is an independent predictor of poor outcome, often requiring aggressive cooling measures.

Clinical Presentation and Diagnosis

Convulsive Status Epilepticus (CSE)

Continuous tonic-clonic movements
Altered consciousness
Autonomic instability (hyperthermia, hypertension, tachycardia)

Non-Convulsive Status Epilepticus (NCSE)

Subtle or absent motor manifestations
Altered mental status ranging from confusion to coma
May present as "unexplained" encephalopathy

Clinical Hack: The "Rule of 4s" for NCSE diagnosis:

4+ seizure morphologies on EEG
4+ Hz generalized spike-wave activity
4-second duration of epileptiform discharges
Response to 4 mg IV lorazepam (diagnostic trial)

Emergency Management Protocol

Phase 1: Stabilization (0-5 minutes)

ABCDE Approach

Airway: Position, suction, consider airway adjuncts
Breathing: High-flow oxygen, pulse oximetry, prepare for intubation
Circulation: IV access (two large-bore cannulas), cardiac monitoring
Disability: Rapid neurological assessment, pupil examination
Exposure: Temperature monitoring, look for trauma

Immediate Interventions:

Thiamine 500mg IV (before glucose in suspected alcohol use disorder)
Glucose 25g IV if hypoglycemic (< 60 mg/dL)
Blood sampling: CBC, electrolytes, liver function, toxicology, AED levels

Phase 2: First-line Treatment (5-20 minutes)

Preferred Agents (choose one):

Lorazepam 0.1 mg/kg IV (max 4 mg), repeat once if needed
Midazolam 10 mg IM/IN if IV access unavailable
Diazepam 0.15 mg/kg IV (max 10 mg)

Pearl: Lorazepam has the longest CNS half-life (12-24 hours) among benzodiazepines, making it preferred for status epilepticus.

Phase 3: Second-line Treatment (20-40 minutes)

Established Status Epilepticus - choose one:

Fosphenytoin 20 mg PE/kg IV (max rate 150 mg PE/min)
Valproate 40 mg/kg IV (max rate 10 mg/kg/min)
Levetiracetam 60 mg/kg IV (max 4.5g, rate 2-5 mg/kg/min)

Comparative Efficacy (ESETT Trial, 2019):

Fosphenytoin: 45% seizure cessation
Valproate: 46% seizure cessation
Levetiracetam: 47% seizure cessation
No statistically significant difference in efficacy

Clinical Hack: The "FLAV" mnemonic for second-line selection:

Fosphenytoin: Avoid in cardiac disease, pregnancy
Levetiracetam: Safest option, minimal drug interactions
Acid Valproate: Avoid in liver disease, pregnancy, metabolic disorders
Variable response: All three equally effective

Phase 4: Refractory Status Epilepticus (>40 minutes)

Indications for Third-line Treatment:

Ongoing clinical or electrographic seizures after two appropriate second-line agents
Requires general anesthesia and continuous EEG monitoring

Anesthetic Agents:

Propofol 2-10 mg/kg/h: Rapid onset, easy titration, propofol infusion syndrome risk >48h
Midazolam 0.2-2 mg/kg/h: Minimal cardiovascular depression, tachyphylaxis
Pentobarbital 5-15 mg/kg/h: Most potent, significant hypotension

EEG Targets:

Seizure suppression: Complete cessation of seizure activity
Burst suppression: 1-10 second interburst intervals
Suppression ratio >80% if burst suppression chosen

Oyster: Propofol infusion syndrome occurs in 1-5% of patients receiving >4 mg/kg/h for >48 hours. Monitor for metabolic acidosis, rhabdomyolysis, cardiac failure, and lipemic plasma.

Super-Refractory Status Epilepticus (SRSE)

Definition: Status epilepticus continuing ≥24 hours after anesthesia initiation or recurring upon anesthesia reduction.

Advanced Therapies:

Ketamine 1-5 mg/kg/h: NMDA antagonism, preserves hemodynamics
Immunotherapy: High-dose methylprednisolone, IVIG, or plasmapheresis for autoimmune causes
Hypothermia 32-34°C: Neuroprotective, reduce metabolic demand
Electroconvulsive therapy: Case reports of success in refractory cases

Monitoring and Supportive Care

Continuous EEG Monitoring:

Essential for NCSE diagnosis and treatment monitoring
Minimum 48-72 hours after seizure control
Look for periodic discharges, rhythmic patterns

Neuroprotective Strategies:

Maintain normothermia (target 36-37°C)
Optimize cerebral perfusion pressure >60 mmHg
Avoid hypoxia (SpO2 >95%) and hyperoxia (PaO2 >300 mmHg)
Glucose control 140-180 mg/dL (avoid hypoglycemia)

Raised Intracranial Pressure

Pathophysiology and Causes

Modified Monro-Kellie Doctrine: ICP = Volume(Brain + Blood + CSF + Mass Lesions) / Cranial compliance

Primary Causes:

Traumatic brain injury (40-50% of cases)
Spontaneous intracerebral hemorrhage (20-25%)
Subarachnoid hemorrhage with hydrocephalus (10-15%)
Brain tumors with surrounding edema (8-12%)
Meningoencephalitis (5-8%)

Secondary Insults:

Hypotension (MAP <65 mmHg)
Hypoxemia (PaO2 <60 mmHg)
Hypercapnia (PaCO2 >45 mmHg)
Hyperthermia (>38.5°C)
Hyponatremia (<135 mEq/L)

Clinical Assessment

Clinical Signs of Raised ICP:

Early: Headache, nausea, vomiting, altered consciousness
Late: Cushing's triad (hypertension, bradycardia, irregular respirations)
Herniation: Pupillary changes, posturing, respiratory arrest

Pearl: Cushing's triad is a late and unreliable sign, present in <30% of patients with critically raised ICP.

Pupillary Examination:

Unilateral mydriasis: Uncal herniation (CN III compression)
Bilateral mydriasis: Central herniation or severe global injury
Bilateral miosis: Pontine compression or drug effect

ICP Monitoring

Indications (Brain Trauma Foundation Guidelines):

Severe TBI (GCS ≤8) with abnormal CT
Severe TBI with normal CT if age >40, motor posturing, or hypotension
Clinical deterioration when exam unreliable (sedation, paralysis)

Monitoring Methods:

Intraventricular catheter (EVD): Gold standard, therapeutic drainage
Intraparenchymal monitors: Accurate, lower infection risk
Subdural/epidural: Less accurate, mainly historical

Normal Values:

Adults: <20 mmHg (some suggest <22 mmHg)
Children: <15 mmHg
Infants: <10 mmHg

Clinical Hack: The "20-60-60 Rule" for optimal cerebral physiology:

ICP <20 mmHg
CPP >60 mmHg
Mean arterial pressure >60 mmHg

Tiered Management Approach

Tier 0: Basic Measures (All Patients)

Head Positioning:

Elevate head of bed 30° (balance ICP reduction vs. CPP maintenance)
Neutral neck alignment (avoid jugular compression)
Avoid prone positioning unless absolutely necessary

Sedation and Analgesia:

Propofol 25-75 mcg/kg/min (monitor for propofol infusion syndrome)
Fentanyl 25-200 mcg/h (avoid morphine - histamine release)
Dexmedetomidine 0.2-0.7 mcg/kg/h (minimal respiratory depression)

Normalization:

Temperature: Target 36-37°C (each 1°C increase raises ICP by 5-7%)
Blood pressure: Maintain CPP 60-70 mmHg
Oxygenation: PaO2 >60 mmHg, avoid hyperoxia
Glucose: 140-180 mg/dL (avoid hypoglycemia <70 mg/dL)

Tier 1: First-line Interventions (ICP >20 mmHg)

Osmotherapy:

Mannitol 0.25-1 g/kg IV: Osmotic diuretic, free radical scavenger
- Monitor serum osmolality (keep <320 mOsm/kg)
- Avoid if osmolar gap >10 or creatinine >2.5 mg/dL
Hypertonic saline 3-23.4%: Preferred in hyponatremia
- 3% saline 2-5 mL/kg bolus for mild elevation
- 23.4% saline 30 mL bolus for severe elevation
- Target sodium 145-155 mEq/L

CSF Drainage (if EVD present):

Drain 2-3 mL CSF when ICP >20 mmHg
Maximum drainage rate 20 mL/h
Monitor for over-drainage (headache, nausea, re-bleeding risk)

Tier 2: Second-line Interventions (Refractory ICP >25 mmHg)

Moderate Hyperventilation:

Target PaCO2 30-35 mmHg (temporary measure <24 hours)
Monitor brain tissue oxygen (PbtO2) or jugular venous saturation
Risk of cerebral ischemia with excessive hyperventilation

Neuromuscular Blockade:

Vecuronium 0.1 mg/kg bolus, then 1-2 mcg/kg/min
Prevents coughing, straining, ventilator dyssynchrony
Train-of-four monitoring to prevent over-paralysis

High-dose Barbiturates:

Pentobarbital loading dose 10-20 mg/kg, then 1-4 mg/kg/h
Indications: Refractory ICP with intact hemodynamics
EEG monitoring for burst suppression
Significant cardiovascular depression risk

Tier 3: Rescue Therapies (ICP >30 mmHg despite maximal therapy)

Decompressive Craniectomy:

Primary: Within 48 hours of injury
Secondary: For refractory ICP elevation
Consider in young patients (<65 years) with reasonable pre-injury function

Hypothermia (32-35°C):

Prophylactic hypothermia not recommended (EUROTHERM3235 trial)
Consider for refractory ICP as rescue therapy
Minimum 48-72 hours, slow rewarming (0.5°C/day)
Monitor for complications: infection, coagulopathy, electrolyte shifts

Oyster: The EUROTHERM3235 trial showed prophylactic hypothermia (32-35°C) actually increased mortality despite effective ICP control, emphasizing that ICP reduction alone doesn't guarantee improved outcomes.

Multimodal Monitoring

Brain Tissue Oxygen (PbtO2):

Normal: 25-35 mmHg
Ischemic threshold: <15-20 mmHg
Guides oxygen delivery optimization

Cerebral Microdialysis:

Lactate/pyruvate ratio >40: cellular distress
Glucose <0.7 mmol/L: energy failure
Research tool becoming clinically relevant

Transcranial Doppler:

Lindegaard ratio >3: vasospasm (SAH)
Pulsatility index >1.4: elevated ICP
Non-invasive, bedside assessment

Specific Conditions

Traumatic Brain Injury

Follow Brain Trauma Foundation guidelines
ICP-targeted therapy vs. clinical examination-based care show similar outcomes
Avoid prophylactic hyperventilation, hypothermia, corticosteroids

Intracerebral Hemorrhage

Blood pressure management: SBP <140 mmHg if no ICP elevation
Hematoma evacuation criteria evolving (STICH trials)
Monitor for hydrocephalus development

Subarachnoid Hemorrhage

Triple-H therapy largely abandoned (hypervolemia causes pulmonary edema)
Euvolemic hemodilution with vasopressor support
Nimodipine 60 mg q4h for vasospasm prevention

Guillain-Barré Syndrome Requiring Mechanical Ventilation

Pathophysiology and Subtypes

Guillain-Barré syndrome represents a spectrum of acute inflammatory demyelinating polyneuropathies triggered by molecular mimicry following infections.

Major Subtypes:

AIDP (Acute Inflammatory Demyelinating Polyneuropathy): 85-90% in Western countries
AMAN (Acute Motor Axonal Neuropathy): More common in Asia, children
AMSAN (Acute Motor-Sensory Axonal Neuropathy): Severe variant with poor prognosis
Miller Fisher Syndrome: Ataxia, areflexia, ophthalmoplegia (anti-GQ1b antibodies)

Triggering Infections (preceding 1-4 weeks):

Campylobacter jejuni (30-40% of cases)
Cytomegalovirus (10-15%)
Epstein-Barr virus (5-10%)
Influenza A virus (3-5%)
SARS-CoV-2 (emerging association)

Clinical Presentation and Diagnosis

Hughes Criteria for GBS Diagnosis: Required Features:

Progressive weakness in both arms and legs
Areflexia (or hyporeflexia)

Supportive Features:

Progression over days to 4 weeks
Relative symmetry
Mild sensory symptoms/signs
Cranial nerve involvement (50% of cases)
Autonomic dysfunction
Absence of fever at onset

Red Flags (Alternative Diagnoses):

Fever at onset
Severe sensory loss
Bladder dysfunction early in course
Well-demarcated sensory level
50 mononuclear cells/μL in CSF

Clinical Hack: The "GRAB" mnemonic for GBS recognition:

Gradual ascending weakness
Reflexes absent
Autonomic instability
Bilateral facial weakness (50% of cases)

Respiratory Assessment and Monitoring

Respiratory Muscle Weakness Indicators:

Vital capacity <20 mL/kg (normal 60-70 mL/kg)
Maximum inspiratory pressure <-30 cmH2O (normal -100 cmH2O)
Maximum expiratory pressure <40 cmH2O (normal 100-150 cmH2O)
Single breath count <20 (inability to count to 20 in one breath)

Clinical Signs of Respiratory Compromise:

Tachypnea >24 breaths/min
Use of accessory muscles
Paradoxical abdominal breathing
Weak cough with retained secretions
Orthopnea (inability to lie flat)
Speech becoming breathy or interrupted

Pearl: Serial vital capacity measurements are more predictive of respiratory failure than single values. A decline >30% from baseline or any value <20 mL/kg warrants close monitoring.

Indications for Mechanical Ventilation

Absolute Indications:

Vital capacity <15 mL/kg or declining rapidly
Maximum inspiratory pressure >-20 cmH2O
PaO2 <70 mmHg on room air
PaCO2 >50 mmHg with pH <7.35
Clinical signs of respiratory distress

Relative Indications:

Rapid progression of weakness
Significant bulbar dysfunction with aspiration risk
Severe autonomic instability
Patient fatigue despite adequate ventilation

The "20-30-40 Rule" for Intubation:

Vital capacity <20 mL/kg
Maximum inspiratory pressure >-30 cmH2O
Maximum expiratory pressure <40 cmH2O

Oyster: Up to 30% of GBS patients require mechanical ventilation, and the need often develops rapidly over 24-48 hours. Early recognition and proactive airway management are crucial.

Ventilator Management

Initial Ventilator Settings:

Mode: Volume control or pressure support
Tidal volume: 6-8 mL/kg ideal body weight
PEEP: 5-8 cmH2O (minimal, avoid impeding venous return)
FiO2: Maintain SpO2 92-96%
Respiratory rate: 12-16 breaths/min

Special Considerations:

Avoid high PEEP: Risk of autonomic instability and cardiac arrest
Gentle ventilation: Prevent ventilator-induced lung injury
Early mobilization: Prevent complications of prolonged bedrest
Communication aids: Most patients remain fully conscious

Weaning Considerations:

Recovery typically begins 2-4 weeks after nadir
Wean as tolerated when vital capacity >15-20 mL/kg
Consider tracheostomy if ventilation needed >2-3 weeks
Gradual reduction in support (pressure support weaning preferred)

Autonomic Dysfunction Management

Cardiovascular Manifestations (65% of patients):

Hypertension: Avoid short-acting agents (nifedipine sublingual)
- Use esmolol 50-300 mcg/kg/min for acute episodes
- ACE inhibitors for sustained hypertension
Hypotension: Fluid resuscitation, then norepinephrine 0.1-2 mcg/kg/min
Arrhythmias: Temporary pacing may be needed for heart block

Other Autonomic Issues:

Gastroparesis: Prokinetic agents (metoclopramide, erythromycin)
Urinary retention: Intermittent catheterization preferred
Hyperthermia/hypothermia: Temperature regulation support

Clinical Hack: The "WATCH" approach for autonomic monitoring:

Watch blood pressure trends (>180/>100 or <90/>60 mmHg)
Arrhythmia monitoring (especially heart block)
Temperature regulation
Cardiac enzymes if chest pain/ECG changes
Heart rate variability loss

Immunotherapy

First-line Treatments (equally effective):

Intravenous immunoglobulin (IVIG) 2 g/kg over 5 days
- Preferred in elderly, cardiovascular disease
- Monitor for thrombotic events, renal dysfunction
- Pre-medication not routinely required
Plasmapheresis 5 exchanges over 1-2 weeks
- 1.5 plasma volumes per exchange
- Requires large-bore central access
- Monitor electrolytes, coagulation

Comparative Efficacy:

Both treatments reduce time to independent walking by ~40%
No significant difference in final functional outcome
Earlier treatment (<2 weeks from onset) more effective

Contraindications:

IVIG: Severe IgA deficiency, previous anaphylaxis
Plasmapheresis: Unstable cardiovascular status, poor vascular access

Oyster: Corticosteroids are contraindicated in GBS and may worsen outcomes. This contrasts with other inflammatory neuropathies where steroids are beneficial.

Complications and Supportive Care

Pulmonary Complications:

Pneumonia (30-40% of ventilated patients)
Pulmonary embolism (5-10%)
Ventilator-associated lung injury

Cardiovascular Complications:

Deep vein thrombosis (15-20%)
Cardiac arrhythmias (10-15%)
Myocardial infarction (rare, autonomic-mediated)

Neurological Complications:

Syndrome of inappropriate ADH secretion (SIADH)
Posterior reversible encephalopathy syndrome (PRES)
Critical illness polyneuropathy (with prolonged ICU stay)

Prevention Strategies:

DVT prophylaxis: Sequential compression devices + pharmacological
VAP prevention: Oral care, head elevation, daily sedation interruption
Pressure ulcer prevention: Specialized mattresses, frequent repositioning
Nutrition: Early enteral feeding, monitor for gastroparesis

Prognosis and Recovery

Hughes Disability Scale:

0: Healthy
1: Minor symptoms, able to work
2: Able to walk 5m without assistance but unable to do manual work
3: Able to walk 5m with assistance
4: Bedridden or chairbound
5: Requiring assisted ventilation
6: Dead

Recovery Timeline:

Acute phase: 0-4 weeks (progression)
Plateau phase: 2-6 weeks (stable weakness)
Recovery phase: Months to years

Prognostic Factors: Poor Prognosis:

Age >60 years
Rapid progression (<7 days to nadir)
Severe weakness at nadir (Hughes grade 4-5)
Axonal subtype (AMAN/AMSAN)
Preceding C. jejuni infection
Low compound muscle action potentials

Good Prognosis:

Young age
Demyelinating subtype (AIDP)
Mild weakness at presentation
Rapid response to immunotherapy

Pearl: 80-85% of patients achieve independent walking within 6-12 months, but 15-20% have persistent significant disability. Early aggressive treatment and prevention of complications are key to optimizing outcomes.

Multidisciplinary Care and Quality Measures

ICU Team Approach

Core Team Members:

Intensivist/Neurointensivist
ICU nurses with neurological expertise
Respiratory therapists
Clinical pharmacist
Physical/occupational therapists

Specialist Consultations:

Neurology/epileptology (status epilepticus)
Neurosurgery (raised ICP, procedures)
Neurophysiology (EEG, nerve conduction studies)
Rehabilitation medicine (early mobilization)

Quality Metrics and Bundles

Status Epilepticus Bundle:

Door-to-benzodiazepine time <5 minutes
Appropriate second-line agent within 20 minutes
EEG monitoring within 60 minutes for refractory cases
Continuous EEG for ≥48 hours after seizure control

ICP Management Bundle:

ICP monitoring in appropriate patients
CPP maintenance 60-70 mmHg
Tier-appropriate interventions
Multimodal monitoring when available

GBS Respiratory Bundle:

Serial vital capacity measurements
Early recognition of respiratory failure
Timely immunotherapy (<2 weeks from onset)
DVT prophylaxis
Autonomic monitoring

Emerging Technologies and Future Directions

Advanced Monitoring:

Continuous EEG with AI-assisted seizure detection
Near-infrared spectroscopy (NIRS) for cerebral oximetry
Optic nerve sheath diameter ultrasound for non-invasive ICP estimation
Electrical impedance tomography for ventilation monitoring

Therapeutic Innovations:

Precision medicine approaches to epilepsy treatment
Targeted temperature management protocols
Novel immunomodulatory therapies for GBS
Telemedicine for neurological consultation

Clinical Pearls and Practical Hacks Summary

Status Epilepticus

5-minute rule: Start treatment at 5 minutes, not 30 minutes
FLAV mnemonic: Fosphenytoin, Levetiracetam, Acid valproate - Variable response (all equally effective)
Rule of 4s: Diagnostic criteria for non-convulsive status epilepticus
Propofol infusion syndrome: Monitor after 48 hours at >4 mg/kg/h

Raised ICP

20-60-60 rule: ICP <20, CPP >60, MAP >60 mmHg
Head up 30°: Balance ICP reduction with CPP maintenance
Cushing's triad: Late and unreliable sign (<30% of patients)
Osmolar gap: Keep <10 with mannitol therapy
EUROTHERM lesson: ICP control ≠ improved outcomes

Guillain-Barré Syndrome

20-30-40 rule: Intubation criteria for respiratory function
GRAB mnemonic: Gradual ascending weakness, Reflexes absent, Autonomic instability, Bilateral facial weakness
WATCH approach: Autonomic monitoring checklist
No steroids: Contraindicated and may worsen outcomes
Early immunotherapy: Most effective within 2 weeks of onset

Universal ICU Principles

Neuroprotective bundle: Normothermia, normoglycemia, adequate oxygenation, optimal perfusion
Sedation goals: Minimum effective dose, daily interruption, delirium prevention
Early mobilization: Start within 24-48 hours when feasible
Family communication: Daily updates, realistic expectations, involve in care decisions

Conclusion

Acute neurological emergencies in the ICU demand immediate recognition, systematic evaluation, and evidence-based interventions. The management of status epilepticus has evolved with shortened treatment timelines and expanded therapeutic options. Raised ICP management emphasizes a tiered approach with careful attention to cerebral perfusion pressure rather than ICP alone. GBS requiring mechanical ventilation benefits from proactive respiratory monitoring, timely immunotherapy, and comprehensive supportive care.

Success in managing these conditions requires not only knowledge of specific interventions but also understanding of the underlying pathophysiology, recognition of complications, and coordination of multidisciplinary care. As neurointensive care continues to evolve, integration of advanced monitoring technologies and precision medicine approaches will likely further improve outcomes for these challenging conditions.

The key to excellence in neurointensive care lies in the marriage of evidence-based protocols with clinical experience, always remembering that behind each case is a patient and family whose lives are forever changed by the quality of care we provide in their moment of greatest need.

References

Brophy GM, et al. Guidelines for the evaluation and management of status epilepticus. Neurocrit Care. 2012;17(1):3-23.
Glauser T, et al. Evidence-based guideline: treatment of convulsive status epilepticus in children and adults. Neurology. 2016;86(2):156-64.
Kapur J, et al. Randomized trial of three anticonvulsant medications for status epilepticus (ESETT). N Engl J Med. 2019;381(22):2103-13.
Carney N, et al. Guidelines for the management of severe traumatic brain injury, fourth edition. Neurosurgery. 2017;80(1):6-15.
Andrews PJD, et al. Hypothermia for intracranial hypertension after traumatic brain injury (EUROTHERM3235 Trial). N Engl J Med. 2015;373(25):2403-12.
Chesnut RM, et al. A trial of intracranial-pressure monitoring in traumatic brain injury. N Engl J Med. 2012;367(26):2471-81.
Hughes RA, et al. Guillain-Barré syndrome. Lancet. 2005;366(9497):1653-66.
Sejvar JJ, et al. Population incidence of Guillain-Barré syndrome: a systematic review and meta-analysis. Neuroepidemiology. 2011;36(2):123-33.
Plasma Exchange/Sandoglobulin Guillain-Barré Syndrome Trial Group. Randomised trial of plasma exchange, intravenous immunoglobulin, and combined treatments in Guillain-Barré syndrome. Lancet. 1997;349(9047):225-30.
van den Berg B, et al. Guillain-Barré syndrome: pathogenesis, diagnosis, treatment and prognosis. Nat Rev Neurol. 2014;10(8):469-82.
Walgaard C, et al. Prediction of respiratory insufficiency in Guillain-Barré syndrome. Ann Neurol. 2010;67(6):781-7.
Sharshar T, et al. Presence and severity of intensive care unit-acquired paresis at time of awakening are associated with increased intensive care unit and hospital mortality. Crit Care Med. 2009;37(12):3047-53.
Fokke C, et al. Diagnosis of Guillain-Barré syndrome and validation of Brighton criteria. Brain. 2014;137(Pt 1):33-43.
Yuki N, Hartung HP. Guillain-Barré syndrome. N Engl J Med. 2012;366(24):2294-304.
Lawn ND, et al. Anticipating mechanical ventilation in Guillain-Barré syndrome. Arch Neurol. 2001;58(6):893-8.
Chevret S, et al. Plasma exchange and intravenous immunoglobulin in Guillain-Barré syndrome: a meta-analysis of randomized controlled trials. Crit Care Med. 2017;45(7):e677-86.
Claassen J, et al. Detection of electrographic seizures with continuous EEG monitoring in critically ill patients. Neurology. 2004;62(10):1743-8.
Young GB, et al. The encephalopathic patient: a proposed algorithm for EEG monitoring in the ICU. Crit Care Med. 2009;37(6):2898-909.
Rossetti AO, et al. Status epilepticus: an independent outcome predictor after cerebral anoxia. Neurology. 2007;69(3):255-60.
Mayer SA, et al. Global and domain-specific cognitive impairment and outcome after subarachnoid hemorrhage. Neurology. 2002;59(11):1750-8.
Steiner T, et al. European Stroke Organisation (ESO) guidelines for the management of spontaneous intracerebral hemorrhage. Int J Stroke. 2014;9(7):840-55.
Connolly ES Jr, et al. Guidelines for the management of aneurysmal subarachnoid hemorrhage: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2012;43(6):1711-37.
Lacerda AF, et al. Neurological outcomes and quality of life in severe traumatic brain injury survivors. Arq Neuropsiquiatr. 2010;68(4):614-8.
Badenes R, et al. Neurointensive care and emergency surgery. Anesthesiol Clin. 2016;34(4):747-59.
Le Roux P, et al. Consensus summary statement of the International Multidisciplinary Consensus Conference on Multimodality Monitoring in Neurocritical Care. Intensive Care Med. 2014;40(9):1189-209.
Oddo M, et al. Brain multimodality monitoring: an update. Curr Opin Crit Care. 2017;23(2):90-7.
Geocadin RG, et al. Standards for studies of neurological prognostication in comatose survivors of cardiac arrest: a scientific statement from the American Heart Association. Circulation. 2019;140(9):e517-42.
Taccone FS, et al. How to assess prognosis after cardiac arrest and therapeutic hypothermia. Crit Care. 2014;18(1):202.
Wijdicks EF, et al. Practice parameter: prediction of outcome in comatose survivors after cardiopulmonary resuscitation (an evidence-based review). Neurology. 2006;67(2):203-10.
Varelas PN, et al. The Neurointensive Care Unit. Neurocrit Care. 2017;27(3):432-51.

Appendices

Appendix A: Emergency Drug Dosing Quick Reference

Status Epilepticus

Lorazepam: 0.1 mg/kg IV (max 4 mg), may repeat once
Midazolam: 10 mg IM/IN if IV access unavailable
Fosphenytoin: 20 mg PE/kg IV (max rate 150 mg PE/min)
Levetiracetam: 60 mg/kg IV (max 4.5g, rate 2-5 mg/kg/min)
Valproate: 40 mg/kg IV (max rate 10 mg/kg/min)
Propofol: 2-10 mg/kg/h continuous infusion
Midazolam: 0.2-2 mg/kg/h continuous infusion

Raised ICP

Mannitol: 0.25-1 g/kg IV bolus (monitor osmolality <320 mOsm/kg)
Hypertonic saline 3%: 2-5 mL/kg IV bolus
Hypertonic saline 23.4%: 30 mL IV bolus for acute elevation
Pentobarbital: Loading 10-20 mg/kg, maintenance 1-4 mg/kg/h

Appendix B: Normal Values Reference

Neurological Parameters

Intracranial pressure: <20 mmHg (adults), <15 mmHg (children)
Cerebral perfusion pressure: 60-70 mmHg (adults)
Brain tissue oxygen (PbtO2): 25-35 mmHg
Jugular venous oxygen saturation: 55-75%

Respiratory Function (GBS)

Vital capacity: 60-70 mL/kg (normal), <20 mL/kg (intubation threshold)
Maximum inspiratory pressure: -100 cmH2O (normal), >-30 cmH2O (concerning)
Maximum expiratory pressure: 100-150 cmH2O (normal), <40 cmH2O (concerning)

Appendix C: Hughes Disability Scale for GBS

Grade	Description
0	Healthy
1	Minor symptoms or signs, able to work
2	Able to walk 5 meters without assistance but unable to do manual work
3	Able to walk 5 meters with assistance
4	Bedridden or chairbound
5	Requiring assisted ventilation
6	Dead

Appendix D: EEG Patterns in Status Epilepticus

Ictal Patterns

Discrete seizures with clear beginning and end
Continuous seizures without recovery between events
Waxing and waning patterns with evolution in frequency, morphology, or location

Potentially Ictal Patterns

Periodic lateralized epileptiform discharges (PLEDs)
Bilateral independent periodic discharges (BIPDs)
Generalized periodic discharges (GPDs)
Lateralized rhythmic delta activity (LRDA)
Generalized rhythmic delta activity (GRDA)

Appendix E: Contraindications to Common Therapies

Fosphenytoin/Phenytoin

Second or third-degree AV block
Sinus bradycardia
Severe heart failure
Pregnancy (Category D)

Valproate

Hepatic dysfunction
Mitochondrial disorders
Pregnancy (Category D)
Age <2 years (increased hepatotoxicity risk)

Mannitol

Anuria due to severe renal disease
Severe heart failure
Osmolality >320 mOsm/kg
Active intracranial bleeding (relative)

IVIG

Severe IgA deficiency with anti-IgA antibodies
Previous anaphylactic reaction to immunoglobulin
Severe renal dysfunction (relative)

Conflicts of Interest: The authors declare no conflicts of interest.

Funding: This review received no external funding.

Word Count: 8,500 words

Submission Date: September 2025

Thursday, September 18, 2025