Study guide
EMG, Nerve Conduction & Acute Muscle Disease
ABPN Neurocritical Care Study Guide Exam
Track your progress as you read
Finished sections get a check mark.
1 Chapter 1: Neurologic Examination & Coma Assessment in the ICU
Current Examination, Blueprint & Preparation Neurologic Examination in Critically Ill Patients Coma Evaluation & Consciousness Alterations Delirium & Toxic-Metabolic Encephalopathy in the ICU
2 Chapter 2: Cerebral Physiology & Intracranial Dynamics
Cerebral Blood Flow, Metabolism & Autoregulation Intracranial Pressure & Compliance Cerebral Edema & Herniation Syndromes
3 Chapter 3: Intracranial Hypertension & Cerebral Perfusion Management
Tiered ICP Management Protocols Hyperosmolar Therapy & Fluid Management Advanced & Refractory ICP Interventions
4 Chapter 4: Airway, Mechanical Ventilation & Pulmonary ICU Management
Emergency Airway Management & Neuro-Intubation Mechanical Ventilation Strategies in Acute Brain Injury Tracheostomy & Ventilator Weaning in Neurocritical Care Pulmonary Complications in the Neuro-ICU Obstructive Lung Disease, Pulmonary Hypertension & Bronchoscopy
5 Chapter 5: Hemodynamics, Shock & Cardiovascular Management
Hemodynamic Monitoring & Blood Pressure Targets Vasoactive Agents: Inotropes, Vasopressors & Antihypertensives Cardiac Complications of Brain Injury
6 Chapter 6: Neuropharmacology, Analgesia & Sedation
ICU Sedation & Analgesia Neuromuscular Blockade & Monitoring Propofol Infusion Syndrome & Drug Toxicities Antiseizure Drug Pharmacology in the ICU
7 Bleeding, Thrombosis & Hematologic Emergencies
Warfarin & Heparin Reversal Direct Oral Anticoagulant (DOAC) Reversal Antiplatelet Management & Platelet Dysfunction Venous Thromboembolism Prophylaxis & Management Transfusion, Coagulopathy, TMA & Cellular-Therapy Neurotoxicity
8 Chapter 8: Systemic ICU Care, Fluids, Electrolytes & Endocrine
Hyponatremia & Osmoregulation: SIADH vs Cerebral Salt Wasting Diabetes Insipidus, Hypernatremia & Endocrine Crises Critical Care Prophylaxis, Nutrition & Infection Prevention
9 Systemic Trauma & Environmental Injury
Polytrauma, Chest Injury & Abdominal Hemorrhage Burns, Electrical Injury & Hanging
10 Cardiac Emergencies & Mechanical Support
IABP, Ventricular Devices & ECMO Acute Coronary, Valvular, Rhythm & Aortic Emergencies
11 Kidney Injury, Acid–Base & Renal Replacement
Acute Kidney Injury & Renal Drug Clearance Acid–Base Disorders, Electrolytes & Renal Replacement
12 Systemic Infection & Endocrine Emergencies
Sepsis, Endocarditis & Antimicrobial Principles Thyroid, Adrenal & Dysglycemic Emergencies
13 Gastrointestinal & Hepatic Emergencies
Acute Abdomen, GI Bleeding & Abdominal Compartment Syndrome Acute Liver Failure, Cirrhosis & Hepatic Drug Effects
14 Chapter 9: Neuroimaging in the Neuro-ICU
Non-Contrast CT & CT Angiography CT Perfusion & Advanced Perfusion Imaging Magnetic Resonance Imaging in Critical Illness
15 Chapter 10: Electrophysiology & Neuromonitoring
Continuous EEG & ACNS Standardized Critical Care Terminology Invasive Neuromonitoring: ICP & External Ventricular Drains Multimodal Monitoring: PbtO2, Microdialysis & Transcranial Doppler
16 Angiography, Electrodiagnosis & CSF Analysis
Conventional Angiography & Cranial–Spinal Shunts EMG, Nerve Conduction & Acute Muscle Disease CSF Analysis: Infection, Inflammation & Hemorrhage
17 Chapter 11: Bedside Procedures, Ultrasound & Death by Neurologic Criteria
Critical Care Procedural Skills Critical Care Ultrasound & Echocardiography Determination of Death by Neurologic Criteria
18 Chapter 12: Acute Ischemic Stroke & Reperfusion Therapies
Acute Ischemic Stroke Management & Thrombolysis Endovascular Thrombectomy & Large Vessel Occlusion Malignant Hemispheric & Cerebellar Infarction
19 Chapter 13: Spontaneous Intracerebral Hemorrhage & Intraventricular Hemorrhage
Acute Intraparenchymal Hemorrhage Management Intraventricular Hemorrhage & Hydrocephalus Surgical Evacuation & Minimally Invasive Surgery in ICH
20 Chapter 14: Aneurysmal Subarachnoid Hemorrhage & Delayed Cerebral Ischemia
Aneurysmal Subarachnoid Hemorrhage: Acute Resuscitation & Securing Delayed Cerebral Ischemia & Cerebral Vasospasm Non-Aneurysmal Subarachnoid Hemorrhage & Vascular Malformations
21 Venous, Spinal & Traumatic Vascular Disease
Cerebral Venous Thrombosis & Spinal Cord Infarction Traumatic Dissection, Carotid–Cavernous Fistula & Penetrating Injury
22 Chapter 15: Traumatic Brain & Spinal Cord Injury
Severe Traumatic Brain Injury & Contusions Acute Traumatic Spinal Cord Injury & Neurogenic Shock Spine Trauma, Fractures & Cord Syndromes
23 Chapter 16: Status Epilepticus, Seizures & Neuromuscular Emergencies
Status Epilepticus: Convulsive & Non-Convulsive Refractory & Super-Refractory Status Epilepticus Acute Neuromuscular Respiratory Failure
24 Chapter 17: Post-Cardiac Arrest Care, CNS Infections & Encephalitis
Targeted Temperature Management & Post-Cardiac Arrest Care Post-Cardiac Arrest Neuroprognostication Acute CNS Infections, Encephalitis & Inflammatory Emergencies
25 Neuroinflammation & Neurooncology
Fulminant Demyelination & Autoimmune Encephalitis Brain, Spinal & Leptomeningeal Cancer Emergencies
26 Pregnancy, Transplantation & Pediatric Care
Pregnancy, Postpartum & Post-Transplant Neurologic Care Pediatric Neurocritical Care
27 Chapter 18: Neurosurgical & Perioperative Emergencies
Postoperative Neurosurgical Complications Device Complications: EVDs, Shunts & ICP Monitors Cerebral Hyperperfusion Syndrome & Post-Interventional Emergencies
28 Chapter 19: Ethics, Palliative Care & Organ Donation in the Neuro-ICU
Communication, Surrogate Decision-Making & Conflict Resolution Neuroprognostication Ethics, Withdrawal of Life Support & Palliative Care Organ Donation & Management of the Deceased Donor
EMG, Nerve Conduction & Acute Muscle Disease
Key Takeaways Explain This Topic AI
Demyelination generally affects conduction speed, latency, dispersion, or block; axonal loss often reduces response amplitudes.
Preserved sensory responses with myopathic motor units support a muscle process, whereas reduced sensory responses support a peripheral sensory-motor neuropathy in context.
Motor neuron disease can cause ventilatory and bulbar failure despite preserved sensation.
Rhabdomyolysis requires assessment of potassium, kidney function, volume status, and the precipitating cause.
Last updated: October 2026
What the Tests Measure
The outline requires basic electromyography (EMG) interpretation and recognition of motor neuron disease, acute myopathies, rhabdomyolysis, and critical illness neuromyopathy. Nerve conduction studies assess evoked responses; needle EMG assesses spontaneous activity and motor-unit behavior. They complement the examination rather than replacing localization or emergency airway assessment.
A compound muscle action potential (CMAP) is the recorded muscle response to motor-nerve stimulation. A sensory nerve action potential (SNAP) reflects a sensory-nerve response. Reduced amplitude can suggest axonal loss or reduced excitable tissue, but technical factors also matter. Latency, conduction velocity, temporal dispersion, conduction block, and late responses provide additional information about myelin and proximal conduction.
Axonal Versus Demyelinating Patterns
Pattern Typical electrodiagnostic features Important caution
Axonal neuropathy Reduced CMAP or SNAP amplitudes, with less prominent slowing Early studies and technical limitations can obscure the pattern
Demyelinating neuropathy Slowed conduction, prolonged distal or late latencies, dispersion or block Formal criteria require multiple findings, not one slow segment
Myopathy Often low CMAP with preserved SNAP; short-duration, low-amplitude recruited motor units when assessable A sedated patient may not recruit voluntarily
Junctional disorder Abnormal decrement or other transmission findings on specialized testing Use a suitable protocol and clinical context
In Guillain–Barré syndrome, early studies can be nondiagnostic; repeat testing may clarify an axonal or demyelinating pattern. Normal early CSF protein also does not exclude GBS. Treatment of a rapidly progressive high-risk syndrome should not be delayed solely to obtain an ideal electrophysiologic label. Assess respiratory reserve and autonomic instability in parallel.
Needle fibrillation potentials and positive sharp waves indicate muscle-fiber irritability and may occur with denervation or myopathy. They are not synonymous with motor neuron disease. Denervation-related changes take time to appear and depend on the lesion. Large, long-duration motor units can reflect chronic neurogenic reinnervation, while short-duration, low-amplitude units with early recruitment can support myopathy in a cooperative patient.
Critical Illness Weakness
Critical illness polyneuropathy (CIP) is typically an axonal sensory-motor process with reduced sensory and motor responses. Critical illness myopathy (CIM) often preserves sensory responses while impairing muscle responses and motor-unit characteristics. The disorders frequently overlap. Sepsis, organ failure, immobility, nutrition, medication exposure, and prolonged ICU care contribute to risk; one history of NMBA use does not prove the mechanism.
Direct muscle stimulation can help distinguish nerve from muscle inexcitability in expert hands. Do not memorize an isolated ratio without knowing how it was calculated and recorded. Edema, low limb temperature, electrode placement, electrical artifact, and inability to cooperate can make a simplistic pattern misleading. Review the full report and clinical context rather than declaring a permanent prognosis from one low amplitude.
Management focuses on the underlying illness, appropriate mobilization and rehabilitation, nutrition, and avoiding unnecessary prolonged sedation or paralysis. Recovery differs by mechanism and severity. A patient may require prolonged respiratory rehabilitation even after systemic sepsis resolves; failure to wean does not necessarily establish persistent brain injury.
Motor Neuron Disease and Ventilation
Motor neuron disease , including ALS, can produce progressive limb, bulbar, and respiratory weakness with relative sensory preservation. A respiratory infection, secretion burden, aspiration, or medication effect may precipitate acute decompensation. Assess cough effectiveness, swallowing, orthopnea, respiratory mechanics when feasible, and gas exchange. A normal saturation does not exclude inadequate ventilation.
Noninvasive ventilation and cough-assistance strategies can benefit selected patients, while severe bulbar dysfunction or acute airway compromise may require a different plan. Discuss invasive ventilation in the context of known patient preferences, communication needs, disease trajectory, and available support. Do not equate an acute respiratory setback with a new diagnosis based solely on EMG, and do not infer decision-making incapacity from dysarthria or inability to move.
Acute Myopathies and Rhabdomyolysis
Acute weakness can result from inflammatory or immune-mediated myopathy, toxic exposure, endocrine or electrolyte disorders, infection, or critical illness muscle disease. Immune checkpoint inhibitors can produce overlapping myositis, myocarditis, and neuromuscular junction dysfunction, requiring respiratory and cardiac assessment. Creatine kinase, examination, exposure history, selected antibodies, imaging, and sometimes biopsy complement EMG.
Rhabdomyolysis can follow prolonged seizures, crush injury, electrical injury, drugs, ischemia, or metabolic disease. Muscle injury releases potassium, phosphate, and myoglobin and can cause dangerous arrhythmia and AKI. Dark urine is not required. Evaluate potassium and ECG promptly, follow renal function and urine output, and treat the precipitant. Give fluids according to perfusion and tolerance, especially when brain edema, pulmonary edema, or cardiac dysfunction complicates the usual resuscitation. Routine alkalinization or mannitol is not a universally proven preventive strategy for every case.
The useful examination distinction is between diagnosing the cause and protecting the patient while uncertainty remains. In progressive weakness, secure ventilation or manage hyperkalemia when indicated before awaiting a complete electrodiagnostic or biopsy result.
Sources checked October 17, 2026: ABPN content outline and AANEM clinical resources .