Study guide

EMG, Nerve Conduction & Acute Muscle Disease

ABPN Neurocritical Care Study Guide Exam

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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 .