18.1 Coma and Other States of Altered Consciousness (03.A)

ABIM Neurocritical Care Subspecialty Certification Exam

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1 Introduction & Exam Overview

1.1 Current Exam Facts 1.2 Eligibility, Practice Pathway, and the IM Training Route 1.3 Format, Scoring, Pearson VUE, and Score Reports 1.4 How to Use This Independent Study Guide

2 ICU Neurologic Exam, Cerebral Physiology, and CSF

2.1 Neurological Examination in the ICU 2.2 Cerebral Physiology, ICP, CBF, and Autoregulation 2.3 CSF Physiology

3 Core Neuropharmacology

3.1 Osmotic Agents 3.2 Anti-Seizure Drugs 3.3 Anesthetics, Sedatives, Analgesia, and Paralytics 3.4 Antihypertensives, Vasopressors, and Inotropes

4 Reperfusion Drugs, Airway, and Ventilation

4.1 Thrombolytics, Anticoagulants, and Antiplatelets 4.2 Reversal of Anticoagulation After Acute Hemorrhage 4.3 Airway Management and Tracheostomy 4.4 Mechanical Ventilation

5 Hemodynamics and Shock

5.1 Hemodynamic Monitoring 5.2 IABP, Temporary VADs, LVAD, and ECMO 5.3 Diagnosis and Management of Shock

6 Nutrition, Temperature, and ICU Prophylaxis

6.1 Nutrition (01.J) 6.2 Temperature Control (01.K) 6.3 ICU Prophylaxis, Delirium, and Early Mobility (01.L)

7 General Trauma

7.1 Emergency Evaluation of Polytrauma, Chest, and Abdominal Trauma 7.2 Long-Bone Fractures and Fat Embolism 7.3 Burns, Electrical Injury, and Hanging/Strangulation

8 Pulmonary Critical Care

8.1 Pulmonary Physiology and ARDS (01.N.1–2) 8.2 PE, Pneumonia, and Pulmonary Edema (01.N.3, 7–8) 8.3 COPD, Asthma, PAH, and Bronchoscopy Basics (01.N.4–6, 9)

9 Cardiovascular Critical Care

9.1 Cardiovascular Physiology, Stress Cardiomyopathy, ACS, and Valves 9.2 Arrhythmias and Pacing 9.3 Acute Aortic Dissection and Cardiac Ultrasound

10 Renal and Infectious Disease

10.1 AKI, RRT, and Renal Drug Dosing 10.2 Acid-Base and Electrolyte Disorders 10.3 Severe Sepsis, Septic Shock, and Infective Endocarditis 10.4 Antimicrobial Use and Infection in the Immunosuppressed

11 Endocrine and Salt-Water Disorders

11.1 Pituitary Apoplexy, DI, and Panhypopituitarism (01.R.1–4) 11.2 SIADH and Cerebral Salt Wasting (01.R.5–6) 11.3 Thyrotoxicosis, Myxedema, Adrenal Crisis, and Dysglycemia (01.R.7–9)

12 Gastrointestinal Critical Care

12.1 GI Physiology, Acute Abdomen, Bleed, Ileus, and Perforation (01.S.1–5) 12.2 Mesenteric Ischemia and Abdominal Compartment Syndrome (01.S.6–7) 12.3 Fulminant Liver Failure, Cirrhosis Decompensation, and Hepatic Dosing (01.S.8–10)

13 Hematologic Disorders

13.1 Anemia, Transfusion, Thrombocytopenia, Coagulopathy, and DIC (01.T.1–4) 13.2 VTE in the Neuro ICU (01.T.5) 13.3 Chemo/Immune, SCT, CAR-T, Sickle Cell, and TMA (01.T.6–10)

14 Neuroimaging

14.1 CT of Brain and Spine 14.2 MRI and CT/MR Perfusion 14.3 Noninvasive Angiography and Catheter Angiography

15 EEG, EMG, and CSF Analysis

15.1 EEG, Standard and Processed (02.B) 15.2 Basic EMG Interpretation (02.G) 15.3 CSF Analysis (02.H)

16 ICP, TCD, and Multimodality Monitoring

16.1 ICP Monitoring (02.C) 16.2 Transcranial Doppler (02.D) 16.3 Brain-Tissue Oxygen and Multimodality Monitoring (02.E–F)

17 Brain Death and Bedside Procedures

17.1 Brain Death Prerequisites and Clinical Exam (02.I) 17.2 Apnea Testing and Ancillary Studies (02.I) 17.3 Vascular Access, Thoracic Echo, and Lung Ultrasound (02.J–L)

18 Coma, Anoxia, and Intracranial Hypertension

18.1 Coma and Other States of Altered Consciousness (03.A) 18.2 Global Anoxia-Ischemia and Post-Resuscitation Encephalopathy (03.A.1) 18.3 Toxidromes, ICU Delirium, and Hypertensive Encephalopathy (03.A.2–4) 18.4 Intracranial Hypertension as a Disease State (03.B)

19 Acute Ischemic Stroke

19.1 IV Reperfusion Therapy (03.C.3) 19.2 Mechanical Thrombectomy Windows and Imaging Selection (03.C.3) 19.3 Malignant Hemispheric Infarction and Basilar Artery Occlusion (03.C.1–2)

20 Intraparenchymal Hemorrhage

20.1 Intracerebral Hematoma (03.D.1) 20.2 Cerebellar Hematoma (03.D.2) 20.3 Intraventricular Hemorrhage (03.D.3)

21 SAH, CVST, and Spinal Cord Infarction

21.1 Aneurysmal Subarachnoid Hemorrhage (03.E.1) 21.2 Non-Aneurysmal SAH (03.E.2) 21.3 Cerebral Venous Sinus Thrombosis (03.F) 21.4 Spinal Cord Infarction (03.G)

22 Vascular Anomalies and Traumatic Brain Injury

22.1 Unruptured Aneurysm, Cavernoma, AVM, and Dural AVF (03.H) 22.2 Diffuse Axonal Injury and Cerebral Contusions (03.I.1–2) 22.3 Epidural Hematoma, Subdural Hematoma, and Penetrating Injury (03.I.3–4, 7) 22.4 Arterial Dissection and Carotid-Cavernous Fistula (03.I.5–6)

23 Spine, Hydrocephalus, and CNS Infection

23.1 Spinal Cord Injury, Central Cord, and Neurogenic Shock (03.J) 23.2 Unstable Spine Fractures (03.K) 23.3 Hydrocephalus and CSF Diversion (03.L) 23.4 Acute CNS Infections (03.M)

24 Seizures and Neuromuscular Emergencies

24.1 Status Epilepticus and Seizures (03.N) 24.2 Guillain-Barré Syndrome (03.O.1) 24.3 Myasthenic Crisis (03.O.2) 24.4 Motor Neuron Disease, Acute Myopathies, Rhabdomyolysis, and CINM (03.O.3–6)

25 Inflammatory Disease, Neuro-Oncology, and Special Populations

25.1 Fulminant Demyelinating Diseases (03.P) 25.2 Autoimmune Encephalitis and Acute Autonomic Hyperactivity (03.Q–R) 25.3 Neuro-Oncology and Treatment Complications (03.S) 25.4 Pregnancy/Post-Partum, Post-Transplant, and Pediatric Patients (03.T–U)

26 Neurosurgical and Perioperative Complications

26.1 Postoperative Seizures, Hemorrhage, Ischemia, and Hyperperfusion (04.A, C, D, H) 26.2 Infection, CSF Leak, and Pneumocephalus (04.B, E, F) 26.3 Complications of EVD and Lumbar Drain (04.G, I)

27 Ethics, Prognostication, and Organ Donation

27.1 Communication, Decision-Makers, Advance Directives, and DNR (05.A, B, G) 27.2 Uncertainties of Prognostication and the Self-Fulfilling Prophecy (05.C) 27.3 Palliative Care, Withdrawal, Withholding, and Futility (05.D–F) 27.4 Donation After Cardiac Death and Care of the Organ Donor (05.H–I)

18.1 Coma and Other States of Altered Consciousness (03.A)

Key Takeaways Explain This Topic AI

Coma is unarousable unresponsiveness with eyes closed and no sleep–wake cycle; it is not the same as a vegetative/unresponsive wakefulness syndrome, MCS, locked-in syndrome, or akinetic mutism.

Locked-in syndrome is ventral pontine injury with preserved awareness, typically vertical eye movements and blinking; calling it coma is a localization and ethics error.

True coma localizes to bilateral hemispheres (or diencephalon) or to the brainstem ascending reticular activating system in the paramedian midbrain or rostral pons; a single cerebral hemisphere does not produce coma unless the brainstem is compressed.

The first laboratory in undifferentiated coma is a point-of-care glucose, obtained while airway, breathing, and circulation are secured.

MCS requires inconsistent but reproducible evidence of awareness; vegetative/unresponsive wakefulness has sleep–wake cycles without awareness.

Last updated: September 2026

Coma and Other States of Altered Consciousness

Quick Answer: Coma means unarousable unresponsiveness with eyes closed and no sleep–wake cycle . Vegetative state / unresponsive wakefulness syndrome (UWS) has eyes open and sleep–wake without awareness. Minimally conscious state (MCS) has inconsistent but reproducible awareness. Locked-in syndrome is aware ventral pontine injury — not coma . Akinetic mutism is a frontal/cingulate paucity of movement with wakefulness. True coma localizes to both hemispheres (or diencephalon) or to the brainstem ARAS . Check glucose with the ABCs.

A silent, motionless patient in the neuro ICU is not automatically “in coma.” On the ABIM Neurocritical Care examination, stems mix a locked-in basilar occlusion, a vegetative survivor after anoxia, an MCS patient who inconsistently follows a command, and a hypoglycemic patient who looks brainstem-dead until the glucometer reads 28 mg/dL. Independent ExamFinch teaching here covers coma and other states of altered consciousness as listed among Neurocritical care diseases in the ABPN Content Specifications. This guide is not an ABIM or ABPN product.

Why the label matters

The word coma is a localization claim and a communication claim. Families hear “coma” as unconsciousness. If the patient can hear you, track vertically, and spell with eye blinks, you have just described locked-in syndrome as if the person were gone. Prognostication, rehabilitation, and whether you talk to the patient at the bedside all change with the correct syndrome name. The Glasgow Coma Scale (GCS) and FOUR score grade responsiveness; they do not by themselves name the syndrome. A GCS of 5T can be bihemispheric anoxia, a pontine hemorrhage, or residual neuromuscular blockade. Report subscores , pupils, tracking, and whether sleep–wake is present.

Named states you must not collapse into one word

Syndrome Wakefulness (eyes / sleep–wake) Awareness Typical localization Bedside signature

Coma Eyes closed; no sleep–wake cycle None that can be demonstrated Bilateral hemispheres/diencephalon, or brainstem ARAS Unarousable; no tracking; no command following

Vegetative / UWS Eyes open; sleep–wake present None Widespread cortex, relatively spared brainstem Eyes open, roving or untracking; startle without reproducible command following

MCS Eyes often open Inconsistent but reproducible Severe but incomplete cortico-thalamic injury Visual pursuit, contingent smiling/crying, localization, or simple command following

Emergence from MCS Awake Reliable Recovering networks Functional communication or functional object use

Locked-in Awake; often appears “coma-like” if you never look at the eyes Preserved Ventral pons (classically basilar artery) Quadriplegia and anarthria with vertical eye movement and/or blinking

Akinetic mutism Awake, eyes open Reduced initiation, not true unawareness Bilateral ACA / cingulate , or paramedian thalamus Almost no spontaneous speech or movement; may track; not flaccid coma

Coma , in the Plum and Posner sense still used at the bedside, is unarousable unresponsiveness . The patient does not open eyes to voice or pain in a sustained way, does not have a sleep–wake cycle, and shows no purposeful behavior. Duration is hours to (by convention) about 2–4 weeks; after that, if the brainstem supports wakefulness without awareness, the label usually moves to vegetative/UWS or MCS rather than “chronic coma.”

Vegetative state and unresponsive wakefulness syndrome describe the same clinical picture: wakefulness without awareness . Eyes open, sleep–wake cycling returns, breathing may be spontaneous, and there may be startle, grimace, or roving eyes, but there is no reproducible evidence that the person understands or intends . Do not call this coma. Do not call a few days of eyes-closed unresponsiveness after cardiac arrest “vegetative” either — that diagnosis is not a day-1 label.

Minimally conscious state , defined in the Aspen and later Giacino work, requires inconsistent but reproducible signs of awareness. MCS− is often visual pursuit, localization to noxious stimulation, or contingent affective behavior. MCS+ includes command following, intelligible words, or yes/no (even if unreliable). One lucky twitch is not MCS. You need a behavior you can elicit again . Emergence from MCS is scored when the patient has functional interactive communication or functional use of two different objects.

Locked-in syndrome is the highest-stakes trap on this list. The lesion is the ventral pons : corticospinal and corticobulbar fibers are destroyed; the tegmentum , including the ascending reticular activating system (ARAS) and much of the horizontal gaze machinery, may be relatively spared, and vertical gaze and eyelid opening (midbrain) often remain. The patient is awake and aware , cannot move limbs or speak, and communicates with vertical eye movements or blinks . EEG is typically near-normal for the awake state. Do not call locked-in “coma.” Do not give a FOUR eye score of 0 without checking whether the eyes open and track vertically. Cover the “coma” label in the note and you will miss both the basilar occlusion and the person in the bed.

Akinetic mutism looks like a quiet, awake patient who does not speak or move much. It is a disorder of initiation , classically from bilateral anterior cerebral artery infarction, cingulate injury, or paramedian thalamic lesions. Eyes may be open and may track. Tone is not the flaccid silence of medullary failure. It is not locked-in (the face and limbs can often be shown to move if sufficiently stimulated) and it is not coma.

Loading diagram... First branch point: is this unarousable coma or another silent syndrome?

Localization: two hemispheres or the brainstem core

Consciousness requires a functioning ARAS in the paramedian tegmentum of the midbrain and rostral pons , plus at least one working cerebral hemisphere (in practice, bihemispheric or thalamic integrity). That anatomy yields two coma localizations:

1. Bihemispheric (or bilateral diencephalic) coma. Diffuse anoxia, hypoglycemia, hepatic encephalopathy, meningitis/encephalitis, bilateral subdural hematomas, and bi-thalamic infarcts shut down both hemispheres. Brainstem reflexes are often preserved early : pupils may be small and reactive, corneal and oculocephalic reflexes present, and breathing regular or Cheyne–Stokes. Motor findings may be symmetric (withdrawal, or nothing). A unilateral cortical stroke does not cause coma unless there is herniation with brainstem compression , massive edema with diencephalic failure, seizure/post-ictal state, or a second lesion. If the stem gives a dense left hemiparesis, a blown right pupil, and unresponsiveness, you are no longer in “left MCA coma” — you are in uncal herniation .

2. Brainstem coma. A paramedian midbrain or pontine tegmental lesion knocks out ARAS. Look for asymmetric or lost cranial-nerve signs : midposition or pinpoint pupils, lost corneal reflexes, lost oculocephalics, skew, internuclear ophthalmoplegia, ataxic or apneustic breathing, or hyperthermia from pontine injury. Ventral pontine injury without tegmental destruction is locked-in, not brainstem coma — the pupils and vertical gaze save the diagnosis.

Psychogenic unresponsiveness and catatonia can mimic coma. The eyes often close actively, vestibulo-ocular testing may show nystagmus (which requires a working cortex), and laboratory and imaging are unrevealing. Do not lead with that diagnosis in a febrile, acidotic, or post-arrest patient.

Confounders that fake a dead brainstem — residual sedation , hypothermia , neuromuscular blockade , and profound metabolic failure — are taught with the ICU examination. Subtract them before you name a syndrome or discuss death by neurologic criteria (a later chapter).

First-hour workup: treat the reversible while you image

Stabilization is not a slogan. Airway, breathing, circulation come first because hypoxia and hypotension make every later scan worse. In parallel, check a point-of-care glucose . Hypoglycemia is common, immediately reversible, and will produce a “brainstem-dead” exam until the sugar is up. Give dextrose when the glucose is low or unobtainable. Give thiamine when malnutrition or alcohol use is plausible — before or with glucose — so you do not precipitate Wernicke encephalopathy. Naloxone belongs in the opioid-looking patient (pinpoint pupils, hypoventilation), not as a reflex for every GCS of 6.

Then obtain a noncontrast head CT unless the cause is already obvious and immediately treatable (documented hypoglycemia that is already correcting with a now-arousing patient). CT finds hemorrhage, hydrocephalus, large infarct with edema, and mass effect. If the story is sudden collapse with pinpoint pupils or locked-in features, add vascular imaging for basilar occlusion. Send CBC, chemistry, liver enzymes, ammonia when indicated, ABG, blood and urine toxicology, cultures if febrile, and consider lumbar puncture after imaging when meningitis or encephalitis is in play. EEG is next when nonconvulsive status epilepticus is possible (subtle twitching, unexplained coma after a seizure, or a flat-looking patient with a history of epilepsy). MRI is for the unclear case after CT, not a substitute for glucose and an airway.

Worked stems

A 62-year-old is found down. GCS E1 V1 M2, pupils 2 mm and reactive, glucose 32 mg/dL . The next action is dextrose (and thiamine if risk is present), not an immediate brain-death discussion and not a first-line MRI.

A 55-year-old with atrial fibrillation is mute and quadriplegic. Eyes are open and look up and down to command . This is locked-in syndrome from ventral pontine ischemia. Call it that. Image the basilar artery . Speak to the patient.

A 40-year-old opens eyes, has sleep–wake cycles three weeks after anoxia, and never follows a command despite off sedation. That is UWS/vegetative , not coma and not MCS until you document a reproducible aware behavior.

Exam traps

Calling locked-in “coma.” Diagnosing vegetative state on hospital day 1. Treating a unilateral hemisphere infarct as an adequate explanation for coma without herniation or a second lesion. Skipping glucose. Using GCS total without pupils or tracking. Independent practice items at /practice/abim-neurocritical-care drill these distinctions; they are a study bank, not the computer-based examination administered by ABPN.