14.1 CT of Brain and Spine

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)

14.1 CT of Brain and Spine

Key Takeaways Explain This Topic AI

Noncontrast CT is the first neuro-ICU study for hemorrhage, hydrocephalus, herniation, and fracture because it is fast and shows acute clotted blood as hyperdensity.

Acute hematoma typically measures about 50–90 Hounsfield units and fades toward brain density over 1–3 weeks, so a subacute subdural collection can be isodense on a narrow brain window.

ASPECTS starts at 10 and subtracts one point for early ischemic hypoattenuation in each of 10 MCA-territory regions: caudate, lentiform, internal capsule, insula, and M1–M6.

Noncontrast CT often misses hyperacute ischemia; diffusion-weighted MRI is the study that becomes positive within minutes.

Iodinated contrast is not required to find blood; when eGFR is below about 30 mL/min/1.73 m², prefer noncontrast CT or noncontrast MRI/time-of-flight MRA over reflexive CTA.

Last updated: September 2026

CT of Brain and Spine

Quick Answer: Noncontrast CT (NCCT) is the first neuro-ICU study for hemorrhage, hydrocephalus, herniation, and fracture . Acute clotted blood is hyperdense (~50–90 HU) . Density falls toward brain over 1–3 weeks , so a subacute subdural can vanish on a narrow window. ASPECTS is a 10-point MCA early-ischemia score, not a perfusion map. Hyperacute infarct is often invisible on NCCT; diffusion-weighted MRI (DWI) is the sequence that turns positive in minutes. CT angiography (CTA) and CT perfusion (CTP) are named here only as pointers to the next two sections.

On the ABIM Neurocritical Care examination, a stem that starts with an unstable, unequal-pupil, ventilated patient is almost always an NCCT problem first, not an MRI problem. Independent ExamFinch teaching in this section covers CT of brain and spine listed under Diagnostic studies and procedural skills in the ABPN Content Specifications (02.A.1). This guide is not an ABIM or ABPN product.

Why NCCT is the first study

NCCT is available in minutes, does not require a ferromagnetic-safety checklist, tolerates pumps and metal hardware, and shows acute blood as bright . That combination is why you send the crashing patient to CT, not to a 30-minute magnet. You are looking for four immediately actionable patterns:

Hemorrhage — intraparenchymal, extra-axial, intraventricular, or subarachnoid
Hydrocephalus — temporal horns, ballooned third or fourth ventricle, transependymal hypodensity

Herniation — subfalcine shift, uncal encroachment, tonsillar descent, external herniation through a craniectomy

Fracture — calvarium, skull base, and, when the neck is uncleared, cervical and often thoracolumbar spine CT

Contrast is not required for any of those four. Iodinated CTA and CTP answer vessel-occlusion and penumbra questions; those techniques are taught in the MRI/perfusion and angiography sections that follow. Do not delay a noncontrast scan to add a CTA protocol if the patient is herniating from a hematoma you have not even seen.

Hounsfield units and windows

Hounsfield units (HU) are the CT density scale, with water near 0 HU and air near −1000 HU .

Material Typical HU How you use it
Air ~−1000 Pneumocephalus, sinus air, open skull
Fat ~−50 to −100 Orbits, lipoma
CSF ~0 to 15 Ventricles, cisterns, chronic hygroma
White matter ~20 to 30 Hypodense relative to cortex
Gray matter ~30 to 45 Loss of gray–white = early ischemia or edema
Acute clotted blood ~50 to 90 ICH, SDH, EDH, SAH, hyperdense vessel
Calcium >100–150 Choroid, pineal, old cavernoma
Iodinated contrast / bone hundreds to 1000+ Vessels on CTA, fractures on bone window

Read every head CT on at least three windows: brain (about WL 40, WW 80), subdural/blood (a wider window, for example WW 150–200, so thin extra-axial blood along the inner table is not lost), and bone . A normal-looking brain window with a missed 4 mm convexity subdural hematoma is a classic trap.

Hyperdensity timeline of blood

Fresh unclotted blood can be only mildly dense. As clot retracts over minutes to hours, attenuation rises (the hematoma looks brightest in the first 1–3 days). Hemoglobin breakdown and serum resorption then lower HU toward cortex and finally toward CSF.

Stage Clock Typical CT look

Hyperacute Minutes to a few hours 40–60 HU possible; mixed density if still bleeding ( swirl sign = unclotted hypoattenuating blood inside a hyperdense clot)

Acute Hours to ~3 days Peak hyperdensity ~60–90 HU ; sharp margins
Subacute ~3–21 days Progressive fade; isodense to cortex around 1–3 weeks , especially extra-axial
Chronic Weeks to months Hypodense, CSF-like; chronic SDH or encephalomalacia

Worked example: a day-0 basal ganglia hematoma measures 72 HU . On day 12 a contralateral crescent along the inner table measures 38 HU —the same as adjacent cortex—and is easy to miss unless you open a subdural window or look for sulcal buckling. Anticoagulated or actively expanding hematomas stay heterogeneous because unclotted blood sits closer to circulating blood (~30–45 HU) than to retracted clot.

Hyperdense vessel sign (MCA or basilar) is thrombus in a large artery, not parenchyma. It is a clue to large-vessel occlusion, not an ASPECTS region. Polycythemia and unenhanced vessels in a dehydrated patient can mimic it; compare with the contralateral artery.

Subarachnoid blood is hyperdense in cisterns and sulci. Sensitivity of NCCT for SAH is highest in the first 24 hours (often taught near 90–95% or higher) and falls over subsequent days. A delayed thunderclap with a normal CT still needs CSF testing or MRI (FLAIR/SWI), not reassurance from a single late scan.

Hemorrhage geometry, hydrocephalus, and herniation

Pattern CT geometry Immediate worry
Epidural Lentiform; usually stops at sutures Arterial (middle meningeal) expansion, lucid interval
Subdural Crescent; crosses sutures, not the midline falx freely Mass effect; isodense subacute miss
SAH Cisterns, sylvian fissures, sulci Aneurysm until the vascular workup says otherwise
ICH Parenchymal hyperdensity Volume, mixed-density expansion, IVH, herniation
IVH Cast in ventricles Obstructive hydrocephalus

Hydrocephalus looks like temporal horns out of proportion, a ballooned third ventricle, and periventricular hypodensity (transependymal flow). A full fourth ventricle with small laterals is a posterior-fossa outlet problem until proven otherwise.

Herniation on CT: subfalcine (septum pellucidum shift, cingulate under falx, ACA crowding), uncal (ambient cistern effacement, temporal uncus over the tentorial notch, PCA crowding), tonsillar (foramen magnum packing), upward (cerebellum crowding the tentorial notch, often after a tight posterior fossa or over-drainage), and external (brain through a craniectomy defect). Millimeters of midline shift plus a newly dilated pupil is an operative conversation, not a repeat-MRI-in-the-morning conversation.

Loading diagram... First-pass noncontrast CT decision path

Typical hematoma attenuation on noncontrast CT over time (teaching curve, not a single-patient tracing)

ASPECTS, conceptually

The Alberta Stroke Program Early CT Score (ASPECTS) estimates early ischemic change in the middle cerebral artery (MCA) territory on NCCT. Start at 10 . Subtract 1 for hypoattenuation or gray–white loss in each involved region:

Level Regions (1 point each)

Basal ganglia / insula cut Caudate (C) , lentiform (L) , internal capsule (IC) , insular ribbon (I) , M1, M2, M3

Immediately above the ganglia M4, M5, M6 (anterior, lateral, posterior MCA cortex)

Worked example: loss of the right insular ribbon and lentiform nucleus only means two regions, so ASPECTS 8 . Add M2 hypodensity and the score is ASPECTS 7 . A hyperdense MCA does not cost an ASPECTS point by itself.

ASPECTS is a burden score , not a perfusion map and not a treatment algorithm. Lower scores mean more established MCA infarct on that scan. Posterior-circulation infarcts use a separate pc-ASPECTS construct; do not force a brainstem stroke onto the MCA 10-point grid. Decisions about thrombolysis or thrombectomy belong in the acute ischemic stroke chapter. Here you only need to read the scan and report the early-change burden honestly.

When NCCT misses early ischemia

Cytotoxic edema takes time to drop HU enough to see. In the first hours, NCCT sensitivity for acute infarct is modest; a normal scan does not exclude stroke . What NCCT is excellent at in that same window is excluding hemorrhage so reperfusion discussions can start.

Missed-infarct patterns:

Hyperacute hemispheric ischemia (minutes to about 3–6 hours) with only subtle loss of the insular ribbon, or with nothing at all

Brainstem and cerebellum , where beam-hardening from petrous bone hides hypodensity
Small lacunar and cortical ribbon infarcts below CT resolution
Hyperacute posterior-circulation syndromes with a normal-looking cut through the pons

The study that detects ischemia in minutes is DWI , taught in the next section. If the stem is hemiparesis at 90 minutes, NCCT without blood and without hypodensity, the imaging diagnosis of infarct is not wait for a 24-hour CT. It is DWI, or a perfusion protocol if MRI is unavailable and you are selecting for late-window therapy—again, later sections.

Spine CT for unstable fracture screening

An uncleared, obtunded, or high-risk trauma patient gets multidetector CT of the spine , not a single lateral radiograph. CT is the bone screen: you are hunting unstable fractures that will injure the cord during a turn, a family visit, or an MRI transfer.

Denis three-column teaching: anterior column (anterior two-thirds of the body and anterior longitudinal ligament), middle column (posterior third of the body and posterior longitudinal ligament), and posterior column (posterior elements and ligaments). Disruption of two columns is treated as unstable until a spine surgeon says otherwise.

Pattern Why it is unstable on a test
Atlanto-occipital dissociation Craniocervical junction shear; immediately life-threatening
Jefferson (C1 burst) Stability hinges on the transverse atlantal ligament
Type II odontoid High nonunion; dens separated from the body
Hangman (C2 pars) with displacement Traumatic spondylolisthesis; types II/III more unstable
Flexion teardrop Posterior-ligament failure plus a retropulsed body
Bilateral facet dislocation Locked facets, often cord injury
Chance (flexion–distraction) Horizontal shear through bone or ligament
Burst with retropulsion Middle-column failure and canal compromise

CT misses isolated ligamentous disruption, cord contusion, traumatic disc, and spinal epidural hematoma . Those are MRI questions when there is a neurologic level, unexplained hypotension with bradycardia (neurogenic shock), or a CT-negative cord. Do not claim CT cleared the cord; it cleared bone .

Contrast, kidneys, and when MRI is the better next picture

Iodinated contrast is for CTA, CTP, and contrast-enhanced CT, not for finding acute blood. Contrast-associated acute kidney injury is a real but over-called problem. Contemporary radiology–nephrology consensus (ACR/NKF 2020) places the clinically important risk mainly at eGFR <30 mL/min/1.73 m² , plus AKI already in progress. Isotonic volume expansion is the prophylaxis that still makes sense in high-risk patients who truly need iodine.

When GFR is low:

Need to exclude ICH, SAH, hydrocephalus, or herniation → NCCT , no iodine

Need early infarct confirmation and the patient is MRI-safe → noncontrast MRI with DWI (no gadolinium required for that question)

Need vessels and iodine is unattractive → time-of-flight MRA (angiography section) rather than reflexive CTA

Need gadolinium MRI in advanced CKD → prefer group II macrocyclic agents; nephrogenic systemic fibrosis risk is concentrated in older group I agents at eGFR <30

An unstable, ventilated patient with a blown pupil does not go to MRI to spare the kidneys. MRI contraindications and logistics are the next section. The point here is that NCCT has no contrast nephropathy and answers the hemorrhage question.

Exam-style traps
Calling a day-12 isodense SDH no extra-axial collection because you never opened a wide window
Treating a normal NCCT at 2 hours as proof there is no infarct
Scoring a hyperdense MCA as an ASPECTS point
Giving iodinated contrast to better see the hematoma
Clearing an obtunded neck with a single radiograph
Sending a herniating patient to MRI as the first test

Independent practice items at /practice/abim-neurocritical-care are a study bank for this reasoning, not the computer-based examination administered by ABPN.