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Non-Contrast CT & CT Angiography

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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

Non-Contrast CT & CT Angiography

Key Takeaways Explain This Topic AI

Non-contrast computed tomography (NCCT) remains the initial neuroimaging modality of choice in emergent neurologic presentations, utilizing calibrated Hounsfield units (HU) to instantly differentiate acute hemorrhage ( 60 – 80 HU 60\text{--}80\text{ HU} 60 – 80 HU ) from cytotoxic edema and ischemic hypodensity ( < 25 HU <25\text{ HU} < 25 HU ).

Early ischemic changes on NCCT include loss of the insular ribbon, obscuration of the lentiform nucleus, sulcal effacement, and the hyperdense MCA sign; each 1 % 1\% 1% increase in tissue water content from cytotoxic edema decreases attenuation by approximately 2.5 HU 2.5\text{ HU} 2.5 HU .

The Alberta Stroke Program Early CT Score (ASPECTS) semiquantitatively evaluates middle cerebral artery (MCA) territory ischemia across 10 regions; landmark trials (SELECT2, ANGEL-ASPECT, TESLA) demonstrated substantial functional benefit of endovascular thrombectomy (EVT) even in large-core infarctions (ASPECTS 3–5), expanding indications beyond the historical ≥ 6 \ge 6 ≥ 6 cutoff.

Extra-axial hemorrhage morphology reflects distinct anatomic compartments: epidural hematomas are biconvex, suture-limited collections typically from middle meningeal artery rupture where an internal 'swirl sign' denotes hyperacute unclotted bleeding, whereas subdural hematomas are crescentic collections from torn bridging veins that cross suture lines.

CT angiography (CTA) provides rapid detection of large vessel occlusion (LVO) and collateral adequacy; in spontaneous intracerebral hemorrhage (ICH), the CTA 'spot sign' represents active contrast extravasation within the hematoma and serves as the most potent independent predictor of hematoma expansion and early neurological mortality.

Last updated: October 2026

Non-Contrast CT & CT Angiography in Neurocritical Emergencies

Non-contrast computed tomography (NCCT) and CT angiography (CTA) represent the foundational diagnostic workhorses of neurocritical care. Due to near-universal emergency department availability, rapid scan acquisition ( < 1 minute <1\text{ minute} < 1 minute ), and absence of contraindications related to implanted ferromagnetic devices, NCCT remains the undisputed first-line imaging modality for acute coma, traumatic brain injury (TBI), suspected intracranial hemorrhage, and acute ischemic stroke.

Physical Principles & Hounsfield Unit Calibration

Computed tomography maps tissue x-ray attenuation coefficients relative to water and air, quantified via the Hounsfield Unit (HU) scale: HU = 1000 × μ tissue − μ water μ water \text{HU} = 1000 \times \frac{\mu_{\text{tissue}} - \mu_{\text{water}}}{\mu_{\text{water}}} HU = 1000 × μ water ​ μ tissue ​ − μ water ​ ​

On this linear scale, air is calibrated to − 1000 HU -1000\text{ HU} − 1000 HU , distilled water to 0 HU 0\text{ HU} 0 HU , and dense cortical bone to + 1000 HU +1000\text{ HU} + 1000 HU .

  • Intracranial Tissue / Substance Typical Attenuation Range (HU) Diagnostic Relevance in Neuro-ICU
  • Air − 1000 -1000 − 1000 Pneumocephalus, skull base fractures, open penetrating trauma
  • Fat − 100 to − 50 -100\text{ to }-50 − 100 to − 50 Dermoid cysts, lipomas, intraventricular fat droplets
  • Cerebrospinal Fluid (CSF) 0 to 10 0\text{ to }10 0 to 10 Ventricular enlargement, effacement, hydrocephalus
  • Ischemic / Infarcted Brain 15 to 25 15\text{ to }25 15 to 25 Cytotoxic edema, loss of gray-white junction

Normal Cerebral White Matter 25 to 30 25\text{ to }30 25 to 30 Lower protein and higher myelin/lipid content than cortex

Normal Cerebral Gray Matter 35 to 40 35\text{ to }40 35 to 40 High cellularity and vascularity; distinct gray-white boundary

Subacute / Lytic Hematoma 30 to 45 30\text{ to }45 30 to 45 Protein degradation and hemoglobin breakdown (isodense to gray matter)

Acute Clotted Blood 60 to 80 60\text{ to }80 60 to 80 Globin protein concentration and clot retraction in hyperacute hematoma

Calcification / Atheroma 100 to 400 100\text{ to }400 100 to 400 Basal ganglia calcification, vascular atheroma

Dense Cortical Bone Variable, often above +1000 Calvarial fractures, skull base integrity

Note

Tailored windowing is vital for bedside image interpretation. Standard brain windows (width ≈ 80 HU \approx 80\text{ HU} ≈ 80 HU , level ≈ 35 HU \approx 35\text{ HU} ≈ 35 HU ) provide general survey; however, dedicated stroke windows (narrow width 30 – 40 HU 30\text{--}40\text{ HU} 30 – 40 HU , level 30 – 35 HU 30\text{--}35\text{ HU} 30 – 35 HU ) amplify subtle density differentials, rendering early cytotoxic parenchymal hypodensity readily distinguishable from adjacent normal gray matter.

Early Ischemic Changes on Non-Contrast CT

In hyperacute ischemic stroke, energy failure secondary to hypoperfusion induces Na + / K + \text{Na}^+/\text{K}^+ Na + / K + -ATPase shutdown, driving intracellular sodium accumulation and cytotoxic edema. Each 1 % 1\% 1% increase in tissue water decreases parenchymal CT attenuation by approximately 2.5 HU 2.5\text{ HU} 2.5 HU .

Early ischemic changes become detectable within 1 – 3 hours 1\text{--}3\text{ hours} 1 – 3 hours of vessel occlusion:

Loss of the Insular Ribbon: The insular cortex has vulnerable end-arteriolar supply from terminal M2/M3 branches with minimal collateral overlap. Edema creates early blurring and hypodensity of the insular gray-white interface.

Obscuration of the Lentiform Nucleus: The putamen and globus pallidus lose demarcation against the surrounding internal and external capsules due to ischemia in deep lenticulostriate arterial distributions.

Cortical Sulcal Effacement: Swelling of cortical gyri compresses subarachnoid spaces and effaces sulci over the hemispheric convexity.

Hyperdense Vessel Signs: High attenuation within an intracranial arterial lumen denotes acute, intraluminal stagnant thromboembolism ( 70 – 80 HU 70\text{--}80\text{ HU} 70 – 80 HU ) prior to parenchymal tissue changes. The classic hyperdense MCA sign appears along the horizontal M1 segment; the MCA dot sign represents thrombus within Sylvian fissure M2/M3 branches viewed in cross-section; and the hyperdense basilar sign indicates life-threatening vertebrobasilar occlusion.

Warning

A false-positive hyperdense MCA sign may occur in patients with marked polycythemia (elevated hematocrit), heavy concentric vascular calcification, or localized hemoconcentration. Comparing attenuation against the contralateral MCA and verifying absence of generalized high vascular attenuation prevents misdiagnosis.

The Alberta Stroke Program Early CT Score (ASPECTS)

The Alberta Stroke Program Early CT Score is an established, validated 10-point quantitative topological scoring system evaluating ischemic changes across the middle cerebral artery (MCA) territory.

Anatomic Topography & Scoring Rules

ASPECTS divides the MCA territory across two defined axial CT planes:

Ganglionic Cut (at the level of the basal ganglia and internal capsule):

  • C: Caudate head
  • L: Lentiform nucleus (putamen and globus pallidus)
  • IC: Internal capsule (posterior limb)
  • I: Insular ribbon
  • M1: Anterior MCA cortex
  • M2: Lateral temporal MCA cortex
  • M3: Posterior temporal MCA cortex

Supraganglionic Cut ( 2 cm 2\text{ cm} 2 cm rostral to the basal ganglia, at the level of the corona radiata and bodies of lateral ventricles):

  • M4: Rostral anterior MCA cortex
  • M5: Rostral lateral MCA cortex
  • M6: Rostral posterior MCA cortex

Scoring starts at 10 points. For each defined region demonstrating distinct parenchymal hypodensity and loss of gray-white differentiation, exactly 1 point is subtracted. An ASPECTS of 10 indicates a completely normal MCA territory; an ASPECTS of 0 denotes complete, pan-territorial infarction.

Large-core evidence: SELECT2, ANGEL-ASPECT, and other trials support expanded EVT eligibility in selected large cores. TESLA did not meet its primary superiority threshold. Do not claim that every trial proved independence or reduced mortality; assess the current guideline and the actual study population.

Traumatic Brain Injury & Intracranial Hemorrhage Patterns

Rapid characterization of extra-axial and intra-axial bleeding compartments guides emergency surgical decompression:

Hemorrhage Type Anatomic Compartment Vascular Etiology CT Morphology & Characteristics Suture Limitation High-Risk Clinical Features

Epidural Hematoma (EDH) Potential space between inner skull table and periosteal dura Middle meningeal artery (85%) or dural venous sinus / skull fracture Biconvex (lens-shaped), uniformly hyperdense ( 60 – 80 HU 60\text{--}80\text{ HU} 60 – 80 HU ) Yes (dura is anchored at calvarial suture lines) Swirl sign (active extravasation); classic lucid interval followed by rapid uncal herniation

Subdural Hematoma (SDH) Space between meningeal dura and arachnoid mater Cortical bridging veins sheared during rotational acceleration Crescentic, concave inner margin conforming to hemispheric contour No (freely crosses cranial sutures; limited only by dural reflections) Acute-on-chronic rebleeding, membrane formation, midline shift disproportionate to thickness

Subarachnoid Hemorrhage (SAH) Space between arachnoid and pia mater Ruptured saccular aneurysm (85%), vascular malformation, or TBI Hyperdensity filling basilar cisterns, Sylvian fissures, and sulci No (diffuses throughout CSF cisterns and ventricular spaces) Vasospasm and delayed cerebral ischemia; intraventricular clot predisposing to acute obstructive hydrocephalus

Important

A swirl or other heterogeneous hemorrhage pattern raises concern for active or evolving bleeding and requires urgent clinical and neurosurgical assessment. It does not independently mandate the same surgical intervention for every lesion; examination, volume, shift, and other indications determine the plan.

The Modified Fisher Scale stratifies aneurysmal SAH vasospasm risk based on cisternal blood thickness and intraventricular hemorrhage (IVH):

Grade 1: Minimal / thin subarachnoid clot; no IVH.

Grade 2: Minimal / thin subarachnoid clot; IVH present.

Grade 3: Thick cisternal clot (filling cistern/fissure ≥ 1 mm \ge 1\text{ mm} ≥ 1 mm in vertical dimension); no IVH.

Grade 4: Thick cisternal clot; IVH present (conferring the highest risk of delayed cerebral ischemia).

CT Angiography (CTA) in Acute Neurocritical Care

CTA combines rapid helical volumetric scanning with a timed intravenous iodinated contrast bolus ( 60 – 80 mL 60\text{--}80\text{ mL} 60 – 80 mL at 4 – 5 mL/s 4\text{--}5\text{ mL/s} 4 – 5 mL/s ) from the aortic arch through the circle of Willis to the vertex.

Large Vessel Occlusion & Collateral Assessment

LVO Identification: CTA achieves > 95 % >95\% > 95% sensitivity and specificity for acute occlusions of the internal carotid artery (ICA) terminus ("T" or "L" occlusions), middle cerebral artery mainstem (M1) and primary divisions (M2), anterior cerebral artery (A1), and basilar artery.

Collateral Assessment (Single-Phase vs. Multiphase CTA):

Single-phase CTA captures contrast at a single peak arterial timepoint. However, retrograde pial collateral filling is hemodynamically delayed. Single-phase acquisition often underestimates true collateral capacity in vessels where blood arrives seconds later.

Multiphase CTA records three sequential phases: peak arterial, peak venous, and late venous. By capturing delayed wash-in and wash-out across pial collaterals, multiphase CTA differentiates true absent collaterals from delayed but robust collateral filling, correlating tightly with penumbral preservation and clinical outcomes.

Vascular Pathologies: Dissection & Aneurysms

Cervical Arterial Dissection: CTA demonstrates eccentric arterial wall thickening, an intimal flap, irregular luminal tapering ("string sign"), pseudoaneurysm formation, or an intramural hematoma visible as a hyperdense crescent on non-contrast imaging.

Aneurysms and AVMs: Identifies aneurysm neck anatomy, incorporation of branch vessels, and draining vein patterns of arteriovenous malformations or dural arteriovenous fistulas (dAVF).

The CTA "Spot Sign" in Spontaneous Intracerebral Hemorrhage

In spontaneous intracerebral hemorrhage (ICH), hematoma expansion occurs in up to 30 % 30\% 30% of patients within the initial hours, driving severe neurological worsening and death.

Definition: The spot sign is defined as one or more discrete, punctate foci of contrast extravasation ( ≥ 1 – 2 mm \ge 1\text{--}2\text{ mm} ≥ 1 – 2 mm ) within the interior of an acute parenchymal hematoma on source CTA images, without connection to surrounding intact normal blood vessels, and exhibiting attenuation > 120 HU >120\text{ HU} > 120 HU .

Clinical Significance: The spot sign represents active microvascular pseudoaneurysm rupture and ongoing arterial leakage. It is the most robust independent imaging predictor of hematoma expansion ( > 33 % >33\% > 33% or > 6 mL >6\text{ mL} > 6 mL ), early neurological deterioration, and in-hospital mortality. Its presence guides aggressive early systolic blood pressure lowering ( < 140 mmHg <140\text{ mmHg} < 140 mmHg ) and identifies candidates for ultra-early hemostatic intervention.