Study guide
21.2 Non-Aneurysmal SAH (03.E.2)
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)
21.2 Non-Aneurysmal SAH (03.E.2)
Key Takeaways Explain This Topic AI
Perimesencephalic nonaneurysmal SAH is prepontine or perimesencephalic blood with a negative high-quality vascular study; prognosis is generally far better than aSAH, but a vascular workup is still required.
AHA/ASA 2023 notes equipoise between CTA alone and CTA plus catheter DSA for a strictly perimesencephalic pattern; many centers still perform at least one catheter angiogram.
CTA-negative SAH with an aneurysmal (diffuse basal) blood pattern needs catheter DSA and often delayed repeat imaging, because occult aneurysm, dissection, and dural fistula can hide on the first study.
Convexity (sulcal) SAH is a different disease family: reversible cerebral vasoconstriction syndrome, cerebral amyloid angiopathy, endocarditis/mycotic aneurysm, trauma, PRES, and cortical venous thrombosis lead the list — not a typical berry aneurysm.
Do not label a patient nonaneurysmal until the blood pattern and a complete vascular evaluation match; the ICU complications of true aSAH are uncommon in strictly perimesencephalic disease but still appear if you missed an aneurysm.
Last updated: September 2026
Not every CT that shows subarachnoid blood is a ruptured saccular aneurysm. Roughly 15% of spontaneous SAH angiograms are negative on the first pass; a slice of those are truly perimesencephalic nonaneurysmal SAH , some are occult aneurysms that appear on a second study, and a growing fraction are convexity (sulcal) SAH from a completely different mechanism. ABIM Neurocritical Care items punish two errors equally: treating a perimesencephalic bleed as if it were ISAT-grade aSAH with 21 days of induced hypertension, and sending home a CTA-negative aneurysmal-pattern bleed without catheter angiography.
Independent ExamFinch teaching for this section is pattern recognition plus a workup rule: the distribution of blood tells you which test is still owed.
Three CT patterns that are not interchangeable
Pattern Where the blood lives First vascular concern Usual next step after negative CTA
Perimesencephalic Anterior to midbrain/pons; may lick ambient cisterns; does not fill sylvian or interhemispheric fissures or pack the ventricles Venous or capillary bleed; rare hidden basilar aneurysm High-quality CTA; many centers still add DSA; AHA/ASA 2023 notes equipoise
Diffuse / aneurysmal Basal cisterns, sylvian fissures, interhemispheric fissure, often IVH Missed aneurysm, dissection, blister, dural AVF Catheter DSA required; repeat delayed DSA and MRI/MRA if first DSA is negative
Convexity / sulcal Focal cortical sulcus, often unilateral, spares basal cisterns RCVS, amyloid, trauma, endocarditis, PRES, cortical vein thrombosis CTA/MRA, MRI with vascular imaging, infectious and reversible-vasoconstriction workup; DSA yield is lower than in basal SAH
If blood has already filled both sylvian fissures, calling it perimesencephalic is a grading error, not a philosophy difference.
Perimesencephalic nonaneurysmal SAH
Perimesencephalic nonaneurysmal subarachnoid hemorrhage (PM-NASAH) was defined by van Gijn and colleagues: CT blood centered in front of the midbrain, with only limited extension into the ambient cisterns, and no aneurysm on a high-quality angiogram. Patients are typically Hunt-Hess 1–2. Headache is still sudden, so the history alone does not separate them from a small posterior-circulation aneurysm.
The leading hypothesis is rupture of a fragile perimesencephalic vein, sometimes in patients with a primitive venous drainage pattern around the vein of Galen. That story explains the modest blood volume and the low rate of rebleeding once an aneurysm has been excluded.
Prognosis is the reason this entity exists as a separate exam topic. Rebleeding is rare after a truly negative workup. Delayed cerebral ischemia and chronic shunt-dependent hydrocephalus are far less common than after thick aneurysmal SAH. Many patients leave the ICU quickly. That better outlook is conditional on not missing a basilar-tip or superior cerebellar artery aneurysm that can mimic the same cistern on a sloppy CT read.
Vascular workup: CTA, DSA, and equipoise
Modern thin-cut CTA has high sensitivity for aneurysms ≥3 mm. Meta-analyses in strictly defined PM-NASAH have argued that a negative high-quality CTA may be enough. The 2023 AHA/ASA aSAH guideline, discussing this pattern, states there is currently equipoise between CTA alone and CTA followed by catheter-based digital subtraction angiography (DSA) . Centers still vary. A defensible ICU approach for the exam:
Confirm the CT pattern is truly perimesencephalic (not diffuse basal blood).
Obtain high-quality CTA (and often DSA) during the index admission.
If CTA is negative but the pattern is not strictly perimesencephalic, proceed to DSA.
If the first angiogram is negative and the pattern was aneurysmal, plan repeat vascular imaging (delayed DSA around day 7, plus MRI/MRA looking for thrombosed aneurysm, dissection, or spinal/dural fistula).
Nimodipine is often started until the aneurysm is excluded, then stopped if the diagnosis is bona fide PM-NASAH and the team is confident. There is no 21-day outcome trial in this subgroup equivalent to the British nimodipine trial in aSAH. Short ICU observation for hydrocephalus is still reasonable. Do not run a full DCI-induced-hypertension protocol on a negative-workup perimesencephalic patient with a normal exam.
CTA-negative aneurysmal-pattern SAH
This is the dangerous cousin. CT looks like aSAH — blood in the sylvian and interhemispheric fissures, maybe IVH — but CTA shows no aneurysm. Causes include:
- Small or blister aneurysm missed on CTA
- Thrombosed aneurysm that will recanalize
- Intracranial arterial dissection
- Dural arteriovenous fistula with retrograde leptomeningeal drainage
Cervical or intracranial vascular lesion better seen on catheter runs or spinal imaging (rare, but consider if there is a prominent cervical clue)
Repeat imaging is not optional decoration. A second DSA after the blood has cleared, 3-D rotational angiography, and MRI of brain and sometimes cervical spine raise the yield. Until that workup is complete, treat blood pressure, hydrocephalus, and ICU complications as you would for unsecured aSAH. The exam stem that says "CTA negative, thick basal SAH, discharged without DSA" is describing a miss.
Convexity SAH: a different differential
Convexity SAH (also called sulcal or cortical SAH) is blood confined to one or a few cerebral sulci, typically over the convexity, without filling the basal cisterns. Berry aneurysms at the circle of Willis almost never present this way. Forcing an ISAT-style coiling discussion is the wrong algorithm.
Cause Typical patient Clues
Reversible cerebral vasoconstriction syndrome (RCVS) Middle-aged, often women; thunderclap, recurrent; vasoactive drugs, postpartum Multifocal segmental vasoconstriction on CTA/DSA that reverses in ~3 months; convexity SAH is a classic imaging partner
Cerebral amyloid angiopathy (CAA) Older adult, often with prior lobar ICH or microbleeds Cortical superficial siderosis, APOE context, no vasoconstriction
Infective endocarditis / mycotic aneurysm Fever, bacteremia, regurgitant valve Distal mycotic aneurysm, infarcts of different ages, hemorrhage
Trauma Fall, assault, anticoagulation Adjacent skull or cortical contusion; history may be missing in the elderly
PRES Hypertension, eclampsia, calcineurin inhibitors, chemotherapy Posterior-predominant edema; convexity blood can accompany the arteriopathy
Cortical venous thrombosis Prothrombotic state Isolated cortical vein on SWI/MRV, seizure, not arterial-territory infarct
Primary angiitis of the CNS Subacute, stepwise, younger than CAA Irregular distal vessels, infarcts, CSF inflammation; least common on this list
Hyperperfusion after carotid revascularization Recent CEA or stent Unilateral headache, ipsilateral hemorrhage or sulcal blood
RCVS deserves extra lines because it is both common in the differential and easy to confuse with aneurysmal SAH or with primary vasculitis. Thunderclap headache that recurs over days, exposure to cannabis, cocaine, triptans, ergots, or SSRIs, and postpartum status are historical gold. Imaging shows "sausage-string" vasoconstriction that is dynamic. Treatment is typically calcium-channel blockade (nimodipine or verapamil, depending on local practice), blood-pressure control, and removal of the trigger — not aneurysm coiling and not cyclophosphamide. Distinguishing RCVS from CNS vasculitis matters because steroids can worsen RCVS in some series.
CAA-related convexity SAH in an 78-year-old with cortical microbleeds is a small-vessel process. DSA is low-yield. Antithrombotic decisions are individualized and painful; the exam still wants you to name amyloid rather than a middle-cerebral-artery berry aneurysm.
Endocarditis can produce convexity blood from a mycotic aneurysm or from hemorrhagic transformation of an embolic infarct. Blood cultures, echocardiography, and prolonged antibiotics share the stage with cautious vascular imaging. A mycotic aneurysm that is ruptured may need endovascular or surgical treatment, but the substrate is infection, not a congenital saccular aneurysm of the anterior communicating artery.
PRES (posterior reversible encephalopathy syndrome) overlaps with RCVS. If "PRES" seems to cause convexity SAH, look for concomitant vasoconstriction. Treat blood pressure, seizures, and the precipitant (including lowering calcineurin inhibitors when that is the cause).
Trauma remains the most common overall cause of SAH in emergency departments. Traumatic SAH is often sulcal, adjacent to a contusion or fracture, and does not follow the basal-cistern aneurysm map. That does not exempt you from thinking about dissection when the neck mechanism is violent.
What "still need a vascular workup" means in the ICU
A useful exam heuristic:
Perimesencephalic pattern + high-quality negative CTA: document the pattern, discuss DSA given AHA/ASA 2023 equipoise, and do not promise aSAH-level DCI risk.
Aneurysmal pattern + negative CTA: this is not "nonaneurysmal" yet. DSA now, repeat later if negative.
Convexity SAH: aneurysm protocol is the wrong first frame. MRI, vascular imaging for RCVS, infection workup, and amyloid features come first; DSA is selective when noninvasive studies fail or a fistula/mycotic aneurysm remains plausible.
Hydrocephalus and vasospasm monitoring are titrated to the true diagnosis. A patient with isolated left-frontal sulcal blood from RCVS does not need a 21-day TCD protocol designed for modified-Fisher-4 aSAH. A patient with cisternal blood and a still-negative angiogram does.
In practice
A 46-year-old has a thunderclap headache after lifting a box. CT shows blood anterior to the pons only. CTA is negative. You keep the patient, obtain catheter angiography (or a documented high-quality CTA pathway plus observation, depending on institutional reading of the 2023 equipoise), and expect a good outcome if no aneurysm appears. Contrast a 46-year-old whose CT fills both sylvian fissures, CTA is negative, and someone writes "nonaneurysmal SAH, discharge." That second patient still owes DSA and a delayed look. Contrast again a 38-year-old postpartum patient with recurrent thunderclap headaches and right-convexity sulcal blood: think RCVS, get vascular imaging for vasoconstriction, and do not coil an aneurysm that is not there.