Study guide
Cerebral Venous Thrombosis & Spinal Cord Infarction
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
Cerebral Venous Thrombosis & Spinal Cord Infarction
Key Takeaways Explain This Topic AI
CVT may cause headache, seizures, papilledema, focal deficits, or hemorrhagic lesions outside a single arterial territory.
Anticoagulation is generally used for CVT even when the venous infarct contains hemorrhage, after considering individual contraindications.
Acute spinal cord infarction often reaches severe deficits rapidly and requires exclusion of compression.
An initially unrevealing spinal MRI does not exclude early cord ischemia.
Last updated: October 2026
Cerebral Venous Outflow Failure
Cerebral venous thrombosis (CVT) includes thrombosis of a dural sinus, cortical vein, or deep venous system. Obstructed drainage raises venous pressure, impairs CSF absorption, and can produce edema, infarction, and hemorrhage. Unlike an arterial infarct, a venous lesion may cross conventional arterial territories or be parasagittal or bilateral. Deep venous thrombosis can produce bilateral thalamic abnormalities and altered consciousness.
Presentations include progressive or thunderclap headache, papilledema, seizures, focal deficits, and encephalopathy. Pregnancy and the postpartum period, estrogen exposure, infection, malignancy, inflammatory disease, and inherited or acquired thrombophilia are relevant risks. A normal noncontrast CT does not exclude CVT. D-dimer can be misleading, particularly with isolated headache or a delayed presentation, and should not replace imaging when clinical suspicion is meaningful.
Diagnose and Treat CVT
Use CT venography or MRI with appropriate venous imaging. Distinguish a true thrombus from normal sinus asymmetry, flow artifacts, or an arachnoid granulation. MRI also evaluates associated edema, infarction, and hemorrhage. Conventional angiography is reserved for selected diagnostic or interventional situations rather than required routinely.
Therapeutic anticoagulation is a principal treatment even when the venous infarct has hemorrhagic components, because the underlying problem is thrombosis and congestion. This differs from routine management of a primary anticoagulant-associated parenchymal hemorrhage. Select the agent and subsequent oral strategy according to pregnancy, renal function, procedures, thrombophilia, and bleeding risks with the stroke team. The presence of a hemorrhagic venous infarct is not an automatic instruction to withhold all anticoagulation.
Treat seizures when present and assess intracranial hypertension, visual risk, and the underlying trigger. If there is life-threatening mass effect, urgent decompressive surgery may be required. Endovascular rescue can be considered for selected patients deteriorating despite appropriate management; it is not routine for every CVT. A patient with impending herniation needs simultaneous stabilization and specialist decisions rather than waiting for anticoagulation alone to reverse the mass effect.
- Feature Ordinary arterial cerebral infarction Venous cerebral infarction
- Vascular problem Arterial inflow interruption Venous outflow obstruction
Imaging distribution Often a recognizable arterial territory May cross arterial boundaries; parasagittal or bilateral patterns
Hemorrhage Can complicate infarction or reperfusion Can result directly from venous congestion
Treatment implication Reperfusion eligibility and cause-specific prevention Anticoagulation is usually central despite hemorrhagic venous injury
Spinal Cord Infarction
Spinal cord infarction can follow aortic disease or intervention, profound hypoperfusion, embolism, dissection, or other vascular mechanisms. Some spontaneous cases have no immediately established cause. Abrupt back or neck pain, rapid weakness, sensory change, and bladder dysfunction should prompt consideration, but no single symptom is obligatory. Deficits often become severe over minutes to hours rather than evolving over many days.
An anterior spinal artery pattern can produce weakness and loss of pain and temperature below the lesion with relative preservation of vibration and position sense. Actual patterns vary because vascular anatomy and lesion extent vary. Early flaccidity and absent reflexes do not exclude a spinal cord lesion; upper motor neuron signs may emerge later. Differentiate the syndrome from cauda equina disease, inflammatory myelitis, spinal hemorrhage, abscess, and compressive tumor or disc disease.
Imaging and Immediate Priorities
Urgent MRI should exclude mechanical compression , a potentially treatable emergency. T2 and diffusion sequences may support ischemia, but small cord size and artifacts limit diffusion sensitivity. An early normal MRI does not settle the diagnosis; repeat imaging may be needed when the clinical pattern remains compelling. A vertebral body infarct or adjacent vascular lesion can strengthen the vascular explanation. CSF is often less inflammatory than in myelitis, but laboratory findings must be interpreted with timing and the differential.
Restore oxygenation and adequate perfusion, evaluate aortic pathology or another treatable vascular cause, and involve appropriate vascular, spine, and neurologic teams. Do not assume that IV cerebral thrombolysis or traumatic-SCI MAP augmentation evidence establishes a proven protocol for every spontaneous spinal infarct. Antithrombotic selection, CSF drainage after aortic procedures, and specific perfusion interventions depend on cause and local expertise.
Prevent secondary complications through respiratory assessment for high lesions, bladder care, pressure-injury prevention, thromboprophylaxis when safe, bowel management, and rehabilitation. Discuss uncertainty honestly: the initial clinical picture and imaging do not provide an exact personal recovery forecast.
Contrast the Two Vignettes
A postpartum patient with headache, seizure, and a hemorrhagic parasagittal lesion needs venous imaging and a CVT treatment assessment. An older patient with sudden paraplegia after an aortic procedure needs urgent cord and vascular evaluation, including exclusion of compression and correction of perfusion problems. Both can be missed if the clinician insists that all strokes must present as a unilateral MCA syndrome.
Sources checked October 17, 2026: AHA 2024 CVT statement and original spinal infarction diagnostic study .