ABEM Neurocritical Care key terms

A 10-point CT scoring system that subtracts one point for each of ten defined middle cerebral artery territory regions showing early ischemic change; lower scores indicate larger established infarction and worse expected outcome.

Blockage of a major intracranial artery such as the internal carotid, proximal middle cerebral, or basilar artery, usually by thrombus; it produces severe deficits and is the target of endovascular therapy.

Endovascular removal of clot from a large intracranial artery using a stent retriever or aspiration catheter, selected by imaging and time from onset; it improves functional outcome in eligible patients.

A large hemispheric infarct that swells over the first days, causing mass effect, midline shift, and raised intracranial pressure with high mortality; decompressive surgery may be offered to selected patients.

Bleeding into the subarachnoid space from a ruptured intracranial aneurysm, typically presenting with sudden severe headache; complications include rebleeding, vasospasm, hydrocephalus, and delayed cerebral ischemia.

New focal deficit or imaging infarction developing days after subarachnoid hemorrhage through vasospasm, microthrombosis, and impaired autoregulation; nimodipine, surveillance, and careful blood pressure support reduce its impact.

The principle that the skull is a fixed container holding brain, blood, and cerebrospinal fluid at constant total volume; expansion of one compartment must be offset by another or intracranial pressure rises.

The gradient driving cerebral blood flow, calculated as mean arterial pressure minus intracranial pressure; it is supported with sedation, osmotherapy, and vasopressors to keep the injured brain perfused.

Widespread shearing damage to white matter tracts from rotational acceleration-deceleration forces, often with punctate hemorrhages at gray-white junctions; patients may have prolonged coma despite a relatively unremarkable initial CT.

A six-category system describing traumatic brain injury on CT by presence of mass lesions, midline shift, and basal cistern effacement; it stratifies severity and helps predict outcome.

Loss of sympathetic vascular tone after high cervical or upper thoracic cord injury, producing hypotension with bradycardia and warm skin; treated with cautious fluids and vasopressors such as norepinephrine.

A hypertensive emergency in chronic spinal cord injury above T6, triggered by a noxious stimulus below the lesion and marked by severe hypertension, headache, and bradycardia; treat by removing the trigger and lowering pressure.

A standardized bedside examination grading spinal cord injury from A (complete) to E (normal) using sacral sparing of motor, sensory, and anal function; it guides prognosis and communicates deficits reliably.

Continuous seizure activity, or repeated seizures without recovery between them, lasting five minutes or more; treated in stages with benzodiazepines, then antiseizure drugs, then anesthetic infusions.

Ongoing electrographic seizure activity without prominent motor signs, often presenting as unexplained altered consciousness; diagnosis requires EEG and treatment follows the same escalating pathway as convulsive status.

Seizures that persist despite adequate first- and second-line antiseizure medication, requiring anesthetic infusions such as midazolam, propofol, or ketamine under continuous EEG monitoring.

EEG patterns such as lateralized periodic discharges that are neither definite seizures nor clearly benign; management requires clinical correlation and sometimes a treatment trial for subtle clinical change.

Severe worsening of myasthenia gravis causing respiratory muscle weakness and airway compromise, often triggered by infection or medication change; managed with ventilation, plasma exchange or IVIG, and avoidance of harmful drugs.

An acute immune-mediated polyneuropathy causing ascending weakness and areflexia, with risk of respiratory failure and dysautonomia; treated with plasma exchange or IVIG, not corticosteroids.

Weakness of breathing muscles from nerve, neuromuscular junction, or muscle disease, detected by falling vital capacity and inspiratory force; tracked with serial bedside measurements and supported with noninvasive or invasive ventilation.

Prolonged bedside electroencephalographic recording used to detect nonconvulsive seizures, follow treatment of status epilepticus, and assess background reactivity in patients who cannot be examined reliably.

Ultrasound through skull windows measuring blood flow velocity in major cerebral arteries; rising middle cerebral artery velocities suggest vasospasm after subarachnoid hemorrhage.

Contrast CT with post-processing that estimates cerebral blood flow, blood volume, and tissue transit time, separating infarct core from salvageable penumbra before reperfusion therapy.

A catheter placed into a lateral ventricle to measure intracranial pressure and drain cerebrospinal fluid; risks include infection, hemorrhage, and malposition.

A probe placed in white matter measuring local partial pressure of oxygen; low values prompt correction of hypoxemia, anemia, and inadequate perfusion pressure in severe traumatic brain injury.

A device that objectively measures pupil size and reactivity to a light stimulus, yielding a numeric index used to detect herniation and to inform neurological prognosis.

Transient left ventricular dysfunction with regional wall motion abnormalities and troponin release after acute brain injury, driven by catecholamine surge; it can cause hypotension and pulmonary edema.

Renal sodium loss after brain injury or hemorrhage causing hyponatremia with reduced circulating volume; treated with saline and sodium replacement rather than fluid restriction.

Excess antidiuretic hormone causing euvolemic hyponatremia with concentrated urine; in neurocritical care it is distinguished from cerebral salt wasting by volume status and managed with fluid restriction.

A rare but often fatal complication of high-dose prolonged propofol causing metabolic acidosis, rhabdomyolysis, arrhythmias, and renal failure; prevented by limiting dose and duration and monitoring laboratory values.

Generalized limb and respiratory muscle weakness developing during critical illness from disuse, inflammation, and medication effects; it prolongs ventilation and complicates weaning and rehabilitation.

Controlled cooling or maintenance of a set body temperature for a defined period, used after cardiac arrest and in selected refractory intracranial hypertension, with attention to shivering, electrolytes, and hemodynamics.

Combining examination, EEG, somatosensory evoked potentials, and blood biomarkers at defined time points to estimate neurological outcome after cardiac arrest, avoiding reliance on any single test.

Loss of the cortical response after median nerve stimulation, assessed at least 24 to 72 hours after arrest; a strong but imperfect predictor of poor outcome that must be interpreted alongside other findings.

A neuronal enzyme released into blood after brain injury; high values after cardiac arrest support a poor prognosis, though hemolysis and sampling timing affect the result.

The final clinical step of brain death determination: disconnecting the patient from the ventilator while monitoring for respiratory effort as carbon dioxide rises above a threshold.

Decisions to stop or limit therapies judged non-beneficial, ideally after multimodal assessment and family discussion; in neurocritical care it strongly shapes observed outcomes.

Bias in prognosis when early pessimistic predictions lead to withdrawal of treatment, making the predicted poor outcome more likely and inflating the apparent accuracy of the predictor.