ABPN Neurocritical Care key terms

The net pressure driving blood through the brain, calculated as mean arterial pressure minus intracranial pressure. Targets are set to preserve cerebral blood flow, typically 60 to 70 mmHg in adults after severe traumatic brain injury.

The principle that the skull is a rigid container holding brain, blood, and cerebrospinal fluid at constant total volume. Any increase in one component must be offset by a decrease in another or intracranial pressure rises.

The intrinsic ability of cerebral arterioles to dilate and constrict so that blood flow stays relatively constant across a range of mean arterial pressures. This mechanism is often impaired after severe brain injury.

A moving correlation between slow waves of intracranial pressure and arterial blood pressure used to gauge whether autoregulation is intact. Positive values suggest impaired reactivity and help individualize perfusion pressure targets.

The rate at which the brain consumes oxygen, reflecting neuronal activity and workload. It falls with sedation, hypothermia, and coma and rises with seizures or fever, coupling metabolic demand to blood flow.

The local matching of blood flow to neuronal activity, producing regional flow increases where neurons are active. It underlies functional imaging signals and is disrupted in several acute brain injuries.

The pressure within the cranial vault, normally under roughly 15 mmHg in adults. Sustained elevation threatens perfusion and can cause herniation, so it is monitored and treated in many acute brain injuries.

The change in intracranial volume per unit change in pressure, describing how well the brain tolerates added volume. Low compliance means small volume increases cause large pressure rises, signaling exhausted compensatory reserve.

Ultrasound through the skull that measures blood flow velocity in major cerebral arteries. It is used to detect vasospasm after subarachnoid hemorrhage and to assess flow patterns in raised intracranial pressure.

A calculated ratio of systolic-to-diastolic velocity difference over mean velocity in a cerebral artery. Rising values suggest increased distal resistance, as seen with elevated intracranial pressure or vasospasm.

New focal neurologic deficit or infarction occurring days after subarachnoid hemorrhage, often from vasospasm and microvascular dysfunction. It is a leading cause of poor outcome and drives nimodipine use and monitoring.

Bleeding into the subarachnoid space from a ruptured intracranial aneurysm, typically presenting with sudden severe headache. Management includes securing the aneurysm, preventing rebleeding, and treating hydrocephalus and vasospasm.

A dihydropyridine calcium channel blocker given orally or enterally after subarachnoid hemorrhage to reduce poor outcomes from delayed ischemia. It lowers blood pressure modestly and is not given intravenously.

Surgical removal of a skull flap to allow a swollen brain to expand and lower intracranial pressure. It is used for malignant cerebral edema, such as large hemispheric infarcts or severe traumatic contusions.

A large hemispheric ischemic stroke with progressive edema causing mass effect, herniation, and high mortality. Early decompressive surgery in selected patients reduces death and severe disability.

A catheter placed into the cerebral ventricles to measure intracranial pressure and drain cerebrospinal fluid. It is used for hydrocephalus, intraventricular hemorrhage, and refractory intracranial hypertension.

Infection of the ventricular system and ependyma, often complicating an external ventricular drain or shunt. It presents with fever, altered mentation, and cerebrospinal fluid pleocytosis and requires targeted antibiotics and device management.

Acute infection of the meninges requiring prompt empiric antibiotics and often dexamethasone before lumbar puncture when bacterial causes are suspected. Critical care focuses on sepsis, seizures, and raised intracranial pressure.

A continuous seizure or recurrent seizures without recovery lasting long enough to risk neuronal injury, conventionally five minutes for generalized convulsive events. It is a medical emergency requiring staged antiseizure and anesthetic therapy.

Seizures that persist despite adequate first- and second-line antiseizure drugs, requiring continuous intravenous anesthetic agents. These patients need airway support, continuous EEG, and monitoring for hemodynamic and metabolic complications.

Ongoing electrographic seizure activity without prominent motor signs, often presenting as unexplained altered consciousness. Diagnosis requires EEG, and it is common in critically ill patients with prior brain injury.

Prolonged bedside electroencephalography used to detect nonconvulsive seizures, track treatment response, and identify ischemia or encephalopathy patterns. It is central to managing coma, status epilepticus, and cardiac arrest survivors.

An EEG pattern of high-amplitude bursts separated by periods of near-flat suppression, produced by deep anesthesia or severe encephalopathy. It is a target for treating refractory status epilepticus with titrated anesthetics.

The fraction of an EEG epoch occupied by suppressed activity, used to quantify depth of anesthesia or encephalopathy. Higher ratios indicate deeper suppression and help titrate therapy in refractory status epilepticus.

A broad-spectrum antiseizure medication available intravenously with minimal drug interactions, commonly used for seizures in critically ill patients. It is often chosen for prophylaxis or treatment when hepatic metabolism and interactions are concerns.

Short-term antiseizure drug use after traumatic brain injury or neurosurgery to prevent early seizures. Prolonged prophylaxis is generally avoided because it does not prevent late epilepsy and adds adverse effects.

A 15-point bedside score of eye opening, verbal response, and motor response used to grade level of consciousness. It guides triage, prognosis, and brain death evaluation in acute neurologic injury.

The clinical process establishing irreversible loss of all brain function, including brainstem reflexes and the capacity to breathe. It requires a known cause, exclusion of confounders, and an apnea test with adequate preoxygenation.

A procedure confirming absence of respiratory drive during brain death evaluation by disconnecting ventilator support while monitoring carbon dioxide rise. Adequate preoxygenation and hemodynamic stability are required to avoid false results or cardiac arrest.

A state of unresponsiveness in which the eyes remain closed and there is no awareness of self or environment. It results from dysfunction of the reticular activating system or bilateral cerebral hemispheres.

A syndrome after severe brain injury with episodic fever, tachycardia, hypertension, tachypnea, and posturing triggered by stimulation. It is diagnosed after excluding other causes and treated with agents that blunt sympathetic outflow.

Transient left ventricular dysfunction with reduced ejection fraction and troponin release after acute brain injury, especially subarachnoid hemorrhage. It can cause pulmonary edema and shock and usually recovers over days to weeks.

Deficient antidiuretic hormone causing large volumes of dilute urine, hypernatremia, and volume depletion. It commonly follows pituitary injury or brain death and is managed with fluid replacement and desmopressin.

Renal sodium loss after brain injury causing hyponatremia and volume depletion, distinguished from SIADH by low effective circulating volume. Treatment is volume and sodium repletion rather than fluid restriction.

Low serum sodium that can worsen cerebral edema and trigger seizures, often from SIADH, cerebral salt wasting, or diuretics. Correction must be gradual to avoid osmotic demyelination, especially in malnourished patients.

Demyelination of the pons and extrapontine structures caused by overly rapid correction of chronic hyponatremia. It presents with dysarthria, dysphagia, quadriparesis, and locked-in features days after correction.

A concentrated sodium solution used to raise serum osmolality and reduce cerebral edema and intracranial pressure. It requires monitoring of sodium, osmolality, and renal function and is often given as boluses.

An osmotic diuretic given intravenously to lower intracranial pressure by drawing water from brain tissue. It can cause hypovolemia, hypernatremia, and renal injury, and serum osmolality is monitored during use.

Controlled cooling to a set temperature after cardiac arrest or for refractory intracranial hypertension, aimed at limiting secondary brain injury. It requires shivering control and careful rewarming to avoid hemodynamic and metabolic instability.

Hypoxic-ischemic damage to the brain after resuscitation from cardiac arrest, causing coma, seizures, and poor outcomes. Care includes temperature control, hemodynamic support, and multimodal prognostication before withdrawal decisions.

Combining clinical examination, EEG, somatosensory evoked potentials, imaging, and biomarkers to estimate neurologic outcome after coma from cardiac arrest. Multiple concordant findings are required before limiting life-sustaining treatment.

An ethically accepted decision to discontinue interventions that no longer provide acceptable benefit, after shared decision-making with surrogates. It is distinguished from euthanasia because the underlying disease causes death.

An opioid receptor antagonist that rapidly reverses opioid-induced respiratory depression and coma. It may precipitate withdrawal and agitation, so titrated dosing with monitoring is preferred in dependent patients.

Unconsciousness caused by drugs or poisons, often with characteristic pupil, respiratory, and motor findings. Management prioritizes airway protection, glucose and temperature control, antidotes when available, and prolonged observation.

A syndrome of headache, seizures, visual loss, and altered mentation with vasogenic edema on imaging, often from severe hypertension or immunosuppressants. Treatment targets the trigger and blood pressure control.

Hypotension and bradycardia from loss of sympathetic tone after cervical or high thoracic cord injury. It is treated with fluids, vasopressors, and atropine for bradycardia, after hemorrhagic shock is excluded.

A hemodynamic goal of maintaining mean arterial pressure around 85 to 90 mmHg for several days after acute spinal cord injury. The aim is to preserve cord perfusion, though evidence for benefit is limited.

Weakness of respiratory muscles from disorders such as Guillain-Barre syndrome or myasthenia gravis, leading to hypoventilation and aspiration risk. Monitoring vital capacity and negative inspiratory force guides intubation timing.

An acute immune-mediated polyneuropathy causing ascending weakness, areflexia, and sometimes autonomic instability. ICU care focuses on respiratory monitoring, pain control, and immunotherapy with IVIG or plasma exchange.

Severe weakness from myasthenia gravis with respiratory or bulbar compromise requiring ventilatory support. Triggers such as infection or medication changes are sought, and treatment includes plasma exchange or IVIG.