Arab Board Neurosurgery Part 1 key terms

The difference between mean arterial pressure and intracranial pressure, representing the pressure gradient that drives blood flow through the brain. It is the target variable in managing raised intracranial pressure after head injury.

The principle that the skull is a rigid container holding brain, blood and cerebrospinal fluid, so an increase in one component must be offset by a decrease in another. It explains why expanding mass lesions raise intracranial pressure.

The pressure exerted within the cranial vault, normally kept low by compensatory displacement of cerebrospinal fluid and venous blood. Sustained elevation risks herniation and reduced cerebral blood flow.

A 3-to-15-point bedside score summing eye opening, verbal response and motor response. It grades depth of impaired consciousness and is used to classify and track traumatic brain injury severity.

Widespread traumatic shearing of white matter tracts from rotational acceleration-deceleration forces, often with hemorrhage at the grey-white junction. It causes prolonged coma disproportionate to findings on initial CT.

A collection of blood between the skull and dura, usually from a torn middle meningeal artery after temporal bone fracture. It classically produces a lucid interval followed by rapid deterioration and a biconvex CT appearance.

Blood accumulating between the dura and arachnoid, typically from torn bridging cortical veins. It appears crescent-shaped on CT and is classified as acute, subacute or chronic.

Patterns of brain tissue displacement across intracranial compartments when pressure gradients develop, such as uncal, subfalcine, transtentorial and tonsillar herniation. Each produces characteristic focal signs and risk of brainstem compromise.

The intrinsic ability of cerebral arterioles to adjust caliber and keep blood flow relatively constant across a range of perfusion pressures. It can be impaired by trauma, ischemia and severe hypertension.

The volume of blood delivered to brain tissue per unit time, normally about 50 mL per 100 g per minute. Flow below roughly 20 mL/100 g/min produces electrical failure and below 10 mL/100 g/min produces infarction.

Hypoperfused brain tissue that is electrically silent but still viable around an infarct core. It is the target of reperfusion therapy because rapid restoration of flow can salvage it.

Flow of fluid produced mainly by choroid plexus through the ventricles and subarachnoid spaces to be absorbed by arachnoid granulations. Obstruction anywhere along this route causes hydrocephalus.

Ventricular enlargement from impaired absorption of cerebrospinal fluid at the arachnoid granulations or from venous hypertension, without obstruction within the ventricular system. The ventricles and subarachnoid spaces are in continuity.

A minimally invasive operation creating a stoma in the floor of the third ventricle to let cerebrospinal fluid bypass an obstruction in the aqueduct. It is preferred in obstructive hydrocephalus when anatomy permits.

A selective interface formed by tight junctions between capillary endothelial cells, astrocyte end-feet and pericytes that restricts entry of many solutes into brain parenchyma. Its disruption underlies vasogenic edema and affects drug delivery.

Extracellular fluid accumulation in white matter caused by breakdown of the blood-brain barrier and leakage of plasma proteins. It spreads along white matter tracts and responds to corticosteroids in tumor-related cases.

Intracellular swelling of neurons and glia from failure of energy-dependent ion pumps, as in acute ischemia. Water shifts into cells, so the tissue becomes swollen with reduced extracellular space.

The most common malignant primary brain tumor in adults, an astrocytic neoplasm with necrosis and microvascular proliferation. It is infiltrative, typically treated with resection, radiotherapy and temozolomide.

A usually benign extra-axial tumor arising from arachnoid cap cells, often dural-based and enhancing homogeneously with a dural tail. It compresses adjacent brain rather than invading it.

An abnormal focal outpouching of a cerebral artery wall, most often at branch points of the circle of Willis. Rupture causes subarachnoid hemorrhage, and treatment options are clipping or endovascular coiling.

Bleeding into the subarachnoid space, classically from a ruptured aneurysm and presenting with sudden severe headache. Complications include rebleeding, vasospasm and hydrocephalus.

Delayed narrowing of cerebral arteries after subarachnoid hemorrhage, usually peaking several days after the bleed. It can cause secondary ischemic deficits and is managed with nimodipine and hemodynamic support.

A congenital tangle of abnormal vessels with direct arterial-to-venous shunting and no intervening capillary bed. It carries risks of hemorrhage and is treated by embolization, radiosurgery or microsurgical excision.

Delivery of highly focused, image-guided radiation in a single session to ablate a target while sparing surrounding tissue. It is used for small tumors, arteriovenous malformations and selected functional disorders.

Implantation of electrodes into deep brain nuclei with programmable electrical stimulation to modulate abnormal circuits. It is used in Parkinson disease, essential tremor and dystonia.

A descending motor pathway from motor cortex through the internal capsule, cerebral peduncle, pyramid and decussation to synapse on lower motor neurons. Its fibers cross in the medulla, so each hemisphere controls the opposite side.

Damage to descending motor pathways above the anterior horn cell, producing spastic weakness, hyperreflexia, extensor plantar responses and loss of fine dexterity. Findings are contralateral to a hemispheric lesion.

Injury to the anterior horn cell, nerve root or peripheral nerve, producing flaccid weakness, muscle wasting, fasciculations and reduced reflexes. It localizes the lesion to the final common pathway.

Symptoms from compression or irritation of a spinal nerve root, causing pain and sensory change in a dermatomal pattern with weakness in the corresponding myotome. Common causes are disc herniation and foraminal stenosis.

Dysfunction of the spinal cord itself, producing a sensory level, spastic weakness, sphincter disturbance and gait difficulty. Causes include compressive spondylosis, tumor, trauma and inflammation.

Incomplete spinal cord injury, often after hyperextension in a stenotic canal, damaging central cord fibers first. It causes greater weakness in the arms than the legs with variable sensory loss.

Compression of the lumbosacral nerve roots below the conus medullaris, causing saddle anesthesia, bladder retention and lower limb weakness. It is a surgical emergency requiring urgent decompression.

Downward displacement of cerebellar tonsils through the foramen magnum, often with syringomyelia or hydrocephalus. It can cause tussive headache, brainstem signs and progressive myelopathy.

A fluid-filled cavity within the spinal cord that expands and damages crossing spinothalamic fibers, producing a cape-like loss of pain and temperature sensation. It often accompanies Chiari malformation or cord tethering.

Premature fusion of one or more cranial sutures, restricting skull growth and producing characteristic head shapes. It may raise intracranial pressure or cause airway, orbital and developmental problems.

Compression of the median nerve within the carpal tunnel, causing nocturnal numbness and pain in the thumb, index and middle fingers with thenar weakness. Diagnosis is clinical, supported by nerve conduction studies.

Electrical recordings of responses from the auditory nerve and brainstem pathways to sound stimuli. They assess brainstem function and are used in intraoperative monitoring and hearing evaluation.

Signals recorded over the scalp after electrical stimulation of a peripheral nerve, reflecting conduction through the dorsal columns and sensory cortex. They are used for intraoperative monitoring and prognostic assessment.