SCRN Exam

This chapter maps the arterial ring at the base of the brain, the territory supplied by each major artery, the collateral systems that keep the penumbra alive, and the venous sinuses that drain the brain. Expect SCRN items that ask you to match a deficit pattern to a territory or to explain why two patients with the same occlusion have very different outcomes.

The circle of Willis is an arterial ring at the base of the brain around the optic chiasm and pituitary stalk. It connects the two carotid systems with each other and with the vertebrobasilar system. Its components are the two ICAs, the two proximal (A1) segments of the ACAs joined by the anterior communicating artery (ACom), the two posterior communicating arteries (PCom) linking each ICA to the ipsilateral PCA, and the two proximal (P1) segments of the PCAs arising from the basilar tip.

The circle works as a pressure equalizer: if one ICA slowly narrows, blood can cross from the opposite carotid through the ACom or come forward from the basilar through a PCom. Only a minority of people have a complete, symmetric circle, and a patient with hypoplastic communicating segments may suffer a larger stroke from the same occlusion. In a fetal PCA, the PCA fills mainly from the ICA, so a carotid embolus can cause an occipital infarct.

The junctions of the circle are also the favorite sites of saccular (berry) aneurysms. The most common locations are the ACom, the junction of the ICA and PCom, the MCA bifurcation and the basilar tip. A PCom aneurysm can compress the oculomotor nerve, producing a dilated pupil with ptosis and a "down and out" eye, sometimes before rupture.

Each major cerebral artery has a predictable territory, and the SCRN expects you to link a territory to a deficit pattern quickly.

The MCA is the largest ICA branch and the most common site of embolic stroke because it continues the straight line of ICA flow. Its M1 segment gives off the lenticulostriate perforators to the basal ganglia and internal capsule, then divides into M2 branches. The superior division supplies the lateral frontal lobe (face and arm motor and sensory cortex, Broca area on the dominant side); the inferior division supplies the lateral temporal and inferior parietal lobes (Wernicke area on the dominant side, optic radiations).

The ACA travels forward and then over the corpus callosum along the medial surface of the hemisphere. It supplies the medial frontal and parietal lobes, including the part of the motor and sensory cortex that represents the leg and foot, the supplementary motor area and frontal micturition centers. The recurrent artery of Heubner, a branch near the ACom, supplies part of the caudate and the anterior limb of the internal capsule.

The PCA wraps around the midbrain to supply the occipital lobe (primary visual cortex), the medial and inferior temporal lobe (including the hippocampus, which handles new memory), and through thalamoperforating and thalamogeniculate branches much of the thalamus.

Watershed zones are the edges between two arterial territories, such as ACA-MCA or MCA-PCA borders, and receive the lowest perfusion pressure. With global hypotension (cardiac arrest, surgery, severe dehydration) or a severe carotid stenosis, they infarct first. An ACA-MCA watershed infarct can cause proximal arm and shoulder weakness with sparing of hand and face ("man in a barrel"); internal border-zone infarcts form a chain of small deep white matter lesions.

Collaterals are alternative channels that deliver blood to tissue when its main artery is blocked. They determine how long the penumbra survives and therefore how much brain a thrombectomy can save. Three levels are described.

Patients with robust leptomeningeal collaterals ("slow progressors") have a smaller core and larger penumbra at any time after onset, while those with poor collaterals ("fast progressors") lose tissue quickly. Collateral flow is pressure-passive, which is one reason permissive hypertension is used in patients who are not reperfused and why aggressive BP lowering before reperfusion can enlarge an infarct.

Brain venous blood drains first into superficial cortical veins and deep veins, then into the dural venous sinuses, channels between the two layers of dura. The superior sagittal sinus runs along the top of the falx in the midline and receives most cortical veins; the arachnoid granulations that absorb CSF project into it. The inferior sagittal sinus runs along the lower edge of the falx and joins the great cerebral vein (of Galen), which drains the deep structures, to form the straight sinus. The superior sagittal, straight and occipital sinuses meet at the confluence of sinuses (torcula) at the back of the skull. From there the paired transverse sinuses run laterally, become the S-shaped sigmoid sinuses and exit through the jugular foramen as the internal jugular veins. The cavernous sinuses lie on either side of the sella turcica and contain the ICA and cranial nerves III, IV, V1, V2 and VI.

Sinus occlusion raises venous pressure and impairs CSF absorption, producing headache, papilledema, seizures and hemorrhagic venous infarcts that ignore arterial territories. Keeping the head midline and avoiding neck flexion or tight endotracheal tube ties protects jugular outflow, which is why these measures are part of ICP management.

• The circle of Willis links both carotids and the basilar through the ACom and PComs, but many people have incomplete circles.
• MCA strokes affect face and arm more than leg; ACA strokes affect leg more than arm; PCA strokes cause contralateral hemianopia and memory problems.
• Watershed areas infarct first with global hypotension or severe proximal stenosis.
• Leptomeningeal collaterals keep the penumbra alive, are pressure-dependent, and explain why some patients benefit from late thrombectomy.
• Venous blood drains through dural sinuses to the internal jugular veins; the superior sagittal sinus is the most common site of venous thrombosis.