Fig. 1.2–3 Arterial supply to the telencephalon. Left: lateral view of the left hemisphere; right: medial view of the left hemisphere.
Fig. 1.2–4 Parts of the vertebral artery.
The right and left anterior cerebral artery are connected through the usually very short, thin anterior communicating artery, which rests directly in front of the pituitary stalk on the skull base. From the precommunicating part (the A1 segment), fine branches pass to the adjoining parts of the frontal lobe and to the hypothalamus and thalamus. The postcommunicating part (the A2 segment) follows the contour of the corpus callosum as far as its splenium, and branches arising from it supply the medial surface of the cerebral hemispheres to above their superior margin—with the exception of the corpus callosum itself.
Four parts of the vertebral artery are also distinguished (Fig. 1.2-4). The first segment, the prevertebral part, is generally given off dorsally as the last branch from the subclavian artery. Infrequently it arises directly from the aortic arch. In its transverse part, it enters the transverse foramen of the C6 vertebra from the caudal direction in 90% of cases and runs upward in the series of foramina as far as the transverse foramen of the atlas. Between C1 and C2, it always forms a loop, which often extends far laterally—a sign of the mobility of the atlantoaxial joint. The short atlantic part bends sharply at the posterior arch of the atlas and embeds itself there into the vertebral artery groove, surrounded by a dense venous plexus and lying tightly on the suboccipital nerve. At the medial end of the groove, which is sometimes closed to form a canal, it bends ventrally and—after penetrating the atlanto-occipital membrane and spinal dura mater—it reaches the subarachnoid space as the intracranial part. From the vertebral artery, which has a diameter of approximately 2.5 mm intracranially, the basilar artery forms in the pontocerebellar cistern, resting on the clivus, after the posterior inferior cerebellar artery has been given off (Figs. 1.2-2, 1.2-5). It is originally paired during embryonic development, and this explains some rare variations. From it emerge—in addition to the anterior inferior cerebellar artery and the superior cerebellar artery—numerous branches to the brain stem and inner ear, as well as to the meninges. Just before reaching the dorsum sellae, the basilar artery finally divides into the two posterior cerebral arteries, which in turn are connected to the two middle meningeal arteries via the posterior communicating arteries.
Fig. 1.2–5 The arterial circle.
From the precommunicating part (the P1 segment), small branches enter the posterior part of the mesencephalon, parts of the hypothalamus and internal capsule, as well as the posterior part of the thalamus. Branches from the postcommunicating part (the P2 segment) pass to the anterior part of the mesencephalon and to the thalamus. Finally, the terminal branch of the artery (the P3 and P4 segments) supplies the medial surface of the parietal lobe and the inferior surface of the temporal lobe, as well as the posterior pole of the telencephalon (Fig. 1.2-3b).
The arterial circle lies centrally at the base of the skull or brain (Figs. 1.2-2, 1.2-5). It is formed bilaterally from the anterior cerebral artery, the trunk of the internal carotid artery, the middle cerebral artery, the posterior communicating artery, and the posterior cerebral artery. The ring is closed anteriorly by the anterior communicating artery. The sizes of the individual arteries involved differ widely even in normal conditions. The communicating arteries are usually very thin, and bilateral circulatory compensation is thus hardly possible. Almost every conceivable variant is also found, from a different origin of the cerebral arteries to a complete absence of individual arteries.
1.2.2 Clinical picture
In Europe, stroke is the third most frequent cause of early invalidity, after cardiovascular and malignant diseases. Ischemic stroke is the most frequent etiological and pathologic cause, representing 85% of cases. Arteriosclerosis in the intracranial vessels is the cause of approximately 8–10% of all cases of ischemic stroke. The annual risk of stroke in patients with intracranial stenosis of more than 50% who have already suffered stroke or a transient ischemic attack (TIA) lies in the range of 12–14% even with drug treatment. In high-risk patients (those with higher-grade stenoses > 70%, those with current symptoms, and women), the annual risk may be as high as up to 23%. Clinically asymptomatic stenoses are associated with a low annual risk of stroke (< 3.5%). Due to the narrow caliber of the intracranial vessels, the exact percentage of stenoses is difficult to assess. Strictures of approximately 50% of the vascular lumen may already lead to clinical symptoms. The findings of the Warfarin-Aspirin Symptomatic Intracranial Disease (WASID) study showed that stenosis greater than 70% markedly increased the relative risk of suffering a subsequent ischemic stroke. Three percent of patients with low-grade stenoses (50–69%) suffered a TIA within 1 year, in comparison with 14% of those with higher-grade stenoses (> 70%). Cases of manifest stroke within 1 year occurred in 8% of patients with low-grade stenoses and in more than 23% of those with high-grade stenoses. The most frequent locations for intracranial stenoses are the internal carotid artery at the level of the siphon, the main trunk of the middle cerebral artery, the distal vertebral artery and the middle segment of the basilar artery. The significance of tandem stenoses and multiple intracranial stenoses is as yet unclear, but there is considerable evidence to suggest that each individual stenosis carries the corresponding risk of infarction and that the risk is then increased.
Intracranial vascular occlusions often arise due to emboli that originate in the heart or aortic arch or from stenotic cervical arteries. Rarer causes include thrombotic occlusions of existing stenoses. The site of an intracranial occlusion is often influenced by wall changes and stenoses that are already present.
1.2.2.1 Clinical symptoms
Vascular occlusion can lead to loss of neurological function (hemiplegia, speech disturbance, visual disturbance, ataxia, and unconsciousness), but it can also produce nonspecific symptoms such as headache and vertigo. The clinical symptoms depend on the capacity of the intracranial collateral circulation and the extent and location of the occluded vascular segment.
Ischemic stroke is classified according to its temporal course. If the symptoms completely resolve within 24 hours, it is called a transient ischemic attack (TIA). Otherwise it represents ischemic stroke syndrome. However, magnetic resonance imaging shows diffusion disturbances as the correlate of cerebral ischemia in up to 50% of cases that are clinically classified as TIAs. Additional classifications into prolonged reversible ischemic neurological deficit (PRIND) and reversible ischemic neurological deficit (RIND) have been abandoned.
1.2.3 Differential diagnosis
Intracranial stenoses and occlusions need not always be caused by arteriosclerosis. Other causes may include dissection, vasculitis, vasculopathy (e.g., fibromuscular dysplasia, moyamoya), vasospasm and vascular compression by extravascular space-occupying lesions.
Dissection is the most frequent cause of ischemic stroke in young adults. However, it is not always possible to confirm intracranial dissection beyond doubt using imaging diagnosis,