Fig. 1.3–1 Sites of predilection for saccular intracranial aneurysms. 1, anterior communicating artery (25%); 2, origin of the posterior communicating artery (20%); 3, division point of the middle cerebral artery (15%); 4, supraclinoid internal carotid artery (10%); 5, tip of the basilar artery (< 10%).
1.3.1.2 Clinical findings
Patients are at risk from intracranial aneurysms, as they may rupture, usually leading to what is known as subarachnoid bleeding. This may also be associated with intraparenchymal bleeding. The acute clinical symptoms of subarachnoid bleeding (SAB) are highly varied, depending on its extent. They range from mild headache to sudden coma. Typically, there is a sudden-onset headache (thunderclap headache), accompanied by nausea and stiff neck. Neurological deficits and various degrees of disturbance of consciousness may also occur. The Hunt and Hess scale (Table 1.3-1) describes the severity of SAB and the surgical mortality risk. Associated vascular spasm with consequent circulatory disturbances and imminent infarction, as well as disturbed cerebrospinal fluid resorption with resultant hydrocephalus, can aggravate the clinical findings as well as the outcome. In the worst case, the bleeding may be so extensive that immediate relief of cerebral pressure becomes absolutely necessary.
Unruptured aneurysms are asymptomatic, or may become apparent as a result of their space-occupying character (known as paralytic aneurysms). These are usually very large or medium-sized aneurysms in the corresponding locations; typical examples include aneurysms in the posterior communicating artery with compression of the oculomotor nerve and consequent paresis of the ocularmuscles, and large aneurysms in the anterior circulation in contact with cranial nerves. Figure 1.3-10 shows an aneurysm in the anterior communicating branch with space-occupying effects on the optic nerve. Figure 1.3-5 illustrates the state after surgical treatment. In extremely rare cases, stroke may occur in association with very large, partly thrombosed aneurysms, due to thrombi embolizing of the aneurysm after forming at its neck when stenosis develop there, or simply due to the aneurysms’ space-occupying effect.
Table 1.3–1 The Hunt and Hess (HH) scale for assessing the severity and surgical risk of subarachnoid bleeding, correlated with the Glasgow Coma Scale (GCS) and World Federation of Neurologic Surgeons scale (WFNS).
Table 1.3–2 The Fisher CT classification of subarachnoid bleeding (SAB).
| Fisher 1 | No bleeding |
| Fisher 2 | SAB < 1 mm thick |
| Fisher 3 | SAB > 1 mm thick |
| Fisher 4 | SAB of any thickness with intraventricular spread or intracranial bleeding |
1.3.1.3 Diagnosis
SAB is usually demonstrated using a noncontrast CT (Fig. 1.3-2). Typically, reversal of contrast is seen between the brain parenchyma and the subarachnoid space. The Fisher classification of SAB describes its extent in the brain and postulates a connection with the occurrence of vasospasm (large amounts of blood = extensive spasm). In questionable cases, and particularly when the bleeding was a considerable time before, lumbar puncture may be necessary in order to demonstrate blood or siderophages in the cerebrospinal fluid.
In the acute setting, the vessels are usually imaged using CT angiography (CTA) or digital subtraction angiography (DSA). Many incidental aneurysms are identified using magnetic resonance angiography (MRA).
However, the gold standard is still DSA, in which the aneurysm is displayed directly with a catheter, usually introduced via the femoral access route. Very small aneurysms in particular can be identified in this way with greater certainty. Modern DSA workstations are equipped with solid-state detectors that allow direct digital imaging for three-dimensional rotation angiography or for measuring the aneurysm. Biplanar examination systems that allow simultaneous radiography at two levels are usually used (Fig. 1.3-3). DSA also has the advantage that endovascular treatment can be added or vasospasm can be treated in the same session. In some cases (approximately 10%), an aneurysm is not identified as the bleeding source in patients with clearly confirmed SAB. Two patterns need to be distinguished: in a typical case of perimesencephalic SAB (also known as a prepontine SAB), a little blood is seen on the CT immediately in front of the brainstem/mesencephalon.
Fig. 1.3–2a, b Subarachnoid bleeding in a patient with an aneurysm in the anterior communicating artery. (a) The CT shows subarachnoid bleeding as a hyperdensity in the basal cisterns, with a spherical gap in the position of the anterior communicating branch (arrow). There is a typical reversal of contrast between the cerebrospinal fluid and brain parenchyma. (b) The gap corresponds to the angiographically demonstrated aneurysm in the anterior communicating artery (anteroposterior projection) (arrow).
Fig. 1.3–3a-f Imaging of an aneurysm using three-dimensional techniques in digital subtraction angiography (DSA) and computed-tomographic angiography (CTA). (a) DSA imaging of a middle cerebral artery aneurysm on the right side. (b) CTA of the same aneurysm. (c, d) AP and lateral radiographic images of an aneurysm at the tip of the basilar artery. (e, f) 3D reconstruction of the aneurysm at the tip of the basilar artery before coiling (e) and after (f).
With this type of finding, no aneurysm is identified later either and the follow-up examination can be scheduled at a longer interval after the hemorrhage. When there is extensive SAB and an aneurysm is not identified, a repeat examination should be carried out at an early stage and further examinations should follow at appropriate intervals in order to exclude aneurysm with certainty.
1.3.1.4 Differential diagnosis
An SAB is considered to be excluded if the CT is negative and there is no evidence of erythrocytes on lumbar puncture. Differential-diagnostic considerations should then turn toward other causes of SAB, if there is no evidence of an SAB in connection with craniocerebral trauma.
Other vascular causes of spontaneous SABs include other types of cerebral or spinal vascular malformation (arteriovenous malformations, dural fistulas), vasculitides or dissections of intracranial vessels, rare brain tumors, coagulation disturbances, and thromboses in the venous sinuses.
When SAB occurs in connection with craniocerebral trauma, the following question always needs to be raised: did the accident occur because the patient had an SAB, or was the SAB exclusively a consequence of the trauma? In unclear cases, CTA, MRA, and/or DSA should be carried out.
Larger aneurysms may resemble a contrast-absorbing tumor of the skull base on imaging morphology and may be confused with meningioma or pituitary adenoma. This can usually be unambiguously