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2Brain

which normally appears black on this se-quence. Conventional or CT angiography isindicated for diagnosis and evaluation of anyunderlying cerebral aneurysm. These aretreated by surgical clipping or endovascularcoiling to prevent rehemorrhage. False-neg-ative angiograms may be due to vasospasm,incomplete visualization of the cerebral cir-culation, or suboptimal technique.

Perimesencephalic nonaneurysmal SAH is due to rupture of small arterioles or venules about the midbrain and pons. Pa-tients present with acute headache but without the depressed sensorium and se-vere neurologic symptoms of patients with acutely ruptured aneurysm.

Blood is usually small in volume and re-stricted to the perimesencephalic cisterns. Hydrocephalus or blood extending to the sylvian fissure or convexity sulci is uncom-mon and would be more typical of a rup-tured aneurysm. Given the consequences of failing to diagnose an acutely ruptured aneurysm, high-quality conventional an-giography is indicated. Because small an-eurysms can be missed due to suboptimal technique or vasospasm, angiography may need to be repeated, particularly if the study is less than perfect or if subtle vascu-lar abnormalities are detected.

Treatment of nonaneurysmal hemor-rhage is conservative and consists of symp-tomatic pain management. Ischemia or rebleeding rarely occurs (less than 1%), and the prognosis is excellent (Fig. 2.19).

◆Subarachnoid Hemorrhage

Most acute spontaneous SAH are due torupture of a saccular aneurysm, usually onearising from the branch points of the cere-bral arteries that make up the circle of Wil-lis. Blood fills the adjacent cerebral cisterns and can extend to the sylvian fissures and convexity subarachnoid space. Occasion-ally the jet of blood can lacerate the adja-cent brain, resulting in intraparenchymal,subdural, or intraventricular hemorrhage.

Patients are most often middle-aged and present with the sudden onset of se-vere headache, accompanied by variable depression of consciousness, meningis-mus, nausea/vomiting, or photophobia. The most immediate complication is acute hydrocephalus from obstruction of arach-noid granulations and compromise of CSF resorption, which may require urgent ven-triculostomy. Vasospasm develops hours to days after acute SAH and can lead to cere-bral ischemia and infarct.

CT shows hyperdense blood in the sub-arachnoid space in > 90% of patients imagedshortly after symptom onset but becomesless sensitive after 24–48 hours. If a lumbar puncture is performed, CSF will show ele-vated numbers of red blood cells in SAH, butthe study may be nondiagnostic in the first 12 hours because of procedure-inducedhemorrhage. CSF obtained after 12 hourswill be xanthochromic in true SAH, as redcell lysis will have taken place by that time.FLAIR MRI can sensitively identify SAH asincreased signal in the subarachnoid space,

Fig. 2.19a–fa–d Subarachnoid hemorrhage due to ruptured anterior communicating artery aneurysm. Nonen-hanced CT shows extensive blood within the suprasellar and perimesencephalic cisterns, intraparenchy-mal hemorrhage, intraventricular hemorrhage, and communicating hydrocephalus due to obstruction at the level of the arachnoid granulations. CTA and conventional angiograms demonstrate an 8-mm aneu-rysm interposed between the proximal right and left anterior cerebral arteries near their origin.

e,f Benign perimesencephalic subarachnoid hemorrhage. Blood is limited to the prepontine and interpe-duncular cisterns; no hydrocephalus.