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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.
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is designated as compact. In diuse AVM a well-formed nidus is absent, and vessels traverse potentially eloquent brain.
It is dicult to detect small unruptured AVMs with noncontrast CT, and the radi-ologist should be sensitive to the subtle findings of asymmetrically enlarged feed-ing vessels and draining veins to do so. Up to 25% of AVMs have a calcified nidus, and this is sometimes the only NCCT finding. CT or MR angiography is useful for local-izing and determining the vascular supply of most AVMs, but comprehensive evalua-tion usually requires conventional catheter angiography, which can be performed in concert with therapeutic embolization.
Management depends on the anatomy, size, and location of the AVM. Options in-clude embolization, focused radiotherapy, surgical excision and combinations of these methods. In general, AVMs with superficial venous drainage have a better progno-sis than those with deep venous drainage (Fig. 2.20).
◆Arteriovenous Malformation
Arteriovenous malformations (AVMs) are developmental anomalies consisting of abnormal arteries and veins without in-tervening capillaries. They appear as a complex tangle of small vessels, the nidus, with enlarged feeding arteries and drain-ing veins. High-flow, rapid arteriovenous shunting is a physiologic feature, and most AVMs are presumed to enlarge over time. In an individual, an AVM may remain static, grow, or even regress, but the annual risk of hemorrhage for an untreated AVM is ap-proximately 3%, is cumulative, and increas-es with age. They are typically solitary, and if a patient has more than one, syndromes associated with vascular malformations, such as Wyburn-Mason and Osler-Weber-Rendu (hereditary hemorrhagic telangiec-tasia), should be considered.
Most AVMs are supratentorial and can be classified as either compact or diuse with respect to the nidus of anomalous vessels. If the nidus is small and contains little if any interposed neuronal tissue, it
Fig. 2.20a–f a,b Incidentally detected arteriovenous malformation. (a) NCCT. Focal hyperdensity along the anterior margin of the right anterior temporal lobe with subtle tubular elements. (b) T2WI. A small tangle of vas-cular ow voids in the right anteromedial temporal lobe is supplied by dilated feeding arteries arising from the middle cerebral artery and drained by a large subtemporal cortical vein that courses along the oor of the middle cranial fossa.
c–f Ruptured arteriovenous malformation. (c) NCCT. Right frontal parenchymal hemorrhage with intra-ventricular and subarachnoid extension. (d–f) CT and conventional angiograms. Small nidus of enlarged vessels at the posterolateral aspect of the hematoma along the dorsal aspect of the thalamus.
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incidentally. Symptomatic patients present with seizures or, if the malformation is lo-cated in an eloquent portion of the brain, focal neurologic deficits related to hemor-rhage or thrombosis.
CT findings are subtle and nonspecific. When visible, cavernous malformations usually appear as a vague, hyperdense, nonenhancing, subcentimeter parenchy-mal nodule and are sometimes mistaken for subacute traumatic hemorrhage. MRI is diagnostic and reveals a characteristic mulberry-like collection of blood products in dierent stages of evolution, often with a rim of surrounding low-signal