Emerg Radiol DOI 10.1007/s10140-014-1251-z

PICTORIAL ESSAY

Cerebral convexity subarachnoid hemorrhage: various causes and role of diagnostic imaging Rajiv Mangla & Douglas Drumsta & Jeevak Alamst & Manisha Mangla & Michael Potchen

Received: 8 April 2014 / Accepted: 17 June 2014 # American Society of Emergency Radiology 2014

Abstract Computed tomography (CT) and magnetic resonance imaging (MRI) have made it relatively easy to diagnose cortical convexity subarachnoid hemorrhages (cSAH); however, the evaluation of these hemorrhages should not be limited to size and location. It is imperative that possible underlying etiologies be identified so that clinicians may properly treat and prevent this potentially catastrophic event. The goal of this article is to review etiologies of cortical convexity subarachnoid hemorrhages, from common causes such as cerebral amyloid angiopathy to less common causes such as reversible cerebral vasoconstriction syndrome and moyamoya. The specific imaging findings of each etiology that may be responsible for these hemorrhages are described in this article so that the radiologist may properly aid in the diagnosis of the underlying cause.

R. Mangla (*) : D. Drumsta : J. Alamst : M. Mangla : M. Potchen Department of Imaging Sciences, University of Rochester Medical Center, 601 Elmwood Avenue, Box 648, Rochester, NY 14642, USA e-mail: [email protected] D. Drumsta e-mail: [email protected] J. Alamst e-mail: [email protected]

Keywords Subarachnoid hemorrhage . Cerebral amyloid angiopathy . Stroke . Cerebral hemorrhage

Introduction Cerebral convexity subarachnoid hemorrhages are commonly seen secondary to trauma; however, there are also a variety of nontraumatic causes. Nontraumatic cerebral convexity subarachnoid hemorrhage (cSAH) is a less reported condition. This type of hemorrhage is usually located in one or few cortical sulci of the brain and does not involve the basal cisterns, the sylvian fissure, or the ventricles. It has been associated with various symptoms and etiologies. Focal neurological deficits are often the presenting symptom. Headaches and nuchal rigidity which are typical for other subarachnoid hemorrhages can occur but may not be the sole clinical symptom at onset [1]. Once cSAH is seen on computed tomography (CT) or magnetic resonance imaging (MRI), it needs to be further investigated with a complete noninvasive parenchymal as well as vascular imaging protocol. Moreover, there is often a need for a systematic and multimodal approach in recognizing underlying causative disorders. The goal of this paper is to illustrate many of the causes of nontraumatic cortical convexity subarachnoid hemorrhages so that the interpreting physician can develop an accurate differential diagnosis.

M. Mangla e-mail: [email protected]

Etiologies of cSAH

M. Potchen e-mail: [email protected]

Radiologically, spontaneous cSAH carries a broad differential diagnosis. It has been more frequently reported

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in the setting of reversible vasoconstriction syndrome in younger patients and with amyloid angiopathy in the

Fig. 1 Mimics of SAH on FLAIR images: T2 FLAIR images in various patents showing mimics of cSAH. In a, the hyperintensity in sulci in frontal lobes is related to susceptibility from the frontal sinus, while in b, it is related to susceptibility from mastoid air cells on the right side. c Hyperintensity due to supplemental oxygen. The hyperintensities in cerebral sulci noted in 1 day are related to collateral vessels in a moyamoya patient

older population [2]. Many other causes have been associated with cSAH.

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Clinical presentation

Neuroimaging

The clinical presentation of cSAH differs from that of basal subarachnoid hemorrhage (SAH). Sudden onset of intense headache and nuchal rigidity, both classical signs of aneurysmal SAH, occurs less frequently in cSAH which may be due to the lack of blood in the basal cisterns or posterior fossa. Moreover, cSAH has comparably a smaller amount of blood. Onset can be sudden or gradual, and symptoms are usually in form of altered mental status or focal neurological defects like weakness, numbness, dysarthria, aphasia, or ataxia [3]. Focal or generalized seizures can also occur in these patients. The seizures and focal neurologic deficits may be due to the local effect of subarachnoid blood adjacent to the cortex. The clinical symptoms relate closely to the location of the SAH. For example, recurrent partial seizures with motor signs contralateral to the cSAH in the central sulcus have been reported [4]. Many times, symptoms may not be related to the SAH itself but possibly due to the underlying disease, such as cerebral thrombosis or posterior reversible encephalopathy syndrome.

Convexity subarachnoid hemorrhage is usually seen in one or a few of the sulci in convexity of the brain and is unilateral in most cases. The radiological presentation of cSAH is thus different from that of ruptured aneurysms and nonaneurysmal perimesencephalic SAH where blood is centered in the basal cisterns and fissures. Nonenhanced head CT is the first investigation performed, but the sensitivity declines rapidly if small hemorrhage is present [5]. Brain MRI is usually crucial to the detection of the underlying cause. At the author’s institution, once cSAH is detected on CT, it is usually further investigated with computed tomography angiography (CTA) and MRI of the brain which include susceptibility-weighted imaging. Eventually, catheter angiography is done if no cause is detected on MRI or noninvasive angiography. These investigations deem to be appropriate in proven SAH as per ACR practice guidelines. Contrast-enhanced MR venography is included in the protocol if clinical symptoms suggest venous sinus or cortical vein thrombosis (CVT). Despite extensive workup, no apparent cause of cSAH may be detected in up to 40 % cases [6].

Fig. 2 A 68-year-old male presented with transient rightsided weakness. CT showed subarachnoid hemorrhage. The T2 FLAIR images confirmed the cSAH. GRE images show small SAH (a). The enhanced susceptibility images SWAN in this case (b) revealed microbleeds and superficial siderosis suggesting the diagnosis of cerebral amyloid angiopathy

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MR imaging has better sensitivity for small cSAH. The MR protocol should include T2 fluid attenuated inversion recovery (FLAIR), gradient echo sequence (GRE) T2, T1 sequences, diffusion weighted imaging (DWI), magnetic resonance angiography (MRA), and post-gadolinium T1weighted imaging [7]. The T2 FLAIR sequence has been found to be superior but nonspecific for the diagnosis of SAH. In the study on lowgrade subarachnoid hemorrhage, CT could detect it only in 66 % of cases while FLAIR had sensitivity of 100 % [8]. Besides SAH, the hyperintensity of cerebrospinal fluid on FLAIR sequence may also be encountered in many important pathological conditions like meningitis and leptomeningeal metastasis. Gadolinium-enhanced MRI can be useful in distinguishing SAH from other conditions. However, certain nonpathological states in which there is no definite cerebrospinal fluid abnormality can also present with hyperintense cerebrospinal fluid [9]. For example, intravenously administered propofol and inhaled 100 % oxygen can commonly mimic SAH on FLAIR images. The various artifacts like

Fig. 3 CAA: T2 FLAIR (a) and GRE (b) sequences demonstrate a left frontoparietal subarachnoid hemorrhage. Further analysis of the GRE sequence (c) reveals punctate foci of susceptibility artifact in the left cerebral hemisphere, consistent with microhemorrhages from Bamyloid deposition

cerebrospinal fluid flow-related artifacts, magnetic susceptibility artifact, truncation artifact, chemical shift artifact, and technical factors like suboptimal inversion time and overlapping of imaging planes can also mimic SAH. Knowledge of these artifacts and mimics is also essential to arrive at the correct diagnosis of cSAH [10] (Fig. 1). GRE T2 is also a very important sequence in neuroimaging of cSAH due to its exquisite sensitivity to the magnetic susceptibility effect from the decomposition products of hemoglobin. Although GRE T2 is less sensitive than FLAIR for the detection of acute SAH, the former is still extremely useful because it may confirm the hemorrhagic nature of the sulcal abnormality. Thus, GRE T2 rules out other causes of hyperintense sulcal abnormality which can be seen in conditions like meningitis, leptomeningeal collaterals, or meningeal carcinomatosis. This sequence is also extremely helpful in diagnosing superficial siderosis, old intraparenchymal hemorrhage cerebral microbleeds. In these situations, GRE has about 100 % sensitivity as compared to the T1-weighted images (36.4 %) and FLAIR (33.3 %) [11]. Moreover, it can

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help in the diagnosis of possible cerebral cortical or dural venous thrombosis and microbleed seen in infective endocarditis [12]. Enhanced susceptibility imaging (ESI) techniques have recently gained popularity for being more reliable and more sensitive for cerebral microbleed (CMB) detection as compared to GRE [13]. These have been commercialized as susceptibility-weighted imaging (SWI) by Siemens (T2-star susceptibility-weighted angiography (SWAN) by General Electric and phase differenceenhanced imaging (PADRE) by Philips imaging. Improved detection of CMBs by these “high-end” sequences may contribute to more accurate identification of the underlying cause of cSAH (Fig. 2). If available, these should be the preferred sequences and be included in the MRI protocol. If these sequences are not available, the section thicknesses of GRE sequence may be reduced to 2–3 mm or imaging can be performed on higher magnetic field strengths to improve the lesion detection. Noninvasive angiography (CTA or MRA) of the brain should always be included in the workup of cSAH. With

Fig. 4 Reversible cerebral vasoconstriction syndrome (CallFleming syndrome: CT 4 (a) and T2 FLAIR 4 (b) images of the brain demonstrate a left frontal subarachnoid hemorrhage (arrow). Subsequent cerebral angiogram image 4 (c) demonstrates multifocal stenosis (arrow). A follow-up cerebral angiogram image 4 (d) performed 1 month later reveals resolution of the multifocal stenosis (arrow), consistent with RCVS

better resolution and easy availability, CTA is preferred over MRA. However, due to radiation dose, MRA could be the preferred modality in pediatric population. Brain angiography may suggest vascular malformation, vasculitis, or vasospasm. Significant internal carotid artery (ICA) atheromatous disease causing stenosis or complete thrombosis has also been reported as a cause, and therefore, imaging of the extracranial vasculature is essential in the diagnostic workup. Digital subtraction angiogram (DSA) should follow CT and MRI, if an underlying pathology cannot be identified. DSA is superior to CTA and MRA to detect various vascular abnormalities which many times cannot be detected by non invasive imaging. Pial arteriovenous malformations and dural arteriovenous fistulae can be missed on noninvasive imaging. The abnormalities in medium- or small-sized arteries, suspicious of vasculitis, and circumscribed cortical venous thrombosis can also be better detected with DSA. Black-blood fat-suppressed pre- and postcontrast T1weighted images can potentially improve better visualization of the arterial wall from the lumen and the

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surrounding tissue. It has been shown that thickening and contrast uptake in the arterial wall can be suggestive active cerebral vasculitis [14]. Serologic and cerebrospinal fluid (CSF) evaluation Serological evaluation and CSF analysis can provide corroborative information in support of a specific diagnosis. The pleocytosis, elevated protein, and increased IgG in CSF may suggest vasculitis. Thrombocytopenia secondary to end-stage liver failure and coagulopathy due to various causes need to be evaluated in diagnostic work up of SAH [1]. Various etiologies of cSAH Cerebral amyloid angiopathy Cerebral amyloid angiopathy (CAA) is the most common cause of cSAH in more than 60-year-old patients. Prevalence and severity of the sporadic form increase with age. The hereditary form has a

Fig. 5 Postpartum cerebral angiopathy: CT image 5 (a) and T2 FLAIR 5 (b) images of the brain demonstrate a right occipital and left parieto-occipital subarachnoid hemorrhage. A subsequent cerebral angiogram of image 5 (c, d) was performed which revealed multifocal stenosis (arrows) of the mediumand small-caliber cerebral arteries in the anterior circulation which is suggestive of postpartum cerebral angiopathy

broader range of clinical symptoms and can be seen at a much younger age. Headache is usually not the presenting symptom, and patients usually present with transient focal neurologic symptoms resembling TIAs or with a sudden neurologic deficit secondary to intracranial hemorrhage [15]. On imaging, the hemorrhage is restricted to a few sulci. CT is not sensitive for the diagnosis of CAA and SAH may not be seen at all or it can be seen as subtle hyperdensity within a sulcus which may initiate a series of investigations. The GRE sequence is also extremely helpful in diagnosing superficial siderosis, old intraparenchymal hemorrhage (>5 mm), or cerebral microbleeds (≤5 mm). The vast majority of patients may also have multifocal and confluent areas of white matter hyperintensity on T2/FLAIR scans. Identification of old CMB is very important for the diagnosis of CAA as per the Boston criteria [15]. Cortical hemosiderosis (CHS) along with microbleeds particularly in a

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superficial location without any other evident cause are considered strongly suggestive of CAA [16]. Cerebellar microbleeds are much less common in CAA as compared to hypertensive microhemorrhages. It has also been reported that the sulcal hemorrhage in CAA might have a propensity to involve the central sulcus [17]. Once the SAH is diagnosed in a case of CAA, it needs to be followed up closely as large subcortical hemorrhage can occur [18]. The pathogenesis of CAA-related cSAH remains unclear. It is still debated whether primary bleeding occurs in the cerebral

Fig. 6 Posterior reversible encephalopathy syndrome (PRES): CT (a) and T2 FLAIR (b) images through the brain demonstrate a left frontal subarachnoid hemorrhage. T2 FLAIR images (c) through the brain in the same patient demonstrate cortical and subcortical areas of increased signal in the occipital and temporal lobes. T2 washout (arrows) is seen on the DWI (d) and ADC (e) maps

cortex rather than directly in the subarachnoid space as a consequence of ruptured meningeal vessels. Several pathological studies on CAA have demonstrated a more severe involvement of leptomeningeal than cortical arteries [19] (Fig. 3).

Vasculopathies Vasculopathies are heterogeneous group of conditions with considerable diversity.

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Vasoconstriction syndromes These are the most common causes of cSAH in the young population. Reversible cerebral vasoconstriction syndrome (RCVS) (CallFleming syndrome) Patients present with a “thunderclap headache” and focal neurologic deficits. In a series of 67 consecutive patients with RCVS, cSAH has been reported in 22 % of patients [20]. Multifocal segmental narrowing alternating with normal-caliber arteries or focal dilations can be seen with MRA, CTA, or DSA. DSA is the most sensitive due to higher resolution. The timing of the angiography is also important and initial angiograms may be normal. Angiographic findings may be more apparent during days to weeks after the onset of symptoms. The absence of serologic or spinal CSF abnormalities is important and rules out inflammation of the vessels. The exact pathophysiology is unknown; however, the suspected etiology involves a transient disturbance in the control of cerebral vascular tone. It

Fig. 7 CNS vasculitis: CT (a) and T2 FLAIR (b) images of the brain demonstrate a right frontal subarachnoid hemorrhage (arrows). A subsequent cerebral angiogram (c, d) was performed which reveals multifocal stenosis (arrows) consistent with the diagnosis of CNS vasculitis

has been associated with a postpartum state and vasoactive substances such as cocaine, SSRIs, cyclophosphamide, and amphetamine derivatives among others (Fig. 4). Postpartum cerebral angiopathy Postpartum cerebral angiopathy (PCA) occurs in normotensive postpartum women within 1–4 weeks of delivery. The angiographic features are characterized by reversible multifocal stenoses and a beaded appearance of the medium- and small-caliber cerebral arteries in the anterior circulation. This is in contradistinction to eclampsia, which affects large- and medium-sized arteries in the posterior circulation [21] (Fig. 5). Posterior reversible encephalopathy syndrome (PRES) The exact etiology is controversial but theories include hypertension with failed autoregulation and hyperperfusion and alternatively endothelial injury with hypoperfusion and vasoconstriction. PRES most commonly involves the parietal and occipital lobes (Fig. 6). Hemorrhage occurs in approximately 15 % of patients [22].

Emerg Radiol Fig. 8 High-grade arterial stenosis/occlusion: CT (a) and T2 FLAIR (b) images of the head demonstrate a subtle subarachnoid hemorrhage within the left watershed region of the middle cerebral artery and posterior cerebral artery (red arrow). CTA of the neck (c) demonstrates occlusion of the left ICA at its origin

Vasculitis Vasculitis is a generic term which denotes inflammation of blood vessels affecting arteries, veins, or both and is

Fig. 9 Arterial dissection: CT scan of the head image 9 (a) demonstrates a right temporal subarachnoid hemorrhage. Cerebral angiogram image 9 (b, c) reveals irregularity of the V4 segment of the right vertebral artery (white arrow) consistent with a dissection. Also, there is a resulting pseudoaneurysm (red arrow)

characterized histopathologically by inflammation of the blood vessel walls. In most cases, patients present with nonspecific neurologic symptoms like headache and encephalopathy. In a few cases, the first imaging manifestation of

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vasculitis can be cSAH. MRI may show multifocal lesions involving the hemispheric cortex and subcortical white matter together with the basal ganglia. Diffusion-weighted image may reveal restriction of diffusion in a gyriform pattern. T2 GRE or SWI may show parenchymal microbleeds in some cases. Angiography usually reveals multiple segmental arterial narrowing and lumen irregularities mainly involving the medium- and small-sized arteries [23, 24]. The pattern of abnormal findings on catheter angiography is often nonspecific. The important differential diagnosis could include intracranial atherosclerotic disease (ASD) and vasospasm. ASD usually has involvement of the extracranial carotid arteries and carotid siphons.

However, even a negative brain biopsy does not rule out isolated CNS vasculitis [25]. Secondary CNS vasculitis Secondary CNS vasculitis may be due to a variety of conditions including collagen-vascular disease, infection, drug abuse, malignancy, or autoimmune diseases. The most common presentation is stroke-related symptoms.

Abnormalities of cervicocerebral arteries Carotid artery stenosis or occlusion

Primary central nervous system (PCNS) vasculitis The diagnosis of PCNS vasculitis is often challenging. The changes on MRI and angiography can be nonspecific. The changes are usually best depicted on catheter angiogram (Fig. 7). In many cases, brain biopsy is the only useful diagnostic study.

Fig. 10 dAVF: T2 FLAIR image 10 (a) and GRE image 10 (b) sequences demonstrate a small subarachnoid hemorrhage in the left temporal region. MRA images of the head image 10 (c, d) demonstrate left occipital intraosseous collaterals (orange arrow). Also, there is an enlarged posterior branch of the left middle meningeal artery (yellow arrow) which feeds the left transverse sinus. There is retrograde flow in the cerebral veins (red arrow). These findings are consistent with a dural AVF

Cortical convexity subarachnoid hemorrhage has been reported to be found in high-grade atherosclerotic stenosis of the extracranial cerebral arteries, acute ICA occlusion, and cervical ICA stenosis which can be

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bilateral. These patients are acutely symptomatic and present with sudden onset of aphasia/dysarthria, and or numbness and may continue to have recurrent events. The initial CT may reveal SAH in one or a few of the cerebral convexity sulci. Further imaging may reveal significant atherosclerotic disease causing narrowing or complete occlusion [26, 27]. The hemorrhage usually occurs on the symptomatic side or on the side with the more severe anatomic narrowing [28]. It has been proposed that cSAH may derive from an acute alteration in hemodynamics which may cause rupture of dilated fragile compensatory pial vessels, in distal cortical arteries territories and often localizes to the watershed region of the PCA and MCA as seen in this case (Fig. 8). Moyamoya Moyamoya (puff of cigarette smoke in Japanese) is a distinctive form of collateralization of vessels seen on angiography that develops in response to an underlying vasculopathy leading to progressive occlusion of the supraclinoid ICA and proximal ACA and MCA. SAH in moyamoya is Fig. 11 Mycotic aneurysm: T2 FLAIR (a) and GRE (b) sequences in a patient with endocarditis demonstrate a small left frontal subarachnoid hemorrhage. A subsequent cerebral angiogram (c) was performed which reveals a mycotic aneurysm in a branch of the left MCA

mainly distributed in the basal cisterns, due to rupture of saccular aneurysms which are formed due to high hemodynamic stress in the posterior circulation. Acute cSAH in moyamoya is quite rare and only a few cases in the literature have been reported [29]. However, other studies have reported more prevalence of old SAH which is better visualized as susceptibility on T2*-weighted or ESI sequences [30]. The cSAH has been attributed to the rupture of dilated, fragile collateral arterioles associated with moyamoya as progressive stenosis of the distal ICA occurs [31]. Dissection Although very rare, intradural vertebral dissection presents with SAH. The hemorrhage is usually seen in the posterior fossa. Rarely, cSAH can be seen. Pseudoaneurysms may develop when the dissection occurs (Fig. 9).

Vascular malformations Small arteriovenous malformations (AVM) and cavernous malformation usually present as cortical hemorrhages. Rarely,

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these can be source of cSAH without parenchymal involvement. Dural arteriovenous fistula (dAVF) Dural AVFs have been most frequently described at the transverse sinus and cavernous sinus. Dural AVFs account for approximately 10–15 % of all intracranial vascular abnormalities [32]. It is a rare cause of cSAH but should be considered when other sources are not found. In most cases, this is thought to occur as a result of venous hypertension. MR imaging can depict edema, flow-void clustering, dilated vessels, and prominent vascular enhancement. Any suspicion of dAVF on MRI may prompt additional evaluation with dynamic 4D CTA or time-resolved MRA [33]. However, despite significant technical improvements in noninvasive techniques, catheter angiography remains the most accurate method for detection and classification of dAVFs (Fig. 10). Mycotic aneurysms cSAH has been rarely reported as a presenting feature of infective endocarditis. It may or may not be associated with mycotic aneurysm [34]. MRI findings are very

Fig. 12 Hemorrhagic meningioma: Incidentally noted on a prior CT and MRI is an extra axial right frontal mass which is hyperintense on CT image 12 (a) and isointense on T1 image 12 (b). At a later date, the mass demonstrates intratumoral hemorrhage in addition to subarachnoid hemorrhage (red arrows) as seen on the T2 FLAIR image 12 (c) and GRE image 12 (d) sequences. This was a pathologically proven meningioma

helpful in symptomatic or asymptomatic patients with IE and can reveal multiple CMBs located in superficial areas of the brain which can be seen on GRE images. Multiple small infracts in watershed territories can also be seen due to cerebral emboli [35]. These aneurysms are most commonly located in the peripheral branches of the cerebral arteries. Although mycotic aneurysms can be visualized on CTA, still the catheter angiography remains the gold standard (Fig. 11).

Brain tumors Although rare, primary brain tumors, both benign and malignant, have been associated with subarachnoid hemorrhage (FF). Hemorrhagic meningioma Intracranial hemorrhage in meningiomas accounts for approximately 1.3–2.4 % and can be seen as intratumoral, intracerebral, subdural, or subarachnoid hemorrhage. cSAH in menigioma has previously been described [36, 37] (Fig. 12).

Emerg Radiol Fig. 13 Metastases: CT scan of the head image 13 (a) in a patient with metastatic lung cancer demonstrates a right frontoparietal subarachnoid hemorrhage. Postcontrast T1weighted images of the brain images 13 (b) and 13 (c) reveal several small enhancing metastatic lesions (red arrows)

Metastatic disease In a known patient with primary malignancy, cSAH may be due to various reasons like leptomeningeal metastases, coagulopathies, cerebral vein thrombosis, PRES, or RCVS secondary to chemotherapy. A careful evaluation is therefore recommended. Gadolinium-enhanced T1 with fat saturation and thin sections (3 mm) may be acquired to see enhancing leptomeningeal metastasis and involvement of cranial nerves [7] (Fig. 13).

Coagulation abnormalities Cerebral venous sinus and cortical vein thrombosis Venous pathologies may induce cSAH, namely thrombosis of cortical bridging veins or sinus thrombosis [12]. Usually, the bleeding is located in close vicinity to the thrombosed vein, and the diagnosis is mainly based on clinical suspicion and imaging confirmation. Plain CT or

MRI may suggest diagnosis of CVT. Susceptibility on GRE sequence is noted within the sinus or in the cortical vein and has been proven to be the most sensitive sequence to diagnose the acute thrombus among the various MRI sequences [38]. The T1-weighted spin echo shows hyperintensity at the site of thrombosis which progressively increases during the first week and is very helpful in the early subacute period. Nevertheless, a negative CT or MRI examination does not rule out CVT, and venographic study either CT venogram (CTV) or MR venogram (MRV) needs to be performed in suspected CVT [39] (Fig. 14). It has been presumed that like dAVF, sinus or venous thrombosis may produce dilatation of the cortical veins, leading to rupture and bleeding into the subarachnoid space thus producing SAH. Coagulation disorders Intracerebral and subdural hemorrhages occur more often in patients with coagulation disorder and rarely cSAH can occur [40, 41].

Emerg Radiol Fig. 14 Cerebral venous sinus thrombosis: T2 FLAIR images (a) reveal a right temporoparietal subarachnoid hemorrhage. T2 FLAIR (b) and GRE (c) sequences demonstrate right sigmoid and transverse sinus thrombosis. The right sigmoid sinuses fail to opacify

Thrombocytopenia secondary to liver failure, HELLP syndrome, and ITP with markedly low platelet counts may also cause cSAH.

Conflict of interest The authors declare that they have no conflict of interest.

References Conclusion In conclusion, nontraumatic cSAH is a rare condition, but the diagnosis of underlying cause is very important for further treatment and follow-ups of the patient. The imaging plays a crucial role, and knowing about the various modalities needed for workup and characteristic appearance of various underlying conditions can help in management of these patients. Acknowledgments The authors are grateful to Sarah Klingenberger, Graphic Designer, Department of Imaging Sciences, University of Rochester Medical Center.

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Cerebral convexity subarachnoid hemorrhage: various causes and role of diagnostic imaging.

Computed tomography (CT) and magnetic resonance imaging (MRI) have made it relatively easy to diagnose cortical convexity subarachnoid hemorrhages (cS...
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