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Manual Pearls and Pitfalls in Abdominal Imaging: Pseudotumors, Variants and Other Difficult Diagnoses

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Imaging description Most cases of non-traumatic subarachnoid hemorrhage SAH are caused by aneurysm rupture. In these patients, it is important to assess the pattern of SAH. There are other patterns of hemorrhage which have been described as compatible with NAPH. Hemorrhage centered anterior to the pons has been referred to as pretruncal and is considered a variant of NAPH [3]. There is also a variant described in which the hemorrhage is centered within the quadrigeminal plate cistern [4].

Importance Patients with NAPH have a much more favorable outcome and can be managed less aggressively. They usually demonstrate complete recovery without complications from vasospasm or hydrocephalus [5]. Their risk of repeat hemorrhage is equivalent to the general population. Thus, identification of this pattern is important for risk stratification. Identification of NAPH is also important in directing further imaging.

A study evaluating the inter- and intra-observer agreement in CT characterization of NAPH found a small level of disagreement [7]. Thus, there should be a high level of confidence that the pattern fulfills the established criteria before suggesting NAPH as the diagnosis. The patients are more likely to be younger and less likely to be hypertensive than those presenting with aneurysmal hemorrhage.

Differential diagnosis The differential diagnosis for non-traumatic CTA-negative SAH includes occult vascular abnormalities such as an aneurysm or vascular malformation, particularly if the SAH is in a pattern that does not fulfill the criteria of NAPH. These patients require DSA for further evaluation. Teaching point Identification of NAPH is important in determining the prognosis and need for follow-up imaging. Nonaneurysmal perimesencephalic subarachnoid hemorrhage: CT and MR patterns that differ from aneurysmal rupture.

Perimesencephalic hemorrhage. Exclusion of vertebrobasilar aneurysms with CT angiography. Pretruncal nonaneurysmal subarachnoid hemorrhage. Mayo Clin Proc. Quadrigeminal variant of perimesencephalic nonaneurysmal subarachnoid hemorrhage. Clinical differences between angiographically negative, diffuse subarachnoid hemorrhage and perimesencephalic subarachnoid hemorrhage.

Neurocrit Care. Negative CT angiography findings in patients with spontaneous subarachnoid hemorrhage: When is digital subtraction angiography still needed? Inter- and intraobserver agreement in CT characterization of nonaneurysmal perimesencephalic subarachnoid hemorrhage.

Figure 2. Axial non-enhanced CT image from a year-old man with an acute headache shows hemorrhage centered anterior to the midbrain, filling the interpeduncular cistern.

There is a small amount of hemorrhage extending across the left ambient cistern into the left aspect of the quadrigeminal plate cistern arrow. Volume rendered image from a CTA demonstrates a small infundibulum at the origin of the right superior cerebellar artery arrow , a normal variant, but no aneurysm.

The remainder of the CTA was negative as well. This is a typical example of NAPH. Axial non-enhanced CT image from a year-old woman with an acute headache shows SAH in the perimesencephalic cisterns, but there is more hemorrhage within the Sylvian fissures. Also notice that the hemorrhage extends laterally within the Sylvian fissures. CTA is recommended for further evaluation. Coronal maximum intensity projection MIP image of the basilar artery demonstrates a small basilar tip aneurysm arrow , which is responsible for the SAH.

Traumatic head injuries may result in intraparenchymal, intraventricular, subarachnoid, subdural, or epidural hemorrhage. Acute hemorrhage is characterized by hyperattenuation on CT, and the classic appearances of the various types of hemorrhage are well known. However, certain types of hemorrhage may be overlooked, especially subdural and subarachnoid hemorrhages.

Images from a head CT are routinely reviewed in the axial plane. However, important findings may be missed on axial images alone. In particular, hemorrhages oriented in a horizontal plane are prone to volume-averaging effects which may result in false-negative results. This is especially true of hemorrhages which occur adjacent to bone, such as the floor of the anterior and middle cranial fossae, where volume-averaging with adjacent bone leads to decreased detection Figure 3.

This issue is compounded by the fact that hemorrhages have a tendency to occur adjacent to bony structures in certain mechanisms of injury [1]. The addition of coronal and sagittal reformations may improve the diagnostic accuracy by reducing both falsenegative and false-positive results Figure 3. Another cause of missed hemorrhage involves the use of inappropriate window and level values Figure 3.

If the window is too narrow, a small subdural hemorrhage may be difficult to distinguish from the adjacent bone. Optimal values for the window and level will vary among scanners, but a reasonable starting point may be a window of and a level of Small quantities of subarachnoid hemorrhage may be overlooked. Subarachnoid hemorrhage tends to accumulate in dependent areas.

Thus, the occipital horns of the lateral ventricles and the interpeduncular cistern should also be specifically evaluated, as these are sites where a tiny amount of hemorrhage may be seen Figure 3. The detection of intracranial hemorrhage is important for accurate treatment and appropriate follow-up of the patient.

Many of these patients will have associated intracranial hemorrhage. A study of radiology residents found that the types of hemorrhages most often missed were subdural hemorrhages especially frontal and parafalcine hemorrhages and subarachnoid hemorrhages especially interpeduncular cistern hemorrhage [4]. Thus, when reviewing images, it is prudent to search specifically for signs of subdural and subarachnoid hemorrhage. Differential diagnosis Imaging artifacts may occasionally be misinterpreted as intracranial hemorrhage.

Experience with interpreting head CTs allows one to predict the usual location and appearance of such artifacts. Reformatted images are also useful. Teaching point The additional of coronal and sagittal reformations, and the use of appropriate window and level values, can lead to a more accurate diagnosis of intracranial hemorrhage. Hardman JM, Manoukian A. Pathology of head trauma. Neuroimaging Clin N Am. Value of coronal reformations in the CT evaluation of acute head trauma.

Lee B, Newberg A. Neuroimaging in traumatic brain imaging. Overnight preliminary head CT interpretations provided by residents: locations of misidentified intracranial hemorrhage.

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Figure 3. Axial non-enhanced CT image from a 9-year-old boy with head trauma from a motor vehicle accident shows no obvious hemorrhage. This was a low-dose exam, reducing the signal-to-noise ratio. Sagittal reformatted CT image shows a subdural hematoma extending along the floor of the left middle cranial fossa arrow. This hemorrhage was initially overlooked on the axial images.

Axial non-enhanced CT image from a year-old man shows subtle increased density along the right aspect of the tentorium arrow. However, it is difficult to be certain that this represents hemorrhage. Coronal reformatted CT image shows obvious thickening and increased density of the right aspect of the tentorium, consistent with a tentorial subdural hematoma. This case illustrates the importance of reformatted images. The image on the left has a window of 80 and level of 40; the middle image has a window of and level of 50; the right image has a window of and level of Notice that as the window widens, the subdural hemorrhage becomes more distinct from the adjacent bone.

Axial non-enhanced CT image from a year-old woman with head trauma shows a tiny amount of hemorrhage within the right occipital horn arrow. Axial non-enhanced CT image in the same patient shows a tiny amount of hemorrhage within the interpeduncular cistern arrow. These were the only foci of hemorrhage, and could have been missed if these sites were not specifically evaluated. Pseudo-subarachnoid hemorrhage pseudo-SAH refers to increased attenuation within the basal cisterns and subarachnoid spaces that mimics subarachnoid hemorrhage SAH , but has a different etiology.

The causes of pseudo-SAH include diffuse cerebral edema, meningitis, and intrathecal contrast [1]. Diffuse cerebral edema is the most common cause of pseudo-SAH. Cerebral edema leads to decreased attenuation of the brain parenchyma. There is also compression of the dural venous sinuses, which may lead to venous congestion and engorgement of the superficial veins.

The combination of decreased brain attenuation and venous engorgement is postulated to be the etiology of pseudo-SAH in the setting of cerebral edema Figure 4. The measured attenuation of the subarachnoid spaces will be lower than that seen with true SAH. Venous engorgement will demonstrate attenuation coefficients of HU. SAH will demonstrate higher attenuation. Therefore, if accurate measurements can be made, the distinction of pseudo-SAH from true SAH can be made in the setting of cerebral edema [3].

When cerebral edema is caused by a hypoxic event, there may be loss of the graywhite matter differentiation, especially involving the basal ganglia Figure 4. Exudative meningitis leads to increased protein content within the subarachnoid space. This may rarely produce a pattern of pseudo-SAH [4]. Similar findings may be seen along the pachymeninges Figure 4. The clinical scenario is helpful in arriving at the correct diagnosis. Patients with pseudo-SAH often have a history of an anoxic event, such as cardiac arrest. The rare cases of meningitis that may cause pseudo-SAH will usually have supporting clinical signs and symptoms.

However, post-mortem studies have proven that the appearance is not caused by the presence of SAH [5]. Therefore, it is important to be aware of this pitfall in order to avoid misdiagnosis. Additionally, it has been shown that patients with post-resuscitation encephalopathy and findings of pseudo-SAH may have a poorer prognosis than those without pseudo-SAH [3]. Teaching point Pseudo-SAH is a rare but important pitfall that is most commonly encountered in the setting of diffuse cerebral edema.

Pseudo-subarachnoid hemorrhage: a potential imaging pitfall associated with diffuse cerebral edema. CT diagnosis of non-traumatic subarachnoid haemorrhage in patients with brain edema. Eur J Radiol. Pseudo-subarachnoid hemorrhage found in patients with postresuscitation encephalopathy: characteristics of CT findings and clinical importance.

Pseudo-subarachnoid hemorrhage: report of three cases and review of the literature. Pseudo-subarachnoid hemorrhage of the head diagnosed by computerized axial tomography: a postmortem study of ten medical examiner cases. J Forensic Sci. Figure 4. Axial non-enhanced CT image from a year-old man with cardiac arrest shows diffusely increased attenuation within the subarachnoid spaces. Notice the decreased attenuation of the basal ganglia. Coronal reformatted CT image again demonstrates diffusely increased attenuation within the subarachnoid spaces, especially prominent in the Sylvian fissures.


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The subarachnoid spaces appeared normal in signal on all MR sequences. Axial apparent diffusion coefficient map shows decreased diffusivity diffusely, most pronounced centrally within the basal ganglia. These findings illustrate the presence of pseudo-SAH in the setting of anoxic injury. Notice the decreased attenuation within the medial temporal lobes arrows , as well as the diffusely decreased graywhite matter differentiation.

These findings are typical of pseudo-SAH. Axial non-enhanced CT image from a year-old man with tuberculous meningitis shows increased attenuation along the tentorium which simulates the appearance of subdural hemorrhage arrows. Axial contrast-enhanced T1-weighted image shows diffuse pachymeningeal enhancement and thickening. Imaging description Arachnoid villi represent the normal sites of cerebrospinal fluid CSF resorption from the subarachnoid space into the venous sinuses. The villi are not visible radiologically, but they may enlarge over time due to distension with CSF.

This causes progressive penetration of the arachnoid membrane into the dura, beneath the vascular endothelium of the venous sinus. The result is formation of an arachnoid granulation. These granulations tend to increase in size and number with age. Arachnoid granulations are most commonly located within the transverse sinuses, superior sagittal sinus, and parasagittal venous lacunae [1].

They usually range in size from 2 to 8mm [2], though may be larger than 10mm at which time they are referred to as giant arachnoid granulations. Contrast-enhanced CT demonstrates a round or oval filling defect within a dural venous sinus. An arachnoid granulation typically occurs where a superficial vein drains into the venous sinus, which is thought to induce a focal weakness in the sinus wall.

There may be a smooth corticated erosion of the adjacent calvarium. A granulation will never demonstrate hyperattenuation on non-enhanced CT, unlike dural venous sinus thrombosis, which commonly demonstrates increased attenuation Figures 5. However, several studies have demonstrated that this rule does not always hold true, especially with giant granulations. In these cases, the characteristic shape, location, and lack of solid enhancement are helpful clues to the correct diagnosis [4]. Importance Arachnoid granulations are common. Autopsy series have reported their occurrence in up to two-thirds of people.

Imaging studies report a widely varying incidence. However, with the increased use of high-resolution MRI, they are encountered more commonly. A study of 90 patients found arachnoid granulations using contrast-enhanced magnetization prepared rapid acquisition gradient-echo MPRAGE sequences [5]. It is important to recognize an arachnoid granulation as a normal structure, and not to misinterpret it as an extra-axial mass or venous thrombosis.

Typical clinical scenario Arachnoid granulations are almost always incidental findings. Rarely, a giant arachnoid granulation may functionally. In such cases, if there is no other finding to explain symptoms of increased intracranial pressure, venous sinus pressure measurements proximal and distal to the lesion may be obtained to assess for the presence of obstruction [6]. Differential diagnosis The primary differential considerations include dural venous sinus thrombosis Figure 5. Most dilemmas will arise in the setting of a giant arachnoid granulation, which may not follow CSF on all MR sequences.

However, they will always be similar to CSF attenuation on CT and should not demonstrate enhancement. The characteristic location at the site of superficial vein penetration is also helpful. However, larger arachnoid granulations may differ in signal from CSF, and other findings may be required for the correct diagnosis. Arachnoid granulations of the posterior temporal bone wall: imaging appearance and differential diagnosis. Br J Radiol. Roche J, Warner D. Arachnoid granulations in the transverse and sigmoid sinuses: CT, MR, and MR angiographic appearance of a normal anatomic variation.

Giant arachnoid granulations just like CSF? Normal structures in the intracranial dural sinuses: delineation with 3D contrast-enhanced magnetization prepared rapid acquisition gradient-echo imaging sequence. Incidental giant arachnoid granulation. Figure 5. The central focus of enhancement represents a penetrating superficial vein. This is the characteristic appearance of an arachnoid granulation. Notice the prominent penetrating superficial vein coursing through the granulation arrow. Axial T2-weighted MR image from a year-old man with an incidental arachnoid granulation of the right transverse sinus arrow.

Notice that the granulation is isointense to CSF. Notice the enhancing penetrating superficial vein arrow. The granulation itself does not enhance. Axial non-enhanced CT image from a year-old female on oral contraceptives shows hyperattenuation within the right transverse and straight sinuses arrows. An arachnoid granulation is never hyperdense. Axial contrast-enhanced CT image shows only thin peripheral enhancement of the right transverse sinus white arrow. The left transverse sinus enhances normally black arrow.

This is a typical example of dural venous sinus thrombosis. Imaging description Enlarged ventricles can be caused by hydrocephalus or parenchymal loss. Hydrocephalus is classified as noncommunicating obstructive or communicating. It is important to try and distinguish among these different patterns, as this will direct further workup and management. Non-communicating hydrocephalus results from obstruction of the ventricular outflow of cerebrospinal fluid CSF.

Frequent causes include neoplasms, aqueductal stenosis, and intraventricular hemorrhage. The site of obstruction can be implied by which ventricles are enlarged. Communicating hydrocephalus usually results from obstruction of CSF resorption at the arachnoid granulations. Less common causes include overproduction of CSF and compromised venous outflow. Normal-pressure hydrocephalus NPH is a specific form of communicating hydrocephalus which is associated with the clinical triad of dementia, ataxia, and urinary incontinence.

Hydrocephalus may lead to transpendymal edema, caused by transpendymal resorption of CSF. This usually indicates an acute enlargement of the ventricles [1]. Some apparent cases of communicating hydrocephalus are caused by fourth ventricular outflow obstruction. An apparent obstructive lesion may not be evident; CT and conventional MRI may miss small webs which obstruct outflow at the foramina of Luschka and Magendie. The addition of 3D constructive interference in the steady state CISS images may allow for improved detection of small membranes at the suspected site of obstruction Figure 6.

Parenchymal volume loss can result in focal or diffuse ventricular enlargement. Diffuse ventricular enlargement caused by volume loss may sometimes be difficult to distinguish from hydrocephalus. Widening of the third ventricular recesses Thinning and displacement of the corpus callosum Decrease in the mammillopontine distance Depression of the fornix. Normal-pressure hydrocephalus is a unique form of communicating hydrocephalus which can be difficult to distinguish from parenchymal atrophy.

The findings described above may be useful in making the distinction. An additional finding which is sometimes present in NPH is focal dilation of the subarachnoid spaces over the convexity or medial surface of the cerebrum in the setting of compressed subarachnoid. There may also be isolated enlargement of the Sylvian fissures or basal cisterns Figure 6. Importance It is important to distinguish true hydrocephalus from atrophy, as this will direct clinical management. Patients with hydrocephalus may require surgical intervention. In particular, patients with NPH will often improve after ventricular shunting [5].

Typical clinical scenario The clinical presentation varies widely based upon the underlying abnormality. Hydrocephalus may be associated with symptoms of increased intracranial pressure, such as headache, nausea, vomiting, seizures, and visual changes. NPH may be associated with the clinical triad of dementia, ataxia, and urinary incontinence. Parenchymal loss may be associated with other forms of dementia, such as Alzheimer's dementia or vascular dementia Figure 6. Differential diagnosis The differential diagnosis of enlarged ventricles includes communicating hydrocephalus including NPH , noncommunicating hydrocephalus, and ex vacuo dilation due to parenchymal loss.

Features that help distinguish between these entities are described above. Teaching point It may not always be possible to distinguish hydrocephalus from enlarged ventricles due to atrophy. It is important to use clinical signs and symptoms to help direct the diagnosis in difficult cases. Diffusion imaging in obstructive hydrocephalus. Is all communicating hydrocephalus really communicating? Prospective study on the value of 3D-constructive interference in steady state sequence at 3T. Morphometric study of the midsagittal MR imaging plane in cases of hydrocephalus and atrophy and in normal brains.

CSF spaces in idiopathic normal pressure hydrocephalus: morphology and volumetry. Postshunt cognitive and functional improvement in idiopathic normal pressure hydrocephalus. Figure 6. Axial FLAIR image from a year-old man with a posterior fossa tumor not shown shows a normal size of the lateral ventricles. Axial FLAIR image obtained six months later shows interval enlargement of the ventricles, with transependymal edema arrow.

The posterior fossa tumor had enlarged and obstructed CSF outflow from the fourth ventricle. Axial T2-weighted image from a year-old man with headaches and visual changes shows enlargement of the lateral and third ventricles which is out of proportion to the size of the sulci. Sagittal T1-weighted image demonstrates the typical findings of hydrocephalus, including upward displacement and thinning of the corpus callosum black arrow , downward displacement of the fornices arrowhead , enlargement of the anterior third ventricular recesses white arrow , and decrease in the mammillopontine distance asterisk.

Sagittal 3D-CISS image demonstrates a thin web within the cerebral aqueduct arrow which is responsible for the obstructive hydrocephalus. Axial non-enhanced CT image from a year-old woman with clinical symptoms of NPH demonstrates enlargement of the ventricles and focal enlargement of a few isolated sulci. Axial T2-weighted image confirms the findings seen on CT. This pattern of isolated sulcal enlargement is often associated with NPH. Axial T2-weighted image from a year-old man with symptoms of Alzheimers dementia demonstrates mild enlargement of the lateral ventricles and mild diffuse sulcal enlargement.

The ventricular enlargement is not out of proportion to the sulcal enlargement. Axial PET image demonstrates hypometabolism in the parietal lobes bilaterally, a pattern supportive of the clinical diagnosis of Alzheimers dementia. Imaging description Blunt cerebrovascular injury BCVI may present as a range of clinical and radiologic manifestations.

The various imaging manifestations of BCVI include minimal intimal injury, raised intimal flap, dissection with intramural hematoma, occlusion, pseudoaneurysm, transection, and arteriovenous fistula. The carotid artery is most often injured in the cervical segment, just inferior to the skull base. The vertebral artery is most often injured in the cervical segment. Multi-vessel injury is common Figure 7. A grading system was developed by Biffl et al.

Five grades are defined, and with regards to the carotid artery, a higher grade is associated with a higher likelihood of cerebral infarction Table 7. In patients who do not exhibit clinical symptoms of BCVI, there are several imaging findings that warrant vascular screening. In general, any severe facial or cervical injury can be associated with BCVI.

Pitfalls in Brain Imaging - CT

Several specific findings which warrant vascular screening have been grouped together as the Denver criteria. These include Le Fort II or III facial fractures; carotid canal fractures; diffuse axonal injury with a Glasgow Coma Scale GCS less than 6; near hanging with anoxic brain injury; cervical fractures of C1 through C3 or involving a transverse foramen; and cervical spine subluxation Figure 7.

Importance There is a high rate of morbidity and mortality from BCVI related to brain infarction [4]. Treatment with antithrombotic medications and carotid artery stenting in eligible patients has been shown to be effective in reducing cerebral infarction [5]. Therefore, it is important to recognize these injuries and understand when vascular imaging is warranted.

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Some studies have found CTA inferior to Table 7. Grades of blunt cerebrovascular injury. DSA [6]. However, CTA will remain an important screening and diagnostic tool, and the majority of cases will be initially detected by CTA. The diagnosis is often suspected clinically based upon the presence of focal neurologic deficits. However, some patients will be asymptomatic or may develop delayed symptoms related to subsequent cerebral infarction [8].

The presence of calcification and a characteristic location help in the distinction. Beam-hardening artifact may also be confused with injury. Therefore, there should be a relatively low threshold for screening at-risk patients. Sliker CW. Blunt cerebrovascular injuries: imaging with multidetector CT angiography.

Blunt carotid arterial injuries: implications of a new grading scale. J Trauma. Blunt cerebrovascular injuries. Clinics Sao Paulo. Screening for blunt cerebrovascular injuries is cost-effective. Am J Surg. Antithrombotic therapy and endovascular stents are effective treatment for blunt carotid injuries: results from longterm followup.

J Am Coll Surg. Blunt cerebrovascular injury screening with channel multidetector computed tomography: more slices still don't cut it. Ann Surg. Utility of screening for blunt vascular neck injuries with computed tomographic angiography. Blunt carotid and vertebral arterial injuries. World J Surg. Figure 7. Curved reformatted image of the right internal carotid artery demonstrates mild luminal irregularities arrows.

This is a young patient, and there are no findings to suggest the presence of atherosclerosis. This would be classified as a grade I injury in the Biffl classification. Curved reformatted image of the left internal carotid artery shows irregular narrowing over a long segment of the artery arrows.

This would be classified as a grade II injury. Multi-vessel injury is common, so injury in one vessel should prompt a careful evaluation of the other vessels. Sagittal non-enhanced CT image of the cervical spine from a year-old man demonstrates a comminuted left-sided facet fracture with subluxation arrow. This injury should prompt further evaluation with CTA. Axial CTA image at the level of the fracture demonstrates occlusion of the left vertebral artery arrow.

This is a grade IV injury. Internal carotid artery dissection presenting as subacute ischemic stroke Michael J. Imaging description Internal carotid artery ICA dissection may be clinically unsuspected as a cause of subacute ischemic stroke, but there are imaging manifestations that suggest this diagnosis. A watershed distribution of hypodensity Figure 8. MRI typically demonstrates restriction bright signal on diffusion-weighted images and decreased signal on the apparent diffusion coefficient ADC map which corresponds to acute cytotoxic edema in the areas of hypodensity Figure 8.

This indicates subacute ischemia. Corresponding gyriform or superficial enhancement in the affected cortex and subcortical white matter Figure 8. Gyriform enhancement is usually caused by vascular or inflammatory processes and is rarely neoplastic. Finding bright signal within the ipsilateral carotid artery on T1-weighted images, corresponding to loss of the normally visualized signal void, suggests slow flow or thrombus as the etiology for the acute ischemic event Figure 8.

If the vascular flow voids are normal on the brain MR study, MR angiography MRA of the neck vasculature will often reveal the source of the ischemic event. In the majority of cases, carotid artery dissection involves the extracranial ICA, sparing the bifurcation. Three-dimensional maximum intensity projection images will usually demonstrate flowrelated signal loss or smooth tapering of the ICA lumen distal to the bifurcation.

On CTA, ICA dissection is characterized by eccentric luminal narrowing with an increase in the external diameter of the artery from mural thrombus, producing a target appearance [1]. Typical clinical scenario ICA dissection has two typical presentations: spontaneous or the sequelae of blunt trauma. Spontaneous ICA dissection can present with ipsilateral frontotemporal headache that can mimic the headache associated with subarachnoid hemorrhage [2, 3].


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This is accompanied by Horners syndrome [3] in less than half of patients. These symptoms can be followed. Ischemia is caused by either thromboembolic events or hypoperfusion. Early recognition of the clinical and imaging manifestations of ICA dissection is critical for early intervention and differentiation from other disease processes. Once ICA dissection is recognized, immediate anticoagulation is the first-line treatment to prevent thromboembolism and allow restoration of vessel anatomy. Differential diagnosis The imaging manifestations of acute stroke can have considerable variation, and can resemble other vascular, neurologic, or neoplastic processes.

Scattered, bilateral multifocal lesions, predominantly in the subcortical and periventricular white matter without a predilection for the watershed zone. Confluent lesions are usually found around the atria of the lateral ventricles and are common in hypertensive patients. No enhancement on post-contrast images and typically spares the cortex. Diffusion-weighted imaging will show a vasogenic pattern of edema diffusion restriction bright signal and increased signal on ADC map. Typically lacks diffusion restriction. Noncontrast CT is often negative.

MRI typically shows abnormal T2 hyperintensity involving both cortical gray and subcortical white matter. Can present as a large, poorly defined area of involvement. Diffusion-weighted imaging shows a vasogenic rather than a cytotoxic pattern of edema. Late cerebritis often demonstrates ring enhancement. Clinical history is often helpful. Can simulate an intimal flap near the distal cervical ICA. Symptoms are related to tight stenosis, subarachnoid hemorrhage, or craniocervical artery dissection.

CTA and MRA usually demonstrate focal or long, tubular, multifocal stenosis with adjunct dilation, the socalled string of beads sign. Diagnosis is strongly suggested when the carotid canal is absent or hypoplastic. Teaching point A young patient presenting with headache, Horners syndrome, or focal neurologic deficits with initial imaging showing ischemia in a watershed distribution should raise the suspicion for ICA dissection.

The presence of intrinsic ribbon-like cortical high signal on T1weighted images with corresponding gyrifom cortical contrast enhancement suggests a subacute ischemic or inflammatory process. Spontaneous dissection of the cervical internal carotid artery: correlation of arteriography, CT, and pathology. Headache and neck pain in spontaneous internal carotid and vertebral artery dissections.

Schievink WI. Spontaneous dissection of the carotid and vertebral arteries. N Engl J Med. Cervical carotid artery dissection: current review of diagnosis and treatment. Cardiol Rev. Incidence and outcome of cervical artery dissection: a population-based study. Carotid and vertebral artery dissections: three-dimensional time-of-flight MR angiography and MRI versus conventional angiography. Figure 8.

Axial non-contrast CT of the head from a year-old woman with headache and upper extremity weakness shows poor gray white matter differentiation in the left posterior parietal lobe black arrowhead as well as ill-defined foci of hypodensity in the left frontal and parietal subcortical white matter white arrowheads corresponding to a watershed infarct. Axial diffusion-weighted MR image shows increased signal in the left frontal and parietal subcortical white matter arrows , corresponding to the hypodensities seen on non-contrast CT.

Axial T1-weighted C , axial FLAIR D , axial E and coronal F post-contrast contrast T1-weighted MR images show ribbon-like intrinsic T1 hyperintensity outlining the affected cortex arrow with intense contrast enhancement in the left posterior parietal lobe arrows and left frontal subcortical white matter arrowheads.

These findings represent laminar necrosis and early gyriform enhancement of subacute ischemic infarct in a watershed distribution. Axial fat-saturated T1-weighted images from MRA demonstrates bright signal in the left internal carotid artery consistent with slow or no flow arrow.

Corresponding axial 2D time-of-flight MR image shows focal signal loss corresponding to absent cephalad blood flow in the ipsilateral ICA. These findings are consistent with left internal carotid artery dissection. Absence of blood flow secondary to sinus aplasia or hypoplasia can be confused with venous sinus thrombosis on noncontrast CT of the brain.

Sinus hypoplasia or atresia is one of the most common anatomic variations of the dural venous sinuses. In most patients, the right transverse sinus is larger than the left [1]. When transverse sinus hypoplasia or aplasia is found, the ipsilateral sigmoid and jugular sinuses are usually also hypoplastic or aplastic [2]. When these findings are present, examination of the sigmoid sinus and jugular sinus for thrombus is mandatory.

A pitfall of MRV is T1 hyperintense subacute thrombus resembling normal flow. Evaluation of pre-contrast MR sequences and source images will help avoid this. Phase contrast MRV sequences are not limited by T1 hyperintense thrombus and should be obtained in difficult cases. Arachnoid granulations are normal structures that invade the dural sinus lumen, mimicking a focal sinus thrombus on contrast-enhanced CT venogram or contrast-enhanced MR.

They typically, but do not always, have signal intensity and attenuation similar to cerebrospinal fluid CSF. They are most typically seen in the far lateral transverse sinuses at the junction of the vein of Labbe and lateral tentoral sinus; however, they occur with equal frequency in the sagittal and sigmoid sinuses, and have a typical imaging appearance [3]. Arachnoid granulations are covered thoroughly in Case 5.

High or asymmetric bifurcation of the venous sinuses at the confluence can resemble an intraluminal thrombus, particularly on contrast-enhanced CT examinations. The empty delta sign refers to a filling defect surrounded by enhancing dura at the sinus confluence that is seen' on contrast-enhanced CT or contrast-enhanced MR [5]. This sign should not be described on non-contrast CT, as hypodensity at the confluence surrounded by normal hyperdense dura is commonly a normal finding.

Difficult cases should be evaluated with CT or MR venography for full evaluation of the venous sinuses. Importance The wide range of variants of intracranial veins and venous sinuses makes identification of venous thrombosis problematic. Variations are generally subdivided into three major categories: variants that mimic venous occlusion, asymmetric or variant sinus drainage, or normal sinus filling defects.

Incorrect diagnosis of venous thrombosis can lead to unnecessary patient anxiety, treatment, and complications of anticoagulation. Typical clinical scenario Venous sinus thrombosis mimics are generally encountered incidentally. The clinical presentation of venous sinus thrombosis is extremely variable and can be non-specific. Headache, nausea, and vomiting are the most common symptoms; however, altered mental status, coma, and death are possible in patients with large cerebral infarcts.

Differential diagnosis Sinus hypoplasia and aplasia and arachnoid granulations generally have characteristic imaging findings. Dural venous sinus thrombosis is the major differential consideration in cases where there is absence of flow or a filling defect in one of the venous sinuses. Teaching point Transverse venous sinus aplasia and arachnoid granulations are commonly mistaken for venous sinus thrombosis. Knowledge of their typical appearance and lack of additional findings associated with sinus thrombus can help avoid this pitfall.

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Cerebral venous sinuses: anatomical variants or thrombosis? Acta Anat Basel. Importance of anatomical asymmetries of transverse sinuses: an MR venographic study. Cerebrovasc Dis. Normal appearance of arachnoid granulations on contrast-enhanced CT and MR of the brain: differentiation from dural sinus disease. The pseudodelta sign in acute head trauma. Lee EJ. The empty delta sign. Figure 9. Axial maximum intensity projection MIP confirms complete absence of flow within the left transverse sinus arrowhead.

Coronal MIP image compares the caliber of the left and right sigmoid and jugular sinuses. T1-weighted images were normal, further supporting the diagnosis of left transverse sinus aplasia. Axial 2D TOF image from an MR venogram in a year-old man with headache and weakness shows absence of contrast and complex heterogeneous hypointense signal in the enlarged left transverse arrowhead and sigmoid arrow venous sinuses. Normal flow enhancement is seen in the right transverse sinus.

Coronal MIP image from a TOF MR venogram shows absence of flow within the left transverse sinus and recanalization of subjacent venous collaterals arrowheads. Axial contrast-enhanced T1-weighted image shows clot extending into the deep venous system arrow with a large parenchymal hypointensity consistent with extensive temporal lobe venous infarct arrowhead. Axial gradient-echo MR image shows blooming of thrombosed blood in both the temporal lobe arrowhead and deep venous system. Axial T1-weighted MR image from a year-old postpartum woman with headache shows intrinsic high signal at the sinus confluence arrow.

More inferiorly, at the junction of the right transverse and sigmoid sinuses, there is high signal filling the sinus lumen arrow , suggesting thrombus. Note the normal flow void on the contralateral side arrowhead C. They are round or oval in shape, and may be unilocular or multilocular. On CT, the cyst will demonstrate hypoattenuation compared with brain parenchyma, and there may be pineal calcifications adjacent to the cyst periphery.

Most cysts are mm in diameter. Thin-section images and sagittal reformatted images are often helpful in their evaluation Figures Sometimes it is difficult to confirm the benign nature of a cystic pineal lesion on a routine head CT, so a MRI is obtained. Features of a benign pineal cyst include thin walls and lack of a solid internal component.

The cyst walls will normally enhance, but the enhancement should be smooth and linear. High-resolution MR sequences, such as balanced steady state free precession SSFP and constructive interference steady state CISS sequences, may demonstrate internal architecture such as thin internal septations and smaller internal cysts. These findings should not be viewed as suspicious for malignancy [1]. A cyst may enlarge over time due to hemorrhage or accumulation of fluid. This may result in local mass effect. Compression of the superior colliculus may result in upward gaze palsy Parinaud syndrome , and effacement of the cerebral aqueduct may lead to obstructive hydrocephalus Figure Thus, it is important to assess the relationship of the cyst to adjacent structures, specifically the tectal plate and cerebral aqueduct.

Therefore, it is clear that pineal cysts are common entities. Small cysts are incidental findings and unlikely to be related to symptoms. Cysts have been reportedly associated with headaches [8]. However, given the common occurrence of headache and the common occurrence of pineal cysts, a causal relationship is difficult to verify. Rarely, a patient will present with ocular gaze disturbance or symptoms related to hydrocephalus. In such cases, the cyst will be large with local mass effect.

Importance There have been several studies designed to determine the natural history of pineal cysts. These studies suggest that follow-up of cysts with benign features is not necessary, in both adults [2, 3] and children [4]. Another study evaluated pineal cystic lesions which were not clearly benign, and thus characterized as indeterminate.

Follow-up was obtained in 26 lesions over a course ranging from seven months to eight years. There was no change in size or appearance of these indeterminate lesions on follow-up imaging [5]. However, there are no standard guidelines on follow-up, and follow-up remains controversial. Some authors recommend follow-up of cysts that are larger than 10mm [6]. If there are atypical features, such as nodular enhancing internal components, follow-up may be prudent Figure Differential diagnosis The primary differential consideration is a cystic pineal neoplasm.

However, if high-quality MRI is performed, a pineocytoma will not demonstrate the features of a benign cyst [9]. Other cystic lesions may occur in the pineal region, most commonly an arachnoid cyst Figures Rarely, an epidermoid will be encountered [10]. Teaching point Small benign-appearing pineal cysts require no follow-up. Internal structure in pineal cysts on high-resolution magnetic resonance imaging: not a sign of malignancy. J Neurosurg Pediatr.

Prevalence and natural history of pineal cysts in adults. Serial MR imaging of pineal cysts: implications for natural history and follow-up. The natural history of pineal cysts in children and young adults. Serial follow-up MRI of indeterminate cystic lesions of the pineal region: experience at a rural tertiary care referral center. From the archives of the AFIP: lesions of the pineal region: radiologic-pathologic correlation. High prevalence of pineal cysts in healthy adults demonstrated by high-resolution, non-contrast brain MR. Headaches and pineal cyst: a case-control study.

Fakhran S, Escott EJ. Pineocytoma mimicking a pineal cyst on imaging: true diagnostic dilemma or a case of incomplete imaging? Intracranial cysts: radiologic-pathologic correlation and imaging approach. Figure Sagittal contrast-enhanced T1-weighted image from a year-old woman shows an incidental pineal cyst.

Notice the thin peripheral enhancement arrow , an expected finding. Sagittal CISS image demonstrates the cystic nature of the lesion. Notice that the signal differs from CSF. This lesion requires no follow-up. Axial non-enhanced CT image from a year-old man shows an incidental low-attenuation pineal lesion arrow. Axial contrast-enhanced T1-weighted image shows the typical appearance of a benign pineal cyst. Follow-up was not suggested. Axial non-enhanced CT image from a year-old woman with headaches shows a low-attenuation lesion within the pineal gland with a dense fluid level layering dependently white arrow.

Also notice the adjacent pineal calcifications black arrow. The lateral and third ventricles are enlarged. Sagittal contrastenhanced T1-weighted image shows no evidence of nodular enhancement within the cyst asterisk. There is complete effacement of the cerebral aqueduct arrow.

This represents a benign pineal cyst which underwent hemorrhage, increased in size, and caused acute obstructive hydrocephalus. Axial non-enhanced CT image from a year-old man with headaches shows a low-attenuation lesion within the pineal gland arrow , with prominent pineal calcifications posteriorly. Sagittal contrast-enhanced T1-weighted image shows a large area of nodular enhancement arrow adjacent to an irregular cyst.

These findings are not compatible with a benign cyst, and follow-up was suggested. Notice that the cyst is posterior to the pineal gland white arrow. Also notice the effacement of the cerebral aqueduct black arrow. This space extends anteriorly from the quadrigeminal plate cistern, superior to the pineal gland. Notice the inferior displacement of the fornix white arrow and internal cerebral vein black arrow. Virchow-Robin VR spaces, also commonly referred to as perivascular spaces, are pia-lined extensions of the subarachnoid space surrounding the walls of cerebral vessels.

Different theories have been proposed for their mechanism of expansion; however, it remains unknown. The typical appearance varies depending on the patients age. Generally, VR spaces are well-defined, round or oval fluid-filled structures with smooth margins and they usually measure 5mm or less [2].

They are typically found in the inferior third of the anterior perforated substance and basal ganglia [2]. There is no restriction on diffusion-weighted imaging DWI. The dilated spaces do not enhance on postcontrast images [3]. Dilated VR spaces typically occur in three characteristic locations, which determine their type Table Atypical appearances of VR spaces have been reported. They can present as clusters of type II enlarged spaces in one hemisphere or unilateral spaces high in one hemisphere Figure Rarely, VR spaces can be markedly enlarged, cause mass effect, and assume bizarre cystic configurations.

Type I: Along the lenticulostriate arteries entering the basal ganglia through the anterior perforated substance. Importance Recognition of their typical location and imaging appearance will allow them to be dismissed as an anatomic variant, avoiding misdiagnosis. Typical clinical scenario Virchow-Robin spaces are usually encountered as an incidental finding or during a work-up for a non-specific symptom.

Occasionally, a patient presents with non-specific, non-localizing symptoms and an atypical enlarged VR lesion is reported as a bizarre multi cystic neoplasm. Differential diagnosis Perivascular spaces mimic several other diseases that present with focal parenchymal signal abnormality. Type II: Along the path of the perforating medullary arteries as they enter the cortical gray matter over the high cerebral convexities and extend into the white matter Type III: In the midbrain Figure These tend to be larger than VR spaces and wedge-shaped on CT [5]. Enhancement can be seen up to 8 weeks after the acute event.

The findings are usually subtle on T1-weighted images Figure The lesions can have rim or solid enhancement, depending on the degree of lesion inflammation Figure The signal does not exactly follow CSF and there are usually associated parenchymal signal abnormalities edema. Cystic neoplasms may have an enhancing component or nodule. Cyst walls can enhance and there is often surrounding parenchymal edema present.

Common locations include the middle cranial fossa, the perisellar cisterns and the subarachnoid space over the convexities. They can be differentiated from VR spaces by their typical location. Teaching point Perivascular spaces are typically found in the inferior third of the anterior perforated substance and can range in size from 2mm up to 10mm in size.

They follow CSF on all pulse sequences, allowing differentiation from focal acute lacunar infarcts and chronic microvascular ischemic disease. Large Virchow-Robin spaces: MR-clinical correlation. Normal perivascular spaces mimicking lacunar infarction: MR imaging. Brain MR: pathologic correlation with gross and histopathology. Lacunar infarction and Virchow-Robin spaces. Unusual widening of Virchow-Robin spaces: MR appearance. MR and CT of lacunar infarcts. Recommended diagnostic criteria for multiple sclerosis: guidelines from the International Panel on the diagnosis of multiple sclerosis.

Ann Neurol. Note the density of this lesion is similar to CSF seen in the neighboring Sylvian fissure. There is ill-defined hypodensity in the bilateral frontal periventricular white matter. Axial non-contrast CT at the junction of the midbrain and pons demonstrates a small round hypodensity that is isodense to CSF arrow. The surrounding brain parenchyma is normal. These represent atypical type II perivascular spaces.

The arrowhead depicts microvascular ischemic white matter change. There is confluent abnormally increased FLAIR signal in the subcortical and periventricular white matter bilaterally. The white matter changes are subtle iso- to slightly hypointense on T1-weighted images. The oval plaques typically project from the corpus callosum and show increased signal on T2-weighted and FLAIR images with corresponding hypointensity on T1-weighted images arrowheads.

Axial T1-weighted post-contrast image demonstrates peripheral enhancement after the administration of gadolinium consistent with an actively demyelinating lesion arrowhead. Imaging description Non-contrast head CT is often the first study for evaluation of acute cognitive decline in the emergent setting. Tumefactive multiple sclerosis TMS typically shows a large area of confluent hypodensity in the periventricular white matter, often extending from the body of the corpus callosum. This area of hypodensity can extend to the subcortical white matter and, in some cases, exhibit mass effect on the neighboring ventricle, distorting the overlying cortex.

While tumefactive lesions can be large enough to exhibit some mass effect, the mass effect is often less than would be expected for the size of the lesion. Post-contrast images can show subtle, discontinuous edge enhancement Figure Further characterization with MRI Figure The confluent hypodensity seen on CT will correlate to a similar territory of intrinsic hypointensity on T1-weighted images. There will be corresponding central hyperintensity with a thin edge of hypointensity on T2-weighted images.

Post-contrast MRI yields a characteristic horseshoe-shaped leading edge of enhancement that is open towards the cortex. Corresponding restriction on diffusion-weighted imaging DWI occurs in the region of enhancement Figure Physiologic permeability and hemodynamic blood volume parameters on perfusion CT have been used to discriminate TMS from high-grade neoplasms. Tumefactive multiple sclerosis typically lacks neo-angiogenesis and vascular endothelial proliferation, and thus shows a low permeability surface-area-product and low blood volume on CT perfusion.

These perfusion studies can also demonstrate vascular structures, usually veins, within the lesions, only present in TMS [3]. Importance Tumefactive demyelination is a spectrum of disease that includes multiple sclerosis and acute disseminated encephalomyelitis ADEM [4]. These lesions can present a diagnostic dilemma to both the clinician and radiologist. Prompt recognition or suspicion can prevent unnecessary surgical biopsy or intervention. These patients often respond well to high-dose corticosteroids, with regression of the demyelinating lesion.

Tumefactive demyelination can share imaging findings with high-grade intracranial neoplasms and infections: contrast enhancement, perilesional edema, and mass effect. Correlation with clinical history, patient demographics, and diagnostic imaging is valuable to differentiate these diseases. When present, recognition of the typical features of TMS is critical:.