Vasogenic Edema

Vasogenic Edema Cytotoxic Edema

4.5 Vasogenic or Interstitial Edema

Vasogenic edema is characterized by dysfunction of the blood-brain barrier, allowing an abnormal passage of proteins, electrolytes and water into the extracellular compartments. Fluid leaving the capillaries enlarges the extracellular space, predominantly in the white matter. Osmotic and hydrostatic gradients will also cause interstitial edema, increasing the extracellular space as water shifts from blood vessels and/or ventricles. Intracellular components are rela tively preserved (Fig. 4.14), although some swelling of myelin sheaths and astrogliosis may be seen histologically [3].

In vasogenic and interstitial edema, electron microscopy has shown an increase of interstitial spaces in white matter amounting to 1000 nm, versus 60 nm in normal white matter [33].These enlarged extracellular spaces, with free water, may be the dominant source for the total brain water signal, resulting in increased ADC.

Figure 4.14

Vasogenic or interstitial edema. There is enlarged extracellular space as water shifts from the blood vessels and/or ventricles. Intracellular compartments are relatively preserved

Vessel v

Vasogenic edema

Cytotoxic Vasogenic EdemaVasogenic Edema

Figure 4.15

Vasogenic edema, as shown on this tissue stain of a trauma case (arrows), is the result of plasma leakage through the blood vessel walls. The increase in extracellular space osmolarity will result in a marked increase in extracellular water, i.e. vasogenic edema (hematoxylin-eosin stain, original magnification x200).(From [36])

Cytotoxic Edema Brain

4.5.1 Conditions that Cause Vasogenic Edema

Vasogenic edema is related to multiple pathological conditions. It typically occurs in the vicinity of brain tumors, intracerebral hematomas, infarctions, cerebral abscesses, contusions and in the reversible posterior leukoencephalopathy syndrome [34]. Venous ischemia at first shows a vasogenic edema due to venous congestion and a breakdown of the normal blood-brain barrier. Progressive venous ischemia re sults in reduced capillary perfusion pressure and cy-totoxic edema [35].

Pathological specimens of vasogenic edema show leakage of plasma from the vessel and diffuse expansion of the extracellular space in the white matter (Fig. 4.15).

Diffusion-weighted images show low signal intensity, isointensity or slightly increased intensity, depending on T2 contrast, and an increase in ADC that reflects free water in the enlarged extracellular space (Fig. 4.16).

Toxoplasma Cerebri

Figure 4.16 a-c

Cerebral toxoplasmosis and vasogenic edema in an 18-year-old woman with headache. a T2-weighted image shows central necrosis as slightly hyperintense (arrow) and peripheral vasogenic edema as very hyperintense in the left hemisphere (arrowheads).Multiple lesions of toxoplasmosis are also seen in the right occipital and left periventricular areas.b DW image reveals vasogenic edema as hypointense, while the central necrosis shows hyperintensity on DW image. c ADC map shows increased ADC from the vasogenic edema.Decreased ADC of the central necrosis is probably due to hyperviscosity of the coagulative necrosis

4.6 Conclusion

4.6.1 Cytotoxic or Cellular Edema

Cytotoxic or cellular edema is hyperintense on DW images and associated with decreased ADC. It can occur in neurons, glial cells, axons (axonal swelling) and myelin sheaths (intramyelinic edema). Cytotoxic edema may be present not only in infarction/ischemia and trauma, but also in status epilepticus, the acute phase of multiple sclerosis, toxic or metabolic leuko-encephalopathy, osmotic myelinolysis, encephalitis, and presumably in the early phase of transneuronal or wallerian degeneration and Creutzfeldt-Jakob disease. The differential diagnosis for hyperintense DW images also includes tumor, abscess and hemorrhage, conditions that also may have decreased ADC. The decreased ADC in these latter conditions may be due to hypercellularity and/or hyperviscosity rather than the cytotoxic edema.

4.6.2 Vasogenic Edema

Vasogenic edema has a variable appearance on DW images, with increased ADC. It is reversible but occasionally associated with cytotoxic edema, which usually is not reversible. DW images and ADC maps are useful for understanding MR images of various diseases with cytotoxic and/or vasogenic edema. These images are more sensitive than conventional MRI to determine the extent of edema in both gray and white matter.

References

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2. Ebisu T,Naruse S, Horikawa Y, et al. (1993) Discrimination between different types of white matter edema with diffusion-weighted MR imaging. J Magn Res Imaging 3:863-868

3. Ironside JW, Pickard JD (2002) Raised intracranial pressure, oedema and hydrocephalus. In: Graham DI, Lantos PL (eds) Greenfield's neuropathology, 7th edn,pp 193-231

4. Lipton SA, Rosenberg PA (1994) Excitatory amino acids as a final common pathway for neurologic disorders. N Engl J Med 330:613-622

5. Chan S, et al. (1996) Reversible signal abnormalities in the hippocampus and neocortex after prolonged seizures. AJNR Am J Neuroradiol 17:1725-1731

6. Mark LP, Prost RW, Ulmer JL, et al. (2001) Pictorial review of glutamate excitotoxicity: fundamental concepts for neu-roimaging. AJNR Am J Neuroradiol 22:1813-1824

7. Moritani T, Shrier D, Wang H, et al. (2002) Excitotoxic mechanism in pediatric brain. Neurographics Vol. 2, Article 1, http://foundation.asnr.org/neurographics/

8. Sharp FR, Swanson RA, Honkaniemi J, et al. (1998) Neuro-chemistry and molecular biology. In: Barnett HJM, Mohr JP, Stein BM, et al. (eds) Stroke pathophysiology, diagnosis, and management, pp 54-56

9. Duong TO,Ackerman JJH,Ying HS,et al.(1998) Evaluation of extra- and intracellular apparent diffusion in normal and globally ischemic rat brain via 19F NMR. Magn Reson Med 40:1-13

10. van der Toorn A, Sykova EDRM,Vorisek I, et al. (1996) Dynamic changes in water ADC, energy metabolism, extracellular space volume, and tortuosity in neonatal rat brain during global ischemia. Magn Reson Med 36:52-56

11. Tien RD, Felsberg GJ, Friedman H, et al. (1993) MR imaging of high-grade cerebral gliomas: value of diffusion weighted echoplanar pulse sequence.AJR Am J Roentgenol 162:671-677

12. Desprechins B, Stadnik T, Koerts G, et al. (1999) Use of diffusion-weighted MR imaging in differential diagnosis between intracerebral necrotic tumors and cerebral abscess-es.AJNR Am J Neuroradiol 20:1252-1257

13. Desmond PM, Lovell AC, Rawlinson AA, et al. (2001) The value of apparent diffusion coefficient maps in early cerebral ischemia. AJNR Am J Neuroradiol 22:1260-1267

14. Burdette JH, Ricci PE, Petitti N, et al. (1998) Cerebral infarction: Time course of signal intensity changes on diffusion-weighted MR images. AJR Am J Roentgenol 171: 791-795

15. Kamal AK, Segal AZ, Ulug AM (2002) Quantitative diffusion-weighted MR imaging in transient ischemic attacks. AJNR Am J Neuroradiol 23:1533-1538

16. Forbes KP, Pipe JG, Heiserman JE (2001) Evidence for cy-totoxic edema in the pathogenesis of cerebral venous infarction. AJNR Am J Neuroradiol 22:450-455

17. Arbelaez A, Castillo M, Mukheri SK (1999) Diffusion-weighted MR imaging of global cerebral anoxia. AJNR Am J Neuroradiol 20:999-1007

18. Wolf RL, Zimmerman RA, Clancy R, et al. (2001) Quantitative apparent diffusion coefficient measurements in term neonates for early detection of hypoxic-ischemic brain injury: initial experience. Radiology 218:825-833

19. Barzo P,Marmarou A,Fatouros P,et al.(1997) Contribution of vasogenic and cellular edema to traumatic brain swelling measured by diffusion-weighted imaging. J Neu-rosurg 87:900-907

20. Liu AY, Maldjian JA, Bagley LJ, Sinson GP, et al. (1999) Traumatic brain injury: diffusion-weighted MR imaging find-ings.AJNR Am J Neuroradiol 20:1636-1641

21. Kim JA, Chung JI,Yoon PH, et al. (2001) Transient MR signal changes in patients with generalized tonicoclonic seizure or status epilepticus: periictal diffusion-weighted imaging. AJNR Am J Neuroradiol 22:1149-1160

22. Men S, Lee DH, Barron JR, et al. (2000) Selective neuronal necrosis associated with status epilepticus; MR findings. AJNR Am J Neuroradiol 21:1837-1840

23. Tsuchiya K, Katase S, Yoshino A, et al. (1999) Diffusion-weighted MR imaging of encephalitis. AJR Am J Roentgenol 173:1097-1099

24. Demaerel P, Baert AL,Vanopdenbosch L, et al. (1997) Diffusion-weighted magnetic resonance imaging in Creutzfeldt-Jakob disease. Lancet 349:847-848

25. Bahn MM, Parchi P. (1999) Abnormal diffusion-weighted magnetic resonance images in Creutzfeldt-Jakob disease. Arch Neurol 56:577-583

26. Castillo M, Mukheriji SK (1999) Early abnormalities related to postinfarction wallerian degeneration: evaluation with MR diffusion-weighted imaging. JCAT 23:1004-1007

27. Verity MA (1997) Toxic disorders. In: Graham DI, Lantos PL (eds) Greenfield's neuropathology, 6th edn,pp 755-811

28. Tievsky AL, Ptak T, Farkas J (1999) Investigation of apparent diffusion coefficient and diffusion tenser anisotropy in acute and chronic multiple sclerosis lesion. AJNR Am J Neuroradiol 20:1491-1499

29. Matsumoto S, Nishizawa S, Murakami S, et al. (1995) Car-mofur-induced leukoencephalopathy: MRI. Neuroradiolo-gy 37:649-652

30. Phillips MD, McGraw P, Lowe MJ, et al. (2001) Diffusion-weighted imaging of white matter abnormalities in patients with phenylketonuria. AJNR Am J Neuroradiol 22:1583-1586

31. Sener RN (2002) Metachromatic leukodystrophy: diffusion MR imaging findings. AJNR Am J Neuroradiol 23:1424-1426

32. Cramer SC, Stegbauer KC, Schneider A, et al. (2001) Decreased diffusion in central pontine myelinolysis. AJNR Am J Neuroradiol 22:1476-1479

33. Gonatas NK, Zimmerman HM, Levine S (1963) Ultrastructure of inflammation with edema in the rat brain. Am J Pathol 42:455-469

34. Mukherjee P, McKinstry RC (2001) Reversible posterior leukoencephalopathy syndrome: evaluation with diffusion-tensor MR imaging. Radiology 219:756-765

35. Keller E, Flancke S, Urbach H, et al. (1999) Diffusion- and perfusion-weighted magnetic resonance imaging in deep cerebral venous thrombosis. Stroke 30:1144-1146

36. Moritani T (2002) Classification of brain edema. In Koredewakaru Diffusion MRI, Tokyo: Shujunsha pp 128137

37. Moritani T, Shrier DA, (2000) Numaguchi Y, et al. Diffusion-weighted echo-planar MR imaging: clinical applications and pitfalls - a pictorial essay. Clin Imaging 24: 181-92.

Infarction

In collaboration with R.de Guzman

5.1 Clinical Significance and Therapeutic Considerations for Brain Infarcts

Stroke is the third leading cause of death in the USA, and cerebral infarction is the most common cause of disability among adult Americans. Until recently these patients were mainly imaged with computed tomography (CT) to establish if the cause of stroke was ischemic or hemorrhagic. Treatment was above all aimed to reduce the risk for further embolic events. In a few instances intra-arterial or intravenous thrombolysis has been instituted, but in most cases this is not feasible because of the narrow therapeutic window. Thrombolytic treatment has a risk of hemorrhagic complications, which is why it has become important to establish the potential benefit of thrombolysis for the individual patient. CT as well as conventional MR imaging have sensitivities below 50% with regard to detection of infarcts in the hyper-acute stage, within 6 hours.

5.1.1 Stroke Mimickers

There is a long list of conditions that mimic the symptoms of an acute ischemic stroke. The most common ones include intracranial hemorrhage, mi-graines,seizures,functional and metabolic disorders, and also vasogenic edema syndromes. It is important to visualize and verify that an ischemic lesion is indeed the cause of the clinical symptoms before therapy is initiated, as these non-ischemic stroke mimickers should not be treated with thrombolysis and such therapy could actually be harmful. Moreover, in older patients it is not uncommon to detect older lesions with prolonged T2 that are indistinguishable from acute lesions using conventional MR imaging.

5.1.2 Diffusion-Weighted Imaging

In recent years, diffusion-weighted (DW) imaging has been proven as the most sensitive MR imaging technique to diagnose hyperacute cerebral infarction. The detection of acute ischemic lesions is based on alterations in motion of water molecules. It is a very sensitive technique,which is not significantly affected by patient motion. DW imaging of the brain can usually be accomplished in less than 2 minutes.

The ischemic event results in restricted diffusion of the affected tissue, which can be seen as early as 30 minutes after ictus. A few rare cases of false-negative DW imaging have been reported [1,2]. These infarcts were seen on perfusion-weighted images and later on DW imaging [1,2].

5.2 Diffusion-Weighted Imaging and Pathophysiology of Cerebral Infarction

The abnormal imaging finding of cerebral and cere-bellar infarctions is an area of hyperintensity on DW imaging of the involved vascular territory. This hy-perintensity is presumed to be caused by cytotoxic edema as a result of cessation of ATP production. Under normal circumstances,ATP maintains the Na+/K+ pump activity and other intracellular energy-related processes. When the Na+/K+ pump is not functioning properly, an inability to remove excess water from the cells develops, resulting in intracellular edema. The outcome of this on DW imaging is restriction of water diffusion,which results in a signal increase on DW imaging and a decrease in diffusion shown as a reduced apparent diffusion coefficient (ADC) [3]. These findings in acute stroke usually represent irreversible damage of brain tissue, or infarction [4].

5.3 Apparent Diffusion Coefficient

The ADC is used to determine whether the signal abnormality on DW images is caused by restricted diffusion or a T2 shine-through effect, as seen in suba-cute-chronic infarctions. ADC represents the degree of diffusibility of water molecules and aids in detecting subtle fluid changes in the hyperacute-acute stages of ischemic stroke. Reduced diffusion is seen as an area of low signal intensity on ADC maps.

5.3.1 Explanation for Restricted Diffusion

Several mechanisms have been proposed to explain the restricted diffusion in ischemia. These include cellular necrosis, shift of fluid from extra- to intracel-lular spaces causing a reduction in size and increase in tortuosity of the extracellular space, but there is also rather strong evidence that at least parts of these findings relate to a reduction in intracellular diffusion [5].

Regions of decreased or restricted diffusion are best seen on DW imaging, while ADC maps will verify the findings by eliminating the T2 shine-through effect as a cause of the increased signal intensity on DW imaging. DW imaging and ADC can also show changes in diffusion that vary for the different stages of a stroke [6], and they can possibly distinguish between multiple strokes over time versus a single, progressive stroke by determining the time course of a cerebral infarction.

Apparent diffusion coefficient values may also be of help in the future to assist in selecting patients with salvageable tissue within an ischemic penumbra for thrombolysis. Intermediate ADC values are noted in the ischemic penumbra, indicating tissue at risk of infarction [7].An approach that is used more often to select patients who may benefit from thrombolysis is by comparing DW imaging and perfusion MR imaging to look for hypoperfused but not diffusion-restricted regions. The mismatch between DW imaging and perfusion demonstrates affected tissue that is still salvageable and not yet infarcted: the penumbra.

5.4 Time Course of Infarction

Infarctions may be classified as hyperacute (less than 6 hours from time of onset of symptoms), acute (6 hours to 3 days), subacute (3 days to 3 weeks), or chronic (3 weeks to 3 months), each having its characteristic signal abnormalities (Table 5.1).

One of the main clinical applications of DW imaging is to detect a hyperacute cerebral infarction. This information is critical,particularly in cases of territorial thromboembolic infarction, as thrombolytic therapy can be started within the golden period of 3 hours from onset of symptoms. Such treatment can result in early reperfusion and reduce the extension of the infarction [3,8]. The DW signal intensity is increased during the hyperacute stage (<6 hours), with corresponding low ADC,manifested as a dark area on the ADC map (Fig. 5.1).

Table 5.1. Time course of thromboembolic infarction of the middle cerebral artery [7]

< 6 hours

3 days

7 days

30 days

T2

Isointense

Bright

Bright

Bright

DW imaging

Bright

Very bright

Bright

Isointense

ADC

Dark

Very dark

Dark

Hyperacute infarction (2 hours after onset) in a 39-year-old woman with decreased consciousness. The symptoms improved after intra-arterial fibrinolytic therapy. a T2-weighted image appears normal. b DW image shows a hyperintense lesion in the right corona radiata (arrows) and a slightly hyperin-tense lesion in the right middle cerebral artery (MCA) territory (arrowheads). c ADC map shows decreased ADC in the corona ra-diata (arrows) and slightly decreased ADC in the cortical area of the MCA territory (arrowheads). d On DW image after fibrinolytic therapy (3 days after onset), the hyperintense lesion in the cortical area mostly resolved with peripheral small infarcts. Early cytotoxic edema with mild decreased ADC does not always result in infarction after treatment

Pictures Peri Heral EdemaEdema Toxin

Almost all acute (6 hours to 3 days) stroke patients examined within 24 hours of onset of symptoms show abnormal signal intensity on DW imaging [9]. At this stage the infarctions show a further increase in DW signal intensity and also a lower ADC than in the hyperacute stage (Fig. 5.2).

Vasogenic Edema Symptoms
Figure 5.2 a-c

Acute infarction (24 hours after onset) in a 56-year-old man with left hemiparesis. a T2-weighted image shows hyperintense lesions preferentially involving the right posterior frontal cortex and the right caudate region, sparing the right corona radiata (arrows).This finding is consistent with a relatively greater involvement of gray matter in the early infarction. b DW image shows the entire right MCA territory as hyperintense.c Decreased ADC is seen in the right MCA territory (arrows). However, some cortical lesions seem to be isointense or have a slightly increased ADC (arrowheads).This may reflect relative vulnerability for brain tissue. Hyperintensity on DW image of these cortical lesions is due to a T2 shine-through effect. DW images and ADC maps are more sensitive than conventional MRI for showing both gray and white matter involvement. ADC maps precisely reflect diffusion restrictions of the lesion within the gray and white matter

5.4.3 Subacute (3 Days to 3 Weeks)

As the infarct continues to evolve into the subacute stage (3 days to 3 weeks), there is pseudo-normalization of the ADC, most likely attributed to a combination of (a) persistence of cytotoxic edema, and (b) development of vasogenic edema and cell membrane disruption, which results in increased amounts of extracellular water. The hyperintensity on DW imaging usually decreases within 1-2 weeks [10], but is still slightly hyperintense, while ADC is usually normalized within 10 days [11]. This time gap is thought to result from T2 shine-through effects on DW imaging in the late subacute infarction (Fig. 5.3).

Figure 5.3 a-d

Subacute infarction (10 days after onset) in a 19-year-old woman with loss of consciousness due to cerebral embolism after cardiac surgery for endocarditis. a T2-weighted image shows hyperintense lesions in the gray (arrowheads) and white matter (arrows) in the right hemisphere and left frontal region. b Gadolinium T1-weight-ed image with magnetization transfer contrast shows gyral enhancement in the cortical lesions, representing subacute infarcts. c DW image also shows hyperintense lesions in the right deep white matter (arrows), and gray matter of both frontal and right parieto-occipital regions (arrowheads). d The ADC map shows decreased ADC in the right deep white matter lesion (arrows), and normal or slightly increased ADC in the gray matter lesions (arrowheads). The prolonged decreased ADC in the white matter may reflect edema of myelin sheaths or axons

Myelin Sheath Edema

5.4.4 Chronic (3 Weeks to 3 Months)

In the chronic stage (3 weeks to 3 months) of infarction, there is a more or less complete necrosis of the cells and at this stage there is an increase in ADC with a bright signal on the ADC map. On T2-weighted imaging the infarction is seen as a bright signal and this, in combination with the increased ADC, will result in a decrease in the signal on DW imaging; the infarction is isointense with surrounding tissue (Fig. 5.4).

Stage Edema
Figure 5.4 a-d

Chronic infarction (10 months after onset) in a 54-year-old man with numbness and weakness of the left lower extremity. a Fluid-attenuated inversion-recovery (FLAIR) image shows chronic infarction in the right MCA territory as a cystic lesion with low signal intensity (cystic necrosis) and peripheral mild hyperinten-sity (gliosis) with atrophy (arrows). b b0 image shows the hy-perintense cystic lesion (arrow). c DW image shows chronic infarction as hypointense cystic areas, and iso- or slightly hyper-intense areas representing glio-sis. d The ADC map shows marked increased ADC in the cystic necrosis (arrow), and slightly increased ADC in the gli-otic periphery of the lesion (arrowheads)

5.5 Diffusion-Weighted Imaging and ADC Characteristics of Gray and White Matter Ischemia

Diffusion-weighted imaging and ADC maps are more sensitive than conventional MR imaging in demonstrating both gray and white matter ischemia (Figs. 5.1, 5.2 and 5.3). Changes in ADC values in acute infarctions seem to be different for gray matter and white matter. Thus, there is a more prominent decrease in ADC in white matter than in gray matter. This decrease also remains for a longer period than in gray matter (Figs. 5.2 and 5.3). One of the explanations for these phenomena is that necrosis may be completed earlier in gray matter infarctions than in white matter infarctions. Another explanation is that the prominent and prolonged decrease in ADC in white matter may reflect cytotoxic edema in different cell types, such as myelin sheaths, axons and glial cells [5,6,11].

5.5.1 Relative ADC

The time course of relative ADC is slightly different in gray matter when compared with the relative ADC in white matter [6]. Fiebach et al. observed a decrease in the relative ADC up to 3 days after the stroke and an increase in relative ADC from the third to the tenth day. The relative ADC increased slightly faster in gray matter than in white, which may be due to the variability between these two tissue types at any stage in the ischemic process, which leads to an altered diffusion. The observed diffusion contrast in gray and white matter could be caused by differences in the mismatch between blood supply and metabolic demand, the type and/or severity of the histopatholog-ic response to ischemic injury (vulnerability) or mechanisms by which histopathologic changes lead to altered diffusion [12]. Regarding the histopatholo-gic response, gray matter has traditionally been considered to be more vulnerable than white matter to early ischemia. More recent findings in experimental models of stroke have demonstrated that is-chemic damage to white matter occurs earlier and with greater severity than previously appreciated [13]. However, if this is true for humans as well is to our knowledge, not yet established.

5.6 Reversibility and Treatment

Reversible ADC is rare but can be found in cases of transient ischemic attack in which imaging was performed within 4 hours, venous infarction, hemiplegic migraine and transient global amnesia. In these rare clinical settings, ischemia does not progress to complete necrosis but a minor subclinical, irreversible injury cannot be ruled out [5].

Clinically, the area of cytotoxic edema with bright DW signal seems to be irreversibly damaged resulting in permanent infarction. In early cerebral ischemia, mildly decreased ADC in the ischemic penumbra is indicative of viable tissue, but hypoper-fused tissue at risk of infarction [14]. After intra-ar-terial or intravenous fibrinolytic therapy, or spontaneous lysis of a clot, abnormal signal in such areas is occasionally reversed, partially or completely (Figs. 5.4 and 5.5).

Vasogenic Edema Alzheimer
Figure 5.5 a-f

Reversible ischemia with cytotoxic edema (2 h from onset) in a 39-year-old man with left internal carotid artery dissection, presenting with right-sided weakness.a FLAIR image shows a subtle hyperintensity in the left frontoparietal white matter (arrows), and linear hyperintensity representing slow flow in the peripheral arteries (arrowheads). b, c DW image (b) shows a hyperintense lesion with decreased ADC (c) in the left frontoparietal white matter, representing cytotoxic edema (arrows).d Perfusion-weighted image shows increase in mean transit time of the entire left anterior and MCA territories. e Follow-up DW image 2 days later shows only a very subtle hyperintensity in the left frontal white matter (arrows). f ADC was normalized,which is in accordance with clinical improvement.Early ischemia with cytotoxic edema may have spontaneously resolved

5.7 Watershed Infarction

Watershed infarction may develop between two major vascular territories or within a single territory in the supraganglionic white matter, a border zone of the superficial and deep penetrating arterioles (Fig. 5.6). As mentioned above, thrombolytic therapy within the first 3 hours from acute onset of symptoms can be effective to limit the size of the infarct under those circumstances. This is, however, not the case in watershed infarctions, as the basic etiology for these lesions is a significant reduction in perfusion second ary to an overall decrease in cerebral blood flow with subsequent poor perfusion pressure distally [7].

There is a difference in the evolution time of ADC between watershed and thromboembolic infarction, the latter having an earlier normalization (Table 5.2). However, T2 signal intensity is the same for both types of infarction. The reason for this difference most likely lies in the different pathophysiologic features and cerebral perfusion of the two stroke subtypes. It is important to note that strokes with different pathogenetic, hemodynamic mechanisms may have different evolution in the ADC courses as well [7].

Watershed Stroke

Watershed infarction. 66-year old man presented with stroke and seizure. a T2-weighted image shows multiple hyperintense lesions in the right frontoparietal area (arrows). b, c DW image shows these lesions as very hyperintense with decreased ADC, representing acute infarcts in the watershed area between anterior and middle cerebral arteries (arrows).d MRA shows bilateral stenoses of internal carotid, and middle and anterior cerebral arteries (arrows).

Bilateral Watershed Stroke
Figure 5.6 a-d

Watershed infarction. 66-year old man presented with stroke and seizure. a T2-weighted image shows multiple hyperintense lesions in the right frontoparietal area (arrows). b, c DW image shows these lesions as very hyperintense with decreased ADC, representing acute infarcts in the watershed area between anterior and middle cerebral arteries (arrows).d MRA shows bilateral stenoses of internal carotid, and middle and anterior cerebral arteries (arrows).

Table 5.2. Time course of watershed infarction of middle cerebral arterial territory [7]

3 days

7 days

14 days

30 days

T2

Bright

Bright

Bright

Bright

DW imaging

Bright

Bright

Bright

Bright

ADC

Dark

Dark

Dark

Less dark

5.8 Perfusion Versus Diffusion Imaging

Perfusion MR imaging may be more sensitive than DW imaging in the detection of a hyperacute cerebral infarction, but it currently entails extensive post-processing to create interpretable perfusion maps (Figs. 5.5 and 5.6). Moreover, MR perfusion determines the degree of blood flow reduction at the level of the cerebral microvasculature, but it will not tell if a hypop-erfused area represents an area of infarction or severe hypoperfusion. Perfusion MR can, however, be matched with the infarcted area on DW images and can demonstrate the area of hypoperfusion outside the infarction - the so-called penumbra. This is the area where neural tissue is at risk for infarction if perfusion is not re-established and ischemic penumbra is assumed to be salvageable by means of thrombolysis.

5.9 Venous Infarction

Cerebral venous sinus thrombosis accounts for only a small percentage of cerebral infarctions in general. Because of its non-specific presentation, cerebral venous sinus thrombosis can be difficult to diagnose. In about 50% of cases, cerebral venous sinus thrombosis results in cerebral venous infarction. This usually presents as a hemorrhagic infarction or focal edema in regions that are not typical for an arterial vascular distribution, usually occurring within the white matter or at the gray-white matter junction (Fig. 5.7).

5.9.1 Predisposing Factors

There are several predisposing factors for thrombus formation within the cerebral venous sinuses. These include pregnancy, infection, extrinsic compression or local invasion by tumor, dehydration, oral contraceptives, hypercoagulable state, trauma, drug abuse. It may also be idiopathic. Thrombus initially forms within the venous sinuses, eventually extending to the veins draining into the sinuses, leading to infarction.

5.9.2 Pathophysiology

The pathophysiological mechanisms that lead to cerebral venous infarction are unclear. It has been postulated that: (1) retrograde venous pressure may cause breakdown of the blood-brain barrier, with leakage of fluid (vasogenic edema) and hemorrhage into the extracellular space or, (2) retrograde venous pressure may cause a decrease in cerebral blood flow, causing tissue damage similar to that seen in arterial infarctions. Restricted water diffusion suggesting cy-totoxic edema is found in patients with acute cerebral venous infarction [2]. However, in cases with only va-sogenic edema, ADC is increased with variable DW signals (Fig. 5.7). Preferred imaging modalities when suspecting cerebral venous sinus thrombosis are conventional MR imaging combined with MR venog-raphy.

Sagittal Sinus Thrombosis Nmr

111 IASMI^i

Figure 5.7 a-d

Venous infarction in a 57-year-old man with dysarthria. a Sagittal T1-weighted image shows a large area of hyperintensity in the left temporal lobe (arrows) with a small area (hemorrhage).The hyperintensity in the left transverse sinus represents sinus thrombosis (arrowhead). b T2-weighted image shows a hyperintense lesion in the left temporal lobe (arrow). c DW image reveals this lesion as mildly hyperintense. d ADC is increased, representing vasogenic edema. On DW image, the lesion is overlapped with diamagnetic susceptibility artifacts from air in the mastoid cells

Small Vessel Infarct

5.10 Small Vessel Infarcts

These are small infarcts measuring approximately 5-15 mm, usually seen in the basal ganglia, internal capsule, thalamus, pons and corona radiata. They account for about 20% of all infarctions and are secondary to an embolus,thrombus or atheroma-tous lesion within long, single, penetrating end arte-rioles.

These infarcts show increased signal in DW imaging with low ADC values (Fig. 5.8). However, unlike the usual time course of cerebral infarctions, they may show a prolonged increase in DW imaging signal and decrease in ADC values, sometimes seen beyond 60 days after onset of symptoms [15].

Differential diagnoses include widened perivascu-lar spaces (Virchow-Robin spaces) and subependymal myelin pallor.

Diffusion Restriction Multiple SclerosisBrain Swelling Imegs
Figure 5.8 a-d

Small vessel infarcts in a 69-year-old man. a, b T2-weighted and FLAIR images show periventricular hyperintensities; however, it is difficult to detect acute small infarcts. c DW image clearly shows multiple hyperintensity spots in the white matter, representing the acute phase of small vessel infarcts. d ADC

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Responses

  • mikaela
    What causes increased signal on ADC map?
    5 years ago
  • mentha
    What Is Vasogenic Edema?
    4 years ago
  • eric
    What is cytotoxic edema?
    3 years ago
  • primula
    How to cure gyral edema?
    1 year ago
  • juan
    Why are pediatric DKA's more sensitive to cerebral edema?
    1 year ago

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