The author: Professor Yasser Metwally

http://yassermetwally.com

INTRODUCTION

November 10, 2009 — Differential diagnoses of a cerebellopontine angle mass on MRI

CONDITION	RADIOLOGIC FINDINGS
Acoustic neuroma	Isointense or slightly hypointense lesion on T1-weighted images. Prominent contrast enhancement permits demonstration of even small intracanalicular masses on coronal or axial images. Hyperintense signal on T2-weighted images.
Meningioma	Usually hypointense to white matter on T1- Prominent and homogeneous contrast enhancement. weighted images. At 1.5 the lesion is hyperintense to white matter on T2-weighted images. Typically larger and more broadly based along the petrous bone than an acoustic neuroma.
Epidermoid	Heterogeneous texture and variable signal intensity. most are of slightly hypersignal than CSF on both T1- and T2-weighted images.
Metastasis	Generally hypointense on T1 -weighted images and of increased signal intensity on T2-weighted. Intratumoral hemorrhage and cystic necrosis may occur.
Arachnoid cyst	Smoothly marginated and homogeneous lesion Typically displaces adjacent brainstem and cerebellar containing cyst fluid that is isointense to CSF on all pulse sequences.
Arterial ectasia	Curvilinear flow void that may simulate a cerebellopontine angle tumor.
Aneurysm of basilar or Vertebrae artery	Flow void that may be surrounded by heterogeneous signal intensity representing turbulence or a thrombus.
Glomus jugulare tumor	Isointense lesion on T1-weighted images.and hyperintense on the T2 weighted images. The tumour is highly vascular and contains multiple signal voids representing enlarged vessels. There is marked contract enhancement.
Lipoma	On CT scan lipomas are characteristically hypodense (fat density) with positive mass effect. On MRI lipomas are hyperintense on precontrast T1 images and diffusely hypointense on MRI T2 images. A hypointense rim is seen on MRI T1,T2 images surrounding lipomas, this hypointense rim could represent the fibrocollagenous tumour capsule. Lipomas characteristically do not enhance after contrast injection.

1. Metwally, MYM: Textbook of neuroimaging, A CD-ROM publication, (Metwally, MYM editor) WEB-CD agency for electronic publication, version 10.4a October 2009 [Click to have a look at the home page]

The author: Professor Yasser Metwally

http://yassermetwally.com

INTRODUCTION

November 10, 2009 — The differential diagnosis of dilated cerebral ventricles

1. Metwally, MYM: Textbook of neuroimaging, A CD-ROM publication, (Metwally, MYM editor) WEB-CD agency for electronic publication, version 10.4a October 2009 [Click to have a look at the home page]

The author: Professor Yasser Metwally

http://yassermetwally.com

INTRODUCTION

November 10, 2009 — Differential diagnosis of a supratentorial mass on MR imaging.

TUMOURS

CONDITION	RADIOLOGIC FINDINGS
Astrocytoma	Hypointense lesion on T1-weighted images. High intensity signal on proton-density and T2-weighted images.Low-grade tumors tend to be homogeneous and lack central necrosis. They may contain large cystic components that have smooth walls and contain uniform-signal fluid, unlike the heterogeneous appearance of necrosis.
Glioblastoma multiforme	Hypointense lesion on T1-weighted images. Hyperintense signal on proton-density and T2-weighted images.These high-grade gliomas appear heterogeneous as a result of central necrosis with cellular debris, fluid,and hemorrhage. These tumors infiltrate along white matter fiber tracts. Deeper lesions frequently extend across the corpus callosum into the opposite hemisphere.
Oligodendroglioma	Hypointense lesion on T1 weighted images. Hyperintense signal on proton-density and T2 weighted images.
Metastasis	Generally hypointense on T1-weighted images and of increased signal intensity on proton-density and T2-weighted images. Peritumoral edema is usually prominent, but unlike infiltrative gliomas, the edema accompanying a metastasis usually does not cross the corpus callosum or involve the cortex.
Lymphoma	Hypointense or isointense mass on T1-weighted images. Typically a homogeneous, slightly high-signal to isointense mass deep in the brain on T2-weighted images.The mild T2 prolongation is probably related to dense cell packing in the tumor, leaving relatively little interstitial space for the accumulation of water.
Meningioma	Usually hypointense to white matter on T1 weighted images. At 1.5 Tesla the lesion is hyperintense to white matter on T2 weighted images.
Epidermoid	Heterogeneous texture and variable signal intensity. Most are of slightly higher signal than CSF on both T1 and T2-weighted images.
Dermoid	Heterogeneous texture as a result of the multiple cell types in it.Fatty components are common and produce high signal on T1 weighted images. A characteristic fat-fluid level may be seen.
Lipoma	High signal intensity on T1 weighted images. Isointense or mildly hyperintense on proton-density images. Low intensity on T2-weighted sequences.
Colloid cyst	Smoothly marginated spherical mass with two signal patterns: low density on CT, isointense on T1 weighted MR images, and hyperintense on T2 weighted MR images; and isodense or slightly hyperdense on CT with a high-signal capsule and a hypointense center on T2 weighted MR images.

INFLAMMATORY LESIONS

Cerebral abscess	Hypointense mass with isointense capsule surrounded by low-signal edema on T1 weighted images. Hyperintense mass surrounded by a hypointense capsule and high-signal edema on T2- weighted images.
Herpes simplex encephalitis	Ill-defined areas of high signal intensity on T1 weighted images. This process usually begins unilaterally but progresses to become bilateral. MRI can demonstrate positive findings more quickly(as soon as 2 days) and more definitively than CT.

INTRACEREBRAL HAEMORRHAGE

Very acute (0-3 hours)	lsointense to slightly hyperintense on T1 weight images. lsointense to bright signal on T2 weighted images.
Acute (3 hours-3 days)	lsointense or hypointense on T1 weighted images. Markedly hypointense on T2 weighted images.
Subacute (3 days 3 Weeks)	Bright rim of hyperintense signal on T1 weighted images that extends inward to fill the entire lesion. Increased signal on T2-weighted images, although to a lesser extent.
Chronic (3 weeks-3months or more)	Variable appearance on T1 weighted images. Pronounced hypointense rim or completely low-signal lesion on T2 weighted images.

VASCULAR DISEASE

Infarction	Hypointense on T1-weighted images. Hyperintense on proton-density and T2-weighted images.Old infarcts may have a more complex signal pattern that is related both to hemorrhagic components and to the evolution of infarcts, the latter resulting in areas of microcystic and macrocystic encephalomalacia and gliosis.
Arteriovenous malformation	Cluster of serpiginous flow voids (representing rapid blood flow) and areas of high signal (slow flow in draining veins).
Aneurysm	Flow void that may be surrounded by a heterogeneous signal intensity pattern representing turbulence or thrombus

1. Metwally, MYM: Textbook of neuroimaging, A CD-ROM publication, (Metwally, MYM editor) WEB-CD agency for electronic publication, version 10.4a October 2009 [Click to have a look at the home page]

The author: Professor Yasser Metwally

http://yassermetwally.com

INTRODUCTION

November 9, 2009 —  Vasogenic edema is characterized by increased permeability of brain capillary endothelial cells (as consequence of vascular injury with disruption of the BBB, or due to defective endothelial lining of the newly formed blood vessels in brain neoplasms) to macromolecules, such as the plasma proteins and various other molecules, whose entry is limited by the capillary endothelial cells (blood brain barrier). Grossly, the gyri are flattened and the sulci narrowed; the white matter is moist and swollen. Microscopically, there is micro-vacuolization of the white matter, poor staining, and "halo’s" around nuclei.

Vasogenic edema is the most common type of edema associated with brain tumors, venous congestion and other causes and results from local disruption of the blood brain barrier. This leads to extravasation of protein-rich filtrate of plasma into the interstitial space, with subsequent accumulation of vascular fluid. This disruption results from loosening of the tight junctions between endothelial cells, and the neoformation of pinocytic vesicles. Once the barrier is breached, hydrostatic and osmotic forces work together to extravasate intravascular fluid. Once extravasated, fluid is retained outside the vasculature, mostly in the white matter of the brain, and within the bundles of myelinated axons of long tracts and commissural fibers. This is because axons run in parallel bundles of fibers with loose extracellular space (that offer low resistance and facilitates the extension of vasogenic edema along myelinated axons which are spreaded apart by the edema) as opposed to gray matter, which has high cell density and is enmeshed in an interwoven network of connecting fibers that offer high resistance to the formation and spread of edema. By definition, this type of edema is confined to the extracellular space. (70)

• More detailed information about the pathophysiology of vasogenic brain edema

Cerebral edema may be defined broadly as a pathologic increase in the amount of total brain water content leading to an increase in brain volume ³⁹. It occurs when plasma-like fluid enters the brain extracellular space through impaired capillary endothelial tight junctions in tumors (vasogenic edema) ⁴⁰ and is a significant cause of morbidity and mortality. The molecular constituents of brain endothelial tight junctions consist of transmembrane proteins occludin, claudin 1 and 5, and junctional adhesion molecules that bind their counterparts on neighboring cells, “gluing” the cells together and creating the blood-brain barrier (BBB) ⁴⁰. Intracellularly, the occludins and claudins bind to zonula occluden (ZO) 1, ZO2, and ZO3, which in turn are attached to the actin cytoskeleton ⁴⁰. Normal astrocytes help to maintain a normal BBB ⁴¹, which is illustrated in Plate. 1. In high-grade tumors, the deficiency of normal astrocytes leads to defective endothelial tight junctions, resulting in BBB disruption, allowing passage of fluid into the extracellular space ⁴⁰. In addition, tumor cells produce factors, such as vascular endothelial growth factor (VEGF) ^42,43 and scatter factor/hepatocyte growth factor ^44,45, which increase the permeability of tumor vessels by downregulation of occludin and ZO1 ^40,44,46,47. In addition, the membrane water channel protein, aquaporin-4 (AQP4), is upregulated around malignant brain tumors ⁴⁰. AQP4-mediated transcellular water movement is important for fluid clearance in vasogenic brain edema, suggesting AQP4 activation or upregulation as a novel therapeutic target in vasogenic brain edema ^40,48. High VEGF expression is reported in human anaplastic astrocytoma and glioblastoma (GBM) ^49,50 meningiomas ⁴⁴, and brain metastases ⁵¹. VEGF is important especially when tumors outgrow their blood supply. Hypoxia is the driving force for VEGF production in glioblastomas and the most important trigger for angiogenesis and cerebral edema formation in glioblastoma ⁵².

Plate 1. The BBB. Normal BBB demonstrating tight junctions between endothelial cells forming a barrier between the circulation and the brain parenchyma. Peritumoral edema formation occurs through defective endothelial junctions of an abnormal BBB. (Click to enlarge figure)

• Neuroimaging of vasogenic brain edema

Increased capillary permeability to large molecules is the corner stone in the aetiopathogenesis of vasogenic edema. The increase in permeability is visualized when contrast enhancement is observed with CT or MRI.

The increase in permeability is visualized when contrast enhancement is observed with CT or MRI. Increased CSF protein levels are also indicative of increased endothelial permeability. MRI is more sensitive than CT in demonstrating the increased brain water and increased extracellular volume that characterize vasogenic edema. Vasogenic edema is characteristic of clinical disorders in which there is frequently a positive contrast-enhanced CT or increased signal intensity with MRI, including brain tumor, abscess, hemorrhage, infarction, and contusion. It also occurs with lead encephalopathy or purulent meningitis.

Figure 1. A, Loss of the gray-white interface with obscuration of the lentiform nucleus, loss of the insular ribbon, sulcal effacement and mass effect are seen in the left hemisphere due to vasogenic edema, B, Grossly , the gyri are flattened and the sulci narrowed; the white matter is moist and swollen. Notice uncal herniation (arrow). (Click to enlarge figure)

The functional manifestations of vasogenic edema include focal neurologic deficits, focal EEG slowing, disturbances of consciousness, and severe intracranial hypertension. In patients with brain tumor, whether primary or metastatic, the clinical signs are often caused more by the surrounding edema than by the tumor mass itself. Ultimately, these changes can lead to herniation.

Figure 2. Occipital glioblastoma surrounded by vasogenic edema involving only the white matter. (Click to enlarge figure)

Highly aggressive tumors (glioblastomas, metastatic tumours, etc.) occur at all ages; however, there is a strong trend toward increasing malignancy with age. Highly malignant tumours and rapidly growing tumours are more commonly surrounded by vasogenic tumours than more benign tumours and tumours with a lower grade of malignancy. Highly aggressive tumors are diffusely invasive tumors that typically have a destructive cellular core. Radiological signs characteristic of vasogenic brain edema is described in the following table.

Table 1. Radiological signs characteristic of vasogenic brain edema

RADIOLOGICAL SIGN	COMMENT
Contrast enhancement.	Contrast enhancement is due to break down of blood brain barrier which is the corner stone in the aetiopathogenesis of vasogenic edema. The microscopic correlate of enhancement is hypercellularity, mitotic activity, neovascularity (in brain tumours) and breakdown of blood brain barrier resulting in increased permeability of brain capillary endothelial cells to macromolecules, such as the plasma proteins and various other molecules, whose entry is limited by the capillary endothelial cells (blood brain barrier)
Diffuse low density on CT scan, diffuse MRI T1 hypointensity and diffuse MRI T2 hyperintensity with loss of the gray-white interface, obscuration of the lentiform nucleus, loss of the insular ribbon.	Obscuration of the lentiform nucleus, loss of the insular ribbon is simply due to loss of the gray-white interface.
Sulcal effacement.	Grossly , the gyri are flattened and the sulci narrowed; the white matter is moist and swollen. Microscopically, there is micro-vacuolization of the white matter, poor staining, and "halo’s" around nuclei.
Mass effect, with ventricular effacement.	Is a common cause of brain herniation.

The relationship between neuroimaging actual tumor extent is critical to the use of these studies in diagnosis and treatment design. In general three zones are identified in malignant brain tumours (1) A central zone (hypointense on the MRI T1 images, hyperintense on the MRI T2 images and hypodense on CT scan) (2) A peripheral enhanced rim with multiple enhanced mural nodules and (3) An ill-defined diffuse large zone surrounding the first two zones. (hypointense on the T1 images, hyperintense on the T2 images and hypodense on CT scan). The first zone corresponds to the necrotic tumour tissues, the microscopic correlate of enhancement is hypercellularity, mitotic activity, and neovascularity with breakdown of blood brain barrier resulting in increased permeability of brain capillary endothelial cells to macromolecules, such as the plasma proteins and various other molecules, whose entry is limited by the capillary endothelial cells (blood brain barrier), while the third zone corresponds to edema, malignant glial cell infiltrations and reactive gliosis. The surrounding zone of edema demonstrates a decreasing gradient of infiltrating tumor cells. The infiltrating tumor cells primarily follow white matter tracts, accompanied by vasogenic edema that may facilitate migration. ^1,2,3,4,5 Although tumor cells may spread a great distance, typically, most are within 2 cm of the enhancing margin.⁶

Table 2. In general three zones are identified in malignant brain tumours

ZONE	DESCRIPTION
Central zone	Formed of necrotic tumour tissue
Intermediate contrast enhancing rim	Formed of viable tumour tissue
Peripheral diffuse zone	Formed of edema, reactive gliosis and malignant cell infiltrations

Glioblastomas characteristically send malignant cells streaming into the surrounding brain. This mode of spread is apparently facilitated by the widened extracellular spaces created through vasogenic edema.

• Vasogenic edema and peritumoral cyst formation

Two types of cysts—peritumoral and intratumoral— are associated with CNS tumors. Peritumoral cysts develop within the brain or spinal cord and form at the margin of the tumor. Alternatively, intratumoral cysts develop within the tumor itself and are usually the result of intratumoral necrosis. Overall, cysts are associated with approximately 10% of benign, malignant, and metastatic tumors of the CNS. They are most frequently associated with hemangioblastomas (83%), cerebellar astrocytomas (77%), and cerebral astrocytomas (29%). The presence of peritumoral cysts can lead to significant neurological impairment due to mass effect and increased intracranial pressure. Based on advances in imaging, histological, and molecular techniques, insight into the mechanism behind peritumoral cyst formation has been provided, and evidence indicates that peritumoral edema precedes and underlies the propagation of these cysts.

Peritumoral cysts (those arising immediately adjacent to the tumor mass) are frequently associated with benign and malignant tumors of the brain and spinal cord (syringomyelia). The cystic component of central nervous system (CNS) tumors and associated peritumoral cysts are often the cause of clinical symptoms. Because of the common occurrence of peritumoral cysts with CNS neoplasms and the morbidity associated with them, advanced imaging, histological, and molecular techniques have been used to determine the mechanism underlying cyst formation and propagation. Based on evidence from such studies, edema appears to be a common precursor to peritumoral cyst formation in the CNS. Mediators of vascular permeability acting locally in the tumor and/or hydrodynamic forces within abnormal tumor vasculature appear to drive fluid extravasation. When these forces overcome the ability of surrounding tissue to resorb fluid, edema and subsequent cyst formation occur. These findings support the concept that the tumor itself is the source of the edema that precedes cyst formation and that resection of tumors or medical therapies directed at decreasing their vascular permeability will result in the resolution of edema and cysts.

• Management of vasogenic edema

Cerebral edema tends to extend along white matter tracts. CT and MRI are helpful in the diagnosis of edema. Therapy includes tumor-directed measures, such as debulking surgery, radiotherapy (RT), chemotherapy, and the use of corticosteroids. Ingraham and coworkers pioneered the use of cortisone to treat postoperative cerebral edema in neurosurgical patients in 1952. He first used steroids in an attempt to ameliorate postoperative adrenal insufficiency in patients undergoing craniotomy for craniopharyngioma resection and noted the favorable effect on postoperative cerebral edema ⁵³. Galicich and colleagues ⁵⁴ and French and Galicich ⁵⁵ introduced dexamethasone therapy as the standard treatment for tumor-associated edema. Despite their well-known side effects, better alternatives do not exist and corticosteroids have remained the mainstay of treatment ever since.

The mechanism of action of corticosteroids is not well understood. It has been argued that their antiedema effect is the result of reduction of the permeability of tumor capillaries by causing dephosphorylation of the tight junction component proteins occludin and ZO1 ⁴⁰. Corticosteroids usually are indicated in any patients who have brain tumor who have symptomatic peritumoral edema. Dexamethasone is used most commonly as it has little mineralocorticoid activity and, possibly, a lower risk for infection and cognitive impairment compared with other corticosteroids ⁵⁷. The choice of starting dose of a corticosteroid largely is arbitrary and depends on the clinical context. The usual starting dose is a 10-mg load, followed by 16 mg per day in patients who have significant symptomatic edema. Lower doses may be as effective, especially for less severe edema ⁵⁸. The dose may be increased up to 100 mg per day if necessary ⁵⁹. Dexamethasone can be given twice daily, although many clinicians prescribe it 4 times daily. As a general rule, patients should be treated with the smallest effective dose for the shortest time possible to avoid the harmful effects of steroids. For asymptomatic patients who have peritumoral edema on imaging studies, corticosteroids are unnecessary. Dexamethasone usually produces symptomatic improvement within 24 to 72 hours. Generalized symptoms, such as headache and lethargy, tend to respond better than focal ones. Improvement on CT and MRI studies often lags behind clinical improvement. Contrast enhancement of tumors typically decreases, suggesting partial restoration of the BBB ⁶⁰, whereas tumor perfusion can increase because of reduced peritumoral water content and local tissue pressure ⁶¹. Using diffusion tensor MRI, administration of corticosteroids decreases peritumoral extracellular water content in edematous brain without affecting the water content of contralateral normal brain. ⁶²

Occasionally, when there is significant mass effect and impending herniation, other measures may be required until corticosteroids have had a chance to take effect or until patients undergo debulking surgery. These include elevation of the head of the bed, fluid restriction, mannitol, hypertonic saline, diuretics, and hyperventilation ^63,64.

After more surgical debulking, steroids should be tapered. The taper can start within a week after surgery but should be delayed in symptomatic patients undergoing RT. In general, patients who have brain tumors exerting significant mass effect should receive steroids for 24 hours before starting RT to reduce intracranial pressure and minimize neurologic symptoms.

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70. The blood brain barrier [Online free full text]

71. Cerebral edema associated with nontraumatic cerebral hemorrhage [Online free full text]

The author: Professor Yasser Metwally

http://yassermetwally.com

INTRODUCTION

November 9, 2009 —  Carbon monoxide (CO) is encountered frequently as a by-product of the burning of many different substances. It is present in automobile exhaust and cigarette smoke and is a metabolite of methylene chloride, which is commonly found in solvents. CO has long been known to cause both short- and long-term CNS effects. This toxic gas causes neural damage by way of tissue hypoxia and free radical production. It binds to hemoglobin in the blood, decreasing the ability of blood to deliver oxygen to body tissues. It also disrupts oxidative phosphorylation in mitochondria, leading to indirect damage to the brain and other tissues with high metabolic demands. CO exerts direct neurotoxic effects at the cellular level and has been shown to cause lipid peroxidation, leading to white matter destruction [1–3].

Headache, dizziness, confusion, and visual changes are common symptoms of CO exposure, but signs of cerebral dysfunction may be absent acutely. Nausea, abdominal pain, shortness of breath, and generalized weakness are commonly reported [1]. Delayed onset of encephalopathic features after apparent full recovery has been estimated to occur in up to 30% of CO victims. Symptoms of cognitive decline, personality changes, psychosis, and parkinsonism may begin anywhere from a few days to several months following the exposure. The mechanisms for this syndrome are not well defined, but recovery occurs in 50% to 75% of victims within a year [4,5].

CO levels in exhaled air can be measured by emergency personnel at the scene of exposure. Blood level of carboxyhemoglobin is the most sensitive marker for confirming the diagnosis and determining level of toxic exposure. It should be noted that smokers have elevated levels of carboxyhemoglobin at baseline. Furthermore, blood carboxyhemoglobin levels begin to decline quickly after removal of the exposure. Levels should therefore be drawn as soon as possible when an accurate estimation of level of exposure is needed [1]. Following stabilization of the victim, neuropsychologic testing is recommended and provides a means of following the clinical course thereafter. The Carbon Monoxide Neuropsychological Screening Battery is an easy-to-use test developed specifically for evaluation of CO victims [6].

After the source of exposure has been removed, providing fresh air is the first priority in treatment. Hyperbaric oxygen therapy greatly enhances recovery from acute symptoms; however, it is unclear whether it decreases the incidence of the delayed neuropsychiatric syndrome or improves long-term outcome. It is nonetheless recommended when the victim is unconscious for any period of time, has an abnormal score on the Carbon Monoxide Neuropsychological Screening Battery, has a carboxyhemoglobin level>40%, or in the presence of certain other complicating medical factors [1].

Figure 1. MRI study in a patient with carbon monoxide poisoning showing symmetric abnormal signal in the globi pallidi. (Click to enlarge figure)

References

1. Ernst A, Zibrak JD. Carbon monoxide poisoning. N Engl J Med. 1998;339:1603–1608.
2. Thom SR. Carbon monoxide-mediated brain lipid peroxidation in the rat. J Appl Phys. 1990;68:997–1003.
3. Thom SR. Leukocytes in carbon monoxide-mediated brain oxidative injury. Toxicol Appl Pharmacol. 1993;123:234–247.
4. Choi IS. Delayed neurologic sequelae in carbon monoxide intoxication. Arch Neurol. 1983;40:433–435.
5. Min SK. A brain syndrome associated with delayed neuropsychiatric sequelae following acute carbon monoxide intoxication. Acta Psychiatr Scand. 1986;73:80–86.
6. Messiers LD, Myers RAM. A neuropsychological screening battery for emergent assessment of carbon-monoxide poisoned patients. J Clin Psychol. 1991;47:675–684.
7. Metwally, MYM: Textbook of neuroimaging, A CD-ROM publication, (Metwally, MYM editor) WEB-CD agency for electronic publication, version 10.4a October 2009 [Click to have a look at the home page]

The author: Professor Yasser Metwally

http://yassermetwally.com

INTRODUCTION

November 9, 2009 — In this case record professor Metwally discusses a case presented with the clinical diagnosis of Paraneoplastic leukoencephalopathy. The case is presented online and in downloadable PDF format.

A 48-year-old female patient was admitted to our hospital due to sudden gait disturbance. One month prior to the admission, She suddenly began to experience difficulty performing simple calculations and dressing himself. This patient visited a local hospital, where She was diagnosed with cerebral infarction and treated with anticoagulation therapy; no relevant disease, medication, smoking, or alcohol history was noted. She had lost 8 kg in the 6 months prior to this event, and She was easily fatigued and experienced night sweating and general weakness. Her cognitive impairment worsened over the next several weeks. She visited our hospital in order to obtain a second opinion.

Click here to download the case record in PDF format (802 KB) 

Click here to download the short case version of this case record in PDF format (107 KB)

Lecture 1. Paraneoplastic leukoencephalopathy

Slide show 1. Case radiology

Click here to download the case record in PDF format (802 KB)

Click here to download the short case version of this case record in PDF format (107 KB)

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References

1. Glass J. Neurologic complications of lymphoma and leukemia. Semin Oncol. 2006;33:342–347.

2. Yoon JH, Bang OY, Kim HS. Progressive multifocal leukoencephalopathy in AIDS: proton MR spectroscopy patterns of asynchronous lesions confirmed by serial diffusion weighted imaging and apparent diffusion coefficient mapping. J Clin Neurol. 2007;3:200–203.

3. Phanthumchinda K, Rungruxsirivorn S. Encephaloradiculopathy: a non-metastatic complication of hepatocellular carcinoma. J Med Assoc Thai. 1991;74:288–291.

4. Gonzales N, Jarboe E, Kleinschmidt-DeMasters BK, Bosque P. Acute multifocal CNS demyelination as first presentation of systemic malignancy. Neurology. 2005;65:166.

5. Song DK, Boulis NM, McKeever PE, Quint DJ. Angiotropic large cell lymphoma with imaging characteristics of CNS vasculitis. AJNR Am J Neuroradiol. 2002;23:239–242.

6. Brecher K, Hochberg FH, Louis DN, de la Monte S, Riskind P. Case report of unusual leukoencephalopathy preceding primary CNS lymphoma. J Neurol Neurosurg Psychiatry. 1998;65:917–920.

7. Lövblad KO, Laubach HJ, Baird AE, Curtin F, Schlaug G, Edelman RR, et al. Clinical experience with diffusion-weighted MR in patients with acute stroke. AJNR Am J Neuroradiol. 1998;19:1061–1066.

8. Fleming JO, Keegan BM, Parisi JE. A 52-year-old man with progressive left-sided weakness and white matter disease. Neurology. 2007;69:600–606.

9. Karaarslan E, Arslan A. Diffusion weighted MR imaging in non-infarct lesions of the brain. Eur J Radiol. 2008;65:402–416.

10. Baehring JM, Henchcliffe C, Ledezma CJ, Fulbright R, Hochberg FH. Intravascular lymphoma: magnetic resonance imaging correlates of disease dynamics within the central nervous system. J Neurol Neurosurg Psychiatry. 2005;76:540–544.

11. Palmedo H, Urbach H, Bender H, Schlegel U, Schmidt-Wolf IG, Matthies A, et al. FDG-PET in immunocompetent patients with primary central nervous system lymphoma: correlation with MRI and clinical follow-up. Eur J Nucl Med Mol Imaging. 2006;33:164–168.

12. Tenembaum S, Chitnis T, Ness J, Hahn JS. International Pediatric MS Study Group. Acute disseminated encephalomyelitis. Neurology. 2007;68(16) Suppl 2:S23–S36.

13. jean WC, Dalmau J, Ho A, Posner JB: Analysis of the IgG subclass distribution and inflammatory infiltrates in patients with anti-Hu-associated paraneoplastic encephalomyelitis. Neurology 44:140-147,1994

14. Bird Sj, Brown Mj, Shy ME, Scherer SS: Chronic inflammatory demyelinating polyneuropathy associated with malignant melanoma. Neurology 46:822-824,1996

15. Metwally, MYM: Textbook of neuroimaging, A CD-ROM publication, (Metwally, MYM editor) WEB-CD agency for electronic publication, version 10.4a October 2009 [Click to have a look at the home page]

16. Praneoplastic neurological syndromes [Full text in PDF format...420]

The author: Professor Yasser Metwally

http://yassermetwally.com

INTRODUCTION

November 8, 2009 —  Temporal lobe epilepsy

Lecture 1. Temporal lobe epilepsy  (Click to download in PDF format ..270 KB)

1. Metwally, MYM: Textbook of neuroimaging, A CD-ROM publication, (Metwally, MYM editor) WEB-CD agency for electronic publication, version 10.4a October 2009 [Click to have a look at the home page]

2. EEG in the evaluation of focal cerebral dysfunction (April 2009) ( 280 KB)  (Click to download in PDF format)

3. Brainmapping and focal epileptic disorders (February 2009) (410 KB) (Click to download in PDF format)

4. Issues in brainmapping [Get connected]

5. Issues in brainmapping [Get connected]

The author: Professor Yasser Metwally

http://yassermetwally.com

INTRODUCTION

November 8, 2009 —  Brainmapping and focal epileptic disorders

Lecture 1. Brainmapping and focal epileptic disorders (Click to download in PDF format ..410 KB)

1. Metwally, MYM: Textbook of neuroimaging, A CD-ROM publication, (Metwally, MYM editor) WEB-CD agency for electronic publication, version 10.4a October 2009 [Click to have a look at the home page]

2. Temporal lobe epilepsy (January 2009) (270 KB) (Click to download in PDF format)

3. Issues in brainmapping [Get connected]

4. Issues in brainmapping [Get connected]

The author: Professor Yasser Metwally

http://yassermetwally.com

INTRODUCTION

November 8, 2009 —  Generalized epilepsies

Lecture 1. Generalized epilepsies (Click to download in PDF format ..237 KB)

1. Metwally, MYM: Textbook of neuroimaging, A CD-ROM publication, (Metwally, MYM editor) WEB-CD agency for electronic publication, version 10.4a October 2009 [Click to have a look at the home page]

2. Brainmapping and focal epileptic disorders (February 2009) (410 KB) (Click to download in PDF format)

3. Temporal lobe epilepsy (January 2009) (270 KB) (Click to download in PDF format)

4. Issues in brainmapping [Get connected]

5. Issues in brainmapping [Get connected]

The author: Professor Yasser Metwally

http://yassermetwally.com

INTRODUCTION

November 8, 2009 — Differential diagnosis of ring-enhancing lesions on neuroimaging

References

1. Metwally, MYM: Textbook of neuroimaging, A CD-ROM publication, (Metwally, MYM editor) WEB-CD agency for electronic publication, version 10.4a October 2009 [Click to have a look at the home page]