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Microvascular Diseases of the Brain: An Update
Nov 4th, 2013 by Administrator

The author: Professor Yasser Metwally

http://yassermetwally.com


INTRODUCTION

October 1, 2013 — Thesis section: Microvascular Diseases of the Brain: An Update

This master degree thesis was presented by Dr. Mohammed Regab and supervised by Professor Yasser Metwally. The thesis discusses the subject of “Microvascular Diseases of the Brain”, The thesis can be viewed online or downloaded in PDF format

Click here to download thesis in PDF format (2020 KB)

Lecture 1. View thesis online…Thesis section: Microvascular Diseases of the Brain: An Update

Click here to download thesis in PDF format (2020 KB)


References

  1. Metwally, MYM: Textbook of neuroimaging, A CD-ROM publication, (Metwally, MYM editor) yassermetwally.com corporation, version 14.1 January 2013 [Click to have a look at the home page]

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MRI picture of subarachnoid hemorrhage
May 23rd, 2013 by Administrator

The author: Professor Yasser Metwally

http://yassermetwally.com


INTRODUCTION

May 23, 2013 — The pathophysiology of subarachnoid hemorrhage and the physical principles of CT explain the change in sensitivity of CT in detecting subarachnoid hemorrhage with time from ictus. X Ray techniques including CT produce tissue contrast because of the proportion of the incident X ray beam that is stopped (attenuated) by the tissue. This relies on two factors: the amount of tissue traversed by the beam and the attenuation coefficient of the tissue. The attenuation coefficient bears a direct relation to the electron density of the tissue. Fresh haemorrhage has the same electron density as brain and other soft tissues and so hyperacute (within 2 hours of ictus) subarachnoid hemorrhage may not be seen directly on CT. As reabsorption of serum from a haematoma progresses the local packed cell volume, and hence electron density, increases making acute subarachnoid hemorrhage visible as a high attenuating “white” area. With the passage of further time subarachnoid hemorrhage becomes less visible on CT principally because of two processes. Firstly, CSF circulation redistributes focal subarachnoid hemorrhage into other parts of the subarachnoid space and ventricular system. The resulting dilution reduces the conspicuity on CT. Secondly, reabsorption of serum is followed by reabsorption of the protein component, which also leads to reduced conspicuity. Consequently the sensitivity of CT to subarachnoid hemorrhage falls drastically over the first 14 days from ictus. [4]

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Magnetic resonance imaging does not directly rely on the electron density of substances for its contrast resolution. The MR signal principally relies on proton (hydrogen nuclei) density, and T1 and T2* (which includes the T2 component) relaxation times. The different physical and chemical states of iron within haemorrhage have profound effects on the MR signal. [14] Standard spin echo MR sequences are considered to be insensitive in detecting acute haemorrhage; however, MR imaging offers two possibilities for improved detection of subarachnoid hemorrhage, both of which depend on the appearance of haemoglobin and its breakdown products.

The protein component produces high T2 signal which is swamped by the bright T2 signal from CSF on a conventional T2 weighted image. FLAIR sequences suppress the CSF signal and allow the signal from globin and its breakdown products to be seen. FLAIR has been reported to be a sensitive test for subarachnoid hemorrhage in the subacute phase. [7]

Iron in the form of Fe3+ or Fe2+ is paramagnetic. The presence of paramagnetic species in the CSF leads to localised perturbations in the magnetic field “seen” by the MR visible hydrogen nuclei. This leads to an increase in the precession rate in the immediate vicinity of Fe ions on the atomic scale and hence a faster dephasing and loss of T2* signal. Gradient echo sequences with significant T2* weighting are particularly sensitive to this localised change and are thus suited to detecting subarachnoid hemorrhage, even in the acute stage.

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Figure 1. MRI T1 image showing a precontrast hyperintensity in the right parieto-occipital region and in the 4th ventricle due to the presence of methemoglobin in the subarachnoid spaces secondary to subarachnoid hemorrhage

The combination of lumbar puncture and CT is sensitive and specific for acute subarachnoid hemorrhage. CT suffers from a loss of sensitivity to subarachnoid hemorrhage in the subacute phase. MRI, particularly FLAIR and T2*, may be able to supplement CT in this situation. Both FLAIR and T2* can be performed on standard MR scanners.

Appropriately selected MR sequences are sensitive and specific in the detection of subarachnoid hemorrhage. This is by contrast with the widespread view in the clinical neuroscience literature, although some reports [7] show the value of FLAIR in detecting subarachnoid hemorrhage. one practical point of view in this chapter is that MR using FLAIR and T2* sequences together is a valuable tool in the detection of subarachnoid hemorrhage.

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Figure 2. An acute subarachnoid hemorrhage. Brain CT was performed on the day of the haemorrhage; MR scans were taken 48 hours later. (A) CT shows blood in the interhemispheric fissure which is not seen on a comparable MR cut with (B) a T1 weighting sequence or (C) a fast spin echo T2 weighting sequence. (D) subarachnoid hemorrhage is seen on the gradient echo T2* image as an area of low signal. Lower cuts on the same patient show interhemispheric, sylvian, and cisternal blood on (E) CT and (F) T2* MR.

  • Conclusions

Sensitivity to subarachnoid hemorrhage varied among the five MR sequences studied from 50% to 94% in acute subarachnoid hemorrhage and from 33% to 100% in subacute subarachnoid hemorrhage. The most sensitive sequences were FLAIR and T2* with T2* performing slightly better than FLAIR. The sensitivity of T2* was 94% under 4 days from the ictus and 100% between 4 and 14 days.

Fluid-attenuated inversion recovery (FLAIR) is the most sensitive MRI pulse sequence for the detection of subarachnoid hemorrhage (subarachnoid hemorrhage). On FLAIR images, subarachnoid hemorrhage appears as high signal-intensity (white) in normally low signal-intensity (black) CSF spaces. In cases of subarachnoid hemorrhage, FLAIR and CT scanning have similar findings. T2- and T2*-weighted images can potentially demonstrate subarachnoid hemorrhage as low signal-intensity in normally high signal-intensity subarachnoid spaces. On T1-weighted images, acute subarachnoid hemorrhage may appear as intermediate-intensity or high-intensity signal in the subarachnoid space.

MRA may be useful for evaluating aneurysms and other vascular lesions that cause subarachnoid hemorrhage. The low sensitivity for aneurysms smaller than 5 mm, the inability to evaluate small aneurysm contour irregularities, and difficulty in obtaining high-quality images in patients who are agitated or confused limits the utility of MRI in the diagnosis of acute subarachnoid hemorrhage.

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Figure 3. A subtle subacute subarachnoid hemorrhage. (A) Brain CT was done 7 days after the haemorrhage and shows abnormal isointense material in the suprasellar cistern and along the path of the left middle cerebral artery towards the sylvian fissure. (B) A comparable slice of FLAIR MR imaging done 24 hours after the CT. It shows the abnormality more clearly as high signal material in the left side of the suprasellar cistern and left sylvian fissure (arrows) in keeping with subacute subarachnoid hemorrhage. (C) The same area shows as low signal on T2* MR imaging (arrow). (D) One slice down from C illustrates a problem with the T2* images. The low signal arising from the boundary between tissues of differing susceptibility—in this case the surface of the right lesser sphenoid wing (arrow)—obscures any additional low signal due to blood in the sylvian fissure and could be misinterpreted as blood. This is one reason why we regard the FLAIR and T2* sequences as complementary rather than alternatives.

Degree of confidence of FLAIR images

In vivo and in vitro studies suggest that FLAIR MRI is as sensitive as or more sensitive than CT scanning in the evaluation of acute subarachnoid hemorrhage; however, compared with lumbar puncture, FLAIR MRI cannot exclude subarachnoid hemorrhage. Relative to CT scanning, MRI is often more valuable in the subacute phase of subarachnoid hemorrhage, in which the density of hemorrhage on CT scans decreases. In patients with equivocal findings on CT scanning or angiography or in those patients who cannot undergo CT scanning or conventional angiography, MRI and/or MRA may provide clinically useful information.

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Figure 4. A CT negative subarachnoid hemorrhage as confirmed by lumbar puncture. (A) Brain CT taken 4 days after the onset of headache is normal. The MR scans were done within 1 hour of the CT. (B) The T2* image closest to the slice of A. It shows an area of low signal (arrow). (C) The corresponding FLAIR image shows high signal from the same area (arrow). Note the different angulation used for CT and MR images.

False positives/negatives of Flair images

Magnetic field inhomogeneity can lead to artifactual increase in signal intensity in sulci over the cerebral convexities on FLAIR images, which can mimic subarachnoid hemorrhage. CSF flow artifacts can mimic the appearance of subarachnoid hemorrhage on either T1- or T2-weighted images. Intracranial thrombus can appear similar in signal to flowing blood on time-of-flight (TOF) gradient-echo (GRE) MRA. In uncooperative patients, motion artifacts may produce images that can lead to either false-positive or false-negative interpretations.

Hyperintensity in the subarachnoid space on FLAIR images can also be secondary to other pathologies, such as meningitis or meningeal carcinomatosis. It is important to know whether recent contrast-enhanced MRIs have been performed, as delayed leakage of gadolinium into the subarachnoid space can result in hyperintense signal on FLAIR images. This has been reported to result from contrast studies performed 24-48 hours before MRI scanning in patients without renal failure and without abnormalities known to disrupt the blood-brain barrier. Substantial increases in subarachnoid FLAIR signal have also been reported in patients receiving 100% supplemental oxygen.


References

1.Vermeulen M, van Gijn J (1990) The diagnosis of subarachnoid haemorrhage. J Neurol Neurosurg Psychiatry 53:365–372.

2. Morgenstern LB, Luna-Gonzales H, Huber JC, Jr, et al. (1998) Worst headache and subarachnoid hemorrhage: prospective, modern computed tomography and spinal fluid analysis. Ann Emerg Med 32:297–304.

3. Sidman R, Connolly E, Lemke T (1996) Subarachnoid hemorrhage diagnosis: lumbar puncture is still needed when the computed tomography scan is normal. Acad Emerg Med 3:827–831.

4. van Gijn J, van Dongen KJ (1982) The time course of aneurysmal haemorrhage on computed tomograms. Neuroradiology 23:153–156.

5. van Gijn J, van Dongen KJ (1980) Computed tomography in the diagnosis of subarachnoid haemorrhage and ruptured aneurysm. Clin Neurol Neurosurg 82:11–24.

6. Vermeulen M, Hasan D, Blijenberg BG, et al. (1989) Xanthochromia after subarachnoid haemorrhage needs no revisitation. J Neurol Neurosurg Psychiatry 52:826–828.

7. Noguchi K, Ogawa T, Inugami A, et al. (1994) MR of acute subarachnoid hemorrhage: a preliminary report of fluid-attenuated inversion-recovery pulse sequences. AJNR Am J Neuroradiol 15:1940–1943.

8. Singer MB, Atlas SW, Drayer BP (1998) Subarachnoid space disease: diagnosis with fluid-attenuated inversion-recovery MR imaging and comparison with gadolinium-enhanced spin-echo MR imaging-blinded reader study. Radiology 208:417–422.

9. Noguchi K, Ogawa T, Seto H, et al. (1997) Subacute and chronic subarachnoid hemorrhage: diagnosis with fluid-attenuated inversion-recovery MR imaging. Radiology 203:257–262.

10. Noguchi K, Ogawa T, Inugami A, et al. (1995) Acute subarachnoid hemorrhage: MR imaging with fluid-attenuated inversion recovery pulse sequences. Radiology 196:773–777.

11. Kates R, Atkinson D, Brant-Zawadzki M (1996) Fluid-attenuated inversion recovery (FLAIR): clinical prospectus of current and future applications. Top Magn Reson Imaging 8:389–396.

12. Chrysikopoulos H, Papanikolaou N, Pappas J, et al. (1996) Acute subarachnoid haemorrhage: detection with magnetic resonance imaging. Br J Radiol 69:601–609.

13. Ogawa T, Inugami A, Fujita H, et al. (1995) MR diagnosis of subacute and chronic subarachnoid hemorrhage: comparison with CT. AJR Am J Roentgenol 5:1257–1262.

14. Vymazal J, Brooks RA, Baumgarner C, et al. (1996) The relation between brain iron and NMR relaxation times: an in vitro study. Magn Reson Med 35:56–61.

15. Mikami T, Saito K, Okuyama T, et al. (1996) FLAIR images of subarachnoid hemorrhage. No Shinkei Geka 24:1087–1092, . (In Japanese.).

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Role of Oxidative Stress in the pathogenesis of neurodegenerative disorders
Mar 13th, 2013 by Administrator

The author: Professor Yasser Metwally

http://yassermetwally.com


INTRODUCTION

March 13, 2013 — Thesis section: Role of Oxidative Stress in the pathogenesis of neurodegenerative disorders

This master degree thesis was presented by Dr. David kamel and supervised by Professor Yasser Metwally. The thesis discusses the subject of “Role of Oxidative Stress in the pathogenesis of neurodegenerative disorders”, The thesis can be viewed online or downloaded in PDF format

Click here to download thesis in PDF format (1020 KB)

 

Lecture 1. View thesis online…Thesis section: Role of Oxidative Stress in the pathogenesis of neurodegenerative disorders

Click here to download thesis in PDF format (1020 KB)


References

  1. Metwally, MYM: Textbook of neuroimaging, A CD-ROM publication, (Metwally, MYM editor) yassermetwally.com corporation, version 14.1 January 2013 [Click to have a look at the home page]

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Radiological pathology of Radiological pathology of multisystem atrophy
Feb 12th, 2013 by Administrator

The author: Professor Yasser Metwally

http://yassermetwally.com


INTRODUCTION

February 12, 2012 — Radiological pathology of Radiological pathology of multisystem atrophy

In this topic Professor Yasser Metwally discusses the pathology and pathogenesis of multisystem atrophy and its radiological picture.

Click here to download file in PDF format

 

Lecture 1. View topic online…Topic of the month: Radiological pathology of multisystem atrophy

Click here to download file in PDF format



References

  1. Metwally, MYM: Textbook of neuroimaging, A CD-ROM publication, (Metwally, MYM editor) yassermetwally.com corporation, version 14.1 January 2013 [Click to have a look at the home page]

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Neuroimaging of intracranial hydatid disease
Feb 11th, 2013 by Administrator

The author: Professor Yasser Metwally

http://yassermetwally.com


INTRODUCTION

February 11, 2013 — Hydatidosis in humans occurs when the eggs of Echinococcus granulosus from canine faeces are accidentally ingested. The eggs loose their enveloping layer in the stomach, releasing the larvae. The larvae pass through the wall of the gut into the portal system and are carried to the liver where 65% of the larval load is filtered. Of the rest, 25% are trapped in the lungs (second filter) and less than 10% reach various organs through the systemic circulation [2].

Hydatid disease is caused by two echinococcus organisms. Most are caused by Echinococcus granulosus and less frequently by Echinococcus multilocularis. E. granulosus has a dog or other carnivore as its definite host, and a sheep or other ruminant as the intermediate host. The organism resides within the intestine of the definite host and is anchored to the mucosa by hooklets. The distal aspect of the organism, called the proglottid, contains numerous amounts of eggs, which get excreted in the feces after they detach themselves from the proglottid. Grazing animals ingest the eggs, and after ingestion, the protective chitinous layer of the egg releases the embryo, which moves through the bowel wall into the portal venous or lymphatic system. The liver is the most involved organ in hydatid disease. After establishing itself in the liver, the embryo matures into a cyst. When the intermediate host dies, its organs are eaten by the definite host, and the life cycle is completed. Human infection occurs by contact with the definite host or by drinking or eating contaminated water or vegetables.

  • E. granulosus

The cyst formed by E. granulosus has three layers. The host’s reaction and formation of the fibrous capsule form the outer layer, or pericyst. The size of the fibrous capsule varies between the different infected organs; in the liver, the capsule is thicker than those formed in the brain. The pericyst layer, containing blood vessels, provides nutrients for the parasite. The middle layer, a laminated membrane, is acellular and permits the flow of nutrients inward but does not allow the parasite to cross the membrane. Infection occurs when the middle layer is disrupted. The inner germinal layer produces the middle laminated layer and produces the scolex or larval stage. The scolices may also be manufactured by brood capsules (small spheres of disrupted germinal membrane) and can persist attached to the germinal membrane or combine with free-floating brood capsules to form hydatid sand or white sediment. The fluid contained within the cyst is a clear, antigenic, transudative serum-containing protein. Cyst rupture can occur and may produce no symptoms or symptoms ranging from eosinophilia to anaphylaxis.

Most hydatid cysts are acquired in childhood but are not diagnosed until the 20s or 30s. Ten percent to 25% may present in childhood. 1 Many cysts are found incidentally, but most symptomatic cysts have ruptured and may be secondarily infected. The most commonly affected organ systems are the liver (65% to 75%) and lung (15% to 20%) with the remaining 5% to 20% encompassing the entire body. Central nervous system involvement occurs in 5% of cases.

Cardiac contraction provides an unfavorable environment for the cysts in the heart, thus cardiac implantation is uncommon. The majority of patients with cardiac hydatidosis are asymptomatic and present due to embolic dissemination of hydatid cysts elsewhere. In a case report by Turgut et al the patient presented with cerebral hydatidosis and acute vascular occlusion of the right femoral and left internal carotid arteries, consequent to embolic dissemination from a left ventricular hydatid cyst. [3]. Trehan et al reported a case, which presented with a left basal ganglionic infarct secondary to a left atrial hydatid cyst [2]. However, sudden death resulting from anaphylactic shock and cardiac tamponade due to rupture of cysts into the blood stream or pericardium respectively has been reported. Location wise the left ventricle (75%), right ventricle (18%) and interventricular septum (7%) are the usual sites. Two-dimensional echocardiography is the best diagnostic procedure for demonstration of cardiac hydatid cysts [2].

Orbital hydatid cysts typically present with gradually progressive proptosis and diminished extra ocular motility. MR and CT imaging characteristics are non-specific, and the differential diagnosis includes congenital cysts like colobomatous cysts, optic nerve sheath meningoceles and hematic cysts. Colobomatous cysts are usually associated with micropthalmia while a hematic cyst contains blood and has a typical appearance on MRI. An optic nerve sheath meningoceles may occur primarily or secondarily (in association a optic nerve pilocytic astrocytoma or meningioma). These meningoceles can be associated with empty sella or enlarged subarachnoid cistern, such as gasserian cistern. [4] In a hydatid endemic area, a unilateral intraconal cystic mass in the presence of a positive hydatid serology should prompt a diagnosis of orbital hydatid cyst [5].

Intracranial hydatid cysts are classified as primary or secondary. The primary cysts, which are the commoner variety, are formed as a result of direct infestation of the larvae in the brain without demonstrable involvement of other organs and are mostly solitary. Supratentorial location is most frequent with a preference for the parietal lobe. These primary cysts are fertile as they contain scolices and brood capsules, hence rupture of primary cyst (e.g. during surgery) can result in dissemination. The secondary cysts on the other hand are less common and are always multiple. They arise from the rupture of a primary hydatid cyst (which may be intracranial or extra cranial). These cysts lack brood capsule and scolices and therefore are infertile and the resultant risk of recurrence after their rupture is negligible. However, recurrent secondary cysts formation can occur from repeated embolic phenomenon from a viable primary source. In the case report by Turgut et al [3], the patient underwent 5 surgeries over a period of 8 years for recurrent multiple intracranial hydatid cysts before the primary cardiac source was detected. Thus, it is essential to look for a primary source in case of multiple intracerebral hydatidosis, as only by eradicating the primary cysts will a cure be achieved.

MR and CT cannot distinguish primary from secondary cysts. Generally, multiplicity of the cysts strongly favors the diagnosis of secondary cysts and should prompt a search for a primary source elsewhere. Both modalities characteristically show hydatid cyst as a spherical, well-defined, non-enhancing cystic lesion without peripheral edema[6,7]. The fluid density is generally equal to that of CSF on both CT and MR scan. A fine rim of peripheral enhancement with perilesional edema may be seen in the presence of active inflammation [8] MR scan may show a low density cyst wall [7] and relations with surrounding structures are better delineated than on CT scan [6,7]. Kohli et al [8] performed in vivo and in vitro MR spectroscopy (MRS) studies in a patient of intracranial hydatid cyst. Besides lactate, alanine and acetate, a large resonance for pyruvate was observed. MRS pattern appeared different from the other cystic lesions of brain and they suggested MRS as an adjunct to imaging in the differential diagnosis of intracranial hydatid. Role of MRS in monitoring drug therapy was also discussed.

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Figure 1. A, Contrast enhanced CT scan of the orbits demonstrating a large non-enhancing intraconal cystic mass on the left side displacing the globe outwards. C,D, Contrast enhanced CT scan of the brain demonstrating multiple non-enhancing, varying sized, water density cysts without perifocal edema. Observe the mild effacement of the surrounding sulci.

  • Conclusion

In conclusion, multiple hydatid cysts in the central nervous system are invariably secondary. A primary source should always be looked for. A cure can be achieved only by eradicating the primary source. An occult cardiac source can be overlooked and hence it is important to think about this possibility when dealing with central nervous system hydatidosis.

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Figure 2. Postcontrast CT scan showing a huge fronto-parietal hydatid cyst, notice absence of wall enhancement, mural nodules, multiloculations or perifocal edema

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Figure 3. CT scan (A) and TI -weighted (B) and T2-weighted (C) MR images demonstrate a large cystic mass in a patient with a suspected brain tumor. Note the lack of surrounding edema. On the T2 image there is a thin, low signal intensity rim, representing the capsule.

Table 1. Characteristic radiological picture of hydatid disease

  • Absence of wall enhancement

  • Absence of perilesional edema

  • Absence of mural nodule

  • T2-weighted MR images, the best for imaging these lesions, shows a thin, low signal intensity rim, representing the capsule, surrounding a hyperintense lesion.

  • E. multilocularis (E. alveolaris)

The second Echinococcus organism is E. multilocularis. It is similar to E. granulosus except that it grows by external budding of the germinal membrane. The budding causes progressive infiltration of surrounding tissues, giving rise to an amorphous semisolid or multiloculated cystic structure. Ninety-five percent of lesions occur in the liver. Brain involvement has been reported in 5% of cases and vertebral involvement in less than 1%. Surrounding edema and calcification in the wall are more common, helping to distinguish it from E. granulosus. In addition, peripheral enhancement is commonly seen. The differential diagnosis includes metastases, abscesses (including tuberculomas and fungal infection), and gliomas. A primary hepatic focus may help to distinguish these lesions from the others on the list.

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Figure 4. 42-year-old man with headache and weakness attributed to cerebral alveolar hydatid disease. A,CT scan of head shows calcified nodular lesions surrounded by edema in right frontoparietal and left occipital regions. B, Enhanced CT scan shows nodular enhancing lesions. C1, Axial TI-weighted contiguous MR sections show heterogeneous lesions of low signal intensity.C2, Axial T2-weighted contiguous MR sections show lesions of low signal intensity. Note surrounding edema. Calcified areas produce low signal intensity and surrounding edema produces high signal intensity. D, Axial contrast-enhanced TI weighted MR image shows heterogeneous contrast enhancement.

  • Management of Hydatidosis in humans

Albendazole and mebendazole are the only anthelmintics effective against cystic echinococcosis. Albendazole is the drug of choice against this disease because its degree of systemic absorption and penetration into hydatid cysts is superior to that of mebendazole. Albendazole in combination with percutaneous aspiration or PAIR therapy can lead to a reduction in cyst size, and, in one study, it improved efficacy over albendazole alone against hydatid cysts. When surgery cannot be avoided, presurgical use of albendazole in echinococcus infestations reduced risk of recurrence and/or facilitated surgery by reducing intracystic pressure.

Treatment of echinococcosis for patients weighing more than 60 kg is albendazole administered PO with meals in a dose of 400 mg twice daily for 28 days. A dose of 15 mg/kg of body weight daily in 2 divided doses (not to exceed total daily dose of 800 mg) has been suggested for patients weighing less than 60 kg. For CE, the 28-day course may be repeated after 14 days without treatment to a total of 3 treatment cycles..


References

  1. Onal C, Orhan B, Metis O et al , Three unusual cases of intracranial hydatid cysts in paediatric age group. Pediatr Neurosurg 1997; 26 : 208-213.

  2. Trehan V, Shah P, Yusuf J, Mukhopadhyay S, et al, Thromboembolism: A Rare Complication of Cardiac Hydatidosis. Indian Heart J 2002; 54: 199-201

  3. Turgut M, Benli K, Eryilmaz M et al, Secondary multiple intracranial hydatid cysts caused by intracerebral embolism of cardiac ecchinococcosis. Neurosurgery 1997; 86:714-718

  4. Kaufman LM, Villablanca P,Mafee MF, Diagnostic imaging of cystic lesions in the child’s orbit. RCNA 1998; 36:1149-1162

  5. El-Nasser A, Mohammad A,Ray CJ et al,Echinococcus cyst of the orbit and substernum. AJO 1994; 118: 676-678

  6. Nurchi G, Francesco F, Montaldo C et al , Multiple cerebral hydatid disease : case report with magnetic resonance imaging study. Neurosurgery 1992; 30 : 436-438.

  7. Coates R, Von Sinner W, Rahm B : MR imaging of an intracranial hydatid cyst. AJNR1990; 11 : 1249-1250.

  8. Kohli A, Gupta RK, Poptani H et al : In vivo proton magnetic resonance spectroscopy in a case of intracranial hydatid cyst. Neurology 1995; 45 : 562-564.

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