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Definition of Some conventional EEG terminologies
Feb 15th, 2013 by Administrator

The author: Professor Yasser Metwally

http://yassermetwally.com


INTRODUCTION

February 15, 2013 — Definition of Some conventional EEG terminologies. While inspecting an EEG record, have you ever asked your self what exactly is meant by sharp wave, spike, spike/wave discharge, hypsarrhythmia, triphasic waves, etc…?

In this slide show Professor Yasser Metwally discusses the Definition of Some conventional EEG terminologies.

Click here to download file in PDF format

Lecture 1. Definition of Some conventional EEG terminologies

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]

  2. The secrets of conventional EEG (Click to download in PDF format]

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Thesis section: Current status of Quantitative EEG
Feb 13th, 2013 by Administrator

The author: Professor Yasser Metwally

http://yassermetwally.com


INTRODUCTION

February 13, 2013 — Thesis section: Current status of Quantitative EEG

This master degree thesis was presented by Dr. Ayman Amin and supervised by Professor Yasser Metwally. The thesis discusses the subject of “Current status of Quantitative EEG”, The thesis can be viewed online or downloaded in PDF format

Click here to download thesis in PDF format (3200 KB)

 

Lecture 1. View thesis online…Thesis section: Current status of Quantitative EEG

Click here to download thesis in PDF format (3200 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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Ehlers-Danlos syndrome
Dec 15th, 2012 by Administrator

The author: Professor Yasser Metwally

http://yassermetwally.com


INTRODUCTION

December 15, 2012 — Ehlers-Danlos syndrome constitutes a group of connective tissue disorders characterized by clinical and genetic variability.[3] Mutations in 8 separate genes contribute to these phenotypes. Earlier reports were focused on the skin and ocular abnormalities. The heterogeneity began to be appreciated in the past few decades, from the insights gained from biochemical and molecular genetic studies.[1]

Ehlers-Danlos syndrome type 1 has an autosomal dominant inheritance and affected individuals have soft, velvety, hyperextensible skin, joint hypermobility, easy bruisablility and thin, atrophic ‘cigarette-paper’ scars following trauma. About 50% of the infants with EDS 1 are born 4 to 8 weeks prematurely because of the fragile fetal membranes as in our Patient 3. [1] Neurological manifestation other than stroke and hypotonia include peripheral neuropathy,[4] epilepsy,[5] neuronal migration disorders,[3,6] Melkerson – Rosenthal syndrome,[7] familial spastic ataxia[8] and dentatopallido luysian atrophy.[9] EDS has a prevalence of 1 in 10,000 persons. It is therefore possible that these neurological illnesses coexist rather than causally linked.[1] Rare manifestations like neuropathy, optic atrophy, deafness, cerebellar ataxia, chorea, myotonia, calf hypertrophy, polymicrogyria and mirror movements ale also noted.

Defects in extra cellular matrix proteins have been proposed as a mechanism for arterial aneurysms and EDS IV.[10] Disruption between the extracellular matrix and cytoskeleton causes aberrations in cellular migration. This might result in various congenital malformations of the brain parenchyma like neuronal migration disorders.[5] The extracellular matrix proteins involved may affect collagen or tenascins, a family of glycoproteins expressed in the surface of neurons and glial cells.[6] Mice deficient in small leucine rich proteoglycans develop osteoporosis, EDS, muscular dystrophy and corneal diseases. This may be the link between some cases of muscular dystrophy and EDS.[11]

Ehlers-Danlos syndrome may affect all level of neuraxis. A careful search may reveal asymptomatic and unrecognized abnormalities, which offer better explanations for the patient’s symptoms and may alter prognosis.


References

1. Byers PH. Disorders of collagen biosynthesis and structure. In: Scriver CR, Beaudet AL, Sly WS, Valle D, editors. The Metabolic and molecular bases of inherited disease. 7th ed. New York: McGraw Hill; 1995;5241-71.

2. Pretorius ME, Butler IJ. Neurologic manifestations of Ehlers-Danlos syndrome. Neurology 1983;33:1087-89.

3. Thomas P, Bossan A, Lacour JP, Chanalet S, Ortonne JP, Chatel M. Ehlers-Danlos syndrome with subependymal periventricular heterotopias. Neurology 1996;46:1165-67.

4. Muellbacher W, Finisterer J, Mamoli B, Bittner RE, Trautinger F. Axonal neuropathy in Ehlers -Danlos syndrome. Muscle Nerve 1998; 21:972-4.

5. Jacome DE. Epilepsy in Ehlers – Danlos Syndrome. Epilepsia 1999;40:467-73.

6. Echaniz-Laguna A, de Saint-Martin A, Lafontaine A L, Tasch E, Thomas P, Hirsh E et al. Bilateral Focal Polymicrogyria in Ehlers – Danlos syndrome. Arch Neurol 2000;57:123-7.

7. Caksen H, Cesur Y, Tombul T, Uner A, Kirimi E, Tuncer O et al. A case of Melkersson-Rosenthal syndrome associated with Ehlers – Danlos syndrome. Genet Couns 2002;13:183-6.

8. Chouza C, Caamano JL, De Medina O, Bogacz J, Oehninger C, Vignale R et al. Familial spastic ataxia associated with Ehlers-Danlos syndrome with platelet dysfunction. Can J Neurol Sci 1984;11:541-549.

9. Sugie K, Nakamuro T, Harada N, Suzumura A, Takayanagi T. A report of two siblings with both maternal dentate-rubro – pallido – luysian atrophy and paternal Ehlers – Danlos syndrome type III. Rinsho Shinkeigaku 1998;38:233-7.

10. North KN, Whiteman DAH, Pepin MG, Byers PH. Cerebrovascular complications in Ehlers-Danlos syndrome type IV. Ann Neurol 1995;38:960-4.

11. Ameye L, Young MF. Mice deficient in small leucine – rich proteoglycans: novel in vivo model for osteoporosis, Ehlers – Danlos syndrome, muscular dystrophy and corneal disease. Glycobiology 2002;12:107-16

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Embolic brain infarction
Nov 20th, 2012 by Administrator

The author: Professor Yasser Metwally

http://yassermetwally.com


INTRODUCTION

November 20, 2012 — In embolic cerebral infarction, the occlusive material originates from an area proximal to the occluded artery. Emboli most frequently arise from the heart or from atherosclerotic plaques involving the carotid bifurcation or vertebral arteries. The common causes of cardiac emboli include thrombi associated with myocardial infarction or cardiac arrhythmias, valvular disease (including prosthetic valves), bacterial or nonbacterial endocarditis, and atrial myxomas. The ulceration of atherosclerotic plaques produces cholesterol or calcific emboli. Rare embolic causes of infarction are nitrogen emboli from rapid decomposition, fat emboli from long bone fractures, and iatrogenic air emboli.

The location and temporal evolution of embolic infarction differ from thrombotic infarction. Embolic particles shower the intracranial cerebral circulation, often causing multiple peripheral infarcts in different major arterial distributions. Embolic occlusions frequently fragment and lyse between the first and fifth days, which re-establishes normal circulation. These findings differ from the relatively permanent occlusion of a single major vascular distribution with atherosclerotic thrombotic infarction. Fragmentation and lysis of embolic occlusion produces a higher perfusion pressure than that seen with simple occlusion (in which collateral vessels supply the circulation). There is also a loss of normal autoregulation of the cerebral vasculature, which can persist for several weeks. These factors produce hyperemia or luxury perfusion, with blood flow to the infarcted region greater than its metabolic requirements. This higher perfusion pressure can also cause hemorrhage into the infarct and conversion of a bland anemic infarct into a hemorrhagic one. This hemorrhage usually occurs between 6 hours and 2 weeks after the embolic event. Anticoagulant treatment of bland anemic infarcts can also result in hemorrhage.

Click to enlarge figure Click to enlarge figure

Figure 1. Haemorrhagic embolic infarctions. They have frankly hemorrhagic features which consist of petechial zones that are frequently confluent and are situated in the cortex.

Click to enlarge figure Click to enlarge figure

Figure 2. A, Plain CT scan showing middle cerebral artery embolic hemorrhagic infarction, notice petechial zones situated in the basal ganglia, B, MRI T2 image showing a left sided hemorrhagic infarction, notice cortical hypointense petechial zones composed mainly of deoxyhemoglobin

Before lysis of the embolus, the MRI appearance of embolic infarction is similar to that of thrombotic infarction. However, in contrast to thrombotic infarctions, embolic infarctions are often multiple, may be located in more than one vascular distribution, and are approximately of the same age. After fragmentation of the embolus and the subsequent increase in perfusion pressure, a hemorrhagic infarction often develops. Most commonly, the hemorrhage in a hemorrhagic embolic infarction is petechial in nature and cortical in location. Occasionally, an intraparenchymal hematoma develops in the infarcted region. Development of secondary hemorrhage is characteristic of embolic infarction but can be seen with thrombotic or hemodynamic infarction.



References

  1. Metwally, MYM: Textbook of neuroimaging, A CD-ROM publication, (Metwally, MYM editor) WEB-CD agency for electronic publication, version 12.4 October 22 [Click to have a look at the home page]

  2. Case of the week: Hemorrhagic embolic infarction. Click here to download case record in PDF format

  3. CT scan imaging of acute cerebral infarction: Hemorrhagic infarction [Full text]

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Textbook of clinical electroencephalography
Sep 12th, 2012 by Administrator

The author: Professor Yasser Metwally

http://yassermetwally.com


INTRODUCTION

September 12, 2012 — This publication covers the clinical aspect of conventional EEG. It simply reflects thing the way I understand, deals with and interpret a conventional EEG tracing. The textbook is composed of 410 pages that can be printed.

Conventional EEG has fallen short of expectation not because of its limited value, but rather because it is rarely ordered by a Knowledgeable clinician and interpreted by an electroencephalographer in a way most useful to the patient.

Another reason why Conventional EEG have fallen short of expectation, is its impressionistic, qualitative nature and this strongly reflects the needs for quantitative EEG. Quantitative EEG (Also called brainmapping, EEG cartography, Brain electrical activity mapping, BEAM) is a wonderful way that reflects the brain function in real time and in a totally non-invasive way. A short notice is given to brainmapping at the end of this textbook.

I really hope you will find this publication as useful as a truly wish. This publication is distributed free of charge, it is placed in the public domain as soon as it is uploaded and can be freely distributed on two conditions;

1- It is not changed in any way

2- It is distributed free of charge

Click to download PDF version of the publication (Server 1) 10 MB

Click to download PDF version of the publication (Server2) 10 MB

Click to download software version of the publication (10 MB)

Click to download PDF version of the publication (Server 1) 10 MB

Click to download PDF version of the publication (Server2) 10 MB

Click to download software version of the publication (10 MB)


  1. Metwally, MYM: Textbook of neuroimaging, A CD-ROM publication, (Metwally, MYM editor) WEB-CD agency for electronic publication, version 13.1 July 2012 [Click to have a look at the home page]

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