Coronal and Axial T1-Weighted MRI Scan Showing Right Hippocampal Sclerosis (Arrow)http://www.ncbi.nlm.nih.gov/bookshelf/br.fcgi?book=epi&part=ch3&rendertype=figure&id=ch3.f1
Showing posts with label causes of epilepsis. Show all posts
Showing posts with label causes of epilepsis. Show all posts
Friday, June 18, 2010
Wednesday, June 16, 2010
1. Cingulate gyrus2. Corpus callosum
3. Internal capsule
4. Putamen
5. Anterior thalamic nucleus
6. Amygdala
7. Insula
8. Temporal lobe
9. Caudate nucleus
10. External capsule
11. Claustrum
12. Anterior commissure
13. Medial segment of globus pallidus
14. Infundibulum
15. Column of fornix
16. Optic tract
17. Inferior (temporal) horn of lateral ventricle
18. Lateral ventricle
19. Fornix
http://www.bing.com/search?q=anatomy+of+hippocampus&src=IE-SearchBox&FORM=IE8SRC
Major anatomical boundaries of mesial temporal lobe on coronal MRI. A is the most rostral and H is the most caudal MRI section. Only MRIs displaying critical landmarks are shown. (A) The anterior border of the perirhinal cortex (PC) is located at the level of the limen insulae (LI). (B) The anterior border of the entorhinal cortex (EC) begins on average 2 mm behind the limen insulae. This coincides with the appearance of the temporal stem (TS). (C) Section through the hippocampal head (HH). (D) The posterior border of the EC is located at the posterior limit of the gyrus intralimbicus (GI) and coincides with the anterior border of the hippocampal body (HB). (E) The posterior border of the PC is situated 2 mm caudal to the posterior end of the EC. (F) The rostral border of the posterior parahippocampal cortex (PPC) is situated 1 mm caudal to the posterior end of the PC. (G) The anterior border of the hippocampal tail (HT) coincides with the crus fornix (CF) becoming fully visible. (H) The posterior border of the PPC is situated at the level of the posterior end of the hippocampal tail (HT). AM = amygdala; CS = collateral sulcus; FI = fimbria
hippocampus
It is important for converting short term memory to more permanent memory, and for recalling spatial relationships in the world about us.
The hippocampus consists of the complex interfolded layers of the dentate gyrus (1) and cornu ammonis (2). Their three layered cortex is continuous below with the subiculum (3) which has four, five then six layers as it merges with the parahippocampal gyrus (4).
Diagram of the hippocampal anatomy and adjacent structures in the mesial temporal lobe. The cornu ammonis, a part of the hippocampus, can be divided into four fields: CA1, CA2, CA3, and CA4.http://emedicine.medscape.com/article/342150-overview
hippocampal anatomy
The hippocampus, or intralimbic gyrus, is formed by 2 cortical laminae embedded in each other: the cornu ammonis (CA), also called the hippocampus proper or Ammon horn, and the dentate gyrus. The CA can be divided into regions, or fields, depending on the appearance of pyramidal neurons.
The 4 fields (named by Lorente de No in 1934) are characterized as follows8 :
1-CA1, or the Sommer sector, is the most vulnerable region; it is the most sensitive to hypoxia.
2-CA2 is the most resistant and well-preserved sector.
3-CA3, which enters the concavity of the dentate gyrus, is slightly vulnerable.
4-CA4, sometimes called the endfolium, has intermediate vulnerability to insults.
The following 3 patterns of cell loss are described in the hippocampus:
1-Classic Ammon horn sclerosis - Primary neuronal loss involves CA1 and CA4; occurs less often in C3 and least often in CA2
2-Total Ammon horn sclerosis - Severe neuronal loss in all of the hippocampal zones, CA1 to CA4
3-Endfolium sclerosis - Cell loss restricted to CA4
http://emedicine.medscape.com/article/342150-overview
The 4 fields (named by Lorente de No in 1934) are characterized as follows8 :
1-CA1, or the Sommer sector, is the most vulnerable region; it is the most sensitive to hypoxia.
2-CA2 is the most resistant and well-preserved sector.
3-CA3, which enters the concavity of the dentate gyrus, is slightly vulnerable.
4-CA4, sometimes called the endfolium, has intermediate vulnerability to insults.
The following 3 patterns of cell loss are described in the hippocampus:
1-Classic Ammon horn sclerosis - Primary neuronal loss involves CA1 and CA4; occurs less often in C3 and least often in CA2
2-Total Ammon horn sclerosis - Severe neuronal loss in all of the hippocampal zones, CA1 to CA4
3-Endfolium sclerosis - Cell loss restricted to CA4
http://emedicine.medscape.com/article/342150-overview
Coronal T2-weighted magnetic resonance images demonstrate mesial temporal sclerosis on the right, as well as associated findings of a small right mammillary body and a small right fornix.http://emedicine.medscape.com/article/342150-overview
Mesial Temporal Sclerosis
Fluid-attenuated inversion recovery (FLAIR) magnetic resonance images in a 40-year-old patient with complex partial seizures. The right hippocampus is atrophic and has increased signal intensity that is compatible with mesial temporal sclerosis. Other associated findings of mesial temporal sclerosis are present and are better demonstrated on coronal T2-weighted magnetic resonance images than they are on these images.http://emedicine.medscape.com/article/342150-overview
Temporal Lobe Epilepsy
1-Temporal lobe epilepsy (TLE) was defined in 1985 by the International League Against Epilepsy (ILAE) as a condition characterized by recurrent unprovoked seizures originating from the medial or lateral temporal lobe. The seizures associated with temporal lobe epilepsy consist of simple partial seizures without loss of awareness and complex partial seizures (ie, with loss of awareness). The individual loses awareness during a complex partial seizure because the seizure spreads to involve both temporal lobes, which causes impairment of memory. The partial seizures may secondarily generalize.
2-Although the causes of temporal lobe epilepsy are widely varied, hippocampal sclerosis is the most common pathologic finding. Hippocampal sclerosis involves hippocampal cell loss in the CA1 and CA3 regions and the dentate hilus. The CA2 region is relatively spared. The clinical correlate on neuroimaging on MRI is called mesial temporal lobe sclerosis.
3-The etiologies of temporal lobe epilepsy include the following:
a-Infections, eg, herpes encephalitis, bacterial meningitis, neurocysticercosis
b-Trauma producing contusion or hemorrhage that results in encephalomalacia or cortical scarring; difficult traumatic delivery such as forceps deliveries
c-Malignancies (eg, meningiomas, gliomas, gangliomas)
d-Vascular malformations (ie, arteriovenous malformation, cavernous angioma)
e-Cryptogenic: A cause is presumed but has not been identified.
f-Idiopathic (genetic): This is rare. Familial temporal lobe epilepsy was described by Berkovic and colleagues3 , and partial epilepsy with auditory features was described by Scheffer and colleagues.
4-Hippocampal sclerosis produces a clinical syndrome called mesial temporal lobe epilepsy (MTLE).
http://emedicine.medscape.com/article/1184509-overview
2-Although the causes of temporal lobe epilepsy are widely varied, hippocampal sclerosis is the most common pathologic finding. Hippocampal sclerosis involves hippocampal cell loss in the CA1 and CA3 regions and the dentate hilus. The CA2 region is relatively spared. The clinical correlate on neuroimaging on MRI is called mesial temporal lobe sclerosis.
3-The etiologies of temporal lobe epilepsy include the following:
a-Infections, eg, herpes encephalitis, bacterial meningitis, neurocysticercosis
b-Trauma producing contusion or hemorrhage that results in encephalomalacia or cortical scarring; difficult traumatic delivery such as forceps deliveries
c-Malignancies (eg, meningiomas, gliomas, gangliomas)
d-Vascular malformations (ie, arteriovenous malformation, cavernous angioma)
e-Cryptogenic: A cause is presumed but has not been identified.
f-Idiopathic (genetic): This is rare. Familial temporal lobe epilepsy was described by Berkovic and colleagues3 , and partial epilepsy with auditory features was described by Scheffer and colleagues.
4-Hippocampal sclerosis produces a clinical syndrome called mesial temporal lobe epilepsy (MTLE).
http://emedicine.medscape.com/article/1184509-overview
Tuesday, June 15, 2010
Cavernoma on the left (coronal 3.0 T MRI). (A) IRprep T1 weighted image. (B) T2 weighted FLAIR image. Both acquisitions demonstrate heterogeneous hyperintense signal caused by blood products in different stages of evolution, surrounded by a rim of low signal intensity from haemosiderin. (Click here to magnify the figure)
low grade astrocytoma
Dysembryoplastic neuroepithelial tumour on the left (coronal 3.0 T MRI). (A) T2 weighted FLAIR image. (B) Dual echo late echo image (TE 120). The images show a circumscribed multicystic mass with hyperintense signal in the region of the left amygdala. (Click here to magnify the figure)http://yassermetwally.wordpress.com/epilepsy-and-seizure-disorders/neuroimaging-of-seizure-disorders/
Left hippocampal sclerosis (3.0 T MRI). (A) Inversion recovery prepared (IRprep) T1 weighted acquisition showing an atrophic hippocampus (on right of image: arrow). (B) T2 weighted fluid attenuated inversion recovery (FLAIR) image demonstrating increased T2 weighted signal within the sclerotic hippocampus. (C) Early echo image from dual echo data (TE 30 ms). (D) Later echo image from the same dual echo data (TE 120 ms). Hippocampal T2 relaxation times may be obtained using the data from the dual echo sequence. (Click here to magnify the figure)
Hippocampal sclerosis is characterised by neuronal cell loss and gliosis in CA1, CA3, and dentate hilus subfields of the hippocampus, and can be reliably identified with MRI. The hippocampus is best visualised by acquiring thin slices (1–3 mm) orthogonal to its long axis. The primary MRI features of HS are hippocampal atrophy, demonstrated with coronal T1 weighted images, and increased signal intensity within the hippocampus on T2 weighted images . Additionally, decreased T1 weighted signal intensity and disruption of the internal structure of the hippocampus may be present. Other MRI abnormalities associated with hippocampal damage include atrophy of temporal lobe white matter and cortex, dilatation of the temporal horn, and a blurring of the grey-white border in the temporal neocortex. Atrophy of the amygdala and entorhinal cortex variably accompany hippocampal damage but may also occur in patients with TLE and normal hippocampi. FLAIR images provide an increased contrast between grey and white matter and facilitate differentiation of the amygdala from the hippocampus.
http://yassermetwally.wordpress.com/epilepsy-and-seizure-disorders/neuroimaging-of-seizure-disorders/
http://yassermetwally.wordpress.com/epilepsy-and-seizure-disorders/neuroimaging-of-seizure-disorders/
MRI technique for epilepsy diagnosis:
The sensitivity of MRI for detecting abnormalities depends on the pathological substrate, the MRI techniques applied, and the experience of the interpreting physician. A routine optimal MRI protocol should include T1 and T2 weighted, proton density and fluid attenuated inversion recovery (FLAIR) sequences. These contrasts need to be acquired in at least two orthogonal planes covering the whole brain, using the minimum slice thickness possible. An oblique coronal plane, orientated perpendicular to the long axis of the hippocampus, gives the best definition of medial temporal lobe structures. In general, T1 weighted images give the best definition of the anatomy and differentiate grey and white matter, while T2 weighted images provide high sensitivity for detecting pathology in the brain. A three dimensional T1 weighted volume sequence with a partition size of 1.5 mm or less should be included as these images may be reformatted in any orientation and used for post-acquisition processing such as measuring hippocampal volumes. FLAIR imaging produces heavy T2 weighting and suppresses signal from cerebrospinal fluid (CSF). This provides high lesion contrast in areas close to CSF and enables anatomical detail to be seen with greater conspicuity than with conventional T2 weighted sequences. Gadolinium does not improve the sensitivity of MRI in patients with epilepsy, but may be useful to characterise intracerebral lesions associated with breakdown of the blood–brain barrier.
The sensitivity of MRI for detecting abnormalities depends on the pathological substrate, the MRI techniques applied, and the experience of the interpreting physician. A routine optimal MRI protocol should include T1 and T2 weighted, proton density and fluid attenuated inversion recovery (FLAIR) sequences. These contrasts need to be acquired in at least two orthogonal planes covering the whole brain, using the minimum slice thickness possible. An oblique coronal plane, orientated perpendicular to the long axis of the hippocampus, gives the best definition of medial temporal lobe structures. In general, T1 weighted images give the best definition of the anatomy and differentiate grey and white matter, while T2 weighted images provide high sensitivity for detecting pathology in the brain. A three dimensional T1 weighted volume sequence with a partition size of 1.5 mm or less should be included as these images may be reformatted in any orientation and used for post-acquisition processing such as measuring hippocampal volumes. FLAIR imaging produces heavy T2 weighting and suppresses signal from cerebrospinal fluid (CSF). This provides high lesion contrast in areas close to CSF and enables anatomical detail to be seen with greater conspicuity than with conventional T2 weighted sequences. Gadolinium does not improve the sensitivity of MRI in patients with epilepsy, but may be useful to characterise intracerebral lesions associated with breakdown of the blood–brain barrier.
Sunday, June 13, 2010
- The most frequent MRI finding was a focal thinning at the isthmus of the corpus callosum-The second most frequent MRI finding was ventricular asymmetry in the axial and coronal plane
-The next most frequent MRI finding was leukomalacia associated or not with other lesions in the periventricular region . These lesions presented hyperintensity on T2-weighted and FLAIR acquisitions.
-Another frequent finding identified in 12 (16%) of the L children was gliosis, defined as the presence of a round or oval white matter lesions that presented isointensity on T1-weighted images and hyperintensity on T2-weighted and FLAIR images.
-Arachnoid cysts
http://www.google.com.eg/imgres?imgurl=http://www.scielo.br/img/revistas/anp/v64n2a/a03fig02.gif&imgrefurl=http://www.scielo.br/scielo.php%3Fscript%3Dsci_arttext%26pid%3DS0004-282X2006000200003&usg=__aMFhBUWip9a_tq7814OL_mEvhwk=&h=607&w=440&sz=174&hl=en&start=4&itbs=1&tbnid=KWsxgXUebWQBkM:&tbnh=136&tbnw=99&prev=/images%3Fq%3Dcerebral%2Bpalsy,mri%26hl%3Den%26tbs%3Disch:1
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