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

1. Cingulate gyrus
2. 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

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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).

http://biology.about.com/gi/dynamic/offsite.htm?site=http://anatomy.uams.edu/anatomyhtml/atlas%5Fhtml/n1a7p4.html

Anatomic diagram depicts the relationship of the hippocampus to other structures in the limbic system. Note that the cingulate gyrus is continuous with the parahippocampal gyrus.

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

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

- 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


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Top: Coronal and axial T1-weighted MRI demonstrating parietal subcortical heterotopia (arrows).
Bottom left: Coronal T2-weighted MRI demonstrating bilateral perisylvian polymicrogyria.
Bottom right: Coronal inverted T2-weighted MRI demonstrating abnormal signal changes (post-traumatic in nature) in the left parietal lobe involving the white matter.

http://www.ncbi.nlm.nih.gov/bookshelf/br.fcgi?book=epi&part=ch12&rendertype=figure&id=ch12.f16

MRI in two patients with symptomatic frontal lobe epilepsy.
Left: Coronal FLAIR MRI showing focal cortical dysplasia in the supplementary motor area of the left frontal lobe. Note the tail extending down towards the frontal horn of the lateral ventricle. This patient was 60 years old and had had left SMA seizures for 7 years. All previous MRI studies were negative.
Right: Axial T2-weighted MRI showing an heterogeneous lesion in the left precentral area. The signal changes are consistent with haemosiderosis suggestive of a cavernous angioma.

http://www.ncbi.nlm.nih.gov/bookshelf/br.fcgi?book=epi&part=ch12&rendertype=figure&id=ch12.f8

Axial proton density-weighted MRI showing left temporal lobe cavernoma in a patient with LTLE.(lateral temporal lobe epilepsy).

http://www.ncbi.nlm.nih.gov/bookshelf/br.fcgi?book=epi&part=ch12&rendertype=figure&id=ch12.f7

MRI findings in hippocampal sclerosis.

Left: Coronal T1-weighted MRI scan showing right hippocampal sclerosis (arrow).

Right: Coronal T2-weighted and magnified T1-weighted MRI scan showing left hippocampal sclerosis.

http://www.ncbi.nlm.nih.gov/bookshelf/br.fcgi?book=epi&part=ch12&rendertype=figure&id=ch12.f7

MRIs of two patients with mesial (right) and lateral (left) temporal lobe epilepsy due to dysembryoplastic neuroepithelial tumours (DNET).
Left: Coronal FLAIR MRI showing a discrete ring-like lesion in the lateral aspects of the right middle temporal gyrus consistent with a small neoplasm. Pathology revealed a DNET.
Right: Coronal T1-weighted MRI showing a large DNET occupying the left hippocampal areas and adjacent mesial temporal lobe gyri and white matter.

Temporal lobe epilepsies comprise a heterogeneous group of disorders sharing the same topographical seizure onset (the temporal lobe), but often of diverse aetiology, age at onset, prognosis, and response to medical or surgical management. Anatomically they are broadly divided into those originating from the lateral or mesial regions of the temporal lobe (Figures 12.1 and 12.2). Mesial (or medial) is far more common (accounting for two-thirds of cases) than lateral temporal lobe epilepsy (LTLE). The most common of all is hippocampal epilepsy, which probably constitutes a disease with known pathology rather than a syndrome. Other causes of temporal lobe epilepsy, mesial or lateral, are benign or malignant tumours, viral and other infectious and parasitic diseases, cerebrovascular disorders, malformations of cortical development, trauma and other injuries

http://www.ncbi.nlm.nih.gov/bookshelf/br.fcgi?book=epi&part=ch12