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Imaging of Patients with Hippocampal Sclerosis at 7 Tesla

Posted Mar 31, 2010 Updated Apr 7, 2023
By Tobias Breyer MD , Isabel Wanke MD , Stefan Maderwald PhD , Friedrich G. Woermann MD , Oliver Kraff PhD , Jens M. Theysohn MD , Alois Ebner MD , Michael Forsting MD , Mark E. Ladd PhD , Marc Schlamann MD
8 min read

Rationale and Objectives

Focal epilepsies potentially can be cured by neurosurgery; other treatment options usually remain symptomatic. High-resolution magnetic resonance (MR) imaging is the central imaging strategy in the evaluation of focal epilepsy. The most common substrate of temporal epilepsies is hippocampal sclerosis (HS), which cannot always be sufficiently characterized with current MR field strengths. Therefore, the purpose of our study was to demonstrate the feasibility of high-resolution MR imaging at 7 Tesla in patients with focal epilepsy resulting from a HS and to improve image resolution at 7 Tesla in patients with HS.

Materials and Methods

Six patients with known HS were investigated with T1-, T2-, T2 ∗ -, and fluid-attenuated inversion recovery–weighted sequences at 7 Tesla with an eight-channel transmit-receive head coil. Total imaging time did not exceed 90 minutes per patient.

Results

High-resolution imaging at 7 Tesla is feasible and reveals high resolution of intrahippocampal structures in vivo. HS was confirmed in all patients. The maximum non-interpolated in-plane resolution reached 0.2 × 0.2 mm 2 in T2 ∗ -weighted images. The increased susceptibility effects at 7 Tesla revealed identification of intrahippocampal structures in more detail than at 1.5 Tesla, but otherwise led to stronger artifacts. Imaging revealed regional differences in hippocampal atrophy between patients. The scan volume was limited because of specific absorption rate restrictions, scanning time was reasonable.

Conclusions

High-resolution imaging at 7 Tesla is promising in presurgical epilepsy imaging. “New” contrasts may further improve detection of even very small intrahippocampal structural changes. Therefore, further investigations will be necessary to demonstrate the potential benefit for presurgical selection of patients with various lesion patterns in mesial temporal epilepsies resulting from a unilateral HS.

Although the causes of temporal lobe seizures are manifold, the most common finding in patients with severe, medically intractable temporal lobe epilepsy is mesial temporal or hippocampal sclerosis (HS) . HS can occur either as a cause or consequence of focal epileptic seizures . Clinical and neuropathological findings, however, suggest different underlying etiologies and subsequent clinical presentations . Any changes of normal cortical architecture can be associated with severe epileptic syndromes, not restricted to the hippocampus. In general, epileptogenic lesions can be very small and either developmental or acquired.

Epilepsy patients are primarily treated pharmacologically to control seizures. But pharmacological treatment remains symptomatic and fails to sufficiently control seizures in about 20%–25% of patients . To date, the only curative treatment option is the neurosurgical resection of an epileptic lesion . Therefore, the precise presurgical anatomical and functional delineation of epileptogenic lesions by magnetic resonance (MR) imaging as well as by electroencephalographic studies is crucial for diagnosis and mandatory before surgical treatment. In addition, precise delineation of epileptic lesions in relation to functionally important surrounding structures such as eloquent areas, fiber tracts, or vessels may minimize surgical complications.

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Materials and methods

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Table 1

Summary of Basic Patient Characteristics with Respect to Sex, Age, Age at Onset of Seizures, Side of the Hippocampal Sclerosis, and Current Semiology of Seizures

Number Sex Age Age at Onset Side Aura Semiology 1 F 39 4 L Abdominal CPS, GTC 2 F 55 NA R Abdominal CPS 3 F 44 39 R Abdominal CPS, GTC 4 F 60 NA R Abdominal CPS 5 M 26 10 R No CPS 6 F 28 24 L Deja-/jamais-vu CPS, GTC

NA, no data available; CPS, complex partial seizure; GTC, focally induced, secondarily generalized tonic-clonic seizures.

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Results

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Figure 1, Anatomy of an unaffected, contralateral hippocampus in a magnified section of a coronal, high-resolution T2 ∗ -weighted image (echo time 20.4 ms, repetition time 750 ms, non-interpolated voxel size 0.2 × 0.2 × 2.5 mm 3 , TA 2:45 minutes). CA1–4, cornu ammonis ( lat. = hippocampus) cortical fields 1–4; CA4, “end folium” are clearly visible.

Figure 2, Corresponding coronal T2-weighted images in a patient with left-sided hippocampal sclerosis at 1.5 T (echo time 85 ms, repetition time 3070 ms, FA 150°, resolution 1 × 1 × 5 mm 3 , TA 4:10 minutes) and 7 Tesla (as described in the Methods section, resolution 0.5 × 0.5 × 3 mm 3 , TA 4:15 minutes); magnification of the left hippocampus in the upper right corner. Note the strong increase in detailed anatomical delineation, especially of the hippocampal sulcus, subiculum, and cortical area CA1 and 4; CA2–3 is clearly atrophic.

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Figure 3, Corresponding T2-, T2 ∗ -, non–contrast-enhanced T1-, and fluid-attenuated inversion recovery (FLAIR)-weighted coronal planes in one patient with right-sided hippocampal sclerosis acquired at 7 Tesla. The T1-weighted image was coronally reformatted from the sagittally acquired isotropic T1 magnetization prepared rapid gradient echo (MPRAGE) sequence.

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Figure 4, Characteristic examples of sclerosed hippocampi from four different patients on corresponding T2 ∗ -weighted coronal images acquired at 7 Tesla showing regional differences of the intrahippocampal atrophy with respect to the CA1, which is markedly atrophied in patient a and d, but to a far lesser extent in patients b and c. Note the atrophy of CA2 in patient c although according to the current literature CA2 should be spared in HS.

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Figure 5, Differences in the extent of T2 ∗ -susceptibility artefacts at the skull base and significant inhomogeneities in the gray/white matter contrast between patient (a) and healthy volunteer (b) . Both T2 ∗ images were obtained at 7 Tesla with identical imaging parameters. The temporal lobes can be identified on (b) but not adequately on (a) , although the signal increase and intrahippocampal structures of the affected, sclerosed hippocampus on the left side of (a) can nevertheless be seen.

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Discussion

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Conclusion

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Academic Radiology, Volume 17, Issue 4
Journals General Radiology
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