CASE 980 Published on 03.04.2001

MR spectroscopy in acute temporal lobe seizures

Section

Neuroradiology

Case Type

Clinical Cases

Authors

R.N.Sener

Patient

13 years, male

Categories

No Area of Interest ; Imaging Technique MR-Spectroscopy

No Procedure ; No Special Focus ;

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Clinical History

Partial complex seizures

Imaging Findings

The patient had partial complex seizures of left temporal lobe origin. He underwent an MRI study including proton MR spectroscopy (TR=1500 msec, and TE=135 msec), 8 hours after the last seizure. Proton MR spectroscopy was repeated 1 month later using the same imaging parameters, when the patient was seizure-free.

Discussion

The most common cause of temporal epilepsy is atrophy in the hippocampus, which is referred to as hippocampal sclerosis. Other causes include tumors, arteriovenous malformations, neuronal migration anomalies, and encephalomalacia. On the other hand, it should be noted that an epileptogenic condition referred to as nonspecific cortical gliosis, in which surgically resected tissue specimens reveal no definite abnormality, can also occur with relatively high prevalances. In patients with hippocampal sclerosis main spectroscopy findings include decreases in N-acetyl aspartate (NAA), and increases in lactate and lipids. In the current patient with MRI evidence of hippocampal sclerosis, decreased NAA levels were noted in two spectroscopy examinations one month apart. Lipids were increased in the initial examination obtained 8 hours after the last seizure, and they returned to normal in the spectroscopy examination one month later, when the patient was seizure-free. These findings suggest that lipids may be a sensitive marker for acute temporal lobe seizures.

Differential Diagnosis List

Decreased NAA, and increased lipids in hippocampal sclerosis

Final Diagnosis

Decreased NAA, and increased lipids in hippocampal sclerosis

References

[1] Achten E. Aspects of proton MR spectroscopy in the seizure patient.
Neuroimaging Clin N Am. 1998 Nov;8(4):849-62. (PMID: 9769346)

[2] Achten E, Santens P, Boon P, De Coo D, Van De Kerckhove T, De Reuck J, Caemaert J, Kunnen M. Single-voxel proton MR spectroscopy and positron emission tomography for lateralization of refractory temporal lobe epilepsy.
AJNR Am J Neuroradiol. 1998 Jan;19(1):1-8. (PMID: 9432150)

[3] Achten E. Aspects of proton MR spectroscopy in the seizure patient.
Neuroimaging Clin N Am. 1998 Nov;8(4):849-62. (PMID: 9769346)

[4] Castillo M, Smith JK, Kwock L. Proton MR spectroscopy in patients with acute temporal lobe seizures. AJNR Am J Neuroradiol. 2001 Jan;22(1):152-7.

[5] Savas R, Sommer A, Georgi M, Sener RN. Prominent occipitotemporal vein: an association with temporal lobe epilepsy?
Comput Med Imaging Graph. 1996 Jan-Feb;20(1):15-8. (PMID: 8891418)

Case information

URL:	https://www.eurorad.org/case/980
DOI:	10.1594/EURORAD/CASE.980
ISSN:	1563-4086

Figure 1

Metabolite Image and Spectra

Metabolite image showing the distribution of NAA, reveals a defective region in the left hippocampus.

Spectrum (TR=1500, and TE=135 msec) at 8th hour after seizures, reveals a decreased NAA peak (at 2.0 ppm), and prominent peaks belonging to lipids at 1.0-1.2 ppm (arrow). Note that lipids resonate between 0.9 and 1.40 ppm, and they are upright (above the baseline) with TE=135 msec, and with other TE values, as well. For comparison, note that lactate resonates at 1.33 ppm, and is inverted (below the baseline with TE=135 msec), and upright with TE=270, and 10-40 msec.

Spectrum (TR=1500, and TE=135 msec) 1 month later, when the patient was seizure-free. NAA peak is still low, however, the prominent peaks belonging to lipids have disappeared. This finding suggests that lipids may be sensitive markers for acute temporal lobe seizures. The literature suggests similar evidence with regard to lactic acid.