Sex: female
Age: 44 years
History
None pertinent.
Laboratory data
Unremarkable.
Physical findings
Minor motor deficit of right arm and leg.
Case text
The patient was admitted to another hospital with seizures. CT Scan examination of the brain without contrast administration performed the first day, was negative. She was referred to our department of radiology for an MRI of the brain.
Image 1-8
MRI of the brain.
1 and 2- Axial, proton density- weighted (3400/22/5) FSE images.
3 and 4- Axial, T2- weighted (3400/90/5) FSE images.
5 and 6- Axial, gadolinium-enhanced, T1-weighted (660/17) SE images.
7 and 8- Coronal, gadolinium-enhanced, T1-weighted (660/17) SE images.
Image 9-16
Follow-up MRI of the brain, performed 5 months after the first MRI.
9 and 10- Axial, proton density-weighted (3400/22/5) FSE images.
11 and 12- Axial, T2-weighted (3400/90/5) FSE images.
13- Axial, gadolinium-enhanced, T1-weighted (560/17) SE image.
14- Coronal, gadolinium-enhanced, T1-weighted (560/17) SE image.
15 and 16- Coronal, T2-weighted (5600/90/180) STIR images.
Image 1-8
1. How would you describe the changes of the brain?
An area of hyperintensity on the proton density and T2-weighted images is shown in the left temporal lobe. There is some mass effect. The T1-weighted images after administration of IV gadolinium demonstrate poorly delineated little contrast enhancement .
2. What anatomical structure is most affected?
Left medial temporal lobe, hippocampal area
3. What is your differential diagnosis?
Tumor (low grade astrocytoma), inflammatory changes (herpes encephalitis), acute ischemic changes (unlikely, doesn't correspond to a vascular territory).
4. Given the character of the lesion, the clinical presentation and lack of laboratory data to support herpes encephalitis, what is your next diagnostic step?
Brain biopsy. Pathologic examination of the biopsy specimen demonstrated a histiocytic clearing secondary to necrosis. This can be compatible with inflammatory changes. The motor deficiency of the right arm and leg resolved a few days later and the patient stayed seizure-free with a daily dose of natrium-valproate 300 mg.
Image 9-16
5. How would you describe the changes of the brain?
A hyperintense signal and important atrophy of left hippocampal area is shown on proton density and T2-weighted images as well as on coronal STIR images. There is no contrast enhancement anymore.
6. What is your (differential) diagnosis?
Mesial temporal sclerosis.
Final diagnosis
Mesial temporal sclerosis.
Differential diagnosis
None.
Discussion
Most authors agree that hippocampal sclerosis is the cause, not the consequence, of seizures. However, the etiology of mesial temporal sclerosis is not well known. Some investigators suggested parturitional brain injury. Also Hodgkin’s disease can result in hippocampal destruction. A significant correlation is suggested between serious childhood illness and hippocampal sclerosis in adults with complex partial seizures. A clear pathophysiologic mechanism for mesial temporal sclerosis has not been established. This pathologically confirmed case of mesial temporal sclerosis provides insight on the evolution of MRI changes going form a non-specific inflammatory lesion to the usual mesial temporal sclerosis findings.