Thalamic laminar necrosis
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NEURO-IMAGES
Thalamic laminar necrosis Dimitri Renard • Guillaume Taieb • Anne Le Floch • Chantal Campello
Received: 23 July 2012 / Accepted: 10 October 2012 / Published online: 31 October 2012 Ó Belgian Neurological Society 2012
We present two cases, one after status epilepticus and one after brain radiation therapy, with bilateral hyperintense thalamic lesions on T1-weighted imaging. The first patient (54-year-old woman) presented with a generalized status epilepticus following diffuse hemispheric subarachnoid hemorrhage. Initial brain MRI showed multifocal hyperintense cerebral cortex and thalami on FLAIR and DWI sequences (probably related to status epilepticus), in absence of T1-weighted signal changes. After successful antiepileptic treatment, MRI, 24 days later, showed near normalization of FLAIR/DWI abnormalities, but now showed hyperintense thalami and rightsided parietal cortex (Fig. 1). MRI, 5 months later, continued to show stable T1-weighted abnormalities. The second patient (37-year-old woman) with a history of cerebellar astrocytoma was (WHO grade III) treated at age 18 by complete surgical resection and large-field radiation therapy (including the occipital lobes and both thalami). Her clinical and radiological state (follow-up was performed with low field MRI scans) was stable for many years. There was no history of status epilepticus.
D. Renard (&) G. Taieb A. Le Floch C. Campello Department of Neurology, CHU Nıˆmes, Hoˆpital Caremeau, Place du Pr Debre´, 30029 Nıˆmes Cedex 4, France e-mail: [email protected]
A follow-up MRI, this time with a high-field 3T MRI scan at age 33, showed hyperintense occipital cortex and thalami on T1-weighted imaging (Fig. 1), still in the absence of tumor recurrence. 3T MRI, 4 years later, was stable.
Fig. 1 T1-weighted 3T MRI of patient 1 (a and b) and patient 2 (c and d) showing laminar necrosis of both thalami (a and b, arrows) associated with laminar necrosis in the right-sided parietal cortex (b, arrows) and in the bilateral occipital cortex (c, arrowheads). d The cerebellar cavity due to cerebellar astrocystoma resection. A preexisting ischemic lacunar left-sided thalamic infarction can also be seen in patient 2 (Panel c)
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None of our patients had sequellary sensory abnormalities, cognitive deficit, or other symptoms potentially related to thalamic dysfunction. Hyperintense thalami on T1-weighted imaging in both patients corresponded probably to laminar necrosis. The proposed mechanism of laminar necrosis is cytolysis, necrosis, and edema, followed by resorption and phagocytosis of necrotic material, resulting in fat-laden macrophages depositions, explaining probably the delayed T1 shortening on MRI. Gray matter (especially the cortex) is probably more vulnerable than white matter, explaining why laminar necrosis is most often seen in the cortex. The most frequently reported risk factors associated with laminar necrosis are ischemia/hypoxia, status epilepticus, and metabolic changes. Radiation therapy is a less frequent cause of lam
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