Hyperacute Seizure 09 - Clinical Case Summary
Hyperacute Seizure 09 - Clinical Case Summary
Hyperacute Seizure 09 - Clinical Case Summary
SummaryHistory
41 yo male presenting with a déjà vu feeling then loss of consciouness. The patient was diagnosed with seizure related to a low grade glioma (which was later resected).
Exams Performed
MR T1-w post contrast only; MR Coronal T2-w spin echo and MR FLAIR; MR diffusion
Prior available imaging reports
CT Head was not obtained
MR T1-w post contrast only
1. There is remodeling (enlargement) of the left middle cranial fossa presumably related to chronic enlargement of the left temporal lobe. These findings are nonspecific, since no clear expansile lesion is identified.
MR Coronal T2-w spin echo and MR FLAIR
1. Findings are consistent with a low-grade mass (glial or gray matter types) involving the anterior and medial aspects of the left temporal lobe. Chronicity it Is implied by the lack of abnormal contrast enhancement on the T1 weighted post contrast MR, and the remodeling of the left temporal fossa.
2. There are features of recent seizure event involving the left hippocampus, which exhibits feature different than those of diffuse tumoral infiltration.
MR Diffusion (DWI)
1. There is increased MR diffusion signal in the anterior temporal lobe and hippocampus on the left consistent with tumoral infiltration resulting in signal produced by T2-w shine-through rather than water restriction. The tumor extension from the T2-w sequences involved the the left uncus, the left amygdala and head of the hippocampus. Recent seizure changes caused edema in the body and body- tail transition zone. MR diffusion exhibits increased T2-w shine-through signal increase, but dos not differentiate the two on the basis of T2 shine-through. Thus, MR diffusion DWI map recognizes both abnormalities, but cannot offer any additional differential information.
MR Susceptibility (SWI) is not available
MR T1-w post contrast only
1. There is remodeling (enlargement) of the left middle cranial fossa presumably related to chronic enlargement of the left temporal lobe. These findings are nonspecific, since no clear expansile lesion is identified.
MR Coronal T2-w spin echo and MR FLAIR
1. Findings are consistent with a low-grade mass (glial or gray matter types) involving the anterior and medial aspects of the left temporal lobe. Chronicity it Is implied by the lack of abnormal contrast enhancement on the T1 weighted post contrast MR, and the remodeling of the left temporal fossa.
2. There are features of recent seizure event involving the left hippocampus, which exhibits feature different than those of diffuse tumoral infiltration.
MR Diffusion (DWI)
1. There is increased MR diffusion signal in the anterior temporal lobe and hippocampus on the left consistent with tumoral infiltration resulting in signal produced by T2-w shine-through rather than water restriction. The tumor extension from the T2-w sequences involved the the left uncus, the left amygdala and head of the hippocampus. Recent seizure changes caused edema in the body and body- tail transition zone. MR diffusion exhibits increased T2-w shine-through signal increase, but dos not differentiate the two on the basis of T2 shine-through. Thus, MR diffusion DWI map recognizes both abnormalities, but cannot offer any additional differential information.
MR Susceptibility (SWI) is not available
Overall impression
1. In this case there is an infiltrative mass in the uncus and amygdala on the left side. The findings are consistent with a low-grade astrocytoma (or DNET or microcystic glioma). The infiltrative uncal mass does invade the rostral hippocampus causing change in T2 signal. However, the uninvolved portion of the left hippocampus is abnormal. There is effacement of both the internal and external white matter tracts. The volume of the left hippocampus is just above normal. Findings are consistent with recent (subacute) post seizure hippocampal post seizure activity. As yet, there is no evidence of chronic mesial sclerosis.
Lessons to be Learned
Infiltrative brain tumors, of any grade, frequently present with seizures. In most cases the seizures eminated from infiltrated cortex in the adjacent brain and they frequently do not have hippocampal changes in the absence of status epilepticus. However, infiltrative mass involving the hippocampus can present with seizure activity and actually have evidence of post seizure hippocampal injury, as well as the tumoral hippocampal infiltration, as is evident in this case.