INTRODUCTION: Transient alterations have been described in neuroimaging (MRI) studies of the non-convulsive focal status (NCFS). We report a case of NCFS together with the MRI findings. CASE REPORT: We describe the case of a 63-year-old female who had a sister and two female cousins with epilepsy; the patient was admitted to hospital after being in state of confusion for 72 hours. Two similar bouts of delirium were reported as having occurred in the 2 preceding years, both of which lasted only a few minutes, and at that time a cardiology study, EEG and MRI scans of the head were performed with normal results. The EEG was compatible with left temporal status and MRI, and presented hyperintensity in the left temporal lobe in T2 and Flair, with no mass effect, with gadolinium uptake in leptomeninges and cortex. CSF was acellular and there were high protein levels in cerebrospinal fluid with a value of 1 g/dL. The patient's situation continued for 10 days, and did not respond initially to antiepileptic treatment. Temporal NCFS was diagnosed, with a cryptogenic rather than idiopathic aetiology. A preliminary MRI scan was normal and another scan performed 10 days after resolution showed a clear regression of the lesion. We related these findings to vasogenic and cytotoxic oedema secondary to the status. An MRI scan carried out at 3 months was normal. CONCLUSIONS: This case lends support to reports, in relation to the appearance of NCFS, of MR images compatible with oedema secondary to rupture of the blood-brain barrier. We base it on sequential MRI studies and on high protein levels in CSF.
INTRODUCTION: Transient alterations have been described in neuroimaging (MRI) studies of the non-convulsive focal status (NCFS). We report a case of NCFS together with the MRI findings. CASE REPORT: We describe the case of a 63-year-old female who had a sister and two female cousins with epilepsy; the patient was admitted to hospital after being in state of confusion for 72 hours. Two similar bouts of delirium were reported as having occurred in the 2 preceding years, both of which lasted only a few minutes, and at that time a cardiology study, EEG and MRI scans of the head were performed with normal results. The EEG was compatible with left temporal status and MRI, and presented hyperintensity in the left temporal lobe in T2 and Flair, with no mass effect, with gadolinium uptake in leptomeninges and cortex. CSF was acellular and there were high protein levels in cerebrospinal fluid with a value of 1 g/dL. The patient's situation continued for 10 days, and did not respond initially to antiepileptic treatment. Temporal NCFS was diagnosed, with a cryptogenic rather than idiopathic aetiology. A preliminary MRI scan was normal and another scan performed 10 days after resolution showed a clear regression of the lesion. We related these findings to vasogenic and cytotoxic oedema secondary to the status. An MRI scan carried out at 3 months was normal. CONCLUSIONS: This case lends support to reports, in relation to the appearance of NCFS, of MR images compatible with oedema secondary to rupture of the blood-brain barrier. We base it on sequential MRI studies and on high protein levels in CSF.
Authors: V Cuvinciuc; A Viguier; L Calviere; N Raposo; V Larrue; C Cognard; F Bonneville Journal: AJNR Am J Neuroradiol Date: 2010-01-21 Impact factor: 3.825