IS THERE A RELATIONSHIP BETWEEN MESIAL TEMPORAL SCLEROSIS, REVERSIBLE POSTERIOR LEUKOENCEPHALOPATHY, AND BENIGN INTRACRANIAL HYPERTENSION?
Abstract number :
2.156
Submission category :
Year :
2005
Submission ID :
5460
Source :
www.aesnet.org
Presentation date :
12/3/2005 12:00:00 AM
Published date :
Dec 2, 2005, 06:00 AM
Authors :
Carl R. Barr, and Ron G. Davis
We report a case of a 14 y/o with known right Mesial Temporal Sclerosis (MTS) discovered after status epilepticus in 2000. EEG showed a right temporal discharge and MRI had increased T2 signal in the right hippocampus. He presented again in March 2005 with status epilepticus requiring pentobarbital coma for control. Post-coma MRI on March 21, 2005 showed no changes. On March 28, 2005 he had acute onset of headache, generalized seizure, delerium and visual disturbance. CT showed bilateral diffuse white matter edema and right occipital hemorrhage. Lumbar puncture showed an opening pressure [gt] 50 cm H20. The patient was ultimately treated with shunting. MRI of the brain showed high T2 and FLAIR signal of the white matter and multiple punctate hemorrhages suggestive of posterior reversible leukoencephalopathy syndrome (RPLS).
A PubMed search was done to determine if an association among (MTS), (RPLS) and/or benign intracranial hypertension(BIH) existed. A literature review using key words mesial temporal sclerosis (MTS), hypertensive encephalopathy(HE), and posterior leukoencephalopathy was done to determine previously reported cases showing an association between these entities. Retrieved articles were reviewed for report of increased CSF pressure or BIH. In 1996, Hinchey et al coined the term [quot]Reversible Posterior Leukoencephalopathy Syndrome[quot] in 15 patients with headache, altered mental status, seizures, and vision abnormalities associated with neuroimaging showing posterior leukoencephalopathy. There was no intent to show an association between MTS and RPL as the majority had hypertension, eclampsia or immunosuppressive agents as cause. No evidence of elevated CSF pressure was given. Pavlakis and colleagues reported on 52 cases of RPLS in children and proposed that hypertension may not be necessary to develop RPLS. They also noted gray matter may be involved, but the syndrome is essentially the same as in adults. Solinas et al in 2003 suggested that hypertensive encephalopathy might be the cause of hippocampal sclerosis (HS) in a report of 3 patients with temporal lobe epilepsy(TLE) and HS. N.Lawn and colleagues report 9 women who had anterior temporal lobectomy for TLE after having eclampsia as there only risk factor. Our patient clearly had (RPLS) although clinical records showed no significant elevations in blood pressure. He also had elevated CSF pressure coinciding with his RPLS. Search of the literature has not previously reported this association. Although our patients MTS preceded this episode of RPLS, the question remains as to whether RPLS, HE, eclampsia or BIH inluence the development of MTS, or if MTS might predispose one to develop RPLS. Our patient presented evidence of the coexistence of MTS, RPL, and BIH and raised questions regarding the relationship among these clinical entities. Further research is necessary to clarify the mechanism of how one might influence the others.