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ARTICLES: D. Donati, N. Akhyani, A. Fogdell–Hahn, C. Cermelli, R. Cassiani-Ingoni, A. Vortmeyer, J. D. Heiss, P. Cogen, W. D. Gaillard, S. Sato, W. H. Theodore, and S. Jacobson Detection of human herpesvirus-6 in mesial temporal lobe epilepsy surgical brain resections Neurology 2003; 61: 1405-1411 [Abstract] [Full text] [PDF]

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Detection of human herpesvirus-6 in mesial temporal lobe epilepsy surgical brain resections

Jonathan M Schott, Martin N. Rossor   (28 January 2004)

Detection of human herpesvirus-6 in mesial temporal lobe epilepsy surgical brain resections 28 January 2004
Jonathan M Schott, Dementia Research Group, Institute of Neurology Box 16, Institute of Neurology, Queen Square, London WC1N 3BG, UK, Martin N. Rossor Send Correspondence to journal: Re: Detection of human herpesvirus-6 in mesial temporal lobe epilepsy surgical brain resections jschott{at}dementia.ion.ucl.ac.uk Jonathan M Schott, et al.	We read with interest the report by Donati et al describing the presence of human herpesvirus-6 (HHV-6) in a significant proportion of temporal lobe biopsy samples from patients with intractable mesial temporal lobe epilepsy. [1] These findings may also be relevant to patients with late onset transient epileptic amnesia (TEA). TEA has been defined as episodic transient amnesia (commonly with a persistent impairment of retrograde or autobiographical memory) in the absence of other cognitive impairment, with an epileptic basis. [2] The epileptic activity underlying this syndrome is thought to originate from the mesial temporal lobes [2,3]. Although treatment with anticonvulsants may ameliorate the amnesia in some cases, our experience shows that some patients suffer persistent and occasionally progressive deficits. TEA is a syndrome generally beginning in later life in patients who have not had seizures [2]. In many cases, the etiology of the temporal lobe seizure disorder remains unclear. HHV-6 can (in the context of acute limbic encephalitis in immunosupressed patients) be associated with temporal lobe seizures and amnesia [4], may invade the central nervous system and remain latent [5], and is now demonstrated in patients with intractable medial temporal lobe epilepsy. [1] We hypothesize that TEA might be caused, at least in some cases, by HHV-6 either due to subacute infection or reactivation. If this hypothesis were confirmed, it might suggest that early treatment with antiviral agents, in addition to anticonvulsants, could improve outcome in some of these patients. References 1. Donati D, Akhyani N, Fogdell-Hahn A et al. Detection of human herpesvirus-6 in mesial temporal lobe epilepsy surgical brain resections. Neurology. 2003; 61 :1405-11 2. Zeman AZ, Boniface SJ, Hodges JR. Transient epileptic amnesia: a description of the clinical and neuropsychological features in 10 cases and a review of the literature. J Neurol Neurosurg Psychiatry. Apr; 64 :435-43. 3. Hogh P, Smith SJ, Scahill RI et al. Epilepsy presenting as AD: neuroimaging, electroclinical features, and response to treatment. Neurology. 2002 22; 58 :298-301. 4. Wainwright MS, Martin PL, Morse RP et al. Human herpesvirus 6 limbic encephalitis after stem cell transplantation. Ann Neurol. 2001 ;50:612-9. 5. Yoshikawa T, Asano Y. Central nervous system complications in human herpesvirus-6 infection. Brain and Development 2000; 22: 307-314