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BRIEF COMMUNICATIONS: T. Nagasaka, K. Shindo, M. Hiraide, T. Sugimoto, and Z. Shiozawa Ipsilateral thalamic MRI abnormality in an epilepsy patient Neurology 2002; 58: 641-644 [Abstract] [Full text] [PDF]

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Reply to Letter to the Editor

Takamura Nagasaka, Kazumasa Shindo, and Zenji Shiozawa   (21 October 2002)

Ipsilateral thalamic MRI abnormality in an epilepsy patient

Morris H Scantlebury, Lionel Carmant   (21 October 2002)

Reply to Letter to the Editor 21 October 2002
Takamura Nagasaka Yamanashi Medical University Nakakoma-gun, Yamanashi Japan, Kazumasa Shindo, and Zenji Shiozawa Send Correspondence to journal: Re: Reply to Letter to the Editor nagat{at}res.yamanashi-med.ac.jp Takamura Nagasaka, et al.	Our report simply revealed reversible thalamic abnormal intensity using MRI without permanent changes, e.g. thalamic atrophy. Moreover, we demonstrated reversible cerebral abnormal intensity of right temporoparietal cortex on MRI, not cerebral hemiatrophy. Recent studies identified thalamic abnormality in the patient with epilepsy in either the interictal state or after status epilepticus neuroradiologically and pathologically. [1, 2, 3] The view that the thalamus plays a significant role in epilepsy is now widely accepted. We presented our case assuming that thalamic changes are well known fact. We did not claim that ours was the first report suggesting that the thalamus is a key site of functional abnormality in epileptic patients. We would emphasize three points about the MRI thalamic abnormality in our patients. It (1) was reversible, (2)occurred during status epilepticus, not the Interictal state or after status epilepticus, (3) occurred in a patient with complex partial seizures originating from parietal sensory neocortex. References 1. Conlon P, Trimble MR, Rogers D, et al. Magnetic resonance imaging in epilepsy: a controlled study. Epilepsy Res 1988; 2:37-43. 2 .Henry TR, Mazziotta JC, Engel J. Interictal metabolic anatomy of mesial temporal lobe epilepsy. Arch Neurol 1993; 50:582-589. 3 .Yune MJ, Lee JD, Ryu YH, et al. Ipsilateral thalamic hypoperfusion on interictal SPECT in temporal lobe epilepsy. J Nucl Med 1998;39:281-285.
Ipsilateral thalamic MRI abnormality in an epilepsy patient 21 October 2002
Morris H Scantlebury Hopietal Sainte-Justine Montrel Quebec, Lionel Carmant Send Correspondence to journal: Re: Ipsilateral thalamic MRI abnormality in an epilepsy patient lionel.carmant{at}umontreal.ca Morris H Scantlebury, et al.	We read with interest the case report published in Neurology [1] that proposed to have reported for the first time a case of status epilepticus, and thalamic atrophy in a 19 year-old female following a one month prior history of repetitive complex partial seizures. Other associated findings were right cerebral hemiatrophy and contralateral cerebellar hemiatrophy. In a study from Tan and Urich [2], the following history of seizures was reported prior to admission: (1) febrile status epilepticus, (2) hemiconvulsions lasting several hours (3) repetitive hemiconvulsions, and (4) "severe" febrile convulsions. All were diagnosed with cerebral hemiatrophy, ipsilateral thalamic atrophy and mesial temporal sclerosis (MTS). [2] A more recent review of 23 patients, between the ages of 1-64 years old with HHE, demonstrated a significant relationship between cerebral hemiatrophy and thalamic atrophy. [3] MRI findings in all patients were cerebral hemiatrophy, 11 patients had ipsilateral MTS of which all had ipsilateral thalamic atrophy. Nine of the eleven patients with MTS had a past history of prolonged febrile seizures. We recently reported two patients with HHE; one with bilateral thalamic lesions on MRI diagnosed following febrile status epilepticus. [4] In addition, damage to the temporal cortex, hippocampus and thalamic structures have been demonstrated in an animal model of self-sustained status epilepticus induced by repetitive electrical stimulation of the amygdala. [5] The possibility remains that damage to the thalamus may contribute to the progression to status epilepticus, which may be prevented by early intervention directed at the thalamo-cortical circuitry. To this extent, we agree with the authors that further research is required to elucidate the role the thalamus plays in status epilepticus and other forms of intractable epilepsy. References: 1. Nagasaka T, Shindo k, Hiriade M, et al. Ipsilateral thalamic MRI abnormality in an epilepsy patient. Neurology 2002;58:641-644. 2. Tan N, Urich H. Postictal cerebral hemiatrophy: with a contribution to the problem of crossed cerebellar atrophy. Acta Neuropathol 1984; 62:332-339. 3. Dix JE, Wayne CS. Cerebral hemi-atrophy: Classification on the basis of MR findings of mesial temporal sclerosis and childhood febrile seizures. Radiology 1997;203:266-274. 4. Scantlebury MH, David M, Carmant L. Association between factor V Leiden and the hemiconvulsion-hemiplegia-epilepsy (HHE) syndrome: A report of two cases. In Press J Child Neurol. 5. Nissinen J, Halonen T, Koivisto E et. al. A new model of chronic temporal lobe epilepsy induced by electrical stimulation of the amygdala in the rat. Epilepsy Research 2000;38(2-3):177-205.