Journal of Neurology https://doi.org/10.1007/s00415-018-9010-9 LETTER TO THE EDITORS Subacute encephalopathy with seizures in alcoholics (SESA) syndrome: further evidence supporting that may lie on the ictal-interictal continuum José L. Fernández‑Torre1,2,3 · Ignacio Banzo4 · Fernando Ortega‑Valín5 · Ernesto Orozco‑Sevilla1 · Isabel Martínez‑Rodríguez4 · Enrique Marco de Lucas6 Received: 19 June 2018 / Revised: 5 August 2018 / Accepted: 7 August 2018 © Springer-Verlag GmbH Germany, part of Springer Nature 2018 Dear Sirs, Subacute encephalopathy with seizures in alcoholics (SESA) syndrome is an unrecognized epileptic condition occurring in chronic alcoholism with specific features that include encephalopathy, lateralized periodic discharges (LPDs) on the electroencephalograhy (EEG), chronic microvascular ischemia on neuroimaging studies and possible recurrence when chronic anti-seizure treatment is stopped [1, 2]. This syndrome can be precipitated by alcohol intake or withdrawal. In the last 15 years, Fernández-Torre and colleagues [2–6] have importantly contributed to delineate the clinical, EEG and neuroimaging features, hypothesizing that SESA syndrome represents a well-defined subtype of focal nonconvulsive status epilepticus (NCSE). Awareness of this particular entity is essential in making an appropriate diagnosis that in turn leads to correct and prompt treatment. Neuroimaging findings of SESA syndrome include transient cortical–subcortical T2-hyperintense areas with restricted diffusion observed in a patient with atrophy and chronic multifocal vascular lesions [5]. In few cases, * José L. Fernández‑Torre jlfernandez@humv.es; ftorrenfc@hotmail.com 1 Department of Clinical Neurophysiology, Marqués de Valdecilla University Hospital, Avda. Valdecilla, s/n, 39008 Santander, Cantabria, Spain 2 Department of Physiology and Pharmacology, University of Cantabria (UNICAN), Santander, Cantabria, Spain 3 Biomedical Research Institute (IDIVAL), Santander, Spain 4 Department of Nuclear Medicine, Marqués de Valdecilla University Hospital, Santander, Cantabria, Spain 5 Department of Neurology, Marqués de Valdecilla University Hospital, Santander, Cantabria, Spain 6 Department of Radiology, Marqués de Valdecilla University Hospital, Santander, Cantabria, Spain angiography or cerebral photon emission computed tomography (SPECT) studies revealed hyperperfusion [4, 7]. Nevertheless, data correlating cerebral blood flow and brain metabolism with EEG in this entity are absent. Herein, we describe a new patient with SESA syndrome focusing our attention on the correlation between EEG and SPECT and 18F-fludeoxyglucose-positron emission tomography (18F-FDG-PET) scan images. A 66-year-old woman with heavy chronic alcohol abuse and depression was transferred from a local hospital to our neurology ward due to disorientation, speech disturbances, and refractory seizures. She had a past history of partial motor, generalized tonic–clonic seizures (GTCSs), and convulsive status epilepticus. She was on treatment with levetiracetam (1000 mg/12 h) and lacosamide (50 mg/12 h), but she had poor medical compliance. On neurological examination, she was alert, but her speech was repetitive with semantic paraphasias and a visual deficit with right-sided homonymous hemianopsia became evident. EEG showed continuous LPDs-proper involving the left temporo-parietooccipital junction (Fig. 1a). Periodic anomalies adopted an association in groups conforming tripleds and polypleds [8]. Head magnetic resonance imaging (MRI) revealed cortical–subcortical areas of increased T2/FLAIR signal and restricted diffusion over the left parieto-occipital region and moderate diffuse cerebral atrophy (Fig. 1b). In view of these findings, a diagnosis of SESA syndrome was proposed. To best determine the significance (interictal versus ictal) of EEG features, we carried out a brain 99Tc-hexamethylpropylenamine oxime SPECT and 18F-FDG-PET. Cerebral SPECT disclosed marked regional cerebral hyperperfusion in the left temporal and occipital lobe with increased glucose metabolism in the 18F-FDG-PET study (Fig. 2a, b). In the following days, her seizures were well controlled after increasing the dose of lacosamide, and finally, she was discharged with limb and gait ataxia and normal speech. 13 Vol.:(0123456789) Journal of Neurology Fig. 1  a EEG revealing continuous LPDs involving the left temporo-parieto-occipital junction; b axial diffusion-weighted images show mild restricted diffusion in the left temporo-occipital cortex Fig. 2  99mTc-HMPAO cerebral SPECT (a) and 18F-FDG-PET (b) showing increased cerebral blood flow and glucose hypermetabolism in the left temporal lobe extending to the occipital region, respectively Our case further contributes to understand the underlying pathophysiology in SESA syndrome. Both left temporo-occipital hyperperfusion and hypermetabolism are strongly suggestive of an epileptic event with ictal nature [9]. It is possible that the existence of recurrent complex partial seizures (CPSs) was unrecognized, since continuous EEG monitoring was not performed. Certainly, not 13 all reported SESA cases met criteria for NCSE based on EEG findings alone but rather due to failure to return to baseline in between clinical seizures. With the findings described above of conditions that lie along an ictal–interictal continuum, ranging from periodic discharges in the form of LPDs, to focal complex partial status epilepticus, a different picture emerges. The term ictal–interictal continuum encompasses EEG patterns that are potentially harmful and can cause neuronal injury or increase a preexisting cerebral lesion [10]. Most authors believe that LPDs largely represent an interictal phenomenon; however, recent studies suggest that LPDs > 2.0 Hz in acute brain injury patients are associated with tissue hypoxia [11]. Of note, aggressive treatment for LPDs when hyperperfusion is detected led to clinical improvement [12]. In summary, cerebral SPECT and PET closely correlated with EEG can play an important role in the optimization of anti-seizure drug therapy and diagnosis of SESA syndrome. Taking in account our considerations, continuous EEG appears ideal for revealing this pathophysiological electro-clinical evolution. A meticulous clinical evaluation and a high level of suspicion during the first 24–48 h Journal of Neurology after admission are then essential for expedited diagnosis and management of this epileptic condition. Compliance with ethical standards Conflicts of interest None of the authors has any conflict of interest to disclose. 5. 6. Ethical standard statement All human studies have been approved by the appropriate ethics committee and have, therefore, been performed in accordance with the ethical standards laid down in the 1964 Declaration of Helsinki. 7. References 9. 1. 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