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An aura is a subjective ictal phenomenon that precedes an observable seizure, which can be localizing, pseudolocalizing, or a network phenomenon. Somatosensory auras (SSA) arise from primary and secondary sensory areas (SI, SII) and insula as evident from cortical stimulation studies.1 Here, we describe SSA originating from the hippocampus, demonstrated during invasive EEG monitoring for a suspected extra temporal epilepsy. A 30-year-old left-handed male, with no antecedents, presented with history of seizures from the second day of his life. His habitual events comprised an aura of paresthesias involving the forehead and right upper limb, without a clear sensory march, followed by a sensation of fear and automatisms like covering his face, holding objects, or interlocking his hands. He also had incoherent speech, restlessness, and impaired awareness, and no postictal recollection. A left hemispheric seizure onset with temporal or pseudo-temporal (parietal or insular) localization secondary to perinatal insult was initially hypothesized. Video EEG demonstrated interictal discharges from the left anterior and mid-temporal regions and captured six clinical seizures with left temporal ictal onset. MRI brain epilepsy protocol revealed left mesial temporal sclerosis with gliosis involving the left parietal operculum. Given the discordant features – sensory aura, aura of fear, and insulo-opercular gliosis – stereo-EEG (SEEG) was undertaken to localize the ictal onset zone, map eloquent cortex, assess probable right-hemispheric language lateralization, record spontaneous seizures, and to proceed with thermocoagulation if possible. Using Brainlab planning software and Leksell stereotactic frame, 10 depth electrodes with 10 contacts each were implanted into the head and body of the hippocampus, Heschl gyrus, angular gyrus, supramarginal gyrus, secondary somatosensory area and perilesional areas (Figure 1A). Interictally, spikes, sharp waves, intermittent positive spikes (Figure 2) and 8–11 Hz brief intermittent rhythmic potentially ictal discharges (Figure 3) were recorded from the head and body of the hippocampus along with focal slowing. High frequency oscillations and sharp waves originated from perilesional areas. The patient reported multiple auras, predominantly paresthesias involving the right side of the face, descending to the right upper and lower limbs and few episodes of fear with ictal correlation of fast rhythmic activity from the head of the hippocampus, followed by a sharp theta rhythm that persisted for 5–8 s. Five habitual events were recorded with ictal onset from the body of the hippocampus and propagation to the head of the hippocampus after 10–12 s, later involving the posterior perilesional area and supramarginal gyrus. Ictal propagation to the insula or somatosensory area was absent (Figure 1B–D). On cortical stimulation, from the head of hippocampus (biphasic stimuli; pulse duration – 0.5 ms, train duration of 4 s, stimulus intensity of 2–5 mA, at 50 Hz) the patient developed his habitual sensory aura consisting of upper limb paresthesias and cephalic sensations, associated with afterdischarges. Other findings included electrographic seizure from the body of hippocampus (3 mA and 50 Hz), non-habitual sensory phenomenon and sustained afterdischarges from the insula and anterosuperior perilesional area (3–4 mA, 50 Hz), afterdischarges and electrographic seizures from angular gyrus and non-habitual clinical seizures from posterosuperior perilesional area (50 Hz and 4 mA). No clinical responses or afterdischarges were elicited from the secondary somatosensory area, likely due to the extensive gliosis. An incomplete insular sampling could also be a reason, as only one electrode was implanted in the insula. Despite the clinical suspicion of a widespread network involving sensory, limbic, and temporal regions, SEEG findings were localized to the left hippocampus and demonstrated sensory aura arising from the hippocampus. Radiofrequency ablation was performed at head and body of hippocampus, insula, perilesional regions, and angular gyrus. The incidence of SSAs ranges from 1.4% to 80%, with the highest rates reported in parietal lobe epilepsy.2, 3 In temporal lobe epilepsy, the incidence ranges from 1.7% to 11%4-6 Proposed mechanisms include rapid ictal spread to extratemporal structures and intrinsic epileptogenicity of the primary or supplementary somatosensory cortices.6, 7 In a cortical stimulation study of mesial temporal structures, 39 of 44 elicited responses were sensory in nature, although the specific sensory types were not detailed.8 Merinder TV et al. reported reproduction of a habitual sensory aura with stimulation of the amygdala and anterior hippocampus; however, the habitual events showed ictal propagation to the insula during SSA.9 Sensory phenomena may also arise directly from the hippocampus itself, as demonstrated by Fish DR et al.10 In their seminal study, sensory responses were elicited from stimulation of the hippocampus and amygdala in 20 of 46 patients undergoing chronic intracranial recordings. These responses were often vague – ipsilateral, contralateral, or bilateral – and lacked the strict somatotopic localization seen with postcentral gyrus stimulation. The authors postulated this to be due to malleable connections within the limbic structures and the temporal lobe rendering the responses more idiosyncratic and reflective of plastic changes occurring over an individual's lifetime due to physiological experiences or pathological conditions such as recurrent seizures. In our patient, although the large cutaneous sensory aura and insular gliosis suggested an extratemporal localization, SEEG findings were paradoxical, with ictal onset from the body of the hippocampus, corroborated by cortical stimulation findings. The occurrence of SSA arising directly from the hippocampal body, in the absence of ictal propagation to sensory cortices, constitutes a unique finding. This observation is indicative of the role of the hippocampus in the generation of somatosensory auras. Nil. Nil. The patient consented fully to the anonymized use of his clinical details, image findings, and EEG for academic purposes and in medical journals. The data that support the findings of this study are available from the corresponding author upon reasonable request. Data S1. Data S2. Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article. Which of the following areas are least likely to produce sensory aura? Which of the following features are most suggestive of origin of sensory aura from the post central gyrus? In this clinical vignette, why were the SEEG findings described as paradoxical? Answers may be found in the supporting information