RESUMO
Pure amnestic seizures are defined as self-limited episodes with isolated, anterograde memory loss and have been attributed to bilateral dysfunction of mesial temporal structures. This type of seizure can occur in patients with different forms of temporal lobe epilepsy and has been more recently associated with a late-onset epileptic syndrome, called transient epileptic amnesia (TEA). The mechanisms of such prolonged manifestations are not well known and notably its ictal or post-ictal origin remains poorly understood. We report a case of prolonged anterograde amnesia (lasting several hours) following a brief seizure induced by stimulation of the left entorhinal cortex, recorded during stereo-EEG (SEEG). This episode was associated with prolonged changes in the intracerebral EEG signal complexity (entropy) within bilateral mesial temporal structures, particularly the entorhinal cortices, with a progressive normalization paralleling the clinical recovery. Our case shows that long-lasting (hours) memory impairment may follow brief seizure that led to prolonged electrophysiological signals alterations in bilateral mesial temporal structures.
Assuntos
Epilepsia do Lobo Temporal , Epilepsia , Humanos , Convulsões , Epilepsia do Lobo Temporal/diagnóstico por imagem , Amnésia/diagnóstico por imagem , Amnésia/complicações , EletroencefalografiaRESUMO
OBJECTIVES: Despite the success of recanalization by bridging therapy, about half of treated stroke patients remain disabled. While numerous reports propose clinical predictors of stroke clinical outcome in this context, we originally aimed to study pre-therapeutic factors influencing infarct growth (IG) and poor clinical outcome in strokes due to large vessel occlusion (LVO) successfully recanalized. MATERIALS AND METHODS: We enrolled 87 consecutive successfully recanalized patients (mTICI: 2b/2c/3) by mechanical thrombectomy (±rt-PA) after stroke due to middle cerebral artery (M1) occlusion within 6 h according to AHA guidelines. IG was defined by subtracting the initial DWI volume to the final 24 h-TDM volume. Statistical associations between poor clinical outcome (mRS≥2), IG and pertinent clinico-radiological variables, were measured using logistic and linear regression models. RESULTS: Among 87 enrolled patients (Age(y): 68.4 ± 17.5; NIHSS: 16.0 ± 5.4), 42/87 (48,28%) patients had a mRS ≥ 2 at 3 months. Diabetic history (OR: 3.70 CI95%[1.03;14.29] and initial NIHSS (/1 point: OR: 1.16 CI95%[1.05;1.27]) were independently associated with poor outcome. IG was significantly higher in stroke patients with poor outcome (+7.57 ± 4.52 vs -7.81 ± 1.67; p = 0.0024). Initial volumes were not significantly different (mRS≥2: 16.18 ± 2.67; mRS[0-1]: 14.70 ± 2.30; p = 0.6771). Explanatory variables of IG in linear regression were diabetic history (ß: 21.26 CI95%[5.43; 37.09]) and NIHSS (ß: 0.83 CI95%[0.02; 1.64]). IG was higher in diabetic stroke patients (23.54 ± 1.43 vs -6.20 ± 9.36; p = 0.0061). CONCLUSIONS: We conclude that diabetes leads to continued IG after complete recanalization, conditioning clinical outcome in LVO strokes successfully recanalized by bridging therapy. We suggest that poor tissular reperfusion by diabetic microangiopathy could explain this result.