[Acute global amnesia as an exclusive presenting symptom of thalamic infarct: a diagnostic challenge]. / Amnesia global aguda como forma exclusiva de presentacion de infarto talamico: un reto diagnostico.

INTRODUCTION: Isolated acute amnesia is an exceptional presenting symptom of thalamic stroke. This study analyses the clinical profile, the diagnosis, the treatment and the prognosis of these patients. CASE REPORTS: We conducted a retrospective review of the cases of thalamic infarct that presented exclusively as acute amnesia in our university tertiary hospital (n = 3) and a review of similar cases in PubMed (n = 20). 48% presented at least one risk factor of stroke (arterial hypertension, dyslipidaemia, diabetes mellitus, atrial fibrillation or a previous stroke). Amnesia was anterograde in three cases (13%) and global in the remaining 20 (87%). The infarct was detected in neuroimaging studies carried out within the first 24 hours in one patient (4%) and later in all the others; the average time until a diagnosis was established was 11 days. The initial CT scan was normal in five patients (22%). Eight cases (35%) required magnetic resonance imaging to detect the infarct. Of these, four subjects were studied directly with MR imaging. Amnesia clearly improved in eight patients (35%), and three of them (13%) made a full recovery. Fifteen patients (65%) presented mnemonic sequelae that interfered with their functional capacity. The clinical picture lasted less than 24 hours in two patients (9%). None of the cases received revasculisation therapy in the acute phase. CONCLUSION: The diagnosis of thalamic infarcts that begin exclusively with amnesia is very difficult and this has negative repercussions on their treatment in the acute phase. These infarcts can produce a functionally disabling memory deficit in a high percentage of patients.

TITLE: Amnesia global aguda como forma exclusiva de presentacion de infarto talamico: un reto diagnostico.Introduccion. La amnesia aguda aislada es una forma excepcional de presentacion del ictus talamico. Se analizan el perfil clinico, el diagnostico, el tratamiento y el pronostico de estos pacientes. Casos clinicos. Revision retrospectiva de los casos de infarto talamico que se presentaron exclusivamente como amnesia aguda en nuestro hospital terciario universitario (n = 3) y revision de casos similares en PubMed (n = 20). El 48% presentaba al menos un factor de riesgo de ictus (hipertension arterial, dislipidemia, diabetes mellitus, fibrilacion auricular o ictus previo). La amnesia fue anterograda en tres casos (13%) y global en los otros 20 (87%). El infarto se detecto en estudio de neuroimagen en las primeras 24 horas en un paciente (4%) y posteriormente en los demas, y la media de dias hasta el diagnostico fue de 11. La tomografia computarizada inicial fue normal en cinco (22%) pacientes. Precisaron estudio por resonancia magnetica ocho (35%) casos para detectar el infarto. De estos, cuatro sujetos se estudiaron directamente con resonancia magnetica. La amnesia presento una mejoria clara en ocho (35%) pacientes, y la recuperacion fue completa en tres (13%). Las secuelas mnesicas que interferian la capacidad funcional se presentaron en 15 pacientes (65%). La clinica persistio menos de 24 horas en dos pacientes (9%). Ningun caso recibio tratamiento revascularizador en fase aguda. Conclusion. Los infartos talamicos que comienzan de forma exclusiva con amnesia presentan notables dificultades diagnosticas que repercuten negativamente en su tratamiento en la fase aguda. Estos infartos pueden producir un deficit mnesico funcionalmente discapacitante en un porcentaje elevado de pacientes.

EGB1212 post-treatment ameliorates hippocampal CA1 neuronal death and memory impairment induced by transient global cerebral ischemia/reperfusion.

Extracts of Ginkgo biloba have been used in traditional medicines for centuries, and have potential for clinical applications in cerebral ischemia/reperfusion injury. However, standardized extracts have proven protective only as pre-treatments, and the major mechanisms of action remain unclear. We explored the potential of the novel extract EGB1212, which meets the United States Pharmacopeia (USP) 31 standardization criteria for pharmaceutical use, as a post-treatment after global cerebral ischemia/reperfusion (GCI/R) injury in a rat model. The pre-treated group was administered EGB1212 for 7 d prior to common carotid artery occlusion (i.e., ischemia, for 20 min). Post-treated rats received the same but starting 2 h after ischemia and continuing for 7 d. Seven days after GCI/R, brains of each group were processed for H&E staining of hippocampal CA1 neurons. Remaining rats underwent the Morris water maze and Y-maze tests of spatial learning and memory, beginning eight days after reperfusion. To assess hippocampal autophagy, light chain (LC)-3-I/LC3-II and Akt/pAkt were determined via a Western blot of rat hippocampi harvested 12, 24, or 72 h after reperfusion. EGB1212 pre- and post-treatments both improved neuronal survival and spatial learning and memory functions. Pre-treatment effectively reduced LC3-II levels and post-treatment resulted in significantly elevated pAkt levels. We conclude that EGB1212 exerted significant neuroprotection in GCI/R in both preventative and post-treatment settings. This extract shows great potential for clinical applications.

[Transient global amnesia]. / Ictus amnésique (amnésie globale transitoire).

UNLABELLED: A DISTINCTIVE SYNDROME: Transient global amnesia is a very distinctive amnesic syndrome. The attack begins abruptly with massive anterograde verbal and non-verbal amnesia. Retrograde amnesia, variable in extent, is also present. A repetitive questioning behavior is usual. The memory impairment gradually resolves after almost always less than 12 hours. WELL-DEFINED CRITERIA: Specific criteria make it possible to distinguish transient global amnesia from psychogenic amnesia, acute confusional state and transient epileptic amnesia. "Pure" transient global amnesia is usually idiopathic and has a good prognosis. It is also distinguishable from symptomatic transient global amnesia. PATHOGENESIS: Functional imaging studies detect hippocampic or thalamic hypoperfusion. This oligemia may be secondary to neuronal dysfunction compatible with spreading depression. The pathogenic mechanisms remain unclear.