Simultaneous transient global amnesia and Takotsubo syndrome after death of a relative: a case report.

INTRODUCTION: Simultaneous occurrence of transient global amnesia and Takotsubo syndrome has been only rarely reported. Here we report another patient with a transient global amnesia and concomitant Takotsubo syndrome. CASE PRESENTATION: Our patient is a 64-year-old white man with a previous history of myocarditis from borreliosis who developed sudden-onset confusional state with perseverations and repetition of the same questions during a funeral for his brother-in-law. Upon neurological work-up and after spontaneous resolution of most of the neurological deficits, transient global amnesia was diagnosed. Blood tests revealed moderate renal insufficiency, elevated troponin-T, and elevated N-terminal prohormone of brain natriuretic peptide. Electrocardiography showed left anterior hemiblock and negative T-waves in V2-V6. Upon transthoracic echocardiography the apical type of a Takotsubo syndrome was suspected. Since coronary angiography was normal and electrocardiography and echocardiographic abnormalities resolved under candesartan, bisoprolol, acetyl-salicylic acid, and atorvastatin within a few days after onset, Takotsubo syndrome was diagnosed. CONCLUSIONS: Since Takotsubo syndrome may be associated with transient global amnesia a causal relation may exist. A possible trigger for both conditions could be severe emotional stress from the loss of a close relative. A possible common pathomechanism could be overstimulation of adrenergic receptors in the myocardium, the cerebrum, or the coronary or cerebral arteries. Whether pre-existing myocardial compromise promotes the development of Takotsubo syndrome requires further investigations.

Pharmacological modulation of spreading depolarizations.

Spreading depolarization (SD) is a wave of almost complete depolarization of the neuronal and glial cells. Nowadays there is sufficient evidence demonstrating its pathophysiological effect in migraine with aura, transient global amnesia, stroke, subarachnoid hemorrhage, intracerebral hemorrhage, and traumatic brain injury. In these cases, occurrence of SD has been associated with functional neuronal damage, neuronal necrosis, neurological degeneration, and poor clinical outcome. Animal models show that SD can be modulated by drugs that interfere with its initiation and propagation. There are many pharmacological targets that may help to suppress SD occurrence, such as Na⁺, K⁺, Cl⁻, and Ca²âº channels; Na⁺/K⁺ -ATPase; gap junctions; and ligand-based receptors, for example, adrenergic, serotonin, sigma-1, calcitonin gene-related peptide, GABAA, and glutamate receptors. In this regard, N-methyl-d-aspartate (NMDA) receptor blockers, in particular, ketamine, have shown promising results. Therefore, theoretically pharmacologic modulation of SD could help diminish its pathological effects.

Transient epileptic amnesia: clinical report of a cohort of patients.

Transient epileptic amnesia is a seizure disorder, usually with onset in the middle-elderly and good response to low dosages of antiepileptic drugs. We describe the clinical, electroencephalography (EEG), and neuroimaging features of 11 patients with a temporal lobe epilepsy characterized by amnesic seizures as the sole or the main symptom. We outline the relevance of a detailed clinical history to recognize amnesic seizures and to avoid the more frequent misdiagnoses. Moreover, the response to monotherapy was usually good, although the epileptic disorder was symptomatic of acquired lesions in the majority of patients.

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.

Neuroprotective effect of Bacopa monniera on ischemia induced brain injury.

PURPOSE: Brain stroke is a leading cause of death without effective treatment. B. monniera, an Indian herbal medicine, exerts antioxidant activity and antistress activity by modulating the antioxidative defence system. We wanted to test if B. monniera could alleviate the ischemia induced brain injury and cognitive dysfunction in Wistar rats. PROCEDURE: We studied the effect of B. monniera (120mg kg(-1), 160mg kg(-1) and 240mg kg(-1) P.O.) on transient intracarotid artery (ICA) occlusion induced ischemia by testing the neurobehavioral and biochemical parameters on treated and control rats. FINDINGS: B. monniera attenuated the reduced transfer latency in ischemic rats in a step through test and showed a protective effect on ischemia induced memory impairment in the plus maze task. It also showed a marginal improvement in neurodeficit score and fore limb muscle grip strength. B. monniera reduced the infarct size in the ischemic brain. It also decreased nitrite, nitrate and lipid peroxidation and significantly improved catalase activity. CONCLUSION: These observations suggest the neuroprotective and antioxidant activity of B. monniera on ischemia induced brain injury and pave the way for future investigations.

A case of transient epileptic amnesia with radiological localization.

BACKGROUND: A 54-year-old man presented to a cognitive disorders clinic having experienced recurrent episodes of transient amnesia over a number of years. The attacks often occurred on waking, did not affect other cognitive abilities such as perception, language or judgment, and typically lasted about half an hour. The attacks were sometimes associated with olfactory hallucinations. Between amnestic episodes, the patient noticed a gradual deterioration in his recall of remote events, despite normal performance on standard memory tests. INVESTIGATIONS: Physical examination, laboratory tests, EEG, MRI brain scan, PET imaging, and neuropsychological assessment. DIAGNOSIS: Transient epileptic amnesia. MANAGEMENT: Anticonvulsant medication.

Recurrent orthostatic global amnesia in a patient with postoperative hyperfibrinogenemia.

Transient global amnesia (TGA) is characterized by sudden, temporary dysfunction of antegrade and recent retrograde memory without other neurologic deficits. Although there is sometimes a precipitating event, the origin of TGA remains controversial. We encountered a patient who developed recurrent TGA when upright, in whom the symptom promptly and regularly resolved when supine. Symptoms began about a week after cardiac surgery concurrent with marked hyperfibrinogenemia and acceleration of the erythrocyte sedimentation rate, and abated without recurrence when these laboratory abnormalities were ameliorated by anticoagulant and corticosteroid therapy. Diagnostic studies, including temporal artery biopsy and cerebral angiography, disclosed no anatomic vascular pathology. This is the first report of TGA associated with postoperative inflammation in which amnesia was provoked by orthostatic positioning. In conclusion, these observations implicate ischemia caused by hemodynamic vascular insufficiency as a possible cause of TGA.

Recovery of long-term anterograde amnesia, but not retrograde amnesia, after initiation of an anti-epileptic drug in a case of transient epileptic amnesia.

Transient epileptic amnesia (TEA) is characterised by recurrent brief episodes of amnesia and atypical amnesic symptoms, known as long-term anterograde amnesia and dense retrograde amnesia. It has been proposed that an antiepileptic drug (AED) can prevent not only epileptiform activity, but also accelerated forgetting. However, there have been no reports regarding the effects of such drugs on retrograde amnesia. We found that an AED prevented accelerated forgetting, but not dense retrograde amnesia, suggesting that accelerated forgetting in TEA was treatable, but retrograde amnesia was an irreversible process.

Transient global amnesia in a patient with high and persistent levels of antiphospholipid antibodies.

Cerebrovascular disease is one of the most common symptoms associated with anticardiolipin antibodies (ACA) and lupus anticoagulant (LA), usually in the form of ischemic stroke. However, many other neurologic disorders have been described in patients with antiphospholipid syndrome or ACA. So far, the precise relation between the presence of antibodies and the development of the disease in many of these cases remain unknown. Transient global amnesia (TGA) is an infrequent neurologic disturbance whose precise pathophysiology is not known. It is characterized by a sudden inability to acquire new information, usually lasting no more than 12 h, and it is not accompanied by any other focal neurological signs or symptoms. We report a patient with TGA with persistent and high levels of ACA and LA and suggest that in patients with TGA, investigation of the possible presence of ACA and/or LA may be warranted because a higher prevalence of TGA in the patients with antiphospholipidic syndrome with respect to the general population may lead to further insights into pathogenesis of neurologic disease associated with antiphospholipidic antibodies.

The effect of calcineurin activator, extracted from Chinese herbal medicine, on memory and immunity in mice.

Calcineurin (CN) is a highly abundant phosphatase in the brain and it is the only Ca(2+)- and calmodulin-dependent protein serine/threonine phosphatase. There is considerable evidence to suggest that CN plays an essential role in activity-dependent modulation of synaptic efficacy. It has been shown recently that inhibitors of CN, such as CsA or FK506, impair memory formation in day-old chicks. In our present study, extract of Fructus cannabis (EFC) with activation of CN, extracted from Chinese traditional medicine, was used to determine the effects on memory and immunity. In the step-down-type passive avoidance test, the plant extract (0.2 g/kg) significantly improved amnesia induced by chemical drugs in mice, and greatly enhanced the ability of cell-mediated type hypersensitivity and nonspecific immune responses in normal mice. The present study provided pharmacological evidence for Chinese herbal medicine screening from molecular model.