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Deep brain stimulation and memory

Deep brain stimulation (DBS) involves the delivery of electrical current into specific brain areas through implanted electrodes. Over the last few decades, this therapy has been successfully used to treat Parkinson’s disease, essential tremor and dystonia, with more than 100,000 patients implanted worldwide. Clinical applications of DBS in psychiatry and other fields of neurology are still investigational. Memory deficits are a hallmark of numerous neuropsychiatric disorders, including dementias. Alzheimer’s disease (AD) is the most common form of dementia accounting for 50–60% of cases. With the anticipated increase in life expectancy of the population, it is estimated that around 66 million people worldwide will be diagnosed with some form of dementia by 2030 [1]. In addition to human suffering, the socioeconomic burden of these disorders is enormous, with more than US$600 billion spent per year in healthcare costs around the world [1]. As with other dementias, the clinical symptomatology of AD is fairly complex, involving multiple cognitive domains. To date, the most commonly used medications to treat AD are the acetylcholinesterase inhibitors [2]. The benefits of these drugs on memory, however, are limited [2]. A few clinical reports have been published over the years studying the effects of electrical stimulation on memory. Improvements have been described in a patient with obesity treated with hypothalamic–forniceal DBS [3] and in a few reports in which epilepsy patients received entorhinal cortex [4] or anterior thalamic nucleus stimulation [5]. By contrast, a series of studies have described memory impairment in patients with epilepsy or brain tumors receiving stimulation in the hippocampal or mesial temporal lobe structures [6–8]. Two studies have been conducted using DBS to treat AD. In the first, a single patient treated with unilateral stimulation of the nucleus basalis of Meynert did not report significant changes in memory [9]. The second consisted of a Phase I trial to assess the safety of DBS in the region of the fornix in six patients with AD. Overall, stimulation was shown to improve and/or slow the rate of cognitive decline in 30% of patients at 6 and 12 months [10]. This was associated with a reversal of the typical temporoparietal hypometabolism of AD [10]. Reasons for the discrepancies described above are still unknown. Targets stimulated across studies are all part of the same limbic networks, which suggests that differences in outcome cannot be solely attributed to the circuitry influenced by DBS.