Cognitive enhancement with central thalamic electrical stimulation

Shirvalkar, Prasad; Seth, Malika; Schiff, Nicholas D.; Herrera, Daniel

doi:10.1073/pnas.0604811103

Cited by 134 publications

(116 citation statements)

References 36 publications

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“…Appropriate electrical stimulation of the central lateral nucleus can facilitate spontaneous object recognition (Shrivalkar et al 2006). This facilitation occurred when stimulation was applied during recognition testing but not during the sample period or during the retention interval.…”

Section: Intralaminar Thalamic Nucleimentioning

confidence: 99%

Unraveling the contributions of the diencephalon to recognition memory: A review

Aggleton¹,

Dumont²,

Warburton³

2011

Learn. Mem.

139

111

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Both clinical investigations and studies with animals reveal nuclei within the diencephalon that are vital for recognition memory (the judgment of prior occurrence). This review seeks to identify these nuclei and to consider why they might be important for recognition memory. Despite the lack of clinical cases with circumscribed pathology within the diencephalon and apparent species differences, convergent evidence from a variety of sources implicates a subgroup of medial diencephalic nuclei. It is supposed that the key functional interactions of this subgroup of diencephalic nuclei are with the medial temporal lobe, the prefrontal cortex, and with cingulate regions. In addition, some of the clinical evidence most readily supports dual-process models of recognition, which assume two independent cognitive processes (recollective-based and familiarity-based) that combine to direct recognition judgments. From this array of information a "multi-effect multinuclei" model is proposed, in which the mammillary bodies and the anterior thalamic nuclei are of preeminent importance for recollective-based recognition. The medial dorsal thalamic nucleus is thought to contribute to familiarity-based recognition, but this nucleus, along with various midline and intralaminar thalamic nuclei, is also assumed to have broader, indirect effects upon both recollective-based and familiarity-based recognition.Clinical studies repeatedly show that diencephalic pathology can impair recognition memory. Even so, there is no agreed locus within the diencephalon responsible for this memory loss and, hence, no agreed mechanism to explain the impairment. The present review examines both clinical and animal findings, and from this information a multi-effect multi-nuclei (MEMN) model emerges to explain the contributions of the diencephalon to recognition memory.At the outset, it is necessary to refine the focus of this review and to define some of its principal terms. The diencephalon comprises the thalamus and hypothalamus but, as will be explained, only the more medial parts of the diencephalon will be considered in detail. Recognition memory refers to the ability to detect whether a stimulus (e.g., a word, face, picture, object, or sound) has previously been encountered. As a consequence, this review is not about item identification (sometimes also confusingly referred to as recognition). Likewise, conditions that have broad disruptive effects on cognition, e.g., dementia, will not be considered even though recognition is typically impaired. Distinctions will be made between "item recognition," where the task is to determine if an individual item is novel or familiar, and "associative recognition," where all the individual items being experienced are familiar, but their particular combination is novel. A further, distinct ability is "recency" discrimination-the ability to determine which of two familiar stimuli has been experienced more recently. Both studies of amnesia and electrophysiological recordings show how recency memory and recogniti...

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Section: Intralaminar Thalamic Nucleimentioning

confidence: 99%

Unraveling the contributions of the diencephalon to recognition memory: A review

Aggleton¹,

Dumont²,

Warburton³

2011

Learn. Mem.

139

111

View full text Add to dashboard Cite

show abstract

“…Detailed electrophysiological studies and clinical observations further indicate a key role of these neuronal populations in maintaining an alert wakeful state [10]. Further, the relevance of activation of these circuits as a therapeutic strategy for acquired cognitive disabilities associated with non-progressive brain injuries has been proposed [3].…”

Section: Discussionmentioning

confidence: 99%

Deep brain stimulation facilitates memory in a model of Alzheimer’s disease

Arrieta‐Cruz

Pavlides

Pasinetti³

2010

Translational Neuroscience

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Based on evidence suggesting that deep brain stimulation (DBS) may promote certain cognitive processes, we have been interested in developing DBS as a means of mitigating memory and learning impairments in Alzheimer's disease (AD). In this study we used an animal model of AD (TgCRND8 mice) to determine the effects of high-frequency stimulation (HFS) on non-amyloidogenic α-secretase activity and DBS in short-term memory. We tested our hypothesis using hippocampal slices (in vitro studies) from TgCRND8 mice to evaluate whether HFS increases α-secretase activity (non-amyloidogenic pathway) in the CA1 region. In a second set of experiments, we performed in vivo studies to evaluate whether DBS in midline thalamic region re-establishes hippocampal dependent short-term memory in TgCRND8 mice. The results showed that application of HFS to isolated hippocampal slices significantly increased synaptic plasticity in the CA1 region and promoted a 2-fold increase of non-amyloidogenic α-secretase activity, in comparison to low frequency stimulated controls from TgCRND8 mice. In the in vivo studies, DBS treatment facilitated acquisition memory in TgCRND8 mice, in comparison to their own baseline before treatment. These results provide evidence that DBS could enhance short-term memory in a mouse model of AD by increasing synaptic transmission and α-secretase activity in the CA1 region of hippocampus.

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“…Left thalamus stimulation appears to improve verbal memory when audition is delivered to the contralateral ear [168]. Continuous high-frequency (100 Hz) electrical stimulation of the central thalamus generates widespread cortical activation and facilitates global arousal, goal-directed seeking behavior, and object recognition memory in rodents [141]. DBS targeting the central thalamus could restore sustained attention, working memory and awareness in patients with traumatic brain injury [126] and appears to have achieved some of these goals in at least one patient [127].…”

Section: Subcortical and Peripheral Stimulationmentioning

confidence: 99%

Techniques and devices to restore cognition

Serruya

Kahana

2008

Behavioural Brain Research

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Executive planning, the ability to direct and sustain attention, language and several types of memory may be compromised by conditions such as stroke, traumatic brain injury, cancer, autism, cerebral palsy and Alzheimer's disease. No medical devices are currently available to help restore these cognitive functions. Recent findings about the neurophysiology of these conditions in humans coupled with progress in engineering devices to treat refractory neurological conditions imply that the time has arrived to consider the design and evaluation of a new class of devices. Like their neuromotor counterparts, neurocognitive prostheses might sense or modulate neural function in a non-invasive manner or by means of implanted electrodes. In order to paint a vision for future device development, it is essential to first review what can be achieved using behavioral and external modulatory techniques. While non-invasive approaches might strengthen a patient's remaining intact cognitive abilities, neurocognitive prosthetics comprised of direct brain-computer interfaces could in theory physically reconstitute and augment the substrate of cognition itself.

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Cognitive enhancement with central thalamic electrical stimulation

Cited by 134 publications

References 36 publications

Unraveling the contributions of the diencephalon to recognition memory: A review

Unraveling the contributions of the diencephalon to recognition memory: A review

Deep brain stimulation facilitates memory in a model of Alzheimer’s disease

Techniques and devices to restore cognition

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