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Background and objectives. Cancer-related cognitive impairment has been acknowledged as a substantial limiting factor in quality of life among cancer patients and survivors. In addition to deficits on behavioral measures, abnormalities in neurologic structure and function have been reported. In this paper, we review findings from the literature on cognitive impairment and cancer, potential interventions, meditation and cognitive function, and meditation and cancer. In addition, we offer our hypotheses on how meditation practice may help to alleviate objective and subjective cognitive function, as well as the advantages of incorporating a meditation program into the treatment of cancer patients and survivors for cancer-related cognitive deficits. Findings. Various factors have been hypothesized to play a role in cancer-related cognitive impairment including chemotherapy, reduced hormone levels, proinflammatory immune response, fatigue, and distress. Pharmacotherapies such as methylphenidate or modafinil have been suggested to alleviate cognitive deficits. While initial reports suggest they are effective, some pharmacotherapies have side effects and may not relieve other symptoms associated with multimodal cancer treatment including sleep disturbance, nausea and pain. Several recent studies investigating the effects of meditation programs have reported behavioral and corresponding neurophysiological modulations that may be particularly effective in alleviating cancer-related cognitive impairment. Such programs also have been shown to reduce stress, fatigue, nausea and pain, and improve mood and sleep quality. Conclusions. With the increasing success of cancer treatment and the ability to return to previous family, social, and work activities, symptom management and quality of life are an essential part of survivorship. We propose that meditation may help to improve cancer-related cognitive dysfunction, alleviate other cancer-related sequelae, and should be fully investigated as an adjuvant to cancer treatment.

Lesions of the dorsal hippocampus have been shown to disrupt both the acquisition and the consolidation of memories associated with contextual fear (fear of the place of conditioning), but do not affect fear conditioning to discrete cues (e.g., a tone). Blockade of central muscarinic cholinergic receptor activation results in selective acquisition deficits of contextual fear conditioning, but reportedly has little effect on consolidation. Here we show for the first time that direct infusion of the muscarinic cholinergic receptor antagonist, scopolamine, into the dorsal hippocampus produces a dose-dependent deficit in both acquisition and consolidation of contextual fear conditioning, while having no impact on simple tone conditioning.
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OBJECTIVE: The purpose of this study was to use functional magnetic resonance imaging (fMRI) to probe the neural circuitry associated with reactivity to negative and positive affective stimuli in patients with major depressive disorder before treatment and after 2 and 8 weeks of treatment with venlafaxine. Relations between baseline neural activation and response to treatment were also evaluated. METHOD: Patients with major depressive disorder (N=12) and healthy comparison subjects (N=5) were scanned on three occasions, during which trials of alternating blocks of affective and neutral pictorial visual stimuli were presented. Symptoms were evaluated at each testing occasion, and both groups completed self-report measures of mood. Statistical parametric mapping was used to examine the fMRI data with a focus on the group-by-time interactions. RESULTS: Patients showed a significant reduction in depressive symptoms with treatment. Group-by-time interactions in response to the negative versus neutral stimuli were found in the left insular cortex and the left anterior cingulate. At baseline, both groups showed bilateral activation in the visual cortices, lateral prefrontal cortex, and amygdala in response to the negative versus neutral stimuli, with patients showing greater activation in the visual cortex and less activation in the left lateral prefrontal cortex. Patients with greater relative anterior cingulate activation at baseline in response to the negative versus neutral stimuli showed the most robust treatment response. CONCLUSIONS: The findings underscore the importance of the neural circuitry activated by negative affect in depression and indicate that components of this circuitry can be changed within 2 weeks of treatment with antidepressant medication.
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Subregional analyses of the hippocampus have suggested a selective role for the CA1 subregion in intermediate/long-term spatial memory and consolidation, but not short-term acquisition or encoding processes. It remains unclear how the direct cortical projection to CA1 via the perforant path (pp) contributes to these CA1-dependent processes. It has been suggested that dopamine selectively modulates the pp projection to CA1 while having little to no effect on the Schaffer collateral (SC) projection to CA1. This series of behavioral and electrophysiological experiments takes advantage of this pharmacological dissociation to demonstrate that the direct pp inputs to CA1 are critical in CA1-dependent intermediate-term retention and retrieval function. Here we demonstrate that local infusion of the nonselective dopamine agonist, apomorphine (10, 15 microg), into the CA1 subregion of awake animals produces impairments in between-day retention and retrieval, sparing within-day encoding of a modified Hebb-Williams maze and contextual conditioning of fear. In contrast, apomorphine produces no deficits when infused into the CA3 subregion. To complement the behavioral analyses, electrophysiological data was collected. In anesthetized animals, local infusion of the same doses of apomorphine significantly modifies evoked responses in the distal dendrites of CA1 following angular bundle stimulation, but produces no significant effects in the more proximal dendritic layer following stimulation of the SC. These results support a modulatory role for dopamine in the EC-CA1, but not CA3-CA1 circuitry, and suggest the possibility of a more fundamental role for EC-CA1 synaptic transmission in terms of intermediate-term, but not short-term spatial memory.
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