Thalamic contributions to anterograde, retrograde, and implicit memory: A case study
ABSTRACT Learning and memory deficits are typically associated with damage or dysfunction of medial temporal lobe structures; however, diencephalic lesions are another common cause of severe and persistent memory deficits. We focus specifically on the thalamus and review the pathological and neuropsychological characteristics of two common causes of such damage: Korsakoff's syndrome and stroke. We then present a patient who had sustained bilateral medial thalamic infarctions that affected the medial dorsal nucleus and internal medullary lamina. This patient demonstrated the characteristic temporally graded retrograde amnesia and a profound anterograde memory (i.e., explicit memory) deficit within the context of relatively preserved implicit memory. Implications of this explicit-implicit discrepancy are discussed within the context of cognitive rehabilitation techniques that hold promise for more severely impaired patients.
- SourceAvailable from: Olivier Piguet
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- "While amnesia is often observed in patients who have sustained a stroke involving AT or MD and the MTT (for a review see, Carlesimo et al., 2011), the unique contribution of thalamic nuclei to amnesia is still not very well understood. With a couple of exceptions (Van der Werf et al., 2003; Perren et al., 2005), reports of memory impairment in patients with focal thalamic lesions have been mostly confined to case studies (Kishiyama et al., 2005; Edelstyn et al., 2006; Carlesimo et al., 2007; Cipolotti et al., 2008; Hampstead and Koffler, 2009). This is partly attributed to the low patient incidence, and variability in the size and location of lesions (i.e. "
ABSTRACT: Effects of thalamic nuclei damage and related white matter tracts on memory performance are still debated. This is particularly evident for the medio-dorsal thalamus which has been less clear in predicting amnesia than anterior thalamus changes. The current study addresses this issue by assessing 7 thalamic stroke patients with consistent unilateral lesions focal to the left medio-dorsal nuclei for immediate and delayed memory performance on standard visual and verbal tests of anterograde memory, and over the long-term (>24 h) on an object-location associative memory task. Thalamic patients showed selective impairment to delayed recall, but intact recognition memory. Patients also showed accelerated forgetting of contextual details after a 24 h delay, compared to controls. Importantly, the mammillothalamic tract was intact in all patients, which suggests a role for the medio-dorsal nuclei in recall and early consolidation memory processes.Frontiers in Behavioral Neuroscience 09/2014; 8:320. DOI:10.3389/fnbeh.2014.00320 · 4.16 Impact Factor
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- "Memory impairment is one of the various neurological manifestations in patients with thalamic hemorrhage (Choi et al., 1983; Kawahara et al., 1986; Waxman et al., 1986; Hankey and Stewart- Wynne, 1988; Kumral et al., 1995; Chen et al., 1996; Chung et al., 1996; Exner et al., 2001; Summers, 2002; Kuljic-Obradovic et al., 2007; Kalefa et al., 2008). Injury of the MTT has been suggested as one of the plausible pathogenic mechanisms of memory impairment in patients with thalamic lesions along with injury of the ventral amygdalofugal pathway and the thalamocortical pathway between the mediodorsal nucleus of the thalamus and the prefrontal cortex (Kawahara et al., 1986; Hankey and Stewart-Wynne, 1988; Graff-Radford et al., 1990; Chen et al., 1996; Exner et al., 2001; Hampstead and Koffler, 2009). However, it has not been clearly demonstrated so far. "
ABSTRACT: Objective: Injury of the mammillothalamic tract (MTT) has been suggested as one of the plausible pathogenic mechanisms of memory impairment in patients with thalamic hemorrhage; however, it has not been clearly demonstrated so far. We attempted to investigate whether injury of the MTT documented by diffusion tensor tractography following thalamic hemorrhage correlates with cognitive impairment. Methods: We recruited 22 patients with a thalamic hemorrhage and 20 control subjects. MTTs were reconstructed using the probabilistic tractography method. Patients were classified into two subgroups: reconstructed group, patients whose MTT was reconstructed in the affected hemisphere, and non-reconstructed group, patients whose MTT was not reconstructed. Results: Mammillothalamic tract was reconstructed in 5 (22.7%, reconstructed group) patients in the affected hemisphere and was not reconstructed in the remaining 17 patients (77.3%, non-reconstructed group). In addition, the MTT was not reconstructed even in the unaffected hemisphere in four patients (23.5%) in non-reconstructed group. Fractional anisotropy and mean diffusivity values of the affected hemisphere in reconstructed group also did not show significant differences from those in the unaffected hemisphere of reconstructed group and the control group (p > 0.05). However, the tract volume of the affected hemisphere in reconstructed group was significantly lower than that of the unaffected hemisphere in reconstructed group and the control group (p < 0.05). Conclusion: A large portion of patients with thalamic hemorrhage appeared to suffer severe injury of the ipsilesional MTT (77.3%) and 18.2% of them appeared to suffer severe injury even in the contralesional MTT. In addition, the remaining 22.7% of patients who had preserved integrity of the ipsilesional MTT appeared to suffer partial injury of the ipsilesional MTT.Frontiers in Human Neuroscience 04/2014; 8:259. DOI:10.3389/fnhum.2014.00259 · 2.90 Impact Factor
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- "This region is believed to play an important role in learning and memory (Gabriel et al., 1983) since lesions in this area are known to impair mnestic functions (inducing diencephalic amnesia; Van der Werf et al., 2003), possibly through a disruption of neural plasticity processes in distal limbic brain regions (Dumont et al., 2012). In particular, damage to this region induces severe anterograde and temporally graded retrograde amnesia, along with impaired subjective memory, resembling patients with hippocampal system injury (Hampstead and Koffler, 2009). Furthermore, lesions in this region have also been associated with impaired regulation of affective responses to environmental conditions, through its connection with medial prefrontal limbic regions (Dupire et al., 2013). "
ABSTRACT: The primary and secondary damage to neural tissue inflicted by traumatic brain injury is a leading cause of death and disability. The secondary processes, in particular, are of great clinical interest because of their potential susceptibility to intervention. We address the dynamics of tissue degeneration in cortico-subcortical circuits after severe brain injury by assessing volume change in individual thalamic nuclei over the first six-months post-injury in a sample of 25 moderate to severe traumatic brain injury patients. Using tensor-based morphometry, we observed significant localized thalamic atrophy over the six-month period in antero-dorsal limbic nuclei as well as in medio-dorsal association nuclei. Importantly, the degree of atrophy in these nuclei was predictive, even after controlling for full-brain volume change, of behavioral outcome at six-months post-injury. Furthermore, employing a data-driven decision tree model, we found that physiological measures, namely the extent of atrophy in the anterior thalamic nucleus, were the most predictive variables of whether patients had regained consciousness by six-months, followed by behavioral measures. Overall, these findings suggest that the secondary non-mechanical degenerative processes triggered by severe brain injury are still ongoing after the first week post-trauma and target specifically antero-medial and dorsal thalamic nuclei. This result therefore offers a potential window of intervention, and a specific target region, in agreement with the view that specific cortico-thalamo-cortical circuits are crucial to the maintenance of large-scale network neural activity and thereby the restoration of cognitive function after severe brain injury.Clinical neuroimaging 10/2013; 3:396-404. DOI:10.1016/j.nicl.2013.09.010 · 2.53 Impact Factor