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Spitz, G.

Publications and source records attributed to Spitz, G..

3 recordsLinked to original sources

Aberrant modulation of brain activity underlies impaired working memory following traumatic brain injury

Impaired working memory capacity is a common and disabling consequence of traumatic brain injury (TBI) that is caused by aberrant neural processing. However, due to high heterogeneity in results across studies, it is challenging to conclude whether impaired working memory in this population is driven by neural hypo- or hyper-activation, and the extent to which deficits are perpetuated by specific working memory subprocesses. Using a combined functional magnetic resonance imaging and working memory paradigm, we tested the hypothesis that the pattern of neural activation subserving working memory following TBI would interact with both task demands and specific working memory subcomponents: encoding, maintenance, and retrieval. Behaviourally, we found that working memory deficits were confined to the high cognitive load trials. Our results confirmed our key prediction. Overall, TBI participants showed reduced brain activity while performing the working memory task. However, interrogation of the subcomponents of working memory revealed a more nuanced pattern of activation. When we simply averaged across all task trials, regardless of cognitive load or subcomponent, TBI participants showed reduced neural activation. When examined more closely, patterns of brain activity following TBI were found to interact with both task demands and working memory subcomponent. Participants with TBI demonstrated an inability to appropriately modulate brain activity between low and high demand conditions necessary during encoding and maintenance stages. Therefore, we demonstrate that conclusions about aberrant neural processing are dependent upon the level of analysis and the extent to which general cognitive domains can be parcellated into its constituent parts.

neuroscience

Age-related decline in cortical inhibitory tone strengthens motor memory

Ageing disrupts the finely tuned excitation/inhibition balance (E:I) across cortex, driven by a natural decline in inhibitory tone ({gamma}-amino butyric acid, GABA). This causes functional decrements. However, in young adults, experimentally lowering GABA in sensorimotor cortex enhances adaptation memory. Therefore, using a cross-sectional design, here we tested the hypothesis that as sensorimotor cortical GABA declines naturally with age, adaptation memory would increase, and the former would explain the latter. Results confirmed this prediction. To probe causality, we used brain stimulation to further lower sensorimotor cortical GABA during adaptation. Across individuals, how stimulation changed memory depended on sensorimotor cortical E:I. In those with low E:I, stimulation increased memory; in those with high E:I stimulation reduced memory. Thus, we identify a form of motor memory that improves naturally with age, depends causally on sensorimotor cortex neurochemistry, and may be a potent target for motor skill preservation strategies in healthy ageing and neurore-habilitation.

neuroscience

Temporal Lobe Activation Predicts Episodic Memory Following Traumatic Brain Injury

The temporal lobes are critical for episodic memories and are preferentially affected following a traumatic brain injury (TBI). As such, episodic memory difficulties are common following TBI; however, the underlying neural changes that precipitate or maintain these difficulties in the early phase of recovery remains poorly understood. Here, we use functional magnetic resonance imaging (fMRI) to interrogate the relationship of temporal lobe activation in response to face, scene, and animal stimuli. Twenty-five patients with moderate to severe TBI were recruited an average of 2 months post-injury and compared with 21 demographically similar healthy controls. Findings indicate that memory for faces was preferentially impaired, compared to scene and animal stimuli. Decreased activity in temporal lobe structures was present for both face (right transverse temporal gyrus) and scene stimuli (right fusiform gyrus), but not for animals. Greater activation in these structures was associated with better long-term recognition. These findings provide evidence to suggest that TBI: a) preferentially affects memory for complex stimuli such as faces and scenes, and b) causes aberrant neuronal processes despite lack of evidence of significant impairment in behavioural performance. The mechanisms underpinning these findings are discussed in terms of differences in strategy use and reduced neural efficiency.

neuroscience