MRI factors associated with cognitive functioning after acute onset brain injury: Systematic review and meta-analysis.

Impairments of memory, attention, and executive functioning are frequently reported after acute onset brain injury. MRI markers hold potential to contribute to identification of patients at risk for cognitive impairments and clarification of mechanisms. The aim of this systematic review was to summarize and value the evidence on MRI markers of memory, attention, and executive functioning after acute onset brain injury. We included ninety-eight studies, on six classes of MRI factors (location and severity of damage (n = 15), volume/atrophy (n = 36), signs of small vessel disease (n = 15), diffusion-weighted imaging measures (n = 36), resting-state functional MRI measures (n = 13), and arterial spin labeling measures (n = 1)). Three measures showed consistent results regarding their association with cognition. Smaller hippocampal volume was associated with worse memory in fourteen studies (pooled correlation 0.58 [95% CI: 0.46-0.68] for whole, 0.11 [95% CI: 0.04-0.19] for left, and 0.34 [95% CI: 0.17-0.49] for right hippocampus). Lower fractional anisotropy in cingulum and fornix was associated with worse memory in six and five studies (pooled correlation 0.20 [95% CI: 0.08-0.32] and 0.29 [95% CI: 0.20-0.37], respectively). Lower functional connectivity within the default-mode network was associated with worse cognition in four studies. In conclusion, hippocampal volume, fractional anisotropy in cingulum and fornix, and functional connectivity within the default-mode network showed consistent associations with cognitive performance in all types of acute onset brain injury. External validation and cut off values for predicting cognitive impairments are needed for clinical implementation.

Role of dopamine and clinical heterogeneity in cognitive dysfunction in Parkinson's disease.

Parkinson's disease (PD) is commonly treated with dopaminergic medication, which enhances some, while impairing other cognitive functions. It can even contribute to impulse control disorder and addiction. We describe the history of research supporting the dopamine overdose hypothesis, which accounts for the large within-patient variability in dopaminergic medication effects across different tasks by referring to the spatially non-uniform pattern of dopamine depletion in dorsal versus ventral striatum. However, there is tremendous variability in dopaminergic medication effects not just within patients across distinct tasks, but also across different patients. In the second part of this chapter we review recent studies addressing the large individual variability in the negative side effects of dopaminergic medication on functions that implicate dopamine, such as value-based learning and choice. These studies begin to unravel the mechanisms of dopamine overdosing, thus revising the strict version of the overdose hypothesis. For example, the work shows that the canonical boosting of reward-versus punishment-based choice by medication is greater in patients with depression and a non-tremor phenotype, which both implicate, among other pathology, more rather than less severe dysregulation of the mesolimbic dopamine system. Future longitudinal cohort studies are needed to identify how to optimally combine different clinical, personality, cognitive, neural, genetic and molecular predictors of detrimental medication effects in order to account for as much of the relevant variability as possible. This will provide a useful tool for precision neurology, allowing individual and contextual tailoring of (the dose of) dopaminergic medication in order to maximize its cognitive benefits, yet minimize its side effects.

The role of the cerebellum in degenerative ataxias and essential tremor: Insights from noninvasive modulation of cerebellar activity.

Over the last three decades, measuring and modulating cerebellar activity and its connectivity with other brain regions has become an emerging research topic in clinical neuroscience. The most important connection is the cerebellothalamocortical pathway, which can be functionally interrogated using a paired-pulse transcranial magnetic stimulation paradigm. Cerebellar brain inhibition reflects the magnitude of suppression of motor cortex excitability after stimulating the contralateral cerebellar hemisphere and therefore represents a neurophysiological marker of the integrity of the efferent cerebellar tract. Observations that cerebellar noninvasive stimulation techniques enhanced performance of certain motor and cognitive tasks in healthy individuals have inspired attempts to modulate cerebellar activity and connectivity in patients with cerebellar diseases in order to achieve clinical benefit. We here comprehensively explore the therapeutic potential of these techniques in two movement disorders characterized by prominent cerebellar involvement, namely the degenerative ataxias and essential tremor. The article aims to illustrate the (patho)physiological insights obtained from these studies and how these translate into clinical practice, where possible by addressing the association with cerebellar brain inhibition. Finally, possible explanations for some discordant interstudy findings, shortcomings in our current understanding, and recommendations for future research will be provided. © 2019 The Authors. Movement Disorders published by Wiley Periodicals, Inc. on behalf of International Parkinson and Movement Disorder Society.

Ischemic neuropathy and rhabdomyolysis as presenting symptoms of postpartum cardiomyopathy.

Rhabdomyolysis and peripheral neuropathy are two distinct disease entities which are rarely encountered in combination. We present a woman with rhabdomyolysis and peripheral neuropathy 3 weeks postpartum. Her symptoms were caused by bilateral femoral artery thrombosis due to postpartum cardiomyopathy (PPCM). This demonstrates that PPCM may present with predominantly non-cardial symptoms and underscores the importance of rapidly recognizing this disorder.