JNS.jpgThe July issue of the Journal of the Neurological Sciences Vol 402 is now available online.

 

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Issue highlights

Do acute stroke patients develop hypocapnia? A systematic review and meta-analysis

Carbon dioxide (CO2) is a potent cerebral vasomotor agent. Despite reduction in CO2 levels (hypocapnia) being described in several acute diseases, there is no clear data on baseline CO2 values in acute stroke.

The aim of the study was to systematically assess CO2 levels in acute stroke. The evidence from this review suggests that acute stroke patients are significantly more likely than controls to be hypocapnic, supporting the value of routine CO2 assessment in the acute stroke setting. Further studies are required in order to evaluate the clinical impact of these findings.


Targeting kinases in Parkinson's disease: A mechanism shared by LRRK2, neurotrophins, exenatide, urate, nilotinib and lithium

Several kinases have been implicated in the pathogenesis of Parkinson's disease (PD), most notably leucine-rich repeat kinase 2 (LRRK2), as LRRK2 mutations are the most common genetic cause of a late-onset parkinsonism that is clinically indistinguishable from sporadic PD.

More recently, several other kinases have emerged as promising disease-modifying targets in PD based on both preclinical studies and clinical reports on exenatide, the urate precursor inosine, nilotinib and lithium use in PD patients. These kinases include protein kinase B (Akt), glycogen synthase kinases-3β and -3α (GSK-3β and GSK-3α), c-Abelson kinase (c-Abl) and cyclin-dependent kinase 5 (cdk5). Activities of each of these kinases are involved either directly or indirectly in phosphorylating tau or increasing α-synuclein levels, intracellular proteins whose toxic oligomeric forms are strongly implicated in the pathogenesis of PD. GSK-3β, GSK-3α and cdk5 are the principle kinases involved in phosphorylating tau at sites critical for the formation of tau oligomers.

Exenatide analogues, urate, nilotinib and lithium have been shown to affect one or more of the above kinases, actions that can decrease the formation and increase the clearance of intraneuronal phosphorylated tau and α-synuclein.

Here we review the current preclinical and clinical evidence supporting kinase-targeting agents as potential disease-modifying therapies for PD patients enriched with these therapeutic targets and incorporate LRRK2 physiology into this novel model.


Cingulate infarction: A neuropsychological and neuroimaging study

Ischemic lesions rarely affect the cingulate cortex (CC) in isolation, restricting human lesion/behavioural change correlational analysis. The aim of this study was to determine clinical, neuropsychological and neuroimaging features of isolated cingulate infarcts.

According rarely seen CC infarction events, we suggest that anterior and posterior CC are functionally separated and differences in clinical presentation are explained by considering; ACC plays a role in executive functions, episodic and working memory, set maintenance, and PCC is focused on spatial and verbal attention, and memory system. We considered that different patterns of cingulate infarcts are the result of variation in cingulate arterial supply or suggest a source of embolism.


Impact of cerebral large-artery disease and blood flow in the posterior cerebral artery territory on cognitive function

The purpose of this study was to elucidate the association of cerebral large artery disease (CLAD) with cerebral blood flow (CBF) in the posterior cerebral artery (PCA) territory and cognitive performance.

We prospectively registered 60 patients with CLAD who had internal carotid or middle cerebral artery (MCA) with the degree of stenosis ≥50%. Automated brain segmentation was used to quantify CBF in the thalamus, hippocampus, and PCA and MCA territories.

CBF of the PCA territory was significantly inversely correlated with the degree of stenosis in CLAD patients. Low CBF of the PCA territory was significantly associated with reduced cognitive and memory functions.