Maintenance of adequate tissue perfusion through a dense network of cerebral microvessels is critical for the perseveration of normal brain function. Regulation of the cerebral blood flow has to ensure adequate delivery of nutrients and oxygen with moment-to-moment adjustments to avoid both hypo- and hyper-perfusion of the brain tissue. Even mild impairments of cerebral blood flow regulation can have significant implications on brain function. Evidence suggests that chronic stress and depression elicits multifaceted functional impairments to the cerebral microcirculation, which plays a critical role in brain health and the pathogenesis of stress-related cognitive impairment and cerebrovascular events. Identifying the functional and structural changes to the brain that are induced by stress is crucial for achieving a realistic understanding of how related illnesses, which are highly disabling and with a large economic cost, can be managed or reversed. This overview discusses the stress-induced alterations in neurovascular coupling with specific attention to cerebrovascular regulation (endothelial dependent and independent vasomotor function, microvessel density). The pathophysiological consequences of cerebral microvascular dysfunction with stress and depression are explored.

Stroke and cardiac arrest result in cerebral ischemia, a highly prevalent medical issue around the world, which is characterized by a reduction or loss of blood flow to the brain. The loss of adequate nutrient supply in the brain during ischemia results in neuronal cell death contributing to cognitive and motor deficits that are usually permanent. Current effective therapies for cerebral ischemia are only applicable after the fact. Thus, the development of preventative therapies of ischemia is imperative. A field of research that continues to show promise in developing therapies for cerebral ischemia is ischemic preconditioning (IPC). IPC is described as exposure to sublethal ischemic events, which induce adaptive changes that provide tolerance to future ischemic events. Through either transient sub-lethal ischemic events, or the actions of a preconditioning molecular mimetic, IPC typically results in augmented gene expression and cellular metabolism. A pivotal target of such changes in gene expression and metabolism is the mitochondrion. Direct and indirect effects on mitochondria by IPC can result in the activation of 5' adenosine monophosphate-activated protein kinase (AMPK), a master regulator of cellular metabolism. Changes in the activity of the posttranslational modifiers, SIRT1 and SIRT5, also contribute to the overall adaptive processes in cellular metabolism and mitochondrial functioning. In this review, we present recently collected evidence to highlight the neuroprotective interactions of mitochondria with AMPK, SIRT1, and SIRT5 in IPC. To produce this review, we utilized PubMed and previous reviews to target and to consolidate the relevant studies and lines of evidence.

Phantom limb pain (PLP) and phantom limb sensations are common complications postamputation. PLP is defined as persistent painful sensations perceived in the missing portion of the amputated limb. Low-temperature plasma radiofrequency ablation (coblation) technology is a relatively new technology that has shown promise in treating neuropathic pain. This report illustrates the use of coblation technology on cervical nerve roots for PLP. Coblation of the cervical nerve root was performed. Three 17G puncture trocars were placed near the C5–C6, C6–C7, and C7–T1 intervertebral foramen with computed tomography (CT) guidance. Then, a coblation needle attached to low-temperature plasma multifunctional operation system was placed near the C8 nerve root through the puncture trocars. To locate the target nerve, single stimulation (lasting for 5 s, at 1 intensity) in “cut” and “coagulation” model was given to serve as a sensory stimulation test. The stimulation induced radiating pain of the stimulated nerve away from the stimulation site to confirm our target nerve. The needle location was redirected based on the reproduction of the patient's symptoms with minimal intensity. A CT-guided cervical nerve root coblation was performed to obtain longer PLP relief. The patient reported pain relief in PLP after the operation. At 1-, 3-, and 6-month postoperative review, PLP relief was achieved. Overall activity was improved and there was necessarily need for pain medications. However, the doses of medicine significantly decreased. The analgesic effect was stable during the 6-month follow-up period. Our report demonstrates that coblation technology is successful treatment for PLP in this case. It will supply us a novel navigation in PLP treatments. Meanwhile, this finding still needs additional study for confirmation.

Ischemic stroke as an initial presentation of malignancy is extremely rare and the underlying etiology is often ignored. The aim of this study is to outline the clues to occult malignancy in patients presenting with cerebral infarction initially. The clinical characteristics of total 19 patients with Trousseau's Syndrome presenting with cerebral infarction initially were analyzed. Among those patients, no conventional vascular risk factors were detected in 68% (13/19) of patients, and infarction occurring in multiple vascular distributions was found in 84% (16/19). Blood test showed thrombophilia in 79% (15/19) of patients with significantly elevated D-dimer, disseminated intravascular coagulopathy (DIC) in 59% (11/19), and elevated levels of tumor makers in 47% (9/19). The prognosis of the 19 patients was poor, with 68% (13/19) of patients undergoing a relapse of stroke in short interval, and 84% (16/19) being reportedly to die in 6 months. In patients, who developed unexplained recurrent brain infarction involving multiple arterial territory, with laboratory evidence suggesting hypercoagulability (higher level of D-dimer, or DIC), Trousseau's Syndrome should be considered, and investigation for an occult malignancy was required.