RESUMEN
After craniectomy, patients are generally advised to wear a helmet when mobilising to protect the unshielded brain from damage. However, there exists limited guidance regarding head protection for patients at rest and when being transferred or turned. Here, we emphasise the need for such protocols and utilise evidence from several sources to affirm our viewpoint. A literature search was first performed using MEDLINE and EMBASE, looking for published material relating to head protection for patients post-craniectomy during rest, transfer or turning. No articles were identified using a wide-ranging search strategy. Next, we surveyed and interviewed staff and patients from our neurosurgical centre to ascertain how often their craniectomy site was exposed to external pressure and the precautions taken to prevent this. 59% of patients admitted resting in contact with the craniectomy site, in agreement with the observations of 67% of staff. In 63% of these patients, this occurred on a daily basis and for some, was associated with symptoms suggestive of raised intracranial pressure. 44% of staff did not use a method to prevent craniectomy site contact while 65% utilised no additional precautions during transfer or turning. 63% of patients received no information about avoiding craniectomy site contact upon discharge, and almost all surveyed wished for resting head protection if it were available. We argue that pragmatic guidelines are needed and that our results support this perspective. As such, we offer a simple, practical protocol which can be adopted and iteratively improved as further evidence becomes available in this area.
RESUMEN
Pericyte-mediated capillary constriction decreases cerebral blood flow in stroke after an occluded artery is unblocked. The determinants of pericyte tone are poorly understood. We show that a small rise in cytoplasmic Ca2+ concentration ([Ca2+]i) in pericytes activated chloride efflux through the Ca2+-gated anion channel TMEM16A, thus depolarizing the cell and opening voltage-gated calcium channels. This mechanism strongly amplified the pericyte [Ca2+]i rise and capillary constriction evoked by contractile agonists and ischemia. In a rodent stroke model, TMEM16A inhibition slowed the ischemia-evoked pericyte [Ca2+]i rise, capillary constriction, and pericyte death; reduced neutrophil stalling; and improved cerebrovascular reperfusion. Genetic analysis implicated altered TMEM16A expression in poor patient recovery from ischemic stroke. Thus, pericyte TMEM16A is a crucial regulator of cerebral capillary function and a potential therapeutic target for stroke and possibly other disorders of impaired microvascular flow, such as Alzheimer's disease and vascular dementia.
