Background Decompressive craniectomy (DC) is used in cases of severe intracranial hypertension or impending intracranial herniation. DC effectively lowers intracranial pressure (ICP) but carries a risk of severe complications related to abnormal ICP and/or cerebrospinal fluid (CSF) circulation, eg, hygroma formation, hydrocephalus, and "syndrome of the trephined." Objective To study the long-term effect of DC on ICP, postural ICP regulation, and intracranial pulse wave amplitude (PWA). Methods Prospective observational study including patients undergoing DC during a 12-mo period. Telemetric ICP sensors (Neurovent-P-tel; Raumedic, Helmbrechts, Germany) were implanted in all patients. Following discharge from the neuro intensive care unit (NICU), scheduled weekly ICP monitoring sessions were performed during the rehabilitation phase. Results A total of 16 patients (traumatic brain injury: 7, stroke: 9) were included (median age: 55 yr, range: 19-71 yr). Median time from NICU discharge to cranioplasty was 48 d (range: 16-98 d) and during this period, mean ICP gradually decreased from 7.8 ± 2.0 mm Hg to -1.8 ± 3.3 mm Hg (P = .02). The most pronounced decrease occurred during the first month. Normal postural ICP change was abolished after DC for the entire follow-up period, ie, there was no difference between ICP in supine and sitting position (P = .67). PWA was markedly reduced and decreased from initially 1.2 ± 0.7 mm Hg to 0.4 ± 0.3 mm Hg (P = .05). Conclusion Following NICU discharge, ICP decreases to negative values within 4 wk, normal postural ICP regulation is lost and intracranial PWA is diminished significantly. These abnormalities might have implications for intracranial fluid movements (eg, CSF and/or glymphatic flow) following DC and warrants further investigations.

Long-Term Effect of Decompressive Craniectomy on Intracranial Pressure and Possible Implications for Intracranial Fluid Movements

The purposes of this narrative review are to (1) summarize a contemporary view of cerebral edema pathophysiology, (2) present a synopsis of current management strategies in the context of their historical roots (many of which date back multiple centuries), and (3) discuss contributions of key molecular pathways to overlapping edema endophenotypes. This may facilitate identification of important therapeutic targets. Cerebral edema and resultant intracranial hypertension are major contributors to morbidity and mortality following traumatic brain injury. Although Starling forces are physical drivers of edema based on differences in intravascular vs extracellular hydrostatic and oncotic pressures, the molecular pathophysiology underlying cerebral edema is complex and remains incompletely understood. Current management protocols are guided by intracranial pressure measurements, an imperfect proxy for cerebral edema. These include decompressive craniectomy, external ventricular drainage, hyperosmolar therapy, hypothermia, and sedation. Results of contemporary clinical trials assessing these treatments are summarized, with an emphasis on the gap between intermediate measures of edema and meaningful clinical outcomes. This is followed by a brief statement summarizing the most recent guidelines from the Brain Trauma Foundation (4th edition). While many molecular mechanisms and networks contributing to cerebral edema after TBI are still being elucidated, we highlight some promising molecular mechanism-based targets based on recent research including SUR1-TRPM4, NKCC1, AQP4, and AVP1. This review outlines the origins of our understanding of cerebral edema, chronicles the history behind many current treatment approaches, and discusses promising molecular mechanism-based targeted treatments.

Cerebral Edema in Traumatic Brain Injury: a Historical Framework for Current Therapy.

Background Research is a central component of neurosurgical training and practice and is increasingly viewed as a quintessential indicator of academic productivity. In this study, we focus on identifying the current status and challenges of neurosurgical research in Iraq. Methods An online PubMed Medline database search was conducted to identify all articles published by Iraq-based neurosurgeons between 2003 and 2020. Information was extracted in relation to the following parameters: authors, year of publication, author's affiliation, author's specialty, article type, article citation, journal name, journal impact factor, and topic. This data were then tabulated and analyzed. Results Between 2003 and 2021, a total of 52 PubMed indexed papers were published from Iraq. All publications have been clustered in the period of 2012-2020. From 2012 to 2016, only four papers were published, one per year. The number of publications increased from 2017 to 2021, with an average of 12 publications per year. The most common article type was "case reports" (n = 14). Neurotrauma (n = 10) and vascular neurosurgery (n = 10) were the two most common topics. Most of the studies came from the city of Bagdad (n = 46), with just nine studies coming from peripheral governorates. The Neurosurgery Teaching Hospital in Bagdad was the neurosurgery center with the highest research output (n = 38). Conclusion The number of publications per year has been showing a, relatively, promising trend since 2012. However, to promote sustained growth in academic productivity, a strategic plan that acknowledges the political, financial, and health-system-related challenges are urgently needed.

PubMed-indexed neurosurgical research productivity of Iraq-based neurosurgeons.

In Reply: A Bibliometric Analysis of Neurosurgical Practice Guidelines

Anatoli Dimitrov

Papers

Commentary: Therapeutic Hypothermia in Patients With Severe Traumatic Brain Injury: Where Do We Go Now?

Dos and Don'ts of virtual reality-based simulators for cranial tumor surgery

Letter: Long-Term Effect of Decompressive Craniectomy on Intracranial Pressure and Possible Implications for Intracranial Fluid Movements.

Letter: A Bibliometric Analysis of Neurosurgical Practice Guidelines

Role of neuroimaging in initial assessment of subarachnoid hemorrhage