Update: Curcumin for Traumatic Brain Injury

A study determined whether the neuroprotective role of curcumin in mouse TBI is dependent on the NF-E2-related factor (Nrf2) pathway. The Feeney weight-drop contusion model was used to mimic TBI. Curcumin was administered intraperitoneally 15 min after TBI induction, and brains were collected at 24 h after TBI. The levels of Nrf2 and its downstream genes (Hmox-1, Nqo1, Gclm, and Gclc) were detected by Western blot and qRT-PCR at 24 h after TBI. In addition, edema, oxidative damage, cell apoptosis and inflammatory reactions were evaluated in wild type (WT) and Nrf2-knockout (Nrf2-KO) mice to explore the role of Nrf2 signaling after curcumin treatment. In wild type mice, curcumin treatment resulted in reduced ipsilateral cortex injury, neutrophil infiltration, and microglia activation, improving neuron survival against TBI-induced apoptosis and degeneration. These effects were accompanied by increased expression and nuclear translocation of Nrf2, and enhanced expression of antioxidant enzymes. However, Nrf2 deletion attenuated the neuroprotective effects of curcumin in Nrf2-KO mice after TBI. These findings demonstrated that curcumin effects on TBI are associated with the activation the Nrf2 pathway, providing novel insights into the neuroprotective role of Nrf2 and the potential therapeutic use of curcumin for TBI 1).


The protective effect of tetrahydrocurcumin (THC) after experimental traumatic brain injury (TBI) has been demonstrated, as demonstrated by the inhibition of oxidative stress, mitochondrial dysfunction, and apoptosis. However, the mechanisms underlying this effect are still not well understood.

A study was to investigate the neuroprotective effects of THC, and its potential mechanisms, in a rat model of TBI. To this end, rats were divided into 4 groups: the sham group, the TBI group, the TBI + vehicle (V) group, and the TBI + THC group. THC or V was administered via intraperitoneal injection to rats in the TBI + V and TBI + THC groups 30 min after TBI. After euthanasia (24 h after TBI), neurological scores, brain water content, and neuronal cell death in the cerebral cortex were recorded. Brain samples were collected after neurological scoring for further analysis. THC treatment alleviated brain edema, attenuated TBI-induced neuronal cell apoptosis, and improved neurobehavioral function. In addition, NFE2-related factor 2 (Nrf2) expression was upregulated following TBI. These results suggest that THC improves neurological outcome after TBI, possibly by activating the Nrf2 signaling pathway 2).


The aim of a study was to investigate the potential neuroprotection of curcumin and the possible role of Nrf2-ARE pathway in the weight-drop model of TBI. The administration of curcumin significantly ameliorated secondary brain injury induced by TBI, such as brain water content, oxidative stress, neurological severity score, and neuronal apoptosis. Curcumin possessed anti-apoptotic character evidenced by elevating Bcl-2 content and reducing that of cleaved caspase-3. Moreover, curcumin markedly enhanced the translocation of Nrf2 from the cytoplasm to the nucleus, proved by the results of western blot and immunohistochemistry, subsequently increased the expression of downstream factors such as heme oxygenase 1 (HO1) and NAD(P)H: quinone oxidoreductase 1 (NQO1) and prevented the decline of antioxidant enzyme activities. In conclusion, curcumin could increase the activities of antioxidant enzymes and attenuate brain injury in the model of TBI, possibly via the activation of the Nrf2-ARE pathway 3).


In a study, Huang et al., evaluated the therapeutic potential of curcumin for the treatment of DAI and investigated the mechanisms underlying the protective effects of curcumin against neural cell death and axonal injury after DAI. Rats subjected to a model of DAI by head rotational acceleration were treated with vehicle or curcumin to evaluate the effect of curcumin on neuronal and axonal injury. We observed that curcumin (20 mg/kg intraperitoneal) administered 1 h after DAI induction alleviated the aggregation of p-tau and β-APP in neurons, reduced ER-stress-related cell apoptosis, and ameliorated neurological deficits. Further investigation showed that the protective effect of curcumin in DAI was mediated by the PERK/Nrf2 pathway. Curcumin promoted PERK phosphorylation, and then Nrf2 dissociated from Keap1 and was translocated to the nucleus, which activated ATF4, an important bZIP transcription factor that maintains intracellular homeostasis, but inhibited the CHOP, a hallmark of ER stress and ER-associated programmed cell death. In summary, we demonstrate for the first time that curcumin confers protection against abnormal proteins and neuronal apoptosis after DAI, that the process is mediated by strengthening of the unfolded protein response to overcome ER stress, and that the protective effect of curcumin against DAI is dependent on the activation of Nrf2 4).


Neurological function, brain water content and cytokine levels were tested in TLR4⁻/⁻ mice subjected to weight-drop contusion injury. Wild-type (WT) mice were injected intraperitoneally with different concentrations of curcumin or vehicle 15 minutes after TBI. At 24 hours post-injury, the activation of microglia/macrophages and TLR4 was detected by immunohistochemistry; neuronal apoptosis was measured by FJB and TUNEL staining; cytokines were assayed by ELISA; and TLR4, MyD88 and NF-κB levels were measured by Western blotting. In vitro, a co-culture system comprised of microglia and neurons was treated with curcumin following lipopolysaccharide (LPS) stimulation. TLR4 expression and morphological activation in microglia and morphological damage to neurons were detected by immunohistochemistry 24 hours post-stimulation.

The protein expression of TLR4 in pericontusional tissue reached a maximum at 24 hours post-TBI. Compared with WT mice, TLR4⁻/⁻ mice showed attenuated functional impairment, brain edema and cytokine release post-TBI. In addition to improvement in the above aspects, 100 mg/kg curcumin treatment post-TBI significantly reduced the number of TLR4-positive microglia/macrophages as well as inflammatory mediator release and neuronal apoptosis in WT mice. Furthermore, Western blot analysis indicated that the levels of TLR4 and its known downstream effectors (MyD88, and NF-κB) were also decreased after curcumin treatment. Similar outcomes were observed in the microglia and neuron co-culture following treatment with curcumin after LPS stimulation. LPS increased TLR4 immunoreactivity and morphological activation in microglia and increased neuronal apoptosis, whereas curcumin normalized this upregulation. The increased protein levels of TLR4, MyD88 and NF-κB in microglia were attenuated by curcumin treatment.

The results suggest that post-injury, curcumin administration may improve patient outcome by reducing acute activation of microglia/macrophages and neuronal apoptosis through a mechanism involving the TLR4/MyD88/NF-κB signaling pathway in microglia/macrophages in TBI 5).


The neuroprotective effects of curcumin were evaluated in a weight drop model of cortical contusion trauma in rat. Male Wistar rats (350-400 g, n=9) were anesthetized with sodium pentobarbital (60 mg/kg i.p.) and subjected to head injury. Five days before injury, animals randomly received an i.p. bolus of either curcumin (50 and 100 mg/kg/day, n=9) or vehicle (n=9). Two weeks after the injury and drug treatment, animals were sacrificed and a series of brain sections, stained with hematoxylin and eosin (H&E) were evaluated for quantitative brain lesion volume. Two weeks after the injury, oxidative stress parameter (malondialdehyde) was also measured in the brain. Curcumin (100 mg/kg) significantly reduced the size of brain injury-induced lesions (P<0.05). Neurological examinations (rotarod and inclined-plane tests) were performed on days 1, 3, 7 and 14 post-brain injury. Control injured rats had a significant neurological deficit during 2 weeks (P<0.001). The injury increased brain levels of the malondialdehyde by 35.6% and these increases were attenuated by curcumin (100 mg/kg). Curcumin treatment significantly improved the neurological status evaluated during 2 weeks after brain injury. The study demonstrates the protective efficacy of curcumin in rat traumatic brain injury model 6).


In a study, pre-treatment with curcumin (75, 150 mg/kg) or 30 min post-treatment with 300 mg/kg significantly reduced brain water content and improved neurological outcome following a moderate controlled cortical impact in mice. The protective effect of curcumin was associated with a significant attenuation in the acute pericontusional expression of interleukin-1beta, a pro-inflammatory cytokine, after injury. Curcumin also reversed the induction of aquaporin-4, an astrocytic water channel implicated in the development of cellular edema following head trauma. Notably, curcumin blocked IL-1beta-induced aquaporin-4 expression in cultured astrocytes, an effect mediated, at least in part, by reduced activation of the p50 and p65 subunits of nuclear factor kappaB. Consistent with this notion, curcumin preferentially attenuated phosphorylated p65 immunoreactivity in pericontusional astrocytes and decreased the expression of glial fibrillary acidic protein, a reactive astrocyte marker. As a whole, these data suggest clinically achievable concentrations of curcumin reduce glial activation and cerebral edema following neurotrauma, a finding which warrants further investigation 7).


In a study Rats were exposed to a regular diet or a diet high in saturated fat, with or without 500 ppm curcumin for 4 weeks (n = 8/group), before a mild fluid percussion injury (FPI) was performed. The high-fat diet has been shown to exacerbate the effects of TBI on synaptic plasticity and cognitive function. Supplementation of curcumin in the diet dramatically reduced oxidative damage and normalized levels of BDNF, synapsin I, and CREB that had been altered after TBI. Furthermore, curcumin supplementation counteracted the cognitive impairment caused by TBI. These results are in agreement with previous evidence, showing that oxidative stress can affect the injured brain by acting through the BDNF system to affect synaptic plasticity and cognition. The fact that oxidative stress is an intrinsic component of the neurological sequel of TBI and other insults indicates that dietary antioxidant therapy is a realistic approach to promote protective mechanisms in the injured brain 8).

1)

Dong W, Yang B, Wang L, Li B, Guo X, Zhang M, Jiang Z, Fu J, Pi J, Guan D, Zhao R. Curcumin plays neuroprotective roles against traumatic brain injury partly via Nrf2 signaling. Toxicol Appl Pharmacol. 2018 May 1;346:28-36. doi: 10.1016/j.taap.2018.03.020. Epub 2018 Mar 21. PubMed PMID: 29571711.
2)

Wei G, Chen B, Lin Q, Li Y, Luo L, He H, Fu H. Tetrahydrocurcumin Provides Neuroprotection in Experimental Traumatic Brain Injury and the Nrf2 Signaling Pathway as a Potential Mechanism. Neuroimmunomodulation. 2018 Apr 18. doi: 10.1159/000487998. [Epub ahead of print] PubMed PMID: 29669346.
3)

Dai W, Wang H, Fang J, Zhu Y, Zhou J, Wang X, Zhou Y, Zhou M. Curcumin provides neuroprotection in models of traumatic brain injury via the Nrf2-ARE signaling pathway. Brain Res Bull. 2018 Apr 4. pii: S0361-9230(17)30417-3. doi: 10.1016/j.brainresbull.2018.03.020. [Epub ahead of print] PubMed PMID: 29626606.
4)

Huang T, Zhao J, Guo D, Pang H, Zhao Y, Song J. Curcumin mitigates axonal injury and neuronal cell apoptosis through the PERK/Nrf2 signaling pathway following diffuse axonal injury. Neuroreport. 2018 Mar 22. doi: 10.1097/WNR.0000000000001015. [Epub ahead of print] PubMed PMID: 29570500.
5)

Zhu HT, Bian C, Yuan JC, Chu WH, Xiang X, Chen F, Wang CS, Feng H, Lin JK. Curcumin attenuates acute inflammatory injury by inhibiting the TLR4/MyD88/NF-κB signaling pathway in experimental traumatic brain injury. J Neuroinflammation. 2014 Mar 27;11:59. doi: 10.1186/1742-2094-11-59. PubMed PMID: 24669820; PubMed Central PMCID: PMC3986937.
6)

Samini F, Samarghandian S, Borji A, Mohammadi G, bakaian M. Curcumin pretreatment attenuates brain lesion size and improves neurological function following traumatic brain injury in the rat. Pharmacol Biochem Behav. 2013 Sep;110:238-44. doi: 10.1016/j.pbb.2013.07.019. Epub 2013 Aug 7. PubMed PMID: 23932920.
7)

Laird MD, Sukumari-Ramesh S, Swift AE, Meiler SE, Vender JR, Dhandapani KM. Curcumin attenuates cerebral edema following traumatic brain injury in mice: a possible role for aquaporin-4? J Neurochem. 2010 May;113(3):637-48. doi: 10.1111/j.1471-4159.2010.06630.x. Epub 2010 Jan 20. PubMed PMID: 20132469; PubMed Central PMCID: PMC2911034.
8)

Wu A, Ying Z, Gomez-Pinilla F. Dietary curcumin counteracts the outcome of traumatic brain injury on oxidative stress, synaptic plasticity, and cognition. Exp Neurol. 2006 Feb;197(2):309-17. Epub 2005 Dec 20. PubMed PMID: 16364299

Neurotrauma and Critical Care of the Brain

Neurotrauma and Critical Care of the Brain

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“This book really is a complete primer on the head injured patient. Without a map such as the one this book metaphorically provides, the voyage to mastery can be hazardous for both practitioner and patient.”— Journal of the American Medical Association

Neurotrauma and Critical Care of the Brain, 2nd edition by renowned neurosurgeons Jack Jallo and Christopher Loftus incorporates salient components of the highly praised first edition. The updated text reflects cutting-edge discussion on traumatic brain injury management in a neurocritical care setting. Contributions from top experts in neurosurgery, neurology, critical care, cardiac and pulmonary care, and trauma surgery provide a concise review of a complex and evolving field.

The book lays a solid foundation with discussion of TBI classification, pathophysiology, key blood biomarkers, noninvasive neuromonitoring in severe TBI patients, multimodality monitoring in neurocritical care, and brain imaging modalities. From the prehospital setting to intensive care, top experts share clinical pearls and core guidelines on the management of mild, moderate, and severe TBI and complications. Chapters new to this edition include concomitant injuries, orbital/facial fractures, vascular injuries, spine fractures, autonomic dysfunction, and temperature management.

Key Highlights

  • Specialized topics include wartime penetrating injuries, cardiovascular complications of TBI, venous thromboembolism prophylaxis, ethical considerations, TBI costs in the U.S. and the financial return on helmets
  • Management of pediatric brain injuries in the NICU with illustrative cases
  • Nearly 200 high quality illustrations facilitate understanding of complex anatomy and techniques
  • Summary tables provide a handy overview of injury type, causes, characteristics, and recommended imaging modalities

This remarkable resource is essential reading for neurosurgeons, neurologists, trauma physicians, critical care and rehabilitation medicine specialists, and residents in these specialties. Paired with Neurotrauma and Critical Care of the Spine, 2nd edition, this dynamic duo is the most up-to-date neurocritical care reference available today.

Trends in Reconstructive Neurosurgery: Neurorehabilitation, Restoration and Reconstruction (Acta Neurochirurgica Supplement) 1st Edition

Trends in Reconstructive Neurosurgery: Neurorehabilitation, Restoration and Reconstruction (Acta Neurochirurgica Supplement) 1st Edition

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These proceeding cover new trends presented at the IV Congress of the International Society of Reconstructive Neurosurgery (ISRN), 2015. ISRN is an “open” multidisciplinary society that deals with advances in spine and peripheral-nerve reconstructive surgery, central nervous system revascularization (surgical, radio interventional), neuromodulation, bioengineering and transplantation, which are the latest tools used to promote reconstruction, restoration and rehabilitation.

Update: Posttraumatic epilepsy in children

Posttraumatic epilepsy in children

Posttraumatic epilepsy (PTE) after a traumatic brain injury occurs in 10%-20% of children.

Among children with moderate traumatic brain injury or severe traumatic brain injury, the presence of additional CT findings, other than skull fractures, seem to increase the risk of PTE. In the cohort of Keret et al, the occurrence of an early seizure did not confer an increased risk of PTE 1).

Mild traumatic brain injury (MTBI) was found to confer increased risk for the development of PTE and intractable PTE, of 4.5 and 8 times higher, respectively. As has been established in adults, these findings confirm that MTBI increases the risk for PTE in the pediatric population 2).

There is a a need for biomarkers in children following traumatic brain injury to reliably evaluate the risk of post-traumatic epilepsy 3).

Classification

Literature recognizes several posttraumatic seizure subtypes based on time of presentation and the underlying pathophysiology: impact, immediate, delayed early, and late/posttraumatic epilepsy. Appropriate classification of pediatric posttraumatic seizure subtypes can be helpful for appropriate management and prognosis.

A review of Arndt et al focused on early posttraumatic seizures, and the subtypes of early posttraumatic seizure. Incidence, risk factors, diagnosis, seizure semiology, status epilepticus, management, risk of recurrence, and prognosis were reviewed. The integration of continuous electroencephalographic (EEG) monitoring into pediatric traumatic brain injury management may hold the key to better characterizing and understanding pediatric early posttraumatic seizures 4).

Treatment

The aim of a rapid evidence review was to provide a synthesis of existing evidence on the effectiveness of treatment interventions for the prevention of PTE in people who have suffered a moderate/severe TBI to increase awareness and understanding among consumers. Electronic medical databases (n = 5) and gray literature published between January 2010 and April 2015 were searched for studies on the management of PTE. Twenty-two eligible studies were identified that met the inclusion criteria. No evidence was found for the effectiveness of any pharmacological treatments in the prevention or treatment of symptomatic seizures in adults with PTE. However, limited high-level evidence for the effectiveness of the antiepileptic drug levetiracetam was identified for PTE in children. Low-level evidence was identified for nonpharmacological interventions in significantly reducing seizures in patients with PTE, but only in a minority of cases, requiring further high-level studies to confirm the results 5).

Case series

2018

During a median follow-up period of 7.3 years, 9 (9%) of 95 children with moderate-to-severe TBI developed PTE; 4 developed intractable epilepsy. The odds for developing PTE was 2.9 in patients with severe compared to moderate TBI. CT findings showed fractures in 7/9 (78%) of patients with PTE, compared to 40/86 (47%) of those without PTE (p = 0.09). Of the patients with fractures, all those with PTE had additional features on CT (such as haemorrhage, contusion and mass effect), compared to 29/40 (73%) of those without PTE. One of nine (11%) PTE patients and 10 of 86 (12%) patients without PTE had immediate seizures. Two (22%) children with PTE had their first seizure more than 2 years after the TBI.

Among children with moderate or severe TBI, the presence of additional CT findings, other than skull fractures, seem to increase the risk of PTE. In this cohort, the occurrence of an early seizure did not confer an increased risk of PTE 6).

2017

Data were collected from electronic medical records of children 0-17 years of age, who were admitted to a single medical center between 2007 and 2009 with a diagnosis of MTBI. This prospective research consisted of a telephone survey between 2015 and 2016 of children or their caregivers, querying for information about epileptic episodes and current seizure and neurological status. The primary outcome measure was the incidence of epilepsy following TBI, which was defined as ≥ 2 unprovoked seizure episodes. Posttraumatic seizure (PTS) was defined as a single, nonrecurrent convulsive episode that occurred > 24 hours following injury. Seizures within 24 hours of the injury were defined as immediate PTS.

Of 290 children eligible for this study, 191 of them or their caregivers were reached by telephone survey and were included in the analysis. Most injuries (80.6%) were due to falls. Six children had immediate PTS. All children underwent CT imaging; of them, 72.8% demonstrated fractures and 10.5% did not demonstrate acute findings. The mean follow-up was 7.4 years. Seven children (3.7%) experienced PTS; of them, 6 (85.7%) developed epilepsy and 3 (42.9%) developed intractable epilepsy. The overall incidence of epilepsy and intractable epilepsy in this cohort was 3.1% and 1.6%, respectively. None of the children who had immediate PTS developed epilepsy. Children who developed epilepsy spent an average of 2 extra days in the hospital at the time of the injury. The mean time between trauma and onset of seizures was 3.1 years. Immediate PTS was not correlated with PTE.

In this analysis of data from medical records and long-term follow-up, MTBI was found to confer increased risk for the development of PTE and intractable PTE, of 4.5 and 8 times higher, respectively. As has been established in adults, these findings confirm that MTBI increases the risk for PTE in the pediatric population 7).

2015

Park et al. performed a retrospective electronic chart review of patients who had suffered traumatic brain injury and subsequently evaluated at Children’s Hospital of Michigan from 2002 to 2012. Various epidemiologic and clinical variables were analyzed.

Patients who had severe traumatic brain injury and post-traumatic epilepsy had an abnormal acute head computed tomography. These patients had increased number of different seizure types, increased risk of intractability of epilepsy, and were on multiple antiepileptic drugs. Hypomotor seizure was the most common seizure type in these patients. There was a high prevalence of patients who suffered nonaccidental trauma, all of whom had severe traumatic brain injury.

This study demonstrates a need for biomarkers in children following traumatic brain injury to reliably evaluate the risk of post-traumatic epilepsy 8).

2013

Children ages 6-17 years with one or more risk factors for the development of posttraumatic epilepsy, including presence of intracranial hemorrhage, depressed skull fracture, penetrating injury, or occurrence of posttraumatic seizure were recruited into a phase II study. Treatment subjects received levetiracetam 55 mg/kg/day, b.i.d., for 30 days, starting within 8 h postinjury. The recruitment goal was 20 treated patients. Twenty patients who presented within 8-24 h post-TBI and otherwise met eligibility criteria were recruited for observation. Follow-up was for 2 years. Forty-five patients screened within 8 h of head injury met eligibility criteria and 20 were recruited into the treatment arm. The most common risk factor present for pediatric inclusion following TBI was an immediate seizure. Medication compliance was 95%. No patients died; 19 of 20 treatment patients were retained and one observation patient was lost to follow-up. The most common severe adverse events in treatment subjects were headache, fatigue, drowsiness, and irritability. There was no higher incidence of infection, mood changes, or behavior problems among treatment subjects compared to observation subjects. Only 1 (2.5%) of 40 subjects developed posttraumatic epilepsy (defined as seizures >7 days after trauma). This study demonstrates the feasibility of a pediatric posttraumatic epilepsy prevention study in an at-risk traumatic brain injury population. Levetiracetam was safe and well tolerated in this population. This study sets the stage for implementation of a prospective study to prevent posttraumatic epilepsy in an at-risk population 9).

1) , 6)

Keret A, Shweiki M, Bennett-Back O, Abed-Fteiha F, Matoth I, Shoshan Y, Benifla M. The clinical characteristics of posttraumatic epilepsy following moderate-to-severe traumatic brain injury in children. Seizure. 2018 Mar 20;58:29-34. doi: 10.1016/j.seizure.2018.03.018. [Epub ahead of print] PubMed PMID: 29609147.
2) , 7)

Keret A, Bennett-Back O, Rosenthal G, Gilboa T, Shweiki M, Shoshan Y, Benifla M. Posttraumatic epilepsy: long-term follow-up of children with mild traumatic brain injury. J Neurosurg Pediatr. 2017 Jul;20(1):64-70. doi: 10.3171/2017.2.PEDS16585. Epub 2017 May 5. PubMed PMID: 28474982.
3) , 8)

Park JT, Chugani HT. Post-traumatic epilepsy in children-experience from a tertiary referral center. Pediatr Neurol. 2015 Feb;52(2):174-81. doi: 10.1016/j.pediatrneurol.2014.09.013. Epub 2014 Oct 12. PubMed PMID: 25693582.
4)

Arndt DH, Goodkin HP, Giza CC. Early Posttraumatic Seizures in the Pediatric Population. J Child Neurol. 2016 Jan;31(1):46-56. doi: 10.1177/0883073814562249. Epub 2015 Jan 6. Review. PubMed PMID: 25564481.
5)

Piccenna L, Shears G, O’Brien TJ. Management of post-traumatic epilepsy: An evidence review over the last 5 years and future directions. Epilepsia Open. 2017 Mar 17;2(2):123-144. doi: 10.1002/epi4.12049. eCollection 2017 Jun. PubMed PMID: 29588942; PubMed Central PMCID: PMC5719843.
9)

Pearl PL, McCarter R, McGavin CL, Yu Y, Sandoval F, Trzcinski S, Atabaki SM, Tsuchida T, van den Anker J, He J, Klein P. Results of phase II levetiracetam trial following acute head injury in children at risk for posttraumatic epilepsy. Epilepsia. 2013 Sep;54(9):e135-7. doi: 10.1111/epi.12326. Epub 2013 Jul 22. PubMed PMID: 23876024; PubMed Central PMCID: PMC3769484.

Intracranial Pressure & Neuromonitoring XVI (Acta Neurochirurgica Supplement) 1st ed. 2018 Edition

Intracranial Pressure & Neuromonitoring XVI (Acta Neurochirurgica Supplement) 1st ed. 2018 Edition

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This book introduces the latest advances relating to the pathophysiology, biophysics, monitoring and treatment of traumatic brain injury, hydrocephalus, and stroke presented at the 16th International Conference on Intracranial Pressure and Neuromonitoring (the “ICP Conference”), held in Cambridge, Massachusetts, in June 2016 in conjunction with the 6th Annual Meeting of the Cerebral Autoregulation Research Network. Additionally, the conference held special sessions on neurocritical care informatics and cerebrovascular autoregulation. The peer-reviewed papers included were written by leading experts in neurosurgery, neurointensive care, anesthesiology, physiology, clinical engineering, clinical informatics and mathematics who have made important contributions in this translational area of research, and their focus ranges from the latest research findings and developments to clinical trials and experimental studies. The book continues the proud tradition of publishing key work from the ICP Conferences and is a must-read for anyone wishing to stay abreast of recent advances in the field.

Neurocritical Care, An Issue of Neurosurgery Clinics of North America, 1e (The Clinics: Surgery)

Neurocritical Care, An Issue of Neurosurgery Clinics of North America, 1e (The Clinics: Surgery)

by Alejandro A. Rabinstein MD FAAN

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This issue of Neurosurgery Clinics, edited by Alejandro A. Rabinstein, will focus on Neurocritical Care. Topics will include Anoxic-Ischemic Brain Injury, Practical Approach to Posttraumatic Intracranial Hypertension According to Pathophysiologic Reasoning, Management of Traumatic Brain Injury: An Update, Cortical Spreading Depression and Ischemia in Neurocritical Patients, Targeted Temperature Management in Brain-Injured Patients, Herpes Virus Encephalitis in Adults: Current Knowledge and Old Myths, Primary Acute Neuromuscular Respiratory Failure, Intensive Care Unit–Acquired Weakness, Recent Advances in the Acute Management of Intracerebral Hemorrhage, New Developments in Refractory Status Epilepticus, Acute Cardiac Complications in Critical Brain Disease, Nosocomial Infections in the Neurointensive Care Unit, Neurologic Complications of Solid Organ Transplantation, and Shared Decision Making in Neurocritical Care.