Category Archives: Neurotrauma

Update: Chronic subdural hematoma recurrence

Chronic subdural hematoma recurrence

Epidemiology

Recurrence rates after chronic subdural hematoma (CSDH) evacuation with any of actual techniques twist drill craniostomy (TDC), burr hole craniostomy, craniotomy range from 5% to 30%. 1)

Risk factors

Chon et al. shown that postoperative midline shifting (≥5 mm), diabetes mellitus, preoperative seizure, preoperative width of hematoma (≥20 mm), and anticoagulant therapy were independent predictors of the recurrence of chronic subdural hematoma. According to internal architecture of hematoma, the rate of recurrence was significantly lower in the homogeneous and the trabecular type than the laminar and separated type 2).

The recurrence rate of chronic subdural hematoma cSDH seems to be related to the excessive neoangiogenesis in the parietal membrane, which is mediated via vascular endothelial growth factor (VEGF). This is found to be elevated in the hematoma fluid and is dependent on eicosanoid/prostaglandin and thromboxane synthesis via cyclooxygenase-2 (COX-2).


Antiplatelet therapy

Antiplatelet therapy significantly influences the recurrence of CSDH 3).

Pneumocephalus

Remaining pneumocephalus is seen as an approved factor of recurrence 4) 5).

Septation

Jack et al.found a 12% reoperation rate. CSDH septation (seen on computed tomogram scan) was found to be an independent risk factor for recurrence requiring reoperation (p=0.04). Larger post-operative subdural haematoma volume was also significantly associated with requiring a second drainage procedure (p<0.001). Independent risk factors of larger post-operative haematoma volume included septations within a CSDH (p<0.01), increased pre-operative haematoma volume (p<0.01), and a greater amount of parenchymal atrophy (p=0.04). A simple scoring system for quantifying recurrence risk was created and validated based on patient age (< or ≥80 years), haematoma volume (< or ≥160cc), and presence of septations within the subdural collection (yes or no).

Septations within CSDHs are associated with larger post-operative residual haematoma collections requiring repeat drainage. When septations are clearly visible within a CSDH, craniotomy might be more suitable as a primary procedure as it allows greater access to a septated subdural collection. The proposed scoring system combining haematoma volume, age, and presence of septations might be useful in identifying patients at higher risk for recurrence 6).

Membranectomy

Opening the internal hematoma membrane does not alter the rate of patients requiring revision surgery and the number of patients showing a marked residual hematoma six weeks after evacuation of a CSDH 7).

In the study of Lee et al, an extended surgical approach with partial membranectomy has no advantages regarding the rate of reoperation and the outcome. As initial treatment, burr-hole drainage with irrigation of the hematoma cavity and closed-system drainage is recommended. Extended craniotomy with membranectomy is now reserved for instances of acute rebleeding with solid hematoma 8).

Diabetes

Surgeons should consider informing patients with diabetes mellitus that this comorbidity is associated with an increased likelihood of recurrence

9) 10) 11).


Balser et al. report 11% recurrence, which included individuals who recurred as late as 3 years after initial diagnosis 12).

Close imaging follow-up is important for CSDH patients for recurrence prediction. Using quantitative CT volumetric analysis, strong evidence was provided that changes in the residual fluid volume during the ‘self-resolution’ period can be used as significantly radiological predictors of recurrence 13).

A structural equation model showed a significant association between increased antiinflammatory activity in hematoma fluid samples and a lower risk of recurrence, but this relationship was not statistically significant in venous blood samples. Moreover, these findings indicate that anti-inflammatory activities in the hematoma may play a role in the risk of a recurrence of CSDH 14).

Irrigation with artificial cerebrospinal fluid (ACF) decreased the rate of CSDH recurrence 15).

Treatment

There is no definite operative procedure for patients with intractable chronic subdural hematoma (CSDH).

Most recurrent hematomas are managed successfully with burr hole craniostomies with postoperative closed-system drainage. Refractory hematomas may be managed with a variety of techniques, including craniotomy or subdural-peritoneal shunt placement 16).

Although many studies have reported risk factors or treatments in efforts to prevent recurrence, those have focused on single recurrence, and little cumulative data is available to analyze refractory CSDH.

Matsumoto et al. defined refractory CSDH as ≥2 recurrences, then analyzed and compared clinical factors between patients with single recurrence and those with refractory CSDH in a cohort study, to clarify whether patients with refractory CSDH experience different or more risk factors than patients with single recurrence, and whether burr-hole irrigation with closed-system drainage reduces refractory CSDH.

Seventy-five patients had at least one recurrence, with single recurrence in 62 patients and ≥2 recurrences in 13 patients. In comparing clinical characteristics, patients with refractory CSDH were significantly younger (P=0.04) and showed shorter interval to first recurrence (P<0.001). Organized CSDH was also significantly associated with refractory CSDH (P=0.02). Multivariate logistic regression analysis identified first recurrence interval <1 month (OR 6.66, P<0.001) and age <71 years (OR 4.16, P<0.001) as independent risk factors for refractory CSDH. On the other hand, burr-hole irrigation with closed-system drainage did not reduce refractory CSDH.

When patients with risk factors for refractory CSDH experience recurrence, alternative surgical procedures may be considered as the second surgery, because burr-hole irrigation with closed-system drainage did not reduce refractory CSDH 17).

Implantation of a reservoir 18) 19) 20).

Subdural-peritoneal shunt 21).

Middle meningeal artery embolization

Embolization of the MMA is effective for refractory CSDH or CSDH patients with a risk of recurrence, and is considered an effective therapeutic method to stop hematoma enlargement and promote resolution 22) 23) 24) 25) 26) 27).

A pilot study indicated that perioperative middle meningeal artery (MMA) embolization could be offered as the least invasive and most effectual means of treatment for resistant patients of CSDHs with 1 or more recurrences 28).

Chihara et al. have treated three cases of CSDH with MMA embolization to date, but there was a postoperative recurrence in one patient, which required a craniotomy for hematoma removal and capsulectomy. MMA embolization blocks the blood supply from the dura to the hematoma outer membrane in order to prevent recurrences of refractory CSDH. Histopathologic examination of the outer membrane of the hematoma excised during craniotomy showed foreign-body giant cells and neovascular proliferation associated with embolization. Because part of the hematoma was organized in this case, the CSDH did not resolve when the MMA was occluded, and the development of new collateral pathways in the hematoma outer membrane probably contributed to the recurrence. Therefore, in CSDH with some organized hematoma, MMA embolization may not be effective. Magnetic resonance imaging (MRI) should be performed in these patients before embolization 29).

Case series

2016

Chronic subdural hematomas (cSDHs) have shown an increasing incidence in an ageing population over the last 20 years, while unacceptable recurrence rates of up to 30 % persist. The chronic subdural hematoma recurrence rate seems to be related to the excessive neoangiogenesis in the parietal membrane, which is mediated via vascular endothelial growth factor (VEGF). This is found to be elevated in the haematoma fluid and is dependent on eicosanoid/prostaglandin and thromboxane synthesis via cyclooxygenase-2 (COX 2). With this investigator-initiated trial (IIT) it was thought to diminish the recurrence rate of operated-on cSDHs by administering a selective COX-2 inhibitor (Celecoxib) over 4 weeks’ time postoperatively in comparison to a control group.

The thesis of risk reduction of cSDH recurrence in COX-2-inhibited patients was to be determined in a prospective, randomised, two-armed, open phase-II/III study with inclusion of 180 patients over a 2-year time period in four German university hospitals. The treated- and untreated-patient data were to be analysed by Fisher’s exact test (significance level of alpha, 0.05 [two-sided]).

After screening of 246 patients from January 2009 to April 2010, the study had to be terminated prematurely as only 23 patients (9.3 %) could be enrolled because of on-going non-steroid anti-rheumatic (NSAR) drug treatment or contraindication to Celecoxib medication. In the study population, 13 patients were treated in the control group (six women, seven men; average age 66.8 years; one adverse event (AE)/serious adverse event (SAE) needing one re-operation because of progressive cSDH (7.7 %); ten patients were treated in the treatment group (one woman, nine men; average age 64.7 years; five AEs/SAEs needing two re-operations because of one progressive cSDH and one wound infection [20 %]). Significance levels are obsolete because of insufficient patient numbers.

The theoretical advantage of COX-2 inhibition in the recurrent cSDH could not be transferred into the treatment of German cSDH patients as 66.6 % of the patients showed strict contraindications for Celecoxib. Furthermore, 55 % of the patients were already treated with some kind of COX-2 inhibition and, nevertheless, developed cSDH. Thus, although conceptually appealing, an anti-angiogenic therapy with COX-2 inhibitors for cSDH could not be realised in this patient population due to the high prevalence of comorbidities excluding the administration of COX2 inhibitors 30).

2010

Recurrence rates after chronic subdural hematoma (CSDH) evacuation with any of actual techniques twist drill craniostomy (TDC), burr holecraniostomy, craniotomy range from 5% to 30%. Use of drain has improved recurrence rates when used with burr-hole craniostomy. Now, we analyze predictors of recurrence of TDC with drain.

Three hundred twelve consecutive patients with CSDH have been studied in a retrospective study. Operative technique in all patients consisted in TDC with drain. Data recorded included any associated comorbidity. Radiologic measures of the CSDH before and after the procedure were studied. Clinical evaluation included Modified Rankin Scale, Glasgow Coma Scale (GCS), and neurological deficits. Two groups were compared: recurrence group and nonrecurrence group. Follow-up was for at least 1 year.

Twelve percent experienced recurrence. Preoperative CSDH width, preoperative midline shift, postoperative midline width, postoperative CSDH width, and residual CSDH 1 month later were significantly associated with CSDH recurrence. The logistic regression model for the multivariate analysis revealed that postoperative midline shift and postoperative neurological deficit were significantly associated with CSDH recurrence. The duration of treatment with dexamethasone was found not to be related with recurrence. Mortality before hospital discharge was 1%. Hospital stay was 2.5 days.

TDC with drain has similar results in recurrence rates, morbidity, mortality, and outcome as other techniques as burr-hole craniostomy with drain. Preoperative and postoperative hematoma width and midline shift are independent predictors of recurrence. Brain re-expansion and time of drain maintenance are important factors related with recurrence of CSDH. Future CSDH reservoirs must avoid negative pressure and sudden pressure changes inside the whole closed drain system 31).

Case reports

2016

Mewada et al. report a case with right hemiparesis and aphasia 1 month after a fall from a bicycle. Computed tomography scan of the head showed left chronic subdural hematoma, which was evacuated by burr-hole drainage. The postoperative course was complicated by reaccumulation within short period of time. On superselective digital subtraction angiography of MMA, iatrogenic dAVF was found on left side. We embolized successfully it using n-butyl cyanoacrylate after a third irrigation. No reaccumulation found in the postoperative period or at last follow-up. They proposed a treatment protocol based on the own experience and literature review.

Refractory chronic subdural hematoma with reaccumulation within a short interval should be subjected to digital subtraction angiography of the MMA. Embolization of ipsilateral MMA is safe, effective, and a useful option for the treatment of iatrogenic dAVF and resolution of hematoma 32).


An 85-year-old male presented with left CSDH, which recurred five times. The hematoma was irrigated and drained through a left frontal burr hole during the first to third surgery and through a left parietal burr hole during the fourth and fifth surgery. The hematoma had no septation and was well-evacuated during each surgery. Antiplatelet therapy for preventing ischemic heart disease was stopped after the second surgery, the hematoma cavity was irrigated with artificial cerebrospinal fluid at the third surgery, and the direction of the drainage tube was changed to reduce the postoperative subdural air collection at the fourth surgery. However, none of these interventions was effective. He was successfully treated by fibrin glue injection into the hematoma cavity after the fifth surgery.

This procedure may be effective for refractory CSDH in elderly patients 33).


A 67-year-old man with dural arteriovenous fistula (AVF) presenting as a non-traumatic chronic subdural hematoma (CSDH). This previously healthy patient was hospitalized due to progressive headache with subacute onset. He underwent burr-hole surgery twice for evacuating the left CSDH that was thickest at the posterior temporal area. The operative procedure and finding was not extraordinary, but subdural hematoma slowly progressed for days following the revision surgery. After investigation by super-selective external carotid angiography, a dural AVF found near the transverse-sigmoid sinus was diagnosed. Dural AVF was completely occluded with trans-arterial injecting polyvinyl alchol particles into the petrosquamosal branch of the middle meningeal artery. The patient showed a good neurological outcome with no additional intervention. Brain surgeons have to consider the possibility of dural AVF and perform cerebral angiogram if necessary when they manage the cases that have a spontaneously occurred and repeatedly recurring CSDH 34).

2007

Spontaneous intracranial hypotension (SIH) is reported to cause chronic subdural hematoma (SDH), however diagnosis of SIH in patients with SDH is not always easy.

Takahashi et al. report a case of chronic SDH refractory to repeated drainage, which was attributed to SIH. A forty-five-year-old man who had been suffering from orthostatic headache for one month was admitted to our hospital presenting with unconsciousness and hemiparesis. CT on admission revealed a chronic subdural hematoma, which was successfully treated once with subdural drainage. However, the patient fell into unconscious again with recurrence of the hematoma within several days. After two more sessions of drainage, SIH due to cerebrospinal fluid leakage was diagnosed with spinal magnetic resonance imaging (MRI) and radionuclide cisternography. Spinal MRI demonstrated abnormal fluid accumulation in the thoracic epidural space, and the radionuclide cisternogram showed early excretion of tracer into urine as well as absence of intracranial tracer filling. After treatment with epidural blood patching, the hematoma rapidly disappeared and he was discharged without symptoms. In the treatment of chronic SDH, especially in young to middle aged patient without preceding trauma or hematological disorders, physicians should pay attention to underlying SIH to avoid multiple surgery. MRI of the spine as well as radionuclide cisternography is useful in evaluation of this condition 35).

1) , 31)

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Pang CH, Lee SE, Kim CH, Kim JE, Kang HS, Park CK, Paek SH, Kim CH, Jahng TA, Kim JW, Kim YH, Kim DG, Chung CK, Jung HW, Yoo H. Acute intracranial bleeding and recurrence after bur hole craniostomy for chronic subdural hematoma. J Neurosurg. 2015 Jul;123(1):65-74. doi: 10.3171/2014.12.JNS141189. Epub 2015 Feb 13. PubMed PMID: 25679282.

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Balser D, Rodgers SD, Johnson B, Shi C, Tabak E, Samadani U. Evolving management of symptomatic chronic subdural hematoma: experience of a single institution and review of the literature. Neurol Res. 2013 Apr;35(3):233-42. doi: 10.1179/1743132813Y.0000000166. Review. PubMed PMID: 23485050.

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Xu FF, Chen JH, Leung GK, Hao SY, Xu L, Hou ZG, Mao X, Shi GZ, Li JS, Liu BY. Quantitative computer tomography analysis of post-operative subdural fluid volume predicts recurrence of chronic subdural haematoma. Brain Inj. 2014;28(8):1121-6. doi: 10.3109/02699052.2014.910702. Epub 2014 May 6. PubMed PMID: 24801643.

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Pripp AH, Stanišić M. The Correlation between Pro- and Anti-Inflammatory Cytokines in Chronic Subdural Hematoma Patients Assessed with Factor Analysis. PLoS One. 2014 Feb 27;9(2):e90149. doi: 10.1371/journal.pone.0090149. eCollection 2014. PubMed PMID: 24587250.

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Adachi A, Higuchi Y, Fujikawa A, Machida T, Sueyoshi S, Harigaya K, Ono J, Saeki N. Risk factors in chronic subdural hematoma: comparison of irrigation with artificial cerebrospinal fluid and normal saline in a cohort analysis. PLoS One. 2014 Aug 4;9(8):e103703. doi: 10.1371/journal.pone.0103703. eCollection 2014. PubMed PMID: 25089621; PubMed Central PMCID: PMC4121178.

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Desai VR, Scranton RA, Britz GW. Management of Recurrent Subdural Hematomas. Neurosurg Clin N Am. 2017 Apr;28(2):279-286. doi: 10.1016/j.nec.2016.11.010. Epub 2017 Jan 4. Review. PubMed PMID: 28325462.

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Matsumoto H, Hanayama H, Okada T, Sakurai Y, Minami H, Masuda A, Tominaga S, Miyaji K, Yamaura I, Yoshida Y, Yoshida K. Clinical investigation of refractory chronic subdural hematoma: a comparison of clinical factors between single and repeated recurrences. World Neurosurg. 2017 Aug 24. pii: S1878-8750(17)31402-X. doi: 10.1016/j.wneu.2017.08.101. [Epub ahead of print] PubMed PMID: 28844917.

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Sato M, Iwatsuki K, Akiyama C, Masana Y, Yoshimine T, Hayakawa T. [Use of Ommaya CSF reservoir for refractory chronic subdural hematoma]. No Shinkei Geka. 1999 Apr;27(4):323-8. Japanese. PubMed PMID: 10347846.

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Laumer R. Implantation of a reservoir for refractory chronic subdural hematoma. Neurosurgery. 2002 Mar;50(3):672. PubMed PMID: 11841742.

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Misra M, Salazar JL, Bloom DM. Subdural-peritoneal shunt: treatment for bilateral chronic subdural hematoma. Surg Neurol. 1996 Oct;46(4):378-83. PubMed PMID: 8876720.

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Mandai S, Sakurai M, Matsumoto Y. Middle meningeal artery embolization for refractory chronic subdural hematoma. Case report. J Neurosurg. 2000 Oct;93(4):686-8. PubMed PMID: 11014549.

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Mino M, Nishimura S, Hori E, Kohama M, Yonezawa S, Midorikawa H, Kaimori M, Tanaka T, Nishijima M. Efficacy of middle meningeal artery embolization in the treatment of refractory chronic subdural hematoma. Surg Neurol Int. 2010 Dec 13;1:78. doi: 10.4103/2152-7806.73801. PubMed PMID: 21206540; PubMed Central PMCID: PMC3011107.

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Neurocritical Care for the Advanced Practice Clinician

Neurocritical Care for the Advanced Practice Clinician

Neurocritical Care for the Advanced Practice Clinician

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  • Published on: 2017-08-21
  • Original language: English
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From the Back Cover

By utilizing a review of case-based studies and providing concise management recommendations from leaders in the field, this book provides essential knowledge for those practicing in a dynamic specialty. In the rapidly developing field of Neurocritical Care, Advanced Practice Clinicians have become an integral component of the multi-disciplinary team. This essential volume provides a frame of reference for advanced practice nurses, physician assistants, physicians, and students on a wide range of common Neuro ICU diagnoses and management strategies.

About the Author

Jessica White is a physician assistant in the Neuroscience ICU at Yale New Haven Hospital.  She has served as part-time faculty at Yale University and Quinnipiac University physician assistant programs, teaching topics of neurology and neurocritical care. Her research interests include family satisfaction and the role of the physician assistant in the multi-disciplinary team. Her training was completed at Midwestern University with a Master of Medical Science from the Physician Assistant program.

 

Dr. Sheth graduated from Johns Hopkins University and the University of Pennsylvania School of Medicine. He was recruited to Yale as the founding chief of the Division of Neurocritical Care and Emergency Neurology and Chief of Clinical Research. His interests are in the advancement of therapies and care of patients with devastating acute neurological syndromes. He is a recognized clinical, a translational scientist, has directed multicenter studies testing potential therapies against brain swelling, stroke, and hemorrhage. He is the winner of the Robert Siekert Award from the American Heart Association, and his research has been funded by the NIH, American Academy of Neurology, American Heart Association(AHA). He has written over 100 publications in critical care neurology and stroke. His collaborative work is dedicated to the improved understanding of neurological disease in the critically ill.

 

Update: Decompressive craniectomy for traumatic brain injury

Decompressive craniectomy for traumatic brain injury

Intracranial hypertension is the largest cause of death in young patients with severe traumatic brain injury 1).

The management of traumatic brain injury progressed significantly in the 1980s and 1990s due to advances in neuroimaging (widespread introduction of CT scanning), prehospital management, neurointensive care (widespread adoption of ICP monitoring and tiered therapeutic protocols) and rehabilitation. This led to a renaissance of interest in decompressive craniectomy (DC) with many uncontrolled studies reporting a survival benefit with DC 2) 3).

Since that time, DC has been increasingly studied in the setting of different conditions, including subarachnoid hemorrhage, and malignant middle cerebral artery infarction.

Furthermore, dural opening, usually followed by insertion of a dural graft (duraplasty), has meanwhile become an integral part of the decompressive surgery technique 4).

The 21st century, so far, has seen consistent efforts to improve the evidence base for DC following TBI with the conduct of randomized clinical trials5).

In severely head injured children, a study has shown that decompressive craniectomy resulted in good recovery in all children in the study, suggesting the procedure has an advantage over non-surgical treatment in children.

In one of the largest studies on pediatric patients, Jagannathan et al. found a net 65% favorable outcomes rate in pediatric patients for accidental trauma after craniectomy when followed for more than five years. Only three patients were dependent on caregivers.

This is the only prospective randomised controlled study to date to support the potential benefit of decompressive craniectomy following traumatic brain injury.

Outcome

Early decompressive craniectomy (DC) has been used as the first stage treatment to prevent secondary injuries in cases of severe traumatic brain injury (TBI). Postoperative management is the major factor that influences outcome.

Intracranial pressure monitoring in conjunction with postoperative treatment, after early DC, is associated with a significantly reduced risk of death6).

Patients surviving from DC need a second operation to repair the bone defect.

In the 2010s the use of decompressive craniectomy (DC) in everyday neurosurgical practice has largely increased, even though the effectiveness of this procedure is still uncertain 7).

Complications

The conversion of the cranium from a “closed box” to an “open box” alters the barometric pressure, cerebrospinal fluid (CSF), and cerebral blood flow (CBF) and may or may not lead to syndrome of the trephined (sinking skin flap syndrome) 8).

Trials

The claim that decompressive craniectomy increases unfavourable outcome is overstated and not supported by the data presented in DECRA trial.

Sahuquillo et al. believe it premature to change clinical practice. Given the dismal outcome in these patients, it is reasonable to include this technique as a last resort in any type of protocol-driven management when conventional therapeutic measures have failed to control ICP, the presence of operable masses has been ruled out and the patient may still have a chance of a functional outcome. The main lesson to be learned from this study is that an upper threshold for ICP must be used as a cut-off for selecting decompressive craniectomy candidates 9).

see RescueICP Study.

Systematic review and meta-analysis

Although many studies have been conducted in this topic, there is still much uncertainty about the effectiveness of surgical treatment in TBI 10).

Zhang et al. aimed to perform a systematic review and metaanalysis to examine the prognostic value of decompressive craniectomy (DC) in patients with traumatic intracranial hypertension. PubMed, EMBASE, Cochrane Controlled Trials Register, Web of Science, http://clinicaltrials.gov/ were searched for eligible studies. Ten studies were included in the systematic review, with four randomized controlled trials involved in the meta-analysis, where compared with medical therapies, DC could significantly reduce mortality rate [risk ratio (RR), 0.59; 95% confidence interval (CI), 0.47-0.74, P < 0.001], lower intracranial pressure (ICP) [mean difference (MD), -2.12 mmHg; 95% CI, -2.81 to -1.43, P < 0.001], decrease the length of ICU stay (MD, -4.63 days; 95% CI, -6.62 to -2.65, P < 0.001) and hospital stay (MD, -14.39 days; 95% CI, -26.00 to -2.78, P = 0.02), but increase complications rate (RR, 1.94; 95% CI, 1.31-2.87, P < 0.001). No significant difference was detected for Glasgow Outcome Scale at six months (RR, 0.85; 95% CI, 0.61-1.18, P = 0.33), while in subgroup analysis, early DC would possibly result in improved prognosis (P = 0.04). Results from observational studies supported pooled results except prolonged length of ICU and hospital stay. Conclusively, DC seemed to effectively lower ICP, reduce mortality rate but increase complications rate, while its benefit on functional outcomes was not statistically significant 11).

Case series

2016

31 patients aged 16-72 of either sex who sustained a severe, non-penetrating TBI and underwent a unilateral DC for evacuation of parenchymal or extra-axial hematoma or for failure of medical therapy to control intracranial pressure (ICP).

Review of the electronic medical record of patients undergoing DC for severe TBI and assessment of extended Glasgow Outcome Score (e-GOS) at 6-months following DC.

The mean age was 39.3y ± 14.5. The initial GCS was 5.8 ± 3.2, and the ISS was 29.7 ± 6.3. Twenty-two patients underwent DC within the first 24 h, two within the next 24 h and seven between the 3rd and 7th day post injury. The pre-DC ICP was 30.7 ± 10.3 and the ICP was 12.1 ± 6.2 post-DC. Cranioplasty was performed in all surviving patients 1-4 months post-DC. Of the 29 survivors following DC, the e-GOS was 8 in seven patients, and 7 in ten patients. The e-GOS was 5-6 in 6 others. Of the 6 survivors with poor outcomes (e-GOS = 2-4), five were the initial patients in the series.

In patients with intractable cerebral hypertension following TBI, unilateral DC in concert with practice guideline directed brain resuscitation is associated with good functional outcome and acceptable-mortality 12).

2009

A case control study comparing a group of patients (n: 16) operated for severe TBI between January 2002 and July 2004 according to an institutional management protocol characterized by an early decompressive craniectomy (DC) approach versus a historical control group (n: 20) managed before the implementation of such protocol. Mortality and Glasgow Outcome Score (GOS) at 6 months were used as the main outcome variables.

An early DC protocol implemented within 12 hours from injury in 16 patients with severe isolated TBI and a Marshall score between III or IV was associated with a lesser mortality than the conventional approach with ventriculostomy and Intensive Care Unit (ICU) management alone. The GOS was significantly better in the DC group (p=0.0002) than in the control group.

The use of an early DC protocol for severe TBI patients (Glasgow Coma Scale <9) had a significantly improved outcome compared with the conventional approach with ventriculostomy and ICU management in Simòn Bolivar Hospital in Bogotá, Colombia 13).

1)

Alvis-Miranda H, Castellar-Leones SM, Moscote-Salazar LR. Decompressive Craniectomy and Traumatic Brain Injury: A Review. Bull Emerg Trauma. 2013 Apr;1(2):60-8. Review. PubMed PMID: 27162826; PubMed Central PMCID: PMC4771225.
2)

Polin RS, Shaffrey ME, Bogaev CA. et al.Decompressive bifrontal craniectomy in the treatment of severe refractory posttraumatic cerebral edema. Neurosurgery 19974184–92.92
3)

Whitfield PC, Patel H, Hutchinson PJ. et al.Bifrontal decompressive craniectomy in the management of posttraumatic intracranial hypertension. Br J Neurosurg 200115500–7.7
4)

Hutchinson P, Timofeev I, Kirkpatrick P. Surgery for brain edema. Neurosurg Focus.2007;22:E14
5)

Kolias AG, Adams H, Timofeev I, Czosnyka M, Corteen EA, Pickard JD, Turner C, Gregson BA, Kirkpatrick PJ, Murray GD, Menon DK, Hutchinson PJ. Decompressive craniectomy following traumatic brain injury: developing the evidence base. Br J Neurosurg. 2016 Apr;30(2):246-50. doi: 10.3109/02688697.2016.1159655. Epub 2016 Mar 14. PubMed PMID: 26972805; PubMed Central PMCID: PMC4841020.
6)

Kim DR, Yang SH, Sung JH, Lee SW, Son BC. Significance of intracranial pressure monitoring after early decompressive craniectomy in patients with severe traumatic brain injury. J Korean Neurosurg Soc. 2014 Jan;55(1):26-31. doi:10.3340/jkns.2014.55.1.26. Epub 2014 Jan 31. PubMed PMID: 24570814.
7)

Aarabi B, Hesdoffer DC, Ahn ES, Aresco C, Scalea TM, Eisenbergh HM: Outcome following decompres- sive craniectomy for malignant swelling due to se- vere head injury. J Neurosurg 104: 469–479, 2006
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Gadde J, Dross P, Spina M. Syndrome of the trephined (sinking skin flap syndrome) with and without paradoxical herniation: a series of case reports and review. Del Med J. 2012 Jul;84(7):213-8. PubMed PMID: 23252092.
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Sahuquillo J, Martínez-Ricarte F, Poca MA. Decompressive craniectomy in traumatic brain injury after the DECRA trial. Where do we stand? Curr Opin Crit Care. 2013 Apr;19(2):101-6. doi: 10.1097/MCC.0b013e32835eba1a. Review. PubMed PMID: 23422159.
10)

Moon JW, Hyun DK. Decompressive Craniectomy in Traumatic Brain Injury: A Review Article. Korean J Neurotrauma. 2017 Apr;13(1):1-8. doi: 10.13004/kjnt.2017.13.1.1. Epub 2017 Apr 30. Review. PubMed PMID: 28512611; PubMed Central PMCID: PMC5432443.
11)

Zhang D, Xue Q, Chen J, Dong Y, Hou L, Jiang Y, Wang J. Decompressive craniectomy in the management of intracranial hypertension after traumatic brain injury: a systematic review and meta-analysis. Sci Rep. 2017 Aug 18;7(1):8800. doi: 10.1038/s41598-017-08959-y. PubMed PMID: 28821777.
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Grindlinger GA, Skavdahl DH, Ecker RD, Sanborn MR. Decompressive craniectomy for severe traumatic brain injury: clinical study, literature review and meta-analysis. Springerplus. 2016 Sep 20;5(1):1605. doi: 10.1186/s40064-016-3251-9. eCollection 2016. PubMed PMID: 27652178; PubMed Central PMCID: PMC5028365.
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Rubiano AM, Villarreal W, Hakim EJ, Aristizabal J, Hakim F, Dìez JC, Peña G, Puyana JC. Early decompressive craniectomy for neurotrauma: an institutional experience. Ulus Travma Acil Cerrahi Derg. 2009 Jan;15(1):28-38. PubMed PMID: 19130336; PubMed Central PMCID: PMC3413286.

Update: Chronic traumatic encephalopathy in American football players

There is tremendous media attention regarding chronic traumatic encephalopathy (CTE), primarily because of the deaths of high profile American football players who were found to have CTE upon neuropathology 1).

Physicians in clinical practice are likely to face an increasing number of retired football players seeking evaluation for chronic neurobehavioral symptoms. Guidelines for the evaluation and treatment of these patients are sparse. Clinical criteria for a diagnosis of CTE are under development. The contribution of CTE vs other neuropathologies to neurobehavioral symptoms in these players remains unclear.

Gardner et al. describe the experience in evaluating and treating a series of 14 self-referred symptomatic players. The aim is to raise awareness in the neurology community regarding the different clinical phenotypes, idiosyncratic but potentially treatable symptoms, and the spectrum of underlying neuropathologies in these players 2).

Altered Corpus Callosum White Matter Microstructure

Forty retired National Football League (NFL) players, ages 40-65, were matched by age and divided into two groups based on their age of first exposure (AFE) to tackle football: before age 12 or at age 12 or older. Participants underwent DTI on a 3 Tesla Siemens (TIM-Verio) magnet. The whole CC and five subregions were defined and seeded using deterministic tractography. Dependent measures were fractional anisotropy (FA), trace, axial diffusivity and radial diffusivity. Results showed that former NFL players in the AFE <12 group had significantly lower FA in anterior three CC regions and higher radial diffusivity in the most anterior CC region than those in the AFE ≥12 group. 3).

Prevention

Findings suggest that regulation of practice equipment could be a fair and effective way to substantially reduce subconcussive head impact in thousands of collegiate football players 4).

Case series

2017

Case series of 202 football players whose brains were donated for research. Neuropathological evaluations and retrospective telephone clinical assessments (including head trauma history) with informants were performed blinded. Online questionnaires ascertained athletic and military history.

Neuropathological diagnoses of neurodegenerative diseases, including CTE, based on defined diagnostic criteria; CTE neuropathological severity (stages I to IV or dichotomized into mild [stages I and II] and severe [stages III and IV]); informant-reported athletic history and, for players who died in 2014 or later, clinical presentation, including behavior, mood, and cognitive symptoms and dementia.

Among 202 deceased former football players (median age at death, 66 years [interquartile range, 47-76 years]), CTE was neuropathologically diagnosed in 177 players (87%; median age at death, 67 years [interquartile range, 52-77 years]; mean years of football participation, 15.1 [SD, 5.2]), including 0 of 2 pre-high school, 3 of 14 high school (21%), 48 of 53 college (91%), 9 of 14 semiprofessional (64%), 7 of 8 Canadian Football League (88%), and 110 of 111 National Football League (99%) players. Neuropathological severity of CTE was distributed across the highest level of play, with all 3 former high school players having mild pathology and the majority of former college (27 [56%]), semiprofessional (5 [56%]), and professional (101 [86%]) players having severe pathology. Among 27 participants with mild CTE pathology, 26 (96%) had behavioral or mood symptoms or both, 23 (85%) had cognitive symptoms, and 9 (33%) had signs of dementia. Among 84 participants with severe CTE pathology, 75 (89%) had behavioral or mood symptoms or both, 80 (95%) had cognitive symptoms, and 71 (85%) had signs of dementia.

In a convenience sample of deceased football players who donated their brains for research, a high proportion had neuropathological evidence of CTE, suggesting that CTE may be related to prior participation in football 5).

1)

Riley DO, Robbins CA, Cantu RC, Stern RA. Chronic traumatic encephalopathy: Contributions from the Boston University Center for the Study of Traumatic Encephalopathy. Brain Inj. 2015;29(2):154-63. doi: 10.3109/02699052.2014.965215. PubMed PMID: 25587744.
2)

Gardner RC, Possin KL, Hess CP, Huang EJ, Grinberg LT, Nolan AL, Cohn-Sheehy BI, Ghosh PM, Lanata S, Merrilees J, Kramer JH, Berger MS, Miller BL, Yaffe K, Rabinovici GD. Evaluating and treating neurobehavioral symptoms in professional American football players: Lessons from a case series. Neurol Clin Pract. 2015 Aug;5(4):285-295. PubMed PMID: 26336629.
3)

Stamm JM, Koerte IK, Muehlmann M, Pasternak O, Bourlas AP, Baugh CM, Giwerc MY, Zhu A, Coleman MJ, Fritts NG, Martin B, Chaisson C, McClean MD, Lin AP, Cantu RC, Tripodis Y, Stern R, Shenton ME. Age at First Exposure to Football is Associated with Altered Corpus Callosum White Matter Microstructure in Former Professional Football Players. J Neurotrauma. 2015 Jul 22. [Epub ahead of print] PubMed PMID: 26200068.
4)

Reynolds BB, Patrie J, Henry EJ, Goodkin HP, Broshek DK, Wintermark M, Druzgal TJ. Practice type effects on head impact in collegiate football. J Neurosurg. 2015 Aug 4:1-10. [Epub ahead of print] PubMed PMID: 26238972.
5)

Mez J, Daneshvar DH, Kiernan PT, Abdolmohammadi B, Alvarez VE, Huber BR, Alosco ML, Solomon TM, Nowinski CJ, McHale L, Cormier KA, Kubilus CA, Martin BM, Murphy L, Baugh CM, Montenigro PH, Chaisson CE, Tripodis Y, Kowall NW, Weuve J, McClean MD, Cantu RC, Goldstein LE, Katz DI, Stern RA, Stein TD, McKee AC. Clinicopathological Evaluation of Chronic Traumatic Encephalopathy in Players of American Football. JAMA. 2017 Jul 25;318(4):360-370. doi: 10.1001/jama.2017.8334. PubMed PMID: 28742910.

Update: Posttraumatic epilepsy

Traumatic brain injury (TBI) is one of the most common causes of acquired epilepsy, and posttraumatic epilepsy (PTE) results in significant somatic and psychosocial morbidity.

The incidence of early post-traumatic seizures after civilian traumatic brain injury ranges 4-25%.

The true incidence of PTE in children is still uncertain, because most research has been based primarily on adults.

PTE in a pediatric population with 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 1).

Risk

The risk of developing PTE relates directly to TBI severity, but the latency to first seizure can be decades after the inciting trauma. Given this “silent period,” much work has focused on identification of molecular and radiographic biomarkers for risk stratification and on development of therapies to prevent epileptogenesis.

Research suggests that there are reciprocal relationships between mental health (MH) disorders and epilepsy risk.

Data suggest that PTE is associated with mental health (MH) outcomes 2years after TBI, findings whose significance may reflect reciprocal, biological, psychological, and/or experiential factors contributing to and resulting from both PTE and MH status post-TBI. Future work should consider temporal and reciprocal relationships between PTE and MH as well as if/how treatment of each condition influences biosusceptibility to the other condition 2).

Treatment

The control of early post-traumatic seizure is mandatory because these acute insults may add secondary damage to the already damaged brain with poor outcome. Prophylactic use of antiepileptic drugs have been found to be have variable efficacy against early post-traumatic seizures.

Based on current studies, however, anticonvulsants have been shown to reduce early PTE occurring within the first 7 days, but little to no benefits have been shown in late PTS occurring after 7 days 3).

Clinical management requires vigilant neurologic surveillance and recognition of the heterogeneous endophenotypes associated with PTE.

Appropriate treatment of patients who have or are at risk for seizures varies as a function of time after TBI, and the clinician’s armamentarium includes an ever-expanding diversity of pharmacological and surgical options.


The lack of evidence on which antiepileptic drug to use in PTE is surprising given the number of patients prescribed an antiepileptic drug therapy for TBI. On the basis of currently available Level III evidence, patients treated with either levetiracetam or phenytoin have similar incidences of early seizures after TBI 4).

There is no statistically significant difference in the efficacy of Phenytoin and Levetiracetam in prophylaxis of early posttraumatic seizures in cases of moderate to severe traumatic brain injury 5).


Most recently, neuromodulation with implantable devices has emerged as a promising therapeutic strategy for some patients with refractory PTE 6).

Systematic review

During June and July 2015, a systematic literature search was performed that identified 6097 articles. Of these, 7 met inclusion criteria. A random-effects meta-analysis was performed. A total of 1186 patients were included. The rate of seizure was 35 of 654 (5.4%) in the levetiracetam cohort and 18 of 532 (3.4%) in the phenytoin cohort. The meta-analysis revealed no change in the rate of early PTS with levetiracetam compared with phenytoin (relative risk, 1.02; 95% confidence interval, 0.53-1.95; P = .96).

The lack of evidence on which antiepileptic drug to use in PTS is surprising given the number of patients prescribed an antiepileptic drug therapy for TBI. On the basis of currently available Level III evidence, patients treated with either levetiracetam or phenytoin have similar incidences of early seizures after TBI 7)

Case series

2016

In a retrospective multicenter cohort study including 5 regional pediatric trauma centers affiliated with academic medical centers, the authors examined data from 236 children (age < 18 years) with severe traumatic brain injury (TBI) (admission Glasgow Coma Scale score ≤ 8, ICD-9 diagnosis codes of 800.0-801.9, 803.0-804.9, 850.0-854.1, 959.01, 950.1-950.3, 995.55, maximum head Abbreviated Injury Scale score ≥ 3) who received tracheal intubation for ≥ 48 hours in the ICU between 2007 and 2011.

Of 236 patients, 187 (79%) received seizure prophylaxis. In 2 of the 5 centers, 100% of the patients received seizure prophylaxis medication. Use of seizure prophylaxis was associated with younger patient age (p < 0.001), inflicted TBI (p < 0.001), subdural hematoma (p = 0.02), cerebral infarction (p < 0.001), and use of electroencephalography (p = 0.023), but not higher Injury Severity Score. In 63% cases in which seizure prophylaxis was used, the patients were given the first medication within 24 hours of injury, and 50% of the patients received the first dose in the prehospital or emergency department setting. Initial seizure prophylaxis was most commonly with fosphenytoin (47%), followed by phenytoin (40%).

While fosphenytoin was the most commonly used medication for seizure prophylaxis, there was large variation within and between trauma centers with respect to timing and choice of seizure prophylaxis in severe pediatric TBI. The heterogeneity in seizure prophylaxis use may explain the previously observed lack of relationship between seizure prophylaxis and outcomes 8).

1)

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.

2)

Juengst SB, Wagner AK, Ritter AC, Szaflarski JP, Walker WC, Zafonte RD, Brown AW, Hammond FM, Pugh MJ, Shea T, Krellman JW, Bushnik T, Arenth PM. Post-traumatic epilepsy associations with mental health outcomes in the first two years after moderate to severe TBI: A TBI Model Systems analysis. Epilepsy Behav. 2017 Jun 25;73:240-246. doi: 10.1016/j.yebeh.2017.06.001. [Epub ahead of print] PubMed PMID: 28658654.

3)

Kirmani BF, Robinson DM, Fonkem E, Graf K, Huang JH. Role of Anticonvulsants in the Management of Posttraumatic Epilepsy. Front Neurol. 2016 Mar 22;7:32. eCollection 2016. Review. PubMed PMID: 27047441.

4)

Khan NR, VanLandingham MA, Fierst TM, Hymel C, Hoes K, Evans LT, Mayer R, Barker F, Klimo P Jr. Should Levetiracetam or Phenytoin Be Used for Posttraumatic Seizure Prophylaxis? A Systematic Review of the Literature and Meta-analysis. Neurosurgery. 2016 Sep 30. PubMed PMID: 27749510.

5)

Khan SA, Bhatti SN, Khan AA, Khan Afridi EA, Muhammad G, Gul N, Zadran KK, Alam S, Aurangzeb A. Comparison Of Efficacy Of Phenytoin And Levetiracetam For Prevention Of Early Post Traumatic Seizures. J Ayub Med Coll Abbottabad. 2016 Jul-Sep;28(3):455-460. PubMed PMID: 28712212.

6)

Rao VR, Parko KL. Clinical Approach to Posttraumatic Epilepsy. Semin Neurol. 2015 Feb;35(1):57-63. Epub 2015 Feb 25. PubMed PMID: 25714868.

7)

Khan NR, VanLandingham MA, Fierst TM, Hymel C, Hoes K, Evans LT, Mayer R, Barker F, Klimo P Jr. Should Levetiracetam or Phenytoin Be Used for Posttraumatic Seizure Prophylaxis? A Systematic Review of the Literature and Meta-analysis. Neurosurgery. 2016 Dec;79(6):775-782. PubMed PMID: 27749510.

8)

Ostahowski PJ, Kannan N, Wainwright MS, Qiu Q, Mink RB, Groner JI, Bell MJ, Giza CC, Zatzick DF, Ellenbogen RG, Boyle LN, Mitchell PH, Vavilala MS; PEGASUS (Pediatric Guideline Adherence and Outcomes) Study.. Variation in seizure prophylaxis in severe pediatric traumatic brain injury. J Neurosurg Pediatr. 2016 Oct;18(4):499-506. PubMed PMID: 27258588.