Reversible monoparesis following decompressive hemicraniectomy for traumatic brain injury

2008 ◽  
Vol 109 (2) ◽  
pp. 245-254 ◽  
Author(s):  
Shirley I. Stiver ◽  
Max Wintermark ◽  
Geoffrey T. Manley
Keyword(s):  
Traumatic Brain Injury ◽  
Cerebrospinal Fluid ◽  
Brain Injury ◽  
Motor Function ◽  
Ct Perfusion ◽  
Motor Deficits ◽  
Decompressive Hemicraniectomy ◽  
Number Of Patients ◽  
Motor Strength

Object The “syndrome of the trephined” is an uncommon and poorly understood disorder of delayed neurological deficit following craniectomy. From the authors' extensive experience with decompressive hemicraniectomy for traumatic brain injury (TBI), they have encountered a number of patients who developed delayed motor deficits, also called “motor trephine syndrome,” and reversal of the weakness following cranioplasty repair. The authors set out to study motor function systematically in this patient population to define the incidence, contributing factors, and outcome of patients with motor trephine syndrome. Methods The authors evaluated patient demographics, injury characteristics, detailed motor examinations, and CT scans in 38 patients with long-term follow-up after decompressive hemicraniectomy for TBI. Results Ten patients (26%) experienced delayed contralateral upper-extremity weakness, beginning 4.9 ± 0.4 months (mean ± standard error) after decompressive hemicraniectomy. Motor deficits improved markedly within 72 hours of cranioplasty repair, and all patients recovered full motor function. The CT perfusion scans, performed in 2 patients, demonstrated improvements in cerebral blood flow commensurate with resolution of cerebrospinal fluid flow disturbances on CT scanning and return of motor strength. Comparisons between 10 patients with and 20 patients (53%) without delayed motor deficits identified 3 factors—ipsilateral contusions, abnormal cerebrospinal fluid circulation, and longer intervals to cranioplasty repair—to be strongly associated with delayed, reversible monoparesis following decompressive hemicraniectomy. Conclusions Delayed, reversible monoparesis, also called motor trephine syndrome, is common following decompressive hemicraniectomy for TBI. The results of this study suggest that close follow-up of motor strength with early cranioplasty repair may prevent delayed motor complications of decompressive hemicraniectomy.

scholarly journals Cortical re-organization after traumatic brain injury elicited using functional electrical stimulation therapy: A case report

2020 ◽  
Author(s):  
Matija Milosevic ◽  
Tomoya Nakanishi ◽  
Atsushi Sasaki ◽  
Akiko Yamaguchi ◽  
Milos R. Popovic ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Electrical Stimulation ◽  
Brain Injury ◽  
Motor Function ◽  
Upper Limb ◽  
Functional Electrical Stimulation ◽  
Short Term ◽  
Electrical Stimulation Therapy

AbstractFunctional electrical stimulation therapy (FEST) can improve motor function after neurological injuries. However, little is known about cortical re-organization after FEST and weather it can improve upper-limb motor function after traumatic brain injury (TBI). Therefore, our study examined cortical and motor changes in a single male participant with chronic TBI suffering from mild motor impairment during 3-months of FEST and at 3-months follow-up. FEST was applied to enable upper-limb grasping and reaching movements during each session, which was performed for 45-60 min, 3 days per week, over 12-weeks. Short-term assessments were examined before and after each session, while long-term assessments were performed at baseline, after 6- and 12-weeks of FEST, and during follow-up 6- and 12-weeks after completing FEST. Short-term assessments carried out using transcranial magnetic stimulation (TMS) showed reduced cortical silent period (CSP), which is related to cortical and/or subcortical inhibition. At the same time, no changes in motor evoked potentials (MEP) were observed, suggesting corticospinal excitability was unaffected. Long-term assessments indicate increased MEP corticospinal excitability after 12-weeks of FEST, which remained during both follow-ups, while no changes in CSP were observed. Similarly, long-term assessments using TMS mapping showed larger hand MEP area in the primary motor cortex (M1) after 12-weeks of FEST as well as during both follow-ups. Corroborating TMS results, fMRI imaging data showed M1, as well as sensory, premotor, parietal area, and supplementary motor area activations increased after 12-weeks of FEST and during both follow-ups. While clinical scores did not change considerably, writing test performance indicates mild improvements after FEST. Our results suggest that FEST can effectively increase cortical activations, while writing tests confirmed functional improvements in fine motor function even after chronic TBI. These results demonstrated long-term recovery mechanisms of FEST, which include cortical re-organization or neuroplasticity to improve motors function after neurological injury.

scholarly journals Psychotropic and pain medication use in individuals with traumatic brain injury—a Swedish total population cohort study of 240 000 persons

2021 ◽  
Vol 92 (5) ◽  
pp. 519-527
Author(s):  
Yasmina Molero ◽  
David James Sharp ◽  
Brian Matthew D'Onofrio ◽  
Henrik Larsson ◽  
Seena Fazel
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Total Population ◽  
Medication Use ◽  
Population Based ◽  
Pain Medication ◽  
Short Term ◽  
Pain Medications ◽  
Before And After

ObjectiveTo examine psychotropic and pain medication use in a population-based cohort of individuals with traumatic brain injury (TBI), and compare them with controls from similar backgrounds.MethodsWe assessed Swedish nationwide registers to include all individuals diagnosed with incident TBI between 2006 and 2012 in hospitals or specialist outpatient care. Full siblings never diagnosed with TBI acted as controls. We examined dispensed prescriptions for psychotropic and pain medications for the 12 months before and after the TBI.ResultsWe identified 239 425 individuals with incident TBI, and 199 658 unaffected sibling controls. In the TBI cohort, 36.6% had collected at least one prescription for a psychotropic or pain medication in the 12 months before the TBI. In the 12 months after, medication use increased to 45.0%, an absolute rate increase of 8.4% (p<0.001). The largest post-TBI increases were found for opioids (from 16.3% to 21.6%, p<0.001), and non-opioid pain medications (from 20.3% to 26.6%, p<0.001). The majority of prescriptions were short-term; 20.6% of those prescribed opioids and 37.3% of those with benzodiazepines collected prescriptions for more than 6 months. Increased odds of any psychotropic or pain medication were associated with individuals before (OR: 1.62, 95% CI: 1.59 to 1.65), and after the TBI (OR: 2.30, 95% CI: 2.26 to 2.34) as compared with sibling controls, and ORs were consistently increased for all medication classes.ConclusionHigh rates of psychotropic and pain medications after a TBI suggest that medical follow-up should be routine and review medication use.

Epidemiology of traumatic brain injury in children 15 years and younger in South-Eastern Norway in 2015–16. Implications for prevention and follow-up needs

2021 ◽  
Vol 31 ◽  
pp. 70-77
Author(s):  
Hilde Margrete Dahl ◽  
Nada Andelic ◽  
Marianne Løvstad ◽  
Ingvil Laberg Holthe ◽  
Morten Hestnes ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
South Eastern ◽  
Eastern Norway

scholarly journals Early diagnosis of mortality using admission CT perfusion in severe traumatic brain injury patients (ACT-TBI): protocol for a prospective cohort study

BMJ Open ◽  
2021 ◽  
Vol 11 (6) ◽  
pp. e047305
Author(s):  
Susan Alcock ◽  
Divjeet Batoo ◽  
Sudharsana Rao Ande ◽  
Rob Grierson ◽  
Marco Essig ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Cohort Study ◽  
Brain Injury ◽  
Early Diagnosis ◽  
Hospital Mortality ◽  
Brain Death ◽  
Severe Traumatic Brain Injury ◽  
Health Research ◽  
Ct Perfusion ◽  
Severe Tbi

IntroductionSevere traumatic brain injury (TBI) is a catastrophic neurological condition with significant economic burden. Early in-hospital mortality (<48 hours) with severe TBI is estimated at 50%. Several clinical examinations exist to determine brain death; however, most are difficult to elicit in the acute setting in patients with severe TBI. Having a definitive assessment tool would help predict early in-hospital mortality in this population. CT perfusion (CTP) has shown promise diagnosing early in-hospital mortality in patients with severe TBI and other populations. The purpose of this study is to validate admission CTP features of brain death relative to the clinical examination outcome for characterizing early in-hospital mortality in patients with severe TBI.Methods and analysisThe Early Diagnosis of Mortality using Admission CT Perfusion in Severe Traumatic Brain Injury Patients study, is a prospective cohort study in patients with severe TBI funded by a grant from the Canadian Institute of Health Research. Adults aged 18 or older, with evidence of a severe TBI (Glasgow Coma Scale score ≤8 before initial resuscitation) and, on mechanical ventilation at the time of imaging are eligible. Patients will undergo CTP at the time of first imaging on their hospital admission. Admission CTP compares with the reference standard of an accepted bedside clinical assessment for brainstem function. Deferred consent will be used. The primary outcome is a binary outcome of mortality (dead) or survival (not dead) in the first 48 hours of admission. The planned sample size for achieving a sensitivity of 75% and a specificity of 95% with a CI of ±5% is 200 patients.Ethics and disseminationThis study has been approved by the University of Manitoba Health Research Ethics Board. The findings from our study will be disseminated through peer-reviewed journals and presentations at local rounds, national and international conferences. The public will be informed through forums at the end of the study.Trial registration numberNCT04318665

scholarly journals Three Month Follow-Up of Rat Mild Traumatic Brain Injury: A Combined [18F]FDG and [11C]PK11195 Positron Emission Study

2016 ◽  
Vol 33 (20) ◽  
pp. 1855-1865 ◽  
Author(s):  
David Vállez García ◽  
Andreas Otte ◽  
Rudi A.J.O. Dierckx ◽  
Janine Doorduin
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Mild Traumatic Brain Injury ◽  
Positron Emission ◽  
18F Fdg ◽  
Emission Study

scholarly journals ELEVATION OF MATRIX METALLOPROTEINASES 3 AND 9 IN CEREBROSPINAL FLUID AND BLOOD IN PATIENTS WITH SEVERE TRAUMATIC BRAIN INJURY

Neurosurgery ◽  
2009 ◽  
Vol 65 (4) ◽  
pp. 702-708 ◽  
Author(s):  
Mark Grossetete ◽  
Jeremy Phelps ◽  
Leopold Arko ◽  
Howard Yonas ◽  
Gary A. Rosenberg
Keyword(s):  
Traumatic Brain Injury ◽  
Cerebrospinal Fluid ◽  
Brain Injury ◽  
Matrix Metalloproteinases ◽  
Blood Brain Barrier ◽  
Normal Pressure Hydrocephalus ◽  
Normal Pressure ◽  
Brain Barrier ◽  
Western Immunoblot ◽  
Blood Brain

Abstract OBJECTIVE Traumatic brain injury (TBI) causes an increase in matrix metalloproteinases (MMPs), which are associated with neuroinflammation, blood-brain barrier disruption, hemorrhage, and cell death. We hypothesized that patients with TBI have an increase in MMPs in ventricular cerebrospinal fluid (CSF) and plasma. METHODS Patients with TBI and a ventricular catheter were entered into the study. Samples of CSF and plasma were collected at the time of catheter placement and at 24 and 72 hours after admission. Seven TBI patients were entered into the study, with 6 having complete data for analysis. Only patients who had a known time of insult that fell within a 6-hour window from initial insult to ventriculostomy were accepted into the study. Control CSF came from ventricular fluid in patients undergoing shunt placement for normal pressure hydrocephalus. Both MMP-2 and MMP-9 were measured with gelatin zymography and MMP-3 with Western immunoblot. RESULTS We found a significant elevation in the levels of the latent form of MMP-9 (92-kD) in the CSF obtained at the time of arrival (P &lt; 0.05). Elevated levels of MMP-2 were detected in plasma at 72 hours, but not in the CSF. Using albumin from both CSF and blood, we calculated the MMP-9 index, which was significantly increased in the CSF, indicating endogenous MMP production. Western immunoblot showed elevated levels of MMP-3 in CSF at all times measured, whereas MMP-3 was not detected in the CSF of normal pressure hydrocephalus. CONCLUSION We show that MMPs are increased in the CSF of TBI patients. Although the number of patients was small, the results were robust and clearly demonstrated increases in MMP-3 and MMP-9 in ventricular CSF in TBI patients compared with controls. Although these preliminary results will need to be replicated, we propose that MMPs may be important in blood-brain barrier opening and hemorrhage secondary to brain injury in patients.

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