Part Ii – Neurological Disorders
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Management of the Head Injury Patient
Management of the Head Injury Patient William Schecter, MD Epidemilogy • 1.6 million head injury patients in the U.S. annually • 250,000 head injury hospital admissions annually • 60,000 deaths • 70-90,000 permanent disability • Estimated cost: $100 billion per year Causes of Brain Injury • Motor Vehicle Accidents • Falls • Anoxic Encephalopathy • Penetrating Trauma • Air Embolus after blast injury • Ischemia • Intracerebral hemorrhage from Htn/aneurysm • Infection • tumor Brain Injury • Primary Brain Injury • Secondary Brain Injury Primary Brain Injury • Focal Brain Injury – Skull Fracture – Epidural Hematoma – Subdural Hematoma – Subarachnoid Hemorrhage – Intracerebral Hematorma – Cerebral Contusion • Diffuse Axonal Injury Fracture at the Base of the Skull Battle’s Sign • Periorbital Hematoma • Battle’s Sign • CSF Rhinorhea • CSF Otorrhea • Hemotympanum • Possible cranial nerve palsy http://health.allrefer.com/pictures-images/ Fracture of maxillary sinus causing CSF Rhinorrhea battles-sign-behind-the-ear.html Skull Fractures Non-depressed vs Depressed Open vs Closed Linear vs Egg Shell Linear and Depressed Normal Depressed http://www.emedicine.com/med/topic2894.htm Temporal Bone Fracture http://www.vh.org/adult/provider/anatomy/ http://www.bartleby.com/107/illus510.html AnatomicVariants/Cardiovascular/Images0300/0386.html Epidural Hematoma http://www.chestjournal.org/cgi/content/full/122/2/699 http://www.bartleby.com/107/illus769.html Epidural Hematoma • Uncommon (<1% of all head injuries, 10% of post traumatic coma patients) • Located -
Cervical Spine Injury Risk Factors in Children with Blunt Trauma Julie C
Cervical Spine Injury Risk Factors in Children With Blunt Trauma Julie C. Leonard, MD, MPH,a Lorin R. Browne, DO,b Fahd A. Ahmad, MD, MSCI,c Hamilton Schwartz, MD, MEd,d Michael Wallendorf, PhD,e Jeffrey R. Leonard, MD,f E. Brooke Lerner, PhD,b Nathan Kuppermann, MD, MPHg BACKGROUND: Adult prediction rules for cervical spine injury (CSI) exist; however, pediatric rules abstract do not. Our objectives were to determine test accuracies of retrospectively identified CSI risk factors in a prospective pediatric cohort and compare them to a de novo risk model. METHODS: We conducted a 4-center, prospective observational study of children 0 to 17 years old who experienced blunt trauma and underwent emergency medical services scene response, trauma evaluation, and/or cervical imaging. Emergency department providers recorded CSI risk factors. CSIs were classified by reviewing imaging, consultations, and/or telephone follow-up. We calculated bivariable relative risks, multivariable odds ratios, and test characteristics for the retrospective risk model and a de novo model. RESULTS: Of 4091 enrolled children, 74 (1.8%) had CSIs. Fourteen factors had bivariable associations with CSIs: diving, axial load, clotheslining, loss of consciousness, neck pain, inability to move neck, altered mental status, signs of basilar skull fracture, torso injury, thoracic injury, intubation, respiratory distress, decreased oxygen saturation, and neurologic deficits. The retrospective model (high-risk motor vehicle crash, diving, predisposing condition, neck pain, decreased neck mobility (report or exam), altered mental status, neurologic deficits, or torso injury) was 90.5% (95% confidence interval: 83.9%–97.2%) sensitive and 45.6% (44.0%–47.1%) specific for CSIs. -
A Review of Traumatic Axonal Injury
Acta Medica 2021; 52(2): 102-108 acta medica REVIEW A Review of Traumatic Axonal Injury Dicle Karakaya1, [MD] ABSTRACT ORCID: 0000-0003-1939-6802 Traumatic brain injury is a major cause of mortality and neurological Ahmet İlkay Işıkay2, [MD] disability worldwide and varies according to its cause, pathogenesis, ORCID: 0000-0001-7790-4735 severity and clinical outcome. This review summarizes a significant aspect of diffuse brain injuries – traumatic axonal injury – important cause of severe disability and vegetative state. Traumatic axonal injury is a type of traumatic brain injury caused by blunt head trauma. It is defined both clinically (immediate and prolonged unconsciousness, characteristically in the absence of space-occupying lesions) and pathologically (widespread and diffuse damage of axons). Following traumatic brain injury, progressive axonal degeneration starts with 1Hacettepe University, Faculty of Medicine, Department disruption of axonal transport, axonal swelling, secondary axonal of Neurosurgery, Ankara, Turkey disconnection and Wallerian degeneration, respectively. However, traumatic axonal injury is difficult to define clinically, it should be Corresponding Author: Ahmet İlkay Işıkay considered in patients with Glasgow coma score < 8 for more than six Hacettepe University, Faculty of Medicine, Department hours after trauma and diffuse tensor imaging and sensitivity-weighted of Neurosurgery, Sıhhiye/Ankara, Turkey imaging MRI sequences are highly sensitive in its diagnosis. Glasgow Phone: +90 312 305 17 15 coma score at the time of presentation, location and severity of axonal E-mail: [email protected] damage are prognostic factors for clinical outcome. https://doi.org/10.32552/2021.ActaMedica.467 Keywords: Diffuse, traumatic, axonal, injury. Received: 29 May 2020, Accepted: 9 March 2021, Published online: 8 June 2021 INTRODUCTION Traumatic axonal injury (TAI) is a distinct it is not diffuse but actually widespread and/or clinicopathological topic that can cause severe multifocal [3]. -
The Dynamic Impact Behavior of the Human Neurocranium
www.nature.com/scientificreports OPEN The dynamic impact behavior of the human neurocranium Johann Zwirner1,2*, Benjamin Ondruschka2,3, Mario Scholze4,5, Joshua Workman6, Ashvin Thambyah6 & Niels Hammer5,7,8 Realistic biomechanical models of the human head should accurately refect the mechanical properties of all neurocranial bones. Previous studies predominantly focused on static testing setups, males, restricted age ranges and scarcely investigated the temporal area. This given study determined the biomechanical properties of 64 human neurocranial samples (age range of 3 weeks to 94 years) using testing velocities of 2.5, 3.0 and 3.5 m/s in a three-point bending setup. Maximum forces were higher with increasing testing velocities (p ≤ 0.031) but bending strengths only revealed insignifcant increases (p ≥ 0.052). The maximum force positively correlated with the sample thickness (p ≤ 0.012 at 2.0 m/s and 3.0 m/s) and bending strength negatively correlated with both age (p ≤ 0.041) and sample thickness (p ≤ 0.036). All parameters were independent of sex (p ≥ 0.120) apart from a higher bending strength of females (p = 0.040) for the 3.5 -m/s group. All parameters were independent of the post mortem interval (p ≥ 0.061). This study provides novel insights into the dynamic mechanical properties of distinct neurocranial bones over an age range spanning almost one century. It is concluded that the former are age-, site- and thickness-dependent, whereas sex dependence needs further investigation. Biomechanical parameters characterizing the load-deformation behavior of the human neurocranium are crucial for building physical models 1–3 and high-quality computational simulations 4–6 of the human head to answer com- plex biomechanical research questions to the best possible extent. -
What to Expect After Having a Subarachnoid Hemorrhage (SAH) Information for Patients and Families Table of Contents
What to expect after having a subarachnoid hemorrhage (SAH) Information for patients and families Table of contents What is a subarachnoid hemorrhage (SAH)? .......................................... 3 What are the signs that I may have had an SAH? .................................. 4 How did I get this aneurysm? ..................................................................... 4 Why do aneurysms need to be treated?.................................................... 4 What is an angiogram? .................................................................................. 5 How are aneurysms repaired? ..................................................................... 6 What are common complications after having an SAH? ..................... 8 What is vasospasm? ...................................................................................... 8 What is hydrocephalus? ............................................................................... 10 What is hyponatremia? ................................................................................ 12 What happens as I begin to get better? .................................................... 13 What can I expect after I leave the hospital? .......................................... 13 How will the SAH change my health? ........................................................ 14 Will the SAH cause any long-term effects? ............................................. 14 How will my emotions be affected? .......................................................... 15 When should -
Clinical Features and Treatment of Pediatric Orbit Fractures
ORIGINAL INVESTIGATION Clinical Features and Treatment of Pediatric Orbit Fractures Eric M. Hink, M.D.*, Leslie A. Wei, M.D.*, and Vikram D. Durairaj, M.D., F.A.C.S.*† Departments of *Ophthalmology, and †Otolaryngology and Head and Neck Surgery, University of Colorado Denver, Aurora, Colorado, U.S.A. of craniofacial skeletal development.1 Orbit fractures may be Purpose: To describe a series of orbital fractures and associated with ophthalmic, neurologic, and craniofacial inju- associated ophthalmic and craniofacial injuries in the pediatric ries that may require intervention. The result is that pediatric population. facial trauma is often managed by a diverse group of specialists, Methods: A retrospective case series of 312 pediatric and each service may have their own bias as to the ideal man- patients over a 9-year period (2002–2011) with orbit fractures agement plan.4 In addition, children’s skeletal morphology and diagnosed by CT. physiology are quite different from adults, and the benefits of Results: Five hundred ninety-one fractures in 312 patients surgery must be weighed against the possibility of detrimental were evaluated. There were 192 boys (62%) and 120 girls (38%) changes to facial skeletal growth and development. The purpose with an average age of 7.3 years (range 4 months to 16 years). of this study was to describe a series of pediatric orbital frac- Orbit fractures associated with other craniofacial fractures were tures; associated ophthalmic, neurologic, and craniofacial inju- more common (62%) than isolated orbit fractures (internal ries; and fracture management and outcomes. fractures and fractures involving the orbital rim but without extension beyond the orbit) (38%). -
NIH Public Access Author Manuscript J Neuropathol Exp Neurol
NIH Public Access Author Manuscript J Neuropathol Exp Neurol. Author manuscript; available in PMC 2010 September 24. NIH-PA Author ManuscriptPublished NIH-PA Author Manuscript in final edited NIH-PA Author Manuscript form as: J Neuropathol Exp Neurol. 2009 July ; 68(7): 709±735. doi:10.1097/NEN.0b013e3181a9d503. Chronic Traumatic Encephalopathy in Athletes: Progressive Tauopathy following Repetitive Head Injury Ann C. McKee, MD1,2,3,4, Robert C. Cantu, MD3,5,6,7, Christopher J. Nowinski, AB3,5, E. Tessa Hedley-Whyte, MD8, Brandon E. Gavett, PhD1, Andrew E. Budson, MD1,4, Veronica E. Santini, MD1, Hyo-Soon Lee, MD1, Caroline A. Kubilus1,3, and Robert A. Stern, PhD1,3 1 Department of Neurology, Boston University School of Medicine, Boston, Massachusetts 2 Department of Pathology, Boston University School of Medicine, Boston, Massachusetts 3 Center for the Study of Traumatic Encephalopathy, Boston University School of Medicine, Boston, Massachusetts 4 Geriatric Research Education Clinical Center, Bedford Veterans Administration Medical Center, Bedford, Massachusetts 5 Sports Legacy Institute, Waltham, MA 6 Department of Neurosurgery, Boston University School of Medicine, Boston, Massachusetts 7 Department of Neurosurgery, Emerson Hospital, Concord, MA 8 CS Kubik Laboratory for Neuropathology, Department of Pathology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts Abstract Since the 1920s, it has been known that the repetitive brain trauma associated with boxing may produce a progressive neurological deterioration, originally termed “dementia pugilistica” and more recently, chronic traumatic encephalopathy (CTE). We review the 47 cases of neuropathologically verified CTE recorded in the literature and document the detailed findings of CTE in 3 professional athletes: one football player and 2 boxers. -
What%Is%Epilepsy?%
What%is%Epilepsy?% Epilepsy(is(a(brain(disorder(in(which(a(person(has(repeated(seizures((convulsions)(over(time.(Seizures(are( episodes(of(disturbed(brain(activity(that(cause(changes(in(attention(or(behavior.( Causes( Epilepsy(occurs(when(permanent(changes(in(brain(tissue(cause(the(brain(to(be(too(excitable(or(jumpy.( The(brain(sends(out(abnormal(signals.(This(results(in(repeated,(unpredictable(seizures.((A(single(seizure( that(does(not(happen(again(is(not(epilepsy.)( Epilepsy(may(be(due(to(a(medical(condition(or(injury(that(affects(the(brain,(or(the(cause(may(be( unknown((idiopathic).( Common(causes(of(epilepsy(include:( •Stroke(or(transient(ischemic(attack((TIA)( •Dementia,(such(as(Alzheimer's(disease( •Traumatic(brain(injury( •Infections,(including(brain(abscess,(meningitis,(encephalitis,(and(AIDS( •Brain(problems(that(are(present(at(birth((congenital(brain(defect)( •Brain(injury(that(occurs(during(or(near(birth( •Metabolism(disorders(present(at(birth((such(as(phenylketonuria)( •Brain(tumor( •Abnormal(blood(vessels(in(the(brain( •Other(illness(that(damage(or(destroy(brain(tissue( •Use(of(certain(medications,(including(antidepressants,(tramadol,(cocaine,(and(amphetamines( Epilepsy(seizures(usually(begin(between(ages(5(and(20,(but(they(can(happen(at(any(age.(There(may(be(a( family(history(of(seizures(or(epilepsy.( Symptoms( Symptoms(vary(from(person(to(person.(Some(people(may(have(simple(staring(spells,(while(others(have( violent(shaking(and(loss(of(alertness.(The(type(of(seizure(depends(on(the(part(of(the(brain(affected(and( cause(of(epilepsy.( -
In Drivers of Open-Wheel Open Cockpit Race Cars
SPORTS MEDICINE SPINE FRACTURES IN DRIVERS OF OPEN-WHEEL OPEN COCKPIT RACE CARS – Written by Terry Trammell and Kathy Flint, USA This paper is intended to explain the mechanisms responsible for production of spinal fracture in the driver of an open cockpit single seat, open-wheel racing car (Indy Car) and what can be done to lessen the risk of fracture. In a report of fractures in multiple racing • Seated angle (approximately 45°) • Lumbar spine flexed series drivers (Championship Auto Racing • Hips and knees flexed • Seated semi-reclining Cars [CART]/Champ cars, Toyota Atlantics, Indy Racing League [IRL], Indy Lights and Figure 1: Body alignment in the Indy Car. Formula 1 [F1]), full details of the crash and mechanism of injury were captured and analysed. This author was the treating physician in all cases from 1996 to 2011. All images, medical records, data available BASILAR SKULL FRACTURE Use of this specific safety feature from the Accident Data Recorder-2 (ADR), Following a fatal distractive basilar is compulsory in most professional crash video, specific on track information, skull fracture in 1999, the Head and Neck motorsport sanctions and has resulted in a post-accident investigation of damage and Support (HANS) device was introduced into dramatic reduction to near elimination of direction of major impact correlated with Indy Cars. Basilar skull fracture occurs when fatal basilar skull fractures. No basilar skull ADR-2 data were analysed. Results provided neck tension exceeds 3113.75 N forces. fractures have occurred in the IRL since the groundwork for understanding spine No data demonstrates that HANS introduction of the HANS and since 2006 fracture and forces applied to the driver in predisposes the wearer to other cervical there has been only one cervical fracture. -
Depressed Skull Fracture (Let's Talk About
In partnership with Primary Children’s Hospital Let’s Talk About... Depressed Skull Fracture B. A. Depressed skull Indentation fracture C. Concussion A depressed skull fracture happens when one or more to be removed. Before the surgery, your child’s head fragments of the skull bone are pushed inward (see is shaved so the surgery can be completely clean. Your “B” on the illustration). An indentation (A) with no child also receives some medicine to help him or her breaks in the bone happens more often in babies. relax and sleep. During surgery, small metal plates Since the brain is beneath the skull, the skull bone and screws may be used to hold the bone fragments fragments may injure the brain (C). Your child may in place. The skin over the surgical area is closed with have a bruise on the brain (called a contusion), and sutures (SOO-churs) or skin staples. a swollen black-and-blue area on the skin. What happens after the surgery? How do you treat a depressed After the surgery, your child will stay in the hospital skull fracture? for a few days. There is a lot of equipment around To find out if your child has a skull fracture, a special the bed. This helps the staff care for your child. x-ray called a CT Scan (short for computerized While your child is in the hospital, the nurses tomography) is needed. The CT scan takes pictures of frequently check your child’s temperature, pulse, your child’s brain and skull bones. blood pressure, and alertness. -
Biomechanics of Temporo-Parietal Skull Fracture Narayan Yoganandan *, Frank A
Clinical Biomechanics 19 (2004) 225–239 www.elsevier.com/locate/clinbiomech Review Biomechanics of temporo-parietal skull fracture Narayan Yoganandan *, Frank A. Pintar Department of Neurosurgery, Medical College of Wisconsin, 9200 West Wisconsin Avenue, Milwaukee, WI 53226, USA Received 16 December 2003; accepted 16 December 2003 Abstract This paper presents an analysis of research on the biomechanics of head injury with an emphasis on the tolerance of the skull to lateral impacts. The anatomy of this region of the skull is briefly described from a biomechanical perspective. Human cadaver investigations using unembalmed and embalmed and intact and isolated specimens subjected to static and various types of dynamic loading (e.g., drop, impactor) are described. Fracture tolerances in the form of biomechanical variables such as peak force, peak acceleration, and head injury criteria are used in the presentation. Lateral impact data are compared, where possible, with other regions of the cranial vault (e.g., frontal and occipital bones) to provide a perspective on relative variations between different anatomic regions of the human skull. The importance of using appropriate instrumentation to derive injury metrics is underscored to guide future experiments. Relevance A unique advantage of human cadaver tests is the ability to obtain fundamental data for delineating the biomechanics of the structure and establishing tolerance limits. Force–deflection curves and acceleration time histories are used to derive secondary variables such as head injury criteria. These parameters have direct application in safety engineering, for example, in designing vehicular interiors for occupant protection. Differences in regional biomechanical tolerances of the human head have implications in clinical and biomechanical applications. -
Diffuse Axonal Injury in Head Trauma
J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.52.7.838 on 1 July 1989. Downloaded from Journal ofNeurology, Neurosurgery, and Psychiatry 1989;52:838-841 Diffuse axonal injury in head trauma PETER C BLUMBERGS, NIGEL R JONES, JOHN B NORTH From the Neuropathology Laboratory, Institute ofMedical and Veterinary Science and Neurosurgery Department, Royal Adelaide Hospital, Adelaide, South Australia SUMMARY Diffuse axonal injury (DAI) as defined by detailed microscopic examination was found in 34 of 80 consecutive cases of head trauma surviving for a sufficient length of time to be clinically assessed by the Royal Adelaide Hospital Neurosurgery Unit. The findings indicate that there is a spectrum ofaxonal injury and that one third ofcases ofDAI recovered sufficiently to talk between the initial head injury producing coma and subsequent death. The macroscopic "marker" lesions in the corpus callosum and dorsolateral quadrants of the brainstem were present in only 15/34 of the cases and represented the most severe end of the spectrum of DAI. Diffuse axonal injury (DAI) that is, widespread superior cerebellar peduncles, (2) evidence of diffuse damage to axons in the white matter of the brain, was damage to axons. originally defined by Strich' and the concept was Patients who sustain severe DAI are unconscious expanded by Adams et al.2 Strich described diffuse from the moment ofimpact, do not experience a lucid Protected by copyright. degeneration ofthe cerebral white matter in a series of interval, and remain unconscious, vegetative