Acquired Brain Injury PDF

Acquired Brain Injury Hua Bi, OD, PhD, FAAO, Dipl AAO Diplomate, American Board of Optometry Acquired Brain Injury Traumatic Brain Injury Disruption in brain function, or other evidence of brain pathology, caused by an external physical force Non-traumatic Brain Injury...

Acquired Brain Injury Hua Bi, OD, PhD, FAAO, Dipl AAO Diplomate, American Board of Optometry Acquired Brain Injury Traumatic Brain Injury Disruption in brain function, or other evidence of brain pathology, caused by an external physical force Non-traumatic Brain Injury Caused by an internal event Common causes include: Stroke Infections, such as meningitis or encephalitis Hypoxia or anoxia Brain tumors Drugs or toxins Traumatic Brain Injury Clinical assessment for acute TBI Glasgow Coma Scale * Alteration of mental status must be immediately related to the trauma to the head. Typical symptoms would be: looking and feeling dazed and uncertain of what is happening, confusion, difficulty thinking clearly or responding appropriately to mental status questions, and being unable to describe events immediately before or after the trauma event. Glasgow Coma Scale (GCS) Etiological classification by physical mechanism of injury: Contact or “impact” loading Noncontact or “inertial” loading The magnitude and direction of each type or combination of loading forces may predict type and severity of injury  Primary vs. secondary injury Primary injury Secondary injury Often the direct mechanical Disruption of the blood brain barrier, damage caused by trauma generation of reactive oxygen species and resultant oxidative stress, metabolic Usually apparent acutely such as dysfunction, inflammation and excitotoxicity fractures, intracranial hemorrhage, The processes are mediated at the contusion and traumatic axonal cellular/molecular level injury, vascular injury Best detected with conventional CT Macroscopic manifestations may become and MRI apparent as diffuse cerebral hyperemia, cytotoxic and/or vasogenic edema, and tissue ischemia (due to microvascular changes, systemic hypotension or hypoxia, or elevated intracranial pressure) Imaging Evaluation of Acute Traumatic Brain Injury Epidural hematoma Subdural hematoma Subarachnoid hemorrhage Skull Fracture Intraventricular Brain Contusion Diffuse axonal injury hemorrhage Traumatic Vascular Injury Can result from several mechanisms including: Laceration by fracture fragments Blunt or penetrating trauma Vascular compression from brain herniation Arterial strain Arterial Dissection Results from a tear in the tunica intima or vasa vasorum allowing blood to accumulate within the vessel wall Laceration Arteriovenous fistula Secondary Injuries Cerebral swelling (vasogenic and cytotoxic edema) Brain herniation (the displacement of brain parenchyma into a different compartment) Hydrocephalus Ischemia or infarction CSF leak Leptomeningeal cyst Encephalomalacia Advanced imaging: Diffusion tensor imaging (DTI) a newly developed magnetic resonance imaging (MRI) technique that generates exquisite structural images of brain white matter tracts via measurement of water molecule diffusion within white matter Anisotropy Advanced imaging: Functional Magnetic Resonance Imaging (fMRI) Blood-oxygen-level-dependent (BOLD) fMRI detects changes in the oxygenation state of hemoglobin, thereby capturing oxygen consumption associated with neuronal activation Positron emission tomography (PET) Uses radiolabeled metabolic analogs to measure the rate of brain glucose metabolism Magnetic resonance spectroscopy (MRS) Measures the concentrations of molecules associated with brain metabolism Visual dysfunction and visual symptoms are common sequelae of traumatic brain injury (TBI) Major cortical areas in control of eye movements and visual processing Frontal, parietal, supplementary eye field (FEF, PEF, SEF) Dorsolateral prefrontal cortex (DLPC) Superior colliculus (SC) Brainstem gaze center (BGC) Caudate nucleus (CN) Substantia nigra pars reticulata (SNPR) Visual dysfunction and visual symptoms are common sequelae of traumatic brain injury (TBI) Because the large amount of cortical circuits involved in vision, a wide range of visual symptoms might follow TBI: Physical: headache, nausea, vomiting, dizziness, fatigue, visual disturbance, sleep disturbance, sensitivity to light/noise, balance problems, transient neurological abnormalities Cognitive Behavioral/emotional The visual dysfunctions most often identified: Convergence insufficiency Accommodative dysfunction Photosensitivity Pursuit/saccade disorder Visual field loss Cranial nerve disorder Tests involving high cortical visual functioning increase sensitivity in detecting changes in brain function Cognitive control evaluation of saccadic movement Attention Visually/symbolically cued saccades Gap saccade test Memory Memory-guided saccades Memory-guided sequences of saccades Executive function Antisaccades Cognitive control evaluation of smooth pursuit Predictive visual tracking Smooth pursuit requires attention, anticipation, working memory, as well as smooth, and at times saccadic eye movements to maintain gaze on a fixed target Smooth pursuit deficits in mild TBI: decreased target prediction, increased eye position error, and variability of eye position Adapted from published materials of Walter Reed National Military Medical Center/Vision Center of Excellence. 2016 Photosensitivity Treatment Tinted lenses: Decrease discomfort from many sources of light (e.g. sun, indoor lights, and computer screens) while retaining details of sensory information TINTED Visual field loss Hemianopia Quadrantanopia Central scotoma Peripheral scotoma Monocular vision Visual neglect Inability to orient, report or respond to objects in contralesional space Most frequently follows right cerebral hemisphere injury Reflects visuospatial attention deficits Evaluation: cancellation tests, tasks of line bisection, copying & drawing objects Treatment and rehabilitation: scanning therapy, prism adaptation Visual midline shift test Visual information processing dysfunction after TBI e.g. longer reaction times, reduced accuracy, slowed information processing speed Function Examples of testing Visual spatial Line bisection Copy picture Letter cancellation Visual analysis Visual closure Visual memory Visual motor integration Writing skills Tangrams Vision Therapy A sequence of neurosensory and neuromuscular activities individually prescribed and monitored to develop, rehabilitate, and enhance visual skills and processing Acquired Brain Injury Traumatic Brain Injury Disruption in brain function, or other evidence of brain pathology, caused by an external physical force Non-traumatic Brain Injury Caused by an internal event Common causes include: Stroke Infections, such as meningitis or encephalitis Hypoxia or anoxia Brain tumors Drugs or toxins Stroke (cerebrovascular accident ) An acute interruption of the cerebral blood flow Key features: Sudden onset Involvement of the central nervous system Lack of rapid resolution Vascular cause Classification: Ischemic stroke Hemorrhagic stroke 1. Ischemic stroke Classification based on the mechanism of injury: A. Large-artery atherosclerosis (embolus or thrombosis) Frequent sites of atherosclerosis The carotid system the origin of the internal carotid artery (ICA) the carotid siphon at the base of the brain the main stem of the middle cerebral artery (MCA) and the anterior cerebral artery (ACA) The vertebrobasilar system the origins of the vertebral arteries in the neck and the distal portion of the intracranial vertebral arteries the basilar artery and origins of the posterior cerebral arteries (PCAs) B. Cardiogenic embolism C. Small vessel occlusion (e.g. lacune) D. Other determined cause E. Undetermined cause 1. Ischemic stroke Imaging of acute ischemic stroke 2. Hemorrhagic stroke Bleeding directly into brain parenchyma resulting from rupture of small arteries and arterioles 2.1. Intracerebral Hemorrhage Common causes: Hypertension Arteriovenous malformations Pathophysiology of brain injury caused by Intracerebral Hemorrhage: Mechanical destruction of brain tissue by hematoma Mass effect of hematoma expansion à induced ischemia and vasogenic edema Inflammatory response & free radical formation à breakdown of BBB Hemoglobin degradation products Activation of coagulation cascade à VEGF release à increased vascular permeability AVM: arteriovenous malformation 2.2. Subarachnoid hemorrhage (SAH) The most common cause: Rupture of an intracranial aneurysm Other causes: vascular malformations Terson’s syndrome: Posterior segment hemorrhages occurring as a consequence of subarachnoid or intracranial hemorrhage Advantages and limitations of CT and MR imaging in acute stroke NCCT: non-contrast CT; GRE: gradient-recalled echo SWI: susceptibility weighted imaging; DWI: diffusion-weighted imaging Modifiable risk factors for ischemic stroke: Hypertension Diabetes Smoking Atrial fibrillation Potentially modifiable risk factors for ischemic stroke: Asymptomatic carotid stenosis Dyslipidemia Cardiac disease Sickle cell disease Diet Physical inactivity Obesity Alcohol use Hormone replacement therapy Hyperhomocysteinemia Hypercoagulability Elevated lipoprotein Inflammation Infection Geography Non-modifiable risk factors for ischemic stroke: Aging Hereditary Modifiable risk factors for intracerebral hemorrhage: Hypertension Cerebral amyloid angiopathy Cholesterol Anticoagulation Antiplatelets Alcohol Smoking Diabetes Microbleeds Dialysis Drugs The ABCD2 scoring system for evaluating risk of stroke after transient ischemic attack: includes factors including age, blood pressure, clinical symptoms, duration, and diabetes: § Age: older than 60 years (1 point) § Blood pressure greater than or equal to 140/90 mmHg on first evaluation (1 point) § Clinical symptoms: a focal weakness with the spell (2 points) or speech impairment without weakness (1 point) § Duration greater than 60 min (2 points), or 10 min to 59 min (1 point) § Diabetes mellitus (1 point) Brain tumors Primary and metastatic tumors More than 100 histologic types based on cell of origin and other histopathologic features The World Health Organization (WHO) classification specifies a grading system, ranging from grade I through grade IV. Grade I/II tumors are considered benign or low grade, whereas grade III/IV tumors are malignant or high grade. MRI provides information, such as tumor localization, vascular permeability, cell density, and tumor perfusion. Meningioma Meningioma Glioblastoma This image shows disruption of the blood-brain barrier (BBB) integrity, with a combination of cellular infiltration & vasogenic edema Neuroinflammatory diseases Multiple sclerosis (MS) The most common chronic disabling immunologic disease of the central nervous system in the young population Common MS lesion locations in the brain: Periventricular region Juxtacortical region Corpus callosum Other regions such as brainstem, cerebellar peduncles Common brain infection Bacterial Meningitis Typically, bacteria seed the leptomeninges (the arachnoid mater and the pia mater) via the bloodstream or from a contiguous site of infection Microorganisms commonly responsible CSF analysis abnormalities: for meningitis: Increased CSF opening pressure In adults The fluid color is usually turbid or Streptococcus pneumoniae frankly purulent N. meningitidis Containing predominantly Listeria monocytogenes polymorphonuclear leukocytes Haemophilus influenzae Low CSF glucose level In neonates Increased CSF protein levels Escherichia coli Group B β-hemolytic streptococci In immunocompromised patients L. monocytogenes Herpes Simplex Encephalitis