Acute Disorders of Brain Function PDF

Acute Disorders of Brain Function  Case Study A 19-year-old female was brought to the ED after suffering a road traffic accident. Eyewitnesses report that the patient lost consciousness briefly after the accident but regained consciousness soon after. While being transpo...

Acute Disorders of Brain Function  Case Study A 19-year-old female was brought to the ED after suffering a road traffic accident. Eyewitnesses report that the patient lost consciousness briefly after the accident but regained consciousness soon after. While being transported to the hospital, the patient’s level of consciousness declined rapidly. Physical examination revealed a Glasgow Coma Scale (GCS) of 6, and a dilated nonreactive left pupil. CT scan of the head revealed a biconvex high density compressing the left parietal lobe and a fractured left temporal bone.  Case Study (cont.) What is your diagnosis? Epidural hematoma The patient regained consciousness for a brief interval before losing consciousness again. Why? She had a lucid interval following the initial injury; this is followed by a decline in her level of consciousness as the hematoma expands and compresses the brain, resulting in transtentorial herniation Which blood vessel was injured in this patient? Middle meningeal artery  Intracranial Hematomas Intracranial hematomas Copstead, Pathophysiology (2019)  Mechanisms of Brain Injury Primary brain injury Secondary brain injury Occurs as a direct result of the initial Progressive damage resulting from the insult body’s response to the initial insult Traumatic brain injury Ischemia and hypoxia Concussion Excitatory amino acids Contusion Intracranial hematomas Cellular energy failure Nontraumatic Reperfusion injury Cerebrovascular disease Abnormal autoregulation Cerebral aneurysm Arteriovenous malformation Increased intracranial pressure (ICP) CNS infection Brain compression and herniation Traumatic Primary Brain Injury  Traumatic Brain Injury Traumatic brain injury (TBI) is a leading cause of death and disability in the United States Most head injuries occur in transportation-related accidents, falls, firearms, and sports accidents Severity of TBI is classified by the Glasgow Coma Scale (GCS) on admission or the lowest in the first 48 hours after admission: Mild GCS score 13-15 Moderate GCS score 9-12 Severe GCS score 3-8 Glasgow Coma Scale (GCS) Glasgow Coma Scale (GCS) Netter’s Neurology (2020)  Traumatic Brain Injury Concussion Mild traumatic brain injury; most common injury encountered by military personnel and athletes Alteration or loss of consciousness (less than 30 minutes) but no evidence of brain damage on CT Headache, nausea, vomiting, dizziness, fatigue, blurred vision, cognitive and emotional disturbances Post-concussion syndrome Secondary impact syndrome Normal brain CT scan Netter’s Neurology (2020)  Traumatic Brain Injury: Contusion An area of brain tissue damage (necrosis, laceration, bruising) Focal injuries (coup) localized to site of impact Polar injuries (coup– countercoup) due to acceleration– Brain contusions deceleration movement Youmans and Winn Neurological Surgery (2017) of the brain within the skull, resulting in double injury (usually opposite focal injury)  Traumatic Brain Injury Diffuse axonal injury Due to movement of the brain within the skull Estimated to occur in over 50% of all comatose head trauma patients; however, Diffuse axonal injury Rosen’s Emergency Medicine (2018) in milder cases, there is no specific acute focal traumatic lesion noted on a head CT scan or on structural MRI scan  Traumatic Brain Injury: Epidural Hematoma Collection of blood between dura and skull Primary injury is minor, suffer only a brief period of disturbed consciousness followed by a period of normal cognition (lucid interval), then consciousness rapidly deteriorates Typically involves arterial injury thus rapid onset of symptoms Diagnosis: CT scan Treatment: surgery to remove hematoma Epidural hematoma Netter’s Neurology (2020)  Traumatic Brain Injury: Subdural Hematoma Collection of blood between dura and outer layer of arachnoid membrane Typically involves bridging veins; symptom onset may be slower Acute: symptoms within 24 hours of injury Subacute: increased ICP (headache, vomiting, blurred vision) 2–10 days later Chronic: variable presentation. Days to weeks. Prone to rebleeding Diagnosis: CT, MRI Treatment: remove tissue and clot Subdural hematoma Netter’s Neurology (2020)  Traumatic Brain Injury: Subarachnoid Hemorrhage Collection of blood between arachnoid and the pia mater Traumatic: due to rupture of bridging veins that pass through the subarachnoid space Nontraumatic: more commonly associated with rupture of cerebral aneurysms or arteriovenous malformations; arterial in origin Blood spreads throughout CSF, causing meningeal irritation, hydrocephalus, headache, vasospasms, ischemia Intracranial hematomas Copstead, Pathophysiology (2019)  Cerebral Aneurysm Congenital defects weaken the medial layer of the artery, the dilated portion fills with blood and eventually burst, causing hemorrhage; most found in circle of Willis High blood pressure, acute alcohol intoxication, and recreational drug use (especially cocaine) are implicated 60% will either die or suffer permanent disability Cerebral aneurysm The Netter Collection of Medical Illustrations: Brain (2013)  Arteriovenous Malformation Capillary system fails to develop appropriately with arterial blood shunted directly into the venous system; causes the vessels to progressively enlarge; becomes a congested mass of enlarged vessels that can burst Arteriovenous malformations Ferri’s Clinical Advisor (2020) Nontraumatic Primary Brain Injury  Cerebrovascular Disease Cerebrovascular disease causes abnormal blood flow to the brain Cerebrovascular disease includes: Transient ischemic attacks (TIA) Cerebrovascular accident (CVA): Ischemic stroke Hemorrhagic stroke Types of stroke The Netter Collection of Medical Illustrations: Brain (2013) Transient Ischemic Attacks (TIA) Neurologic deficits completely resolve. Neurologic symptoms typically last only minutes, but they may last as long as 24 hours. TIAs are important warning signs of thrombotic disease and carry a significant risk for subsequent stroke.  Cerebrovascular Accident (CVA) (Also Known as Stroke) Sudden onset of neurologic dysfunction due to brain infarction as a result of cardiovascular disease The fifth leading cause of death in the United States Most common form of stroke is ischemic More common in men than women Risk factors are similar to other atherosclerotic vascular diseases (hypertension, DM, hyperlipidemia, smoking, advancing age, family history)  Ischemic Stroke Results from sudden occlusion of a cerebral artery secondary to thrombus formation or emboli Thrombotic strokes associated with atherosclerosis and coagulopathies Embolic strokes associated with cardiac dysfunction or dysrhythmias (atrial fibrillation) Types of stroke The Netter Collection of Medical Illustrations: Brain (2013)  Hemorrhagic Stroke Hemorrhage within the brain parenchyma Usually occurs secondary to severe, chronic hypertension Most occur in basal ganglia or thalamus Degree of secondary injury and associated morbidity and mortality is much higher in Hemorrhagic stroke The Netter Collection of Medical hemorrhagic stroke than Illustrations: Brain (2013) ischemic stroke  Clinical Manifestations of CVA Clinical manifestations vary depending on the blood vessel affected but generally contralateral hemiplegia and hemisensory loss, aphasia, and partial visual field defects Clinical manifestations of stroke Treatment The Netter Collection of Medical Illustrations: Brain (2013) Ischemic stroke: angioplasty or thrombotic therapy Hemorrhagic stroke: hypertension management  Stroke Sequelae Motor and sensory deficits (contralateral) Motor: flaccidity or paralysis; recovery occurs with onset of spasticity Sensory: may involve neglect or visual impairment Language deficits Aphasia occurs with brain damage to the dominant cerebral hemisphere Cognitive deficits Impaired language skills, spatial relationship skills, concentration, reasoning, and short-term memory  CNS Infections Organisms may gain access to the CNS in the following ways: Hematogenous (through the bloodstream) Direct extension from a middle ear or paranasal sinuses, along peripheral and cranial nerves Vertical (through maternal–fetal exchange) Risk factors: immunocompromise, debilitation, poor nutrition, radiation, steroid therapy, contact with vectors Meningitis commonly associated with bacterial infections (most life- threatening); encephalitis usually viral Sources of bacterial meningitis The Netter Collection of Medical Illustrations: Brain (2013)  Bacterial Meningitis Classic presentations: headache, fever, stiff neck (meningismus), and signs of cerebral dysfunction (confusion, delirium) Kernig’s sign and Brudzinski’s sign Netter’s Infectious Diseases (2012)  Bacterial Meningitis Causative bacteria depends on age group, but most common bacteria are Streptococcus pneumoniae Common causative bacteria by age group The Netter Collection of Medical Illustrations: Brain (2013)  Encephalitis Inflammation of the brain commonly caused by viruses such as West Nile virus, Western equine encephalitis, herpes simplex Treatment: supportive with control of symptoms, antiviral, steroids, antiseizure, Herpes simplex encephalitis fluid resuscitation The Netter Collection of Medical Illustrations: Brain (2013)