NURS 324 Acute Neuro abnormal motor responses ANS decorticate posture decerebrate posture acute bacterial meningitis ANS rapidly destroys capillary structure and invades brain leads to cerebral edema and alterations in cerebral blood flow release of endotoxins due to bacterial replication and lysis in CSF massive recruitment of neutrophils to pia mater acute subdural hematoma ANS seen within 24 hours after injury can lead to brain herniation anterior cord syndrome ANS infarction of anterior spinal artery or pressure by disk damage to anterior 2 3 of cord posterior 1 3 preserved assessing pupils ANS PERRLA shape size symmetry reactivity to light change in size with accommodation autonomic dysreflexia ANS a sudden massive reflex sympathetic discharge associated with spinal cord injury at level T6 or above where descending inhibition is blocked in response to sensory input below level of SCI full bladder or rectum painful stimuli may occur after spinal shock resolves and be a recurrent complication autoreglation ANS compensatory alteration in the diameter of the intracranial blood vessels maintains a constant blood flow during changes in cerebral perfusion pressure lost with increased ICP bacterial meningitis interventions ANS urgent antibiotic therapy with broad spectrum 3rd gen cephalosporins vanc and or ampicillin bacterial meningitis organisms ANS pneumococcus Strep pneumoniae meningococcus Neisseria meningitidis Brown Sequard syndrome ANS incomplete sci penetrating injury damage to hemi section of anterior and posterior cord hyperextension or flexion injury compression fracture loss of voluntary motor function loss of proprioception on ipsilateral side contralateral loss of pain and temp sensation C2 C3 level sci ANS some neck control but none lower intermittent ventilation categories of diffuse brain injury ANS mild concussion classic concussion mild DAI moderate DAI severe DAI cauda equina ANS fracture or dislocation of spine or large disk herniation damage to conus meduallaris flaccid bowel blaccid bladder and or sexual dysfunction cause of cerebral edema ANS changes to vascular permeability trauma tumors hypoxia infection hemorrhage infarction movement of proteins to ECF cause of increased ICP ANS increased volume CSF mass effects bleeding edema causes other structures to be compressed causes of TBI ANS trauma MVA and falls tumors stroke infection central cord syndrome ANS acute cord compression injury to central gray or white matter fibers in corticospinal tract that control arms more centrally located than those controlling legs cerebral edema ANS increase in the fluid content in the brain tissue increases ICP cerebral perfusion pressure CPP ANS difference between MAP and ICP CPP MAP ICP normal is 70 90 mmHg pressure gradient that drives blood into the brain chronic subdural hematoma ANS symptoms may not arise for weeks post injury may need surgical evacuation of gelatinous blood chronic traumatic encephalopathy CTE ANS progressive dementing disease secondary to repeated head trauma sport related blast injuries in soldiers work related tau neurofibrillary tangles present in brain cingulate herniation ANS less severe cerebrum moves across center classic concussion ANS loss of consciousness 6 hours amnesia headache for days brief period of bradycardia hypotension clinical manifestations of increased ICP ANS decreased LOC widened pulse pressure bradycardia clinical manifestations of level of arousal ANS LOC breathing pattern pupillary reaction and oculomotor response motor responses clinical presentation of meningitis ANS severe onset of headache fever nuchal neck rigidity may have nausea projectile vomiting photophobia and altered LOC petechial rash sign of DIC clinical presentation of stroke ANS depends on extent of blood flow interruption hemiplegia or hemiparesis one sided weakness or paralysis sudden confusion changes in speech or swallowing sudden vision changes in one or both eyes sudden trouble walking dizziness or loss of balance sudden severe headache common pathways of brain damage ANS hypoxic and ischemic injury excitatory amino acid injury cerebral edema increased intracranial pressure often overlap complete SCI ANS complete loss of motor sensory reflex and autonomic function below level of injury spinal shock complications of DAI s ANS post concussion syndrome post traumatic seizures chronic traumatic encephalopathy CTE conditions that can lead to meningitis ANS basilar skull fractures otitis media sinusitis sepsis neurosurgery immunocompromised contra coup injury ANS secondary impact of brain onto cranium when head snaps back into position cytotoxic cerebral edema ANS actual swelling of neurons increase in intracellular fluid hypo osmotic states water intoxication damage to anterolateral tract leads to ANS loss of pain temperature coarse sensation damage to corticospinal tract leads to ANS loss of motor function decerebrate posture ANS upper extremity extension means there is severe damage involving the midbrain and upper pons decorticate posture ANS upper extremity flexion means there is hemispheric damage above the midbrain delirium ANS acute stage of confusion usually associated with ANS overstimulation neurotransmitter imbalance develops slowly over 2 3 days common in acute care settings determining level of sci ANS motor and somatosensory testing discriminative touch and temperature diagnosing meningitis ANS history and physical blood and nasal cultures CSF analysis diffuse brain injury diffuse axonal injury ANS mechanical injury from high levels of acceleration and deceleration or rotational forces causes shearing of delicate axonal fibers and white matter tracts that project to the cerebral cortex dysphasia ANS alteration in speech caused by abnormal impact on L MC artery expressive vs receptive effects of brain herniation ANS rising ICP leads to rostal to caudal head to tail failure from diencephalon to midbrain ocular followed by pons motor and eventually medullary respiratory function altered pupillary reaction to light decerebrate posturing death due to respiratory failure effects of diffuse brain injury ANS acute brain swelling caused by increased intravascular blood flow vasodilation increased cerebral blood volume widespread affective and cognitive dysfunction effects of LMN syndrome ANS absent tone atrophy paralysis paresis fasciculation common no Babinski may involve on one limb and progress effects of primary brain injury ANS cerebral