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Neuro Cranial Nerves  Cerebrovascular Disease · most frequent neurological disorder of adults 3rd of leading morbidity & mortality in US · cause - 1st heart di...

Neuro Cranial Nerves  Cerebrovascular Disease · most frequent neurological disorder of adults 3rd of leading morbidity & mortality in US · cause - 1st heart disease - IndCancer Any pathological · disorder that involves the blood vessels of the brain hemounage ↳ thrombosis, embolism,  Stroke · National Stroke Association of permanent stroke is leading cause disability - 15% are institutionalized - not 30%% dependent on activities of needed daily living - for exam 60%decreased socialization outside home - · American Heart Association $15-20 billion spent annually - on stroke and stroke related disorders stroke Spotting a Balance Loss Eye sight changes Face drooping Arm Weakness Speech Difficulty Time toCall all stept Stroke Etiology ovascullar Obstruction 3/1 (thrombi or emboli) ↳ Lischemia infartion I Tissue Hemo naghoxygen · dying Yu(hypertensive vascular disease -uptured aneurysm ↳arteriovenous malformation Lsubarachnoid or intracerebral bleeds Epidemiology 0750 ,000 strokes annually omenswomen Risk Factors · Cardias Disease (a fib) smoking - - ↑Cholesterol Hypertension - - DM BC pills Obesity - - - Prevention - Increase cranial pressure > call- · - dilated pupils > herniations lifestyle changes - - pushes increased brain I as - warfarin or aspirin stem down further-inhibits La fil function Brocas Area (breathing etc) , strokes Infarct vs Ischemic Stroke Infarct - Results of thrombus or embolus Oxygen deprivation of cerebral tissue - microscopic necrosis of neuron Lnecrotic area is infarcted in the first 12-24 hrs but Ischemic I can't see anything - Decline in cerebral blood flow can hemorrhagic for - zone of irreversible infarction surrounded salvageable by potentially area - lischemic penumbra Clinical Manifestations & - sudden onset of neurological impairment Local - weakness dysphagia - aphasia - Resolves within 24hrs TIusually last minutes LIWV Stroke Diagnosisa Must be Rapid · Identify I patients who can receive thrombolytic therapy 3hr from time of symptom onset to thrombolytics time to needle when was normal last Goal · ↳save damaged brain tissue and minimize permanent deficits Diagnostic Test-no contrast i is makesurether · CT Scan who contrast · Neurological Exam of Health Stroke scale national institutes score gives severity of stroke. LoG gaze,, visual , motor, sensory language Clinical Management Four · Primary Goals - Restoration of Cerebral blood flor Prevention of recurrent thrombosis NeuroprotectionIncreased I supportivearea ~ I · save as much ischemic area as possible - Oxygen - Blood flow - Glucose stocot- Pharmacological Managemento PA - should be started within 3hrs of onset of When pt was last seen symptom free Symptons - Older than lay /0 - UHSS Score-deficits tumors negative for - O bleeds or Antiplatelet · Anticoagulants · Anti-hypertension · -Lower BP gradually ~ In acute stroke brain is accustomed to higher BP Lower iP too fast leads to decreased cerebral perfusion & Nursing · Assessment uneurologic changes · Administer +-PA · Monitor oxygen and glucose lls= 100 glucose case status · Prevention commu bedsores, aspiration , contractures,thrombophlebitis mos status , collaborative care · social workers;POTiNutrition : Spiritual care etc.  C Stroke P+  Intracranial Pressure Monitoring LICP) * Monitors the pressures within the skull · to be made measurements allow for decisions - as to what interventions should occur in order to prevent further cerebral ischemia -help to prevent herniation of the brain stem Imonitoringar Catheter (IVC) most common of ICP type monitoring · Normal measurements L OtOmmHy - upperlimitsmmmmy coughing os is Lsymptomatic 20-25mmlty · Monitor for obstruction of the catheter Indications for ICP · Head Injury-GCS : 9 Stroke · Bran Tumor · ippt2 ICpTherapy · Mannitol Hypertonic crystalloid decreases cerebral edema Bolus 10 25-2. g/kg body weight I Don't need to knowl Lmust -concentration of fluid measure semm Iserum OSMO> osmolarity every bloons 320mOsm may develop acute tribular Holey Cath necrosis ↳ Diuresis ICP Care positioning · CHOB 38 Respiratory · Hyperventilation to lower PaDe to 30mmily situations ↳But only in emergency Pain/Agitation/Moxious Stimuli · minimize Temperature · maintain normal Monitor diastolic) pressure systolic - -VIS and ICP (pulle Os Signs and Symptoms of Increased IC · change in LOC · Headache Confusion-lethargy vomiting · · not associated volhaused Pupil changes · L size and crisually projectile response to light seizure · Visual Disturbances Cushings Triad (veffe) * · Hypertension/Widened - pulse pressure Bradycardia higher (bounding) - Cheyne-Stoke respiration score - -worst · Posture decerebrate /decorticateto the core - Continued · decraway foc(Istupor(coma)  Head Trauma Types · Acceleration · when a moving object hits non-moving head a · Acceleration Deceleration - ·whenamoving head hits a stationary obsethe When the read - isstruck causing the brain to more within the cranial vault Rational · - Forces cause the brain to twist within the skull  Defining the Severity of Head Injury · Mild-GCS 13to 15. - may have Loc or amnesia for 5-homins no ct changes - Moderate GCS 9 to 12 · - - LOC or amnesia for 1-24hrs have abnormal CT may - · severe-GCS 3702 i We must intubate LOC or amnesia for >24hrs - may have contusion , laceration , intracranial hematoma - On CT # *  Concussion Mild traumatic · brain injury (TBI) have LOC may or may to not - - often unable recall events that lead toTBI - often short term memory problem problems after event - often do not seek medical attention Signs · and symptoms - normal CT - headache - decreased attention span dizzyness - emotional lability/Irritability -  contusion Focal injury that ranges in severity · - Result of laceration of microvessels on the surface of cortex - Found on CT - May result in Cerebral Edema speaks 24-72 hr Signs and Symptoms - Altered LOC - Headache - Nausea/Vomiting  Epidural Hematoma# Collection of blood between the dura · skull laceration of the extradural - caused by artery intervention require surgical - Signs Symptoms · and - Classic LLOC-regain consciousness-rapid deterioration - Posture to unconsciousness - unilateral dilation of pupil late ;  Subdural Hematoma D · collection of blood below the dura and above the arachnoid covering common in most elderly and alcoholics - -venous bleed ; bridging veins Three Categories Acuteneeds surgical intervention ~ Symptoms within 24-48hrs HA Worsening - focal neurological deficit - - unilateral pupil abnormality - decreasing LOC - increased ICP Subacute days a -sympomsonset we of slow onset symptoms very - chronic - Initial small bleed that does not cause symptoms of the - overtime capillary ofleaking causes expansion masse symptoms increased ICP ofteninedrywhstofrequentfas ace drains - head of bed flat; decrease tension on bridging veins  Secondary Brain Injury All events that lead to further brain after damage · the initial Increased ICP - injury - Cerebral ischemia - systemic hypotension - local or systemic infections · Results in - cerebral infarction - coma - herniation · Prevention maintain BP avoid hypotension = - - maintain good ventilation Lavoid hypercaphia and hypoxia - avoid seizures Monro-Kellie Doctrine The contents of the cranium-brain , CSF, and blood have - a fixed volume ; any addition to the volume must be balanced by a reduction in one of the other components  Herniation Syndrome Cushing's · Triad Thethreatestagesofherniatioause pressure - Ldecreased heart rate pattern Lirregular respiratory earl Must · be recognized  Causes of TBI of TBI Management - monitor LOC - monitor US - monitor for increased ICP as with strokes prevent further complications - - - maintain oxygenation and nutrition  * Guillan-Barre' Syndrome autoimmune response , causing myelin to Inflammatory peripheral go cowny) · neuropathy -Lymphocytes and macrophages strip myelin from axon : be seen in May · G Gradual peripheral nervous system i of - - cranial nerves B Block Spinal nerve roots Si sensation - Etiology · nuclear Lautoimmune response is suspected · Occasionally vaccinations ; Flu shot · Half patients have febrile illness 2-3ks prior to onset of = symptoms Respiratory or gastrointestinal associated ~ campylobacter jejuni LCMV Virus ↳ Epstein-Barr - St Group · 2ndgroup Pure motor sensory system mostly distal motor cranial nerves predominantly - rapid onset of weakness proximal muscles - ↳ par Guillain-Barre' syndrome Epidemiology montwomen - any age - - annually 2 cases per 100, 000 population Pathophysiology the axon is lost sheath surrounding myelin myelin sheath - closs of newe impulses T-cells inflammation problem lymphocyte causes - cells the vessel walls to the migrate through peripheral - newve edema and perivascular inflammation - then break down the - macrophage myelin  & parts Guillain-Barre' Syndrome Clinical Manifestations Symmetrical - weakness/tingling in extremities - weakness prominentinproximal musdesbeginnis - - paresthesias occur , DT2 disappear within first few days of symptoms extend to involve the cranial may neves - interferes with the drive - frequently respiratory - autonomic disturbances retention Lurinary zorthostatic hypotension symptoms progress over several loks - at - level of paralysis may stop any point - most function returns in descending order - Demyelination occurs rapidly -remyelination occurs 1-2mm per day part 4 Guillain-Barre Syndrome Diagnosis- Based on clinical symptoms - MG studies - Lumbar puncture for CSE studies celevated protein Lelevated LBCS Pulmonary Function studies - Management Hursing Supportive Clinical Management Mechanical ventilation - - heparin 5000 units - compression devices - nutrition/ fluids - intubation/ventilator pain assessment Intervention plasmapheresis (Plasma Exchange - - Hegretol 3 neurontin -change - skin eye care - bowel/bladder IgG and IgA nerve - com exercises complications Given over 3-3 days endings Preventing - DUT Pneumonia Psychological Issues cannot move-but they can near is feel that the patient pain · Be aware Anticipated needs · sedation Consider · using · Find for the patient to call for assistance a way  Guillain-Barre Syndrome sparts Favorable · Low Morality Rate 2 s% during the acute phase · Disability Deficits -210-20 % have significant disabilities o Recovery L80 % have full recovery months within 6-12 renal Hong term ↳ may have life long weakness - vapid Demylinezation Graduaa sensation · · oremyelinzation gradual sensation -Imm a day -autoimmune disease · parettesislegst) · inflammation of myelin sheath , respiratoryorgas is cause · peripheral system - recover 6-12months urinary retention meds ; pain · · · orthostatic hypotension Tegrefor · Diagnosisprotein colnormalis Neurotin Lumbar