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Pathophysiology of Neurological DisordersNervous System A&PCentral nervous systemBrainSpinal cordPeripheral nervous systemCranial nervesSpinal nervesNervous System PathwaysAfferent pathwaysAscending → carry sensory impulses toward the CNSEfferent pathwaysDescending → transmit motor impulses away from the CNSNerve PathwaysPeripheral Nervous SystemFunctionally → divided into:Somatic nervous system → pathways that regulate voluntary motor control (Ex: skeletal muscles)Autonomic nervous system → pathways that regulate body’s internal environment via involuntary control of organ systems (Ex: heart/circulatory system)Autonomic Nervous SystemANS further divided into:Sympathetic nervous system (SNS)Parasympathetic nervous system (PNS)Innervation of OrgansOrgans innervated by specific components of nervous system:Effector organs (Name an organ—ANY ORGAN!) organ that nerves go to and have an effect on.Cells of Nervous SystemNeuron → primary cellNeuroglia → “nerve glue” → supporting cell in CNS → provide structural support & nutritionSchwann cell → supporting cell in PNS → provide structural support & nutritionNeuronsNerve Injury & RegenerationMature nerve cells do not divide (once they are in place)Injury can cause permanent loss of functionSevered axon → swelling in portion distal to cut → neurofilaments hypertrophy → myelin sheath shrinks / disintegrates → axon degenerates & disappearsMyelin sheaths reform into Schwann cells that line up in a column between cut & effector organProximal to cut (similar changes back to next node of Ranvier)→ swelling/disperses Nissl substance → cell increases metabolic activity / protein synthesis → 7-14 days later, new terminal sprouts project from the proximal segment & may enter remaining Schwann cell pathway (limited to myelinated fibers & generally occurs only in the PNS)Regeneration in CNS limited by ↑ incidence of scar formation & different nature of myelin formedRegeneration depends on many factors—location, type of injury, inflammatory response, process of scarringThe closer (of injury) to cell body, greater chances of cell dying/not regenerating ConsciousnessArousal + Content of thoughtArousal: State of awakeness of individual (*Reticular activating system)Content of thought: Awareness of self, environment, and responsiveness (Ex: Cognition)Alterations in ArousalCaused by:Structural damage (trauma, vascular, infection)Metabolic disturbances (hypoxia, electrolyte disturbances, drugs, toxins)Psychogenic (rare--psychiatric)Patho of Alterations in ArousalProcesses depend on locationDysfunction may be diffuse (Ex: Encephalitis)Dysfunction may be localized (Ex: Tumor / Mass)Traumatic Brain InjuryBlunt force/closed head traumaCoup / contrecoup Extradural (Epidural)hematomaSubdural hematomaIntracerebral hemorrhageOpen/penetrating traumaBullets, knives, screwdrivers, etc.Coup-ContrecoupPatho of Coup/Contrecoup InjuryAcceleration impact→injury to local areaDeceleration impact→injury to opposite sideHematomas may form→increased intracranial pressure (↑ICP)Edema forms around & in damaged neural tissue→ ↑ICPBrain structures may be exposed to environmentInjury to brain tissue significantHigh risk for infectionSigns/Symptoms of Brain TraumaHeadache w/increasing severityVomiting (projectile/uncontrollable)Drowsiness ConfusionSeizure activityRespiratory depression/failureLoss of consciousnessLoss of reflexesPupillary dilationSpinal Cord InjuryCause: Pulling, twisting, severing, or compressing neural tissue of spinal cordLevel of injury will determine clinical manifestations (S/S) (Ex: hyperextension/hyperflexion of neck)See pictures on p. 397 in Patho book Most frequent area of fracture is c5-c7(whiplashOther common areas are T12, L1Peripheral Nerve TraumaCause: Crushing or cutting of neuronsSigns/Symptoms:NumbnessParesthesia (abnormal sensation ie. burning, pricking, tingling, tickling)PainSuccess for regeneration much higher in crushing injuries Cerebrovascular DisordersTransient ischemic attack (TIA)Brief period of inadequate cerebral perfusion→sudden focal loss of neurologic functionFull recovery usually within 24 hoursCerebrovascular accident (CVA)Stroke often causes permanent neurological deficitsDamage occurs within seconds to minutes due to loss of perfusionSigns / Symptoms of CVADepend on brain hemisphere & location of occurrence (right brain affects left half of body)Loss of consciousnessWeaknessDifficulty speakingDifficulty swallowingImpaired visionParesthesias Infectious CNS DisordersMeningitis (in the meninges)Causes: Bacteria, viruses, fungusEncephalitisCause: Usually viralPatho of MeningitisBacteria normally found in nasopharynxUsually starts w/upper respiratory infection → bacteria become blood borne →(thought to)enter CNS through choroid plexus → bacteria (or toxins) cause inflammation in meninges→ exudate causes thickening of CSF→ impedes flow, disrupts blood flow due to swelling Bacterial MeningitisSigns/Symptoms of Bacterial MeningitisTypical symptoms for infection +Severe headachePhotophobiaNuchal rigidity↓consciousnessSeizuresPetechial rashViral symptoms usually less severeFungal symptoms much slower & insidiousEncephalitisCause: usually viral—mosquito borne viruses & herpes simplex type IPatho: Virus reaches meninges → edema develops → ↑ICP → widespread nerve cell degenerationS/S: fever, delirium, confusion → unconsciousness, seizure activity, involuntary movement, abnormal reflexes, paresis & paralysis Alterations in Cognition and Motor FunctionDegenerative diseasesAlzheimer’s diseaseParkinson’s diseaseAlzheimer’s DiseaseMost common neurodegenerative disorder / most frequent cause of dementia in elderlyExact cause unknown → ?loss of neurotransmitter stimulation“Neurofibrillary tangles” & “senile plaques” found in cerebral cortex & hippocampusSigns/Symptoms of Alzheimer’s DiseaseEarly signs mimic natural aging processes:Memory lossLanguage lossConfusionRestlessnessMood swingsDifficulty in interpreting visual informationLater signs:Loss of personalityLoss of functionPsychotic symptomsRigidity/flexion posturingParkinson’s DiseaseChronic, progressive degeneration of neurons in the basal ganglia (corpus striatum)Associated with impaired motor functionOnset predominantly middle to old agePatho of Parkinson’s DiseaseCause: UnknownDegeneration of nigrostriatal pathway → reduction in neurotransmitter dopamine → alters excitability of striatum & release of other neurotransmitters (acetylcholine)Neurons in substantia nigra lose pigment & characteristic black colorSigns/Symptoms of Parkinson’s Disease{Most neural degeneration occurs before the onset of symptoms}Tremors (hands, arms, legs, face)RigidityBradykinesia (slowed movement)—may progress to akinesia (inability to move)Postural instabilityLate symptom: Dementia ................
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