Basics of Brain Anatomy amp Physiology Nervous system divisions See your flow Chart Neurotransmitter Action Vascular Disorders Ischemic or Hemorrhagic in Origin Vascular Disorders Interference with blood supply ID: 1040134
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1. Nervous System Disorders
2. Basics of Brain Anatomy & Physiology
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8. Nervous system divisionsSee your flow Chart
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10. Neurotransmitter Action
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13. Vascular DisordersIschemic or Hemorrhagic in Origin
14. Vascular DisordersInterference with blood supplySpecific area of ischemia leads to local damage and manifestations dependant on cerebral artery involvedHemorrhage Increased intracranial pressure will cause local ischemia and generalized symptoms.Global cerebral ischemiaImpaired perfusion of entire brainLoss of function and generalized cerebral edemaBrain death if not reversed quickly
15. Transient Ischemic Attacks (TIAs)May occur singly or in a seriesResult from temporary & localized reduction of blood flow in the brainWarning sign of impending strokeRecovery typically within 24 hours
16. Transient Ischemic Attacks (TIAs)Partial occlusion of an artery due to :AtherosclerosisSmall embolusVascular spasmLocal loss of autoregulation
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18. Signs & symptoms of tiaDifficult to diagnose after the attackDirectly related to location of ischemiaIntermittent short episodes of impaired functionExamples:muscle weakness in arm or legVisual disturbancesNumbness and paresthesia (abnormal sensations) in faceTransient aphasia or confusion may develop.
19. Cerebrovascular Accidents (CVAs)A CVA (stroke) is an infarction of brain tissue that results from lack of blood.Occlusion of a cerebral blood vesselRupture of cerebral vessel
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21. Cerebrovascular Accidents (CVAs)5 minutes of ischemia causes irreversible nerve cell damage.Central area of necrosis develops, tissue liquefies leaving a cavityAll function lost in this area.Surrounded by an area of inflammation. This zone will regain function following healing.
22. Types of CVAsOcclusion of an artery by an atheromaOften develop in large arteriesSudden obstruction by an embolus lodging in a cerebral arteryIntracerebral hemorrhage: most severe & destructive Caused by rupture of a cerebral artery in patient with severe hypertensionEffects are evident in both hemispheres.Complicated by secondary effects of bleeding
23. Types of CVAs: Know this info
24. 1st 48-72 hours:Edema & inflammation increase neurological deficitsTo limit permanent damage:Inflammation & pressure must be minimized rapidlyAdequate perfusion must be regainedComplications common including:Recurrent CVAImmobility issuesParalysis issues
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26. Risk factors include:Diabetes, hypertension, systemic lupus erythematosus, atherosclerosis, history of TIAs, increasing age, obstructive sleep apnea, heart disease, smoking, sedentary lifestyleCombination of oral contraceptives and cigarette smokingCongenital malformation of blood vesselsIncreasing age
27. Signs and symptomsDepend on the location of obstructionSize of artery involvedPresence of collateral circulation may diminish size of affected areaLack of voluntary movement or sensation on opposite side of the body.Initially flaccid paralysisSpastic paralysis develops weeks later
28. Emergency First Aid for Stroke
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30. TreatmentClot-busting agentsSurgical interventionGlucocorticoidsSupportive treatmentOccupational and physical therapists; speech-language pathologistsTreat underlying problem to prevent recurrences.Rehabilitation begins immediately.
31. Cerebral Aneurysms Localized weakness & dilation in the wall of an arteryCerebral aneurysms are frequently multiple.Usually at the points of bifurcation (branching points) on the circle of WillisKnown as Berry aneurysms
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33. Berry aneurysm
34. pathophysiologyRupture can result from sudden increase in BP due to exertion or hypertension Bleeding into subarachnoid space
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36. Signs & symptomsEnlarging aneurysm increases pressure on optic chiasm or cranial nervesLoss of visual fieldsVisual disturbancesIncreasing tension on BV wall & meningesLeads to headache
37. Signs & symptomsSmall, slow bleedHeadachePhotophobiaIntermittent dysfunction, slurred speech, weaknessNuchal rigidityStiff extended neck – blood irritates spinal nerves causing muscle contractions in neck
38. Massive tear leads to subarachnoid hemorrhageImmediate severe headacheVomitingPhotophobiaSeizures & loss of consciousnessSudden fatal increase in ICP and death
39. treatmentCT scan, MRI, Angiogram can locate aneurysmSmall unruptured asymptomatic aneurysms may be monitored with imaging scansIf diagnosed BEFORE rupture:Clipping or tying offClipped & bypassedPacked to eliminate blood flow
40. treatmentInitial rupture = 35% mortality2nd rupture = additional 15% mortality
41. Brain & Spinal cord Injuries
42. Types of Head InjuriesConcussion (minimal brain trauma)Cause: sudden excessive movement of the brainResult of mild blow to the head or whiplash-type injuryReversible interference with brain functionAmnesia and headaches may follow.Recovery usually within 24 hours, without permanent damageContusionBruising of brain tissue, rupture of small blood vessels, and edemaPossible residual damage
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44. Types of Head Injuries (Cont.)Closed head injurySkull is not fractured in injury.Brain tissue is injured and blood vessels may be ruptured.Extensive damage may occur when head is rotated. Open head injuries Involve fractures or penetration of the brain
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48. Types of head injuriesLinear fracture: simple cracks in the boneComminuted fracture: several fracture lines, may be fragmentedCompound fracture: brain tissue is exposed to environment, infection risk is high, severe damage if bone fragment penetrates brain tissue
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50. Types of Head Injuries (Cont.)Depressed skull fracturesInvolve displacement of a piece of bone below the level of the skull Compression of brain tissueBlood supply to area often impaired—pressure to brain
51. Types of Head Injuries (Cont.)Basilar fracturesOccur at the base of the skull Leakage of CSF through ears or nose is possibleContrecoup injury Area of the brain contralateral to the site of direct damage is injuredAs brain bounces off the skullMay be secondary to acceleration or deceleration injuries
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55. Etiologyi. Contact sports injuries (incl. multiple concussions)ii. Car/motorcycle accidentsiii. Fallsiv. Shaken baby syndromev. Alcohol (along with other systemic factors) can mask signs of injury, delay onset of cerebral edema and increased ICP but create a greater onset at later time.
56. Primary brain injuriesDirect injuriesLaceration or compression of brain tissueRupture or compression of cerebral blood vesselsRotational shear forcesCell damage & bleeding – leads to inflammation leads to increased ICP leads to ischemia leads to dysfunctionsCentral area necrotic & replaced by scar tissue or cystSurrounding area of inflammation may recover
57. Secondary injuriesResult from additional effects of cerebral edema, hemorrhage, hematoma, cerebral vasospasm, infection, ischemia related to systemic factors
58. HematomasClassified by location in relation to the meninges
59. Types of Hematomas
60. Epidural hematomaResults from bleeding between dura and skullSigns usually arise within few hours of injurySubdural hematomaDevelops between dura and arachnoidHematoma may be acute or subacuteTear in arachnoid may allow CSF to leak into subdural spaceCreates additional pressureHematoma disintegrates about 7 days postinjury.Hemolysis increases osmotic pressure → ICP
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63. Subarachnoid hemorrhageOccurs in space between arachnoid and piaAssociated with traumatic bleeding from the blood vessels at the base of the brainBlood mixes with CSF—no localized hematoma formationIntracerebral hematomaResults from contusions or shearing injuriesMay develop several days after injury
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66. Acute: signs present in about 24 hoursSubacute: increasing ICP develops over a week or so
67. Signs and symptomsFocal signs based on locationGeneral signs of increased ICPSeizures - Often focal but may be generalizedCranial nerve impairment may occurOtorrhea (otorrhagia) or rhinorrheaLeaking of CSF from ear or noseFever - May be sign of hypothalamic impairment or cranial or systemic infection Immobility complications
68. CT and MRI - Useful to determine extent of brain injuryTreatment Glucocorticoid agents - Decrease edemaAntibiotics - Reduce risk of infection Surgery may be necessary - Reduction in ICPBlood products and oxygen - Used to protect remaining brain tissue
69. Spinal Cord Injuries
70. Spinal Cord InjuriesResults from vertebral fracture or dislocationInjury of spinal cord, intervertebral disc, or supporting ligamentsEtiologyCar accidents, sports injuries, forceful traumas
71. Spinal Cord InjuryResults from fracture, dislocation of vertebraeCompresses, stretches, or tears spinal cordCervical spine injuriesMay result from hyperextension or hyperflexion of neck with possible fractureDislocation of vertebraMay crush or compress spinal cordCompression Causes injury to spinal cord when great force is applied to top of the skull or to the feet
72. Types of Spinal Cord Injuries
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75. Classification of vertebral fracturesSimpleSingle line breakCompressionCrushed or shattered bone in multiple fragmentsWedgeDisplaced angular section of boneDislocation Vertebra forced out of its normal position
76. Damage may be temporary or permanent.Axonal regrowth may occur.Laceration of nerve tissue by bone fragmentsUsually permanent loss of conduction in affected tractsComplete transsection or crushing of cordIrreversible loss of all sensory and motor function at and below the level of injuryPartial transection or crushingMay allow recovery of some function
77. BruisingReversible damageProlonged ischemia and necrosisLead to permanent damageRelease of norepinephrine, serotonin, histamineReleased by damaged tissue—vasoconstrictionAssessment using dermatome mapAssessment of movement and sensory responsesCan determine the degree of damage or recovery
78. Dermatomes
79. Spinal shockInitial period after injury—ANS reflexes absentConduction of impulses ceasesRecovery dependent on amount of bleeding and surgical intervention Inflammation gradually subsides.Damaged tissue removed by phagocytesScar tissue formationReflex activity resumes below level of injury.No communication with higher levels of brainControl of reflexes below the level of damage is lost.
80. Effects of Spinal Cord Damage
81. Effects of Spinal Cord Damage (Cont.)
82. Two stages in post-traumatic periodSpinal shockRecovery and recognition of extent of functional lossSpinal shockInitially, all neurological activity ceases below and slightly above the level of injury.No reflexes presentCondition may persist for days or weeksFlaccid paralysisSensory loss at and below injured areaAbsence of all reflexesLoss of central control of autonomic function
83. RecoveryGradual return of reflex activity below level of injuryNo impulses through specific area of damageHyperreflexia may develop. Gradually, extent of damage will be revealed. Voluntary motor activity and sensory impulses are blocked at and below the level of damage.Many injuries are incomplete, and permanent damage varies among individuals.
84. Tetraplegia (quadriplegia)Paralysis of all four extremitiesParaplegiaParalysis of the lower part of the trunk and legsIpsilateral paralysis and contralateral loss of pain and temperature sensationDepends on the point of decussation and location
85. Autonomic DysreflexiaMassive sympathetic reflex response that cannot be controlled from the brainOften initiated by infection, genital stimulation, or other stimuli Leads to:Increased blood pressureVasoconstriction below the injuryVasodilation above the injuryTachycardia
86. Autonomic Dysreflexia Following Spinal Cord Damage
87. Complications of Spinal Cord InjuryUrinary tract infectionsPneumoniaSkin breakdownSpasm and painDepression
88. Treatment Treatment and rehabilitation begin at the time of injury.Immobilize spine.Maintain breathing and prevent shock.Hospital traction or surgeryRelieve pressure and repair tissuesGlucocorticoidsReduce edema and stabilize vascular systemOngoing care to prevent complications related to immobility
89. Intracranial pressure (ICP)
90. ICPSkull contains brain tissue, blood & CSFAt normal volumes = normal pressures remain constantTemporary fluctuations occur with activities
91. Monro-Kellie doctrineFluids are NOT compressible AND the Cranial vault is non-expandable – so its volume remains constant.Therefore: Blood, CSF & Brain Tissue must remain in constant equilibriumAn increase in one aspect must cause a corresponding decrease in other aspects.
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94. ICPNotes Example: cerebrospinal fluid = intracranial pressure = arterial blood flow = space for brain tissue (which gets compressed & eventually dies due to ischemia)
95. ICP Monitoring
96. Response to ischemiaPulse pressure – difference between systolic & diastolic pressureBP dropAbnormal respiratory patterns: Cheyne-StokesPtosis
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98. Response to ischemiaIpsilateral (same side) pupil becomes fixed & dilated then both pupils (“blown”)NystagmusElevated CSF pressure with composition/color changeBrain herniation & death
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100. Alzheimer’s Disease
101. characteristicsNeurofibrillary tangles and beta-amyloid protein plaques# and distribution are significant factors
102. characteristicsCortical atrophy, dilated ventricles & widening of sulciDeficit of neurotransmitter ACh
103. etiologyUnknown: genetic, viral, metabolic, exposure to toxins4 defective genes (on chromosomes 1,4,19, 21) associated with early onset AD as an autosomal dominant trait.
104. Signs & symptomsOnset – insidious over 10-20 yearsEarly stage: gradual loss of memory & lack of concentration, ability to learn new info& to reason is impaired, behavioral changes & mood swings
105. Signs & symptomsMiddle stage: cognitive function, memory & language skills continue to decline problem solving, mathematical ability & judgement are poor. Daily activities difficultApathy, indifference, & confusion
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107. Signs & symptomsLate stage:Lack of awareness or interest in environmentLack of familial recognition & relationshipsIncontinence & degenerative motor functions (due to decrease in Ach.
108. treatmentMedications show some temporary improvementProvide for safe environment: daily routine & secure environment is importantTreat physical/emotional symptoms as neededClinical trials continue focusing on plaque development