neurology
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Neurology
1The SkullThe brains protector
2Made of 8 irregularly fused bonesSmooth on the outside, folds and ridges on the inner surface
The Skull3
The Cranial Vault4Foramen magnum
5The Brain (80%)
6Increased Brain Volume MassCerebral Swelling
7Blood (10%)Normally about 750cc of circulating volume
20% of the Cardiac Output
8Increased Blood VolumeHemorrhageVasodilatation
9Cerebrospinal Fluid (10%)
10
HydrocephalusIncreased CSF Volume11Intracranial Pressure (ICP)The pressure exerted by the brain tissue, intracranial blood, & CSF
12Normal ICP0-15 mm Hg
13
Tough MotherDura Mater14Dura MaterDouble layered
Inelastic, fibrous membrane
Holds the brain in place
15Epidural SpaceSpace that is directly above the Dura
Middle Meningeal Artery is present here
16Epidural Hematoma
17
Subdural Space18Cerebral lobes
19
MovementImpulsesFrontal lobe20
Spoken LanguagePersonalityFrontal lobe21
Sight UnderstandingTouch UnderstandingParietal lobe22
Distance and Position to ObjectsParietal lobe23Temporal lobeMemory
HearingWritten Words24
25
Controls Balance26
Damage Causes Ipsilateral Movement27
PonsMid BrainMedulla Oblongata
Brainstem28Neuro Assessment
29
ABCs FirstQuick HistoryLOCVital SignsPupilsEarly or Late?Early: restlessness, disorientation, lethargyLate: Increase BP, pupillary changes, seizures
Down and Dirty30AssessmentGLASGOW COMA SCALEBest Eye OpeningBest Verbal ResponseBest Motor Response
Best Eye Opening
Spontaneously-4To Verbal Command-3To Pain-2No Response-1
Best Verbal Response
Oriented, Converses-5Disoriented, Converses-4Inappropriate words-3Incomprehensible sounds-2No Response-1
Best Motor Response
Obeys Commands-6To PainLocalizes Pain-5Flexion Withdrawal-4Abnormal Flexion-3Abnormal Extension-2No Response-1
Glasgow Coma Scale
PediatricsVerbal (2 to 5 years)Appropriate words or -5Inappropriate words-4Persistent cries and/or screams-3
Glasgow Coma Scale
PediatricsVerbal (0 to 23 months)Smiles or coos appropriately-5Cries and consolable-4Persistent inappropriate crying and / or screaming-3
MildGCS Score 14-15
ModerateGSC Score 9-13
SevereGCS Score 3-8Severity of Injury
A desk scores a 3
Loss of ConsciousnessA,E,I,O,U TIPSAAlcoholEEpilepsyIInsulin (too much, too little)OOxygen (too much, too little)UUremia or other metabolic issuesTTrauma, toxicity, tumors, thermoregulationIInfections, ischemiaPPsychiatric, poisoningsSStroke, syncope or other neurologic / cardiovascular causes
Babinskis ReflexPresent when stroking of Planter surface of foot causes Flexing of great toeFanning of other toesNormally present in children 2yo indicates problem in corticospinal tract (nerve path spine to brain)
Abnormal posturing is a late sign of increasing ICP
DecorticateAbnormal flexionDecerebrateAbnormal extension
Meningeal SignsNuchal rigidityStiff neck, pain on flexionPhotophobiaPositive Brudzinskis Involuntary flexion of knees/hips when neck flexedPositive KernigsUnable to straighten leg when hip fully flexed in supine patient
Increased Intracranial Pressure
Neurological EmergenciesJuly 30, 2004CEN Review Course43Compensatory mechanisms are depleted. Results in rapid increase in ICP with only a small increase in volume.Produces a shift of brain contents to area of lesser pressure, herniation then occurs.Intracranial PressureIntracranial pressure reflectsBrainCerebrospinal fluidBloodAs intracranial pressure increases, cerebral perfusion pressure decreasesLeads to cerebral ischemia and hypoxiaIn a hypotensive patient, even a marginally elevated ICP can be harmful
Adequacy of cerebral perfusion pressure is most important
Increased Intracranial PressureInitially -intracranial volume increases-ICP remains stable.System becomes less compliant, or less able to tolerate increases in volumeLater, intracranial volume conts to increase, less compliance will be unable to buffer the increases and ICP will riseIncreased Intracranial PressureAssessmentEarly picture of increased intracranial pressure (IICP)LOCLoss of insightLoss of recent memoryRestless, irritable, uncooperative behaviorRequires more stimulation to get same responseSpeech less distinct Sudden quietness in a very restless patient
Increased Intracranial PressureEarly Increasing ICP Motor functionUsually contralateral to lesionPronator driftLoss of one or more grades on the strength scaleIncreased tone
Increased Intracranial PressureEarly Increasing ICPPupilsSluggish to light responseUsually unilateral Ipsilateral to lesionPapilledema or bulging of optic discsBlurred vision
Increased Intracranial PressureEarly Increasing ICPVital signsOccasionally tachycardicOccasional hypertensive swings
Increased Intracranial PressureLate Increasing ICPLOCArousable only with deep pain UnarousableMotor functionDense hemiparesisAbnormal flexionAbnormal extensionNo response (flaccidity preliminary to death)
Abnormal posturing is a late sign of increasing ICPDecorticateAbnormal flexionDecerebrateAbnormal extension
Increased Intracranial PressureDecreased LOCMotor DysfunctionsPupillary abnormalitiesImpaired ReflexesChanges in Vital SignsIrregular respirationsSign & Symptoms-Impending Herniation
Increased Intracranial PressureLate Signs Increasing ICP Vital signsCushings triadVery late sign of increasing ICP, last ditch effort to perfuse brainElevated SBPBradycardiaWidening pulse pressure
Increased Intracranial PressureInterventionsABCsMechanically decrease ICPOxygenateOsmotic Agents
Increased Intracranial PressureOsmotic Agents
Mannitol:reduces ICP within 15 minutes with continued effectiveness for 2-3 hoursMonitor serum osmolarity
Increased Intracranial PressureTreatment of ICPEasiest to manipulate is BP and CSFproper head alignment sedationSurgery
GoalKeep SBP>90Traumatic Brain Injury
58Traumatic Brain InjuryInjury to skull, brain, or both that is of enough magnitude to interfere with normal neurological function
59TRAUMATIC BRAIN INJURYNearly 2 million people sustain head injuries each year
60
70,000 die prior to hospitalization61
TBIAnother 25,000 die following hospitalization6290,000 people will have significant permanent neurological disabilities for the rest of their lives
63Traumatic Brain InjuryThe peak age for neurotrama is 15 to 30 years of age
64Causes of TBI65Highlight most involve vehicle of some sort or some violence
Primary Injury66ConcussionTransient impairment of neurological function caused by a mechanical forceRapid acceleration-deceleration
if repeated can produce a permanent deterioration in intellect
recent studies suggest long term impairment even with moderateconcussion moderate if loss of consciousness
ConcussionDiagnosisCT scanRule out other injuryClinical pictureHistory of injury
ConcussionInterventionsAssess neuro statusPatient/Family education return to facilityChange in LOCChange in pupilsProjectile vomitingSeizureInability to arouse
InterventionsEducate patient/familyPost concussion syndromeH/ADizziness (positional)TinnitusInability to concentratePersonality changeMemory disturbances
InterventionsEducate patient/familyPost concussion syndromeDurationDays to yearsSocial/occupationalDifficulty school/work
Skull Fractures
72Diastatic Skull FracturesFracture along suture line
Often seen in children
73Depressed Skull FractureA break in a cranial bone (or "crushed" portion of skull) with depression of the bone in toward the brainMay require surgical elevation
74
75Compound Skull FractureA break in or loss of skin and splintering of the bone.
76Basilar Skull FractureA Fracture that occurs somewhere in the Cranial Vault
77Basal Skull FracturesPeriorbital ecchymosis (Raccoon sign)
Anterior fracture
Basal Skull fractureRetroauricular ecchymosis (Battles sign)--Posterior fracture
Blood behind tympanic membrane--Middle Fracture
Basilar Fractures contdIf Basilar skull fracture suspectedNO nasal intubationNO nasal gastric tubes
Basal Skull FracturesCSF leaksrhinorrhea (nose)otorrhea (ear)Tests for CSF: Positve glucose Positive HaloBasal Skull FractureVIIth (Facial) Nerve PalsyOccur immediatelyOccur a few days after initial injury
Cerebral ContusionCerebral contusions fairly commonMostly occur in frontal and temporal lobesBruising of the brain tissue without puncture of pia Petechial hemorrhagesExtravasation of fluid from vessels
Cerebral ContusionDistinction between contusion and traumatic intracerebral hematoma ill defined.Contusions, can evolve into an intracerebral hematoma
Cerebral Contusion
Blunt forceHigh velocityLow velocityCerebral ContusionInterventionDecrease ICPMannitol to decrease water content in brainIncrease venous outflowDiscuss with family/patient evolution of contusion and need for monitoringDiscuss bizarre behavior- frontal lobeAssist family in understanding a contusion to brain stem has injured awake center in brainEpidural HematomaLocated outside the dura, within the skullBiconvex or lenticular in shapeMostly located in temporal or temporoparietal region
Epidural HematomaResult from tearing of middle meningeal artery D/T fractureBleeds arterial in originDoes not tamponade50% mortality
Epidural HematomaBrief loss of consciousness followed by lucid interval then rapidly progressive deteriorationTalk and die
Epidural HematomaBleeding can rapidly become mass lesionCause IICPBrain shiftUncal herniation
Subdural HematomaMore common than epidural hematomas30% of severe head injuriesTearing of bridging vein between cerebral cortex and a draining venous sinus
Subdural HematomaCover entire surface of hemisphere
Subdural HematomaPresentation can beAcute < 48 hoursSubacute 2 days to 3 weeksMore frequent in elderlyChronic > 3 weeks
Subdural HematomaClinical findings range from headache with nausea to comatose and flaccid
Subdural HematomaNon-contrast CT scanCrescent shaped massAncillary testsCBCChemistryCoag studiesT&C
Subdural HematomaInterventionsAcuteDecrease ICPNonacuteBurr holes
Subarachnoid Hemorrhage/Aneurysm ruptureworst h/a of my lifeAneurysms result from thinning vascular wallPrecipitated by hypertensive eventStrainingSexHeavy lifting
Subarachnoid Hemorrhage/Aneurysm ruptureAfter rupture vessel clamps down to prevent further bleedingResult inIschemia/infarctionBlood in subarachnoid space is irritantMeningeal signs
Subarachnoid Hemorrhage/Aneurysm ruptureComplicationsIncreased ICPVasospasmRebleedingIschemiaInfarctionHydrocephalus
Subarachnoid Hemorrhage/Aneurysm ruptureInterventionsABCsMonitor neuro statusFluids within normal range avoid dehydration increases hemoconcentration, increases vasospasmMonitor sodium usually fallsNormotensive BP until clipped then can be elevated
Penetrating/Perforating InjuriesA foreign object penetrates into the skull and brain
101Perforating & Penetrating Trauma
PerforatingPenetrating102Secondary Injury
103Causes of Secondary InjuryHypoxia
104Causes of Secondary InjuryHypotension
105Causes of Secondary InjuryCerebral edema1.Cerebrum
2. Skull
3. Cerebellum
4. Herniation of Brain Into Spinal Column
106Causes of Secondary InjurySustained hypertension
107Causes of Secondary InjuryHypercapnia
108Causes of Secondary InjurySeizures
109Causes of Secondary InjuryVasospasm
110Causes of Secondary InjuryMetabolic abnormalities (hypoglycemia)
111Causes of Secondary InjuryIschemia (#1 cause)
Normal Ischemic
112MAP & ICP GO HAND IN HAND
MAP=Diastolic x2Plus SystolicDivide that by 3ICP=The BrainThe CSFThe Blood 113Cerebral Perfusion Pressure (CPP)Pressure required to maintain adequate perfusion to cerebral tissues
MAP ICP = CPPNormal: 70-100 mmHg114CPP < 50 mmHgResults in Ischemia
115Spinal Cord InjuriesInvolve bruising or tearing of spinal cord substance from penetrating trauma or a fracture/dislocation of spinal column15-35 year oldsUsually due to trauma
Spinal Cord InjuriesMechanism of InjuryAxial loadingHyperflexionHyperextension Injury may involve onlySpinal cordVertebral bodyBoth
Spinal Cord InjuriesDamage to cordFrom extrinsic(bony and soft tissue injury)From intrinsic (hemorrhage, edema, hypoxia, biochemical changes
Spinal Cord InjuriesClassification CompleteTransection of the cord, no preservation of motor or sensory functionIncompleteSome cord sparing
Spinal Cord InjuriesRespiratory ComplicationsPhrenic nerve innervates diaphragm, exits cervical cord at C-3, C-4, C-5 if involved diaphragm involvedCompromises ability to breathIntercostal muscles (T-1 to T-12) involved becomes difficult to deep breath, cough
Neurogenic ShockEliminates the fight or flight protective response and permits the parasympathetic system to function unopposedResults in vasodilation below level of the injury, pooling of blood, decreased venous return to the heart, and decreased cardiac output
Neurogenic ShockLoss of ability to sweatBelow level of injuryD/T lack of innervation of sweat glandsTemperature lower than normalD/T break in connection between hypothalamus and sympathetic nervous systemLoss of body heat by passively dilated vascular bed of skin
Neurogenic ShockBlood pressure may not be restored by fluids aloneIn trying to normalize BP may cause fluid overload, pulmonary edemaBP best restored by judicious use of vasopressorsMay perfuse adequately without normal BP
Intravenous FluidsQuadriplegic patients-may fail to become tachycardic or may even become bradycardic in the presence of shock- due to loss of cardiac sympathetic tone.
Intravenous FluidsHypovolemic ShockPatient usually presents with tachycardiaNeurogenic ShockPatient usually presents with bradycardiaOverzealous fluids may cause PULMONARY EDEMA in Spinal Cord Injury PatientsIf blood pressure does not improve after fluid challenge, judicious use of vasopressors, may be indicated
Neurogenic ShockOrthostatic HypotensionRapid drop in BP when vertical position assumed.Blood supply to brain inadequate, syncope results. (brain damage and death can result)D/T loss of arteriole vasomotor tone below level of lesion so there is pooling of blood in abdomen and LEs when upright.Seen in patients with lesions above T-7
Spinal Cord InjuriesInterventionsABCsCervical Spine ImmobilizationO2Monitor VS, CO2Mechanical ventilation if neededMonitor LOC, UOPEnhance venous return to the heart
InterventionsSupport BP if neededAtropine if neededMethylprednisoloneNG tubeFoleyAttempt to have someone with patient most of the time
Autonomic HyperreflexiaNoxious stimuli produces sympathetic discharge that causes reflex vasoconstriction of blood vessels in skin and visceral bed below level of the injury
Vasoconstriction of visceral bed distends baroreceptors in the carotid sinus and aortic arch, body attempts to lower hypertension by superficial dilation of vessels above level of injury
Neurological EmergenciesJuly 30, 2004CEN Review Course128Autonomic HyperreflexiaAs spinal shock reverses, potential for dysreflexia should be considered in patients with injuries T-6 or above
Nursing intervention prevent conditions that are know to trigger autonomic hyperreflexia
Causative noxious stimulus most commonDistended bladder d/t kinked drainage tube
Autonomic HyperreflexiaClinicallySudden hypertension 240/120Pounding headacheAnxious Flushed face, neck, upper chest moistened with perspirationBlurred visionNasal congestionNauseaLower extremities goose flesh, cold
Autonomic HyperreflexiaInterventionsElevate HOBRelieve trigger mechanismTreat hypertension as neededResources for family/patient for self care
HeadachesOccur when there is traction, pressure, displacement, inflammation or dilation of pain receptors in brain or surrounding tissuesTwo types:PrimaryNo organic cause consistently identified (migraines, cluster, tension)SecondaryOrganic etiology (tumor, aneurysm, meningitis, temporal arteritis)
HeadachesAffects up to 75% population per year5% will seek treatment50 % of people with headache suffer migraineMechanism unknownBlood vessels that supply brain and surrounding tissue narrow, reduced blood flow, followed by reflex vasodilatation, swelling, and inflammation of cerebral blood vesselsHeadachesAssessmentHx of present illnessTime frameonset (migraines early morning)Occurrence (in groups, then period of remission)Aura (migraines with/without aura)Duration (tension 7 days, migraine 4-72 hours)
HeadachesPainCharacter and qualityIntensityTherapeutic measures implementedSuccess of therapeutic measuresLocationUnilateral (migraine), bilateral (tension), hatband
HeadacheSymptoms with migrainesAura possiblewithout aura most commonNausea/vomitingPhotophobiaDifficulty concentratingVisual changesMay see neurodeficits in complicated migraine
HeadacheCluster HeadachesBurning, sharp, severe unilateral orbital or temporal painPhotophobiaTearing, nasal congestion on affected sideMay have lid edema, red eye on affected side.Usually lasts < 1 hour, but may have multiple per day
HeadachesTensionDull, nonpulsating painNo photophobia, auraUsually starts at occiput and moves around bilaterally to frontal area (band like)
HeadachesPrecipitating eventEmotional (stress/depression)Metabolic (fever/menses)Flickering lights/televisionAlcohol abuse/withdrawalFoodFatigue or altered sleep wake cycle
HeadachesPhysical ExamNeuro examEdema over the sinusesDistended, twitching scalp vesselsFlushed, pale, or shiny skin
HeadachesDiagnostic procedures (organic)Skull x-raysCT scan
HeadachesInterventions/PlanningPhysical measuresHeat (muscular) or cold (vascular)Darkened roomMassagePsychological measuresStress mgtRelaxation techniquesBehavior modification
HeadachesInterventionsPharmacological measuresPreventive drugsVasoconstrictor agentsBeta blockersAnticonvulsantsAnalgesicsOxygen
Stroke
144This slide series, developed by American Stroke Association, a division of the American Heart Association, is a comprehensive overview of stroke:
Prevalence of stroke
Descriptions of the two major types of stroke
Risk factors for stroke
Warning signs of stroke
Effects of a stroke
Treatment of stroke
Prevention of stroke
Stroke rehabilitationWhat Is Stroke ?A stroke occurs when blood flow to the brain is interrupted by a blocked or burst blood vessel.
145If the human brain is to function at peak levels, blood must flow through its many vessels. If blood flow is obstructed at any point within the vessels, the brain loses its energy supply and becomes injured. If blood is obstructed for more than several minutes, the injury sustained by the brain cells becomes permanent and results in tissue death of the affected region. The loss or alteration of bodily function that results from an insufficient supply of blood to part of the brain is a stroke.What Is the Impact of Stroke? Stroke is the third leading cause of death in the United States
On average, someone suffers a stroke every 53 seconds
About 600,000 Americans suffer strokes each year
Every 3.3 minutes, someone dies of a stroke
146Stroke is the third leading cause of death in the United States, ranked behind heart disease and cancer.
Additional statistics regarding stroke include:
Someone suffers a stroke every 53 seconds.
About 600,000 Americans suffer strokes each year.
Someone dies of a stroke every 3.3 minutes.
What Is the Impact of Stroke? Stroke is a leading cause of serious, long-term disability
About 4 million Americans are stroke survivors
Stroke costs the U.S. $30 to $40 billion a year147Stroke is also one of the leading causes of serious, long-term disability and accounts for more than half of all patients hospitalized for neurological disease that is sudden in onset.
About 4.4 million stroke survivors are alive today (2.1 million are male; 2.2 million are female).
Stroke costs the U.S. between $30 to $40 billion a year.StrokeClinical syndrome consisting of a neurological deficit resulting from an interuption of blood flow to an area of the brain, rapid or gradual in onset, which persists for more than 24 hours.Two typesIschemic: Thrombotic or embolic occlusion of a cerebral artery resulting in infarctionHemorrhagic: Spontaneous rupture of a vessel resulting in intracerebral or subarachnoid hemorrhage
Neurological EmergenciesJuly 30, 2004CEN Review Course148
StrokeAssessmentHx present illness (time pattern)Classifications of stroke:TIA brief, lasting seconds to hours; < 24 hrsRIND lasting 48 hours or less, complete resolution of deficit, reversible ischemic neuro deficitStroke in evolution/progressive Symptoms last >24 hrs with progressive neurologic deterioration. Completed stroke permanent neurologic damageStrokeMedical HistoryDiabetesRheumatic heart diseaseRecent MICHFMigrainesHypertensionA-Fib
StrokePhysical ExamAnterior CirculationAlteration in LOCMotor deficitContralateral hemiparesis, hemiplegiaSensory deficitContralateral
StrokePhysical ExamAnterior CirculationSpeech deficitDysphasiaExpressive or receptive Dominant hemisphereVisual deficitLoss of vision in half of the visual field on same side
StrokePhysical ExamPosterior Circulation (vertebral basilar)Alteration in LOCMotor deficitmore than one limb
StrokePhysical ExamCranial nerve deficitDysphoniadifficulty producing voice soundsDysarthriadifficulty in articulationDysphagiadifficulty in swallowing
StrokePhysical ExamPosterior Circulation (vertebral basilar)Visual deficitsfield defects, cortical blindnessdiplopiaLoss of coordinationAtaxia
StrokeIschemicSudden, rapid onsetOccurs at sleep, rest
HemorrhagicSevere headacheMore gradual onsetSymptoms of increasing ICPOccurs during activity
StrokeInterventionsMaintain airway, breathing, circulationMonitor neuro status for changeMaintain venous outflow (head neutral position)Frequently monitorCerebral functionLOCBlood pressure
StrokeInterventionsSupplemental oxygen, pulse oximetryRSI: sedation, neuromuscular blockers, analgesicsInitiate measures to normalize blood pressure Keep SBP < 180, DBP
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