PowerPoint Presentation

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