2Rapid Neurologic Assessment Glasgow Coma ScaleResponse to painful stimuli—sternal rub, trapezius squeezeLevel of consciousness—even a subtle change is the first indicator of a decline in neurologic statusDecortication—abnormal posturing seen in the client with lesions that interrupt the corticospinal pathways. The patient’s arms, wrists, and fingers are flexed with internal rotation and plantar flexion of the legs.
3Rapid Neurologic Assessment cont. Decerebration-abnormal posturing and rigidity characterized by extension of the arms and legs,pronation of the arms, plantar flexion and opisthotonos (kind of spasm with head and feet bent backward and body bowed forward). Indicates dysfunction of the brainstem.
5Brain Disorders—Migraines Caused by a phenomenon called “cortical spreading depression” whereby neurological activity is depressed over a specific area of the cortex—formerly felt to be related to dilation of cerebral blood vesselsResults in release of inflammatory mediators leading to irritation of the nerve roots, especially the trigeminal nerveSerotonin release involved in the causationDiagnosis is based on H&P, neurologic exam and imaging.
6MigrainesTriggersTyramine-containing food and beverages such as beer, wine, aged cheeses, chocolate, yeast, MSG, nitrates, artificial sweeteners, smoked fishMedications:estrogens, nitroglycerine, nifedipine, cimetidineOther: fatigue, hormonal fluctuations, missed meals, sleeping problems, varying altitudes
7Commonly Used Drugs for Migraines NSAIDsBeta blockers such as inderalCalcium channel blockers-verapamilAbortive drugs such as ASA, acetaminophenErgotamine preparationsTriptansOpioidsInvestigational—droperidol (Inapsine)
8SeizuresAbnormal, sudden, excessive, uncontrolled electrical discharge of neurons within the brain. May cause change in LOC, motor or sensory ability, and/or behavior.Epilepsy—chronic disorder characterized by recurrent, unprovoked seizure activity
9Types of Seizures Generalized Absence—petit mal Tonic-clonic—grand mal. Muscle stiffening followed by jerkingMyoclonic—contractions of body musclesAtonic—go “limp”, drop attacksPartial—simple partial, complex partialothers
10Antiepileptic Drugs Tegretol—partial or generalized seizures Klonopin—absence, myoclonic and akinetic seizuresValium—status epilepticusDepakote—all typesZarontin-absence seizuresNeurontin—partial seizuresDilantin-all typesTopamax—for intractable partial seizuresKeppra—adjunct in partial seizures
11Common side effects of anti-epileptics (AEDs) Teratogenic potentialMedication interactionsBlood dyscrasiasAltered liver functionEffects on renal functionWt. gain or lossSometimes sedation
12Surgical optionsIdentify seizure area by EEG, insert electrodes, surgically excisecorpuscallostomy
13Characteristics of Seizures Important to observe and document:How often?DescriptionProgressionDurationLast time occurredPreceded by aura?What does patient do post-seizure?Time elapsed before returns to baseline
14Seizure Precautions Stay with patient O2 Airway Suction IV access Siderails up, paddedBed in lowest positionTurn patient to sideLoosen restrictive clothingDo not force anything into the mouthFollowing seizure—do neuro checks
15Status EpilepticusCharacterized by prolonged seizures lasting more than 5 minutes or repeated seizures over the course of 30 minutesIs a medical emergency. Brain damage and death can ensue.Untreated can cause hypoxia, hypotension, hypoglycemia, dysrhythmias and lactic acidosis. Rhabdomyolysis can occur with effects on the kidneys.
16Treatment of Status Epilepticus Lorazepam is the drug of choice due to rapid onset of action and long duration of actionValiumPhenobarbitalDilantinSupportive/safety care
17Meningitis Inflammation of the meninges or brain covering Entry is via the bloodstream at the blood-brain barrier. May be direct route or via skull fracture. Exudate will develop.Viral is most commonFungal-Cryptococcal. Can be caused by sinusitisBacterial-mortality rate+25%. Most commonly caused by Neisseria meningitidis and Streptococcus pneumoniae.
18Meningitis—S/S LOC Disorientation Photophobia Nystagmus hemiparesis CN dysfunctionPersonality changesN/VFever and chillsRed macular rashNuchal rigidity, positive Kernig’s (hamstring pain w/extension) and Brudzinski’s (flexion of the hips when the neck is flexed)
19Review of CSF findings Pressure <20cm of H2O Clear, colorless. Cloudy indicates infection. Pink to orange==RBCsCells 0-5 lymphocytes normal.Glucose—50-75mg/dL normal, less than 50 indicates infectionProteins normal, paraventricular tumor, viral, more than 500=bacterial infection
21Meningitis May display s/s of increased ICP ( see following slide) Left untreated, can result in brain herniation or damage
22MeningitisTreatment according to causative pathogen as found by LP (lumbar puncture)BedrestIV fluids, analgesics for pain and feverAnticonvulsantsCorticosteroidsPathogen specific abx—meningococcus penicillin or cephalosporins, contacts rifampin or cipro; pneumococcal—PCN, cephalosporins and also vancomycin
23ICPPressure-volume relationship between ICP, volume of CSF, blood, brain tissue and cerebral perfusion pressure (Monroe-Kellie Hypothesis)Cranial compartment is incompressible and cranial contents should have a fixed volumeEquilibrium must be maintained. Increased volume will result in downward displacement of the brain
24Key Features of Increased Intracranial Pressure Lethargy to comaBehavioral changesHeadacheN/VChange in speech patternAphasiaPupillary changes--papilledemaCranial nerve dysfunctionSeizuresAbnormal posturingCushing’s Triad—elevated BP, decreased pulse and decreased respirations
25Treatment of increased ICP Maintain airwayHyperventilate patient to “blow off” CO2 (CO2 dilates blood vessels)Raise HOB to allow for venous drainageDecrease metabolic demands by paralyzing and sedating patientMannitolcorticosteroidsPain managementIntracranial monitoring (in ventricle)CraniotomiesDecompressive craniectomy
26Brain Attacks (Strokes or CVAs) Affects over 550, 000 Americans per yearTwo major types—ischemic and hemorrhagicCaused by disruption of the normal blood supply to the brainMay be preventable if causes discovered early
27Risk Factors for Brain Attacks ObesityHeart diseaseDiabetes mellitusHypercholesterolemiaHypercoagulable statesCocaine, illicit drug useAtrial fibrillation
28Differential Features of the Types of Stroke Thrombotic—onset is gradualUsually related to ASHD and hypertensionIntact LOCMay have speech and visual changesSlight HANo seizuresDeficits may be permanent
29Differential of strokes EmbolicAbruptSteady progressionAwakeMay be associated with cardiac diseaseMaximal deficits at onsetNo seizuresRapid improvements
30Differentials of strokes HemorrhagicSudden onsetDeepening stupor or comaMay have hypertensionFocal deficitsSeizures possiblePermanent deficits possibleMay result from an aneurysm, rupture of an AV malformation or severe hypertension
31Ishemic Stroke Caused by a blockage of a blood vessel Generally caused by atherosclerosisEarly warning signs include: transient loss of vision, transient ischemic attack (called silent strokes)Risk factors: atrial fibrillation, ASHD, cocaine use/abuse, hx of “blood clots”Treatment—”clot buster” TPA, streptokinase,others
32Transient ischemic attack vs. reversible ischemic neurologic deficit Ischemic strokes are often preceded by warning signs such as TIAs or RINDsBoth cause transient focal neurologic dysfunction from a brief interruption in cerebral blood flowTIAs last minutes to <24hRINDs last >24h but less than a week
33Hemorrhagic strokesIf survive event, recovery from hemorrhagic stroke better than ischemicCaused by vascular disruption e.g. aneurysms, AVMSurgical decompression
34Assessment of patient with brain attack Neurologic examMotor exam—hemiplegia vs. hemiparesisSensory changes-neglect syndrome (most notable in right cerebral hemispheric injuries)Amaurosis fugax—temporary loss of vision in one eyeHemianopsia—blindness in one half of visual fieldCranial nerve functionCardiovascular assessment—abrupt reduction of BP not advised
35AssessmentBaseline CT, MRI even better (want to ensure that the stroke is not hemorrhagic)ECGEchocardiogramCardiac enzymes
36Interventions Depending of type of brain attack: Anticoagulants (assuming not a bleed)Catheter directed thrombolytic therapy—may use if systemic tx not effectiveEndarterectomyCraniotomySystemic thrombolytic tx—must meet strict criteria. Must give within 3hours of onset of s/sWire coils in aneurysms—seals the area
37Key considerations Impaired physical mobility; self care deficit Disturbed sensory perceptionUnilateral neglect—in rt cerebral stroke. May have lack of proprioception and failure to recognize their impairmentImpaired verbal communication—expressive aphasia (Broca’s), receptive aphasia (Wernicke’s)
38Parkinson’s disease Genetic and environmental contributors Associated with four cardinal s/s: tremor, rigidity, akinesia (slow movements), and postural instabilityDegeneration of substantia nigra—decreased dopamine. Acetylcholine will predominate. Also with norepinephrine loss thus the postural hypotension.
39Parkinson’s Key Features Stooped postureSlow and shuffling gaitPill-rolling, mask-like facies, uncontrolled drooling, rare arm swinging with walkingChange in voice, dysarthria and echolaliaLabile and depressed, sleep disturbancesOily skin, excessive perspiration, orthostatic hypotension
40Parkinson’s Disease Stages Initial-hand and arm trembling, weakness, unilateral involvementMild-masklike facies, shuffling, bilateral involvementModerate—increased gait disturbancesSevere—akinesia, rigidityComplete dependence
41InterventionsEldepryl (MAO inhibitor which decreases the breakdown of dopamine)Dopamine agonists—stimulate dopamine receptors but have side effects such as nausea, drowsiness, postural hypotension and hallucinations. Mirapex and Requip mimic the actions of dopamine.
42Interventions cont.Levodopa/carbidopa. Used as disease progresses. “Wearing off” phenomenon.Amantadine—used to treat the “wearing off” s/s.Stavelo—(carbidopa/levodopa/entacapone). Dopa-decarboxylase inhibitor/dopamine precursor/COMT inhibitor. Useful in end-stage disease.
43Drug toxicity/tolerance in PD Reduce medication dosageChange of medications or in the frequency of administrationDrug holiday up to 10 days
44Nursing considerations Maintain mobility and flexibility by ROMEncourage self-care as much as possibleMonitor sleep patterns to avoid injuryNutrition-may need soft or thickened foods.ConstipationSpeech therapy may be neededPsychosocial support—impaired memory cognition
45Surgical Management in PD Stereotactic pallidotomyDeep brain stimulation when meds no longer work. Electrode is implanted and connected to a “pacemaker” in chest.Fetal tissue transplantation using fetal substantia nigra (implanted in the caudate nucleus of the brain).
46Alzheimer’s DiseaseChronic progressive degenerative disease usually seen in individuals older than 65Characterized by loss of memory, judgment, and visuospatial perception and by a change in personalityProgressively physically and cognitively impaired resulting ultimately in death
47AD Increased amount of beta amyloid Neurofibrillary tangles throughout the neuronsNeuritic plaquesGranulovascular degenerationReduced levels of acetylcholine? Increased levels of glutamate
48Key Features of ADEarly-forgets names, misplaces household items, mild memory loss, short attention span, subtle changes in personality, wanders, impaired judgmentMiddle—cognition vitally impaired; disoriented to time, place and event; agitated; unable to care for self, incontinentSevere-incapacitated; motor and verbal skills lost
49Physical Assessment of AD Observe for stage of progressionObserve for changes in cognition—attention, judgment, learning and memory, communication/languageObserve for changes in behaviorChanges in self-care skillsPsychosocial assessmentDx of exclusion. Check CMP, CBC, B12, folate, TSH, RPR, drug toxicities and levels, alcohol screeningPET or MRI to r/o pathology
50Mini-mental state examination—orientation, registration (repeat three words), naming, reading and following directions.Good one is to have them draw a clock with an indicated time
51Interventions for ADProvide environmental stimulation through contact with people, provide a clock and calendar, present change gradually, allow for rest periods, use repetitionBe concreteLimit informationPrevent overstimulation and provide structure
52Interventions cont. Promote independence in ADL Be consistent Promote bowel and bladder contenence fy offering rest room breaks q2h daytime, limit fluids at hsAdminister cholinesterase inhibitors such as Aricept, Reminyl and Exelon. Maintains functionality for a few more months.
53Interventions cont. Provide ID band Monitor to ensure safety from wanderingWalk patient to reduce restlessnessInvolve in activitiesRestraints only as last resort
54Multiple Sclerosis (MS) Also called disseminated sclerosis or encephalomyelitis disseminataChronic, inflammatory disease of CNSCauses gradual destruction of myelin sheath of neurons. Results in scars or sclerosis on the myelin sheaths.Results from autoimmune processBetween attacks, s/s may resolve but permanent injury occurs as disease progresses
55MS Usually affects adults 20-40 years of age More common in women than menOccurs in more temperate climatesNo cure
56MS signs and symptoms Changes in sensation* Muscle weakness Incoordination, loss of balance*DysarthriaDysphagiaVisual problems (diplopia)*FatigueBladder and bowel problemsCognitive impairmentHeat intolerance*indicates initial or presenting symptoms
57Diagnosis of MS MRI CSF testing will show oligoclonal bands Visual evoked potentials and somatosensory evoked potentials (sensory and visual nerves respond less actively in MS)Antibody testing for myelin oligodendrocyte glycoprotein and myelin basic protein—in formative stages for testing at this time
58Types Relapsing-remitting--charac. by remissions and relapses Secondary progressivePrimary progressive—no remissions, gradual declineProgressive relapsing—steady decline with superimposed attacks
59---Copaxone (immunomodulator that targets T-cells, decreases inflammation), Avonex (interferon beta), Betaseron (interferon beta), Tysabri (immunotherapy)Avoidance of over-heating (Uththoff’s phenomenon)
60Spinal Cord InjuryForce applied to spinal cord will result in neurologic deficitsInjury may be direct insult to the spinal cord or may be secondary to a contusion, compression or to a concussion (loss of function resulting from a blow)
61Primary mechanisms of injury Hyperflexion injury occurs when the head is suddenly and forcefully accelerated forward, causing extreme flexion of the neck. Often occurs in head-on collisions and diving accidents
62Primary mechanisms of Injury Hyperextension injuries occur most often in automobile accidents in which the client’s vehicle is struck from behind or during falls when the client’s chin is struck. The head is accelerated and decelerated. Results in stretching or tearing longitudinal ligament, fractures or subluxates vertebrae and may rupture the disc.
63Primary mechanisms of injury cont. Axial loading (vertical compression) occurs from diving accidents, falls on the buttocks, or a jump in which a person landed on their feet. The blow may cause the vertebrae to shatter. Pieves of bone enter the spinal canal and damage the cord.
65Extent of Injury Most spinal cord injuries are incomplete lesions Specific syndrome result from incomplete lesions
66Cervical Injuries May produce: Anterior cord syndrome Posterior cord syndromeBrown-Sequard syndromeCentral cord syndromeCauda equina syndromes are associated with injuries to the lumbar and sacral cord
67Cervical InjuriesAnterior cord syndrome results from damage to the anterior portion of both gray and white matter of the spinal cord, generally 2ndary to decreased blood supply. Motor function, pain and temperature sensation are lost below the level of injury but touch, position and vibration remain intact.
68Posterior cord lesion—rare Posterior cord lesion—rare. Results from damage to the posterior gray and white matter of the spinal cord. Motor function remains intact but the patient loses the sense of position sensation, of crude touch and of vibration.
69Brown-Sequard—results from a penetrating injury that causes hemisection of the spinal cord or injuries that affect half of the spinal cord. Motor function, proprioception, vibration and deep touch sensations are lost on the same side of the body as the lesion. On the opposite of the lesion, the sensations of pain, temperature and light touch are affected.
70Central cord syndrome—results from a lesion of the central portion of the sc. Loss of motor function is more pronounced in the upper extremities than in the lower extremities. Sensation varies.
71Lumbosacral Injuries—damage to the cauda equina or conus medullaris produces a variable pattern of motor or sensory loss as the peripheral nerves have the potential for recovery and regrowth. This injury generally results in a neurogenic bowel and bladder.
72Vital statistics of spinal cord injuries Primary cause is trauma secondary to MVAUnmarried male between 16-30Generally are CauscasianMost injuries are cervical
73AssessmentThorough history including mechanism of injury, any changes since initial responder, previous medical history, hx of osteoporosis, osteomyelitis or previous neck or back injuries or surgeries
74AssessmentFirst priority for the client with a SCI is assessment of the respiratory pattern and airwayEnsure neck is stabilizedAssess for evidence of abdominal hemorrhage or other sites of injury/hemorrhageGlasgow Coma ScaleDetailed assessment of the client’s motor and sensory status
75Spinal ShockOccurs immediately after injury as a result of disruption of pathways between upper motor neurons (lie in cerebral cortex) and lower motor neurons (lie in spinal cord).Characterized by:Flaccid paralysisLoss of reflex activity below level of lesionBradycardiaPossible paralytic ileusHypotension.May last days to weeks; reversal indicated by return of reflex activity
76Assessment Sensory function C4-5 can shrug C5-6 can pull up arms against resistanceC7 can overcome resistance with arms flexedC8 can grasp objectsL2-4 can raise legs straight up against resistanceL5 apply resistance when patient dorsiflexesS1apply resistance while the client plantar flexes his feet
77CardiovascularDysfunction r/t disruption of the autonomic nervous system, especially if above T-6Bradycardia, hypotension and hypothermia may result from disruption of sympathetic inputBP < 90 torr requires intervention to ensure satisfactory perfusion of the spinal ccord
78RespiratoryCan develop from both immobility and from interruption of spinal innervation to the respiratory musclesC3-5 innervate the diaphragm
79Gastrointestinal and Genitourinary assessment Must assess the patient’s abdomen for indications of hemorrhage, distention or paralytic ileusIleus may develop within 72h of the injury. Can cause areflexic bladder which can lead to urinary retention and a neurogenic bladder.
80Musculoskeletal Assessment Assess muscle tone and sizeMuscle wasting is 2ndary to long-term flaccid paralysis seen in lower motor neuron lesions (cell body lies in ant. gray column of spinal cord. Innervates striated muscles).Upper motor neuron lesions (neuron body lies in cortex, axon synapses with lower motor neuron). Causes spasticity.
81Interventions for Patients with Spinal Cord Injuries Immobilization for cervical injuries—fixed skeletal traction such as halo fixation or tongsMaintain proper alignment of head, neck and bodyTurn using the log roll techniqueMonitor skin integrityTraction pin insertion site careIf thoracic or lumbosacral injury—immobilize with corset or braceMedications—supportive, may use steroids, baclofen, other meds under investigation
82Interventions for patients with SCIs Surgical decompression and stabilization—spinal fusion, insertion of Harrington rods, laminectomy (excision of a posterior vertebral arch)Prevent complications of immobilityPromote self-careBladder retraining—spastic (UMN) or flaccid (LMN) may be able to initiate voiding or may need I&O catherterizations
83Interventions cont.Bowel retraining—LMN may have to have manual disimpactions, see p. 993.Rehab, involve community resourcesHome care managementPsychosocial implications
84Autonomic Dysreflexia or Hyperreflexia Commonly seen in patients with injury to the upper spinal cord (T5 and above). Caused by massive sympathetic discharge of stimuli from the autonomic nervous system.Stimulus sends nerve impulses to sc, travel upward until blocked by lesion at level of injury. Can’t reach brain so reflex is activated that increases activity of sympaathetic portion of ANS.
85Autonomic dysreflexia cont. Increased activity of sympathetic portion of ANS results in spasms and a narrowing of blood vessels with resultant rise in BP. Brain perceives elevated BP, sends message to heart which slows down and dilates vessels above level of injury to dilate. Brain cannot send messages below level of injury so BP cannot be regulated.
86Autonomic Dysreflexia Precipitated by distension of the bladder or colon; catheterization of or irrigation of the bladderIs a medical emergency
87Key Features of Autonomic Dysreflexia Sudden onset of severe, throbbing headacheSevere, rapidly occurring hypertensionBradycardiaFlushing above the level of the lesionPale extremities below the lesionNauseaBlurred visionPiloerectionFeeling of apprehension
88Care of Patient experiencing Autonomic Dysreflexia Place in sitting positionNotify physicianLoosen tight clothingAssess for causeCheck foley cathIf no cath, check bladder for distentionPlace anesthetic ointment on tip of catheter before insertion
89Care of Patient with Autonomic Dysreflexia cont. Check for fecal impaction, disimpact with anesthetic ointment if presentCheck room to ensure not too coolMonitor BP q15 minutesGive nitrates or hydralazine as ordered
90Myasthenia Gravis (MG) Autoimmune disease of neuromuscular junction. Characterized by flare-ups and remissions. Caused by auto antibody attack on the acetylcholine receptors. May be related to hyperplasia of the thymus.Presents with muscle weakness that improves with rest, poor posture, ocular palsies, ptosis, diplopia, respiratory compromise, bowel and bladder problems
91MGDiagnosis based on H&P, labs which include thyroid studies, tests to R/O inflammatory illnesses, (RA, SLE, polymyositis), acetylcholine receptor antibodies (positive confirms but negative does not rule out)
92MGTesting with cholinesterase inhibitors (Tensilon). Baseline muscle strength tested then injection given. Within seconds, most myasthenic patients show a marked improvement in muscle tone that lasts several minutes.May be used to distinguish between myasthenic crisis and cholinergic crisis.
93Myasthenic Crisis Undermedicated with anticholinesterase drugs. Increased pulse and respirationsRise in BPAnoxiaCyanosisBowel and bladder incontinenceAbsence of cough and swallowing reflex
94Cholinergic crisis Like being tx with chemical weapons Too much acetylcholineNausea, vomiting, diarrheaAbdominal crampsMuscle twitchingHypotensionBlurred vision
95Treatment of MG Immunosuppression with steroids, Imuran or Cytoxan PlasmapheresisResp. supportNutritional supportEye protection if unable to close eyes completelyThymectomyMaintanance—cholinesterase inhibitor drugs such as Mestinon