- def
    - two types
    - bacterial
    - increased risk
    • Inflammation of the membranes of the spinal cord andbrain AKA meninges.
    • Two types, septic and aseptic. Septic=bacterial.Aseptic=viral or secondary to lymphoma, leukemia orHIV.
    • Bacterial meningitis outbreaks common with densepopulated communities (college campuses). ↓incidencew/H. influenza 2nd to vaccinations.
    • Increased risk: smoking, viral URI, otitis media,mastoiditis, immunodeficiencies
    • Meningeal infections: originate either through thebloodstream OR by direct spread (traumatic injury orinvasive procedures)•
    • Concentrates in the nasopharynx and transmitted bysecrection or aerosol contamination.•
    • Bacterial or meningococcal meningitis occurs as anopportunistic infection in patients w/AIDS or LymeDisease.•
    • Causative organism enters the bloodstream crosses theblood-brain barrier and proliferates in the CSF.•
    • CSF studies=decreased glucose, increased proteinlevels and WBC levels
    Meningeal infections: originate either through the
    bloodstream OR by direct spread (traumatic injury or
    invasive procedures)
    • Concentrates in the nasopharynx and transmitted by
    secrection or aerosol contamination.
    • Bacterial or meningococcal meningitis occurs as an
    opportunistic infection in patients w/AIDS or Lyme
    • Causative organism enters the bloodstream crosses the
    blood-brain barrier and proliferates in the CSF.
    • CSF studies=decreased glucose, increased protein
    levels and WBC levels
    Severe headache (steady, throbbing)• High Fever• Nuchal Rigidity• +Kernig’s Sign=lying w/thigh flexed onabdomen, leg cannot be completely extended• Photophobia• +Brudzinski’s Sign=neck flexed results in flexedknees and hips• Rash, Disorientation and Memory Impairment• Behavioral Manifestations• Later in illness=lethargy,unresponsiveness, and coma can develop• Seizures in 30% w/ S. Pneumoniae• Increased ICP due to accumulation ofpurulent excudate• Can experience rapid decline in only a fewhours resulting in death
    High doses of IV antibiotic therapy that crossesthe blood-brain barrier• Dexamethasone in conjunction w/antibiotic• Identification/treatment of seizures• Neuro and vital sign checks• Lab values, I&O, pulse oximetry• Information to family or significant other• Droplet precautions until 24 hours of antibiotic• Monitor for fluid overload
  5. Herpes Simplex Virus Encephalitis
    Acute inflammatory process of brain tissue• HSV most common cause in US• Two Types: HSV-1=children & adultsHSV-2=neonatesHSV-1=follows a retrograde intraneuronalpath to the brain (olfactory and trigeminalnerves) most common
  6. HSV Encephalitis
    Diagnosis: CSF examination, EEG, MRI• CSF=high pressure, low glucose, highprotein• Treatment-Antiviral agent ie. Acyclovir• Nursing considerations: monitor forprogression of disease & symptoms,comfort measures (dimmed lights,decreased noise) Cautious use of opioidsdue to masking of neuro symptoms
  7. Arthropod Borne Virus Encephalitis
    MOSQUITO (primary vector)• West Nile and St. Louis most common• Affects adults primarily, climate/human behavior ie.warm weather=crawfish boils• West Nile birds primary host, humans secondary• Symptoms: early flu like symptoms with both West Nileand St. Louis• West Nile specific symptoms: maculopapular ormorbilliform rash to neck, trunk, arms, and legs. Flaccidparalysis.• Symptoms common to West Nile and St. Louis areParkinsonian type movements, reflecting inflammation ofthe basal ganglia. Seizures (poor prognositic indicator)
  8. Arthropod-Borne Virus Encephalitis
    • • Diagnosis: CSF examination, MRI (St.Louis=inflammation of basal
    • ganglia or WestNile=inflammation of periventricular
    • areas),Immunoglobulin M antibodies to WNV in serumand CSF• No medication
    • treatment known• Treat symptoms, control seizures, monitor forincreased
    • ICP• Nursing interventions: Neuro checks, seizuremonitoring,
  9. Fungal Encephalitis
    Primarily with the immunocompromised• Fungal spores enter body via inhalation, infectlungs (resp. symptoms). May enterblood=fungemia. Spreads to CNS=meningitis,encephalitis, or abscess.• Clinical presentation: fever, malaise, HA, changein LOC, symptoms of increased ICP.• Diagnostics: immunocompromised, occupationaland travel history, CSF=elevated WBCs&protein levels, decreased glucose, MRI, +culture.
  10. Fungal EncephalitisNursing and Medical Management
    Antifungal agents=Amphotericin B orDiflucan. Amophotericin requires premedwith Benadryl & Tylenol due to “flu-like”symptoms.• Monitor for renal insufficiency, increasedICP• Provide family support and education
  11. Creutzfeldt-Jakob Disease
    Rare degenerative infectious neurologic disordertransmissiable spongiform encephalitis (TSE).• From ingestion by humans of prions(proteinaceous particles smaller than a virus) ininfected beef• Can be dormant for decades before causingneurologic degeneration• “Mad Cow” disease• NO TREATMENT, pallative measures only
    Autoimmune process• Immune mediated progressive demyelinatingdisease of the CNS• Demyelination causes impaired transmission ofnerve impulses• Factors: geographic prevalence highest in all ofEurope, New Zealand, Southern Australia,Northern US and Southern Canada,women>men, young 20-40yo, research possiblegenetic predisposition, early age environmentalexposure
  13. Multiple Sclerosis Pathophysiology
    Sensitized T cells remain in CNS & promoteinfiltration of other agents that damage theimmune system which causes demyelination.• Demyelination=interruption of the flow of nerveimpulses• Commonly affected areas: optic nerves, chiasmtracts, cerebrum, brain stem, cerebellum &spinal cord.• Axons eventually begin to degenerate whichresults in permanent and irreversible damage.
  14. Multiple SclerosisClinical Manifestations
    - Relapsing Remitting MS
    80% to 85% of all multiple sclerosis– Acute attacks with full recovery or w/sequelae &residual deficits.– Periods b/w relapses have no disease progression– Residual deficits accumulate over time.– 50% with Relapsing Remitting MS progress to asecondary progressive course
  15. Multiple SclerosisClinical Manifestations•
    Primary Progressive MS
    Progression of disease/disability from onsetwithout plateaus, remissions OR RAREplateau or temporary improvement ofcondition– 10% of MS cases– Deficits include: quadriparesis, cognitiveimpairment, visual loss, brainstemdysfunctions
  16. Multiple SclerosisClinical Manifestations
    • Secondary Progressive MS - Begins with initial course of RR MSFollowed by progression of variable ratewhich may include occasional relapses &minor remissions
    • Progressive Relapsing MS - 5% of all MSHas progression of disability from onset withclear acute relapses with or without recovery
  17. Multiple SclerosisSigns and Symptoms
    Vary dependent on location of lesion(s)• Commonly seen: fatigue, depression,weakness, numbness, difficulty incoordination, loss of balance, pain, visualdisturbances including blurring of vision,diplopia, patchy blindness (scotoma), andtotal blindness, pain, spasticity (musclehypertonicity of the extremities)
  18. Multiple SclerosisLocation of lesion=Presentation
    Pyramidal Tracts of Spinal Cord=spasticityof extremities, loss of abdominal reflexes• Sensory Axons=parasthesias, pain• Frontal or Parietal lobe=cognitive &psychosocial problems• Cerebellum or basal ganglia=ataxia• Cortex/basal ganglia/spinal cord=bladder,bowel, sexual dysfunction
  19. Multiple SclerosisDiagnostics/Assessment
    MRI-presence of plaques in CNS• Electrophoresis of CSF• Urodynamics (baseline)• NCS (baseline)• Neuropsychological testing (baseline)• Sexual counseling
  20. Multiple SclerosisMedical Management
    NO CURE, treat symptoms• Goal of treatment: delay progression of disease,management of chronic symptoms, treat acuteexacerbations• Pharmacologic Therapy– Interferon (Rebif and Betaseron) IM weekly w/complaints of flulike symptoms, depression, monitor LFTs– Copaxone decreases rate of relapses in RR, # of plaques,increases time b/w relapses. Daily SubQ injection, costs $1,400without insurance– IV Methylprednisolone (key in treating acute relapses in RR,shortens duration of relapse) Tx for 3 days, then change to oralfor tapering doses– Novantrone IV every three months, decreases frequency ofclinical relapses w/secondary progressive or worsening RR
  21. Multiple SclerosisNursing Management
    Individualized plan of care• PT, OT, ST, Rehab• Family/significant other education (MS/chronic)• Emotional support• Exercises• Prevention of spasticity and contractures• Activity/Rest• Minimize effects of immobility• Prevent Injury• Bladder and bowel education/management
  22. Myasthenia Gravis
    Autoimmune disorder affecting myoneural junctionresulting in varying degrees of weakness of thevoluntary muscles• Female>male; Female (ages 20 to 40); Male (ages 60 to70)• 60,000 cases in US• Pathophys:antibiodies directed at the acetylcholinereceptor sites impair transmission of impulses across themyoneural junction. Resulting in fewer receptorsavailable resulting in voluntary muscle weakness thatescalates with continued activity.• 80% have thymic hyperplasia or a thymic tumor (thymusgland believed to be sight of antibody production)
  23. Myasthenia Gravis• Clinical manifestations
    typically involvesocular muscles=diplopia, ptosis (droopingof eyelids); facial weakness, throatweakness; dysphonia (laryngealinvolvement), increased risk for choking &aspiration, generalized weakness ofextremities & intercostalmuscles=respiratory compromise• Only MOTOR, no sensory involvement
  24. Myasthenia Gravis• Treatments with Meds
    – Mestinon (pyridostigmine bromide)-anticholinesterase medication (1st line of tx)– Prednisone (immunosuppressive therapy)– Cytotoxic meds (Imuran, Neoral, Cytoxan)
  25. Myasthenia Gravis• Treatment with Plasmaphersis
    Plasma exchange (decreases the number ofantibodies in the bloodstream)Improves symptoms temporarily (a few wks)IVIG (intravenous gamma globulin) used to treatexacerbationsNO Cure for myasthenia gravisSurgical intervention: Thymectomy (3 years to seeaffect due to long life of T cells)
  26. Myasthenia GravisNursing Management
    Education of patient and family– Medication management, energyconservation, prevention of complication,ocular manifestation management– Educate on recognition of Myasthenic Crisis
  27. Guillain-Barre’ Syndrome
    Autoimmune attack on peripheral nerve myelin.• Acute, rapid demyelination of peripheral nerves andsome cranial nerves.• Preceded by a viral infection (typically 2 weeks prior)• Question re: flu vaccine• Males>females, ages 16 to 25 and also ages 45 to 60.• 75% recover completely• 25% residual deficits (severe to mild)• Higher incident of permanent disability when >60yo,require mech vent support, rapid progression of onset• Recovery may take up to 2 years
  28. Guillian-Barre’ Syndrome
    Weakness presents distally and progressesproximally.• Usually begins in legs• Monitor closely for respiratory compromise• Monitor vital capacity• CSF=elevated proteins, otherwise WNL• Nerve conduction tests (sequential)• GBS is a medical emergency• Medical management: IVIG and Plasmaphersis
  29. Guillian-Barre’ SyndromeNursing Management
    Maintaining respiratory function-monitorfor decline resulting in need for vent• VS and swallowing ability• Physical mobility (skin too)• Nutrition• Communication• Education (patient and family)• Depression, anxiety, fear
  30. Trigeminal NeuralgiaTic Douloureux (painful twitch)
    5th CN resulting in PAIN, unilateral• Abrupt onset and end• Women>Men; ages 50 to 60• Pain free intervals (can be measured fromminutes to weeks)• As patient ages attacks more frequent• Paroxysms (attack) occur with anystimulation of the nerve (trigger points)
  31. Trigeminal Neuralgia• Treatments/Nursing Management
    Anticonvulsant-Tegretol, Neurontin, Dilantin– Microvascular Decompression of the nerve– Gamma Knife Surgery– Percutaneous radiofrequency coagulation– Percutaneous balloon microcompression– Pain prevention– Postop care
  32. Bell’s Palsy
    7th CN unilateral inflammation• Unilateral weakness/paralysis of affected side (oftenconfused with CVA)• Unable to wrinkle forehead, eye does not close• Cause unknown• Occurrence higher with age and third trimesterpregnancy• Usually a complete recovery (4 to 6 weeks)• Rare reoccurence• Nursing-protection of the eye• Med-Prednisone, pain management
  33. Peripheral Neuropathy
    Bilateral, symmetric dysfunction of peripheralmotor and sensory nerves• Most common cause diabetes (poor glycemiccontrol)• Starts in feet and hands• Symptoms: loss of sensation, pain, parathesias,weakness, muscle atrophy, hypoactive reflexes• NO cure or specific treatment• Nursing Management: pain control, safety
  34. Primary Brain Tumors
    Originate from brain tissue (not mets) butmuch less common than metastaticlesions• Etiology unknown• 18,000 new cases of malignant braintumors each year• Male=Female, ages 50 to 70• Most common type, glial tumors
  35. Types of Primary Brain Tumorssee chart 65-1 page 2302• Gliomas (most common type)
    Astrocytomas– Glioblastoma Multiforme– Oligodendrocytoma– Ependymoma– Medulloblastoma
  36. Type of Primary Brain Tumors
    Meningomas (15 to 20% of all braintumors)• Neuromas• Pituitary adenomas (7 to 12% of all braintumors)• Angiomas (masses composed largely ofabnormal blood vessels)=risk forhemorrhagic stroke
  37. Primary Brain TumorsClinical Manifestations
    Focal or generalized neurologicalsymptoms• Increased ICP (N/V, HA, papilledema)• Focal: hemiparesis, seizures, mentalstatus changes. All depends on locationof tumor. Visual changes, vertigo, ataxia,personality changes
  38. Primary Brain Tumor Diagnosticsand Medical Management
    Neuro Exam• CT Scan w/contrast• MRI• PET scan (complements MRI)• EEG• Radiation Therapy• Chemotherapy• Bone Marrow• Surgical intervention• Gamma Knife
  39. Primary Brain TumorNursing Management
    Aspiration Prevention• Neuro checks• Protection from seizures• Motor and sensory function
  40. Cerebral Metastases
    Most common neurological complication ismetastatic brain lesions• Neuro signs/symptoms-HA, gait disturbances,visual impairment, personality changes, alteredmental status, focal weakness, paralysis,aphasia• Need patient/family support and education• Pallative treatments which can include radiation,chemo, surgical intervention• Pain management and Corticosteroids• Nutrition, self care deficits, anxiety/depression
  41. Spinal Cord Tumors
    Classified by anatomical relation to the spinalcord• Symptoms: pain, weakness, paralysis (motorand sensory)• Diagnostics: MRI, CT, Biopsy, Neuro exam• Medical-treatment depends on type and locationof tumor• Surgical intervention primary treatment, alsochemo and radiation. Might only opt for pallative• Nursing-neuro checks, assessments, painmanagement, respiratory, education
  42. Parkinson’s Disease
    Slow progressive neurodegenerative dz• Etiology unknown• Symptoms appear usually 5th decade oflife, can be earlier• 4th most common neurodegenerative dz• Males>Females, rare onset after age 65• Loss of dopamine results in destruction ofpigmented neuronal cells
  43. Parkinson’s DiseaseClinical Manifestations
    Gradual onset, slow progression=chronicprolonged course• Cardinal signs: tremor, rigidity (cogwheel)bradykinesia (abnormally slow movements) andpostural instability• Autonomic symptoms: orthostatic hypotension,uncontrolled sweating, gastric and urinaryretention, sexual dysfunction• Sleep disturbances, dementia (40% to 70%)• Mask like face, expressionless, shuffling gait,dsyphonia, dysphagia, drooling
  44. Parkinson’s DiseaseDiagnostics/Medical Management
    Diagnosed from history and presence oftwo of the four cardinal signs: tremor,rigidity, bradykinesia, and posturalchanges.• Early diagnosis difficult• Medical management-control symptoms• Pharmacological measures: multipleoptions/trials (page 2314)
  45. Parkinson’s DiseaseSurgical Management
    Limitations of levodopa therapy andimprovements in stereotactic surgery andnew approaches in transplantation haveincreased surgical interventions• Stereotactic-(see figure 65-5, page 2315)– Only available if other measures failed, strictcriteria (thalamotomy and pallidotomy),improvement in rigidity, bradykinesia,dyskinesia
  46. Parkinson’s DiseaseSurgical Management
    Neural Transplantation (research)• Deep Brain Stimulation-pacemaker typedevice implanted deep into the brain tissueand is used to control tremors (see figure65-6) performed here in Shreveport
  47. Parkinson’s Disease• Nursing:
    Mobility– Self care deficits– Nutrition– Swallowing– Communication– Family/Significant others– Psych
  48. Huntington’s Disease
    Chronic, progressive hereditary disease of thenervous system (each offspring with a parentwith Huntington’s disease has a 50% chance ofinheriting the disorder-autosomal dominantgenetic disorder)• Causes progressive involuntary choreiformmovement and dementia• Male=Female, b/w 35 and 45 yo, however 10%are children, emaciated appearing• Fatal 10 to 20 years following diagnosis due toheart failure, choking, falling, infection
  49. Huntington’s Disease• Clinical manifestations
    chorea (abnormallyinvoluntary movements of the wholemusculature of the body), constant movements,tics, grimaces, speech slurred, drooling, evenmovement with sleep, loss of bladder/bowelcontrol, decrease cognition, personalitychanges,• Suicidal ideations• Diagnosis-clinical presentation, +family history,and exclusion of other disease processes. Nowa DNA marker test
  50. Huntington’s Disease• Medical Management
    No treatment reverses orstop progression of disease• Medications: given to reduce chorea (see pages2319-2320); must monitor motor response toavoid AKATHISIA (motor restlessness) indicatesovermedication and often mistaken for thefidgeting of the disease itself• Patient & family/significant other education• Current on services available in community aswell as financial resources.
  51. Amyotrophic Lateral Sclerosis(ALS)-”Lou Gehring”
    Unknown etiology, life expectancy 25 months after initialdiagnosis• Loss of motor neurons (nerve cellls controlling muscles)anterior horn of SC and motor nuclei of lower brain stem• Males>females, 50 to 60yo, smoking?• Clinical manifestations (depends on which muscleaffected): fatigue, progressive muscle weakness,cramps, fasciculations (twitches), incoordination. 25% ofpatients present w/swallowing difficulties (affecting CNfirst) weakness of soft palate and upper esophagealweakness regurg of liquids through nose
  52. ALS
    Diagnosis: Signs/symptoms, MRI, EMG, musclebiopsy• Nursing: maintain highest quality of life possible,lots of education, community referrals toresources such as MDA• Pharm: med trials, meds for symptoms• Respiratory:need decisions made early indisease regarding life support measures asdecline in respiratory status (musculature anddysphagia) common cause of death
  53. Muscular Dystrophies
    Multiple types, onsets, ages and outcomes• Resources-MDA• Incurable diseases, most progressive weakness• Diagnostics: Muscle biopsy, genetic testing• Medical Management: prolong quality of life andfunctional status• Nursing: EDUCATION, enhance quality of life,prevention of complications
  54. Degenerative Disk Disease
    Common, prevalent• Most adults will experience an episode of backpain or neck pain within lifetime• Costly $$$$$ (medical, loss of income, etc)• Pathophysiology: Page 2324• Clinical manifestations: herniated disk(cartilaginous plate b/w disks) w/pain anylocation on the spine (C, T, L). Manifestationsdependent on location
  55. Degenerative Disk Disease• Diagnostics/Assessment:
    History, exam, MRI,CT, rare myelography, EMG• Medical: conservative measures (therapy, rest,meds). Surgery last resort• Surgeries: disectomy, laminectomy,hemilaminectomy, fusion, foraminotomy all ofwhich are “decompression”• Pharm: analgesics,muscle relaxants, ESI• Nursing: pain management, mobility,maintaining precautions, monitor for postopcomplications
  56. Degenerative Disk Disease• Terms to know
    Radiculopathy– Nucleus pulposus– Herniated nucleus pulposus– Sciatica– Myelography– Spondylosis– Parathesias
  57. Post Polio Syndrome
    Patients who are now elderly and hadpolio as a child or young adult developingweakness, fatigue, musculoskeletal pain• Common 60-80% of polio survivors• Cause unknown• Diagnostics: symptoms, history of polio• Medical-no cure, no meds, treat symptoms• Nursing: education, rehab, quality of life
Card Set
Neuro test 3