Neuro

• 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

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

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

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

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)

• • 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,
• PREVENTION=DEET

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.

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

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

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.

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

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

• 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

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)

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

MRI-presence of plaques in CNS• Electrophoresis of CSF• Urodynamics (baseline)• NCS (baseline)• Neuropsychological testing (baseline)• Sexual counseling

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

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

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)

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

– Mestinon (pyridostigmine bromide)-anticholinesterase medication (1st line of tx)– Prednisone (immunosuppressive therapy)– Cytotoxic meds (Imuran, Neoral, Cytoxan)

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)

Education of patient and family– Medication management, energyconservation, prevention of complication,ocular manifestation management– Educate on recognition of Myasthenic Crisis

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

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

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

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)

Anticonvulsant-Tegretol, Neurontin, Dilantin– Microvascular Decompression of the nerve– Gamma Knife Surgery– Percutaneous radiofrequency coagulation– Percutaneous balloon microcompression– Pain prevention– Postop care

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

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

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

Astrocytomas– Glioblastoma Multiforme– Oligodendrocytoma– Ependymoma– Medulloblastoma

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

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

Neuro Exam• CT Scan w/contrast• MRI• PET scan (complements MRI)• EEG• Radiation Therapy• Chemotherapy• Bone Marrow• Surgical intervention• Gamma Knife

Aspiration Prevention• Neuro checks• Protection from seizures• Motor and sensory function

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

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

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

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

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)

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

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

Mobility– Self care deficits– Nutrition– Swallowing– Communication– Family/Significant others– Psych

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

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

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.

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

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

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

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

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

Radiculopathy– Nucleus pulposus– Herniated nucleus pulposus– Sciatica– Myelography– Spondylosis– Parathesias

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