Neurology Chapter 64 Management of Patients with neurologic infection, autoimmune disorders and neuropathies.

Neurology Chapter 64 Management of Patients with neurologic infection, autoimmune disorders and neuropathies

Meningitis Pathophysiology Meningitis Encephalitis
Infection/ inflammation of the meninges Encephalitis Infection/inflammation of the brain tissue

Meningitis Pathophysiology Meningitis/ encephalitis  Infection 
Immune response  Swelling/edema  I –ICP  Etc.

Meningitis Is meningitis a disorder of the CNS, PNS or both? CNS PNS

Meningitis The most common bacterial pathogens are:
Haemonphili influenzai Affected kids < 5 yrs H influenzae vaccine (Hib) Streptococcus pneumoniae Affects age 19-59 Neisseria meningitides Easily transmitted to others Least lethal

Meningitis Two ways the infectious agent can inter the meninges
Blood stream Most common Usually d/t URI Direct extension TBI Invasive procedures

Meningitis The viral type of meningitis is usually
Self limiting Benign Bacterial meningitis is potentially Fatal

Meningitis Clinical manifestations Onset: General S&S Abrupt
Nuchal rigidity Positive Kernig's Positive Brudzinski’s Photophobia

Meningitis Clinical Manifestations S&S of infection Fever Chills

Meningitis Clinical manifestations S&S of I-ICP H/A i LOC Vomiting
Papilledema Hydrocephalus

Meningitis Clinical manifestations N. Meningitidis Rash Petechial
Purpuric lesion Ecchymosis

Meningitis Clinical manifestations Infants/young children Seizures
High-pitched cry Bulging fontanels

Meningitis Mr. Jones has encephalitis. Would you expect his signs and symptoms to be more or les severe than a person with meningitis? More severe Less severe Encephalitis signs and symptoms are more severe with delirium & seizures.

Meningitis Diagnosis Lumbar tap Positive Kernig’s Positive Brudzinski
C&S of CSF Positive Kernig’s Positive Brudzinski

Meningitis Treatment Broad spectrum antibiotics Intrathecally
Penicillin Cephalosporin's Intrathecally Early intervention crucial!

Meningitis Nursing interventions Isolation Assessment
? Causative agent Assessment V/S Neuro check Cranial nerve involvement Abn sleep patterns Behavioral changes ABG’s Opisthotonus

Meningitis Nursing management I-ICP protocol I&O
Quiet environment: Dark Limit visitors Nutrition No constipation Pad side rails Emotional support Alkalosis

Meningitis Prevention Haemonphilus vaccine
HiB meningococcal conjugate vaccine persons aged 11 to 55 years. designed to offer protection against four serogroups of Neisseria meningitidis (A, C, Y, W-135), which account for approximately 70 percent of cases in the United States.

Meningitis Complications Thrombosis i cerebral blood flow Brain damage
Death

Meningitis What do bulging fontanel’s in an infant indicate?
What type of meningitis occurs most frequently and is considered the milder form? What are the symptoms of meningitis? To facilitate performing the lumbar puncture, on the patient who may have meningitis, it is best for the nurse to place the patient in what position? After the lumbar puncture has been performed, it is best for the nurse to do

Meningitis What standard vaccine is administered to infants to prevent meningitis? Identify the bacteria most commonly associated with meningitis What is the most severe form of meningitis? What affect does meningitis have of the physiology of the brain? Name six signs and symptoms of bacteria meningitis Is meningitis a disease of the CNS or PNS

Brain Abscess Pathophysiology
A collection of infectious material within the tissue of the brain Infection  I-ICP  Brain shift

Brain Abscess 2 ways infection can enter the brain Direct invasion
Spread from nearby sight Sinuses Ears Teeth

Tongue piercing causes brain abscess
13 December 2001 New Scientist Parents now have another reason to frown on tongue piercing - a potentially fatal brain abscess suffered by a young woman in Connecticut. The woman's tongue became sore and swollen two or three days after it was pierced, and she reported a foul-tasting discharge from the pierced region. The infection healed in a few days after she removed the stud from her tongue, but a month later she suffered severe headaches, fever, nausea and vomiting. A scan at the Yale University hospital revealed the brain abscess, which physicians drained. She recovered after six weeks of intravenous antibiotic treatment.

Brain Abscess Clinical manifestations I-ICP Infection Fever? Sometimes
Sometimes not!

Brain Abscess Diagnostic findings CT MRI

Brain Abscess Medical Management Antimicrobial therapy Surgery
Large IV doses Surgery Anti-convulsant

Brain Abscess Nursing management I-ICP protocol Neuro assessment
Safety protocol seizures

Brain Abscess Who is most at risk for brain abscesses?
Describe the medical treatment for a patient with a brain abscess? Is a brain abscess a diseases of the CNS, PNS or both?

Multiple Sclerosis Pathophysiology Autoimmune disease
Demyelination of the myelin covering that protects the neurons of the brain and spinal cord

Multiple Sclerosis Demyelination Destruction of the myelin sheath 
Impaired transmission of nerve impulses Both the axon & myelin are attacked

Multiple Sclerosis Is multiple sclerosis a disorder of the CNS, PNS or both? CNS PNS Both CNS & PNS

Multiple Sclerosis Etiology / Contributing factors Unknown cause
Men vs women Men < women Age of onset 20-40

Multiple Sclerosis Clinical manifestations
Usually slow, progressive disease Relapsing-remitting course Patient may experience remission & exacerbation’s Exacerbation of symptoms  Partial/full remission  Symptoms return

Multiple Sclerosis Clinical Manifestations
Episodes of motor, visual or sensory disturbance Visual disturbances Diplopia Blurred vision Paresthesia Fatigue Dizziness

Multiple Sclerosis Clinical Manifestations Emotional disturbances
Scanning speech Incontinence Sexual disorders Spasticity Muscle hypertonicity

Multiple Sclerosis Diagnosis MRI CT scan Lumbar puncture Sm. Plaque
Patches CT scan Lumbar puncture Immunoglobulin abnormalities

Multiple Sclerosis Medical management No cure Goal Manage symptoms
Delay progress Manage symptoms

Multiple Sclerosis Pharmaceutical Interferons ABC&R

Multiple Sclerosis Pharmaceutical Skeletal muscle relaxants
Baclofen/lioresal i transmission of impulses from the spinal cord to the skeletal muscle  i spasticity S/E Drowsiness, weak

Multiple Sclerosis Pharmaceutical Corticosteriods Immunosuppressants
Dexamethasone, prednisone Action Decreased imflammation S/E Poor wound healing Na+ & H20 retention h glucose levels

Multiple Sclerosis Nursing Interventions Individualized B&B management
Avoid stress Stress Fatigue Extreme temp. Exercise Fluids Diet High roughage

Multiple Sclerosis Complications Pneumonia Decubitis ulcers
Contractures Dependency

Multiple Sclerosis What is the pathophysiology of MS?
Is MS a disease of the CNS, PNS, or both? Explain what demyelination refers to. What role does temperature play in multiple sclerosis? Identify 5 common signs and symptoms of MS.

Multiple Sclerosis What classifications of medications are used in treating MS? What is the progression of multiple sclerosis What is the most common symptom associated with MS? When does the individual usually seed medical help? What can exacerbate MS? What is a long term goal for a patient with MS?

Myasthenia Gravis Pathophysiology Auto-immune
Progressive disease Remission & exacerbation Flaw in transmission of impulses from the nerve to the muscle Neuro-muscular junction Most often affects the muscles regulated by the cranial nerves

Myasthenia Gravis Pathophysiology
Specifically attacks receptors for acetylcholine  Prevents muscle contraction  Progressive weakness & fatigue

Myasthenia Gravis Is myasthenia Gravis a disorder of the CNS, PNS or both? CNS PNS Both CNS & PNS

Myasthenia Gravis Clinical manifestations Onset Early Progressive
Gradual Early Ptosis Diplopia Progressive May be fast or slow With or without remission Dysphonia Difficulty chewing & swallowing Extreme muscle weakness

Myasthenia Gravis Clinical manifestations
Resp. paralysis (Bulbar paralysis) Vital capacity i Resp. failure  Deathmosis

Myasthenia Gravis “Myasthenia gravis is purely a motor disorder with no effect on sensation or coordination.”

Myasthenia Gravis Etiology Men vs Women Age 20-40 Thymus
Men < women Age 20-40 Thymus enlarged

Myasthenia Gravis Diagnostic exams Positive response to Tensilon
IV Tensilon Prevents Acetylcholine from being broken down Muscle function improves within 60 sec. & lasts 30 mins.

Myasthenia Gravis Treatment No cure Anticholinesterase agents
Neostigmine, Mestinon, Prostigmin, Mytelase Prevents the destruction of Acetylcholine, thereby increasing the muscle to nerve response and muscle strength S/E: Sweating, weakness, bradycardia, hypotension

Myasthenia Gravis Treatment Corticosteroids Thymus Plasmapheresis
radiation Plasmapheresis Plasma exchange

Myasthenia Gravis Nursing interventions Planned activities
Avoid stress Rest periods Resp. baseline Tidal volume Vital capacity Inspiratory force

Myasthenia Gravis Nursing interventions
Do not administer barbiturates, tranquilizers, muscle relaxants, morphine etc. Eye care

Myasthenia Gravis Complications Myasthenic crisis Caused by S&S
Not enough med. Stress S&S Rapid onset of weakness  Resp. distress Treatment Medication IV or IM Resp. support Intubation PEEP Suction NG tube

Myasthenia Gravis Complications Cholinergic crisis Caused by S&S
Too much med. S&S Rapid onset of weakness  Resp. distress Treatment Hold medication Resp. support Intubation PEEP Suction NG tube

Myasthenia Gravis How can you tell the difference between Myasthenic crisis and a Cholinergic crisis? Tensilon test If they respond to tensilon with increased muscle strength… Myasthenic Crisis They need more medications If they respond to the tensilon with increased muscle weakness… Cholinergic crisis Hold medications

Myasthenia Gravis What can cause a cholinergic crisis?
What are the S&S of a cholinergic crisis? What is the treatment of a cholinergic crisis? MG is a disorder of the CNS, PNS or both? What are the clinical manifestations of MG How do you confirm the diagnosis of MG?

Myasthenia Gravis Myasthenic crisis is caused by what?
What are the S&S of a Myasthenic crisis? What is the treatment of a Myasthenic crisis? What is the difference between MG and MS? (besides the letter G&S) When you give a Tensilon test how would you know if they were under medicated? What meds are used to treat MG?

Guillain-Barre Syndrome
Pathophysiology Autoimmune disease The myelin sheath of the spinal and cranial nerves are destroyed by diffuse inflammatory reaction

Is Guillain-Barre Syndrome a disorder of the CNS, PNS or Both? CNS PNS Both CNS and PNS

Pathophysiology Demyelination Axon atrophy Starts distal nerves Remyelination Slow Descending pattern

Pathophysiology Sudden attack on myelin  Inflammation  Axon damaged  Paralysis / paresis  Remyelination  If cell body (soma) NOT destroyed  Recovery If sell body (soma) IS destroyed  Some degree of permanent disability

Etiology Unknown In most patients it is preceded by viral infection Men vs. Women =

Clinical manifestations Onset Abrupt Symmetrical paresis that progresses to paralysis Begins with lower extremities Paresthesias Weakness Dyskinesia Paralysis

Clinical manifestations Progresses upward Resp failure Bulbar weakness Recovery

Diagnostic exam CSF Increased protein EEG Slowing of nerve conduction

Treatment Considered a medical emergency Mechanical ventilation Immunosuppressant Anti-coagulants Plasmapheresis

Nursing interventions Respiratory function ROM TED hose Nutrition Communication Anxiety

Complications Resp. failure PE Anxiety

What is the pathophysiology of GB? What is demyelination? Is GB a disorder of the CNS, PNS or both? What are the S&S of GB? What are the initial symptoms of GB? What is the outcome of GB? What are the complications associated with GB?

Trigeminal Neuralgia AKA Pathophysiology Tic Douloueux
Condition of CN 5 Neuralgia = Nerve pain

Trigeminal Neuralgia Clinical manifestation
Pain occurs when trigger points are stimulated, causing periods of intense pain and facial twitching Begins and ends suddenly Worst pain known!

PAIN!!! Trigeminal Neuralgia Clinical Manifestations Sudden Stabbing
Burning Knife-like

Trigeminal Neuralgia Etiology Unknown Men vs Women Age of onset
Men < women Age of onset 50’s Dental work

Trigeminal Neuralgia Diagnostic exams Hx MRI

Trigeminal Neuralgia Treatment Anticonvulsants Examples Action S/E
Tegretol Dilantin Action i transmission of nerve impulse S/E Drowsiness

Trigeminal Neuralgia Nerve block Surgery
Alcohol and phenol injected into the nerve Destroys the nerve – temporarily Surgery

Trigeminal Neuralgia Nursing Interventions Goal Avoid Triggers
Relieve pain Avoid Triggers Hot & cold foods Draft areas Brushing teeth Chewing food Self-care deficit Depression Suicide

Trigeminal Neuralgia Complications Paralysis Infection

Trigeminal Neuralgia What cranial nerve is involved with trigeminal neuralgia? What is the primary nursing diagnosis with a patient with Trigeminal Neuralgia? What can trigger Trigeminal neuralgia? That is Tic Douloureux? What is Dilantin? What are the side effects of Dilantin? What are the S&S is Trigeminal neuralgia? What is the treatment for trigeminal neuralgia?

Bell’s Palsy Pathophysiology Inflammation of CN -7
Resulting in weakness or paralysis of one side of the face Usually resolve in 2-8 weeks

Bell’s Palsy Clinical Manifestations
Facial pain that radiates to the eye & ear h eye tearing Speech difficulties Distortion of the face Diminished blink reflex

Bell’s Palsy Etiology Unknown

Bell’s Palsy Medical Treatment Corticosteriods Eye drops Analgesics

Bell’s Palsy Nursing interventions Eye care Moist heat to face Massage
Patch Drops Moist heat to face Massage Electric stim

Bell’s Palsy What cranial nerve is involved with Bell’s palsy?
What is the primary nursing diagnosis with a patient with Bell’s palsy? What can trigger Bell’s palsy? What are the S&S is Bell’s palsy? What is the treatment for Bell’s palsy?

Neurology Chapter 64 Management of Patients with neurologic infection, autoimmune disorders and neuropathies.

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Neurology Chapter 64 Management of Patients with neurologic infection, autoimmune disorders and neuropathies.

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