Neurologic Function

Management of Patients with Neurologic Infections and Autoimmune Disorders

Meningitis
Inflammation of arachnoid/pia mater of brain, spinal cord, and CSF Septic (bacterial) or Aseptic (viral) Enter CNS indirectly or directly Resulting inflammatory response can ICP Exudate may spread to cranial/spinal nerves and cause neurologic deterioration

Clinical Manifestations
Headache Fever Nuchal rigidity Positive Kernigs sign Positive Brudinskis sign Photophobia Rash with N. meningitidis Disorientation Seizures

Diagnostics What diagnostics would you expect to be ordered?

What findings would you expect?

Prevention
Haemophilus influenzae meningitis is now rarely seen do to childhood vaccination College freshmen are targeted for vaccination against N. meningitidis Close contacts of patients with meningococcal meningitis (N. meningitidis) are treated prophylactically with rifampin (Rifadin), ciprofloxacin (Cipro) or ceftriaxone (Rocephin)

Management
Medical Early administration of antibiotics Dexamethasone Fluid volume expanders Dilantin for seizure control Nursing Neurological checks Monitor VS, SpO2, ABGs Maintain adequate tissue oxygenation Monitor arterial BP Rapid fluid replacement Prevent ICP Seizure management Prevent complications Maintain Infection Control

Encephalitis
Acute inflammation of brain tissue Most often viral
Herpes Simplex Virus Enteroviruses Arboviruses

Can also be caused by: bacteria, fungi, paracytes No exudate Can result in death

Diagnostics
The specific diagnostics will vary by cause Common diagnostics include
CSF analysis Neuroimaging (MRI) EEG

Assessment
Use GCS Clinical manifestations: fever, n/v, nuchal rigidity, headache, vertigo Seizure activity Cranial nerve involvement Indicators of ICP

What is the GCS? What does a GCS 15 tell you? A GCS 3? What signs are indicative of increased intracranial pressure?

Treatment

What is the treatment of encephalitis dependent upon?

Multiple Sclerosis
Progressive, degenerative disease affecting:
Myelin sheath Conduction pathways of CNS

Leading cause of neurologic disability in 20 40 year olds 4 patterns Periods of remission and exacerbation

Pathophysiology
Sensitized T cells cross blood-brain barrier and remain in the CNS and promote entry of other agents that damage immune system Immune system attack leads to inflammation that destroys myelin and oligodendroglial cells Damaged myelin is removed by astrocytes and plaques develop on demyelinated axons

Pathophysiology
White fiber tracts are affected Recovery of myelin will occur with remission Repeated exacerbations will result in permanent damage caused by degeneration of the demyelinated axons

Clinical Manifestations
Fatigue Depression Weakness Numbness Ataxia Loss of balance Pain Absent abdominal reflexes Hyperactive DTRs Visual disturbances
diplopia

Spasticity Cognitive changes

Mild to moderate

Emotional lability Bladder, bowel, and sexual dysfuntion

Secondary Complications
UTI Constipation Pressure ulcer Contractures Dependent pedal edema Pneumonia Reactive depression Decreased bone density Increased risk of osteoporosis

Gerontologic Considerations
Mrs. S is 60 years old and has had relapsing-remitting MS for 35 years. She had just been diagnosed with type 2 diabetes and her BP is now at a level that requires pharmacotherapy. With each exacerbation of her MS she seems to have increased functional deficits. Her functional abilities are also impaired by increasing weakness and a stooped posture. She has been hospitalized for an acute exacerbation and work-up that identified the diabetes mellitus. She has recovered to the point that she can be discharged to home but she is worried about being a burden.

Question As you are planning Mrs. Ss discharge, what factors must be considered?

Assessment and Diagnostic Findings

MRI identifies multiple plaques in CNS Electrophoresis of CSF Evoked potential studies Urodynamic studies Neuropsychological testing

Medication
Disease modifying therapy:
Interferon beta-1a Interferon beta-1b Glatiramer acetate Methylpredinisolone Mitoxantrone

Symptom management:
Baclofen Benzodiazepines Zanaflex Dantrolene Amantadine Pemoline Fluoxetine Alpha-adrenergic blockers Antispasmotics Vitamin C

Nursing Interventions
Promote physical mobiltiy Prevent injury Enhance bladder and bowel control Enhance communication & manage swallowing difficulties Improve sensory and cognitive function Improve home management Promote sexual function

Myasthenia Gravis
Chronic neuromuscular autoimmune disease Weakness of voluntary muscles Remissions and exacerbations Nerve impulse not transmitted to skeletal muscles Development of specific antibodies to one or more Ach receptor sites Degeneration of Ach receptors Thymus gland often abnormal

Clinical Manifestations
Ocular muscle involvement Bulbar weakness Generalized weakness Dysphonia

Describe the clinical presentation of these manifestations. What is a major associated risk?

Assessment/Diagnostics
AchE Inhibitor test: edrophonium (Tensilon) is injected IV Identification of Ach receptor antibodies in serum Repetitive Nerve Stimulation MRI

Medical Management
Medications:
Antichoinesterase Inhibitors (pyridostigmine) Immunosuppresive agents Corticosteroids Cytotoxic agents

Other:
Plasmppheresis Thymectomy

Interventions
Identify at least one strategy to:
Assist with activities Facilitate communication Provide respiratory support Provide nutritional support Provide eye protection Provide psychosocial support

When is the best time to administer AchIs?

Serious Complication
Respiratory Failure
Often precipitated by a respiratory infection Other triggers: medication change, surgery, pregnancy, medications that exacerbate MG

Discuss why respiratory failure would occur. What collaborative interventions would be necessary if respiratory failure occurs?

Myasthenia Gravis: Crisis

Myasthenia Crisis
Exacerbation of myasthenic symptoms Undermedication with AchEIs

Cholinergic Crisis
Acute exacerbation of muscle weakness Overmedication with cholinergic drugs When is the best time for chest physiotherapy? What should the nurse offer after CPT?

Problem Identification Identify the key Collaborative Problem and Nursing Diagnosis associated with Myasthenia Crisis

Guillian-Barr Syndrome
Autoimmune attack on myelin of PNS Ascending weakness most typical Impaired saltatoy conduction Characterized by: dyskinesia, hyporeflexia, and paresthesia Antecedent event Most fully recover, but can result in death

Pathophysiology
Cell mediated and humoral immune attack Molecular mimicry Process results in influx of macrophages and other immune mediated agents that attack myelin Axon looses ability to conduct impulse

Clinical Manifestations
Classic presentation: Areflexia and ascending weakness Paresthesia Pain Blindness Respiratory compromise Autonomic dysfunction

Assessment and Diagnostics

No serum test will diagnose CSF analysis Evoked potential studies
Discuss what CSF finding is diagnostic of GBS. What would evoked potential studies show and why?

Medical Management
Baseline respiratory assessment and close monitoring
Continuous ECG monitoring

Anticipate need for intubation and mechanical ventilation Plasmapheresis and IV Immunoglobulin G (IVIG) Short acting alpha adrenergic beta blockers

Nursing Interventions
Identify interventions that will: Maintain respiratory and cardiovascular function Enhance physical mobility Provide adequate nutrition Improve communication Decrease fear and anxiety Monitor and manage potential complications