neurological alterations notes

7/28/2019 Neurological Alterations Notes

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Flow of CSF

Characteristics of Normal CSF Function Protection, circulate nutrients Pressure 60-150 mm H

2

0

WBC

0-8 per ul

Protein14-45 mg/dL Glucose 45-75 mg/dL Appearance Clear, colorless

LP Analysis Side lying position

Lateral recumbent with chin resting on flexed knees Or bent over, head down Label tubes correctly!!! Usually 5 drawn

Can lose sample or lab will reject if not labeled correctlyInfectious Disorders

Meningitis Most common infectious disorder of brain and spinal cord esp. when school starts in the fall Caused by bacteria, viruses, fungi, and chemicals

Bacterial (Septic) Meningitis Medical emergency Most common causes:

Streptococcus pneumoniae Meisseria meningitidis Haemophilus influenzae vaccine has helped

Meningitis-Viral Agents Enteroviruses Arboviruses Human immunodeficiency virus Herpes Simplex virus (HSV)

Meningitis-Fungal Agents Ex. Candida albicans, Histoplasmosis capsulatum


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Bacterial Meningitis Inflammatory response, CSF, ICP

Be careful with LP and ICP Brain parenchyma involved cerebraledemaand further ICP

Need to use some sort of diuretic to decrease ICP Clinical Manifestations

Meningeal irritation Nuchal rigidity Positive Kernigs, Brudzinskis

Additional Clinical Manifestations Photophobia, fever, H/A, N/V, LOC (confusion), ICP, possible seizures Meningococcus rash, petechiae

Complications Most common- ICP CN alterations:

Papilledea, hemianopsai (blindness in half of visual field), decreased ocular movement Noncommunicating hydrocephalus Waterhouse-Friderichsen syndrome Manifested by DIC (disseminated intravascular coagulation), Rash, petechiae, adrenal hemorrhage and

circulatory collapse (shock) death

Upper Respiratory Tract Complication

Diagnostic Tests Blood Cultures first bleeding times!

Usually done beforeantibiotics given, however if Dr. says GIVE ANTIBIOTICS FIRST, give those andthen blood culture

Lumbar Puncture (LP) with CSF analysis purulent drainage L4/L5 Label correctly!!

Expect pt to be dizzy, headache, position correctly, meds for pain, replace fluid loss WBC- >1000/ul, Protein- >500 mg/dL Glucose- low < 45 mg/dL; cloudy/turbid X-ray


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CT- assess ICP and hydrocephalus MRI

Collaborative Care Medical emergency Placed on respiratory isolation, wear N-95, droplet precautions MENINGOCOCCAL MENINGITIS IS CONTAGIOUS Collect cultures, start antibiotic therapy

Other Medications Decadron decreases inflammation Antipyretics- (fever cerebral edema and seizures)

Tylenol per rectum Analgesics Antiseizure meds Mannitol Diuretics: reduces cerebral edema

Monitor electrolytes, strict I/O, daily weight Nursing Interventions

Resolve infection Depends on organism, however, not a short-term goal! Going to take some time

Control discomfort pain meds Decrease stimuli turning off light, closing blinds, eye covers when sleep

Usually will have photosensitivity Family at BS Seizure precautions Cooling blanket Fluids IVF

Convalescent Nursing Interventions Nutrition Progressive ROM exercises Gradual progression of activity Adequate rest & sleep Assessment of long term sequelae Family support

Recovery after the acute stage takes several weeks. High protein, high calorie foods in small, frequentfeedings are recommended. Muscle rigidity can persist, so warm baths and progressive ROM exercises

can help to loosen muscles. Progress activity gradually as tolerated and encourage adequate rest

periods and sleep. Residual effects from the infection can persist such as dementia, seizures, deafness,

hemiplegia, hydrocephalus. Should also assess vision, hearing, cognitive skills, and motor and sensory

abilities. Infants may have silient sequelae that are not apparent until they start to school and have

learning and behavioral problems. Watching a loved one suffer with meningitis is very stressful to family

members. Family support is needed.

Health Promotion is important in the prevention of meningitis! Prevention of URI via vaccinations forpneumococccal pneumonia and influenza are important. There is also a vaccine for protection againstNeisseria meningitides that is recommended for children ages 11-12, and for teens entering high school

and college who have not been previously vaccinated.

People who have been in close contact with anyone who has bacterial meningitis should be treated withprophylactic antibiotics. Early and vigorous treatment of resp. and ear infections is very important.

Health Promotion Vaccinations

Viral Meningitis Presenting sx similar to bacterial meningitis


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LP shows lymphocytosis Culture- no organisms bc viral Treat sx, prevent ICP Usually full recovery

Encephalitis acute inflammation of the brain Usually caused by a virus Epidemic

West Nile, Equine, anything from ticks & mosquitos Nonepidemic HSV Cytomegalovirus AIDS

Manifestations Fever, headache, N/V CNS abnormalities: hemiparesis, tremors, seizures, personality changes, memory impairment, amnesia,

dysphagia

Diagnostic Tests Brain imaging: CT, MRI, PET PCR:

Early diagnosis of encephalitis from HSV & West Nile Detects viral RNA

Management Mosquito Program HSV- most severe form of viral encephalitis

Meds: Zovirax, Vira-A Seizures- antiseizure meds Cerebral edema- Mannitol and Decadron

Brain Abscess accumulation of pus with in the brain tissue that results from local or systemic infection Primary organisms streptococci or staphylococci Manifestations similar to meningitis and encephalitis

Headache, fever, N/V, confusion, drowsiness, seizures Focal symptoms: vision loss, hallucination if abscess in occipital region

Can be caused from sinus, ear, tooth infection, pulmonary infection, bacterial endocarditis Collaborative and Nursing Care

Diagnostic Tests- CT, MRI Antimicrobial therapy I&D (incision and drainage) Management of sx

Seizure Disorders and Epilepsy Uncontrolled electrical discharge of neurons Etiology

Moves across both hemispheres Results from birth injury, congenital defects, infections, trauma, tumors, vascular disease, stroke, genetic

factors 3/4th

of seizures are idiopathic

Pathophysiology Epilepsy

Spontaneous recurring seizures Etiology


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Group of abnormal neurons (seizure focus) that undergo spontaneous firing, this area usually forms scartissue (gliosis) which lead to additional abnormal firing

Astrocytes release glutamate that triggers firing, so medications are targeted at suppressing astrocytesignaling or decreased glutamate release

Seizures Classification

Generalized bilateral synchronous epileptic discharges Tonic-clonic, Absence (petit mal) seizure, Myoclonic seizure, and Atonic

Partial unilateral focal irritations Simple, complex

Unclassified epileptic Phases of a Seizure

Prodromal signs or activity that precedes a seizure Aura sensory warning Ictal full seizure activity Post Ictal period of recovery after the seizure

Generalized Seizures usually results in a loss of consciousness

Tonic-Clonic Begins with aura, loss of consciousness and rigidity and is followed by tonic-clonic movement

Hyoerventiliation, loss of urinary/bowel control, tongue or cheek biting Usually lasts 2-5 minutes and a full recovery may take several hours

Petit Mal (Absence) Usually only in children however may develop into another seizure disorder

Brief starting period that may or may not result in loss of consciousness Staring/fixation of gaze and blank facial expressions

Seizures Atypical Absence

Staring Myoclonic

Jerk and fall Partial Seizures

Arise from region in motor cortex (posterior frontal lobe), most commonly begins in upper extremities andspreads to face and lower extremities (Jacksonian march)

Noting progression is important in identifying area of cortex involved Simple Partial Seizure- < 1 minute

Affects focal sensory or motor activities without loss of consciousness


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Complex Partial Seizure- Usually temporal lobe, effects cognitive, psychosensory, psychomotor oraffective activities with brief loss of consciousness

Diagnostic Studies Detailed Health History

An accurate diagnosis is crucial due to the socioeconomic, physical, psychological impact on a pt.

Comprehensive description of the seizures is most important. Asking questions to observer and pt. Ex incontinence, aura, progression of sx, postictal behaviors. Electroencephalogram (EEG)

Diagnostic test done to record the electrical activity of the surface cortical neurons of the brain 8 16 electrodes are placed on specific areas of the scalp and connected to a machine that converts the

electical signals into a written printout for interpretation

Various stimuli such as flashing bright lights and loud noises may be given to evaluate the effect on brainactivity.

Done to evaluate cerebral disease as well as brain death. Not a definitive test b/c some people without seizures have abnormalities and some people with

seizures have normal findings b/w seizures


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Pt. preparation: Teach pt. that test is painless, no electrical shocks are given. Avoid caffeine and other stimulants before test. Determine if antiseizure drugs or tranquilizing meds need to be held prior to test. Post test:

Resume all meds after test. Assist pt. to wash electrode gel out of hair.

Serum Lab studies Lab tests such as CBC, chemistries, liver and renal function, and urinalysis are done to rule out metabolicdisorders that can also cause seizures.

CT, MRI CT scan or MRI are done to rule out structural lesions as a cause, ie. tumors.

Complications Status epilepticus Continuous seizure Energy demand greater than supply EEG

Collaborative Care Drug Therapy (pg. 1538)

Generalized and Partial Seizures Dilantin (phenytoin)

Side effects hyperplasia, blood dyscrasias, elevated glucose, alopecia, hirsutism Follow up blood tests with doctor!!

Therapeutic drug level: 10-20 Tegretol

Side effects drowsiness, visual disturbances, dry mouth, headache Do not take with grapefruit juice, report visual abnormalities, abrupt withdrawal may precipitate

seizures

Absence or Myoclonic Depakote (hepatotoxicity) or Klonopin (ataxia, respiratory or cardiac depression)

Status epilepticus Requires initiation rapid acting drug that can be given IV

Ativan and Valium used most often (short acting) Must be followed by long acting drugs like Dilantin

Surgical Intervention When drug therapy is not effective at preventing seizures, surgical removal of focal area may be done. Surgery is not beneficial for everyone. Removing Focus

A definitive area of focus must be identified along with failure of drug therapy before surgery can beconsidered.

Vagal Nerve Stimulation This involves implantation of an electrode around the left vagus nerve in the neck which is connected to

a battery placed beneath the skin in the upper chest

The device is programmed to deliver intermittent electrical stimulation to the brain to reduce thefrequency and severity of seizures

The exact mechanism of action is unknown, although stimulation may interrupt synchronization ofepileptic brain-wave activity

This is similar to a pacemaker implantation in the heart for slow heart beats. Nursing Interventions

Airway, Safety


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Monitor vitals, loosen clothing, protect pts head, raise side rails or move patient to floor if not in bed,do not restrain the patient, if possible (or immediately post-seizure) place pt on their side with head

flexed forward which allows tongue to fall forward facilitating drainage of saliva and mucous and helps

prevent aspirating

Do not place objects in the patients mouth or attempt to pry jaws open

Multiple Sclerosis Chronic degenerative disorder of CNS that is characterized by inflammation, demyelination and scarring in

multiple areas of the brain and spinal cord

Pathophysiologymyelin Clinical manifestationsrelapses and remissions

See picture** Motor, sensory, cerebellar, emotional

Diplopia double vision Ataxia lack of voluntary coordination of muscle movements Flaccid

Diagnostic Tests

No definitive dx Hx, manifestations CSFmay show increased immunoglobulin G, lymphocytes and monocytes (elevated protein and WBCs) MRI sclerotic plaques

Drug Therapy (Pg. 1544-45) Corticoids- ACTH

Helps prevent exacerbations Restrict salt intake Cannot discontinue these medication abruptly

Immunomodulators- Self Injections Interferron-B

Reduce frequency of relapse Immunosuppressants- Toxicities

Monitor for hypertension and kidney dysfunction Anticholinergics

Treat bladder symptoms Cholinergics

Treat cognitive impairment Muscle relaxants

Treats muscle spasticity CNS Stimulants

Treat fatigue Antiviral/ Antiparkinsonian

Symptom Management Neurectomy Baclofen pump

Symptom Management Urinary elimination

Nursing Interventions Immobility Independence Neuromuscular function Fatigue


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Psychosocial well-being Prevent exacerbations Nutrition Symptom management

Parkinsons disease (PD) Triad

Bradykinesia: slowness in the initiation and execution of movement Rigidity: Increased muscle tone Tremors Also Postural Instability

Degeneration ofdopamine Allows acetylcholine to dominate in the substantia nigra making smooth, controlled movements difficult

Clinical Manifestations Drug Therapy

AnticholinergicsCogentin Treats tremors by blocking cholinergic receptors

Orthostatic hypotension and sedation effect poorly tolerated by elderly

Fall risk! Monitor for anticholinergic effects

blurred vision, drowsiness, constipation, urinary retention, dry mouth and cognitive impairment AntihistamineBenadryl

Has anticholinergic effect Helps tremors & rigidity MAOs

Inhibits metabolism of dopamine Used in early PD

Monitor for insomnia, N/V and exacerbation of dyskinesia ** do not give with Demerol

COMT InhibitorsEntacapone (Comtan) Decreases breakdown of levodopa making more available in the brain as dopamine

Can be used with dopaminergic or dopamine agonist for better results Monitor for dyskinesia/hyperkinesia when used with levodopa Assess for diarrhea Dark urine is a normal finding ** do not give with Demerol

Dopaminergic Levodopa Converted to DA in basal gangliaimproves triad symptoms: Bradykinesia, tremor, rigidity Monitor for ortho. Hypotension, N/V, on-off phenomenon, hallucinations, paranoia, nightmares

Administered @ exact time ordered (very short half-life) Effect decreased in presence of dietary protein (give on empty stomach)

DDC (dopa decarboxylase inhibitors) Carbidopa (Sinemet) Used with levodopa to decrease the breakdown of the levodopa before it reaches the brain

Less levodopa is needed, less side effects Avoid sudden changes in movement, avoid alcohol, see s/e of levodopa

Antivirals amantadine (Symmetrel) Stimulate the release of dopamine and prevent its reuptake

Monitor fro swollen ankles and discoloration of the skin Surgical Intervention

Ablation stereotactic destruction of areas in thalamus, globus pallidus, and subthalamic nucleus Deep Brain Stimulation placing electrodes on areas listed above to decrease neuronal activity produced by DA

depletion


10/12

Shown to improve motor function, reduce dyskinesias and reduce medication usage Transplantation fetal neural tissue implanted into basal ganglia and is designed to provide DA-producing cells

Still in experimental stages Nursing Interventions

Altered mobilitymarching in place, stepping over logs, do not pul client Bradykinesia Safety- falls (orthostasis) Dysphagia Constipation Dementia

Myasthenia Gravis (MG) Pathophysiology- acetylcholine receptors

Caused by antibodies that interfere with the transmission of Actyl @ neuromuscular junction MG Clinical Manifestations

Ocular eyelid or extraocular muscles Bulbar difficulty swallowing and articulating words Generalized

Manifestations

Fluctuating weakness

muscle weakness improves with rest Muscles involved Proximal more than distal No sensory loss Exacerbations

Complications Myasthenic Crisis- undermedication

Exacerbation of muscle weakness triggered by infection, surgery, emotional distress, inadequate drugs Sx

Myasthenic symptoms(weakness, incontinence, fatigue), Respiratory muscle weaknessmechanical ventilation, Hypertension

RX Anticholinesterase drug TENSILON improves symptoms

Cholinergic Crisis- overmedication Sx: muscle twitching followed by same symptoms of muscle weakness and respiratory failure

Hypersecretions (nausea diarrhea, respiratory secretions and bowel hypermotility), Hypotension RX: does not improve when tensilon is given, need anticholinergic medication ATROPINE

Diagnosis H&P Electromyography shows decreased response to repeated stimulation indicative of muscle fatigue Tensilon Test give anticholinesterase medication and see if symptoms improve Atropine cholinergic antagonist needs to be available to counteract effects of Tensilon in Cholinergic

Crisis

Collaborative Care & Drug Therapy Anticholinesterase Inhibitors Tensilon

Enhances function at neuromuscular junction Take same time each day, take with food to decrease GI upset, eat within 45 minutes to strengthen

chewing and reduce risk for aspiration

If observe periods of weakness, discuss strength and times of administration Use cautiously for those w asthma or cardiac dysrhythmias

Corticosteroids used to decrease autoimmune response of disease Immunosuppressants used to decrease autoimmune response of disease


11/12

Surgical removal of thymus gland Nursing Interventions

Muscle endurance Manage fatigue Avoid complications Maintain quality Manage respiratory status Nutrition MG Foundation

Amyotrophic Lateral Sclerosis (ALS) Loss ofmotor neurons

Clinical Manifestations Progressive No sensory loss intellectual function remains intact Atrophy- respiratory concern; eventually die of respiratory failure

Diagnostic tests CK-BB levels increased, EMG

Drug Therapy Riluzole slows progression, does not cure!

Glutamate antagonist that slows deterioration of motor neurons by decreasing the release of glutamicacid

Monitor LFT (hepatotoxic risk), avoid alcohol, take @ evenly spaced intervals as prescribed, soteaway from bight light

Management Huntingtons disease

Progessive, degenerative brain disorder caused by a deficiency of Ach and GABA that leads to an excess ofDopamine

Symptoms opposite of PD Genetically transmitted autosomal dominant disorder Clinical Manifestations

Chorea abnormal excessive involuntary movement Interventions

No cure; all care is palliative Haldol, Risperdal, Valium

Pts need extremely high caloric (400-500calories/day) intake bc of constant movement Alzheimers disease (AD)

Pathophysiology Plaques & tangles

Clinical manifestations MildShort term memory loss, forgetfulness, decreased judgment, geographic disorientation Moderatewandering, getting lost, confusion, agitation, receptive & expressive aphasia, apraxia Late unable to process new info, little memory left, cannot understand words, repetitious words/sounds,

immobility, difficulty eating/swallowing

Diagnostic Tests H & P (The diagnosis of AD is primarily a DX of exclusion) Screening for vitamin B12 deficiency; mental status testing Neuroimaging (CT scan or MRI) shows presence of vascular brain lesions SPECT, MRS, & PET detect changes early in the disease, as well as monitoring the TX response

Management


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Drug Therapy Cholinesterase inhibitors donepezil (Aricept) Memantine (Namenda) Antipsychotics controls hallucinations/delusions Antidepressants for the depression associated with dementia

AimImprove memory Nursing Interventions

Reorient Routines Safety Behavioral problems Communication Comfort Nutrition Oral care Skin care Elimination Caregiver support

Sundowning PT becomes more confused & agitated in the late afternoon or evening

Interventions Create calm environment Maximize daylight exposure Evaluate meds Limit naps & caffeine

Guillain- Barre syndrome Pathophysiology

Peripheral nervous system is damaged Manifestations

Remyelinization Begins ascending Improves descending Complications:

Respiratory Immobility

Interventions Maintain ventilation No Aspiration Manage pain Communication Nutrition Psychosocial Elimination ROM/ Skin Care Safety Return to optimal status

**Emergency MGMT of seizures, diagnostic test, more Pharm. questions than Beerman, Blue Boxes (nursing care

plans),

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