Flow of CSF

Characteristics of Normal CSF Function Protection, circulate nutrients Pressure 60-150 mm H 0

2

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 correctly Infectious 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

 Bacterial Meningitis Inflammatory response, CSF, ICP Be careful with LP and ICP Brain parenchyma involved cerebral edema and 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 before antibiotics given, however if Dr. says GIVE ANTIBIOTICS FIRST, give those and then 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

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, frequent feedings 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 for pneumococccal pneumonia and influenza are important. There is also a vaccine for protection against Neisseria 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 with prophylactic antibiotics. Early and vigorous treatment of resp. and ear infections is very important.

Health Promotion Vaccinations Viral Meningitis Presenting sx similar to bacterial meningitis

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

 Group of abnormal neurons (seizure focus) that undergo spontaneous firing, this area usually forms scar tissue (gliosis) which lead to additional abnormal firing Astrocytes release glutamate that triggers firing, so medications are targeted at suppressing astrocyte signaling 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 and spreads 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

 Complex Partial Seizure- Usually temporal lobe, effects cognitive, psychosensory, psychomotor or affective 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 brain activity. 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

 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 metabolic disorders 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 be considered. 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 the frequency and severity of seizures The exact mechanism of action is unknown, although stimulation may interrupt synchronization of epileptic brain-wave activity This is similar to a pacemaker implantation in the heart for slow heart beats. Nursing Interventions Airway, Safety

 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 Pathophysiology myelin Clinical manifestations relapses 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 CSF may 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

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 of dopamine Allows acetylcholine to dominate in the substantia nigra making smooth, controlled movements difficult Clinical Manifestations Drug Therapy Anticholinergics Cogentin 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 Antihistamine Benadryl 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 Inhibitors Entacapone (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 ganglia improves 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

 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 mobility marching 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 weakness mechanical 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

 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 of motor 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 glutamic acid Monitor LFT (hepatotoxic risk), avoid alcohol, take @ evenly spaced intervals as prescribed, sote away from bight light Management Huntingtons disease Progessive, degenerative brain disorder caused by a deficiency of Ach and GABA that leads to an excess of Dopamine 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 Mild Short term memory loss, forgetfulness, decreased judgment, geographic disorientation Moderate wandering, 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

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),