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Confidence Test taking strategies Ample test preparation and study habits Review of frequent board examination topics Focus on your goals Above all- PRAYERS
1.Central nervous system (CNS): brain and spinal cord 2.Peripheral nervous system (PNS): cranial nerves, spinal nerves and autonomic nervous system
Function of the nervous system are
NERVOUS SYSTEM
Brain
Spinal Cord
Peripheral
BRAIN : Diencephalon
BRAIN: Diencephalon
Thalamus largest part, influences mood
and registers an unlocalized, uncomfortable perception of pain. Epithalamus small area superior and posterior to the thalamus, involved in the emotional and visceral response to odors, pineal body (onset of puberty)
in maintaining homeostasis, plays a central role in the control of body temperature, hunger and thirst, plays a major role in controlling the secretion of hormones from the pituitary gland.
Diencephalon
BRAIN : Brainstem
Connects the spinal cord to the remainder of
the brain Consists of the medulla oblongata, pons, and midbrain Involved in vital body functions such as the control of HR, BP, and breathing
BRAIN : Brainstem
magnum to the pons CN 9, 10, 11, 12 Specific functions: regulation of HR and BV diameter, breathing, swallowing, vomiting, coughing, sneezing, balance and coordination
Brainstem : Pons
Immediately superior to the medulla
oblongata Means bridge CN 5, 6, 7, 8 Lower part of the pons: breathing, swallowing and balance Other nuclei in the pons control functions such as chewing and salivation
Brainstem : Midbrain
Superior to the pons Smallest region of the brainstem CN 3 and 4 Found superior and inferior colliculus Superior colliculi involved in visual reflexes,
turning the head, a sudden loud noise, bright flash of light Inferior colliculi major relay centers for the auditory nerve pathways in the CNS
movements and in the control of pupil diameter and lens shape Contains a nuclear black mass called Substantia Nigra
BRAIN : Cerebrum
BRAIN : Cerebrum
Largest part of the brain Divided into left and right hemisphere by a
longitudinal fissures The surface of each hemisphere is wrinkled by presence of eminences known as Gyri and furrows called Sulci or Fissures
lobes:
Frontal lobes Principal motor area (4) Important in the control of voluntary motor functions, motivation, aggression, mood, and olfactory (smell) reception Brocas area (44,45) Brocas aphasia (executive, motor, nonfluent, anterior)
Parietal lobe Principal center for the reception and conscious perception of most sensory information, such as touch, pain, temperature, balance and taste Principal sensory area (3,1,2)
Occipital lobe Functions in the reception and perception of visual input Principal visual cortex (17)
Temporal lobe Involved in olfactory (smell) and auditory (hearing) sensations and plays an important role in memory They associated in abstract thought and judgement Primary auditory cortex (41,42) Wernickes area (22) wernickes aphasia (receptive, sensory, fluent, posterior)
Brain: Cerebellum
BRAIN : cerebellum
Composed of gray matters Posterior and inferior to the cerebrum Involved in balance, maintenance of muscle
tone and coordination of fine motor movements Major function of the cerebellum is that of comparator Also involves learning motor skills (riding a bicycle/playing a piano)
Cerebellar comparator
magnum to the 2nd lumbar vertebra below which is the cauda equina It has a central gray part organized into horns and a peripheral white part forming nerve tracts Roots of spinal nerves extend out of the cord
outside the brain and spinal cord Divided into two groups:
12 pairs of CN 31 pairs of SN
Sensory Motor
Cranial nerves sensory I,II,VIII motor III, IV, VI, XI, XII mixed V, VII, IX, X
Feel A is
Girls Vagina
Such Heaven
Some Say Marry Money But My Brother Says Big Boobs Matter Most
region of vertebral column 31 pairs (c8, t12, l5, s5, c1) Organized into 3 plexuses
spinal cord (thoracolumbar) Utilized by the body for FLIGHT and FIGHT response Neurotransmitter agents are Epinephrine and Norepinephrine (coming from the adrenal gland) ADRENERGIC system
Sympathetic Responses:
Increased:
HR RR BP Visual Acuity (Pupillary Dilation) Smooth Muscle tone sphincters are contracted Vasoconstriction - peripheral Metabolism glucose, fatty acids
Sympathetic Responses:
Decreased
Peristalsis Salivary
secretions
Ejaculation
Parasympathetic Responses
Decreased:
HR RR BP Visual Acuity (Pupillary constriction) Smooth Muscle tone sphincters are relaxed Vasodilation = peripheral Metabolism dec glucose, fatty acids
Parasympathetic Responses:
Increased:
Peristalsis Salivary
secretions
Erection
abnormal reflexes
reflexes
Meninges
Meninges
Dura mater Dural venous sinuses Epidural space (SC)
Meninges
Arachnoid Subdural space (space between dura mater and arachnoid, contains small amount of serous fluid)
Meninges
Pia mater Tightly bound to the surface of brain and SC Subarachnoid space (bet. Arachnoid and pia mater, filled with CSF and BV)
Cerebrospinal Fluid
Bathes the brain and spinal cord Protective cushion aound the CNS Produced by the Choroid plexus of the lateral,
third, and fourth ventricles Clear, colorless, SG of 1.007 In normal adult, approximately 500 ml of CSF produced each day, all but 125 to 150 ml is absorbed by the villi
CSF Flow
Cerebral Circulation
Receives approximately 15% of the cardiac
output or 750 ml per minute Does not store nutrients and has a high metabololic demand that requires high blood flow Unique BF bec. It flows against gravity Poor collateral BF
BLOOD-BRAIN BARRIER
CNS is inaccessible to many substances Many substances cannot reach the neurons
of the CNS Formed by the endothelial cells of the brains capillaries, which form continuous tight junctions, creating BBB to macromolecules Must filter through the capillary endothelial cells and astrocytes Can be altered by trauma, cerebral edema and hypoxia
NEURONS
Basic functional unit
Dendrite- branch
type structure with synapses for receiving electrochemical messages Axon long projection that carries impulses away from the cell body
Neurotransmitters
Acetycholine Dopamine Epinephrine and Norepinephrine GABA (inhibitory) Serotonin ( depression, Glutamine (excitatory
manic)
5 categories:
1. Cerebral function- LOC, mental status 2. Cranial nerves 3. Motor function 4. Sensory function 5. Reflexes
source of history
A. Health assessment interview to collect subjective data 1. If clients ability to communicate is challenged by altered level of consciousness, interviewer may discuss with family member or close friend 2. If client has a health problem involving neurologic function, determine a. Onset b. Characteristics and course c. Severity d. Precipitating and relieving factors e. Associated symptoms noting timing and circumstances
3. Questions about present health status include a. Numbness or tingling sensations b. Tremors, problems with coordination or balance c. Loss of movement of any part of the body d. Difficulty with speaking or senses e. Information about memory f. Feeling state, e.g. anxious, depressed g. Changes in sleep patterns h. Ability to perform self-care and ADL i. Sexual activity j. Weight changes k. Prescribed and over the counter medications, frequency of use and duration
4. Determine history of a. Seizures, fainting, dizziness, headaches b. Trauma, tumors, surgery involving brain, spinal cord, nerves c. Diseases that might affect neurologic function 1. Cardiac disease 2. Strokes 3. Pernicious anemia 4. Sinus infections 5. Liver dysfunctions 6. Diabetes mellitus 7. HPT 8. Mental health problems
B. Physical assessment to collect objective data a. Unilateral neglect b. Poor hygiene and grooming c. Abnormal gait and posture d. Emotional swings, personality changes e. Masklike appearance on face f. Apathy
g. Aphasia (defective or absent language function): TIAs, strokes; strokes involving posterior or anterior artery involve receptive aphasia h. Dysphonia (change in tone of voice): strokes of posterior inferior cerebral artery, paralysis of vocal cords, cranial nerve X
i. Dysarthria (difficulty in speaking): strokes involving anterior inferior and superior cerebral arteries, lesions involving UMN, LMN, cerebellum, extrapyramidal tract j. Decreased level of consciousness: brain trauma, infections, TIAs, stroke, brain tumors k. Confusion, coma: strokes affecting vertebralbasilar arteries
2. Cognitive function assessment with abnormal findings a. Disorientation to time and place: stroke of right cerebral hemisphere b. Memory deficits: anterior cerebral artery and vertebralbasilar artery c. Perceptual deficits: strokes of middle cerebral artery, brain trauma, dementing conditions d. Impaired cognition: strokes of middle cerebral artery, cerebral trauma, brain tumors
CEREBRAL FUNCTION
Assess the degree of wakefulness/alertness Note the intensity of stimulus to cause a
response Apply a painful stimulus over the nailbeds with a blunt instrument Ask questions to assess orientation to person, place and time
Cerebral function
Utilize the Glasgow Coma Scale An easy method of describing mental status
and abnormality detection Tests 3 areas- eye opening, verbal response and motor response Scores are evaluated- range from 3-15 No ZERO score
identification Repeat with the other nostrils PROBLEM- ANOSMIA- loss of smell
Snellen chart Check for visual field by confrontation test Check for pupillary reflex- direct and consensual Fundoscopy to check for papilledema
Snellen chart
extra-ocular muscles Deviations: Opthalmoplegia- inability to move the eye in a direction Diplopia- complaint of double vision
facial skin Motor portion- assess the muscles of mastication Assess corneal reflex
Place each substance in the anterior two thirds of the tongue, rinsing the mouth with water Motor portion- ask the client to make facial expressions, ask to forcefully close the eyelids
balance
the client to say AH The posterior one-third of the tongue is supplied by the glossopharyngeal nerve
for symmetry
patient to flex or extend the extremities while the examiner places resistance Grading of muscle strength
Biceps (C5-C6) Triceps (C6-C8) Brachioradialis (C5-C6) Patellar Assessing the sensory function Achilles
Grading of reflexes
Deep tendon reflex 0- absent + present but diminished ++ normal average +++ increased but not necessary abnormal ++++ hyperactive or clonic Superficial reflex 0 absent +present
. Reflex assessment with abnormal findings a. Hyperactive reflexes: lesions affecting UMN b. Decreased reflexes: LMN involvement c. Clonus of foot (hyperactive, rhythmic dorsiflexion and plantar flexion of foot): UMN disease d. Superficial reflexes (such as abdominal) and cremasteric reflex may be absent with LMN and UMN diseases e. Positive Babinski reflex (dorsiflexion of big toe with fanning of other toes): UMN diseases of pyramidal tract
Special neurologic assessment with abnormal findings Positive Brudzinskis sign (pain, resistance, flexion of hips and knees when head flexed to chest with client supine) indicates meningeal irritation
Abnormal Reflex
Positive Brudzinskis sign (pain, resistance, flexion of hips and knees when head flexed to chest with client supine) indicates meningeal irritation
Positive Kernigs sign (excessive pain and/or resistance when examiner attempts to straighten knees with client supine and knees and hips flexed) indicates meningeal irritation
Positive Babinski reflex (dorsiflexion of big toe with fanning of other toes): UMN diseases of pyramidal tract
sides, elbows, wrists and fingers flexes, legs extended with internal rotation, feet are flexed: body parts pulled into core of body): lesions of corticospinal tracts
Decerebrate posturing (neck extended with jaw clenched, arms pronated, extended, close to sides, legs are extended straight out and feet plantar flexed): lesions of midbrain, pons, diencephalon
b. Positive Kernigs sign (excessive pain and/or resistance when examiner attempts to straighten knees with client supine and knees and hips flexed) indicates meningeal irritation c. Decorticate posturing (upper arms close to sides, elbows, wrists and fingers flexes, legs extended with internal rotation, feet are flexed: body parts pulled into core of body): lesions of corticospinal tracts d. Decerebrate posturing (neck extended with jaw clenched, arms pronated, extended, close to sides, legs are extended straight out and feet plantar flexed): lesions of midbrain, pons, diencephalon
Diagnostic Test
a.
Skull and spinal x-ray - identify fractures dislocation. Compression, spinal cord problem Nursing Care - provide nursing support for the confused or combative patient - maintain immobilization - remove metal items
b. CT Scan - detect intracranial bleeding, space occupying lesion, cerebral edema. Hydrocephalus, infarction Nursing Care a. Assess for allergies b. Instruct to lie still and flat c. Inform pt that there may be hot, flushed sensation and metallic taste in the mouth d. Treat allergic reaction
c. Magnetic Resonance Imaging - provides more detailed pictures -Patients with pacemakers, orthopedic metal prosthesis and implanted metal devices cannot undergo this procedure
EEG
Withhold medications that may interfere with the results- anticonvulsants, sedatives and stimulants Wash hair thoroughly before procedure
Unstable vital signs or cardiopulmonary compromise space occupying lesions infections on the site hematologic problems
Don't let people drive you crazy when you know it's in walking distance.
Thank You.
pathophysiologic phenomena Not a disorder Causes: head injury, toxicity and metabolic derangement Disruption in the basic functional units or neurotransmitters results in faulty impulse transmission
LEVEL OF CONSCIOUSNESS - awake, alert and responsive? - Assess different LOCs: 1. ALERT - speak in a normal voice - patient opens eyes, looks at you and responds fully and appropriately to stimuli
GENERAL SURVEY
2. LETHARGY - Speak in a loud voice - Appears drowsy but opens the eyes and looks at you, responds to questions, and then falls asleep
GENERAL SURVEY
3. OBTUNDED - Shake patient gently as if awakening the sleeper - Opens the eyes and looks at you, but responds slowly and is somewhat confused - Alertness and interest in the environment are decreased
GENERAL SURVEY
4. STUPOROUS
-
Pinching a tendon Rubbing the sternum Roll a pencil across a nail bed
Arouses from sleep after a painful stimulus Verbal responses are slow or absent Minimal awareness of self or environment
GENERAL SURVEY
5. COMA - Apply repeated painful stimuli - Remains unarousable with eyes closed - No evident response to inner need or external stimuli
Decerebrate Decorticate
Sensory function
Patient is not oriented Patient does not follow command Patient needs persistent stimuli to be awake COMA= clinical state of unconsciousness
unresponsiveness to the environment in which the patient makes no movement or sound but sometimes opens the eyes PERSISTENT VEGETATIVE condition in which the patient is described as wakeful but devoid of conscious content, w/o cognitive or affective mental function
1. 2. 3. 4. 5. 6.
Etiologic Factors Head injury Stroke Drug overdose Alcoholic intoxication Diabetic ketoacidosis Hepatic failure
ASSESSMENT 1. Behavioral changes initially 2. Pupils are slowly reactive 3. Then , patient becomes unresponsive and pupils become fixed dilated
Complications
Nursing intervention
Nursing Intervention 1. Maintain patent airway Elevate the head of the bed to 30 degrees Suctioning 2. Protect the patient Pad side rails Prevent injury from equipments, restraints and etc.
Nursing Intervention 3. Maintain fluid and nutritional balance Input an output monitoring IVF therapy Feeding through NGT 4. Provide mouth care Cleansing and rinsing of mouth Petrolatum on the lips
Nursing Intervention 5. Maintain skin integrity Regular turning every 2 hours 30 degrees bed elevation Maintain correct body alignment by using trochanter rolls, foot board 6. Preserve corneal integrity Use of artificial tears every 2 hours
Nursing Intervention 7. Achieve thermoregulation Minimum amount of beddings Rectal or tympanic temperature Administer acetaminophen as prescribed 8. Prevent urinary retention Use of intermittent catheterization
Nursing Intervention 9. Promote bowel function High fiber diet Stool softeners and suppository 10. Provide sensory stimulation Touch and communication Frequent reorientation
Nursing diagnosis
Ineffective airway clearance related to altered
LOC Risk of injury related to decreased LOC Deficient fluid volume related to inability to take fluids by mouth Risk for impaired skin integrity related to immobility
Headache
One of the most common ailments Generally classified into 3 categories:
Acute SAH, hemorrhagic stroke, meningitis, seizure, acutely elevated ICP, hypertensive encephalopathy, post-LP, ocular dse., new migraine headache
Subacute temporal arteritis, intracranial tumor, subdural hematoma, pseudotumor cerebri, trigeminal/glossopharyngeal neuralgia, postherpetic neuralgia, HTN
chronic/episodic migraine, cluster headache, tension headache, sinusitis, dental dse., neck pain
Evaluation:Headache
Is the headache new or old? Characteristics? Intensity, quality, location,
duration Associated symptoms? Neurologic symptoms? If an SAH is suspected with negative head CT, LP is mandatory CT w/out contrast
Migraine headache
Most commonly affects women (+) family history Unkonwn cause but likely related to vascular
and brain neurotransmitters (serotonin) Triggers include: foods, fasting stress, menses, OCPs, bright-lights
Assessment:
a. gradual onset severe unilateral b. throbbing pain that may become bilateral c. lasts 4 to 72 hours d. maybe preceded by sensory, motor, or mood alterations (AURA) e. nausea, vomiting and photophobia
Cluster headache
Men > women Pathogenesis: increased HISTAMINE
Assessment:
a. pain is severe, unilateral, involving the face, occurs on the same side and on the same time of the day, sometimes at night b. attacks last 20 minutes to 2 hours c. occurs in clusters of 2 to 8 weeks d. associated with unilateral excessive tearing, redness of the eye, nasal congestion, facial swelling, flushing and sweating
Tension headache
Most common type of headache diagnosed in
adults Result from irritation of sensitive nerve endings in the head, jaw and neck caused by prolonged muscle contraction
Assessment:
a. dull, bandlike pain and pressure in the back of the head and neck, across forehead, bitemporal areas; dull persistent ache; tender spots of head and neck
Collaborative Management:
Therapeutic interventions:
1. non-pharmacologic: relaxation techniques 2. avoidance of TYRAMINE containing foods (cheese or chocolates) 3. identification of other triggers such as skipping of meals, intake of certain spices and preservatives, withdrawal from caffeine 4. inhalation of 100% O2 to abort cluster headache
Pharmacologic interventions:
1. aspirin, acetaminophen, NSAIDs 2. antihistamines and decongestant 3. methysergide, ergotamine, sumatriptan 4. beta-adrenergic blockers, Ca channel blockers or antidepressants 5. corticosteroids 6. opioid analgesics, muscle relaxants and antianxiety
Drug Alert: vasoconstrictors and 5HT agonists are contraindicated in patients with uncontrolled HTN, CAD, hemiplegic migraine and PVD
Nursing Diagnoses:
Acute pain Disturbed sensory perception Ineffective coping Nausea
Nursing Interventions:
Supportive care:
1. reduce environmental stimuli 2. to relieve tension headaches: a. suggest light massage of tight muscles in neck, scalp, and back b. apply warm, moist heat to areas of muscle tension c. teach progressive muscle relaxation
3. administer abortive and preventive medications as directed 4. encourage pt. to lie down and attempt to sleep 5. encourage adequate nutrition, rest and relaxation 6. review coping mechanisms and strengthen positive ones
1. teach proper administration of medications: a. Sumatriptan SC with autoinjection for quick relief or given orally b. oral and nasal fomulations 5HT agonist c. Ergotamine metered dose inhaler
2. teach patient about the adverse effects of headache medications. a. Ergot derivatives - numbness, coldness, paresthesias and pain of extremities b. Sumatriptan chest pain, wheezing, swelling of lips and flushing c. Beta-adrenergic blocker & Ca channel light headeness and hypotension
Intracranial Pressure
A.Intracranial Pressure (ICP) 1. Pressure within cranial cavity measured within lateral ventricles 2. Transient increases occur with normal activities coughing, sneezing, straining, bending forward
3. a. b. c. d. e. f. g.
Sustained increases associated with Cerebral edema Head trauma Tumors Abscesses Stroke Inflammation Hemorrhage
B. Monro-Kellie hypothesis 1. Within skull there are 3 components that maintain state of dynamic equilibrium a. Brain (80%) b. Cerebrospinal fluid (10%) c. Blood (10%) 2. If volume of any one increases the volume of others must decrease to maintain normal pressure
C. Normal intracranial pressure 1. 5 15 mm Hg, with pressure transducer with head elevated 30 degrees 10-20mmHg (Brunner)
D. Background regarding regulation of ICP Pathophysiology The cranium only contains the brain substance, the CSF and the blood/blood vessels MONRO-KELLIE hypothesis- an increase in any one of the components causes a change in the volume of the other Any increase or alteration in these structures will cause increased ICP
Pathophysiology Compensatory mechanisms: 1. Increased CSF absorption 2. Blood shunting 3. Decreased CSF production
Pathophysiology Decompensatory mechanisms: 1. Decreased cerebral perfusion 2. Decreased PO2 leading to brain hypoxia 3. Cerebral edema 4. Brain herniation
slow bounding pulses Increased concentration of carbon dioxide will cause VASODILATION increased flow increased ICP
CEREBRAL EDEMA
Abnormal accumulation of fluid in the intracellular space, extracellular space or both.
Herniation
Results from an excessive increase in ICP when the pressure builds up and the brain tissue presses down on the brain stem
Vasomotor center triggers rise in BP to increase ICP Sympathetic response is increased BP but the heart rate is SLOW Respiration becomes SLOW
CLINICAL MANIFESTATIONS Early manifestations: Changes in the LOC- usually the earliest Pupillary changes- fixed, slowed response Headache vomiting
CLINICAL MANIFESTATIONS late manifestations: Cushing reflex- systolic hypertension, bradycardia and wide pulse pressure bradypnea Hyperthermia Abnormal posturing
Nursing interventions: Maintain patent airway 1. Elevate the head of the bed 15-30 degrees- to promote venous drainage 2. assists in administering 100% oxygen or controlled hyperventilation- to reduce the CO2 blood levels constricts blood vessels reduces edema
Mannitol- to produce negative fluid balance corticosteroid- to reduce edema anticonvulsants-p to prevent seizures
Nursing interventions 4. Reduce environmental stimuli 5. Avoid activities that can increase ICP like valsalva, coughing, shivering, and vigorous suctioning
Nursing interventions 6. Keep head on a neutral position. AVOIDextreme flexion, valsalva 7. monitor for secondary complications
Seizure Disorder
also known as convulsions, epileptic
Sudden alterations in normal brain activity that cause distinct behavior and body function Pathophysio: poorly understood but may be related to metabolic and electrochemical factors at the cellular level(fever, rapid withdrawal from alcohol, electrolyte imbalance, brain pathology)
PREDISPOSING FACTORS: 1. head or brain trauma 2. tumors 3. cranial surgery 4. metabolic disorders 5. CNS infections 6. circulatory disorders 7. drug toxicity/drug withdrawal states 8. congenital neurodegenerative disorders
classified as: a. partial seizures INVOLVES 1 HEMISPHERE 1. simple partial motor, somatosensory an psychomotor symptoms w/o impairment of consciousness - can progress to complex partial
2. COMPLEX PARTIAL SEIZURES - manifest impairment of consciousness w/ or w/o simple partial symptoms - can secondarily become generalized
2. Generalized seizures: involves both brain hemispheres; consciousness always impaired a. Absence seizures (petit mal) - characterized by sudden brief cessation of all motor activity, blank stare and unresponsiveness often with eye fluttering - lost of contact w/ environment for 5 to 30 secs. - resumes activity and is not aware of seizure
b. Tonic-clonic seizures (GRAND MAL) 1. Most common type in adults 2. Preceded by aura, sudden loss of consciousness 3. Tonic phase: rigid muscles, incontinence (LAST 30 TO 60 SECS.) 4. Clonic phase: altered contraction, relaxation; eyes roll back, froths at mouth (LAST SEVERAL MINUTES) 5. Postictal phase: unconscious and unresponsive to stimuli (UP TO SEVERAL HOURS)
Complications:
Status Epilepticus - acute, prolonged, repetitive seizure activity - series of generalized seizures w/o return to consciousness between attacks - continuous clinical or electrical seizures lasting at least 5 minutes, even w/o impairment of consciousness
FEBRILE SEIZURES
CRITERIA: 1. Age: 9 mos. To 5 yrs. 2. Generalized tonic-clonic lasting not more than 15 mins 3. Onset of fever > 39C within hours of the seizure 4. Family history of BFC 5. No neurologic deficit that would explain the seizure
Diagnostic Tests 1. Neurologic exam 2. EEG to confirm diagnosis and locate lesion 3. Xray, MRI, CT scan identify any neurologic abnormalities 4. Lumbar puncture may be done if infection suspected 5. CBC, electrolytes, BUN, blood glucose 6. ECG to determine cardiac dysrhythmias
Therapeutic Interventions:
1. Maintain good nutrition/sleep hygiene/avoid stress 2. Ketogenic diet a. precisely calculated portions of CHON and fats w/o CHO b. IV fluids should be dextrose free, and all medications should be in sugarfree suspensions
Pharmacologic:
a. Antiepileptic drugs Phenytoin (Dilantin) for partial and generalized seizures except absence seizures Nsg. Considerations: 1. Encourage good oral hygiene 2. therapeutic range is 10 to 20 mcg/ml, administer IV w/ normal saline 3. watchout SE: rash, nystagmus, ataxia, drug-induced lupus, anemia,
Phenobarbital(Luminal) - for partial and generalized seizures (tonic-clonic) Nsg. Considerations: 1. contraindicated in hepatic or renal dysfunction 2. avoid use w/ other CNS depressants 3. watchout SE: hyperactivity, sedation, nystagmus, ataxia
Valproic Acid (Depakene)/Divalproex Na (Depakote) sole therapy for absence seizures and adjunct therapy for partial and generalized seizures Nsg. Considerations: 1. liver function test and platelet count should be monitored monthly for at least 1st 6 months 2. take w/ food to minimize adverse effect 3. avoid use w/ other CNS depressants 4. watchout SE: hepatotoxicity, nausea and vomiting, abdominal pain, anemia, decreased WBC & platelet
Carbamazepine (Tegretol) refractory partial and generalized seizures Nsg. Considerations: 1. use cautiously in patients w/ existing cardiac, renal, or liver probs. 2. give w/ food 3. watchout SE: dizziness, nausea and vomiting, liver dysfunction, anemia, decreased WBC & platelet
Gabapentin (Neurontin) adjunct treatment of partial and secondarily generalized seizures Nsg. Considerations: 1. serum levels not necessary 2. watchout SE: somnolence, dizziness, ataxia, headache, tremor, vomiting, nystagmus, fatigue
NURSING INTERVENTIONS: 1. Monitor the entire seizure event, including prodromal signs, seizure behavior, and postictal state 2. Monitor serum levels for therapeutic range of medications 3. Monitor pt. for adverse reactions of medications 4. Monitor CBC, UA, and liver function
Surgery: if all attempts to control seizures are not successful 1. May attempt to excise tissue involved in seizure activity 2. EEG done during surgery to identify epileptogenic focus
Care of client during a seizure 1. Protect client from injury and maintain airway 2. Do not force anything into clients mouth 3. Loosen clothing around neck
Health Promotion: Stress the following to clients 1. Importance of medical follow-up, taking prescribed medications 2. Driving privileges are prohibited in clients with seizure disorders; drivers licenses are reinstated after seizure free period and statement from health care practitioner 3. Client needs proper identification 4. Family members need to be educated in preventing injury if seizure occurs
Nursing Diagnoses 1. Risk for Ineffective Airway Clearance 2. Anxiety Home Care 1. Education of client and family regarding seizure disorder; safety measures, avoidance of alcohol and caffeine 2. Referral to support group, national organizations
B. Mechanisms of trauma 1. Acceleration injury: head struck by moving object 2. Deceleration injury: head hits stationary object 3. Acceleration-deceleration (coup-contrecoup phenomenon): head hits object and brain rebounds within skull 4. Deformation: force deforms and disrupts body integrity: skull fracture
c. Basilar: 1. Involves base of skull and usually involve extension of adjacent fractures 2. If dura disrupted may have leakage of CSF occurring as a. Rhinorrhea: through nose b. Otorrhea: through ear
CNS infection
A. CNS infections 1. Most common is bacterial meningitis 2. Mortality rate 25% in adults 3. Meningococcal occurs in epidemics with people living in close contact 4. Pneumococcal effects very young and very old
B. Risk Factors 1. High risk for old and young 2. High risk for clients with debilitating diseases, or immunosuppressed
C. Pathophysiology 1. Pathogens enter CNS and meninges causing inflammatory process, which leads to inflammation and increased ICP 2. May result in brain damage and lifethreatening complications
D. Meningitis 1. Inflammation of pia mater, arachnoid, and subarachnoid space 2. Spreads rapidly through CNS because of circulation of CSF around brain and spinal cord 3. May be bacterial, viral, fungal, parasitic in origin 4. Infection enters CNS though invasive procedure or through bloodstream, secondary to another infection in body
E. Bacterial meningitis 1. Causative organisms: Neisseria meningitis, meningoccus, Streptococcus pneumoniae, Haemophilus influenzae, E. Coli 2. Risk factors: head trauma with basilar skull fracture, otitis media, sinusitis, immunocompromised, neurosurgery, systemic sepsis
3. Manifestations a. Fever chills b. Headache, back and abdominal pain c. Nausea and vomiting d. Meningeal irritation: nuchal rigidity, positive Brudzinskis sign, Kernigs sign, photophobia e. Meningococcal meningitis: rapidly spreading petechial rash of skin and mucous membranes f. Increased ICP: decreased LOC, papilledema
4. a. b. c.
F. Viral meningitis 1. Less severe, benign course with short duration 2. Intense headache with malaise, nausea, vomiting, lethargy 3. Signs of meningeal irritation
G. Encephalitis 1. Acute inflammation of parenchyma of brain or spinal cord 2. Usually caused by virus 3. Inflammation occurs with manifestations similar to meningitis 4. LOC deteriorates and client may become comatose 5. Arboviruses are agents including West Nile virus
H. Brain abscess 1. Infection with a collection of purulent material within brain tissue usually in cerebrum 2. Causes include open trauma and neurosurgery; infections of ear, sinuses 3. Common pathogens are streptococci, staphylococci, bacteroids
4. Becomes space-occupying lesion 5. At risk for infection and increased ICP 6. Manifestations a. General symptoms associated with acute infectious process b. Client develops seizures, altered LOC, signs of increased ICP c. Specific neurologic symptoms are related to location 7. May be drained surgically, if considered feasible
I. Collaborative Care 1. Bacterial meningitis: requires immediate treatment and isolation of client 2. Viral meningitis: supportive treatment and management of client symptoms 3. Brain abscess treatment focuses on antibiotic therapy
J. Diagnostic Tests 1. Lumbar puncture: definitive test for bacterial meningitis demonstrating infection: turbid cloudy appearance, increased WBC, gram stain, culture 2. CT scan, MRI
K. Medications 1. Meningitis: immediate treatment with effective antibiotics for 7 21 days; according to culture results; dexamethasone to suppress inflammation 2. Encephalitis: viral treated with anti-viral medications 3. Brain abscess: antibiotic therapy, which may include intraventricular administration; anticonvulsant medications, antipyretics
L. Health Promotion 1. Vaccinations for meningococcal, pneumococcal, hemophilic meningitis 2. Prophytlactic rifampin for persons exposed to meningococcal meningitis 3. Mosquito control 4. Prompt diagnosis and treatment of clients with infections 5. Asepsis care for clients with open head injury or neurosurgery
N. Home Care 1. Client education for future prevention 2. Complete medications and treatment plan
Brain Tumor
A. Description 1. Growths within cranium including tumors of brain tissue, meninges, pituitary gland, blood vessels 2. May be benign or malignant, primary or metastatic 3. May be lethal, due to location (inaccessible to treatment) and capacity to impinge on CNS structures
4. In adults most common tumor is glioblastoma followed by meningioma and cytoma 5. Cause is unknown: factor associated include heredity, cranial irradiation, exposure to some chemicals
6. Tumors within brain a. Compress or destroy brain tissue b. Cause edema in adjacent tissues c. Cause hemorrhage d. Obstruct circulation of CSF, causing hydrocephalus 7. Estimated 25% persons with cancer develop brain metastasis, often multiple sites throughout the brain
B. Manifestations: Multiple depending on location of lesion and rate of growth 1. Changes in cognition and LOC 2. Headache usually worse in morning 3. Seizures 4. Vomiting 5. Manifestations associated with cerebral edema, increased ICP, cerebral ischemia leading to brain herniation syndromes
C. Collaborative Care 1. Effective treatment includes chemotherapy, radiation therapy, and/or surgery 2. Treatment depends on size and location of tumor, type of tumor, neurologic deficits, and clients over all condition
D. Diagnostic Tests 1. CT scan or MRI: determine tumor location and extent 2. Arteriography 3. EEG: information about cerebral function, seizure data 4. Endocrine studies if pituitary tumor suspected
E. Treatment 1. Medications: Chemotherapy, corticosteroids, anticonvulsants 2. Surgery a. Purposes include tumor excision, reduction, or for symptom relief b. Craniotomy: location according to approach to tumor 3. Radiation: Alone or as adjunctive therapy
F. Nursing Care 1. Support during diagnosis and management through selected treatment 2. Nursing care involves interventions to deal with altered LOC, increased ICP, and seizures
G. 1. 2. 3. 4. 5.
Nursing Diagnoses Anxiety Risk for Infection Ineffective Protection Acute Pain Disturbed Self-esteem
H. Home Care 1. Education, support to client and family 2. Instructions for treatment plan and followup care 3. Referral to home care agencies 4. Referrals to therapies, community resources, support groups as appropriate
CHILLAX!
CEREBROVASCULAR ACCIDENTS
An umbrella term that refers to any
functional abnormality of the CNS related to disrupted blood supply Similaraties between The 2 broad types, overall the etiology, pathophysiology, medical & surgical management, and nursing care differs
CEREBROVASCULAR ACCIDENTS
Can be divided into two major categories
1. Ischemic stroke- caused by thrombus and embolus 2. Hemorrhagic stroke- caused commonly by hypertensive bleeding
Stroke (CVA)
Ischemic (85%)
Hemorrhagic (15%)
Cerebral thrombosis
Cerebral embolus(20%)
Intracerebral Hge
SAH
Lacunar infarct(25%)
CEREBROVASCULAR ACCIDENTS
The stroke continuum 1. TIA- transient ischemic attack, temporary neurologic loss less than 24 hours duration 2. Reversible Neurologic deficits- s/sx last more the 24 hrs. resolve in days w/o permanent neurologic deficit 3. Stroke in evolution- worsening of neuro s/sx over several minutes or hours 4. Completed stroke- indicates no further progression of the hypoxic insult
General manifestations
Localization
Anterior cerebral artery: Weakness Numbness on the opposite side Personality changes Impaired motor and sensory function
Localization
Middle cerebral artery: Aphasia Dysphagia HEMIPARESIS on the OPPOSITE side- more severe on the face and arm than on the legs
Localization
Posterior cerebral artery: Visual field defects Sensory impairment Coma Less likely paralysis
RISKS FACTORS
Non-modifiable Advanced age Gender race Modifiable Hypertension Cardio disease Obesity Smoking Diabetes mellitus hypercholesterolemia
COMPARISON:
LEFT HEMISPHERIC
Paralysis/weakness on
RIGHT HEMISPHERIC
Paralysis/weakness on
the right side Right visual field deficit Aphasia Altered intellectual ability Slow, cautious behavior
the left side Left visual field deficit Spatial-perceptual deficits Increased distractibility Impulsive behaviour and poor judgement Lack of awareness of deficits
Place pillow under axilla Hand is placed in slight supination Change position every 2 hours
Aspirin Diazepam to prevent seizures Thrombolytics Stool softeners Antihypertensives Analgesics, Muscle relaxants, STEROIDS
MEDICAL MGNT: 1. TIA/Mild stroke non surgical approach -- platelet inhibiting medications 2. Thrombolytic therapy t-PA administration -- eligibility criteria for t-PA administration -- should be done w/in 3 hrs. -- VS impt -- bleeding- most common S.E.
thromboplastin time Platelet ct. 100,000/mm No prior intracranial Hge, neoplasms, AV malformation, or aneurysms
No major surgical procedures w/in 14 days No stroke, serious head injury or intracranial
interruption of blood supply, compression and increased ICP More sever deficits and longer recovery time Pathophysio depends on the cause
Intracerebral Hemorrhage
Most common in patients w/ HPN and
cerebral atherosclerosis ---causing rupture of the vessels involve usually ARTERIAL Occurs most commonly in the cerebral lobes, basal ganglia, thalamus and brainstem Arterial pathology, brain tumor and the use of meds (oral anticoagulant, amphetamines, crack and coccaines)
develops as a result of weakness in the arterial wall Unknown Usually happens in the bifurcation of the large Artery at the circle of willis
development that leads to a tangle of arteries and veins in the brain w/o capillary bed (-) capillary beds leads to dilation of the AV and eventual RUPTURES Cause of He in young adult
Subarachnoid Hemorrhage
May occur as a result of an AVM, intracranial
aneurysms, trauma, or HPN Most common cause is a leaking aneurysm in the area of the circle of Willis or a congenital AVM
UNIQUE CLINICAL MANIFESTATIONS: 1. sudden, unusually severe headache and often LOC 2. (+) meningeal irritation 3. Visual disturbances adjacent of oculomotor nerve
Medical management: 1. Complete bed rest w/ elastic compression stockings 2. Management of vasospams 3. Surgical and medical treatment to prevent rebleeding
Acute Stroke
1. Anticoagulant therapy a. Ordered for thrombotic stroke during strokein-evolution b. Contraindicated in completed stroke c. Never used in hemorrhagic stroke d. Prevent further extension of clot ; Heparin, warfarin sodium (Coumadin)
Acute Stroke
2. Thrombolytic therapy: must be given within 3 hours of onset of manifestations and will dissolve clot; recombinant altephase (Activase rt-pa) 3. Antithrombotic: inhibit platelet phase of clot formation; contraindicated with hemorrhagic stroke (aspirin, dipyidamole) 4. Calcium channel blockers: reduce ischemic deficits, death (Nimodipine (Nimotop)) 5. Corticosteroids: used to treat cerebral edema 6. Diuretics: reduce increased intracranial pressure: mannitol, furosemide 7. Anticonvulsants: phenytoin (Dilantin)
Ancillary:
1. Surgery a. Carotid endarterectomy: in clients who have had TIAs b. Extracranial-intracranial bypass 2. Physical therapy: prevents contractures, improves muscle strength and coordination 3. Occupational therapy: provides assistive devices and plans for regaining lost motor skills 4. Speech therapy: improves communication disorder
Nursing Diagnoses
1. Ineffective Tissue Perfusion: Cerebral; frequent monitoring of neurologic status, cardiac status 2. Impaired Physical Mobility 3. Self-care Deficit 4. Impaired Verbal Communication 5. Impaired Urinary Elimination and Risk for Constipation 6. Impaired Swallowing
Complications
1. Motor Deficits a. Affects connections involving motor areas of cerebral cortex, basal ganglia, cerebellum, peripheral nerves b. Produce effects in contralateral side ranging from mild weakness to severe limitation c. Hemiplegia: paralysis of half of body d. Hemiparesis: weakness of half of body e. Flaccidity: absence of muscle tone (hypotonia)
Complications
f. Spasticity: increased muscle tone usually with some degree of weakness g. Affected arm and leg are initially flaccid and become spastic in 6 8 weeks, causes characteristic body positioning: 1. Adduction of shoulder 2. Pronation of forearm 3. Flexion of fingers 4. Extension of hip and knee 5. Foot drop, outward rotation of leg, with dependent edema
Sensory-perceptual Deficits
a. Hemianopsia: loss of half of visual field on
one or both eyes; homonymous hemianopia: same half missing in each eye b. Agnosia: inability to recognize one or more subjects that were previously familiar: includes visual, tactile, auditory
Sensory-perceptual Deficits
c.
Apraxia: inability to carry out some motor pattern even when strength and coordination is adequate (e.g. getting dressed) d. Neglect syndrome (unilateral neglect): attention disorder in which client ignores affected part of body; client cannot integrate or use perceptions from affected side of body or from environment on affected side
Communication Disorders
a. Usually result of stroke affecting dominant hemisphere (left hemisphere dominant in 95% right-handed persons; 70% left-handed persons) b. Aphasia: inability to use or understand language
Communication Disorders
1.
Expressive: motor speech problem; client understands what is said but can only respond verbally in short phases: Brocas aphasia 2. Receptive aphasia: sensory speech problem in which one cannot understand spoken or written word; speech may be fluent but with inappropriate content: Wenickes aphasia 3. Mixed or global aphasia: language dysfunction in both understand and expression
5. Maintain urinary elimination 6. Improve bowel function 7. Provide Comfort measures 8. Monitor and manage complications
Degenerative disorders-
NON-demyelinating
neurologic disorder that affects the brain resulting in cognitive impairments - Not exclusive in the elderly - 1 10% occurs in middle age 7th decade of life
CAUSES: Unknown Potential factors- Amyloid plaques in the brain, Oxidative stress, neurochemical deficiencies
3 stages:
Mild/Early
Amnesia Forgetfulness and have diffulty retaining new information Word finding difficulty Poor abstract reasoning Perseveration Floating around
Moderate
Latent/ Severe
Fragmented memory loss Increase irritability Urinary and fecal incontinence Unresponsiveness or coma
CLINICAL MANIFESTATIONS 1. Forgetfulness 2. Recent memory loss 3. Difficulty learning 4. Deterioration in personal hygiene 5. Inability to concentrate
LATE CLINICAL MANIFESTATIONS 6. Difficulty in abstract thinking 7. Difficulty communicating 8. Severe deterioration in memory, language and motor function 9. repetitive action 10. personality changes
DIAGNOSTIC TEST Health history = Neurologic examination PET scan EEG, CT and MRI Other tests to rule out Vit B deficiencies and hypothyroidism Autopsy is the most definitive
Drug therapy 1. drugs to treat behavioral symptomsantipsychotics 2. anxiolytics 3. Tacrine HCL(cognex) first meds used, 1993 4. Donepezil (Aricept) 2nd meds, 1997 5. Rivastigmine (Exelon) - 2000
3. Establish an effective communication system with the patient and family Use short simple sentences, words and gestures Maintain a calm and consistent approach Attempt to analyze behavior for meaning
4. protect the patient from injury Provide a safe and structured environment Requests a family member to accompany client if he wanders around Keep bed in low position Provide adequate lightning Assign consistent caregivers = nightlights are helpful
5. Encourage exercise to maintain mobility 6. Promoting independence in self-care activities - simplify daily activities by organizing them into short, achievable steps so that the patient experience a sense of accomplishment
demyelinating disease of the CNS The myelin sheath is destroyed and replaced by sclerotic tissue (sclerosis)
factors, geographic location and genetic predisposition Exacerbations and remissions Common in WOMEN ages 20-40
PATHOPHYSIOLOGY Sensitized T cells will enter the brain and promote antibody production that damages the myelin sheath Plaques of sclerotic tissues appear on the demyelinated axons interrupting the neuronal transmission
CLINICAL MANIFESTATIONS 1. Primary symptomsa. fatigue- throughout the course b. depression as reaction to diagnosis c. weakness, numbness, difficulty in coordination, loss of balance d. pain occurs in 66% due to demyelination of pain fibers
2. Visual disturbances lesion in the optic nerve a. blurring of vision b. Diplopia initial sign c. patchy blindness (scotoma) d. total blindness CHARCOTS TRIAD Scanning speech Intentional tremors Nystagmus
3. Spasticity (muscle hypertonicity) of the extremities and loss of abdominal reflexes 4. Ataxia 5. Emotional lability and euphoria 6. bladder, bowel and sexual dysfunction
NURSING INTERVENTIONS 1. Promote physical mobility Exercise Schedule activity and rest periods Warm packs over the spastic area Swimming and cycling are very useful
Set a voiding schedule Intermittent bladder catheterization Adequate fluids, dietary fibers and bowel training program
Vision- use eye patch for diplopia Obtain large printed reading materials Offer emotional support Involve the family in the care
Interferons beta 1a (Avonex) and beta 1b (Betaseron), Glatiramer Acetate (Copaxone), Rebif
Immunosuppresants to stabilize disease process Corticosteroids to reduce edema and inflammatory porcess BACLOFEN for muscle spasms NSAIDS for pain Antidepressants
movement disorder The degenerative idiopathic form is the most common form
CAUSATIVE FACTORS: unknown Potential factors: genetics, atherosclerosis, free radical stress, viral infection, head trauma and environmental factors
Parkinsonian symptoms occur in the 5th
decade of life
Pathophysiology Decreased levels of dopamine due to destruction of pigmented neuronal cells in the substantia nigra in the basal ganglia Clinical symptoms do not appear until 60% of the neurons have disappeared
CLINICAL MANIFESTATIONS 1. Tremor- resting, pill-rolling, unilateral (70%) 2. Rigidity- cog-wheel, lead-pipe 3. Bradykinesia- abnormally slow movement
Postural Changes
4. Dementia, depression, sleep disturbances and hallucinations 5. excessive sweating, paroxysmal flushing, orthostatic hypotension
cholinegic neurons on the extrapyramidal tract to restore balance between cholinergic and dopaminergic activities.
Acting on neurotransmitter pathways other
Medical management 1. Anti-parkinsonian drugs- Levodopa, Carbidopa 2. Anti-cholinergic therapy(Biperiden) 3. Antiviral therapy- Amantadine 4. Dopamine Agonists- bromocriptine and Pergolide, Ropirinole anmd Pramipexole
PHARMACOLOGIC:
Cogentin tremor and rigidity Artane tremor and rigidity Parlodel/Permex useful in postponing L-Dopa Akineton Benadryl - tremors Eldepryl (MAOI) inhibits dopamine
NURSING INTERVENTIONS
1. Improve mobility 2. Enhance Self- care activities 3. Improve bowel elimination 4. Improve nutrition 5. Enhance swallowing 6. Encourage the use of assistive devices
NURSING INTERVENTIONS
low protein Excessive vitamin B6 intake (pyridoxine) intake effectiveness of L-dopa Sinemet can discolor urine and perspiration
Can increase urine glucose intake
abnormal fatigability of striated muscles which are exacerbated by exercise and repetitive movements Autoimmune disorder affecting the myoneural junction Characterized by varying degrees of weakness of the voluntary muscles
ETIOLOGY Autoimmune disease Thymoma Women suffer at an earlier age (20-40) compared to men (60-70) and are more affected
Pathophysiology: 1. Acetylcholine receptor antibodies interfere with impulse transmission 2. Follows an unpredictable course of periodic exacerbations and remissions
ASSESSMENT FINDINGS 1. Involves the ocular muscles a. diplopia double vision b. ptosis drooping of the eyelids 2. Bulbar symptoms weakness of the muscles of the face and throat 3. Generalized weakness a. bland facial expression b. dysphonia c. decrease vital capacity PURELY MOTOR WITH NO EFFECT ON SENSATION OR COORDINATION
DIAGNOSTIC TESTS 1. EMG 2. TENSILON TEST (Edrophonium) 3. CT scan 4. Serum anti-AchReceptor antibodies
SHOULD BE GIVEN ON TIME 30 MINS. BEFORE MEALS W/ MILK AND CRACKERS TO PREVENT CRISIS
NURSING INTERVENTIONS 1. Administer prescribed medication as scheduled 2. Prevent problems with chewing and swallowing 3. Promote respiratory function 4. Encourage adjustments in lifestyle to prevent fatigue 5.maximize functional abilities
crisis and cholinergic crisis 7. prevent problems associated with impaired vision resulting from ptosis of eyelids 8. provide client teaching 9. promote client and family coping
nerve myelin Acute, rapid segmental demyelination of peripheral nerves and some cranial nerves producing ascending weakness POTENTIALLY FATAL!
unknown origin commonly follows viral infection (66%) Assoc. with Gastrointestinal infection (Campylobacter Jejuni) and respiratory infection
PATHOPHYSIOLOGY
Cell-mediated immune attack to the myelin sheath of the peripheral nerves Infectious agent may elicit antibody production that can also destroy the myelin sheath of the PERIPHERAL NERVES!!
and degenerative changes in the posterior and anterior nerve roots, MOTOR and SENSORY losses occur SIMULTANEOUSLY!
CLINICAL MANIFESTATIONS: occurs 2 weeks before symptoms begins 1. Ascending weakness and paralysis: Leg affected first (1 month) 2. AREFLEXIA of the lower extremities 3. paresthesia 4. potential respiratory failure Duration of symptoms are variable:complete functional recovery may take up to 2 yrs.
LABORATORY EXAMINATION 1. CSF protein level is INCREASED but the WBC remains normal in the CSF 2. EMG and nerve conduction velocity studies
NURSING INTERVENTIONS 1. Maintain respiratory function Chest physiotherapy and incentive spirometry Mechanical ventilator
Support paralyzed extremities Provide passive range of motion exercise Prevent DVT and pulmonary embolism Padding over bony prominences
4. Improve communication
Provide Referrals Answer questions Provide diversional activities DVT, Urinary retention, pulmonary embolism, respiratory failure
MEDICAL MANAGEMENT ICU admission Mechanical Ventilation TPN and IVF PLASMAPHERESIS IV IMMUNOGLOBULIN
paroxysms of pain Most commonly occurs in the 2nd and 3rd branch CAUSES:NOT CERTAIN, chronic compression or irritation of 5th CN 400x more common in MS
Pain is more often cyclic Most often in the 5th decade of life Paroxsyms can occur with any stimulation of
the affected nerves, such as washing of face, shaving, brushing the teeth, eating and drinking
ASSESSMENT 1. Pain history (UNILATERAL) 2. Searing or burning jabs of pain lasting from 1-15 minutes in an area innervated by the trigeminal nerve (shooting/stabbing) DIAGNOSTIC TESTS Skull x-ray or CT scan
Medical management: 1. Carbamazepine (Tegretol) - taken w/ meals - serum levels must be monitored - S.E. nausea, dizziness, drowsiness and aplastic anemia 2. Gabapentin (Neurontin)
Surgical Management: 1. Microvascular decompression of the trigeminal nerve 2. Percutaneous radiofrequency trigeminal gangliolysis TRIGEMINAL RHIZOTOMY - surgical treatment of choice
NURSING INTERVENTIONS 1. provide emotional support 2. encourage to express feelings 3. provide adequate nutrition in small frequent meals at room temperature
MANIFESTATIONS 1. Unilateral facial weakness 2. Mouth drooping 3. Distorted taste perception 4. Smooth forehead 5. Inability to close eyelid on the affected side 6. Incomplete eye closure 7. excessive tearing when attempting to close the eyes 8. Inability to raise eyebrows, puff out the cheek
Nursing Interventions 1. Apply moist heat to reduce pain 2. Massage the face to maintain muscle tone 3. Give frequent mouth care 4. protect the eye with an eye patch. Eyelid can be taped at night 5. instruct to chew on unaffected side Reassure that no stroke has occurred and recovery occurs w/in 3-5 weeks
neurologic disease characterized by increasing dementia and chorea (rapid, jerky involuntary movements) 1. Cause unknown 2. No cure 3. Usually asymptomatic until age of 30 40
Pathophysiology: involves destruction of cells in basal ganglia and other brain areas, decrease in acetylcholine
Manifestations 1. Abnormal movement and progressive dementia 2. Early signs are personality change with severe depression, memory loss; mood swings, signs of dementia
environmental stimuli and emotional stress; arms and face and entire body develops choreiform movements, lurching gait; difficulty swallowing, chewing, speaking
dependence 5. Death usually results from aspiration pneumonia or another infectious process
long-term care
Nursing Care 1. Very challenging: physiological, psychosocial and ethical problems 2. Genetic counseling
Nursing Diagnoses 1. Risk for Aspiration 2. Imbalanced Nutrition: Less than body requirements 3. Impaired Skin Integrity 4. Impaired Verbal Communication
Progressive, degenerative neurologic disease characterized by weakness and wasting of muscles without sensory or cognitive changes 2. Several types of disease including a familial type; onset is usually between age of 40 60; higher incidence in males at earlier ages but equally post menopause 3. Physiologic problems involve swallowing, managing secretions, communication, respiratory muscle dysfunction 4. Death usually occurs in 2 5 years due to respiratory failure
Pathophysiology 1. Degeneration and demyelination of motor neurons in anterior horn of spinal cord, brain stem and cerebral cortex 2. Involves upper and lower motor neurons 3. Reinnervation occurs in the early course of disease, but fails as disease progresses
Manifestations
increased DTRs (UMN involvement); muscle flaccidity, paresis, paralysis, atrophy (LMN involvement); clients note muscle weakness and fasciculations (twitching of involved muscles); muscles weaken, atrophy; client complains of progressive fatigue; usually involves hands, shoulders, upper arms, and then legs
result in dysphagia and dysarthria; emotional lability and loss of control occur 3. 50% of clients die within 2 5 years of diagnosis, often from respiratory failure or aspiration pneumonia
Collaborative Care 1. Evaluation to make the diagnosis 2. Referrals for home health support; 3. Client needs to make decisions regarding gastrostomy tube, ventilator support
Diagnostic Test 1. Testing rules out other conditions that may mimic early ALS such as hyperthyroidism, compression of spinal cord, infections, neoplasms 2. EMG to differentiate neuropathy from myopathy 3. Muscle biopsy shows atrophy and loss of muscle fiber 4. Serum creatine kinase if elevated (non-specific) 5. Pulmonary function tests: to determine degree of respiratory involvement
Medications: Rilutek (Riluzole) antiglutamate 1. Prescribed to slow muscle degeneration 2. Requires monitoring of liver function, blood count, chemistries, alkaline phosphatase
Nursing Care 1. Help client and family deal with current health problems 2. Plan for future needs including inability to communicate
Nursing Diagnoses 1. Risk for Disuse Syndrome 2. Ineffective Breathing Pattern: may require mechanical ventilation and tracheostomy
community resources for health care assistance and dealing with disabilities
4. Rare in USA affecting persons 55 - 74 5. Variant form of CJD is mad cow disease:
believed transmitted by consumption of beef contaminated with bovine form of disease; none identified in USA as of yet 6. Pathophysiology: spongiform degeneration of gray matter of brain
Manifestations 1. Onset: memory changes, exaggerated startle reflex, sleep disturbances 2. Rapid deterioration in motor, sensory, language function 3. Confusion progresses to dementia 4. Terminal states: clients are comatose with decorticate and decerebrate posturing
Diagnostic Tests 1. Clinical pictures, suggestive changes on EEG and CT scan 2. Similar to Alzheimers in early stages 3. Final diagnosis made on postmortem exam
Nursing Care 1. Use of standard precautions with blood and body fluids 2. Support and assistance to client and family
The end.