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Neurologic nursing

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all about neurologic nursing, the concept of perception and coordination.

all about neurologic nursing, the concept of perception and coordination.

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  • 1. THE CONCEPT OF PERCEPTIONAND COORDINATION (NEUROLOGIC NURSING)
  • 2. Perception- is defined as the perception and awareness of sensory stimuli.-          it is a mental act involving memory and the intellectual interpretation of new sensory data in terms of previously encountered information.Coordination- maybe defined as “the working together of muscles to produce movement or of systems to accomplish a given process.-         it implies perception of the movement or reaction that is necessary and the subsequent completion of that action via the appropriate bodily activity.Management of coordination and perception within the human body is controlled by the Central Nervous System, the Peripheral, the Autonomic Nervous System and the Neuro-endocrine System.
  • 3. ANATOMY ANDPHYSIOLOGY
  • 4. DIVISION
  • 5. BASIC STRUCTURES NEURONS NEUROGLIA NEUROTRANSMITTERS NERVE
  • 6. NEURON Cell body - contains nucleus and cytoplasm where metabolic activity takes place. Collection clusters of nerve cells bodies are called ganglia or nuclei. Ganglia with same functions are called centers. Axons- generate and conduct impulses away from the cell body and release a neurotransmitter Dendrites- carry electrical current towards the cell body
  • 7. NEURONS Types:Based on Function (direction of impulse transmission1. Sensory neurons (afferent)2. Motor neurons (efferent)Based on Structure1. Unipolar: most sensory neurons2. Bipolar: sensory neurons- ear and eye3. Multipolar: motor and association neurons
  • 8. Classification 1. Based on Function (direction of impulse transmission  A. Sensory neurons (afferent)  B. Motor neurons (efferent) 2. Based on Structure  A. Unipolar: most sensory neurons  B. Bipolar: sensory neurons- ear and eye  C. Multipolar: motor and association neurons
  • 9. NEUROGLIA– makes up about 85 % of the CNS cells. They provide, nourishment, support and protection to the neurons Types:1. Astrocytes– star-shaped supportive cells2. Oligodendrocytes3. Microglia4. Ependymal cells
  • 10. NEUROTRANSMITTERS – chemicals that carry messages between different nerve cells or between nerve cells and muscles. Released by an axon across the synaptic cleft to bind to specific receptors in the postsynaptic bulbs of another neuron or cell.- It acts to potentiate, terminate or modulate a specific action. Types:1. Excitatory – acetylcholine (PNS), Norepinephrine (SNS), Gamma-aminobutyric acid, enkephalins or endorphins2. Inhibitory – acetylcholine (Heart via vagal nerve), Dopamine, Serotonin Concentration:1. PSNS – acetylcholine2. SNS – norepinephrine
  • 11. NERVES- bundles of neurons processes wrapped in connective tissue coverings found outside the CNS.
  • 12. MAJOR PARTS CNS1. Brain2. Spinal Cord PNS1. Cranial Nerves2. Spinal Nerves ANS1. Parasympathetic2. Sympathetic
  • 13. CNS:BRAIN
  • 14. PARTS OF BRAIN CEREBRUM CEREBELLUM DIENCEPHALON BRAIN STEM
  • 15. PROTECTION OF BRAIN SKULL MENINGES CSF BLOOD BRAIN BARRIER
  • 16. BLOOD-BRAIN BARRIER CNS is inaccessible to many substances that circulate in the blood plasma (dye, meds). Barrier is formed by the endothelial cells of brain capillaries, which form continuous tight junctions, creating a barrier to macromolecules and many compounds. Has an implication in the tx and selection of meds for CNS disorders as well as serving a protective function.
  • 17. CEREBRAL CIRCULATION Receives 15% of cardiac output or 750ml/min. Brain does not store nutrients and has high metabolic demands that require high blood flow. Blood flow is against gravity as arteries fill in below and veins drain from above. Can’t tolerate decreased blood flow for it will result to irreversible tissue damage when blood flow is occluded even for a short period of time.
  • 18. CIRCLE OF WILLIS Located at the base of the brain surrounding the pituitary gland. It is a formed ring of arteries between vertebral and internal carotid artery chains (internal carotid, anterior and middle cerebral artery, anterior and posterior communicating artery) The most frequent site of aneurysm – weakening or bulge in the arterial wall.
  • 19. CNS:SPINAL CORD
  • 20. - reflex center and conductionSpinal cord pathway -located within the vertebral canal -extends from the foramen magnum to L1 to L2 -has central area of gray mater surrounded by columns of white mater, which carry motor and sensory tracts from the brain. - Serves as a connection bet. brain and the periphery. - About 45cm (18in) long and about the thickness of a finger. - Surrounded by meninges, dura, arachnoid and pia layers.
  • 21. SPINAL CORD PROTECTION MENINGES VERTEBRAL COLUMN- The bones of the vertebral column surround and protect the spinal cord.- It consists of 7 cervical, 12 thoracic, 5 lumbar, 1 sacrum, and 1 coccyx.- They are all separated by disks except for the 1st (atlas) and the 2nd (axis), sacral and coccygeal.
  • 22. PNS:CRANIALNERVES
  • 23. CRANIAL NERVES (12) - 3 Sensory (1, 2 and 8) - 5 motor (3, 4, 6, 11 and 12) - 4 mixed (5, 7, 9 and 10)
  • 24. I. Olfactory sensory smellII. Optic sensory visual acuityIII. Oculomotor motor muscle that move the eye & lid pupillary constriction.IV. Trochlear motor muscle that move the eyeV. Trigeminal mixed facial sensation, mastication, corneal reflex
  • 25. VI. Abducens motor muscle that move the eyeVII. Facial motor facial expression and movement, salvation and tearing, ear sensationVIII. Acoustic sensory hearing and equilibriumIX. Glossopharyngeal mixed taste, sensation in pharynx and tongue, pharyngeal muscles
  • 26. X. Vagus mixed muscles of pharynx and larynx, soft palate, external ear sense, pharynx, larynx, thoracic, abdominal viscera, parasympathetic innervation of thoracic and abdominal organs.
  • 27. XI. Spinal accessory motor sternocleidomastoid and trapezius muscleXII. Hypoglossal motor tongue movement
  • 28. PNS:SPINALNERVES
  • 29. SPINAL NERVES -thirty one (31) pairs of nerves formed by the union of the dorsal and ventral roots of the spinal cord on each side -splits into:a. dorsal rami – serve the posterior body trunkb. ventral rami – serve the limbs through the plexuses (cervical, brachial , lumbar, sacral)
  • 30. AUTONOMIC NERVOUS SYSTEM
  • 31. ANS - regulates the activity of smooth muscles,cardiac muscles and glands2 divisions:1. Sympathetic ”fight or flight” response; prepares the body to cope with stress e.g. increased heart rate, blood pressure pre ganglionic neurons are in the sympathetic chains or in collateral ganglia post ganglionic axons secrete norepinephrine2. Parasympathetic ”house keeping” system; in control most of the time maintains homeostasis first motor neurons are in the brain or the sacral region of the cord second motor neurons are in the terminal ganglia close to the organ served post ganglionic axons secrete acetylcholine
  • 32. EFFECTS OF ANS PNS SNSPupil of eye constricted dilatedHR decreased increasedHeart vessels constricted dilatedVessels in:Skeletal mus. No effect dilatedAbd’l viscera/skin No effect constrictedBP decreased increasedBronchioles constricted dilatedBreathing decreased increasedDigestive peristalsis increased decreasedd. Tube sphincter relaxed constricted
  • 33. Secretion of glands thin, watery saliva thick, viscid salivaDigestive secretion increased no effectGlycogen-glucogenConversion of liver no effect increasedUrinary bladder wall contracted relaxedUrinary sphincter relaxed contractedUterine mus. Relaxed; variable contracted; varies in mens & pregnancyExt. genitalia mus. Dilated no effectSecretion of sweat no effect increasedPilomotor mus. no effect contracted (goose flesh)Adrenal medullae no effect secretion of epinephrine and norepinephrine
  • 34. ASSESSMENT: NEUROLOGICASSESSMENT
  • 35. I. NURSING HEALTH HISTORY history of present illness (COLD SPA) review of medical history system by system evaluation ***are important and critical in order to come up with to an accurate diagnosis.
  • 36. II. CLINICAL MANIFESTATIONS1. Pain - a multidimensional unpleasant experience which may occur from neurologic disorders like: Acute - Spinal disk disease, Trigeminal neuralgia, Painful neuropathies Chronic - Cerebral palsy2. Seizures - results from abnormal paroxysmal discharges or neuronal firing in the cerebral cortex, which then manifest as an alteration in consciousness, sensation, behavior, movement or perception. It may also be a sing of brain lesion.3. Dizziness and Vertigo Dizziness - abnormal sensation of balance or movement, fairly common in elderly and most common complaint encountered by health professionals, can be caused by virus, hot weather, roller coaster ride, middle ear infection, etc. Vertigo – specific form of dizziness, usually a manifestation of vestibular dysfunction, can be severe as to result in spatial disorientation, loss of equilibrium, and nausea and vomiting.
  • 37. II. CLINICAL MANIFESTATIONS4. Visual disturbances - visual effects that cause people to seek health care, can range from decreased visual acuity associated with aging to sudden blindness caused by glaucoma, normal vision depends upon functioning visual pathways through the retina and optic chiasm and the radiations into the visual cortex in the occipital lobe, lesions of the eye itself (cataract), lesion along the pathway (tumor), lesion in the visual cortex (from stroke) interfere with normal visual acuity, abnormality of eye movement (nystagmus associated with multiple sclerosis) can compromise vision by causing diplopia or double vision.5. Weakness - especially muscle weakness is a common manifestation of neurologic disorder. Frequently coexists with other symptoms of disease and can affect variety of muscles causing a wide range of disability. It can be sudden or permanent as in stroke, or progressive as in amyotrophic lateral sclerosis.
  • 38. II. CLINICAL MANIFESTATIONS6. Abnormal Sensation - numbness, abnormal or loss of sensation is a neurologic manifestation of both central & peripheral nervous system disease. It can significantly affect balance and coordination.7. Impact on lifestyle - limitations imposed to the patient by any deficit & the patient’s role in society including family & community roles. Plan of care that the nurse develops to address & support adaptation to the neurologic deficit & continued function to the extent possible within patient’s support system.
  • 39. III. CEREBRAL FUNCTIONS1. Mental status – Assess patient’s appearance, behavior, dressing, grooming, personal hygiene, posture, gesture, movements, facial expressions and motor activity. Assess orientation to time, place and person.2. Intellectual Function – Assess IQ, serial 7 test (100 minus 7), capacity to interpret well – known proverbs, ability to recognize similarities and make judgments. Check also for the memory (remote and recent).3. Thought content – Assess if thought are spontaneous, natural, clear, relevant and coherent. Assess for presence of fixed ideas, illusions, hallucinations, preoccupations with morbid and paranoid ideation.4. Emotional status – Assess the affect or the external manifestation of mood: natural and even, irritable or angry, anxious, apathetic, flat, euphoric, jumping of ideas, and consistency between verbal and non verbal cues.
  • 40. III. CEREBRAL FUNCTIONS5. Perception – having an insight into the patient’s cortical ability Agnosia – inability to interpret or recognize objects seen through the special senses. Types of agnosia Affected cortical area Visual (show pencil) occipital lobe Auditory temporal (lateral/superior) Tactile (hold coin) parietal Body parts/relationship parietal (postero-inferior)6. Motor Ability - asking the patient to perform a skilled act (throw a ball, move a chair), failure means cerebral dysfunction7. Language Ability- person with normal neurologic function can understand and communicate in written & spoken language. Aphasia – a deficiency in language function Types of aphasia Brain area involved Auditory-receptive temporal lobe Visual-receptive parietal-occipital lobe Expressive speaking inferior posterior frontal areas Expressive writing posterior frontal areas
  • 41. IV. CRANIAL NERVE FUNCTIONCranial Nerve Clinical ExamI. Olfactory - with eyes closed, the pt. identifies familiar odor (coffee, tobacco). Each nostril is tested separatelyII. Optic - Snellen eye chart; visual fields, opthalmoscopic examIII. Oculomotor - for CNs 3, 4 & 6; tests for ocularIV. Trochlear rotations, conjugate mov’ts.,VI. Abducens nystagmus. Test for pupillary reflexes & inspect eyelids for ptosisV. Trigeminal - have pt. close the eyes. Touch a wisp of cotton to forehead, cheeks & jaw. Sensitivity to superficial pain is tested the sharp & dull ends of a broken tongue blade.
  • 42. V. Trigeminal - alternate bet. the sharp & dull end - patient reports dull & sharp with each mov’t. If reports are incorrect, test for temp sensation. - while the patient looks up, lightly touch a wisp of cotton against the temporal surface of each cornea. A blink and tearing are normal responses. - have the patient clench & move the jaw from side to side. Palpate the masseter & temporal muscles, noting strength & equality.VII. Facial - observe symmetry while patient performs facial mov’t.; smiles, whistles, elevates eyebrows, frowns, tightly closes eyes (examiner opens them); flaccidity
  • 43. VIII. Acoustic - whisper or watch-tick technique; test for lateralization (weber); test for air & bone conduction (Rinne)IX. Glossopharyngeal - assess patient’s ability to discriminate bet. Sugar & salt on posterior 3rd of the tongueX. Vagus - depress a tongue blade on posterior tongue or stimulate posterior pharynx to elicit gag reflex note any harshness in voice. Have pt. say “ah”, observe for symmetric rise of uvula & soft palate.XI. Spinal Accessory - palpate & note strength of trapezius muscle on shrugging & sternocleidomastoid muscle as pt. turns head against pressure
  • 44. XII. Hypoglossal - while pt. protrudes tongue, any deviation or tremors are noted. Strength of the tongue is tested by having the protruded tongue move from side to side against a tongue depressor.
  • 45. V. REFLEXES Involuntary contractions of muscle in response to abrupt stretching or striking with a reflex or percussion hammer near the site of muscle insertion. Valid findings depend on proper use of reflex hammer, proper positioning of extremities & a relax patient. 2 TYPES: Superficial, Deep Tendon Reflexes1. Superficial or Cutaneous Reflexes - graded as (+) or (-) Corneal reflex – cotton wisp is touched to outer sclera of each eye. Normal response is a blink. Gag reflex – tongue depressor is touched to uvula. Normal response is gag. Cremasteric reflex – inner thigh of male client is stroked. Normal response is penile erection. Plantar or Babinski reflex – lateral sole is stroked with tongue blade, normal response is toe flexion or negative babinski.
  • 46. V. REFLEXES 2 TYPES: Superficial, Deep Tendon Reflexes2. Deep tendon reflex – graded as:+4 -hyperactive+3 -more brisk than avg. maybe normal or indicative of a dse.+2 -average or normal response+1 -hypoactive or diminished 0 -No response Biceps reflex (C5C6) -Arm is slightly flexed at the elbow with the palm down. The examiners thumb is placed on the biceps tendon and a blow is stuck over the thumb. The biceps muscles should contact and flexion of the forearm at the elbow should occur. Brachioradialis reflex (C5C6) - The forearm should rest in the person’s lap. The hand is supported in a semi prone position and the tendon over the radius is struck about 1 to 2 inches above the wrist. The result should be flexion and supination of the forearm.
  • 47. V. REFLEXES Triceps reflex (C7C8) - The client’s arm is flexed at the elbow with forearm held across the abdomen. The hand of that arm is supported with the palm toward the body and a blow is struck over the triceps tendon. The triceps muscle should extend at the elbow. Patellar reflex (L2L3L4) Ankle reflex (S1S2) - With the person’s leg somewhat flexed at the knees and the foot supported with the examiner’s hand the Achilles tendon is struck above the heel. Normal response is plantar flexion. Clonus – very hyperactive reflexes which may indicate CNS disease abd require further evaluation
  • 48. VI. MOTOR FUNCTIONS1. Muscle Strength2. Balance and coordination1. Muscle Strength- Patient is asked to walk across the room while examiner observes for posture & gait. Muscles are palpated for size & symmetry. Any evidence of atrophy or involuntary mov’t. (tremors, tic), muscle tone (tension present in a muscle at rest) is evaluated by palpating various muscle groups @ rest & during passive mov’t. Abnormalities include spasticity (inc. Muscle tone), rigidity (resistance to passive stretch) & flaccidity. Strength is assessed to know the ability to flex or extend against resistance. Graded as: 0- no contractility 1- some contractility but no joint motion 2- complete ROM without gravity 3- complete ROM with gravity 4- complete ROM with some resistance 5- normal function against full resistance
  • 49. VI. MOTOR FUNCTIONS2. Balance & Coordination - Cerebellar influence on the motor system is reflected in balance, control & coordination. Hand & extremity coordination is tested by having the pt. perform alternating mov’ts & point to point testing (thigh patting with alternate hands, pronate & supinate, thumb with each fingers). Speed, symmetry & degree of difficulty are noted. Patient’s finger then examiner’s finger touching) Check for Ataxia - incoordination of voluntary muscle action, particularly of muscle group used in activity (rhythmic, involuntary mov’ts) Check for maintenance of standing position: (Romberg’s test)- screening test for balance. Patient stands with feet together with arms @ the side, with eyes open first then both eyes closed for 20-30 seconds. Loss of balance means (+) Romberg test. Ask the person to stand erect with both heels together and both eyes open. Note any swaying or loss of balance. Ask the person to maintain that position but to close both eyes. Note any abnormal swaying or tendency to fall.
  • 50. VII. SENSORY FUNCTIONSGENERAL TYPES OF SENSATION:1. Superficial - concerned with touch, pain, temperature2. Deep sensation - concerned with muscle and joint sense3. Combined – superficial and deep sensory mechanism combined in steriognosis (recognition and naming of familiar objects placed on hand) and in the ability to localize cutaneous stimuli
  • 51. VII. SENSORY FUNCTIONS1. Tactile Sensation – lightly touch a cotton wisp to a body part. Compare proximal to distal sensation.2. Vibration Sensation - Ask the client to close both eyes. Vibrate a tuning fork by knocking it against the palm of the hand. Apply the tuning fork to the bony prominences to ensure that the person is responding to vibration and not sound both eats should be blocked from receiving sound. Ask the client to report the feeling of a “buzz” and to say when the “buzz” stop3. Pain and Temperature Sensation3. Position Sensation or Proprioception – moves toes up, down, side to side
  • 52. VII. SENSORY FUNCTIONS5. Integration of Sensation Two point discrimination - Ask the client to close both eyes. Hold one pin in each hand and apply them so that the fingers of the examiner slide down the pin. Simultaneously apply the two pins to the same body part. Ask the person to report when one or two pins is/are felt Test for stereognosis – the ability to recognize an object of touch Test for extinction phenomenon - Ask the client to close both eyes and to report where he or she is touched. The answer should not just state “on the side” but should state which side it is.
  • 53. VIII. BOWEL FUNCTIONSIX. BLADDER FUNCTIONS
  • 54. ASSESSMENT:KEY SYMPTOMSOF NEUROLOGIC DISORDERS
  • 55. 1. Altered Level of Consciousness2. Altered memory, orientation, concentration3. Speech difficulties4. Altered movement and coordination (weakness, paralysis)5. Pain6. Seizures7. Dizziness (Vertigo)8. Visual disturbances9. Taste & Smell alterations10. Abnormal Sensation (numbness, paresthesia)11. Altered temp regulation12. Altered pain perception13. Altered bowel and bladder elimination
  • 56. DIAGNOSIS:DIAGNOSTIC TESTS
  • 57. I. GLASGOW COMA SCALE1. Verbal responseOriented 5Confused 4Inappropriate words 3Incomprehensible sounds 2None 12. Eye openingSpontaneous 4To voice 3To pain 2None 1
  • 58. 3. Best motor responseObeys command 6Localizes pain 5Withdraws from pain 4Abnormal flexion (decorticate) 3Abnormal extension 2None 1Levels of consciousnessDeep coma 3 -5Coma 6 -8Lethargic 9 - 11Stuporous 12 -14Normal 15
  • 59. Coma – a clinical state of unconsciousness in which the patient is unaware of self or the environment for prolonged periods (days to months or even years)Persistent vegetative state – condition in which the patient is described as wakeful but devoid of conscious content, without cognitive or affective mental functionBrain Death – irreversible loss of all functions of the entire brain, including the brain stem
  • 60. II. LUMBAR PUNCTURE AND CSF ANALYSIS Carried out by inserting a needle into the lumbar SA space to withdraw CSF. Done to obtain CSF for examination, measure & reduce CSF pressure, determine the presence or absence, detect spinal SAB & administer medications intrathecally. Needle is inserted into the SA space between 3rd & 4th or 4th & 5th lumbar vertebrae. Specimens are obtained for cell count, culture & glucose & protein testing. Specimen should be sent to lab immediately because changes will take place & alter result if allowed to stand. Other form include Queckenstedt’s test.
  • 61. II. LUMBAR PUNCTURE AND CSF ANALYSIS RESULT:a. 70-200mmH20- normal CSF pressure with the pt in lateral recumbentb. Should be clear & colorlessc. Pink, blood-tinged or grossly bloody CSF may indicate a cerebral contusion, laceration or SA hemorrhage COMPLICATIONS:a. Herniation of intracranial contentsb. Spinal epidural abscess/hematomac. Meningitisd. Temporary voiding problemse. Slight increase of temperaturef. Backache or spasmsg. Stiffness of neckh. Post lumbar puncture headache
  • 62. II. LUMBAR PUNCTURE AND CSF ANALYSIS POST LUMBAR PUNCTURE HEADACHE : Caused by CSF leakage @ the puncture site. The fluid continues to escape into the tissues by way of the needle track, from the spinal canal. It is then absorbed promptly by the lymphatics. As a result, the supply of CSF in the cranium is depleted @ point @ which it is insufficient to maintain proper mechanical stabilization of the brain. This leakage of CSF allows settling of the brain when the patient assumes an upright position, producing tension & stretching the venous sinuses & pain-sensitive structures. Both traction & pain are lessened & the leakage is reduced when the pt lies down.
  • 63. II. LUMBAR PUNCTURE AND CSF ANALYSIS NURSING INTERVENTIONS:1. Signed consent and void before the procedure. Use small gauged needles2. Instruct to relax to avoid traumatic or bloody tap, fetal position. A local anesthetic will be used.3. Patient remains on prone position 2 – 3 hours post procedure4. Headache is managed by rest, analgesics & hydration5. Assist with EPIDURAL BLOOD PATCH – blood is withdrawn from antecubital area & injected into the epidural space, usually @ the site of previous spinal puncture *** Blood acts as gelatinous plug to seal the hole in the dura, preventing further loss of CSF
  • 64. III. CT SCAN- a non-invasive & painless procedure & has a highdegree of sensitivity for detecting lesions.- makes use of a narrow x-ray beam to scan the headin successive layers. The images provide crosssectional views of the brain or other organs.- performed first without contrast then with IV contrastenhancement.- patient lies in adjustable table with the head in fixedposition while the scan system rotates around thehead & produces cross-sectional images. The patientmust stay still because motion will distort the image
  • 65. III. CT SCAN NURSING INTERVENTIONS:1. teaching the pt about the need to lie quietly & still throughout the procedure2. sedation can be used if agitation, restlessness or confusion will interfere with a successful study3. instruct pt to be on NPO for at least 4 hours4. monitoring pt for allergic reaction of contrast agent & other side effects5. increase hydration to flush out contrast
  • 66. IV. POSITRON EMISSION TOMOGRAPHY Computerized nuclear imaging technique that produces images of actual organ functioning. Patient either inhales radioactive gas or injected, that emits positively charged particles. It is useful in showing metabolic changes in the brain (Alzheimer’s dse), locating lesion (tumor, epileptogenic lesion), identifying blood flow & O2 metabolism in pts with strokes, evaluating new therapies for brain tumors & revealing biochemical abnormalities associated with mental illness. NURSING INTERVENTIONS:1. Patient preparation; explanation of the test & teaching patient of inhalation techniques & sensation (dizziness, lightheadedness, headache)
  • 67. V. ELECTROENCEPHALOGRAPHY Represents a record of the electrical activity generated in the brain. Obtained through electrodes applied in the scalp or through electrodes applied within the brain tissue. Provides a physiologic assessment of cerebral activity. Useful test for diagnosing & evaluating seizure disorders, coma, or organic brain syndromes. Tumors brain abscesses, blood clots, & infection may cause abnormal patterns in electrical activity NURSING INTERVENTIONS:1. Patient is deprived of sleep2. Anti-seizures, tranquilizers, stimulants, depressants are withheld 24-48 hours (can alter/mask abnormal wave patterns of seizure disorders.3. No coffee, tea, chocolate & cola (all stimulants)4. Meal should NOT be omitted - altered blood glucose change brain wave5. Patient is informed that it would take 45-60 minutes for awake & 12 hours for sleep EEG.
  • 68. VI. MYELOGRAPHY An x-ray of the spinal subarachnoid space taken after the injection of contrast agent into the spinal subarachnoid space through a lumbar puncture. Shows any distortion of the spinal cord or spinal dural sac caused by tumors, cysts, herniated vertebral disks or other lesions NURSING INTERVENTIONS:1. Information of the procedure; meal prior to procedure is omitted; sedative may be given2. After procedure, pt may lie in bed with HOB @ 30-45 degrees for 3 hours
  • 69. VII. ELECTROMYELOGRAPHY Obtained by introducing needle electrodes into the skeletal muscles to measure changes in the electrical potential of the muscle & the nerves leading to them. Useful in determining the presence of neuromuscular disorders & myopathies and help distinguish weakness due to neuropathy from weakness due to other causes NURSING INTERVENTIONS:1. Explanation of the procedure & patient is warned to expect a sensation similar to that of an IM injection as the needle is inserted into the muscle2. Inform that muscles examined may ache for a short of time after the procedure
  • 70. VIII. MAGNETIC RESONANCE IMAGING Helps identify cerebral abnormality more early and clearly than other test by using a highly magnetic field. The test may be done with or without a contrast. The magnet causes hydrogen ions in the body (protons) to align like small magnets and emit signals which are converted into images. NURSING REPONSIBILITIES:1. Remove all metal objects from the patient and inside the examination room.2. Instruct patient that it is painless but he may hear loud thumping3. Inform that he or she may communicate to the staff via a microphone inside the scanner.4. For claustrophobic patients, sedation may be used.
  • 71. IX. CEREBRAL ANGIOGRAPHY X- ray study of cerebral circulation after injection of a dye to a selected artery (usually femoral artery) under local anesthesia and heparinized saline. Valuable for detection of aneurysm, AV malformations and other vascular diseases. NURSING RESPONSIBILITIES:1. Ensure well hydration and clear liquids before the test2. Instruct to void before the test3. Location of peripheral pulses are marked with a felt – tip pen4. Shave the are (groin)5. Instruct to remain immobile during the test, brief feeling of warmth behind the eyes, face, jaw, teeth, tongue and lips and a metallic taste after dye injection.6. After the test, monitor VS, affected extremity for s/s of occlusion, apply cold compress to relive hematoma.
  • 72. X. NON – INVASIVE CAROTID FLOW STUDIES & TRANSCRANIAL DOPPLER Uses UTZ imagery and Doppler measurements of arterial blood flow to assess carotid and deep orbital circulation and presence of Stenosis or obstruction. Transcranial Doppler assesses flow velocities in deep cranial arteries and helpful in detection of vasospasm. NURSING RESPONSIBILITIES:1. Inform that it is non – invasive, hand held transducer is placed over the neck and orbits of the eyes with water soluble jelly.2. It is done at bedside.
  • 73. XI. CHEST X - RAY Makes images of the heart, lungs, airway, blood vessels and the bones of the spine and chest. An x-ray (radiograph) is a painless medical test that helps physicians diagnose and treat medical conditions. Radiography involves exposing a part of the body to a small dose of ionizing radiation to produce pictures of the inside of the body. X-rays are the oldest and most frequently used form of medical imaging. NURSING RESPONSIBILITIES:1. Check the doctor’s order.2. Inform the patient about the procedure.3. Provide privacy.4. Instruct the patient to remove clothing’s and jewelries.5. Instruct the patient to take full inspiration during the procedure.
  • 74. DIAGNOSIS: NURSINGDIAGNOSES
  • 75. 1. Altered Cerebral Tissue Perfusion2. Impaired Physical Mobility3. Ineffective Breathing Pattern4. Ineffective Airway Clearance5. Impaired Gas Exchange6. Pain7. Self – Care Deficit8. Activity Intolerance9. Impaired Urinary / Bowel Elimination, Incontinence, Retention10. Altered Nutrition Less than Body Requirement11. Impaired / Risk for Impaired Skin Integrity12. Risk for Injury13. Impaired Verbal Communication14. Disturbed Sensory Perception15. Altered Thought Process16. Confusion: Acute / Chronic17. Anxiety18. Low Self Esteem19. Ineffective Individual Coping20. Risk for Ineffective Family coping21. Sexual Dysfunction
  • 76. MANAGEMENT OFNEUROLOGIC DISORDERS
  • 77. INTRACRANIAL SURGERIES LAYERS OF SCALP & MENINGES: (SCALP – SKULL - DAP)1. Skin2. Connective tissue3. Aponeurosis4. Loose Connective Tissue (vascular layers)5. Pericranium (skull)6. Dura, Arachnoid, Pia matter TYPES OF SURGERIES:1. Supratentorial2. Infratentorial3. Transphenoidal4. Burr Holes
  • 78. I. UNCONSCIOUSNESS & COMA TERMS:1. Altered LOC – disorientation, difficulty in following commands and needs persistent stimuli to achieve a state of alertness.2. Coma – state of unarousable unconsciousness wherein purposeful response to external and internal stimuli are absent except for involuntary responses to painful stimuli and brain stem reflexes.3. Akinetic mutism – unresponsiveness to the environment in which the patient makes no voluntary movements.4. Persistent vegetative state - condition in which the unresponsive patient is described as wakeful or resumes sleep – wake cycles after coma but is devoid of conscious content, without cognitive or affective mental function.5. Locked-in syndrome - inability to speak, tetraplegia but with intact vertical eye movements and eyelid elevation . Results from lesions in Pons.
  • 79. I. UNCONSCIOUSNESS & COMA S/S:1. Glasgow coma scale result below 152. Presence of multiple pathophysiologic phenomenon3. Comatose w/ localized abnormal pupillary & motor response – neurologic problem4. Comatose but w/ pupillary light reflexes – toxic or metabolic disorder COMPLICATIONS:1. Respiratory failure2. Pneumonia3. Pressure ulcers4. Venous stasis5. Musculoskeletal deterioration6. Disturbed GI Functions7. Aspiration
  • 80. I. UNCONSCIOUSNESS & COMA MEDICAL/SURGICAL/NURSING MGT:1. Maintain patent airway Semi – Fowler’s position, lateral or semi-prone position, suction secretions with hyper-oxygenation, monitor breath sounds, prepare intubation set.2. Protect the client Side rails: 2 @ day, 3 @ night, privacy during nursing activities3. Maintain fluid balance and proper nutrition IV (slow), NGT, gastrostomy4. Mouth care Cleanse, rinse, remove secretions, apply thin petrolatum on lips, move ET tube to side regularly5. Maintain skin and joint integrity Regular turning, proper moving in bed, passive ROM, assistive devices, proper positioning, fluidized or low – air loss bed
  • 81. I. UNCONSCIOUSNESS & COMA MEDICAL/SURGICAL/NURSING MGT:6. Preserve corneal integrity Cleanse with cotton moistened w/ NSS, artificial tears every 2 hours, cold compress for periorbital edema, proper eye patching7. Maintain Body temperature Proper ventilation, clothes, TSB, IV hydration, antipyretics, monitor temperature8. Prevent urinary retention Regular palpation of bladder, IFC, bladder training9. Promote bowel function Monitor bowel sounds and movements, rectal exam, fecal collection bags, stool softeners; glycerin suppositories, enema.10. Provide sensory stimulation Orientation, patience11. Meet family’s needs12. Monitor and manage complications
  • 82. II. INCREASED ICP PREDISPOSING FACTORS:1. Cerebral edema2. Head injury3. Hydrocephalus4. Inflammatory conditions5. Tumor SITUATION: Imbalance among the 3 major determinants of ICP. ICP exceeds 20 mmHg (normal is 10 – 20 mmHg ,measured at the lateral ventricles)
  • 83. II. INCREASED ICP3 major determinants of ICP:1. Brain tissue – 1,400 grams (increased by space occupying lesions/tumor, abscess, edema)2. Blood supply – 75 ml (affected by thrombosis, embolism, aneurysm, AV malformation)3. CSF – 75 ml (increased by obstruction to flow or overproduction d/t a tumor in choroid plexuses)**** CSF and Blood supply undergo constant minor changes due to increase in the intra-thoracic pressure when the person sneezes, coughs, strains; posture, BP, systemic oxygen and CO2 levels.
  • 84. II. INCREASED ICP CEREBRAL RESPONSE TO INCREASED ICP:1. Monro – Kellie Hypothesis2. Autoregulation3. Cushing’s Reflex EFFECTS:1. Ischemia – cell death2. Cerebral edema3. Fatal complication - Herniation of brain tissue (brain stem)4. Secondary complications – SIADH, Diabetes insipidus (> 250ml urine/hour in 2 consecutive hours)
  • 85. II. INCREASED ICP Early Signs:1. Change in LOC – earliest sign, restlessness to confusion2. Slowing of speech – delayed response to verbal suggestions3. Pupillary changes – anisocuria4. Constant Headache Late Signs:1. Change in VS – Cushing’s triad plus hyperthermia2. Deterioration of LOC - disorientation to lethargy, stupor to coma3. Cheyne-stokes breathing4. Ataxic breathing – irregular with random sequence of deep and shallow respiration5. Projectile vomiting6. Decorticate and Decebrate posture, flaccidity, hemiplegia7. Loss of brainstem reflexes – pupillary (fixed, dilated pupils), corneal reflex, gag, swallowing reflex
  • 86. II. INCREASED ICP Medical Nursing1. Monitoring ICP and Cerebral Oxygenationa. Ventriculostomy a. Evaluate ICP as orderedb. Subarachnoid screw or bolt b. Perform regular neurologic ICP checkc. Epidural monitor c. Prompt referral ofd. Fiberoptic monitor significant abnormale. Jugular Venous Bulb (SjvO2) findingsf. LICOX - measures O2 and
  • 87. II. INCREASED ICP Medical Nursing2. Decreasing cerebral edemaa. Osmotic diuretics – mannitol a. Administer meds ad orderedb. Loop diuretics – furosemide b. Monitor for electrolytec. Potassium sparing diuretics – imbalance with use of spironolactone diuretics especiallyd. For Hypokalemia – KCL Potassiume. For Hyperklaemia – Insulin, c. Record I and O kayexalate, Na CHO3, Calcium d. Emphasize fluid restriction Gluconate to patient and SOf. Corticosteroids e. Position properly to facilitateg. Negative fluid balance - Fluid drainage – HOPB elevated restrictions by 30 degreesh. Ventriculostomy f. Regulate IVF properlyi. IFC g. Oral care during fluid restrictions
  • 88. II. INCREASED ICP Medical Nursing3. Maintaining Cerebral Perfusion and oxygenationa. Inotropic agents - a. Administer meds as Dobutamine HCL (dobutrex) ordered and Norepi. bitartrate b. Proper positioning, (Levophed) use of cervical collarb. Oxygenation administration c. Maintain oxygen as mechanical ventilation orderedc. CPP monitoringd. ABG, Hgb, Pulse oximetry
  • 89. II. INCREASED ICP Medical Nursing4. Reducing CSF and Intracranial Blood Volumea. CSF drainage a. Proper positioningb. Promoting mild cerebral b. Maintain integrity of vasoconstriction – PaCO2 at intraventricular 30 – 35 mmHg catheter for CSF drainage
  • 90. II. INCREASED ICP Medical Nursing5. Preventing further increase in ICPa. Cough suppressants a. Proper positioning, use (dextrometorphan) of cervical collar,b. Antivomiting (plasil) preventing hip flexionc. Stool softeners (dulcolax) b. Instruct to consciousd. Surgery – burr hole client to avoid valsalva maneuver, bending, stooping, lifting heavy objects c. Prevent vomiting and coughing
  • 91. II. INCREASED ICP Medical Nursing6. Controlling Fever and reducing metabolic demandsa. Antipyretics a. Monitor VS esp. Temperatureb. Hypothermic blanket – use rectal or tympanicc. High doses of barbiturates – thermometer Pentobarbital (nembutal), b. Provide adequate ventilation Thiopental (pentothal) c. Administer meds as orderedd. Paralyzing agents – propofol d. Monitor for adverse effects of (Diprivan) with analgesia and paralyzing agents and sedation barbituratese. Induced hypothermia e. Assist in induction of hypothermia
  • 92. II. INCREASED ICP Medical Nursing7. Maintaining a patent airway a. Suction secretions as needed –a. Intubation with oxygenation b. Monitor breath sounds8. Preventing Infectiona. Prophylactic antibiotics a. Maintain aseptic technique when especially if with caring for tubes and intraventricular catheter intraventricular catheter b. Monitor for signs and symptoms of meningitis and other infections
  • 93. II. INCREASED ICP Medical Nursing9. Monitoring and managing complicationsa. Diabetes Insipidus – a. Perform frequent and regular electrolyte replacement, neurologic assessments vasopressin b. Monitor urine and record outputb. SIADH – fluid restriction, c. Proper use of monitoring devices monitoring F & E status d. Educate family regarding monitoring technology/equipment and their purposes.
  • 94. III. HEADACHE/CEPHALGIA DEFINITION: A symptom rather than a disease which may indicate organic disease, stress response, vasodilatation, skeletal muscle tension, or combination of factors. TYPES:1. PRIMARY HEADACHE – no organic cause is identified. Includes: Migraine Tension – type headache Cluster headaches Cranial arteritis Other primary headaches2. SECONDARY HEADACHE - associated with organic cause such as brain tumor or aneurysm.
  • 95. III. HEADACHE/CEPHALGIA ASSESSMENT:1. Migrainea. Prodromeb. Aura Phasec. Headache Phased. Recovery and Postdrome2. Other headache typesa. Tension headacheb. Cluster headachesc. Cranial arteritis
  • 96. III. HEADACHE/CEPHALGIA Medical Nursing1. PreventionMigraine: a. Educate patients1. Beta blockers – propanolol, regarding causes and metoprolol predisposing factors2. Calcium channel blockers for clients and the need to avoid with asthma, DM, bradycardia – them. verapamil b. Teach relaxation3. Amitriptyline HCL (elavil) techniques c. Administer meds as4. Divalproex (valproate) ordered5. Flunarizine6. Serotonin antagonist (pizotyline)Others:a. Ergotamine tartrateb. Lithium naproxen (naprosyn)c. Methysergide (sansert)
  • 97. III. HEADACHE/CEPHALGIA Medical Nursing2. Relieve Paina. 100 % oxygen via face a. Provide comfort mask for 15 minutes measures, quiet, darkb. Ergotamine tartrate environmentc. Corticosteroids b. Assist with comfortabled. Other analgesics positioning – usually HOB elevated by 30 degrees c. Apply warm compress and massage to area with muscle tension d. Administer meds as ordered
  • 98. IV. SEIZURE DISORDER Convulsion Seizure Epilepsy- can be best described as - includes clinical - when seizuresa sudden, excessive, manifestation such become recurrent ordisorderly discharge of as disturbances in chronic in natureneurons in either a sensation, alteration - a paroxysmalstructurally normal or in perception and or disturbance indiseases cortex which coordination, LOC, consciousness witharises from an instability convulsive autonomic, sensoryof the neuronal movements or a and /or motormembrane caused by an combination of any dysfunctionexcess of excitation or a or all of the - a manifestation ofdeficiency of normal aforementioned. excessiveinhibitory mechanism. neurological-refers only to those discharge in the brain.violent, involuntarymuscular contraction ofvoluntary muscle.
  • 99. IV. SEIZURE DISORDER Convulsion Seizure Epilepsy- can be best described as - includes clinical - when seizuresa sudden, excessive, manifestation such become recurrent ordisorderly discharge of as disturbances in chronic in natureneurons in either a sensation, alteration - a paroxysmalstructurally normal or in perception and or disturbance indiseases cortex which coordination, LOC, consciousness witharises from an instability convulsive autonomic, sensoryof the neuronal movements or a and /or motormembrane caused by an combination of any dysfunctionexcess of excitation or a or all of the - a manifestation ofdeficiency of normal aforementioned. excessiveinhibitory mechanism. neurological-refers only to those discharge in the brain.violent, involuntarymuscular contraction ofvoluntary muscle.
  • 100. IV. SEIZURE DISORDER CAUSES: 1. Idiopathic 2. Acquireda. Cerebrovascular diseaseb. Hypoxemia of any causec. Fever (childhood)d. Head injurye. Hypertensionf. CNs infectionsg. Brain tumorh. Drug and alcohol withdrawali. Agents - (INH) isoniazidj. Allergiesk. Metabolic and toxic conditions – hypoglycaemia, hypocalcemia, hyponatremia, renal failure, pesticides
  • 101. IV. SEIZURE DISORDER PATHOPHYSIOLOGY:1. Depletion of K+ and a gain of Na+ in the neuronal cell produce seizure2. Alteration in the blood brain barrier system can precipitate a shift in K+ concentration lowering the convulsive threshold3. An altered O2 and glucose concentration – produce rapid marked potassium loss and a sodium accumulation within the cells depolarizing the membrane and producing those paroxysmal discharges.4. Infectious process – as a result of cell destruction, fever, inflammation and possible bacterial toxicity.5. Vitamin B6 deficiency whether dietary or drug antagonized. Since Vit B6 is involved in the metabolism of GABA, a shift of the normal excitatory inhibitory balance occur with excitation prevailing and a results to seizure.6. The duration of a seizure varies greatly. It may last a few seconds or persists for several minutes. Although investigators do not know why seizure stops at a given time. It is thought to be related to exhaustion of the neurons involved and to certain unknown factor which inhibits further electrochemical transmission. Some individuals may experience them once or twice a year, while others may have 2 or 3 episodes in a single day. It is unpredictable which is especially frightening to the individual.
  • 102. IV. SEIZURE DISORDER CLASSIFICATION:1. Generalized seizure Grand mal or major motor Petit mal Myoclonic seizure Infantile spasms Atoning seizure Tonic seizure Febrile seizures Status epilepticus2. Partial seizure Localized motor seizures or Jacksonian seizure Psychomotor (complex partial seizure) Partial seizure with secondary generalization3. Unilateral4. Unclassified epileptic seizures
  • 103. IV. SEIZURE DISORDER MEDICAL MANAGEMENT:1. Prevention – removal of precipitating factors2. Anticonvulsant Therapy Phenytoin (Dilantin) – DOC Phenobarbital (Luminal) Mephobarbital (Mebaral) Primidone (Mysoline) Succinamides Ethosiximide (Zarontin) Methsuximide (Celontin) Others Diazepam (Valium) Clonazepam (Clonopin) Valproic Acid (Depakene) Acetazolamide (Diamox) Carbamazepine (Tegretol)3. Surgery
  • 104. IV. SEIZURE DISORDER NURSING MANAGEMENT:1. General – C-A-E-S-A-R2. During the Seizure3. After the Seizure
  • 105. V. CEREBROVASCULAR ACCIDENT (STROKE) SITUATION: Sudden loss of brain function resulting from a disruption of blood supply to part of the brain causing temporary or permanent dysfunction. May be caused by thrombosis, embolism, hemorrhage. Also known as Ischemic stroke and brain attack MAJOR CAUSES:1. Ischemic2. Hemorrhagic
  • 106. V. CVA/STROKE RISK FACTORS:1. HPN2. DM3. MI4. Aortic valve disease5. CHF6. Arterio/Atherosclerosis TYPES ACCORDING TO TIME:1. Transient Ischemic Attack (TIA)2. Reversible ischemic Neurologic deficit3. Stroke in Evolution4. Completed Stroke TYPES ACCORDING TO CAUSE:1. Ischemic2. Hemorrhagic
  • 107. STROKE CLASSIFICATION ACCORDING TO TIME1. Transient Ischemic Attack (TIA) - temporary episode of neurologic dysfunction (loss of motor, sensory & visual dysfunction) Management: Anticoagulant therapy heparin, coumadin, aspirin2. Reversible ischemic Neurologic deficit - signs & symptoms are consistent with but more pronounced than TIA. S/Sx resolve in days without neurologic deficit3. Stroke in Evolution - worsening of neurologic S/Sx over several minutes or hours. Also called Progressing stroke4. Completed Stroke - stabilization of neurologic S/Sx. No further progression of hypoxic insult to the brain.
  • 108. TYPES ACCORDING TO CAUSE (ISCHEMIC):1. Large artery thrombosis – due to atherosclerotic plaques in the large blood vessels of the brain. Thrombus formation & occlusion @ the site of atherosclerosis result in ischemia & infarction.2. Small penetrating artery thrombosis - affect one or more vessels & are the most common type of ischemic stroke. - also called lacunar stroke.3. Cardiogenic Embolic stroke - associated with cardiac dysrhytmias, usually atrial fibrillation. Emboli originate from the heart & circulate to the cerebral vasculature, most commonly the left middle cerebral artery, resulting in a stroke. Embolic strokes may be prevented with use of anticoagulants.4. Cryptogenic - no known cause5. Others - cocaine use, coagulopathies, migraine & spontaneous dissection of the carotid or vertebral arteries.
  • 109. Pathophysiology: Obstruction of blood vessels (of different causes) ↓ Ischemia ↓ Energy failure Acidosis ↓ Ion imbalance ↓ inc. glutamate depolarization Intracellular calcium increase ↓ Cell membranes & protein breakdown Formation of free radicals; Decrease protein production ↓ Cell injury & death
  • 110.  Ischemic cascade begins when cerebral blood flow falls to less than 25 ml/100g/min. at this point, neurons can no longer maintain aerobe respiration. Mitochondria switches to anaerobic respiration which generates large amounts of lactic acid, causing change in Ph, also renders the neuron incapable of producing large quantities of ATP to fuel depolarization process. Membranes pump that maintain electrolyte balance begin to fail & cells cease to function. An area of low cerebral blood flow (penumbra region) exists around the area of infarction. It is ischemic brain tissue that can be salvaged with timely intervention.
  • 111. TYPES ACCORDING TO CAUSE:(HEMORRHAGIC STROKE)1. Intracerebral Hemorrhage2. Intracranial/Cerebral Aneurysm3. Subarachnoid Hemorrhage4. Arterio-Venous Malformation
  • 112. V. CVA/STROKE RISK FACTORS1. HPN – BP vasoconstriction pressure in blood vessels rupture of vessels thrombus in the blood vessel of brain blood supply to the brain2. DM - blood sugar levels viscosity of blood perfusion of blood stasis of blood flow thrombus formation blood supply to the brain
  • 113. 3. MI – decrease O2 to myocardium decreased cardiac output decreased perfusion stasis thrombus decreased blood supply to brain4. Aortic valve dse - decreased cardiac output decreased perfusion stasis thrombus decreased blood supply to brain5. CHF – inability of heart to pump sufficient amount of blood back to heart decreased cardiac output decreased perfusion stasis thrombus decreased blood supply to brain6. Arterio/Atherosclerosis – narrowing of blood vessels decreased cardiac output decreased perfusion stasis thrombus decreased blood supply to brain
  • 114. V. CVA/STROKE CLINICAL MANIFESTATIONS Stroke can cause a wide variety of neurologic deficits, depending on the location of lesion, size of area of inadequate perfusion & the amount of collateral blood flow.1. Ischemic2. Hemorrhagic3. Motor disturbances4. Communication problems5. Perceptual/ Sensory disturbance lesion; numbness & tingling of extremities.6. Cognitive deficit7. Emotional deficits
  • 115. V. CVA/STROKE CLINICAL MANIFESTATIONS Ischemic: Numbness or weakness of face, arm or leg especially on one side of the body Hemorrhagic: “Exploding headache”, decreased LOC, focal seizures, nuchal rigidity
  • 116. V. CVA/STROKE CLINICAL MANIFESTATIONSMOTOR hemiplegia – most common motor dysfunction, due to lesion of the opposite side of the brain (paralysis of one side of the body) hemiparesis – weakness of one side of the body. Ataxia – staggering, unsteady gait; unable to keep feet together, needs a broad base to stand Dysphagia – swallowing difficulty. apraxia – inability to perform a previously learned action (picks up a fork but attempts to comb hair)
  • 117. V. CVA/STROKE CLINICAL MANIFESTATIONSCOMMUNICATION dysarthria – difficulty in speaking, caused by paralysis of muscles responsible for producing speech dysphasia/aphasia – defective or loss of speech. Could either be expressive, receptive or mixed/global
  • 118. V. CVA/STROKE CLINICAL MANIFESTATIONSPERCEPTUAL DISTURBANCE - Perception is the ability to interpret sensation. Disturbances are due to disturbances of primary sensory pathways between the eye & cerebral cortex. Homonymous hemianopsia – loss of half of the visual field. It corresponds to the paralyzed side of the body. Loss of peripheral vision – difficulty seeing @ night. Diplopia – double vision, unaware of objects or borders of objects. Paresthesia – occurs on side opposite to lesion; numbness & tingling of extremities.
  • 119. PERCEPTUAL DISTURBANCE
  • 120. PERCEPTUAL DISTURBANCE
  • 121. V. CVA/STROKE CLINICAL MANIFESTATIONSCOGNITIVE DEFICIT Short & long term memory loss Decreased attention span Impaired ability to concentrate Poor abstract reasoning Altered abstract reasoningEMOTIONAL DEFICITS Loss of self control Emotional lability Decreased tolerance to stressful situations Depression Withdrawal Fear, hostility & anger Feelings of isolation
  • 122. V. CVA/STROKE CLINICAL MANIFESTATIONSUSUAL SIGNS & SYMPTOMS 1. Headache 2. Vomiting 3. Seizures 4. Confusion 5. Decreased LOC 6. Nuchal rigidity 7. Fever 8. Hypertension 9. Slow bounding pulse 10. Cheyne-stokes respirations
  • 123. V. CVA/STROKE DIAGNOSTIC TESTS1. CT scan show lesion – to determine if the event is ischemic or hemorrhagic; to determine treatment2. 12 lead ECG3. Carotid Ultrasound4. Cerebral arteriography shows occlusion or malformation of vessels5. Transcranial Doppler6. Transthoracic or transesophageal echocardiogram7. MRI of brain8. Single photon emission CT
  • 124. V. CVA/STROKE MEDICAL MANAGEMENT Ischemic Stroke1. Thrombolytic therapy – Recombinant t-PA2. Anticoagulants – heparin – Coumadin (after 24 hours)3. Antiplatelets - Aspirin4. Statins - simvastatin5. AntiHPN – ACE Inhibitors6. Thiazide Diuretics7. Intubation8. Surgery: Carotid Endarterectomy – removal of an atherosclerotic plaque or thrombus from carotid artery to prevent stroke in patients with occlusive diseases of the extracranial cerebral arteries.9. Manage complication – pulmonary care, maintenance of patent airway, & administration of supplemental oxygen
  • 125. V. CVA/STROKE MEDICAL MANAGEMENT Hemorrhagic Stroke1. Analgesics – codeine, acetaminophen2. Sequential compression devices – prevent DVT3. Surgery: endovascular treatment, aneurysm coiling, removal of aneurysm
  • 126. V. CVA/STROKE MEDICAL MANAGEMENTCOMMUNICATION: Aphasia right hemiplegics Receptive – inability to decode spoken word (WERNICKE”S area affectation) give one command at a time, simple instructions, non verbal communication Expressive – inability to speak (BROCA’S area affected) encourage attempts at speech – anticipate needs, allow to verbalize, no matter how long it takes, do not finish sentences for himHOMONYMOUS HEMIANOPSIA AND LOSS OF HALF OF EACH VISUAL FIELD - approach patient on unaffected side place belongings on unaffected side teach scanning technique (turn head to sides)
  • 127. V. CVA/STROKE MEDICAL MANAGEMENTMANAGING COMPLICATIONS: - pulmonary care, maintenance of patent airway, & administration of supplemental oxygenENDARTERECTOMY – removal of an atherosclerotic plaque or thrombus from carotid artery to prevent stroke in patients with occlusive diseases of the extracranial cerebral arteries.NURSING MANAGEMENT POST OP 1. Close cardiac monitoring 2. Maintenance of adequate BP
  • 128. V. CVA/STROKE NURSING MANAGEMENT1. Maintain Patent airway2. Monitor VS , neurological checks3. Promote Bed rest4. Perform GI decompression (NGT)as ordered5. Maintain Fluid electrolyte balance6. Reposition q2h7. Promote Skin integrity8. Improve mobility9. Support Elimination – offer bed pan every 2 hours – catheterize if necessary – stool softeners and suppositories10. Ensure safety11. Facilitate Communication12. Administer drugs as ordered
  • 129. VI. NEUROLOGIC TRAUMA CLASSIFICATION:1. Brain Trauma Primary trauma –is the direct result of some force applied to the skull resulting in a fracture, hemorrhage, contusion, or concussion. Secondary trauma - is one in which some other medical condition causes a person to fall or otherwise to sustain a blow to the head. These conditions include diabetic, cardiac, epileptic or hysterical problems and situations following drug and/or alcohol ingestion in which the person falls, strikes the head and loses consciousness.a. Fractureb. Hemorrhagec. Contussiond. Concussion2. Spinal Cord Injury
  • 130. BRAIN TRAUMA: FRACTURES
  • 131. BRAIN TRAUMA: FRACTURES1. Linear fracture- are those in which there is a simple break in the continuity of the bone/skull2. Comminuted fracture- are fragmented interruptions of the skull from multiple linear fractures3. Depressed fracture - comminuted bone fragments penetrate the brain tissue4. Compound fracture- any of the preceding which also has an opening through the sinuses, eardrums or scalp.
  • 132. BRAIN TRAUMA: HEMORRHAGE1. Linear fracture- are those in which there is a simple break in the continuity of the bone/skull2. Comminuted fracture- are fragmented interruptions of the skull from multiple linear fractures3. Depressed fracture - comminuted bone fragments penetrate the brain tissue4. Compound fracture- any of the preceding which also has an opening through the sinuses, eardrums or scalp.
  • 133. BRAIN TRAUMA: HEMORRHAGE1. Epidural Hematoma2. Subdural Hematoma3. Intra-cerebral Hematoma
  • 134. BRAIN TRAUMA: CONCUSSION Concussion- It is essentially a disruption of normal activity among some of the synapses of the neurons. It is a temporary disarrangement of normal neurons activity. Muscular activity and mental clarity usually return within a few minutes after trauma, although there may be residual amnesia for the event. BRAIN TRAUMA: CONTUSIONContusions- Resemble bruises. There is only slight injury to small vessels with a small amount of bleeding into the surrounding tissues. The resulting effects of increased ICP are dependent upon the amount of contused brain tissue.
  • 135. SPINAL CORD INJURY Primary Injury - results from initial insult or trauma and produces permanent damage Secondary Injury – results from contusion or tear injury in which nerve fibers begin to swell and disintegrate. Damage is reversible up to 4 – 6 hours after the injury. Effects:1. Central Cord Syndrome2. Anterior Cord Syndrome3. Brown Sequard Syndrome
  • 136. SPINAL CORD INJURY COMPLICATIONS:1. Spinal and Neurogenic shock “areflexia”2. Autonomic Dysreflexia “hyperreflexia”3. Tetraplegia and Paraplegia4. Deep Vein Thrombosis and Thrombophlebitis5. Orthostatic Hypotension
  • 137. SPINAL CORD INJURY MANAGEMENT:1. Cord Damage – immobilize2. Respiration – stabilize, intubation3. Urinary and bowel function – training, IFC, enema, suppositories, don’t allow bladder to distend4. Thrombosis – anticoagulants, elastic compression stockings5. Cardiovascular stability6. Help assess meurologic status7. Encourage adequate fluid, nutrition8. Support skin to prevent breakdown, watch out for Shock
  • 138. VII. HYDROCEPHALUS DEFINITION: A.k.a. water on the brain Can be caused by impaired CSF flow and re- absorption, or excessive CSF production. Flow obstruction, hindering free passage of CSF through the Ventricular System & SA space (e.g. stenosis of cerebral aqueduct or obstruction of Foramen of Monro) due to tumors hemorrhages, infection or congenital malformations. Overproduction of CSF (e.g. papilloma of choroid plexus)
  • 139. VII. HYDROCEPHALUS TYPES:1. Congenital2. Acquired3. Communicating or Non – obstructive4. Non – communicating or Obstructive
  • 140. VII. HYDROCEPHALUS MEDICAL MANAGEMENT:1. Drugs2. Surgical removal of obstruction3. Surgical placement of shunting devicesa. VP shuntb. VA shuntc. EVD MEDICAL MANAGEMENT:1. Prevent Increase ICP2. Prevent Infection3. Promote proper nutrition4. Educate SO5. Post – op care
  • 141. VIII. NEURAL TUBE DEFECTS DEFINITION: Failure of neural tube to close or fully develop at 3 – 5 weeks of gestation. CAUSE: Genetics, heredity, drugs, radiation, chemicals or toxins, maternal malnutrition, maternal use of antiepileptic drugs, infectious diseases and FOLIC ACID DEFICIENCY (normal intake 0.4 - 4 mg/day). CLASSIFICATION:1. Anencephaly - cerebrum2. Encephalocele – cerebrum, meninges, glial cells3. Spina Bifida – spinal cord, meninges, usually L5 and S1 regiona. Spina Bifida occultab. Spina Bifida cystic Meningocele Myelomeningocele
  • 142. VIII. NEURAL TUBE DEFECTS GENERAL MANAGEMENT FOR NTD:1. All – protect from LATEX allergy, NO to balloons, vinyl gloves2. Anencephaly – no cure, support parents3. Encephalocele – protect from infection, support perio-peratively, and educate parents about possible intellectual impairment.4. Spina bifida occulta - facilitate work ups, referral to surgery, monitor for development of s/s.5. Meningocele – protect sac from rupture, drying or infection, place in prone position, facilitate early sac excision (24 – 48 hours of life), complete closure of spinal column, monitor for development of complications.6. Myelomeningocele – cover sac with non-adhesive, sterile, moist saline gauze, place infant in prone position, facilitate surgery (repair and shunt placement), emphasize to parents that surgery has its risks (lower extremities paralysis), monitor for development of complications like increase ICP and HYDROCEPHALUS.
  • 143. IX. MULTIPLE SCLEROSIS DEFINITION: Immune-mediated progressive demyelination or destruction of myelin sheath that surrounds certain nerve fibers in brain and spinal cords resulting to impaired transmission of nerve impulses. Affects the CNS. May be Relapsing-remitting, Primary progressive, Secondary progressive, Progressive-relapsing. CAUSE: Possibly Human Leukocyte Antigen in cell wall, presence of sensitized T – Cells that remain within the CNS. DX: MRI, Electophoresis of CSF (several bands of IG G) MAIN S/S: FATIGUE, CHARCOAT’S TRIAD MGT: Analgesics, immunosuppressive agents and steroids, GABA agonist, Benzodiazepines (valium), Symmetrel, Cylert, Prozac, Inderal, Vitamin C, antibiotics. NSG. CARE: AVOID FATIGUE, AVOID PREGNANCY during remission
  • 144. MULTIPLE SCLEROSIS A degenerative disease characterized by demyelination of nerve fibers within the spinal cord and brain. Destruction of an area of a myelin sheath occurs, followed by a proliferation of neuroglial cells, scar formation and damage to the nerve fiber with ensuing loss of transmission of impulses.Etiology and incidence: The cause is unknown. At present theories undergoing investigation are concerned with auto immune mechanisms and viral infections as possible etiologic factors. It most prevalent in colder climates. It has a slightly higher incidence in females between 20 to 40 years of age.
  • 145. Course and manifestations: Characterized by remissions and relapses, and the course is extremely variable and unpredictable.Early symptoms: Transient tingling sensations, numbness and muscular weakness in one or both arms and legs and visual disturbances (nystagmus, diplopia or blurring of vision); emotional lability, evidenced bv alternating periods of euphoria, depression, irritability.Late symptoms: With relapses and increasing damage, the patient may develop paralysis, impaired speech, dysphagia, increasing loss of sensation, bladder and bowel incontinence, increasing visual difficulties, personality changes, and intellectual impairment. Weakness of the respiratory muscles and cough reflex may also be present, predisposing him to pulmonary complication.
  • 146. Diagnostic test: At present there are no specific diagnostic tests. The CSF shows an elevated gamma globulin and a positive colloidal gold precipitation test (Lange colloidal gold curve)Treatment and Nursing Care: During remissions – the patient is encouraged to resume his usual pattern of life modifying it as necessary to avoid fatigue, emotional stress and infection. Well balanced diet adequate rest and learning to accept what cannot be readily change are stressed. Avoid pregnancy. During relapses – confine to bed for a period of 2 to 3 weeks or until symptoms begin to disappear. Warm baths, massage, pleasant quiet surroundings, encouraging reading and listening to radio, chat. The limbs are passively moved through the full range of motion twice daily.Steroid therapy: Dexamethasone (Decadron), Adrenocorticotropin (ACTH) or Prednisone
  • 147. X. MYASTHENIA GRAVIS DEFINITION: Immune-mediated varying degrees of voluntary muscle weakness. Affects the MYONEURAL JUNCTION. CAUSE: Presence of ANTIBODIES directed towards Ach receptors. DX: Achetylcholinesterase inhibitor test: TENSILON TEST, Presence of Ach receptor antibodies in serum, Successive nerve stimulation, Evaluation of Thymus gland. S/S: Ptosis, descending paralysis, muscle weakness in late afternoon, risk for respiratory failure. COMPLICATIONS: Respiratory Failure and Crisis:  Myasthenic crisis  Cholinergic crisis  Brittle Crisis – extreme under meds
  • 148. Etiology: Predisposing factor:- autoimmune - auto immune disease - viral infection, Thymoma, rheumatoid arthritis, - systemic lupus erythematous │--------------------------------------------------------------------------------------│ ↓ auto antibodies ↓ blocking the binding of acetylcholine ↓ destruction of ACH receptor ↓ impaired transmission of impulses across the myoneural junction ---------------------------------------------------------------------------------------------------------------------- ↓ ↓ ↓ ↓ ↓ ↓ facial expression limb movements laryngeal chewing & eye & eyelid involvement swallowing movements -myasthenic smile - unstable - dysphonia - dysphagia - diplopia - waddling gait - dysarthria - choking - ptosis - weak arms, - slurred speech - aspiration legs, hands & fingers Diaphragm- Shortness of breathComplications:- Myasthenia crisis or Brittle Crisis- Cholinergic crisis
  • 149. PTOSIS
  • 150. CRISIS: acute episodes to severe muscular weakness in which respiratory insufficiency and the inability to swallow are manifested.Categories: Myasthenic type – is attributed to a temporary resistance to or inadequate dosage of the cholinergic preparation being administered. Manifested by extreme weakenss. Tensilon relieves symptoms Cholinergic crisis – is caused by excess of anticholinesterase medication. Patient becomes pale and manifests diarrhea, nausea, vomiting, diaphoresis, increased salivation and bronchial secretions, abdominal cramps and blurred vision. Symptoms worsen in Tensilon. Atropine as antidote.
  • 151. X. MYASTHENIA GRAVIS MGT:1. Drugs – ANTICHOLINESTERASE/pyridostigmine bromide (Mestinon) and Neostigmine (Prostigmin), immunosuppressive agents (Prednisone), cytotoxic agents NO TO MORPHINE, CURARE, QUININE, NEOMYCIN, STREPTOMYCIN2. IVIG, Plasmapheresis, Thymectomy, Intubation, Mechanical Ventilation NSG. CARE:1. Avoid overfatigue.2. Support nutrition.3. Administer meds at precise time. 20 – 30 minutes before meals.4. Protect patient from fall.5. Aspiration precaution.6. Monitor respiratory status and provide adequate ventilation.7. Avoid exposure to infection.8. Provide eye care. “Crutches” to eyelids, patch one eye and give artificial tears.
  • 152. XI. GUILLAIN BARRE SYNDROME DEFINITION: An acute inflammatory demyelinating disease of the peripheral nervous system. CAUSE: Unclear. It is believed to be associated with an viral infections 1-4 weeks before. DX: Spinal Tap - High Protein levels in CSF, EMG – slow conduction of impulses to muscles S/S: 1. Initial phase - Bilateral muscle weakness in the lower extremities, with an ascending pattern. Can result in potential life-threatening respiratory compromise. 2. Plateau phase - May last days to weeks. It is an interim period in which no changes occur. 3. Recovery phase - Synonymous with re myelination and axonal regeneration. Paralysis resolves gradually in a descending symmetrical pattern following a proximal to distal pattern.
  • 153.  Pathophysiology: Schwann cells, which cover the nerve axons, form the myelin sheath. Degeneration of these cells occurs, causing a flaccid paralysis, which is usually in an ascending pattern. It is primarily the motor neurons affected. Sensory involvement is limited and is usually confined to the hands and feet in what is termed the glove and stocking pattern. Spontaneous regeneration of the myelin sheath occurs with complete recovery within 6 months to 1 year. Management is aimed at supporting body functions and preventing complications associated with paralysis until recovery occurs.
  • 154. GB Planning and Intervention:1. Assess for respiratory compromises - evaluate ABGs and pulse oximetry2. Be prepared to provide respiratory support – mech. vent and later on, intubation3. Perform pulmonary toilet to prevent pneumonia, suction as necessary, hyperoxygenate/hyperventilate4. Monitor Vital signs, ECG5. Assess for urinary retention6. Maintain optimal positioning a. Elevate head of bed as tolerated to promote lung expansion and decrease risk for aspiration b. Turn and reposition every 2 hours c. Assist with active and passive ROM7. Prevent DVT & pulmonary embolism – Anti-embolic stockings, sequential compression boots, anticoagulants
  • 155. 8. Administer medications as indicated and ordered, including: 1. IVIG – therapy of choice, followed by plasmapheresis 2. Analgesics 3. Anti-anxiety agents 4. Corticosteroids 5. Antibiotics for prophylaxis 6. Antacids to control gastric irritation 7. H2 blockers to reduce gastric acid secretion and prevent ulcer 8. Anticoagulants 9. A short – acting alpha adrenergic blockers for HPN in autonomic dysfunction
  • 156. XII. PARKINSON’S DISEASE DEFINITION: A progressive degenerative neurologic disorder affecting the brain centers that are responsible for control and regulation of movement (extrapyramidal) caused by deficiency of dopamine. Occurs in the elderly. CAUSE: Dopamine deficiency DX: EEG, CT Scan, SPECT (PET) S/S:1. Resting tremors2. Rigidity3. Bradykinesia4. Postural instability
  • 157.  Manifestations:1. Tremors of the upper limbs; “Pill rolling”2. Rigidity; “cogwheel rigidity”3. Bradykinesia (moves slowly)to hypokinesia (diminished movements)4. Stooped posture, loss of postural reflexes5. “Shuffling, propulsive gait/ festinating” gait6. Monotone speech; “microphonia, dysphonia”7. Mask like facial expression8. Increased salivation, drooling, dysphagia9. Excessive sweating, seborrhea10. Lacrimation, constipation11. Decreased sexual capacity12. Alteration in handwriting; “micrographia”13. Dementia, depression, sleep disturbances and hallucinations
  • 158. XII. PARKINSON’S DISEASE MGT: Drugs, Surgery 1. Antiparkinsonians 2. Anticholinergics 3. Antihistamines 4. Dopamine agonist 5. Antidepressants 6. MAO Inhibitors 7. Antiviral 8. Stereotactic Procedures - Thalamotomy and Pallidotomy 9. Neural Tranplantation 10. Deep Brain Stimulation NSG. CARE:1. Aspiration precaution2. Educate on drug therapy3. Physical therapy and gait training4. Diet5. Safety6. Emotional support7. Promote independence8. Skin care
  • 159. Drug Function Generic Name (Trade Name)Levodopa Enhances conversion of levodopa to Levodopa (Laradopa); dopamine in the brain. levodopa/carbidopa (Sinemet, Sineme CR,Atamet); levodopa/benserazide (Madopar)Dopamine agonist Mimics the action of dopamine by Bromocriptine (Ergoset, Parlodel); activating nerve cells in the brain. pergolide (Permax); pramipexole (Mirapex); ropinirole (Requip)Anticholinergic Blocks action of acetylcholine, a brain Trihexiphenidyl (Artane, Trihexy); chemical that becomes overactive when biperidine (Akineton); benztropine dopamine levels drop. (Congentin)MAO-B inhibitor Blocks action of an enzyme that breaks Selegiline (Eldepryl, Movergan) down dopamine in the brain.COMT inhibitor Blocks action of an enzyme that breaks Tolcapone (Tasmar); entacapone down levodopa in the body, permitting (Comtan) more levodopa to reach the brain.Amantadine Stimulates release of dopamine from Amantadine (Symadine, Symmetrel) nerve cells in the brain and may block acetylcholine action.
  • 160. BELL’S PALSY It is a lower motor neuron lesion of the 7th cranial nerve, resulting in paralysis of one side of the face. It is usually self-limiting to a few weeks.Manifestations: Facial paralysis involving the eye Tearing of eye Painful sensations in the face Sagging of one side of mouth; droolingManagement: Steroids and analgesics Protect involved eye Active facial exercises
  • 161. CEREBRAL PALSY- Is an umbrella term encompassing a group ofnon-progressive, non-contagious neurologicaldisorders that cause physical disability inhuman development, specifically movement &posture.- Neurological disability or difficulty controllingvoluntary muscles (caused by damage to someportion of the brain, with associated sensory,intellectual, emotional or convulsive disorders.
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  • 163. THANKS!