You are on page 1of 21
Neurologic Review 1. Review neurologic A&P. Pay particular attention to: a. Transmission of nerve impulses and the role of myelin i. Neuron- the basic unit of the nervous system transmits impulses or “messages”.  Each neuron produces a specific transmitter capable of either enhancing or inhibiting an impulse.  Transmission of nerve impulses are affected by: strength, distance, oxygen, pH, and/or medications/stimulants. a. Strength and Distance- synapses on or near the body of the cell have greater influence than those farther along the dendrite. Strength can also be influenced by inhibition by another neuron, adequate supply of transmitter substance, and extracellular fluid changes. b. Oxygen- lack of O2 or the effects of hypnotics and anesthetics can quickly depress nerve cell activity. i. In older adults, lack of O2 to the brain often causes changes in mental state. c. pH- changes in pH of ECF: acidosis depresses nerve cell activity; alkalosis excites nerve cells. i. Increased nerve cell activity occurs with the use of some drugs, such as caffeine (in coffee), theophylline (in tea and some asthma drugs), and theobromine (in cocoa). d. SAMEi. Dendrites synapse with other neurons via an afferent pathway to bring impulses to the cell body ii. Axons synapse with other neurons via an efferent pathway to transmit impulses away from the body.  Many axons are covered by a myelin sheath—a white lipid covering. Myelinated axons are referred to as white matter. a. Non-myelinated axons have a grayish cast and are called gray matter. b. Myelinated axons have gaps in the myelin called nodes of Ranvier. The nodes of Ranvier play a major role in impulse conduction.  When the myelin is impaired, the impulses cannot travel from the brain to the rest of the body, such as in patients with multiple sclerosis or GBS, which are autoimmune diseases. b. Characteristics and functions of neurons and neuroglial cells i. Neuroglial cells provide protection, structure, and nutrition for the neurons. These cells are part of the blood brain barrier and help regulate cerebrospinal fluid (CSF).  Astroglial cells  Oligodendrocytes- help form myelin sheath  Microglial cells- scavenger cells, macrophages that help clean up debris and fight infection.  Ependymal cells- CSF production and storage. c. Parts of the brain (cerebrum, cerebellum, brainstem, etc.), their functions, and roles i. Cerebrum- right and left hemispheres of cerebrum are joined by the corpus callosum. Left hemisphere is dominant in most people. At base of cerebrum near the ventricles is a group of neurons called the basal ganglia, which regulate the human needs for mobility.  Cerebral cortex- outermost layer of cerebrum; houses centers for most higher brain functions (learning, reasoning, deduction, and emotion).  Cerebrum- crossing motor tracts in medulla oblongata- contralateral impairment- left side stroke  right sided weakness ii. Cerebellum- controls voluntary movement and maintains equilibrium. Interprets movement directives from the motor cortex, and is responsible for maintaining posture, muscle tone, and storing some types of memory.  Cerebellar control of the body is ipsilateral- situated on the same side- right side of the cerebellum controls right side of the body and vice versa. iii. Brainstem- controls all cardiac and respiratory ability. Reticular activating system (RAS)controls awareness and alertness.  Midbrain- relay impulses to CNS; auditory and visual reflex; location of periaqueductal gray, which may abolish pain when stimulated; cerebral aqueduct  Pons- relay impulses to higher cortical structures, cardiac acceleration and vasoconstriction center; pneumotaxic center- controls respiratory pattern and rate.  Medulla- crossing of motor tracks; coughing, swallowing, gag; cardiac slowing, respiratory, and vasomotor center. d. Cerebral lobes (frontal, temporal, etc.) and their main roles i. Frontal lobe:  Primary motor area (motor cortex) controls voluntary movement.  Broca’s area (speech center)- formation of words or speech. Expressive aphagia  Access to past info or experience  Judgment, reasoning, concentration ii. Parietal lobe: includes somatosensory area, responsible for processing and storing sensory information from pain, touch, pressure, and temperature, important for singing, playing instruments, perception of body parts and body position awareness (proprioception).  ND: Risk for injury iii. Temporal lobe- auditory center for sound interpretation, complicated memory patterns, Wernicke’s area for speech- processing of words into coherent thought and understanding of written or spoken words (receptive aphagia). iv. Occipital lobe- primary visual center; receives and processes visual information and maps it onto the cerebral cortex in a complex network. v. Limbic lobe- emotional and visceral patterns connected with survival; also learning, memory, and olfaction. e. The role and function of the BBB and CSF i. Blood brain barrier (BBB)- cerebral capillaries tightly joined; only certain substances from bloodstream allowed into cerebrospinal circulation. ii. Cerebrospinal fluid circulation (CSF)- produced by choroid plexus in ventricles; reabsorbed by arachnoid villi. Circulates, surrounds, cushions brain and spinal cord within the subarachnoid space. f. The role of the autonomic nervous system in neurologic function i. Autonomic nervous system- two parts: sympathetic nervous system (SNS) and parasympathetic nervous system (PNS). ANS functions are not usually under conscious control.  SNS- thoracolumbar- fight or flight response- increased rate and contractility a. Adrenergic responses- Assessment: increased pulse and blood pressure, dilated pupils, decreased peristalsis, increased perspiration.  PNS- craniosacral (originates in the gray matter of the sacral area of spinal cord)Rest and digest-- involuntary reactions. a. Cholinergic responses- Assessment: decreased pulse and blood pressure, constricted pupils, increased salivation, increased peristalsis, dilated blood vessels, bladder contraction. 2. Describe a thorough neurologic assessment, how the various tests and techniques would be provided, and what their findings suggest. Pay particular attention to: a. Assessing LOC—must determine a baseline for patient before any assessment. LOC observed through responsiveness and mental status. Assessment becomes increasingly invasive as the client is less responsive-- begin with least noxious stimuli and progress to most noxious stimuli: walk in room call name touch pt clavicular pinch sternal rub (most noxious). i. A change in LOC is very important because it is the first indicator and most sensitive indicator of a neurologic problem. b. Memory- loss of memory, especially recent memory, tends to be an early sign of neurologic problems. i. Long term (remote)- birth date, city of birth, things from past. ii. Recall (recent)- tested during the history and checked on the medical record; mode of transport to the hospital, time of admission. Early sign of neurologic problem. iii. Immediate (new)- give three unrelated words and have pt. repeat, ask pt. to recall three words after 5 minutes. c. Glasgow Coma Scale—rapid neurologic assessment—establishes baseline data in each of these areas: eye opening, motor response, and verbal response. A score of 15 represents normal neurologic functioning. A score of 7 represents a comatose state. For patients who are intubated and cannot talk, record their score with a “t” after the number—the best possible score for this patient would be 11t. i. A rapid neurologic assessment “neuro check” will also assess for other signs of altered mental status (headache, restlessness, irritability, and slurred speech) and also posturing and pupil assessment would be included. d. Posturing-- decerebrate or decorticate posturing, as well as pinpoint or dilated and non-reactive pupils, is a late mental deterioration sign. i. Decorticate (Flexor) is abnormal posturing seen in the patient with lesions that interrupt the corticospinal pathways. Client flexes one or both arms on the chest and may extend the legs stiffly. Flexor posturing indicates a nonfunctioning cortex. ii. Decerebrate (Extensor) is abnormal posturing and rigidity characterized by extension of the arms and legs, pronation of the arms, plantar flexion, and opisthotonos (body spasm  in which body is bowed forward). Extensor posturing indicates dysfunction/lesion in the brainstem area. e. Pupillary assessment- pupil constriction is a function of cranial nerve III. PERRLA. i. Lack of pupil symmetry usually means brain herniated. f. Sensory function—assessed when problems affecting spinal cord or nerves. Pain, superficial and deep sensation, light touch, and proprioception. Pain and temperature are transmitted by the same nerve endings; therefore, if one is intact, can assume other intact. g. Motor function—assess for involuntary tremors or movements; grip strength; strength against resistance; pronator drift (cerebral motor or brainstem injury). h. Cerebellar function—fine coordination (finger to nose); gait and equilibrium; Romberg sign (sways with eyes closed but not when eyes are open) i. Reflex activity—deep tendon reflexes of biceps, triceps, brachioradialis, quadriceps, Achilles i. Cutaneous (superficial) reflexes- Babinski’s sign- dorsiflexion of great toe and fanning of other toes- abnormal sign in anyone older than 2 years and represents the presence of CNS disease. ii. Hyperactive- upper motor neuron disease, tetanus, hypocalcemia iii. Hypoactive- lower motor neuron disease, disease of neuromuscular junction, muscle disease, DM, hypothyroidism, or hypokalemia iv. Also assess for asymmetry— may indicate a disease process  0- absent, no response  1 (+)- weaker than normal, hypoactive  2 (++)- normal  3 (+++)- stronger or more brisk than normal  4 (++++)- hyperactive  Note: 1 and 3 may be normal for some individuals 3. Discuss the necessity of various neurologic diagnostic tests and describe important pre and post-op nursing considerations when relevant. a. X-ray vs. CT Scan vs. MRI vs. PET Scan i. X-rays of skull and spine- rule out cervical fracture in trauma. In head trauma and multiple injuries, one of the first priorities is to rule out cervical spine fracture. ii. CT (computed tomography) scan- accurate, quick, easy, noninvasive, painless, and least expensive method of diagnosing neurologic problems. Uses ionizing radiation. Provides us with info about structure of CNS, distinguishes between bone, soft tissue (brain, vascular system, and ventricular system), and fluids such as CSF or blood. Tumors, infarctions, hemorrhage, hydrocephalus, and bone malformations can also be identified.  Contrast enhanced CT is useful in locating and identifying tumor types and abscesses. For situations in which bleeding is the only concern (trauma patients), contrast scans are not usually required. iii. MRI (magnetic resonance imaging)- different dimensions of the brain—uses magnet instead of ionizing radiation and non-iodine based contrast. Better than CT but expensive and takes longer.  A functional MRI can assess blood flow to the brain rather than merely show its anatomical structure. Contraindicated in patients with cardiac pacemakers, other implanted pumps or devices, and ion-containing metal aneurysm clips. May also be contraindicated in patients who are confused or agitated, have unstable vital signs, are on continuous life support, or have older tattoos (which contain lead). iv. PET (positron emission tomography)- provides image of brain function, specifically glucose and oxygen metabolism and cerebral blood flow. Patient injected with IV deoxyglucose, which is tagged to an isotope. The isotope emits activity, which are scanned and converted into a color image by computer. The more active a given part of the brain, the greater the glucose uptake.  Used to evaluate drug metabolism and detect areas of metabolic alteration that occur in dementia, epilepsy, psychiatric and degenerative disorders, neoplasms, and Alzheimer’s disease.  Teach pt that he/she will be NPO the night before morning testing and 4 hours before afternoon testing. Patients with diabetes have their tests in the morning before taking their antidiabetic drugs. Withhold caffeine, alcohol, and tobacco 24 hrs before test. Do not give any glucose solutions and any other drugs that alter glucose metabolism before test. Insert 2 IV lines.  Post op—the radioisotope is eliminated in the urine so encourage the patient to increase fluid intake unless contraindicated. b. Cerebral angiography—done to visualize the cerebral circulation to detect blockages in the arteries or veins in the brain, head, or neck. Injection of dye then X-rays. i. Risks for the procedure are contrast reaction (including hives and flushing), thrombosis (clotting), and bleeding from the entry site. Patients with known contrast sensitivity are pre-treated with steroids. ii. Pre op- ensure patient is NPO 4-6 hrs before test. Assess and document neurologic sings, vital signs, and neurovascular checks.  Reinforce these important points: your head is immobilized during the procedure, do not move during procedure, you will feel a warm or hot sensation when dye is injected—this is normal, you will be able to talk to the physician—let him/her know if you are in pain or have any concerns. iii. Post op—  Care of injection site- check dressing for bleeding and swelling around site, apply ice pack to site, keep extremity straight and immobilized, maintain pressure dressing for 2 hours.  Check extremity for adequate circulation to include skin color and temperature, pulses distal to the injection site, and capillary refill.  If bleeding is present maintain manual pressure on site and notify physician immediately.  Assess vital signs and “neuro” signs per orders  Increase oral or IV fluid intake unless contraindicated  Document assessments and interventions c. Lumbar puncture—needle inserted between 3rd and 4th or 4th and 5th lumbar vertebrae in subarachnoid space. Used to obtain CSF for sample or pressure reading, inject spinal anesthetics,  drugs, or contrast medium. It can also reduce mild to moderate increased ICP in certain conditions. i. Contraindicated in patients with symptoms indicating increased ICP—change in LOC, headache, blurred vision. Also not performed in patients with skin infections at or near the puncture site because of the danger of introducing infective organisms into the CSF.  Normal level of CSF—less than 20 cm H2O ii. Pre Op- explain procedure, noting that some discomfort may be felt when the local anesthetic is injected or that pain may occur in the legs when the spinal needle is inserted.  Place the patient in the fetal position, and remind pt to remain still. iii. Post Op- obtain vital signs and complete neurologic checks; pt must remain flat for 4-8 hrs to prevent hematoma or CSF leak; increase fluids; monitor for spinal headache.  Monitor for complications, especially increased ICP (severe headache, nausea, vomiting, photophobia, change in LOC).  Observe needle insertion site for leakage. Notify physician if occurs.  Provide drug for headache. Notify physician if drug does not relieve pain. 4. Describe the pathophysiology of various types of headaches, their S&S, diagnosis, and treatment a. Migraines—mediated via trigeminal vascular system. i. Spasm in cerebral arteries r/t overreaction to stimulus. This response is followed by arterial constriction and a decrease in cerebral blood flow. Cerebral hypoxia may occur. Platelets clump together, and serotonin, a vasoconstrictor, is released. Other arteries dilate, which triggers the release of prostaglandins (chemicals that cause inflammation and swelling) that increase sensitivity to pain. Also a role of excessive synaptic glutamate (excitatory neurotransmitter) release or decreased removal of glutamate and potassium from the synaptic cleft. ii. Chronic, episodic, long duration (usually lasts longer than 4 hrs); women>men; familial iii. May or may not have aura—halo around vision iv. Unilateral, fronto-temporal, throbbing pain usually behind one eye or ear; anorexia; photophobia, phonophobia (sensitivity to noise), N/V v. Treatment: avoid triggers!!! Lie in quiet, dark room, with cool cloth, sleep  Antiemetics  Mild headache—NSAIDs (ibuprofen and naproxen)  Severe—Triptans (Imitrex), Ergotamine derivatives, antiepileptics a. Triptans (Imitrex) contraindicated in patients with actual or suspected ischemic heart disease, cerebrovascular ischemia, hypertension, and peripheral vascular disease. i. Teach pts take as soon as migraine symptoms develop. Report chest pain or tightness immediately because may develop angina. Use contraception because may not be safe for women who are pregnant. ii. Common side effects: flushing, tingling, and a hot sensation. iii. Triptan drugs should not be taken with selective serotonin reuptake inhibitor (SSRI) antidepressants or St. John’s wort, an herb used commonly for depression. b. Cluster (histamine cephaliga)—episodic- occurs around same time for period of 4-12 weeks; generally in spring/fall; men>women i. Short duration (less than 4 hrs), excruciating, nonthrobbing, boring (constant pain), unilateral pain in and around eye  Occurs with ipsilateral tearing of eye, rhinorrhea or congestion, ptosis, eyelid edema. ii. May be attributed to vasoreactivity and oxyhemoglobin desaturation or an overactive hypothalamus. iii. The onset of the pain is associated with relaxation, napping, or rapid eye movement (REM) sleep. iv. Treatment—meds same as migraine plus calcium channel blockers, corticosteroids, and oxygen.  Calcium channel blockers—especially verapamil (Calan)  Oxygen—100% oxygen via mast at 7 to 10 L/min administered to patient in a sitting position. O2 reduces cerebral blood flow and inhibits activity of the carotid bodies c. Tension—most common type of chronic, long duration (more than 4 hrs) headaches; caused by stress and tension. i. Neck and shoulder tenderness, bilateral pain at skull base and forehead, similar symptoms to migraine. ii. Treatment—NSAIDs, caffeine, muscle relaxants  A combination of ibuprofen plus caffeine may be more effective in relieving pain than NSAIDs alone.  Muscle relaxants—tizanidine (Zanaflex), divalproex (Depakote) an antiepileptic drug 5. Seizures- Discuss the differences between epilepsy and seizures as well as describe the similarities/differences between seizure types. a. Seizure- an abnormal, sudden, excessive, uncontrolled electrical discharge of neurons within the brain that may result in a change in LOC, motor or sensory ability, and/or behavior. i. Caused by a pathological condition; once treated no more seizures. ii. Trauma, tumor, metabolic disorder, electrolyte imbalance, fever stroke, or substance abuse b. Epilepsy—two or more seizures experienced by a person. A chronic disorder in which repeated unprovoked seizure activity occurs. Results from brain or CNS irritation. i. Abnormality in electrical neuronal activity, an imbalance of neurotransmitters (GABA), or a combination of both ii. GABA is an inhibitory neurotransmitter Generalized seizures- involve both hemispheres of cerebrum 1. Tonic-Clonic (grand mal)         3. Clonic                Lasts 2- 5 mins Begins with tonic phase; particularly of arms and legs and LossOC Followed by clonic phase of all extr. May have incontinence/ bite tongue Fatigue, confusion, lethargy post sz. Abrupt increase in muscle tone (tightening) with LossOC 30 seconds to several minutes May have autonomic changes (variability of HR increase then decrease, skin flushing, GI upset) Violent muscle contraction and relaxation, rhythmic jerking of arms and legs Lasts 30 seconds to several minutes May or may not lose consciousness Brief jerking or stiffening of extr. (singular or muscle group) Lasts only a few seconds Symmetric (both sides) or asymmetric (1 side) Sudden loss of muscle tone Lasts seconds Followed by postictal (after seizure) confusion May result in falls—Risk for injury Most resistant to drug therapy Most common in children; familial Brief LossOC manifests as blank staring Possible automatisms (involuntary behaviors) lip smacking and picking at clothes Lasts for seconds then return to baseline Partial seizure (focal or local sz.)- begins in one cerebral hemisphere  Generally seen in adults  Less responsive to medical treatment 1. Complex  May cause LOC or “black out”  Lasts 1-3 minutes  Automatisms  Affects awareness and memory  Often in temporal lobe  Patient starts to wander  Similar to Absence sz.  Remain conscious  Aura- unusual sensation- “déjà vu”, perception of an offensive smell, or sudden onset of pain  One-sided movement of extremity  Autonomic changes (change in HR, skin flushing, GI upset)  No affect on awareness or memory 2. Tonic 4. Myoclonic 2. Simple 5. Atonic (akinetic) 6. Absence c. How is status epilepticus defined? i. A medical emergency and is a prolonged seizure lasting longer than 5 minutes or repeated seizures over the course of 30 minutes. A potential complication of all types of seizures. Seizures lasting longer than 10 minutes can cause death from hypoxia. ii. Causes—sudden withdrawal from antiepileptic drugs, infections, acute alcohol or drug withdrawal, head trauma, cerebral edema, metabolic disturbances. iii. Convulsive status epilepticus—priority-nursing intervention is establishing an airway and then notifying the health care provider. d. What are the treatment options for all of the above? i. #1 is to remove the underlying cause ii. Seizure precautions—  ABCs!!!!  Padded side rails  Turn to side if lose consciousness to prevent aspiration Protect from injury- don’t restrain, no tongue blade, remove objects from immediate environment  Be sure that oxygen and suctioning equipment with an airway are readily available.  If patient does not have IV access insert a saline lock. iii. Drug Therapy Drug Diazepam (Valium), Lorazepam (Ativan) Indication for use Status epilepticus Nursing interventions Monitor airway, breathing, circulation (ABCs) Give Given as 4 mg over a 2-minute period, process may be repeated until a total of 8 mg is reached Monitor for hair loss, tremor, increased liver enzymes, bruising, and N/V. Monitor CBC, PT, PTT, and AST Monitor for gastric distress, gingival hyperplasia, anemia, ataxia, and nystagmus. Check CBC and calcium levels; monitor for therapeutic drug levels (10-20 mcg/mL) and toxic levels (>30 mcg/mL) Major drug-drug interaction with Coumadin Only give with 0.9% NS To prevent additional tonic-clonic seizures in status epilepticus give IV loading dose bolus (100 ccs) and after administer oral doses of Dilantin Monitor renal function carefully Notify health care provider for gait or coordination problems.  Divalproex (Depakote) All types of seizures Phenytoin (Dilantin) All types, except absence, myoclonic and atonic sz. Used for status epilepticus Levetiracetam (Keppra) Adjunct management of partial seizures iv. Vagal nerve stimulation—surgical implant in left chest wall; lead attached to vagus nerve.  Only used in people who experience simple or complex partial seizures.  Manually triggered with magnet when aura occurs; change in voice quality signifies stimulation.  Side effects: hoarseness, dysphagia, dyspnea, neck pain, and cough 6. Discuss the pathophysiology, sim/diff between meningitis (viral and bacterial) vs. encephalitis, S&S, diagnosis, and treatment. a. Meningitis—inflammation of the meninges (protective covering) that surround the brain and spinal cord. Caused by direct invasion or indirect invasion (crossing BBB). b. Assessment—classic signs: fever/chills, headache, N/V, photophobia, altered mental status. i. Nuchal rigidity- neck stiffness, Kernig’s sign, Brudzinski sign positive ii. Assess for increased ICP resulting from the presence of exudate (Pus), which can lead to hydrocephalus and cerebral edema. Left untreated increased ICP can lead to herniation of the brain and death. iii. Seizure activity r/t irritation of the cerebral cortex iv. Increased ICP may lead to decreased LOC v. SIADH r/t to hypothalamic stimulation—excessive amounts of ADH produced and results in water retention and dilution of serum sodium caused by increased sodium loss by the kidneys vi. Lab tests:  CSF via lumbar puncture (LP)  Blood cultures  CBC  Electrolytes vii. Interventions: padding side rails, make sure O2 available, IV access  Neuro checks, vital signs, vascular assessment  Antibiotics, antiepileptics  Droplet precautions Type Definition Viral Meningitis (Aseptic) Most common type Bacterial Meningitis Life threatening needs to be caught early Encephalitis Cause Results from virus- measles, mumps, herpes simplex, or zoster Side effects Usually self-limiting; Altered mental status, fever, chills, photophobia, headache, aches, N/V, genital lesions (Herpes simplex 2) Treatment Symptomatic; if genital lesions present acyclovir may be prescribed CSF Findings Appearance WBC Protein Glucose CSF Pressure Clear Increased Increased, slightly elevated Normal Varies Inflammation of brain tissue and often surrounding meninges Occurs most commonly in fall Most often- virus and winter with predisposing Degeneration of cortex neurons condition- URI, ear infection, resulting in demyelination, pneumonia, sinusitis hemorrhage, edema, and necrosis Similar to viral meningitis but Long term- persistent neuro also includes formation of problems- learning deficits, exudate which can cause epilepsy, memory, and/or fine increased ICP as a result of motor deficits blockage of the flow of CSF, Fever, change in mental status change in cerebral blood flow, or (more severe), signs of thrombus (blood clot) formation increased ICP, photophobia, motor dysfunction, focal neurologic deficits Meningococcal meningitisDiagnose with CSF specimen occurs in highly populated areas Care similar to meningitis and requires a vaccine ABCs and supportive care; (Menomune) monitor ICP Influenza vaccine Turn patient every 2 hours Elevate HOB 30-45 unless Cloudy turbid contraindicated (after LP or in Increased patient with severe Increased hypotension) Keep room dark and quiet to promote comfort and decrease Decreased agitation Elevated Acyclovir for herpes encephalitis; no cure for West Nile 7. Discuss the pathophysiology, S&S, diagnosis, and treatment for the following CNS diseases Type Definition Parkinson’s Disease Progressive, neurodegeneration affecting motor ability Dopamine (inhibitory) and acetylcholine (excitatory) in a relationship of checks and balances allows for refined, coordinated movement. Degeneration of substantia nigra results in decreased dopamine Alzheimer’s Disease Chronic, progressive, degenerative disease of brain w significant changes in cognition, behavior, and personality Affects of aging greatly accelerated resulting in structural changes to the brain and changes in neurotransmitters- increased glutamate decreased acetylcholine Microscopic changes- neurofibrillary tangles, neuritic plaques (reduction in Ach), and granulovascular degeneration Exact cause unknown, with no means of prevention Loss of memory, attention, concentration, judgment, visuospatial perception, communication, personality, severe physical deterioration over time Risks- age, women>men, family history, environment (virus, metals), head trauma/injury, chemical imbalance, Xcess Glut. Diagnosis: true diagnosis can only be done by autopsy, mini mental state exam (assess cognitive status), Genetic testing (apolipoprotein E4), amyloid beta, protein precursor, CT scan, PET scan, EEG  Structured and consistent environment  Reality orientation (early) vs. validation therapy (Late)  Assisting with facial recognition (prosopagnosia)  Promote communication and minimize agitation  Exercise and rest  Wear identification bracelet, GPS, or enroll in Safe Return Program  Prevent caregiver role strain!!! Huntington’s Disease Autosomal dominant disorder of movement with neurologic and behavioral symptoms R/T to decrease in amount of GABA and increase in glutamate Disease manifests itself between the ages of 35-50 yrs old. It’s a combination between Alzheimer’s and Parkinson’s disease Diagnosis- family history (genetic) and clinical assessment Progressive mental status changes leading to dementia, choreiform movements (rapid jerky movements) Pathophysiology Cause Signs and Symptoms Treatment and Nursing interventions Environmental, genetics, >40, reduced estrogen levels Secondary causes: antipsychotic drugs or brain tumor Loss of voluntary control and initiation of fine motor movements Decrease in SNS stimulation of heart and blood vessels 4 cardinal symptoms: resting tremor, rigidity, bradykinesia or akinesia (slow movement/no movement), and postural instability Drug therapy is essential part of management Exercise and ambulation Self management Injury prevention Nutrition—swallow evaluation Communication Surgery: results in decreased need of meds  Stereotactic pallindotomy- electrode inserted into area (det. By CT or MRI)- receives mild electrical stimulation; pt assessed for reduction of tremor/rigidity; when correct spot found, permanent lesion made to destroy tissue  Deep Brain Stimulation- electrode implanted in thalamus and connected to pacemaker that interferes with tremor cells; similar to vagal nerve stimulation No cure or treatment; need to prevent transmission (genetic counseling) Drug therapy to manage symptoms:  Psychotropics (Haldol) for movement abnormalities, agitation, hallucination, and delusions  Antidepressants, antianxiety meds, glutamate blockers (Namenda) Parkinson’s Disease Drug Therapy Dopamine agonists (Mirapex, Requip) LevodopaCarbidopa (Sinemet) Dopamine receptor antagonist (Parlodel) Antiviral drugs (Symmetrel) Mimics dopamine, fewer incidents of dyskinesia and wearing off phenomenon #1 used, less expensive better at improving motor fxn.; long term use leads to dyskinesia (inability to perform voluntary movement) Promotes release of dopamine when other drugs no longer effective; useful w/ dyskinesia Alzheimer’s Disease Cholinesterase inhibitors (Aricept) N-methyl-D-aspartate receptor antagonist (NMDA) (Namenda) Antidepressants Delay destruction of Ach; slows onset of cognitive decline Indicated for advanced AD, slows rate of deterioration Blocks excess amounts of glutamate SSRIs Don’t give tricyclics because have anticholinergic effect Reserved for patients with emotional or behavioral problems (hallucinations/delusions) Not used often; used early in disease; reduces symptoms Combined with Sinemet to reduce dyskinesia Psychotropic drugschemical restraints (Haldol) Anticholinergic (Cogentin) No longer used because side effects in elderly are high—causes constipation, confusion, urinary retention Treats severe motor symptoms (tremors/rigidity) 8. Discuss the pathophysiology of lumbosacral back pain, causes, risk factors, treatment, and care for a patient receiving back surgery a. Lumbosacral back pain—motor and sensory disease. More common than cervical pain. i. Acute- self limiting; Chronic > 3 months—generally results from injury or trauma ii. Low back pain (LBP)- muscle strain or spasm, ligament sprain, disk degeneration, stenosis, or herniation of nucleus pulposus (center of disk)  Bulging disk can compress nerves (sciatic nerve) resulting in pain, numbness, tingling, weakness, and bowel and bladder dysfunction.  Prevention best measure—Ergonomics!!!!! a. Good posture, proper lifting techniques, exercise iii. Diagnosis—X-ray, CT, MRI iv. Treatment:  Patient becomes tolerant and dependent on medication so try to stay away from narcotics and opioids for chronic long-term management of back pain.  NSAIDS, short-term steroids, antiepileptic, muscle relaxants  Williams position—HOB > 30 degrees and pillow under the knees  Heat, physical therapy, weight control v. Surgery:  Minimally invasive surgery—advantages: less muscle injury, decreased blood loss, and decreased post-operative pain. a. Local anesthetic with use of fluoroscopy to insert arthroscope to remove compressed disk.  Open procedure- Diskectomy, laminectomy, spinal fusion a. Post-op—vital signs, must lie flat so difficulty voiding in addition to opioid analgesics via PCA or epidural. b. Assess surgical dressing for bleeding and leakage of CSF c. Log rolling, pulmonary management (cough and deep breathing Q 2h), DVT management (Lovenox & Heparin, SCDs) d. Patients will need brace or orthotic device 9. Describe the various mechanisms behind spinal cord injury. a. Discuss relevant assessment findings by body system including assessment findings particular to cervical injuries (anterior, posterior, central, and Brown-Sequard syndrome). i. Spinal cord injury—loss of mobility, sensation, reflex activity, and bowel and bladder control. Trauma is the leading cause of SCIs and motor vehicle accidents are leading cause of trauma.  Complete—spinal cord severed or severely damaged; no innervation of motor or sensory below level of injury.  Incomplete—more common; some function maintained  Types of primary injury: a. Penetrating injuries to cord, hyperflexion, hyperextension, axial loading or vertical compression, excessive rotation b. Secondary injuries worsen the primary injury: hemorrhage, ischemia, hypovolemia, neurogenic shock Type Anterior cord Syndrome Definition Damage to anterior portion of gray and white matter r/t decreased blood supply Symptoms Loss of motor function, pain, and temp sensation; retains touch, position and vibration sensation Posterior cord syndrome Rare; damage to posterior gray and white matter Brown- Sequard syndrome Results from penetrating injury causing hemisection of cord Motor function intact Motor function, but loss of vibratory proprioception, sense, touch, and vibration and deep position sensation touch lost ipsilaterally; contralaterally pain, temp, and light touch are lost Intact Lost ipsilaterally Lost contralaterally Lost contralaterally Deep touch- lost ipsilaterally Light touch- Lost contralaterally Lost ipsilaterally Central cord syndrome Lesion to central portion of cord Loss of motor function more severe in upper extremities, varying degrees of sensation remain Motor function Pain Temp Touch Lost Lost Lost Intact Lost Lost more severe in upper extremities Varying degree Varying degree Varying degree Vibration Intact Lost Position Intact Lost Spinal Cord injury assessment: ABCs!!!! Airway, breathing pattern, and circulation status   Varying degree Varying degree   Respiratory assessment (PRIORITY)—ensure adequate airway; especially with cervical injuries. o C3-C5 innervates phrenic nerve and control diaphragm—intubation may be required Cardiovascular assessment—possibility of hemorrhage and disruption of sympathetic fibers of ANS o Injury T6 and above o Hypothermia, hypotension, brady/tachycardia o Neurogenic shock o Vasopressors given to maintain vital signs GI/GU assessment—T6 and above o Paralytic ileus or hypotonic bowel o Neurogenic bladder- no reflex ability for bladder contraction urinary retention o Autonomic dysreflexia Neurologic status o LOC (GCS) o Motor and sensory function—start distally o Deep tendon reflexes o Muscle tone and size o Spinal shock- flaccid paralysis and loss of reflex activity below the level of the lesion b. Discuss severe complications associated with SCI and their treatments (autonomic dysreflexia, neurogenic shock, spinal shock). i. Autonomic dysreflexia (hyperreflexia)—above level of T6; excessive uncontrolled sympathetic output. May be permanent. A strict toileting regimen is very important.  Severe HTN and headache, bradycardia, nasal stiffness, and flushing  Caused by a noxious stimulus- a distended bladder or constipation  Neurologic emergency and must be promptly treated to prevent a hypertensive stroke. ii. Neurogenic shock—type of hypovolemic shock; disruption in communication between upper and lower motor neurons  Severe hypotension, bradycardia, warm, dry skin  Treated symptomatically by restoring fluids to the circulating blood volume. iii. Spinal Shock—concussive response immediately following injury (48 hrs-several wks)  Flaccid paralysis and loss of reflexes; muscle spasticity upon resolution in those with cervical and high thoracic injuries. c. How are these deficits managed, paying attention to medical and surgical management? i. Ineffective (Spinal Cord) Tissue perfusion  Assess vital signs, neuro checks, respiratory status and pain minimally every 4 hours.  Position in proper body alignment  Cervical immobilization a. Halo fixator (static traction device)—4 pins/screws inserted into skull; metal halo ring attached to screws and then to plastic vest or cast. i. Skin and screw care—Risk for infection  Thoracic and lumbar/sacral—ORIF then halo fixation device for upper thoracic injury a. For lower thoracic, lumbar, and sacral injury; immobilization with brace when out of bed (TSLO)  Drug Therapy Drug Methylprednisolone (Solu-Medrol) Action Decreases inflammation to the spinal cord Nursing Interventions Monitor closely for adverse drug reactions, including infection, elevated serum glucose, and stress ulcers Dextran (plasma expanders) and inotropes Atropine sulfate  Dantrium & Lioresal (Baclofen) Surgery o Laminectomy—removal of vertebral laminae to allow for cord expansion when edema present o Spinal fusion—stabilize/support spine o Post-op: TLSO, brace, or corset for immobilization Increase capillary blood flow w/in spinal cord and to prevent or treat hypotension Treat bradycardia if pulse rate falls below 60 bpm Treat muscle spasms  Assess neuro status and vital signs minimally every 4 hours  Complications of surgery (DVT, pneumonia)  Cardiovascular assessment r/t loss of SNS innervation  Logroll  Ineffective Airway Clearance; Ineffective Breathing Pattern; Impaired Gas Exchange o Vital signs/ lung sounds q 4 hrs o Tracheostomy, ventilator o Incentive spirometer o Suctioning o Cough & Deep Breathing (cough assist) o Turn Q2H o Increased risk for atelectasis, pneumonia, and PE  Impaired physical mobility; Self-care Deficit o Pressure ulcers—turn Q2h, ROM q4-8h  Sitting—reposition frequently, minimally every hour  Pressure relief devices o DVTs—SCDs, Heparin o Prevent Orthostatic Hypotension—change positions slowly, dangle at side of bed  Altered urinary elimination; Constipation—injury T6 and above o Always look for symptoms of autonomic dysreflexia o Flaccid bladder- lumbosacral area lesion of lower motor neuron  Valsalva maneuver or tightening of abdominal muscles  High level SCI may require catheterization  Upper motor neuron- spasticity  Lower motor neuron- flaccidity- push pressure over patient bladder o Bladder Training—Q4h intermittent catheterization  Medication- Urecholine o Bowel Training—encourage fluid (2000-2500cc); high fiber diet  Rectal stimulation, stool softener (Colace, Peri-colace)  Schedule toileting 30 minutes to 1 hour after meals 10. Discuss the pathophysiology, S&S, diagnosis, and treatment of the following PNS diseases a. Multiple sclerosis b. Amyotrophic Lateral Sclerosis c. Guillain Barre d. Myasthenia Gravis Multiple Sclerosis Amyotrophic Lateral Sclerosis Adult onset upper and lower motor neuron disease characterized by progressive weakness, muscle wasting/spasticity leading to paralysis Symptoms begin in one area of body and spread until entire body involved—until pt goes into respiratory failure. No known cause, no cure, no specific treatment or prevention Guillain Barre Syndrome Myasthenia Gravis- attacks acetylcholine receptors Pathophys iology Chronic, autoimmune disease characterized by inflammation; diffuse plaque formation in white matter resulting in demyelinization Periods of exacerbation/remission Signs & Symptoms  Muscle weakness, spasticity, and extreme fatigue (hallmark symptom) associated with sensitivity to temperature; intention tremor, loss of balance and coordination  Tinnitus (ringing in the ears), vertigo (dizziness), hearing loss  Cognitive changes- loss of memory  Dysphagia, dysarthria (slurred speech), blurred vision, diplopia, nystagmus (involuntary eye movements)  Hypalgesia (decreased sensitivity to pain), paresthesia (numbness or tingling sensations), decreased temp sensation  Bowel and bladder dysfunction, alteration in sexuality Diagnosis Looks like other neuro diseases making  Creatinine kinase dx difficult and prolonged increased  CSF- elevated protein and slightly  EMG- fibrillation and increased WBCs, presence of IgG fasiculations of bands muscles  CT scan- increased density in white  Muscle biopsy- small, matter and MS plaques atrophic fibers  MRI- diagnostic for MS: plaques  EMG- abnormal results Chronic, autoimmune disease of neuromuscular junction. Fatigue and weakness in muscles innervated by cranial nerves and skeletal and respiratory muscles Risk: Familial, hyperplasia of thymus gland, hyperthyroidism, PCN, interferonalpha, bone marrow transplant  Ascending paralysis- starts in feet  Peak: 20-30 yo.; women 3x> men and legs and moves up to  Periods of exacerbation and remissionrespiratory system. Pts can still feel No cure and think but body is like a tomb.  Progressive muscle weakness that  History of acute illness, virus, improves with rest more noticed in trauma, surgery, or immunization 1 proximal muscles, fatigue to 3 weeks before onset  Ocular palsy, ptosis, lid lag, diplopia  Usually affects 30-50 years old  Respiratory compromise  Abrupt onset  Paresthesias, decreased smell and taste  Does not affect LOC, cerebral  Dysphagia, problems chewing function, or pupillary signs  Ascending symmetric muscle weakness leading to flaccid paralysis w/out muscle atrophy  Decreased/absent DTRs  Respiratory compromise  Loss of bowel/bladder control  Paresthesias, pain  Cranial nerve manifestations- can’t chew, swallow, or communicate  Autonomic manifestations  Anxiety and depression Labs- thyroid function, serum protein CSF- increase in protein without electrophoresis to rule out other increase (or only slightly) in cell immunologic dx (RA, lupus), check for Ach count receptor antibodies Moderate leukocytosis early in EMG to test neuromuscular junction illness Tensilon testing- injection of tensilon Electrophysiologic studiesresults in improvement in muscle tone in demyelination of nerves MG patients; determines if sudden increase in weakness in MG patient r/t cholinergic crisis or myasthenic crisis Acute autoimmune process characterized by varying degrees of motor weakness and paralysis. Demyelination of peripheral nerves through immune mediated response; results in progressive motor and sensory problems Treatment  PT/OT, ROM, stretching and strengthening exercises  Avoid extremes in temperature or activities that cause fatigue  Speech language pathology  Bladder training program Drug therapy for symptom managementpain, fatigue, sleep, spasticity, excess secretions PT/OT/SLP Eventual ventilator management and palliative care Plasmapheresis—remove circulating antibodies from plasma, pts need port similar to dialysis port Airway- positioning, suctioning, CPT, turn Q2h, C&DB, incentive spirometer Cardiac dysfunction- vital signs, cardiac monitor, meds for labile BP Mobility- PT/OT/SLP, nutrition assessment, prevent skin breakdown and DVTs Respiratory support: monitor for distress, depression, and aspiration. C&DB, suctioning, CPT, postural drainage, O2, intubation Plasmapheresis or IVIG (immunoglobulin) Promote mobility and self carPT/OT/SLP Nutritional support Eye care Surgery- Thymectomy early in diseasetake out the problem before onset Cholinesterase inhibitors- pyridostigmine (Mestinon)- first line managementprevent decrease of Ach- given before eating to prevent aspiration Immunosuppressants- corticosteroids (prednisone) or chemotherapeutic agents Cholinergic crisis- too much cholinesterase inhibitor drug S&S during crisis:  N/V  Diarrhea  Abdominal cramps  Blurred vision  Hypotension  Facial twitching Myasthenic crisis- too little cholinesterase inhibitor drugs S&S during crisis:  Increased BP (Hypertension)  Increased pulse  Increased respirations  Anoxia  Cyanosis  Incontinence  Absent cough/swallow reflex Drug Therapy Interferon beta (Avonex) Natalizumab (Tysabri) Glatiramer acetate (Copaxone) Immunomodulator ; modifies course of disease; has antiviral effects Monoclonal antibody; binds to WBCs to prevent further damage to myelin Synthetic protein similar to myelin based protein Riluzole (Rilutek)- only  Immunoglobulins (IVIG)- just as approved med for ALS; effective as plasmapharesis; safer, extends survival time and more available (only 2-3 months); o Monitor for chills, fever, monitor for liver myalgia, anaphylaxis, ARF toxicity  Corticosteroids  Pain- PCA pump o Neurontin- helps with nerve related pain Immunosuppressi ve therapycyclophosphamide (Cytoxan) & SoluMedrol Baclofen (Lioresal) or diazepam (Valium) Tergretol Stabilizes disease process- shut off immune system so can’t attack itself Decrease muscle spasticity Paresthesia 11. Describe the pathophysiology of stroke. Focus on sim/diff between right and left cerebral damage, S&S, and relevant nursing considerations. a. When is a carotid endarectomy indicated and what are important nursing considerations pre and post procedure? i. Most widely performed surgical procedure to prevent progression of TIA to a stroke. ii. Removal of atherosclerotic plaque from carotid artery iii. Patient usually stays in hospital for 2 nights  Post-op: monitor vital signs, neuro checks, and peripheral pulses. Check incision site for bleeding. Monitor for cerebral hyperperfusion, which may occur because increased vascular pressure (from the open artery) and lead to intracranial hemorrhage (stroke). Stroke—disruption of blood supply (oxygen and glucose) to brain and removal of metabolic waste. Results in tissue death; deficits r/t location and amount of tissue damaged; effects are ipsilateral and contralateral Often preceded by warning- TIA (transient ischemic attack) or RIND (reversible ischemic neurologic deficit) Ischemic Hemorrhagic General Assessment  Occlusion of cerebral artery  Less common  Pt should be assessed within 10 by thrombus or embolus. minutes of arrival  Bleeding into brain tissue or areas surrounding brain  Thrombotic caused by  ABCs atherosclerosis over many  Ruptured aneurysm or AV  Neuro assessment via specialized years with compensation by malformation, or severe HTN in stroke scale collateral circulation weakened vessel wall  Cognitive changes, motor changes,  Embolic generally originates sensory changes, cranial nerve fxn,  Long-term residual effects more from emboli from heart; paralysis or weakness, pupillary likely middle cerebral artery most abnormalities, emotional lability  Prone to re-bleeding and common site- acute blockage  Cardiovascular assessment—HTN, rupture all of a sudden dysrhythmia, heart murmur  Look for change in LOC, N/V, VS  Keep BP less than 150 systolic  Keep BP between 120-150  Diagnostics—CT or CT angiographyidentify hemorrhage or aneurysms systolic o MRI- presence of edema, ischemia, necrosis earlier than CT Right CVA—right hemisphere Left CVA—left hemisphere center Treatment: Altered Cerebral Tissue Perfusion involved with visual and spatial for language, math skills, and GOAL- Restore Blood flow to brain awareness and proprioception analytic thinking  Weakness/paralysis to left  Weakness/paralysis to right side Thrombolytic therapy (fibrinolytic therapy)— side  Aphasia, agraphia, alexia  Retavase- tx for ischemic stroke- activates  Disoriented to person, place,  Inability to discriminate words plasminogen (breaks down thrombi) and time and letters, reading problems  Drug must be started w/in 3 hrs of  Impaired sense of humor  Visual deficits in right visual symptoms  Visual spatial deficits field  Monitor for hemorrhage Intra-arterial thrombolysis  Loss of depth perception  Slow, cautious behavior  Impulsive  Anxiety, depression, guilt, worry  Thrombolytic agent injected directly into thrombus- BP must be <185/110 give  Neglect syndrome  Quickly angered and frustrated Betalol  Euphoria, constant smiling  Intellectual impairment  Within 6 hours of symptoms  Poor judgment and Calcium channel blockers overestimation of abilities  Prevention of Cerebral vasospasm 12. When discussing traumatic brain injury, what is the mechanism of injury in each and how is the damage manifested in the brain? a. Closed head injury—result of blunt trauma; most serious i. Concussion- falls and motor vehicle accidents  Shaky movement in brain  May lose consciousness  Mild or severe (diffuse axonal injury) ii. Contusion- bruising of brain tissue iii. Laceration- tearing of cortical surface vessels b. Open head injury—mostly worried about risk for infection of brain tissue i. Fractured or pierced by penetrating object; exposure to outside contaminants ii. Linear, depressed, open, and comminuted iii. Basilar skull fracture—base of skull; results in leakage of CSF from nose or ears; potential for hemorrhage 13. Discuss the various levels of cerebral hemorrhage (epidural, subdural, and intracerebral) and the manifestations of each. a. Epidural—arterial bleed between dura/skull. Often from fracture of temporal bone and bleed of MMA. Fluctuates between lucid and unconscious. Progress to coma. b. Subdural—venous bleed between dura and arachnoid. Tearing of veins in cerebral hemispheres from laceration. Bleed slow. Highest mortality rate c. Intracerebral—accumulation of blood in brain tissue from tearing of arteries and veins in white matter. Subarachnoid (SAH) most common. d. All act as space occupying lesions--- increase ICP. 14. Discuss increased ICP- what are the contributing factors, nursing assessment for detection, compensatory measures for correction, and potential complications of the imbalance? a. Cranial contents: brain, blood, CSF i. Little room for any of the contents to increase in volume or expand; increase in one means decrease in other  Compensation: first-CSF shunting, second- decreased blood volume, lastlybrain herniation ii. Normal ICP 10-15 mmHg; when compliance no longer takes place, ICP increases  Decreased cerebral perfusion, tissue hypoxia, acidosis, and hypercarbia lead to cerebral vasodilation, edema, and further increases in ICP. b. Monitoring for increased ICP r/t cerebral edema i. Neuro checks q4h ii. HOB elevated no more than 30 degrees iii. Avoid extreme hip or neck flexion iv. Quiet, dark environment v. Cluster care; avoid suctioning and client coughing vi. Manage HTN c. How is ICP treated/managed? i. ABC management  Mechanical ventilation- maintain PaCO2 35-38 and PaO2 80-100  Suction with care to avoid increasing ICP or creating hypoxia  Monitor vital signs and treat fever ii. Prevention of increased ICP  Maintain neck in neutral position; log roll; keep HOB >30 degrees iii. Drug therapy  Mannitol (Osmitrol) and Lasix—strictly measure I&Os, osmolarity, and electrolytes  Opioids (morphine or fentanyl)—decreases agitation and restlessness caused by pain  Neuromuscular blocking agents a. Nimbex- paralysis without pain control or sedation! b. Patient experiencing dangerous agitation  Antiepileptic drugs  Barbiturate coma iv. Fluid and electrolyte management  Monitor for DI and SIADH