Chapter 53 Care of the Patient with a Neurologic Disorder

Chapter 53 Care of the Patient with a Neurologic Disorder
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Overview of Anatomy and Physiology
Structural divisions – 2 main Central nervous system (CNS) Brain and spinal cord Peripheral nervous system – 2 main Somatic nervous system Sends messages from the CNS to the skeletal muscles; voluntary Autonomic nervous system Sends messages from the CNS to the smooth muscle, cardiac muscle, and certain glands; involuntary The nervous system functions as a switchboard for the body. It receives messages from the environment and transfers them to the brain for interpretation and action.

Cells of the nervous system – 2 broad categories Category one: neurons – transmitter cells Space between each neuron is called a synapse Category two: neuroglial or glial cells – support cells The basic nerve cell in the body is known as a neuron. Neurons act under the “all or none law.” Explain this phenomenon.

Neuron (nerve cell) : 3 Main structures Cell Body: contains a nucleus surrounded by cytoplasm Axon: cylindric extension of the nerve cell that conducts impulses away from the neuron cell body Dendrites: branching structures that extend from a cell body and receive impulses

Neuromuscular junction: is the area of contact between the ends of a large myelinated nerve fiber and a fiber of skeletal muscle. The neurotransmitters act to make sure that the neurological impulse passes from the nerve to the muscle.

Neurotransmitters: chemicals that modify or result in the transmission of impulses between synapses Acetylcholine: role in nerve impulse transmission; spills into the synapses area and speeds up transmission of the impulse. Enzyme cholinesterase is then released to deactivate the acetylcholine once the message or impulse has been sent. Norepinephrine: has an effect on maintaining arousal (awakening from a deep sleep), dreaming, and regulation of mood (happiness or sadness).

Neurotransmitters: cont. Dopamine: affects motor function (gross subconscious movements of the skeletal muscles), also plays a role in emotional response. Parkinson’s disease there is a decrease in dopamine levels. This causes the tremors, or involuntary, trembling muscles Serotonin: induces sleep, affects sensory perception, controls temperature, and helps regulate mood

Neuron coverings: Myelin – white, waxy, fatty material covering many nerve fibers (axons and dendrites). Increases rate of transmission of impulses and protects and insulates the fibers. Axons leaving the CNS are wrapped in layers of myelin with indentations called Nodes of Ranvier; which further increase the rate of transmission, because the impulse can jump from node to node. In the Peripheral nervous system the myelin is produced by Schwann cells. Outer membrane of the Schwann cells gives rise to another layer called the neurilemma. Neurilemma is a very important layer, because it helps regenerate injured axons. This only occurs in the peripheral nervous system. Cells damaged in the CNS result in permanent damage (paralysis), because they do not have neurilemma and are not able to regenerate.

A, Diagram of a typical neuron. B, Myelinated axon.
Figure 54-1 The neuron is composed of three main structures. These structures are the cell body, the axon, and the dendrites. What roles are played by each of the parts? (A, B, from Thibodeau, G.A., Patton, K.T. [2007]. Anatomy and physiology. [6th ed.]. St. Louis: Mosby. ) A, Diagram of a typical neuron. B, Myelinated axon.

Central nervous system: One of two main divisions of the nervous system and composed of the brain and spinal cord. Cranium protects the brain. Vertebral column protects the spinal cord Brain: specialized cells in the brain’s mass of convoluted, soft, gray or white tissue coordinate and regulate the functions of the CNS. One of largest organs weighing approximately 3 pounds (6.6 kg). Divided into 4 principal parts: the cerebrum, diencephalon, cerebellum, and the brainstem. The central nervous system is one of the divisions of the nervous system. The brain is one of the body’s largest organs. What are the functions of each of the structures identified? What is the impact on the body if the key areas identified are injured or unable to adequately function?

Cerebrum Largest part of the brain. Divided into Right and Left hemispheres. Outer portion of brain composed of gray matter and is called the cerebral cortex. Arranged in folds call gyri, grooves are sulci (fissures). Connecting structure is the corpus callosum, divides the two hemispheres into 4 lobes. Controls initiation of movement on the opposite side of the body.

Diencephalon: often called the interbrain, it lies beneath the cerebrum. It contains the thalamus and the hypothalamus. Thalamus serves as a relay station for some sensory impulses while interpreting other sensory messages such as pain, light touch, and pressure. Hypothalamus lies beneath the thalamus, plays vital role in control of body temperature, fluid balance, appetite, and certain emotions, such as fear, pleasure, and pain. Both the sympathetic and parasympathetic divisions are under the control of the hypothalamus. The hypothalamus influences heartbeat, contraction and relaxation of the walls of the blood vessels, hormone secretion, and other vital body functions.

Cerebellum: lies posterior and inferior to the cerebrum and is the second largest portion of the brain. Contains 2 hemispheres. Responsible for coordination of voluntary movement and maintenance of balance, equilibrium, and muscle tone. Sensory messages form the semicircular canals in the inner ear send their messages to the cerebellum

Brain stem: located at the base of the brain and contains the midbrain, pons, and medulla oblongata Midbrain: forms the superior portion of the brainstem. Responsible for motor movement, relay of impulses, and auditory and visual reflexes. Is the origin of cranial nerves III and IV. Pons: connects the midbrain to the medulla oblongata. Is the origin of cranial nerves V through VIII. Composed of myelinated nerve fibers and responsible for sending impulses to the structures that are inferior and superior to it. Also contains the respiratory center and compliments the respiratory center in the medulla.

Brain Stem cont. Medulla oblongata: distal portion of the brainstem. Origin of cranial nerves IX and XII. Controls heartbeat, rhythm of breathing, swallowing, coughing, sneezing, vomiting, and hiccups (singultus). A vasomotor center regulates the diameter of the blood vessels, which aids in the control of the blood pressure Coverings of the brain and spinal cord: Brain and spinal cord are surrounded by three protective coverings called the meninges: 1) the dura mater (the outer layer) 2) arachnoid membrane (second layer) 3) pia mater (the inner most layer) which provides oxygen and nourishment to the nervous tissue. These layers also bathe the spinal cord and brain in CSF

Ventricles: 4 in all, are spaces located in the brain. The CSF, which is clear and resembles plasma, flows into the subarachnoid spaces around the brain and the spinal cord and cushions them. Contains proteins, glucose, urea, and salts; it also contains certain substances that form a protective barrier that prevents harmful substances from entering the brain and spinal cord.

Spinal cord: is a 17”-18” cord that extends from the brainstem to the second lumbar vertebra. 2 main functions: conducting impulses to and from the brain and serving as a center for reflex actions. Responsible for reflex activities, such as knee jerks. Sensory neuron sends information to the cord, a central neuron interprets the impulse, and motoneuron sends the message back to the muscle or organ involved. Thus message is sent, interpreted, and acted upon without traveling to the brain

Sagittal section of the brain (note position of midbrain).
Figure 54-2 (From Thibodeau, G.A., Patton, K.T. [2007]. Anatomy and physiology. [6th ed.]. St. Louis: Mosby.) Sagittal section of the brain (note position of midbrain).

Peripheral nervous system: comprises the motor nerves, sensory nerves, and ganglia outside the brain and spinal cord. Spinal nerves: 31 pairs, all mixed nerves. This means that they transmit sensory information to the spinal cord through afferent neurons and motor information from the CNS to the various areas of the body through efferent neurons. Spinal nerves are named according to the corresponding vertebra (e.g. C1, C2). Cranial nerves: 12 pairs, attach to the posterior surface of the brain, mainly the brainstem. Conduct impulses between the head, neck, and brain, excluding the vagus nerve (X), also serves organs in the thoracic and abdominal cavaties.

Autonomic nervous system: controls the activities of the smooth muscle, cardiac muscle, and all glands. Is a subdivision of the peripheral nervous system. Primary function is to maintain internal homeostasis; EX. Maintain a normal heartbeat, constant body temperature, and a normal respiratory rate. Has 2 divisions that are antagonistic. One slows and one accelerates the action. Sympathetic nervous system: prepares the body for “fight or flight” Parasympathetic nervous system: Calms the body after a crisis

Neural pathway involved in the patellar reflex.
Figure 54-4 (From Thibodeau, G. A., Patton, K. T. Anthony’s textbook of anatomy and physiology. [18th ed.]. St. Louis: Mosby.) Neural pathway involved in the patellar reflex.

Effects of normal aging on the nervous system Loss of brain weight Loss of neurons (1% a year after age 50) Reduction in cerebral blood flow Decrease in brain metabolism and oxygen utilization Decreased blood supply to spinal cord causes decreased reflexes Older Adult Considerations: Neurological Disorders List p 1933 (5th ed) p1892 (6th ed) As the body ages, there is a gradual reduction in the effectiveness of neurological functioning. An estimated 1% loss of neurons occurs after age 50. Outline the implications when factoring in this loss for an adult at age 65. Ask those who have grandparents to estimate their ages and discuss the implication of a 1% loss in neurons for them. What safety implications arise when considering the neurological changes in an older adult?

Prevention of neurological problems Avoid drug and alcohol use Safe use of motor vehicles Safe swimming practices Safe handling and storage of firearms Use of hardhats in dangerous construction areas Use of protective padding as needed for sports Preventing neurological Injuries List p1933 (5th ed) p1892 (6th ed) Some of the disorders in the neurological system are the result of a disease process. Other illnesses occur in response to an injury or are the impact of a chosen lifestyle. What populations are associated with unhealthy neurological behaviors? What opportunities exist for health teaching in these populations?

Assessment of the Neurological System
History: Comprehensive history essential for diagnosing neurological disease. Be specific about symptoms experienced as well as pt. understanding. Information from family may also be helpful. Symptoms/Subjective data that may be significant include: A) Headaches – especially those that first occur after middle age or those that change in character; headaches that are worse in the morning or awaken a person from a sleep are especially significant. B) Clumsiness or loss of function in an extremity C) Change in visual acuity D) Any new or worsened seizure activity E) Numbness or tingling in one or more extremities F) Pain in an extremity or other part of the body G) Personality changes or mood swings H) Extreme fatigue or tiredness When collecting neurological data, a comprehensive approach is best. Input from both the patient and family can provide invaluable clues regarding behavior indicative of neurological changes. What elements in a patient’s health history are beneficial? The Glasgow coma scale is performed to assess the patient’s level of consciousness. It is important to note that the Glasgow coma scale results are on a potentially changing continuum. What factors are assessed in the Glasgow coma scale? What techniques can be utilized to review cranial nerve function?

Mental status: Assessment of the neurological pt’s mental status is important and is done with every assessment. It generally includes: Orientation to person, place, time, and purpose Mood and behavior General knowledge (such as names of presidents) Short and long term memory Attention span Ability to concentrate DOCUMENTATION: is key to determining a change. Nurse should vary orientation questions so pt doesn’t memorize answers through repetition.

Level of consciousness (LOC): is the earliest and most sensitive indicator that something is changing. A decrease in LOC is the earliest sign of increased intracranial pressure. LOC has 2 components, arousal and awareness. Wakefulness is controlled by the brainstem and most fundamental part of LOC. If pt can open eyes to voice or to pain the wakefulness center in the brainstem is still functioning. Awareness, a higher function controlled by the reticular activating system in the brainstem, is the ability to interact with others. Has 4 parts: 1. Orientation – person, place, time, and purpose 2. Memory: Assess short-term memory; do not ask yes or no question 3. Calculation: example, “If you had $2 and your apple costs $1.25, how many quarters would you get back?” 4. Fund a knowledge: Ask the patient to name the president and to tell you what’s on the national news Restlessness, disorientation, and lethargy may be seen first. Table LOC (p1934 5th ed) p1894 (6th ed)

Glasgow coma scale: quick, practical and standardized system for assessing the degree of consciousness impairment in the critically ill and for predicting the duration and ultimate outcome of coma, particularly with head injuries.

Language and speech Speech is a function of the dominant hemisphere, on the left side of the brain for all right-handed people and most left-handed people. Aphasia is an abnormal neurological condition in which the language function is defective or absent due to injury of certain areas of the cerebral cortex. Broca’s area in the frontal lobe responsible for speech production Wernicke’s area in the posterior part of the temporal lobe responsible for understanding speech

Language and speech Aphasia includes all areas of language, including speech, reading, writing, and understanding. Aphasia has been subdivided as follows: 1. Sensory aphasia or receptive aphasia: inability to comprehend the spoken word or written word 2. Motor aphasia: inability to use symbols of speech (aka expressive aphasia) 3. Global aphasia: inability to understand the spoken word or to speak Anomia is a form of aphasia characterized by inability to name objects. Dysarthria is defined as difficult, poorly articulated speech that usually results from interference in the control over the muscles of speech caused by damage to a central or peripheral nerve.

Cranial nerve function: 12 pairs of nerves emerge from the cranial cavity through openings in the skull (Table 54-1 p1932 (5th ed) p1896 (6th ed)) Motor Function: will detect abnormalities in the normal functioning of nerves and muscles. Motor status exam includes: Gait and stance Muscle tone Coordination Involuntary movements Muscle stretch reflexes (push-pull)

Motor function cont. Paralysis – a loss of function Paresis – a lesser degree of movement deficit from partial or incomplete paralysis Flaccid – weak, soft, and flabby and lacking normal muscle with absent deep tendon reflexes Spastic – involuntary, sudden movement or muscular contraction with increased reflexes. Fasciculations – small, localized, spontaneous, and involuntary contractions

Sensory and perceptual status: most difficult part of the neurological exam. Alterations in sensation should be assessed include: Pain, touch, temperature, and proprioception (the sensation pertaining to spatial-position and muscular-activity stimuli originating from within the body or to the sensory receptors that those stimuli activate. Unilateral neglect – condition in which an individual is perceptually unaware of and inattentive to oneside of the body Hemianopia – characterized by defective vision or blindness in half of the visual field.

Blood and urine Culture- may rule out infection Drug screens – rule out use of drugs w/ lethargy or to identify specific drugs ingested. Arterial blood gases - used in monitoring O2 levels of the blood. Gases may be altered with neurological diseases such as Guillain-Barre’ syndrome, in which breathing patterns are altered. Cerebrospinal fluid: Normally up to 10 lymphocytes/ml of spinal fluid. An increase of the number of lymphocytes can indicate infection such as tuberculosis, meningitis or a viral infection. Bacterial infections often lower the glucose level as well as the chloride levels. A culture is done to determine the causative organism for meningitis. Spinal-fluid protein is elevated when degenerative diseases or a brain tumor is present. Blood in the spinal-fluid indicates hemorrhage from somewhere in the ventricle system. Protein electrophoresis eval may give evident of neurological diseases such as multiple sclerosis (MS) The patient’s direct reports of neurological impairments and changes are combined with diagnostic testing to determine a diagnosis. Testing can include serum values or electronic scanning to obtain a physical picture. What are the nursing implications for each of the tests listed?

Computed tomography (CT [aka.cat scan]): detect pathologic conditions of the cerebrum and spinal cord using a technique of scanning without radioisotopes. Takes minutes w/o contrast and up to 60 minutes w/ contrast and is painless (except with some discomfort with the injection of dye) NOTE: check allergies to shellfish, seafood, and/or iodine. Brain scan: detecting pathologic conditions of the cerebrum. Uses radioactive isotopes and a scanner. Takes about minutes. (If mercury is used as the isotope indicator, a mercurial diuretic Meralluride (aka..Mercuhydrin) is administered several hrs before the procedure to allow a greater concentration of the mercury to circulate to brain tissue because meralluride minimizes the uptake of mercury by the kidneys. Used less often because CT’s and MRI’s give excellent results

MRI scan: Magnetic resonance imaging Uses magnetic forces to image body structures Relevance in the nervous system as a way to detect pathologic conditions of the cerebrum and spinal cord Used to detect Stroke, multiple sclerosis, tumors, trauma, herniation, and seizure. Greater contrast of soft-tissue vs CT scan Diagnostic choice for neurological diseases Caution: remove watches, credit cards, and any metal from clothing and body before entering the scanning room Takes about minutes PET scan: Positron Emission Tomography Scan Uses injection of deoxyglucose with radioactive fluorine Gives color composite of questioned area. Shades of color give an indication of the level of glucose metabolism Used for patients w/ stroke, Alzheimer’s disease, tumors, epilepsy, and Parkinson’s disease Takes about 45 – 60 minutes

Lumbar puncture To obtain CSF for examination, to relieve pressure, or introduce dye or medication Takes about minutes at the bedside Caution: sharp shooting pain down one leg may occur, caused by the needle coming close to a nerve. Usually done between L4-L5 or L5-S1 Post procedure pt lays flat for several hours. Headache may occur (opioids are usually not helpful). MRA: Magnetic Resonance Angiography Differential signal characteristic of flowing blood to evaluate extracranial and intracranial blood vessels. Provides anatomic and hemodynamic information With or without contrast Rapidly replacing cerebral angiography for use in dx CVA

Laboratory and Diagnostic Examinations
Electroencephalogram Myelogram Angiogram Carotid duplex Digital subtraction angiography Electromyogram Echoencephalogram Diagnostic examinations used for the nervous system often employ scanning techniques to view an area of concern. What patient teaching will be needed for each of the listed exams?

Electroencephalogram (EEG) To provide function by measuring the electrical activity of the brain. Disease assessed by EEG: epilepsy, mass lesions (tumors, abscess, hematoma), cerebrovascular lesions, and brain injury. Myelogram Used to identify lesions in the intradural or extradural compartments of the spinal canal by observing the flow of radiopaque dye through the subarachnoid space Most common use is dx of herniated or protruding intervertebral disk. Other lesions include spinal tumors, adhesions, bony deformations, and arteriovenous malformations. Water soluble iodine dyes are more often used because they are absorbed into the bloodstream and excreted by the kidneys Site of puncture to be monitored for leakage of CSF

Angiogram Used to visualize the cerbral arterial system by injecting radiopaque material. For detection of arterial aneurysms, vessel anomalies, ruptured vessels and displacement of vessels by tumors or masses Takes about 2-3 hours Carotid Duplex Uses ultrasound and pulsed doppler technology Noninvasive procedure that evaluates carotid occlusive disease Electromyogram Used to measure the contraction of a muscle in response to electrical stimulation Takes about minutes for one muscle study Echoencephalogram Uses ultrasound to depict the intracranial structures of the brain. Helpful in detecting ventricular dilation and major shift of midline structures in the brain as a result of an expanding lesion.

Position and angle of the needle when lumbar puncture is performed.
Figure 54-6 The lumbar puncture is an invasive exam. It can be done at the patient’s bedside. A frequently voiced concern relates to the possibility of paralysis if done incorrectly or if the patient moves. Review the reasoning that should be shared with the patient and family as to why paralysis should not be a concern. (From Elkin, M.K., Perry, A.G., Potter, P.A. [2004]. Nursing interventions and clinical skills. [4th ed.]. St. Louis: Mosby.) Position and angle of the needle when lumbar puncture is performed.

Common Disorders of the Neurological System
Headaches Common neurological complaint; has many different causes Etiology/pathophysiology Skull and brain tissues are not able to feel sensory pain Vascular headaches Migraine Pre-Migraine: visual field defects, unusual smells or sounds, disorientation, paresthesias During Migraine: nausea, vomiting, sensitivity to light, chills, fatigue, irritability, diaphoresis, edema Cause includes abnormal metabolism of serotonin, a vasoactive neurotransmitter found in platelets and cells of the brain, plays a major role. Cluster Aka alarm clock headache : known to wake up pt in the middle of the night with intense pain in or around the eye on one side of your head Pain is described as sharp, penetrating or burning. A cluster period generally lasts from six to 12 weeks Risk factors include: Gender (men) Age (late 20’s) Smoking/Alcohol use, family history Hypertensive Elevated blood pressure cause increased pressure Tension headaches – caused by tension, stress, or cervical arthritis Traction-inflammation headaches – caused by an infection, intracranial causes, occlusive vascular structures and temporal arthritis Headaches are a frequent complaint in both men and women. They can be caused by a variety of events. Headaches are classified according to their underlying cause. What population is most at risk of experiencing each of the headache types?

Headaches (continued) Clinical manifestations/assessment Head pain Migraine headaches Prodromal (early sign/symptom) Visual field defects, unusual smells or sounds, disorientation, paresthesias During headache Nausea, vomiting, light sensitivity, chilliness, fatigue, irritability, diaphoresis, edema To diagnose and classify the type of headaches, an accurate accounting of the clinical manifestations is important. What data should be collected from the patient regarding the headache?

Headaches (continued) Medical management/nursing interventions Pharmacological management Migraine headaches Aspirin, acetaminophen, ibuprofen Ergotamine tartrate Codeine; Inderal Dietary recommendations Limit MSG, vinegar, chocolate, yogurt, alcohol, fermented or marinated foods, ripened cheese, cured sandwich meat, caffeine, and pork Psychotherapy Treatment options for headaches can be pharmacological or nonpharmacological. What nondrug interventions can be employed for managing headaches? What is the underlying rationale for each of the interventions? Why are caffeine restrictions recommended in headache sufferers and yet caffeine is one of the leading ingredients in migraine relief medications?

Headaches (continued) Medical management/nursing interventions Cluster headaches Narcotic analgesics Tension headaches Non-narcotic analgesics Traction-inflammatory headaches Treat cause Comfort measures Cold packs to forehead or base of skull Pressure to temporal arteries Dark room; limit auditory stimulation What is the underlying rationale for each of the interventions? Why are narcotic analgesics avoided in patients with tension headaches?

Neuropathic pain Etiology and pathophysiology May arise from several occurrences The pain transmission is not fully understood Clinical manifestations Ranges from mild to excruciating Changes in ability to carry out ADLs Medical management/nursing implications Pharmacological management Anticonvulsants; nonopioid analgesics; antidepressants Comfort measures Neuropathic pain is common. A number of factors may contribute to its development. These factors include postherpetic neuralgia, phantom limb pain, diabetic neuropathies, and trigeminal neuralgia. What tests may be implemented to diagnose the disorder?

Increased intracranial pressure Etiology/pathophysiology Increase in any content of the cranium Space-occupying lesions, cerebrospinal problems, cerebral edema Clinical manifestations/assessment Diplopia Headache Decreased level of consciousness Pupillary signs The structure of the cranium does not allow for expansion as it is housed within the rigid skull. Any increase in the contents will result in an increase in intracranial pressure. What are normal contents of the cranium? What are some causes of intracranial pressure? Does intracranial pressure occur suddenly with rapid onset or is it slow, taking place over a period of time?

Increased intracranial pressure (continued) Clinical manifestations/assessment (continued) Widening pulse pressure (increased systolic/decreased diastolic) Bradycardia (pulse less than 60) Respiratory problems (poss. Cheyne stoking) High, uncontrolled temperatures Positive Babinski’s reflex (extension of the big toe while fanning the other toes.) Seizures Posturing (Decorticate, Decerebrate, or both) Vomiting Singultus (ordinary hiccup) The onset of symptoms associated with intracranial pressure will vary. They will become increasingly evident as the pressure intensifies. Initially the body attempts to compensate for the changes. What actions does the body take into account for the alteration in homeostasis? In what order will the signs and symptoms manifest? Why? At what point do these clinical manifestations become ominous?

Increased intracranial pressure (continued) Medical management/nursing interventions Treat cause if possible Pharmacological management Corticosteroids (dexmethasone) Antacids; histamine-receptor blockers Anticonvulsants (dilantin, cerebyx(short-term IV or IM use)) AVOID opioids and other drugs that cause respiratory depression Mechanical decompression Craniotomy (surgical operation in which a bone flap is temporarily removed from the skull to access the brain) Craniectomy (Surgical removal of a portion of the cranium) Internal monitoring devices Ventricular pressure monitoring – catheter inserted through a burr hole into the lateral ventricle and attached to a transducer and oscilloscope to monitor ICP Subarachnoid screw – inserted through a burr hole in skull and attached to a transducer and oscilloscope for continuous monitoring Once it is identified, there may be limited time to treat intracranial pressure. What diagnostic testing can be utilized for increased intracranial pressure? Why is prompt treatment such a priority? Discuss the use of pharmacological agents in the management of intracranial pressure. What physiological symptoms indicate that the medical interventions have been effective? What is the prognosis for increased intracranial pressure?

Disturbances in muscle tone and motor function Etiology/pathophysiology Damage to the nervous system causes serious problems in mobility Clinical manifestations/assessment Flaccid or hyperreflexic muscle tone Clumsiness or incoordination Abnormal gait Patients experiencing neurological system disorders can present with a variety of signs and symptoms. The assessment will be key in making a determination of the exact problem and developing a plan of care. Review the assessments that will be performed. What types of questions should be asked during the patient interview?

Disturbances in muscle tone and motor function (continued) Medical management/nursing interventions Muscle relaxants Protect from falls Assess skin integrity Positioning Sit up and tuck chin when eating Encourage patient to assist with ADLs Emotional support Safety is a key part of a successful plan of care for the neurologically impaired patient. The risk of injury is great. What are priority safety-related goals for the neurologically impaired patient?

Other Disorders of the Neurological System
Epilepsy or seizures Etiology/pathophysiology Transitory disturbance in consciousness or in motor, sensory, or autonomic function due to sudden, excessive, and disorderly discharges in the neurons of the brain; results in sudden, violent, involuntary contraction of a group of muscles Types: grand mal; petit mal; psychomotor; Jacksonian-focal; myoclonic; akinetic Status epilepticus Seizures affect both men and women of all races and ages. Identify some potential causes of seizures. Recurrent generalized seizures will result in status epilepticus. Sudden withdrawal from the prescribed anticonvulsant therapies is the #1 cause of its occurrence. Status epilepticus is a “9-1-1” event. Emergency intervention is needed to prevent brain damage or death. What events occur during status epilepticus that will result in neurological death?

Epilepsy or seizures (continued) Clinical manifestations/assessment Depends on type of seizure Aura Postictal period Medical management/nursing interventions During seizure: Protect from aspiration and injury Anticonvulsant medications Surgery Removal of brain tissue where seizure occurs Seizures have predictable stages. The seizure might begin with an aura (the predictor of the seizure), followed by the ictal phase (seizure), and ending with the postictal period. An estimated 50% of people experience auras. An aura is a sensation that indicates impending seizure activity. Auras are individualized and can include psychic, olfactory, visual, auditory, or taste hallucinations. What is the value of an aura? What should the patient do after experiencing the aura? After the seizure activity ends, a patient might experience a postictal period. The postictal period can be characterized by feelings of fatigue, lethargy, and disorientation.

Epilepsy or seizures (continued) Medical management/nursing interventions (continued) Adequate rest Good nutrition Avoid alcohol Avoid driving, operating machinery, and swimming until seizures are controlled Good oral hygiene Medic Alert tag The diagnosis of a seizure disorder is traumatic to the patient and family. What are the long-range implications of a seizure disorder diagnosis? What are the nursing responsibilities when caring for the patient during and after seizure activity?

Degenerative Diseases
Multiple sclerosis Etiology/pathophysiology Degenerative neurological disorder with demyelination of the brain stem, spinal cord, optic nerves, and cerebrum Multiple sclerosis is a chronic, progressive neurological disease. The disease initially begins between the ages of 15 and 50 years. Women are affected more than men.

Pathogenesis of multiple sclerosis.
Figure 54-13 In multiple sclerosis, the myelin sheath becomes damaged. This loss of myelin integrity results in impaired transmission of nerve impulses. What theories do scientists support regarding the cause of multiple sclerosis? (From Lewis, S.M., Heitkemper, M.M., Dirksen, S.R. [2007]. Medical-surgical nursing: assessment and management of clinical problems. [7th ed.]. St. Louis: Mosby.) Pathogenesis of multiple sclerosis.

Multiple sclerosis (continued) Clinical manifestations/assessment Visual problems Urinary incontinence Fatigue Weakness Incoordination Sexual problems Swallowing difficulties The clinical manifestations are typically vague and gradually increase in severity and regularity. Several body systems are affected as multiple sclerosis progresses. The disease is associated with periods of remissions and exacerbations. What diagnostic procedures can be implemented when multiple sclerosis is suspected?

Multiple sclerosis (continued) Medical management/nursing interventions No specific treatment Pharmacological management Adrenocorticotropic hormone (ACTH) Steroids Valium Betaseron (interferon beta-1b) Avonex (interferon beta-1a) Pro-banthine; urecholine Bactrim, Septra, and Macrodantin The prescribed pharmacological treatments will vary among practitioners. Drug therapy will also be affected by the stage and severity of the disease. What are goals of nursing interventions when caring for the patient experiencing an exacerbation of multiple sclerosis? Outline the prognosis associated with multiple sclerosis.

Multiple sclerosis (continued) Medical management/nursing interventions Nutrition Skin care Activity Environmental controls Patient teaching What are goals of nursing interventions when caring for the patient experiencing an exacerbation of multiple sclerosis? Outline the prognosis associated with multiple sclerosis.

Parkinson’s disease Etiology/pathophysiology Deficiency of dopamine Clinical manifestations/assessment Muscular tremors; bradykinesia (slow movement) Rigidity; propulsive gait (a stooped, stiff posture with the head and neck bent forward) Emotional instability Heat intolerance Decreased blinking “Pill-rolling” motions of fingers Parkinson’s disease is a chronic neurological disorder. It occurs most frequently in middle-aged and older adults. Explain the pathology of the disease. There is no known cure.

Nigrostriatal disorders produce parkinsonism.
Figure 54-14 (From Lewis, S.M., Heitkemper, M.M., Dirksen, S.R. [2007]. Medical-surgical nursing: assessment and management of clinical problems. [7th ed.]. St. Louis: Mosby.) Nigrostriatal disorders produce parkinsonism.

Parkinson’s disease (continued) Medical management/nursing interventions Pharmacological management Levodopa Sinemet Artane Cogentin Symmetrol Surgery – ablation of affected area vs deep brain stimulator Activity – posture is important, best to not use a pillow Should walk with hands behind back to maintain erect spine and decrease incidence of falling Nutrition – malnutrition and constipation can be severe Need foods that are appetizing and easily chewed and swallowed Encourage 5-6 small meals a day Elimination may feel urgency and hesitancy in voiding Should be on a high fiber diet to help prevent chronic constipation Encourage fluids and take a stool softener, suppositories, prune juice, or milk of magnesia Treatment goals for Parkinson’s disease focus on managing symptoms. Long-term drug therapy for the management of the disease can eventually result in an overabundance of side effects. A “drug holiday” might be indicated. Discuss the purpose of the drug holiday. Considering the treatment modalities available, what are the implications of a diagnosis of Parkinson’s disease for patients and families?

Nursing Diagnosis: Impaired physical mobility, related to rigidity, bradykineia, and akinesia Risk for aspiration related to disease process Patient Teaching: Important to take medication as prescribed Good skin care Proper ambulation and positioning Proper feeding and eating technique to reduce risk of aspiration Prognosis Chronic degenerative disorder with no acute exacerbations If pt compliant with treatment, signs and symptoms can be managed for a long period of time.

Alzheimer’s disease (AD) Etiology/pathophysiology Is a chronic, progressive, degenerative disorder Impaired intellectual functioning Common cause of dementia in the older person and affects men and women equally. Chronic, progressive degeneration of the cells of the brain Brain changes include plaques in the cortex, neurofibrillary tangles, and the loss of connections between cells and cell death. Decrease in brain size 10% age 65 or older and 50% age 85 and older have AD Genetic link Increased plasma levels of homocysteine are associated with a significantly increased risk of AD or dementia Blood homocysteine levels can be lowered by eating foods rich in folic acid, such as fruits and green leafy vegetables. Alzheimer’s disease is a chronic, progressive disease that impacts men and women in equal numbers. Review available theories relating to potential causes of Alzheimer’s disease.

Alzheimer’s disease (continued) Clinical manifestations/assessment = 7 stages Stage 1 Mild memory lapses; decreased attention span Difficulty in using the correct word Disinterest in surroundings and possibly depression No impairment (normal function) The person does not experience any memory problems. An interview with a medical professional does not show any evidence of symptoms of dementia. A series of four stages is used to outline the progression of Alzheimer’s disease. The stages chronicle the clinical manifestations being experienced by the patient. As the disease progresses, the characteristics of the stages worsen. What are the goals of nursing care for each of the stages?

Alzheimer’s disease (continued) Clinical manifestations/assessment = 7 stages Stage 2 Obvious memory lapses, especially short-term memory Disoriented to time Loss of personal objects Loss of impulse control , behavioral manifestations of AD result from changes in brain (agitation) Some pts develop psychotic manifestations Decrease in sleep Very mild cognitive decline (may be normal age-related changes or earliest signs of Alzheimer's disease) The person may feel as if he or she is having memory lapses — forgetting familiar words or the location of everyday objects. But no symptoms of dementia can be detected during a medical examination or by friends, family or co-workers.

Alzheimer’s disease (continued) Clinical manifestations/assessment = 7 stages Stage 3 Total disorientation to person, place, and time Apraxia ( impairment in the ability to perform purposeful acts or to use objects properly ); visual agnosia (inability to recognize objects by sight); dysgraphia (difficulty communicating via writing); wandering Awake most of the night Mild cognitive decline (early-stage Alzheimer's can be diagnosed in some, but not all, individuals with these symptoms) Friends, family or co-workers begin to notice difficulties. During a detailed medical interview, doctors may be able to detect problems in memory or concentration. Common stage 3 difficulties include: Noticeable problems coming up with the right word or name Trouble remembering names when introduced to new people Having noticeably greater difficulty performing tasks in social or work settings Forgetting material that one has just read Losing or misplacing a valuable object Increasing trouble with planning or organizing

Alzheimer’s disease (continued) Clinical manifestations/assessment = 7 stages Stage 4 Moderate cognitive decline (Mild or early-stage Alzheimer's disease) At this point, a careful medical interview should be able to detect clear-cut symptoms in several areas: Forgetfulness of recent events Impaired ability to perform challenging mental arithmetic — for example, counting backward from 100 by 7s Greater difficulty performing complex tasks, such as planning dinner for guests, paying bills or managing finances Forgetfulness about one's own personal history Becoming moody or withdrawn, especially in socially or mentally challenging situations

Alzheimer’s disease (continued) Clinical manifestations/assessment = 7 stages Stage 5 Moderately severe cognitive decline (Moderate or mid-stage Alzheimer's disease) Gaps in memory and thinking are noticeable, and individuals begin to need help with day-to-day activities. At this stage, those with Alzheimer's may: Be unable to recall their own address or telephone number or the high school or college from which they graduated Become confused about where they are or what day it is Have trouble with less challenging mental arithmetic; such as counting backward from 40 by subtracting 4s or from 20 by 2s Need help choosing proper clothing for the season or the occasion Still remember significant details about themselves and their family Still require no assistance with eating or using the toilet

Alzheimer’s disease (continued) Clinical manifestations/assessment = 7 stages Stage 6 Severe cognitive decline (Moderately severe or mid-stage Alzheimer's disease) Memory continues to worsen, personality changes may take place and individuals need extensive help with daily activities. At this stage, individuals may: Lose awareness of recent experiences as well as of their surroundings Remember their own name but have difficulty with their personal history Distinguish familiar and unfamiliar faces but have trouble remembering the name of a spouse or caregiver Need help dressing properly and may, without supervision, make mistakes such as putting pajamas over daytime clothes or shoes on the wrong feet

Alzheimer’s disease (continued) Clinical manifestations/assessment = 7 stages Stage 6 (cont) Experience major changes in sleep patterns — sleeping during the day and becoming restless at night Need help handling details of toileting (for example, flushing the toilet, wiping or disposing of tissue properly) Have increasingly frequent trouble controlling their bladder or bowels Experience major personality and behavioral changes, including suspiciousness and delusions (such as believing that their caregiver is an impostor)or compulsive, repetitive behavior like hand-wringing or tissue shredding Tend to wander or become lost

Alzheimer’s disease (continued) Clinical manifestations/assessment = 7 stages Stage 7 (Terminal stage) Severe mental and physical deterioration Hospice appropriate Very severe cognitive decline (Severe or late-stage Alzheimer's disease) In the final stage of this disease, individuals lose the ability to respond to their environment, to carry on a conversation and, eventually, to control movement. They may still say words or phrases. At this stage, individuals need help with much of their daily personal care, including eating or using the toilet. They may also lose the ability to smile, to sit without support and to hold their heads up. Reflexes become abnormal. Muscles grow rigid. Swallowing impaired.

Alzheimer’s disease (continued) Assessment Memory loss initial sign combined w/ inability to carry out normal activities. Diagnostic Tests No specific test for AD CT, EEG, MRI, and PET may be used to rule out other pathologic conditions At times only confirmation is at autopsy

Alzheimer’s disease (continued) Medical management/nursing interventions Pharmacological management Agitation: Lorazepam; Haldol Dementia: Cognex ; Aricept (short-term benefit for mild cognitive impairment (MCI) , slows progression by up to 3 yrs) Namenda used for moderate to sever (only slows symptoms not MCI) Nutrition Finger foods; frequent feedings; encourage fluids (2000 ml/day) Increase foods high in folic acid and vitamin B12 to reduce homocysteine levels Safety Remove burner controls at night Double-lock all doors and windows Constant supervision Prognosis NO effective treatment to stop progression Lifespan w/ disease 5-20 yrs; cost is approximately $19,000 annually Most pt die from complications related to the disease such as pneumonia, malnutrition, or dehydration Presently there is no cure for the disease. Pharmacological therapies focus on controlling symptoms. Nonmedication therapies seek to promote and prolong functioning for the patient. What are the psychosocial implications of a diagnosis of Alzheimer’s disease?

Myasthenia gravis Etiology/pathophysiology Autoimmune disease of the neuromuscular junction Neuromuscular disorder; nerve impulses fail to pass at the myoneural junction; causes muscular weakness Can occur at any age but common between ages 10 to 65. Peak in women age 20 – 30. Women more affected than men in young but equals out at older age Infants of mothers with MG may be symptomatic at birth 25% patient have Thymoma (cancer of the thymus) 80% have cellular structure of the thymus gland Clinical manifestations/assessment Ptosis (eyelid drooping); diplopia (double vision); 15% of cases confined to the eye muscles Skeletal weakness; ataxia (lack of voluntary coordination of muscle movements) Dysarthria (difficulty w/ speech); dysphagia (difficulty swallowing) Bowel and bladder incontinence Exacerbations may be initiated by upper respiratory infections, emotional tension, and menstuation Myasthenia gravis is a disorder of the nervous system associated with neuromuscular weakness. It is considered an autoimmune disease. What is meant by the term “autoimmune”? How is an individual affected by an autoimmune disease such as myasthenia gravis?

Myasthenia gravis (continued) Medical management/nursing interventions Pharmacological management Anticholinesterase drugs (promote nerve impulse transmission and quite effective of alleviating symptoms) Prostigmin Mestinon Corticosteroids (adjunct therapy d/t immune component) Imuran Cyclosporine Caution with certain drugs: Anesthetics, antidysrhythimics, antibiotics, quinine, antipsychotics, barbituates, sedatives, hypnotics, opioids, tranquilizers, and thyroid prep Plasmapheresis removes antibodies produced by the autoimmune response…short term fix Thymectomy if thymoma is present Intravenous immune globulin to reduce production of acetylcholine antibodies used only in severe relapse of MG May require mechanical ventilation Prognosis: chronic disease Myasthenia gravis characteristically has a slow onset, and diagnosis may be difficult or mistaken for other disorders. What tests are employed to assess for myasthenia gravis?

Amyotrophic lateral sclerosis (ALS) Etiology/pathophysiology Motor neurons in the brain stem and spinal cord gradually degenerate Electrical and chemical messages originating in the brain do not reach the muscles to activate them Lou Gehrig’s disease famous baseball player stricken in early 1940’s Onset between ages (2:1 men:women) 10% of cases is genetic defect Effects 5 out of every 100,000 people worldwide Amyotrophic lateral sclerosis (ALS) involves the destruction of motor neurons in the brain stem and spinal cord. The loss of motor neurons impairs the body’s ability to respond to messages from the brain. The disorder is often referred to as Lou Gehrig’s disease, named after a professional baseball player who developed the disease in the 1940s.

Amyotrophic lateral sclerosis (ALS) (continued) Clinical manifestations/assessment Weakness of the upper extremities Head drop due to weak neck muscles Muscle cramps Muscle contractions called fasciculations Dysarthria (speech difficulty) Dysphagia (difficulty swallowing) Choking easily Drooling Gagging Muscle wasting paralysis Compromised respiratory function Difficulty breathing Weight loss DOES NOT AFFECT THE SENSES (sight, smell, taste, hearing, touch) The progression of ALS is made increasingly difficult because as the body begins to fail, the patient’s mind remains intact and fully functioning. There is no cure. Therapies seek to manage symptoms and promote functioning. What nursing interventions should be incorporated into the care of the patient experiencing ALS?

Amyotrophic lateral sclerosis (ALS) (continued) Medical management/nursing interventions Diagnostics Medical Hx. w/ strength and endurance eval (muscle tremors , spasms, twitching, or loss of muscle tissue (atrophy), twitching of tongue is common) Abnormal reflexes, stiffness and clumsiness Emotional incontinence Tests may be done to rule out other causes (i.e. blood, CT or MRI, Electromyography, spinal tap, swallow studies, nerve conduction)

Amyotrophic lateral sclerosis (ALS) (continued) Medical management/nursing interventions NO CURE Rilutec (Riluzole): slows the progression of ALS and prolongs life. Helps protect motoneurons damaged by the disease Baclofen or diazepam: used to control spasticity that interferes with daily activities Trihexyphenidyl or amitriptyline: used for people w/ problems of swallowing their own saliva G-Tube placement due to choking Complications: Aspiration Loss of abilty to care for self Lung failure (ARDS) Pneumonia Pressure sores Weight loss Multidisciplinary ALS teams; emotional support; Part of the Muscular Dystrophy Foundation ALS Associan Prognosis Death. Lifespan post diagnosis typically ranges 2-6 years. Approximately 25% patients live for more than 5 years (up to 7 years)

Huntington’s disease Etiology/pathophysiology Like Parkinson’s disease involves the basal ganglia and the extrapyramidal motor system Overactivity of the dopamine pathways Genetically transmitted autosomal dominant disorder that affects both men and women of all races. Defect on chromosome 4 Offspring of person w/ disease has 50% chance of developing disease Two forms: Adult-onset (most common) symptoms in mid 30s-40s Early-onset symptoms occur during childhood or adolescence Huntington’s disease is genetically transmitted. It is an autosomal dominant disorder. The children of an affected parent have a 50% chance of inheriting it. Given the rate of transmission between parents and children, what genetic counseling should be provided to potential carriers?

Huntington’s disease (continued) Clinical manifestations/assessment Behavioral Hallucinations Irritability Moodiness Restlessness or fidgeting Paranoia psychosis Abnormal and excessive involuntary movements (chorea) Facial movements, including grimaces Head turning to shift eye position Wild jerking of extremities face and other body parts Slow, uncontrolled movement Abnormal reflexes Hesitant speech or poor enunciation Ataxia to immobility Unsteady gait “Prancing” and wide walk

Huntington’s disease (continued) Clinical manifestations/assessment Deterioration in mental functions Dementia Disorientation or confusion Loss of judgment Loss of memory Personality changes Speech changes Symptoms in children Rigidity Slow movements Tremors

Huntington’s disease (continued) Medical management/nursing interventions Diagnostics CT of head may show loss of brain tissue MRI or PET of brain Genetic tests Treatment NO CURE; palliative care (treat the symptoms) Pharmacological management Antipsychotics: Dopamine blockers may reduce abnormal behaviors (Azilect, Clozaril, Reglan, Haloperidol) Antidepressants (Depression and suicide common (assess for S&S)) Antichoreas (Amantadine & tetrabenzine: used to control extra movements) Co-enzyme Q10: help slow down the course of the disease (but not conclusive)

Huntington’s disease (continued) Medical management/nursing interventions Safe environment Emotional support Huntington’s Disease Society of America High-calorie diet As much as kcal/day to maintain body weight due to involuntary body movements Complications Loss of ability to care for self Loss of ability to interact Injury to self or others Increased risk for infection Depression death Prognosis Causes disability that gets worse overtime Average lifespan from onset of symptoms is years. Cause of death is often infection or suicide The disease has no cure. The goals of treatment seek to manage the symptoms and reduce injury. What are the primary needs of the patient? How can the nurse meet these needs?

Vascular Problems Stroke (cerebrovascular accident [CVA])
Etiology/pathophysiology: Blood flow to a part of the brain stops. Aka.. Brain attack Abnormal condition of the blood vessels of the brain: 2 types 85% thrombosis & embolism = ischemic stroke 15% hemorrhage = hemorrhagic stroke (weak and bursts open, aneurysm, arteriovenous malformation) Results in ischemia of the brain tissue Most common disease of nervous system (estimated 700,000 suffer strokes each yr. and the cause of 158,000 deaths annually) All ages affected Greatest number between ages 75-85 Residual effects vary from mild deficits to severe disabilities Hemiparesis (weakness or paralysis of one side of the body), inability to walk, complete or partial dependence with ADL’s and aphasia Stroke is the most prevalent neurological disorder. It ranks as the third leading cause of death in the United States. The clinical manifestations of a stroke vary by cause and individual. Some of the more common symptoms can include disturbances in motor activity, intellectual functioning, or communication abilities. What factors can determine the types and degree of impairments that will be experienced?

Figure 54-17 Three types of stroke.
Strokes are classified by their underlying cause. Strokes can be ischemic, thrombotic, or embolic. How do the types of strokes differ? (From Lewis, S.M., Heitkemper, M.M., Dirksen, S.R. [2007]. Medical-surgical nursing: assessment and management of clinical problems. [7th ed.]. St. Louis: Mosby.) Three types of stroke.

Vascular Problems Stroke (cerebrovascular accident [CVA]) cont.
Risk Factors Atrial Fibrillation Diabetes Family Hx of stroke High Cholesterol Increasing age >65 Race (black people are more likely to die of a stroke) Unhealthy lifestyle Overweight or obese Drinking heavily To much fat or salt in diet Smoking Illegal drugs (cocaine) Birth control pills

Vascular Problems Stroke (cerebrovascular accident [CVA]) cont.
Clinical manifestations/assessment Headache Sensory deficit Hemiparesis; hemiplegia Dysphasia or aphasia *See handout page 2 Symptoms Diagnostics CT – primary test for diagnosis. Used to differentiate between ischemic vs hemmorhagic CT angiography (CTA) provides visualization of vasculature MRI or PET used to determine extent of damage Doppler, CTA, or MRA may be done to assess cartoids post TIA may result in cerebral angiogram

Vascular Problems Stroke (cerebrovascular accident) (continued)
Medical management/nursing interventions Hemorrhagic Surgery to repair damage May cause vasospasm (narrowing of blood vessel, decreasing perfusion) Occurring in 30-60% of cases post-operatively (between days 4-12). Mortality rate as high as 50% If not tx rapidly can cause cerebral ischemia or cerebral anoxia which leads to severe mental and physical deficits or death. Thrombosis or embolism Thrombolytics (plasmnogen activator t-PA, alteplase) causes lyses of clot Must be administered within 3 hours of the onset of symptoms. The longer the wait the less effective. TIME IS A FACTOR Heparin, Lovenox, and Coumadin (platelet inhibitors and anticoagulants PATIENTS MUST BE SCREENED CAREFULLY BEFORE TX BEGINS Recent hx. Of GI bleed, CT or MRI to rule out hemorrahagic stroke Decadron to reduce ICP Neurological checks at regular intervals Q8 hrs Nutritional interventions: tube feeding may be necessary or TPN Physical, occupational, and/or speech therapy Bobath approach: designed to normalize muscle tone by providing as many sensations of normal muscle tone, posture, and movement as possible Support Groups American Stroke Association The greatest chance for a positive prognosis involves early intervention. Currently there are pharmacological interventions, if provided in the early stages, that can improve the patient’s chances for recovery. These therapies involve the use of thrombolytics. Explain their uses and parameters for successful intervention. What nursing assessments are needed for the patient who has had a stroke?

Vascular Problems Stroke (cerebrovascular accident) (continued)
Complications Aspiration Dementia Falls Loss of mobility Loss of movement or feeling in one or more parts of the body Muscle spasticity Poor nutrition Pressure ulcers Problems speaking and understanding (effects on Broca or Wernike’s area of brain) Problems thinking and/or focusing

Cranial and Peripheral Nerve Disorders
Trigeminal neuralgia Etiology/pathophysiology Degeneration of or pressure on the trigeminal nerve; tic douloureux Occurs at any age Caused by Multiple Scleroisis Pressure on the trigeminal nerve from a swollen blood vessel or tumor Clinical manifestations/assessment Excruciating, burning facial pain, electric-like spasms that last a few seconds or minutes Pain usually one side of face May be triggered by touch or sounds Can be triggered by Brushing teeth, chewing, drinking, eating, lightly touching the face, shavingl Trigeminal neuralgia is a disorder of the peripheral nervous system. It is most common in women in middle and late adulthood. Patients having trigeminal neuralgia experience severe pain when trigger points along the trigeminal nerve are activated. What activities can cause this pain?

Trigeminal neuralgia Medical management/nursing interventions Diagnostics: Blood tests MRI of the head Trigeminal reflex testing: electrical stimulation of the divisions of the trigeminal nerve and measurement of the response with standard electromyography apparatus. This testing is not readily available to most physicians, and its indications and clinical utility are still unclear Pharmacological Management Anti-seizure drugs (carbamazepine (Tegratol), gabapentin, phenytoin, valproate, and pregabalin) Muscle relaxants (baclofen, clonazepam) Tricyclic antidepressants (amitriptyline, nortriptyline) Surgical resection of the trigeminal nerve Within 24 hrs of resection of 5th nerve pt develops herpes simplex of the lips (cold sores) heals in about a week (5-14 days) Avoid stimulation of face on affected side

Trigeminal neuralgia Medical management/nursing interventions Comfort measures Keep room free of drafts Avoid walking briskly to bedside of patient Place bed out of traffic area to prevent jarring of bed avoid touching the patients face Don’t urge pts to wash or shave the affected area or to comb the hair Avoid hot or cold liquids, may trigger pain Puree food and ensure that it is lukewarm. Suggest food be taken through a straw Prognosis Depends on cause. Pain varies and permanent relief of pain is obtained only by surgery Pain can be disruptive to lifestyle. Can be total physical and psychological dysfunction or even suicide.

Bell’s palsy (peripheral facial paralysis) Etiology/pathophysiology Inflammatory process involving the facial nerve VII from the nucleus in the brain to the periphery Damage to this nerve causes weakness or paralysis of these muscles Evidence the reactivated herpes simplex (HSV) may be involved. Causing inflammation, edema, ischemia, and demyelination of the facial nerve. Can be unilateral (one side) or bilateral (both sides) Causes, Incidence, and risk factors Affects 30,000-40,000 people in the USA Cause is not clear. But may be caused by other disease processes such as: Herpes simplex HIV infection Middle ear infection Sarcoidosis - inflammation occurs in the lymph nodes, lungs, liver, eyes, skin, or other tissues Bell’s palsy occurs as a result of inflammation of the facial nerve (cranial nerve V). No exact cause has been identified. What theories concerning a cause of this disease have been identified?

Bell’s palsy (peripheral facial paralysis) Clinical manifestations/assessment Facial numbness or stiffness Hard to close one eye Problems w/ smiling, grimacing, or making facial expressions Drawing sensation of the face Twitching Unilateral weakness of facial muscles Drooping of face Reduction of saliva Drooling Pain behind the ear Ringing in ear or other hearing loss

Bell’s palsy (peripheral facial paralysis) (continued) Medical management/nursing interventions Diagnostics CT scan or MRI of the head Electromyography (EMG) or Nerve conduction test to check nerves that supply the muscles of the face Treatment Often no tx needed. Begins to resolve immediately but may take up to months to get full muscle strength Eye drops to lubricate if needed or an eye patch when sleeping Pharmacological management Corticosteroids may reduce swelling around the facial nerve Antiviral medications in an attempt to fight off virus that may be causing bell’s palsy There is no exact course of therapy to treat Bell’s palsy. Medical interventions seek to reduce inflammation and manage symptoms. What are the nursing responsibilities in the care of this disorder? What is the prognosis for patients diagnosed with Bell’s palsy?

Bell’s palsy (peripheral facial paralysis) (continued) Medical management/nursing interventions Electrical stimulation Moist heat Massage of the affected area Facial exercises Prognosis Usually resolve on own Long term changes in taste Spasms of muscles or eyelids Weakness that remains in facial muscles Complications Excess drying of the eye surface, leading to eye ulcer or infections

Guillain-Barré syndrome Etiology/pathophysiology Inflammation and demyelination of the peripheral nervous system Possibly viral or autoimmune reaction Most common in people of both sexes between the ages of 30-50 Often follows a minor infection, such as lung or GI infection Nerve damage causes tingling, muscle weakness, and paralysis. Guillian-Barre syndrome most often affects the nerves’ covering (myelin sheath) and causes nerve signals to move more slowly or not at all. Guillain-Barré syndrome involves the loss of myelin sheaths in the peripheral nervous system. Myelin acts as insulation for nerves, and the loss of myelin results in alterations of nerve conduction. Although no exact cause has been pinpointed, commonality has been noted between at least 50% of people diagnosed. Review this “common ground.”

Guillain-Barré syndrome (continued) Clinical manifestations/assessment Symptoms are progressive Paralysis usually starts in the lower extremities and moves upward; may stop at any point Respiratory failure if intercostal muscles are affected May have difficulty swallowing, breathing, and speaking Diagnostics Lumbar puncture ECG Electroyography (EMG) Nerve conduction velocity test Pulmonary function tests

Guillain-Barré syndrome (continued) Medical management/nursing interventions Adrenocortical steroids Apheresis Mechanical ventilation Gastrostomy tube Meticulous skin care Range-of-motion exercises Complications: Respiratory failure DVT Increased risk of infections Low or unstable bp Paralysis that is permanent Pneumonia Skin damage aspiration Prognosis: Most recover completely but can take weeks, months, or years. 30% of cases will have some residual effects The vast majority of people diagnosed with Guillain-Barré syndrome will fully recover. What are the goals of treatment during the acute phase of the disease?

Meningitis Etiology/pathophysiology Acute infection of the meninges Bacterial or aseptic Increased incidence in winter and fall months

Meningitis (continued) Clinical manifestations/assessment Headache; stiff neck Irritability; restlessness Malaise Nausea and vomiting Delirium Elevated temperature, pulse, and respirations Kernig’s and Brudzinski’s signs The clinical manifestations seen in meningitis largely occur as a result of the impact of the inflammatory process on the meninges. What diagnostic testing can be used to confirm diagnosis?

Meningitis (continued) Medical management/nursing interventions Pharmacological management Antibiotics Massive doses Multiple types IV or intrathecal Corticosteroids Anticonvulsants Antipyretics Dark, quiet room Treatment of meningitis uses a variety of different classifications of medications. What is the desired effect/purpose for the use of each of the potential drug classifications? What is the prognosis for the patient diagnosed with meningitis?

Encephalitis Etiology and pathophysiology Acute inflammation of the brain caused by a virus Clinical manifestations Headache Fever Seizures Change in LOC Medical management and nursing interventions Primarily supportive Encephalitis may be associated with certain seasons and endemic to certain geographic locations. What are potential causes of nonepidemic encephalitis? The best prognosis is associated with early diagnosis. What tests may be utilized to confirm a diagnosis?

West Nile virus Etiology and pathophysiology Principal route of infection through the bite of an infected mosquito Clinical manifestations Fever Headache Back pain Myalgia Prevention Certain individuals infected with West Nile virus will become affected with West Nile virus meningitis or encephalitis. What is the prognosis for this disease? What population has the most harsh prognosis?

Brain abscess Etiology and pathophysiology Accumulation of pus within the brain tissue Clinical manifestations Headache Fever Drowsiness, changes in LOC Seizures Medical management/nursing interventions Antimicrobial therapy Supportive care

Acquired immunodeficiency syndrome Etiology and pathophysiology Symptoms may develop from the infection with HIV or as a result of an associated infection Clinical manifestations AIDS dementia complex (ADC) Memory loss Global cognitive dysfunction Medical management/nursing interventions Antiviral, antifungal, antibacterial agents Anticonvulsants Safety What opportunistic infections may be associated with this disorder? What diagnostic tests may be utilized in the care of the patient suspected of having this condition?

Brain tumors Etiology/pathophysiology Benign or malignant Primary or metastatic May affect any area of the brain Brain tumors can originate in the brain tissue or spread there from some other location of the body. What terminology would be used to describe those tissues originating in the brain? What would tumors that spread to the brain be referred to as?

Brain tumors (continued) Clinical manifestations/assessment Headache Hearing loss Motor weakness Ataxia Decreased alertness and consciousness Abnormal pupil response and/or unequal size Seizures Speech abnormalities The clinical manifestations of a brain tumor will vary according to size and location.

Brain tumors (continued) Medical management/nursing interventions Surgical removal of tumor Craniotomy Intracranial endoscopy Radiation Chemotherapy Combination of above Management of brain tumors is individualized. The physician and patient chart a path unique to the individual’s degree of involvement and personal wishes. What nursing care will be needed for the patient after surgical intervention for a brain tumor?

Trauma Craniocerebral trauma Etiology/pathophysiology
Motor vehicle and motorcycle accidents, falls, industrial accidents, assaults, and sports trauma Direct trauma: Head is directly injured Indirect trauma: Tension strains and shearing forces Open head injuries Closed head injuries Hematomas Trauma to the brain can result in disability or death. It is a major cause of neurological impairment. How do acceleration and deceleration injuries differ? Provide examples of each type of injury. A hematoma can occur as a result of a brain injury. Compare and contrast an epidural and a subdural hematoma.

Trauma Craniocerebral trauma Clinical manifestations/assessment
Headache Nausea Vomiting Abnormal sensations Loss of consciousness Bleeding from ears or nose Abnormal pupil size and/or reaction Battle’s sign In addition to the assessment of objective and subjective data, diagnostic tools can be employed to assess a craniocerebral injury. What tests can be anticipated?

Trauma Craniocerebral trauma (continued)
Medical management/nursing interventions Maintain airway Oxygen Mannitol and dexamethasone Analgesics Anticonvulsants When a head injury occurs, the priorities employ the ABCs of health care—Airway, Breathing, and Circulation. Once the patient has been stabilized, pain management might be needed. Care must be given to medicate the patient while avoiding medications that reduce respirations or mask neurological changes. What are the preferred analgesic medications when caring for the patient who has experienced a head injury? What analgesics should be avoided? Anticonvulsants can also be administered. What is the rationale for their use?

Trauma Spinal cord trauma Etiology/pathophysiology
Automobile, motorcycle, diving, surfing, other athletic accidents, and gunshot wounds Fracture of vertebra Complete cord injury Incomplete cord injury An estimated 10% of traumatic injuries to the nervous system involve the spinal cord. What populations are at greatest risk of spinal cord injury? Compare and contrast a complete spinal cord injury with an incomplete spinal cord injury.

Mechanisms of spinal injury.
Figure 54-24 (From Lewis, S.M., Heitkemper, M.M., Dirksen, S.R. [2007]. Medical-surgical nursing: assessment and management of clinical problems. [7th ed.]. St. Louis: Mosby.) Mechanisms of spinal injury.

Trauma Spinal cord trauma (continued)
Clinical manifestations/assessment Loss of muscle function depends on level of injury Spinal shock Autonomic dysreflexia Sexual dysfunction The level of spinal cord injury will determine the degree of functioning lost. The higher the injury, the greater the loss. Outline the types of impairments that would be associated with injuries to the cervical, thoracic, lumbar, and sacral regions. Spinal shock is a common early occurrence in most spinal cord injuries. What additional needs might the patient have during this period? Autonomic dysreflexia is a serious complication experienced when damage at or above T-6 occurs. Review the signs and symptoms of autonomic dysreflexia. What stimuli can promote this problem?

Trauma Spinal cord trauma (continued)
Medical management/nursing interventions Realignment of bony column for fractures or dislocations: Immobilization; skeletal traction Surgery for spinal decompression Methylprednisolone Mobility: Slowly increase sitting up Urinary function: Foley catheter; bladder training Intermittent catheterization Bowel program A spinal cord injury is a traumatic event for the patient and family. What psychosocial supports will be indicated? What are the responsibilities of the nurse regarding emotional support?

Nursing Process Nursing diagnoses Autonomic dysreflexia
Communication, impaired Coping, compromised family Disuse syndrome, risk for Grieving Infection, risk for Knowledge, deficient Memory, impaired

Nursing Process Nursing diagnoses (continued)
Mobility, impaired physical Nutrition, imbalanced: less than body requirements Pain, acute, chronic Self-care deficit Swallowing, impaired Thought process, disturbed Tissue perfusion (cerebral), ineffective

Chapter 53 Care of the Patient with a Neurologic Disorder

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