Help
Options
Didn't know it?
click below
click below
Knew it?
click below
click below
Don't Know
Remaining cards (0)
Know
retry
shuffle
restart
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
355 test 4
| Question | Answer |
|---|---|
| Stroke | either ischemia (inadequate blood flow) to a part of the brain hemorrhage (bleeding) into the brain that results in the death of brain cells, terms brain attack and cerebrovascular accident are also used to describe stroke |
| what functions are impaired from a stroke? | movement, sensation, thinking, talking, or emotions |
| FAST warning signs of a stroke | Facial drooping Arm weakness speech slurred Time is CRITICAL! If someone shows any of these signs , call 911 Note the time when the signs first appeared. |
| stroke non modifiable risk factors | Age, gender, ethnicity or race, and family history or heredity common in men, but more women die from stroke African Americans have twice the incidence of stroke A person with a family history of stroke has an increased risk of having a stroke |
| stroke modifiable risk factors | Hypertension, heart disease, diabetes, smoking, obesity, sleep apnea, metabolic syndrome, lack of exercise, poor diet, and drug/ alcohol HTN is most important modifiable risk factor. Heart disease, including atrial fibrillation (blood clot), MI |
| Illicit drug use, especially | cocaine use, increases stroke risk. |
| Never, low-dose what? | oral contraceptives have lower risks for stroke except in those who have hypertension and smoke. Women who have migraines with aura have an increased risk for stroke. |
| Transient (temporary) Ischemic Attack (TIA) | caused by focal brain, spinal cord, or retinal ischemia, but without acute infarction of the brain S/S typically last < 1 hour Teach patient to seek treatment for any stroke S/S TIAs may be due to microemboli that temporarily block the blood flow. |
| Unlike a TIA, in which ischemia occurs without infarction, a stroke results in | infarction (cell death). We classify strokes as ischemic or hemorrhagic |
| Ischemic Stroke | Results from inadequate blood flow to the brain from partial or complete occlusion of an artery Classified as thrombotic or embolic |
| Ischemic Stroke Thrombotic | injury to a blood vessel wall and formation of a blood clot lumen of vessel becomes narrowed, and, if it becomes occluded, infarction occurs. Thrombosis develops readily where atherosclerotic plaques have already narrowed blood vessels Most common |
| Thrombotic stroke signs | depends on rapidity of onset, size of the damaged area, collateral circulation Most do not have a decreased level of consciousness (LOC) in the first 24 hours Manifestations may progress in the first 72 hours as infarction and cerebral edema increase. |
| Ischemic Stroke Embolic | embolus lodges in and occludes a cerebral artery, resulting in infarction and edema Most emboli originate in the endocardial layer of heart when a plaque breaks off and enters circulation Embolus travels upward to the cerebral circulation and lodges |
| what causes most embolic strokes | Heart conditions like A. Fib, MI, infective endocarditis, valvular heart prostheses, patent foramen ovale, and atrial septal defects |
| embolic strokes signs | can affect any age Severe manifestations occur suddenly rapidly, giving little time to accommodate an obstructed blood vessel by developing collateral circulation Initially characterized by severe neurologic deficits |
| Hemorrhagic Stroke | Result from bleeding into the brain tissue itself (intracerebral or intraparenchymal hemorrhage) or into the subarachnoid space or ventricles (SAH or intraventricular hemorrhage). |
| Hemorrhagic Stroke Intracerebral Hemorrhage | Bleeding within the brain caused by a rupture of a vessel HTN is common cause Other causes- vascular malformations, coagulation disorders, anticoagulant and thrombolytic drugs, trauma, brain tumors, and ruptured aneurysms- during periods of activity |
| Hemorrhagic Stroke Intracerebral Hemorrhage signs | neurologic deficits, headache, nausea, vomiting, decreased LOC, and hypertension,↑ ICP, displace brain tissue, and decrease CBF, Initially, severe HA and N/V severe hemorrhage-hemiplegia, fixed and dilated pupils, abnormal body posturing, and coma |
| Hemorrhagic Stroke Subarachnoid Hemorrhage (SAH) | there is intracranial bleeding into the cerebrospinal fluid–filled subarachnoid space.caused by rupture of a cerebral aneurysm Other causes-trauma and cocaine “silent killer” since people do not have warning S/S, poor prognosis |
| Hemorrhagic Stroke Subarachnoid Hemorrhage (SAH) manifestations | LOC may range from alert to comatose, focal neurologic deficits (including cranial nerve deficits), nausea, vomiting, seizures, HA, and stiff neck Complications of aneurysmal SAH include rebleeding and cerebral vasospasms, which can lead to infarction |
| stroke manifestations | Neuro manifestations do not significantly differ between ischemic and hemorrhagic stroke Both cause neural tissue destruction → neurologic dysfunction Can affect bladder and bowel function, intellect, spatial perception, sensation, swallowing |
| right brain damage stroke | paralyzed on left side, hemiplegia, left sided neglect, spatial deficits, denies problems, rapid performance, short attention span, impulsive, impaired judgement, impaired time |
| left brain damage stroke | paralyzed on right side, impaired speech, impaired right/left discrimination, cautious, slow, aware of deficits, depression, impaired comprehension |
| stroke motor function manifestations | motor- impaired mobility, (2) respiratory function, (3) swallowing and speech, (4) gag reflex, and (5) self-care abilities caused by the destruction of motor neurons in the pyramidal pathway |
| stroke motor function manifestations pt 2 | Characteristic deficits include loss of skilled voluntary movement (akinesia), impaired integration of movements, changes in muscle tone, and altered reflexes Initially have hyporeflexia, then progresses to hyperreflexia |
| A lesion on 1 side of the brain affects | motor function on the opposite side of the body (contralateral) Affected extremities may be weakened or paralyzed to different degrees |
| stroke communication manifestations | Receptive aphasia (Wernicke's): loss of language comprehension, temporal lobe Expressive aphasia (Broca’s): inability to produce language Global: total inability Nonfluent: minimal speech wt slow speech Fluent: speech present, little communication |
| what side of brain dominates communication | left |
| dysarthria in stroke pt | : a problem with the muscular control of speech Impairment may involve pronunciation, articulation, and phonation Does not affect the meaning of communication or language comprehension Affects the mechanics of speech |
| Broca's aphasia | nonfluent aphasia, Damage to frontal lobe short phrases that make sense but take effort • Often omit small words • Typically understands others’ speech • Often aware of their difficulties and can become easily frustrated |
| global aphasia | Type of nonfluent aphasia • Results from damage to extensive portions of language areas of brain • Have severe communication difficulties • May be limited in ability to speak or understand language |
| wernickes aphasia | fluent aphasia • Damage occurs in left temporal lobe, although it can result from damage to right lobe • May speak in long sentences that have no meaning, add unnecessary words difficulty understanding speech • Often unaware of their mistakes |
| affect stroke manifestations | May have difficulty controlling emotions Emotional responses may be exaggerated or unpredictable Depression and frustration from loss of function and communication problems |
| Intellectual Function manifestations stroke | Stroke may impair memory, judgement, and ability to learn. Left brain stroke: more likely to have memory problems; cautious Right brain stroke: impulsive; unpredictable actions |
| Spatial-Perceptual Problems stroke | Incorrect perception of self and illness. Spatial neglect: patient neglects all input from the affected side Agnosia: inability to recognize an object by sight, touch, or hearing Apraxia: inability to carry out learned movements on command |
| Elimination manifestations stroke | Most urinary and bowel elimination problems are temporary Patient may have frequency, urgency, and incontinence Constipation is associated with immobility, weak abdominal muscles, dehydration, and decreased response to the defecation reflex |
| Diagnostic Studies stroke | Non contrast head CT or MRI CT scan is a rapid diagnostic tool to rule out hemorrhage MRI is more effective in identifying ischemic stroke than CT (CTA) provides visualization of cerebral vessels MRA can detect vascular lesions and blockages |
| Stroke Prevention | goals of stroke prevention include adopting a healthy lifestyle and managing modifiable risk factors Focuses on (1) healthy diet, (2) weight control, (3) regular exercise, (4) no smoking, (5) limiting alcohol use, and (6) BP management |
| Preventative Drug Therapy stroke | prevent thrombus or embolus development Antiplatelets are first line treatment Aspirin 81mg/day Anticoagulants warfarin (Coumadin), rivaroxaban (Xarelto), dabigatran (Pradaxa), and apixaban (Eliquis) Statins |
| Surgical/Endovascular Therapy for Stroke Prevention | Carotid endarterectomy- atheromatous lesion is removed from carotid artery to improve blood flow Transluminal angioplasty-balloon to open a stenosed artery in brain-improve blood flow Stenting-ntravascular stent to try to maintain patency |
| Care after stenting or angioplasty | includes neurovascular assessment and BP management Monitor for bleeding |
| Acute Care For Ischemic Stroke | most important point in the pt history is the time of onset of symptoms.Elevated BP is common right after a stroke BP goal for ischemic stroke NOT receiving fibrinolytics:220/120 BP RECEIVING fibrinolytics< 180/105-so ischemic doesn’t turn hemorrhagic |
| IV antihypertensives such as | labetalol and nicardipine are preferred for stroke |
| Acute Care for Ischemic Stroke electrolytes | Maintain careful fluid and electrolyte balance Adequate hydration promotes perfusion Overhydration can ↑ ICP Hypotonic IVF are avoided Increased ICP is more likely to occur with hemorrhagic strokes but can occur with ischemic strokes |
| Drug Therapy for Ischemic Stroke Fibrinolytic Therapy | Tissue plasminogen activator (tPA) produces fibrinolysis (clot break down) IV tPA can re-establish blood flow through a blocked artery and prevent cell death in patients with the acute onset of ischemic stroke Must be given within 3-4.5 hours of onset |
| Fibrinolytic Therapy prior | head CT or MRI to r/o hemorrhagic stroke Contraindications: coagulation disorders; GI bleeding, stroke, or head trauma within the past 3 months; major surgery within 14 days; or recent internal bleeding within 22 days. Closely monitor neuro status |
| Fibrinolytic Therapy BP and anticoag use | Maintain SBP < 180-185 mmHg May be given intra-arterially Anticoagulant use in the emergency phase after an ischemic stroke is not recommended because of the risk for intracranial hemorrhage. |
| Drug Therapy for Hemorrhagic Stroke | Anticoagulants and platelet inhibitors are contraindicated Drug therapy involves managing HTN Oral and IV agents to maintain SBP < 160 |
| Surgical Therapy for Hemorrhagic Stroke | Immediate evacuation of hematomas > 3 cm Surgical resection, radiosurgery, or embolization of arteriovenous malformations (AVMs) Clipping or coiling of aneurysm to prevent rebleeding |
| stroke assessment | Cardiac and respiratory Health history Comprehensive neuro exam LOC, cognition, motor abilities, CN function, sensation, proprioception, cerebellar function, DTRs National Institute of Health Stroke Scale (NIHSS) measures stroke severity |
| stroke resp system | Patients at risk for atelectasis and pneumonia Mechanical ventilation may be needed Oral care; suction as needed Encourage deep breathing Risk for aspiration pneumonia due to dysphagia or ↓ LOC Keep NPO until swallow evaluation elevate HOB |
| stroke cardio system | Manage HTN per guidelines Risk for venous thromboembolism (VTE) in weakened or paralyzed extremity ROM exercises, compression devices, low-molecular weight heparin (enoxaparin) |
| stroke Integumentary System | High risk of skin breakdown Frequent position changes, good skin hygiene, wheelchair cushions, float heels, cushion bony prominences, frequent skin assessments Position the patient on the weak or paralyzed side for only 30 minutes at a time |
| stroke Musculoskeletal System | ROM exercises Careful positioning to prevent joint contractures trochanter roll at the hip to prevent external rotation hand cones (not rolled washcloths) to prevent hand contracture arm supports and lap boards to prevent shoulder displacement |
| stroke GI system | Constipation is common Increased fluid and fiber intake, prophylactic stool softeners or fiber and physical activity may help Enemas are only used if other measures are ineffective as they cause vagal stimulation and ↑ ICP |
| stroke urinary system | Poor bladder control and incontinence during acute phase of stroke Avoid the use of indwelling catheters Avoid bladder overdistention An intermittent catheterization program may be used for patients with urinary retention, schedule toileting q 2 hr |
| stroke nutrition | NPO until swallowing evaluation Foods should be easy to swallow and provide enough texture, temperature, and flavor to stimulate a swallow reflex high-Fowler’s position for the feeding and 30 min after head flexed forward; food in the unaffected side |
| stroke nutrition pt 2 | teach the patient to swallow and then swallow again, If the patient is unable to take in an adequate oral diet and dysphagia persists, a PEG tube may be used removing unnecessary items from the tray or table |
| stroke communication | Assess patient ability to speak and understand Use gestures to support verbal cues Verbal stimuli can easily overwhelm the patient with aphasia Give the patient extra time to understand and respond to communication A picture board may be helpful |
| Sensory Perceptual Problems: Right Brain Stroke | Difficulty judging position, distance, and rate of movement Impulsive and impatient Tend to deny problems related to strokes May not correlate spatial-perceptual problems with the inability to perform activities One-sided neglect is common |
| Sensory Perceptual Problems: Left Brain Stroke | Slower in organizing and performing tasks Impaired spatial discrimination Usually admit to deficits and have a fearful, anxious response to a stroke Behaviors are slow and cautious |
| Sensory Perceptual Problems stroke | Homonymous hemianopsia: blindness in the same half of visual fields of both eyes Pt has trouble wt spatial orientation disregard of objects in part of visual field first, help pt to compensate by arranging the environment within pt perceptual field |
| Sensory Perceptual Problems stroke pt 2 | diplopia (double vision), loss of the corneal reflex, and ptosis (drooping eyelid) Diplopia is often treated with an eye patch If the corneal reflex is absent, the patient is at risk for corneal abrasion Artificial tears or gel, eye shield |
| stroke coping | Affects the family emotionally, socially, and financially and changes roles Nurses promote coping through education and emotional support Update the family daily, advocate for patient wishes and advanced directives during decision making |
| Rehabilitation stroke | Rehabilitation is the process of maximizing the patient’s capabilities and resources to promote optimal functioning related to physical, mental, and social well-being Goals of rehabilitation are to prevent deformity and maintain and improve function |
| Occupational therapy emphasizes | retraining for skills of daily living, including eating, dressing, hygiene, and cooking |
| Ambulatory Care Musculoskeletal Function stroke | Spasticity with exaggerated reflexes within 48 hours after the stroke denotes progress toward recovery Continued flaccidity weeks after stroke indicates poor functional prognosis last stage of recovery when pt has voluntary control of muscle groups. |
| Musculoskeletal Function stroke | Interventions advance in a manner of progressive activity Balance training and posture first, then transferring from bed to chair, etc… Supportive or assistive equipment, such as canes, walkers, and leg braces, may be needed |
| Stroke Survivorship and Coping | Patients often grieve sensory, intellectual, communicative, functional, role behavior, emotional, social, and vocational losses. Some patients develop long-term depression Loss of independence may be a major concern. |
| The nervous system is made up of 2 types of cells | neurons and supportive glial cells. |
| Neurons: | The main functional unit of the nervous system Cell body contains the nucleus and cytoplasm Dendrites are short processes extending from the cell body, they receive impulses from other neurons and conduct them to the cell body |
| axon | tail-like projection from the cell body that carries impulses to other neurons or end organs Many axons are covered with a white, lipid protein substance called the myelin sheath The myelin sheath speeds the conduction of nerve impulses |
| Nodes of Ranvier | gaps in the myelin sheath that allow the action potential to travel faster by jumping from node to node |
| Glial Cells (glia): | Provide support, nourishment, and protection to neurons Make up about half of brain and spinal cord mass |
| Nerve Regeneration: | Certain portions of neurons and some subsets of glial cells can regenerate in optimal conditions. Neurogenesis may also occur from stem cells. These findings support that a patient will have a certain amount of recovery |
| The purpose of a neuron is to | initiate, receive, and process nerve impulses or messages. |
| Synapse | junction between two neurons, where nerve impulses are transmitted from one neuron to the next or to glands or muscles |
| Neurotransmitters | chemicals that affect the transmission of impulses across the synaptic cleft |
| Excitatory neurotransmitters activate | postsynaptic receptors to increase the chances of an action potential being generated. Epinephrine, norepinephrine, glutamate |
| Inhibitory neurotransmitters activate | postsynaptic receptors to decrease the chance that an action potential will be generated-Serotonin, dopamine, y-aminobutyric acid (GABA) |
| The CNS consists of the | brain, spinal cord, and cranial nerves I and II. |
| The brain has three components: | cerebrum, brainstem, and cerebellum. |
| The cerebrum is composed of the | right and left hemispheres and 4 lobes: Frontal: memory, higher cognitive functioning, speech production Temporal: integrates visual and auditory data, speech reception Parietal: interprets spatial information Occipital: processes sight |
| Basal ganglia | voluntary movements, automatic skeletal muscle activity |
| Limbic system | concerned with emotion, aggression, feeding behavior, and sexual response |
| Diencephalon | Thalamus: major relay center for sensory input Hypothalamus: directly influences release of hormones from the anterior pituitary gland; regulates appetite, body temperature, water balance, and circadian rhythm |
| The brainstem includes the | midbrain, pons, and medulla. Contains centers for sneezing, coughing, swallowing, hiccupping, and vomiting. The medulla is concerned with respiratory, vasomotor, and heart function. |
| the Reticular Activating System (RAS) | regulates arousal, alertness, and sleep-wake transitions |
| The cerebellum coordinates | voluntary movement and maintains stability and equilibrium |
| The brain contains 4 interconnected, CSF-filled cavities called | ventricles |
| Cerebrospinal fluid (CSF) circulates within the | circulates within the subarachnoid space surrounding the brain and flows into the spinal cavity. CSF cushions the brain and spinal cord and carries nutrients to these structures. CSF is produced at an average rate of 500ml per day |
| The spinal cord is continuous with the | brainstem and exits the skull through the foramen magnum. The center of the spinal cord is composed of gray matter that contains motor neurons. The gray matter is surrounded by white matter that contains sensory and motor fibers. |
| Spinal Nerves | Nerves originating from the spinal cord that contain a pair of sensory (afferent) nerve fibers and motor (efferent) fibers Each spinal nerve innervates a specific region of the body |
| Dermatome | Area of skin innervated by the sensory fibers of a spinal nerve |
| Myotome | Muscle group innervated by the motor fibers of a spinal nerve |
| Cranial Nerves | 12 paired nerves composed of cell bodies with fibers that exit from the cranial cavity Unlike the spinal nerves, which always have both afferent sensory and efferent motor fibers, some CNs are only sensory, some only motor, and some both. |
| Autonomic Nervous System (ANS) | involuntary functions of heart muscle, smooth muscle, and glands through both efferent and afferent pathways Divided into sympathetic and parasympathetic Sympathetic NS- norepinephrine secretion Parasympathetic NS-acetylcholine secretion |
| The ANS provides | dual and often reciprocal innervation to many structures. Example: SNS increases HR and force of contraction while the PSNS decreases HR and force of contraction |
| The brain’s blood supply arises from the | internal carotid arteries (anterior circulation) and the vertebral arteries (posterior circulation) Internal carotid arteries perfuse the anterior and middle portions of the cerebrum. |
| The Circle of Willis is formed by | by communicating arteries within the brain - plays a key role in cerebral blood flow. Venous blood drains from the brain through the dural sinuses, which form channels that drain into the 2 jugular veins. |
| Blood Brain Barrier | Physiologic barrier between blood capillaries and brain tissue Protects the brain from harmful agents, while allowing nutrients and gases to enter Lipid-soluble compounds enter the brain easily. Water-soluble enter brain and the spinal cord slowly. |
| Meninges | protective membranes Dura mater: outermost layer Arachnoid: fragile, web-like membrane that lies between the dura mater and pia mater Subarachnoid space: CSF area between the arachnoid layer and pia mater Pia mater: innermost layer vascular |
| skull | Protects the brain from external trauma Composed of 8 cranial bones and 14 facial bones Foramen magnum Hole through which the brain stem extends to the spinal cord. |
| Vertebral Column | Protects the spinal cord, supports the head, and provides flexibility. Made up of 33 individual vertebrae: 7 cervical, 12 thoracic, 5 lumbar, 5 sacral (fused into 1), and 4 coccygeal (fused into 1). |
| Gerontologic Considerations neuro | Loss of neurons begins in early adulthood Ventricles enlarge, brain weight and cerebral blood flow decrease, and CSF production declines In the PNS, the myelin sheath degenerates. Cordinated neuromuscular activity like maintain BP and body temp altrd |
| ask abt what meds and surgery neuro | Sedatives, opioids, tranquilizers, and mood-elevating drugs Many drugs have neurologic side effects Surgical History Ask about any surgery involving any part of the nervous system, such as head, spine, or sensory organs or eye surgery |
| A comprehensive neuro assessment looks at | 6 categories of function: mental status, CN function, motor function, sensory function, cerebellar function, and reflexes. Neurologic assessment helps determine the presence, location, and nature of nervous system disease |
| mental status | General appearance and behavior: LOC, posture, motor activity, hygiene and dress, facial expressions, speech pattern Cognition: orientation x 4, memory, general knowledge, insight, judgement, problem solving Mood and affect: note any agitation |
| CN I | olfactory, sensory assess- close 1 nostril at a time and identify easily recognized smells |
| CN II | Optic, sensory assess- visual fields- position yourself opposite of pt. ask them to look at bridge of ur nose and indicate when an object is presneted from periphery of each of visual fields. snellen chart |
| CN III | oculomotor, MOTOR assess- pupil constriction and accommodation, cardinal fields |
| CN IV | trochlear, motor assess- test same as III |
| CN V | trigeminal, sensory and motor assess- sensory- pt closes eyes and identify light touch on both sides of face. motor- clench teeth and then palpate masseter muscle. corneal blink reflex- pt look up and away touch cornea wt cotton wisp and look for blink |
| CN VI | abducens, MOTOR assess- test same as CN III |
| CN VII | facial, sensory and motor assess- ot raises eyebrows, close eyes tight, purse lips, draw back corners of mouth in a smile, frown, note asymmetry |
| CN VIII | vestibulocochlear, sensory assess-pt closes eyes and indicate when they hear rustling of fingers. weber and rhine test |
| CN IX | glossopharyngeal, sensory and motor assess- test gag reflex, touch sides of posterior pharynx with tongue blade, pt say ah |
| CN X | vagus, sensory and motor, testing for IX |
| CN XI | accessory, motor pt shrug shoulders and turn head to side against resistance |
| CN XII | hypoglossal, motor assess- pt protrude tongue, move tongue up and down |
| Motor Function assess | Assessment includes strength, tone, coordination, and symmetry of the major muscle groups. Test muscle strength by asking the patient to push and pull against the resistance of your arm as it opposes flexion and extension of the patient’s muscle. |
| Test cerebellar function by | assessing balance and coordination finger-to-nose test (having the patient alternately touch the nose, then touch the examiner’s finger) heel-to-shin test (having the patient stroke the heel of 1 foot up and down the shin of the opposite leg) |
| Sensory Function assess | Touch, pain, and temperature: Light touch assessed with a cotton wisp or light pinprick- ask the patient to indicate when they feel the stimulus. Test pain by alternately touching the skin with the sharp and dull end of a pin. |
| Extinction is assessed by | simultaneously touching both sides of the body symmetrically. Normally, the simultaneous stimuli are both perceived. |
| Sensory Function | Position sense (proprioception) Gently move great toe or index finger up or down- ask patient to indicate direction digit was moved |
| romberg test | Patient stands with feet together and eyes closed. If the patient can maintain balance with the eyes open but sways or falls with the eyes closed (i.e., a positive Romberg test), vestibulocochlear problems may be present |
| Cortical sensory function test | graphesthesia by having the patient identify numbers traced on the palm Test stereognosis (ability to perceive the form and nature of objects) by having the patient close the eyes and identify the size and shape of easily recognized objects |
| Reflexes | 0 to 5 scale as follows: 0 = absent reflex; 1 = weak response, seen only with reinforcement; 2 = normal response; 3 = brisk response; 4 = hyperreflexia with non sustained clonus; and 5 = hyperreflexia with clonus. |
| CSF Analysis | CSF is obtained through a lumbar puncture (LP) HCP inserts needle into the L3-4 or L4-5 interspace to aspirate CSF A manometer attached to the needle is used to measure CSF pressure Normal CSF is clear, colorless, odorless |
| LP is contraindicated in the | presence of increased intracranial pressure |
| Preprocedure LP | vital signs and a baseline neurologic assessment. Notify HCP of signs of increased intracranial pressure (see Chapter 61). • Assess coagulation studies to reduce the risk for epidural hematoma.• Have patient void. • Place patient in a side-lying |
| postprocedure LP | Monitor neurologic signs and vital signs. • Monitor for headache intensity and drainage from the puncture site. • Apply pressure and a pressure dressing to the puncture site. |
| postprocedure LP pt 2 | Keep the patient in a reclining position for 1 hour or up to several hours to decrease the risk for spinal headache. The patient may to turn from side to side as long as the head is not raised. • Properly label CSF specimens and send to laboratory. |
| cerebral angiography | serial x ray visulization of intracranial and extracranial blood vessels to detect vascular lesions. catheter insterted into femoral artery for injection of contrast. |
| cerebral angiography nurse responsibilities | before- assess for stroke risk, NPO maybe, during- contrast can cause burning. monitor VS every 15-30 min first 2 hrs, every hour for next 6 hrs. assess bleeding |
| CT scan | rapid means of radiographic brain images. |
| CT scan nurse | note renal function before. assess shellfish allergy. drink plenty of fluids post |
| CTA | noninvasive imaging of vascualar system. evaluates blood volume, flow, and mean transit time |
| MRI | imaging of brain, spinal cord, spinal canal by magnetic energy. greater detail than CT |
| MRI nurse | check for pregnancy beofre, allergies, and renal function. remove all metal |
| MRA | differential signal characteristics of flowing blood to evaluate extracranial and intracranial blood vessels. |
| PET | measures metabolic avtivity of brain to assess cell death or damage. uses radioactive material that shows up as bright spot on image. |
| PET nurse | empty bladder, 2 IV lines |
| carotid artery duplex scam | noninvasive, assess degree of stenosis of carotid artery, combines ultrasound and doppler |
| EEG | electrical activity of brain using scalp electrodes. evaluates seziures, cerebral diease, CNS effects of systemic dieases, brain injury. |
| EMG | recording electrical activity associated with innervation of skeletal muscle. needle electrodes inserted into the muscle. restrict stimulants 2-3 hrs before, assess for hematoma after |
| The skull is an enclosed space with | 3 volume components: Brain tissue- 78% of total volume Blood- 12% CSF- 10% |
| Intracranial Pressure (ICP) | Hydrostatic force measured in the brain CSF compartment Balance of brain tissue, blood, and CSF maintains normal ICP Normal ICP: 5-15 mmHg; sustained ICP > 20 abnormal |
| Factors that influence ICP: | arterial pressure, venous pressure, intra-abdominal and intrathoracic pressure, posture, temperature, and blood gasses (CO2) We can measure ICP in the ventricles, subarachnoid space, subdural space, epidural space |
| Monro-Kellie Doctrine | 3 components (brain, blood, CSF) must stay at a constant volume within the enclosed skull If 1 component increases and the volume of another is displaced, the total intracranial volume will not change. Only applicable if skull is closed. |
| Normal Compensatory Adaptations | Changing CSF volume Altering absorption or production; displacement Changing intracranial blood volume Cerebral vasoconstriction or dilation, collapse of cerebral veins, altering venous outflow Altering brain tissue volume |
| Cerebral Blood Flow | Amount of blood (in mL) passing through 100g of brain tissue in 1 minute 50 mL/min/100g of brain tissue Maintaining CBF is critical because the brain requires a constant supply of O2 and glucose |
| Autoregulation of Cerebral Blood Flow | Automatic adjustment in cerebral blood vessel diameter by the brain to maintain constant blood flow with changes in arterial BP Ensures consistent CBF and maintains cerebral perfusion pressure WNL Autoregulation effective when MAP between 70-150 mmHg |
| Cerebral Perfusion Pressure (CPP) | Pressure needed to ensure blood flow to the brain CPP = MAP - ICP Normal CPP 60-100 mmHg As CPP decreases, autoregulation fails and CBF decreases CPP may not reflect perfusion pressure in all parts of the brain |
| MAP= | SBP+ 2 (DBP)/3 |
| Factors Affecting Cerebral Blood Flow (CBF) | Arterial blood CO2 PaCO2 ↑ = vasodilation and ↑ CBF PaCO2 ↓ = vasoconstriction and ↓ CBF Arterial blood O2 (PaO2) PaO2 ↓ = vasodilation and ↑ CBF, which ↑ PaO2 Hydrogen ion concentration vasodilate in response to increased hydrogen |
| Increased Intracranial Pressure | Results from an increase in any or all of the 3 components (brain tissue, blood, CSF) within the skull ↑ ICP = decreased CPP and increased risk for brain ischemia and infarction Life threatening, poor prognosis |
| Common causes of increased ICP include a | mass (e.g., hematoma, contusion, abscess, tumor) and cerebral edema (from brain tumors, hydrocephalus, head injury, brain inflammation). |
| Herniation occurs as the | brain tissue is forcibly shifted from a compartment of greater pressure to a compartment of less pressure. Herniation forces the cerebellum and brainstem downward through the foramen magnum. Compression of respiratory center causes respiratory arrest |
| Cerebral Edema | Increased accumulation of fluid in the extravascular spaces of brain tissue Cerebral edema = increase in brain tissue volume and ↑ ICP |
| Increased Intracranial Pressure manifestations | Change in LOC Most sensitive and reliable indicator of neurologic status Result of impaired CBF, which causes O2 deprivation to reticular activating system (RAS) Changes may be subtle or dramatic (coma) Changes in Vital Signs-Cushing’s Triad |
| Cushing’s Triad | systolic HTN with widening pulse pressure, bradycardia, irregular respirations Medical emergency, sign of impending death |
| Increased Intracranial Pressure manifestations pt 2 | Ocular Signs Result of compression of CN II, III, IV, and VI Pupillary changes, changes in eye movements, diplopia, blurred vision Fixed, dilated (blown) pupil is a neurologic emergency that indicates severe brain damage |
| Increased Intracranial Pressure manifestations pt 3 | Decorticate (flexor): internal rotation and adduction of the arms with flexion of the elbows, wrists, and fingers, extension of the legs Decerebrate (extensor): arms are stiffly extended, adducted, and hyperpronated; hyperextension of legs plantar feet |
| Increased Intracranial Pressure manifestations pt 4 | Headache Compression of intracranial structures, such as arteries, veins, and CNs, can cause a headache Nocturnal headache and/or a headache in the morning may indicate a tumor Unexpected vomiting not preceded by nausea |
| Increased Intracranial Pressure diagnostics | CT and MRI may identify a cause EEG, cerebral angiography, PET scan, ICP measurement and transcranial doppler LP is contraindicated with suspected increased ICP Risk of cerebral herniation from sudden release in pressure |
| Monitoring ICP | Ventriculostomy: specialized catheter inserted into ventricle, connected to an external transducer Measures the pressure within the ventricles, facilitates removal of CSF |
| Monitoring ICP infection | Infection is a serious complication with ICP monitoring. Routinely assess the insertion site and use aseptic technique. Monitor the CSF for a change in drainage color or clarity. |
| Increased Intracranial Pressure management | Identify and treat the underlying cause Support brain function Patient may need mechanical ventilation ABGs guide O2 therapy Maintain PaO2 ≥ 100 Maintain PaCO2 between 35-45 |
| Increased Intracranial Pressure management pt 2 | Metabolic demands, such as fever (greater than 100.4°F [38°C]), agitation, shivering, pain, and seizures, can increase ICP. Prophylactic anti-seizure medication Antipyretics, cool baths or ice packs keep temp 96.8- 98.6°F Prevent shivering |
| Increased Intracranial Pressure Mannitol (Osmitrol) | Osmotic diuretic, given IV Pulls fluid from brain tissue into blood vessels → reduces brain fluid content and ↓ ICP Monitor fluid and electrolyte status May be contraindicated with renal disease |
| Increased Intracranial Pressure drugs Hypertonic Saline | Causes massive movement of water out of edematous swollen brain cells and into blood vessels Reduces cerebral edema, ↑ CBF, and ↓ ICP Monitor serum Na, BP, and S/S of fluid volume overload |
| Increased Intracranial Pressure drugs Corticosteroids (dexamethasone) | Used to treat edema around tumors and abscesses May cause hyperglycemia, infections, and GI bleeding |
| Increased Intracranial Pressure drugs 0.9% normal saline | preferred solution for giving secondary medications. D5W or 0.45% NS may decrease serum osmolality and increase cerebral edema |
| Increased Intracranial Pressure Nutrition Therapy | Malnutrition promotes cerebral edema Early feeding and nutritional support may improve patient outcomes Supplements, electrolyte replacements, and enteral or parenteral nutrition may be needed |
| Increased Intracranial Pressure assessment | Glasgow Coma Scale (GCS) Quick, standard assessment of LOC Assesses 3 areas: eye opening, best verbal response, best motor response The total GCS score is the sum of the numeric values assigned to each of the 3 areas |
| GCS score of | 8 or less generally indicates coma. |
| Increased Intracranial Pressure pupils | Fixed pupil unresponsive to light stimulus usually indicates increased ICP If corneal reflex is absent, routine eye care is needed. |
| Oculocephalic/ Doll’s Eye Reflex | Turn the patient’s head briskly to the left or right while holding the eyelids open A normal response is movement of the eyes across the midline in the direction opposite that of the turning- Positive reflex Negative reflex: eyes remain midline |
| Oculovestibular/ Cold Caloric Reflex ICP | Instill a syringe of ice-cold water into the external auditory ear canal Assess the patient’s eyes for a total of 1 minute. A normal response is nystagmus or jerking movements of the eye absence of eye movement or response indicates neurologic demise |
| ICP Respiratory Function care | Maintain a patent airway GCS < 8 requires intubation for airway protection Snoring sounds indicate obstruction and require immediate intervention. Minimize frequency and duration of suctioning; < 10 seconds in duration |
| Increased Intracranial Pressure sedation | Pain, anxiety, therapeutic procedures, or noxious stimuli can increase ICP Minimize stimulation Opioids, IV sedation (propofol, dexmedetomidine), paralytics (vecuronium), benzodiazepines may be used |
| Increased Intracranial Pressure body position | Keep head midline, avoiding extreme neck flexion Position HOB so that it lowers ICP while optimizing CPP Elevating HOB promotes drainage from head and can decrease cerebral edema Elevating HOB > 30° can decrease CPP |
| ICP Monitoring and safety | Avoid coughing, straining, sneezing, and the Valsalva maneuver Safety Increased risk of injury from confusion, agitation, and seizures Use restraints carefully Seizure precautions Calm, reassuring approach |
| Head Injury | Most common causes are falls and motor vehicle accidents Deaths from head trauma occur at 3 points after injury: immediately after the injury, within 2 hours after injury, and about 3 weeks after injury. Scalp Lacerations Profuse bleeding occurs |
| Comminuted | Multiple linear fractures with fragmentation of bone into many pieces |
| Compound | Depressed skull fracture and scalp laceration with communicating pathway to intracranial cavity |
| Depressed fracture | Inward indentation of skull |
| Basilar Skull Fracture | Linear fracture involving the base of the skull Battle’s Sign: postauricular bruising Periorbital bruising (raccoon eyes) Dura tear and subsequent leakage of CSF |
| Rhinorrhea or otorrhea confirms that | fracture has extended into dura CSF leak = high risk for meningitis; prophylactic antibiotics How to test for CSF in ear or nose drainage: Test for glucose with test strips; CSF will be positive for glucose |
| Halo sign | Collect drainage on gauze pad Blood will pool to the center, and CSF creates a yellowish ring, encircling the blood |
| Head Trauma | Brain injuries are categorized as diffuse (generalized) or focal (localized) Diffuse: not localized to 1 area of the brain, more widespread Focal: damage is localized to a specific area of the brain |
| Concussion | Sudden transient mechanical head injury with disruption of neural activity and a change in LOC Brief disruption in LOC, amnesia about the event, and headache Patient may or may not lose consciousness Short duration; resolves spontaneously |
| Post-concussion syndrome | may develop 2 weeks to 2 months after injury persistent headache, lethargy, personality and behavior changes, shortened attention span, decreased short-term memory, and changes in intellectual ability |
| Laceration | Tearing of the brain tissue Often occur in depressed and open fractures and penetrating injuries; severe tissue damage Management consists of antibiotics (until meningitis is ruled out) and preventing secondary injury from increased ICP. |
| Laceration surgery is | impossible |
| Contusion | Bruising of the brain tissue within a focal area Usually associated with a closed head injury; often occurs at a fracture site May be areas of bleeding, infarction, necrosis, and edema Increased bleeding and mortality rate with anticoagulant use |
| Coup-Contrecoup Injury | Damage occurs when brain moves inside the skull from high-impact injuries Contusions or lacerations at site of direct impact of brain on skull- coup Second area of damage on opposite side- contrecoup Leads to multiple contused areas |
| Epidural Hematoma | Bleeding occurs in epidural space between dura mater and skull Neurologic emergency Can be venous or arterial Venous: tear of dural venous sinus; develop slowly Arterial: tear of middle meningeal artery; develops rapidly |
| Epidural Hematoma signs | initial period of unconsciousness at the scene → brief lucid period → decrease in LOC; headache, nausea, vomiting, focal deficits Requires rapid surgical intervention to evacuate hematoma and ↓ ICP |
| Subdural Hematoma | Bleeding in the subdural space between the dura mater and arachnoid layer of meninges Usually a venous bleed; typically develop more slowly May be acute, subacute, or chronic |
| Subdural Hematoma acute s/s | : manifests within 24-48 hours after injury S/S include ↓ LOC and headache from ↑ ICP and brain tissue compression Size of hematoma determines prognosis and presentation LOC may range from drowsy to confused to unconscious Ipsilateral pupil fixed |
| Subdural Hematoma | Subacute: manifests 2-14 days after injury Gradual decline in mental status as hematoma develops Hematoma may appear to enlarge over time as the breakdown products of the blood draw fluid into the subdural space |
| Subdural Hematoma chronic | develops over weeks or months after seemingly minor head injury More common in older adults Larger subdural space in older adults = ↓ ICP More focal S/S |
| Intracerebral Hematoma | Bleeding within the brain tissue; usually from a laceration Unconsciousness, hemiplegia on contralateral side, dilated pupil on ipsilateral side |
| Subarachnoid Hemorrhage | Bleeding in subarachnoid space |
| Head Trauma diagnostics | CT scan is the best test to evaluate head trauma Allows for rapid diagnosis and intervention MRI scan is more sensitive at detecting small lesions Cervical spine trauma often occurs with a head injury Cervical spine X-rays; CT or MRI of spine |
| Head Trauma diagnostics Interprofessional Care | Rapid diagnosis Surgery if indicated Prevent secondary injury by treating cerebral edema and managing ICP Skull fractures usually treated conservatively; surgery if depressed fracture or loose fragments |
| Head Injury Nursing Management | Prevention of head injuries is key Teach about distracted, drunk, or drugged driving; helmet use when riding bikes or motorcycles, and seatbelt use to prevent injuries from car and motorcycle crashes. |
| Head Injury acute care | Frequent neuro assessments and GCS; report any signs of deteriorating neuro state, even if subtle Lubricating eye drops or taping eyes shut if loss of corneal reflex Interventions to prevent/reduce fever and prevent shivering Fever ↑ ICP and metabolic |
| Head Injury ambulatory care | Patients usually require rehabilitation after they are stabilized May have chronic problems related to motor and sensory deficits, communication, memory, and intellectual functioning Posttraumatic seizures may develop within hours to years after |
| primary brain tumors | arise from tissues within the brain Classified according to the tissue from which they arise Meningiomas are most common Rarely metastasize outside of the CNS |
| secondary brain tumors | result from metastasis of cancer from elsewhere in the body Metastatic brain tumors are most common Lung and breast cancer most commonly metastasize to the brain. |
| Brain Tumors manifestations | Headache- worse at night; usually dull and constant Seizures Nausea/vomiting Memory problems, mood/personality changes Muscle weakness, aphasia, sensory losses Hydrocephalus |
| Brain Tumors diagnostics | CT and MRI to identify location and size of lesions MRI and PET scans allows for detection of small tumors and may provide better diagnostic information than a CT Cerebral angiography can assess blood flow to the tumor and further localize the tumor |
| brain tumors surgical therapy | Surgical removal is preferred treatment Complete removal is not always possible Can reduce mass, ↓ ICP, relieve S/S, and extend survival time |
| brain tumors Ventricular Shunts | Placed to treat hydrocephalus from obstructive tumor Catheter with 1-way valve placed in lateral ventricle and tunneled under skin to drain CSF into peritoneal cavity Avoid rapid drainage by gradually changing patient position when sitting upright |
| Shunt malfunction s/s | : HA, restlessness, ↓ LOC, vomiting |
| Brain Tumors radiation | May be used after surgery Radiation seeds can be implanted into brain Radiation may cause cerebral edema and rapidly ↑ ICP Treated with high dose corticosteroids |
| Stereotactic Radiosurgery | Method of delivering a highly concentrated dose of radiation to a precise location within the brain |
| Brain Tumors chemo | Cancerous tumors may cause a breakdown of the blood-brain barrier in the area of the tumor, allow chemotherapy to target the area. Chemotherapy wafers can be implanted during surgery and deliver treatment directly to tumor |
| Indications for cranial surgery: | Aneurysm repair Arteriovenous (AV) malformation Brain abscess Tumor Hydrocephalus Bleeding Skull fracture |
| Craniotomy | Opening into cranium with removal of bone flap and opening the dura to remove a lesion, repair a damaged area, drain blood, or relieve ↑ ICP. After surgery, the bone flap is secured with small plates or wired shut. |
| Stereotactic Procedures | Computer guided to precisely target an area of the brain Used for removal of small brain tumors and abscesses, drainage of hematomas, ablative procedures for extrapyramidal diseases (e.g., Parkinson disease), and repair of arteriovenous malformations |
| Burr hole | Opening into the cranium with a drill. Used to remove localized fluid and blood beneath the dura. |
| Cranioplasty | Repair of cranial defect resulting from trauma, malformation, or previous surgery. Artificial material used to replace damaged or lost bone. |
| Bacterial Meningitis | Acute inflammation of the meningeal tissues surrounding the brain and spinal cord College students living in dormitories and people living in institutions (e.g., prisoners) have a high risk for meningitis Streptococus pneumonia and Neisseria causes it |
| Bacterial Meningitis Organisms usually gain entry to the | CNS through the upper respiratory tract or bloodstream Can also enter by direct extension from penetrating skull wounds or through fractured sinuses in basilar skull fractures. |
| Bacterial Meningitis pt 2 | Inflammatory response to the infection increases CSF production with a moderate increase in ICP Purulent secretions quickly spread to other areas of the brain through the CSF; cerebral edema and increased ICP become more of a problem |
| Bacterial Meningitis Manifestations | Fever, severe headache, nausea, vomiting, and nuchal rigidity (neck stiffness) are key signs of meningitis Photophobia, a decreased LOC, and signs of increased ICP may be present Seizures, coma If the infecting organism is a meningococcus, a skin rash |
| Bacterial Meningitis Complications | ↑ ICP, major cause of AMS Residual neurologic dysfunction involving CNs Papilledema, blindness, unequal pupils, tinnitus, vertigo, deafness (may be permanent) Hemiparesis, dysphasia, and hemianopsia- usually resolve over time Chronic headaches |
| Bacterial Meningitis Diagnostics | Blood cultures Head CT CT scans may show signs of increased ICP or hydrocephalus LP with CSF analysis Specimens of the CSF, sputum, and nasopharyngeal secretions are taken for culture before the start of antibiotic therapy |
| Bacterial Meningitis Interprofessional Care | Medical emergency Rapid diagnosis is crucial Ampicillin, penicillin, vancomycin, cefuroxime, ceftriaxone, and ceftazidime Dexamethasone |
| Bacterial Meningitis Health Promotion | Prevention of respiratory tract infections through vaccination for pneumococcal pneumonia and influenza Meningococcal vaccines are available that protect against the serogroups |
| Bacterial Meningitis Acute Care | Administer antibiotics, analgesics, anti-seizure drugs, and antipyretics Codeine may be used for head and neck pain without excess sedation Fever increases cerebral edema droplet isolation slighty elevate HOB Seizure precautions-prevent shivering |
| Bacterial Meningitis Ambulatory Care | Patients require several weeks of recovery before resuming normal activities High protein, high calorie diet Muscle rigidity may persist in neck and legs ROM exercises Increase activity as tolerated, frequent rest periods |
| Viral Meningitis | Most common causes are enteroviruses, arboviruses, human immunodeficiency virus, and herpes simplex virus (HSV) Headache, fever, photophobia, and stiff neck Xpert EV test rapidly diagnose viral meningitis CSF can be clear or cloudy,lymphocytosis |
| Brain Abscess | Accumulation of pus within the brain tissue from a local or systemic infection Direct extension from an ear, tooth, mastoid, or sinus infection is the main cause Streptococci and Staphylococcus aureus are the most common infective organisms |
| Brain Abscess s/s/treat | HA, fever, and nausea and vomiting. Signs of increased ICP may include drowsiness, confusion, and seizures Focal S/S Treated with antibiotics Abscess may have to be drained or removed if encapsulated |
| Encephalitis | Acute inflammation of the brain Usually caused by a virus Ticks and mosquitoes transmit epidemic encephalitis Eastern equine, La Crosse, St. Louis, West Nile, and Western equine Non-epidemic encephalitis may occur as a complication of mumps |
| HSV encephalitis is the most | most common cause of acute non-epidemic viral encephalitis |
| Encephalitis s/s | May be acute or subacute Fever, headache, nausea, and vomiting CNS signs appear on day 2 or 3 Range from minimal changes in mental status to coma |
| Encephalitis diagnose | CT or MRI PCR test for West Nile Virus and HSV West Nile virus should be strongly considered in adults over 50 years old who develop encephalitis or meningitis in summer or early fall |
| Encephalitis Nursing Management | Prevention focuses on mosquito control Removing standing water where mosquitoes can breed Insect repellent Symptomatic treatment Acyclovir (Zovirax) is used to treat encephalitis caused by HSV infection |
| Dementia | Disorder characterized by a decline from the previous level of function in 1 or more cognitive domains: complex attention, executive function, language, learning and memory, perceptual-motor, and social cognition Interferes with ADLs |
| Dementia patho | Caused by treatable and untreatable conditions Most commonly caused by neurodegenerative conditions that cannot be reversed Alzheimer’s, dementia with Lewy bodies, frontotemporal dementia , Parkinson’s Disease with dementia, vascular dementia |
| dementia manifestations | Onset of symptoms depends on cause of dementia Neurologic degeneration usually occurs gradually and progresses over time Symptoms of vascular dementia may appear abruptly (stroke) Acute changes that occur over weeks or months may indicate infection |
| dementia diagnostics | Thorough medical, neurologic, and psychologic history Pay special attention to cognitive and behavioral changes Family members or significant others can give important information, diet, tremors, CT/MRI, LFTs, CBC, thyroid, genetic test |
| Alzheimer Disease | Chronic, progressive, irreversible neurodegenerative brain disease Most often affects persons age 65 and older Early onset AD occurs in patients younger than 60 Progresses slowly |
| Alzheimer Disease etiology | Exact cause is unknown, likely multiple factors involved Age is the greatest risk factor but AD is not a normal part of aging Women are more likely to develop AD than men, mainly because they live longer, onset before 60, rapid course |
| Alzheimer Disease etiology pt 2 | Diabetes increases the risk of developing AD Insulin resistance may interfere with body’s ability to break down amyloid. DM damages small blood vessels in the brain. High blood glucose and high cholesterol have a role in atherosclerosis |
| Alzheimer Disease patho | amyloid plaques, neurofibrillary tangles, loss of connections between neurons, and (4) neuron death In AD, excess plaques develop first in areas of the brain used for memory and cognitive function, including the hippocampus.then attacks cerebral cortex |
| Alzheimer Disease patho pt 2 | Plaques consist of clusters of insoluble deposits of a protein called β-amyloid Overproduction of β-amyloid is an important risk factor for AD. Abnormally high levels of β-amyloid cause cell damage and ultimately neuron death. |
| Alzheimer Disease patho pt 3 | Neurofibrillary tangles are abnormal collections of twisted protein threads inside nerve cells. The main component of these structures is a protein called tau. In AD, tau protein is altered. As a result, the microtubules twist together |
| Alzheimer Disease s/s | Initial manifestations: Memory loss, mild disorientation, or trouble with words and numbers- often first reported by a family member Memory loss initially relates to recent events, with remote memories still intact. |
| Alzheimer Disease s/s pt 2 | Unpredictable behaviors, aggression, agitation result from ongoing neuron loss Delusions, hallucinations Aphasia, apraxia, visual agnosia, and dysgraphia develop as AD progresses Eventually, long term memories are lost |
| Alzheimer Disease-Retrogenesis | Process in which the decline in AD mirrors, in reverse order, brain development that occurs from birth Compares the developmental stages of childhood with the deterioration of patients with AD |
| Alzheimer Disease diagnosis | AD is considered on a spectrum Stages are preclinical AD, mild cognitive impairment, and dementia |
| Alzheimer Disease-Preclinical Stage | A long lag exists between pathologic changes in the brain and manifestations of AD. Brain changes, including amyloid buildup and other early neuron changes, may already be in process No significant symptoms yet |
| Alzheimer Disease-Mild Cognitive Impairment (MCI) | problems with memory, language, or other essential cognitive functions Problems are severe enough to be noticed by the person having them and by others and can be found on tests do not interfere with daily activities, no dementia |
| Alzheimer Disease Diagnostic Studies | diagnosis of exclusion Health history, physical assessment, neurologic, and mental status exams, and lab tests A definitive diagnosis of AD requires an examination of brain tissue at autopsy and findings of neurofibrillary tangles and plaques. |
| Alzheimer Disease Diagnostic Studies pt 2 | Repeated at regular intervals during the course of care to assess changes in cognitive status Mini-Cog-repeat 3 words, draw clock, repeat 3 words, Mini Mental State Exam,Montreal Cognitive Assessment |
| Alzheimer Disease Interprofessional Care | No cure for AD Treatment does not stop neurodegeneration Care is aimed at controlling undesirable behavior manifestations and providing support for family and caregivers |
| Cholinesterase Inhibitors | for AD, Block cholinesterase, the enzyme that breaks down acetylcholine in the synaptic cleft donepezil (Aricept), rivastigmine (Exelon), and galantamine (Razadyne). Rivastigmine is available as a patch |
| N-methyl-d-aspartate (NMDA) receptor antagonist | for AD, memantine (Namenda) Protects the brain’s nerve cells by blocking the action of glutamate Large amounts of glutamate are released in AD, leading to cellular degeneration |
| Selective Serotonin Reuptake Inhibitors (SSRIs) | for AD depression, fluoxetine (Prozac), sertraline (Zoloft), and citalopram (Celexa), Atypical antidepressants trazodone, mirtazapine (Remeron) |
| Antipsychotics | for AD behavior problems, Should only be used when agitation and psychosis are severe, dangerous, and cause significant distress Aripiprazole (Abilify), haloperidol (Haldol), olanzapine (Zyprexa), quetiapine,risperidone |
| Benzodiazepines | For AD behavior issues, Clonazepam (Klonopin), lorazepam (Ativan) |
| Alzheimer Disease Behavioral Problems | Occur in 90% of patients with AD Repetitiveness, delusions, hallucinations, agitation, aggression, wandering, hoarding, sleeping problems, resisting care Behaviors may be unpredictable; not intentional |
| Sundowning AD | patient becomes more confused and agitated in the late afternoon or evening Behaviors related to sundowning include agitation, aggressiveness, wandering, resistance to redirection, and increased verbal activity, such as yelling |
| Sundowning interventions | creating a quiet, calm environment; (2) maximizing exposure to daylight by opening blinds and turning on lights during the day; (3) evaluating medications to determine if any could cause sleep problems; (4) limiting naps and caffeine |
| Infection Prevention AD | UTIs and pneumonia are most common Risk for aspiration pneumonia Manifested by change in behavior, fever, cough, or pain on urination |
| Delirium | State of confusion that develops over days to hours Decreased ability to direct, focus, sustain, and shift attention and awareness Deficits in memory, orientation, language, visuospatial ability, or perception may be present Sleep may be disturbed |
| Delirium patho | contributing factor is impaired cerebral oxidative metabolism, in which the brain gets less oxygen and has problems using it. Neurotransmitter abnormalities may be involved: Cholinergic deficiency, excess dopamine, increased or decreased serotonin |
| delirium risk factors | Risk factors include age, pre-existing dementia, hypertension, alcohol use, and severe illness on admission Dementia is the leading risk factor for delirium. |
| Delirium etiology | Sleep deprivation, stress, sensory overload, immobilization, electrolyte imbalances, infection, and drug use can lead to delirium Most often occurs among hospitalized older adults May be the first symptom of life-threatening problems |
| Delirium s/s | Usually develops over a 2- to 3-day period Delirium can last from 1 to 7 days Memory, judgment, and orientation are impaired Speech is rapid, rambling, and/or incoherent Disorganized thinking, irritability, insomnia |
| Delirium diagnostics | The Confusion Assessment Method (CAM) is a reliable tool for assessing delirium (Table 64.19) Explore potential causes Laboratory tests include CBC, serum electrolytes, BUN, and creatinine levels; ECG; urinalysis; liver and thyroid function tests O2 |
| Delirium management | Many cases of delirium are potentially reversible Eliminate precipitating factors Discontinue medications, correct fluid and electrolyte disturbances and nutritional deficiencies, antibiotics for suspected infection |
| Delirium drug therapy | for severe agitation, cautiously due to psychoactive properties Dexmedetomidine (Precedex), an α-adrenergic receptor agonist, has been used in ICU settings for sedation Low-dose antipsychotics (e.g., haloperidol, risperidone [Risperdal]) |
| can be used to treat delirium from sedative and alcohol withdrawal | Short-acting benzodiazepines (e.g., lorazepam [Ativan]) |
| Primary Headaches | are not caused by a disease or another medical problem Tension-type, migraine, and cluster headaches |
| Secondary Headaches | are caused by another disease or problem, such as sinus infection, neck injury, or brain tumor. |
| Tension-Type Headache (TTH) | Most common type Presents bilaterally with pressing or tightening quality Mild to moderate in severity Can last for minutes to days Episodic or chronic |
| Tension-Type Headache (TTH) Etiology and Pathophysiology | Cause is unknown May be triggered by stress, depression, anxiety, smoking, or caffeine |
| Tension-Type Headache (TTH) s/s | Bilateral frontal-occipital bandlike pain or dull pressure May have neck pain, photophobia, or sensitivity to sound (phonophobia) No prodromal symptoms |
| Migraine Headaches | Recurring headache characterized by unilateral throbbing pain Most common between the ages of 25 and 55 2 categories: migraine without aura and migraine with aura |
| Migraine Headaches Etiology and Pathophysiology | Interactions between trigeminal nerve, vascular, genetic, hormonal, and environment factors causing vasodilation and inflammation in the brain State of neuron hyperexcitability in the cerebral cortex Risk factors include age, female gender, obesity |
| Migraine Headaches Manifestations | Change in activity level, depression, fatigue, pallor, yawning, or difficulty concentrating Pain is unilateral, pounding is synchronous pulse and worsens with movement 4 - 72 hours |
| aura | neurologic symptoms that occur before a headache begins Visual, sensory, aphasic Visual: flashes of bright lights, blind spots, distortions, or zigzag lines Sensory: tingling or numbness in the fingers or in the mouth, voices that do not exist |
| Cluster Headache | Most severe Affects the trigeminal nerve (CN V) Has associated autonomic symptoms (e.g., tears, stuffy nose) Age at onset is often 20 to 50 years More common in smokers and men |
| Cluster Headache Etiology and Pathophysiology | May be genetic component Many attacks occur at night, waking patient from sleep Alcohol, caffeine, and tyramine foods-older fermented food, strong odors, getting overheated, and high altitudes can be triggers |
| Cluster Headache Manifestations | Severe, intense pain lasting from 15 minutes to 3 hours Pain is sharp and stabbing, described as excruciating Usually around the eye, radiating to the temple, forehead, cheek, nose, teeth, or jaw along the CN V pathway swelling around eye, pallor,flush |
| Cluster Headache Manifestations pt 2 | be agitated and restless, unable to sit still or relax Headaches occur in clusters, recurring regularly A cluster typically lasts 4 to 12 weeks, then the patient goes into remission for months to years usually occur at the same time in the day |
| Headaches diagnostics | No specific laboratory or radiologic test can diagnose or differentiate headache types A headache diary can be useful CT scan, MRI, or magnetic resonance angiography (MRA) may rule out an aneurysm, tumor, or infection |
| Drug Therapy: Tension-Type Headaches Symptomatic/Abortive | Aspirin, acetaminophen, or NSAIDs used alone or in combination with caffeine, a sedative, or a muscle relaxant Combination drugs: butalbital/acetaminophen/caffeine (Fioricet) and butalbital/aspirin/caffeine (Fiorinal) |
| Drug Therapy: Tension-Type Headaches Preventative | Tricyclic antidepressants (amitriptyline, doxepin, nortriptyline) Anti-seizure medications (topiramate [Topamax], divalproex [Depakote]) Muscle relaxants |
| Drug Therapy- Migraine Headaches Abortive/Symptomatic Treatment | Serotonin receptor agonists (triptans)-vasoconstrict First treatment severe migraines Reduce neurogenic inflammation of cerebral blood vessels Most effective when taken at start of a migraine or during aura,Contraindicated for people with heart disease |
| Drug Therapy- Migraine Headaches Abortive/Symptomatic MEDS | Serotonin receptor agonists (triptans) almotriptan eletriptan (Relpax) frovatriptan (Frova) naratriptan (Amerge) rizatriptan (Maxalt) |
| Drug Therapy- Migraine Headaches Abortive/Symptomatic Treatment part 2 | Alpha-Adrenergic Blockers Vasoconstrict vessels in brain Ergotamine and dihydroergotamine Contraindicated with cardiovascular disease and other vasoconstricting medications |
| Drug Therapy- Migraine Headaches Preventative | Anti-Seizure Drugs topiramate, divalproex, valproate Taken daily Side effects include hypoglycemia and cognitive changes Take 2 to 3 months to reach full effectiveness dont stop abruptly |
| beta blockers for migraine | preventative, propranolol (Inderal), metoprolol (Lopressor), and atenolol (Tenormin) |
| Tricyclic Antidepressants for migraine | Amitriptyline, doxepin, nortriptyline PREVENTIVE |
| Botulinum toxin A (Botox) for migraines | preventive, Given by multiple injections around the head and neck into the pain fibers involved in HAs Maximum benefit may not be seen for up to 6 months Injections are usually given every 3 months |
| CGRP Antagonists for migraines | preventative, Block the effect of CGRP, a small protein involved with pain transmission CGRP levels increase during a migraine attack Injectable agents include erenumab (Aimovig), fremanezumab (Ajovy), and galcanezumab (Emgality) Ubrogepant orally |
| Drug Therapy- Cluster Headaches Abortive/Symptomatic Treatment | Triptans Alpha Adrenergic Blockers High flow O2 therapy 100% O2 at 7-12 L/min per non rebreather mask for 20 minutes relieves pain by causing vasoconstriction and reducing inflammation in the brain |
| Drug Therapy- Cluster Headaches Preventative | High-dose verapamil is the first-choice drug to prevent cluster headache Anti-seizure meds, and CGRP antagonists may be used |
| Seizure | Sudden abnormal, excessive, electrical discharge of neurons in the brain During a seizure, multiple neurons fire at a rate much faster than normal → involuntary movements, sensory phenomena, emotional expression, and unusual behaviors |
| Seizure disorder (epilepsy) | Group of neurologic diseases marked by recurring seizures 2 or more seizures more than 24 hours apart without an underlying problem that caused the seizure |
| Seizures patho | idiopathic generalized epilepsy (IGE) Known causes include stroke, brain tumors, cerebral infection, traumatic brain injury, hypoxic birth injury, neurodevelopmental disorders or neurodegenerative disease. Acute causes include low or very high glucose |
| Seizure disorder is characterized by a | group of abnormal neurons that seem to fire without a clear cause May happen due to the release of excitatory neurotransmitters or by an absence of neuro inhibitory activity |
| seizure focus | the place where the seizure originates |
| Localizing the seizure focus (the place where the seizure originates) is | critical to the success of any surgical treatment. |
| Seizures s/s | Prodromal phase: sensations changes that precede a seizure by hours Aural phase: sensory warning that is similar each time a seizure occurs Ictal phase: from 1st symptoms to the end of seizure activity Postictal phase: recovery |
| 3 major classes based on where the seizure activity begins: | generalized onset, focal onset, and unknown onset Seizures within each classification can be motor or nonmotor. Seizures may begin with a single focus but may spread and become generalized throughout the brain. |
| Generalized-onset seizures | Start over wide areas of both sides of the brain Characterized by bilateral, synchronous neural discharges Patient has impaired consciousness for few seconds to several minutes |
| types of generalized seizures | Generalized onset motor seizure = Tonic Clonic seizure Generalized onset non-motor seizure = Absence seizure |
| Tonic-clonic seizures | Most common generalized onset motor seizure Patient loses consciousness and, if upright, falls to the ground Body stiffens (tonic phase) for 10 to 20 seconds and then the extremities jerk (clonic phase) May last 30 to 40 seconds up to several minutes, |
| Typical absence seizure: | sudden onset brief staring spell that resembles daydreaming and sudden recovery Often goes unnoticed because it lasts less than 10 to 20 seconds. Usually, the patient is unresponsive when spoken to during the seizure |
| Atypical absence seizure: | staring spell is accompanied by other signs and symptoms Eye blinking or jerking movements of the lips and repetitive finger movements (automatisms) |
| Focal Onset Seizures | Begin in 1 hemisphere of the brain in a localized region of the cortex Cause sensory, motor, cognitive, or emotional manifestations based on the function of the involved area of the brain May be motor or non-motor |
| Focal Onset Seizures: Motor | Tonic: sustained stiffening; increased muscle tone Clonic: rhythmic jerking or clonus/twitching Myoclonic: very rapid, irregular, brief jerking Atonic: loss of tone, relaxed muscles/flaccidity |
| Focal Onset Seizures: nonMotor | emotional manifestations or autonomic symptoms |
| Psychogenic Nonepileptic Seizures | Imitate seizures but are triggered by emotional events, not neuronal activity May be misdiagnosed as a seizure disorder Proper diagnosis usually requires video-EEG monitoring during the attack A history of emotional or physical abuse |
| Psychogenic Nonepileptic Seizures treat | cognitive behavioral therapy and serotonin reuptake inhibitors. |
| Status Epilepticus | State of continuous seizure activity Defined as any seizure lasting longer than 5 minutes or occurring so close together the patient cannot recover between them Patient does not return to consciousness between seizures |
| Status Epilepticus pt 2 | Neurologic emergency During repeated seizures, the brain uses more energy than the body can supply → neurons become exhausted and cease to function → permanent brain damage |
| Without treatment of status epilepticus | CSE can lead to respiratory insufficiency, hypoxemia, dysrhythmias, hyperthermia, and systemic acidosis → death |
| seizures diagnostics | EEG May be normal between seizures Abnormal EEG can help determine type of seizure and pinpoint focal location Video or continuous EEG may be needed CBC, serum chemistries, liver and kidney function test for metabolic issues, CT, MRI |
| seizures drug therapy | Goal of therapy is to prevent seizures with minimal drug side effects Most drugs stabilize nerve cell membranes and prevent spread of the epileptic discharge Therapy should begin with a single drug and dosage increased until seizures are under control |
| Treatment of status epilepticus and active tonic-clonic seizures requires a | rapid-acting antiseizure drug Benzodiazepines are most common: IV lorazepam (Ativan) is preferred, IV diazepam (Valium) Followed up with long acting drugs |
| Benzodiazepines effects | vision changes, drowsiness, ataxia, and mental slowness |
| Patient must be seizure free for a | prolonged period (e.g., 2–5 years) and have a normal neurologic assessment and EEG before drug weaning can be considered. |
| Common side effects of seizure medications: | Blood dyscrasias: abnormal blood counts ↓ platelets and ↑ WBC Monitor CBC Monitor for bruising and bleeding Slurred speech, confusion, sedation, drowsiness Implement safety measures and fall prevention Liver toxicity Avoid alcohol |
| Hydantoins for seizures | - Phenytoin (Dilantin) - Fosphenytoin -May turn urine pink-red/brown -Hirsutism -Gingival hyperplasia - good oral care with soft toothbrush |
| Iminostilbenes for seizures | carbamazepine (Tegretol) -oxcarbazepine (Trileptal) |
| Succinimides for seizures | -ethosuximide -methsuximide -stop if rash occurs |
| valproates for seizures | -valproic acid (Depakene) -divalproex (Depakote) -Suicidal thoughts -Weight gain |
| Miscellaneous Anti-seizure Medications | gabapentin (Neurontin) lacosamide (Vimpat) lamotrigine (Lamictal) levetiracetam (Keppra) pregabalin (Lyrica) tiagabine (Gabitril) topiramate (Topamax) |
| Acute Care During seizure: | Anticipate giving benzodiazepines to stop an active seizure Assist with ventilations if patient does not start breathing spontaneously Assess for hypoglycemia. Maintain NPO till awake with gag reflex. Monitor VS |
| When seizure occurs outside the hospital setting | activate EMS if (1) the duration is greater than 5 min; (2) events recur without the patient recovering to baseline; (3) the patient is unable to establish a normal breathing pattern, is injured or pregnant |
| Restless Leg Syndrome | Movement disorder with unpleasant sensory (paresthesia) and motor abnormalities of 1 or both legs Primary (idiopathic): cause is unknown, thought to be a problem with dopamine levels Symptoms may be worsened by sleep deprivation, sleep apnea |
| Restless Leg Syndrome s/s | Severity of symptoms ranges from infrequent minor discomfort (numbness, tingling, “pins and needles”) to severe pain Tingling, itching, “creepy- crawling,” or throbbing feeling in calf muscle |
| Restless Leg Syndrome s/s part 2 | Most common at night; may disrupt sleep Physical activity, such as walking, stretching, rocking, or kicking, often relieves the pain Fatigue worsens symptoms |
| Restless Leg Syndrome diagnostics | Diagnosis based on history Sleep diary may be helpful Diagnostic Criteria overwhelming urge to move the legs, often accompanied by uncomfortable or unpleasant sensations in the legs |
| Restless Leg Syndrome Interprofessional Care | Gabapentin or pregabalin are first-line drugs for RLS Dopamine agonists may also be used Increase amount of DA in the brain ropinirole [Requip], pramipexole [Mirapex], rotigotine [Neupro] |
| Multiple Sclerosis | Chronic, unpredictable, progressive, degenerative disorder of the CNS Characterized by disseminated demyelination of nerve fibers of the brain and spinal cord Onset is usually between ages 20 and 40 years |
| Multiple Sclerosis patho | Primary problem is an autoimmune process Immune system attacks myelin proteins causing damage to the myelin sheath Transmission of nerve impulses is slowed Inflammation continues or recurs and myelin loses the ability to regenerate |
| Multiple Sclerosis s/s | May be slow and gradual or rapid and progressive Vision changes like blurred or double vision, red-green color distortion, or blindness in 1 eye may be the first sign Extremity weakness and problems with coordination, tremors, hearing loss, ataxia |
| Multiple Sclerosis s/s part 2 | Problems with bowel or bladder function Problems with sexual function Problems with cognitive function Multitasking, concentration, short-term memory, speed of processing, and word finding Emotional changes, such as anger, depression, or euphoria |
| Multiple Sclerosis diagnostics | MRI with contrast of the brain and spinal cord may show plaques, inflammation, atrophy, and tissue destruction Diagnostic criteria for MS Evidence of at least 2 inflammatory demyelinating lesions in at least 2 different locations within the CNS |
| Multiple Sclerosis drug therapy | Disease Modifying Drugs (DMDs) Suppress the immune system in order to modify disease progression and prevent relapses More effective when started early in the course of MS May be injectable, oral, or IV |
| Disease Modifying Drugs injectables | β-1a interferon (Rebif, Plegridy, Avonex) β-1b interferon (Betaseron, Extavia) |
| Disease Modifying Drugs IV infusions | alemtuzumab (Lemtrada) natalizumab (Tysabri) ocrelizumab (Ocrevus) |
| Multiple Sclerosis Disease Modifying Drugs teach | self-injection techniques Rotate injection sites Monitor LFTs Avoid pregnancy Follow cancer screening guidelines No contact with large crowds and people who have an infection Protect skin from sun exposure with SPF, flu s/s |
| Corticosteroids (prednisone) | Used to treat acute MS exacerbations Reduce edema and acute inflammation at the site of demyelination |
| Multiple Sclerosis management | Help patient identify and avoid triggers Provide emotional support Assist with ADLs during exacerbation Prevent complications of immobility Promote balance of activity and rest |
| Parkinson Disease (PD) | Chronic, progressive neurodegenerative disorder characterized by slowness in the initiation and execution of movement (bradykinesia), increased muscle tone (rigidity), tremor at rest, and gait changes |
| Parkinson Disease patho | Combination of genetic and environmental risk factors; increased risk with TBI Degeneration of the DA-producing neurons Disrupts the normal balance between DA and acetylcholine (ACh) DA is essential for normal function of the extrapyramidal motor |
| Parkinson Disease s/s | Onset is gradual with ongoing progression Tremors, rigidity, bradykinesia, and postural instability |
| tremor parkinsons | More prominent at rest and lessens with purposeful movement Worsened by stress or increased concentration Hand tremor is described as “pill rolling” because the thumb and forefinger look like rolling a pill |
| Bradykinesia parkinsons | Slowness of movement; slowing of ADLs Stooped, bent forward posture, masked face/flat affect (deadpan expression), drooling of saliva, and shuffling gait |
| Rigidity parkinsons | Increased resistance to passive motion Jerky quality (cogwheel rigidity), as if there were occasional catches in the passive movement of a joint |
| Postural Instability parkinsons | Unable to stop themselves from going forward or backward Increased risk of falls |
| Parkinson Disease Non-Motor Manifestations | Depression, anxiety, apathy, fatigue, inability to plan, poor attention Pain, urinary incontinence, constipation, and memory changes Trouble communicating due to a lack of expressive voice and low volume (hypophonia) Sleep disruptions |
| parkinson's complications | Dysphagia, malnutrition, and aspiration Immobility, falls, injuries Depression, hallucinations Dementia |
| Parkinson Disease diagnostics | Diagnosis is based on the history and clinical features MRI and CT are usually normal Diagnosis requires the presence of 2 of the 4 main manifestations |
| Parkinson Disease drug therapy | either enhance the release or supply of DA or block effects of the overactive cholinergic neurons (anticholinergic) Dopaminergics, anticholinergics, COMT Inhibitors Excess dopaminergic drugs can worsen rather than relieve symptoms.Monitor for dyskinesia |
| Dopamine Precursors parkinsons | Levodopa, levodopa/carbidopa (Sinemet) Primary treatment for symptomatic patients |
| Dopamine Receptor Agonists parkinsons | pramipexole (Mirapex), ropinirole (Requip, Requip XL), rotigotine (Neupro [transdermal patch] |
| Dopamine Agonists parkinsons | amantadine, apomorphine (Apokyn) |
| Dopaminergics parkinsons | May cause dyskinesias, dry mouth, orthostatic hypotension, hallucinations Protein ingestion can impair the absorption of levodopa. Limiting protein intake to the evening meal can decrease this problem. |
| Anticholinergics parkinsons | Decrease the activity of acetylcholine, balancing cholinergic and dopaminergic actions benztropine (Cogentin), trihexyphenidyl Diphenhydramine is an antihistamine that has anticholinergic effects May cause blurred vision, urinary retention, tachy, |
| Catechol O-Methyltransferase (COMT) Inhibitors parkinsons | breaks down levodopa in the peripheral circulation COMT inhibitors block COMT, prolonging the effect of carbidopa/levodopa Used as adjuncts to therapy when the patient’s response to levodopa is wearing off entacapone (Comtan), opicapone (Ongentys) |
| Myasthenia Gravis | Autoimmune disease of the neuromuscular junction marked by fluctuating weakness of certain skeletal muscles that worsens with activity |
| Myasthenia Gravis patho | Autoimmune process in which antibodies attack and destroy ACh receptors Prevents ACh molecules from attaching to receptors and stimulating muscle contraction |
| Myasthenia Gravis s/s | weakness of skeletal muscles Affects multiple muscle groups Muscles used to move the eyes and eyelids, chew, swallow, speak, and breathe Muscles are often strongest in the morning and become exhausted with continued activity |
| First muscles involved are the Myasthenia Gravis s/s | ocular muscles, causing ptosis (drooping of the eyelids) in 1 or both eyes and double vision Facial mobility and expression can be impaired, difficulty chewing and swallowing food Speech is affected No sensory loss normal reflexes |
| Myasthenic Crisis | Acute worsening of muscle weakness triggered by respiratory infection, surgery, exposure to certain drugs, or starting corticosteroid treatment Complications result from muscle weakness in areas that affect swallowing and breathing. lead to aspiration |
| Myasthenia Gravis diagnostics | Edrophonium test Edrophonium, an anticholinesterase agent, is given IV Edrophonium blocks the enzyme acetylcholinesterase, the enzyme that breaks down ACh A patient with MG will have rapid improvement in muscle strength,atropine be readily available |
| Myasthenia Gravis drugs | Anticholinesterase drugs Inhibit acetylcholinesterase to prolong the action of ACh and improve impulse transmission at the neuromuscular junction Pyridostigmine (Mestinon)-excessive cause cholinergic crisis-weakness, flaccidity, sweat, salivation |
| Myasthenia Gravis Surgical Therapy | Thymectomy Thymus gland in the patient with MG appears to enhance the production of AChR antibodies Removal results in improvement in most patients |
| Myasthenia Gravis meds part 2 | Corticosteroids (specifically prednisone) are used to suppress the immune response. Immunosuppressants azathioprine (Imuran), mycophenolate (CellCept), and cyclosporine (Sandimmune) |
| Amyotrophic Lateral Sclerosis (ALS) | Rare progressive neuromuscular disorder marked by loss of motor neurons Upper and lower motor neurons in the brainstem and spinal cord gradually degenerate Excess glutamate (an excitatory neurotransmitter) damages the neurons |
| ALS s/s | Progressive muscle weakness, wasting and atrophy; involuntary contractions or twitching As the ability to move decreases, swallowing is impaired leading to aspiration Death often results from compromised respiratory function |
| Huntington Disease | , degenerative brain disorder causing deterioration of physical, emotional, and cognitive abilities Genetically transmitted, autosomal dominant disorder → offspring of a person with HD have a 50% risk Caused by mutation in HTT found on chromosome 4 |
| Huntington Disease tests | Genetic testing confirms diagnosis Deficiency of the neurotransmitters ACh and γ-aminobutyric acid (GABA) → excess DA |
| Huntington Disease s/s | opposite of parkinsons, movement disorder and cognitive and psychiatric problems. Abnormal and excessive involuntary movements (chorea) Writhing, twisting movements of the face, limbs, and body Speech, chewing, and swallowing are affected |
| Huntington Disease Psychiatric symptoms | include depression, anxiety, agitation, impulsivity, apathy, social withdrawal, moodiness, and stubbornness At the end of the disease, the patient will be nonverbal, bedridden, and require help with all ADLs. |
| Huntington Disease management | Most common cause of death is pneumonia, followed by suicide No cure, treatment is palliative Because of the chorea, caloric requirements are high. End-of life issues and advanced directives must be addressed |
| Spinal Cord Injury (SCI) | Caused by trauma or damage to the spinal cord Can result in temporary or permanent alteration in spinal cord function Usually a result of trauma motor vehicle collisions, falls, violence, and sports injuries |
| Spinal Shock | May occur shortly after acute SCI Characterized by loss of deep tendon and sphincter reflexes, loss of sensation, and flaccid paralysis below the level of injury Lasts days to weeks |
| Neurogenic (vasogenic) Shock | Can occur in cervical or high thoracic injury (T6 or higher) Caused by unopposed parasympathetic response due to loss of sympathetic nervous system (SNS) innervation causes peripheral vasodilation, venous pooling, and decreased cardiac output |
| Neurogenic (vasogenic) Shock s/s | Manifestations: hypotension (<90 mm Hg), bradycardia, and temperature dysregulation May persist for as long as 5 weeks after injury |
| Classification of SCI Level of Injury | Level of injury may be cervical, thoracic, lumbar, or sacral Cervical and lumbar injuries are most common Injury from C1 to T1 can cause paralysis of all 4 extremities, resulting in tetraplegia (formerly called quadriplegia) |
| Paraplegia | (paralysis and loss of sensation in the legs) can occur in SCI below the level of T2 |
| C4 injury | tetraplegia, complete paralysis below the neck |
| C6 injury | partial paralysis of hands and arms as well as lower body |
| T6 injury | paraplegia, paralysis below the chest |
| L1 injury | paraplegia, paralysis below the waist |
| SCI respiratory manifestations | Respiratory complications closely correspond to the level of injury. Injuries above C3 result in total loss of respiratory muscle function Respiratory arrest within minutes of injury if not intubated |
| High cervical injury (C3–5) | respiratory insufficiency due to loss of phrenic nerve innervation to the diaphragm and decreased chest and abdominal wall strength |
| Cervical and thoracic injuries cause | paralysis of abdominal and often intercostal muscles Ineffective cough → cannot clear secretions Increased risk for aspiration, atelectasis, and pneumonia Hypoventilation → decreased tidal volume |
| Spinal Cord Injury (SCI) Manifestations Cardiovascular System | Injuries above T6 lead to SNS dysfunction → bradycardia, peripheral vasodilation, and hypotension (neurogenic shock) Cardiac output decreases Thermoregulation Poikilothermia: inability to maintain a constant core temperature |
| Spinal Cord Injury (SCI) Manifestations Urinary System | Neurogenic bladder: any type of bladder dysfunction related to abnormal or absent bladder innervation Both the detrusor muscle (bladder wall) and urethral sphincter may be affected Flaccid: no reflex detrusor contractions → overdistension and retention |
| Spinal Cord Injury (SCI) Manifestations GI System | Decreased GI motor activity → gastric distention and paralytic ileus Delayed gastric emptying Dysphagia may be present, neurogenic bowel- lead to stool retention, constipation, impaction, and incontinence |
| Spinal Cord Injury (SCI) Metabolic Needs | Lean body mass decreases and muscles atrophy, leading to weight loss Increased nutrition needs due to increased metabolism and more protein breakdown Start nutrition support within 72 hours after injury |
| SCI Peripheral Vascular Problems | Increased risk of VTE due to immobility, hypercoagulability, venous stasis Decreased sensation makes it difficult to detect |
| SCI pain manifestations | Neuropathic pain: occurs from damage to the spinal cord or nerve roots hot, burning, tingling, pins and needles, cold, and/or shooting |
| Spinal Cord Injury (SCI) diagnostics | CT scan is the preferred imaging study Cervical x-rays are done when a CT scan is not readily available MRI can assess soft tissue injury, neurologic changes, unexplained neurologic deficits |
| Spinal Cord Injury (SCI) Prehospital | ABCs Rigid cervical collar and a supportive backboard to restrict spinal movement- supine position Intubation ASAP for respiratory distress |
| Spinal Cord Injury (SCI) acute care | SCI of the thoracic and lumbar vertebrae requires less intense support than cervical SCI Neurogenic shock is treated with IV fluids and vasopressors to maintain SBP greater than 90 mm Hg Perform full neuro assessment including motor |
| signs of internal bleeding | Rapidly ↓ BP and ↑ HR |
| SCI Non-Operative Stabilization | Nonoperative treatments involve stabilization of the injured spinal segment and decompression, either through traction or realignment Stabilization eliminates damaging motion at the injury site |
| SCI surgical therapy | Used to manage instability and decompress the spinal cord Can access spine from the back (posterior approach) or from the front of the spine (anterior approach) Fixation involves attaching metal screws, plates, or other devices |
| Acute Care Immobilization | Maintain neck and spine in neutral position Logroll patient to prevent movement of the spine For cervical injuries, skeletal traction is used for early realignment (reduction).Crutchfield or Gardner-Wells tongs or halo (halo ring) |
| SCI immobilization | Skeletal Traction A rope extends from the center of the device over a pulley to weights attached at the end. Traction must be maintained at all times. Patients need serial x-rays to evaluate the effects of traction. |
| Halo vest immobilizes a | cervical fracture while the bones fuse while still allowing for ambulation Meticulous wound care at site of tong or pin insertion to prevent infection. Carefully assess areas under halo vest or cervical collar for skin breakdown, set of wrenches close |
| SCI corticosteroids | High dose methylprednisolone to decrease swelling from SCI Use is controversial |
| SCI VTE prevention meds | Low molecular weight heparin (enoxaparin) or heparin unless contraindicated |
| SCI vasopressors | phenylephrine, norepinephrine Used in acute phase of injury to maintain the MAP to improve perfusion to the spinal cord Pregabalin (Lyrica) and Gabapentin (Neurontin) for neuropathic pain |
| During the first 48 hours after injury | spinal cord edema may increase the level of dysfunction, causing respiratory distress. Frequent and thorough assessment of respiratory system is required |
| SCI respiratory care | Apply supplemental O2 as needed Endotracheal intubation and mechanical ventilation may be needed at C5 or above Patients who have chest trauma or difficulty weaning from the ventilator may need a tracheostomy for airway management.suctioning as needed |
| SCI Cardiovascular Instability | Bradycardia (HR < 60) is common due to unopposed vagal response Increase in vagal stimulation, (turning or suctioning) can cause cardiac arrest Atropine (anticholinergic), temporary, or permanent pacemaker for symptomatic bradycardia |
| SCI Cardiovascular Instability care | Loss of tone in peripheral vessels results in chronic low BP with orthostatic hypotension Salt tablets, fludrocortisone, or midodrine to ↑ BP Compression stockings or abdominal binder to increase venous return and prevent orthostatic hypotension |
| SCI Cardiovascular Instability care part 2 | Manage hypotension with fluid replacement and a vasopressor agent (phenylephrine or norepinephrine) Keep SBP > 90 and MAP 85-90 |
| SCI Fluid and Nutrition Management | During the first 48 to 72 hours after the injury, a paralytic ileus may develop NG tube for severe ileus Nutrition should be started within the first 72 hours after injury High-protein, high-calorie diet is needed for energy and tissue repair |
| Spinal Cord Injury (SCI) Bladder and Bowel Management | Immediately after the injury, urine retention occurs because of the loss of autonomic and reflex control of the bladder and sphincter (neurogenic bladder). Indwelling urinary catheters used during this time for retention |
| SCI urine residual should be | less than 500mL |
| Bladder and Bowel Management care SCI | Start a bowel program to combat constipation from neurogenic bowel Involves inserting a rectal stimulant (suppository or small-volume enema) daily at a regular time Increase fluids, fiber, and physical activity to prevent constipation |
| SCI skin care | The most common long-term complication in SCI is a pressure injury (PI) Areas most vulnerable to breakdown include the sacrum, ischia, trochanters, and heels. Daily skin assessment: including areas under collars and braces. Assess nutritional status |
| SCI reflexes | Once spinal cord shock is resolved, return of reflexes may complicate rehabilitation. Reflexes are often hyperactive and have exaggerated responses Spasms ranging from mild twitches to convulsive movements below the level of injury may occur |
| reflex SCI meds | Antispasmodic drugs, such as baclofen (Lioresal), dantrolene (Dantrium), and tizanidine (Zanaflex), may help control spasms. Botulism toxin injections may be given to treat severe spasticity |
| Autonomic Dysreflexia SCI | Massive, uncompensated cardiovascular reaction mediated by the SNS Can occur after the resolution of spinal shock in patients with injury at T6 or higher Occurs in response to stimulation of sensory receptors below the level of the SCI |
| Baroreceptors in the | carotid and aorta sense the hypertension and stimulate the parasympathetic system. This causes a decrease in heart rate. |
| Autonomic Dysreflexia SCI s/s | hypertension, throbbing headache, marked diaphoresis above the level of injury, bradycardia (30 to 40 beats/min),, flushing of the skin above the level of injury, blurred vision or spots, nasal congestion, anxiety, and nausea Life-threatening |
| Autonomic Dysreflexia Management | Elevate HOB or sit patient upright to decrease BP Determine and eliminate the cause (bowel impaction, urinary retention, UTI, PI, tight clothing) Catheterization to relieve bladder distention Remove stool impaction if present Remove all skin stimuli |
| Autonomic Dysreflexia Management part 2 | BP often during the episode. If symptoms persist after the source has been relieved, give a rapid-onset and short-duration agent, such as nitroglycerin, nitroprusside, or hydralazine |
| Spinal Cord Tumors | Can be primary or secondary Most are slow growing Symptoms are due to the mechanical effects of slow compression and irritation of nerve roots, spinal cord displacement, or gradual obstruction of the blood supply |
| Spinal Cord Tumors s/s | Both sensory and motor problems may result The most common early symptom of a spinal cord tumor is back pain or pain radiating along the compressed nerve route Pain may worsen with activity, coughing, straining, and/or lying down, cold, tingles |
| Spinal Cord Tumors Interprofessional Care | Diagnosed by x-ray, MRI, or CT; CSF analysis may reveal tumor cells Spinal cord compression is a medical emergency - patients may need emergency surgery to decompress spinal cord, corticosteroids to reduce edema |
| Trigeminal Neuralgia | Characterized by sudden, usually unilateral, severe, brief, stabbing, recurrent episodes of pain in the distribution of the trigeminal nerve The pain intensity and lifestyle disruption that accompany TN cause dysfunction |
| Trigeminal Neuralgia Etiology and Pathophysiology | TN most often affects the sensory (afferent) branches of the second and third divisions (maxillary and mandibular branches) Most cases result from vascular compression of the trigeminal nerve root Constant compression appears to lead to chronic injury |
| Trigeminal Neuralgia Manifestations | Abrupt onset excruciating pain burning, knifelike, lightning-like shock in lips, upper or lower gums, cheek, forehead Facial twitching, frequent blinking usually brief, seconds to 2 or 3 minutes. Frequency ranges from 1 to over 50 times a day |
| Trigeminal Neuralgia Manifestations | are triggered by light touch at a specific point (trigger zone) along the distribution of the nerve branches Precipitating stimuli include chewing, brushing the teeth, feeling a hot or cold blast of air on the face, washing the face, yawn |
| Trigeminal Neuralgia meds | Antiseizure drug therapy may reduce pain by stabilizing the neuronal membrane and blocking nerve firing First-line drugs include carbamazepine (Tegretol) and oxcarbazepine (Trileptal) Tricyclic antidepressants (amitriptyline or nortriptyline) for pain |
| Trigeminal Neuralgia management | Assess characteristics, frequency, and pain management techniques. Evaluate the degree of pain and its effects on the patient’s lifestyle, drug use, emotional state, and suicidal tendencies. Hygiene best when analgesia is at its peak |
| Bell’s Palsy | Acute, usually temporary, facial paresis (or palsy) resulting from damage or trauma of the facial nerve (CN VII) Usually affects only 1 side of the face High incidence during pregnancy and in persons with upper respiratory tract conditions |
| Bell’s Palsy cause | Exact cause unknown Potentially a reactivation of HSV or HZV, causing inflammation and nerve compression |
| Bell’s Palsy recovery | Recovery usually begins within 2 weeks of symptom onset Most patients will recover some or all facial function within 6 months May be residual effects in some cases, including facial asymmetry or abnormal facial movements. |
| Bell’s Palsy Manifestations | Acute onset of unilateral lower motor facial weakness Drooping of the eyelid and corner of the mouth, drooling, facial twitching, dryness of the eye or mouth, facial numbness, altered taste, hearing loss, and excessive tearing in 1 eye |
| Bell’s Palsy diagnosis | MRI or CT to rule out other causes of facial paralysis Oral corticosteroid therapy to reduce inflammation and swelling should be started with 72 hours of onset |
| Bell’s Palsy management | Active facial muscle exercises are done several times a day when function returns Protect the face from cold and drafts because trigeminal hyperesthesia (extreme sensitivity to pain or touch) may occur. Eye protection is important |
| Guillain-Barré Syndrome (GBS) | Autoimmune process that occurs a few days or weeks after a viral or bacterial infection Most common type of GBS is acute inflammatory demyelinating polyneuropathy (AIDP) |
| Guillain-Barré Syndrome (GBS) etiology | After an infection, immune responses cause injury to the myelin sheath Segmental loss of the myelin sheath → Transmission of nerve impulses is stopped or slowed |
| Guillain-Barré Syndrome (GBS) Manifestations | Acute, ascending, rapidly progressive, symmetric weakness of the limbs 1st S/S are weakness, paresthesia (numbness and tingling), and hypotonia (reduced muscle tone) of the limbs Reflexes are weak, resp failure Autonomic nervous system dysfunction,pain |
| Guillain-Barré Syndrome (GBS) management | May need intubation and mechanical ventilation Plasmapheresis or high-dose IV immunoglobulin (IVIG), are most effective if used within the first 2 weeks of symptom onset Enteral or parenteral nutrition may be used to ensure adequate caloric intake. |
| Tetanus | Severe nervous system infection affecting spinal and cranial nerves Results from the effects of a potent neurotoxin (tetanospasmin) released by the anaerobic bacillus Clostridium tetani Binds to motor nerves → causes sustained muscle contraction |
| hallmark tetanus | tetanus is muscle rigidity and spasms Facial muscles are affected first with stiffness in the jaw |
| Tetanus manage | Laryngeal and respiratory spasms cause apnea and anoxia May require mechanical ventilation Adults should receive a tetanus and diphtheria toxoid booster every 10 years. Immediate, thorough cleansing of all wounds with soap and water |
| If an open wound occurs and the patient has not been immunized within | 5 years, tetanus booster is needed Treated with tetanus immune globulin (TIG) and 10-14 day course of antibiotics |
| Triptans first line for | symptomatic or abortive migraines |
| High flow O2 for | cluster HA bc it vasoconstricts arteries |
| Give thrombolytic | 3-4.5 hrs with onset of symptoms |
| too acidotic= | high ICP |
| Rule for suctioning with ICP | minimize to less than 10 sec at a time, hyperoxygenate before and after Start nutrition within 72 hours of head injury |
| Order of meninges from outer to inner | skull, dura mater, arachnoid layer, pia mater, brain |
| Lumbar puncture to diagnose | bacterial meningitis, will be cloudy and discolored, low glucose |
| Oculovestibular/Cold Caloric Reflex | Instill a syringe of ice-cold water into the external auditory ear canal ○ Assess the patient’s eyes for a total of 1 minute. ○ A normal response is nystagmus or jerking movements of the eye ○ An abnormal response is the absence of eye movement |
| ICP Monitoring | A ventriculostomy is the gold standard ○ Catheter inserted in ventricle and connected to an external transducer. ● The transducer must be level with the tragus of the ear for accurate pressure readings. ● Risk for infection! |
| monitor what for mannitol | fluid and electrolyte status: BP, urine output, daily weights, electrolyte |
| A CSF leak with a head injury indicates that the | dura mater has been torn (dural tear) |
| embolic stroke has no chance of | collateral circulation |
| Triptans and Alpha Adrenergic Blockers are contraindicated with | heart disease and hx of stroke because they vasoconstrict* |
| Overmedication ↑ ACh too much, leading to a | Cholinergic crisis ○ Muscle weakness, sweating, N/V/D, stomach cramping |
Created by:
cwehner125