Neurological Alterations

Describe the oculocephalic reflex..

-Absent doll eyes means brainstem activity is active but processing is abnormal -Eyes move in the opposite direction as the head when turned is a positive finding -Do not test when increased ICP or cervical injuries are present

What are brain tumors and what causes them?

-Exact cause is unknown. Could be genetic mutations or environmental factors (cell phones) -Can occur anywhere in the brain structures and are named according to the cell tissue or where they are located (cerebral tumors are most common) Can be primary or secondary -Primary originate in the CNS and rarely spread outside this area -Secondary result from metastasis from other areas of the body Complications of Cerebral Tumors -Cerebral edema/brain tissue inflammation -ICP -Neurologic deficits -Hydrocephalus -Pituitary dysfunction

What are the S/S of brain tumors and how are they diagnosed?

-Manifestations vary with site of the tumor S/S -Headaches are more severe on awaking in the morning -N&V -Visual symptoms -Seizures -Changes in mentation or personality -Papilledema -Neurologic deficits result from destruction, distortion, or compression of brain tissue --Supratentorial cerebral tumors: paralysis, seizures, memory loss, cognitive impairment, language impairment, or vision problems --Infratential tumors: ataxia, autonomic nervous system dysfunction, vomiting, drooling, hearing loss, and vision impairment Diagnosis -Based on the history, neurologic assessment, clinical examination, and results of neurodiagnostic testing -Non-invasive (CT, MRI, skull films) conducted first. These test identify size, location, and extent of tumor. MRI is good for initial diagnostic; CT used for follow up -Cerebral angiography provides info about tumor blood supply -EEG, LP, brain scan, and PET provide info about size, location, and characteristics -Labs evaluate endocrine, renal, and electrolyte status **LP should NOT be performed is exhibiting S/S of ICP elevation**

What are the main types of spinal tumors and what causes them?

-Most often found in the thoracic area, but can occur in the lumbar and cervical areas. -Pathological effects are more often related to compression of the cord than to invasion of the spinal cord itself. As the tumor expands, it compresses the cord or the spinal nerve roots. Further growth leads to movement of the cord. In addition, a large tumor may affect the blood supply to the cord by compression or obstruct the normal flow of CSF. Venous occlusion by the tumor may lead to spinal cord congestion and infarction (tissue death) -Classified as Primary or Secondary --Primary tumors include the epidural vessels, spinal meninges, or glial cells of the cord. Their cause is unknown but they can be cancerous or benign. Usually can be removed but may cause permanent damage due to effects ICP from tumor --Secondary tumors are more common. They develop as a result of metastasis or of a cancer that originated from another part of the body. The metastasis compresses the spinal cord or nerve roots from the inside -Anatomically, Can be Intramedullary or Extramedullary Tumors --Intramedullary tumors account for a small number spinal cord tumors and are usually cancerous. They start within the spinal cord itself, in the central gray matter --Extramedullary tumors, representing most spinal cord tumors, are found with in the spinal dura but outside of the cord. They are further defined anatomically as extradural and intradural tumors. Extradural and epidural tumors occur between the vertebrae and the spinal dura. They develop in the surrounding bone and cause destruction of the vertebral bodies. Intradural tumors are located within the dura and originate from the pia-arachnoid, spinal roots, or ligaments. -Tumors involving the bones of the vertebrae typically develop as a consequence of metastatic tumors from the lung, breast, colon, and uterus

Describe interventions used for spinal cord tumors.

-Nursing care focuses on careful monitoring of VS and neurologic status at least every 4 hrs or more 1. Surgery (primary management) -Goal is to remove as much of tumor ass possible (often not possible and other treatment is needed like chemotherapy) -**Emergency surgery is indicated if: rapid loss of sensory and motor function or a loss of bladder or bowel control. Surgical decompression may be performed to maintain bladder, bowel, or motor function and to preserve quality of life--even with a poor prognosis** -Laminectomy and surgical decompression and total or partial resection of the tumor is performed -Spinal fusion may be necessary -Rarely, a cordotomy or palliative sectioning of sensory roots is done to control intractable pain -Post-op assess vitals and neuro checks every 1-2 hrs until they are stable and then every 4 hrs. Turn by log roll and reposition every 2 hrs. Inspect incision site for compromise (especially leakage of CSF), monitor respiratory pattern for compromise (cervical cord tumor), see p. 964 2. Radiation Therapy -Used with low-grade malignant tumors that are not completely removed, metastatic tumors, or with recurrent tumors or when there is no other treatment option -Spinal cord cannot tolerate high doses of radiation. Overexposure can result in spinal damage, which can develop over 6-12 mo after therapy -S/S or radiation overdose: spastic paralysis, loss of sensation, and bowel and bladder dysfunction. Death may occur. -Radiation therapy is described in Chapter 24 3. Chemotherapy -Use is very limited -Alkylating agents are effective for CNS tumors because the cross the blood-brain barrier -Some patients may receive carmustin (BCNU) or lomustine (CCNU) -Combination therapy with procarbazine, vincristine, and carmustine may be used (PVC therapy) -May be used as an adjunctive therapy for metastatic tumors -Meningeal involvement may benefit from intrathecal (spinal) chemotherapy -Nursing care for Chemotherapy is described in Chapter 24 Community-Based Care -Collaborate with patient and family and suggest ways to eliminate potential hazards in the home -Referral to social worker or case manager for ambulatory aids -May be discharged to rehab -Teaching plan depends on level of dysfunction -Nurse should be able to answer questions or correct misinformation about sexuality -Prognosis for metastatic and malignant tumors is poor -Encourage patient to express feelings

Describe interventions used for herniated disc.

-Pain usually managed with Non-steroidal anti-inflammatory drugs (NSAIDS), muscle relaxants, and at times, narcotics -Ice may be used for the first 48 hrs -After that heat may be used -Semi-sitting position (in a recliner chair); More comfortable, reduces back strain; promotes forward lumbar spine flexion -Supine with pillows under the legs -Lateral with thin pillow between knees with painful leg flexed -AVOID: prone position, sleeping w/thick pillows under the head -Physical Therapists may be able to relieve pain & spasm with stretching exercises & ultrasonic heat treatments -Spinal manipulation: Use of the hands on the spine to stretch, mobilize, or manipulate the spine -Work space or equipment modifications may be necessary -Progressive muscle relaxation exercises -For severe lumbar disc problems with leg pain -2 to 4 days of bed rest on a firm mattress -Most clients do not require bed rest -> 4 days of BR can be debilitating & slow recovery -Client taught use of proper body mechanics -If have to sit, should change positions often -Aerobic activities prescribed to help avoid debilitation -Walking, stationary bicycling, & back strengthening -Begin within first 2 weeks after injury (perform for 20 to 30 minutes, 2 or 3 times per week) -Work activities individualized -Back brace or corset may be prescribed -Usually not recommended once clinical manifestations are relieved -Exercise to strengthen the back and abdominal muscles helps prevent further problems if the exercises are done daily throughout life Surgical Management -Surgery indicated in clients with spinal disc problems when Sciatica is severe & disabling -Manifestations of sciatica persist without improvement or worsen, and physiologic evidence of specific nerve root dysfunction; also used to stabilize spinal fractures -Chemonucleolysis Chymopapain - a proteolytic enzyme isolated from papaya latex - is used as a meat tenderizer; Injected into the disc, it digests the protein in the disc & shrinks it; Contraindicated in people with multiple allergies & in people allergic to papaya; Immediate & delayed(after 15 days) allergic responses; Use abandoned by most practitioners Complications -General potential complications after spinal disc surgery at any level include: Infection and inflammation, injury to nerve roots, dural tears, and hematoma -Non-union of the surgical area also is a risk; Is associated with smoking Some surgeons assess serum nicotine levels prior to surgery to reduce risk of non-union & validate statements of smoking cessation

Describe interventions used for encephalitis.

-Protect against West nile virus -Acyclovir (Zovirax) it the antiviral drug of choice for herpes encephalitis -Drug therapy must begun early before patient becomes stuporous or comatose (usually occurs 4-6 days after initial neurologic symptoms) -Prompt recognition and treatment of increased ICP -**Maintain patent airway to prevent development of atelectasis or pneumonia, which can lead to brain hypoxia and brain damage** -TCDB every 2 hrs -Perform deep tracheal suctioning in the presence of ICP or compromised respiratory status -Elevate HOB 30-45 degrees unless contraindicated (after LP or sever hypotension) -Keep room dark and quiet -Promote comfort -Keep bed in lowest position -Assess family needs and need for rehab

Describe the assessment findings and S/S of spinal tumors and how they are diagnosed.

-S/S depend on the location of the tumor and is speed of growth. Tumors that involve the bones of the vertebral column usually occur as a result of metastasis (cancer spread) from other parts of the body -The appearance of neurologic S/S is related to the rate of tumor growth. The spinal cord can often accommodate a slowly growing lesion. With time, the cord may become significantly misshapen and displaced, but the patient surprisingly has few symptoms. However a rapidly growing tumor quickly leads to spinal cord compression and edema and the development of neurological symptoms such as numbness and paralysis S/S -Pain (most common) results from cord compression, infiltration of spinal tracts, or irritation of the spinal roots. Assess quality, severity, and intensity of pain, alleviating/aggravating factors, and location. Radicular (nerve pain) is stabbing or dull with intermittent episodes of sharp, piercing pain. The pain may increase during coughing, straining, or sneezing. Lying flat may increase the pain as a consequence of stretching the involved spinal roots -Assess Weakness, clumsiness, spasticity, and hyperactive reflexes and compare bilaterally (may indicate mobility problems involving the corticospinal tract) -Ataxia (staggered gait) -Hyptonia (decreased muscle tone) -Positive Babinski reflex -Spastic paralysis -Flaccid paralysis (may indicate tumor that affects spinal roots, an intramedullary tumor in the lumbosacral area, or an extramedullary tumor) -Assess sensory loss and compare bilaterally. Early symptoms include a slowly progressive numbness or tingling, pain, and temperature loss. The sensory deficit is further marked by a decreased touch perception, and inability to sense vibration, and loss of positional sense. The patient reports a tight, band-like feeling around the trunk -Loss of bladder control occurs before loss of bowel control. Assess for urinary hesitancy, dribbling, incontinence, urgency, or acute retention. -Bowel dysfunction is manifested by constipation. Keep in mind that the patient is embarrassed to admit bladder or bowel dysfunction -Decrease in genital sensation that affects sexual function, enjoyment, or ability to have erection or to ejaculate (caused by a lesion on the sacral area) Diagnosis -Radiographic examinations or scans of the spine detect narrowing of the spinal canal, destruction of vertebrae, or the presence of calcification. -Myelogram may be used when block is complete; it indicates the level, extent, and boundaries of the tumor (performed less due to new technology) -Biopsy (may not be used for tumors as a result of metastasis) -MRI provides detailed pathological condition of the spinal cord than either a CT or myelography -Electromyography (EMG) may help make differential diagnosis to rule out MS or ALS

Describe interventions used for brain tumors.

-Small benign tumor may be used may be monitored by CT or MRI -Malignant tumors are managed by chemotherapy, radiation, and/or surgery Drug Therapy -Chemotherapy: when given systemically, the drug must be lipid-soluble to cross the blood-brain barrier; monitor for side effects (see chapter 24 -Analgesics: codeine and acetaminophen given for headache; **Decadron (also given after craniotomy) and glucocorticoids given to control cerebral edema; Dilantin given to treat seizures; protonix given to prevent stress ulcers** Nonsurgical -Stereostatic radiosurgery: ionized radiation used to destroy intracranial lesions selectively without damaging surrounding tissues; great for deep-seated lesions that are hard to get to; procedure takes less than an hr and requires overnight observation --Advantages: Noninvasive, lower risk than craniotomy, surgical precision, decreased cost, decreased morbidity, decreased hospital stay, rapid recovery time --Disadvantages: uncomfortable, rigid head frame Surgical Management 1. Preoperative Care -Biopsy specifies pathophysiology -Patient worried about procedure and body image -Teach expectations (rehab may be indicated) -Patient should not have alcohol, tobacco, anticoagulants, or NSAIDS for at least 5 days before surgery -NPO for at least 8 hrs 2. Operative procedures -Most surgeries are MIS -Local anesthesia (No sensory neurons for pain in the brain) -Craniotomy: Surgeon makes an incision along or behind the hair line after placing the patient's head in a skull fixation device. Several burr holes are drilled into the skull, and a saw is used to remove a piece of bone to expose the affected area. Tumor is removed/debulked. After surgery, the bone flap is replaced and held by small screws or bolts. A drain may inserted. **3. Postoperative care -Monitor patient to detect changes and complications (ICP) -Periorbital edema: ecchymosis treated with cold compress to decrease swelling -Irrigate eye with the affected eye with warm saline solution or artificial tears to promote comfort -May need to be ventilated -Monitor for dysrhythmias caused by fluid and electrolyte imbalance -Strict I&Os (fluids may be restricted to 1500mL) -Range of motion every 2-3 hrs -TCDB every 2hrs -TEDs and SCDs to prevent DVT -Supratentorial surgery: **elevate HOB to 30 degrees to promote venous drainage from head; avoid hip or neck flexion and maintain the head in a midline, neutral position to prevent increased ICP; turn patient side to side every 2 hrs to prevent pneumonia and pressure ulcers; place patient on nonoperative side to prevent displacement of cranial contents by gravity** -Infratentorial surgery: **must lay flat on either side for 24-48 hrs (prevents neck pressure on the neck-area incision site); must be NPO 24 hrs post-op edema around the medulla and lower cranial nerves may cause vomiting and aspiration)** -Check head dressing every 1-2 hrs for drainage -Measure drainage amount, color, and smell -Monitor labs --Low hematocrit and hemoglobin=blood loss --Hyponatremia=fluid volume overload, SIADH, or steroid use --Hypokalemia=cardiac irritability --Hypernatremia=meningitis, dehydration, or diabetes insipidus (manifested by muscle weakness, restlessness, extreme thirst, and dry mouth, dehydration, and decreased urine output. untreated hypernatremia can lead to seizures. DI should be considered if the patient voids large amounts of very dilute urine with an increasing serum osmolarity and electrolyte concentration) -May be ventilated to control ICP (PaCO2 kept about 35 mm Hg to prevent vasodilation from increased carbon dioxide with increased ICP) -Suction PRN (remember to hyperoxygenate) -Monitor for complications** 4. Preventing and Managing Complications A. Increased ICP -Severe headache, deteriorating LOC, restlessness, irritability, and dilated or pinpoint pupils that are slow to react to light or nonreactive, B. Hematomas and intracranial hemorrhage -Severe headache, rapid decrease in LOC, progressive neurologic deficits, and herniation syndrome (brain tissue shifting, often downward). Bleeding into posterior fossa may lead to sudden cardiovascular and respiratory distress. Treatment requires surgical removal. C. Hydrocephalus (increased CSF in the brain) -Increased ICP, headache, decreased LOC, irritability, blurred vision, and urinary incontinence. Ventriculostomy may be placed as an emergency procedure to reduce CSF. long term shunt may be placed (risk of subdural hematoma and tearing veins. D. Respirator Complications -Atelectasis, pneumonia, and neurogenic pulmonary edema (interventions may cause ICP); neurogenic pulmonary edema is *life-threatening* and has symptoms of pulmonary edema w/o cardiac involvement. E. Wound infection -Complicated by other disease process (diabetes). Check for signs of infection. F. Meningitis -See meningitis section G. Fluid and Electrolyte Imbalance -**DI (supratentorial surgery involving pituitary or hypothalamus), SIADH (failure of posterior pituitary gland), and CSW. Urine output increases drastically (up to 10L/day), Specific gravity drops below 1.005, dehydration, hypovolemic shock. Fluid replacement and hormone therapy (fluid loss greater than 6 L/24hrs. May need vasopressin if urine output is greater than 50 mL/hr. -SIADH: sodium concentration in urine normal or elevated, serum sodium level falls, loss of thirst, weight gain, irritability, muscle weakness, and decreased LOC. Treated by fluid restriction and volume replacement with 3% hypertonic sodium.** -CWS (cerebral salt wasting): hyponatremia, decreased serum osmolarity, and decreased blood volume. Serum vasopressin and ANF levels differentiate CSW and SIADH. Treated with sodium and isotonic fluid replacement. -Strict I&O and daily weight. Assess for fluid volume overload or dehydration Community-Based Care -May be treated at home -May need assistive devices (walker, wheelchair) -Make environment safe (fall precautions) and add grab bars -May need rehab for physical and cognitive impairments -Make sure family and patient understand discharge instructions and documentation should include the name of the person that received the teaching -Avoid taking OTC unless approved by HP -Maintain regular exercise and proper diet -Implement seizure precautions

Describe interventions used for meningitis.

-The most important interventions are to accurately monitor and document neurologic status -Cranial nerve testing (CN VI involvement may indicate development of hydrocephalus -Drug therapy initiated with 2 hrs after prescribed -Broad-spectrum antibiotic -2 wk use of IV antibiotics -Monitor response -Steroids recommended for S. pneumoniae -Prophylaxis for those exposed to N. menigitides and H. infuenzae meningitis -Perform complete vascular assessment every 4 hrs to detect compromise from systemic emboli (most severe in the hands) -Assess temperature, color, pulses, and capillary refill -Gnagrene can develop if not caught early -Monitor for complications such as septic shock, coagulation disorders, ARDS, and systemic arthritis. Notify HP immediately -Isolate until results of CSF analysis are obtained. -Bacterial is very contagious -ABX -Anticonvulsants -Fluid and electrolyte replacement -Monitor for increased ICP -Provide quiet environment -Analgesics may be avoided if they have CNS depressant actions—will mask CNS changes **Contact Precautions** -Standard precautions unless patient has bacterial type that is transmitted by droplets

What are the S/S of TIAs and how are they diagnosed?

-Typically symptoms resolve within 30-60 min -Diagnosis is made upon assessment of symptoms and CT and MRI indicate brain tissue damage and risk for stroke

Describe interventions used for TIAs.

-Upon admission to the ED, patient is stabilized and complete neurologic exam is performed -Routine laboratory work, CT, and ECG are done -Patients over 65, diabetics, those with symptoms lasting longer than 10 mins, or motor speech difficulties are often admitted -Patient usually placed on anticoagulation therapy (Plavix) unless contraindicated -Teach bleeding precautions -Reinforce need for follow up exam

Describe interventions used for cluster headaches.

1. Drug therapy -Usually similar to that used for migraines -Additional drugs include: calcium-channel blockers (Calan), lithium, and corticosteroids. OTC drugs such as capsacin (civamide), melatonin, and glucosamine. 2. Teaching -Wear sunglasses and sit facing away from window to help decrease exposure to light and glare -100% oxygen via mask 7-10 L/min in sitting position (if prescribed) for 15-30 mins and D/C when headache is relieved. Oxygen reduces cerebral blood flow and inhibits activity of the carotid bodies, which are sensitive to oxygen levels in the body. Teach oxygen use precautions -Avoid triggers like bursts of anger, prolonged anticipation, excessive physical activity, and excitement -Explain need for consistent sleep-wake cycle 3. Surgical Interventions -Indicated for chronic drug-resistant cluster headaches -Percutaneous stereotactic rhizotomy (invasive procedure) -Long-term high frequency electrical stimulation of the hypothalamus (deep brain stimulation) may reduce or eliminate pain -Not approved by FDA and may cause permanent brain or nerve damage and are done as a last resort

What is a seizure and what causes it?

A seizure is an abnormal, sudden, excessive, uncontrolled electrical discharge of neurons within the brain that may result in a change of LOC, motor or sensory ability, and/or behavior -May occur for no known reason or pathological cause (brain tumor) Types of Seizure **1. "Grand Mal" or Generalized tonic-clonic- loss of consciousness, convulsions, muscle rigidity; lasts 2-5 mins** 2. Absence- brief loss of consciousness; daydreaming 3. Myoclonic- sporadic (isolated), jerking movements; may be unilateral or bilateral 4. Clonic- repetitive, jerking movements; may become incontinent; may bite their tongue; lasts several minutes 5. Tonic- muscle stiffness, rigidity; lasts 30 secs to several min 6. Atonic- loss of muscle tone;often followed by confusion Partial Seizures 1. Simple (awareness is retained) a. Simple Motor- Jerking, muscle rigidity, spasms, head-turning b. Simple Sensory- Unusual sensations affecting either the vision, hearing, smell taste, or touch c. Simple Psychological- Memory or emotional disturbances **2. Complex (Impairment of awareness) Automatisms such as lip smacking, chewing, fidgeting, walking and other repetitive, involuntary but coordinated movements; black out; may last 1-3 mins** 3. Partial seizure with secondary generalization Symptoms that are initially associated with a preservation of consciousness that then evolves into a loss of consciousness and convulsions; may occur with an aura -Secondary seizures result from underlying brain lesions, most commonly a tumor or trauma: metabolic disorders, acute alcohol withdrawal, electrolyte imbalance; high fever, stroke, head injury, substance abuse, heart disease -Can be triggered by physical activity, emotional stress, excessive fatigue, caffeine, alcohol, or certain foods and chemicals

What is a stroke and what causes it?

A stroke is a condition in which the brain cells suddenly die because of a lack of oxygen. A stroke can be caused by an obstruction in the blood flow, or the rupture of an artery that feeds the brain. -**Any stroke is a medical emergency that strikes suddenly, and it should be treated immediately to prevent neurologic deficit and permanent disability** -Caused by combination of genetics and environment risk factors (modifiable and non modifiable) -Rise in occurrence of younger adult population due to chronic IV drug abuse an crack cocaine -3rd leading cause of death in US -Those who have had a stroke are likely to have another one within a yr -South=Stroke Belt (obesity) -Circadian pattern peak between 6am and noon (lowest incidence between midnight and 6am) Pathological Changes in the Brain -Cerebral tissue dies from lack of oxygenation (infarction) -Brain is affected on the infarction side as well as the opposite side -Effects on nonaffected side may be due to brain swelling and further changes to blood flow (may develop manifestations of increased ICP) Types of Stroke -Ischemic: caused by the occlusion (blockage) of a cerebral artery by a thrombus (clot) or embolus (dislodged clot); often occur during sleep --Thrombotic; account for more than half of all strokes; associated with atherosclerosis (fatty plaques occlude vessel); because blockage is gradual, thrombotic strokes have slow onset; may have history of TIAs --Embolic: caused by thrombus that breaks off from one area and travels to the cerebral arteries; usual source is the heart; can also be from plaque that breaks off; emboli tend to become lodged at points of bifurcation; middle cerebral artery is most commonly involved; characterized by sudden onset and rapid occurrence of neurologic deficits; pressure on artery from embolus can cause hemorrhage, causing bleeding directly within brain tissue; history of afib increases risk -Hemorrhagic: bleeding occurs in the brain (usually intracerebral or subarachnoid --Intracerebral: results from severe hypertension, causing vessels to rupture; damage to the brain occurs from bleeding, causing edema, distortion, and displacement, which are irritants to the brain tissue; occur usually with sudden, drastic BP elevations (cocaine use) --Subarachnoid: more common; usually caused by mild aneurysm or arteriovenous malformation ~Aneurysm: abnormal ballooning or blister along a normal artery, which usually develops in a weak spot on the artery wall; larger aneurysms are more likely to rupture than smaller ones; leads to cerebral ischemia, infarction, and neurologic dysfunction ~Arteriovenous Malformation: abnormality that occurs during embryonic development; tangled or spaghetti-like mass of malformed, thin-walled, dilated vessels; absence of capillary network; may eventually rupture, causing bleeding into brain Health Promotion -Reduce modifiable risk factors -Healthy diet low in saturated and trans fat -Avoid sedentary lifestyle -Smoking cessation

What are transient ischemic attacks and what causes them?

A transient ischemic attack (TIA) is a transient episode of neurologic dysfunction caused by ischemia (loss of blood flow) - either focal brain, spinal cord or retinal - without acute infarction (tissue death). -Warning sign for stroke -Differentiated from reversible ischemic attack by length of time patient is symptomatic --TIA lasts from a few minutes to less than 24 hrs --RIND last longer than 24 hrs but less than a week

What is a migraine and what causes it?

An episodic familial disorder manifested by a unilateral, frontotemporal, throbbing pain that is often worse behind one eye or ear. Its is often accompanied by a sensitive scalp, anorexia, photophobia, and nausea without vomiting. Also classified as a "long-duration headache" because it usually lasts 4-72 hrs. --Familial (women are affected more than men--especially those with history of anxiety or depression) --Sufferers are at risk for stroke and epilepsy --The cause is likely a combination of vascular, genetic, neurologic, hormonal, and environmental factors. It is generally agreed that migraines are mediated via the trigeminal vascular system and central projections. Blood vessels in the brain overact to a triggering event, causing spasm in the arteries at the base of the brain. This response is followed by arterial constriction and a decrease in cerebral blood flow. Cerebral hypoxia may occur. Platelets clump together, and serotonin, a vasoconstrictor, is released. Other arteries dilate, which triggers the release of prostaglandins (chemicals that cause inflammation and swelling) and other substances that increase sensitivity to pain. --Triggers: -Caffeine -Red wine -Stress -MSG -Environmental factors -Weather changes Three categories of migraine headache are migraines with aura, migraines without aura, and atypical migraines. --Aura: a sensation that signals the onset of a headache or seizure; the patient may experience visual changes, flashing lights, or double vision. Aura occurs immediately before migraine episode. **Most headaches are migraines without aura** --Atypical: the least common of the three types of migraine headaches and includes menstrual and cluster migraines

What is a disc herniation and what causes it?

An intervertebral disc is a pad composed of three parts that rests between the centers of two adjacent vertebrae. -Discs provide cushions for spinal movement. -Strenuous activity or degeneration of the disc or vertebrae can allow the disc to move from its normal location. -Displacement of intervertebral disc material may be referred to as: Prolapse, herniation, rupture, or extrusion -Ruptured intervertebral discs may occur at any level of the spine. -Lumbar discs are more likely to rupture than cervical discs because of the: Force of gravity; continual movement in this region; and improper movements of the spine, as with lifting or turning -Thoracic disc disorders are the least common -More than half of patients give a hx of a previous back injury. -Heavy physical labor, strenuous exercise, & weak abdominal and back muscles increase risk -Repeated stress progressively weakens the disc, resulting in bulging and herniation

What are the S/S of stroke and how are they diagnosed?

Assessment **-Ask about onset and S/S (determines course of interventions)** -Embolic and hemorrhagic stroke have abrupt onset -Thrombotic strokes have gradual progression -Determine the severity of the symptoms, such as whether they worsened after the initial onset (hemorrhagic) or began to improve (embolic stroke) -Observe LOC and indications of neurologic impairment -Obtain information about history (diabetes, head trauma, HTN, heart disease, anemia, and obesity) -Obtain list of medications including OTC, herbal, recreational, and nutritional supplements -Obtain info about smoking, alcohol use, diet, and activity level S/S 1. Cerebral Aneurysm -Sudden severe headache ("the worst headache of my life") -N&V -Photophobia -Cranial neuropathy -Stiff neck -Change in mental status -May have family history of aneurysm 2. Stroke A. Cognitive Changes -Change in LOC (most important area to access); use GCS -Denial of illness -Spatial and proprioceptive dysfunction (right cerebral hemisphere) -Impairment of memory, judgment, or problem-solving, and decision-making abilities -Decreased ability to concentrate and attend to tasks -Right cerebral hemisphere is more involved with visual and spatial awareness and proprioception; may be unaware of deficits and disoriented to time and place; personality changes like impulsivity and poor judgment -Left cerebral hemisphere (most dominant hemisphere) is center of language, mathematic skills, and analytical thinking; left-sided involvement results in aphasia, alexia or dyslexia, agraphia, and acalculia (may need speech pathology consult) B. Motor Changes -Right hemiplegia/hemiparesis indicates stroke involving the left cerebral hemisphere because the motor fibers cross in the medulla before entering the spinal cord and periphery -Left hemiplegia/hemiparesis indicate stroke in right cerebral hemisphere -If brainstem or cerebellum is involved may experience hemiparesis or quadriparesis and ataxia -Patient w hypotonia or flaccid paralysis cannot overcome the forces of gravity and the extremities fall to the side; extremities may feel heavy and muscle tone is inadequate for balance, equilibrium, and protective mechanisms **-Hypertonia (spastic paralysis) tends to cause fixed positions or contractures of the involved extremities; ROM of the joints is restricted and shoulder subluxation may easily occur from either spasticity or flaccidity** -Assess proprioception, head and truck control, balance, coordination, and gait -May be unable to use an object correctly (agnosia) -May not be able to carry out a purposeful motor activity or speech (apraxia) -Loss of neurologic control by the cerebral cortex causes a spastic (upper motor neuron) uninhibited bladder; bowel function may also be affected; assess for incontinence (most common) or retention of urine and stool C. Sensory Changes -Evaluate response to touch and painful stimuli, diminished motor function, and decreased sensation (usually unilateral) -Evaluate for unilateral body neglect syndrome (right cerebral hemisphere); patient unaware of left paralyzed side -Assess visual ability; infarction or ischemia involving the carotid artery may cause pupil constriction or dilation, ptosis, visual field deficits, or pallor or petechiae of the conjunctiva; brief episode of blindness (amaurosis fugax) in one eye results from cerebral ischemia caused by ophthalmic or carotid artery insufficiency; hemianopsia (blindness in half the visual field) results from damage to the optic tract or occipital lobe. usually this occurs bilaterally (homonymous hemianopsia). The patient must turn their head to scan the complete range of vision (may not see all of their food); may have abnormal eye movements (nystagmus) D. Cranial Nerve Function -Ability to chew (CN V) -Ability to swallow (CN IX and X) -facial paresis (CN VII) -Absent gag reflex (CN IX) -Impaired tongue movement (CN XII) -Difficulty chewing, swallowing food and liquid (dysphagia); risk for aspiration and constipation E. Cardiovascular -Embolic stroke may cause murmurs, dysrhythmias (afib), or HTN -High blood pressure is needed after ischemic stroke (too high may lead to another stroke 3. Psychosocial Assessment -May have severe neurologic deficits that are permanent -Assess coping -Explain behavioral changes to family; emotional lability (frontal lobe) is described as laughing and crying for no reason 4. Laboratory Assessment -Elevated hematocrit and hemoglobin -Elevated WBC -PT/INR is used to asses clotting ability 5. Imaging Assessment -CT without contrast done initially (negative for thrombotic and embolic stroke; may detect hemorrhagic); after 24 hrs CT shows signs of brain damage -MRI detects ischemic damage before CT 6. Other Assessment -ECG -Cardiac enzymes

Describe the assessment findings and S/S of cluster headaches and how they are diagnosed.

Assessment Questions -Ask about prescribed drugs for both the prevention and relief of the headache as well as OTC drugs and herb usage -Ask about interventions such as relaxation techniques, meditation, acupuncture, and massage therapy -Ask the patient to recall a typical week's activities and any change in lifestyle -Ask about bedtime and waking time to help assess changes in activity or lack of continuity in the sleep-wake cycle S/S -Unilateral occulotemporal or oculofrontal headaches -May be described as excruciating, boring, and non-throbbing -Intense pain is felt deep in and around the eye -Occur at about the same time a day for about 4-12 wks followed by a period of remission for 9 mo to a yr (rarely does not follow this cycle) -Pain may radiate to the forehead, temple, or cheek (to a lesser extent to the ear and neck) -Temporal artery may be prominent and tender -Patient often paces, walks, or sits and rocks during the attack (only headache in which this behavior occurs) -During periods of remission, alcohol does not cause a headache (as it does during the headache period) -Onset is associated with relaxation, napping, or REM sleep -Ipsilateral (same side)tearing of the eye -Rhinorrhea (diarrhea of the nose) or congestion -Ptosis (may become permanent) -Eyelid edema -Facial sweating -Miosis (constriction of the pupils) -Bradycardia -Flushing or pallor in the face -Increased ICP -Increased skin temperature -N&V -Restlessness or agitation caused from pain

What are the S/S of seizures and how are they diagnosed?

Assessment Questions -How many seizures has the patient had, how long they last, and what triggers them -Ask family to describe seizure -Ask about presence of aura -Ask about any herbs the patient may be taking -Ask about recent head injuries -Asses alcohol and illicit drug use -Ask about medical history (HTN and previous stroke) Diagnosis -Based of history and physical -ECG, MRI, CT, and PET scan

Describe the assessment findings and S/S of migraine headaches and how they are diagnosed.

Assessment Questions: -When do the headaches occur? -How often? -How long do they last? -Do certain foods, alcohol, or other things trigger the headaches? -Have there been any recent changes in your headaches? -How do you treat the headaches? Does this treatment work? -How often and what drug or herbal remedy do you take? -Is there a family history of headaches? -Where do the headaches begin? Do they spread to other areas? -Do you experience other symptoms with the headaches, such as weakness or change in speech? -How does this impact your activities of daily living? Diagnosis is bases on the patient's history and on physical, neurologic, and psychological assessment. MRI is indicated if the patient has other neurological findings, a history of seizures, findings not consistent with a migraine, or a change in the severity of the symptoms of frequency of the attack. Neuroimaging is also recommended in patients over 50 with a new onset of headaches, especially women (**increased risk for stroke--explain cardiovascular risk and S/S of stroke**).

What is a cluster headache and what causes it?

Cluster headaches are manifested by brief (30 min-2hrs), intense unilateral pain that generally occurs in the spring and fall without warning. --Far less common than migraines --Usually develop between 20-50 yrs of age --May be attributed to vasoreactivity and neurogenic inflammation --Can be related to an overactive hypothalamus

Describe nursing interventions associated with brain abscess.

Drug Therapy -Antibiotics (combinations) -Dilantin to prevent seizures -Analgesic to treat headache -Drug level must be followed as prescribed to maintain therapeutic blood levels Surgical Interventions -Drainage of encapsulated abscess via burr hole -Craniotomy to remove abscess -Patients are discharged home when no neurologic deficits are noted -May require long term care -May have permanent neurologic deficits

What is encephalitis and what causes it?

Encephalitis: Inflammation of the brain tissue and often surrounding meninges -**Usually caused by viral infection** though can be fungal or bacterial -Causative agents include herpes, arboviruses (viruses spread from mosquito/tick to human), West Nile virus, and amebae Naegleria and Acanthamobea -Can be spread by blood products, breast milk, and organ transplant

Describe interventions used for the treatment of Increased ICP.

Goal is to maintain ICP less than 20 mm Hg while maintaining CPP above 70 1. Nursing Interventions: Manage ICP -Elevate HOB to 30 degrees, keep the head in a neutral. midline position to facilitate thee drainage of venous pressure and decrease the risk for venous obstruction -Monitor BP response to head elevation (raising HOB may decrease MAP and decrease CPP) -Whenever patient is moved monitor ICP response; if CPP does not return to baseline within 5 mins move patient back to previous position to elevate CPP -Only suction the patient when necessary; hyperoxygenate between passes and for 1 min after; each suction attempt should be no more than 2 seconds; no more than 2 passes; head kept in neutral position -**Turning, repositioning, and hygiene measures may increase ICP; space nursing care activities ** -Family presence has been shown to decrease ICP but need to maintain calm environment 2. Medical Management -Adequate oxygenation and ventilation -Cautious, limited use of hyperoxygenation -Osmotic and loop diuretics -Euvolemic fluid administration -Maintenance of BP -Reduction of metabolic demands -Corticosteroids 3. Adequate Oxygenation **-Maintain PaO2 above 80 mm Hg (below 50 mm Hg can increase ICP)** -May have endotracheal tube or may have mechanical ventilation -PEEP may be added to facilitate oxygenation but should be used with caution because it may prevent venous outflow and increase ICP -May need long term trach -Adequate hematocrit and hemoglobin are indications of adequate oxygenation 4. Management of Carbon Dioxide -PaCO2 kept at 35-45 mm Hg 5. Diuretics -Osmotic diuretics draw water from extracellular space; Should note decrease in ICP and increase in urine output; Side effects: hypotension, electrolyte imbalance, and rebound in increased ICP -When using Mannitol, patient must be assed for adequate intravascular volume to prevent hypotension; contraindicated in patient with kidney injury -Loop diuretics remove sodium and water from damaged brain cells 6. Optimal Fluid Administration -Normal saline and isotonic fluids are preferred -Hypotonic solutions=bad -Strict I&Os -Monitor sodium, potassium, and osmolality (below 320 mOsm/L) -Colloids or blood products may need to be administered -Hemodynamic monitoring may be required 7. Blood Pressure Management -MAP kept between 70-90 mm Hg -Important to monitor ICP and MAP collectively -CPP kept at 70 mm Hg at least -Hypotension leads to brain ischemia (Vasopressor may be needed) -HTN=bad (may need antihypertensive drug; some drugs can cause vasodilation; vasodilation=bad) 8. Reduce Metabolic Demands **-Temperature control: Avoid fever; may need medically induced hypothermia; may cause coagulation problems and electrolyte imbalance** -Sedation: May receive propofol or Benzos; morphine added for pain relief and sedation -Seizure prophylaxis: AEDs and seizure precautions -Neuromuscular blockade and barbiturate therapy: used for patients who are not responsive to other treatments

What are the S/S of a head injury and how is it diagnosed?

History -May be difficult to assess due to presence of amnesia or decreased LOC -Always ask when, where, and how the injury occurred -Did the patient lose consciousness? for how long? -Has there been a change in LOC -Drug or alcohol abuse? (may mask S/S of increased ICP) -Check indications of lucid interval -Seizure history? -History of falls? -Hand dominance? -Disease or injury to eyes? -Allergies (seafood) -Must be screened for abuse and neglect S/S **-Priority is airway (ABCs); always check airway first** **-Increased ICP (hypertension, hypoxemia, hypercapnia, changes in neurologic status, ovoid pupils, papilledema)** -All patients are treated as though they may have cervical spine injury until ruled out by x-ray -Symptoms of cervical involvement: loss of motor and sensory function, tenderness along the spine, and abnormal head tilt -Older adults prone to cervical injury at the first or second vertebral level (life threatening) -Cheyne-Stokes, central neurogenic hyperventilation, and/or apnea (injury to brainstem) -Monitor BP and HR to detect changes in cerebral blood flow -May have hypotension or hypertension -Cushing's triad (severe hypertension with a widened pulse pressure and bradycardia) may be sign of increased ICP -Thready pulse, irregular, rapid pulse (increased ICP) -Increased cerebral bloodflow in response to hypertension -Vasogenic edema (further increases ICP) -Hypotension and tachycardia suggest hypovolemic shock which may lead to ischemia and infarction of brain tissue -Dysrhythmias from severe ICP **-Assess GCS (Most important variable is LOC which indicates pressure on the rectiular activating system within the brainstem) -Early indicators of change in LOC include subtle behavior changes (restlessness, irritability) and disorientation may be caused by temporal fracture** -Anticholinergics and adrenergics effect pupil dilation -Pinpoint and nonresponsive pupils indicate brainstem dysfunction at the level of the pons -Assymetric, loss of light reaction, or unilateral or bilateral dilated pupils are treated as herniation -Pupils that are fixed and dilated are a poor prognostic sign, resulting from marked increase in ICP ("blown pupils") -Check gross vision -Test CN III, IV, and VI (may be diminished from increased ICP and hydrocephalus) -Visual-field deficits and diplopia (damage to optic chiasm or optic tract) -Late signs of ICP (severe headache, N&V, seizures, and papilledema/choked disc); may be days after the event -Decerebrate or decorticate posturing or flaccidity -Ataxia -Changes in motor function -Leakage of CSF from ears and nose; distinguished by "halo" sign; test positive on glucose strip; assess for nuchal rigidity when spinal cord injury is ruled out -Palpable fractures -Ecchymosis and tenderness Psychosocial Assessment -May have long-term or permanent disability -May have personality changes -Memory may be affected -Ability to talk and communicate may be affected -Assess coping skills -Assess family dynamics and ability to cope Laboratory Assessment -CT indicates scope on injury and hematoma -Radiography and CT used to rule out cervical fractures and dislocations -Chest x-ray rules out chest injuries -MRI for diagnosis of axonal injury (not recommended for patients with ICP or other invasive monitoring devices) -Abdominal ultrasound detects abdominal bleeding or bowel laceration Other Diagnostic Assessment -Doppler flow studies or arteriogram (measures integrity of cerebral vessels) -Cerebral blood flow studies measure cerebral perfusion -Evoked potentials provide information on functioning od sensory pathways; may be useful in predicting outcomes

Describe interventions used for strokes.

Improving Cerebral Perfusion -Ischemic: start two IV lines running non dextrose isotonic saline -Assess for increasing ICP 1. Nonsurgical Management -Monitor for neurologic changes and complications -Ischemic: fibrinolytic therapy and endovascular interventions -Monitor for hyperglycemia, UTIs, and pneumonia -Implement fall precautions A. Fibrinolytic Therapy: "clot-busting drug"; success depends on how quickly agent is administered after symptoms present (given within 3 hrs); Recombinant tissue plasminogen activator (rtPA, Retavase) only approved agent; may be contraindicated if patient: is over 80, INR less than or equal to 1.7, stroke scale greater than 25, history of both stroke and diabetes; must obtain consent; dosage based on weight B. Endovascular interventions: includes intra-arterial thrombolysis using drug therapy of mechanical clot removal; can be given 6 hrs after onset C. Monitor for Increasing ICP: highest risk 24-48 hrs after stroke; keep HOB between 25-30 degrees; provide oxygen therapy and keep O2 sat at >92%; maintain head at neutral, midline position; Turn to side to prevent aspiration; avoid activities that increase ICP (extreme flexion); allow breaks in between ADLs and procedures; hyperoxygenate before suctioning; provide calm environment and keep lights low; monitor vitals every 1-2 hrs; Notify HP for high BP; fever can cause increased ICP; hypothermia may cause decreased cerebral perfusion; monitor for dysrhythmias like afib that increase risk for emboli D. Monitor for Other Complications: monitor for aneurysm or AVM; monitor for hydrocephalus observe manifestations similar to increasing ICP (change in LOC,, headache, pupil changes, seizures, poor concentration, gait disturbances, and behavioral changes); monitor for vasospasm (decreased LOC, motor and reflex changes, increased neurologic deficits); monitor ruptured aneurysm of AVM (severe headache, N&V, decreased LOC, neurologic deficits) E. Ongoing Drug Therapy: Anticoagulants (Warfarin--level at 2-3 times control value); Aspirin within 24-48 hrs after onset (should not be given within 24 hrs of clot-buster); teach anticoagulant teaching; Plavix is used for ischemic strokes; Antiepileptic drugs for seizures (Ativan, Neurotin, Topamax); CCBs treat vasospasm (Nicardipine); Stool softeners promote defecation F. Other Nonsurgical Interventions: Stents are used to prevent stroke; postoperative complications symptoms include temporal headache, HTN, seizure, and focal neurologic deficits; may occur 1 hr-1wk postop 2. Surgical Management -Few are candidates for surgical intervention -Carotid endarterectomy: thrombus removed mechanically; usually monitored for 2 days postop; monitor VS, check peripheral pulse, check insertion site for bleeding; monitor for cerebral hyperperfusion -Extracranial-intracranial bypass: craniotomy is performed to unclog vessels limit visitors and reduce stress **3. Managing Impaired Swallowing -Aspiration maybe silent and may not be noticed until after pulmonary symptoms occur -NPO until swallowing is assessed -All liquids and medications should be assessed for swallowing -Observe for facial drooping, drooling, impaired voluntary cough, hoarseness, incomplete closure of the mouth, or cranial nerve palsies -Collaborate with speech therapist to conduct bedside barium swallow -Make sure UAP are aware of dietary needs -Massage throat when patient swallows to stimulate tactile feedback -Reduce stimuli when eating or drinking -Observe for indications of fatigue when feeding -Collaborate with dietician to ensure adequate nutrition** 4. Improving Mobility and Promoting Self-Care -May have mobility impairments that can lead to respiratory problems (pneumonia) -Risk for pressure ulcers -Risk for clots (compression hose and promote ambulation) -Promote independence as mush as possible **5. Promoting Effective Communication -May need to incorporate pictures and nonverbal language (left hemisphere) -May need speech pathologist to incorporate exercises that strengthen facial muscles used for speech -Expressive aphasia (Broca's) can understand what is said but cannot verbalize back; may also have trouble writing; damage to frontal lobe -Receptive aphasia (Wernike's) cannot under stand the spoken of often written word; damage to temporoparietal area; may make up words -Often has mixed aphasia -Present one idea at a time, use simple one step explanations, speak slowly but not loudly, use gestures, avoid "yes" and "no," and use alternate forms of communication** 6. Promoting Continence -Use bladder training program -Use bladder scanner to check for residual urine (can lead to UTI) -Determine normal time for BM and voiding -Encourage intake of apple juice, prune juice, and high fiber diet to promote bowel elimination -Remove catheter ASAP to prevent infection -May need stool softeners 7. Managing Sensory Perception -Visual deficits come from right brain involvement -May have problem with depth perception -Use verbal and tactile cues -Always approach patient from unaffected side which should face the door -Place objects in field of vision -Mirror may be used to increase visualization -Patch may be used to prevent blurred vision -Maintain hazard free environment -Reorient often -Use structured schedule 8. Preventing Unilateral Neglect -Risk for injury and falls -Teach patient to touch and use both sides of body -Wash and dress affected side first -Teach patient to scan entire field of gaze Community-Based Care -May need extensive rehab Home Care Management -Provide hazard free home with assisted devices -Modifications to home should be made before discharge Teaching for Self-Care -Teach about post stroke depression (onset 3 mo after stroke) -Teach about drugs, how to ambulate, how to facilitate swallowing -Left sided involvement can cause patient to be anxious, slow, cautious, and hesitant -Family may need time away from patient

What is increased ICP and what causes it?

Increased intracranial pressure in the brain -Normal ICP ranges from 0-15 mm Hg -Increased ICP is defined as pressure 20 mm Hg persisting for 5 mins of more (life threatening) Causes 1. Increased Brain Volume -Brain swelling 2. Increased Cerebral Blood Volume 3. Increased CSF

What is meningitis and what causes it?

Meningitis-inflammation of the meninges that surround the brain and spinal cord. -Can be viral or bacterial (symptoms are the same but bacterial causes more severe presentation) **--Meningococcal meningitis is medical emergency. Outbreaks in high population density and crowded living conditions.** Predisposing Conditions -Middle ear infection -Pneumonia -Acute or chronic sinusitis -Sickle cell anemia -Spinal or brain surgery -Immunosuppression (AIDS patients may get Cryptococcus neoformans) -Infections elsewhere in the body -Tongue piercings -Foreign travel Bacterial Routes of entry -Penetrating trauma -Surgical procedures -Ruptured cerebral abscess -Ear discharge -Nasal discharge -Basilar skull fracture -Saliva and snot exchange -Foreign travel Viral Routes of Entry -Measles -Mumps -Herpes

Describe interventions used for head injury.

Nonsurgical Management -Priority is maintaining airway, breathing, and circulation 1. Preventing and detecting ICP -Take vitals ever 1-2 hrs or more -Drug therapy may prevent severe hypertension and hypotension -Monitor for dysrhythmias (ST-segment and T-wave changes); report irregularities to HP -Assess for hypothalamic fever (absence of sweating, and no diural variation); can last several days to weeks; responds better to cooling (monitor for S/S of adverse effects of hypothermia); higher morbidity and mortality rates -Prophylactic hyperventilation during first 20 hrs is generally avoided but may be used for ICP -Maintain PaCO2 at 35-38 mm Hg; Carbon dioxide is powerful vasodilator that increases ICP -Arterial oxygen levels (Pao2) is maintained at 80-100 to prevent vasodilation from hypoxemia -Monitor ABGs and vent settings -Chest physiotherapy used for thick secretions **-Hyperventilate before performing suction; overly aggressive suctioning can increase ICP** -Always administer paralytics with a sedative -Lidocaine my be used to suppress the cough reflex (coughing increases ICP) -Maintain in midline neutral position; log roll; keep HOB at 30 degrees -Determine donor status before brain death occurs 2. Determining Brain Death -Four prerequisites of brain death: --Coma of unknown cause established by history, clinical examination, laboratory testing, and neuroimaging --Normal or near-normal core body temperature (higher than 36 degrees Celsius) --Normal systolic blood pressure (higher than or equal to 100 mm Hg) --At least one neurologic examination (some state require two) -Neuroimaging not necessary but desirable 3. Drug Therapy -Glucocorticoids have no benefit to decrease ICP -Mannitol is used to treat cerebral edema; **administer through filter needle to eliminate microscopic crystals**; Lasix may also be used; monitor I&O, severe dehydration, and indications of acute renal failure, weakness, edema, and changes in urine output; electrolytes and osmolarity measured ever 6 hrs (keep osmolarity between 310-320 mOsm/L) -Opioids (morphine, fentanyl, versed, ativan) may be used with ventilated patients to decrease agitation and control restlessness; reversed with Narcan; give opioids in small doses -Antiepileptic drugs (Dilantin) prevent seizures 4. Inducing Barbiturate Coma -Used for intracranial hypertension/ICP not controlled bay any other means (pentobarbital sodium/Neembutal, Novopentobarb or thiapentone) -Complete unresponsiveness; may be hard to detect subtle or obvious neurologic changes -Requires mechanical ventilation, hemodynamic monitoring, and ICP monitoring -Complications: decreased GI mobility, cardiac dysrhythmias from hypokalemia, hypotension, and fluctuations in body temperature -Decreases brain function to facilitate recovery 5. Maintaining Fluid and Electrolyte Balance -Fluid loss from DI or SIADH -Fluid overload causes increased cerebral edema -Fluids must be tittered -Check urine specific gravity ever 1-4 hrs -Monitor serum osmolarity and electrolytes once a day 6. Managing Nutritional Status -Changes occur in taste, smell, swallowing, sensation, vision, pain, and temperature -May not be able to chew or swallow -Weigh patient daily -Monitor albumin level and provide adequate protein intake -Assess for dehydration (dry mucosal membranes and weight loss) -Make mealtime enjoyable -Position to maximize swallowing ability -Soft food and thickened liquids -Caloric supplements and shakes 7. Managing Sensory, Cognitive, and Behavioral Changes -May experience loss of sensation, temperature, touch, and position sense -Provide hazard-free environment -Prevent injury (make sure food isn't too hot) -Provide sensory stimulation to comatose patient -May have short-term memory loss (always introduce yourself) -Maintain sleep wake cycle with rest periods -May have cognitive impairment -Maintain seizure precautions -Use restraints and mittens when necessary -Moderate to sever TBI patients may never be the same Surgical Management -IC monitoring (assess the patient not the monitor) -Burr hole (subdural hematomas) -Craniotomy (extreme cases--epidural hematomas) Community-Based Care -Goal is to return to highest level of functioning -May need rehab -Reduce home hazards (smoke alarms bc of lost sense of smell) Teaching for Self-Management -Seizure precautions -Explain drug therapy and drug schedule -Assess coping -Encourage activities as tolerated -Stress follow-ups -Provide structured environment for personality and cognitive changes/deficits -Reinforce positive behaviors -May have post trauma syndrome for up to yrs after concussion -Patients w behavioral changes may need constant supervision -Family may need respite care

Describe interventions used for seizures.

Nonsurgical Management 1. Drug Therapy -Most are completely controlled by anti-epileptic drugs -Teach patients to take their drugs at the same time to maintain therapeutic levels -Take as prescribed -Can build up sensitivity to drugs as they age -Keep scheduled lab appointments **-Be aware of drug and food interactions (warfarin cannot be given with dilantin; grapefruit juice can deceased drug metabolism, which can effect drug levels)** 2. Teaching for Self-Management **-Never stop taking AEDs (may cause severe seizure)** -Balanced diet, proper rest, and stress-reduction minimizes breakthrough seizure -Keep a seizure diary -May be restricted with driving -May need to find another job -See box **3. Seizure Precautions -Padded side rails (debatable; may embarrass client) -Padded tongue blade is NEVER the right answer -Have suction equipment at bed side -Bed rails up -Ensure IV access is maintained -See box** 4. Seizure Management -Observe to determine type of seizure and duration -Redirect patient's attention away from injury **-Turn patient to side to facilitate drainage of secretions** -Remove objects that may cause harm -May need supplemental oxygenation -Do not restrain patient 5. Emergency Care: Acute Seizure and Status Epilepticus Management -Seizures that occur in greater intensity, number, or length than the patient's normal are considered acute -Treated with Ativan (status epilepticus), Valium; IV Dilantin or Cerebyx -Status epilepticus medical emergency and is a prolonged seizure lasting longer than 5 mins (seizures lasting more than 20 mins can cause death) or repeated seizures over the course of 30 mins -Causes of status epilepticus: sudden withdrawal of AEDs, infections, acute alcohol or drug withdrawal, head trauma, cerebral edema, metabolic disturbances -Blood is drawn to find pathological etiology -Symptoms of untreated/severe status epilepticus: brain damage or death (tonic-clonic), hypoxia, hypotension, hypoglycemia, cardiac dysrhythmias, lactic acidosis, kidney failure and electrolyte imbalance (older adults) -Drug levels checked every 6-12 hrs after loading dose Surgical Management 1. Vagal Nerve Stimulation -May result in severe neurologic deficits -Pacemaker-like device attached to left chest and vagus nerve -Patients may carry magnet to activate device during aura -Change in voice may indicate vagus nerve may be stimulated -Complications of procedure include: hoarseness (most common), cough, dyspnea, neck pain, or dysphagia -Teach patient to avoid MRIs, microwaves, shortwave radios, and ultrasound diathermy 2. Conventional Surgery Procedures -Operative care similar for that of craniotomy -Monitor for neurological deficits after surgical procedures

Describe interventions used with spinal cord injury.

Nursing -Focused on maintaining spinal alignment, preserving airway, and preventing complications associated with immobility -SCI above T6 should be monitored for autonomic dysreflexia (see box) -Maintain spinal cord perfusion -Keep MAP at 85-90 mm Hg -Systolic BP less than 90 is avoided (may need vasopressors and fluid therapy) -Glucosteroids (prednisone) -Dextran may be given to treat hypotension -Atropine used for bradycardia -Muscle relaxants (tizanidine, Zanaflex) used for severe muscle spasticity (may cause downiness and sedation) -Intrathecal baclofen (Lioresal) which is administered via programmable pump; monitor for adverse effects (sedation, fatigue, dizziness, and changes in mental status); seizures and hallucinations may occur if ITB is withdrawn suddenly -Celebrex given to prevent heterotopic ossification -Gastric decomposition for first 72 hrs or until bowel sounds return -Prophylaxis for stress ulcers (PPIs) -May need bowel program -Maintain skin integrity -May need catheter -Provide adequate nutrition -May need antithrombosis prophylaxis -May have orthostatic hypotension -Reposition frequently ("wheel chair push-ups"); may need special positioning devices Surgical -Indicated for fractures, spinal misalignment and incomplete injury -May need bone graft or rods and pins -May need external immobilization devices

What is a brain abscess and what causes it?

Purulent infection of the brain in which pus forms in the extradural, subdural, or extracerebral area of the brain. The causative organisms are usually bacteria that invade the brain directly or indirectly. Cerebral abscesses may be a complication of meningitis, penetrating head injury, systemic infection, AIDS. -Can be caused by bacteria (streptococci), yeast, or fungi -Most occur in frontal or temporal lobes

What are the S/S of brain abscess and how are they diagnosed?

S/S -Begin slowly and are similar to meningitis -Headache, fever, and neurologic deficits, or nonspecific S/S 9perform ongoing assessments) -Patient maybe lethargic or confused -Pupils start out equal but may become compromised as ICP increases -LOC progressively declines -Airway and respiratory function may be altered -May have blindness in periphery **-Nystagmus (cerebral hemisphere involvement) -Ataxic gait (cerebral hemisphere involvement) -Motor weakness (hemiplegia indicates frontal lobe involvement) -Seizures (irritation of cortical tissue) -Most often has no sensory impairment -Varying degrees of aphasia (frontal or temporal lobe involvement)** -Late in disease process may have S/S of increased ICP: severe headache, decreased LOC (coma), widened pulse pressure, bradycardia, and irregular respirations -AIDS patient may present with systemic infection, lymphoma, and CNS involvement -Some patients (older adults and immunosuppressed) have atypical symptoms and symptoms may not be present until late in disease process Diagnostic Assessment -Increased WBC and ESR -Culture of ear, nose, throat, and blood may indicate source of infection -CT indicates cerebritis, hydrocephalus, or midline shift -MRI can detects abscess early -EEG can localize lesion (decreased electrical activity around abscess) -Radiography of sinuses -Lumbar puncture if meningitis is suspected or if increased ICP is not present -Needle biopsy may indicate source of infection

What are the S/S of increased ICP, how is it monitored, and how is it diagnosed?

S/S -Emphasis on LOC and motor/cranial nerve function -HTN as a compensatory response to augment CPP -Cushing triad is late sign (systolic HTN w/widening pulse pressure, bradycardia, and irregular respirations) that signifies irreversible damage Monitoring Techniques 1. ICP Monitoring -Indicated for patients with GCS of 3-8 -Used to assess response to therapy (such as administering Mannitol) -Classified by device type -Nurse monitors waveform (correlates with arterial pulse) -Never flush -Zero-reference the transducer system at the level of the foramen Munro 2. Cerebral Oxygenation Monitoring -Monitored by jugular oxygenation -Placement confirmed by neck x-ray -Normal value is 60-70% (less than 50% indicates cerebral ischemia) -Normal values doesn't ensure that all areas of the brain are perfused -PbtO2 value must be greater than 20 mm Hg 3. Other Physiological Monitoring -Hemodynamic monitoring -Continuous EEG (records electrical activity in the brain) Diagnostic Testing 1. Laboratory Tests -ABGs, SpO2, end-tidal carbon dioxide -CBC (emphasis on hemoglobin, hematocrit, and platelets) -Coagulation profile -Electrolytes, blood urea, nitrogen, creatine, liver function, and serum osmolality 2. Radiological Studies and Other Diagnostic Tests -CT scan (asses potential for worsening) -MRI provides anatomical detail -Cerebral blood flow monitoring (noninvasive) via Doppler to assess response to treatment and monitor for vasospasm (increased velocity) -Evoked potential monitoring (noninvasive) records sensation to stimuli to evaluate spinal cord function -EEG monitors for seizure activity or lack brain activity

What are the S/S of meningitis and how is it diagnosed?

S/S -Fever -Headache -Altered mental status -Photophobia -ICP (decreasing LOC) -Nuchal rigidity (classic sign) -Positive Kernig's (Client is in a recumbent position and the thigh is flexed at a right angle to the abdomen and the knee is flexed at a 90 degree angle to the thigh. Extend the leg upward and the patient will experience pain, spasm of the hamstring muscle and resistance to further extension of the leg at the knee.) and Brudinski's (With the client in a supine position, lift the head up from the bed. If positive, the forward neck flexion will cause flexion of both thighs at the hip and flexure movements of the ankles and knees.) signs -Seizure activity (particularly in bacterial) is caused by irritation of cerebral cortex -Older adults and those treated with antibiotics may not have fever -Water retention and dilution of serum sodium by increased sodium loss by kidney caused by excessive secretion of ADH. SIADH may cause increased ICP -Petechial or hemorrhagic rash may develop (systemic) -CSF is cloudy with bacterial Assess for Complications -Increased ICP from pus which can lead to hydrocephalus and cerebral edema (ICP can lead to death) -Observe temperature of extremities -Check peripheral pulses -Check for signs of abnormal bleeding -Signs of septic emboli -Signs of DIC -Seizures -Hemiparesis -Hydrocephalus: increased ICP, urinary incontinence, decreasing LOC Diagnosis 1. Laboratory Assessment **-Definitive diagnosis comes from analysis of CSF** -Older adults or immunosuppressed patient may get CT scan before LP -Broad spectrum antibiotic may be given before LP -WBC is usually elevated -Dilutional hyponatremia is an indicator 2. Other Diagnostics -Chest x-ray -CT or MRI -**Lumbar puncture: Bacterial: increased protein, decreased glucose, cloudy, increased leukocytes; Viral: increased protein, normal glucose, clear, increased lymphocytes** -May culture other areas: blood, wounds, sinuses, etc.

What are the S/S of herniated disc and how are they diagnosed?

S/S -Lower back pain that radiates down the sciatic nerve into the posterior thigh. -Typically begins in the buttocks & extends down the back of the thigh and leg to the ankle. -Can also lead to groin pain -Muscle spasms & hyperesthesia (numbness & tingling) in areas of distribution of affected nerve roots -Pain exacerbated by straining (coughing, sneezing, defecation, bending, lifting, & straight-leg raising) or prolonged sitting & -Pain is relieved by side-lying with the knees flexed -Any movement of lower extremities that stretches the nerve causes pain & involuntary resistance -Straight-leg raising on the affected side is limited -Complete extension of the leg is not possible when the thigh is flexed on the abdomen. -May have depression of deep tendon reflexes Diagnosis -X-Ray Studies -May show spinal degenerative changes -Usually do not show a ruptured disc -Magnetic resonance imaging (MRI) -May show extrusion of disc material into the spinal canal and impingement of a spinal nerve root -Discography injection of a water-soluble imaging material into the nucleus pulposus; used to determine internal changes in the disc. -Electromyography of the peripheral nerves to localize the site of the ruptured disc

What are the S/S of encephalitis and how is it diagnosed?

S/S -N&V -Stiff neck -High fever -Changes in mental status (agitation) -Motor dysfunction (dysphagia) -Focal (specific) neurologic deficits -Photphobia -Phonophobia -Fatigue -Symptoms of increased ICP (decreased LOC) -Joint pain -Headache Other Assessment -Assess LOC using GCS -Mental status changes are more extensive than meningitis -Acute confusion, irritability, and personality changes (especially w herpes simplex) -Monitor for signs of meningeal irritation (nuchal rigidity) -Motor changes vary from mild weakness to hemiplegia -May have muscle tremors, spasticity, ataxic gait, myoclonic jerks, and increased deep tendon reflexes -Observe for CN involvement such as ocular palsies, facial weakness, and nystagmus -Herpes zoster effects may cause rash, severe pain, itching, burning, and tingling in the areas that are affected Diagnosis -LP is done to analyze offending organism -PCR test may detect viral DNA or RNA in CSF -Specificity and sensitivity is used to diagnose encephalitis caused by herpes simplex virus -Electroencephalogram is done to evaluate brain wave activity to detect seizures -CT scan detects increasing ICP or obstructive hydrocephalus

What are the S/S of spinal cord injury and how are they diagnosed?

S/S 1. Respiratory -Assessment of respiratory and neurologic function is priority -Respiratory problems are common with thoracic and cervical injury -Paralysis of diaphragm and intercostal muscles -Baseline ABGs are obtained -Assess adequacy of airway and ventilation (SpO2) -May need trach or ventilator **-Complete lesions are associated with C1-C3 (ventilator dependency), C4-C5 (phrenic nerve impairment and may be treated with phrenic pacemaker), below C5-C6 (intact diaphragmatic breathing with varying impairment of intercostal and abdominal muscles)** -Injuries above T6 may cause respiratory problems -Teach tetraplegics to cough by placing hands on either side of rib cage or upper abdomen below the diaphragm ("cough assist of "quad cough") -Encourage incentive spirometer use -Monitor for complications (pneumonia, pulmonary emboli, atelectasis) 2. Neurological -Emphasis of motor, sensory, and reflex responses -Assess major muscle groups and sensory level -Assess LOC (GCS) -Neurogenic shock (injury at T6 and above) is characterized by inability to regulate body temperature (poikilothermia); should be kept warm with blankets to prevent hypothermia; hyperthermia can occur if patient is warmed too quickly -Ask sensory and motor function and compare bilaterally -May have decreased (hypoesthia) or increased (hyperesthia) sensation 3. Hemodynamic Assessment -Assess for hemorrhage -Managed in CCU 7-14 days after injury to assess hemodynamic injury -Decreased HR may be associated with hypothermia, neurogenic shock, and hypoxia -Venous stasis occurs as a result los of vasomotor tone and paralysis, increasing risk for venous thromboembolism 4. Bowel and Bladder -Atony of bowel and bladder -Urinary retention (catheter may be required) -Risk for paralytic ileus -May require gastrointestinal decompression -Assess for bowel sounds and flatus -Bowel program may be implemented -Flaccid bladder-use Valvasa maneuver (injury to lumbosacral area) --Only perform digital rectal exam when ordered by HP (may cause vagal response) -High fiber diet 5. Skin Assessment -Risk for skin breakdown (skin assessment every 4 hrs) -Inspect halo pins carefully -May cause quadriparesis, tetraplegia, paraplegia or paraparesis 6. Psychosocial Assessment -May be cognitively impaired -May be permanently disabled -May experience, denial, anger, or depression -Man with injuries above T6 are often able to have erection by stimulating reflex activity; ejaculate is less common and may be mixed with urine -Women may be come pregnant (may need invitro); some women report vaginal dryness (may need lubricant) -May need to use special sexual positions -May achieve need for sexuality by nonintercourse Diagnostic Studies -Baseline electrolytes, CBC, PT, platelet count, and ABGs -X-ray, CT, MRI, and myelography used to assess damage -Somatosensory-cortical evoked potential done to assess sensory pathways

What is a spinal cord injury and what causes it?

SCI occurs with or without vertebral injury, resulting in complex and multifaceted biochemical changes in the spinal cord. Hemorrhage and edema damages the spinal cord -Most common causes are MVAs, falls, acts of violence (GSW), and sports injuries -Most commonly occur between ages 16-30 Two Types of Shock 1. Spinal Shock: an electrical silence of the cord below the level of injury that causes complete loss of motor, sensory, and reflex activity; begins within a minute and lasts 4-6 weeks; extent of injury is not known until spinal shock resolve; resolution is signaled by return of deep tendon reflexes; rarely motor and sensory function return **2. Neurogenic shock: occurs from disruption of autonomic pathways, resulting temporary loss of autonomic function below the injury; sympathetic input is lost, causing vasodilation and distributive shock, which manifests as hypotension, bradycardia (pacemaker may be required), and hypothermia; duration is variable; resolution is signaled by return of sympathetic tone** Two Types of Lesions 1. Complete Lesion: causes total, permanent loss of motor and sensory function below the level of injury 2. Incomplete Lesion: more common; results in sparing of some motor and sensory function below the level of injury; have potential for partial recovery; three types (central, anterior, and Brown-sequard)

Describe interventions used for migraines.

Three "R" approach -Recognize migraine symptoms -Respond and see the health care provider -Relieve pain and associated symptoms (**pain relief is a priority**). 1. Abortive Therapy: aimed at alleviating pain during the aura phase (if present) or soon after the headache has started. -Drug therapy started on a low dose that is increased until the desired clinical effect is obtained -Mild migraines may be relieved by acetaminophen, NSAIDS, caffeine, antiemetics. For severe migraines triptan preparations, ergotamine derivatives, and isometheptene combinations (can cause rebound headache/medication overuse headache in which another headache occurs after the drug relieves the initial pain). -**Triptans are contraindicated in patients with actual or suspected ischemic heart disease, CVA, HTN, PVD, and those with Prinzmetal's angina because of potential for coronary spasm** -Ergotine (Cafergot) is taken at the start of a headache -Dihydroergotamine (DHE) should not be given within 24 hrs of a triptan drug -Midrin (a combination drug) is given when ergotamine preparations are not tolerated or do not work -Opioids and barbiturates can be used but should be avoided because they can be addictive--some opioids actually cause a migraine 2. Preventative Therapy -Used when a migraine occurs more than twice a week, interferes with ADLs, or is not relieved with acute treatment -HP may prescribe an NSAID, beta-adrenergic, calcium-channel blocker (beta-adrenergics and calcium-channel blockers can lower blood pressure and heart rate). It is important to take medications as ordered to prevent migraines. --HP may prescribe an anti-epileptic drug like Topamax. Topamax should be used in small doses and can be linked suicide when given in large doses (particularly to bipolar patients) -Trigger avoidance therapy (see box 44-2) --Include healthy diet and exercise to prevent headaches 3. Complementary and Alternative Therapies -Yoga, meditation, massage, exercise, biofeedback, acupuncture, laying in a darkened room, and herbs. Teach patients that all herbs and nutritional therapies should be approved by HP because they may interact with prescriptions. There is no evidence to support any herb or natural remedy, but some patients have had positive results.

What is a head injury and what causes it?

Traumatic brain injury is caused by a blow or jolt to the head or by a penetrating injury (bullet or foreign object). Patient may have short-term or long-term physical, cognitive, financial, and emotional consequences -Direct injury is caused by a force produced by a blow to the head -Indirect injury is caused by force applied to another body part with a rebound effect too the brain -Damage most commonly occurs to the frontal and temporal lobes -Drugs and alcohol are contributing factors -Young males are more likely to be affected -Can be prevented by using fall precautions, wearing seat belts, and wearing helmet Types of Injury 1. Primary Brain Injury -May be mild (GCS 13-15 w loss of consciousness for 15 min), moderate (long period of lost LOC and GCS 9-12), or severe (GCS 3-8 and loss of consciousness more than 6 hrs) -Open head injury occurs when the skull is fractured or when it is pierced by a penetrating object --Three types of fractures: linear (simple clean break), depressed (pressed inward), open (direct opening to the brain), and comminuted (fragmented bone with depression into brain tissue) --Basilar skull fracture occurs at base of skull; results from CSF leakage from the nose or ears; raccoon eyes, rhinorrhea, and preorbital edema; **potential for hemorrhage caused by damage to carotid; damage to cranial nerves I, II, VII, and VIII; potential for infection** --Most penetrating injuries caused by GSW or knife injuries; speed, mass, and velocity determine extent of damage; high risk for infection -Closed head injury is the result of blunt trauma; the integrity of the skull is not violated; more serious that open head injury --Contusion-bruising of the brain tissue most commonly found at the site of impact (croup injury) or in a line opposite of the site of impact (contrecoup injury) --Concussion is a shaky movement of the brain and may be mild or more severe. Some patients lose consciousness for a short time --Diffuse axonal injury seen in high-speed acceleration/deceleration, typically in MVA; significant damage to white matter; may present with immediate coma and most survivors require long-term care --Laceration causes actual tearing of the cortical surface vessels, which may lead to secondary hemorrhage and significant cerebral edema and inflammation; more serious than a contusion 2. Types of Force -Acceleration injury is caused by an external force contacting the head, suddenly placing the head in motion -Deceleration injury occurs when the moving head is suddenly stopped or hits a stationary object -Hyperflexion: Most often seen cervical area at level of C5 to C6; Sudden deceleration motions -Hyperextension: Involve backward & downward motion of the head; Often seen in rear-end collisions or diving accidents -Rotation: Often occur in conjunction with a flexion or extension injury -Axial loading: Vertical compression; Falls & lands on feet -Penetrating injuries: Bullet, knife, etc; Cause permanent damage by anatomical transection 3. Secondary Injury -Includes any processes that occur after the initial injury and worsen or negatively influence patient outcomes --Increased ICP: ICP is maintained at normal level of 10-15 mm Hg; increased ICP is the leading cause of death from head trauma in patients who reach the hospital alive; occurs when the brain can no longer accommodate further volume changes; as ICP increases, cerebral perfusion decreases, leading to tissue hypoxia, a decreased serum pH level, and increase in the level of carbon dioxide, which cause cerebral vasodilation, edema, and further increased ICP; can cause irreversible brain damage (brain herniation syndromes) --Edema: vasogenic, cytotoxic, and interstitial; **cerebral perfusion pressure (CPP) is maintained at 70 mm Hg** --Hemorrhage: causes a brain hematoma or clot; all hematomas are potentially life threatening because they act as a space-occupying lesions and are surrounded by edema; can be epidural, subdural, and intracerebral ~Epidural:A collection of blood between the inner table of the skull & the outermost layer of the dura; Most often associated with: Skull fractures, middle meningeal artery laceration; may have "lucid intervals"; Dilated, fixed pupil on the same side as the impact area is a hallmark of EDH ~Subdural: venous bleeding into the space beneath the dura and above the arachnoid; bleeding occurs more slowly; may present 48 hrs-2wks after impact or 2 weeks to several months after injury; highest mortality rate ~Intracerebral: accumulation of blood within the brain tissue caused by a tearing of small arteries and veins in the subsubcortical white matter; may produce significant brain edema and ICP elevations; brain stem injury have poor prognosis --Hydocephalus is abnormal increase in CSF volume; if not treated may cause increased ICP --Brain Herniation brain shifts and herniates downward as a result of increased ICP ~Uncal herniation creates pressure on CNIII; Late findings include dilated and nonreactive pupils, ptosis, and rapidly deteriorating LOC ~Central herniation manifested Cheyne-Stokes respirations, pinpoint and nonreactive pupils, and potential hemodynamic instability ~All herniations are potentially life threatening, and HP must be notified when they are suspected -Hypercapnia is a powerful vasodilator; results in cerebral vasodilatation & increased cerebral blood volume & ICP; significant hypotension causes inadequate perfusion to neural tissue *Not typical to be hypotensive with TBI If hypotensive, need to rule out internal injuries