Neuron & parts of neuron and their function



Neuro Study Guide neuron & parts of neuron and their functionSensory neuron (afferent)From receptors?in the skin, skeletal muscles, and joints are called somatic. Sensory neurons from receptors in internal organs are called visceral sensory neurons.?Detect stimuli-such as touch, pressure, heat, cold, or chemicals-and then transmit information about the stimuli to the CNS. A motor neuron (efferent) Motor neurons that innervate skeletal muscle are called somatic. Motor neurons that innervate smooth muscle, cardiac muscle, and glands are called visceral.Relay messages from the brain to the muscle or gland cellsInterneuronFound only in the CNSConnect the incoming sensory pathways with the outgoing motor pathways. Besides receiving, processing, and storing informationLearning TipTo remember the difference between?afferent?and?efferent:Afferent: A is for affect or sense.Efferent: E is for effect (action).Or think of the alphabet—A?before?E: You have to feel or sense (afferent) a stimulus before you can take action (efferent).Neuron StructureCell body: control center of the neuron and contains the nucleus. Dendrites: receive signals from other neurons and conduct the information to the cell body. Axon: carries nerve signals away from the body,Myelin sheath: consist mostly of lipid, myelin acts to insulate the axon.Bell’s palsyPathophysiology The facial nerve (cranial nerve VII) becomes inflamed and edematous, causing interruption of nerve impulses. The cause is thought to be nerve trauma from a viral infection such as Epstein-Barr, herpes simplex, or herpes zoster. Loss of motor control typically occurs on one side of the face; bilateral facial palsy occurs rarely. Contracture of facial muscles can occur if recovery is slow. Men and women are affected equally. Bell palsy is more common in women in the third trimester of pregnancy, in people with immune disorders such as HIV, and in people with diabetes. It occurs in all ages (including children).Signs and SymptomsPain behind the ear may precede the?onset of facial paralysis. Dry eye or tingling around the lips.Unable to close the eyelid, wrinkle the forehead, smile, raise the eyebrow, or close the lips effectively. The mouth is pulled toward the unaffected side. Drooling of saliva occurs, and the affected eye has constant tearing. Sense of taste is lost over the anterior two-thirds of the tongue. Speech difficulties occur. Most patients recover completely within 6 months?Therapeutic Measures Prevention of complications is the goal of treatment. Prednisone may be given over 7 to 10 days to decrease inflammation. Antiviral agents such as acyclovir (Zovirax) may be used to fight the virus and can shorten the course of the disease. Analgesics are given for pain control. Moist heat and gentle massage to the face and ear can ease pain. A facial sling can be used to aid in eating and support of facial muscles.stroke PathophysiologyIf the supply of oxygen and glucose is stopped, brain tissue dies. When a stroke occurs, brain cells begin dying immediately. There is an area of brain tissue surrounding the damage called the?penumbra.?It contains brain cells that are “stunned” and can be revived if the brain is reperfused quickly. However, the brain cells will die if the blood supply is not restored.The particular vessel or vessels involved determine the area of the brain affected and symptoms that result. The duration of ischemia determines whether the symptoms are transient or permanent. TIA symptoms generally resolve within 24 hours; however, a TIA can be a warning of an impending stroke.Etiology Strokes are classified as either ischemic or hemorrhagic. Ischemic strokes are more common, accounting for about 87% of all strokes. Hemorrhagic strokes account for the remaining 13% of strokes.Ischemic Stroke Occurs when the blood supply to the brain is blocked or significantly slowed. There are two major types: thrombotic or embolicThrombotic Stroke:Occur when an occlusion builds up in an artery until it significantly decreases or stops blood flow to the brain. Thrombotic strokes most often occur in the internal or common carotid arteries.Embolic Stroke Typically caused by a blood clot that is created somewhere in the body, often within the heart. It then travels through the arteries until it becomes trapped in a smaller vessel, preventing the passage of blood. Typically, the?embolism?will travel and become lodged in the middle, anterior, or posterior cerebral arteries.Risk factors of ischemic stroke:Are classified as modifiable or nonmodifiable. Nonmodifiable risk factors are those that cannot be altered, such as age or gender. Modifiable risk factors are those that can be changed with treatment, such as high blood pressure. Women have additional risks due to hormone changes in pregnancy and menopause. Children with sickle cell disease, cardiac anomaly, and hyperlipidemia are also at risk for stroke. Minimizing or eliminating these modifiable risk factors can significantly lower risk of a stroke. Hemorrhagic StrokeAre caused by the rupture of a cerebral blood vessel that allows blood to escape into brain tissue and not travel beyond the point of the rupture. It can be further classified into two major types: subarachnoid hemorrhage and intracerebral hemorrhage.Subarachnoid Hemorrhage A stroke that occurs on the surface of the brain. It is most often the result of a ruptured cerebral aneurysm.Strokes caused by subarachnoid hemorrhage usually are very serious and require surgery to correct. They are often fatal.Intracerebral HemorrhageA stroke that occurs in the deeper tissues of the brain.It usually is caused by uncontrolled hypertension. Maintaining blood pressure below 120/80 mm Hg should be the goal for these patients.Patients can experience multiple undetected intracerebral hemorrhages, with minimal deficits noted. However, damage will eventually accumulate, and the patient will develop major?deficits. Box 49.1 Modifiable Risk factors for StrokeMen and WomenCigarette smokingHigh blood pressureDiabetes mellitusCardiovascular diseaseHigh total cholesterolLow high-density lipoprotein (HDL) cholesterolDyslipidemiaAtrial fibrillationAsymptomatic carotid stenosisSickle cell diseaseObesityExcessive alcohol intakePoor diet (e.g., high sodium, high fat, low potassium)Physical inactivityWomen Pregnancy Oral contraceptivesHormone replacement therapyHigh triglyceridesHistory of migrainesThick waistWarning Signs for a Stroke The acronym FAST, which states for?Face,?Arms,?Speech, and?Time?Sudden numbness or weakness of face, arm, or leg, especially on one side of the bodySudden confusion or trouble speaking or understandingSudden trouble seeing in one or both eyesSudden trouble walking, dizziness, loss of balance, or coordinationSudden severe headache with no known causeWomen may have other unique symptoms, such as sudden onset of the following:NauseaFacial and limb painSudden behavioral changesHallucinationsGeneral weaknessChest painShortness of breathHiccupsPalpitations?Signs and Symptoms Symptoms are varied and depend on the area of the brain affected. Common symptoms include visual disturbanceslanguage disturbancesweakness or paralysis on one side of the bodydifficulty swallowing (dysphagia). Signs and symptoms are generally the same for both ischemic and hemorrhagic stroke. Patients may have drowsiness and a severe headache, often described as “the worst headache of my life.”Diagnostic Tests On arrival at the emergency department, a computed tomography (CT) scan will be performed immediately. The purpose of the CT scan is to identify whether symptoms are caused by a hemorrhagic stroke so that the health care provider can determine the appropriate course of treatment. Ischemic stroke changes will not be visible on a CT until several days after the event. Interventions for hemorrhagic strokes are different than for ischemic strokes.Patients may have an electrocardiogram (ECG) to determine whether atrial fibrillation is present. An echocardiogram may be done to determine the presence of other heart disease that increases the risk of thrombus formation. Other tests that may be performed in the ED include complete blood count (CBC), blood glucose level, metabolic panel, blood typing, prothrombin time (PT), international normalized ratio (INR), and serum pregnancy, if indicated. Stools and emesis may be checked for blood if indicated. The patient will be placed on a cardiac monitor and pulse oximeter. The ED nurse will complete a dysphagia screen before the patient consumes any food or fluids.Therapeutic Measures Initial emergency care is supportive while test results are pending. ABCs (Airway,?Breathing, and?Circulation) are monitored. Oxygen is administered to maintain oxygen saturation at or above 94% and the patient’s level of consciousness (LOC) is reduced. Vital signs and heart rhythm are monitored. A temperature greater than 99.6°F is treated because hyperthermia is associated with poorer patient outcomes. When test results verify whether the stroke is hemorrhagic or ischemic, therapeutic interventions are begun.Some hospitals have a stroke team that evaluates all patients who arrive at the hospital within 2 hours of symptom onset. The stroke team will assess the patient within the first 15 minutes of arrival. Lab tests, ECG, and CT scans will be done, with results back within 45 minutes after assessment. The HCP will make a decision regarding thrombolytic therapy within 1 hour of arrival.If the patient is hyperglycemic, blood glucose should be lowered to 140 to 180 mg/dL. Hyperglycemia during the first 24 hours following ischemic stroke is associated with worse outcomes. If intravenous (IV) fluids are needed, only solutions without glucose are used, such as normal saline solution.Patients suffering from a stroke can develop increased intracranial pressure (ICP), which further adds to brain damage. Stroke patients are also at risk for repeated strokes. Careful serial neurologic assessments and vital signs are needed to promptly detect and report changes.Thrombolytic Therapy This is a “clotbuster” medication (alteplase [tissue plasminogen activator; tPA]) that can lyse (or break down) a thrombus (clot) and potentially completely reverse stroke symptoms. tPA works best when administered within 3 to 4.5 hours of symptom onset, so it is only an option if the patient arrives at the ED quickly after symptoms begin. Some patients awaken after a night’s sleep to discover they have had a stroke; their symptom onset is considered the time they went to bed, so they are not candidates for thrombolytic therapy.Thrombolytic agents can lyse a thrombus by causing conversion of plasminogen to plasmin. Plasmin is the enzyme that causes thrombi to break down.Patients treated effectively with tPA may be able to leave the hospital within 1 or 2 days with no residual effects from the stroke. Thrombolytics are associated with a significant risk of hemorrhage, so all risk of bleeding must be ruled out before these drugs will be considered. They are used very cautiously. If a patient is experiencing an ischemic stroke involving a large blood vessel of the brain, a stent-retrieval device might be used to remove any remnants of the thrombus after the tPA is used. The device is inserted through the groin and advanced to the affected cerebral vessel.Pharmacological ManagementBlood pressure control is vital for the stroke patient. Because of the lack of perfusion to certain areas of the brain, the body’s response is to increase the systolic blood pressure to force blood into the affected areas. If the patient will receive tPA, the blood pressure must be maintained below 185/110 mm Hg to reduce the risk of bleeding. This is often done through the use of a beta blocker (labetalol) or calcium channel blocker (nicardipine), because of their fast-acting effects and ability to be given via IVIf tPA is not being given, the HCP may allow the blood pressure to remain high for a period of time to help salvage brain tissue, depending on the source of the stroke and location of the thrombus. This “permissive hypertension” helps blood travel through collateral blood vessels in the brain to reach the affected area. Antihypertensive agents should be given if the systolic pressure exceeds 220 mm Hg or the diastolic pressure exceeds 120 mm Hg?Postemergent Care Medical management focuses on controlling the cause of the TIA or stroke. The results of the diagnostic tests help the HCP determine the course of treatment. If the patient has residual physical deficits, the HCP will order physical, occupational, and speech therapy consultations to evaluate the patient’s functional status and make recommendations for further treatment and rehabilitation.Patients who have a minor stroke receive dual antiplatelet therapy with aspirin and clopidogrel (Plavix) within 24 hours of symptom?onset. Decreasing platelet aggregation lessens the likelihood of another stroke. The patient in atrial fibrillation may also receive an anticoagulant to prevent thrombus development. Cholesterol-lowering medication, preferably a statin, will be ordered for patients who have a low-density lipoprotein (LDL) cholesterol level greater than 100 mg/dL. This will also help minimize the development of atherosclerotic plaques. Statins also may have a neuroprotective effect and may further decrease risk of a stroke.Deep vein?thrombosis?(DVT) is of concern when caring for patients who have had a stroke. The decrease in movement, confinement to a hospital bed, and hypercoagulable state all increase risk of DVT. Not only can DVTs cause severe pain and complications in the affected leg, but the thrombus can dislodge and travel to the lungs and cause a pulmonary embolism. Prevention involves anticoagulant medication or nondrug treatments such as sequential compression devices.Stroke patients are at risk for respiratory complications for several reasons, such as an increase in ICP. Patients with stroke are prone to aspiration because of a decreased LOC and possibly impaired swallowing ability. Patients should be orally suctioned as needed to keep the airway clear. A patient who vomits should be turned to the side to reduce the risk of aspiration. Oral feedings should be started carefully and progressed slowly. Feedings should begin only after the patient is alert and the ability to swallow safely has been determined by an appropriate swallowing evaluation.Surgery Patients with warning signs of stroke or patients who have been stabilized after a stroke may be candidates for surgery. In patients with significant carotid artery occlusion, a carotid?endarterectomy?may be performed. This involves a small incision in the neck and surgical removal of the occlusion from the artery.Alternatively, a patient who is at high risk for complications with a carotid endarterectomy may have a carotid stent placed. This is placed during a carotid angiogram procedure. A catheter is advanced to the carotid artery, where a balloon is inflated to open the artery by pushing on the plaque. Then a stent (a tiny metal or polymer-based tube) is expanded inside the artery to keep it open and allow better blood flow to the brain. A risk from either procedure is an ischemic stroke.Seizures/Epilepsy PathophysiologyThe normal stability of the neuron cell membrane is impaired in individuals with seizures. This instability allows for abnormal electrical discharges to occur, causing the characteristic symptoms seen during a seizure.Seizures can be classified as partial or generalized. Partial seizures begin on one side of the cerebral cortex. In some cases, the electrical discharge spreads to the other hemisphere and the seizure becomes generalized. Generalized seizures are characterized by involvement of both cerebral hemispheres.Etiology Epilepsy can be acquired or idiopathic (unknown cause). Causes of acquired epilepsy include traumatic brain injury and anoxic events. No cause has been identified for idiopathic epilepsy. The most common time for idiopathic epilepsy to begin is before age 20. New-onset seizures after this age are most commonly caused by an underlying neurologic disorder. As the population ages, more older adults are having first-time seizure as a result of bleeding or bruising in the brain related to a fall. Multiple medications in the elder population and untreated hypertension can increase the risk of falls as well as brain injury after a fall.Signs and Symptoms Symptoms of seizure activity correlate with the area of the brain where the seizure begins. Some patients experience an aura or sensation that warns that a seizure is about to occur. An aura can be a visual distortion, a noxious odor, or an unusual sound. Patients who experience an aura may have enough time to sit or lie down before the seizure starts, thereby minimizing the risk of injury.Partial SeizuresRepetitive, purposeless behaviors, called?automatisms,?are the classic symptom of partial seizures. The patient appears to be in a dreamlike state while picking at his or her clothing, chewing, or smacking his or her lips. Patients may be labeled as mentally ill, particularly if automatisms include unacceptable social behaviors such as spitting or fondling themselves. Patients are not aware of their behavior or that it is inappropriate. If the patient does not lose consciousness, the seizure is labeled as simple partial and usually lasts less than 1 minute. If consciousness is lost, it is called a complex partial seizure or psychomotor seizure; it can last from 2 to 15 minutes.Partial seizures arising from the parietal lobe can cause paresthesias on the side of the body opposite the seizure focus. Visual disturbances are seen if the seizure originates in the occipital lobe. Involvement of the motor cortex results in involuntary movements of the opposite side of the body. Typically, movements begin in the arm and hand and can spread to the leg and face.The?postictal?period is the recovery period after a seizure. Following a partial seizure, the postictal phase may be no more than a few minutes of disorientation.Generalized Seizures Affect the entire brain. Two types of generalized seizures are absence seizures and tonic-clonic seizures. Absence seizuressometimes referred to as petit mal seizures, occur most often in children. They are manifested by a period of staring that lasts several seconds.Tonic-clonic seizures are what most people envision when they think of seizures; they are sometimes called grand mal?seizures or convulsions. Tonic-clonic seizures follow a typical progression. Aura and loss of consciousness may or may not occur. The tonic phase, lasting 30 to 60 seconds, is characterized by rigidity, causing the patient to fall if not lying down. The pupils are fixed and dilated, the hands and jaws are clenched, and the patient may temporarily stop breathing. The clonic phase is signaled by contraction and relaxation of all muscles in a jerky, rhythmic fashion. The extremities can move forcefully, causing injury if the patient strikes furniture or walls. The patient is often incontinent. Biting the lips or tongue can cause bleeding.Diagnostic TestsAn EEG is the most useful test for evaluating seizures. An EEG can determine where in the brain the seizures start, the frequency and duration of seizures, and the presence of subclinical (asymptomatic) seizures. Sleep deprivation and flashing light stimulation may be used to evaluate the seizure threshold.Therapeutic Measures If an underlying cause for the seizure is identified, treatment focuses on correcting the cause. If no cause is found or if the seizures continue despite treatment of concurrent disorders, treatment focuses on stopping or preventing seizure activity.Numerous anticonvulsant medications are available. Typically, the patient is started on one medication, and the dosage is increased until therapeutic levels are attained or side effects become troublesome. If seizures are not controlled on a single medication, another medication is added. Many anticonvulsants require periodic blood tests to monitor serum levels as well as kidney and liver function. Most of these medications can cause drowsiness, so teach the patient to avoid driving or operating machinery until the effects of the drug are known. Driving is also contraindicated until seizures are under control.If a patient must discontinue an anticonvulsant, it should be tapered slowly according to manufacturer directions. Stopping an anticonvulsant abruptly can result in status epilepticus, discussed later. If seizures continue despite anticonvulsant therapy, surgical intervention may be considered.Surgical Management The success of surgical intervention for epilepsy depends on identification of an epileptic focus within nonvital brain tissue. The surgeon attempts to resect the area affected to prevent spread of seizure activity. In some cases, seizures can be cured, but in others, the goal is to reduce the frequency or severity of the seizures. If no focus is identified or if it is in a vital area such as the motor cortex or speech center, surgery is not feasible.The preoperative assessment for epilepsy surgery is an extensive multistage process. Thorough assessment and teaching are essential. To adequately identify seizure foci, the patient is weaned off anticonvulsant therapy. Increasing the frequency of seizures with weaning is anxiety provoking for patients and family members.Emergency CareIs required when a seizure occurs. The prime objective is to prevent injury during a seizure. Side rails, if used, should be padded to prevent injury if the patient strikes his or her extremities against them. If the patient falls to the floor, move furniture out of the way. Maintain a patent airway, and, if possible, turn the patient on his or her side to prevent aspiration if vomiting occurs. Do not force an airway or anything else into the patient’s mouth once the seizure has begun. Do not restrain the individual because this can also increase the risk of injury. Observe and document the patient’s behavior during the seizure (e.g., which part of the body was first involved, progression of the seizure, length of time the seizure lasted). After the seizure, assess the patient for breathing, suction the oral pharynx if necessary, and, in rare cases, initiate rescue breathing or cardiopulmonary resuscitation (CPR) as indicated.Psychosocial EffectsFinances can be a major concern to patients with seizure disorders. Some patients with epilepsy experience hiring discrimination or may not qualify for some jobs in which safety is a concern. Remind patients that falsifying information on job applications may be grounds for dismissal. Health insurance coverage issues can create financial hardships for patients on long-term medications. Most patients whose seizures are controlled can work and lead productive lives. A social worker can help explore options for financial assistance if needed.Patients with poorly controlled seizures should not operate motor vehicles. Job opportunities may be limited for patients who depend on public transportation. Encourage the patient to obtain a state identification card. This can be used in place of a driver’s license for identification.Patients may limit interpersonal relationships out of fear of having a seizure. The involuntary movements, sounds, and possible incontinence that occur with seizures are embarrassing to patients and can be frightening to laypeople. Role-playing may help the patient determine when and how to confide in others.Language Disturbances Difficulty with language is commonly associated with TIA and stroke.?Aphasia?refers to the absence of language;?dysphasia?refers to difficulty with speech and is not as severe as aphasia. With dysphasia, the patient may experience trouble selecting the correct words, use incomprehensible or nonsense speech, have trouble understanding others’ speech, and have trouble writing or reading. Aphasia can be?expressive,?in which the patient knows what he wants to say but cannot speak or make sense, or?receptive,?which is an inability to understand spoken and/or written words.When both expressive and receptive aphasia are present, it is called?global aphasia.?Slurred or indistinct speech because of a motor problem (lack of coordination) is referred to as?dysarthria.?This speech impairment is often the cause of delay in treatment and emphasizes the importance of observation of symptoms by others.Myasthenia Gravis Pathophysiology Means “grave muscle weakness,” or weakness of the voluntary or skeletal muscles of the body. MG is a chronic disease of the neuromuscular junction. Normally, a neuron releases the chemical neurotransmitter acetylcholine (ACh) at the neuromuscular junction. Receptors on the muscle tissue take up ACh, and contraction of the muscle results. In MG, the body’s immune system is activated, producing antibodies that attack and destroy ACh receptors at the neuromuscular junction. Therefore, ACh cannot stimulate muscle contraction because the number of ACh receptors has been reduced. This results in loss of voluntary muscle strength.Signs and Symptoms MG results in progressive extreme muscle weakness. The classic sign of MG is increased muscle weakness during activity and improvement in muscle strength after rest. Muscles are strongest in the morning, when the person is rested. Activities affected by MG include eye and eyelid movements, chewing, swallowing, speaking, and breathing as well as skeletal muscle function. Patients often present with drooping of the eyelids (ptosis). Facial expressions become masklike. After long conversations, the patient’s voice may fade. Falls occur because of weakness of the arm and leg muscles. Patients with MG experience periods of exacerbation and remission of symptoms, similar to patients with MS. Exacerbations can be caused by emotional or physical stress such as menses, illness, trauma, extremes in temperature, pregnancy, electrolyte imbalance, surgery, and drugs that block action at the neuromuscular junctionTherapeutic MeasuresNo cure is currently available for MG. Treatment is aimed at controlling symptoms. Removal of the thymus gland (thymectomy) can decrease production of ACh receptor antibodies and decrease symptoms in most patients. Medications used to treat MG include the anticholinesterase drugs neostigmine (Prostigmin) and pyridostigmine (Mestinon). These drugs improve MG symptoms by destroying the acetylcholinesterase that breaks down ACh. Remember that ACh causes muscles to contract. If ACh is allowed more time to attach to remaining muscle tissue receptors, the muscle contracts and strength is increased. Steroids such as prednisone and immunosuppressants are used to suppress the body’s immune response. The monoclonal antibody ritux-imab (Rituxan) is an IV-administered medication used in some cases of MG; it works by affecting the immune system. Plasmapheresis can be used to remove antibodies from the patient’s blood. IV immunoglobulin (IVIg) helps restore normal immune function.Intracranial Surgery The primary purpose of intracranial surgery is to remove a mass lesion. These types of lesions include hematomas, tumors, arteriovenous malformations, and, occasionally, contused brain tissue. Other indications for surgery include elevation of a depressed skull fracture, removal of a foreign body, debridement of a wound, or resection of a seizure focus. The term?craniotomy?refers to any surgical opening in the skull. A burr hole is an opening into the cranium made with a drill.?Craniectomy?is the term used to describe removal of part of the cranial bone.?Cranioplasty?refers to repair of bone or use of a prosthesis to replace bone following surgery.The goal of intracranial tumor surgery is gross total resection (removal) of the tumor. This involves removal of all visible tumor, called?debulking.?Even with the use of an operative microscope, viable tumor cells can be left behind that can give rise to recurrence. If the entire tumor cannot be removed, the surgeon debulks as much as possible, giving radiation therapy or chemotherapy less of a burden to combat. In some cases, it is not feasible to attempt more than a biopsy of the tumor. Location of the tumor or the patient’s age or medical condition may not allow the patient to tolerate a full craniotomy. A biopsy may be done under local or general anesthesia, depending on the patient’s condition. The goal of a biopsy is to obtain tissue that allows pathological diagnosis of the tumor, which then guides further treatment.Intracranial surgery is usually performed under general anesthesia. Occasionally, a procedure requires that the patient be awake and cooperative.Preoperative CarePreoperative care of the patient undergoing intracranial surgery is similar to that of patients having other surgeries.The patient undergoes a laboratory workup and anesthesia evaluation. If the patient has cognitive impairments, it is important that a family member be available to provide information and sign consents. A thorough baseline neurologic assessment should be documented.Patient education is important preoperatively. The extent of education depends on the patient’s ability to absorb new information, which is influenced by the disease process, cognitive functioning, anxiety, and education level. Family members are involved as needed. Information about the disease process and surgery is provided by the surgeon. The nurse can play an important role in reinforcing and clarifying the information presented.Anxiety is also a significant concern before surgery. The patient is anticipating serious surgery as well as an unknown outcome. Allow time for the patient and family members to express their fears and ask questions. Honest and accurate information should be provided.Family members should be prepared for how the patient will look after surgery. A preoperative visit to the ICU may help prevent some anxiety postoperatively. Family members should be accompanied on this visit by a knowledgeable nurse who can explain what they are seeing.Surgery can last 2 hours for a biopsy to 12 hours or longer for more involved procedures. Patients and family members should be prepared for the idea that some or all of the patient’s hair will be shaved off. Some people prefer to have all their hair shaved rather than just part. The patient should be prepared to see his or her face swollen after surgery, particularly around the eyes; the periorbital region may be bruised. Many patients wish to wear a scarf or scrub cap after the dressing is removed.Nursing Process for the Postoperative Care of the Patient Having Intracranial SurgeryData CollectionAfter intracranial surgery, the patient will be cared for in the ICU. Plan to assist the RN with frequent neurologic assessments in addition to routine postoperative monitoring. Patients should have their neurologic status assessed every hour for the first 24 hours or as ordered by the health care provider (HCP). Many patients undergo a CT scan within the first 24 hours following surgery to assess cerebral edema. Once the patient is awake and alert, plan to assess the patient’s response to changes in body image and knowledge base related to care that will be required following discharge.Nursing Diagnoses, Planning, and ImplementationThe primary goal after intracranial surgery is prevention of complications. Once the patient is stabilized, goals can change to longer-term outcomes such as acceptance of changes in body image and understanding of self-care following discharge. If the patient has severe deficits following surgery, rehabilitation or long-term care may become necessary. A consultation with a social worker can help with planning for this transition.Parkinson’s Disease Pathophysiology A chronic degenerative movement disorder that arises in the basal ganglia in the cerebrum. Parkinson disease has typically been considered a disease of older adults; however, there are many people with young-onset Parkinson disease.The disease is characterized by tremors, changes in posture and gait, rigidity, and slowness of movements.?The substantia nigra is a group of cells located within the basal ganglia, which is situated deep in the brain. These cells are responsible for the production of dopamine, an inhibitory neurotransmitter. Dopamine facilitates the transmission of impulses from one neuron to another. Parkinson disease is caused by destruction of the cells of the substantia nigra, resulting in decreased dopamine production. Loss of dopamine function results in impairment of semiautomatic movements. Parkinson disease is sometimes referred to as an extrapyramidal disorder because the extrapyramidal tracts in the spinal cord that contain motor neurons are affected.Acetylcholine, an excitatory neurotransmitter, is secreted normally in individuals with Parkinson disease. The normal balance of acetylcholine and dopamine is interrupted in these?patients, causing a relative excess of acetylcholine. This results in the tremor, muscle rigidity, and?akinesia?(loss of muscle movement) characteristic of Parkinson disease.Signs and Symptoms The onset of symptoms in patients with Parkinson disease is usually gradual and subtle. A substantial percentage of the dopamine-producing cells are nonfunctional before the patient becomes symptomatic.The primary symptoms of Parkinson disease are muscular rigiditybradykinesia?(slow movement) or akinesiachanges in postureand tremors. The brain is no longer able to direct the muscles to perform in the usual manner. This lack of communication between the brain and muscles can have a profound impact on the patient’s ability to ambulate safely, perform ADLs and job functions, or enjoy leisure activities. The symptoms may also have a significant negative impact on the patient’s self-esteem.The patient may have difficulty initiating movement; this can be particularly apparent when the patient tries to start walking, rise from a sitting position, or begin dressing. Because considerable effort is required to move the rigid muscles, the patient performs voluntary movements very slowly. At times, the patient can experience freezing of gait and be unable to initiate ambulation or negotiate a turn during ambulation.The extensor muscles are more affected by Parkinson disease than the flexor muscles. This impaired function of the extensor muscles results in the stooped posture typical of patients with Parkinson disease. Flexion of the hips, knees, and neck shifts the center of gravity forward. The gait is characterized by short, shuffling steps that may increase in speed once the patient finally starts walking. Once in motion, the patient may have difficulty stopping. The patient maintains a broad base when making turns to try to compensate for imbalance. These changes place patients at high risk for falls. Slowness of movement and stiff muscles make it much harder for patients to catch themselves if they start to fall or to relax the muscles to minimize injury.Tremors typically begin in the hand and then progress to the?ipsilateral?foot. In most patients, the tremor then moves to the?contralateral?side. Many patients identify one side of the body as being more affected by the tremor than the other. Tremor of the hand has been described as a pill-rolling tremor; the thumb typically moves back and forth across the fingers and looks like the patient is rolling a pill. Tremors typically lessen or disappear during movement and are more noticeable when the extremity is at rest or when trying to hold an object still (this is called a resting tremor). The tremors disappear when the patient is asleep. The inability to hold an object still can make simple acts such as drinking a glass of water or reading a book nearly impossible. The signs and symptoms of Parkinson disease tend to increase in severity when the patient becomes fatigued. Another type of tremor, a benign familial (or essential) tremor, can sometimes be mistaken for Parkinson disease. The secondary symptoms of Parkinson disease include generalized weaknessmuscle fatigue crampingdifficulty with fine motor activities. This fine motor dysfunction can make it difficult for the patient to button a shirt or tie shoes. Handwriting typically deteriorates as the disease progresses. A soft, monotone voice and masklike facial expression can make the patient appear to be lacking in emotional responses. It may be necessary to ask patients about their emotional status and help them develop ways to express their emotions. The normal blink response is diminished, so?the patient and significant others must be educated about eye care to prevent corneal abrasions.Dysfunction of the autonomic system can cause DiaphoresisConstipationorthostatic hypotensiondroolingdysphagiaseborrheafrequent urination. Patients who experience seborrhea and diaphoresis need frequent attention to personal hygiene. Drooling and dysphagia can make the patient reluctant to appear in public. Slowness in initiating walking, balance problems, and frequent urination place the patient at risk for urinary incontinence, which can also increase the patient’s reluctance to leave home.Late in the disease, mental function may become slowed, and the patient may develop dementia. This is compounded by the side effects of many anti-Parkinson drugs. Death is usually from complications of immobility.Therapeutic Measures There is no cure for Parkinson disease. Treatment is aimed at controlling symptoms and maximizing the patient’s functional level. Many patients with Parkinson disease experience fluctuations in motor function related to their drug therapy. This is referred to as the “on–off phenomenon.” Patients may experience a decreased response to levodopa, or off period, particularly as the dose is wearing off. As the disease progresses, patients may notice that the off periods become less predictable and occur more rapidly. The patient may have a delayed or absent response to the next dose of levodopa, resulting in the patient being stuck in the off stage and being significantly disabled for that period. Fluctuations in motor function can be accompanied by other symptoms, such as pain, diaphoresis, anxiety attacks, hallucinations, or mood swings. These symptoms significantly increase the disability associated with the episodes.Patients who are taking maximum doses of medication for Parkinson disease symptoms may benefit from a “drug holiday.” During a drug holiday, patients are taken off all drugs for a time and then restarted on lower doses. Hospitalization may be necessary during this time to maintain patient safety.parts of the brain and their functionBrainConsists of many parts that function as an integrated whole. The four principle areas are the cerebrum, diencephalon (thalamus and hypothalamus), brainstem (midbrain, pons, and medulla oblongata), and cerebellum.MeningesThe meninges are the three layers of connective tissue that cover the CNS. Where they enclose the brain, they are referred to as cranial meninges.Ventricles and Cerebrospinal FluidThe ventricles are four cavities within the brain: two lateral ventricles are located within the cerebral hemispheres, the third ventricle lays midline within the thalamusthe fourth ventricle is midline between the brainstem and cerebellum. CSF is formed from capillaries of the choroid plexus within and circulates through the four ventricles. Circulation of CSF moves inferiorly within the CNS, into the?subarachnoid?space, and ultimately superiorly to drain into the dural venous sinuses. CSF permits the exchange of nutrients and wastes between the blood and CNS neurons. It also acts as a cushion or shock absorber for the CNS. The pressure and constituents of CSF may be determined by means of a lumbar puncture (spinal tap) and may be helpful in the diagnosis of diseases such as meningitis.Brainstem: Midbrain, Pons, and Medulla OblongataPrimarily a reflex center, the midbrain regulates visual reflexes (coordinated movement of the eyes), auditory reflexes (turning the ear toward a sound), and righting reflexes that keep the head upright and contribute to balance. Within the pons are two respiratory centers that work with those in the medulla oblongata to produce a normal breathing rhythm. The medulla oblongata lies just superior to the spinal cord. It regulates the most vital life functions.CerebellumThe cerebellum is posterior to the brainstem. The functions of the cerebellum include the involuntary aspects of voluntary movement: coordination, appropriate direction and endpoint of movements, and maintenance of posture and balance. For maintenance of balance, the cerebellum uses input from vision, proprioceptors, and equilibrium receptors in the inner ear to detect movement and changes in position.Diencephalon: Thalamus and HypothalamusDeep beneath the cerebral hemispheres, the diencephalon consists primarily of the thalamus and hypothalamus. Above the brainstem, the thalamus acts as a gateway for nearly every sensation traveling to the cerebral cortex. The thalamus filters sensory input, permitting the cerebrum to concentrate on more important sensations with less distraction. The hypothalamus suspends the pituitary gland from a stalk called the infundibulum; they are anatomically and physiologically connected.CerebrumThe two cerebral hemispheres form the largest part of the human brain. The right and left hemispheres are connected?primarily by the corpus callosum, a band of about 300 million nerve fibers. The cerebral cortex is folded extensively into convolutions (or gyri) that create more surface area for neurons. The deep grooves between the folds are called fissures; shallow grooves are called sulci. The cerebral cortex is divided into lobes, whose functions have been extensively mappedtrigeminal neuralgia Pathophysiology Involves the fifth cranial (trigeminal) nerve. The fifth cranial nerve has three branches that include both sensory and motor functions. The branches innervate areas of the face, including the forehead, nose, cheek, gums, and jaw. TN affects only the sensory portion of the nerve. Irritation or chronic compression of the nerve is suspected to initiate symptoms. This condition is seen more often in women and usually begins about age 50 to 60.Signs and Symptoms Causes intense recurring episodes of pain, described as sudden, jabbing, burning, or knifelike. Episodes of pain begin and end suddenly, lasting a few seconds to minutes. Attacks occur in clusters from a few times a year to up to hundreds of times daily. Pain is felt in the skin on one side of the face. A slight touch, cold breeze, talking, or chewing can trigger attacks of pain. The areas of the face where pain occurs are referred to as trigger zones. Areas affected include the lips, upper or lower gums, cheeks, forehead, or side of the nose. Sleep provides a period of relief from the pain. Therefore, persons with TN may sleep most of the time to avoid painful attacks. They also may refrain from activities such as talking, face washing, teeth brushing, shaving, and eating to prevent pain. Frequent blinking and tearing of the eye on the affected side also occur.Therapeutic Measures Initial management includes the use of anticonvulsants such as phenytoin (Dilantin), gabapentin (Neurontin), or carbamazepine (Tegretol) to reduce transmission of painful nerve impulses. Baclofen or clonazepam (Klonopin) may also be effective in controlling symptoms. Commonly administered analgesics and opioids are typically not effective in managing the sharp, intense pain.If medications are not effective, surgery to remove the vessel that is irritating the nerve may be done. Other methods such as radiation, injection, or heat may be used to destroy the sensory portion of the trigeminal nerve. These interventions leave the patient with varying degrees of plementary and alternative therapies such as botulinum toxin (Botox) injection, acupuncture, electrical stimulation, and nutritional therapy have been used with varying success.Headaches Migraine Headaches Migraine headaches are a neurologic disorder involving brain chemicals and neurologic pathways. Current thought is that a trigger stimulates a release of chemicals that cause an inflammatory response and overstimulation of the trigeminal nerve, resulting in pain. A migraine may or may not involve an aura, such as vision changes or tingling, that precedes an attack. The tendency to develop migraine headaches is often hereditary. Children who have one or both parents who experience migraines are more likely to experience them as well. Migraines frequently begin in childhood or adolescence and are more common in women. Common migraine triggers include hormones (menses related), changes in barometric pressure, specific foods, noise, bright light, alcohol, and stress.There are two major types of migraine: migraine with aura and migraine without aura. There are four phases generally associated with migraine headaches: prodromal, aura, headache, and resolution. The pre-headache?(prodromal)?phase can include symptoms such as irritability, sleepiness, or food cravings. The aura stage might include visual disturbances, difficulty speaking, and/or numbness or tingling. The?headache that follows is often accompanied by nausea and sometimes vomiting; it can last for hours to days. Commonly used descriptors of migraine pain include?throbbing, boring, viselike,?and?pounding.?The pain is usually on one side of the head. Noise and light tend to worsen the headache, leading patients to find a dark, quiet environment. The final stage, resolution, might be accompanied by sluggishness or confusion. Treatment of migraine may be prophylactic or directed at an acute episode. Prophylactic treatment is usually reserved for those patients experiencing one or more migraine headaches per week. Patients who experience 15 or more days a month with a migraine headache may be treated with botulinum toxin (Botox). Small doses of Botox are injected into specific areas of the head and neck around pain fibers that stimulate the release of the inflammatory chemicals. It may take two or three treatments of Botox for the patient to experience relief. The treatments are repeated every 3 months.Dietary restrictions can be helpful if precipitating foods or beverages can be identified.Several types of medications are available to treat acute migraine headaches. Nonsteroidal anti-inflammatory drugs (NSAIDs) such as naproxen (Naprosyn, Aleve) may be tried first. Ergot (Cafergot), a vasoconstrictor, is effective only if taken before the vessel walls become edematous, usually within 30 to 60 minutes of headache onset. Triptans, such as sumatriptan (Imitrex) and zolmitriptan (Zomig), work at the serotonin receptor sites and have a vasoconstricting action. Treximet combines naproxen and sumatriptan. Opioids are habit forming and are used only as a last resort. The potentially additive effects of multidrug regimens require careful monitoring.A new class of medication is under development for the treatment of migraine headaches. Calcitonin gene-related peptide (CGRP) spikes during migraine attacks. The new medications are aimed at neutralizing CGRP or at blocking its receptor sites.Tension or Muscle Contraction Headaches Persistent contraction of the scalp and facial, cervical, and upper thoracic muscles can cause tension headaches. A cycle of muscle tension, muscle tenderness, and further muscle tension is established. This cycle may or may not be associated with vasodilation of cerebral arteries. Tension headaches can be associated with premenstrual syndrome or psychosocial stressors such as anxiety, emotional distress, or depression. Symptoms typically develop gradually. Radiation of pain to the crown of the head and base of the skull, with variations in location and intensity, is common.?Pressure, aching, steady,?and?tight?are some of the words patients use to describe the pain of tension headaches.Care must be taken to thoroughly rule out physical causes before attributing the headache to psychosocial origins. Symptom management may include the use of relaxation techniques, massage of the affected muscles, rest, localized heat application, nonopioid analgesics, and appropriate counseling.Cluster Headaches Vascular disturbance, stress, anxiety, and emotional distress are all proposed causes of cluster headaches. As indicated by the name, these headaches tend to occur in clusters during a time span of several days to weeks. Months or even years can pass between episodes. Alcohol consumption may worsen the episodes.The patient may state that the headache begins suddenly, typically at the same time of night.?Throbbing?and?excruciating?are often the adjectives used by the patient. The headache tends to be unilateral, affecting the nose, eye, and forehead. A bloodshot, teary appearance of the affected eye is common.Because of the brief nature of cluster headaches, treatment is difficult. A quiet, dark environment and cold compresses can lessen the intensity of the pain. NSAIDs or tricyclic antidepressants may be prescribed.Plasmapheresis Also known as plasma exchange therapy, is a procedure that removes the plasma component from whole blood and replaces it with fresh plasma. The goal is to remove antibodies through plasma exchange, suppressing the immune response and inflammation.Preprocedure Nursing CareTeach the patient about the procedure and what to expect, including what the machine looks like (similar to but smaller than a dialysis machine), the need for arterial and venous access sites, and the length of the procedure (2 to 5 hours).The health care provider may order medications held until after the procedure. Some patients may require premedication, especially if they have experienced complications in the past.Assess baseline vital signs and weight.Assess complete blood cell count (CBC), platelet count, and clotting studies.Check blood type and crossmatch for replacement blood products.Postprocedure Nursing CareObserve the patient for signs of hypovolemia, such as dizziness and hypotension.Apply pressure dressings to the access sites.Monitor the patient for infection and bruits at the access site.Monitor electrolytes and signs of electrolyte loss. Report imbalances, and administer replacement electrolytes as pare preprocedure and postprocedure laboratory data, such as CBC, platelet count, and clotting times.Brain tumorsPathophysiology Brain tumors cause symptoms by either compressing or infiltrating brain tissue. Tumors can arise from CNS cells or can metastasize from other locations in the body. Primary brain tumors rarely metastasize; however, if they do, it is to the spine.There is no established cause for primary brain tumors. It is unclear what causes the cells to begin reproducing in an uncontrolled fashion. Risk factors include age (45 and older), exposure to radiation or industrial chemicals, and family history. Whites are more likely to be diagnosed with a brain tumor than other racial or ethnic groups.Brain tumors can be classified in several ways. The traditional distinction of benign and malignant is less helpful when classifying brain tumors than when classifying other cancers. A benign tumor in the brainstem can be fatal, whereas a malignant tumor in the frontal lobe may not be. Location of the tumor can be just as important a factor in outcome as the cell type.Primary tumors are those arising from cells of the CNS. Intra-axial tumors are those that arise from the glial cells within the cerebrum, cerebellum, or brainstem. These tumors infiltrate and invade brain tissue. Extra-axial tumors arise from the skull, meninges, pituitary gland, or cranial nerves; they place pressure on the brain.Most brain tumors are secondary; that is, they have metastasized from a primary malignancy somewhere else in the body. These tumors commonly spread via the arterial system. If untreated, they cause increased ICP. This can be the cause of the patient’s death rather than the primary malignancy.Signs and Symptoms The symptoms of a brain tumor are directly related to the location of the tumor in the brain and to the rate of growth. Slow-growing types of tumors such as meningiomas (a tumor arising from the meninges can get to be quite large before causing symptoms. Conversely, glioblastoma multiforme or metastatic tumors can abruptly cause seizures or hemiparesis. Other types of tumors include oligodendroglioma, astrocytoma, and acoustic neuroma. The most common early symptom of a brain tumor is fatigue. Other symptoms can include seizuresmotor and sensory deficits,nausea and vomitingheadachespersonality changesconfusion speech and vision disturbances. If the pituitary gland is involved, additional symptoms related to changes in hormone secretion occur, such as abnormal growth or fluid volume imbalances.Diagnostic Tests MRI gives the clearest images of a brain tumor. If the tumor appears to be highly vascular or in proximity to major blood vessels, an angiogram may be performed. It is now possible to do a magnetic resonance angiogram (MRA), which involves IV administration of contrast material. MRA is much less invasive than a traditional angiogram. If the tumor is in the region of the pituitary gland, serum hormone levels are evaluated. Biopsy may be done during surgical removal of the tumor or using needle aspiration. Additional tests may be carried out to find a primary cancer site.Therapeutic Measures Surgery Surgical treatment involves removal of the tumor or as much of the tumor as possibleMedical Treatment Medical treatment is aimed at controlling symptoms. Patients who have a seizure are placed on anticonvulsants. If significant cerebral edema is noted on MRI or if the patient is suffering from headaches or other symptoms, a steroid such as dexamethasone (Decadron) may be prescribed to lessen edema and reduce symptoms. Typically, patients do not require narcotics for pain relief.Radiation Therapy External beam radiation therapy is standard treatment for many patients with a brain tumor.The therapy is typically given 5 days a week for 6 weeks. Some clinicians use a hyperfractionated schedule, in which the patient has therapy twice a day for less time. Brachytherapy is a means of delivering radiation therapy directly to the tumor. Small catheters are implanted in the tumor, and then tiny radioactive particles are inserted into the catheters. The treatment typically takes 3 to 5 days. During this time, the patient is confined to a private room. Interaction with visitors and staff is kept to a minimum to reduce exposure to radioactivity. This therapy is not appropriate for confused individuals because they may not be able to cooperate with restrictions.Stereotactic radiosurgery is a technique that uses small amounts of radiation directed at the tumor from different angles. A metal frame is affixed to the patient’s skull, and the tumor is visualized within the framework on a CT scan or MRI. A computer plan is generated to direct the radiation. Because multiple small sources are used, the normal brain tissue receives very little radiation, while the majority of the radiation accumulates in the tumor.Chemotherapy The blood–brain barrier is a protective mechanism that prevents many injurious substances from reaching brain tissue. Unfortunately, it is also effective in preventing most chemotherapy agents from reaching the brain. To penetrate the blood–brain barrier, large doses of chemotherapy may be required. These doses may not be well tolerated by other body systems. Chemotherapy substances may be placed in the cavity left by surgical resection. Other treatments disrupt the blood–brain barrier with mannitol (an osmotic diuretic) and then deliver intra-arterial chemotherapy under general anesthesia. Targeted drug therapy uses a drug such as bevacizumab (Avastin), which stops formation of new blood vessels that support the tumor. Gene therapy is also being used in an effort to kill malignant cells.Cranial Nerves NumberNameFunctionIOlfactorySense of smellIIOpticSense of sightIIIOculomotorMovement of eyeballConstriction of pupil for bright light or near visionIVTrochlearMovement of eyeballVTrigeminalSensation in face, scalp, and teethContraction of chewing musclesVIAbducensMovement of eyeballVIIFacialSense of tasteContraction of facial musclesSecretion of salivaVIIIVestibulocochlearSense of hearingSense of equilibriumIXGlossopharyngealSense of taste Secretion of salivaSensory input for cardiac, respiratory, and blood pressure reflexesContraction of pharynx, swallowingXVagusSensory input in cardiac, respiratory, and blood pressure reflexesSensory and motor input to larynx (speaking)Decreased heart rateContraction of alimentary tube (swallowing, peristalsis)Increased digestive secretionsXIAccessoryContraction of neck and shoulder musclesMotor input to larynx (speaking)XIIHypoglossalMovement of the tonguestatus epilepticus Status epilepticus is characterized by at least 30 minutes of repetitive seizure activity without a return to consciousness. This is a medical emergency and requires prompt intervention to prevent irreversible neurologic damage. Abruptly stopping anticonvulsant therapy is the usual cause of status epilepticus.Seizure activity precipitates a significant increase in the brain’s need for glucose and oxygen. This metabolic demand is even greater during status epilepticus. Irreversible neuronal?damage can occur if cerebral metabolic needs cannot be fulfilled. Adequate oxygenation must be maintained, if necessary, by intubating and mechanically ventilating the patient. These patients are also at significant risk for aspiration. Therefore, it is important that the nurse assist in airway maintenance and suction as needed to prevent hypoxia and aspiration pneumonia. Intravenous (IV) diazepam (Valium) or lorazepam (Ativan) is administered to stop active seizures. Diazepam can also be given rectally. Because both of these drugs can cause respiratory depression, careful airway management is required. After obtaining serum drug levels, anticonvulsant therapy is adjusted to achieve therapeutic levels.If seizures remain resistant to treatment, a barbiturate coma may be induced with IV pentobarbital. The last line of treatment for status epilepticus is general anesthesia or pharmacological paralysis. Both of these therapies require intubation, mechanical ventilation, and management in an ICU setting. Continuous EEG monitoring is used to verify that the seizures have actually stopped. A patient treated with neuromuscular blockade drugs can still be seizing but have no visible manifestations.Guillain-barre syndrome PathophysiologyA rare neuromuscular disease. Both men and women in the United States are affected equally. Onset is usually between 30 and 50 years of age. GBS is an inflammatory disorder characterized by abrupt onset of symmetrical paresis (weakness) that progresses to paralysis. The myelin sheath of the spinal and cranial nerves is destroyed by a diffuse inflammatory reaction. The peripheral nerves are infiltrated by lymphocytes, which leads to edema and inflammation. Segmental?demyelination?causes atrophy of the axons, resulting in slowed or blocked nerve conduction. Typically, the demyelination begins in the most distal nerves and ascends in a symmetrical fashion.?Remyelination?is a much slower process. It occurs in a descending pattern and is accompanied by a resolution of symptoms.It is characterized by progressive weakness and numbness that begins in the legs and ascends up the body. The numbness tends to be mild, but the muscle weakness usually progresses to paralysis. The paralysis can ascend all the way to the cranial nerves or stop anywhere between the legs and head. Deep tendon reflexes are either depressed or absent. Respiratory function becomes compromised in approximately 50% of patients with ascending GBS.Signs and Symptoms Divided into three stages Stage 1: Onset of SymptomsThe first stage starts with the onset of symptoms and lasts until the progression of symptoms stops. This stage can last from 24 hours to 3 weeks. It is characterized by abrupt and rapid onset of muscle weakness and paralysis, with little or no muscle atrophy. Patients with ascending GBS may gradually notice a reduced ability to take deep breaths or carry on conversations and may feel short of breath. These patients are terrified that they will not be able to breathe and may require intubation and artificial ventilation.The autonomic nervous system is often affected by GBS. Patients can experience unstable blood pressure, cardiac arrhythmias, urine retention, or paralytic ileus. Patient reports of discomfort range from annoying numbness and cramping to severe pain. The discomfort is exacerbated by the patient’s inability to move voluntarily.Stage 2: Plateau The second stage is the plateau stage, when symptoms are most severe but progression has stopped. It can last from 2 to 14 days. Patients may become discouraged if no improvement is evident.Stage 3: Recovery Axonal regeneration and remyelination occur during the third state, recovery. This stage lasts from 6 to 24 months, and symptoms slowly improve. Most patients with GBS recover completely within a few months to a year. A few patients experience chronic disability.Therapeutic Measures During the initial stages, patients are partially or completely dependent for all needs. They are often frightened and anxious. Oxygen and mechanical ventilation may be required. Plasmapheresis may be used to remove the patient’s plasma and replace it with fresh plasma. This procedure is thought to lessen the body’s immune response. Immunoglobulin therapy may help reduce the severity of the disease. Supportive interventions include anticoagulants to prevent deep vein thrombosis and analgesics for pain. Intensive rehabilitation helps the patient regain function during the recovery phase.Nursing Care for the Patient with Gullain-Barre Syndrome Assess the patient’s vital signs, arterial blood gases (ABGs), and oxygen saturation (SpO2) to monitor respiratory status. Monitor gag, corneal, and swallowing reflexes to determine whether safety measures are needed to prevent aspiration or injury to the eyes. Be prepared to teach the patient and family about the disease and treatment.?Glasgow Coma Scale/types of posture Is an international scale used to assess LOC and document findings. The GCS is used to evaluate patients who have a potential for rapid deterioration in consciousness. When assessing LOC, consider the patient’s physical ability to respond, taking into consideration trauma, medical condition, and medications. For example, a patient who cannot open his or her eyes because of facial trauma may still have an intact neurologic system.Motor response is scored in the GCS based on following commands, responding to pain, or displaying abnormal postures. Abnormal postures include decorticate and decerebrate. In?decorticate,?or flexion, posturing, the patient’s arms are flexed at the elbow, the hands are raised toward the chest, and the legs are extended. This posture indicates significant impairment of cerebral functioning. In?decerebrate,?or extension, posturing, both the arms and legs are extended, and the arms are internally rotated. This abnormal posturing indicates damage in the area of the brainstem.The total possible score on the GCS ranges from 3 to 15. A score of less than 7 indicates a comatose patient and a score of 15 indicates the patient is fully alert and oriented. When used to score the effects of a head injury, a score of 13 or 14 indicates mild head injury, 9 to 12 indicates moderate injury, and any score of 8 or below indicates severe head injury. For all categories of the GCS, the type of painful stimuli required to elicit a response should be documented. Deterioration in the patient’s condition (i.e., a lowering of the GCS score) should be reported to the HCP promptly.multiple Sclerosis Pathophysiology A chronic progressive degenerative disease that affects the myelin sheath of the neurons in the CNS. Myelin is responsible for the smooth transmission of nerve impulses. In MS, the myelin sheath begins to break down as a result of activation of the body’s immune system. The affected nerves become inflamed and edematous, which interrupts impulses to the muscles. As the disease progresses, sclerosis or scar tissue damages the nerves. Nerve impulses can become completely blocked, causing permanent loss of muscle function in that area of the body.Signs and Symptoms Symptoms vary greatly among patients. Patients may present with muscle weaknesstingling sensationsnumbnessvisual disturbances, usually in one eye at a time. Symptoms may begin slowly over weeks to months or start suddenly and dramatically. MS affects many body systems. Many factors can trigger the onset of symptoms or aggravate the condition, including extreme heat and coldfatigueinfectionphysical and emotional stress. Hormonal changes after pregnancy can also cause symptom onset or exacerbation.Periods of exacerbation and remission lead patients with MS to be uncertain about when the disease will flare up and what body system will be affected. Intense fatigue is common; therefore, immobility can become a problem. Accidents and falls are common because of muscle weakness or numbness of the trunk and limbs. Some people with MS experience symptoms such as muscle spasticity, bowel or bladder dysfunction, or paralysis. Difficulty with concentration or forgetfulness can also be problematic. Pneumonia can occur from immobility and from weakness of the diaphragm and intercostal muscles. Death, often resulting from respiratory infection, typically occurs 20 to 35 years after diagnosis.Therapeutic Measures No cure, although early treatment can delay progression of the disease. Some drugs can slow disease progression by modifying the immune system, such as interferon therapy (Betaseron or Avonex) or immunoglobulins (ocrelizumab [Ocrevus]). Teriflunomide (Aubagio) and dimethyl fumarate (Tecfidera) can reduce relapses. Each of these medications has serious side effects.Other drugs are given to control symptoms. Steroids such as adrenocorticotropic hormone (ACTH, which triggers the body to make its own steroids) and prednisone are given to decrease inflammation and edema of the neurons, which can relieve some symptoms. Anticonvulsants such as carbamazepine (Tegretol) or duloxetine (Cymbalta) help relieve neuropathic pain. The medications valium (Diazepam), baclofen (Lioresal), and tizanidine (Zanaflex) help control muscle spasms. Bladder problems are treated with parasympathetic agents such as bethanechol (Urecholine) and oxybutynin (Ditropan). Fatigue can be treated with antidepressants or an antiviral agent such as amantadine (Symmetrel). Acute exacerbations are typically treated with high doses of steroids or with ACTH. For those who suffer sudden severe attacks or do not respond to high doses of steroids, plasma exchange or?plasmapheresis?may be used to remove antibodies from the blood that are attacking the myelin.Rehabilitation after acute exacerbation includes physical, speech, and occupational therapies. Physical therapy can help with strength, coordination, and balance. An occupational therapist can help the patient and family adapt the home environment to the patient’s special needs. Assistive devices such as braces, canes, wheelchairs, and splints allow the patient increased mobility and independence. Patients who develop speech difficulties benefit from speech therapy. Exercise also can be beneficialspinal shockA disruption of sympathetic nervous system function, resulting in vasodilation, hypotension, and bradycardiaDilation of the blood vessels allows more blood flow just beneath the skin. This blood cools and is circulated throughout the body, causing hypothermia. The patient is unable to maintain control of body temperature. In addition, all reflexes below the level of the injury are lost, and retention of urine and feces occurs. Spinal shock can last from a week to many weeks in some patients.medications used in cerebrovascular disorders Thrombolytic AgentsDissolve existing clots.Examplesalteplase (tissue plasminogen activator [tPA]; Activase)Nursing ImplicationsMust be administered within 3 to 4.5 hours of symptom onset.Monitor for bleedingAntiplatelet AgentsPrevent formation of clots.Examplesaspirinclopidogrel (Plavix)aspirin/dipyridamole (Aggrenox)Nursing ImplicationsMonitor patient for bruising, change in level of consciousness, and prolonged bleeding time.Anticoagulant AgentsProlong time to form clots; prevent new clots.Exampleswarfarin (Coumadin)heparinNursing ImplicationsMonitor patient for bruising, change in level of consciousness, and prolonged bleeding time.For warfarin (Coumadin), monitor international normalized ratio (INR) frequently until therapeutic, and then monthly.Cholesterol-Lowering AgentsReduce cholesterol level.Examplessimvastatin (Zocor)pravastatin (Pravachol)atorvastatin (Lipitor)lovastatin (Mevacor)Nursing ImplicationsPatient should notify health care provider if muscle pain or weakness occur.babinski reflexTested by firmly stroking the sole of the foot. Normal response is flexion of the great toe. If the great toe extends and the other toes fan out, neurologic dysfunction should be suspected if the patient is more than 6 months old. Deep tendon reflexes are not usually part of a routine nursing assessment. The patient’s gait should be assessed to detect any neurologic dysfunction and to assess ability to ambulate safely. Patients who stagger, weave, or bump into objects may need assistance with walking.increased intracranial pressure (IICP)Pathophysiology and Etiology ICP is the pressure exerted inside the cranial cavity by these components. Normal ICP is 0 to 15 mm Hg. ICP fluctuates with normal physiological changes, such as arterial pulsations, changes in position, and increases in intrathoracic pressure (e.g., coughing or sneezing).If an increase in one component is not accompanied by a decrease in one or both of the other components, the result is increased ICP. Any patient with a pathological intracranial condition is at risk for increased ICP. Common causes of increased ICP include brain traumaintracranial hemorrhagebrain tumors. Prompt detection of changes in neurologic status indicating increased ICP allows intervention aimed at preventing permanent brain damage.The consequences of increased ICP depend on the degree of elevation and the speed with which the ICP increases. Patients with slow-growing tumors can have significantly increased ICP before they develop symptoms. Conversely, patients with a subarachnoid hemorrhage can sustain a sudden sharp increase in ICP.The normal functioning body has several methods of compensating for increased ICP. CSF can be shunted into the spinal subarachnoid space. Hyperventilation can trigger constriction of cerebral blood vessels, decreasing the amount of blood within the cranial vault. These compensatory mechanisms are temporary and not particularly effective if the increase in ICP is sudden or severe.Signs and Symptoms Restlessness irritability,decreased LOC because cerebral cortex function is impaired. If not intubated, the patient can hyperventilate, causing vasoconstriction as the body attempts to compensate. As the pressure increases, the oculomotor nerve can be compressed on the side of the impairment. Compression of the outermost fibers of the oculomotor nerve results in diminished reactivity and dilation of the pupil. As the fibers become increasingly compressed, the pupil stops reacting to light. If the compression continues and the brain tissue exerts pressure on the opposite side of the brain from the injury, both pupils become fixed and dilated.Vital sign changes are a late indication of increasing ICP. The Cushing triad is a classic late sign of increased ICP. It is characterized by bradycardia, irregular respirations, and arterial hypertension (increasing systolic blood pressure while diastolic blood pressure remains the same), resulting in widening pulse pressure. By the time these symptoms appear, the ICP is significantly increased, and interventions may not be successful. VomitingBox 48.1 Signs and Symptoms of IICPHeadacheDilated pupil on affected sideHemiparesis or hemiplegiaDecorticate then decerebrate posturingDecreasing level of consciousnessIncreasing systolic blood pressureIncreasing then decreasing pulse rateRising temperatureMonitoring Allows for early detection of changes in the pressure on the brain, before changes in symptoms are seen. The most common method of monitoring ICP in adults is by placing a catheter in a ventricle of the brain, in the cerebral parenchyma, or in the subdural or subarachnoid space. This can be done at the bedside or in an operating room. Each of these methods requires anesthetizing the scalp and drilling a hole, called a?burr hole,?into the skull.Placement of a catheter into one of the lateral ventricles is referred to as external ventricular drainage. This method allows for pressure monitoring as well as drainage of CSF to reduce ICP. Disadvantages to this method include difficulty in locating the ventricle for insertion of the catheter and clotting of the catheter by blood in the CSF. To allow communication with the subarachnoid space, a subarachnoid bolt can be tightly screwed into the burr hole after the dura has been punctured. The advantage of a subarachnoid bolt is ease of placement. Disadvantages include occlusion of the sensor portion of the bolt with brain tissue and inability to drain CSF. An intraparenchymal monitor is placed directly into brain tissue. Some physicians believe that this most accurately reflects the actual situation within the skull. These monitors cannot be used to drain CSF and can become occluded by brain tissue.Patients with ICP monitors are cared for in an intensive care unit (ICU) and require aggressive nursing care to prevent complications. These patients are often mechanically ventilated and may be pharmacologically paralyzed and sedated. In addition to meeting the patient’s physiological needs and preventing complications, education and emotional support for family members are important.Measures to Prevent Increased Intracranial PressureKeep head of bed elevated 30 degrees unless contraindicated. Avoid flexing the neck; keep head and neck in midline position. Administer antiemetics and antitussives as necessary to prevent vomiting and couch. Administer stool softeners. Minimize suctioning. If absolutely necessary, oxygenate first and limit suction passes to one or two.Avoid hip flexionPrevent unnecessary noise and startling the patientSpace care activities to provide rest between each disturbance. romberg testPerformed by having the patient stand with feet together and eyes closed. A negative Romberg test means that the patient experiences minimal swaying for up to 20 seconds. A patient who sways or leans to one side is said to have a positive Romberg test, which may be seen in cerebellar dysfunction.BE SAFE!A positive Romberg test in an older adult is expected as a result of normal aging changes in the cerebellum. Be sure to protect the patient with a positive result from falls. A gait belt may be helpful when assisting the patient with ambulation.alzheimer’s disease Pathophysiology Viral or bacterial infection and autoimmune dysfunction. Markers associated with Alzheimer disease can be found on several chromosomes. Chromosome 21 in particular has been associated with Alzheimer disease and is also the location of the genetic abnormality responsible for Down syndrome. Patients older than age 40 who have Down syndrome usually develop Alzheimer disease. The exact correlation between the two disorders is still being studied. Lifestyle factors that increase risk of Alzheimer disease include hypertension, hypercholesterolemia, and poorly controlled diabetes.Signs and Symptoms STAGE 1 This early stage lasts from 2 to 4 years and is characterized by increasing forgetfulness. At this stage, the patient may attempt to cope by using lists and reminders. Interest in day-to-day activities, acquaintances, and surroundings tends to diminish. The patient is reluctant to take on tasks because of uncertainty in how to perform them. If the patient is still working, his or her performance deteriorates and can result in being terminated from the job.STAGE 2.?The second stage is the longest in duration, lasting 2 to 12 years. Progressive cognitive deterioration causes difficulty doing simple calculations or answering questions. Patients may become irritable, particularly when asked to perform a task that they know they should be able to perform but cannot. It may help the patient to break down the task into manageable steps. Depression is common. Aphasia and the resulting inability to make themselves understood can exacerbate patients’ irritability. It is during the middle stage, as cognitive function significantly deteriorates, that the patient may become more physically active. The normal sleep–wake cycle is disrupted, and the patient tends to wander aimlessly, particularly at night. The patient may become lost in familiar surroundings, which compounds the anxiety that typically develops during this stage. Hallucinations and seizures can occur. Management of day-to-day activities, such as feeding a pet or paying bills, becomes overwhelming. Personal hygiene deteriorates, as does appropriate social behavior. Patients may make up stories to cover for deficits, saying that possessions they misplaced were stolen. Some patients hoard food or money.STAGE 3.?The third stage of Alzheimer disease is characterized by progression to complete dependency. The patient loses the ability to converse or control bowel or bladder function. If the patient is still mobile, constant supervision is required to protect from wandering and avoid injury. Emotional control and ability to recognize loved ones are lost. This lack of recognition is particularly devastating for family members. Eventually, the patient is unable to move independently, swallow, or express needs. Death usually occurs from complications of immobility.The duration of the final stage of Alzheimer disease, characterized by complete dependence, depends in part on the physical stamina and general health of the individual. The healthier the patient, the longer the body will continue to function. Another factor is the decisions that have been made regarding artificial feeding and respiratory support. Few family members or HCPs advocate intubation and mechanical ventilation for patients with Alzheimer disease. The issue of enteral feedings, however, is an emotional one with few easy answers. The use of enteral feedings can prolong the patient’s life, despite the absence of cognitive functioning. As with patients suffering from Huntington disease, every effort should be made to determine the patient’s wishes before cognitive impairment makes that impossible.Some experts recognize seven stages of Alzheimer disease. Individuals are evaluated using the Global Deterioration Scale for Assessment of Primary Degenerative Dementia (GDS), which presents a more detailed description of each stage. Pre-dementia (Stages 1 through 3) is characterized with no impairment to MCI. In Stages 4 and 5, patients have significant memory loss and confusion. In Stage 5, the person cannot survive without assistance with ADLs. The final stages (6 and 7) are associated with loss of verbal and basic psychomotor skills, and the brain no longer has control over the body.Therapeutic Measures No known cure for Alzheimer disease. Treatment has traditionally focused on minimizing the effects of the disease and maintaining independence as long as possible. Acetylcholinesterase (AChE) inhibitors such as donepezil (Aricept) or rivastigmine (Exelon) are thought to inhibit the breakdown of the neurotransmitter acetylcholine.Increased levels of acetylcholine in the brain allow better functioning of the remaining neurons. They appear to be most effective for those patients who exhibit mild to moderate symptoms of Alzheimer disease. It can take some time to notice any effects?of the drugs. Use of AChE inhibitors diminishes the amount of medical care and social service interventions required and delays admission to skilled nursing facilities. This delay in institutionalization can result in significant positive impact on quality of life as well as financial savings for the patient and family. Another class of medications, NMDA (N-methyl-D-aspartate) antagonists, can prevent overexcitation of NMDA receptors in the brain and allow more normal function. Memantine (Namenda, Axura) is the only drug currently available in this class. These drugs can be given at any stage of Alzheimer disease and, like AChE inhibitors, simply slow the patient’s decline.Antidepressants, antipsychotics, and antianxiety drugs can be used as a last resort to control symptoms of depression and behavioral disturbances, but they do not treat the dementia. Patients should be carefully monitored for drug interactions and side effects.meningitits Pathophysiology and Etiology Inflammation of the meninges that surround the brain and spinal cord. It can be caused by either bacterial or viral infection. Any microorganism that enters the body can result in meningitis. Bacterial meningitis is a serious infection that is spread by direct contact with discharge from the respiratory tract of an infected person. Viral meningitis, also called aseptic meningitis, is more common and rarely serious. It usually presents with flu-like symptoms, and patients recover in 1 to 2 weeks.The most common bacteria that cause meningitis are?Neisseria meningitidis, Streptococcus pneumoniae,?Group B?Streptococcus,?and?Haemophilus influenzae?type b (Hib). Bacterial infection generally begins in another area, such as the upper respiratory tract, enters the blood, and invades the CNS, causing the meninges to become inflamed and intracranial pressure (ICP) to increase. Vessel occlusion and necrosis of areas in the brain can occur. Cranial nerve function can be transiently or permanently affected by meningitisSigns and Symptoms Nuchal rigidityPositive Kernig and Brudzinski signsFeverPhotophobiaPetechial rash on skin and mucous membranesEncephalopathyPrevention Vaccines are available against some pathogens. Hib vaccinations are begun during infancy. A vaccine against?S. pneumoniae?is recommended for people over age 65 and those who have a chronic medical condition. Two doses of meningococcal vaccine (MCV4) for adolescents, one at age 11 or 12 and a booster at age 16. Other groups at increased risk who should be vaccinated are college freshmen living in dormitories, U.S. military recruits, anyone with compromised immunity, laboratory personnel, and those traveling to areas of the world where meningococcal disease is common. Diagnostic Tests L Lumbar puncture with cerebrospinal fluid, analysis, culture and sensitivity (C&S)Complete blood count (CBC)C&S nose and throat Therapeutic Measures Antibiotics such as vancomycin and cephalosporins are administered for bacterial meningitis. It is important to note the sensitivity report when it is complete to confirm that the antibiotic in use is the best choice. Symptom management is the same for viral or bacterial meningitis. Antipyretics such as acetaminophen are used to control fever; a cooling blanket also can be used. Care should be taken to avoid cooling the patient too much because shivering increases the metabolic demand for oxygen and glucose. Analgesics are given to lessen head and neck pain. Corticosteroids and anti-inflammatory agents are given to decrease cerebral swelling. Nausea and vomiting are controlled with antiemetic medications. The patient with meningococcal meningitis should be placed in droplet isolation for at least the first 24 hours of medication administration to prevent transmission to others.Patients can become agitated. A quiet, dark environment lessens the stimulation of a patient who has a headache or photophobia and who is agitated, disoriented, or at risk for seizures. An important aspect of nursing care focuses on keeping patients from harming themselves. It is very upsetting to families to see a loved one acting agitated or disoriented. Therefore, it is important to teach the family about symptoms and treatment goals for the patient.types of brain injuries Concussion Is a mild brain injury. If there is loss of consciousness, it is for 5 minutes or less. Concussion is characterized by headache, dizziness, or nausea and vomiting. The patient may describe amnesia of events before or after the trauma. On clinical examination, there is no skull or dura injury and no abnormality detected on CT scan or MRI.Contusion Characterized by bruising of brain tissue, possibly accompanied by hemorrhage. There can be multiple areas of contusion, depending on the causative mechanism. Severe contusions can result in diffuse axonal injury. The symptoms of a cerebral contusion depend on the area of the brain involved.Brainstem contusions affect LOC. Decreased LOC can be transient or permanent. Respirations, pupil reaction, eye movement, and motor response to stimuli can also be affected. The autonomic nervous system can be affected by edema or by hypothalamic injury, causing rapid heart rate and respiratory rate, fever, and diaphoresis.Hematoma Subdural Hematoma Classified as acute or chronic based on the time interval between injury and onset of symptoms. Acute subdural hematoma is characterized by appearance of symptoms within 24 hours following injury. The bleeding is typically venous in nature and accumulates between the dura and arachnoid membranes. Damage to the brain tissue can cause an altered LOC. Therefore, it can be difficult to recognize a subdural hematoma on the basis of clinical examination alone. As the subdural hematoma increases in size, the patient may exhibit one-sided paralysis of extraocular movement, extremity weakness, or dilation of the pupil. LOC can deteriorate further as ICP increases. Older adults and people with alcoholism are particularly prone to chronic subdural hematomas. Atrophy of the brain, common in these populations, stretches the veins between the brain and dura. A seemingly minor fall or blow to the head can cause these stretched veins to rupture and bleed. Often, there are no other injuries associated with the trauma. Because a chronic subdural hematoma can develop weeks to months after the injury, the patient may not remember an injury occurring.The patient with a chronic subdural hematoma may be forgetful, lethargic, or irritable or may report a headache. If the hematoma persists or increases in size, the patient can develop hemiparesis and pupillary changes. The patient or family members may not associate the symptoms with a previous injury and, therefore, may delay seeking medical care.Epidural Hematoma Blood collects between the dura mater and skull. The blood is usually arterial in nature and is often associated with skull fracture. Arterial bleeding can cause the hematoma to become large very quickly. Patients with epidural hematoma typically exhibit a progressive course of symptoms. The patient loses consciousness directly after the injury; he or she then regains consciousness and is coherent for a brief period. The patient then develops a dilated pupil and paralyzed extraocular muscles on the side of the hematoma and becomes less responsive. If there is no intervention, the patient becomes unresponsive.Seizures or hemiparesis can occur. Once the patient has symptoms, deterioration can be rapid. Airway management and control of ICP must be instituted immediately, or the patient will die.Diagnostic Tests Computed tomography (CT) scan, magnetic resonance imaging (MRI)Skull x-raysRoutine laboratory tests (hemoglobin, electrolytes, coagulation studies, type and crossmatch)Neuropsychological testingTherapeutic Measures Control of ICP and support of body functions. Patients with brain injuries can be partially or completely dependent on assistance with respiration, nutrition, elimination, movement, and skin integrity. A variety of techniques are used to control ICP in the patient with moderate or severe brain injury. The first step is to insert an ICP monitor to allow measurement of the ICP. If ICP remains elevated despite drainage of CSF, the next step is use of an osmotic diuretic. The most commonly used drug is IV mannitol (Osmitrol). Mannitol uses osmosis to pull fluid from the brain into the intravascular space and eliminate?it via the renal system. Serum osmolarity and electrolytes must be carefully monitored when mannitol is being administered. Some patients experience a rebound increase in ICP after the mannitol wears off.Mechanical hyperventilation may be used if the patient is still experiencing increased ICP. Hyperventilation is effective in lowering ICP because it causes cerebral vasoconstriction. Vasoconstriction allows less blood into the cranium, thereby lowering ICP. Research has demonstrated, however, that aggressive hyperventilation, particularly within the first 24 hours after injury, can induce ischemia in the already compromised brain. Therefore, hyperventilation is now reserved for increased ICP that does not respond to other treatments.High-dose barbiturate therapy may be used to induce a therapeutic coma, which reduces the metabolic needs of the brain during the acute phase following injury. These patients are completely dependent for all of their needs and care. They must be mechanically ventilated and cared for in an ICU setting. Vasopressors may be required to maintain blood pressure, and the patient’s temperature should be kept as normal as plications Brain HerniationIf interventions to control ICP are unsuccessful, the patient can experience uncontrolled edema or herniation of brain tissue. Herniation is displacement of brain tissue out of its normal anatomical location. This displacement prevents function of the herniated tissue and places pressure on other vital structures, most commonly the brainstem. Herniation usually results in brain death.Patients who experience brain death may be suitable organ donor candidates. For some family members, the opportunity to donate their loved one’s organs provides some sense of purpose in the death.Diabetes InsipidusEdema or direct injury that affects the posterior portion of the pituitary gland or hypothalamus can result in inadequate release of antidiuretic hormone, causing diabetes insipidus. This results in polyuria and, if the patient is awake, polydipsia. Fluid replacement and IV vasopressin are used to maintain fluid and electrolyte balance. Acute HydrocephalusCerebral edema can interfere with CSF circulation, causing?hydrocephalus.?Initial treatment is use of an external ventricular drain, followed by a ventriculoperitoneal shunt if necessary. A shunt drains excess CSF into the peritoneum, where it is reabsorbed into circulation and excreted.Labile Vital SignsDirect trauma to or pressure on the brainstem can cause fluctuations in blood pressure, cardiac rhythm, or respiratory pattern. Treatment is aimed at control of ICP. Post-Traumatic Stress DisorderPatients who sustain a concussion can experience ongoing, somewhat vague symptoms. They may report headache, fatigue, difficulty concentrating, depression, or memory impairment. Symptoms can be severe enough to interfere with work, school, and interpersonal relationships. Neuropsychological testing can provide objective evidence of cognitive dysfunction and establish the need for cognitive rehabilitation for post-traumatic stress disorder, or PTSD.Symptoms can take 3 to 12 months to resolve.Cognitive and Personality ChangesAlterations in personality and cognition may be the most difficult long-term complication for patients and family members to adjust to. The patient can have significant short-term memory impairment. This limits his or her ability to learn?new information and can interfere with ability to function at work or school. Impaired judgment can make the patient a safety risk to self or others. It also affects social functioning. Emotional lability, loss of social inhibitions, and personality changes may occur. These consequences of TBI have a profound effect on the patient and family members. Spouses may state, “This is not the person I married.” If behavior is violent, bizarre, or profane, children may be unwilling to bring their friends home and can become socially isolated. Young children in particular have difficulty understanding why a parent is behaving so differently. Disintegration of relationships is not uncommon following TBI.Neuropsychological testing objectively identifies problems. These deficits can then be addressed with cognitive rehabilitation. Individual and family counseling can be helpful. Support groups for patients and family members may also help.Motor and speech impairment are additional possible long-term complications of TBI. Intensive rehabilitation provides the best opportunity for maximizing recovery.?Exam of the eyeExamination of the pupils is an important part of the neurologic assessment and cranial nerve evaluation. The size of the pupils at rest is documented in millimeters.If the patient’s pupils are unusually large or small, determine whether the patient has received any medications that can affect pupil size. If the patient’s pupils are unequal in size?(anisocoria),?without a correlating diagnosis or symptoms, ask the patient or significant others whether the patient normally has unequal pupils. Anisocoria may be congenital; it can also be caused by cataract surgery. Development of unequal pupils in a patient who previously had equal pupils is an emergency and should be reported to the HCP immediately. Any deviation from the normal round shape of the pupils is documented. Accommodation?is the process of visual focusing from far to near. To evaluate for accommodation, have the patient focus on an object at a distant point and then refocus on the object at a near point. Pupils should constrict with the adjustment to the near object, and the eyes should converge. Upon completion of the assessment of the pupils, document your findings. PERRLA is a commonly used acronym to note that?pupils are?equal,?round, and?reactive to?light and?accommodation. Next, evaluate for range of motion and for smoothness and coordination of movements. Eyes that move in the same direction in a coordinated manner are said to have a?conjugate?gaze. Conversely, a?dysconjugate?gaze is movement of the eyes in different directions. Some patients may be unable to move one or both eyes in a specific direction; this is called?ophthalmoplegia.?It is often documented as “limited extraocular movements.” Always document what the limitation is (e.g., “Patient is unable to look laterally with left eye”). This allows colleagues to compare findings and recognize changes.Nystagmus?is involuntary movement of the eyes. Nystagmus varies in the speed of the movement and direction. Horizontal nystagmus is the most common. Common causes of nystagmus are phenytoin (Dilantin) toxicity and injury to the brainstem.anticonvulsant MedicationsSuppress abnormal discharge of neurons and suppress spread of seizure activity from focus to other parts of brain.carbamazepine (Tegretol)Monitor complete blood count (CBC).Therapeutic level is 6–12 mcg/mL.Do not crush sustained-release (SR) forms.Lacosamide (Vimpat)Injectable form available.May increase risk of suicidal ideation.Ezogabine (Potiga)May cause retinal abnormalities. Vision exam necessary at baseline and every 6 months.Monitor for urinary retention.Blood levels not necessary.Gabapentin (Neurontin)Blood levels not necessary. Levetiracetam (Keppra)May need reduced dose for older adults.Assess white blood cell, red blood cell, and liver function tests.Lamotrigine (Lamictal)Discontinue therapy and notify health care provider if rash appears.Monitor blood iramate (Topamax)Blood levels not necessary. Phenytoin (dilantin)Regular dental care essential. Therapeutic level is 10–20 mcg/mL.Binds to tube feedings; hold tube feeding 1 hr before and 2 hr after dose.Phenobarbital (Luminal)Monitor vital signs.Therapeutic level is 15–40 mcg/mL.Valproic acid (Depakote)Therapeutic level is 50–100 mcg/mL.Do not crush SR form.cerebral aneurysm, Subarachnoid hemorrhage and intracranial hemorrhage A cerebral aneurysm is a weakness in the wall of a cerebral artery. It may be congenital, traumatic, or the result of disease. If the aneurysm ruptures, the result is often a subarachnoid hemorrhage. It is unknown what causes the formation of congenital aneurysms or what causes them to rupture. Unruptured aneurysms are typically asymptomatic. The exception is a very large aneurysm, which can cause symptoms similar to a brain tumor. Aneurysms can affect children and young, otherwise healthy adults.Pathophysiology and Etiology Aneurysms can occur in any of the cerebral arteries, although most occur in the circle of Willis. The most common site is at the bifurcation of an artery. It is theorized that increased?turbulence at the bifurcation can cause an outpouching of a congenitally weak arterial wall.Subarachnoid hemorrhage is the collection of blood beneath the arachnoid mater following aneurysm rupture. Rupture of an arteriovenous malformation or head trauma may also result in subarachnoid hemorrhage. The presence of blood outside the blood vessels is very irritating to brain tissue. It is believed that irritation from blood breakdown is the major cause of vasospasm, a common complication of subarachnoid hemorrhage.It is unclear what causes an aneurysm to rupture. Some people develop a subarachnoid hemorrhage while performing the Valsalva maneuver, engaging in sexual activity, or physically exerting themselves. For others, the aneurysm ruptures during a quiet, inactive period. If the aneurysm rupture is associated with a particular activity, the patient may be very frightened of engaging in that activity again. This may have a negative effect on the patient’s interpersonal relationships if the associated activity was sexual in nature. The patient’s partner may feel guilty or responsible for the hemorrhage. Education, emotional support, and confidentiality are essential to help both the patient and significant other.Signs and Symptoms Some patients experience a small hemorrhage before diagnosis of subarachnoid hemorrhage. This leakage of blood may cause a mild headache, vomiting, or disorientation. The symptoms may be attributed to a flu-like syndrome. Patients may dismiss the symptoms and not seek medical care.The most common presentation of rupture of an aneurysm is sudden onset of a severe headache. Typically, a patient will state, “I have never had a headache this bad in my life.” Patients may hold their heads and moan or cry in pain. Sensitivity to light is a common finding. This may make patients reluctant to cooperate with pupil examinations. LOC varies based on the severity of the hemorrhage. Patients may be alert and coherent, lose consciousness immediately, or gradually become less responsive. The decreased LOC is caused by ICP and impairment of cerebral blood flow. Patients may experience generalized seizures.Blood in the subarachnoid space causes meningeal irritation. The patient may exhibit nuchal rigidity. The most commonly affected cranial nerves are III and VI. This is manifested as an enlarged pupil or abnormal gaze. Motor dysfunction may involve one or both limbs on the side opposite the hemorrhage.Therapeutic Measures Patients with subarachnoid hemorrhage are cared for in an intensive care unit (ICU) setting. They typically have an arterial line and a central venous pressure monitoring catheter. Blood pressure is carefully monitored because high pressures increase the risk of re-rupture of the aneurysm and low pressures can be associated with ischemia. Values outside parameters identified by the HCP are reported. Typically, the systolic blood pressure is kept between 120 and 160 mm Hg. Vasoactive drugs may be required to maintain blood pressure within the prescribed parameters.There is no cure for subarachnoid hemorrhage. Treatment consists of correcting the cause of the hemorrhage if possible. Preventing or managing complications and providing supportive care are important aspects of nursing care.TIA (Transent ischemic attcks)Is a temporary blockage of blood to the brain that causes a transient (brief) neurologic impairment. The episode typically lasts minutes to hours, and the patient recovers completely. The risk factors, causes, and symptoms of a TIA are identical to those of a stroke. Indeed, if the blockage that causes a TIA does not reverse, an area of the brain is permanently damaged, and the event is a stroke. Urgent evaluation of a TIA is essential to decrease the risk of stroke.Treatment of a TIA is focused on preventing a full stroke. The cause of the TIA may be discovered with diagnostic tests, which can then guide treatment. However, there may be no clear etiology of the TIA. Treatment, therefore, is mostly centered on minimizing the patient’s risk factors for a stroke.ALSPathophysiology A progressive, degenerative condition that affects?motor neurons responsible for the control of voluntary muscles. In the brain and spinal cord, upper and lower motor neurons begin to degenerate and form scar tissue or die, blocking transmission of nerve impulses. Without stimulation, muscles?atrophy, and muscle strength and coordination decrease. As the disease progresses, more muscle groups, including muscles controlling breathing and swallowing, become involved. The heart and gastrointestinal tract are controlled involuntarily and so are not affected by ALS. The ability to think and reason also is not affected. ALS can occur at any age but usually does not appear until adulthood. The cause of ALS is not known, but it is believed to have a genetic component. Smoking and other toxins appear to increase risk.Signs and Symptoms Symptoms are vague early in the course of ALS. Primary symptoms include progressive muscle weakness decreased coordination. This can begin in the arms, legs, or muscles of speech and swallowing. Atrophy of muscles and?fasciculation?(twitching) also occur. Muscle spasms can cause pain. Difficulty with chewing and swallowing places the patient at risk for choking and aspiration as the disease progresses. Inappropriate emotional outbursts of laughing and crying can occur. Speech becomes increasingly difficult. Bladder and bowel functions remain intact, yet problems such as constipation, urinary urgency, hesitancy, or frequency can occur.Late in the disease, communication becomes limited to moving and blinking the eyes in response to questions. Pulmonary function becomes severely compromised to the point of requiring mechanical ventilator assistance if the patient chooses. Other complications can include extreme malnutrition, falls, pulmonary emboli, and heart failure. ALS eventually leads to death from respiratory complications such as atelectasis, respiratory failure, and pneumonia.Therapeutic Measures There is no cure for ALS, and treatments are palliative in nature. Goals of treatment are aimed at maintaining function as long as possible and emotionally supporting the patient and family. Glycopyrrolate (Robinul) may be administered to decrease saliva production. Quinine (Qualaquin) may be used for muscle cramps. Riluzole (Rilutek) slows the progression of the disease and can prolong life by 3 to 4 months. Edaravone (Radicava) reduces the glutamate in the body, which damages the motor nerves, slowing decline in function.Nonpharmacological measures such as physical therapy, massage, position changes, and diversional activities can help control pain. Enteral feedings via a surgically placed gastrostomy tube help provide adequate nutrition. Prevention of infections, such as pneumonia and urinary tract infection (UTI), is vital. Meticulous skin care minimizes the incidence of pressure injuries. Physical, occupational, and speech therapies allow the patient to maximize function for as long as possible. Therapy can also decrease the occurrence of complications such as aspiration, falls, and contractures. As the disease progresses, mechanical ventilation may be needed. Patients may choose supportive hospice care instead of life-prolonging mechanical ventilation.Patients with speech problems may benefit from the use of alternative communication. A variety of such systems are available; most involve laptop computers that patients can use to type in words or symbols to generate speech. Medicare pays at least a portion of the cost for the equipment. Support groups and counseling provide emotional support for the patient and familyPatient educationReinforce information given by the HCP to the patient and family about ALS and its prognosis. Support groups can provide emotional support as the patient and family deal with the likely reality of untimely death. Assistive devices and exercises help prevent complications. Teaching family members how to perform physical therapy and other health care activities allows the patient to spend as much time as possible at home. Teach the patient to avoid exposure to persons with infections because an infection can be deadly to a patient with a debilitating disease. Request a consultation with a palliative care specialist or other resource?personnel to help the patient and family develop an advance directive.Lumbar PunctureCSF may be obtained via lumbar puncture and evaluated for glucose and protein levels, presence of bacteria and WBCs, levels of immunoglobulin, antibodies, and culture and sensitivity. x-raySpinal x-ray (radiograph) examinations are done to determine the status of individual vertebrae and their relationship to one another. If the patient experiences pain with certain movements, he or she may be asked to flex and extend the area of the spine being examined while the radiographs are taken. This allows detection of abnormal movement of the vertebrae. Skull radiographs may be taken to detect skull fractures or foreign bodies. No special nursing care is required.CTA computed tomography (CT) scan is used for diagnosing neurologic disorders of the brain or spine. A CT scan can detect hemorrhage, altered ventricle size, cerebral atrophy, tumors, skull fractures, and abscesses. A CT scan is used when magnetic resonance imaging (MRI) is contraindicated because of metal aneurysm clips or other metal implants.The scan may be performed with or without radiopaque contrast material to enhance the clarity of the images. Contrast material is most commonly used if a tumor is suspected or following surgery in the area to be scanned. CT scans are commonly used in emergency evaluations because they can be done quickly, an important consideration if the patient is mechanically ventilated or has unstable vital signs.Nursing care:During a CT scan, the patient must lie still on a movable table. Noncontrast scans take about 10 minutes; contrast scans take 20 to 30 minutes. Patients who are receiving dye should be warned that they may feel a sensation of warmth following the injection; warmth in the groin area might make them feel as though they have been incontinent of urine. Nausea, diaphoresis, itching, or difficulty breathing can indicate allergy to the dye and should be reported immediately to the HCP. Sedation may be required for patients who are agitated or disoriented. Patients who are in pain may need pain medication before the examination. MRIMRI i s used for diagnosis of degenerative diseases such as multiple sclerosis, arteriovenous malformations, small tumors, hemorrhages, and cerebral and spinal cord edema. An MRI of the mediastinal cavity will determine whether the thymus gland is enlarged and facilitate diagnosis of myasthenia gravis. It is a longer procedure and may be difficult for unstable, disoriented, or mechanically ventilated patients. As with CT scan, MRI can be done with or without contrast material. Some facilities have the capability to perform magnetic resonance angiograms (MRAs). This test allows visualization of blood vessels and assessment of blood flow without being as invasive as a traditional angiogram. angiogram An angiogram in an x-ray following injection of dye that provides information about the structure of specific vessels as well as overall circulation to an area.myelogram Is a n x-ray examination of the spinal canal and its contents after injection of contrast material. Compression of nerve roots, herniation of intravertebral disks, and blockage of CSF circulation can all be detected by myelogram. EEGElectrodes are placed on the scalp to record brain activity during an?electroencephalogram?(EEG). Analysis of the tracing can identify areas of abnormality, such as a seizure focus or areas of slowed activity.?Spinal cord injuries Pathophysiology The spinal cord is made up of nerve fibers that allow communication between the brain and the rest of the body. Damage to the spinal cord results in interference with this communication process. Damage may be caused by bruising, tearing, cutting, edema, or bleeding into the cord. The damage can be caused by external forces or by fragments of fractured bone.Etiology and Types The causes of spinal cord injury are similar to those of TBI. It is not uncommon for a patient to have both a spinal cord injury and TBI. Motor vehicle collisions are the most common causes of spinal cord injury in the United States. Females are more often injured by falls, and males are more often injured during acts of violence or contact sports. Assaults can cause cord injury if a knife or bullet penetrates the spinal cord. Diving into shallow water is a common cause of cervical cord injury.Spinal cord injuries can be classified by location or by degree of damage to the cord. A complete spinal cord injury means that there is no motor or sensory function below the level of the injury. With an incomplete lesion, some function remains. This does not necessarily mean that the remaining function will be useful to the patient. Some patients find that having areas where sensation is intact may be more painful than useful.The cervical and lumbar portions of the spine are injured more often than the thoracic or sacral segments. This is because the cervical and lumbar areas are the most mobile portions of the spine.Signs and Symptoms Cervical InjuriesSigns and symptoms depend on the level at which the cord is damaged. Cervical cord injuries can affect all four extremities, causing paralysis and paresthesias, impaired respiration, and loss of bowel and bladder control. Paralysis of all four extremities is called?quadriplegia;?weakness of all extremities is called?quadriparesis.?If the injury is at C3 or above, the injury is usually fatal because muscles used for breathing are paralyzed. An injury at the fourth or fifth cervical vertebra affects breathing and may necessitate some type of ventilatory support. Such patients typically need long-term assistance with ADLs.Thoracic and Lumbar Injuries Thoracic and lumbar injuries affect the legs, bowel, and bladder. Paralysis of the legs is called?paraplegia;?weakness of the legs is called?paraparesis.?Sacral injuries affect bowel and bladder continence and may affect foot function. Individuals with thoracic, lumbar, and sacral injuries can usually learn to perform ADLs independently. ................
................

In order to avoid copyright disputes, this page is only a partial summary.

Google Online Preview   Download