Neurologic Disorders PDF

NEUROLOGIC DISORDERS ARCHIEVAL S. GUITCHE, RM, RN, LPT, MD  ANATOMY AND PHYSIOLOGY OF BRAIN AND SPINAL CORD ANATOMY AND PHYSIOLOGY A. CEREBRUM The cerebrum consists of the right and left hemispheres Each hemisphere receives sensory information from the opposite side of the...

NEUROLOGIC DISORDERS ARCHIEVAL S. GUITCHE, RM, RN, LPT, MD  ANATOMY AND PHYSIOLOGY OF BRAIN AND SPINAL CORD ANATOMY AND PHYSIOLOGY A. CEREBRUM The cerebrum consists of the right and left hemispheres Each hemisphere receives sensory information from the opposite side of the body and controls the skeletal muscles of the opposite side. The cerebrum governs sensory and motor activity and thought and learning ANATOMY AND PHYSIOLOGY B. CEREBRAL CORTEX The cerebral cortex is the outer gray matter, it is divided into five lobes It is responsible for the conscious activities of the cerebrum ANATOMY AND PHYSIOLOGY C. BASAL GANGLIA Cell bodies in white matter that help the cerebral cortex produce smooth voluntary movements ANATOMY AND PHYSIOLOGY D. DIENCEPHALON 1. THALAMUS Relays sensory impulses to the cortex Provides a pain gate Part of the reticular activating system ANATOMY AND PHYSIOLOGY 2. HYPOTHALAMUS Regulates autonomic responses of the sympathetic and parasympathetic nervous systems Regulates the stress response, sleep, appetite, body temperature, fluid balance, and emotions Responsible for the production of hormones secreted by the pituitary gland and the hypothalamus ANATOMY AND PHYSIOLOGY E. BRAINSTEM 1. MIDBRAIN Responsible for motor coordination Contains the visual reflex and auditory relay centers ANATOMY AND PHYSIOLOGY 2. PONS Contains the respiratory centers and regulates breathing 3. MEDULLA OBLONGATA Contains all afferent and efferent tracts and cardiac, respiratory, vomiting, and vasomotor centers Controls heart rate, respiration, blood vessel diameter, sneezing, swallowing, vomiting, and coughing. ANATOMY AND PHYSIOLOGY F. CEREBELLUM Coordinates muscle movement, posture, equilibrium, and muscle tone ANATOMY AND PHYSIOLOGY G. SPINAL CORD Provides neuron and synapse networks to produce involuntary responses to sensory stimulation Controls body movement and regulates visceral function Carries sensory information to and motor information from the brain ANATOMY AND PHYSIOLOGY G. SPINAL CORD Extends from the first cervical to the second lumbar vertebra Protected by the meninges, cerebrospinal fluid (CSF), and adipose tissue  ANATOMY AND PHYSIOLOGY G. SPINAL CORD Nerve tracts White matter contains the nerve tracts Ascending tracts (sensory pathway) Descending tracts (motor pathway) ANATOMY AND PHYSIOLOGY H. MENINGES The dura mater is a tough and fibrous membrane. The arachnoid membrane is a delicate membrane and contains CSF The pia mater is a vascular membrane The subarachnoid space is formed by the arachnoid membrane and the pia mater ANATOMY AND PHYSIOLOGY I. CEREBROSPINAL FLUID (CSF) Secreted in the ventricles, circulates in the subarachnoid space and through the ventricles to the subarachnoid space of the meninges, where it is reabsorbed. Acts as a protective cushion; aids in the exchange of nutrients and wastes Normal pressure is 6 to 25 cmH2O Normal volume is 125 to 150 mL About 500 mL/day is produced ANATOMY AND PHYSIOLOGY J. VENTRICLES Four ventricles The ventricles communicate between the subarachnoid spaces and produce and circulate CSF ANATOMY AND PHYSIOLOGY K. BLOOD SUPPLY Right and left internal carotid arteries Right and left vertebral arteries These arteries supply the brain via an anastomosis at the base of the brain called the circle of Willis ANATOMY AND PHYSIOLOGY L. NEUROTRANSMITTERS Acetylcholine Epinephrine Norepinephrine Dopamine Serotonin y-aminobutyric acid (GABA) ANATOMY AND PHYSIOLOGY M. NEURONS The neuron consists of the cell body, axon, and dendrites The cell body contains the nucleus ANATOMY AND PHYSIOLOGY M. NEURONS Neurons carrying impulses from the peripheral nervous system to the central nervous system (CNS) are called sensory neurons. Neurons carrying impulses away from the CNS are called motor neurons. Synapse is the chemical transmission of impulses from one neuron to another. ANATOMY AND PHYSIOLOGY N. AXONS AND DENDRITES The axon conducts impulses from the cell body. The dendrites receive stimuli from the body and transmit them to the axon The neurons are protected and insulated by Schwann cells. The Schwann cell sheath is called neurolemma. ANATOMY AND PHYSIOLOGY N. AXONS AND DENDRITES Neurons do not reproduce after the neonatal period If an axon or dendrite is damaged, it will die and be replaced slowly only if the neurolemma is intact and the cell body has not died. ANATOMY AND PHYSIOLOGY O. SPINAL NERVES Afferent (sensory) nerve fibers and efferent (motor) nerve fibers combine to form 31 pairs of spinal nerves. Mixed nerve fibers are formed by the joining of the anterior motor and posterior sensory roots. ANATOMY AND PHYSIOLOGY P. AUTONOMIC NERVOUS SYSTEM (Involuntary Functions) Sympathetic (adrenergic) fibers dilate pupils, increase heart rate and rhythm, contract blood vessels, and relax smooth muscles of the bronchi. Norepinephrine is a major neurotransmitter for the sympathetic nervous system. Parasympathetic (cholinergic) fibers produce the opposite effect, Acetylcholine is a major parasympathetic nervous system transmitter that contracts smooth muscles, dilates blood vessels, increases bodily secretions, and slows heart rate. NEUROLOGICAL ASSESSMENT A. Assessment of risk factors Trauma Hypertension Hemorrhage Cigarette smoking Tumors Stress Infection Aging process Toxicity Chemicals, either Metabolic disorders ingestion or Hypoxic conditions environmental exposure NEUROLOGICAL ASSESSMENT B. Assessment of cranial nerves C. Assessment of level of consciousness (LOC) D. Assessment of vital signs: Monitor for blood pressure or pulse changes, which may indicate increased ICP. E. Assessment of respirations NEUROLOGICAL ASSESSMENT F. Assessment of temperature An elevated temperature increases the metabolic rate of the brain An elevation in temperature may indicate a dysfunction of the hypothalamus or brainstem A slow rise in temperature may indicate infection. NEUROLOGICAL ASSESSMENT G. Assessment of pupils Unilateral pupil dilation indicates compression of cranial nerve III Midposition fixed pupils indicate midbrain injury. Pinpoint fixed pupils indicate pontine damage. NEUROLOGICAL ASSESSMENT H. Assessment for posturing Posturing indicates a deterioration of the condition Flexor (decorticate posturing) Client flexes one or both arms on the chest and may extend the legs stiffly. Flexor posturing indicates a nonfunctioning cortex. NEUROLOGICAL ASSESSMENT Extensor (decerebrate posturing) Client stiffly extends one or both arms and possibly the legs. Extensor posturing indicates a brainstem lesion Flaccid posturing: Client displays no motor response in any extremity. NEUROLOGICAL ASSESSMENT Assessment of reflexes Assessment of meningeal irritation. Assessment of the autonomic system 1. Sympathetic functions, adrenergic responses a. Increased pulse and blood pressure b. Dilated pupils c. Decreased peristalsis d. Increased perspiration NEUROLOGICAL ASSESSMENT 2. Parasympathetic function, cholinergic responses Decreased pulse and blood pressure Constricted pupils Increased salivation Increased peristalsis Dilated blood vessels Bladder contraction NEUROLOGICAL ASSESSMENT Assessment of sensory function: Touch, pressure, pain Glasgow Coma Scale The scale is a method of assessing a client’s neurological condition. The scoring system is based on a scale of 3 to 15 points. A score lower than 8 indicates that coma is present. ALTERED LEVEL OF CONSCIOUSNESS ALTERED LEVEL OF CONSCIOUSNESS GLASSGOW COMA SCALE Objectively documents the client’s level of consciousness Maximum total is 15; minimum is 3. A score of 7 or less indicates coma. Clients with low scores (i.e., 3 to 4) have high mortality rates and poor prognosis. Clients with scores greater than 8 have a good prognosis for recovery GLASSGOW COMA SCALE 2 ALTERED LEVEL OF CONSCIOUSNESS Monitor and evaluate the vital sign changes indicating changes in condition: 1. Pulse: a pulse rate change to 100 bpm can indicate increased intracranial pressure (ICP). A fast rate (>100 bpm) can indicate infection, thrombus formation, or dehydration. 2. BP: rising BP or widening pulse pressure can indicate increased ICP. ALTERED LEVEL OF CONSCIOUSNESS 3. Temperature: report any abnormalities; temperature elevation can indicate worsening condition, damage to temperature-regulating area of brain, or infection. If temperature elevates, take quick measures to decrease it, because fever increases cerebral metabolism and can increase cerebral edema. 4. Level-of-consciousness changes: they may range from active to somnolent. 5. Pupillary changes: they may range from prompt to sluggish or may increase in size. ALTERED LEVEL OF CONSCIOUSNESS Prevent injury and promote safety: 1. Place bed in low position and keep side rails up at all times. 2. Pad side rails if client is agitated or if there is a history of seizure activity. 3. Restrain client if client is trying to remove tubes or attempting to get out of bed. 4. Touch gently, and talk softly and calmly to the client, remembering that hearing is commonly intact. ALTERED LEVEL OF CONSCIOUSNESS 5. Avoid oversedating the client because sedatives and narcotics depress responsiveness and affect pupillary reaction (an important assessment in neurologic vital signs). 6. During all activities, tell the client what you are doing, regardless of the level of consciousness.  INCREASED INTRACRANIAL PRESSURE INCREASED ICP Increased ICP may be caused by trauma, hemorrhage, growths or tumors, hydrocephalus, edema, or inflammation. Increased ICP can impede circulation to the brain, impede the absorption of CSF, affect the functioning of nerve cells, and lead to brainstem compression and death. INCREASED ICP Assessment Altered level of consciousness, which is the most sensitive and earliest indication of increasing ICP Headache Abnormal respirations Rise in blood pressure with widening pulse pressure Slowing of pulse Elevated temperature INCREASED ICP Vomiting Pupil changes Late signs of increased ICP include increased systolic blood pressure, widened pulse pressure, and slowed heart rate. Other late signs include changes in motor function from weakness to hemiplegia, a positive Babinski’s reflex, decorticate or decerebrate posturing, and seizures. INCREASED ICP Interventions Monitor respiratory status and prevent hypoxia. Monitor ICP if a pressure device is in place. Avoid the administration of morphine sulfate to prevent the occurrence of hypoxia. Maintain mechanical ventilation as prescribed; maintaining the PaCO2 at 30 to 35 mm Hg will result in vasoconstriction of the cerebral blood vessels, decreased blood flow, and therefore decreased ICP. INCREASED ICP Maintain body temperature. Prevent shivering, which can increase ICP. Decrease environmental stimuli. Monitor electrolyte levels and acid–base balance. Monitor intake and output. Limit fluid intake to 1200 mL/day. Instruct the client to avoid straining activities, such as coughing and sneezing. Instruct the client to avoid Valsalva’s maneuver. INCREASED ICP For the client with increased ICP, elevate the head of the bed 30 to 40 degrees, avoid the Trendelenburg’s position, and prevent flexion of the neck and hips. Level of consciousness is the most sensitive indicator of neurological status. NEUROLOGIC DISORDERS  01 TRAUMATIC BRAIN INJURY TRAUMATIC BRAIN INJURY Any traumatic damage to the head Open TBI occurs when there is a fracture of the skull or penetration of the skull by an object. Closed TBI is the result of blunt trauma (more serious because of chance of increased ICP in closed vault). Increased ICP is the main concern in head injury; it is related to edema, hemorrhage, impaired cerebral autoregulation, and hydrocephalus. TRAUMATIC BRAIN INJURY TRAUMATIC BRAIN INJURY Types of Head Injury Concussion ▪ Concussion is a jarring of the brain within the skull; there may or may not be a loss of consciousness. Contusion ▪ Contusion is a bruising type of injury to the brain tissue. ▪ Contusion may occur along with other neurological injuries, such as with subdural or extradural collections of blood. TRAUMATIC BRAIN INJURY Skull Fractures Linear Depressed Compound Comminuted TRAUMATIC BRAIN INJURY Epidural Hematoma The most serious type of hematoma, epidural hematoma forms rapidly and results from arterial bleeding. The hematoma forms between the dura and skull from a tear in the meningeal artery. It is often associated with temporary loss of consciousness, followed by a lucid period that then rapidly progresses to coma. Epidural hematoma is a surgical emergency. TRAUMATIC BRAIN INJURY Subdural Hematoma Subdural hematoma forms slowly and results from a venous bleed. It occurs under the dura as a result of tears in the veins crossing the subdural space. TRAUMATIC BRAIN INJURY Intracerebral Hemorrhage Intracerebral hemorrhage occurs when a blood vessel within the brain ruptures, allowing blood to leak inside the brain. Subarachnoid Hemorrhage A subarachnoid hemorrhage is bleeding into the subarachnoid space. It may occur as a result of head trauma or spontaneously, such as from a ruptured cerebral aneurysm. TRAUMATIC BRAIN INJURY NURSING ASSESSMENT A. Unconsciousness or disturbances in consciousness B. Vertigo C. Confusion, delirium, or disorientation D. Symptoms of increased ICP 1. Change in level of responsiveness is the most important indicator of increased ICP. 2. Changes in vital signs a. Slowing of respirations or respiratory irregularities TRAUMATIC BRAIN INJURY b. Increase or decrease in pulse c. Rising BP or widening pulse pressure d. Temperature rise 3. Headache 4. Vomiting (projectile) 5. Pupillary changes reflecting pressure on optic or oculomotor nerves a. Decrease or increase in size or unequal size of pupils b. Lack of conjugate eye movement c. Papilledema TRAUMATIC BRAIN INJURY E. Seizures F. Ataxia – poor muscle control causing clumsy movement G. Abnormal posturing (decerebrate or decorticate) H. Cerebrospinal fluid (CSF) leakage through nose (rhinorrhea) or through ear (otorrhea). I. Hematomas TRAUMATIC BRAIN INJURY Nursing Plans and Interventions A. Maintain adequate ventilation and airway. 1. Monitor PO2 and PCO2 for the development of hypoxia and hypercapnia. 2. Position client semiprone or lateral recumbent to prevent aspiration. 3. Turn from side to side to prevent lung secretion stasis. TRAUMATIC BRAIN INJURY B. Keep head of bed elevated 30 to 45 degrees to aid venous return from the neck and to decrease cerebral volume. C. Obtain neurologic vital signs as prescribed (at least every 1 to 2 hours), and maintain a continuous record of observations and Glasgow Coma Scale ratings. D. Notify physician at first sign of deterioration or improvement in condition. TRAUMATIC BRAIN INJURY E. Avoid activities that increase ICP, such as 1. Change in bed position for caregiving and extreme hip flexion 2. Endotracheal suctioning 3. Compression of jugular veins (keep head straight and not to one side) 4. Coughing, vomiting, or straining of any type (no Valsalva: Increased intrathoracic pressure increases ICP. TRAUMATIC BRAIN INJURY F. If temperature increases, take immediate measures to reduce it (aspirin, acetaminophen, cooling blanket) because increased temperature increases cerebral blood flow drastically; avoid shivering. G. Use intracranial monitoring system when available. 1. A catheter is inserted into the lateral ventricle, a sensor placed on the dura, or a screw into the subarachnoid space attached to a pressure transducer. 2. Elevations of ICP over 20 mm Hg should be reported stat. TRAUMATIC BRAIN INJURY H. Administer medications prescribed by physician to reduce ICP. 1. Hyperosmotic agents and diuretics to dehydrate brain and reduce cerebral edema a. Mannitol b. Urea 2. Steroids - to reduce brain swelling 3. Barbiturates - to reduce brain metabolism and systemic BP TRAUMATIC BRAIN INJURY I. Insert indwelling Foley catheter to prevent restlessness caused by distended bladder and to monitor balance between restricted fluid I&O, especially if placed on osmotic diuretics. J. Try not to use restraints; they only increase restlessness. Avoid narcotics because they mask the level of responsiveness. K. Physician may order passive hyperventilation on ventilator: leads to respiratory alkalosis, which causes cerebral vasoconstriction and decreased cerebral blood flow, and therefore decreased ICP. L. Continue seizure precautions. Health care provider may order prophylactic phenytoin (Dilantin).  02 SPINAL CORD INJURY SPINAL CORD INJURY Disruption in nervous system function, which may result in complete or incomplete loss of motor and sensory function. Changes occur in the function of all physiologic systems. SPINAL CORD INJURY A. Injuries are described by location in the spinal cord. The most common sites are the fifth, sixth, and seventh cervical vertebrae (C5, C6, C7), the twelfth thoracic (T12), and the first lumbar (L1). B. Damage can range from contusion to complete transection. C. Permanent impairment cannot be determined until spinal cord edema has subsided, usually by 1 week. SPINAL CORD INJURY NURSING PLANS AND INTERVENTIONS Maintain client in an extended position with cervical collar on during any transfer. Stabilize the client when transferring between the accident scene and the emergency department. The client will be realigned and stabilized in the emergency room. SPINAL CORD INJURY Maintain a patent airway (most important). In cervical injuries, skeletal traction is maintained by use of skull tongs or a halo ring (Crutchfield tongs or a Gardner-Wells fixation device). High-dose corticosteroids are often given to help control edema during the first 8 to 24 hours. SPINAL CORD INJURY Use a very firm mattress with board underneath. Assess for respiratory failure, especially in clients with high cervical injuries. Further loss of sensory or motor function below injury can indicate additional damage to cord due to edema and should be reported immediately. SPINAL CORD INJURY Evaluate for presence of spinal shock (a complete loss of all reflex, motor, sensory, and autonomic activity below the lesion). This medical emergency occurs immediately after the injury. ○ Hypotension, bradycardia ○ Complete paralysis and lack of sensation below lesion ○ Bladder and bowel distention SPINAL CORD INJURY Evaluate for autonomic dysreflexia (exaggerated autonomic responses to stimuli), which occurs in clients with lesions at or above T6. This medical emergency usually occurs after the period of spinal shock has finished and is usually triggered by a noxious stimulus such as bowel or bladder distention. It may also be triggered by a vaginal examination. ○ Elevated BP ○ Pounding headache, sweating, nasal congestion, goose bumps, bradycardia ○ Bladder and bowel distention SPINAL CORD INJURY Watch for acute paralytic ileus, lack of gastric activity. ○ Assess bowel sounds frequently. ○ Initiate gastric suction to reduce distention, prevent vomiting and aspiration. ○ Use rectal tube to relieve gaseous distention. Suction with caution to prevent vagus nerve stimulation, which can cause cardiac arrest. Administer high-dose corticosteroids intravenously to decrease edema and reduce cord damage.  03 CEREBRAL ANEURYSM CEREBRAL ANEURYSM Dilation of the walls of a weakened cerebral artery; can lead to rupture CEREBRAL ANEURYSM Assessment Headache and pain Irritability Visual changes Tinnitus Hemiparesis Nuchal rigidity Seizures CEREBRAL ANEURYSM Interventions Maintain a patent airway (suction only with a doctor’s prescription). Administer oxygen as prescribed. Monitor vital signs and for hypertension or dysrhythmias. Avoid taking temperatures via the rectum. Initiate aneurysm precautions  04 SEIZURE DISORDER SEIZURE DISORDER Seizures are an abnormal, sudden, excessive discharge of electrical activity within the brain. Epilepsy is a disorder characterized by chronic seizure activity and indicates brain or CNS irritation. Causes include genetic factors, trauma, tumors, circulatory or metabolic disorders, toxicity, and infections. SEIZURE DISORDER Status epilepticus involves a rapid succession of epileptic spasms without intervals of consciousness; it is a potential complication that can occur with any type of seizure, and brain damage may result. It is defined as a seizure with 5 minutes or more of continuous clinical and/or electrographic seizure activity or recurrent seizure activity without recovery between seizures SEIZURE DISORDER TYPES OF SEIZURE TYPES OF SEIZURE DISORDER Generalized Seizures 1. Tonic-Clonic Tonic-clonic seizures may begin with an aura. The tonic phase involves the stiffening or rigidity of the muscles of the arms and legs and usually lasts 10 to 20 seconds, followed by loss of consciousness. The clonic phase consists of hyperventilation and jerking of the extremities and usually lasts about 30 seconds. Full recovery from the seizure may take several hours. TYPES OF SEIZURE DISORDER 2. Absence A brief seizure that lasts seconds, and the individual may or may not lose consciousness No loss or change in muscle tone occurs. Seizures may occur several times during a day. The victim appears to be daydreaming. This type of seizure is more common in children. TYPES OF SEIZURE DISORDER 3. Myoclonic Myoclonic seizures present as a brief generalized jerking or stiffening of extremities. The victim may fall from the seizure 4. Atonic or Akinetic (Drop attacks) An atonic seizure is a sudden momentary loss of muscle tone. The victim may fall as a result of the seizure, TYPES OF SEIZURE DISORDER Partial Seizures 1. Simple Partial The simple partial seizure produces sensory symptoms accompanied by motor symptoms that are localized or confined to a specific area. The client remains conscious and may report an aura. TYPES OF SEIZURE DISORDER 2. Complex Partial The complex partial seizure is a psychomotor seizure. The area of the brain most usually involved is the temporal lobe. The seizure is characterized by periods of altered behavior of which the client is not aware. The client loses consciousness for a few seconds.  SEIZURE DISORDER Assessment Seizure history Type of seizure Occurrences before, during, and after the seizure Prodromal signs, such as mood changes, irritability, and insomnia Aura: Sensation that warns the client of the impending seizure Loss of motor activity or bowel and bladder function or loss of consciousness during the seizure Occurrences during the postictal state, such as headache, loss of consciousness, sleepiness, and impaired speech or thinking SEIZURE DISORDER Interventions Note the time and duration of the seizure. Assess behavior at the onset of the seizure: If the client has experienced an aura, if a change in facial expression occurred, or if a sound or cry occurred from the client. If the client is standing or sitting, place the client on the floor and protect the head and body. SEIZURE DISORDER Support airway, breathing, and circulation. Administer oxygen. Prepare to suction secretions. Turn the client to the side to allow secretions to drain while maintaining the airway. Prevent injury during the seizure. Remain with the client. Do not restrain the client. Loosen restrictive clothing. SEIZURE DISORDER Note the type, character, and progression of the movements during the seizure. Monitor for incontinence. Administer intravenous medications as prescribed to stop the seizure. Document the characteristics of the seizure. Provide privacy. Monitor behavior following the seizure, such as the state of consciousness, motor ability, and speech ability. SEIZURE DISORDER Instruct the client about the importance of life-long medication and the need for follow-up determination of medication blood levels. Instruct the client to avoid alcohol, excessive stress, fatigue, and strobe lights. If the client is having a seizure, maintain a patent airway. Do not force the jaws open or place anything in the client’s mouth. SEIZURE DISORDERS SUPPLEMENTAL VIDEOS 1. https://www.youtube.com/watch?v=8kYJughJXbs 2. https://www.youtube.com/watch?v=otuaPazecDo  05 CEREBROVASCULAR ACCIDENT (STROKE) CEREBROVASCULAR ACCIDENT A stroke, sometimes referred to as a brain attack, manifests as a sudden focal neurological deficit and is caused by cerebrovascular disease. Part of the brain cannot get the blood (and oxygen) it needs, causing brain cells to die. Cerebral anoxia lasting longer than 10 minutes causes cerebral infarction with irreversible change. CEREBROVASCULAR ACCIDENT Transient ischemic attack may be a warning sign of an impending stroke. The permanent disability cannot be determined until the cerebral edema subsides. The order in which function may return is facial, swallowing, lower limbs, speech, and arms. CEREBROVASCULAR ACCIDENT Sudden loss of brain function resulting from a disruption in the blood supply to a part of the brain; classified as thrombotic or hemorrhagic CEREBROVASCULAR ACCIDENT CNS involvement related to cause of stroke includes the following: Hemorrhagic caused by a slow or fast hemorrhage into the brain tissue; often related to HTN Ischemic caused by a clot that has broken away from a vessel and has lodged in one of the arteries of the brain, blocking the blood supply. It is often related to atherosclerosis (so it may occur again). CEREBROVASCULAR ACCIDENT Causes Thrombosis Embolism Thrombotic and embolic strokes are classified as ischemic strokes. Hemorrhage from rupture of a vessel; classified as a hemorrhagic stroke CEREBROVASCULAR ACCIDENT Risk factors HTN Advanced age Previous transient ischemic Diabetes attacks (TIAs) Oral contraceptives and HRT Cardiac disease: Smoking atherosclerosis, valve Alcohol, more than 2 drinks per disease, history of day dysrhythmias (particularly atrial flutter or fibrillation) CEREBROVASCULAR ACCIDENT Diagnosis is made by observation of clinical signs and is confirmed by: Cranial CT scan MRI Doppler flow studies Ultrasound imaging CEREBROVASCULAR ACCIDENT Nursing Assessment A. Change in level of consciousness B. Paresthesia, paralysis C. Aphasia, agraphia D. Memory loss E. Vision impairment F. Bladder and bowel dysfunction G. Behavioral changes CEREBROVASCULAR ACCIDENT H. Assessment of client’s functional abilities, including 1. Mobility 2. Activities of daily living (ADLs) 3. Elimination 4. Communication I. Ability to swallow, eat, and drink without aspiration ASSESSMENT FINDINGS IN A STROKE Agnosia ▪ The inability to recognize familiar objects or persons Apraxia ▪ Called dyspraxia if the condition is mild ▪ Characterized by loss of ability to execute or carry out skilled movements or gestures, despite having the desire and physical ability to perform them ASSESSMENT FINDINGS IN A STROKE Hemianopsia ▪ Blindness in half the visual field Homonymous Hemianopsia ▪ Loss of half of the field of view on the same side in both eyes  Normal Homonymous hemianopsia Bitemporal hemianopsia Binasal hemianopsia ASSESSMENT FINDINGS IN A STROKE Neglect Syndrome (Unilateral Neglect) ▪ Client unaware of the existence of her or his paralyzed side Proprioception Alterations ▪ Altered position sense that places the client at increased risk of injury CEREBROVASCULAR ACCIDENT Clinical Manifestations of Stroke Based on Type Thrombotic Stroke Typically, there is no decreased level of consciousness within the first 24 hours. Symptoms get progressively worse as the infarction and edema increase. CEREBROVASCULAR ACCIDENT Embolic Stroke Sudden, severe symptoms Warning signs are less common. Client remains conscious and may have a headache. CEREBROVASCULAR ACCIDENT Clinical Manifestations of Stroke Based on Type Hemorrhagic Stroke Sudden onset of symptoms Symptoms progress over minutes to hours due to ongoing bleeding. CEREBROVASCULAR ACCIDENT Nursing Plans and Interventions Interventions during the acute phase of stroke: Maintain a patent airway and administer oxygen as prescribed. Monitor vital signs. Usually a blood pressure of 150/100 mm Hg is maintained to ensure cerebral perfusion. Suction secretions to prevent aspiration as prescribed, but never suction nasally or for longer than 10 seconds to prevent increased ICP. CEREBROVASCULAR ACCIDENT Monitor for increased ICP, because the client is most at risk during the first 72 hours following the stroke. Position the client on the side to prevent aspiration, with the head of the bed elevated 15 to 30 degrees as prescribed. Monitor level of consciousness, pupillary response, motor and sensory response, cranial nerve function, and reflexes. Maintain a quiet environment. CEREBROVASCULAR ACCIDENT Insert a urinary catheter as prescribed. Administer intravenous fluids as prescribed. Maintain fluid and electrolyte balance. Prepare to administer anticoagulants, antiplatelets, diuretics, antihypertensives, and antiseizure medications as prescribed depending on the type of stroke that has been diagnosed. CEREBROVASCULAR ACCIDENT Nursing Plans and Interventions Interventions during the postacute phase of stroke: Continue with interventions from the acute phase. Position the client 2 hours on the unaffected side and 20 minutes on the affected side; the prone position may also be prescribed. Provide skin, mouth, and eye care. Perform passive range-of-motion exercises to prevent contractures. CEREBROVASCULAR ACCIDENT Place antiembolism stockings on the client; remove daily to check skin. Monitor the gag reflex and ability to swallow. Provide sips of fluids and slowly advance diet to foods that are easy to chew and swallow. When the client is eating, position the client sitting in a chair or sitting up in bed, with the head and neck positioned slightly forward and flexed. CEREBROVASCULAR ACCIDENT Place food in the back of the mouth on the unaffected side to prevent trapping of food in the affected cheek. Provide soft and semisoft foods and flavored, cool or warm, thickened fluids rather than thin liquids, because the stroke client can tolerate these types of food better; speech therapists may do swallow studies to recommend consistency of food and fluids. CEREBROVASCULAR ACCIDENT Nursing Plans and Interventions Interventions during the chronic phase of stroke: Neglect syndrome a. The client is unaware of the existence of the paralyzed side (unilateral neglect), which places the client at risk for injury. b. Teach the client to touch and use both sides of the body. CEREBROVASCULAR ACCIDENT Hemianopsia a. The client has blindness in half of the visual field. b. Homonymous hemianopsia is blindness in the same visual field of both eyes. c. Encourage the client to turn the head to scan the complete range of vision; otherwise, the client does not see half of the visual field. CEREBROVASCULAR ACCIDENT Approach the client from the unaffected side. Place the client’s personal objects within the visual field. Provide eye care for visual deficits. Place a patch over the affected eye if the client has diplopia. Increase mobility as tolerated. Encourage fluid intake and a high-fiber diet. Administer stool softeners as prescribed. Encourage the client to express feelings. CEREBROVASCULAR ACCIDENT Encourage independence in activities of daily living. Assess the need for assistive devices such as a cane, walker, splint, or braces. Teach transfer technique from bed to chair and from chair to bed. Provide gait training. Initiate physical and occupational therapy for assessment and to determine the need for adaptive equipment or other supports for self-care and mobility. Refer client to a speech and language pathologist as prescribed.  06 MULTIPLE SCLEROSIS MULTIPLE SCLEROSIS Demyelinating disease resulting in the destruction of CNS myelin and consequent disruption in the transmission of nerve impulses It usually occurs between the ages of 20 and 50 years and consists of periods of remissions and exacerbations. The causes are unknown, but the disease is thought to be the result of an autoimmune response or viral infection. MULTIPLE SCLEROSIS Precipitating factors include pregnancy, fatigue, stress, infection, and trauma. Symptoms involving motor function usually begin in the upper extremities with weakness progressing to spastic paralysis. Bowel and bladder dysfunction occurs in 90% of cases. MS is more common in women. MULTIPLE SCLEROSIS Physical assessment to include: 1. Optic neuritis (loss of vision or blind spots) 2. Visual or swallowing difficulties 3. Gait disturbances; intention tremors 4. Unusual fatigue, weakness, and clumsiness 5. Numbness, particularly on one side of face 6. Impaired bladder and bowel control 7. Speech disturbances 8. Scotomas (white spots in visual field, diplopia) MULTIPLE SCLEROSIS NURSING PLANS AND INTERVENTIONS Allow hospitalized client to keep own routine. Orient client to environment and teach strategies to maximize vision. With exercise programs, encourage client to work up to the point just short of fatigue. Teach client that, for muscle spasticity, stretch-hold-relax exercises are helpful, as are riding a stationary bicycle and swimming; take precautions against falls. Initially, work with client on a voiding schedule. MULTIPLE SCLEROSIS Place an eye patch on the eye for diplopia. Encourage adequate fluid intake, high-fiber foods, and a bowel regimen for constipation problems. Anticholinergic agents are used for bladder spasticity and intravenous glucocorticoids for acute flare-ups. Instruct the client in safety measures related to sensory loss, such as regulating the temperature of bath water and avoiding heating pads.  07 MYASTHENIA GRAVIS MYASTHENIA GRAVIS A neuromuscular autoimmune disorder of the neuromuscular junction characterized by considerable weakness and abnormal fatigue of the voluntary muscles A defect in the transmission of nerve impulses at the myoneural junction occurs. MYASTHENIA GRAVIS Causes include 1. Insufficient secretion of acetylcholine; 2. Excessive secretion of cholinesterase; and 3. Unresponsiveness of the muscle fibers to acetylcholine. MYASTHENIA GRAVIS MULTIPLE SCLEROSIS ASSESSMENT Weakness and fatigue Difficulty chewing and swallowing Dysphagia Ptosis Diplopia Weak, hoarse voice Difficulty breathing Diminished breath sounds Respiratory paralysis and failure MYASTHENIA GRAVIS Nursing Plans and Interventions If client is hospitalized, have tracheostomy kit available at bedside for possible myasthenic crisis. Administer cholinergic drugs as prescribed. Schedule nursing activities to conserve energy (e.g., complete daily hygiene activities, administration of medications, and treatments all at once), and allow rest periods. MYASTHENIA GRAVIS Plan activities during high-energy times, often in the early morning. Instruct client to avoid situations that produce fatigue or physical or emotional stress (any type of stress can exacerbate symptoms). Encourage coughing and deep breathing every 4 to 6 hours. (Muscle weakness limits ability to cough up secretions, promotes URTI.) If symptoms worsen, identify type of crisis and report immediately: myasthenic or cholinergic. MYASTHENIA GRAVIS MYASTHENIA CRISIS An acute exacerbation of the disease The crisis is caused by a rapid, unrecognized progression of the disease, inadequate amount of medication, infection, fatigue, or stress. MYASTHENIA GRAVIS Assessment Increased pulse, respirations, and blood pressure Dyspnea, anoxia, and cyanosis Bowel and bladder incontinence Decreased urine output Absent cough and swallow reflex Interventions Assess for signs of myasthenic crisis. Increase anticholinesterase medication, as prescribed. MYASTHENIA GRAVIS CHOLINERGIC CRISIS Results in depolarization of the motor end plates The crisis is caused by overmedication with anticholinesterase (Atropine). MYASTHENIA GRAVIS Assessment Abdominal cramps Nausea, vomiting, and diarrhea Blurred vision Pallor Pupillary miosis Facial muscle twitching Hypotension Increased bronchial secretions, tearing, perspiration Bronchospasm, wheezing, and bradycardia MYASTHENIA GRAVIS Interventions Withhold anticholinesterase medication. Prepare to administer the antidote, atropine sulfate, if prescribed. Monitor vital signs and respiratory status closely; intubation may be necessary. Frequent monitoring of respiratory status is needed, and elective intubation may be initiated. MYASTHENIA GRAVIS MYASTHENIA GRAVIS Edrophonium (Tensilon) test This test is performed by the neurologist and may be done to diagnose myasthenia gravis and to differentiate between myasthenic crisis and cholinergic crisis. The test places the client at risk for ventricular fibrillation and cardiac arrest; emergency equipment needs to be available Have atropine sulfate available when performing the edrophonium test. MYASTHENIA GRAVIS Edrophonium test procedure Edrophonium injection is administered to the client. Positive for myasthenia gravis: Client shows improvement in muscle strength after the administration of edrophonium. Negative for myasthenia gravis: Client shows no improvement in muscle strength, and strength may even deteriorate after injection of edrophonium. MYASTHENIA GRAVIS To differentiate crisis Myasthenic crisis: Edrophonium is administered; if strength improves, the client needs more medication. Cholinergic crisis: Edrophonium is administered; if weakness is more severe, the client is overmedicated; prepare to administer atropine sulfate, the antidote, as prescribed.  08 PARKINSON DISEASE PARKINSON DISEASE Chronic, progressive, debilitating neurologic disease of the basal ganglia and substantia nigra, affecting motor ability and characterized by tremor at rest, increased muscle tone (rigidity), slowness in the initiation and execution of movement (bradykinesia), and postural instability (difficulties with gait and balance) PARKINSON DISEASE The pathophysiology involves an imbalance between acetylcholine and dopamine, so symptoms can be controlled by administering a dopamine precursor (levodopa). PARKINSON DISEASE Nursing Assessment Rigidity of extremities Masklike facial expressions with associated difficulty in chewing, swallowing, and speaking Drooling Stooped posture and slow, shuffling gait Tremors at rest, “pill-rolling” movement (disappears during sleep and purposeful activity) Emotional lability Increased tremors with stress or anxiety PARKINSON DISEASE Nursing Plans and Interventions Schedule activities later in the day to allow sufficient time for client to perform self-care activities without rushing. Encourage activities and exercise. A cane or walker may be needed. Eliminate environmental noise, and encourage the client to speak slowly and clearly, pausing at intervals. Serve a soft diet, which is easy to swallow. Administer antiparkinsonian drugs as prescribed PARKINSON DISEASE Carbidopa-levodopa taken with a monoamine oxidase inhibitor antidepressant can cause a hypertensive crisis. If an anticholinergic medication is discontinued abruptly, the signs and symptoms of Parkinsonism may be intensified. PARKINSON DISEASE PARKINSON DISEASE  09 TRIGEMINAL NEURALGIA TRIGEMINAL NEURALGIA A sensory disorder of the trigeminal (5th cranial nerve) It results in severe, recurrent, sharp facial pain along the trigeminal nerve. TRIGEMINAL NEURALGIA Assessment The client has severe pain on the lips, gums, or nose, or across the cheeks. Situations that stimulate symptoms include cold, washing the face, chewing, or food or fluids of extreme temperatures. TRIGEMINAL NEURALGIA Interventions Instruct the client to avoid hot or cold foods and fluids. Provide small feedings of liquid and soft foods. Instruct the client to chew food on the unaffected side. Administer medications as prescribed TRIGEMINAL NEURALGIA Surgical interventions Microvascular decompression: Surgical relocation of the artery that compresses the trigeminal nerve as it enters the pons, which may relieve pain without compromising facial sensation Radiofrequency waveforms: Create lesions that provide relief of pain without compromising touch or motor function TRIGEMINAL NEURALGIA Rhizotomy: Resection of the root of the nerve to relieve pain Glycerol injection: Destroys the myelinated fibers of the trigeminal nerve (may take up to 3 weeks for pain relief to occur)  10 BELL’S PALSY (FACIAL PARALYSIS) BELL’S PALSY Caused by a lower motor neuron lesion of cranial nerve VII that may result from infection, trauma, hemorrhage, meningitis, or tumor. It results in paralysis of one side of the face. Recovery usually occurs in a few weeks, without residual effect BELL’S PALSY Assessment Flaccid facial muscles Frequently results in inability to raise the eyebrows, frown, smile, close the eyelids, or puff out the cheeks Upward movement of the eye when attempting to close the eyelid Loss of taste BELL’S PALSY Interventions Encourage facial exercises to prevent the loss of muscle tone (a face sling may be prescribed to prevent stretching of weak muscles). Protect the eyes from dryness, and prevent injury. Promote frequent oral care. Instruct the client to chew on the unaffected side.  11 GUILLAIN-BARRE SYNDROME GUILLAIN-BARRE SYNDROME An acute infectious autoimmune neuronitis of the cranial and peripheral nerves. Generally occurs a few days to weeks after viral or bacterial infection. The immune system overreacts to the infection and destroys the myelin sheath. The syndrome usually is preceded by a mild upper respiratory infection or gastroenteritis. The recovery is a slow process and can take years. GUILLAIN-BARRE SYNDROME Nursing Assessment Paresthesia (tingling and numbness) Muscle weakness of legs progressing to the upper extremities, trunk, and face Increasing pulse rate and disturbances in rhythm Possible pain in the back and in calves of legs Weakness or paralysis of the intercostal and diaphragm muscles; may develop quickly GUILLAIN-BARRE SYNDROME Paralysis of the ocular, facial, and oropharyngeal muscles, causing marked difficulty in talking, chewing, and swallowing. Assess for: Breathlessness while talking Shallow and irregular breathing Use of accessory muscles while breathing Any change in respiratory pattern Paradoxical inward movement of the upper abdominal wall while in a supine position, indicating weakness and impending paralysis of the diaphragm GUILLAIN-BARRE SYNDROME NURSING PLANS AND INTERVENTIONS Care is directed toward the treatment of symptoms, including pain management. Monitor respiratory status closely. Provide respiratory treatments. Prepare to initiate respiratory support. Monitor cardiac status. Assess for complications of immobility. The major concern in Guillain-Barré syndrome is difficulty breathing; monitor respiratory status closely.  12 AMYOTROPHIC LATERAL SCLEROSIS AMYOTROPHIC LATERAL SCLEROSIS Also known as Lou Gehrig’s disease It is a progressive, rare, incurable degenerative disease involving the motor system. The sensory and autonomic systems are not involved, and mental status changes do not result from the disease. The cause of the disease may be related to an excess of glutamate, a chemical responsible for relaying messages between the motor neurons. AMYOTROPHIC LATERAL SCLEROSIS As the disease progresses, muscle weakness and atrophy develop until a flaccid tetraplegia develops. Eventually, the respiratory muscles become affected, leading to respiratory compromise, pneumonia, and death. No cure is known, and the treatment is symptomatic. AMYOTROPHIC LATERAL SCLEROSIS Assessment Respiratory difficulty Fatigue while talking Muscle weakness and atrophy Tongue atrophy Dysphagia Weakness of the hands and arms Fasciculations of the face Nasal quality of speech Dysarthria AMYOTROPHIC LATERAL SCLEROSIS Interventions Care is directed toward the treatment of symptoms. Monitor respiratory status and institute measures to prevent aspiration. Provide respiratory treatments. Prepare to initiate respiratory support. Assess for complications of immobility. Address advance directives as appropriate. Provide the client and family with psychosocial support.  13 ENCEPHALITIS & MENINGITIS CNS INFLAMMATION ENCEPHALITIS An inflammation of the brain parenchyma and often of the meninges. It affects the cerebrum, brainstem, and cerebellum. It most often is caused by a viral agent. MENINGITIS An inflammation of the arachnoid and pia mater of the brain and spinal cord It is caused by bacterial and viral organisms, although fungal and protozoan meningitis also occur. CNS INFLAMMATION DIAGNOSIS CSF is analyzed to determine the diagnosis and type of meningitis. In meningitis, CSF is cloudy, with increased protein, increased white blood cells, and decreased glucose counts. CNS INFLAMMATION Transmission Transmission occurs in areas of high population density, crowded living areas such as college dormitories, and prisons. Transmission of meningitis is by direct contact, including droplet spread. CNS INFLAMMATION Assessment Mild lethargy Photophobia Deterioration in the level of consciousness Signs of meningeal irritation, such as nuchal rigidity and a positive Kernig’s sign and Brudzinski’s sign Red, macular rash with meningococcal meningitis Abdominal and chest pain with viral meningitis Kernig’s Sign ▪ Loss of the ability of a supine client to straighten the leg completely when it is fully flexed at the knee and hip; indicates meningeal irritation Brudzinski’s Sign ▪ Involuntary flexion of the hip and knee when the neck is passively flexed; indicates meningeal irritation CNS INFLAMMATION Interventions Monitor vital signs and neurological signs. Assess for signs of increased ICP. Initiate seizure precautions. Monitor for seizure activity. Monitor for signs of meningeal irritation. Perform cranial nerve assessment. Assess peripheral vascular status (septic emboli may block circulation). CNS INFLAMMATION Maintain isolation precautions as necessary with bacterial meningitis. Maintain urine and stool precautions with viral meningitis. Maintain respiratory isolation for the client with pneumococcal meningitis. Elevate the head of the bed 30 degrees, and avoid neck flexion and extreme hip flexion. Prevent stimulation and restrict visitors. Administer analgesics and/or antibiotics as prescribed.