Unit 4 Week 14

cerebellum

is located behind the pons and medulla and is responsible for smooth, coordinated movements. It also influences posture and equilibrium. Unlike the cerebrum, damage to one side of the cerebellum affects the ipsilateral (same) side of the body. Injury to the cerebellum leads to a variety of disorders depending on the affected region. Individuals may present with slurred speech and uncoordinated movements that are jerky and slow. Others may present with an ataxic gait (uncoordinated walking). The cerebellum also plays a role in motor learning. When a motor skill is learned, such as riding a bike, the cerebellum stores this information and later provides individuals with the ability to perform the skill without having to relearn it.

unknown onset seizure

is one in which the time of beginning seizure activity is unknown. It may not be witnessed by anyone or occur when the affected person is alone. As more information is obtained, an unknown onset seizure may later be diagnosed as a focal or generalized seizure.

medulla oblongata

is part of the brainstem between the pons and spinal cord. It is responsible for maintaining vital body functions, such as breathing, sleep-wake cycles, blood pressure, and heart rate.

complementary hemisphere

is referred to as the representational hemisphere; in most persons, this is the right hemisphere. It focuses more on recognition of faces, music, and visual-spatial relationships than the other hemisphere.

spinothalamic tract

is the major region of sensory neurons that travel from the periphery up into the brain. The spinothalamic tract originates in the spinal cord and crosses at some level within the spinal cord before arriving in the brain. This crossover of neurons causes any type of cerebral injury to manifest sensory and motor deficits on the contralateral side of the body.

corticospinal tract

is the major region of upper motor neurons that descend from the brain down into the spinal cord.

diencephalon

is the posterior part of the forebrain that connects the midbrain with the cerebral hemispheres; it consists of the thalamus and hypothalamus. The diencephalon relays sensory information between brain regions and controls many autonomic functions of the PNS. It also connects structures of the endocrine system with the nervous system and works in conjunction with limbic system structures to generate and manage emotions and memories.

Vertebral-basilar insufficiency (VBI)

is the syndrome that occurs when there is decreased vertebral and basilar artery blood flow and consequent decreased blood supply to the cerebellum

Family Coping for ischemic stroke

Encourage to participate in care Encourage counseling Avoid doing activities for the patient that the patient can do herself Assist in developing goals for home setting Will require months of therapy Expect emotional lability Community resources

Cerebrum

makes up most of the brain tissue and is located in the uppermost region of the brain. It is divided into a right and left hemisphere, which are connected by the corpus callosum. Each hemisphere is also divided into the frontal, parietal, temporal, and occipital lobes. Although each lobe has specific functions, there is some overlapping of responsibilities

corticobulbar tract

neurons run parallel to the corticospinal tract; they descend from the cortex down into the brainstem where cranial nerves emerge.

Acetylcholine

is found within the CNS, PNS, and ANS. It can act as either an excitatory or inhibitory neurotransmitter, depending on what neurons secrete it. For example, within the ANS, Ach functions as an inhibitory neurotransmitter to slow the heart rate. However, within the PNS, it behaves as an excitatory neurotransmitter at neuromuscular junctions.

Midbrain

is involved in functions such as vision, hearing, eye movement, and body movement. The anterior part contains the cerebral peduncle, a huge bundle of axons traveling from the cerebral cortex through the brainstem. These fibers, along with other structures, are important for voluntary motor function.

Pons

is involved in motor control and sensory analysis. For example, information from the ear first enters the brain in the pons. It also has parts that are important for level of consciousness and sleep. Some structures within the pons are linked to the cerebellum and are involved in movement and posture.

Glutamate

, is considered a major mediator of excitatory signals in the CNS and is involved in cognition, memory, and learning. Glutamate is kept within the nerve terminal vesicles; after being released from the neuron, specific transporters must rapidly remove it from the extracellular space, as extracellular accumulation of glutamate causes brain cell injury and cell death.

transient ischemic attack (TIA)

. Many persons call this a "mini-stroke," which is an inaccurate label. A TIA is a disruption of cerebral circulation with neurological deficits that are reversible and last for less than 24 hours. In a TIA, the body naturally dissolves the clot that caused the ischemia, circulation returns, and there is no permanent neurological injury. However, TIA is often a warning sign of future stroke.

subarachnoid hemorrhage (SAH),

A specific type of cerebral hemorrhage occurs when an arterial branch in the subarachnoid space ruptures; this event, called a may be the result of head trauma or aneurysm rupture. The most common sites for cerebral aneurysm are in those arteries that make up the circle of Willis within the subarachnoid space

Cerebral Arteriosclerosis

A thrombus is frequently the cause of an ischemic stroke. Thrombi arise from arteriosclerotic plaque; they commonly develop in either the neck or the heart's left atrium and travel up the carotid artery and into the brain. As described in the chapters on cardiovascular disease, endothelial injury usually starts the process of arteriosclerosis. Endothelial injury can be incited by a number of predisposing factors, including free radical injury, hypertension, hyperlipidemia, or high glucose levels in diabetes. As arteriosclerotic plaque builds up, the blood vessel diameter decreases; this, in turn, lessens blood flow to the tissue. Alternatively, arteriosclerotic plaque often breaks and pieces of plaque become emboli. Either as a thrombus or embolus, a piece of plaque can lodge in an arteriole and obstruct blood flow. These mechanisms can occur in cerebrovascular vessels, causing ischemia and infarction of brain tissue.

Motor Hemiplegia Hemiparesis Early stages of stroke may display flaccid paralysis with decreasing deep tendon reflexes Deep tendon reflexes appear within 48 hours and display spasticity and increased tone Communication ◦Aphasia/Dysphagia ◦Dysarthria ◦Apraxia Perceptual disturbances ◦Visual disturbances (hemianopsia) Sensory Loss ◦Impaired touch with proprioception ◦Agnosia Cognitive impairments ◦Frontal Lobe damage: decreased learning, memory, or higher cortical functioning impaired ◦Depression ◦Emotional lability, hostility, frustration, lack of cooperation

Affected Body Functions of cva

Carotid Stenosis

Arteriosclerosis of the carotid artery, called carotid stenosis, is also a common cause of ischemic stroke. In arteriosclerosis of the carotid artery, the lumen of the carotid artery narrows from plaque buildup. Normally, the endothelial lining of the carotid artery is smooth and blood cells travel unencumbered. With carotid artery stenosis, the once-smooth endothelial surface becomes irregular because of accumulated plaque.

•May not present with the "entire" picture •Vision •Hearing •Orientation •Cognitive impairment •Pain •History of seizures, falls, medications, blackouts, communicable diseases •Sensations, range of motion, surgical history •Drug/alcohol use •Trauma to head •Cranial nerve assessment •Full neuro exam •Muscle strength •Gait •Babinski Sign

Assessment of the Neurological System

Atrial Fibrillation

Atrial fibrillation is another cause of ischemic stroke. In left-sided atrial fibrillation, the left atrium is quivering—not contracting sufficiently—and this leads to stasis of blood in the chamber. Stasis of blood increases susceptibility of clot formation in the left atrium. Once formed, clots can travel from the left atrium to the left ventricle and into the aorta. From the aorta, the clot can ascend into the common carotid artery to the internal carotid artery and lodge in a cerebral vessel, most commonly the middle cerebral artery, which leads to brain tissue ischemia (see Fig. 33-9). If ischemia is prolonged, infarction of cerebral tissue and brain cell death occur. Brain cell death leads to loss of neurological functions; this is referred to as a neurological deficit. The travel of a clot from the left atrium to the brain is referred to as a cardioembolic event.

Ischemia and Ischemic Penumbra

Cerebral ischemia often occurs gradually and symptoms are progressive. The process of ischemia can appear over several hours and progress to maximal deficit over several days. The core area of tissue ischemia can increase over time. The survival of this area of ischemia is dependent upon collateral circulation and the length of time that the tissue is ischemic. Restoration of blood flow to the area is critical and can reverse some of the neurological dysfunction. As time passes, brain cells die, so prompt treatment is mandatory. Failure to restore blood flow results in the tissue becoming infarcted with consequent brain cell death. As the brain cells die, they are replaced by scar tissue called neuroglia (gliosis).

Occupational therapist Home modifications Speech therapist Mental health counseling Stroke support groups Caregiver support Respite care

Community care for cva

Cerebral hypoxia ◦Administer oxygen Monitor BP (avoid extremes) Monitor for seizure activity Vasospasm Leading cause of mortality in those surviving the initial insult Bedside transcranial Doppler ultrasound ◦7-10 days after initial insult, clot is dissolved, and chance for re-bleeding increases ◦Nimodipine (Nimotop) is the only drug approved for use with patients experiencing subarachnoid hemorrhage Increased Intracranial Pressure (normal pressure is 7-15 mmHg) ◦Monitor neurologic status Monitor CSF drainage Elevate HOB Sedation Hyperventilation Hypertension BP medication may be administered to prevent enlargement of hematoma at affected site Monitor BP Stool softeners

Complications of hemorrhagic stroke

Manifestations of cva

Depends on area of the brain affected, amount of time affected, size of lesion Present with numbness or weakness to the face, arm, or leg Most often on one side of body Confusion or altered mental state Difficulty speaking Visual disturbances Trouble walking, lack of coordination Sudden and severe onset of headache Motor, sensory, cranial nerves, cognitive, and other functions potentially affected

Clinical Manifestations of seizures

Depends on region of brain effected Generalized seizures involve both brain hemispheres, so both sides of body Intense rigidity of body Epileptic cry Tongue chewed Incontinent After movements stop, patient goes into deep coma-like sleep and loud breathing

Signs and symptoms offer clues to diagnosis Imagining: Blood Urine Spinal fluid Genetic testing Chorionic villus sampling

Diagnosing neurological disorders

CVA Pathophysiology

Disruption of blood flow related to obstruction Penumbra region If edema persists and causes pressure on the brainstem, the respiratory rate, BP, HR, and level of consciousness are altered Cushing's Triad: Hypertension, Bradycardia, Irregular Respirations Loss of 1.9 million neurons each minute left untreated Brain ages 3.6 years for each hour left untreated

Modifiable Risk Factors for cva

Hypertension Atrial fibrillation Dyslipidemia Diabetes Smoking Oral Contraceptives Asymptomatic carotid stenosis Obesity Sedentary lifestyle Sleep apnea Excessive alcohol consumption Periodontal disease

Pathophysiology of hemmorrhagic stroke

Intracerebral hemorrhage - bleeding into the brain Most often with hypertensive and cerebral atherosclerotic patients Intracranial aneurysm - unknown cause Dilation of the walls of the cerebral artery resulting in weaknes Arteriovenous malformations (AVM) - Abnormality in embryonal development Tangle of arteries and veins; common cause of stroke in young people Subarachnoid hemorrhage - May result from AVM, aneurysm, trauma, or hypertension

Cardioembolic Strokes ◦Treated with warfarin (Coumadin), dabigatran (Pradaxa), or rivaroxaban (Xarelto) ◦Aspirin when anticoagulants are contraindicated Thrombolytic Therapy ◦Binds to fibrin and converts plasminogen to plasma ◦Rapids reaction decreases area of ischemia and overall improvement after 3 months ◦Stroke teams ◦IV or Intra-arterial administration ◦Quick determination of eligibility for t-PA ◦Assess on National Institutes of Health Stroke Scale

Medical Management of cva

Bed rest Sedation Promotion of recovery from bleeding and decrease risk of re-bleeding Prevention of complications Monitor for DVT Antihypertensive medications at discharge Not usually surgically treated If ICP continues to increase or neuro responses decrease, craniotomy may occur

Medical Management of hemorrhagic stroke

Clonic

Motor symptoms that include sustained rhythmical jerking movements

Tonic

Muscles may become tense or rigid,

Atonic

Muscles may become weak or limp,

Aphasia,

a language disorder whereby individuals are unable to speak or understand the spoken word, is also a common presentation. In the majority of the population, language is a function of the left hemisphere

Altered LOC is the earliest sign of deterioration Drowsiness, slurring of speech Aneurysm precautions (decrease ICP changes, prevent further bleeding) ◦Quiet, non-stressful, bed rest Bed at 15-30 degrees Avoid sudden activities that may increase BP No enemas Dim lights No caffeine Nurse administers all personal care Educate family and patient on aneurysm precautions Keep the patient/family informed Vasospasm Monitor for intensified headaches Decrease in LOC Aphasia, partial paralysis Administer calcium channel blocker (nimodipine) Seizures Maintain patent airway Re-bleeding ◦Small percent of patients experience re-bleeding after hemorrhagic stroke Monitor BP Most frequently in first 2 weeks after initial insult Severe headache, nausea, vomiting, decreased LOC, decreased neurologic status CT to confirm Home and Community Care Educate patient and family on stroke cause, S/Sx, and consequences Use of assistive devices Modifications to the home Follow-up appointments Home care

Nursing Interventions for hemorrhagic stroke

Goal to improve mobility, achieve self-care, decreased shoulder pain, decreased confusion, improved communication, restored function, absence of complications Holistic care Arms adduct, internal rotation Legs rotate externally Correct positioning of arms, hands, legs Change position every 2 hours ROM 4 to 5 times per day Observe for SOB, chest pain, cyanosis, increased pulse rate Written schedules Assist with balance while sitting before standing May use wheel chair or other mobility aidsParallel barsShoulder pain Do NOT lift by shoulder; no trapeze beds Medications for shoulder pain amitriptyline (Elavil), lamotrigine (Lamictal), pregabalin (Lyrica) Promote personal care Utilize own clothing Visual field may be affected Place objects on side of active sight Nutrition Work with speech therapist Thick liquids Sit up straight, chin down Check placement of enteral feeding tubes, if present Bowel and bladder control◦ Intermittent catheterization Establish routine of eating nutrition education Communication◦ Nurse is supportive Build communication efforts Do not finish sentences Consistent routine Written schedules Checklists Communication board One instruction at a time Talk to the patient during all interactions

Nursing Interventions for ischemic stroke

Monitor blood pressure Suspect thrombus at surgical site if new neuro deficits Assess cranial nerve function Assess LOC, mental functioning Assess pupil response Skin assessment Intake and Output Bleeding Any impairment of daily functions

Nursing Management for ischemic stroke

Manage BP Decreased alcohol consumption Stroke screens Increased age and males are at higher risk

Prevention of hemorrhagic stroke

Can be altered significantly Dysfunction may be physically related to the stroke or mentally relate Talk to the patient about concerns Education Potential medications Alternative expression and satisfaction

Sexual function for cva

Broca's area,

The ability to speak is controlled by this region Dysfunction of Broca's area causes expressive aphasia; the affected individual cannot make words, but he or she does understand what others are saying.

categorical hemisphere;

The cerebral hemisphere associated with language comprehension skills and sequential-analytical processes is referred to as the in most persons, this is the left hemisphere. For most right-handed individuals, the left hemisphere is the categorical hemisphere. The left hemisphere contains areas for language comprehension, speech, and word formation

Glutamate Toxicity

The effect of glutamate in ischemic stroke. (1) In ischemia, the hypoxic brain cells release excess glutamate. (2) The excess glutamate causes overexcitation of the postsynaptic neurons and triggers an influx of calcium. (3). This influx of calcium causes activation of enzymatic degeneration of brain cells.

Ictal period

The episode of the seizure

complementary hemispheric specialization

The location of specific functions within the brain

circle of Willis.

The vertebral arteries are located on both posterior sides of the neck. The vertebral arteries unite to form the basilar artery, which bifurcates to form the posterior cerebral arteries. The anastomosis of the posterior cerebral arteries and the terminal branches of the internal carotids form this. Located at the base of the brain, the circle of Willis provides collateral circulation in the event that one of the major cerebral vascular routes should occlude

ischemic penumbra.

When a cerebral artery is occluded, cerebral perfusion pressure is diminished. Autoregulation of cerebral circulation is nonfunctional and is not able to restore blood flow to the area. Oxygen deprivation allows neurons in the core area of ischemia to progress to irreversible cerebral infarction in minutes. However, brain cells that lie at the perimeter of the stroke region are hypoperfused but are not irreversibly damaged. The perimeter around the core ischemic area is called this. The rapid reperfusion of this area is critical because, if left untreated, the penumbra will also succumb to ischemia and infarction. Within the ischemic penumbra and surrounding brain tissue, some cerebral edema occurs, which also contributes to hypoperfusion and further damage of brain cells.

Focal seizures

arise from a neuronal area localized within one cerebral hemisphere and are restricted to that hemisphere. can cause motor, sensory, autonomic, or psychic symptoms with or without impairment of cognition. Focal seizures are further classified according to patient awareness as either focal onset aware or focal onset impaired awareness seizures. Focal onset aware seizures occur when the affected individual is awake and aware during the seizure. Focal onset impaired awareness seizures occur when the individual is confused or their awareness is affected in some way during the focal seizure.

Generalized seizures

arise within one hemisphere and rapidly involve neurons distributed across both cerebral hemispheres. may have motor and/or nonmotor symptoms. Motor symptoms may include clonic, tonic, or myoclonic muscle activity. Alternatively, muscles can become atonic, or the individual may endure repeated flexion and extension of the whole body called epileptic spasms. Nonmotor symptoms are usually called absence seizures when the patient is unaware of seizure activity. During these episodes the individual has staring spells without movement. Absence seizures can also have brief twitches (myoclonus) that can affect a specific part of the body or just the eyelids.

Obtain a through history Head-to-toe physical and neuro exam CT scan within 25 minutes 12-lead ECG Carotid ultrasound CT angiography MRI Doppler flow studies

assessment of cva

Parietal lobe:

associated with movement, orientation, recognition, and perception of stimuli

Temporal lobe:

associated with perception and recognition of auditory stimuli, memory, and speech

Frontal lobe:

associated with reasoning, planning, parts of speech, movement, emotions, and problem solving

Occipital lobe:

associated with visual processing

Myclonus:

brief muscle twitching

Cerebellum

contributes to coordination, precision, and accuracy of movement. It receives input from sensory systems and from other parts of the brain and spinal cord, and integrates these inputs to fine-tune motor activity. Damage to the cerebellum causes lack of coordination, imbalance, and a gait disturbance termed ataxia.

brainstem.

divided into three regions: the midbrain, pons, and medulla. These regions allow nerve fibers from the spinal cord to connect with the cerebrum. Cranial nerves originate from the different sections of the brainstem and terminate on various organs. Damage to the brainstem can affect cranial nerve function, which includes changes in pupil size. The midbrain controls auditory and visual responses and modulates movement. The pons connects the cerebellum to the rest of the brain and controls arousal, sleep, and autonomic functions. The medulla oblongata, the "vital sign center," regulates vasomotor tone, cardiac, and respiratory functions.

Dopamine

has many functions, including roles in: • Behavior and cognition • Voluntary movement • Motivation • Punishment and reward • Attention • Working memory • Learning Dopaminergic neurons are mainly located in the substantia nigra of the midbrain's basal ganglia region. Dysfunction of dopaminergic neurotransmission in the CNS has been implicated in a variety of neuropsychiatric disorders, including social phobia, Tourette's syndrome, Parkinson's disease, schizophrenia, neuroleptic malignant syndrome, attention deficit-hyperactivity disorder (ADHD), and drug and alcohol dependence.

NIHSS National Institutes of Health Stroke Scale

is a graded neurological examination that evaluates visual fields, ataxia, speech, language, cognition, and motor and sensory function (see Table 33-2). Each section has a graded point scale based on level of function. The points are then added for a total score. Essentially, the higher the score, the greater the neurological deficit. A range of scores correlates with the patient's clinical presentation.

Transcranial Doppler

is a noninvasive ultrasound procedure that can be used on certain areas of the skull. It is used in critical care to assess intracranial pressure, confirm the lack of cerebral circulation in brain death, detect vasospasm in SAH, and monitor blood flow during thrombolytic treatment and carotid endarterectomy.

substantia nigra

is a portion of the basal ganglia that synthesizes dopamine.

basal ganglia

is a portion of the midbrain that modulates voluntary motor function and routine behaviors.

Myelin

is a protective sheath that is formed around axons of some neurons in the nervous system. It acts as an insulator of the electrical signal that is conducted down the axon in neurotransmission and is comparable to the insulation around an electrical wire. The myelin sheath contains a variety of fatty substances called lipids and is considered white matter. In the nervous system, neuron cell bodies are located within the gray matter, whereas axonal tracts and glial cells are within the white matter. allows for a rapid, efficient conduction of a nerve impulse down its axon. Without an even coating of myelin, nerve impulses can become disrupted and potential for conduction can be lost; nerves can eventually wither away. In disorders that cause degeneration of myelin, some regrowth is possible with time, though eventually myelin cannot regenerate; at this point, whole nerve degeneration occurs, causing complete nerve tract disruption.

Seizure

is a sudden, abnormal, disorderly discharge of neurons within the brain that is characterized by a sudden, transient alteration in brain function. A seizure may result in an altered level of consciousness as well as a number of motor, sensory, autonomic, and behavioral manifestations. Seizures have various clinical presentations depending on the specific part of the brain that is affected by the abnormal impulse propagation. A seizure can present as a temporary disruption of the senses, a loss of consciousness, muscle spasms, or repetitive convulsions. Seizures can also occur as a symptom secondary to pathological conditions of the brain, such as tumor, CNS infection, stroke, head injury, metabolic imbalance, substance abuse, and acute alcohol withdrawal Types: Focal Generalized Unknown

Norepinephrine

is an excitatory neurotransmitter in the brain and stress hormone within in the endocrine system. Stress activates a region of the brainstem called the locus coeruleus—the origin of most norepinephrine pathways in the brain. Neurons using norepinephrine project from the locus coeruleus to the cerebral cortex, limbic system, and the spinal cord.,

schemic stroke

is caused by a thrombus or embolus that lodges in a cerebral artery and blocks blood flow to the brain tissue. Ischemia of brain tissue leads to cerebral infarction, which is the death of brain cells.

hemorrhagic stroke

is caused by rupture and hemorrhage of a cerebral artery, leading to compression and toxicity of brain cells and loss of cerebral blood flow. Approximately 85% of strokes are due to ischemia, whereas 15% are hemorrhagic strokes

Maintenance of cerebral hemodynamic Reduce ICP Administer osmotic diuretics Maintain PaCO2 lower Supplemental oxygen if below 92% Elevate HOB 25-30 degrees Potential hemicraniectomy for increasing ICP Intubation Vitals Neuro assessments

what to do when someone is Unable to receive t-PA

Recombinant tissue-type plasminogen activator (rt-PA),

often called a "clot-buster," is the thrombolytic agent most often used. IV administration of rt-PA rapidly dissolves the clot that is causing the ischemia of brain tissue. However, not all ischemic stroke patients are candidates for rt-PA. A strict protocol excludes patients who have a specific set of conditions, which includes susceptibility to bleeding Dosing of t-PA Vitals regularly with systolic BP less than 180 mmHg and diastolic less than 105 mmHg Maintain airway patency Monitor closely for bleeding Delay invasive procedures for 24 hours

Serotonin,

or 5-hydroxytryptamine, is a neurotransmitter chemically derived from tryptophan. It is found primarily in the gastrointestinal tract, platelets, raphe region of the brainstem and is thought to be a contributor to feelings of well-being.

Postictal period:

phase after completion of the seizure. the altered state of consciousness that a person enters after experiencing a seizure, usually lasts between 5 and 30 minutes; however, it can last longer in the case of larger or more severe seizures. The postictal state is characterized by drowsiness, confusion, nausea, hypertension, headache, and other disorienting symptoms. Additionally, emergence from this period is often accompanied by amnesia or other memory defects. During this period, the brain recovers from the trauma of the seizure.

Prevention Healthy lifestyle No smoking Exercise DASH diet Community education on stroke S/Sx Low-dose aspirin Risk increases with age More common in men African Americans

prevention of cva

Babinski reflex,

which is tested with stimulation of the sole of the foot. A negative Babinski reflex, in which the toes flex inward with stimulation of the sole of the foot, is normal in adults. A positive Babinski reflex, where the patient's toes flare in response to stimulation of the sole of the foot, indicates an upper motor neuron disorder.

Carotid Endarterectomy (CEA) ◦Removal of atherosclerotic plaque or thrombus from carotid artery Carotid stenting

surgical options for ischemic stroke

Wernicke's area,

the ability to comprehend language is controlled by which is connected to Broca's area. Dysfunction of Wernicke's area causes receptive aphasia. In receptive aphasia, the affected individual can speak but cannot understand words and uses illogical language.

receptive aphasia,

the affected individual can speak but cannot understand words and uses illogical language.

expressive aphasia;

the affected individual cannot make words, but he or she does understand what others are saying.

Gamma amino butyric acid (GABA),

the chief inhibitory neurotransmitter in the CNS, typically has a relaxing, antianxiety, and anticonvulsive effect on the brain. It also has an inhibitory effect on muscles, which decreases spasms and allows for muscle tone.

upper neurons,

the motor and sensory neurons within the brain

lower neurons.

the neurons of the spinal cord

Epilepsy

| Abnormal electrical discharge of neurons in the brain, an imbalance of neurotransmitters, or both. Ion channel abnormalities causing hyperexcitability of regions of brain neurons, causing seizures. signs and symptoms Group of syndromes characterized by unprovoked and recurring seizures Primary Epilepsy (idiopathic) Secondary Epilepsy (symptom of underlying condition) Same intelligence range as overall population Women seize more often during menses Decrease in effectiveness of contraceptives Congenital fetal anomaly is 2-3 X higher in women with epilepsy Long-term use of Antiseizure medications result in bone mass loss physical assessment Generalized seizure: loss of consciousness and tonic-clonic contractions of muscle. Postictal memory loss. Absence seizure: loss of attentiveness for period of time. Before a seizure, an individual may have unique sensations referred to as an aura. Generalized: loss of consciousness, involuntary muscle contractions, autonomic symptoms, postictal vomiting common. Focal: spasms of a specific muscle group with awareness or lack of awareness. Absence: loss of attentiveness. diagnostic tests Most patients have a normal EEG when not having a seizure. EEG is abnormal during seizure. Brain imaging may exhibit the cerebral hemisphere seizure origin. Metabolic panel is used to rule out electrolyte imbalances or toxicities. treatment Anticonvulsant medications to prevent seizures. Safety measures during seizure activity such as adjusting environment to prevent patient injury. After seizure, patient placed on side to prevent aspiration. Control, not cures Meds used depends on type of seizures experiencing Start treatment with one medication Watch for gingival hyperplasia with longer term use of Dilantin

Ischemic Stroke

| An area of the brain undergoes ischemia and infarction. Two main etiologies: (1) A thromboembolism commonly causes obstruction of a branch of a cerebral artery. Usually, a piece of arteriosclerotic plaque breaks away from an area of carotid artery stenosis and travels up to a branch of the middle cerebral artery. (2) The left atrium undergoes atrial fibrillation with stasis of blood and clot formation. The clot travels from the left atrium into the left ventricle, into the aorta, and upward into the carotid artery into a cerebral artery. Alternatively, an arteriosclerotic cerebral artery causes tissue ischemia. Treatment of thrombolytic therapy occurred in 1996 Treatment must occur within 3 hours (some are expanding) 5 types of ischemic strokes: Large artery thrombosis Small penetrating artery thrombosis Cardiogenic embolic Cryptogenic Other signs and symptoms Motor and sensory loss is evident on the opposite side of the body than the cerebral hemisphere undergoing the ischemia. Hemiparesis (weakness) or hemiplegia (paralysis) is observed. If the left hemisphere undergoes ischemia, most of those affected will suffer aphasia. physical assessment Hemiparesis or hemiplegia of limbs is observed on the opposite side of the cerebral hemisphere affected. Sensation is diminished on one side of the body. Speech problems are evident if the cerebral ischemia is of the left hemisphere. diagnostic tests CT scan without contrast or MRI demonstrates area of injury. treatment Thrombolytic is administered if the ischemic stroke began less than 4.5 hours ago and the patient is eligible. Aspirin is given with anticoagulants to prevent further damage. Some patients are eligible for surgical thrombectomy.

MG

| Autoimmune antibodies directed against muscle acetylcholine receptors. Autoimmune disorder affecting myoneural junctions Weakness of voluntary muscle Most people have thymic tumor or thymic hyperplasia Signs and symptoms Muscle weakness; often manifests as ptosis or easy fatigability. Physical assessment Muscle weakness; ptosis of eyelids; worsens as day continues. Autoimmune disorder affecting myoneural junctions Weakness of voluntary muscles Most people have thymic tumor or thymic hyperplasia Diagnostic tests EMG. Edrophonium (Tensilon®) testing. treatment Acetylcholinesterase inhibitors such as physostigmine to allow more acetylcholine to remain in the synapse. Corticosteroids and immunosuppressive therapy to decrease effects of autoantibodies. No Cure Administration of anticholinesterase medications and immunosuppressive therapy Pyridostigmine bromide (Mestinon) Plasmapheresis Thymectomy Myasthenia Gravis may result in generalized weakness and respiratory failure Endotracheal intubation may be necessary

MS

| Autoimmune, demyelinating disorder that results in inflammation and damage to the myelin and other cells within the CNS, ANS, and PNS. Progressive demyelination of the CNS Impaired transmission of nerve impulses Women more frequent than men 25-35 years of age is peak onset Not proven genetically transmitted but is genetically predisposed Environmental factors of smoking, decreased Vitamin D, exposure to Epstein-Barr virus Demyelination interrupts the flow of nerve impulses Plaque appears on demyelinated axons Affects optic nerves Cerebrum Brain stem, cerebellum, spinal cord Permanent irreversible damage Signs and symptoms Ocular and cerebellar symptoms often are initially present. Vision disturbances and gait and balance problems often are initial symptoms. Symptoms begin mild Relapsing-Remitting Secondary Progressive Primary Progressive Progressive-Relapsing Physical assessment Motor and sensory weakness. Visual problems. Incoordination and gait disturbance (ataxia). Diagnostic tests Condition cannot be diagnosed after only a single symptomatic episode. Symptoms are clues to diagnosis; however, diagnosis requires the appearance of demyelination lesions detected on imaging studies. McDonald criteria are used to diagnose. EMG and evoked potential tests are also used. treatment Immunomodulators and immunosuppressives to decrease autoantibody effects. Corticosteroids to decrease inflammation. No cure exists Disease-modifying therapies◦Reduce frequency and duration of relapse ◦Interferon beta 1a (Rebif) and 1b (Betaseron)◦Administered every-other day ◦Glatiramer acetate (Copaxone) reduces relapsing-remitting; takes 6 months to work ◦Methylprednisolone (IV) shortens acute relapse, but no known long term benefits ◦Others under investigation Symptom Management with Medications◦Baclofen (Lioresal) treats spasticity ◦Benzodiazepines, tizanidine (Zanaflex) and dantrolene (Dantrium) also treat spasticity ◦Nerve blocks and surgical interventions can be used for pain treatment◦ Amantadine (Symmetrel), pemoline (Cylert), and dalfampridine (Amprya) are used for fatigue ◦Ataxia can be treated with anti-seizure medication (Neurotnin) and benzodiazepines ◦Ascorbic acid may be prescribed prophylactically to acidify the urine

HD

| Autosomal-dominant neurological disorder; genetic mutation on chromosome 4 that codes for huntingtin protein; causes progressive lack of muscle control. Chronic, progressive, hereditary disease of nervous system Progressive involuntary choreiform movement and dementia Genetic testing Genetic counseling is important Premature death of cells in the striatum of the basal ganglia Signs and symptoms Involuntary motor symptoms, cognitive decline, and emotional/behavioral symptoms. Chorea (rapid, jerky, involuntary, purposeless movements) Intellectual decline Personality changes Constant writhing Uncontrollable movement of the entire body Tics/grimaces of the face Speech slurring/delays/unintelligible Difficulty swallowing and chewing Gait is unorganized Bowel and bladder control is lost Cognitive function delays Uncontrolled fits of anger in early stages Suicidal depression, anxiety, psychosis Dementia in later stages Physical assessment Motor control deficits. Chorea, athetosis, ballismus, and cognitive impairment. Diagnostic tests Presymptomatic blood test for the presence of the mutated HD gene. treatment Supportive treatment. Based on family history Known genetic marker No known treatment stops progression Medications can decrease chorea Tetrabenazine (Xenazine) is the only approved drug Navane, Haldol, and Benzodiazepines have decreased symptoms SSRI's and Tricyclic Antidepressants have been successful in treating psychotic symptoms

Hemorrhagic Stroke

| Cerebral artery rupture occurs, which causes a large amount of blood to compress the brain tissue and cause brain death. Subarachnoid hemorrhage is one type of hemorrhagic stroke. Approximately 15% of cerebrovascular disorders Bleeding into the brain tissue, ventricles, or subarachnoid space Primarily from the spontaneous rupture of small vessels Cerebral amyloid angiopathy Arteriovenous malformations Intracranial aneurysms Intracranial neoplasm Medication side effects (anticoagulants and amphetamines) signs and symptoms Motor and sensory loss is evident on the opposite side of the body than the cerebral hemisphere undergoing the hemorrhage. Hemiparesis (weakness) or hemiplegia (paralysis) is observed. If the left hemisphere undergoes hemorrhage, most of those affected will suffer aphasia. Subarachnoid hemorrhage causes severe headache with changing level of consciousness. physical assessment Sudden onset. Elevated blood pressure. Rapid deterioration of cognitive function. Motor and sensory loss on opposite side of the affected cerebral hemisphere. If the left hemisphere undergoes hemorrhage, most of those affected will suffer aphasia. Severe headache Motor, sensory, cranial nerve, cognitive, deficits Loss of consciousness Nuchal rigidity Visual disturbances Tinnitus, dizziness, hemiparesis diagnostic tests CT scan or MRI demonstrates specific area of bleeding in the brain. Over the following day, CT scans are done to evaluate bleeding into the brain. Prognosis based on neuro condition of patient and location of hemorrhage/aneurysm Cerebral angiography Lumbar puncture can determine a subarachnoid hemorrhage if CT scan is negative, and there is no evidence of ICP Toxicology screen for younger adults treatment Supportive care. Decrease cerebral edema with IV mannitol or hypertonic saline. Patient may need intubation and mechanical ventilation. Neurosurgery may be possible in some patients.

Migraine Headache

| Hyperexcitability of neurons, cortical spreading depression, trigeminal nerve complex activation, dural blood vessel sensitivity. Ion channel abnormalities may be associated. Migraines are often hereditary, and low magnesium levels May be triggered by menstrual cycles, stress, depression, bright lights, sleep deprivation, MSG in foods, food triggers Oral contraceptives 1. Prodrome: neural hyperexcitability in the brain 2. Aura: cortical spreading depression (CSD) occurs 3. Pain: trigeminovascular complex activation accounting for the pain 4. Postdrome: sensitization of the trigeminovascular complex persists Signs and symptoms Commonly lasts 4 to 72 hours. May or may not be accompanied by an aura. Nausea, vomiting, photophobia, and phonophobia are common. Severe, throbbing pain; nausea, photophobia Physical assessment Normal physical examination. Diagnostic tests Normal laboratory tests and imaging studies. Specific criteria for diagnosis of a migraine headache. treatment NSAIDs to decrease inflammation. Triptans, which are serotonin agonists, are first-choice medications. Avoidance of triggers. Triptans Serotonin receptor agonists Sumatriptan (Imitrex) Naratriptan (Amerge) Rizatriptan (Maxalt) Zolmitriptan (Zomig)Almotriptan (Axert) Takes effect within 20 to 60 minutes May repeat in 2-4 hours Ergotamine preparations (do not take with triptans....prolonged vasoactive reaction)

Transient Ischemic Attack

| Ischemia of the brain that is caused by the same etiologies as ischemic stroke: thromboembolism from carotid stenosis or atrial fibrillation. Ischemia of the brain is caused by a thromboembolus that dissolves within 24 hours. The ischemia is reversible after the thrombus dissolves. Patient may present with acute symptoms that resolve in an hour or less Obvious to bystanders but not necessarily the patient Sudden loss of motor, sensory, or visual function No evidence of ischemia with CT scan Warning sign of stroke signs and symptoms Motor and sensory loss is evident on the opposite side of the body than the cerebral hemisphere undergoing the ischemia. Hemiparesis (weakness) or hemiplegia (paralysis) is observed. If the left hemisphere undergoes ischemia, most of those affected will suffer aphasia. physical assessment Hemiparesis or hemiplegia of limbs is evident on the opposite side of the cerebral hemisphere affected. Loss of sensation on one side of body. Speech problems are evident if cerebral ischemia is of the left hemisphere. Gradually improving neurological examination Neurological examination is back to normal within 24 hours, with no remaining neurological deficits. diagnostic tests CT scan or MRI may not be helpful if ischemia area has resolved. Electrocardiogram. Carotid artery CT scan. treatment Aspirin or anticoagulant therapy is used to prevent recurrence. Carotid stenosis surgery, called endarterectomy, or treatment of atrial fibrillation may be done to prevent recurrence.

Trigeminal Autonomic Cephalgia

| Main type is called a cluster headache. Activation of the trigeminovascular system, autonomic nerves, and hypothalamus play prominent roles. unilateral, 1-8 daily Signs and symptoms Stabbing, unilateral headache. Nasal discharge, tearing of the eye, pallor, and perspiration over one side of the face. Physical assessment Rhinorrhea, conjunctival injection, tearing of the eye, sweating, eyelid edema, and pallor over one side of the face. Restlessness and agitation. Diagnostic tests Diagnosis mainly based on symptoms. treatment 100% oxygen inhalation, or 6 mg subcutaneous or nasal spray sumatriptan. Short course of oral or IV corticosteroids. Preventive medication includes verapamil, lithium carbonate, methylergonovine, and topiramate.

Tension Headache

| Pericranial and cervical muscle tension. steady pressure in forehead/temple/back of neck Signs and symptoms Band of pain around head. Cervicothoracic muscle stiffness. Physical assessment Normal physical examination. Diagnostic tests Diagnosis mainly based on symptoms. treatment Acetaminophen, aspirin, or NSAIDs.

GBS

| Postinfectious disease with resulting neuropathy; ascending paralysis, previous infection evokes an autoimmune response in the peripheral nerve; can occur postimmunization also. Acute, rapidly progressing, potentially fatal polyneuropathy Onset 1-3 wks post URI or GI infection Starts as weakness of lower extremities - moves upward Hypotonia & areflexia Autonomic nervous system dysfunction ◦Severe muscle & respiratory involvement ◦Most dangerous -hypotension, hypertension, abnormal vagal responses (bradycardia, asystole, heart block) ◦Bowel & bladder dysfunction ◦Inappropriate antidiuretic hormone (SIADH) ◦Pain - worse at night COMPLICATIONS COLLABORATIVE CARE Most severe - respiratory failure Respiratory Infections & UTIs Fever (first sign) Immobility ◦Paralytic ileus, muscle atrophy, DVT, pulmonary emboli, skin breakdown, orthostatic hypotension, nutritional deficiencies Signs and symptoms Progressive, usually symmetric, ascending muscle weakness accompanied by absent or depressed deep tendon reflexes, paresthesias, and numbness. Physical assessment Motor and sensory deficits, distal to proximal, starting in lower limbs and moving upward. Diagnostic tests Clinical examination is only diagnostic modality. treatment May require temporary mechanical ventilation, IV immunoglobulin, corticosteroids, or plasmapheresis (plasma exchange). Supportive care Plasma exchange within first 2 weeks High-dose immunoglobin Nutritional therapy r/t difficulty swallowing Nursing Management ◦Make a mind map that includes ◦Nursing Diagnosis ◦Interventions

Parkinson's Disease

| Progressive loss of dopamine-producing cells, especially in the substantia nigra of the basal ganglia that modulates movement and posture. Affects more men Idiopathic cause Research suggests potential causes of genetics, atherosclerosis, excessive accumulation of oxygen free radicals, viral infections, brain trauma, chronic use of antipsychotic medications, and/or certain environmental exposures Accumulation of protein (alpha-synuclein) in Lewy bodies Decreased levels of dopamine in substantia nigra◦Loss of dopamine in this area results in more excitatory neurotransmitters than inhibitory neurotransmitters◦This imbalance of neurotransmitters has an affect on voluntary movement Signs and symptoms Clinical signs TRAP: Tremor at rest, Rigidity, Akinesia or bradykinesia, and Postural/gait instability. Excessive sweating Hypokinesia Orthostatic hypotension Micrographia Gastric retention Mask-like facial expression Urinary retention Blinking decreases Paroxysmal flushing Dysphonia Constipation Dysphagia Sexual dysfunction Drooling Depression, anxiety Choking/aspiration Dementia Hallucination Physical assessment Stiff posture, muscle stiffness, blank expression, gait disturbances, and resting tremor. "Freezing" episodes where individual cannot initiate movement; micrographia, slowed movements, depression, cognitive disturbance. Autonomic disturbances. Cardinal Signs: Tremor, Rigidity, Bradykinesia, Postural Instability Diagnostic tests Diagnosis mainly based on symptoms. Normal laboratory tests and imaging studies. Genetic susceptibility and current research regarding accumulation of mutated protein in brain. Significant symptom improvement with trial of levodopa indicates Parkinson's disease. Diagnosis based on history and the presence of two of the four cardinal manifestations Diagnosis confirmed with positive response to levodopa (Larodopa) medication trial treatment Levodopa-carbidopa medications to replace dopamine in the brain and decrease peripheral effects of dopamine. Dopamine agonists. Catechol-O-methyl transferase inhibitors to decrease breakdown of dopamine. Anticholinergic drugs to balance acetylcholine effects. Individualized Direct management based on controlling of symptoms and functional independence Antiparkinsonian medications Levodopa is most effective Carbidopa used in conjunction with Levodopa Surgical management Stereotactic Procedures Neural Transplantation

ALS

| Progressive neurodegenerative disorder characterized by a loss of upper and lower motor neurons. Unknown etiology leading to loss of motor neurons Lou Gehrig's disease Theory of overexcitation of nerve cells by the neurotransmitter glutamate results in cell injury and neuronal degeneration 5-10% of cases are familial Damages only motor neurons; sensory neurons remain intact Signs and symptoms Gradual loss of control of muscles. Fatigue Progressive muscle weakness Cramps Twitching (fasiculations) Lack of coordination Spasticity Esophageal weakness Respiratory function compromised Physical assessment Muscle weakness and atrophy, dysarthria, dysphagia. Sensation intact. Diagnostic tests Normal laboratory tests and imaging studies. Diagnosed based on signs and symptoms No specific clinical or laboratory tests Death usually is a result of infection, respiratory insufficiency, or aspiration treatment No cure. Riluzole (RilutekR). Supportive and palliative care. No cure Average survival of 3-5 years Riluzole (Rilutek) prolongs survival for 3-6 months Hospitalization resulting from:Dehydration,Pneumonia,Malnutrition,Respiratory failure,End of life issues

Lacunar Infarct

| Small blood vessel infarction associated with hypertension. signs and symptoms No symptoms or evidence of neurological changes are present. physical assessment No symptoms or evidence of neurological changes are evident. diagnositc tests CT scan or MRI demonstrates small area of infarction. treatment Aspirin or anticoagulant therapy is used to prevent further injury.

OCCIPITAL LOBE

• Analyzing and interpreting visual information

TEMPORAL LOBE

• Hearing • Smelling • Learning • Memory • Emotional behavior • Visual recognition

PARIETAL LOBE

• Receiving and interpreting bodily sensations • Governing of proprioception, the awareness of one's body and body parts in space and in relation to each other

FRONTAL LOBE

• Voluntary movements • Memory • Emotion • Social judgment • Decision making • Reasoning • Aggression