Nightingale Cognitive Systems Cerebral Hemodynamics & Motor Function Discussion

Nightingale Cognitive Systems Cerebral Hemodynamics & Motor Function Discussion ORDER NOW FOR CUSTOMIZED AND ORIGINAL ESSAY PAPERS ON Nightingale Cognitive Systems Cerebral Hemodynamics & Motor Function Discussion This week, you will have the opportunity to unleash your creativity in order to help you and your classmates study. For this assignment you will be able to create an infographic or video presentation and upload it here for grading. Nightingale Cognitive Systems Cerebral Hemodynamics & Motor Function Discussion Assignment Instructions: 1. Select one of the topics below. Alterations in Cerebral Hemodynamics, (Chapter 15, p. 373) 2. Explore the topic and gather the information needed to teach your fellow learners. 3. Please create these items using infographics ( Canva.com ) or video ( Powtoon.com ). If you would like to use a different media source, please email your Instructor first for permission. understanding_pathophysiology____sue_e._huether_chapter_15.pdf 15 Alterations in Cognitive Systems, Cerebral Hemodynamics, and Motor Function Barbara J. Boss, Sue E. Huether, Kelly Power-Kean CHAPTER OUTLINE Alterations in Cognitive Systems, 363 Alterations in Arousal, 363 Alterations in Awareness, 369 Data-Processing Deficits, 371 Seizure Disorders, 376 Types of Seizure, 376 Alterations in Cerebral Hemodynamics, 377 Increased Intracranial Pressure, 378 Cerebral Edema, 379 1071 Hydrocephalus, 380 Alterations in Neuromotor Function, 380 Alterations in Muscle Tone, 380 Alterations in Muscle Movement, 381 Upper and Lower Motor Neuron Syndromes, 385 Motor Neuron Diseases, 387 Amyotrophic Lateral Sclerosis, 388 Alterations in Complex Motor Performance, 389 Disorders of Posture (Stance), 389 Disorders of Gait, 389 Disorders of Expression, 389 Extrapyramidal Motor Syndromes, 390 A person achieves cognitive and behavioural functional competence by integrated processes of cognitive systems, sensory systems, and motor systems. The purpose of this chapter is to present the concepts and processes of alterations in these systems as an approach to understanding the manifestations of neurological dysfunction and disease. The neural systems that are essential to cognitive function are (1) attentional systems that provide arousal and maintenance of attention over time; (2) memory and language systems by which information is communicated; and (3) affective or emotive systems that mediate mood, emotion, and intention. These core systems are 1072 fundamental to the processes of abstract thinking and reasoning. The products of abstraction and reasoning are organized and made operational through the executive attentional networks. The normal functioning of these networks manifests through the motor network in a behavioural array viewed by others as appropriate to human activity and successful living. Alterations in Cognitive Systems Full consciousness is a state of awareness both of oneself and of the environment, and a set of responses to that environment. The fully conscious individual initiates spontaneous, purposeful activity independently to a perceived stimulus. Any decrease in this state of awareness and varied responses is a decrease in consciousness. Consciousness has two distinct components: arousal (state of awakeness) and awareness (content of thought). Arousal is mediated by the reticular activating system, which regulates aspects of attention and information processing and maintains consciousness. Awareness encompasses all cognitive functions and is mediated by attentional systems, memory systems, language systems, and executive systems. Alterations in Arousal Alterations in level of arousal may be caused by structural, metabolic, or psychogenic (functional) disorders. Pathophysiology Structural alterations in arousal are divided according to the original location of the pathological condition. Causes include infection, vascular alterations, neoplasms, traumatic injury, congenital alterations, degenerative changes, polygenic traits, and metabolic disorders. Supratentorial disorders (above the tentorium cerebelli) produce changes in arousal by either diffuse or localized dysfunction. Nightingale Cognitive Systems Cerebral Hemodynamics & Motor Function Discussion The tentorium cerebelli is an extension of the dura mater that separates the cerebellum from the inferior portion of the occipital lobes. Diffuse dysfunction may be caused by disease processes affecting the cerebral cortex or the underlying subcortical white matter (e.g., 1073 encephalitis). Disorders outside the brain but within the cranial vault (extracerebral) can produce diffuse dysfunction, including neoplasms, closed-head trauma with subsequent subdural bleeding, and accumulation of pus in the subdural space. Disorders within the brain substance (intracerebral)—bleeding, infarcts, emboli, and tumours—function primarily as masses. Such localized destructive processes directly impair function of the thalamic or hypothalamic activating systems or secondarily compress these structures in a process of herniation. Infratentorial disorders (below the tentorium cerebelli) produce a decline in arousal by (1) direct destruction or compression of the reticular activating system and its pathways (e.g., accumulations of blood or pus, neoplasms, and demyelinating disorders) or (2) destruction of the brainstem (midbrain, pons, medulla) either by direct invasion or by indirect impairment of its blood supply. Metabolic disorders produce a decline in arousal by alterations in delivery of energy substrates as occurs with hypoxia, electrolyte disturbances, or hypoglycemia. Metabolic disorders caused by liver or renal failure cause alterations in neuronal excitability because of failure to metabolize or eliminate medications and toxins. All the systemic diseases that eventually produce nervous system dysfunction are part of this metabolic category. Psychogenic alterations in arousal (unresponsiveness), although uncommon, may signal general psychiatric disorders. Despite apparent unconsciousness, the person actually is physiologically awake and the neurological examination reflects normal responses. Clinical manifestations and evaluation Five patterns of neurological function are critical to the evaluation process: (1) level of consciousness, (2) pattern of breathing, (3) pupillary reaction, (4) oculomotor responses, and (5) motor responses. Patterns of clinical manifestations help in determining the extent of brain dysfunction and serve as indexes for identifying increasing or decreasing central nervous system (CNS) function. Distinctions are made between metabolically induced and structurally induced manifestations (Table 15-1). The types of manifestations suggest the cause of the altered arousal state (Table 15-2). 1074 TABLE 15-1 Clinical Manifestations of Metabolic and Structural Causes of Altered Arousal Manifestations Metabolically Induced Structurally Induced Blink to threat (cranial nerves II, VII) Optic discs (cranial nerve II) Extraocular movement (cranial nerves III, IV, VI) Pupils (cranial nerves II, III) Equal Asymmetrical Flat, good pulsation Papilledema Roving eye movements; normal oculocephalic reflex (Doll’s eyes phenomenon) and oculovestibular reflex (caloric ice water test) Gaze paresis, nerve palsy Equal and reactive; may be dilated (e.g., atropine), pinpoint (e.g., opiates), or midposition and fixed (e.g., benzodiazepines combined with other central nervous system– depressant agents) Symmetrical response Asymmetrical or nonreactive; may be midposition (midbrain injury), pinpoint (pons injury), large (tectal injury). Nightingale Cognitive Systems Cerebral Hemodynamics & Motor Function Discussion Asymmetrical response Corneal reflex (cranial nerves V, VII) Grimace to pain Symmetrical response (cranial nerve VII) Motor function Symmetrical movement Muscle tone Symmetrical Asymmetrical response Asymmetrical Posture Symmetrical Deep tendon reflexes Babinski sign Sensation Symmetrical Paratonic (rigid), spastic, flaccid, especially if asymmetrical Decorticate, especially if symmetrical; decerebrate, especially if asymmetrical (see Figure 15-6) Asymmetrical Absent or symmetrical response Symmetrical Present Asymmetrical TABLE 15-2 Differential Characteristics of States Causing Altered Arousal Mechanism Manifestations Supratentorial mass lesions compressing or displacing diencephalon or brainstem Initiating signs usually of focal cerebral dysfunction: vomiting, headache, hemiparesis, ocular signs, seizures, coma Signs of dysfunction progress rostral to caudal Neurological signs at any given time point to one anatomical area (e.g., diencephalon, mesencephalon, medulla) Motor signs often asymmetrical History of preceding brainstem dysfunction or sudden onset of coma Infratentorial mass of destruction causing coma 1075 Metabolic coma Exogenous toxins (medications) Endogenous toxins (organ system failure) Psychiatric unresponsiveness Localizing brainstem signs precede or accompany onset of coma and always include oculovestibular abnormality Cranial nerve palsies usually manifest “bizarre” respiratory patterns that appear at onset Confusion and stupor commonly precede motor signs Motor signs usually are symmetrical Pupillary reactions usually are preserved Asterixis, myoclonus, tremor, and seizures are common Acid–base imbalance with hyperventilation or hypoventilation is common Lids close actively; pupils reactive or dilated (cycloplegics) Oculocephalic reflexes are unpredictable; oculovestibular reflexes are physiological (nystagmus is present) Motor tone is inconsistent or normal Eupnea or hyperventilation is usual No pathological reflexes are present Electroencephalogram (EEG) is normal Level of consciousness is the most critical clinical index of nervous system function, with changes indicating either improvement or deterioration of the individual’s condition. A person who is alert and oriented to self, others, place, and time is considered to be functioning at the highest level of consciousness, which implies full use of all the person’s cognitive capacities. From this normal alert state, levels of consciousness diminish in stages from confusion and disorientation (which can occur simultaneously) to coma, each of which is clinically defined (Table 15-3). TABLE 15-3 Levels of Altered Consciousness State Definition Confusion Loss of ability to think rapidly and clearly; impaired judgement and decision making Disorientation The person may exhibit restlessness, anxiety, and irritation; disorientation to time occurs first, followed by disorientation to place and familiar others (family members) and impaired memory; recognition of self is lost last Lethargy Limited spontaneous movement or speech; easy arousal with normal speech or touch; may or may not be oriented to time, place, or person Obtundation Mild to moderate reduction in arousal (awakeness) with limited response to environment; falls asleep unless stimulated verbally or tactilely; answers questions with minimal response Stupor Condition of deep sleep or unresponsiveness from which person may be aroused or caused to open eyes only by vigorous and repeated stimulation; response is often withdrawal or grabbing at stimulus Light coma Associated with purposeful movement on stimulation 1076 Coma Deep coma Associated with nonpurposeful movement only on stimulation Associated with unresponsiveness or no response to any stimulus Patterns of breathing help evaluate the level of brain dysfunction and coma (Figure 15-1). Rate, rhythm, and pattern should be evaluated. Breathing patterns can be categorized as hemispheric or brainstem patterns (Table 15-4). FIGURE 15-1 Abnormal Respiratory Patterns With Corresponding Level of Central Nervous System Activity. (From Urden, L.D., Stacy, K.M., & Lough, M.E. [2010]. Nightingale Cognitive Systems Cerebral Hemodynamics & Motor Function Discussion Critical care nursing: Diagnosis and management [6th ed.]. St. Louis: Mosby.) TABLE 15-4 Patterns of Breathing Breathing Pattern Description Location of Injury Hemispheric Breathing Patterns Normal After a period of hyperventilation that lowers partial pressure of carbon dioxide in arterial blood (PaCO2), the individual continues to breathe regularly but with reduced depth. Posthyperventilation Respirations stop after hyperventilation apnea has lowered partial pressure of carbon dioxide (PCO2) level below normal. Rhythmic breathing returns when PCO2 level returns to normal. Cheyne-Stokes Breathing pattern has a smooth increase respirations (crescendo) in rate and depth of breathing (hyperpnea), which peaks and is followed by 1077 Response of nervous system to an external stressor—not associated with injury to central nervous system (CNS) Associated with diffuse bilateral metabolic or structural disease of cerebrum Bilateral dysfunction of deep cerebral or diencephalic structures; a gradual smooth decrease (decrescendo) in rate and depth of breathing to the point of apnea, when the cycle repeats itself. The hyperpneic phase lasts longer than the apneic phase. Brainstem Breathing Patterns Central neurogenic A sustained, deep, rapid, but regular pattern hyperventilation (hyperpnea) occurs, with a decreased PaCO2 and a corresponding increase in pH and PO2. Apneusis Cluster breathing Ataxic breathing Gasping breathing pattern (agonal gasps) seen with supratentorial injury and metabolically induced coma states May result from CNS damage or disease that involves midbrain and upper pons; seen after increased intracranial pressure and blunt head trauma A prolonged inspiratory cramp (a pause at Indicates damage to full inspiration) occurs; a common variant of respiratory control this is a brief end-inspiratory pause of 2 or 3 mechanism located at seconds, often alternating with an endpontine level; most expiratory pause. commonly associated with pontine infarction but documented with hypoglycemia, anoxia, and meningitis A cluster of breaths has a disordered Dysfunction in lower sequence with irregular pauses between pontine and high breaths. medullary areas Completely irregular breathing occurs, with Originates from a primary random shallow and deep breaths and dysfunction of medullary irregular pauses. The rate is often slow. neurons controlling breathing A pattern of deep “all-or-none” breaths is Indicative of a failing accompanied by a slow respiratory rate. medullary respiratory centre With normal breathing, a neural centre in the forebrain (cerebrum) produces a rhythmic pattern. When consciousness decreases, lower brainstem centres regulate the breathing pattern by responding only to changes in partial pressure of carbon dioxide in arterial blood (PaCO2) levels; this breathing pattern is called posthyperventilation apnea. Cheyne-Stokes respiration is an abnormal rhythm of ventilation with alternating periods of tachypnea and apnea (crescendo–decrescendo pattern). Increases in PaCO2 levels lead to tachypnea. The PaCO2 level then decreases to below normal and breathing stops (apnea) until the carbon dioxide reaccumulates and again stimulates tachypnea (see Figure 15-1). In cases of opiate or sedative medication overdose, the respiratory centre is depressed so the rate of breathing gradually decreases until respiratory failure occurs. Pupillary changes indicate the presence and level of brainstem dysfunction because brainstem areas that control arousal are 1078 adjacent to areas that control the pupils (Figure 15-2). For example, severe ischemia and hypoxia usually produce dilated, fixed pupils. Hypothermia may cause fixed pupils. FIGURE 15-2 Appearance of Pupils at Different Levels of Consciousness. Some drugs affect pupils and must be considered in evaluating individuals in comatose states. Nightingale Cognitive Systems Cerebral Hemodynamics & Motor Function Discussion Large doses of atropine and scopolamine fully dilate and fix pupils. Doses of sedatives (e.g., benzodiazepines) in sufficient amounts to produce coma, and taken in combination with other CNS-depressant agents (e.g., alcohol or barbiturates), cause the pupils to become midposition or moderately dilated, unequal, and commonly fixed to light. Opiates cause pinpoint pupils. Severe barbiturate intoxication may produce fixed pupils. Oculomotor responses (resting, spontaneous, and reflexive eye movements) change at various levels of brain dysfunction in comatose individuals. Persons with metabolically induced coma, except with barbiturate-hypnotic and phenytoin poisoning, generally retain ocular reflexes even when other signs of brainstem damage are present. Destructive or compressive injury to the 1079 brainstem causes specific abnormalities of the oculocephalic and oculovestibular reflexes (Figures 15-3 and 15-4). Injuries that involve an oculomotor nucleus or nerve cause the involved eye to deviate outward, producing a resting dysconjugate lateral position of the eye. Test for Oculocephalic Reflex Response (Doll’s Eyes Phenomenon). A, Normal response—eyes turn together to side opposite from turn of head. B, Abnormal response—eyes do not turn in conjugate manner. C, Absent response—eyes move in direction of head movement (brainstem injury). (From Rudy, E.B. [1984]. Advanced neurological FIGURE 15-3 and neurosurgical nursing. St. Louis: Mosby.) 1080 FIGURE 15-4 Test for Oculovestibular Reflex (Caloric Ice Water Test). A, Ice water is injected into the ear canal. Normal response—conjugate eye movements. B, Abnormal response—dysconjugate or asymmetrical eye movements. C, Absent response—no eye movements. Assessment of motor responses helps to evaluate the level of brain dysfunction and determine the most severely damaged side of the brain. The pattern of response noted may be (1) purposeful; (2) inappropriate, generalized motor movement; or (3) not present. Motor signs indicating loss of cortical inhibition that are commonly associated with decreased consciousness include primitive reflexes and rigidity (paratonia) (Figure 15-5). Primitive reflexes include grasping, reflex sucking, snout reflex, and palmomental reflex, all of which are normal in the newborn but disappear in infancy. Abnormal flexor and extensor responses in the upper and lower extremities are defined in Table 15-5 and illustrated in Figure 15-6. FIGURE 15-5 Pathological Reflexes. A, Grasp reflex. B, Snout reflex. C, Palmomental reflex. Nightingale Cognitive Systems Cerebral Hemodynamics & Motor Function Discussion D, Suck reflex. 1081 TABLE 15-5 Abnormal Motor Responses With Decreased Responsiveness Motor Response Description Location of Injury Decorticate posturing/rigidity: upper extremity flexion, lower extremity extension Decerebrate posturing/rigidity: upper and lower extremity extensor responses Slowly developing flexion of arm, wrist, and fingers with adduction in the upper extremity and extension, internal rotation, and plantar flexion of lower extremity Hemispheric damage above midbrain releasing medullary and pontine reticulospinal systems Opisthotonos (hyperextension of vertebral column) with clenching of teeth; extension, abduction, and hyperpronation of arms; and extension of lower extremities In acute brain injury, shivering and hyperpnea may accompany unelicited recurrent decerebrate spasms Associated with severe damage involving midbrain or upper pons Extensor responses in upper extremities accompanied by flexion in lower extremities Flaccid state with little or no motor response to stimuli Acute brain injury often causes limb extension regardless of location Pons Lower pons and upper medulla FIGURE 15-6 Decorticate and Decerebrate Posture/Responses. A, Decorticate posture/response. Flexion of arms, wrists, and fingers with adduction in upper extremities Bilateral extension, internal rotation, and plantar flexion in lower extremities. B, Decerebrate posture/response. All four extremities in rigid extension with hyperpronation of forearms and plantar extension of feet. (From deWit, S.C., 1082 & Kumagai, C.K. [2013]. Medical-surgical nursing [2nd ed.]. St. Louis: Saunders.) Vomiting, yawning, and hiccups are complex reflexlike motor responses that are integrated by neural mechanisms in the lower brainstem. These responses may be produced by compression or diseases involving tissues of the medulla oblongata (e.g., infection, neoplasm, infarction) but also occur relative to other more benign stimuli to the vagal nerve. Most CNS disorders produce nausea and vomiting. Vomiting without nausea indicates direct involvement of the central neural mechanism (or pyloric obstruction; see Chapters 36 and 37). Vomiting often accompanies CNS injuries that (1) involve the vestibular nuclei or its immediate projections, particularly when double vision (diplopia) also is present; (2) impinge directly on the floor of the fourth ventricle; or (3) produce brainstem compression secondary to an increase in intracranial pressure. Quick Check 15-1 1. Why are structural as well as metabolic factors capable of producing coma? 2. Why is level of consciousness the most critical index of central nervous system function? 3. Why does Cheyne-Stokes respiration appear in a comatose individual? 4. Why are oculomotor changes associated with levels of brain injury? … Get a 10 % discount on an order above $ 100 Use the following coupon code : NURSING10

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