By B. Killian. Grand Canyon University. 2018.
In many but not all cases singulair 4 mg without prescription, it involves the use of nicotine buy singulair 4 mg, † alcohol and other drugs buy singulair 5mg overnight delivery. Addiction involving these substances typically originates with use in adolescence when the brain is still developing 2 and is more vulnerable to their effects. If untreated, it can become a chronic and relapsing condition, requiring ongoing professional 3 treatment and management. Although there has been an evolution in scientific understanding of the disease, public attitudes and health care practice have not kept pace with the science. Terms used to describe different levels of substance use and addiction’s many forms lack precision, obscuring important differences in the use of addictive substances and the nature and severity of the illness and complicating our ability to treat it effectively. The term addiction also has been used in reference to compulsive behaviors involving eating, gambling and other activities that affect the brain’s reward system and which may develop independent of or in combination with other manifestations of addiction. This report, however, focuses only on addiction involving nicotine, alcohol and other drugs. Use of these Advances in neuroscientific research, including substances can result from an existing brain animal studies and brain imaging, demonstrate dysfunction; use also can alter the structure and clearly that addiction is a primary and often function of the brain, dramatically affecting * 4 8 chronic disease of the brain. The amount and for developing the disease include a genetic duration of substance use that results in brain predisposition and a range of biological, changes and addiction depends on the individual 5 † 9 psychological and environmental influences. There is a growing body of evidence showing the brain circuits that are implicated in substance As yet, there is no conclusive biological marker addiction in general also are involved in other of addiction; therefore the diagnosis of addiction compulsive or addictive behaviors such as those is based on its symptoms including the related to gambling, certain forms of disordered compulsive use of addictive substances, eating (e. These are beginning to explore whether substance symptoms that characterize addiction are addiction might be part of a syndrome cognitive and behavioral manifestations of the 11 characterized by: underlying disease and its effects on the brain. The foundations of the disease may exist in certain individuals even before they ever use an Shared neurobiological and psychosocial addictive substance and, in some cases, once the antecedents (risk factors); disease develops it persists even when an individual is not actively engaged in substance Production of desirable effects upon 12 use. It is not the substances a person uses † that make them an addict; it is not even the The addictive potential of a substance is quantity or frequency of use. Addiction is about determined not only by its intrinsic ability to what happens in a person’s brain when they are stimulate the reward circuits of the brain, but also by exposed to rewarding substances or rewarding the speed with which it crosses the blood-brain behaviors, and it is more about reward circuitry barrier (i. Other physical signs such as intoxication, withdrawal, needle-related findings, co-infections, and laboratory findings--such as abnormalities in * A primary disease indicates that it is not simply a liver function tests or positive breath or urine tests-- symptom or effect of another disease or condition. With assessment, pleasure seeking, impulse control/ repeated use of addictive substances, the brain inhibition, emotion, learning, memory and stress begins to expect this stimulation and an addicted 15 control. On involving another substance; for example, a neurological level, this reinforcement is a nicotine use can prime the brain, making it more process carried out by chemical messengers that susceptible to developing addiction involving 18 ‡ 22 flood the reward circuits of the brain. Signals in the environment such as Virtually all addictive substances affect the seeing a drug-using friend or passing a bar, or * pleasure and reward circuitry deep in the brain emotional signals such as feeling stressed or sad which is activated by the neurotransmitter also become associated with the addictive † 19 23 dopamine. As use continues, the pleasure associated with Definition of Addiction the dopamine release that results from the American Society of Addiction Medicine ingestion of an addictive substance--or from its anticipation--can become consuming to the point Addiction is a primary, chronic disease of brain reward, motivation, memory and related circuitry. This is reflected in an At the same time, the brains of substance-using individual pathologically pursuing reward and/or individuals may adapt to the unnaturally high relief by substance use and other behaviors. Compared to non-substance users, the addiction often involves cycles of relapse and brains of chronic substance users appear to have remission. Without treatment or engagement in lower baseline levels of dopamine, making it recovery activities, addiction is progressive and difficult for them to achieve feelings of pleasure 24 can result in disability or premature death. The cognitive control of an motivated or directed actions such as attaining addictive substances and also influences dopamine ‡ levels in the brain. Although certain when he or she wants to cut down or stop using specific genetic factors predispose an individual 37 an addictive substance, it becomes extremely to addiction involving a particular substance, 30 difficult to do so. Advances in genetic research have enabled People may choose to take drugs, but no one chooses to be an addict. Genetic variations may affect a person’s ability The Risk Factors for Addiction 41 to metabolize an addictive substance or to 42 tolerate it. Studies have found that genetics Genetic factors play a major role in the account for between half and three quarters of development of addiction as do individual † 43 the risk for addiction. Genetic factors appear biological and psychological characteristics and to be stronger drivers than environmental factors 31 44 environmental conditions. A factor influences them to have a higher tolerance for that is particularly predictive of risk, however, is alcohol are at increased risk of developing the age of first use; almost all cases of addiction begin with substance use before the age of 21, 35 when the brain is still developing. Genetic Risks * Twin and adoption studies confirm a genetic role in the likelihood of substance use and the from environmental similarities. Identical twins are genetically identical and fraternal twins share an * These studies help distinguish the roles of genetics average of 50 percent of their genes, but both types of and environment in the development of addiction. Adopted children with biological tendency toward heightened dopamine response parents who have addiction involving alcohol also are at increased risk because of their are at least twice as likely as are adopted enhanced or above average experience of reward 56 children without such parents to develop or pleasure from engaging in substance use. Individuals Other biological risks may involve damage or † whose genetic makeup produces involuntary deficits in the regions of the brain responsible 57 skin flushing and other unpleasant reactions to for decision making and impulse control. Psychological Risks It’s theoretically possible to take kids before Clinical mental health disorders such as they first drink, find out whether they have any depression and anxiety and psychotic disorders gene variations, and say to them, ‘If you choose such as schizophrenia, as well as behavioral to be a drinker, then be careful because it’s very disorders such as conduct disorder and attention- likely that you’ll need to drink more to have the 58 50 deficit/hyperactivity disorder --and sub-clinical same effect. Individuals whose brain University of California, San Diego development has been altered by stress are more sensitive to the effects of addictive substances and more vulnerable to the development of Other Drugs. Twin military duty, are at increased risk of developing studies have found genetic risks for 62 addiction. People who have risk-taking or hallucinogen, opioid, sedative and stimulant use 63 impulsive personality traits or who have low 53 64 and addiction. Expectations play a role in substance use as well, since people who expect that using In addition to genetic variations, certain addictive substances will be a positive and individuals have neurological, structural or rewarding experience--in terms of physical functional differences that make them more effects, mood or behavior--are likelier to smoke, 54 susceptible to addictive substances. This is in drink alcohol or use other drugs than are those part due to individual differences in how the 67 with more balanced or negative expectations. Some research indicates that individuals with a Environmental Risks naturally low level of dopamine response to addictive substances are at increased risk of Many factors within an individual’s family, engaging in substance use in order to achieve a social circle and community, as well as the greater experience of reward. Other research larger cultural climate, increase the likelihood suggests that individuals with a biological that an individual will use addictive substances and develop addiction. The of cases, addiction originates with substance use 82 nature of the parent-child relationship is key; before the age of 21. Because the parts of the people who come from families with high levels brain responsible for judgment, decision- of parent-child conflict, poor communication, making, emotion and impulse control are not weak family bonds and other indicators of an fully developed until early adulthood, unhealthy parent-child relationship are at adolescents are more likely than adults to take 69 increased risk of substance use and addiction. At the same time, because these or convey approval of such use are at increased regions of the brain are still developing, they are 70 risk as well. Homes where liquor and combination of early initiation of use and medicine cabinets are open to teens increase the genetic, biological, psychological or 73 chances that teens will use these substances. Widespread access to controlled prescription drugs contributes to the misuse of these … [addiction] is not simply a disease of the 75 substances and increased access to marijuana brain, but it is a developmental disorder, and it 71 marketed as medicine is linked to increased begins early in life--during adolescence. Community tolerance of high levels of substance use or of experimenting with and --Nora D. Risky Use and Addiction Exposure to advertising and marketing messages Frequently Co-occur with Other that promote or glamorize smoking and drinking Health Conditions increases the chances that these substances will 78 be used and misused.
Manual Therapy 6(3):170–177 Cautions Abrams A 1922 New concepts in diagnosis and • Acute arthritis and other inﬂammatory treatment singulair 10mg with mastercard. Voprosy Kurortologii singulair 5mg with amex, Fizioterapii discount singulair 10 mg with amex, • Phlebitis Lechebnoi Fizicheskoi Kultury 2:19–20 Naturopathic perspectives Akuthota V, Nadler S 2004 Core strengthening. Mouritz, London Almekinders L 1993 Anti-inﬂammatory treatment of Further reading muscular injuries in sports. Orthopaedic Physical Therapy Taos, New Mexico Clinics of North America 9:395–410 3. Hamwee J 1999 Zero balancing – touching the Anderson R, Wise D, Sawyer T et al 2005 Integration of energy of bone. Francis Lincoln, London myofascial trigger point release and paradoxical relaxation training treatment of chronic pelvic pain in men. Journal of Urology 174(1):155–160 Conclusion Andersson G, Lucente T, Davis A et al 1999 A The summaries of modalities outlined in this chapter comparison of osteopathic spinal manipulation with are far from comprehensive. In the next chapter constitutional Foundation models of manual medicine are explored. Assendelft W, Morton S, Yu E et al 2003 Spinal manipulative therapy for low back pain. Annals of Internal Medicine 138:871–881 Abbate G 2004 Chiropractic neck manipulation linked to woman’s death. Globe and Mail, Toronto, Ontario, Aust G, Fischer K 1997 Changes in body equilibrium January 17. In: Proceedings of National high velocity, low amplitude manipulative technique Conference on Chiropractic Pediatrics. Journal of the American Osteopathic Association 93:203–214 Bailey M, Dick L 1992 Nociceptive considerations in treating with counterstrain. Journal of the American Bogduk N, Twomey L 1991 Clinical anatomy of the Osteopathic Association 92(3):334, 337–341 lumbar spine, 2nd edn. Churchill Livingstone, Edinburgh Baldry P 1993 Acupuncture, trigger points and musculoskeletal pain. Churchill Livingstone, Bolton P, Stick P, Lord R 1989 Failure of clinical tests to Edinburgh, p 91–103 predict cerebral ischemia before neck manipulation. Journal of Manipulative and Physiological Therapeutics Ballantyne F, Fryer G, McLaughlin P 2003 The effect of 12(4):304–307 muscle energy technique on hamstring extensibility: the mechanism of altered ﬂexibility. Spine Barnes J 1996 Myofascial release in treatment of 23:1992–1996 thoracic outlet syndrome. Journal of Bodywork and Movement Therapies 1(1):53–57 Brady L, Henry K, Luth J et al 2001 The effects of Shiatsu on lower back pain. Journal of Holistic Nursing Barnes M 1997 The basic science of myofascial release. Eastland Press, Seattle Brennan G, Fritz J, Hunter S et al 2006 Identifying subgroups of patients with acute/subacute ‘nonspeciﬁc’ Beal M 1985 Viscerosomatic reﬂexes review. Bronfort G, Assendelft W, Evans R et al 2001 Efﬁcacy of Traditional and biomedical concepts in holistic care: spinal manipulation for chronic headache: a systematic history and basic concepts. Journal of Manipulative and Physiological 14:69–78 Therapeutics 27(7):457–466 Bei Y 1993 Clinical observations on the treatment of 98 Brown B, Tissington-Tatlow W 1963 Radiographic cases of peptic ulcer by massage. Chiropractic Techniques 5(2):53–55 Position Paper on Naturopathic Manipulative Therapy. Bhole M 1983 Gastric tone as inﬂuenced by mental American Association of Naturopathic Physicians, states and meditation. Journal of Churchill Livingstone, Edinburgh Physical Education 69:23–28 Butler D 1991b Mobilisation of the nervous system. Bishop E, McKinnon E, Weir E et al 2003 Reﬂexology in Churchill Livingstone, Edinburgh, p 104–105 management of encopresis and chronic constipation. Paediatric Nursing 15:20–21 Churchill Livingstone, Edinburgh, p 137 Blackburn J 2004 Trager® at the table – part 3. Journal Butler D, Gifford L 1989 Adverse mechanical tensions of Bodywork and Movement Therapies 8(3):178–188 in the nervous system. Journal of Chiropractic Education 17:48–49 Caldwell C 1997 Getting in touch: the guide to new body-centered therapies. American the American Osteopathic Association 102(7):371–375 Academy of Osteopathy Journal 7(4):25–29 Chapter 7 • Modalities, Methods and Techniques 283 Cantu R, Grodin A 1992 Myofascial manipulation. Australian Journal stimulation as a treatment for urge incontinence and of Physiotherapy 49:223–241 associated pelvic ﬂoor disorders at a pelvic ﬂoor center: a follow-up study. Journal of the American Proprioceptive neuromuscular facilitation decreases Osteopathic Association 91(3):255–259 muscle activity during the stretch reﬂex in selected posterior thigh muscles. Journal of Sport Rehabilitation Clelland J, Savinar E, Shepard K 1987 Role of physical 9:269–278 therapist in chronic pain management. Hospital Medicine 109(1):78–80 Pharmacist 9:255–260 Chaitow L 1980 Neuromuscular technique. Thorsons, Cohen L, Warneke C, Fouladi R et al 2004 Psychological Wellingborough, p 72–73 adjustment and sleep quality in a randomized trial of Chaitow L 1994 Integrated neuromuscular inhibition the effects of a Tibetan yoga intervention in patients technique. Cancer 100:2253–2260 Chaitow L 2001 Modern neuromuscular techniques, Collins N, Teys P, Vicenzino B 2004 The initial effects 2nd edn. Churchill Livingstone, Edinburgh of a Mulligan’s mobilization with movement technique on dorsiﬂexion and pain in subacute ankle sprains. Manual Therapy 9(2):77–82 Churchill Livingstone, Edinburgh Comeaux Z 2002a Facilitated oscillatory release. Chaitow L 2003 Palpation and assessment skills, 2nd American Academy of Osteopathy Journal 12(2):24–35 edn. Churchill Livingstone, Edinburgh Comeaux Z 2002b Robert Fulford and the philosopher Chaitow L 2005 Cranial manipulation: theory physician. Churchill Livingstone, Edinburgh Comeaux Z 2004 Facilitated oscillatory release – a dynamic method of neuromuscular and ligamentous/ Chaitow L 2006 Muscle energy techniques, 3rd edn. Journal of Churchill Livingstone, Edinburgh Bodywork and Movement Therapies 9(2):88–98 Chaitow L, DeLany J 2000 Clinical applications of Cooke B, Ernst E 2000 Aromatherapy for anxiety: a neuromuscular techniques, vol 1: the upper body. Journal of Bodywork and appropriateness of manipulation and mobilization of Movement Therapies 3(1):11–16 the cervical spine. Journal Journal of Bodywork and Movement Therapies of Manipulative and Physiological Therapeutics 4(3):155–165 25(1):1–9 Cyriax J, Coldham M 1984 Textbook of orthopaedic Dorland’s Medical Dictionary 1985 26th edn. Journal Mosby, St Louis of the American Osteopathic Association 100(5): Deig D 2001 Positional release technique. Butterworth- 285–297 Heinemann, Boston Duval C, LaFontaine D, Herbert J et al 2002 The effect Delaney J, Leong K, Watkins A et al 2002 Short-term of Trager therapy on the level of evoked stretch effects of myofascial trigger point massage therapy on responses in patients with Parkinson’s disease and cardiac autonomic tone in healthy subjects. Journal of Manipulative and Physiological Advanced Nursing 37:364–371 Therapeutics 25(7):455–464 Delitto A, Cibulka M, Erhard R et al 1993 Evidence for Dynamic Chiropractic 2002 Coroner’s Inquest in use of an extension-mobilization category in acute low Canada. Dynamic Chiropractic August 16, 200, Vol 20, back syndrome: a prescriptive validation pilot study. Physical Therapy 75:470–479 29(6):801–805 Derby R, Eek B, Lee S-H et al 2004 Comparison of Eliska O, Eliskova M 1995 Are peripheral lymphatics intradiscal restorative injections and intradiscal damaged by high pressure manual massage? Journal of Pain and Symptom enhancement of leukocyte trafﬁcking to sites of surgery Management 17:65–69 or immune activation.
Isoenzymes of one enzyme group are often expressed to differing extents in different tissues singulair 4 mg with amex. These subunits come together in various combinations order 4mg singulair overnight delivery, leading to ﬁve distinct isoforms effective singulair 10 mg. The all-H isoform is characteristic of that from heart tissue, and the all-M isoform is typically found in skeletal muscle and liver. Isoenzymes all catalyse the same chemical reaction, but with different degrees of efﬁciency. Both enzymes convert glucose to glucose- 6-phosphate, the ﬁrst reaction in glycolysis, but respond to quite different concentrations of glucose. Glucokinase has a high K (low afﬁnity) for glucose, about 2 × 10−2 M, and operates m within the liver. On the other hand, hexokinase has a low K (high afﬁnity) for glucose, about 5 × 10−5 M. It would be fully saturated at a blood glucose m concentration of 5 × 10−3 M (5 mM) and its activity would change little with changes in glucose concentration at this level. Hexokinase is located in muscle, where it is responsible for initiating glycolysis to provide energy for muscle contraction; muscle only imports and uses glucose, it does not export it (Figure 9. Inhibitors of the ﬁrst class usually cause an inactivating, covalent modiﬁcation of enzyme structure. The kinetic effect of irreversible inhibitors is to decrease the concentration of active enzyme. Irreversible inhibitors are usually considered to be poisons and are generally unsuitable for therapeutic purposes. Reversible enzyme inhibitors are usually either competitive or non-competitive; a third type, uncompetitive, is rarely encountered (Table 9. Most therapeutic drugs are reversible competitive inhibitors, which bind at the catalytic (active site) of the enzyme. Competitive inhibitors are especially attractive as clinical modulators of enzyme activity because they offer two routes for the reversal of enzyme inhibition, by decreasing the concentration of inhibitor or by raising the concentration of substrate. Since high concentrations of a substrate can displace its competitive inhibitor, it is apparent that Vmax should be unchanged by competitive inhibitors. This characteristic of competitive inhibitors is reﬂected in the identical vertical-axis intercepts of Lineweaver–Burk plots, with and without inhibitor (Figure 9. Competitive inhibitors often structurally resemble the substrate of the enzyme (structural analogues). The similarity between the structures of folic acid and methotrexate is shown in Figure 9. Most allosteric enzymes are oligomeric (consisting of multiple subunits); generally they are located at or near branch points in metabolic pathways, where they are inﬂuential in directing substrates along one or another of the available metabolic routes. Effectors may control enzyme activity by altering the Vmax or the Km of the enzyme; Km effectors work on K-type enzymes, Vmax effectors work on V-type enzymes. Numerous enzymes of intermediary metabolism are affected by phosphorylation, either positively or negatively. Covalent phosphorylations can be reversed by a separate subclass of enzymes known as phosphatases. The aberrant phosphorylation of growth factor and hormone receptors, as well as of proteins that regulate cell division, often leads to unregulated cell growth or cancer. The usual sites for phosphate addition to proteins are the serine, threonine and tyrosine R-group hydroxyl residues. Post-translation Phosphorylation or glycosylation may be used to activate Rapid modiﬁcation or deactivate an enzyme. In the response to insulin, the phosphorylation of multiple enzymes, including glycogen synthase, helps control the synthesis or degradation of glycogen and allows the cell to respond to changes in blood sugar. Another example of post-translational modiﬁcation is the cleavage of the polypeptide chain. Chymotrypsin is produced in the inactive form, the proenzyme, as chymotrypsinogen. Bacteria may Slow become resistant to penicillin because enzymes called β-lactamases are induced which hydrolyse the crucial β-lactam ring within the penicillin molecule. Compartmental- Fatty acids are synthesised by one set of enzymes in the isation cytosol, and used by a different set of enzymes as a source of energy in the mitochondrion. For example, haemaglutinin, in the inﬂuenza virus, is activated by a conformational change caused by the acidic conditions which occur when it is taken up inside its host cell and enters the lysosome. Many of the proteins that bind calmodulin are themselves unable to bind calcium, and so use calmodulin as a calcium sensor and signal transducer. Calmodulin undergoes a conformational change upon binding of calcium, which enables it to bind to speciﬁc proteins for a speciﬁc response. For example: • allosteric changes in enzyme activity occur in milliseconds or less • transmembrane ion channels open or close in milliseconds or less • G-protein transmembrane signalling operates over a few milliseconds • protein kinases and phosphatases operate over a few seconds • a protein switches compartments in a minute or so • changes in gene expression are evident over about 24 hours • growth/differentiation occurs over a few days. Today, commercially puriﬁed and sometimes immobilised enzymes are used by industry and medicine. A natural event; the gene for lactase (ß-galactosidase) is ‘switched on’ at birth and ‘switched off’ after weaning. As a result, lactose is unabsorbed by the body, ferments in the lower gut and produces intestinal gases (methane), leading to pain and ﬂatulence. In most Europeans, however, the infant condition persists, and the lactase gene remains active (possibly linked with the domestication of cattle and goats in the Near East some 10 000 years ago; the ability to digest lactose throughout life could have conferred some nutritional advantage). The gene encoding lactase in humans is located on chromosome 1; 70% of ‘Westerners’ have a mutation in the gene such that it fails to ‘switch off’, thus conferring lactose tolerance. For those lactose-intolerant individuals, lactase may be added to milk or taken as capsules before a meal; it is supplied as a pro-enzyme called prolactazyme. The pro-enzyme is activated by partial digestion in the stomach, so that it has the opportunity to function in the small intestine. So-called ‘live yogurts’ solve this problem because the lactose (in the yogurt) is digested by the bacteria present. Lactase enzyme is expensive however; nowadays milk can be pre-treated with lactase before distribution. It is useful for diabetics to measure their blood sugar level throughout the day in order to regulate their use of insulin. One test (Clinistix) relies upon a chemical reaction that produces a colour change on a test strip. The test strip contains a chemical indicator called toluidine and the ‘immobilised’ enzyme glucose oxidase. Glucose oxidase converts the glucose in urine to gluconic acid and hydrogen peroxide; hydrogen peroxide reacts with toluidine, causing the colour change. A variety of metabolic diseases are caused by deﬁciencies or malfunctions of enzymes, due originally to gene mutation. Albinism, for example, may be caused by the absence of tyrosinase, an enzyme essential for the production of cel- lular pigments. One such example is Gaucher’s disease type I, caused by a deﬁciency in the enzyme glucocerebrosidase, causing lipids to accumulate, swelling the spleen and liver, and trigger- ing anaemia and low blood platelet counts.
Organisms causing meningitis Population Additional Potential Pathogens Neonate (<1 mo) Group B streptococci buy discount singulair 10mg online, E proven singulair 4 mg. Encephalitis cheap singulair 5 mg with visa, causative organisms Virus Route of Entry Arbovirus Mosquito bite; hematogenous spread (California, W. Louis, West Nile) Herpes virus Herpes simplex type 1 Skin lesions; retrograde neuronal spread Varicella zoster Skin lesions; retrograde neuronal spread E-B virus Mononucleosis Rabies Animal bite; retrograde neuronal spread Measles, mumps Post-infectious Table 4D. Examination • Meningitis • Evaluate the patient’s overall appearance and mental status. Note that papilledema takes time to develop, and this finding can be absent in the majority of patients with bacterial meningitis. In infants <12 mo of age, when meningeal signs are unreliable, the anterior fontanelle should be evaluated for bulging. Neck stiffness is often absent at the extremes of age, or in patients with altered levels of conscious- ness, immunosuppressed, or partially treated disease. Localizing signs are generally absent in bacterial meningitis; their presence suggests the possibility of a focal infection, such as an abscess. The level of consciousness may range from confusion or delirium to stupor or coma. Evaluation 4 • Delay in the diagnosis of bacterial meningitis in the elderly, especially with nonspecific symptoms, is responsible for the high mortality in this population. Normal adult pressures are 5-19 cm H2O, when the patient is in the lateral recumbent position. Empiric therapy should be based on the suspected patho- gen, taking into consideration the patient’s age and risk factors for specific organ- isms. An infectious disease consultant may be helpful for information regarding local drug resistance patterns (Table 4D. Neurosurgical consulta- tion is recommended for possible aspiration or excision (Table 4D. If dexamethasone is given, benefit is greatest when started prior to or concurrent with initial antibiotic therapy. Health care personnel coming into con- tact with respiratory droplets are also candidates for prophylaxis (Table 4D. If a fungal abscess is suspected, ampho- tericin B should be added to the empiric regimen. Neurol Clin North Am 1998; 16:2 Part E: Cerebrovascular Emergencies Basic Anatomy • The anterior circulation, consisting of the paired internal carotid arteries and their branches (ophthalmic, anterior cerebral, and middle cerebral arteries), supplies most of the cerebral hemispheres and the deep cortical gray matter. Clinicoanatomic Correlation • Anterior Circulation • Anterior circulation strokes rarely have associated symptoms; neurologic deficits accompanied by headache, nausea, and vomiting are more suggestive of intracere- bral hemorrhage or posterior circulation stroke. In addition, complications of cerebellar infarcts, such as edema compressing brainstem structures, may cause rapid deterioration (i. Voluntary eye opening, vertical eye movements, and ocular convergence are preserved. Neurologic Emergencies 103 • Neurologic exam may reveal nystagmus; ipsilateral Horner’s syndrome, paralysis of the soft palate and posterior pharynx, and limb ataxia; and impaired pain/ temperature sensation in the ipsilateral face and contralateral limbs. Scope of the Problem • Disruption in the flow of blood to the brain results in ischemia and cell death. The central area of infarction is surrounded by a region of salvageable tissue, referred to as the penumbra. Identifying the etiology of the patient’s symptoms is critical for determining therapy. Risk Factors • Vascular Disorders • Atherosclerosis • Diastolic or isolated systolic hypertension • Hyperlipidemia (hypercholesterolemia) • Cigarette smoking • Oral contraceptive use • Diabetes mellitus • Hereditary predisposition (i. Vital Signs • Hypotension may be the underlying cause of a stroke; markedly elevated blood pres- sure is suggestive but not diagnostic of a hemorrhagic stroke. Neurologic Emergencies 105 Physical Examination • Focus on searching for an underlying systemic cause, especially a treatable one. A patient with a cere- bral hemispheric stroke will typically gaze toward the side of the insult; a brainstem infarct will cause the patient to gaze away from the side of the lesion. Whenever possible, lower extremity strength should be assessed by observing the patient’s gait. Double simultaneous stimulation: assess sensation on both sides of the body simultaneously; patients with cortical infarcts will only notice the unaf- fected side. Evaluation • Pulse Oximetry • Rapid determination of oxygen saturation may reveal impending respiratory failure and the need for mechanical ventilation. Patients with severely depressed mental Neurologic Emergencies 107 status and patients with an unprotected airway may require intubation and me- chanical ventilation. How- ever, in the absence of hypoxia, supplemental oxygen has not been shown to affect outcome. Over the next few hours to days, the blood pressure generally 4 declines spontaneously. The ischemic penumbra may be dependent upon a moder- ately increased blood pressure for adequate perfusion; thus, use of antihypertensive agents may exacerbate the patient’s condition. Aspirin is recommended in patients who are not candidates for thrombolytics or other anticoagulants. However, because this modality is now being described by certain groups as the standard of care, the 108 Emergency Medicine inclusion and exclusion criteria are included here. For this reason, many neurologists are describing symptoms that persist for more than 1 h as an acute stroke. Various guidelines exist, ranging 4 from keeping the diastolic blood pressure at approximately 100 mm Hg to basing the target systolic and diastolic levels on the patient’s premorbid blood pressure. Potential surgical candidates are those with neurologic deterioration, superficial cerebral hemorrhages causing mass effect, and cerebellar hematomas. Neurosurgical consultation is recommended in all patients with intracerebral hemorrhage. Preventing rerupture, by maintaining adequate blood pressure control, is the mainstay of treatment. Eleva- tion of the head of the bed, mild sedation, and analgesics (for headache) may suffice. The blood pressure should be reduced to approximately 160/100 mm Hg, using rap- idly titratable, parenteral medications if necessary. The timing and outcome of sur- gical intervention are determined by the patient’s clinical grade and medical stability, among other factors. Is admission medically justified for all patients with acute stroke or transient ischemic attack? Part F: Dizziness and Vertigo Basic Anatomy • The vestibular system provides input to the brain regarding movement of the head. The vestibular portion of the 8th cranial nerve is composed of the utricle, the saccule, and three semicircular canals that lie at right angles to each other.
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