By H. Topork. Southwest University. 2018.
The campaign led to the establishment of ‘smoke-free’ areas and then smoking bans in workplaces generic liv 52 120 ml otc medicine youkai watch, on public transport and other public spaces buy liv 52 60 ml with visa medicine hat jobs. The award, by Stockport council in 1993, of £15,000 in damages to Veronica Bland, who claimed that her chronic bronchitis resulted from eleven years of exposure to smoking workmates, marked the public affirmation of the status of the passive smoker in Britain. As the medical historian Allan Brandt observed, ‘in less than a decade, American public space was radically subdivided on the basis of the harms of passive smoking’ (Brandt 1998). Despite the growing medical (and political) consensus about the dangers of passive smoking, the issue has remained controversial. The Swedish toxicologist Robert Nilsson, while accepting the plausibility of the ETS-lung cancer link and the fact that numerous studies appear to show a statistically significant increase in risk, has questioned its epidemiological significance (Nilsson 1997). Thus he offered estimates, on the basis of current knowledge, of the annual incidence of cancer in a population of 100,000 resulting from various environmental factors: unknown (177), diet (135), smoking (68), other lifestyle factors (45), sunshine (23), …ETS (2). By contrast, in a population which consumes Japanese seafood (which contains arsenic) this will cause 12 cases of cancer; where there are traces of natural arsenic in drinking water, this will cause five cases; eating mushrooms will cause three cases. In other words, the risk of ETS is comparable with that of environmental agents which are generally regarded as an insignificant threat to health. Even if the more moderate increases are true—and given that passive smoking has been estimated to be equivalent to actively smoking up to half a cigarette a day—the cancer-causing potency of ETS appears to be around ten times greater than mainstream smoke. Another anomaly of passive smoking is that it appears to be associated with an increased risk of a type of lung cancer that arises from glandular tissue (adenocarcinoma) instead of from the cells lining the airways (squamous or oat cell carcinoma) which is the familiar type caused by smoking. This type of tumour appears to be more common in East Asia—where many of the studies of passive smoking have been conducted. The idea that a very low level of smoke inhalation could cause a type of lung cancer in passive smokers that vastly higher levels do not appear to cause in heavy smokers defies biology and common sense. Nilsson also pointed to a number of possible sources of bias or confounding in the conduct and interpretation of studies of passive smoking. He also noted that the increased risk suggested by some surveys implies that passive smoking is more dangerous than smoking up to ten cigarettes a day. Perhaps the most fundamental defect of the presentation of the risk of passive smoking is the failure to distinguish between relative and absolute risk. In a critical commentary, the Australian medical research scientist Raymond Johnstone noted that the annual death rate from lung cancer among the non-smoking wives of non- smoking men is around six per 100,000, whereas among the non- smoking wives of smoking men the corresponding figure is eight per 100,000. Now this may be reported as an increased (relative) risk of 33 per cent. Yet in absolute terms it amounts to an absolute (or exposure) risk of one in 50,000, which is, for practical purposes, negligible. His conclusion was that ‘the most that one can say about the alleged link beween passive smoking and lung cancer is that if there is one, then it is so small that it is difficult to measure it accurately and the risk, if any, is well below the level of those to which we normally pay attention’ (Johnstone 1991:81). The alarming estimates of deaths attributable to passive smoking result from multiplying minuscule risks of dubious validity by vast population numbers—an effective propaganda device but statistical sharp practice. The drive to impose restrictions on smoking in workplaces and in public has not been in the least inhibited by expert doubts about the validity of the evidence on which it is based. Indeed, as medical historian Virginia Berridge has observed, ‘the coalition advocating 40 THE REGULATION OF LIFESTYLE those restrictions pre-dated the evidence’ (Berridge 1998). Yet, as she acknowledged, ‘by the mid-1990s, there was widespread agreement that the epidemiological evidence on passive smoking was at least debatable’. It may have been regarded as debatable among medical experts at an elite symposium, but as far as public policy was concerned ETS was lethal. In a revealing exchange at the same symposium on the history of smoking and health, when Richard Doll was asked to compare the epidemiological evidence on passive smoking with his work in the 1950s, his response was ‘it’s utterly different’ (Doll 1998). Recalling that his study had shown a fifty-fold increase in risk for heavy smokers, he commented that ‘for passive smoking the evidence is qualitatively different’. While indicating that he did believe that passive smoking was harmful, he conceded that ‘the quantitative relationship is very weak’, suggesting that his belief was more grounded in loyalty to the anti- smoking cause than his confidence in the figures. The discovery of the link between smoking and lung cancer gave a great impetus to the quest for some similar causative agent of coronary heart disease (CHD), another condition which caused a rapidly increasing death toll from the 1920s onwards. Mortality from coronary heart disease grew at an even faster rate, reaching twice the rate of lung cancer in the early 1950s and three times the rate in the 1960s. Sudden death from a heart attack, particularly affecting men in middle age—a condition virtually unknown before the First World War—became familiar throughout the Western world. The coronary death rate in Britain reached a plateau in the late 1970s and then slowly declined (in the USA, this fall began a decade earlier). The cause of the rapid increase in CHD was (and largely remains) a mystery, as does the reason for its more recent decline (which began before any of the familiar preventive interventions had been implemented on a large scale).
Cross References Brudzinski’s (neck) sign; Kernig’s sign; Nuchal rigidity Metamorphopsia Metamorphopsia is an illusory visual phenomenon characterized by objects appearing distorted or misshapen in form cheap 60 ml liv 52 with amex medications safe during pregnancy. As with neglect buy 200 ml liv 52 with mastercard treatments for depression, these phenomena may be classified as object- or person-centered: ● Object-centered: affecting size and spatial relationships Macropsia: objects appear larger than normal - 194 - Micrographia M Micropsia: objects appear smaller than normal Pelopsia: objects appear closer to the observer than actual Porropsia: objects appear farther away from the observer than actual ● Person centered: Micro- and macrosomatognosia: body image appears smaller or larger than normal (“Alice in Wonderland” syndrome). Metamorphopsias are often transient and episodic, occurring for example during migraine attacks, epileptic seizures, with psychotropic drug abuse, and following petechial intraparenchymal hemorrhages. Rarely, they are long-lasting or permanent, for example following brain infarction (most commonly involving the occipito-parietal or temporo-parietal cortex: lesions on the right are more likely than those on the left to give metamorphopsia) or tumors. Retinal disease causing displacement of photoreceptors may produce metamorphopsia: micropsia due to receptor separation in retinal edema, macropsia due to receptor approximation in retinal scarring. Occasional cases of metamorphopsia have been reported with lesions of the optic chiasm, optic radiation, and retrosplenial region. Indeed, it seems that meta- morphopsia may occur with pathology at any point along the visual pathway from retina to cortex. Differing patterns of metamorphopsia may assist with clinico-anatomical correlation: ● retinal lesions: ipsilateral monocular ● chiasmal lesions: bitemporal ● occipitoparietal lesions: contralateral homonymous Metamorphopsia may be associated with visual hallucinations. Metamorphopsia and visual hallucinations restricted to the right visual hemifield after a left putaminal hemorrhage. Journal of Neurology, Neurosurgery and Psychiatry 1996; 61: 420-421 Cross References “Alice in Wonderland” syndrome; Hallucination; Illusion; Macropsia; Micropsia; Pelopsia; Porropsia; Telopsia Micrographia Micrographia is small handwriting. It is most often recognized in asso- ciation with the extrapyramidal features of idiopathic Parkinson’s dis- ease (indeed it may be the presenting sign), but may occasionally occur with other parkinsonian syndromes (e. In Parkinson’s disease, handwriting may initially be of normal size but then become progressively smaller, slower, and more illegible as writing proceeds, an example of parkinsonian fatigue, a gradual - 195 - M Micropsia decline in the amplitude and speed of initiation of voluntary move- ments. Such “slow” micrographia may be distinguished from “fast” micrographia in which letters are small throughout although written at normal speed without fatigue, which may be seen in PSP or other pal- lidal pathologies. There is a poor correlation between micrographia and the side, severity or duration of classical parkinsonian features, and its response to levodopa preparations is very variable. These observations, along with reports of isolated micrographia with cortical lesions demon- strated by neuroimaging, suggest that the anatomical basis of micro- graphia may be at the level of the cortex (dominant parietal lobe) rather than the basal ganglia. Micrographia has also been described following large right ante- rior cerebral artery infarcts and lacunar infarcts involving the putamen and genu of the internal capsule. Journal of the Neurological Sciences 1972; 15: 141-152 Scolding NJ, Lees AJ. Micrographia associated with a parietal lobe lesion in multiple sclerosis. Journal of Neurology, Neurosurgery and Psychiatry 1994; 57: 739-741 Cross References Fast micrographia; Fatigue; Parkinsonism Micropsia Micropsia, or “Lilliput sight,” is an illusory phenomenon in which the size of a normally recognized object is underestimated. It is the most common form of metamorphopsia, and is most often associated with lesions of the right temporo-parietal cortex, although macular edema and optic chiasm lesions may also cause micropsia. Hemimicropsia, micropsia confined to one visual hemifield, has been recorded. The entirely subjective nature of the disorder may account for the relative rarity of reports. Seeing objects smaller than they are: micropsia following right temporo-parietal infarction. Selective deficit of visual size per- ception: two cases of hemimicropsia. Journal of Neurology, Neurosurgery and Psychiatry 1994; 57: 73-78 Cross References Metamorphopsia Microsomatognosia - see “ALICE IN WONDERLAND” SYNDROME - 196 - Mirror Agnosia M Milkmaid’s Grip Milkmaid’s grip is the descriptive term applied to the inability to main- tain a firm grip (e. Seen in Huntington’s disease, this may reflect a combination of chorea and motor impersistence. Cross References Chorea, Choreoathetosis; Impersistence; Trombone tongue Miosis Miosis is abnormal reduction in pupillary size, which may be unilateral or bilateral. Philadelphia: Lippincott Williams & Wilkins, 2002: 135-146 Cross References Age-related signs; Anisocoria; Argyll Robertson pupil; Horner’s syn- drome; Mydriasis Mirror Agnosia Mirror agnosia, or the “looking glass syndrome,” is a phenomenon observed in patients with left hemispatial neglect as a result of right parietal lobe lesions. There is inability to point to objects seen in a mirror, with repeated reaching “into” the mirror even when the actual location of the target is shown. In a milder form, known as “mirror ataxia,”patients reach in the direction of the object but with increased errors of reach and grasp, suggesting that visual information is not adequately transformed into a body-centered frame of reference. Mirror agnosia and mirror ataxia constitute different parietal lobe disorders. Annals of Neurology 1999; 46: 51-61 Ramachandran VS, Altschuler EL, Hillyer S.
The cortical topography of human swallowing musculature in health and disease discount liv 52 100 ml on-line medicine you can give dogs. Philadelphia: Lippincott Williams & Wilkins discount liv 52 200 ml mastercard treatment 0f gout, 2002: 227-235 Cross References Bulbar palsy; Dysphonia; Gag reflex; Jugular foramen syndrome; Pseudobulbar palsy Dysphasia - see APHASIA Dysphonia Dysphonia is a disorder of the volume, pitch or quality of the voice resulting from dysfunction of the larynx, i. Hence this is a motor speech disorder and could be considered as a dysarthria if of neurological origin. Dysphonia manifests as hoarseness, or a whispering breathy qual- ity to the voice. Recognized causes of dysphonia include: ● Infection (laryngitis) ● Structural abnormalities, e. Flaccid dysphonia, due to superior laryngeal nerve or vagus nerve (recurrent laryngeal nerve) palsy, bulbar palsy. The use of botulinum toxin in the treatment of adductor spasmodic dyspho- nia. Journal of Neurology, Neurosurgery and Psychiatry 1993; 56: 526-530 Cross References Aphonia; Bulbar palsy; Diplophonia; Dysarthria; Dystonia; Hypophonia; Vocal tremor, Voice tremor Dyspraxia Dyspraxia is difficulty or impairment in the performance of a voluntary motor act despite an intact motor system and level of consciousness. This - 105 - D Dysprosody may be developmental in origin (“clumsy child”), but in adult practice reflects a loss of function (hence apraxia is a better term). Cross References Apraxia Dysprosody - see APROSODIA, APROSODY Dyssynergia - see ASYNERGIA Dystaxia - see ATAXIA Dystonia Dystonia, a term first used by Oppenheim in 1911, is a motor syndrome of sustained involuntary muscle contractions causing twisting and repet- itive movements, sometimes tremor, and/or abnormal postures. Dystonic movements may initially appear with voluntary movement of the affected part (“action dystonia”) but may eventually occur with voluntary move- ment elsewhere in the body (“overflow”). The severity of dystonia may be reduced by sensory tricks (geste antagoniste), using tactile or propriocep- tive stimuli to lessen or eliminate posturing; this feature is unique to dys- tonia. Dystonia may develop after muscle fatiguing activity, and patients with focal dystonias show more rapid fatigue than normals. Dystonic disorders may be classified according to: Age of onset: the most significant predictor of prognosis: worse with earlier onset; Distribution: focal, segmental, multifocal, generalized, hemidystonia; Etiology: primary/idiopathic vs. Peripheral focal dysto- nias, such as torticollis and writer’s cramp, have been suggested to result from abnormal afferent information relayed from “stiff” muscle spindles. The genetic characterization of various dystonic syndromes may facilitate understanding of pathogenesis. From a therapeutic point of view, one of the key questions relates to response to levodopa: dopa-responsive dystonia (DRD) responds very well to levodopa (and response fluctuations do not develop over time; cf. Other treatments which are sometimes helpful include anticholinergics, dopamine antagonists, dopamine agonists, and baclofen. Drug-induced dystonia following antipsychotic, antiemetic, or antidepressant drugs is often relieved within 20 minutes by intramuscular biperiden (5 mg) or procyclidine (5 mg). Surgery for dysto- nia using deep brain stimulation is still at the experimental stage. Advances in Clinical Neuroscience & Rehabilitation 2004; 4(2): 20,22,24 Fahn S, Marsden CD, Calne DB. London, Butterworth 1987: 359-382 Grunewald RA, Yoneda Y, Shipman JM, Sagar HJ. Idiopathic focal dystonia: a disorder of muscle spindle afferent processing? BMJ 1999; 319: 623-626 Cross References Anismus; Blepharospasm; Dysphonia; Eyelid apraxia; Fatigue; Gaping; Geste antagoniste; Hemidystonia; Torticollis; Writer’s cramp - 107 - E Ear Click - see PALATAL MYOCLONUS; TINNITUS Echolalia Echolalia is the involuntary automatic repetition of an interviewer’s speech. This may be observed in a variety of clinical situations: ● Transcortical sensory aphasia: In the context of a fluent aphasia with repetition often well or normally preserved, usually as a result of a vascular lesion of the left hemisphere although an analogous situation may be encountered in Alzheimer’s disease; “incorporational echolalia,” when the patient uses the examiner’s question to help form an answer, may be observed as a feature of “dynamic aphasia” which bears resemblance to transcortical motor aphasia, but may result from a frontal lesion. Cortex 1998; 34: 67-82 Cross References Aphasia; Coprolalia; Dynamic aphasia; Imitation behavior; Jargon aphasia; Logorrhea; Palilalia; Transcortical aphasias Echophenomena - see IMITATION BEHAVIOR - 108 - Emotionalism, Emotional Lability E Echopraxia Echopraxia is the involuntary, automatic, imitation of an interviewer’s movements. This may be observed as a feature of apraxic syndromes, such as corticobasal degeneration, as a complex motor tic in Gilles de la Tourette syndrome, and in frontal lobe disorders (imitation behavior). Cross References Copropraxia; Imitation behavior; Tic Écriture en Double Miroir - see MIRROR WRITING Ectropion - see LID RETRACTION Eidetic Memory Photographic, or eidetic, memory is an enhancement of memory to prodigious capacity, beyond hypermnesia. Synesthesia may be linked to eidetic memory, synesthesia being used as a mnemonic aid.
He immediately made an appointment with a well-known internist in town because he felt his fam- ily doctor was not responsive buy discount liv 52 200 ml treatment using drugs is called. Making the Diagnosis On the day of his appointment order liv 52 60 ml visa medicine 752, Pedro took his Eight Step notebook, his blood test results from the family doctor, his calorie journal, and his sense of humor to the internist’s ofﬁce. He told the doctor he wanted to be so thin he’d have to jump around in the shower to get wet. The internist laughed and after reviewing Pedro’s notebook, he responded that he didn’t know if he could get Pedro that thin, but he was reasonably sure he could make him a lot better. He said he was very impressed with Pedro’s hard work and then gave Pedro a blood and urine test and a computerized tomography (CT) scan. The doctor felt reasonably sure he could give his patient not only a diagnosis but also a cure. When all the test results came back, the doctor told Pedro he had developed Cushing’s syndrome, also known as hypercortisolism. This is a metabolic disorder that occurs when excess cor- tisol circulates in the bloodstream. All the key indicators were found in Pedro’s notebook: the round face and extra fatty tissue in the neck; the thinning skin (which accounted for the bright red stretch marks); the excess beard growth; his obesity, weakness, and fatigability. In fact, Pedro’s metabolic condition causes a certain pecu- liar pattern of obesity that results in a round (moon) face and obesity around the trunk (centripetal obesity). He explained that Pedro’s adrenal glands were producing too much cor- tisol, which in turn caused all his symptoms. The CT scan revealed a small 144 Diagnosing Your Mystery Malady adrenal adenoma, or benign tumor. This tumor was subsequently removed and eventually all Pedro’s symptoms, including his obesity, disappeared. Case Study: Lincoln Fifty-two-year-old Lincoln was a middle school math teacher. Toward the end of the school year, he began to feel sluggish and generally run down. He noticed he was having problems focusing on his lesson plans and was randomly forgetting things. He attributed it to simply needing his summer vacation after a long, tough year. What he couldn’t explain, though, was his gradual weight gain over the past three months. He knew that he had stopped exercising since his heart attack in March, and even though the doctors told him it was perfectly ﬁne for him to start exercising again, he was a little anxious about resuming any activity that required a lot of exertion. He thought this might be the reason for his weight gain, but it just wouldn’t level off and the pounds kept slowly creeping on. He recalled that when he had stopped smoking years earlier, he had gained weight but even that had leveled off after a couple of months. At the last school health fair, he was checked out and was told he was ﬁne. Several times, he visited the hospital clinic where he’d been treated for his heart attack; they drew his blood and even checked for thyroid disease. Lincoln was told it was anxiety after his heart attack, but he knew there was really something wrong with his body. When summer vacation ﬁnally arrived, Lincoln made a concerted effort to get back into his weight lifting and daily two-mile walks around the river in the city where he lived. But after two months of this regimen with no abatement of his symptoms and no weight loss, he decided to take matters into his own hands. He was given a copy of the Eight Steps by a teacher friend and decided to try to solve his mystery malady. He ﬁlled up a notebook, precisely answering all the questions posed by all Eight Steps.