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The remarkable epidemiologic and pathologic similarities between kuru and scrapie were pointed out by Hadlow (1959) arteria bologna 7 dicembre purchase 162.5 mg avalide visa, who suggested that it might be possible to transmit kuru to subhuman primates prehypertension a literature-documented public health concern buy discount avalide on line. This was accomplished in 1966 by Gajdusek and coworkers; inoculation of chimpanzees with brain material from affected humans produced a kuru-like syndrome in chimpanzees after a latency of 18 to 36 months. Since then the disease has been transmitted from one chimpanzee to another and to other primates by using both neural and nonneural tissues. Kuru has gradually disappeared, apparently because of the cessation of ritual cannibalism by which the disease had been transmitted. At least 50 percent of the neurologic disorders in a general hospital are of this type. At some time or other, every physician will be required to examine patients with cerebrovascular disease and should at least know something of the common types- particularly those in which there is a reasonable prospect of successful medical or surgical intervention or the prevention of recurrence. There is another advantage to be gained from the study of this group of diseases- namely, that they have traditionally provided one of the most instructive approaches to neurology. Fisher has aptly remarked, house officers and students learn neurology literally "stroke by stroke. It must also be noted that, in the last two decades, new and extraordinary types of imaging technology have been introduced that allow the physician to make physiologic distinctions between normal, ischemic, and infarcted brain tissue. This biopathologic approach to stroke will likely guide the next generation of treatments and has already had a pronounced impact on the direction of research in the field. Salvageable brain tissue to be protected in the acute phase of stroke can be delineated by these methods. To identify this ischemic but not yet infarcted tissue virtually defines the goal of modern stroke treatment. Which of the sophisticated imaging techniques will contribute to improved clinical outcome is still to be determined, but certain ones, such as diffusionweighted imaging, have already proved invaluable in stroke work. First, all physicians have a role to play in the prevention of stroke by encouraging the reduction in risk factors such as hypertension and the identification of signs of potential stroke, such as transient ischemic attacks, atrial fibrillation, and carotid artery stenosis. Second, careful bedside clinical evaluation integrated with the newer testing methods mentioned above still provide the most promising approach to this category of disease. Finally, the last decade or two have witnessed a departure from the methodical clinicopathologic studies that have been the foundation of our understanding of cerebrovascular disease. Increasingly, randomized studies involving several hundred and even thousands of patients and conducted simultaneously in dozens of institutions have come to dominate investigative activity in this field. These multicenter trials have yielded highly valuable information about the natural history of a variety of cerebrovascular disorders, both symptomatic and asymptomatic. However, this approach suffers from a number of inherent weaknesses, the most important of which is that the homogenized data derived from an aggregate of patients may not be applicable to a specific case at hand. Moreover, many large studies show only marginal differences between treated and control groups. Each of these multicenter studies will therefore be critically appraised at appropriate points in the ensuing discussion. Since 1950, coincident with the introduction of effective treatment for hypertension, there has been a substantial reduction in the frequency of stroke. This was most apparent three decades ago, as treatment for high blood pressure became a public health focus. Among the residents of Rochester, Minnesota, Broderick and colleagues documented a reduction of 46 percent in cerebral infarction and hemorrhage when the period 1975­ 1979 was compared with 1950­ 1954; Nicholls and Johansen reported a 20 percent decline in the United States between 1968 and 1976. During this period, the incidence of coronary artery disease and malignant hypertension also fell significantly. In the last decade, according to the American Heart Association, the mortality rate from stroke has declined by 12 percent, but the total number of strokes may again be rising. Definition of Terms As discussed below, the term stroke is applied to a sudden focal neurologic syndrome, specifically the type due to cerebrovascular disease. The term cerebrovascular disease designates any abnormality of the brain resulting from a pathologic process of the blood vessels. Pathologic process is given an inclusive meaning- namely, occlusion of the lumen by embolus or thrombus, rupture of a vessel, an altered permeability of the vessel wall, or increased viscosity or other change in the quality of the blood flowing through the cerebral vessels. The vascular pathologic process may be considered not only in its grosser aspects- embolism, thrombosis, dissection, or rupture of a vessel- but also in terms of the more basic or primary disorder, i. Equal importance attaches to the secondary parenchymal changes in the brain resulting from the vascular lesion.

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A common and critical cause of sudden monocular blindness blood pressure lowering foods buy cheapest avalide and avalide, especially in elderly persons blood pressure 9555 purchase avalide 162.5 mg without a prescription, is ischemic optic neuropathy. It is due to disease of ciliary vessels that supply the optic nerve; it is therefore considered further on, in the discussion of diseases of the optic nerve. In summary, sudden painless monocular loss of vision should always raise the question of ischemia of the retina, due either to occlusive disease of the central retinal artery or vein or to ischemic optic neuropathy from disease of the ciliary vessels. Detachment of the retina, macular or vitreous hemorrhage, and acute glaucoma are less common but obvious causes. Other Diseases of the Retina Aside from vascular lesions, other alterations of the retina, namely tears and detachments, may impair vision acutely. The most common form of retinal detachment is an intraretinal detachment due to separation of the pigment epithelium layer from the sensory retina with fluid accumulation through a tear or hole in the retina. In so-called traction detachment- observed in cases of premature birth or proliferative retinopathy secondary to diabetes or other vascular disease- contracting fibrous tissue may pull the retina from the choroid. Serous retinopathy, a fairly common disease, and chorioretinitis represent another category of retinal disease. In serous retinopathy, a condition that occurs most often in young or middleaged males, the entire perimacular zone is elevated by edema fluid. Metamorphopsia (distortion of vision) in one eye is a common presentation, and although vision is usually distorted, acuity is not much impaired. The retinal change (leakage of fluid into the subretinal space) causes a loss of visualization of the detail of the choroid and is demonstrated by fluorescein angiography. The condition tends to resolve over several months or may be treated with laser to seal the site of leakage. In chorioretinitis, generally an infectious process, there may also be difficulty in diagnosis and, in a many of our cases, the initial diagnosis had been retrobulbar neuritis. One cannot depend upon the appearance of a macular star (see above) for diagnosis. Infarcts of the nerve-fiber layer (cotton-wool patches), hemorrhages, and perivascular sheathing are the usual findings. Occlusion of the central retinal vein with suffusion of the veins, swelling of the disc, and florid retinal hemorrhages. Both the retina and choroid may be involved by these diseases, in which case the ophthalmoscopic picture is characteristic. Destruction of the retina and the pigment epithelium of the choroid produces "punched-out" lesions, exposing the whitish sclera and deposits of black pigment in various forms. The choroid may be the site of viral and also noninfective inflammatory reactions, often in association with painful recurrent iridocyclitis and lacrimal inflammation. They assume several forms and may be associated with other neurologic abnormalities. The most frequent in youth and middle age is retinitis pigmentosa, a hereditary disease of the outer photoreceptor layer and subjacent pigment epithelium. The retina is thin, and there are fine deposits of black pigment in the shape of bone corpuscles, more in the periphery; later the optic discs become pale. Clinically this disorder is marked by constriction of the fields with relative sparing of central vision ("gun-barrel" vision), metamorphopsia (distorted vision), delayed recovery from glare, and nyctalopia (reduced twilight vision). There are widely diverse causes of retinitis pigmentosa and related retinal degenerations, too numerous to list here; furthermore, these degenerations have been linked to deficits in over 75 different genes. In one form of isolated retinitis pigmentosa, which follows an autosomal dominant pattern of inheritance and is linked to chromosome 3, the gene for rhodopsin (a combination of vitamin A and the rod-cell protein opsin) produces a defective opsin. This results in a diminution of rhodopsin in rod cells, a diminished response to light, and eventual degeneration of the rod cells (Dryja et al). Retinitis pigmentosa may also be associated with the Laurence-Moon-Biedl syndrome, with certain mitochondrial diseases (Kearns-Sayre syndrome, Chap. Another early-life hereditary retinal degeneration, characterized by massive central retinal lesions, is the autosomal recessive Stargardt form of juvenile tapetoretinal degeneration.

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In one such family the illness had occurred in two generations; in another arteria musculophrenica discount avalide 162.5mg mastercard, three brothers in a single generation were afflicted pulse pressure young adults order avalide uk. Skre described two recessive types of hereditary spastic paraplegia in Norway, one with onset in childhood, the other in adult life. In contrast to the dominant form (see further on), the recessive types displayed evidence of more widespread involvement of the nervous system, including dementia, cerebellar ataxia, and epilepsy. Also, Cross and McKusick have observed a recessive type of paraplegia accompanied by dementia beginning in adolescence. Worster-Drought and others have reported the pathologic findings in two cases of this type. Van Bogaert and associates published an account of similar cases that showed the characteristic pathologic features of Alzheimer disease. Adult forms of metachromatic leukodystrophy and adrenoleukodystrophy may present with a similar clinical picture (Chap. Quite rare instances of the same syndrome with adult onset have turned out to be due to phenylketonuria or other aminoacidopathies (see Chap. Another interesting association of familial spastic paraplegia is with progressive cerebellar ataxia. Fully one-third of the cases that we have seen with such a spastic weakness were also ataxic and would fall into the category of spinocerebellar degenerations. Yet another variant of this group of diseases has been described by Farmer and colleagues; the inheritance in their cases was autosomal dominant, and the main clinical features were deafness and dizziness, ataxia, chorea, seizures, and dementia, evolving in that order. Postmortem examinations of two patients disclosed calcification in the globus pallidus, neuronal loss in the dentate nuclei, and destruction of myelinated fibers in the centrum semiovale. Adult Polyglucosan Body Disease Under this title, Robitaille and colleagues have described a distinct type of progressive neurologic disease in adults characterized clinically by spasticity, chorea, dementia, and a predominantly sensory polyneuropathy. Structures that closely resembled Lafora bodies and corpora amylaceae were found in large numbers in both central and peripheral neural processes (mainly in axons) and also in astrocytes. The dementia appears to be relatively mild, consisting of impairment of retentive memory, dysnomia, dyscalculia, and sometimes expressive dysphasia and deficits of "visual integration"; this was overshadowed by the rigidity and spasticity of the limbs and the peripheral nerve disorder. The finding of polyglycosan axon inclusion in biopsied nerve confirms the diagnosis. In his words, it is characterized by "involuntary tremulous motion, with lessened muscular power, in parts not in action and even when supported; with a propensity to bend the trunk forward, and to pass from a walking to a running pace, the senses and intellect being uninjured. As a rule, it begins between 40 and 70 years of age, with the peak age of onset in the sixth decade. It is infrequent before 30 years of age, and most series contain a somewhat larger proportion of men. Trauma, emotional upset, overwork, exposure to cold, "rigid personality," and so on, are among many factors that have been suggested over the years as predisposing to the disease, but there is no convincing evidence to support any such claims. A possible relationship to repeated cerebral trauma and to the "punch-drunk" syndrome (dementia pugilistica, page 863) has been particularly problematic and is unresolved despite several celebrated cases (Lees). Idiopathic Parkinson disease is observed in all countries, all ethnic groups, and all socioeconomic classes, although the incidence in African Americans is only one-quarter that in whites. The disease is frequent in North America, where there are approximately 1 million patients, constituting about 1 percent of the population over the age of 65 years. The incidence in all European countries where vital statistics are kept is similar. Genetic Aspects Considering its frequency, coincidence in a family on the basis of chance occurrence might be as high as 5 percent. These data suggest a more substantial role for an inherited trait in cases of ostensibly sporadic disease (see below regarding the Parkin mutations). Also, Kruger and colЁ leagues have reported a 13-fold increased susceptibility to the disease in patients who harbor a combination of certain -synuclein and apolipoprotein E genotypes, but this awaits confirmation. While familial cases are decidedly rare (Table 39-2), Golbe and colleagues advanced the understanding of the genetic underpinning of the disease by describing two large kindreds (probably related and originating from a small town in southern Italy) in which 41 patients in four generations were affected. The illness in their cases was characteristic of Parkinson disease both clinically and pathologically, the only unusual features being a somewhat earlier onset (mean age 46 years), a relatively rapid course (10 years from onset to death), and a low incidence of tremor (only 8 of the 41 patients).

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This requires that sensory thresholds heart attack people order cheapest avalide and avalide, particularly in the feet and legs blood pressure under stress purchase 162.5mg avalide with amex, always be assessed in relation to age standards. The effect of aging is most evident in relation to vibratory sense, but proprioception, as well as the perception of touch, and fast pain are also diminished with age. Receptors in the skin and special sense organs (taste, smell) also wither with age. Terminology (See also Table 8-1) A few additional terms require definition, since they may be encountered in discussions of sensation. Anesthesia refers to a complete loss and hypesthesia to a partial loss of all forms of sensation. Loss or impairment of specific cutaneous sensations may be indicated by an appropriate prefix or suffix. Careful testing will demonstrate an elevated threshold to tactile, painful, or thermal stimuli; but once the stimulus is perceived, it may have a severely painful or unpleasant quality (hyperpathia). Some clinicians use this last term to denote an exaggerated response to a painful stimulus (hyperalgesia which is subtly different from hyperpathia). In alloesthesia, or allesthesia, a tactile or painful stimulus delivered on the side of hemisensory loss is experienced in a corresponding area of the opposite side or at a distant site on the same side. This phenomenon is observed most frequently with right-sided putaminal lesions (usually hemorrhage) and with anterolateral lesions of the cervical spinal cord; it presumably depends on the existence of an uncrossed ipsilateral spinothalamic pathway (see the original studies of Ray and Wolff). However, a cooperative patient may, if asked to use a pin or his fingertips, outline an analgesic or anesthetic area or determine whether there is a graduated loss of sensation in the distal parts of a leg or arm. Finally, the findings of the sensory examination should be accurately recorded on a chart by shading affected regions on a preprinted figure of the body or a sketch of a hand, foot, face, or limb. With attention to certain details of procedure, these tests are quite sufficient for most clinical purposes. For clinical investigation and research into the physiology of pain, which require the detection of threshold values and quantification of sensory impairment, a wide range of instruments are available. Their use has been described by Dyck et al (see also Lindblom and Ochoa and Bertelsmann et al). The patient is first acquainted with the nature of the stimulus by applying it to a normal part of the body. Then, with eyes closed, he are asked to say "yes" each time various other parts are touched. A patient who is simulating sensory loss may say no in response to a tactile stimulus. Cornified areas of skin, such as the soles and palms, will require a heavier stimulus than other areas and the hair-clad parts a lighter one because of the numerous nerve endings around the follicles. Patients will be more sensitive to a moving contactual stimulus of any kind than to a stationary one. By this method, a stimulus of constant strength can be applied and the threshold for tactile sensation determined by measuring the force required to bend a hair of known length. Special difficulties arise in the testing of tactile perception, when a series of contactual stimuli lead to a decrement of sensation, either through adaptation of the end organ or because the initial sensation outlasts the stimulus and seems to spread. The patient may then fail to report tactile stimuli in an area where they were previously present, or he may report contact without being touched. Testing of Pain Perception this is most efficiently assessed by pinprick, although it may be evoked by a variety of noxious stimuli. Patients must understand that they are to report the feeling of sharpness, not simply the feeling of contact or pressure of the pinpoint. If pinpricks are applied rapidly in one area, their effect may be summated and a heightened perception of pain may result; therefore they should be delivered about one per second and not over the same spot. An effective approach is to ask the patient to compare the pin sensation in two areas on a scale of 1 to 10; a report of "8 or 9" as compared to "10" is usually insignficant. It is almost impossible, using an ordinary pin, to apply each stimulus with equal intensity. A pinwheel is sometimes more effective because it allows the application of a more constant pressure. This difficulty can be overcome to some extent by the use of an algesimeter, which enables one to deliver stimuli of constant intensity and also to grade the intensity and determine threshold values.

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