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By: John Walter Krakauer, M.A., M.D.

  • Director, the Center for the Study of Motor Learning and Brain Repair
  • Professor of Neurology

https://www.hopkinsmedicine.org/profiles/results/directory/profile/9121870/john-krakauer

The result is that the cycle is shortened (or hypertension frequent urination order perindopril 8mg amex, said another way quercetin high blood pressure medication effective perindopril 8 mg, the clock advances) blood pressure youth purchase perindopril paypal. Much remains to blood pressure jadakiss lyrics order perindopril online be explored, including the mechanisms by which the proteins affect the physiology and behavior of the organism. In any case, per and tim are only part of a larger story of biological rhythms, because various rhythms can be uncoupled. For example, rearing flies in continuous bright light completely obliterates the circadian rhythm of emergence of adults illustrated in Figure 17. Although circadian rhythms are extremely widespread, the mechanism of control differs from one species of organism to the next. Mammals also have pronounced circadian rhythms that govern, among other physiological states, the sleep cycle. The phenomenon of jet lag results from the time needed to adjust the sleep cycle after a change of time zone. A mutation called tau in the hamster results in a short 20-hour cycle rather than the normal 23. Prion proteins were originally discovered through their ability to act as infectious agents in the transmission of any of a number of serious neurological diseases. Produced initially as a precursor protein of 253 amino acids, the mature prion protein is found on the surface of neurons and glial cells in the brain. However, that it plays an important role in circadian regulation is supported by the observation that, in transgenic mice produced by genetic engineering (Section 9. Both of these conditions are marked by a mid-life age of onset and by progressive ataxia (loss of control of movement) and dementia (literally, "out of mind"), but their clinical symptoms differ somewhat. In both diseases, parts of the brain lose their normal histology and become full of holes (technically, spongiform encephalopathy). For example, injection of a chimpanzee with prion protein from a Page 724 Table 17. Other infectious diseases once attributed to transmission of a "slow virus" are now known to have prions as the active agent (Table 17. One example is kuru, discovered originally among the Fore people of Papua New Guinea who practiced ritual cannibalism as a rite of mourning in which the brain of the dead was handled and eaten, particularly by the women and children. Another example is scrapie, the equivalent prion-protein disease in sheep and goats, so called because the diseased animal is so intolerably itchy that it rubs and scrapes against any convenient object. A third example is "mad cow disease" (technically, bovine spongiform encephalopathy), whose identification as a prion-protein defect resulted in an eruption of near hysteria over the importation of British beef into Europe. Although the transmissible prion agent is thought to be a protease-resistant, insoluble form of the protein derived from the normal protease-sensitive protein, it is not clear whether the transmissible protein should be regarded as a truly infectious agent or merely as a cytotoxic metabolite. Birds and mammals are especially adept at modifying their behavior in response to environmental cues and previous experiences. Although learning of sorts can be demonstrated in organisms such as Drosophila, the ability is most highly developed in birds and mammals-particularly in human beings and higher primates. Partly because of the importance of learning in human beings, and partly because of its intrinsic interest, psychologists and geneticists have tried to assess the genetic contribution to learning ability in various organisms. Artificial Selection for Learning Ability Selection experiments for learning ability were some of the earliest studies in behavior genetics in animals. In these experiments, the animal is introduced into one end of a maze and must make its way to the other end to find a reward. One apparatus for testing the maze-learning ability of laboratory rats is illustrated in Figure 17. For an animal that has previous experience in getting through the maze, the number of wrong turns ("errors") is a measure of the extent to which the animal has learned the layout of the maze. Artificial selection for better maze-learning ability is carried out by choosing superior learners as the parents in each generation; for poorer maze-learning ability, inferior learners are chosen as parents. The results of 21 generations of selection for better or poorer mazelearning ability are shown in Figure 17. The initial population was a large, genetically heterogeneous strain of laboratory rats. The "maze-bright" population was selected for better learning, and the "maze-dull" population for poorer learning. Each data point gives the average number of errors made by the animals in each population after the same number of learning trials. Those rats that performed best (that is, made the fewest errors after a given number of trials) were mated among themselves to form a "maze-bright" selected line, and in each generation, selection was carried out within this line for the brightest animals. Similarly, those rats that performed worst (made the most errors) were mated among themselves to form a "maze-dull" line, and in each generation, the dullest of the dull were selected to perpetuate the line. By generation 2, there was virtually no overlap in learning ability between the two lines; the dullest "brights" were about equal in maze-learning ability to the brightest "dulls. Crosses between the 'bright" and "dull" lines produced an F1 generation that was intermediate in maze-learning ability. Additional crosses revealed that maze learning is inherited as a typical multifactorial trait of the sort discussed in Chapter 16. First, there was no control experiment consisting of a randomly mated population, unselected for maze-learning ability, established from the same initial population as the selected lines and main-tained with the same population size as the selected lines. An unselected control is necessary to detect possible systematic changes in the environment in the course of the selection. A better set of experiments would have included at least two "bright" selected lines, at least two "dull" selected lines, and at least one unselected control line. The replication is necessary to assess the reproducibility of the result in independently selected populations. Nevertheless, in spite of the technical limitations, the experiments in Figure 17. In the absence of genetic variation, the divergence between the selected lines would be impossible. Roughly speaking, it is the proportion of the total variance in phenotype that is transmitted from parents to offspring. For example, the selected populations differed in their maze-learning ability depending on whether the rats were motivated by hunger or by escape from water. The maze-bright animals learned better than the maze-dull animals when motivated by hunger (the condition in which the selection was carried out), but the maze-dull rats actually learned better than the maze-bright rats when tested in a situation in which getting through the maze allowed them to escape from immersion in water. Furthermore, the maze-bright rats were more active than the maze-dull rats when in mazes, but they were less active than the maze-dull rats when in exercise wheels. The differences between the strains were varied and complex, and it is not clear which of the differences may have been related to maze learning in a causal sense and which were fortuitous differences. Indeed, it is not even clear that the maze-bright rats were in any sense "smarter" than the maze-dull rats. The maze-bright rats may simply have responded better to the specific maze learning test situation. Genotypeenvironment interaction means that the relative performance of different genotypes changes drastically according to the environment. In another set of maze-learning experiments, the bright and dull rats from the thirteenth generation of an experiment like that in Figure 17. An "enriched" environment having cage walls decorated with designs in luminous paint and containing ramps, mirrors, swings, polished balls, marbles, barriers, slides, tunnels, bells, teeter-totters, and springboards-all constructed so that they could be easily shifted to new positions. A "restricted" environment having cages surrounded by drab, gray walls and containing only food and water pans. The maze-learning ability of the rats reared in these three environments is summarized in Figure 17. This difference is expected, because the normal environment is the one in which the selection experiments were carried out. The genotype-environment interaction is observed in the enriched and the restricted environments. Therefore, the difference in maze-learning ability is much diminished in the enriched environment. The result is that in the restricted environment, the maze-learning ability of both strains is approximately equal. The principal conclusion from these experiments is that, though the maze-bright and maze-dull strains certainly differ in genetic factors affecting maze learning, the magnitude of the difference between the strains results as much from their rearing environment as from their difference in genotype.

An exchange event between homologous chromosomes blood pressure chart dental treatment generic 4 mg perindopril mastercard, crossingover pulse pressure classification 4 mg perindopril for sale, results in the recombination of genes in the homologous chromosomes heart attack by one direction buy perindopril 8 mg free shipping. The probability of crossing-over between any two genes serves as a measure of genetic distance between the genes and makes possible the construction of a genetic map blood pressure quickly lower buy 8 mg perindopril visa, a diagram of a chromosome showing the relative positions of the genes. The genetic mapping of linked genes is an important research tool in genetics because it enables a new gene to be assigned to a chromosome and often to a precise position relative to other genes within the same chromosome. Genetic mapping is essential in human genetics for the identification of genes associated with hereditary diseases, such as the genes whose presence predisposes women carriers to the development of breast cancer. When the genes are on different chromosomes, the expected gametes from the Aa Bb parent are as shown in Figure 4. An expected 50 percent of the testcross progeny result from gametes with the same combination of alleles present in the parents of the double heterozygote (parental combinations), and 50 percent result from gametes with new combinations of the alleles (recombinants). In either case, with independent assortment, the genotypes of the testcross progeny are expected in the ratio of 1: 1: 1: 1. In this chapter, we will examine phenomena that cause deviations from this expected ratio. In his early experiments with Drosophila, Morgan found mutations in each of several X-linked genes that provided ideal materials for studying the inheritance of genes in the same chromosome. One of these genes, with alleles w+ and w, determined normal red eye color versus white eyes, as discussed in Chapter 3; another such gene, with the alleles m+ and m, determined whether the size of the wings was normal Page 125 or miniature. The initial cross was between females with white eyes and normal wings and males with red eyes and miniature wings. We will use the slash in this instance to help us follow these X-linked traits: the resulting F1 progeny consisted of wildtype females and white-eyed, nonminiature males. When these were crossed, the female progeny consisted of a 1: 1 ratio of red: white eyes (all were nonminiature), and the male progeny were as follows: Because each male receives his X chromosome from his mother, the phenotype reveals the genotype of the X chromosome that he inherited. The results of the experiment show a great departure from the 1: 1: 1: 1 ratio of the four male phenotypes expected with independent assortment. If genes in the same chromosome tended to remain together in inheritance but were not completely linked, this pattern of deviation might be observed. In this case, the combinations of phenotypic traits in the parents of the original cross (parental phenotypes) were present in 428/644 (66. The recombinant X chromosomes w+ m+ and w m result from crossing-over in meiosis in F females. In this 1 example, the frequency of recombination between the linked w and m genes was 33. The pairs of homologous chromosomes segregate at random with respect to one another, so an A-bearing chromosome is as likely to go to the same anaphase pole with a B-bearing chromosome as with a b-bearing chromosome. The result is that each possible combination of chromatids is equally likely among the gametes: 1/4 each for A B, A b, a B, and a b. Even genes in the same chromosome can undergo independent assortment (frequency of recombination equal to 50 percent) if they are sufficiently far apart. This implies the following principle: Genes with recombination frequencies smaller than 50 percent are present in the same chromosome (linked). Two genes that undergo independent assortment, indicated by a recombination frequency equal to 50 percent, either are in nonhomologous chromosomes or are located far apart in a single chromosome. This notation is a simplification of a more descriptive but cumbersome form: In this form of notation, the horizontal line separates the two homologous chromosomes in which the alleles of the genes are Page 126 located. The linked genes in a chromosome are always written in the same order for consistency. In the system of gene notation used for Drosophila, and in a similar system used for other organisms, this convention makes it possible to indicate the wildtype allele of a gene with a plus sign in the appropriate position. In one configuration, called the trans, or repulsion, configuration, the mutant alleles are in opposite chromosomes, and the genotype is written as w+/+ m (Figure 4. In the alternative configuration, called the cis, or coupling, configuration, the mutant alleles are present in the same chromosomes, and the genotype is written as w m/+ +. He also studied progeny from the cis configuration of the w and m alleles, which results from the cross of white, miniature females with red, non-miniature males: In this case, the F1 females were phenotypically wildtype double heterozygotes, and the males had white eyes and miniature wings. The difference is within the range expected from random variation from experiment to experiment. However, in this case, the phenotypes constituting the parental and recombinant classes of offspring are reversed. In the first cross, the F1 female was the trans double heterozygote (w +/+ m); in the second cross, the F1 female had the cis configuration (w m/+ +). The repeated finding of equal recombination frequencies in experiments of this kind leads to the following conclusion: Recombination between linked genes takes place with the same frequency whether the alleles of the genes are in the trans configuration or in the cis configuration; it is the same no matter how the alleles are arranged. The recessive allele y of another X-linked gene in Drosophila results in yellow body color instead of the usual gray color determined by the y+ allele. When white-eyed females were mated with males having yellow bodies, and the wildtype F1 females were testcrossed with yellow-bodied, white-eyed males, Page 127 the progeny were In a second experiment, yellow-bodied, white-eyed females were crossed with wildtype males, and the F1 wildtype females and F1 yellow-bodied, white-eyed males were intercrossed: In this case, 98. The parental and recombinant phenotypes were reversed in the reciprocal crosses, but the recombination frequency was virtually the same. However, the recombination frequency was much lower between the genes for yellow body and white eyes than between the genes for white eyes and miniature wings (1. These and other experiments have led to the following conclusions: • the recombination frequency is a characteristic of a particular pair of genes. In experiments with other genes, Morgan also discovered that Drosophila is unusual in that recombination does not take place in males. Although it is not known how (or why) crossing-over is prevented in males, the result of the absence of recombination in Drosophila males is that all alleles located in a particular chromosome show complete linkage in the male. For example, the genes cn (cinnabar eyes) and bw (brown eyes) are both in chromosome 2 but are so far apart that, in females, there is 50 percent recombination. Thus the cross yields progeny of genotype + +/cn bw and cn bw/cn bw (the nonrecombinant types) as well as cn +/cn bw and + bw/cn bw (the recombinant types) in the proportions 1: 1: 1: 1. However, because there is no crossing-over in males, the reciprocal cross yields progeny only of the nonrecombinant genotypes + + /cn bw and cn bw/cn bw in equal proportions. The absence of recombination in Drosophila males is a convenience often made use of in experimental design; as shown in the case of cn and bw, all the alleles present in any chromosome in a male must be transmitted as a group, without being recombined with alleles present in the homologous chromosome. The absence of crossing-over in Drosophila males is atypical; in most other animals and plants, recombination takes place in both sexes. The early geneticists understood that recombination between genes takes place by an exchange of Page 128 segments between homologous chromosomes in the process now called crossing-over. Each crossing-over is manifested physically as a chiasma, or cross-shaped configuration, between homologous chromosomes; chiasmata are observed in prophase I of meiosis (Chapter 3). Each chiasma results from the breaking and rejoining of chromatids during synapsis, with the result that there is an exchange of corresponding segments between them. The theory of crossing-over is that each chiasma results in a new association of genetic markers. The unit of distance in a genetic map is called a map unit; 1 map unit is equal to 1 percent recombination. For ease of reference, we list the four completely equivalent ways in which a genetic distance between two genes may be represented. Hence 1 percent recombination means that 1 meiotic cell in 50 has a crossover in the region between the genes. If one meiotic cell in 50 has a crossing-over, the frequency of crossing-over equals 1/50, or 2 percent. The correspondence of 1 percent recombination with 2 percent crossing-over is a little confusing until you consider that a crossover results in two recombinant chromatids and two nonrecombinant chromatids (Figure 4. A frequency of crossing-over of 2 percent means that of the 200 chromosomes that result from meiosis in 50 cells, exactly 2 chromosomes (the two involved in the exchange) are recombinant for genetic markers spanning the particular chromosome segment. To put the matter in another way, 2 percent crossing-over corresponds to 1 percent recombination because only half the chromatids in each cell with an exchange are actually recombinant. In situations in which there are genetic markers along the chromosome, such as the A, a and B, b pairs of alleles in Figure 4. The crossing-over does result in the physical exchange of segments between the innermost chromatids. However, because it is located outside the region between A and B, all of the resulting gametes must carry either the A B or a b allele combinations. The presence of the crossing-over is undetected because it is not in the region between the genetic markers. In some cases, the region between genetic markers is large enough that two (or even more) crossovers can be formed in a single meiotic cell.

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Lesions within the facial canal distal to blood pressure cuff amazon cheap perindopril american express the meatal segment cause both hyperacusis and ageusia; lesions in the facial canal between the nerve to heart attack 60 cheap 4 mg perindopril visa stapedius and the chorda tympani cause ageusia but no hyperacusis; lesions distal to heart attack 99 blockage order discount perindopril online the chorda tympani cause neither ageusia nor hyperacusis arteria dorsalis pedis purchase perindopril 8mg free shipping. Lesions of the cerebellopontine angle cause ipsilateral hearing impairment and corneal refiex depression (afferent limb of refiex arc affected) in addition to facial weakness. There is also a sensory branch to the posterior wall of the external auditory canal which may be affected resulting in local hypoaesthesia (Hitselberg sign). Causes of recurrent facial paresis of lower motor neurone type include • Diabetes mellitus • Lyme disease (neuroborreliosis, Bannwarth’s disease) • Sarcoidosis • Leukaemia, lymphoma In myasthenia gravis, a disorder of neuromuscular transmission at the neuromuscular junction, there may be concurrent ptosis, diplopia, bulbar palsy, and limb weakness and evidence of fatiguable weakness. Emotional facial paresis in temporal lobe epilepsy: its prevalence and lateralizing value. Clinically, facilitation may be demonstrated by the appearance of tendon refiexes which are absent at rest after prolonged (ca. The classic example, and probably the most frequently observed, is abducens nerve palsy (unilateral or bilateral) in the context of raised intracranial pressure, presumed to result from stretching of the nerve over the ridge of the petrous temporal bone. Fasciculations may also be induced by lightly tapping over a partially denervated muscle belly. Facial and perioral fasciculations are highly characteristic of spinal and bulbar muscular atrophy (Kennedy’s disease). Denervation of muscle fibres may lead to nerve fibre sprouting (axonal and collateral) and enlargement of motor units which makes fasciculations more obvious clinically. Fasciculations may be seen in: • Motor neurone disease with lower motor neurone involvement. This pattern has been observed in progressive supranuclear palsy and 139 F Fatigue with globus pallidus lesions, and contrasts with the ‘slow’ micrographia, meaning writing which becomes progressively slower and smaller, as seen in idiopathic Parkinson’s disease. Cross Reference Micrographia Fatigue the term fatigue may be used in different contexts to refer to both a sign and a symptom. This most characteristically occurs in disorders of neuromuscular junction transmission. A gradual decline in the amplitude and speed of initiation of voluntary movements, hypometria and hypokinesia, as seen in disorders of the basal ganglia, especially Parkinson’s disease, may also be described as fatigue. Fatigue may be evaluated with various instruments, such as the Krupp Fatigue Severity Score. Cross Reference Lasegue’s sign Fencer’s Posture, Fencing Posture Epileptic seizures arising in or involving the supplementary motor area may lead to adversial head and eye deviation, abduction and external rotation of the contralateral arm, fiexion at the elbows, and posturing of the legs, with maintained consciousness, a phenomenon christened by Penfield as the ‘fencing posture’ because of its resemblance to the en garde position. A similar phenomenon may be observed if the patient is pulled backwards (retropulsion). It is less common in symptomatic causes of parkinsonism, but has been reported, for example, in aqueduct stenosis. Finger agnosia is most commonly observed with lesions of the dominant parietal lobe. It may occur in association with acalculia, agraphia, and right– left disorientation, with or without alexia and difficulty spelling words, hence as one feature of Gerstmann syndrome. Isolated cases of finger agnosia in association with left corticosubcortical posterior parietal infarction have been reported. It follows non-dominant (right) hemisphere lesions and may accompany emotional dysprosody of speech. Paradoxical pupillary phenomena: a review of patients with pupillary constriction to darkness. This type of behaviour may be displayed by an alien hand, most usually in the context of corticobasal degeneration. Forced groping may be conceptualized as an exploratory refiex which is ‘released’ from frontal lobe control by a pathological process, as in utilization behaviour. Forced upgaze may also be psychogenic, in which case it is overcome by cold caloric stimulation of the ear drums. Cross Reference Oculogyric crisis Forearm and Finger Rolling the forearm and finger rolling tests detect subtle upper motor neurone lesions with high specificity and modest sensitivity. There is no language disorder since comprehension of spoken and written language is preserved; hence it is qualitatively different from Broca’s aphasia. The appearance is a radial array likened to the design of medieval castles, not simply of battlements. The visions of Hildegard von Bingen (1098–1179), illustrated in the twelfth century, are thought possibly to refiect migrainous fortification spectra. Cross References Aura; Hallucination; Photopsia; Teichopsia Foster Kennedy Syndrome the Foster Kennedy syndrome consists of optic atrophy in one eye with optic disc oedema in the other eye, Anosmia ipsilateral to optic atrophy may also be found. Similar clinical appearances may occur with sequential anterior ischaemic optic neuropathy, sometimes called a pseudo-Foster Kennedy syndrome. Retrobulbar neuritis as an exact diagnostic sign of certain tumors and abscesses in the frontal lobe. This is one of the unpredictable motor fiuctuations in late Parkinson’s disease (associated with longer duration of disease and treatment) which may lead to falls, usually forward onto the knees, and injury. Two variants are encountered, occurring either during an off period or wearing off period, or randomly, i. Treatment strategies include use of dopaminergic agents and, anecdotally, L-threodops, but these agents are not reliably helpful, particularly in random freezing. The term is also sometimes used for weakness of little finger adduction (palmar interossei), evident when trying to grip a piece of paper between the ring and little finger. Other phenomena associated with frontal lobe pathology include imitation behaviours (echophenomena) and, less frequently, utilization behaviour, features of the environmental dependency syndrome. Cross References Abulia; Akinesia; Akinetic mutism; Alternating fist closure test; Apathy; Attention; Disinhibition; Dysexecutive syndrome; Emotionalism, Emotional lability; Fist-edge-palm test; Frontal release signs; Hypermetamorphosis; Hyperorality; Hyperphagia; Hypersexuality; Incontinence; Perseveration; Utilization behaviour; Witzelsucht Frontal Release Signs Frontal release signs are so named because of the belief that they are released from frontal inhibition by diffuse pathology within the frontal lobes (usually vascular or degenerative) with which they are often associated, although they may be a feature of normal ageing. Some of these responses are present during infancy but disappear during childhood, hence the terms ‘primitive refiexes’ or ‘developmental signs’ are also used (Babinski’s sign may therefore fall into this category). The term ‘psychomotor signs’ has also been used since there is often accompanying change in mental status. The frontal release signs may be categorized as: • Prehensile: Sucking refiex (tactile, visual) Grasp refiex: hand, foot Rooting refiex (turning of the head towards a tactile stimulus on the face) • Nociceptive: Snout refiex Pout refiex Glabellar (blink) refiex Palmomental refiex the corneomandibular and nuchocephalic refiexes may also be categorized as ‘frontal release’ signs. Fugue may be: • Psychogenic: associated with depression (sometimes with suicide); alcoholism, amnesia; ‘hysteria’ • Epileptic: complex partial seizures • Narcoleptic Some patients with frontotemporal dementia may spend the day walking long distances, and may be found a long way from home, unable to give an account of themselves, and aggressive if challenged; generally they are able to find their way home (spared topographical memory) despite their other cognitive deficits. Cross References Amnesia; Automatism; Dementia; Poriomania; Seizures Functional Weakness and Sensory Disturbance Various signs have been deemed useful indicators of functional or ‘non-organic’ neurological illness, including • Collapsing or ‘give way’ weakness • Hoover’s sign • Babinski’s trunk–thigh test • ‘Arm drop’ • Belle indifference • Sternocleidomastoid sign • Midline splitting sensory loss • Functional postures, gaits: monoplegic ‘dragging’ fiuctuation of impairment 152 Funnel Vision F excessive slowness, hesitation ‘psychogenic Romberg’ sign ‘walking on ice’ uneconomic posture, waste of muscle energy. How to identify psychogenic disorders of stance and gait: a video study in 37 patients. Depressing the tongue with a wooden spatula, and the use of a torch for illumination of the posterior pharynx, may be required to get a good view. There is a palatal response (palatal refiex), consisting of upward movement of the soft palate with ipsilateral deviation of the uvula; and a pharyngeal response (pharyngeal refiex or gag refiex) consisting of visible contraction of the pharyngeal wall. Some studies claim that the refiex is absent in many normal individuals, especially with increasing age, without evident functional impairment; whereas others find it in all healthy individuals, although variable stimulus intensity is required to elicit it. Some argue that absence of the refiex does not predict aspiration and is of little diagnostic value, since this may be a normal finding in elderly individuals, whereas pharyngeal sensation (feeling the stimulus at the back of the pharynx) is rarely absent in normals and is a better predictor of the absence of aspiration. Cross References Bulbar palsy; Dysphagia Gait Apraxia Gait apraxia is a name given to an inability to walk despite intact motor systems and sensorium. These phenomena may be observed with lesions of the frontal lobe and white matter connections, with or without basal ganglia involvement, for example, in diffuse cerebrovascular disease and normal pressure hydrocephalus. In modern classifications of gait disorders, gait apraxia is subsumed into the categories of frontal gait disorder, frontal disequilibrium, and isolated gait ignition failure. Gait apraxia is an important diagnosis to establish since those affiicted generally respond poorly, if at all, to physiotherapy; moreover, because both patient and therapist often become frustrated because of lack of progress, this form of treatment is often best avoided. The neuroanatomical substrates of such decision-making are believed to encompass the prefrontal cortex and the amygdala. Gambling may be defined as pathological when greater risks are taken and potential losses are correspondingly greater; this may be classified as an impulse control disorder. This may occur in psychiatric 156 Gaze Palsy G disease such as depression, schizophrenia, and malingering, and sometimes in neurological disease (head injury, epilepsy). Affiicted individuals may also demonstrate paroxysmal hyperpnoea and upbeating nystagmus, suggesting a brainstem (possibly pontine) localization of pathology. Preservation of the vestibulo-ocular refiexes may help differentiate supranuclear gaze palsies from nuclear/infranucelar causes. However, this is not a form of impaired muscle relaxation akin to myotonia and paramyotonia. For instance, when lifting the legs by placing the hands under the knees, the legs may be held extended at the knees despite encouragement on the part of the examiner for the patient to fiex the knees.

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This type of bladder produces symptoms of urinary frequency hypertension jnc 6 generic perindopril 2 mg amex, urgency pomegranate juice blood pressure medication perindopril 4 mg on line, dribbling and/or incontinence pulse pressure 25 generic perindopril 2 mg without a prescription. This produces symptoms of urinary frequency blood pressure chart when to go to the hospital buy line perindopril, urgency, dribbling, hesitancy and incontinence. Because urine stays in the bladder longer than it ought to, the bladder is prone to infection. Notice that the symptoms of either small or big bladder dysfunction (frequency, urgency, dribbling, incontinence) are similar, so it is not possible to tell, simply on the basis of symptoms, which kind of bladder dysfunction is present. Incoordinated Bladder the third type of bladder problem is the incoordinated bladder (a fancier name is detrusor sphincter dyssynergia). Here, either the sphincter remains closed when the bladder wall contracts, creating a sense of urgency followed by hesitancy in voiding, or the bladder wall relaxes while the sphincter stays open, causing dribbling, incontinence and overflling of the bladder. However, bladder infections, which sometimes spread to the kidneys and even the blood, occur frequently and require prompt investigation and appropriate treatment, including antibiotics. A key way is to 62 the Facts You Need, Fifth Edition fnd out how much urine remains in the bladder after voiding (called the “post-void residual”), either by doing an ultrasound of the bladder at that time or draining it with a catheter (thin hollow tube). If there is a lot (more than 100 cc), you have a faccid big bladder; if there is less than 100 cc, you have a normal or a small spastic bladder. These include oxybutynin, tolterodine, solifenacin succinate, propantheline, favoxate, imipramine and mirabegron. They lengthen the intervals between urinations and decrease the sense of urgency, giving you more time to reach the bathroom and to avoid dribbling and incontinence. To even out the blood levels, some, such as oxybutynin, can be applied as a skin patch. Other approaches to the spastic bladder that can sometimes show great effect include injections of botulinum toxin to specific regions of the muscles surrounding its outlet or even into the wall of the bladder itself. In mild cases, a method that helps you to empty the bladder more completely is the Crede maneuver of bladder massage. After you’ve voided as much urine as possible naturally, you apply downward pressure to the lower abdomen with both hands while bearing down. This technique can be performed only when you’re sitting, which requires a change in behavior for men. If the bladder cannot be emptied suffciently using the Crede maneuver, intermittent self-catheterization may be necessary. A small tube (catheter) is inserted through the urethra (the canal through which urine is discharged) into the bladder to allow the urine to drain. This is much easier to do than it sounds, and it the Facts You Need, Fifth Edition 63 poses very little risk of damage, particularly in women, who tend to have a short urethra. It enables you to decide when to empty the bladder, and thus avoid dribbling or incontinence. Timing varies from person to person, but usually it need not be done more than about every 4 to 6 hours. Medications such as oxybutynin are sometimes used with self-catheterization, to relax the bladder and allow it to fll more completely and to decrease dribbling and incontinence between catheterizations. Self-catheterization also allows a stretched bladder wall to gradually shrink back to normal size and, sometimes, function. The problem with self-catheterization is that you have to have suffcient arm control to insert the tube into the bladder. Chronic use of a Foley catheter carries a signifcant risk of urinary tract infections, so physicians insert it only when absolutely necessary. A permanent in-dwelling catheter has to be changed about once every month by a nurse. A condom catheter—which fts over the penis, like a condom, and is connected by a tube to a collecting bag—may be useful for men, but it will help only if the bladder empties itself automatically. Unfortunately, female condom catheters tend to fall off, and to date are not reliable enough for use. An uncoordinated bladder may result in either too little or too much urine left in the bladder after urination. If there is too little urine, bladder-inhibiting medication such as oxybutynin, propantheline, favoxate or imipramine will be necessary. The examination may be combined with a cystoscopy, in which the urologist inserts a small telescope into the bladder to look at the walls. Alpha blockers were originally developed to treat high blood pressure, but they can also help the bladder work in a slightly more coordinated fashion. Clonidine and terazosin are alpha blockers that are sometimes used to try to improve coordination and increase bladder control. A hormone medication called desmopressin mimics a brain hormone that decreases urine formation in the kidneys and therefore lowers the probability of waking up in a wet bed: it is safest when used as a pill. Other people beneft from imipramine or oxybutynin taken just before bed, to let the bladder fll up more at night. The faccid bladder fails to empty completely and bacteria grow in the remaining urine. Intermittent self-catheterization may introduce bacteria into the bladder, producing infection. Women have a shorter urethra than men and are more prone to develop bladder infections because bacteria can reach the bladder more easily. The presence of bacteria does not mean that the infection requires treatment—anyone with an in-dwelling Foley catheter will test positive for bacteria. But antibiotic treatment is called for when there is urinary frequency or urgency, burning or discomfort when urinating, fever or foul smelling urine. Blood or mucus in the urine also suggests the need for the Facts You Need, Fifth Edition 65 treatment. Intravenous antibiotics are necessary only for severe infections accompanied by fever and malaise. Tips for preventing bladder infections • Empty the bladder completely, using self-catheterization techniques if necessary. Make the urine more acidic by drinking cranberry juice or taking high doses of vitamin C (1,000 to 4,000 mg a day), to retard bacterial growth. If you have a history of urinary tract infections, ask your physician about low-dose antibiotics. If you stop early because you’re feeling better, any remaining bacteria will re-invade and cause problems again. When the rectum, which constitutes the last 5 or 6 inches (12 to 15 cm) of gastrointestinal tract, flls with stool, a “flled” signal is sent to the brain. If the time is appropriate, the external sphincter of the anus relaxes so a bowel movement can occur. If the time is not appropriate, the external sphincter constricts to delay the bowel movement. As in urination, relaxation of the external sphincter is what sets the process in motion. As well, weakness, spasticity or fatigue may signifcantly limit physical activity, which in turn slows bowel activity and causes constipation. Some medicines taken for other problems such as bladder frequency or depression may also slow the bowel. How to Manage Constipation • Drink adequate amounts of liquid (eight to twelve glasses daily). It softens the stool and decreases the amount of time required for the stool to pass through the intestinal tract. Sources include whole-grain breads and cereals, fruits and vegetables, nuts, seeds and beans. But don’t incorthe Facts You Need, Fifth Edition 67 porate high-fber foods too quickly or they may produce gas and, occasionally, diarrhea. Select the time that is most convenient for having a bowel movement—usually shortly after a meal, since the bowel is normally more active then. Drink a cup of hot or lukewarm coffee, tea or water; it frequently encourages a bowel movement. Schedule 15 to 20 minutes of uninterrupted time daily for this activity, and stick to the routine, even if it proves diffcult initially. There is a long list, ranging from mild bulk-forming agents based on fber, through stronger oral stimulants like milk of magnesia, to suppositories and rectal stimulants (enemas). High-fber foods help constipation For a healthy bowel, include in your daily diet: • one serving of fruit (with the skin left on) or vegetable, cooked, raw or dried • one-half to one serving of whole wheat or rye bread or fruit juice • one serving (1 tablespoon/15 mL) of bran, nuts or seeds.

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