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Thus, strictly speaking, in some cases the damage done by these lesions may be more ``metabolic' than structural. On the other hand, subarachnoid hemorrhage and bacterial meningitis are among the most acute emergencies encountered in evaluating comatose patients, and for that reason this class of disorders is considered here. Subarachnoid Hemorrhage Subarachnoid hemorrhage, in which there is little if any intraparenchymal component, is usually due to a rupture of a saccular aneurysm, although it can also occur when a superficial arteriovenous malformation ruptures. Saccular aneurysms occur throughout life, generally at branch points of large cerebral arteries, such as the origin of the anterior communicating artery from the anterior cerebral artery; the origin of the posterior communicating artery from the posterior cerebral artery; the origin of the posterior cerebral artery from the basilar artery; or the origin of the middle cerebral artery from the internal carotid artery. Microscopic examination discloses an incomplete elastic media, which results in an aneurysmal dilation that may enlarge with time. Some ruptures are presaged by a severe headache, a so-called sentinel headache,56,57 presumably resulting from sudden dilation or leakage of blood from the aneurysm. Occasionally an aneurysm of the posterior communicating artery compresses the adjacent third nerve causing ipsilateral pupillary dilation. For this reason, new onset of anisocoria even in an awake patient is considered a medical emergency until the possibility of a posterior communicating artery aneurysm is eliminated. If the hemorrhage is sufficiently large, the sudden pressure wave, as intracranial pressure approximates arterial pressure, may result in impaired cerebral blood flow and loss of consciousness. About 12% of patients with subarachnoid hemorrhage die before reaching medical care. The cause of the behavioral impairment after subarachnoid hemorrhage is not well understood. It is believed that the blood excites an inflammatory response with cytokine expression that may diffusely impair brain metabolism as well as cause brain edema. A 66-year-old man was brought to the Emergency Department after sudden onset of a severe global headache with nausea and vomiting. She did not offer a history of headache, but upon being asked, the patient did admit that she had one. On examination the neck was stiff, but the neurologic examination showed only lethargy and inattention. Lumbar puncture yielded bloody fluid, with 23,000 red blood cells and 500 white blood cells. A cerebral angiogram demonstrated a saccular aneurysm at the junction of the internal carotid and middle cerebral arteries on the right. Signs that suggest that the blood was present before the tap include the persistence of the same number of red cells in tubes 1 and 4, or the presence of crenated red blood cells and/or xanthochromia if the hemorrhage is at least several hours old. Specific Causes of Structural Coma 131 Even in those patients who are not comatose on admission, alterations of consciousness may develop in the ensuing days. Deterioration may occur due to rebleeding, which is particularly common in the first 24 to 48 hours. This delayed cerebral ischemia may result in brain infarction and further edema, thus exacerbating the impairment of consciousness. Acutely developing hydrocephalus66 from obstruction of spinal fluid pathways may also impair consciousness. The patient should be observed carefully for these complications and appropriate treatment applied. Leptomeningeal tumors include lymphomas and leukemias and solid tumors such as breast, renal cell, and lung cancers, as well as medulloblastomas and glial tumors. Many patients with meningeal carcinoma have impairment of consciousness that is difficult to explain on the basis of the distribution of the tumor cells. The diagnosis of subarachnoid tumor is challenging, particularly when the multilevel dysfunctions of the nervous system are the first signs of the tumor. If the scan is negative, the diagnosis is established by the presence of tumor cells77 or tumor markers78 in the spinal fluid. Meningitis can be either acute or chronic and can be caused by a variety of different organisms including bacteria, fungi, rickettsiae, and viruses. Neurologic signs and symptoms caused by meningitis vary depending on the acuity of the infection and the nature of the infecting organisms, but certain aspects are common to all. This is usually done via the bloodstream, and for this reason blood cultures will often identify the organism. Less commonly, meningitis is a result of spread of organisms from structures adjacent to the brain (sinusitis, otitis).
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Posturing responses include several stereotyped postures of the trunk and extremities. Most appear only in response to noxious stimuli or are greatly exaggerated by such stimuli. Seemingly spontaneous posturing most often represents the response to endogenous stimuli, ranging from meningeal irritation to an occult bodily injury to an overdistended bladder. The nature of the posturing ranges from flexor spasms to extensor spasms to rigidity, and may vary according to the site and severity of the brain injury and the site at which the noxious stimulation is applied. In addition, the two sides of the body may show different patterns of response, reflecting the distribution of injury to the brain. Clinical tradition has transferred the terms decorticate rigidity and decerebrate rigidity from experimental physiology to certain patterns of motor abnormality seen in humans. First, these terms imply more than we really know about the site of the underlying neuro- logic impairment. Even in experimental animals, these patterns of motor response may be produced by brain lesions of several different kinds and locations and the patterns of motor response in an individual to any one of these lesions may vary across time. In humans, both types of responses can be produced by supratentorial lesions, although they imply at least incipient brainstem injury. There is a tendency for lesions that cause decorticate rigidity to be more rostral and less severe than those causing decerebrate rigidity. In general, there is much greater agreement among observers if they simply describe the movements that are seen rather than attempt to fit them to complex patterns. Flexor posturing of the upper extremities and extension of the lower extremities corresponds to the pattern of movement also called decorticate posturing. The fully developed response consists of a relatively slow (as opposed to quick withdrawal) flexion of the arm, wrist, and fingers with adduction in the upper extremity and extension, internal rotation, and vigorous plantar flexion of the lower extremity. However, decorticate posturing is often fragmentary or asymmetric, and it may consist of as little as flexion posturing of one arm. Such fragmentary patterns have the same localizing significance as the fully developed postural change, but often reflect either a less irritating or smaller central lesion. The decorticate pattern is generally produced by extensive lesions involving dysfunction of the forebrain down to the level of the rostral midbrain. A similar pattern of motor response may be seen in patients with a variety of metabolic disorders or intoxications. For example, in the series of Jennett and Teasdale, after head trauma only 37% of comatose patients with decorticate posturing recovered. Some patients assume an opisthotonic posture, with teeth clenched and arching of the spine. Tonic neck reflexes (rotation of the head causes hyperextension of the arm on the side toward Examination of the Comatose Patient 75 which the nose is turned and flexion of the other arm; extension of the head may cause extension of the arms and relaxation of the legs, while flexion of the head leads to the opposite response) can usually be elicited. As with decorticate posturing, fragments of decerebrate posturing are sometimes seen. These tend to indicate a lesser degree of injury, but in the same anatomic distribution as the full pattern. It may also be asymmetric, indicating the asymmetry of dysfunction of the brainstem. Although decerebrate posturing usually is seen with noxious stimulation, in some patients it may occur spontaneously, often associated with waves of shivering and hyperpnea. Decerebrate posturing in experimental animals usually results from a transecting lesion at the level between the superior and inferior colliculi. The level of brainstem dysfunction that produces this response in humans may be similar, as in most cases decerebrate posturing is associated with disturbances of ocular motility. However, electrophysiologic, radiologic, or even postmortem examination sometimes reveals pathology that is largely confined to the forebrain and diencephalon. Thus, decerebrate rigidity is a clinical finding that probably represents dysfunction, although not necessarily destruction extending into the upper brainstem. Nevertheless, it represents a more severe finding than decorticate posturing; for example, in the Jennett and Teasdale series, only 10% of comatose patients with head injury who demonstrated decerebrate posturing recovered.
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Overdose Symptoms of hypermagnesaemia may include nausea, vomiting, flushing of the skin, thirst, hypotension due to peripheral vasodilatation, drowsiness, confusion, loss of tendon reflexes and respiratory depression due to neuromuscular blockade, slurred speech, double vision, muscle weakness, bradycardia, cardiac arrhythmias, coma, and cardiac arrest. Forms available from special-order manufacturers include: tablet, chewable tablet, capsule, oral suspension, oral solution, powder l Tablet Magnesium glycerophosphate (Non-proprietary) Magnesium (as Magnesium glycerophosphate) 97. With intravenous use For intravenous infusion, in persistent pulmonary hypertension of the newborn, dilute to a max. Phosphate infusion is occasionally needed in phosphate deficiency arising from use of parenteral nutrition deficient in phosphate supplements; phosphate depletion also occurs in severe diabetic ketoacidosis. It is difficult to provide detailed guidelines for the treatment of severe hypophosphatemia because the extent of total body deficits and response to therapy are difficult to predict. High doses of phosphate may result in a transient serum elevation followed by redistribution into intracellular compartments or bone tissue. It is recommended that severe hypophosphataemia be treated intravenously as large doses of oral phosphate may cause diarrhoea; intestinal absorption may be unreliable and dose adjustment may be necessary. Phosphate is not the first choice for the treatment of hypercalcaemia because of the risk of precipitation of calcium phosphate in the kidney and other tissues. Neonates Phosphate deficiency may occur in very low-birthweight infants and may compromise bone growth if not corrected. Some units routinely supplement expressed breast milk with phosphate, although the effect on the osmolality of the milk should be considered. Aluminium- containing preparations are rarely used as phosphate- binding agents and can cause aluminium accumulation. Sevelamer hydrochloride is licensed for the treatment of hyperphosphataemia in adults on haemodialysis or peritoneal dialysis. Although experience is limited in children sevelamer hydrochloride may be useful when hypercalcaemia prevents the use of calcium carbonate p. Absorption of aluminium from aluminium salts is increased by citrates, which are contained in many effervescent preparations (such as effervescent analgesics). In emergencies in intensive care faster rates may be used- seek specialist advice. For peripheral intravenous administration the concentration of potassium should not usually exceed 40 mmol/litre. Local policies on avoiding inadvertent use of potassium concentrate should be followed. The potassium content of some phosphate preparations may also limit the rate at which they may be administered. With oral use Administer dose (powder) in a small amount of water or honey-do not give with fruit juice or squash, which have a high potassium content. Local policies on avoiding inadvertent use of potassium chloride concentrate should be followed. With intravenous use Potassium chloride concentrate must be diluted with not less than 50 times its volume of sodium chloride intravenous infusion 0. For peripheral intravenous infusion, the concentration of potassium should not usually exceed 40 mmol/L. Higher concentrations of potassium chloride or faster infusion rates may be given in very severe depletion, but require specialist advice. Salt substitutes A number of salt substitutes which contain significant amounts of potassium chloride are readily available as health food products. Exceptionally, if potassium chloride concentrate is used for preparing an infusion, the infusion solution should 562 Metabolic disorders Ruthmol ). These should not be used by patients with renal failure as potassium intoxication may result. Modified-release preparations should be avoided unless effervescent tablets or liquid preparations inappropriate.
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Active vibration damping You know the problems that can be created by the tiniest vibrations. Enabling you to completely, and steadily, focus on what matters most: your treatment. When you require precise repositioning to reexamine previously visualized structures or when you need to align with a pre-mapped trajectory, making use of all six axes, the Robotic Visualization System delivers precise positioning at the push of a button. PositionMemory Save Move Recall When working on a tumor case, you may already have identified regions of concern where you want to protect the functional structure. Image-guided surgery Image with Brainlab Microscope Navigation Software Minimize time-consuming efforts in approaching challenging neurosurgical pathologies. With no way out, you might have to contend with uncomfortable working positions causing fatigue. They share the same high-resolution, digital image to follow the procedure with comparable fidelity. Efficient and effortless access to this comprehensive information is essential for treatment. During a Vestibular Schwannoma case, for instance, it can help identify the course of facial nerves. And, can support inspection of regions that are not directly visualized by a surgical microscope. Imagine being able to identify the blood flow in the tiniest blood vessels with an intraoperative angiogram during any vascular procedure. Or to visualize fluorescence-stained structures while viewing the anatomy in natural-like colors. In challenging neurosurgery, visualization adjuncts are essential for making the right decisions at the right time. For the indicative time: the Delay Map (or Summary Map) provides quick information about the time when the fluorescent signal appeared for each image point in the map. For a complete picture: the Diagram Function outlines assessment of fluorescence intensity variation over time and fast access to the key indicators for further analysis. For instance, removing video sequences with movement artefact, you can now generate a summary map without compromises. It is the first intraoperative fluorescence module to highlight the fluorescence-stained structures while visualizing non-stained tissue in its natural-like color. When we envisioned the all-new Robotic Visualization System, we conceived a design that can deliver so much more without losing its familiarity.
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Iron salts may be harmful and result in iron overload if given alone to patients with anaemias other than those due to iron deficiency. In most forms of sickle-cell disease, varying degrees of haemolytic anaemia are present accompanied by increased erythropoiesis; this may increase folate requirements and folate supplementation may be necessary. The beneficial effects of hydroxycarbamide may not become evident for several months. They are also susceptible to developing acute haemolytic anaemia when they eat fava beans (broad beans, Vicia faba); this is termed favism and can be more severe in children or when the fresh fava beans are eaten raw. Acute complications in the more severe forms include sickle-cell crisis, where infarction of the microvasculature and blood supply to organs results in severe pain. Sickle-cell crisis requires hospitalisation, intravenous fluids, analgesia and treatment of any concurrent infection. Chronic complications include skin ulceration, renal failure, and increased susceptibility to infection. These patients must be regarded as being at high risk of severe exacerbation of haemolysis following administration of any of the drugs listed below. Pyridoxine hydrochloride is indicated in both idiopathic acquired and hereditary sideroblastic anaemias. Although complete cures have not been reported, some increase in haemoglobin can occur with high doses. Reversible sideroblastic anaemias respond to treatment of the underlying cause but pyridoxine hydrochloride is indicated in pregnancy, haemolytic anaemias, or during isoniazid p. Corticosteroids have an important place in the management of haematological disorders including autoimmune haemolytic anaemia, idiopathic thrombocytopenias and neutropenias, and major transfusion reactions. They are also used in chemotherapy schedules for many types of lymphoma, lymphoid leukaemias, and paraproteinaemias, including multiple myeloma. Dapsone and other sulfones (higher doses for dermatitis herpetiformis more likely to cause problems). Primaquine (30 mg weekly for 8 weeks has been found to be without undue harmful effects in African and Asian people). Quinolones (including ciprofloxacin, moxifloxacin, nalidixic acid, norfloxacin, and ofloxacin). Erythropoietins Epoetins (recombinant human erythropoietins) are used to treat the anaemia associated with erythropoietin deficiency in chronic renal failure. There is insufficient information to support the use of erythropoietins in children with leukaemia or in those receiving cancer chemotherapy. Darbepoetin is a glycosylated derivative of epoetin; it persists longer in the body and can be administered less frequently than epoetin. Forms available from special-order manufacturers include: oral suspension Capsule Drugs used in hypoplastic, haemolytic, and renal anaemias Anabolic steroids, pyridoxine hydrochloride p. Severe reactions are common in the first 2 days and profound immunosuppression can occur; antilymphocyte immunoglobulin should be given under specialist supervision with appropriate resuscitation facilities. It is unlikely that dietary deprivation of pyridoxine hydrochloride produces clinically relevant haematological effects. The aim of treatment is to relieve symptoms of anaemia and to avoid the need for blood transfusion. The haemoglobin concentration should not be increased beyond that which provides adequate control of symptoms of anaemia. Pure red cell aplasia There have been very rare reports of pure red cell aplasia in patients treated with erythropoietins. In patients who develop a lack of efficacy with erythropoietin therapy and with a diagnosis of pure red cell aplasia, treatment with erythropoietins must be discontinued and testing for erythropoietin antibodies considered. Patients who develop pure red cell aplasia should not be switched to another form of erythropoietin. Other factors, such as iron or folate deficiency, that contribute to the anaemia of chronic renal failure should be corrected before treatment and monitored during therapy.
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Projecting this scenario to a range of radiogenic tumors in a genetically heterogeneous human population would tend to lead to a situation in which the balance between a certain set of tumor susceptibility (S) and resistance (R) loci in a given subgroup might serve to emphasize risk in a given set of organs. Equally, however, the balance of additional S and R locus combinations might provide a degree of resistance to the induction and development of cancer in other organs. Thus, with this first genetic scenario, major distortions of the distribution of overall cancer risk after radiation might not apply simply because different genetic susceptibilities would tend to "average out" across organs. By contrast, a second hypothetical scenario involves a small subset of common polymorphic loci that exert organ-wide effects on tumor susceptibility or resistance, which might be particularly strong in the specific instance of radiation exposure. In this instance, genetically determined distortion of the distribution of overall cancer risk might be expected. At present, the data available are insufficient to distinguish the likely contributions from these two genetic scenarios. Finally, the large study of cancer concordance in 90,000 Nordic twin pairs should be noted. Lichtenstein and colleagues (2000) and Hoover (2000) make some important points about the difficulties that exist in separating the genetic and environmental components of cancer. In essence, Hoover notes that this Nordic study, like others, is consistent with the presence of low-penetrance cancer-predisposing genes in the general population. However, the confidence intervals for the heritable component of cancers at common sites were wide-all ranged from around 5 to 50%. It was also pointed out that for cancer at common sites, the rate of concordance in monozygotic twins was generally less than 15%. Thus, the absolute risk of concordance of site-specific cancer in identical genotypes sharing some common environmental factors is rather low. In addition to this, a study based on the Swedish Family Cancer Database (Czene and others 2002) has provided further information on the genetic component of organ-specific cancer. With the exception of the thyroid, the environment appears to have the principal causal role for cancer at all sites. One important message that emerges from current data on cancer genes of low penetrance and the overall genetic component of cancer is that predictive genotyping of individuals for the purposes of radiological protection may not Copyright National Academy of Sciences. The data considered in this chapter did not reveal consistent evidence for the involvement of induced genomic instability in radiation tumorigenesis, although telomere-associated processes may account for some tumorigenic phenotypes. A further conclusion was that there is little evidence of specific tumorigenic signatures of radiation causation, but rather that radiation-induced tumors develop in a tumor-specific multistage manner that parallels that of tumors arising spontaneously. However, further cytogenetic and molecular genetic studies are needed to reduce current uncertainties about the specific role of radiation in multistage radiation tumorigenesis; such investigations would include studies with radiation-associated tumors of humans and experimental animals. However, since the induction or development of these two cancer types is believed to proceed via atypical mechanisms involving cell killing, it was judged that the threshold-like responses observed should not be generalized. Radiation-induced life shortening in mice is largely a reflection of cancer mortality, and the data reviewed generally support the concept of a linear dose-response at low doses and low dose rates. However, these data are difficult to interpret, and the implications for radiological protection remain most uncertain. Genetic Susceptibility to Radiation-Induced Cancer the review of cellular, animal, and epidemiologic or clinical studies on the role of genetic factors in radiation tumorigenesis shows that there have been major advances in understanding, albeit with some important knowledge gaps. An important conclusion is that many of the known, strongly expressing, cancer-prone human genetic disorders are likely to show an elevated risk of radiation-induced cancer, probably with a high degree of organ specificity. Cellular and animal studies suggest that the molecular mechanisms underlying these genetically determined radiation effects largely mirror those that apply to spontaneous tumorigenesis be feasible in the medium term. The likely involvement of multiple and relatively organ-specific sets of polymorphisms and gene-gene or gene-environment interactions makes the provision of meaningful judgments on risk most uncertain. For these reasons it may be more realistic at this stage of knowledge to focus attention on general patterns of generadiation interactions and their implications for population risk, rather than risk for specific individuals. Attention has also been given to evidence from various studies on the inherited factors that influence radiation cancer risks. The principal objective of this work was to provide judgments on radiation cancer risk of prime importance to radiological protection, particularly where these judgments serve to couple information about the action of radiation on cells (Chapters 1 and 2) with the epidemiologic measures of risk considered in subsequent chapters. Although less well established, the data available point toward a single-cell (monoclonal) origin for induced tumors and indicate that low-dose radiation acts predominantly as a tumor-initiating agent. These data also provide some evidence on candidate, radiation-associated mutations in tumors. One mechanistic caveat explored was that novel forms of cellular damage response, collectively termed induced genomic instability, might contribute significantly to radiation cancer risk.
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The observation that aP, which induces an immune response mismatched to that induced by natural infection, fails to prevent colonization or transmission provides a plausible explanation for the resurgence of pertussis and suggests that optimal control of pertussis will require the development of improved vaccines. Although a variety of small-animal models have been used to study pertussis, none of them adequately reproduce the human disease (16). To address this gap, we recently developed a nonhuman primate model of pertussis using baboons (Papio anubis) and found the disease is very similar to severe clinical pertussis. The coughing fits last on average >2 wk in the baboon, although this is less than some severely infected children, where the cough can last up to 12 wk (1, 17). Because this is the only model of pertussis to reproduce the cough illness and transmission of the human disease, we believe it provides the unique opportunity to test our hypothesis that aP vaccines fail to prevent B. Using this model we have confirmed that, as in humans, aP vaccines provide excellent protection against severe disease in baboons. However, aP vaccines do not prevent colonization following direct challenge or infection by transmission. In this study, we show nonhuman primates vaccinated with aP were protected from severe symptoms but not infection and readily transmitted Bordetella pertussis to contacts. While all groups possessed robust antibody responses, key differences in T-cell memory suggest that aP vaccination induces a suboptimal immune response that is unable to prevent infection. These data provide a plausible explanation for pertussis resurgence and suggest that attaining herd immunity will require the development of improved vaccination strategies that prevent B. Infection results in a wide spectrum of clinical manifestations ranging from mild respiratory symptoms to a severe cough illness accompanied by marked leukocytosis and the hallmark inspiratory whoop and posttussive emesis (3). Because acellular pertussis vaccines replaced whole-cell vaccines in the 1990s, pertussis has reemerged at a startling rate in the United States despite nationwide vaccine coverage in excess of 95% (4). With a 50-y high of 42,000 reported cases in the United States in 2012, pertussis is the most common of the vaccinepreventable diseases (5). Hampering our ability to counteract this resurgence is the fact that pertussis pathogenesis and immunity to natural infection have not been well studied in humans because typical pertussis is sporadic given high rates of vaccination in developed countries. We also found that aP vaccination induces T helper 2 (Th2) and T helper 1 (Th1) immune memory responses, whereas infection and-to a lesser extent-wP vaccination induce Th17 and Th1 memory. Our results suggest that in addition to the potential contribution of reduced efficacy and waning immunity of aP, the inability of aP to prevent colonization and transmission provides a plausible explanation for pertussis resurgence. Although these data suggest aP vaccine is less effective than wP vaccine at preventing colonization, the rate of undiagnosed B. After 2 wk, colonization gradually decreased, and the infection cleared after 30 d.
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It may be beneficial to consult a veterinary nutritionist who can formulate a diet specific to the patient. Pain in these patients may be due to the cancer itself, a treatment modality being used. Practitioners have at their disposal comprehensive sources of information on pain management. The linear accelerator is the standard device for administering radiation therapy, and functions by accelerating electrons at relativistic speeds. Goals of Radiation Therapy the goal of definitive or curative radiation therapy is eradication of all viable tumor cells within the patient. Its intent is to cure the patient whenever possible and to prolong survival as long as possible. Most palliative protocols Nutrition the nutritional status of all oncology patients should be routinely assessed beginning at diagnosis and throughout treatment. It is characterized by a distinct set of metabolic changes that are nearly impossible to reverse once they are present, although dietary modifications can slow progression. Diets should be tailored to each individual taking into account their cancer diagnosis, any other disease processes. The most important dietary consideration for canine and feline oncology patients is that the ration is palatable and eaten, otherwise it has no benefit. Providing a complete and balanced diet, whether commercially available or homemade, is imperative. A variety of diets have been used for Pet Radiation Therapy Centers Pet radiology centers are available to veterinarians who wish to refer their oncology patients for radiotherapy. In addition to other resources, the Veterinary Cancer Society provides an online list (vetcancersociety. Preoperative radiation therapy has potential advantages over postoperative radiation. These include treatment of well oxygenated tissue rather than scars, decreased tumor seeding, a smaller treatment volume, and, in some situations, less aggressive surgery. Potential disadvantages include increased wound complications and delayed surgical extirpation. The decision to do so is based on tumor location, surgeon preference, and risk of wound complication. Specifically, canine and feline lymphoma, sarcomas, and carcinomas of the nasal cavity respond favorably to radiation. Canine oral tumors, specifically acanthomatous epulis, squamous cell carcinoma, fibrosarcoma, and melanoma, respond to radiation. Canine soft tissue sarcomas, lymphoma, mast cell tumors, ceruminous gland tumors, thyroid carcinomas, bladder tumors, prostate tumors, perianal adenomas, and apocrine gland anal sac adenocarcinomas also respond to radiation, as does localized lymphoma. Factors affecting acute response to radiation in normal tissue include total dose, overall treatment time (dose intensity), and volume of tissue irradiated. Acute effects in healthy tissue are to be expected and will occur if curative doses are administered, but will resolve with time and supportive care. These effects are related to damage to the vascular and connective (stromal) tissue in non- or slowly-proliferating tissue such as the brain, spinal cord, muscle, bone, kidney, and lung. Damage is often progressive and nonreversible, thus limiting the dose that can be given. Tissue destruction is related to dose, treatment volume, and dose-perfraction, and can be limited through the use of fractionated radiation therapy. Newer Technologies 3-D conformal radiation therapy allows the beam to be tightly shaped to the tumor and allows sparing of normal tissues. State of art radiation therapy currently includes stereotactic radiosurgery and stereotactic body radiation therapy. These methods involve more sophisticated technology and delivery of single or several fractions of high-dose radiation therapy with a narrow margin.
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Characteristic imaging signs include inflammatory lesions of the brainstem sometimes extending into the diencephalon, as well as periventricular subcortical white matter lesions in the hemispheres. When the dural venous system is involved and there is no venous infarct, headache is the major symptom and there may be no other neurologic signs. A combination of parenchymal lesions and dural venous infarction should lead to a careful search for a history of genital or oral ulceration. It is characterized by recurrent ischemic episodes, cognitive deficits, behavioral disorders, and migraine-type headaches. The patient may go on to develop focal signs, such as visual field defects or hemiparesis, and then become severely encephalopathic, lapsing into coma. All had a history of migraine with aura and all the episodes seemed to start with an otherwise typical headache. Most primary neuronal and glial disorders cause coma only after a period of profound dementia has led the physician to the appropriate diagnosis. The disorders included below occasionally produce unconsciousness sufficiently early in their course that they may be confused with other conditions described in this book. As a result, a brief discussion of their clinical picture and differential diagnosis seems warranted. Although Multifocal, Diffuse, and Metabolic Brain Diseases Causing Delirium, Stupor, or Coma 277 some of these diseases are caused by transmissible agents. Prion Diseases Prions are infectious proteinaceous particles (membrane glycoproteins) that, when in certain conformations, can cause infectivity without the presence of nucleic acid. Kuru, one of the first prion disorders to be described, occurred among natives of Papua, New Guinea, who reportedly ate the brains of their relatives as part of a funeral ritual. The second third have behavioral or cognitive changes rapidly progressing to dementia. The final third present with focal signs, particularly visual loss, ataxia, aphasia, and motor defects. The illness progresses over a period of weeks to months with severe obtundation, stupor, and finally unresponsiveness; 90% of patients die within 1 year and many within a matter of 6 to 8 weeks of diagnosis. The motor system suffers disproportionately with diffuse paratonic rigid- ity; decorticate posturing and extensor plantar responses develop later. Early in the course, myoclonus appears in response to startle; later the myoclonus occurs spontaneously. A similar appearance of lesions in the pulvinar is also diagnostic (``pulvinar sign'). Unilateral or asymmetric findings are common early in the course of the disease, but eventually become bilateral and more extensive. The hyperintensity on diffusion-weighted imaging is accompanied by a decrease in the apparent diffusion constant, suggesting restricted water diffusion. However, when taken together in the appropriate clinical setting, the disorder may be diagnosed without the need for biopsy. The appearance of subacute dementia with myoclonic twitches in a middle-aged or elderly patient without systemic disease is highly suggestive of the diagnosis. Although there is a tendency to mistake the early symptoms for an involutional depression, the organic nature of the disorder rapidly becomes apparent. The first, called pure adrenal myeloneuropathy, affects myelin in the spinal cord and, to a lesser degree, peripheral nerves. A mild version of this form is also occasionally seen in female carriers (heterozygotes) of the disease. The second form is a rapidly progressive inflammatory myelinopathy beginning in the posterior hemisphere that probably results from an immune response to the very-long-chain fatty acids that accumulate in the disease. Many patients have biochemical evidence of adrenocortical failure even in the absence of clinically apparent insufficiency. Axons may either be preserved or destroyed, and there are an abundance of fatty macrophages without evidence of inflammation in the lesion. About 40% of patients present with the acute onset of stupor or coma, and only half of these have prodromal cognitive or behavioral symptoms. Comatose patients may be rigid, with increased reflexes and extensor plantar responses. Gliomatosis Cerebri Gliomatosis cerebri implies diffuse infiltration of the brain by neoplastic glial cells. Histologically, the tumor can be astrocytic or oligodendroglial and can be low or high grade.
When stimulated vigorously she would answer with her name, but could not answer other questions or follow commands. Pupils were 2 mm bilaterally, with roving eye movements and full responses to oculocephalic maneuvers. She was treated with dexamethasone and whole brain radiation therapy, resulting in rapid clearing of her cognitive function. Intraventricular chemotherapy with methotrexate and cytosine arabinoside was initiated. When she died of a pulmonary embolus 18 months later, autopsy revealed no evidence of residual cancer in the brain. The loss of several tendon reflexes in this setting is a critical clue to the diagnosis. Radiologic evaluation may show nothing, or it may reveal superficial tumor implants along the surface of the brain, the meninges, or the spinal roots. Agents causing delirium or coma may include (1) medicinal agents prescribed but taken in overdose, (2) medicinal agents procured illicitly. However, patients who are stuporous but arousable may deny drug ingestion and, if comatose, no history may be available at all. An increased anion gap is found in toxic ingestion of drugs such as ethylene glycol, propylene glycol, methanol, paraldehyde, and salicylates. A decreased anion gap may be found after ingestion of lithium, bromides, or iodides. The socalled oxygen saturation gap exists when there is more than a 5% difference between calculated saturation, as measured from arterial blood, and that as measured by an oximeter. If the oximeter reading is too high after carbon monoxide intoxication, there may be severe methemoglobinemia. In addition, if the venous blood has a high oxygen content with the appearance of arterial blood, one should consider cyanide or hydrogen sulfide poisoning. Laboratory confirmation of the clinical diagnosis is desirable, but the delay in conducting the tests often means that the information becomes available too late to be useful in guiding treatment. Persons who chronically take these drugs develop a tolerance to their effects and require larger doses with resulting higher blood levels to produce coma. Pharmacologic interaction between drug mixtures and the inability to anticipate the effects of still unabsorbed material in the gut further interfere with making a correlation. Sedatives such as benzodiazepines, neuroleptics, antihistamines, alcohol, and sedating antidepressants, as well as older drugs such as meprobamate and bromides, can all produce coma if enough is taken. The mechanism of action of each drug depends partly on its structure and partly on the dose. These effects may produce autonomic dysfunction, and in fact, the most dangerous effect of overdose with tricyclic antidepressants is their cardiotoxicity. Overdoses with most depressant drugs produce fairly consistent clinical findings; individual drugs usually cause relatively minor clinical differences. Almost all of these agents depress vestibular and cerebellar function as readily as cerebral cortical function so that nystagmus, ataxia, and dysarthria accompany or even precede the first signs of impaired consciousness. Larger amounts of drug produce coma, and at this quantity all the agents depress brainstem autonomic responses. With few exceptions, such as the benzodiazepines or neuroleptics, respiration tends to be depressed at least as much as and sometimes more than somatic motor function. The oculocephalic responses are depressed or absent, and the oculovestibular responses to cold caloric testing are depressed and may be lost altogether in deep coma. Patients with depressant drug poisoning are usually flaccid with stretch reflexes that are diminished or absent.