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Poor accuracy of stroke scoring systems for differential clinical diagnosis of intracranial haemorrhage and infarction zofran arrhythmia purchase betapace with mastercard. Multivariate analysis of predictors of hematoma enlargement in spontaneous intracerebral hemorrhage arrhythmia caffeine buy betapace now. Volume of ventricular blood is an important determinant of outcome in supratentorial intracerebral hemorrhage arrhythmia or anxiety buy genuine betapace online. Relative edema volume is a predictor of outcome in patients with hyperacute spontaneous intracerebral hemorrhage blood pressure rates chart generic betapace 40 mg amex. Edema after intracerebral hemorrhage: correlations with coagulation parameters and treatment. Diagnosis is still frequently overlooked or delayed due to the wide spectrum of clinical symptoms and the often subacute or lingering disease onset. The superficial veins of the brain that drain the cortex and the underlying white matter form a network of anastomoses that drain into the cortical sinuses, but number, diameter and topography of these veins vary among individual patients. However, two major superficial veins can be identified in the majority of patients: the upper anastomotic vein of Trolard, which drains into the superior sagittal sinus, and the lower anastomotic vein of Labbwhich drains into the transverse sinus. Cerebral veins do not possess valves and therefore allow blood flow in both directions. This is the main reason why even larger thrombotic venous occlusions may remain clinically silent for a long time. In contrast, the deep veins that drain the basal ganglia and other deep subcortical structures do not possess the diversity of the superficial venous network. The basal veins of Rosenthal and the internal cerebral veins drain into the great cerebral vein of Galen and the straight sinus, and from there the transverse and sigmoid sinuses, finally reaching the vena cava via the jugular veins. Blood supply to the cerebellum and brainstem is drained from the posterior fossa by veins reaching the vein of Galen, the petrose or the lateral sinus. In contrast to veins, the cerebral sinuses are formed by duplication of the dura mater and are fixed to the osseous cranial structures. Thus, there is no possibility of influencing venous blood flow by means of vasoconstriction or vasodilatation. Cerebral veins have a peculiar anatomy, as they do not follow the arteries as in other parts of the body. The infectious agents reach the cerebral sinuses ascending Anatomy the cerebral venous system consists of two distinct groups the superficial and the deep cerebral veins 165 Section 3: Diagnostics and syndromes Table 11. Potential causes of and risk factors associated with cerebral venous thrombosis [3, 4, 14]. From a pathophysiological point of view, these bleedings are caused by the diapedesis of erythrocytes through the endothelial membrane, following the increase of the venous and capillary transmural pressure after venous thrombosis. Clinical features Abrupt occlusion of a cerebral artery results in the acute manifestation of focal neurological symptoms due to ischemia of the brain tissue perfused by this artery. In contrast, cerebral venous thrombosis may remain clinically silent, as long as venous drainage is maintained by collateral veins or sinuses. Eventually, failure of collateral venous drainage will result in the gradual, fluctuating or progressive clinical manifestation of focal or generalized brain dysfunction. In most prospective clinical series [2, 3, 6, 8], intense and diffuse headache was either the first (> 70%) or the most common (750%) symptom of cortical venous thrombosis. Headache, as well as nausea, papilledema, visual loss or sixth nerve palsy, is due to increased intracranial pressure. Motor symptoms may initially present as a monoparesis that gradually develops into a full-blown hemiparesis. Impairment of the level of consciousness (any degree from somnolence to deep coma) may be present in 300% of patients, and acute delirium or psychotic symptoms are observed in 205% [2, 3, 6, 8]. As a rule, extended thrombosis of cortical sinuses will result in symptoms and signs of generalized brain dysfunction (headache and other signs of increased intracranial pressure, impairment of the level of consciousness, generalized seizures), while isolated cortical venous thrombosis will result in focal neurological signs or focal seizures. The rare thromboses of the inner cerebral veins (veins of Rosenthal, great vein of Galen, straight sinus, etc. Thrombosis of the cavernous sinus may present with the characteristic combination of ocular chemosis, eye protrusion, painful ophthalmoplegia, trigeminal dysfunction, and occasionally papilledema. Cavernous sinus thrombosis may be unilateral, but the good collateralization between the cavernous sinuses usually leads to bilateral symptoms, while extension of the thrombosis into the large sinuses is the exception. Most cases of cavernous sinus thrombosis are due to ascending infection from the orbita, the paranasal sinuses or other structures of the viscerocranium and are accompanied by signs of local or systemic infection. Septic thrombosis of other sinuses is found as a complication of bacterial infection.

Where possible arrhythmia potassium order betapace no prescription, information specific to other etiologies is provided below heart attack white sea remix discount 40mg betapace otc, but the physician should recognize this general limitation when formulating a prognosis for a comatose patient who has not suffered a traumatic brain injury or cardiac arrest blood pressure under 100 cheap betapace 40 mg online. Consciousness heart attack in spanish generic betapace 40mg, Mechanisms Underlying Outcomes, and Ethical Considerations 345 a better prognosis than nontraumatic coma, possibly because patients are usually younger and the pathophysiology differs from other types of coma. Recovery after prolonged traumatic coma is well described and, unlike nontraumatic causes, unconsciousness for 1 month does not necessarily preclude significant recovery. Severe head injury causing 6 hours or more of coma still carries a 40% probability of recovering to a level of moderate disability or better. By 6 hours, motor responses no better than abnormal flexor were associated with a mortality of 63%, while abnormal extensor or flaccid responses predicted an 83% mortality. Paradoxically, elderly patients may require a much longer recovery time, so it is risky to predict ultimate recovery early in the course. This number fell to 39% between age 20 and 59 years and to only 5% among those older than Table 9 Class I Evidence for Early Prognosis in Coma Due to Traumatic Brain Injury I. A meta-analysis of 5,600 patients identified a continuously worsening prognosis with increasing age without a sharp stepwise drop at any point. Data from the Traumatic Coma Data Bank8 reveal an increased incidence of intracranial hemorrhage with age and premorbid medical illnesses, but did not demonstrate a significant statistical association. In one series, 95% of patients who had either bilaterally nonreactive pupils or absent oculocephalic responses at 6 hours after injury died. A single episode of hypotension (arterial line reading) is associated with a doubling of mortality and a significant increase in morbidity. Although length of coma provides a good indication of severity of brain damage, it can be determined only retrospectively when the patient awakens and thus cannot be used for early prognosis of outcome. On the other hand, it can be predicted with some confidence that a patient in prolonged coma is unlikely to recover. The same limitation applies to efforts to correlate outcomes of recovery of cognitive functions with the duration of posttraumatic amnesia. Percentage of patients who recovered full consciousness as a function of duration of coma for several age groups. Logi and associates24 prospectively studied 131 comatose patients of varying etiologies, including head trauma patients (N 22), and found 100% specificity for bilateral absence of cortical responses predicting nonawakening when sedating medications had been withdrawn and there were no other metabolic disturbances. Other electrophysiologic markers, including cognitive event-related potentials,28 might provide better prognostic value in future studies. Jennett and colleagues in Glasgow, undertook prospective studies of the outcome from coma as caused by medical disorders. All patients over 12 years old, save those with head trauma or exogenous intoxication in acute coma, were identified and repeatedly examined. Meticulous efforts were made to examine every patient in coma using examining techniques that guaranteed consistency of observation. The patients were followed for a minimum of 12 months (unless death occurred first) and many for much longer (only two of the 500 patients were lost to follow-up). This large population provided landmark data on substantial numbers of individuals in each of the major disease categories, permitting correlations between outcome and both the severity of early signs of neurologic dysfunction and the specific etiology of coma. Subsequent studies have largely confirmed the conclusions drawn from this patient population, including larger prospective studies of coma following cardiac arrest. Of the 500 patients, 379 (76%) died within the first month and 88% had died by the end of a year. Some of the patients died during that first month of nonneurologic causes, but the table is constructed so as to indicate the highest possible chance of recovery by the brain. The difference is explained by most of the hepatic and miscellaneous patients having reversible biochemical, infectious, or extracerebral intracranial. By contrast, many patients with stroke or global cerebral ischemia suffered destruction of brain structures crucial for consciousness. Reflecting this difference, the metabolic-miscellaneous group of patients showed significantly fewer signs of severe brainstem dysfunction than did those with vascular-ischemic disorders. For example, corneal responses were absent in fewer than 20% of the metabolic group, but in more than 30% of the remaining patients. Furthermore, when patients with hepatic-miscellaneous causes of coma did show abnormal neuro-ophthalmologic signs (see below), their prognosis was as poor as that of patients in the other disease groups with similar signs.

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These studies have identified the etiology of injury blood pressure medication pictures order betapace cheap, the clinical depth of coma blood pressure cuffs for sale generic betapace 40 mg fast delivery, and the length of time that a patient remains comatose as the most critical factors hypertension quotes purchase 40 mg betapace otc. The bold black line indicates emergence from the minimally conscious state heart attack 85 blockage cheap betapace online master card, defined by reliable functional communication. Several limitations, as discussed below, place stringent demands on physicians to carefully consider all available historical details and the reliability of clinical and laboratory evaluations in their consideration of prognosis for an individual patient. Prospective studies of prognosis in adults and children indicate that within a few hours or days after the onset of coma, neurologic signs and electrophysiologic markers in many patients differentiate, with a high degree of probability, the extremes of no improvement or good recovery. Unfortunately, radiologic and biochemical indicators have generally provided less accurate predictions of outcome, with some exceptions discussed below. Accurate prognostication improves over time, but it is still unclear how early one can make accurate predictions within different diagnostic categories. The first section of this chapter details what we now know about prognosis, emphasizing broad outcome categories and shortterm outcomes rather than outcomes beyond a year or longer, although we recognize that rarely, even severely brain-injured patients may improve after many years (see page 371). We use the scheme in Table 9 to assess the reliability of the data presented in this section. The second section addresses mechanisms that may underlie recovery, or lack thereof, from coma. Severe cognitive disabilities can arise from at least two fairly different anatomic injuries: (1) extensive, relatively uniform diffuse axonal injury or hypoxic-ischemic damage causing widespread neuronal death and (2) focal cerebral injuries causing functional al- teration of integrative systems in the upper brainstem and thalamus. New studies suggest that physiologic correlates of brain function in some severely disabled patients with relatively intact cerebral structures may ultimately lead to identification of residual cerebral capacities. The third section addresses important ethical considerations in dealing with comatose patients and their families and caregivers. For the two most carefully studied etiologies of coma, traumatic brain injury and cardiopulmonary arrest, mortality ranges from 40% to 50% and 54% to 88%,2 respectively. These statistics have actually improved since the last edition of Stupor and Coma, because of better acute management both in the field and in intensive care. Beyond mortality statistics, very few studies of prognosis in coma have looked at large numbers of patients for careful evaluation of outcomes other than survival or death. These indicate that patients comatose from traumatic brain injury have a significantly better prognosis than patients with anoxic injuries. For example, of 1,000 trauma patients in coma for at least 6 hours, 39% recovered independent function at 6 months,3 whereas only 16% of 500 patients suffering nontraumatic coma made similar recoveries at 1 year. This section reviews efforts to predict outcome from coma for different etiologies. The reader will find that the literature continues to provide little specific information about the kind of outcome enjoyed or suffered by patients. The definitions attempted to identify fairly precisely what was meant by each grade of outcome. Only a small number of outcomes were chosen in the hope that sufficient numbers of patients would fall into each class to allow statistical analysis, but that important differences in medical and social recovery would not be excessively blurred. There still exists a need for further subdivision and consideration of outcomes in the severely disabled group, as discussed below. For example, when using the prognostic data provided below, care should be taken to distinguish indicators of death from those indicating outcomes including severe disability, which remains a very broad category. Patients who survived medical coma had achieved most of their improvement by the end of the first month. Among the 121 patients still living at 1 month, 61 died within the next year, usually from progression or complication of the illness that caused coma in the first place. Table 9 Best One-Month Outcome Related to Cause of Coma Best One-Month Outcome (%) Cause of Coma All patients (500) Subarachnoid hemorrhage (38) Other cerebrovascular disease (143)* Hypoxia-ischemia (210)* Hepatic encephalopathy (51) Miscellaneous (58)* No Recovery 61 74 74 58 49 45 Vegetative State 12 5 7 20 2 10 Severe Disability 12 13 11 11 16 14 Moderate Disability 5 5 4 3 10 5 Good Recovery 10 3 4 8 23 6 *Hypoxia-ischemia includes 150 patients with cardiac arrest, 38 with profound hypotension, and 22 with respiratory arrest. Other cerebrovascular diseases include 76 with brain infarcts and 67 with brain hemorrhage. Miscellaneous includes 19 patients with mixed metabolic disturbances and 16 with infection. Consciousness, Mechanisms Underlying Outcomes, and Ethical Considerations 349 There were seven moderately disabled patients who improved to a good recovery. Of 39 patients severely disabled at 1 month, nine later improved to a good recovery or moderate disability rating. At the end of the year, three patients remained vegetative and four severely disabled. While current patients may have a greater chance of survival with modern therapies, it is unfortunately not likely that they would have a significantly different natural history after 1 month, suggesting that the data from this series remain relevant.

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Grooming and dress Good habits of grooming and dress may suffer in certain illnesses blood pressure medication hydro order betapace now, sometimes with diagnostically suggestive results arteria magna cheap betapace 40mg line. Depressive patients may find that hopelessness 4 arteria aorta purchase genuine betapace line, fatigue blood pressure spikes betapace 40mg without a prescription, and anhedonia make them give up all hope of maintaining their appearance, with the result that grooming and dress are left in a greater or lesser degree of disarray. Manic patients, overflowing with exuberance, may truly make a spectacle of themselves with decorations of make-up and garish clothing. Rarely, one may see evidence of neglect wherein dress and grooming suffer on only one side of the body (Section 2. Comments should be made on the relationship of the patient to the interviewer, noting, for example, whether the patient is cooperative or uncooperative, guarded, evasive, hostile, or belligerent. For example, as noted by Bleuler (1924), in schizophrenia, there is often a `defect in. Many of these may be determined during the non-directive portion of the interview; however, some, especially those concerning cognition. Psychomotor retardation may range from an almost total quietude and immobility to a mere slowing of speech and behavior. Mere exhaustion may slow patients down, but the response to rest is generally robust. Apathetic patients, lacking in motivation, may evidence little speech or behavior; depressed patients may appear similar but here one also sees a depressed mood. Delirium may be characterized by quietude and inactivity but is distinguished by the presence of confusion and deficits in memory and orientation. Other behavioral disturbances may occur during the interview and examination, including mannerisms, stereotypies, and echopraxia. Mannerisms represent more or less bizarre transformations of speech, gesture, or other behaviors (Section 4. Stereotypies are a kind of perseveration wherein patients repeatedly engage in the same behaviors, to no apparent purpose (Section 4. Echopraxia is said to be present when patients involuntarily mimic what others, such as the examining physician, do (Section 4. Anxious patients are beset with apprehensions, may plead for help, and may complain of tremor and palpitations. Affect has been variously defined as representing either the combination of the immediately present emotion and its accompanying expression in tone of voice, gesture, facial expression, etc. Given that, as with mood, affect may be depressed, euphoric, anxious, or irritable it may appear academic to distinguish between the two; however, disparities between mood and affect may arise. Mood is enduring, whereas affect is relatively changeable: in a sense, mood is to climate p 01. Affect, in addition to being depressed, euphoric, anxious or irritable, may also be flattened or labile. Some investigators believe flattened affect is also present in severe depression; however, in my experience there is little difficulty in distinguishing a flattened from a depressed affect. Labile affect is characterized by swift, and sometimes violent, changes in both felt and expressed emotion. Disturbances of mood are seen in a large number of conditions, as discussed in the chapters on depression, mania, and anxiety. Furthermore, it must be stressed that changes in mood, and especially affect, are also very common in dementia and delirium. This is particularly important to keep in mind, given that effective treatment of delirium typically results in a normalization of affect without the need for treatment with antidepressants or other medications. Incoherence and allied disturbances Normally the thoughts we put into words are coherent, focused, and goal-directed: abnormalities here include incoherence, circumstantiality and tangentiality, and flight of ideas. Incoherence may be found in a number of different syndromes, and it is the presence of other signs and symptoms that alerts the clinician to which syndromal diagnosis should be pursued: cognitive deficits indicate the presence of dementia or delirium; heightened mood, pressure of speech, and hyperactivity suggest mania; and bizarre behavior, hallucinations, or delusions point to a psychosis, such as schizophrenia. In general, patients with loosening of associations spoke freely and at length and, although what they said made little sense, they had no trouble in finding words. By contrast, patients with aphasia often had at least some difficulty in finding words, and their responses to questions were typically brief. Furthermore, whereas patients with loosening of associations had little or no recognition of their incoherence, the aphasic patients often seemed at least somewhat aware of their difficulty.

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