By V. Lares. DeVry University, Columbus.

This feature is not included in the DSM-5 definition discount lanoxin 0.25 mg visa blood pressure chart conversion. The DSM-5 definition makes the point that the behaviour of the individual is “inflexible” generic lanoxin 0.25 mg with amex heart attack cafe menu. It does not make the important point that the individual with a personality has a limited repertoire, or number of ways, of responding to the world. Faced with opposition the normal/average individual has a range of responses: to think of a new approach, work harder and try again when better prepared, to use humour, to be more assertive, to reassess whether the goal is worth further effort or not, etc. The individual with a personality disorder has a limited number of ways of responding (for example, responses may be limited to seduction or aggression). These are applied in all situations, and because of inflexibility, they are applied repeatedly, even when they have already proved unsuccessful. In these circumstances loss and disappointment, and direct and indirect distress are inevitable. Dimensional model The view that we all share personality features/traits, and these can be quantitatively scored, is the basis of dimensional models of personality/personality disorder. The diagnosis/classification of personality disorder is heading in this direction. A categorical approach has and continues to be used – however, the DSM-5, in addition to the categorical account, has introduced “an alternative model of personality disorder” - which is dimensional in nature, and will be discussed in the latter half of this chapter. The Eysenck Personality Inventory (EPI) measures two separate dimensions: extraversion-introversion (which measures reserved, versus outgoing attitude) and neuroticism (which measures tendency to distress). The Cattell 16 Personality factor Test (16PF) measures 16 different dimensions, and the Minnesota Multiphasic Personality Inventory (MMPI) (probably the most widely used personality test) measures 10 different dimensions. McCrae & John (1992) developed a five-factor model (FFM) of personality which was widely accepted. It employs the personality dimensions of 1) openness, 2) conscientiousness, 3) extraversion, 4) agreeableness, and 5) neuroticism, known by the acronym OCEAN. Cloninger et al (1993) described four temperamental dimensions, 1) novelty- seeking, 2) harm avoidance, 3) reward dependence, and 4) persistence), which are present from birth and are essentially stable. In addition, this group described three character dimensions (1, self-direction, 2) co-operation, and 3) self-transcendency) which are variable and modified by experience. He believed that while the temperamental dimensions strongly influence behaviour, it is the character dimensions which determine the presence or absence of personality disorder. It considers personality disorders to be distinct from healthy, no personality disorder. It also considers the different personality disorders to be distinct from each other, such that they can be placed in separate boxes or categories. In this chapter we will focus mainly on the categorical diagnostic method, as this is currently the clinically dominant approach. However, immediately after the section dealing with categorical diagnostic criteria, some details of The Alternative DSM-5 Model for Personality Disorder (apparently - the way of the future? The Diagnostic Criteria The clinical interview with the patient (and those who know the patient) is currently the most useful diagnostic method. A detailed life history provides extensive information regarding previous and likely future responses to the environment, and is invaluable to personality assessment. The skilled interviewer will also make observations regarding her/his own response to the patient, which is likely to be similar to the responses of others. DSM-5 groups the personality disorders into three clusters, based on descriptive similarities. The first task is to identify the appropriate Cluster. Clusters of personality disorder, adapted from DSM-5 Students will have more contact with people with Cluster B personality disorder, as people from this cluster are far more likely than those with Cluster A and C disorders, to present at Emergency Departments and to be admitted to public hospitals. Cluster A – Individuals appear odd or eccentric Paranoid Pervasive distrust and suspiciousness, such that the motives of others are interpreted as malevolent. There must be at least 4 of the following:  Suspects, without sufficient basis, that others are exploiting, harming, or deceiving  Preoccupied with unjustified doubts about the loyalty or trustworthiness of friends or associates  Reluctance to confide in others  Reads hidden demeaning or threatening meanings into benign remarks  Persistently bears grudges (unforgiving of insults or slights)  Perceives attacks on his/her character or reputation which are not perceived by others  Recurrent unjustified suspicions regarding fidelity of spouse or partners Prevalence rate in the general population is 0.

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There was a belt tied to a rafter with the buckle end hanging down discount 0.25 mg lanoxin otc blood pressure readings. The first noise Ellen heard may have been the jerking of the rafter or the chair falling over order lanoxin 0.25mg visa arrhythmia powerpoint presentation, and the second, some moments later, may have been when the buckle broke and Harold landed on the floor. The ambulance officers noted thick purple marks around his neck and that the whites of his eyes were pinkish. The police were shown the hanging belt and Harold was taken to hospital. Harold was orientated in time, place and person and an X-ray of his neck revealed no bony abnormality. He could move all limbs and did not appear to have sustained any permanent physical damage. He cried and said he was just missing “the girls” since they both left home about the same time. Ellen, a neighbour, a hospital doctor and an ambulance officer were discussing the situation in the corridor. Ellen was saying she would take Harold home and perhaps they should take a holiday together, when a nurse passing his cubicle noticed Harold was attempting to strangle himself with the leads of a cardiac monitor. They rushed back, removed the leads and called a psychiatrist. Harold had been drinking excessively over the last month. He denied feeling depressed, but had been moved to tears when watching sentimental television programs. He had been preoccupied with thoughts of his dead parents and dead brother. He had found himself thinking about cemeteries and his own funeral. He then started to experience strong urges to kill himself. He could not explain these urges, nor could he guarantee he would not act on them. Harold was transferred to a psychiatric ward for observation, with a probable diagnosis of major depressive disorder. There was some uncertainty as he denied feeling depressed. However, depressed mood is not always a prominent complaint in major depression, in which case the term “masked depression” may be applied. Supporting the diagnosis of depression was the history of preoccupation with death and sad events, and self-destructive urges. Within and hour of admission to the psychiatric ward Harold again performed self- destructive behaviour. He asked to go to the toilet and was allowed access to a specially designed facility which contained no cloth towels and no suspension points from which one could hang, and no sharp edges with which cutting could be performed. Soon after he had been left alone a heavy thud was heard. Harold was found on the floor outside the toilet cubicle in a pool of blood and with a large laceration on the top of his head. He had climbed up and stood on the wall of the toilet cubicle and divided down head first onto the floor. This was a resourceful and determined attempt and left no doubt that Harold was a danger to himself. He revealed that he had been feeling guilt as if he was responsible for events which he heard about on the news, even events on the other side of the world. He had not admitted this when brought into hospital because he felt ashamed. He left hospital two weeks later, in remission, and returned to work. Colin took Hilda to their general practitioner who referred her to hospital for admission.

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Neuronal depolarization of pre- facilitate an influx of sodium purchase lanoxin 0.25 mg online hypertension 7101. However order lanoxin 0.25 mg online blood pressure 6240, some of the kainate synaptic neurons in turn depends on activation of non- and AMPA receptors are comprised of subunits that allow NMDA receptor-gated channels and other depolarizing calcium permeability (38). This may be relevant to ischemic neurotransmitter receptors. The excitatory action of depo- injury because in neurons after cerebral ischemia, glutamate larizing neurotransmitter receptors is countered by hyperpo- receptor 2 (GR2), a subunit necessary for non-NMDA re- larizing receptor-gated ion channels, such as the GABA ( - FIGURE 92. A simplified neuronal circuit diagram illustrating the ion channels that determine the syn- aptic release of glutamate and intraneuronal Ca2 concentrations in response to ischemia. Chapter 92: Molecular Pathophysiology of Stroke 1321 aminobutyric acid) receptor. Propagation of the action po- progressively less effective; however, such agents are effective tential induced by depolarization of the neuronal cell body up to 2 hours after the onset of middle cerebral artery occlu- requires voltage-dependent sodium channels. In the clinical trials, most patients were release of glutamate itself depends on P- and Q-type voltage- enrolled 6 to 12 hours after the onset of ischemia, long after dependent calcium channels. Glutamate release into the the time that these drugs were effectively administered in synaptic cleft can bind to the NMDA receptor and open animal studies. As a result, calcium enters the cell Whatever the reason for the failure of these anti-excito- driven by its concentration gradient. However, intraneu- toxic drugs in human trials, it has become clear that it may ronal calcium may increase by other mechanisms. Post- be more practical to select treatment approaches that target synaptic voltage-dependent calcium channels may allow cal- mechanisms that are active at longer intervals after ischemia. Also, Na may enter the cell via the NMDA recep- tor-gated channel and depolarize the neuron. Thus, excito- toxicity may be ameliorated at a number of sites in vivo. MECHANISMS OF PROGRAMMED CELL Many drugs that can inhibit excitotoxicity at each of DEATH these steps have been developed. GABA agonists such as clomethazole have been shown to be neuroprotective in vivo Many of the key molecular events in programmed cell death and are currently undergoing clinical trials (47,48). Just as calcium entry dent models of stroke, BW1003,619 and phosphenytoin into the neuron is a key step in excitotoxicity, the release prevent prolonged opening of the voltage-dependent so- of cytochrome c from the mitochondria is a key event in dium channel, ameliorate increases in extracellular gluta- initiating apoptosis in many cell types. Cytosolic cyto- mate, and decrease infarction volume (49–51). Drugs that prevent prolonged opening of P- and Q-type calcium chan- nel antagonists are also neuroprotective in animal models of stroke (52). In contrast to their very limited effects in primary neuronal tissue culture models, non-NMDA antag- onists are very effective in both global and focal ischemia models in rodents. Indeed, such agents have a longer time window of efficacy than do NMDA antagonists when ad- ministered after the onset of ischemia (53,54). Likewise, voltage-dependent calcium channel antagonists are not ef- fective in vitro; however, the voltage-dependent calcium channel antagonist nimodipine is effective in reducing in- farction volume in temporary focal ischemia in rats (55). Blockade of excitotoxicity via all these pharmacologic strategies has proved effective in temporary focal ischemia models in rodents, the model that most closely resembles human stroke. Unfortunately, results with these agents in human trials have to date been very disappointing, for sev- eral possible reasons. First, drugs that affect neurotransmis- sion in the brain have many undesirable side effects, which in turn have led to reductions to doses that may have been ineffective. Side effects include effects on respiration and cardiac rhythm. In addition, agents that directly antagonize the NMDA receptor may injure a circumspect population of neurons in the cingulate and retrosplenial cortex in ro- dents (56), and may induce hallucinations and psychosis in humans (57). Another obvious reason for the lack of efficacy in these drugs in clinical trials is the time interval between the onset of ischemia and the administration of drug. When given before the onset of ischemia, these treatments can spare 50% or more of ischemic rat brain tissue from eventual FIGURE 92.

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Basic Hemodynamic Monitoring of Neurocritical Patients | 57 Oxygen delivery to tissues and organs responds to many local systemic variables to keep cellular homeostasis buy 0.25mg lanoxin with amex blood pressure rises at night. Pulmonary artery balloon flotation catheter insertion may be necessary for full assessment of these parameters cheap lanoxin 0.25mg with amex prehypertension chest pain, and of evaluation of determinants of cardiac output and the oxygen content of circulating blood, on which oxygen delivery is dependent. In the presence of positive pressure ventilation with PEEP, central venous and pulmonary artery occlusion pressures may be falsely elevated and need to be interpreted with caution. The fluid challenge is the only way to interpret Central Venous Pressure (CVP) or Pulmonary Artery Occlusion Pressure (PAOP). Assessment of the determinants of cardiac output will proceed as follows: a. Heart rate and rhythm assisted by pulse oximeter and electrocardiogram. Preload assessed right and left heart; right heart through neck vein distension, liver enlargement and central venous pressure assessment; left heart through dyspnea on exertion, orthopnea, arterial blood pressure; pulmonary artery occlusion pressure and arterial pressure through waveform analysis (Sakr 2005). Afterload assisted by mean arterial blood pressure and systemic vascular resistance; contractility can be assessed by ejection fraction and echocardiography. As discussed earlier, the goal of hemodynamic monitoring in neurocritical care units is to assess the magnitude of physiological derangements in critically ill patients and to institute measures to correct the imbalance. Basic hemodynamic monitoring consists of clinical examination, invasive arterial monitoring, central venous pressure monitoring, hourly urine output, central venous oxygen saturation and echocardiography. Dynamic indices of fluid responsiveness such as the pulse pressure variation and stroke volume variation can guide 58 | Critical Care in Neurology decision making for fluid resuscitation. Cardiac output is traditionally measured using the pulmonary artery catheter; less invasive methods now available include the pulse contour analysis and arterial pulse pressure derived methods. It is essential to determine whether the hemodynamic therapy is resulting in an adequate supply of oxygen to the tissues proportionate to their demand. Mixed and central venous oxygen saturation and lactate levels are commonly used to determine the balance between oxygen supply and demand (Walley 2011). Neurocritical Monitoring Mervat Wahba, Nabil Kitchener, Simin Mansoor Neurocritical care relies on monitoring cerebral functions. Intracranial pressure monitoring may indicate high pressure in several acute neurological conditions. Massive stroke may cause life-threatening brain edema and occur in about 10% of patients with supratentorial stroke. Massive brain edema usually occurs between the second and the fifth day after stroke onset. Neuro-Specific Monitoring Accurate neurological assessment is fundamental for the management of patients with intracranial pathology. This consists of repeated clinical examinations (particularly GCS and pupillary response) and the use of specific monitoring techniques, including serial CT scans of the brain. This chapter provides an overview of the more common monitoring modalities found within the neurocritical care environment. A drop of two or more GCS points (or one or more motor points) should prompt urgent re-evaluation and a repeat CT scan. Eye opening is not synonymous with awareness, and can be seen in both coma and persistent vegetative state (PVS). The important detail is that the patients either open their eyes to a specific command or shows ability to fix eye on a specific target or follows a visual stimulus. Pupillary response Changes in pupil size and reaction may provide useful additional information: – Sudden unilateral fixed pupil: Compression of the third nerve, e. A reduction in sedation level will usually be at the suggestion of the Regional Neurosurgical Center (RNC) and its timing will depend upon a number of factors. Responses such as unilateral pupillary dilatation, extensor posturing, seizures, or severe hypertension should prompt rapid re-sedation, repeat CT scan, and contact with the RNC. In the patient with multiple injuries, consideration must be given to their analgesic requirements prior to any decrease in sedation levels. Invasive Monitoring Cerebral perfusion pressure (CPP) reflects the pressure gradient that drives cerebral blood flow (CBF), and hence cerebral oxygen delivery. Measurement of intracranial pressure (ICP) allows estimation of CPP. Sufficient CPP is needed to allow CBF to meet the metabolic requirements of the brain. An inadequate CPP may result in the failure of autoregulation of flow to meet metabolic needs whilst an artificially induced high CPP may result in hyperemia and vasogenic edema, thereby worsening ICP.

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