By L. Tarok. Belhaven College.

Prediction of reflex sympathetic dystrophy in hemiplegic patients by electromyo- graphic study 100mg provigil overnight delivery. Endarterectomy for moderate symptomatic carotid stenosis: Interim results from the MRC European Carotid Surgery Trial discount 100mg provigil otc. Clinical assessment and management of swallowing difficulties after stroke discount provigil 200 mg line. Three-phase bone studies in hemiplegia with reflex sympathetic dys- trophy and the effect of disuse order provigil 200mg otc. Hamilton MG buy provigil 100mg online, Spetzler RF: The Prospective Application of a Grading System for Arteriovenous Malformations. Reflex sympathetic dystrophy in the hands: clinical and scintographic cri- teria. Low-molecular-weight heparin for the treatment of acute ischemic stroke. Proprioceptive Neuromuscular Facilitation: Patterns and Techniques, 2nd ed. National Institute of Neurologic Disorders and Stroke rt-PA Stroke Study Group. The American Heart Association Consensus Statement on guidelines for carotid endarterec- tomy. Beneficial effect of carotid endarterectomy in symptomatic patients with high-grade carotid stenosis. Brunnstrom’s Movement Therapy in Hemiplegia: A Neurophysiological Approach, 2nd ed. Significance of Factors Contributing to Surgical Complications and to Late Outcome After Elective Surgery of Cerebral Arteriovenous Malformations. Reflex sympathetic dystrophy syndrome in stroke patients with hemilegia—three-phase bone scintography and clinical characteristics. An analysis of perioperative sur- gical mortality and morbidity in the asymptomatic carotid atherosclerosis study. Bethesda, MD; National Institute of Neurologic Disorders and Stroke, National Institutes of Health, 1999. Grand rounds clinical lecture presented at: JFK Johnson Rehabilitation Institute August 1999; presented at Kessler Rehabilitation Institute Board Review Course 2000. INTRODUCTION EPIDEMIOLOGY Trauma is the leading cause of death in ages 1–44 and more than half of these deaths are due to head trauma. Traumatic brain injury (TBI) is arguably the primary cause of neuro- logic mortality and morbidity in the United States About 500,000 per year traumatic brain injuries (requiring hospitalization) in the United States National Health Interview Survey (1985) provided the only national estimate of incidence of nonfatal TBI (hospitalized and non-hospitalized cases) for 1985–1987: – 1. Cranial nerve injury TRAUMATIC BRAIN INJURY 49 Secondary Damage that occurs after the initial trauma and as a result of the injuring event. Most sec- ondary injury occurs during the first 12 to 24 hours after trauma, but may occur up to 5 to 10 days postinjury in very severe brain injury. Because of the delayed presentation, secondary injury may be preventable. Intracranial hemorrhage (epidural, subdural, subarachnoid and intracerebral hematoma) B. Elevated Intracranial Pressure (ICP) – ↑ ICP ↓perfusion ⇒ ischemic brain damage D. Production of free-radical molecules Other secondary causes of brain injury include: Hypotension Hyperemia Electrolyte imbalances Hyponatremia Anemia Infection Hyperthermia Carotid dissection Hyperglycemia Epilepsy/seizures Hypercarbia Vasospasm/ischemia Hypoglycemia Primary Head Injury Contusion—bruising of cerebral (cortical) tissue Occurs on the undersurface of the frontal lobe (inferior frontal or orbitofrontal area) and anterior temporal lobe, regardless of the site of impact (Figure 2–1) May produce focal, cognitive, and sensory-motor deficits Is not directly responsible for loss FIGURE 2–1. Location of Contusions of consciousness following trauma May occur from relatively low velocity impact, such as blows and falls Diffuse axonal injury (DAI): DAI is seen exclusively in TBI Damage seen most often in the corpus callosum and other midline structures involving the parasag- ittal white matter, the interventric- ular septum, the walls of the third ventricle and the brain stem (mid- brain and pons) (Figure 2–2) FIGURE 2–2. Locations of Diffuse Axonal Injury 50 TRAUMATIC BRAIN INJURY Responsible for the initial loss of consciousness seen in acute TBI Results from acceleration-deceleration and rotational forces associated with high-velocity impact (MVAs) The axonal injury seen in severe TBI is thought to be secondary to damage to the axo- plasmic transport in axons (with ↑ Ca++ influx) leading to axonal swelling and detachment Secondary Head Injury Brain Swelling Occurs after acute head injury within 24 hours. Vasogenic edema: – Due to outpouring of protein rich fluid through damaged vessels – Extracellular edema – Related to cerebral contusion 2. Cytogenic edema: – Found in relation to hypoxic and ischemic brain damage – Due to failing of the cells’ energy supply system ↑cell-wall pumping system ⇒ intracellular edema in the dying cells PENETRATING HEAD INJURIES Missile/Fragments Deficits are focal corresponding to location of lesions caused by bullet/fragment If the brain is penetrated at the lower levels of the brain stem, death is instantaneous from respiratory and cardiac arrest. Risk of long-term posttraumatic epilepsy is higher in penetrating head injuries compared to nonpenetrating injuries RECOVERY MECHANISMS Plasticity Brain plasticity is when the damaged brain has the capabilities to repair itself by means of morphologic and physiologic responses Plasticity is influenced by the environment, complexity of stimulation, repetition of tasks, and motivation It occurs via 2 mechanisms: 1) Neuronal regeneration/neuronal (collateral) sprouting 2) Unmasking neural reorganization TRAUMATIC BRAIN INJURY 51 Neuronal Regeneration Intact axons establish synaptic connections through dendritic and axonal sprouting in areas where damage has occurred May enhance recovery of function, may contribute to unwanted symptoms, or may be neutral (with no increase or decrease of function) Thought to occur weeks to months post-injury Functional Reorganization/Unmasking Healthy neural structures not formerly used for a given purpose are developed (or reas- signed) to do functions formerly subserved by the lesioned area. Brain plasticity—remember “PUN” Plasticity = Unmasking + Neuronal sprouting OTHER RELATED PHENOMENA ASSOCIATED WITH HEAD INJURY RECOVERY Synaptic Alterations Includes diaschisis and increased sensitivity to neurotransmitter levels Diaschisis: Mechanism to explain spontaneous return of function (Figure 2–3) 1. Lesions/damage to one central nervous system (CNS) region can produce altered function in other areas of the brain (at a distance from the original site of injury) that were not severed if there is Injury (Site A) connection between the two sites Altered function also occurs here (Site B) (through fiber tracts).

No part of this publication may be translated into other languages best 200 mg provigil, reproduced or utilized in any form or by any means electronic or mechanical cheap provigil 100 mg free shipping, including photocopying discount provigil 100 mg fast delivery, recording order provigil 200 mg line, microcopy- ing cheap provigil 200mg online, or by any information storage and retrieval system, without permission in writing from the publisher. Population-Based Healthcare for Chronic Idiopathic Pain and Fatigue after War Engel, C. Much of the confusion about treatment of pain comes from inad- equate evaluation and understanding of pain and a lack of knowledge about the psychiatric conditions that accompany many pain disorders. The distinction between chronic and acute pain syndromes, as well as the distinction between those in whom the goal of treatment is rehabilitation and those who need to be made comfortable has been poorly appreciated in clinical efforts. The idea that pain must be assessed daily in all patients at every clinical interaction and treated with an opiate-based protocol has caused as many problems as it has solved. Acute pain with a known etiology that is expected in the course of treatment should be vigorously suppressed in most cases. Acute pain of unclear etiology should be evaluated for cause and appropriate treatment. Chronic pain in most patients deserves a comprehensive workup and thoughtful treatment plan which balances comfort with function and rehabilitation. It occurs at high rates in many chronic medical conditions and has been shown to affect recovery, cost, morbidity, and mortality. Depression is often missed in medical settings and is underdiagnosed and undertreated in most studied patient populations. It adds to the costs of treatment, magnifies the subjective experience of noxious stimuli, and retards rehabilitation. Depression is a barrier to patients’ engagement in treatment, and sometimes a barrier to physician engagement in VII patient care. The co-occurrence of these two conditions is well known but the details of phenomenology, interrelationships, and rational therapies remain spec- ulative. This volume focuses on the need for a coherent approach to the formu- lation of patients with chronic pain who suffer from depression. Depression is a personal experience that takes on many forms and emerges from many causes. The Pain Treatment Programs in the Department of Psychiatry and Behavioral Sciences at the Johns Hopkins Medical Institutions have implemented a comprehensive approach to the treatment of patients with chronic pain based on the formulation of each patient’s problems. This formulation recognizes that distress and suffering need to be both explained and understood from several different perspectives. These perspectives organize what we know about patients, both from experience and research, into the different kinds of altered circum- stances that affect individuals. Each perspective offers a distinct but comple- mentary way in which mental life can become disordered. Clark and Treisman discuss these perspectives and their application to patients with chronic pain in the first paper, ‘Perspectives on Pain and Depression’. The recognition that depression is not just an affective disorder or demoral- ization is discussed in detail in the papers by Katz, ‘Function, Disability, and Psychological Well-Being’ and Krueger et al. Katz explores the relationship between function and well-being recognizing that disability in valued life activities produces depressive symptoms. Specifically, this model addresses the individual’s unique interests and wants that chronic pain compromises. The inherent traits of internalizing and externalizing ultimately generate a variety of psychiatric conditions that may vary in symptomatology but share a common essence. Both of these well-developed models offer deeper insights into the formulation of patients with chronic pain and depression but more importantly make explicit how specific interventions could facilitate rehabilitation. Clark and Treisman review the ‘Neurobiology of Pain’ to introduce the next two papers. While basic scientific advances have demonstrated the complexity of the human body, clinical practice must still contend with complicated syndromes such as complex regional pain syndrome (CRPS) and Gulf War syndrome (GWS). Clark/Treisman VIII No exact pathophysiology explains the entire presentation of patients with CRPS and these patients exhibit a wide variety of somatic complaints, psycho- logical symptoms, and abnormal illness behaviors. Population-Based Healthcare for Chronic Idiopathic Pain and Fatigue after War’. The disability and depression manifested by patients with GWS represent one of the most challenging examples of reinforced illness behavior that extends beyond the individual patient into healthcare systems, the military ‘family’, and society itself as legislated by the government. The final three papers discuss issues relating to the use of opioids in the treatment of chronic pain.

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The existence of demonstrable behav- ioral subroutines in animals suggests that the hypothalamus plays a key role in matching behavioral reactions and bodily adjustments to challeng- ing circumstances or biologically relevant stimuli buy provigil 200 mg otc. Moreover proven 200 mg provigil, stress hor- mones at high levels discount 200 mg provigil amex, especially glucocorticoids proven provigil 200mg, may affect central emo- tional arousal provigil 200 mg for sale, lowering startle thresholds and influencing cognition (Sapolsky, 1992). Saphier (1987) observed that cortisol altered the firing rate of neurons in limbic forebrain. Clearly, stress regulation is a complex, feedback-dependent, and coordinated process. The hypothalamus appears to take executive responsibility for coordinating behavioral readiness with physiological capability, awareness, and cognitive function. Chapman and Gavrin (1999) suggested that prolonged nociception may cause a sustained, maladaptive stress response in patients. Signs of this in- clude fatigue, dysphoria, myalgia, nonrestorative sleep, somatic hyper- vigilance, reduced appetite and libido, impaired physical functioning, and impaired concentration. In this way, the emotional dimension of persisting pain may, through its physiological manifestation, contribute heavily to the disability associated with chronic or unrelieved cancer pain. Central Serotonergic Pathways The serotonergic system is the most extensive monoaminergic system in the brain. It originates in the raphé nuclei of the medulla, the pons, and the mesencephalon (Grove, Coplan, & Hollander, 1997; Watson, Khachaturian, Lewis, & Akil, 1986). Descending projections from the raphé nuclei modu- late nociceptive traffic at laminae I and II in the spinal cord and also motor neurons. The raphé nuclei of the midbrain and upper pons project via the medial forebrain bundle to multiple limbic sites such as hypothalamus, sep- tum and hippocampus, cingulate cortex, and cerebral cortex, including frontal cortex. The potential role of serotonergic mechanisms in affective disorders, particularly depression and panic disorder, continues to receive a great 76 CHAPMAN deal of attention (Grove et al. These are important for pain perception because descending endogenous modulatory pathways from the nucleus raphé magnus, the solitary nucleus, and other mesen- cephalic structures can attenuate or gate nociceptive signaling at the level of the dorsal horn, and these pathways are largely serotonergic. Longstand- ing, but thinly supported, speculation holds that depletion of serotonin may result in diminished endogenous modulation of nociception and hypersen- sitivity to noxious events. Currently, the major antidepressant medications are selective serotonin (5-hydroxytryptamine; 5-HT) reuptake inhibitors, often called SSRIs (Asberg & Martensson, 1993). Increased receptor selectivity in the newer drugs helps to maximize benefit and minimize side effects of these medications. It is now clear that the older assumptions of simple bioamine deficiency are insufficient to account for the role of serotonin in affective disorders. Al- though a definitive understanding is still at issue, it has become clear that the serotonergic system influences the actions of the HPA axis, particularly by augmenting cortisol-induced feedback inhibition (Bagdy, Calogero, Mur- phy, & Szemeredi, 1989; Dinan, 1996; Korte, Van, Bouws, Koolhaas, & Bohus, 1991). Moreover, it interacts with noradrenergic pathways in complex ways, including attenuation of firing in LC neurons (Aston-Jones et al. The interdependence of the monoamine systems and the HPA axis indicates that we cannot hope to account for complex patterns of brain or behavioral responses by considering these elements individually. They appear to be components of a larger system that we have yet to conceptualize. TWO STAGES IN THE EMOTIONAL ASPECT OF PAIN The physiology of emotion suggests that the affective dimension of pain in- volves a two-stage mechanism. The primary mechanism generates an im- mediate experience akin to hypervigilance or fear; put simply, it is threat. In nature, this rapid response to injury serves to disrupt ongoing attentional and behavioral patterns. At the same time, efferent messages from the hy- pothalamus, amygdala, and other limbic structures excite the autonomic nervous system, which in turn alters bodily states. Cardiac function, muscle tension, altered visceral function, respiration rate, and trembling all occur, and awareness of these reactions creates a strong negative subjective expe- rience. This body state awareness is the second mechanism of the affective dimension of pain. Damasio (1994) submitted that visceral and other event-related, autonom- ically mediated body state changes constitute “somatic markers.

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TAC1 knockout mice express lower levels of anxiety in various paradigms as well buy provigil 100mg low price. For example cheap 100 mg provigil amex, TAC1 knockout mice are more active in the central area of an open field buy provigil 100 mg online, spend more time in open maze compartments discount provigil 100 mg, show decreased latency to approaching food in a novel environ- ment purchase provigil 200mg on line, and spend more time interacting socially with unfamiliar mice. Knockout studies of the TACR1 gene have also demonstrated the role of neurokinin signaling in regulation of negative emotion. Mice lacking the neu- rokinin receptor gene show decreased levels of anxiety relative to heterozygotes and wild-type mice in a variety of paradigms. TACR1 knockout mice spend more time in open arms of an elevated plus maze, show decreased latency to approaching food in a novel environment, and, as pups, show decreased fre- quency of vocalizations when separated from their mother. Overall, these studies demonstrate the role of neurokinin and neurokinin receptor gene expression in regulation of depression and anxiety. The mecha- nisms by which neurokinin and neurokinin receptor gene expression regulate negative emotion are not well understood, however. There is some indication that neurokinin systems interact with serotonergic pathways, but this is not established. For example, disruption of the TACR1 gene appears to increase firing of serotonergic neurons in the dorsal raphe nucleus, and is associ- ated with desensitization of serotonin autoreceptors in a manner similar to that observed with sustained antidepressant use. However, neurokinin antagonists apparently do not significantly influence serotonergic functioning, and there is some indication that TACR1 disruption influences Structural Models 71 serotonergic functioning indirectly through noradrenergic systems in the locus ceruleus. In addition to neurokinin systems, other neurogenetic substrates are increasingly being implicated in the joint expression of pain and various forms of negative emotion. The opiate neuropeptides in particular represent another important class of neuromodulators involved in both pain and internalizing phe- nomena. Numerous molecular genetic studies suggest that various opiate neu- ropeptides are involved in pain and internalizing phenomena. Preproenkephalin gene knockout mice, for example, have altered nociceptive profiles and exhibit increased anxiety relative to wild-type mice. Similarly, nociceptin knock- out mice demonstrate elevated levels of anxiety in a variety of paradigms, as well as elevated pain thresholds. Molecular genetic studies of pain and negative emotion in mice and other animals provide important information about the neuromolecular systems underlying internalizing phenomena. However, the role of these systems in regulating internalizing phenomena in humans remains poorly understood. As research on the behavioral genomics of negative emotion continues, it will become important to adopt a perspective that comprises a variety of phenomena simultaneously. Linkage and association studies focusing on pain, depression, and anxiety simultaneously, for example, will provide important information that would be missed if each were studied individually. The IE Model of the Structure of Common Mental Disorders: Recent Evidence of a Connection to Pain As described earlier, the IE model is one evolving perspective that has the potential to encompass both pain and internalizing phenomena such as depres- sion and anxiety simultaneously. This model originally emerged from our research on common mental disorders in general population samples, including unipolar mood, anxiety, substance use, and antisocial behavior disorders; chronic pain was not originally a focus of the model. However, we were recently able to study the model in the general health care setting. Specifically, we evaluated the fit of the model to data from the World Health Organization (WHO) Collaborative Study of Psychological Problems in General Health Care, which was carried out in 15 study centers in 14 countries. Participating centers included Rio de Janeiro (Brazil), Santiago (Chile), Shanghai (China), Paris (France), Berlin and Mainz (Germany), Athens (Greece), Bangalore (India), Verona (Italy), Nagasaki (Japan), Groningen (The Netherlands), Ibadan (Nigeria), Ankara (Turkey), Manchester (UK), and Seattle, Wash. We were able to evaluate patterns of comorbidity among depression, somatization, Krueger/Tackett/Markon 72 hypochondriasis, neurasthenia, anxious worry, anxious arousal, and hazardous use of alcohol. The somatization symptom count included a number of pain- related symptoms (abdominal, back, joint, arms or legs, chest, headache, else- where), in addition to symptoms focused on gastrointestinal, cardiopulmonary, pseudoneurological, genitourinary, and skin complaints that were currently pre- sent and not medically explained. In modeling the WHO data, we found that the best fitting model for the data from all the sites, modeled simultaneously, divided the syndromes into two distinct spectra or factors. The first factor (internalizing) was indicated by depression, somatization, hypochondriasis, neurasthenia, anxious worry, and anxious arousal. This factor was found to be separate from a factor indicated by hazardous use of alcohol. In addition, the strengths of the relationships between the underlying factors and their manifestations in specific syndromes (load- ings) did not vary across countries. These findings extend previous research on the IE model in a number of ways. The model fit data from diverse cultures, suggesting that the IE structure of these syndromes is relatively universal. In addition, the general health care setting and international focus of the research resulted in a different set of syn- dromes being modeled (somatization, hypochondriasis, and neurasthenia were not part of the model before this research was undertaken).

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