By T. Rhobar. Castleton State College.
Prevention of mother-to-child transmission of HIV and the health-related Millennium Development Goals: time for a public health approach discount 40 mg paroxetine otc treatment goals for depression. Use of antiretroviral drugs for treating pregnant women and preventing HIV infection in infants discount paroxetine 30mg visa medicine versed. Comparative quantifcation of health risks: Global and regional burden of disease attribution to selected major risk factors order paroxetine 30mg visa treatment jalapeno skin burn. Therapeutic efects of oral zinc in acute and persistent diarrhea in children in developing countries: pooled analysis of randomized controlled trials cheap paroxetine 20mg on line treatment centers of america. The American Journal of Clinical Nutrition, 2000,72:1516-1522. Prevention of diarrhea and pneumonia by zinc supplementation in children in developing countries: pooled analysis of randomized controlled trials. A collection of 104 peer-reviewed perspectives and theoretical underpinnings. In what circumstances is telemedicine appropriate in the developing world? The role of information communication technology (ICT) towards universal health coverage: the first steps of a telemedicine project in Ethiopia. Feasibility of using teleradiology to improve tuberculosis screening and case management in a district hospital in Malawi. Bulletin of the World Health Organization, 2012,90:705-711. Automated real-time nucleic acid amplifcation technology for rapid and simultaneous detection of tuberculosis and rifampicin resistance: Xpert MTB/RIF system. Rapid molecular TB diagnosis: evidence, policy-making and global implementation of Xpert®MTB/RIF. The European Respiratory Journal, 2012, doi: http://dx. WHO monitoring of Xpert MTB/RIF roll-out (web site). Feasibility, diagnostic accuracy, and efectiveness of decentralised use of the Xpert MTB/RIF test for diagnosis of tuberculosis and multidrug resistance: a multicentre implementation study. Xpert MTB/RIF for diagnosis of TB and drug-resistant TB: a cost and afordability analysis. The European Respiratory Journal, 2012,(Epub ahead of print) doi: http://dx. A comprehensive global monitoring framework, including indicators, and a set of voluntary global targets for the preven- tion and control of noncommunicable diseases. Measuring progress on NCDs: one goal and fve targets. A strategy to reduce cardiovascular disease by more than 80%. An international randomised placebo-controlled trial of a four-component combination pill (“polypill”) in people with raised cardiovascular risk. Use of a Multidrug Pill In Reducing cardiovascular Events (UMPIRE): rationale and design of a randomised controlled trial of a cardiovascular preventive polypill-based strategy in India and Europe. European Journal of Preventive Cardiology, 2012, doi: http://dx. Report of a meeting of the WHO Expert Committee on the Control of Leishmaniases, 22–26 March 2010. Geneva, World Health Organization, 2010 (WHO Technical Report Series, No. Visceral leishmaniasis in eastern Africa — current status. Transactions of the Royal Society of Tropical Medicine and Hygiene, 2007,101:1169-1170. Injectable paromomycin for Visceral leishmaniasis in India. The New England Journal of Medicine, 2007,356:2571-2581. Treatment of kala-azar in southern Sudan using a 17-day regimen of sodium stibogluconate combined with paromomycin: a retrospective comparison with 30-day sodium stibogluconate monotherapy. The American Journal of Tropical Medicine and Hygiene, 2007,77:89-94. The world health report 2006– working together for health. Integrated management of childhood illness by outpatient health workers: technical basis and overview. The WHO Working Group on Guidelines for Integrated Management of the Sick Child. Bulletin of the World Health Organization, 1997,75:Suppl 17-24. Lay health workers in primary and community health care for maternal and child health and the manage- ment of infectious diseases. Cochrane Database of Systematic Reviews (Online), 2010,3CD004015. Intrapartum-related stillbirths and neonatal deaths in rural Bangladesh: a prospective, community-based cohort study. WHO recommendations: optimizing health worker roles to improve access to key maternal and newborn health interventions through task shifting. Rates of virological failure in patients treated in a home-based versus a facility-based HIV-care model in Jinja, southeast Uganda: a cluster-randomised equivalence trial. Task shifting of antiretroviral treatment from doctors to primary-care nurses in South Africa (STRETCH): a pragmatic, parallel, cluster-randomised trial. Routine versus clinically driven laboratory monitoring of HIV antiretroviral therapy in Africa (DART): a randomised non-inferiority trial. Measuring maternal mortality: an overview of opportunities and options for developing countries. Maternal mortality is declining, but more needs to be done. Improved access to comprehensive emergency obstetric care and its efect on institutional mater- nal mortality in rural Mali. Bulletin of the World Health Organization, 2009,87:30-38. Can paying for results help to achieve the Millennium Development Goals? A critical review of selected evaluations of results-based fnancing. Efect of a cash transfer programme for schooling on prevalence of HIV and herpes simplex type 2 in Malawi: a cluster randomised trial. Effect of a conditional cash transfer programme on childhood mortality: a nationwide analysis of Brazilian municipalities. Promoting healthy behaviours and improving health outcomes in low and middle income countries: a review of the impact of conditional cash transfer programmes. The cure for cholera - improving access to safe water and sanitation. The New England Journal of Medicine, 2013,368:592-594. Annual Review of Public Health, 2012 (Epub ahead of print). The quest for universal health coverage: achieving social protection for all in Mexico.
Third generic 40mg paroxetine with mastercard symptoms early pregnancy, LTP is readily generated in in vitro prepara- nel buy paroxetine 30mg mastercard treatment variance. Depolarization of the postsynaptic cell (right) relieves the tions of the hippocampus buy 20mg paroxetine amex treatment works, thus making it accessible to rigor- Mg2 block of the NMDA receptor channel and allows Na and Ca2 to flow into the cell buy paroxetine 40 mg with visa treatment 2011. The resultant rise in Ca2 in the den- ous experimental analysis. Indeed, much of what we know dritic spine is a necessary trigger for the subsequent events lead- about the detailed mechanisms of LTP derives from studies ing to LTP. Fourth, LTP has been observed at vir- tually every excitatory synapse in the mammalian brain that has been studied. In con- in which LTP has been demonstrated, and it can be seen trast, as described in Chapter 6, the NMDA receptor ex- that regions thought to be particularly important for various hibits a strong voltage dependence because of the block of forms of learning and memory are prominent. Although its channel at negative membrane potentials by extracellular LTP is not a unitary phenomenon, most synapses appear magnesium. As a result, NMDA receptors contribute little to express a form of LTP that is identical or highly analogous to the postsynaptic response during basal synaptic activity. Thus, this form of LTP is the focus of the remainder ciates from its binding site within the NMDA receptor of this section. The resultant rise in intracellular calcium is a necessary and perhaps sufficient trigger for LTP. This local source of calcium within the dendritic spine ac- Triggering of LTP: A Critical Role for NMDA counts for the input specificity of LTP. Receptors and Calcium The evidence in support of this model for the initial It is well established that the triggering of LTP requires triggering of LTP is compelling. Specific NMDA receptor synaptic activation of postsynaptic N-methyl-d-aspartate antagonists have minimal effects on basal synaptic transmis- (NMDA) receptors, a subtype of ionotropic glutamate re- sion but block the generation of LTP (22,23). Preventing ceptor (see Chapter 6) and postsynaptic depolarization, the rise in calcium by loading cells with calcium chelators which is accomplished experimentally by repetitive tetanic blocks LTP (24,25), whereas directly raising intracellular stimulation of synapses or by directly depolarizing the cell calcium in the postsynaptic cell mimics LTP (25,26). How do these requirements ex- receptor activation causes a large increase in calcium level plain the properties of LTP? During basal low-frequency within dendritic spines (see 23 for references). The exact synaptic transmission, synaptically released glutamate binds properties of the calcium signal that is required to trigger to two different subtypes of ionotropic glutamate receptor, LTP are unknown, but a transient signal lasting only 1 to termed AMPA ( -amino-3-hydroxy-5-methyl-4-isoxazole 3 seconds appears to be sufficient (27). Whether additional propionic acid) and NMDA receptors, which are often, but sources of calcium, such as release from intracellular stores, not always (see later), co-localized on individual dendritic are required for the generation of LTP is unclear. The AMPA receptor has a channel that is permeable uncertain whether additional factors provide by synaptic to monovalent cations (Na and K ), and activation of activity are required. Various neurotransmitters found in AMPA receptors provides most of the inward current that the hippocampus such as acetylcholine and norepinephrine generates the excitatory synaptic response when the cell is can modulate the ability to trigger LTP, and such modula- 150 Neuropsychopharmacology: The Fifth Generation of Progress tion may be of great importance for the functional in vivo to CaMKII, whereas the tyrosine kinases Fyn and Src may roles of LTP. However, there is no compelling evidence to indirectly modulate LTP by affecting NMDA receptor suggest that any neurotransmitter other than glutamate is function (see 23 for references). Signal Transduction Mechanisms in LTP Expression Mechanisms and LTP A bewildering array of signal transduction molecules has been suggested to play a role in translating the calcium signal In the 1990s, tremendous confusion and controversy sur- that is required to trigger LTP into a long-lasting increase rounded the seemingly simple issue of whether LTP is in synaptic strength (28). However, for only a few of these caused primarily by presynaptic or postsynaptic modifica- has compelling evidence of a mandatory role in LTP been tions. The great challenge to answering this question largely presented. A major limitation of much of the work on this stemmed from the great technical difficulties inherent in topic is that investigators have not adequately distinguished examining the changes the occur at individual synapses that molecules that are key components of the signal transduc- are embedded in a complex network in which each cell tion machinery absolutely required for LTP from biochemi- receives 10,000 or more synapses. Most neurobiologists cal processes that modulate the ability to generate LTP or studying this question agree that the simplest postsynaptic play a permissive role. For example, any manipulation that change that could cause LTP would be a change in AMPA modifies the activity of NMDA receptors may affect LTP. First, it must be activated Most studies examining this issue have used electrophysi- or produced by stimuli that trigger LTP but not by stimuli ologic assays, and most of these are inconsistent with the that fail to do so. Second, inhibition of the pathway in hypothesis that the release of glutamate increases signifi- which the molecule participates should block the generation cantly during LTP (23,39). Third, activation of the pathway should lead to mitter release probability invariably influence various forms LTP. To pendent protein kinase II (CaMKII) fulfills these require- measure glutamate release more directly, two approaches ments and is a key component of the molecular machinery were used. One took advantage of the finding that glial for LTP. Inhibiting its activity pharmacologically by directly cells tightly ensheath synapses and respond to synaptically loading postsynaptic cells with CaMKII inhibitors or ge- released glutamate by activation of electrogenic transporters netic knockout of a critical CaMKII subunit blocks the that generate a current directly proportional to the amount ability to generate LTP (29–31). Conversely, acutely in- of glutamate released (40,41). The other took advantage of creasing the postsynaptic concentration of active CaMKII use-dependent antagonists of the NMDA receptor or of a increases synaptic strength and occludes LTP (32,33). Fur- mutant AMPA receptor that lacks the GluR2 subunit. That this autophosphoryla- directly proportional to the probability of transmitter release tion is required for LTP was demonstrated by the finding (42,43). LTP had no discernible effect on these measures, that genetic replacement of endogenous CaMKII with a even though they were affected in the predicted fashion by form lacking the autophosphorylation site prevented LTP manipulations known to increase transmitter release. In addition to these negative findings, certain electro- Several other protein kinases have also been suggested to physiologic and biochemical measures were found to in- play roles in the triggering of LTP, but the experimental crease during LTP. An increase in the amplitude of minia- evidence supporting their role is considerably weaker than ture electrophysiologic synaptic currents (mEPSCs), which for CaMKII. Activation of the cyclic adenosine monophos- represent the postsynaptic response to the spontaneous re- phate–dependent protein kinase (PKA), perhaps by activa- lease of a single quantum of neurotransmitter, normally in- tion of a calmodulin-dependent adenylyl cyclase, has been dicates an increase in the number or function of postsynap- suggested to boost the activity of CaMKII indirectly by tic neurotransmitter receptors. Such an increase occurs decreasing competing protein phosphatase activity (37,38). A more direct way 1, an endogenous protein phosphatase inhibitor (see section of monitoring changes in AMPA receptors is to measure on LTD later). Protein kinase C may play a role analogous the postsynaptic response to direct application of agonist, Chapter 11: Synaptic Plasticity 151 and such responses have also been reported to increase, al- beit gradually (47). That LTP is caused by a modification of AMPA receptors is supported by the finding that LTP causes an increase in the phosphorylation of the AMPA receptor subunit GluR1 at the site that is known to be phosphorylated by CaMKII (as well as PKC) (35,48,49). Using expression systems, this phosphorylation has been shown to increase the single- channel conductance of AMPA receptors (50). Because an increase in single-channel conductance of AMPA receptors has been reported to occur during LTP (51), one mecha- nism that seems likely to contribute to LTP is CaMKII- dependent phosphorylation of GluR1. Consistent with this idea, genetic knockout of GluR1 has been found to prevent the generation of LTP (52). A syn- Transmission apse is functionally silent when it expresses NMDA receptors but notAMPAreceptorsinitsplasma membrane(bottom). Theinduc- Although the evidence presented thus far makes a strong tion of LTPcauses the insertion of AMPA receptors (top) from a case for postsynaptic changes contributing to LTP, there putative cytosolic pool. To the right of each diagram are the syn- remained one reproducible experimental result that was dif- aptic currents (i. This result derived from experiments that took advantage of the finding that the action potential-dependent release of quanta of neurotrans- mitter at individual synapses is probabilistic, and therefore release occurs only 10% to 40% of the time. Therefore, if protocol at such synapses causes the rapid appearance of a single synapse or a very small number of synapses is acti- AMPA receptor-mediated EPSCs (55,56). Second, immu- vated once every few seconds, on some of the trials no post- nocytochemical analysis demonstrates that AMPA receptors synaptic response is recorded, that is, a so-called failure oc- are not found at a significant percentage of hippocampal curs. An extensively replicated finding is that LTP causes a synapses, whereas all synapses appear to contain NMDA decrease in the proportion of failures that occur (see 53 for receptors (see 23 for references).
An open cheap 20 mg paroxetine with amex symptoms xanax, dose ranging decreases cognitive function and catecholamine innervation in study of tomoxetine in children with ADHD buy 40 mg paroxetine with amex symptoms zithromax. Proceedings of the annual meeting of the American Academy 35 generic paroxetine 20 mg otc medicine youtube. Differential distribu- of Child and Adolescent Psychiatry XV buy paroxetine 30mg overnight delivery medicine for runny nose, Chicago, 1999. Psychopharmacology in in the target sites of the mesolimbic system in an animal model children and adolescents. Further evidence of of adults with attention deficit hyperactivity disorder. Am J an association between attention-deficit/hyperactivity disorder Psychiatry 1999;156:1931–1937. Neuropsychopharmacological mechanisms of stim- rette smoking in children and adolescents. J Am Acad Child ulant drug action in attention-deficit hyperactivity disorder: a Adolesc Psychiatry 1997;36:37–44. Noradrenergic hypothesis of atten- ADHD, depression, and non-tobacco substance use disorders to tion deficit disorder with hyperactivity: a critical review. In: nicotine dependence in substance-dependent delinquents. Psychopharmacology: the third generation of Alcohol Depend 1999;54:195–205. Neurobiology of attention deficit during pregnancy a risk factor for attention deficit hyperactivity disorder with hyperactivity: where have we come in 50 years? Catecholamines in attention- prenatal exposure to nicotine in guinea pigs. Neurobehav Toxicol deficity hyperactivity disorder: current perspectives. The biochemical basis striatal dopaminergic and nicotinic systems. Release of dopamine and 5- ject retrieval, and discrimination reversal deficits in chronic low hydroxytryptamine from rat striatal slices following activation dose MPTP-treated monkeys. Effects of dopamine ago- J Pharmacol 1987;141:395-399. Electrodermal correlates of hyper- MPTP-treated monkeys. Pharmacol Biochem Behav 1994;48: activity in children. The role of frontal lobe dysfunction in childhood 29. The clinical use of psychological and Brain Res 1994;60:115–124. Cambridge, MA: Harvard University Press, nergic function in the prefrontal cortex, nucleus accumbens 1988:46–69. Frontal lobe functions hyperactivity disorder: the spontaneously hypertensive rat. Brain in attention deficit disorder with and without hyperactivity: a Res 1995;676:343–351. The nucleus accumbens motor-limbic interface of 163–188. Neurosci Biobehav Rev 2000;24: history and comorbidity on the neuropsychological performance 133–136. Toward defining cleus accumbens slices and monoamine levels in a rat model for a neuropsychology of attention deficit-hyperactivity disorder: attention-deficit hyperactivity disorder. Neurochem Res 1995; performance of children and adolescents from a large clinically 20:427–433. Neuropsychological chrome oxidase mapping study, cross-regional and neurobehav- function in adults with attention-deficit hyperactivity disorder. Psychological adjustment psychosocial risk factors in DSM-III attention deficit disorder. J Atten J Am Acad Child Adolesc Psychiatry 1990;29:526–533. Attention dysfunc- of attention deficit hyperactivity disorder: evidence for single tion and psychopathology in college men. Attention deficit disor- Tohen M, Tsuang MT, Zahner GEP, eds. Further evidence and verbal learning deficits in adults diagnosed with attention for family-genetic risk factors in attention deficit hyperactivity deficit disorder. Neuropsychiatry Neuropsychol Behav Neurol disorder: patterns of comorbidity in probands and relatives psy- 1995;8:282–292. Evidence of familial (ADHD): diagnostic classification estimates for measures of association between attention deficit disorder and major affec- frontal lobe/executive functioning. Neuropsychological assessment of atten- disorder and major depression share familial risk factors? Attention deficit strain I/LnJ: a putative model of ADHD? Neurosci Biobehav disorder and conduct disorder: longitudinal evidence for a famil- Rev 2000;24:45–50. J Am Acad Child Adolesc Psychiatry 1994; cial disorders among relatives of ADHD children: parsing famil- 33:858–868. Attention-deficit vation in ADHD: preschool and elementary school boys and hyperactivity disorder with bipolar disorder: a familial subtype? J Am Acad Child Adolesc Psychiatry 1999;38:1363–1371. J Am Acad Child Adolesc Psychiatry 1997;36:1378–1387;discus- 64. Familial association rine-18]fluorodopa positron emission tomographic study. J between attention deficit disorder and anxiety disorders. Evidence dysfunction in attention deficit/hyperactivity disorder revealed for the independent familial transmission of attention deficit by fMRI and the counting stroop. Biol Psychiatry 1999;45: hyperactivity disorder and learning disabilities: results from a 1542–1552. Refining the ADHD metabolism in adults with hyperactivity of childhood onset. Toward guidelines porter density is elevated in patients with attention deficit hyper- for pedigree selection in genetic studies of attention deficit hy- activity disorder. Neuropsychiatry Neuropsychol Behav Neurol 1997;10: tence and remission of ADHD: results from a four-year prospec- 151–154. Herskovits EH, Megalooikonomou V, Davatzikos C, et al. High risk for attention head injury predictive of subsequent development of attention- deficit hyperactivity disorder among children of parents with deficit/hyperactivity disorder? Analysis with brain-image data- childhood onset of the disorder: a pilot study. Diagnostic continuity anomalies in children with attention-deficit hyperactivity disor- between child and adolescent ADHD: findings from a longitu- der. Demonstration of The aetiological role of genes, family relationships and perinatal vertical transmission of attention deficit disorder.
Ventilated head-injured patients with intracranial pathology on CT require ICP monitoring discount 40mg paroxetine otc symptoms low blood pressure. Invasive or non-invasive neurospecific monitoring requires careful interpretation when assisting goal-directed therapies purchase paroxetine 30mg with amex symptoms ms women. Multimodal monitoring using a combination of techniques can overcome some of the limitations of individual methods discount 30 mg paroxetine fast delivery medications such as seasonale are designed to. Cerebral Edema Nabil Kitchener Cerebral edema is a challenging problem in the neurocritical care setting purchase paroxetine 10mg mastercard medications pregnancy. Different etiologies may cause increased intracranial pressure. Secondary brain injury may ensue as a result of cerebral edema, and may result in different herniation syndromes. Brain monitoring for increased intracranial pressure may by employed in certain patient populations. Serial neuroimaging may be useful in monitoring exacerbations of brain edema. Osmotherapy has been recommended for management of cerebral edema. Mannitol and hypertonic saline are the two agents widely used for this purpose. Knowledge of possible side effects of osmotherapeutic agents is necessary. Common concerns of such therapies include renal insufficiency, pulmonary edema, and exacerbation of congestive heart failure, hypernatremia, hemolysis, and hypotension. Specific measures as controlled ventilation, sedation and analgesia, pharmacologic coma, hypothermia and surgical decompression may be required in patient subpopulations. Important questions still need to be answered regarding the timing of the decompressive surgery and patient selection criteria. Surgical decompression may be applicable in certain patients. Recent studies indicate that surgical decompression may 80 | Critical Care in Neurology significantly reduce mortality in young patients with malignant cerebral infarcts. General medical management is focused toward limiting secondary brain damage. General measures include head and neck position, optimization of cerebral perfusion and oxygenation, management of fever, nutritional support and glycemic control. Abnormalities of intracranial pressure may result in pathology requiring urgent evaluation and intervention to prevent life- threatening consequences. This pathology may represent intracranial hyper- or hypotension, or it may manifest as an abnormality of cerebrospinal fluid (CSF) dynamics, such as hydrocephalus. Elevated intracerebral pressure is the final common pathway for almost all pathology leading to brain death, and interventions to treat ICP may preserve life and improve neurologic function after head trauma, stroke, or other neurologic emergencies. Common causes of raised intracranial pressure are shown in Table 7. Lead encephalopathy Hepatic coma Renal failure Diabetic ketoacidosis Burns Near drowning Hyponatremia Status epilepticus Types of Cerebral Edema Cerebral swelling or edema can complicate many intracranial pathologic processes including neoplasms, hemorrhage, trauma, autoimmune diseases, hyperemia, or ischemia. There are essentially three types of cerebral edema: 1. Cytotoxic edema is associated with cell death and failure of ion homeostasis. Cytotoxic edema results from energy failure of a cell as a result of hypoxic or ischemic stress, 82 | Critical Care in Neurology which leads to cell death. Intracellular swelling occurs and results in the CT and MR appearance of both gray and white matter edema, usually in the distribution of a vascular or borderzone territory after hypoxia or stroke. Vasogenic edema is associated with breakdown of the blood-brain barrier. Vasogenic edema represents breakdown of the blood-brain barrier, appears mostly in the white matter, and is more likely to be associated with neoplasms or cerebral abscesses. In reality, cerebral edema in many situations, usually exhibit a combination of vasogenic and cytotoxic edema. Interstitial (hydrostatic or hydrocephalic) edema is associated with hydrocephalus, in which there is increased tension of CSF across the ependyma. Interstitial edema, or transependymal flow, is radiographically seen with hypodense areas surrounding the ventricular system and is associated with increased CSF volume or pressure. In cytotoxic edema, osmotic therapy with mannitol and hypertonic saline may not reduce edema in the Cerebral Edema | 83 lesion itself, but may reduce the volume of normal brain allowing for some increased margin of safety by decreasing intracranial pressure (Raslan 2007). Steroids are of no value in cytotoxic edema due to stroke, and may be harmful in the settings of brain trauma. Surgical decompression of cytotoxic edema with decompressive craniectomy may be therapeutic, and life-saving (Hofmeijer 2009). Vasogenic edema responds to steroids and surgical resection of the lesion, and may also benefit from osmotic therapy with mannitol or hypertonic saline (Oddo 2009). Hydrostatic edema is treated surgically with CSF removal or shunting, and it is treated medically with agents to decrease production of CSF, such as acetazolamide and furosemide. General Neurological Treatment Strategies Magdy Khalaf, Nabil Kitchener The concept of neurocritical care has been developed to coordinate the management of critically ill neurological patients within a single specialist unit and to include clinical situations such as swallowing disturbances, respiratory problems management in neurocritical care, infection control in the unit, pain relief and sedation in some patients, as well as diagnosing brain death. Acute rehabilitation is important in securing improved long-term neurological outcomes after many brain insults, trauma, ischemia or hemorrhage. Intervention from neurophysiotherapists, as part of the neurocritical care multiprofessional team, must occur as early as possible. Respiratory muscle impairment is the most common reason for admission to the ICU in patients with neuromuscular disorders. Objective measures of respiratory muscle function are necessary because significant respiratory muscle impairment may exist despite a paucity of symptoms. Analgesia in the neurocritical care unit is indicated in many situations such as postoperative pain, traumatic injury, and subacute or chronic pains. Although it is mandatory and beneficial in many situations, precautions must be taken before General Neurological Treatment Strategies | 85 applying many agents; e. Some agents may cause decreased level of consciousness or obtundation leading to impairment of neurological exam. This chapter will cover management of these issues in the neurocritical care setting. Swallowing Disturbances Weakness, spasticity or both of the pharynx and tongue cause dysphagia and tendency for aspiration. A feeding tube through a percutaneous endoscopic gastrostomy (PEG), cervical esophagostomy or jejunostomy is a reliable method of patient feeding when prolonged deficit is expected. Nutrition support by enteral feeding through either a nasogastric or an orogastric tube should be maintained in all intubated patients whenever possible. In patients with a normal baseline nutritional state, support should be initiated within 7 days. In malnourished patients, nutritional support should be initiated within 72 h. Delayed gastric emptying is common in critically ill patients on sedative medications but often responds to promotility agents such as domperidone, and metoclopramide (Gomes 2010). Parenteral nutrition is an alternative to enteral nutrition in patients with severe gastrointestinal pathology. When patients improve the gastrostomy is easy to close.
Serotonergic func- sants in obsessive-compulsive disorder: antiobsessional or anti- tion in obsessive-compulsive disorder: behavioral and neuroen- depressant agents? Biol Psychiatry 1995;38: obsessive-compulsive disorder: a placebo-controlled double- 138–149 buy 30mg paroxetine otc medications zoloft side effects. Clomipramine in fects of tryptophan and m-chlorophenylpiperazine in patients the treatment of patients with obsessive-compulsive disorder purchase paroxetine 10mg without prescription treatment xerosis. Clomipramine treat- ity in obsessive-compulsive disorder: effects of chronic clomi- ment of obsessive-compulsive disorder 10mg paroxetine with mastercard medications and grapefruit interactions. Double blind tine treatment on behavioral and neuroendocrine responses to comparative study of clomipramine and amitriptyline in obses- meta-chlorophenylpiperazine in obsessive-compulsive disorder purchase 20mg paroxetine with visa symptoms 37 weeks pregnant. A double- blind trial of clomipramine and clorgyline. Effect of chronic during pharmacologic treatment of patients with obsessive-com- administration of selective 5-hydroxytryptamine and noradrena- pulsive disorder. A double-blind trial of chlorimipramine and doxepin nin reuptake inhibitors: relevance to treatment of obsessive- in obsessive-compulsive neurosis. Neuropsychopharmacology 1995;13:117– Shen Ko Tsa Chih (in Chinese) 1986;19(5):279–281. A cross-over treatment of obsessive-compulsive neurosis Chapter 114: Current and Experimental Therapeutics of OCD 1661 with imipramine and cholimipramine. Chung Hua Shen Ching DSM-III-R obsessive-compulsive disorder. Eur Neuropsy- Ching Shen Ko Tsa Chih (in Chinese) 1986;19(2):275–278. A control study of clomipramine and amitriptyline 79. Are fluoxetine for treating obsessive-compulsive study Chung Hua Shen Ching plasma levels related to outcome in obsessive-compulsive disor- Ching Shen Ko Tsa Chih (in Chinese) 1991;24(2):67–70, 123. Fluvoxamine treatment inhibitors in anxiety disorder: a double blind comparison of of obsessive-compulsive disorder. Am J Psychiatry 1987;144: clomipramine and fluvoxamine. Controlled comparison mine in obsessive-compulsive disorder. Arch Gen Psychiatry of clomipramine and fluoxetine in the treatment of obsessive- 1989;46:36–44. Zohar J, Judge R, the OCD Paroxetine Study Investigators. Paroxetine versus clomipramine in the treatment of obsessive- 84. Efficacy of fluvoxamine, pa- Am J Psychiatry 1990;147:923–928. Results of a dou- sive disorder: a single blind study. J Clin Psychopharmacol 1997; ble-blind placebo controlled trial of a new serotonin uptake 17:267–271. Double-blind parallel cacy of a serotonin reuptake inhibitor in imagined ugliness. Arch comparison of three dosages of sertraline and placebo in outpa- Gen Psychiatry 1999;56:1033–1039. Current issues in the phar- treatment of obsessive-compulsive disorder: an open pilot study. J Clin Psychopharmacology disorders: practical management. Fluvoxamine in OCD: a multicenter parallel design reuptake inhibitor citalopram in obsessive-compulsive disorder. Treatment of obsessive-compulsive Congress, Nice, France, June, 1992. Review of the cardiovascular treatment and prevention of relapse of obsessive-compulsive dis- effects of heterocyclic antidepressants. Treatment emer- investigation of fixed-dose fluoxetine in the treatment of obses- gent sexual dysfunction with fluoxetine. In: Pollack MH, Otto MW, Rosenbaum comparison of three dosages of sertraline and placebo in outpa- JF, eds. New York: Guilford Press, tients with obsessive-compulsive disorder. Drugs and the treatment of psychiatric disor- fluoxetine. New York: McGraw-Hill, 1996: treatment of obsessive-compulsive disorder. Open trial of fluoxetine interactions of psychotropic drugs. Int J Psychol Med 1991;21: in obsessive-compulsive disorder. J Int Clin Psychopharmacol 1994;14: ment of obsessive-compulsive disorder: an open clinical trial. Am J Psychiatry 1996;153: blind, placebo-controlled study of fluoxetine inpatients with 311–320. Psychopharmacology in the medically sented at the Annual Meeting of the American Psychiatric Asso- ill. Principles of medical psychia- ciation, New York, May 1996. Efficacy of drug treatment in obses- adolescents with obsessive-compulsive disorder (Letter). Am J sive-compulsive disorder: a meta-analytic review. Int Clin Psycho- pulsive disorders: preliminary clinical experience. Fluvoxamine trial of fluoxetine and placebo in children and adolescents with versus clomipramine in the treatment of obsessive-compulsive obsessive-compulsive disorder. J Am Acad Child Adolesc Psychia- disorder: a multi-center, randomized, double-blind, parallel try 1992;31:1062–1069. Fluvoxamine versus to fluoxetine in the treatment of children and adolescents with clomipramine for obsessive-compulsive disorder: a double-blind obsessive-compulsive disorder. Sertraline in children ment of obsessive-compulsive disorder. Br J Psychiatry 1996; and adolescents with obsessive-compulsive disorder: a multicen- 169:468–474. Clomipramine versus fluoxetine 1752–1756 (published erratum appears in JAMA 2000;8: in obsessive-compulsive disorder: a retrospective comparison of 283(10):1293). Riddle MA, Reeve EA, Yaryura-Tobias side effects and efficacy. Fluvoxamine for children and adolescents with obses- 122–124. A review of the efficacy of selective seroto- trial. J Am Acad Child Adolesc Psychiatry 2001;40(2):222–229. Arch Gen Psychiatry 1985;42(10): toms after discontinuation of clomipramine in patients with 977–983. A double-blind der Psychopharmacol Bull 1980;16(3):61–63.