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English to French: Post-Traumatic Stress Disorder, From Neurobiology to Traitment General field: Medical Detailed field: Medical (general)
Source text - English The neurobiology of the stress response involves mechanisms related to bodily survival and adaptation to change. Stress is associated with various types of learning, including the learning of conditioned fear responses and autobiographical memory formation. While these adaptations can have survival value, a failure of another type of learning – the turning off of the fear response (or extinction) when no longer needed – can lead to pathology, including symptoms of PTSD. The breadth of the topic can be appraised by examining the time frames of some of the typical responses. The latter extend from fragments of seconds (e.g., for defense reflexes such as auditory startle), to several seconds (for sympathetic activation), tens of minutes (for activation of the HPA axis), hours (for early gene expression), days (for memory consolidation) and months (for permanent changes in the CNS to occur) (Post, 1992). Furthermore, at each stage, the biological responses to mental stressors are heavily modulated by appraisal (e.g., of the threat and of one’s own resources; Lazarus & Folkman, 1984), controllability, and attribution of meaning, and by the relative success in coping with tasks related to survival and learning. Prior experiences and beliefs are also powerful modulators of the mental and therefore the biological response to adversities. Most adverse mental health consequences of traumatic events result from our immense ability to learn, remember, and reshape our behavior (and the underlying CNS functioning) on the basis of new – including catastrophic – experiences. The meaning conveyed to one’s action (e.g., cowardice, heroism), as well as the meaningfulness of a group effort (e.g., unnecessary war) can either soothe and down-regulate fear responses or maintain and reinforce them (Holloway & Ursano, 1984). Stress results in acute and chronic changes in neurochemical systems and specific brain regions, which result in long-term changes in brain “circuits” involved in the stress response (Bremner, 2011; Vermetten & Bremner, 2002a,b). Brain regions that are felt to play an important role in PTSD include the hippocampus, the amygdala, and the medial prefrontal cortex. Cortisol and norepinephrine are two neurochemical systems that are critical in the stress response.
1.2.1 Cortisol and norepinephrine The corticotropin-releasing factor (CRF)/HPA axis system plays an important role in the stress response (Chrousos & Gold, 1992) (see Chapter 11). CRF is released from the hypothalamus, with stimulation of adrenocorticotropin hormone (ACTH) release from the pituitary, resulting in glucocorticoid (cortisol in man) release from the adrenal, which in turn has a negative feedback effect on the axis at the level of the pituitary, as well as central brain sites including the hypothalamus and hippocampus. Cortisol has a number of effects that facilitate survival and triggers other neurochemical responses to stress, such as the noradrenergic system via the brainstem locus coeruleus (Melia & Duman, 1991). Other responses include an activation of brain areas related to perceiving and responding to the environment. Other players in the immediate response include nuclei controlling facial expression, breathing rhythm, startle response, and parasympathetic modulation of heart rate. This cluster of responses is controlled by the central nucleus of the amygdala – a powerful modulator of fear responses (Davis, 1992; LeDoux, 1993, 1996). Stress also results in activation of the noradrenergic system, centered in the locus coeruleus. Noradrenergic neurons release transmitter throughout the brain which is associated with an increase in alerting and vigilance behaviors, critical for coping with acute threat (Abercrombie & Jacobs, 1987; Bremner et al., 1996a,b). Studies in animals have shown that early stress has lasting effects on the HPA axis and norepinephrine (Plotsky & Meaney, 1993). These effects could be mediated by an increase in synthesis of CRH messenger RNA (mRNA) following stress (Makino et al., 1995). Exposure to chronic stress results in potentiation of noradrenergic responsiveness to subsequent stressors and increased release of norepinephrine in the hippocampus and other brain regions (Abercrombie & Jacobs, 1987). It has been theorized that a failure to mount appropriate levels of cortisol during traumatic events may lead to prolonged adrenergic activation and thereby increase the risk of developing PTSDs (Yehuda, 1998). Abnormally low cortisol levels following trauma were, in fact, reported in vulnerable rape victims and in road accident survivors who were at higher risk for developing PTSD (McFarlane et al., 1997; Resnick et al., 1995), but the causal link with PTSD has not been established. A combination of adrenergic activation and low levels of cortisol has been shown to significantly increase emotional learning in animals (Bohus, 1984; Munck et al., 1984). Importantly, the hormonal stress response seems to “go wrong” in individuals whose prior life experience was particularly stressful (Resnick et al., 1995) – yet this also requires further confirmation. The intensity of biopsychological responses to traumatic events increases in circumstances that are uncontrollable and inescapable (Anisman et al., 1981; Breier, 1989; Seligman & Meier, 1967).
1.2.2 Biology of learning and adaptation in PTSD Immediate alarm responses are followed, in the brain, by a cascade of metabolic and genomic (i.e., expression of new genes) events (Post, 1992). Importantly, the cascade of neuronal changes includes areas of the brain that are not directly involved in stress response. Particularly interesting is the activation of protein synthesis in brain areas related to learning and memory, such as the hippocampus and the amygdala (e.g., Davis, 1994) (seeChapter6). Newly synthesized proteins in these areas constitute the biological basis of long-term memories of stressful events. The distribution of these biological changes in the brain suggests that there are two types of memory traces of stressful events: explicit memories (i.e., verbal and retrievable) and implicit memories (e.g., changes in habits, conditioned responses). This is very important, because non-verbal, implicit memories of traumatic events may shape future behavior in the absence of conscious elaboration and verbal recall (e.g., by causing bodily alarm and emotional fear responses upon exposure to reminders of the traumatic event). Experimental work in animals has shown that a subtype of emotional memories, based on “quick and dirty” processing of sensory information, is acquired and stored in the lateral and basal nuclei of the amygdala (LeDoux, 1993, 1995). LeDoux has also shown that such “emotional” learning (indeed, fear conditioning) is relatively immune to change. Memory traces stored in the basal and lateral nuclei of the amygdala are subsequently used to interpret new sensory signals as to their aversive nature, such that when a stimulus is interpreted as immediately threatening, the central nucleus of the amygdala is activated (see earlier) and the fear response is put in motion. Despite the persistence of emotional learning, the behavioral expression of fear conditioning can be inhibited by the activity of cortical areas of the brain (Morgan et al., 1993 ; Morgan & LeDoux, 1995). This is, in fact, what happens when aversive or conditioned responses subside; the information is not forgotten or erased, but rather put under inhibitory control (Quirketal., 2006). Brain areas involved in such inhibitory control include sensory association areas, areas in the frontal lobe and the hippocampus. Memories of traumatic events, therefore, are not suppressed, but rather controlled and neglected, such that they have no behavioral expression. Subsequent traumatization may activate such memories, yet the strategy of controlling the effect of aversive learning may also be stronger in individuals who recover from traumatic events. Exposure to stressful events, therefore, may either “sensitize” or “immunize” survivors (Solomonetal.,1987). Further experimental work has shown that aversive memories, at the level of the amygdala, can be reinforced by elevated plasma levels of the stress hormone epinephrine (Cahill & McGaugh, 1998; McGaugh, 1985, 2000). An initial hypersecretion of the epinephrine could be involved in an exaggeration and a consolidation of fear-related memories of the traumatic event (Cahill et al., 1994; McGaugh et al., 1990). Moreover, the intensity of the adrenergic “stress” response can also foster emotional (and amygdala-mediated) learning at the expense of rational or declarative, hippocampus-mediated learning (Metcalfe & Jacobs, 1996). Supportive evidence for the link between an initial autonomic activation and subsequent PTSD has been found in a study of patients presenting to the emergency room after a trauma (Shalevetal., 1998). Heart rate levels upon admission were higher in subjects who subsequently developed PTSD. In another study of trauma survivors, the physiological response of heart rate, skin conductance and electromyography (frontalis) to mental imagery recorded a short time following the trauma was shown to differentiate between those who went on to develop PTSD and those who did not (Shalev et al., 1993a). Trauma survivors admitted to the emergency room, who subsequently went on to develop PTSD had higher heart rates at the emergency department and 1 week later, but not after 1 and 4 months (Shalev et al., 1988). PTSD patients can re-access their trauma memories as often as 100 times a day, and elicit these physiological reactions each time. PTSD patients possibly continue to reinforce the initial impact of the trauma by reactivating it in this way. PTSD patients have also been reported to differentiate from normal survivors by poor habituation of skin conductance to a repetition of loud startling noises (Shalev et al., 1992). This may represent a primary defect of the CNS that continues to identify and classify the loud tones as threatening in people with PTSD. PTSD patients, therefore, continue to react, rather than rejecting the noises as redundant information and stopping the reaction to them. In a prospective study of 239 trauma survivors (Shalevetal.,2000), the auditory startle response of all the trauma survivors is normal at 1 week. The response of those patients who go on to develop PTSD becomes abnormal between 1 and 4 months after the trauma, suggesting that this is the critical period during which the CNS adapts its response to ambiguous stimuli (such as loud noises) and determines whether PTSD develops. There are two important questions for the clinician to address when trying to recognize the vulnerable patients who will develop PTSD: why does trauma lead to PTSD for them rather than some other psychiatric disorder or no disorder at all; and what are the risk factors for determining these patients? The acute stress response is universal and non-predictive of PTSD. Moreover, as mentioned, patients who develop PTSD fail to show are mission of these acute symptoms and show abnormally increased heart rates several days after the trauma, as well as other abnormal physiological responses such as the increased startle response. It would therefore appear that PTSD might develop as a failure of the body to reverse the acute stress response. Preclinical and clinical studies have shown alterations in memory function following traumatic stress as well as changes in a circuit of brain areas, including hippocampus, amygdala, and medial prefrontal cortex, that mediate alterations in memory (Bremner, 2003, 2010, 2011; Bremner & Charney, 2010; Garakani et al., 2011). The hippocampus, a brain area involved in verbal declarative memory, is very sensitive to the effects of stress (see Chapter 6). Stress in animals was associated with alterations in neuronal structure in the CA3 region of the hippocampus (which may be mediated by hypercortisolemia, decreased brain-derived neurotrophic factor, and/or elevated glutamate levels) and inhibition of neurogenesis (Magarinos & McEwen, 1995; Nibuya et al., 1995; Sapolsky et al., 1990). As reviewed in Chapter 6, high levels of glucocorticoids seen with stress were also associated with deficits in new learning (Diamond et al., 1996; Luine et al., 1994). Antidepressant treatments block the effects of stress and/or promote neurogenesis in the hippocampus (Nibuya et al., 1995; Santarelli et al., 2003), including phenytoin (Watanabe et al., 1992), tianeptine, dihydroepiandosterone, and fluoxetine (Czeh et al., 2001; D’Sa & Duman, 2002; Duman, 2004; Duman et al., 2001; Garcia, 2002; Lucassen et al., 2004; Malberg et al., 2000; McEwen & Chattarji, 2004), which may represent, at least in part, the mechanism of action of the behavioral effects of antidepressants (Santarelli et al., 2003; Watanabe et al., 1992; although see Henn & Vollmayr, 2004). Changes in the environment have also been shown to modulate neurogenesis in the dentate gyrus of the hippocampus, and slow the normal age-related decline in neurogenesis (Gould et al., 1999; Kempermann et al., 1998). Chapter11ofthisvolumereviewsthelong-termdysregulationoftheHPAaxis associated with PTSD. Findings include low or normal baseline levels of cortisol (Yehudaetal.,1991,1995a) with two studies using multiple serial measurements in plasma showing a loss of normal diurnal rhythm and decreases at specific times of the day (Bremner et al., 1997; Yehuda et al., 1994), elevations in CRF (Bakeretal.,1999;Bremneretal.,1997),increasednegativefeedbackoftheHPA axis after dexamethasone challenge (Stein et al., 1997; Yehuda et al., 1993) and increased cortisol response to stress, especially trauma-specific stressors (Elzinga et al., 2003).
1.2.3 Cognitive function and brain structure in PTSD Studies in PTSD are consistent with changes in cognition and brain structure (see Chapter 12 in this volume for a review of brain imaging studies in PTSD). Multiple studies have demonstrated verbal declarative memory deficits in PTSD (Brewin, 2001; Buckley et al., 2000; Elzinga & Bremner, 2002; Golier & Yehuda, 1998). Patients with PTSD secondary to combat (Bremner et al., 1993a; Golier et al., 1997; Uddo et al., 1993; Vasterling et al., 1998; Yehuda et al., 1995b), rape (Jenkins et al., 1998), the Holocaust (Golier et al., 2002; Yehuda et al., 1995b), and childhood abuse (Bremner et al., 1995a; Bremner et al., 2004; Moradi et al., 1999) were found to have deficits in verbal declarative memory function based on neuropsychological testing with a relative sparing of visual memory and IQ (Barrett et al., 1996 ; Bremner et al., 1993a, 1995a; Gil et al., 1990; Gilbertson et al., 2001; Golier et al., 1997, 2002; Jenkins et al., 1998; Moradi et al., 1999; Roca&Freeman,2001;Sachinvalaetal.,2000;Uddoetal.,1993;Vasterlingetal., 1998, 2002; Yehuda et al., 1995b). Other types of memory disturbance studies in PTSD include gaps in memory for everyday events (dissociative amnesia; Bremner et al., 1993b), deficits in autobiographical memory (McNally et al., 1994), an attentional bias for trauma-related material (Beck et al., 2001; Bryant &Harvey,1995;Cassidayetal.,1992;Foaetal.,1991;Golieretal.,2003;McNally et al., 1990, 1993; McNeil et al., 1999; Moradi et al., 2000; Thrasher et al., 1994) and frontal lobe-related impairments (Beckham et al., 1998). These studies show that PTSD is associated with deficits in verbal declarative memory (Elzinga & Bremner, 2002). Studies have also shown a smaller volume of the hippocampus in PTSD (Bremner & Vermetten, 2012). Vietnam veterans with PTSD were originally shown to have 8% smaller right hippocampal volume based on magnetic resonance imaging (MRI) relative to controls matched for a variety of factors such as alcohol abuse and education (Bremner et al., 1995b). These studies, which are described in detail in Chapter 12 of this volume, were later extended to adults with PTSD from childhood abuse, but not children with PTSD. Other studies in PTSD have found smaller hippocampal volume and/or reductions in N-acetyl aspartate, a marker of neuronal integrity. Meta-analyses, in which data are pooled from all of the published studies, found smaller hippocampal volume for both the left and the right sides, equally in adult men and women with chronic PTSD, and no change in children (Kitayama et al., 2005; Smith, 2005; Woon et al., 2010). Several studies have shown that PTSD patients have deficits in hippocampal activation while performing a verbal declarative memory task (Astur et al., 2006; Bremner et al., 2003; Shin et al., 2004b). In addition to the hippocampus, other brain structures have been implicated in a neural circuitry of stress, including the amygdala and prefrontal cortex. Animal studies also show that early stress is associated with a decrease in branching of neurons in the medial prefrontal cortex (Radley et al., 2004). Studies in PTSD found smaller volumes of the anterior cingulate based on MRI measurements (Kitayama et al., 2006; Rauch et al., 2003). Structural imaging studies in PTSD are reviewed in more detail in Chapter 12.
Translation - French L’incidence des courses marathon répétées sur la fonction cardiovasculaire au sein de la population vieillissante
Erin Karlstedt1 , Anjala Chelvanathan2 , Megan Da Silva1 , Kelby Cleverley1 , Kanwal Kumar3 , Navdeep Bhullar1 , Matthew Lytwyn1 , Sheena Bohonis1 , Sacha Oomah1 , Roman Nepomuceno1 , Xiaozhou Du1 , Steven Melnyk1 , Matthew Zeglinski1 , Robin Ducas2 , Mehdi Sefidgar4 , Scott Mackenzie4 , Sat Sharma5 , Iain D Kirkpatrick6 and Davinder S Jassal1,2,6*
Reçu : 17 avril 2012
Approuvé : 31 juillet 2012
Publié : 20 août 2012 [~]
Contexte clinique : Plusieurs études ont corrélé une augmentation des biomarqueurs cardiaques provenant d’une lésion après avoir participé à un marathon avec une dysfonction systolique ventriculaire droite (VD) transitoire et réversible, tel que démontré par une échocardiographie transthoracique (ETT) et une résonance magnétique cardiovasculaire (RMC). La présence de lésions myocardiques résultant de courses marathon répétées chez la population vieillissante reste un sujet controversé.
Objectifs : Évaluer l’importance et la gravité de la dysfonction cardiaque suite à une course marathon chez les individus de plus de 50 ans à l’aide des biomarqueurs cardiaques, de l’ETT, de la tomodensitométrie (TDM) cardiaque, et de la RMC.
Méthodologie : Un total de 25 volontaires sains (21 hommes, 55 ans ± 4 ans) ayant participé au Marathon du Manitoba (26,2 milles) de 2010 et de 2011 ont participé à l’étude. Les biomarqueurs cardiaques et les ETT ont été réalisés une semaine avant le marathon, tout de suite après le marathon et une semaine plus tard. Une RMC a été réalisée comme point de départ et dans les 24 heures suivant la fin du marathon, puis une TMD cardiaque dans les 3 mois suivant le marathon.
Résultats : Tous les participants présentaient une troponine cardiaque T (TnTc) élevée après le marathon. Les volumes atrial et ventriculaires droits avaient augmentés, alors que la fonction systolique du VD avait diminué considérablement immédiatement après le marathon, revenant aux valeurs de base une semaine plus tard. Une TDM cardiaque a révélé des signes de sténose de l’artère interventriculaire antérieure suite à un rehaussement tardif après gadolinium (RT) dans la région sous-endocardique de la paroi antérieure du ventricule gauche chez seulement deux individus parmi la population étudiée.
Conclusions : La course marathon est associée à une augmentation transitoire, mais réversible des marqueurs biologiques et à une dysfonction systolique du VD chez les individus de plus de 50 ans. La présence de fibrose myocardique chez les marathoniens plus âgés est peu fréquente, mais lorsque présente, elle pourrait être attribuable à une coronaropathie occulte sous-jacente.
Source text - English Grapefruit juice boosts the serum (blood) concentration of many medications. It contains furanocoumarin substances that bind to and inhibit the activity of certain cytochrome enzymes (such as cytochrome P450 and CYP3A4 ) in the small intestine. Usually, the cytochrome enzymes metabolize or partially break down many medications before they are absorbed into the bloodstream. Owing to its particular make-up, grapefruit juice blocks or handcuffs the enzymatic breakdown of many medications, thereby allowing blood levels to the drug to build to greater-than-normal concentrations, with possibly toxic effects.
The ability of grapefruit juice to increase drug absorption was first discovered during trials with felodipine (Plendil), a calcium channel blocker used for heart disease, in which blood levels of Plendil shot up after people drank grapefruit juice. Since then, the list of drugs affected by grapefruit juice has grown to include many familiar and widely used medications such as the cholesterol-lowering statins (including Lipitor, Zocor, Crestor and others), some benzodiazepines (tranquilizers), budesonide, cyclosporine and erythromycin antibiotics, some estrogens, nifedipine (Adalat), sertraline (Zoloft), fluoxetine (Prozac), verapamil and the anticoagulant, warfarin (Coumadin).
Since the drug-boosting effects of grapefruit juice can last several hours, even up to 24 hours, people should be wary when taking medications affected by this citrus fruit. The effect varies according to the type and amount of grapefruit juice swallowed. For example, 1 daily glass of normal-strength white grapefruit juice for 3 days doubled blood levels of some statin drugs (lovastatin and simvastatin); and 3 full glasses a day gave up to fifteenfold increases in these medications.
Most other citrus juices (sweet orange and tangerine) don’t contain furanocoumarins and therefore have no effect on drug concentrations although Seville oranges, tangelos and Indian pomelos can affect medication levels. So it’s best to check with the pharmacist or doctor about possible interactions, especially when blood concentrations need to be carefully controlled
Translation - French Le jus de pamplemousse augmente la concentration de nombreux médicaments dans le sérum (sang). Il contient des furanocoumarines qui se fixent à certaines enzymes cytochromes (telles que les cytochromes P450 et CYP3A4) et inhibent l’activité de ces dernières dans l’intestin grêle. Habituellement, plusieurs médicaments sont métabolisés et dégradés partiellement par les enzymes cytochromes avant leur passage dans la circulation sanguine. En raison de sa composition particulière, le jus de pamplemousse neutralise ou entrave la dégradation enzymatique de plusieurs médicaments, permettant ainsi aux taux de médicament dans le sang de s’élever à des concentrations supérieures à la normale, avec des effets possiblement toxiques.
La propriété du jus de pamplemousse d’augmenter l’absorption des médicaments a été découverte pour la première fois lors d’essais menés sur le félodipine (Plendil), un inhibiteur calcique utilisé pour les maladies cardiaques, au cours desquelles les concentrations de Plendil dans le sang ont augmenté de façon très significative après que les gens aient ingéré du jus de pamplemousse. Depuis, la liste de médicaments interagissant avec le jus de pamplemousse s’est allongée, englobant plusieurs médicaments courants et largement prescrits comme les réducteurs de cholestérol (incluant Lipitor, Zocor, Crestor et autres), certaines benzodiazépines (tranquillisants), le budésonide, la cyclosporine et l’érythromycine (antibiotique), certains œstrogènes, la nifédipine (Adalat), la sertraline (Zoloft), la fluoxétine (Prozac), le vérapamil et l’anticoagulant, la warfarine (Coumadin).
Puisque les effets amplificateurs du jus de pamplemousse sur les médicaments peuvent durer quelques heures, voire même jusqu’à 24 heures, les gens se doivent d’être prudents lorsqu’ils prennent des médicaments affectés par cet agrume. L’effet varie en fonction du type et de la quantité de jus de pamplemousse ingérés. Par exemple, un verre de jus de pamplemousse blanc à concentration normale par jour pendant 3 jours double le taux de médicaments à base de statine (lovastatine et simvastatine) dans le sang ; et en consommant 3 grands verres par jour, l’absorption de ces médicaments peut être multipliée par 15.
La majorité des autres agrumes (oranges sucrées et tangerines) ne contient pas de furanocoumarines et par conséquent ils n’ont aucun effet sur les concentrations médicamenteuses alors que les oranges de Séville, les tangelos et les pomelos peuvent influer sur les concentrations de médicaments. Alors il est préférable de vérifier auprès du pharmacien ou du médecin à propos des interactions possibles, plus particulièrement lorsque la concentration sanguine doit être attentivement surveillée.
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