Author Archives: Stéphane Bastianetto

1. Long-termisme : Un courant salvateur ou une idée destructrice ?

   6 décembre 2022 20 h 34 min Leave a Comment

   Le long-termisme, une philosophie trop ambitieuse ?

   Les précurseurs et les adeptes du long-termisme soutiennent que les décisions importantes que nous prenons actuellement doivent permettre d’améliorer le futur sur le très long terme. Certains y voient une manière de sacrifier le présent pour sauver le futur. D’autres se montrent beaucoup plus sceptiques face aux idéaux prônés par ce courant. Alors que ce mode de pensée est aujourd’hui mis en avant par certaines des plus grandes personnalités de ce monde, la question qui se pose est de savoir si ces personnes font fausse route ou si le long-termisme sauvera vraiment le monde.

   Les casinos en ligne et la question du divertissement immédiat

   Il est difficile de concilier les casinos en ligne, qui se focalisent sur le divertissement à court terme, et le concept même de long-termisme. En effet, les casinos canadiens en ligne sont plus focalisés sur le fait de fournir des sessions de qualité à leurs visiteurs, et ce, en s’appuyant sur les meilleurs jeux et bonus d’argent. Casinofrancaisenligne.com possède même une liste des meilleurs opérateurs au Canada pour tous ceux qui recherchent l’établissement de rêve pour s’amuser et gagner. Le moins qu’on puisse dire, c’est que les casinos canadiens en ligne laissent la porte ouverte au débat quant à savoir si les distractions d’aujourd’hui, aussi qualitatives qu’elles soient sont importantes quand on les compare aux défis de demain.

   Qu’est-ce que le long termisme ?

   Le long-termisme est un courant de pensée qui recherche une amélioration de l’avenir sur le long terme, qu’importent les moyens déployés dans le présent pour y parvenir. Les transhumanistes et les altruistes considèrent le long termisme comme une notion importante dans la mesure où il permet de justifier les efforts effectués afin de limiter la survenue d’évènements pouvant mettre en péril l’humanité tout entière. Les long-termistes prônent donc une idéologie selon laquelle il incombe à ceux qui vivent maintenant et qui en ont les moyens, de s’assurer que les générations à venir survivent et qu’elles s’épanouissent. Seuls comptent les incidences de nos actions futures sur le long terme. Selon ce concept, la génération actuelle est reléguée au second plan, puisqu’elle n’est qu’une étape vers un futur plus radieux selon les long-termistes. Son principal rôle est de déterminer de quelle manière l’histoire des générations futures sera façonnée, si elle y parvient avec succès, ou si elle échoue dans le processus.

   Afin de garantir cet avenir radieux à une génération sans cesse grandissante, le long-termisme compte énormément sur la technologie. Les long-termistes estiment que la technologie pourrait leur permettre de lutter contre les risques existentiels bien que ceux-ci ne menacent pas l’humanité à l’heure actuelle. Ils se préparent plutôt à des menaces très lointaines telles que la guerre biochimique, les pandémies ou encore la prise de pouvoir par les intelligences artificielles.

   Certaines personnes partisanes du long-termisme, pensent que la pire chose qui pourrait arriver à l’humanité, serait une stagnation des progrès scientifiques, car il existe une forte corrélation avec ceux-ci et non conditions de vie. Selon eux la technologie a avancé, à l’exemple des nouvelles technologies qui permettent de lutter contre la maladie de Parkinson, mais elle ne sera pas nécessairement en mesure de tout résoudre. Une proportion de long-termistes plus radicale pense qu’il serait préférable de sacrifier une partie de l’humanité, notamment les plus pauvres, afin de mieux se focaliser sur le futur. Ils nourrissent généralement une fascination pour la conquête spatiale car selon eux, ce serait l’un des moyens pour garantir un meilleur avenir pour les générations à venir.

   Comment améliorer l’avenir sur le long terme

   Les personnes chargées de l’étude sur le long termisme pensent qu’il est possible d’améliorer l’avenir sur le long terme de diverses manières.

   Limiter les risques existentiels

   Un risque existentiel est un danger qui menace de provoquer la destruction du potentiel humain, son extinction ou encore un effondrement sociétal. Lorsqu’on parle de risques existentiels, il s’agit de pandémies artificielles ou naturelles, de guerres nucléaires ou encore de changements climatiques extraordinaires. Réduire drastiquement les chances que l’un de ces risques ne survienne, pourrait permettre aux populations futures de se développer et vivre dans de meilleures conditions. Les adeptes du long-termisme pensent donc que l’humanité amorce un virage où tous les choix qu’elle fera durant ce siècle permettront de bâtir tout son avenir.

   <h3>Changer de trajectoire</h3>

   Les changements de trajectoire sont pour les chercheurs, une version plus légère des risques existentiels. Des économistes célèbres tels que Tyle Cowen soutiennent que l’augmentation du pourcentage de croissance est d’une importance capitale car elle permettra aux générations futures de s’enrichir. Toujours selon lui, le futur s’annonce très sombre pour les classes moyennes. Selon d’autres, l’optimisation d’institutions de gouvernance internationales et nationales et le changement des valeurs sociétales pourraient faciliter ces changements de trajectoire.

   Exploiter l’époque « charnière » dans laquelle nous vivons

   Selon les long-termistes, nous vivons à un moment crucial de l’histoire de l’humanité. Ils estiment que la société n’étant pas encore parvenue à un état stable, est toujours en mesure d’influencer celui dans lequel elle se trouve. Alors l’humanité peinait à influencer son avenir sur le long terme, deux concepts quelque peu récents ont en quelque sorte permis d’inverser la donne. Les armes nucléaires ont offert à l’humanité assez de pouvoir pour s’autodétruire, ce qui constitue un danger pour le développement des générations futures. Par ailleurs, les développements dans les sciences sociales et physiques ont permis à l’humanité de mesurer en quelque sorte l’impact de ses actions présentes sur le futur.

   Pourquoi le long-termisme suscite de la suspicion ?

   Certains considèrent que ce courant de pensée est assez risqué dans la mesure où selon la logique long-termiste, il est préférable d’investir ses ressources dans l’optimisation des conditions de vie des futures générations, peu importe à quel point le futur est lointain. Cela sans compter le sacrifice de nombreuses luttes telles que celles contre le réchauffement climatique, la précarité et la pauvreté, qui sont considérées comme ayant un impact négligeable en comparaison à l’existence même de l’humanité. Il faut remarquer que les précurseurs et les adeptes de ce courant sont puissants, riches qui vivent dans de grands cercles de décisions et qui ont par conséquent des moyens conséquents et nécessaires pour investir dans des projets qui s’inscrivent dans une vision long-termiste.

   On peut prendre l’exemple de Elon Musk ou encore de Sam Bankman-Fried qui a fait fortune dans les cryptomonnaies et qui a ensuite mis en place un fonds philanthropique estimé à plus de 132 millions de dollars. Ce fonds doit cependant servir dans un avenir lointain. Il n’est pas si simple de laisser des traces sur le futur ou encore de juger objectivement de l’impact de certains évènements après plusieurs siècles. Bien que chaque action et chaque évènement impacte le monde d’une certaine manière, dans un monde plutôt changeant, il n’est pas simple de conserver les traces d’actions individuelles dans le temps. Seules les actions collectives de grande envergure perdurent et ont une chance de changer le cours de l’histoire.

   <h2>Sacrifier le présent au détriment du futur</h2>

   Prenons le cas du Future Fund, l’organisation de Sam Bankman-Fried (SBF), dont le but est d’optimiser les perspectives humanitaires sur le long terme. Cette organisation avait pour but d’attribuer un fond d’au moins 100 millions de dollars à la cause long-termiste. Aujourd’hui, elle n’en a plus les moyens. On retient donc dans un premier temps qu’il y a toujours une part d’incertitude dans une promesse future. Par ailleurs, le long termisme ne définit pas de marche à suivre, alors que la liste de ses préoccupations ne cesse de grandir. Les long-termistes ont tendance à négliger les sérieux problèmes que nous rencontrons aujourd’hui, sous prétexte que l’avènement de solutions technologiques avancées, qui n’ont cependant pas encore été inventées, permettront de dépasser ces crises.

   D’aucuns pensent que le danger de cette pensée réside dans cette prévision absurde qui cherche incessamment à répondre à de grands défis dans le futur, tout en minimisant les problèmes actuels. La négligence sur le court terme pourrait pousser les long-termistes à se détourner de leurs objectifs, au point de se compliquer la tâche et d’envenimer des situations déjà existantes.

   L’altruisme repensé par les long-termistes

   Les plus grands partisans du long-termisme pensent qu’il ne faudrait pas gaspiller de l’énergie altruiste pour des projets tels que la découverte d’un traitement contre l’Alzheimer, la lutte contre la faim dans le monde, la lutte contre la pauvreté, le racisme ou encore le droit des femmes et qu’il serait plus important de consacrer cette énergie pour sauver des vies dans les pays riches. En effet, de nombreux long-termistes pensent que puisque l’avenir s’annonce vaste, les habitants des pays riches sont plus susceptibles d’avoir un impact sur celui-ci que ceux des pays pauvres. Il serait donc plus légitime d’accorder une plus grande priorité à la vie des habitants des pays riches.

   Par ailleurs, les altruistes efficaces estiment que la meilleure manière de se rendre utile à la cause humanitaire n’est pas de travailler dans un centre de recherche ou encore dans l’humanitaire. Selon eux, investir dans la recherche spatiale ou encore dans la construction d’une intelligence artificielle éthique sont plus utiles que de tenter de supprimer la faim ou la malaria dans le monde.

2. Mécanismes du plaisir et circuits de récompense du cerveau

   19 h 50 min 1 Comment

   Le circuit de récompense et les mécanismes du plaisir dans le cerveau

   Le désir, le plaisir et le besoin sont autant de sensations qui répondent à des mécanismes et des processus extrêmement complexes tous initiés par le cerveau humain. Tous ces mécanismes interviennent ensuite dans ce que l’on appelle le système de récompense. Aujourd’hui, le circuit de récompense intervient dans la quasi-totalité de ce que nous faisons, que cela soit fait consciemment ou non. Que se passe-t-il concrètement dans le cerveau et comment tout cela peut-il aboutir à l’addiction ?

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   Qu’est-ce que le circuit de la récompense du cerveau ?

   Encore appelé système hédonique, le circuit de la récompense fait référence à un réseau de connexions grâce auxquelles deux groupes de neurones sont interconnectés. Ces groupes de neurones représentent une structure paire dont une partie se trouve dans l’hémisphère gauche et l’autre dans l’hémisphère droit. Il est mis en évidence pour la première fois durant une expérience sur un animal. Il s’agissait d’une série d’expériences d’autostimulation dans laquelle l’animal s’autoadministre des drogues. Le circuit de la récompense participe au renforcement de certaines de nos habitudes, par exemple dans les habitudes sexuelles ou alimentaires. Bien que de nombreux neurotransmetteurs, messagers du cerveau, soient secrétés dans le circuit de la récompense, le principal demeure la dopamine. Viennent ensuite la noradrénaline, la sérotonine et le GABA. Les neurones à dopamine interviennent dans le désir et dans le plaisir.

   Le système de récompense est capital pour la survie puisqu’il fournit la motivation qu’il faut pour générer des comportements ou produire des actions permettant à un être vivant de survivre et de se préserver. Au fil de l’évolution et de la sélection naturelle, de nombreuses sensations de satisfaction ont été associées à ces comportements. Un circuit de récompense s’est naturellement mis en place afin de favoriser ces comportements, surtout ceux reliés à nos besoins fondamentaux. Il s’est ensuite agrandi pour nous contraindre à répéter les actions plaisantes que nous avons expérimentées durant notre vie. Des études en neurosciences ont permis de mettre en évidence les trois composantes qui constituent le système de récompense dans le cerveau.

   La composante affective

   On l’associe généralement au plaisir ou au déplaisir produit par la consommation d’un renforçateur (stimulus provoquant l’apprentissage de réactions autonomes ou de réactions motrices). Ici, le plaisir sexuel et gustatif sont les principales récompenses alors que la peur et la douleur sont les principales punitions.

   La composante motivationnelle

   La composante motivationnelle désigne la motivation qui est enclenchée par le renforçateur. Il peut s’agir de la détection du renforçateur par les organes sensoriels, soit d’une représentation mentale de ce renforçateur qui vient enclencher le désir ou la motivation nécessaire pour obtenir ou bénéficier de la récompense tout en se soustrayant à la punition.

   S’il s’agit de caresses, de chaleur ou de phéromones sexuelles, de renforçateurs inconditionnels en général, on se trouve en présence d’un stimulus qui entraîne l’activation des circuits innés tout en faisant également appel à une motivation innée. Au cas où le renforçateur serait conditionnel, on se trouve dans une situation où c’est le stimulus qui se charge d’activer de nouveau, une sensation déjà expérimentée avec le renforçateur, ce qui provoque parallèlement une envie de fuir le renforçateur ou une envie de le consommer.

   La composante cognitive

   La composante cognitive, c’est l’ensemble des apprentissages qui facilitent la combinaison entre réactions comportementales ou émotionnelles et renforçatrices. Notons que le plaisir et la motivation qu’un individu ressent pour un renforçateur sont conditionnés par l’état de son organisme et par les exigences de celui-ci.

   Par exemple, l’organisme est moins motivé par le sexe lorsqu’il est fatigué, une sensation de dégout peut naitre suite à une indigestion après ingestion de votre nourriture préférée et une nourriture est plus savoureuse au début d’un repas qu’à la fin. Les récompenses et les punitions (renforcements) ne sont pas toujours des phénomènes conscients. Il n’est pas impossible que des renforcements altèrent profondément les comportements et les états émotionnels de l’individu sans que celui-ci s’en rende compte.

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   Casinos en ligne sans dépôt et circuits de récompense du cerveau

   Les établissements de jeux, notamment les casinos en ligne, n’hésitent pas à exploiter le système de récompense pour attirer les clients et pour les fidéliser. Les machines-à-sous ont toujours été conçues, avec les lumières ou les symboles qui clignotent, ainsi que les effets sonores entraînants, pour stimuler les joueurs et associer les gains à une forte dose de dopamine. Le parieur ressent un rush qu’il va chercher à reproduire en jouant encore et encore.

   Les bonus de casinos en ligne interviennent aussi dans ce système de récompense. Les offres sans dépôt en particulier servent à titiller les joueurs avec leur format « zéro risque ». Bien entendu, les meilleurs casinos en ligne sont ceux qui sont suffisamment responsables pour prendre des mesures afin d’éviter les phénomènes d’addiction de leurs joueurs. C’est pour cela qu’il importe de suivre des guides de confiance pour trouver les bonus sans dépôt canadiens les plus en vogue. Vous pourrez ainsi tester gratuitement de nombreuses machines à sous sur les casinos en ligne sans prendre trop de risques.

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   Comprendre le mode de fonctionnement de la dopamine dans le cerveau

   La dopamine fait partie de nos messagers nerveux qui interviennent pour nous fournir une sensation de satisfaction en récompense à certains actes posés. Ce processus intervient dans les actes sexuels, les sentiments amoureux et est à l’origine des addictions. La dopamine est un neurotransmetteur que le corps humain sécrète naturellement. Notre cerveau est un amas de réseaux de neurones. C’est le centre névralgique des données et de toutes les pensées qui nous animent. La communication entre les neurones est possible grâce à un échange de molécules que sont les neurotransmetteurs parmi lesquels figure la dopamine. C’est une neurohormone secrétée par l’hypothalamus, la zone chargée de régulariser le cerveau, mais également par les corps striés à la base du cerveau et par le locus Niger au niveau de la moelle épinière. Une fois secrétée, la dopamine achemine les informations d’un neurone à un autre en la faisant transiter par la synapse, l’espace entre deux neurones.

   La sécrétion de la dopamine permet de mémoriser la sensation ressentie. Factuellement, la libération de la dopamine, son acheminement ou la manière dont elle se connecte aux récepteurs neuronaux, forment un ensemble qui conduit à des prises de décision différentes. La compréhension de notre pensée profonde utilise la dopamine.

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   Les autres neurotransmetteurs du système de récompense du cerveau

   La dopamine n’est pas le seul neurotransmetteur qui intervient dans le système de récompense dans le cerveau. Bien qu’il domine par son impact, de nombreux autres neurotransmetteurs interviennent dans le système de récompense et en dehors de la dopamine, les deux principaux sont les cannabinoïdes et les opioïdes endogènes.

   Les cannabinoïdes endogènes

   Les cannabinoïdes endogènes sont émis par certains organismes. Bien qu’ils aient quasiment les mêmes propriétés que les neurotransmetteurs, ils présentent cependant une différence. Alors que les neurotransmetteurs sont synthétisés continuellement par les cellules nerveuses dans le cytoplasme avant d’être stockés sous forme de vésicules, les cannabinoïdes ne sont synthétisés que lorsqu’il y a une stimulation. Ils font partie des principaux neurotransmetteurs de la composante affective.

   Les opioïdes endogènes

   Il s’agit d’un ensemble de neurotransmetteurs sécrétés naturellement par le corps. Ce groupe de neurotransmetteurs inclut les enképhalines, les dynorphines et les endorphines. L’une de leurs principales fonctions est de participer à la régulation de l’humeur et de la douleur. Ils font partie de la composante affective comme les cannabinoïdes.

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   Les effets de la dopamine sur l’organisme

   En dehors de sa contribution au système de récompense, la dopamine a de nombreux effets sur l’organisme. Certains ont des impacts négatifs alors que d’autres s’avèrent bénéfiques.

   Les addictions

   La dopamine intervient également dans les addictions. La consommation va libérer de la dopamine, motivant le consommateur à ingurgiter toujours plus d’alcool ou à inhaler davantage de drogue. C’est notamment ce qui l’enferme dans un cercle vicieux et fait qu’il est si compliqué d’en finir avec l’addiction à l’alcool. Néanmoins, la dopamine n’est pas responsable à 100 % de l’addiction aux drogues d’une personne. Certaines études prouvent que l’environnement social d’un individu influe également.

   Reproduction et amour

   La dopamine se retrouve également dans le plaisir sexuel et les sentiments amoureux. Son rôle et celui du système de récompense est donc primordial dans l’évolution de la race humaine. En effet, sans désir sexuel, une espèce ne pourrait se reproduire suffisamment, ce qui conduirait à son extinction.

   Autres incidences sur l’organisme

   <p>La fonction de la dopamine ne se limite pas qu’au rôle de molécule du plaisir. En effet, chez les sujets souffrant de la maladie de parkinson par exemple, les organismes chargés de sécréter de la dopamine sont par exemple défaillants, ce qui suscite des tremblements et une mauvaise coordination des membres.

   La dopamine intervient également dans l’arrêt de la production du lait maternel chez la femme. Par ailleurs, bien qu’on ne puisse actuellement l’expliquer, elle joue également un rôle important chez les personnes qui souffrent de stress post-traumatique.

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   Comment fonctionne le système de récompense dans le cerveau

   Le système de récompense s’active au terme de la grossesse et favorise l’apprentissage d’actions motrices, de comportements primordiaux à la survie d’un individu et de son espèce, mais aussi l’apprentissage de réactions émotionnelles. Il agit en quelque sorte comme un baromètre qui vient indiquer dans quel état physique ou psychique un individu se trouve ou peut se trouver. Il est constamment actif lorsque nous éprouvons du plaisir naturellement, c’est-à-dire dans les choses simples telles que le fait de manger, de contempler de beaux paysages, d’écouter de la musique ou d’avoir des rapports sexuels. Il est, en effet, lié à ces besoins essentiels qui sont primaires chez tout être humain. Le plaisir ressenti durant ces actions, stimule leur apprentissage et leur répétition.

3. Lumbar arthritis

   5 décembre 2022 19 h 37 min Leave a Comment

   Osteoarthritis is a degenerative joint disease that causes pain and stiffness in your joints. It usually starts around your hips and knees and can affect any part of your body.

   In some cases, lumbar arthritis may occur when there is damage to the discs between your vertebrae. This type of arthritis is often caused by injury or trauma to the back.

   Lumbar arthritis is a symptom of arthritis that affects the spine. The most common cause is osteoarthritis.

   Also known as spinal arthritis, it is the result of degeneration due to osteoarthritis and inflammation of the joints below the lumbar spine.

   The disease develops gradually and is often associated with degeneration of the vertebrae in the elderly.

   Osteoarthritis is considered a normal part of aging, but the pain and stiffness of low back arthritis can limit a persons’ ability to perform simpler tasks, especially those that require bending and stretching. .

   Lower back arthritis pain results from movement and inactivity.

   It may get worse after standing for long periods of time. Leaning to the side or backwards can also cause pain.

   The pain may begin in the lower back and spread to the pelvic region or the sides of the buttocks. The pain can also spread to the thighs, but it rarely extends to the knees.

   Lumbar arthritis can also cause muscle spasms, cracking joints, stiffness, and a reduced range of motion in the lower back.

   Symptoms are usually slow to develop and not noticeable at first. However, any rapid movement, twisting, or backward movement in the lower back can cause injury to the lumbar region and symptoms to appear in people with this condition.

   Causes and risk factors

   Lumbar arthritis results from specific arthritic conditions. The most common cause of lumbar arthritis symptoms is osteoarthritis, but other types are sometimes involved.

   Osteoarthritis

   Ongoing damage from osteoarthritis in the facet joints of the spine eventually causes these joints to wear and tear. As a result, the bones of the spine begin to wear down.

   Osteoarthritis can result from external factors, including poor diet, being overweight, and genetics.

   Psoriatic arthritis (PSA)

   Lumbar arthritis has also been linked to psoriatic arthritis. Typically, PsA affects people with psoriasis, but the disease appears on its own in some cases.

   Low back pain is a symptom of PSA. Up to 20 percent of people with this condition have spinal involvement. 

   Spondyloarthritis

   This type of arthritis mainly affects the spine and sacroiliac joints and often affects young adults, teenagers or children. 

   Spondyloarthritis is also associated with inflammation of tendons and ligaments.

   Enteropathic arthritis

   Enteropathic arthritis affects people with inflammatory bowel diseases, such as Crohn’s disease and ulcerative colitis. In enteropathic arthritis, the sacroiliac joints are affected, causing lower back pain.

   Rheumatoid arthritis

   Rheumatoid arthritis can affect various joints in the body, including the facet joints of the spine, causing pain. It can also destroy the joints of the spine that it affects.

   Osteoporosis

   Osteoporosis causes loss of bone mass. It is mainly due to aging. When it affects the spine, the outer parts of the vertebrae become weak and painful over time. 

   Diagnosis of lumbar arthritis

   Doctors usually diagnose low back arthritis with a physical exam. They may also order imaging tests, such as X-rays, if needed.

   A doctor will inquire about the patient’s symptoms, pain profile, and range of motion in the lower back.

   Treatments

   Treatment for lumbar arthritis includes:

   • Over-the-counter pain medications
   • lifestyle changes
   • alternative therapies
   • prescription drugs
   • surgery

   If standard medication does not work, doctors may prescribe stronger non-steroidal anti-inflammatory drugs if needed.

   Certain lifestyle changes can keep pressure off the spine and improve a person’s quality of life. Lifestyle changes to relieve symptoms of lower back arthritis include:

   • weightloss
   • healthy diet, including foods that reduce inflammation
   • NO SMOKING
   • do not drink alcohol in excess
   • exercise, especially water aerobics and abdominal strengthening

   Quick relief therapies for lumbar arthritis include hot and cold compresses to improve blood circulation and reduce swelling.

   Prevention of lumbar arthritis

   Certain precautions taken to prevent back pain can also help prevent lumbar arthritis.

   These include:

   • reduce the risk of injury by lifting the load correctly.
   • practice good posture
   • exercise regularly
   • maintain a healthy weight
   • eat a healthy diet
   • wear appropriate shoes, as some shoes can disrupt posture and cause long-term problems
   • stop smoking

4. Dressing apraxia

   19 h 29 min Leave a Comment

   Apraxia is a neurological disorder where people lose the ability to carry out certain actions due to damage to the brain. This includes dressing, eating, writing, speaking, and even walking. It affects about 1% of the population.

   Dressing apraxia is the inability to dress oneself (e.g., sticking one’s head down one’s sleeve or putting one’s pants right side up). 

   This type of apraxia is seen in late forms of Alzheimer’s disease.

   This difficulty is not explained by a primary motor or sensory deficit or by an attention deficit (as can be observed in patients with delirium or severe frontal syndrome). 

   Assessment of dress apraxia

   The clinical assessment consists of asking the patient to dress himself or to dress a doll or a mannequin, or to indicate the correct sequence of the steps of dressing.

   When dressing apraxia is related to a lesion of the posterior parietal right hemisphere (tumor or stroke), the disease is usually associated with attentional or spatial motor difficulties with the left limbs. 

   However, dysfunction in executive functions, motor deficits or constructive apraxia can also contribute. 

   Associated with lesions of the parietal lobe of the left hemisphere, dressing apraxia seems more related to general deficits in gesture planning with both limbs.

   Case study

   A 56-year-old right-handed man developed persistent dressing apraxia following a cerebral infarction. On examination, he showed a considerable difficulty in dressing that did not get better even after many tries. 

   He also showed impaired judgement of orientation, difficulties with constructive task completion, and an apparent impairment in right-left object discrimination when objects were placed in front of him. Interestingly, his right left orientation about his own body was not impaired.  No other neuropsychological signs including aphasia, apraxia, agnosia, asomatognosia and anosognosia were present. His visual imagery and mental operation were impaired in the experimental investigations. For instance, he was unable to rotate an imagery object in his mind. Medical staff concluded that his dressing impairment was related with this difficulty in rotating an imagery object in the mind. 

5. Sleep apnea: risk factor for Alzheimer’s?

   19 h 13 min Leave a Comment

   Sleep apnea is a condition where breathing stops briefly during sleep. The brain doesn’t get enough oxygen and may not wake up until the person starts breathing again. This causes excessive daytime sleepiness and poor concentration.

   It has hypothesized that people with sleep apnea have an increased risk of cognitive decline.

   A new study examines the potential links between sleep apnea and Alzheimer’s disease.

   In a new study, French scientists have scanned the brains of elderly people. They found an association between sleep apnea and the presence of amyloid plaques and other biological changes associated with inflammation and Alzheimer’s disease.

   The scientists published their findings in the journal  Neurology JAMA.

   Tracking changes in the brain

   In this latest research, the scientists recruited 127 retired men and women over the age of 65 living in France and already enrolled in a Europe-wide clinical trial assessing the mental health and well-being of an aging population.

   All participants answered questionnaires about their cognitive function and the quality of their sleep. Only people who had no symptoms of memory loss could participate in the study.

   The researchers gave each person a wearable home device to record their sleep quality and breathing while they slept.

   By measuring the frequency and duration of a decline in the participant’s nasal pressure, the researchers were able to divide the participants into two categories: those with and without sleep-disordered breathing.

   The study team also tested participants’ memory and cognitive function, including executive function.

   All participants underwent brain imaging scans, including magnetic resonance images (MRI) and positron emission tomography (PET) scans. A subgroup of 87 people also underwent an FDG-PET scan to measure glucose metabolism in the brain.

   Link between sleep quality and Alzheimer’s disease

   The study team found that around 75% of the participants had sleep apnea and there was a marked buildup of amyloid protein in their brains, a hallmark of Alzheimer’s disease.

   They also found significantly higher gray matter volume and increased neural activity in brain regions associated with Alzheimer’s disease, including the cingulate cortex. These observations suggest inflammation in this area of ​​the brain.

   When they analyzed the data, the researchers found no difference between self-reported memory problems and feelings of sleepiness between the two groups.

   “At a time when clinical trials of Alzheimer’s disease treatments are not yet successful, the identification of risk factors and protective factors is of interest to a growing number of researchers.”

   “Through the use of multiple brain imaging methods, this study allowed us to clarify the mechanisms explaining the links between sleep quality, risk of cognitive decline and Alzheimer’s disease,” explains the lead author. Dr. Géraldine Rauchs from the University of Caen, France.

   “Although this does not mean that these people will necessarily develop the disease, they are at higher risk. In addition, effective solutions exist to treat sleep apnea. The detection and treatment of sleep disorders, in particular sleep apnea, will therefore be part of the arsenal to promote successful aging,” she explains.

   This is the first study of its kind to use multiple brain imaging methods on a large group of participants from the general community.

   Link between apnea and markers of Alzheimer’s disease

   Researchers have found an association between sleep apnea and Alzheimer’s disease, which may point to a common underlying biological mechanism. However, the study was not intended to show causation or whether people with biological markers of Alzheimer’s developed symptoms of dementia.

   The researchers plan to continue their work by investigating whether there is a difference between brain damage in men and women. They also plan to assess whether treating apnea can make a difference in brain changes.

   Two other studies suggest sleep apnea is a risk factor for Alzheimer’s disease

   Obstructive sleep apnea increases the risk of developing Alzheimer’s disease, possibly by increasing amyloid deposits in the brain.

   It would also precipitate the first memory problems.

   In 2017, a study showed that the severity of obstructive sleep apnea goes hand in hand with a higher level of amyloid (lesions characteristic of Alzheimer’s disease) in the brain. Thus, individuals with more apneas per hour had greater amyloid accumulation in the brain.

   Obstructive sleep apnea affects 30-80% of older people.

   « Several studies have suggested that sleep disturbances may contribute to amyloid deposition and accelerate cognitive decline in at-risk individuals, » said Dr. R. Osorio, MD, lead study author and professor of psychiatry at the Institute. New York University.

   The study included 208 participants, aged 55 to 90, with normal cognition. The researchers performed lumbar punctures to collect cerebrospinal fluid (CSF) from the participants, then used positron emission tomography to measure amyloid deposits directly in the brain.

   The results revealed that more than half of the participants had obstructive sleep apnea, including 36.5% mild and 16.8% moderate to severe. Of the total study sample, 104 participated in a two-year longitudinal study. A correlation has been observed between the severity of apnea and an increase in
   amyloid deposits in the brain.

   The study, however, did not find that the severity of apnea was a predictor of cognitive deterioration in these healthy older adults, which may seem surprising.

   “It is clear that sleep is important for memory,” he adds. “Often people with sleep apnea don’t know. Their airways are temporarily blocked, causing them to wake up unconscious. Some people with sleep apnea can wake up at least 35 times per hour. »

   According to the researchers, nocturnal continuous positive airway pressure ventilation, dental appliances, positional therapy and other treatments for sleep apnea may delay cognitive impairment and dementia in many older individuals. For access to a wide range of CPAP machines, masks, and sleep apnea solutions, visit CPAP Online Australia.

   In 2015, the same team showed in the journal Neurology that untreated sleep apnea advances the appearance of the first signs of memory loss by 13 years on average (77 years instead of 90).

   It confirms a previous study (see below) which showed that older people with sleep apnea – signs of disturbed breathing during sleep – are more likely to be at risk of developing Alzheimer’s disease.

   Sleep apnea also adversely affects the cardiovascular system by increasing the risk of heart disease, type 2 diabetes, high blood pressure and obesity. It would increase the risk of stroke.

   This would explain, at least in part, its deleterious impact on the brain of the elderly.

   The good news is that by treating these nocturnal breathing disorders with a positive pressure mask, its deleterious effect disappears.

   2470 medical records of people aged 55 to 90 participating in a study on Alzheimer’s disease were analyzed.

   The fact that there is a correlation between sleep apnea and Alzheimer’s disease does not mean that there is a causal link.

   Sleep apnea would affect, among the elderly, one in two men and one in four women, many of whom are unaware of it.

   People with untreated sleep apnea snore loudly, stop breathing in the middle of the night, and feel tired during the day.

   Sources. RA Sharma et al. Obstructive Sleep Apnea Severity Affects Amyloid Burden in Cognitively Normal Elderly: A Longitudinal Study. American Journal of Respiratory and Critical Care Medicine, 2017. Osorio RS et al. Alzheimer’s Disease Neuroimaging Initiative. Sleep-disordered breathing advances cognitive decline in the elderly. Neurology, 12;84(19):1964-71, 2015.

6. Primary progressive aphasia

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   Primary progressive aphasia is characterized by gradual deterioration of language, with non-fluent, fluent, and mixed forms. It can be confused with Alzheimer’s disease.

   Primary progressive aphasia includes several neurodegenerative disorders of the dominant hemisphere of language, including Alzheimer’s disease, frontotemporal dementia, and stroke.

   It generally begins between the ages of 45 and 70 with an isolated language disorder and is characterized by a slowly progressive onset language disorder, affecting the production and/or understanding of language. This disorder appears isolated for a few years.

   There are different forms of progressive primary aphasia:

   • Progressive fluent aphasia is characterized by a decline in word comprehension. Spoken language is fluent, though sometimes with difficulty in finding the appropriate word, and grammar is mostly preserved.
   • Progressive logopenic aphasia, characterized by decreased verbal production and difficulty finding words, with grammar remains retained.
   • Progressive non-fluent aphasia. In this case, it is firstly the production of language that is altered. Speech is slowed down and the construction of sentences full of mistakes. There are phonemic paraphasias (difficulties in the sequence of phonemes). Language comprehension remains virtually intact. Progressive nonfluent aphasia is sometimes the first manifestation of corticobasal degeneration;
   • primary progressive aphasia.

   Progressive aphasia can be confused with  Alzheimer’s disease. Verbal comprehension is diminished in progressive fluent aphasias, resulting in a low score on the verbal memory test.

   Conversely, a disorder of the lexical semantic system observed in aphasia is often a symptom in Alzheimer’s disease.

   However, the importance of the semantic deterioration, the absence of true amnesia and alterations of the parietal cerebral areas make it possible often to make the distinction with Alzheimer’s disease.

   A simple cognitive test such as the  Mini Mental Examination (MMSE) or the Five Word Test  can help make this distinction. Unlike Alzheimer’s patients, aphasic patients, for example, have more problems naming objects but find it easier to remember the list of five words or to copy drawings (for example two pentagons).

   Epidemiology

   Between 0.5 and 2.5% of patients with a neurodegenerative disease (e.g. Alzheimer’s disease) have primary progressive aphasia. Its incidence is estimated at 1/100,000 and the average survival is 8 years (minimum 3 years and maximum 17 years).

   Diagnostic criteria

   Most patients consult their doctor for difficulty finding words and names.

   • Gradual onset and slowly progressive difficulty in finding words, naming objects, in syntax or understanding words in conversation or on an established neuropsychological test of language.
   • All the difficulties encountered in everyday life during the first two years following the onset of symptoms can be attributed to the language disorder. Premorbid language function is intact (dyslexia is possible during evolution)
   • Apathy, disinhibition, impaired recent memory, impaired three-dimensional vision, impaired visual recognition, and marked sensorimotor deficits are absent for the first two years of illness, which means that the patient does not meet any diagnostic criteria for another dementia pathology.
   • Other cognitive functions may be affected after the first two years, but language remains the most affected function throughout the course of the disease and deteriorates more rapidly than the other functions.
   • Other causes of aphasia such as stroke or tumor are ruled out by imaging.

   What is the differential diagnosis of primary progressive aphasia?

   If the diagnosis of progressive aphasia is not made, the doctor will look for the following pathologies:

   • Brain tumors.
   • Vascular pathologies (example infarction).
   • Alzheimer’s disease.
   • Frontotemporal dementias.
   • Corticobasal degeneration.
   • Progressive supranuclear palsy.
   • Psychogenic language disorder.

   The most common differential diagnosis of progressive aphasia is Alzheimer’s disease.

   The extent of deterioration in semantics and the absence of alterations in the parietal cortex, however, often allow to distinguish it from Alzheimer’s disease. A cognitive test such as the Mini-Mental State Examination can help make this distinction. 

   Progressive nonfluent aphasia is sometimes the first manifestation of corticobasal degeneration.  

   Progressive supranuclear palsy may be accompanied by progressive nonfluent aphasia. The classic symptoms of progressive supranuclear palsy are parkinsonian disorders with repeated falls, psychomotor retardation, apathy and planning problems.

   Practical case of primary progressive aphasia

   Anamnesis

   In 2008, a retired music teacher (76) presented to a geriatrician. During the interview with her doctor, her spouse noticed that:
   – she showed a lack of interest in the activities she practiced before (playing bridge, going to the museum);
   – she neglected herself;
   – she no longer took care of her bank account, the house (shopping, washing up, etc.);
   – his conversations were limited, but continues to read daily.

   Neuropsychological assessment

   In 2009, her condition not having improved, she carried out a neuropsychological assessment, the results of which were as follows:
   – Score on the cognitive test of the  mini-mental examination (MMSE): 22/30
   –  Clock test : 3/7
   –  5-word test  : 9/10 (immediate recall: 5/5; delayed recall: 4/5)
   – Rapid Assessment of Cognitive Functions (ERFC)
   Item 1. Temporo-spatial orientation: 8/8
   Item 2. Attention and memory: 8/10
   Item 3. Mental calculation: 0/2
   Item 4. Reasoning and judgment: 4/5
   Item 5. Comprehension: 5/5
   Item 6. Naming: 3*/4
   Item 7. Repetition: 2/2
   Item 8. Written order: 1/1
   Item 9. Verbal fluency: 1*/4
   Item 10. Praxies: 6/6
   Item 11. Visual decoding: 1/1
   Item 12. Writing: 0/2

   His score is 39/50.

   Diagnostic

   She suffers from:
   – a lack of fluency in her speech. During a semantic fluency test, the patient gives only two words belonging to the category ‘fruit’ in 2 minutes.
   – Agraphia: writing disorder independently of any motor disorders. neurological disorder of motricity hampering the elementary gestures of writing.
   – alexia (inability of an individual to read and understand a text).
   – semantic paralexia: the subject replaces words in a text with others; language becomes unintelligible.

   The other capacities are intact: episodic memory, conceptualization capacities, to perform gestures, praxis, visuo-spatial capacities, executive functions, temporo-spatial orientation.

   Diagnosis: The patient probably suffers from progressive primary aphasia.

7. Aphasia

   18 h 57 min Leave a Comment

   Aphasia is a language disorder that affects the expression or understanding of spoken or written language.

   Language disability is a condition caused by a brain lesion located, in the vast majority of cases, in the left cerebral hemisphere.

   These lesions can occur at any age, but they are more common in older people with stroke or dementia.

   Aphasia is distinct from voice disorders ( dysphonies) and speech disorders ( dysarthrias), although people with aphasia may experience articulatory difficulties and changes in vocal volume.

   Causes

   A lesion of one or more areas of the brain, such as Broca’s area, the white matter, the caudate nucleus, the temporoparietal cortex, or Wernicke’s area, which can be caused by stroke, ischemic or hemorrhagic origin, head trauma, brain tumor, or dementia ( Alzheimer’s disease ).

   Signs and symptoms

   Despite the integrity of the tongue and larynx, the person has difficulty speaking, articulating, and understanding what is said to him.

   The most characteristic symptom of aphasia is the difficulty of spontaneously finding the right word during a dialogue or in a test intended to name an object that one visualizes.

   This characteristic is distinguished from non-aphasic language disorders (which are observed for example in the context of the dysexecutive syndrome) or from a confusional state.

   The inability to find the correct word usually stems from a difficulty in accessing the correct phonological form. The semantic knowledge concerning the item to be named is intact.

   For example, an aphasic person who cannot name the word “orange” is able to say that it is a citrus fruit, orange in color, and has no difficulty in recognizing the image of an orange. In addition, the missing word is often accompanied by an impression of having the word on the tip of the tongue and can be found by a clue (for example, the word begins with the sound « O »).

   Written language is as much altered as oral language in the majority of cases.

   There are mainly three forms of aphasia:

   • Global aphasia: this is the most severe form of aphasia caused by complete obstruction of the middle cerebral artery; the patient speaks little or not at all. He articulates badly. Verbal communication is almost impossible.
   • Wernicke’s aphasia ¹  : Wernicke’s area is the language comprehension area. The patient expresses himself, but has difficulty understanding language and making himself understood. The person cannot transpose the words read or heard into a coherent thought (verbal productions characterized by jargon or paraphasias). There is also perseveration (repeated use of the same word).
   • Broca’s aphasia: Broca ‘s area is a small area on the left side of the brain (sometimes on the right in left-handed people) that is important in language processing. When damaged, an individual has difficulty speaking but can still understand speech. It works closely with Wernicke’s area (language comprehension area). Broca’s aphasia is often caused by a lesion of the left hemisphere and in particular Broca’s area. The patient has difficulty speaking and/or writing. He is unable to express himself coherently.

   Wernicke’s area located in the left hemisphere.Broca’s area located in the left hemisphere.

   	Fluency	Missing word	Understanding	signs
   Global aphasia	very diminished	Strong inability to find the word	very altered	Speech often limited to a stereotype
   Wernicke’s aphasia	Normal	Fairly strong inability to find the word	very altered	Paraphasias, dyssyntaxia, jargon
   Broca’s aphasia	Diminished	Inability to find the word	Below par	Dysprosody, agrammatism

   Other forms of aphasia are:

   • Anomic aphasia.
   • Conduction aphasia.
   • Transcortical aphasia.
   • Amnesic aphasia.

   Diagnostic

   Examination of the expression and comprehension of oral language.

   Take into account the level of education and the mother tongue.

   • Spontaneous language.
   • Repetition of words, simple or complex, and sentences, to better identify arthritic disorders and paraphasias.
   • Naming and designation of items (objects or images). The test consists of asking patients to name about ten objects presented visually, which makes it possible to detect the patient’s inability to find the word. In the event of failure, the examiner must ensure that the unnamed object has indeed been identified by the patient, by having him designate the object in multiple choice. If the patient cannot name the object because he does not identify it, this is not aphasia, but visual agnosia.
   • Description of a complex image.
   • Story of a story.
   • Execution of simple and complex orders.
   • Listening comprehension test. The examiner gives an order to the patient such as “here are 3 papers a large, a medium, a small, you will give me the large, keep the medium and throw away the small”.

   Written language exam

   • Identification of letters, syllables and words.
   • Read aloud.
   • Understanding of written language.
   • Spontaneous writing.
   • Dictation.

   This examination can be deepened with more complex tests such as the definition of words, the interpretation of a text or the construction of a sentence with words.

   Aphasia caused by stroke

   It seems that fluent aphasias (Wernicke type) are more common than non-fluent aphasias with agrammatism in elderly people who have suffered a stroke.

   The clinical profile can be more complex, with little difficulty in finding the word. Semantic paraphasia and visual errors can occur in patients with associated cognitive, behavioral and mood symptoms (slowing down, attention disorders, executive functions, memory disorders, depression, anxiety, apathy). Moreover, the precise evaluation of these patients is made difficult by the associated disorders and by fatigue.

   Aphasia and dementia

   Aphasia is present in people with different forms of dementia, partly Alzheimer’s disease  and especially  frontotemporal dementias.

   Aphasia can be a symptom among others or, on the contrary, be at the forefront throughout the evolution: we then speak of primary progressive aphasia, a pathology that is part of the frontotemporal dementias.

   Primary progressive aphasia usually affects people in their 60s, with an insidious onset characterized by difficulties in spontaneous speech that get progressively worse. There are two possible forms:

   1. progressive nonfluent aphasia with reduced speech, articulatory difficulties, and agrammatism, while comprehension remains preserved;
   2.  fluent progressive aphasia with fluent speech but difficulty understanding the word.

   A particular form of primary progressive aphasia, logopenic aphasia, appears in Alzheimer’s disease.

   In Alzheimer’s disease, language disorders appear discreetly and are mainly due to a lack of semantic knowledge rather than an inability to find the word.

   Rehabilitation

   • Recovery can occur spontaneously.
   • Speech therapy sessions. They are beneficial and improve the communication capacity of patients. However, the benefit is often limited by comprehension disorders or by factors unrelated to aphasia, such as fatigue, low motivation or sensory disturbances. In most cases, the speech therapist focuses on educating the family circle, so that they communicate as well as possible with the patient. In the case of progressive aphasia, prolonged management is necessary because this form of aphasia evolves, unless the patient presents significant cognitive or comprehension disorders.

8. Hyperosmia

   4 décembre 2022 19 h 31 min Leave a Comment

   The human nose is capable of detecting odors at concentrations down to parts per trillion. This sensitivity allows us to detect smells that would otherwise go unnoticed. However, some people experience heightened olfactory perception, which may result in hyperosmia.

   Hyperosmia is associated with several diseases, such as epilepsy, neurodegenerative diseases, and memory disorders. Loss of smell is more common than hyperosmia. 

   It can occur with no apparent cause, apart from the known diseases that cause this disorder.

   Symptoms

   People with hyperosmia may experience pronounced discomfort. Exposure to chemical odors such as synthetic fragrances, perfumes, and cleaning products can trigger mild to severe discomfort. Even the smell of some shampoos can be unpleasant.

   Exposure to toxic smells and fumes that worsen your hyperosmia can lead to anxiety and depression. Triggers and irritants vary from person to person.

   Complications and associated diseases

   Hyperosmia is sometimes caused by migraines (between 25 and 50% during their migraine attacks according to studies).

   Severe cases can disrupt your life by causing anxiety and depression, especially if you don’t know what smells might be triggering the discomfort. 

   The causes of hyperosmia

   Hyperosmia is associated with several diseases and can trigger a variety of symptoms. Certain diseases associated with this disorder can cause the change in smell, and vice versa. For this reason, it can be difficult to determine whether this disorder is the symptom or the cause.

   Pregnancy

   One of the most common causes of hyperosmia is pregnancy. An early symptom of pregnancy is an increased sense of smell. 

   Migraines

   Migraines can and are caused by hyperosmia. Increased sensitivity to smells can occur between migraine episodes. Sensitivity to smells can also trigger a migraine or make you more likely to get one.

   Lyme disease

   Lyme disease is another disease associated with hyperosmia. In one study, 50% of Lyme disease patients showed an increased sense of smell.

   Autoimmune diseases

   Recently, researchers have begun to study the links between autoimmune diseases such as Addison’s disease. Hyperosmia is also a symptom of untreated adrenal insufficiency, which is a precursor to Addison’s disease.

   Neurological diseases

   Certain neurological conditions have also been linked to hyperosmia, including multiple sclerosis, Parkinson’s disease, Alzheimer’s disease, and epilepsy. Multiple sclerosis is known to affect senses like taste and smell. Loss of smell is most common in these diseases.

   In rare cases, growths such as polyps or tumors may arise intranasally or intracranially. These can affect the olfactory nerve.

   Other possible causes include:

   • allergies
   • Meningitis
   • Diabetes
   • Cushing’s syndrome
   • B-12 deficiency
   • Nutrient deficiencies
   • Certain prescription drugs

   The disease (or predisposition) can also be of genetic origin. 

   Treatment of hyperosmia

   If you have hyperosmia, chewing peppermint gum may help until you can part with the smell.

   Successful long-term treatment involves identifying and treating the underlying cause of the symptom. Treatment based on the root cause should lessen your hypersensitivity to odors. 

   If a polyp or tumor is causing hyperosmia, surgical removal may alleviate symptoms. Migraine medications can help treat hyperosmia when migraines are the main cause. 

   Avoiding specific triggers when possible is valuable. The triggering factors (food, perfumes etc.) are different for each person. Some people are triggered by certain foods.

   It’s possible that your prescription medications are the cause. If you have suffered from hyperosmia after starting a new prescription, you should ask your doctor to switch medications.

   Prognosis

   If you are able to identify and treat the underlying cause, your long-term prognosis looks good. You should be able to fully recover.

   Hyperosmia can be difficult to treat when the underlying cause is hard to find. In these cases, symptom management is the best approach until the cause is found.

9. Apathy

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   Apathy, which is characterized by a loss of motivation and interest, is frequently found in Alzheimer’s disease and Parkinson’s disease.

   Apathy is manifested by several signs, including loss of motivation, initiatives, falling social activities, disinterest, emotional blunting, and a lack of energy. These signs must be systematically identified if they last more than two weeks.

   How to differentiate apathy from depression?

   It is not easy to differentiate apathy from depression, as some symptoms co-exist.

   Here is a summary: 
   – Symptoms of apathy include a loss of motivation and perseverance, a reduction in emotional responses, indifference, and social withdrawal. 
   – Depression is characterized by sadness, anxiety, suicidal ideation, agitation, devaluation, pessimism, feeling of guilt, negative thoughts, dark thoughts, and loss of appetite. 
   – Common symptoms of both disorders: disinterest in the environment, psychomotor retardation, fatigue, lack of energy, hypersomnia, lack of insight, lack of initiative, loss of hope. 
   Apathy is more common than depression in Alzheimer’s disease, frontotemporal dementia, unlike Parkinson’s disease.

   Apathy and Alzheimer’s disease

   Apathy is one of the most common behavioral symptoms of Alzheimer’s disease, affecting up to 75% of patients (the average prevalence is reported to be 55% However, this percentage depends on the method of evaluation and the type of population targeted. 

   It is present at all stages of Alzheimer’s disease, but its frequency increases with the severity of the disease, affecting 40% of patients in the mild stage, 80% in the moderate stage, and more than 90% in the severe stage of the disease.

   It is manifested by a loss of interest in the environment, a drop in motivation, enthusiasm, spontaneity. 

   Some studies have found a correlation between the severity of apathy and executive function disorders (anticipation, selection of an objective, planning, ability to adapt to changes). 

   The link between apathy and cognitive decline has been little explored in Alzheimer’s disease. According to one study, the frequency of apathy increases with the severity of cognitive impairment. 

   Interesting fact: Apathetic people who are considered healthy may perform poorly on cognitive tests, suggesting that apathy may be a warning sign for identifying people at risk. This hypothesis is confirmed by a follow-up study, which showed that apathetic at-risk subjects have a greater probability of later developing Alzheimer’s disease. 

   Similarly, anosognosia (misunderstanding by a patient of a disorder), very common in Alzheimer’s disease, is mainly linked to apathy (for example, the patient is unaware that he lacks initiative, motivation, etc.).

   Apathy and Alzheimer’s: the recommendation of the High Authority for Health

   Apathy is a behavioral disorder that should be better diagnosed, according to the High Authority for Health (HAS, France). Apathy is often confused with depression, which explains why many patients wrongly take antidepressants.

   The French health agency publishes new recommendations on apathy with the dual objective of: “precisely defining the diagnosis” and “recommending management favoring non-drug therapeutic means. »

   According to the HAS, “non-drug interventions should be preferred, as they address the symptoms. These may be cognitive stimulation therapies, psycho-socio-cognitive rehabilitation or even group activities related to daily life…”.

   The HAS recommends reducing drugs at risk of side effects that promote apathy.

   Apathy is accompanied by dysfunction of certain regions of the brain

   Most studies have reported that apathy is accompanied by poor functioning of certain regions of the brain.

   A decrease in metabolism (characterized by a reduction in blood circulation) has been observed in the frontal and temporal cortex of apathetic Alzheimer’s patients.

   There is a correlation between the severity of apathy and reduced frontal cortex activity.

   The nuclear magnetic resonance technique has shown that the thickness of the frontal cortex and the cingulate cortex decreases (reflecting atrophy of these regions) in apathetic Alzheimer’s patients.

   This study demonstrates that apathy is not only a psychological disorder, but that it is accompanied by a dysfunction of certain regions of the brain.

   Parkinson disease

   According to epidemiological data, the prevalence of apathy in Parkinson’s disease is estimated at 16-42%. This variability depends on the instrument used as well as on the composition of the populations examined. 

   Its severity is generally not related to the severity of motor disorders. On the other hand, it seems to be linked to the importance of cognitive disorders, particularly executive ones. 

   Apathy can appear in the parkinsonian without it suffering from depressive disorders and vice versa. 

   Frontotemporal dementia

   Apathy is one of the most common initial signs of  frontotemporal dementia.

   Its prevalence is estimated at 70-90%, and it occurs at all stages of the disease. 

   Patients are usually unaware of this disorder. Therefore, the diagnosis should primarily be based on information provided by the closest caregiver. 

   The presence of apathy in a patient makes it possible to differentiate frontotemporal dementia from other forms of frontotemporal dementia (e.g. semantic dementia and primary progressive aphasia). 

   In frontotemporal dementia, the severity of apathy is related to the severity of disturbances in the frontal cortex.

   Apathy and vascular disease

   A recent study in people over the age of 85 indicates that this category of the elderly population with vascular disease has an increased risk of suffering from apathy, but not depression, suggesting that these two disorders do not have the same cause. 

   Evaluation

   The management of apathy remains difficult today, largely due to the lack of standardized means to detect its presence and assess its severity. 

   The first scale proposed was the Apathy Evaluation Scale (AES) and its abbreviated version, called Apathy Scale (AS).

   The Neuropsychiatric Inventory is a reliable instrument to assess neuropsychiatric disorders in neurological diseases.

   Another more specific scale is also used and is called the Apathy Inventory (AI).

   More recently, two new instruments have been proposed: the Structured Interview for Apathy (SIA) and the Lille Apathy Rating Scale (LARS).

   Apathy would increase the risk of cognitive impairment

   Older people with apathy but without depressive symptoms have greater brain atrophy compared to those who are not apathetic.

   According to the lead author of the study, memory loss is therefore not the only symptom associated with an abnormal decrease in brain volume, characteristic of pathological cerebral aging.

   The researchers showed, using neuroimaging examinations, that the decrease in brain volume concerns both the gray matter (formed by the cell bodies of neurons that store information) and the white matter (formed by the axons and terminals that provide the connection between neurons).

   These results, if confirmed, would identify apathetic people as individuals at risk of developing cognitive disorders. Source: Structural MRI correlates of apathy symptoms in older individuals without dementia: AGES-Reykjavik Study. Neurology, 2014.

10. Generalized anxiety

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    Generalized anxiety is the most frequently encountered mental disorder, especially in the elderly. It is often associated with depressive disorders.

    There is a feeling of apprehension of a danger that is both imminent and unpredictable. This feeling is subjective and appears disproportionately.

    When the anxiety is isolated, it is called primary anxiety. The type of disorder can be determined by considering its causes and how it evolved, as well as the circumstances under which it appeared.

    Primary anxiety disorders are generalized anxiety disorder, panic disorder, obsessive-compulsive disorder, and phobic disorder.

    When anxiety is accompanied by a mental or physical illness (e.g. hypochondria,  depression), it is often referred to as secondary anxiety.

    The symptoms are diverse and neurovegetative: general excitability, tachycardia, palpitations, dyspnea, dry mouth, tremors, excessive sweating, dizziness. They can also be the sign of a medical pathology. For example, palpitations may be the first signs of heart disease, while tremors may suggest Parkinsonian syndrome.

    Certain behavioral disorders are often associated: wandering, wandering, insomnia, alcoholism or abuse of tranquillizers, character disorders. This anxiety can also be observed visually in the form of a worried expression, changes in mimicry, posture and mobility.

    Generalized anxiety is characterized by the presence of several symptoms of excessive anxiety or worry occurring over a period of at least six months.

    Generalized anxiety alone represents 70% of primary anxiety disorders in the elderly. The individual has difficulty controlling his preoccupations, which are associated with somatic symptoms (e.g. irritability, insomnia) and subjective distress.

    Historical

    The terms anxiety and anguish originate from the Indogermanic verbal root “ankh” which means “to tighten”, “to choke”, which recalls certain signs (tight throat, feeling of suffocation).

    The term “panic” originates from the ancient Greek god of forests and riverbanks Pan who according to legend sowed panic among the Persians at the battle of Marathon.

    While anxiety is associated with a physical cause (anxiety of dying during a heart attack) leading to physical manifestations (eg palpitation), anxiety is associated with apprehension of an event and fear of a real external danger (eg a bombardment).

    The description of anxiety appears at the end of the 19th century with the German doctors Bndict and Westphal, the latter introducing the term “agoraphobia”.

    At the beginning of the 20th century, Janet introduced the concept of what would become obsessive compulsive disorder.

    Until the early 1980s, anxiety disorders were part of the non-psychotic disorders called « neuroses », including hysteria, neurasthenia, psychasthenia, anorexia and personality disorders.

    Prevalence

    Anxiety disorders have a lifetime prevalence of about 15%. Anxiety disorders are marked by an early onset, with an age of onset of 11 years. Specific phobias are the earliest, i.e. before the age of 10.

    More specifically, generalized anxiety disorder has a lifetime prevalence of approximately 6% and tends to increase with age.

    The other anxiety disorders appear later, with a median age between 20 and 30 years.

    A quarter of anxiety disorders are considered serious, compared to almost half for mood disorders and obsessive-compulsive disorders and 80% for bipolar disorders.

    Unlike other types of disorders (phobic, obsessive-compulsive or panic), they tend to persist. Women are two times more affected than men.

    However, it is quite possible that GAD is obscured by the symptomatology of other psychiatric conditions.

    It very often coexists with another mental disorder: social or specific phobia, panic disorder or depressive state.

    Due to the presence of somatic disorders, these patients consult not only a general practitioner, but also pulmonologists, gastroenterologists or cardiologists.

    A study finds 46% late onset of generalized anxiety in a population of elderly subjects . Another study reports that symptoms of anxiety are present in about 25% of elderly people in the community, reaching 50% in people placed in medical care.

    Diagnostic criteria for generalized anxiety disorder

    The diagnostic criteria of the American psychiatry manual DSM IV make it possible to differentiate generalized anxiety disorder from normal anxiety. These criteria are:

    1. At least one excessive worry and fearful expectation lasting several days for at least 6 months, and stimulated by events or activities (such as work or school performance).

    2. Anxiety that is difficult to control, even uncontrollable.

    3. At least three of the following six symptoms present for more than one day during the past 6 months): 
    – Agitation, over-excitement 
    – ​​Tiredness 
    – Trouble concentrating 
    – Irritability 
    – Muscle tension 
    – Sleep disturbances (difficulty sleeping or insufficient sleep or restless)

    4. The object of concern is not limited. If the object is limited (eg separation, trauma), the anxiety disorder will be classified differently: separation anxiety disorder, post-traumatic anxiety.

    5. Suffering and impairment of significant social, professional activities

    6. The disorder is not due to substance abuse (drugs, or medications), medical condition (hyperthyroidism), or mental illness.

    Signs and symptoms of generalized anxiety disorder

    Here are the main symptoms:

    • Sleeping troubles.
    • Hustle.
    • Complaints (eg dizziness, pain, headaches) easily evoked by the subject, and concerning his body, which will lead him to consult his doctor often.
    • Increased heart rate
    • rapid breathing
    • Difficulty concentrating
    • Fear of becoming independent or dependent.
    • Loneliness expressed discreetly by the person.

    Comorbidity

    Generalized anxiety in the elderly is associated with comorbidity. Anxiety symptoms can be linked to three types of disorders:

    • physical disorders: cardiac, urinary, digestive symptoms and sleep disorders; 
    • cognitive disorders: attention and concentration disorders; there may also be feelings of derealization, depersonalization and recurring thoughts;
    • behavioral disorders: hyperkinesia, repetitive behaviors, avoidance, hypervigilance.

    Etiology

    The cause is unknown and multifactorial, combining both an alteration of certain neurotransmitters and psychosocial factors.

    Genetic factors: Studies show that the risk is three times higher among first-degree relatives of patients with generalized anxiety.

    Neurochemical factors. The areas that seem to be affected in GAD are the limbic system and the prefrontal cortex and more precisely the cortico-subcortical neural circuit which includes:

    • the prefrontal cortex which is connected to the cingulate cortex
    • The subcortical structures (hippocampae, amygdala and part of the thalamus).

    There is therefore a dysfunction of this coritco-subcortical circuit.

    A neuroimaging study (functional MRI technique) indicates that people prone to generalized anxiety disorder have hyperactivity of the amygdala (brain structure present in the limbic system) and hypoactivity of the prefrontal cortex. Serotonin is a neurotransmitter thought to be involved in anxiety.

    It can be hypothesized that the decreased activity of the GABA inhibitory system leads to hyperactivation of the limbic system which is associated with the symptoms of anxiety. This would explain why benzodiazepines, which inhibit GABA activity, have an anxiolytic effect.

    Psychosocial factors. According to the cognitive-behavioural model, the different parameters processing information would not be perceived in an equitable manner, favoring the negative and threatening representation of an anxiety-provoking situation. The development of an anxiety disorder can occur through observational learning, in which a person develops a disorder (or phobia) by observing a person displaying anxiety (or fear). Parents can play a role in increasing the risk (overprotective mother, parent who is not very warm and critical of the child, separation).

    What are the treatments for anxiety?

    Once you’ve been diagnosed with anxiety, you can explore treatment options with your doctor. For some people, medical treatment is not necessary. Lifestyle changes may be enough to cope with the symptoms.

    In moderate or severe cases, however, treatment can help you overcome symptoms and lead a more manageable daily life.

    Treatment for anxiety falls into two categories: psychotherapy and medication. Meeting with a therapist or psychologist can help you learn tools and strategies for dealing with anxiety when it arises.

    Medications typically used to treat anxiety include antidepressants and benzodiazepines.

    What natural remedies are used to treat generalized anxiety disorder?

    Lifestyle changes can be an effective way to combat some of the stress and anxiety you may face every day. Most of the natural « cures » consist of taking care of your body, participating in healthy activities and eliminating unhealthy ones.

    These include:

    • get enough sleep
    • meditate
    • stay active and exercise
    • eat healthy
    • stay active and train
    • avoid alcohol
    • avoid caffeine
    • stop smoking