Author Archives: Stéphane Bastianetto

1. Tinnitus

   2 décembre 2022 15 h 27 min Leave a Comment

   Tinnitus is the perception of noise or ringing in the ears, affecting about 15 to 20% of people. 

   Tinnitus is not a condition in itself – it is a symptom of an underlying condition, such as age-related hearing loss, ear injury, or circulatory system disorder.

   Although bothersome, tinnitus is generally not something serious. 

   Although it can get worse with age, for many people, tinnitus can get better after treatment. 

   Treating the identified underlying cause sometimes helps. Other treatments reduce or mask noise, making tinnitus less noticeable.

   Symptoms

   Tinnitus involves the sensation of hearing sound in the absence of external sound. Tinnitus symptoms can include phantom noises in the ears, such as:

   • A ring
   • A buzz
   • A roar
   • A click
   • A whistle

   Phantom noise can range from a low-pitched roar to a high-pitched squeal, which can be heard in one or both ears. In some cases, the sound may be so loud that it may interfere with the ability to concentrate or hear external sound. Tinnitus can be present all the time or intermittently.

   There are two types of tinnitus.

   • Subjective tinnitus is the most common type of tinnitus. Ear problems in the outer, middle, or inner part can cause it. Disorders with the auditory (auditory) nerves or the amount of your brain that interprets nerve signals as sound (auditory pathways) can cause issues.
   • Objective tinnitus is tinnitus that your doctor can hear during an exam. A blood vessel disturbance, a bone condition in the middle ear, or muscle twitching can cause this rare tinnitus.

   Not confused with auditory hallucinations.

   Tinnitus Diagnosis

   The doctor examines the ears, head, and neck to look for possible causes of tinnitus. The tests include:

   ·       Hearing test (audiological). The patient sits in a soundproof room with headphones. It indicates when he can hear the sound, and the results are compared to those considered normal for his age. This test can help rule out or identify possible causes of tinnitus.

   ·       Movement. The doctor may ask to move the eyes, clench the jaw, or move the neck, arms, and legs. If the tinnitus changes or worsens, it can help identify an underlying disorder that needs treatment.

   ·       Imaging tests. Depending on the suspected cause of the tinnitus, the patient may need imaging tests (CT scans or MRIs).

   The sounds heard can help the doctor identify a possible underlying cause.

   ·       Clicks. Muscle contractions in and around the ear can cause sharp clicks to be heard in bursts. They can last from a few seconds to a few minutes.

   ·       Humming. These sound fluctuations are generally of vascular origin and occur, for example, when exercising or changing position, for example, when lying down or getting up.

   ·       Heartbeat. Blood vessel problems, such as high blood pressure, aneurysm or tumor, and blockage of the ear canal or eustachian tube, can amplify the heartbeat sound in the ears.

   ·       Low ringtone. Conditions that can cause severe ringing in one ear include Ménière’s disease. Tinnitus can become very loud before an attack of vertigo – a feeling that the environment is spinning or moving.

   ·       High-pitched ringing. Exposure to loud noise or a knock in the ear can cause a high-pitched ringing or buzzing sound that usually subsides after a few hours. However, tinnitus may be permanent if there is also hearing loss. Long-term noise exposure, age-related hearing loss, or medication can cause continuous, high-pitched ringing in both ears. Acoustic neuroma, also called vestibular schwannoma, can cause constant, high-pitched ringing in one ear.

   ·       Other sounds. Stiff bones in the inner ear (otosclerosis) can cause severe tinnitus that may be continuous or come and go. Earwax, foreign bodies, or hair in the ear canal can rub against the eardrum, causing a variety of sounds.

   Often, it is challenging to determine the cause of tinnitus. 

2. Brain abscess

   8 h 59 min Leave a Comment

   Brain abscesses are caused by bacteria entering the bloodstream through a break in the skin. They usually form when there is an injury to the head, neck, face, or teeth.

   This allows bacteria to enter the blood stream and travel to the brain. Once inside the brain, the bacteria multiply and cause swelling.

   This causes pressure on nearby nerves and may lead to seizures.

   Brain abscess is more likely to affect adult males under the age of 30. 

   In children, they most often develop in those between 4 and 7 years old. Vaccination programs have reduced the incidence of brain abscesses in young children.

   Brain Abscess Symptoms

   Brain abscess symptoms include headache, fever, nausea, vomiting, stiff neck, confusion, seizures, loss of consciousness, coma, and death.

   The most common cause of brain abscesses is bacterial infection. Other causes include fungal infections, trauma, tumors, and autoimmune diseases.

   If the headache suddenly gets worse, the abscess may have burst.

   In two-thirds of cases, symptoms last up to 2 weeks. On average, doctors diagnose the disease 8 days after the onset of symptoms.

   The causes of brain abscess

   Brain abscesses are caused by bacteria, fungi, or amoebae that enter the brain.

   Brain abscesses are caused by bacteria, fungi, or amoebae that enter the brain. The most common cause is bacterial meningitis.

   Brain abscesses can also be caused by tuberculosis or fungal infections of the sinuses or ear.

   As the cells accumulate, a wall or membrane develops around the abscess. This isolates the infection and prevents it from spreading to healthy tissue.

   If an abscess swells, it puts increasing pressure on surrounding brain tissue.

   How the infection enters the brain

   Brain infections are quite rare for several reasons.

   One reason is the blood-brain barrier, a protective network of blood vessels and cells. It blocks certain components of blood flowing to the brain.

   Sometimes an infection can cross the blood-brain barrier. This can happen when inflammation damages the barrier.

   The infection enters the brain through three main routes.

   It could:

   • by blood;
   • from a neighboring site, for example the ear;
   • result from traumatic injury or surgery

   Infection from another area of ​​the body

   If an infection occurs elsewhere in the body, infectious organisms can bypass the blood-brain barrier and enter and infect the brain.

   Many bacterial brain abscesses arise from a lesion in the body. 

   A person with a weakened immune system (for example caused by chemotherapy or an organ transplant) has a higher risk of developing a brain abscess as a result of a blood-borne infection.

   The most common infections known to cause brain abscesses are:

   • endocarditis, an infection of the heart valve
   • pneumonia, bronchiectasis and other lung infections
   • an abdominal infection such as peritonitis,
   • cystitis or inflammation of the bladder.

   Direct contagion

   An untreated middle ear infection can lead to a brain abscess. If an infection starts inside the skull, for example in the nose or ear, it can spread to the brain.

   Infections that can trigger a brain abscess include:

   • ear infection;
   • sinusitis;
   • mastoiditis, an infection of the bone behind the ear.

   The location of the abscess may depend on the site and type of the original infection.

   Direct trauma

   A brain abscess can result from neurological surgery or brain injury.

   An abscess can result from:

   • a blow to the head that causes a skull fracture,
   • a complication of surgery, in rare cases.

   Diagnosis of brain abscess

   To diagnose a brain abscess, the doctor will assess the signs and symptoms and review the patient’s medical history and recent movements.

   Symptoms can be similar to those of other illnesses and conditions, so confirming a diagnosis can take time. The diagnosis will be easier if the doctor can determine exactly when the symptoms started and how they progressed.

   Tests may include:

   • a blood test to check for high levels of white blood cells, which may indicate an infection
   • imaging scans, such as an MRI or CT scan,
   • biopsy which consists of taking a sample of pus for analysis.

   The number of deaths from brain abscess has declined over the past decades, due to the increasingly common use of neuroimaging.

   Brain abscess treatment

   Treatment usually involves surgical drainage of the pus through an incision into the skull (craniotomy). Antibiotics should also be given intravenously to fight any infection that might have caused the abscess in the first place. After the infection is eliminated, a long-acting antibiotic may be given orally to help prevent future recurrences.

   If tests show an infection is viral rather than bacterial, the doctor will change treatment accordingly.

   The effectiveness of the treatment will depend on:

   • the size of the abscess
   • number of abscesses
   • the cause of the abscess
   • how the person is healthy

   Surgery

   A person may need surgery if:

   • the pressure in the brain continues to rise
   • the abscess does not respond to medication
   • there is a risk that the abscess will burst

   A craniotomy is a procedure in which the surgeon makes an opening in the skull.

   Medication

   A short course of high-dose corticosteroids can help with increased intracranial pressure and risk of complications, such as meningitis.

   However, doctors do not routinely prescribe corticosteroids.

   A doctor can prescribe anticonvulsants to prevent seizures. A person who has had a brain abscess may need to take anticonvulsants for up to 5 years.

    

3. Wandering in Alzheimer’s disease

   1 décembre 2022 19 h 32 min Leave a Comment

   Wandering is a common behavior among patients suffering from Alzheimer’s disease.

   The wandering may occur during the day or night, and it may be triggered by external stimuli, such as noise, light, or smells. It may also be caused by internal factors, such as sleep disorders, depression, or anxiety.

   The wandering Alzheimer syndrome is a condition where patients lose their sense of direction and wander off without knowing why.

   This happens when there is damage to the hippocampus, a part of the brain responsible for spatial navigation. Patients may become lost and disoriented, unable to find their way back home.

   Wandering becomes a complicated situation for the family and professional environment.

   Indeed, the elderly person can be in danger if the entourage or the police do not find him quickly.

   Running away or wandering?

   It is difficult to know whether a patient leaves voluntarily or by chance, especially since the memory problems from which he suffers make it difficult to distinguish. 

   Moreover, the patient does not have all his faculties of judgment, which does not make it possible to know if the act is voluntary or not.

   The main forms of running away are:

   • Running away due to orientation disorders. The patient is happy to be found.
   • Running away due to behavioral problems. The patient does not realize he is at home (confusion) or thinks he is still working or has a dependent child (delusions).
   • The reactive fugue. The patient does not find his bearings in the establishment he has just joined.
   • Running away due to a hostile environment. The patient does not feel included in the health care establishment in which he does not feels, comfortable, or thinks that the nursing staff will harm him.

   Trompe l’oeil murals to improve the quality of life of patients

   The idea behind trompe l’oeils is to trick your brain into thinking there’s something real when there isn’t. This technique is used in architecture, painting, sculpture, and even in medical treatments. It’s often used to create illusions of depth, which can help people who suffer from conditions like dementia.

   In 2019, the Anna-Laberge Foundation obtained a donation that allowed it to install trompe-l’oeil murals in a residential center, in order to improve the quality of life of patients with Alzheimer’s disease. 

   The murals, made up of different images, make it possible in particular to camouflage the elevator and exit doors of the unit, which, among other things, reduces attempts to run away and the interventions of the staff to counter them.

   A box to help the person in the event of a runaway

   In Belgium, an original solution has been found to find them as quickly as possible. In the event of a worrying disappearance, the investigators inspect a box which is in the fridge in the middle of the food.

   The fridge is indeed the only piece of furniture that is the easiest to find in a house.

   In this box is a booklet in which we find the basic information on the missing person: his photo, the addresses where the person is likely to go, the people to warn.

   The Wandering Alzheimer Project

   The Wandering Alzheimer Project is a project designed to provide a box which will allow people who suffer from Alzheimer’s disease to wander safely. This box contains a GPS tracker, a panic button, and a mobile phone charger. It also includes a map of the area where the user lives, so that if they get lost, someone can find them.

   Optical illusions to reduce runaways in long-term care centers

   More and more accommodation and long-term care centers (CHSLD; equivalent of EPHAD in France) are using trompe-l’oeil murals that allow elevators and exits to be camouflaged.

   This technique aims to reduce runaways and anxiety in people with Alzheimer’s disease.

   It is currently used in a CHSLD in Montreal. Thus, the elevator or the exit door are replaced by a sideboard, a table or a general store.

   « We try to use paints that encourage the recall of old memories », comments the head of unit.

   An anti-fugue sensor in a sock

   A 15-year-old New Yorker has developed a device that allows him to prevent people suffering from Alzheimer’s from running away.
   This idea came to him following the runaways of his grandfather suffering from the disease.

   The principle is as follows: when the Alzheimer’s person gets up at night, a wireless pressure sensor attached to the sock sends an audible alert to a smartphone. This device has been tested 437 times on his grandfather, with 100% success.

   The young Kenneth Shinozuka hopes to be able to quickly provide hundreds of copies to caregivers. According to him, this tool will protect patients and reduce the stress of caregivers. Kenneth Shinozuka won the 2014 Google Science Fair prize worth $50,000.

4. The painkillers are harmful in people with Alzheimer’s

   9 h 51 min Leave a Comment

   Two studies found that people with Alzheimer’s disease and taking opioid painkillers were twice as likely to develop side effects like constipation, nausea, vomiting, dizziness, confusion, hallucinations, and sleep problems. They also identified a mechanism that could explain why this happens.

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   In a randomized controlled trial of 162 Norwegian nursing home residents, researchers from the University of Exeter, King’s College London and the University of Bergen found a significant increase in side effects such as changes in personality changes, confusion and sedation, which can have a serious impact on the lives of people with dementia.

   The team wants studies to be carried out to look at the appropriate dosage of painkillers (e.g. buprenorphine) for people with dementia.

   About half of people with dementia who live in nursing homes experience pain.

   Previous research has recognized that pain is often under diagnosed and poorly managed in people with dementia, impacting quality of life.

   After paracetamol, opioid painkillers are frequently the second choice of treatment for clinicians in people with dementia and are prescribed to nearly 40% of people with dementia living in care homes.

   They provide effective pain relief, but current recommendations do not consider that people with dementia get noticeable pain relief from doses lower than those usually prescribed, and are particularly susceptible to adverse effects.

   The team studied 162 people from 47 Norwegian nursing homes who suffered from dementia and depression. In those given buprenorphine as part of their treatment, harmful side effects more than tripled. The researchers also found that those taking buprenorphine were significantly less active during the day.

   According to Clive Ballard, a professor at the University of Exeter Medical School:

   Pain is a symptom that can cause enormous distress, and it is important that we can provide relief to people with dementia. When we try to relieve their pain, we need more research in this area, and we need to find the right treatment. We need to establish the best course of treatment and consider the appropriate dosage for people with dementia.

   Importantly, research conducted by Professor Ballard’s team and presented at the 2018 Alzheimer’s Disease International Conference (AAIC) sheds light on why people with dementia are more sensitive to opioid painkillers, suggesting that they overproduce the body’s natural opioids.

   A second study in an Alzheimer’s mouse model revealed increased sensitivity to morphine (an opioid painkiller) compared to healthy mice. People with Alzheimer’s disease responded to a much lower dose for pain relief and experienced more adverse effects when the dose was increased to a normal level. Looking further, the study found that the Alzheimer’s mice produced more endorphins (the body’s natural endogenous opioids).

5. The Okinawa Island Diet

   9 h 37 min Leave a Comment

   The Okinawan diet refers to the traditional eating habits of the people of the Japanese island of Okinawa (population 1.3 million).

   It is based on whole grains, legumes, fruits, vegetables, fish, tofu, seaweed, nuts, seeds, and herbs.

   The islanders eat very little meat and avoid processed foods. They drink green tea instead of coffee. They do not smoke and rarely use alcohol. They exercise regularly and maintain a healthy weight.

   Okinawa Island hosts more than 40 centenarians per 100,000 inhabitants, 3 times more than in all of Japan.

   This longevity is not only the consequence of a favorable genetic background but would above all be the conjunction of a protected environment, good eating habits, regular physical activity and a strong social fabric.

   Life expectancy on this island is 82 years with only 2.6 years of disability after 100 years. The difference between men and women is clear, with a woman/man ratio of 5 female centenarians for 1 male centenarian.

   Diabetes is rare on the island of Okinawa, while cancers (colon, breast, prostate, etc.) are nearly 80% less numerous than in Western countries.

   The diet of centenarians on the island of Okinawa

   The inhabitants of the island of Okinawa consume a wide variety of foods, and their calorie consumption is about 300 calories less when in industrialized countries.

   The use of soybeans and rice is very high, as is that of fish, unlike that of meat and dairy products.

   The intakes of vitamins A, B, C and proteins are also very high, unlike those of carbohydrates and salt.

   The following nutrients, known to fight against inflammation and aging, thanks in particular to their antioxidant properties, are also widely consumed:

   • Polyphenols from green tea, certain vegetables, fruits (berries)
   • Omega 3 fatty acids
   • Magnesium (soya, tofu, green vegetables)

   Soy is an excellent source of alpha-linolenic acid, protein and phytoestrogens. These compounds are known to have beneficial effects for the cardiovascular system and have anti-cancer properties.

   Caloric intake has been estimated at just over 1000 calories per day, thanks to the consumption of foods with low energy density which allow the absorption of fewer calories, due to their high content of water, fiber and proteins.

   Physical activity and social life

   The centenarians of the island of Okinawa practice gardening, walking, martial arts and dance, a physical activity which is accompanied by an active social life (third age clubs, parties).

   Genetic factors

   Environmental factors do not explain everything, and it would seem that the frequency of certain alleles is more frequent among the inhabitants of Okinawa.

6. Les neurotransmetteurs

   30 novembre 2022 20 h 56 min Commentaires fermés sur Les neurotransmetteurs

   Les neurotransmetteurs, souvent appelés messagers chimiques, sont des molécules utilisées par le système nerveux pour transmettre des messages entre les neurones ou des neurones aux muscles.

   Ils sont libérés à la terminaison des neurones.

   Les neurotransmetteurs sont les principaux protagonistes de la transmission synaptique,

   Plus d’une cinquantaine de neurotransmetteurs ont été identifiés à ce jour.

   La communication entre deux neurones se produit dans la fente synaptique (le petit espace situé entre les synapses des neurones).

   Puis les signaux électriques qui ont voyagé le long de l’axone sont convertis en signaux chimiques par la libération de neurotransmetteurs, provoquant une réponse spécifique dans le neurone situé en aval.

   Pour provoquer cette réponse, le neurotransmetteur doit se fixer sur le récepteur situé sur le neurone en aval.

   

   Les neuromodulateurs sont un peu différents, car ils ne sont pas limités à la fente synaptique entre deux neurones et peuvent donc affecter un grand nombre de neurones en même temps.

   La plupart des neurotransmetteurs sont des petites molécules d’amines, des acides aminés ou des neuropeptides.

   Il existe à ce jour une douzaine de neurotransmetteurs à petites molécules connus et plus de 100 neuropeptides différents.

   Ces produits chimiques et leurs interactions sont impliqués dans d’innombrables fonctions du système nerveux ainsi que dans le contrôle des fonctions corporelles.

   Un neurone et sa terminaison synaptique sont identifiés par le neurotransmetteur qu’ils produisent et libèrent.

   Par exemple, un neurone cholinergique est un neurone qui libère le neurotransmetteur acétylcholine à hauteur de ses synapses.

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   Les principaux neurotransmetteurs

   Voici les principaux neurotransmetteurs, avec entre parenthèses leurs abréviations et le qualificatif correspondant :

   Neurotransmetteur	Abréviation	Qualificatif
   Acétylcholine	ACh	cholinergique
   Dopamine	DA	dopaminergique
   Noradrénaline	NA	noradrénergique
   Sérotonine	5-HT	sérotoninergique
   Glutamate	Glu	glutamatergique
   Acide gamma aminobutyrique	GABA	gabarergique

   Un neurotransmetteur influence un neurone de trois manières : excitatrice, inhibitrice ou modulatrice.

   Un neurotransmetteur excitateur favorise la génération d’un signal électrique appelé potentiel d’action dans le neurone en aval, tandis qu’un neurotransmetteur inhibiteur l’empêche. Le fait qu’un neurotransmetteur soit excitateur ou inhibiteur dépend du récepteur auquel il se lie.

   Exemples de neurotransmetteurs excitateurs ou inhibiteurs

   Neurotransmetteur
   Acétylcholine	Excitateur
   Dopamine	Excitateur
   Noradrénaline	Excitateur
   Sérotonine	Excitateur
   Glutamate	Excitateur
   GABA	Inhibiteur

   Les neurotransmetteurs exercent diverses fonctions dans le cerveau lorsqu’ils sont libérés ; en voici les principales :

   Neurotransmetteur	Fonctions
   Acétylcholine	Favorise l’attention, la mémoire et l’apprentissage Stimule la contraction des muscles squelettiques Dilatation des vaisseaux Contraction des bronches, de la pupille, des intestins Bradycardie (coeur) Stimule l’excrétion de certaines hormones
   Dopamine	Contrôle la motricité et la posture Coordonne certains processus cognitifs et émotionnels Favorise l’attention Module l’humeur Joue un rôle dans la dépendance
   Noradrénaline	Contrôle la vigilance Favorise l’attention Ajuste certains comportements tels que le stress, l’émotion Agit comme une hormone dans le sang en stimulant la contraction des vaisseaux sanguins et augmentant la fréquence cardiaque.
   Sérotonine	Régule l’humeur Régule le cycle circadien Contrôle de la douleur Régule la température Régule l’appétit
   Glutamate	Favorise l’apprentissage et la mémorisation des informations à long-terme, la plasticité des synapses du cerveau
   GABA	Diminue l’excitabilité des neurones Il est surtout présent dans les neurones du cortex. Contribue au contrôle moteur et à la vision.

   Une altération de leur fonction provoque des dérèglements dans le cerveau, à l’origine de troubles – cognitifs, psychologiques et comportementaux – suivant le neurotransmetteur impliqué.

   Voici quelques exemples de neurotransmetteurs dont la baisse ou l’augmentation est associée à des troubles ou maladies.

   Neurotransmetteur	Altération	Troubles et maladies
   Acétylcholine	Diminution	Maladie d’Alzheimer Maladie de Parkinson
   Dopamine	Diminution	Maladie de Parkinson
   Dopamine	Augmentation	Schizophrénie Troubles psychotiques
   Noradrénaline	Diminution	Maladie d’Alzheimer Dépression
   Sérotonine	Diminution	Dépression
   Glutamate	Augmentation	Accident vasculaire cérébral Maladie d’Alzheimer
   GABA	Diminution	Epilepsie

   Que deviennent les neurotransmetteurs ?

   Les neurotransmetteurs libérés par les vésicules vont diffuser dans la fente synaptique dans laquelle :

   1. Ils sont dégradés par des enzymes, des protéines que l’on peut comparer à des ciseaux coupants en deux un neurotransmetteur pour l’inactiver.
   2. Ils sont recapturés par des molécules (appelés transporteurs) situées sur la membrane du neurone présynaptique. Ces transporteurs ‘pompent’ les neurotransmetteurs afin qu’ils soient réutilisés. Le neurone économise ainsi la synthèse de neurotransmetteur. D’une manière générale, plus la libération de neurotransmetteur est importante, plus l’activité des transporteurs l’est.
   3. Ils se lient à des protéines (appelées récepteurs) situées sur la membrane du neurone présynaptique et postsynaptique.

   Les récepteurs situés sur la membrane du neurone présynaptique (appelés récepteurs présynaptiques) contrôlent la libération, la synthèse et la recapture du neurotransmetteur.

   Par la suite, la quantité restante de neurotransmetteur (c’est-à-dire la quantité qui n’aura été ni dégradée ni recapturée) se liera aux récepteurs situés sur la membrane du neurone postsynaptique (on parle de récepteur post-synaptique).

   Enfin, la liaison du neurotransmetteur avec son récepteur conduira à un effet physiologique (par exemple, à une contraction du muscle si le neurotransmetteur libéré est l’acétylcholine.

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   Où et comment les neurotransmetteurs sont-ils synthétisés ?

   Ils sont synthétisés par les neurones dans la terminaison nerveuse et/ou le corps cellulaire. Dans ce dernier cas, le messager chimique migre librement ou est transporté grâce aux vésicules jusqu’à la terminaison synaptique.

   Cette synthèse se fait à partir d’autres molécules (dites précurseurs) appelées substrats et met en jeu des enzymes (de synthèse) qui accélèrent ces réactions.

   Voici en résumé le devenir d’un neurotransmetteur au niveau de la terminaison nerveuse :

   • 

   • 

   Le dernier neurotransmetteur découvert

   En 2025, des chercheurs ont émis une hypothèse que la créatine fonctionnait comme un neurotransmetteur dans le système nerveux central, du moins chez la souris. Ils ont détecté la créatine dans les vésicules synaptiques et ont observé sa libération lors d’une stimulation neuronale.

7. Can antioxidants protect memory?

   20 h 30 min Leave a Comment

   Antioxidants are nutrients found naturally in foods that help protect against free radicals.

   Free radicals are molecules that cause cell damage and can contribute to aging and disease.

   There are two main categories of antioxidants: vitamins and minerals. Vitamins A, C, E, and K are called fat-soluble vitamins because they need fat to be absorbed into the body. These vitamins are found in fruits, vegetables, nuts, seeds, and whole grains. Minerals such as zinc, iron, copper, manganese, calcium, magnesium, selenium, and iodine are water-soluble vitamins. These vitamins are found mostly in lean meats, fish, beans, and dairy products.

   What are flavonoids?

   Flavonoids are important molecules in herbal medicine that come from plant metabolism, they are found in different parts of the plant at the level of fruits, flowers or leaves. Scientists have already identified more than 8,000 different flavonoids, these molecules belong to the large family of phenolic compounds. They have antioxidant properties. Foods enriched in flavonoids are tea (particularly green tea), red fruits, olive oil, garlic, dark chocolate, grapes and vines, spinash, broccoli and onion.

   Antioxidant flavonoids can prevent memory decline

   Researchers at Rush University Medical Center in Chicago studied more than 960 people with an average age of 81 and found that those who ate foods containing antioxidant flavonoids, found in plant pigments, were healthier. 

   Specifically, participants who consumed the most kaempferol, found in kale, beans, tea, spinach and broccoli, had a 0.4 unit slower rate of cognitive decline per decade compared to those in the lowest group.

   And those who consumed the most quercetin, from sources such as tomatoes, kale, apples and tea, had a slower rate of cognitive decline of 0.2 units per decade.

   Consuming wine, kale, oranges, and tomatoes has also been shown to be beneficial.

   These results were confirmed by other previous studies

   The researchers studied 1,924 people aged 65 and older who were enrolled in the Rush Memory and Aging Project. They looked at how many times each person ate or drank fruit and vegetable servings per day and whether they had high blood levels of antioxidants. After about four years, the participants took tests to measure their cognitive function. Those who ate or drank more fruit and vegetables had better memory than those who didn’t.

   The researchers analyzed data on 2,977 people aged 65 and older who were enrolled in the Health ABC Study. They looked at how much fruit and vegetable intake participants had over the course of five years. Participants who ate the most antioxidants were about half as likely to develop dementia compared to those who ate the least amount of these nutrients.

   The study looked at data on 2,000 people over age 65 who were followed for four years. They found that those who ate or drank more antioxidants had better cognitive function than those who didn’t.

8. Does Anesthesia Promote Memory Loss?

   19 h 37 min Leave a Comment

   It’s not uncommon for people who undergo general anesthesia during surgery to experience some degree of memory impairment afterwards. This is because anesthetics work by blocking certain parts of the brain responsible for memory formation.

   Memory problems are even more common in people over the age of 70 following anesthesia. Symptoms persist for months or years in some patients. Patients with Alzheimer’s disease appear to be particularly at risk of impaired cognition following anesthesia, and some studies suggest that exposure to anesthetics may increase the risk of Alzheimer’s disease.

   People over 70 are more at risk

   In adults over the age of 70, exposure to general anesthesia and surgery is associated with a subtle decline in memory and thinking skills, according to a new study published in 2018. The study analyzed nearly of 2,000 people and found that exposure to anesthesia after age 70 was linked to long-term changes in brain function.

   Although the decline in brain function was small, it may be more pronounced in people with already low cognitive function or pre-existing mild cognitive impairment. In older people whose cognitive impairment is not yet clinically recognized, exposure to anesthesia and surgery may highlight underlying problems with memory and thinking.

   We need to be sure that patients considering surgery, and their families, are properly informed that the risk of cognitive dysfunction is possible,” explains the study’s lead author. Additionally, alternative strategies should be discussed with patients before surgery is performed for those deemed to be at high risk. This study provides further reasons for clinicians to begin performing routine cognitive assessments prior to surgery. operation to further assess the risk of exposure.

   The authors emphasized that it is not possible to determine whether anesthesia, surgery, or underlying conditions requiring surgery caused the decline.

   Source : Schulte PJ et coll. Association between exposure to anaesthesia and surgery and long-term cognitive trajectories in older adults: report from the Mayo Clinic Study of Aging. British Journal of Anaesthesia, 2018.
   

   Anesthesia around the age of 40 does not increase the risk of memory loss

   There is no significant link between being exposed to general anesthesia after age 40 and the development of mild cognitive impairment years later, according to an epidemiological study. 

   The potential link between on the one hand exposure to anesthesia following surgery and on the other hand cognitive decline and dementia has recently been a matter of debate, with previous findings contradicting those recently published. This new study found no link between exposure to anesthesia and cognitive decline when taking into account the number of exposures or the total cumulative duration of exposure. 

   « It is reassuring for the majority of older people who may need surgery to learn that anesthesia and surgery are unlikely to be associated with long-term cognitive decline, » says the lead author of study (David O. Warner, Mayo Clinic, Rochester, Minnesota, USA). 

   The researchers looked at Mayo Clinic data from 1,731 residents between the ages of 70 and 89 whose cognitive functions were assessed every 15 months. Medical records (including surgeries with anesthesia) were obtained for each participant after the age of 40. Of these, 536 (31%) developed mild cognitive decline over a period of 4.8 years. No adverse effects of anesthesia were reported in the study. 

   Although the current results are « comforting », it is quite possible that people at risk are more vulnerable to anesthesia, in particular the elderly with vascular disorders and who are undergoing vascular surgery. Researchers believe that anesthesia produces an inflammatory state in the brain – called neuroinflammation – which would trigger cognitive impairment in people at risk.

   Source : Juraj Sprung et coll. Association of Mild Cognitive Impairment With Exposure to General Anesthesia for Surgical and Nonsurgical Procedures. Mayo Clinic Proceedings, 2016.

   Age-dependent effect

   A study published in the journal Anaesthesia confirmed that anesthesia can cause long-term damage to brain cells and impair memory.  It’s important to note that these results only apply to older adults.  Younger people tend to recover faster after anesthesia because their brains are better able to adapt to the effects of drugs. 

   However, older adults often have weaker immune systems and are more susceptible to infections, which could make them more vulnerable to complications following surgery.  One limitation of this study is that it relied on self-reported information about whether participants had undergone surgery. 

   Anesthesia and risk of dementia

   In 2016, American researchers reported that exposure to anesthesia was not associated with an increased risk of dementia, and Alzheimer’s disease in particular. This prospective study included nearly 4,000 participants aged 65 and older. This result contradicts that published by the European Society of Anaesthesiology (ESA) in June 2013 which reported a 35% increase in the risk of dementia. 

   In order to justify these results, the researchers indicated that some anesthetics would promote the inflammation of neural tissues, resulting in lesions characteristic of Alzheimer’s disease (accumulation of amyloid and tau protein). In this study, the average age of the participants was 75 years old and 62% were women. 632 participants (9%) developed dementia 8 years after follow-up. 

   However, there have been no clinical trials to establish a link between anesthetic exposure and the development of Alzheimer’s disease. Therefore, before drawing firm conclusions, it is necessary to conduct additional studies. However, one should be aware of the potential risks and take precautions with vulnerable elderly patients.

   Source: Mother G et coll. Alzheimer’s disease and anesthesia. Turk J Med Sci 2015;45(5):1026-33).

    

9. Influx nerveux

   16 h 32 min Commentaires fermés sur Influx nerveux

   Le neurone fonctionne en émettant des signaux électriques (on parle également d’influx nerveux). C’est ce qui le différencie des autres cellules.

   Chaque neurone possède un axone qui agit comme un fil électrique, en conduisant l’influx nerveux (sous la forme d’un potentiel d’action) vers le neurone voisin, assurant ainsi l’activité fonctionnelle du cerveau.

   La transmission de l’influx nerveux se fait grâce à la présence, dans la membrane entourant le neurone (cette membrane est une fine couche d’un centième de millième de millimètre d’épaisseur), de canaux ioniques. Ces canaux sont des sortes de vannes laissant passer des ions positifs tels que le calcium et le potassium.

   Pas d’influx nerveux: le neurone est au repos

   Lorsque aucun influx n’existe, le neurone est au repos et sa membrane plasmique est normalement polarisée: on parle de potentiel de repos. A ce moment, l’extérieur du neurone est positif par rapport à l’intérieur, car les ions sodium (qui sont des ions positifs) sont plus importants à l’extérieur qu’à l’intérieur.

   Un influx nerveux arrive: le neurone s’excite

   Lorsqu’un influx nerveux arrive, les canaux ioniques s’activent et laissent entrer, en quelques millièmes de seconde, des ions sodium (des ions potassium sortent peu de temps après): la face interne de la membrane devient alors chargée positivement. Un influx nerveux est généré et se propage du corps cellulaire vers la terminaison de l’axone à une vitesse de 1 à 150 mètres par seconde. Son amplitude est d’environ 100 millivolts et sa durée d’environ 1 à 2 millièmes de seconde.

   Par où le neurone reçoit l’influx nerveux ?

   La réception se fait essentiellement sur la membrane des dendrites (sortes de minces filaments agissant comme des antennes) et du soma (le soma est aussi appelé corps cellulaire) du neurone. Un neurone peut recevoir une information d’environ un millier de neurones. L’axone peut également recevoir des influx.

   Où est généré l’influx nerveux ?

   Le neurone intègre le message et génère, en réponse à ce message, un potentiel d’action qui prend naissance dans la région où l’axone quitte le soma (région appelée segment initial).

   Comment se propage l’influx nerveux ?

   L’ouverture de canaux à sodium en une région donnée (que nous appellerons A) stimule la membrane de la région adjacente qui devient à son tour excitable…et ainsi de suite. C’est de cette manière que l’influx nerveux se propage. Il est à noter que la membrane située dans la région A de l’axone revient à l’état de repos: en effet les canaux à sodium se referment tandis que les canaux à potassium s’ouvrent, laissant sortir les ions potassium.

   L’influx nerveux est transmis) à un autre neurone ou à un autre type de cellule (par exemple une cellule musculaire) par l’intermédiaire de la synapse.

   Le neurone à l’état de repos

   

   Le neurone est à l’état de repos si aucun influx nerveux n’est transmis. Les canaux à sodium et potassium sont fermés et une pompe maintient en l’état ce déséquilibre ionique (les ions sodium sont majoritairement à l’extérieur du neurone tandis que les ions potassium sont plus concentrés à l’intérieur qu’à l’extérieur) : le potentiel d’action est en phase de repos.

   Le neurone à l’état excité

   

   Le neurone est à l’état excité. Lorsqu’un influx nerveux arrive sur les dendrites et le soma du neurone (flèche verte), un nouvel influx prend naissance dans la région où l’axone quitte le corps cellulaire (A), provoquant l’ouverture de canaux sodiques et l’entrée rapide (quelques millisecondes) d’ions sodium (1); puis s’ouvrent les canaux potassiques, laissant sortir les ions potassium (2): la membrane revient à son état de repos. L’entrée d’ions sodium change les propriétés électriques du point voisin (B) de l’axone et provoque à son tour une entrée d’ions sodium, puis une sortie de potassium qui ramène la partie B de l’axone à son état de repos. Et de fil en aiguille, l’influx nerveux se propage sur toute la longueur de l’axone jusqu’à ses terminaisons (flèche rouge).

   La myéline

   Les gaines de myéline sont des membranes formées de tissu adipeux qui protègent les cellules nerveuses Ces membranes sont enroulées en spirale autour de certains axones.
   La myéline est fabriquée par deux types différents de cellules de soutien. Dans le système nerveux central (SNC) – le cerveau et la moelle épinière – des cellules appelées oligodendrocytes s’enroulent autour des axones pour créer une gaine de myéline. Dans les nerfs à l’extérieur de la moelle épinière, les cellules de Schwann produisent de la myéline.

   Peu importe où elle se trouve dans le système nerveux, cette gaine de myéline assure une propagation plus rapide des signaux: la vitesse de conduction de l’influx sur un axone myélinisé (c’est-à-dire un axone avec myéline) est jusqu’à 200 fois plus rapide (100 mètres par seconde) que celle d’un axone sans myéline.

   Les myélines sont séparées (tous les 1 à 3 millimètres) par des espaces appelés noeud de Ranvier (L.-A. Ranvier: histologiste français du XXème siècle). Ces espaces (d’une longueur de quelques millièmes de millimètre) sont très excitables car ils contiennent la majorité des canaux ioniques. 

   Conduction saltatoire

   L’influx nerveux ne se propage pas uniformément mais saute de part en part sur les noeuds de Ranvier : on parle de conduction saltatoire.

   

   Légende:
   A – Axone
   D – Dentrites
   M – Gaine de myéline
   R – Noeud de Ranvier
   S – Soma et son noyau (N)

   La structure et la composition de la membrane neuronale et de la gaine de myéline se modifient lors du vieillissement cérébral « normal », entraînant une diminution de la vitesse de l’influx nerveux. Cette modification serait à l’origine du déclin cognitif observé lors du vieillissement normal.
   

10. Les antalgiques plus nocifs chez les personnes atteintes d’Alzheimer

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    Deux nouvelles études mettent en évidence une augmentation des effets secondaires d’analgésiques opioïdes couramment prescrits chez les personnes atteintes de la maladie d’Alzheimer. Les chercheurs ont également identifié un mécanisme qui pourrait causer le problème.

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    Dans un essai contrôlé randomisé mené auprès de 162 résidents de foyers de soins norvégiens, des chercheurs de l’Université d’Exeter, du King’s College de Londres et de l’Université de Bergen ont constaté une augmentation significative des effets secondaires tels que les changements de personnalité, la confusion et la sédation, qui peuvent avoir de graves répercussions sur la vie des personnes atteintes de démence.

    L’équipe souhaite que des études soient menées pour examiner la posologie appropriée d’analgésiques (ex. buprénorphine) pour les personnes atteintes de démence.

    Environ la moitié des personnes atteintes de démence qui vivent dans des foyers éprouvent une douleur.

    Des recherches antérieures ont reconnu que la douleur est souvent sous-diagnostiquée et mal prise en charge chez les personnes atteintes de démence, ce qui a un impact sur la qualité de vie.

    Après le paracétamol, les analgésiques à base d’opioïdes sont fréquemment le second choix   de traitement pour les cliniciens chez les personnes atteintes de démence et sont prescrits à près de 40 % des personnes atteintes de démence vivant dans des foyers de soins.

    Ils soulagent efficacement la douleur, mais les recommandations actuelles ne tiennent pas compte du fait que les personnes atteintes de démence obtiennent un soulagement notable de la douleur à partir de doses plus faibles que celles habituellement prescrites, et sont particulièrement sensibles aux effets indésirables.

    L’équipe a étudié 162 personnes de 47 foyers de soins norvégiens qui souffraient de démence et de dépression. Chez ceux à qui la buprénorphine a été attribuée dans le cadre de leur traitement, les effets secondaires nocifs ont plus que triplé. Les chercheurs ont également constaté que ceux qui prenaient de la buprénorphine étaient significativement moins actifs pendant la journée.

    Selon Clive Ballard, professeur à l’Université d’Exeter Medical School :

    La douleur est un symptôme qui peut causer une énorme détresse et il est important que nous puissions soulager les personnes atteintes de démence. Lorsque nous essayons de soulager leur douleur, nous avons besoin de plus de recherches dans ce domaine, et nous devons trouver le bon traitement. Nous devons établir la meilleure voie de traitement et examiner la posologie appropriée pour les personnes atteintes de démence.

    Il est important de noter que les recherches menées par l’équipe du professeur Ballard et présentées lors de la conférence internationale sur la maladie d’Alzheimer 2018 (AAIC) permettent de mieux comprendre pourquoi les personnes atteintes de démence sont plus sensibles aux analgésiques opioïdes, ce qui suggère qu’elles surproduisent les opioïdes naturels du corps.

    Une seconde étude portant sur un modèle de souris Alzheimer a révélé une sensibilité accrue à la morphine (analgésique opioïde) par rapport aux souris saines. Les personnes atteintes de la maladie d’Alzheimer ont répondu à une dose beaucoup plus faible pour soulager la douleur et ont éprouvé plus d’effets indésirables lorsque la dose a été augmentée à un niveau normal. En regardant plus loin, l’étude a révélé que les souris Alzheimer produisaient plus d’endorphines (opioïdes endogènes naturels du corps).