Dementia: what are the causes ?

Comment créer un logo ?

Dementia: when is the diagnosis made?

Dementia: behavioral and psychological symptoms

Confusional syndrome

Delusional disorder

Macular degeneration

Corticobasal degeneration

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  1. Dementia: what are the causes ?

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    Dementia is not a disease, but rather a sum of symptoms with very diverse origins.

    There are more than 50 diseases, or infectious and toxic agents which, by affecting the brain, cause dementia.


    Epidemiology

    Dementia affects 5% of people aged 65 and over and around 40-50% of those over 85.


    The main causes of dementia

    CausesTypes of dementia
    Alzheimer’s diseaseAlzheimer-type dementia
    • Pick’s disease
    • Frontal degeneration
    Frontotemporal dementias
    Lewy bodyDementia with Lewy bodies
    Primary progressive aphasiaDementia linked to cortical atrophy
    • Parkinson’s disease
    • Huntington’s disease
    Subcortical dementia
    • Cardiovascular diseases (cerebrovascular accident, arteriosclerosis)
    • Binswanger’s disease
    Vascular dementias including:
    • Single or multiple infarct
    dementia • Subcortical vascular dementia
    • Chronic subdural hematoma
    • Brain tumors
    • Normal pressure hydrocephalus
    • Head trauma
    Dementias related to neurological conditions
    • Syphilis
    • Viral encephalopathy (Creutzfeldt-Jakob, Gerstmann-Straussler-Scheinker diseases)
    • AIDS
    • Meningitis
    Dementia associated with infection
    • Vitamin B6, B12 or folic acid deficiency
    • Hypo or hyperthyroidism
    • Alcoholism
    • Heavy metals (mercury, lead)
    • Drugs or drug intoxication
    • Dehydration, hyperthermia
    Metabolic or toxic agent-related dementias

    Dementia subgroups

    The medical community divides dementia into two subgroups based on their causes:

    • Degenerative dementias: Alzheimer’s disease, Lewy body dementia, frontotemporal lobar dementia (degeneration), dementia associated with Parkinson’s disease or extrapyramidal syndrome
    • Secondary dementias: vascular dementia, neurosyphilis, hypothyroidism, normal pressure hydrocephalus, central nervous system infections, meningitis, encephalitis, HIV, metabolite or toxic attacks (alcohol), Creutzfeldt-Jakob disease.

    The causes can be reversible (depression, delirium, harmful side effects of drugs, infections, etc.) or irreversible (dementia of the Alzheimer type, vascular dementia, frontotemporal dementia, dementia with Lewy bodies, dementia associated with Parkinson’s disease, etc.).


    The prevalence of dementias

    Dementia of the Alzheimer type is the most common dementia (accounting for approximately 50% to 70% of cases), followed by vascular dementia (approximately 20%) and dementia with Lewy bodies. Vascular dementia is often associated with dementia of the Alzheimer type: we then speak of mixed dementia.

    Before the age of 65, half of dementia is due only to Alzheimer’s disease, reaching 70% after the age of 65. 

     Alzheimer’s diseaseDementia with Lewy bodiesFrontotemporal dementiasVascular dementia
    Prevalence 50-70%0-25%8-10%15-30%

    The treatment of dementia

    There is currently no cure for most dementias (such as Alzheimer’s disease). However, cognitive symptoms are treated by alleviating them and/or delaying their progression.
    It is sometimes possible to treat or reduce non-cognitive symptoms (aggressiveness, agitation, sleep disturbances, depression, hallucinations, etc.) using medication or by modifying the living environment (for example lowering the sound and light level in the House).
    Some dementias are treatable, such as those linked to a vitamin B deficiency or following alcoholism.


    The anatomical location of dementias

    Some of these dementias primarily affect either the cortical areas or the areas located under the cortex (subcortical areas); they can, as in the case of vascular dementia, affect both.


    Symptoms associated with dementia

    Their nature, severity and progression differ depending on the type of dementia.  For example, the symptoms associated with dementia with Lewy bodies (Lewy bodies are cells that ubiquitously affect the brain) resemble those of Alzheimer’s disease (memory loss, difficulty speaking, etc.) but generally progress faster. Behavioral disorders appear earlier and more often in frontotemporal dementia or Lewy body dementia than in Alzheimer-type dementia or vascular dementia.


    Clinical characteristics of dementias

    The discovery of biomarkers or the contribution of neuroimaging (e.g., MRI, scanner) made it possible to confirm the clinical diagnosis of each of the tomes of dementia.

     Alzheimer’s diseaseDementia with Lewy bodiesFrontotemporal dementiasVascular dementia
    First signsInsidious cognitive losses (short-term memory)Insidious cognitive and behavioral disturbances (hallucinations)Behavioral and language disorders, apathy, disinhibitionSudden onset (with neurological disorder for example)
    EvolutionprogressiveprogressiveprogressiveStepwise worsening
    Accompanying signs Motor disorders, hallucinations, hypersensitivity to neurolepticsCompulsive behaviors, irritability, physical neglectCardiovascular diseases, cerebrovascular history, focal neurological deficit
    Profile of DisordersSignificant memory disordersAttention disorders (beginning forms)Alterations in executive functions, attention disorders (beginning forms)Variable (beginner forms)
    NeuroimagingTemporal lobe involvementInvolvement of cortical and subcortical regionsLocalized frontal or temporal atrophyCerebrovascular lesions
  2. Comment créer un logo ?

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    Avoir un logo reconnaissable est la marque de l’entreprise par laquelle les personnes la connaissent. Vous pouvez le dessiner vous-même, vous pouvez commander le développement à un designer, ou vous pouvez utiliser l’un des services en ligne spéciaux qui seront discutés dans cet article.


    Qu’est-ce qu’un logo ?

    Le logo est considéré comme l’un des éléments les plus importants de l’identité d’une entreprise. Il forme une image de marque reconnaissable, facilite le choix des produits par les clients et joue un rôle important dans la communication. La nécessité de créer un logo est un fait dont on ne parle plus depuis longtemps.


    Comment faire un logo en ligne ?

    Il y a littéralement dix ou quinze ans, une personne qui décidait de dessiner un logo par elle-même n’avait d’autre choix que de prendre un crayon et du papier. Mais aujourd’hui, l’ensemble du processus est beaucoup plus facile. Il existe de nombreux services en ligne polyvalents comprenant une large gamme d’instruments pour créer un logo en ligne.


    Quelques conseils pour ceux qui décident de créer leur propre logo

    Que doit être le logo ? Simple, unique, reconnaissable, mémorable. Et il doit être apprécié non seulement par le développeur, mais aussi par le public cible. Pour créer un tel logo :

    • Familiarisez-vous avec les bases de la psychologie de la perception des couleurs et des formes ;
    • utilisez des références – elles aident à formuler les exigences de votre logo ;
    • apprenez des exemples de bons logos, mais ne les copiez pas ;
    • réalisez une enquête sur les réseaux sociaux pour connaître les préférences du public cible ;
    • essayez de rester dans les tendances de la catégorie, tout en étant unique ;
    • ne surchargez pas le logo avec de nombreux détails – ils nuisent à la mémorisation et rendent le logo peu évolutif.

    En conclusion. Prendre un modèle et le modifier légèrement ne signifie pas concevoir un logo. Il est important de comprendre que le logo généré est une solution temporaire et qu’un rebranding sera certainement nécessaire à l’avenir. Si vous voulez retarder ce moment autant que possible, utilisez les services du service en ligne Turbologo.


    Créateurs de logos en ligne

    En utilisant l’un d’entre eux, vous pouvez dessiner votre propre image de marque. Pour ce faire, les concepteurs proposent un vaste ensemble d’outils, d’icônes prêtes à l’emploi et d’autres éléments. En les combinant d’une manière ou d’une autre, vous pouvez créer vous-même un logo à partir de zéro dans des créateurs de logos tels que Logotypemaker, Looka, etc.

    Pour : dans la grande majorité des cas, le développement d’un logo dans un concepteur en ligne ne nécessite pas de compétences avancées en matière de conception ou la capacité de travailler avec des outils spécifiques.

    Canva

    Canva est un éditeur de logos en ligne gratuit qui vous permet de créer des logos à partir de rien ou d’utiliser des modèles prêts à l’emploi. Des modèles prêts à l’emploi, convenant aussi bien aux professionnels qu’aux débutants dans ce domaine. Le service dispose d’une grande bibliothèque d’éléments divers (autocollants, formes, lignes, images), de polices de caractères, y compris celles en langue russe, de mises en page et de modèles. 

    L’inscription est nécessaire pour créer un projet. Il est possible de réaliser non seulement des logos, mais également diverses bannières, cartes postales, cartes de visite, ainsi que de monter récemment des vidéos.

    La version gratuite est suffisante pour un travail confortable, un abonnement sera plus probablement nécessaire pour les grandes entreprises ou ceux qui créent des designs de manière professionnelle.

    Générateurs de logos pour les marques ou les produits. 

    Les générateurs ressemblent à un constructeur avec des fonctionnalités réduites. En règle générale, ils proposent de désigner le domaine d’activité et le nom de l’entreprise. Après cela, il ne reste plus qu’à cliquer sur le bouton et obtenir un certain nombre de logos générés automatiquement. Le logo qui vous plaît peut légèrement être modifié manuellement, mais le choix des outils est généralement limité.

    Exemples de générateurs : Turbologo, Logoshi.

    Avantages : prix relativement bas. En outre, il existe des générateurs de logos gratuits pour les entreprises. Le processus le plus simple.


    Conclusion

    Le logo est l’élément central de l’identité visuelle de l’entreprise et le fondement sur lequel la marque elle-même est construite. Le logo parfait ne vieillit pas, il est pour toujours.

    Écartez les options trop décorées. Le design doit être modérément sobre, mais intéressant et mémorable. Le plus important est de maintenir la qualité des services de votre marque afin que les consommateurs puissent avoir confiance en elle.

  3. Dementia: when is the diagnosis made?

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    The diagnosis of dementia is based on an interview with the patient and a physical examination (cognitive functions, neurological examination, autonomy, mental health).

    Examinations: the first step in diagnosing dementia

    It includes basic and clinical examinations. The clinical examination includes a history and physical examination.

    A. Maintenance

    From the start of the interview, the doctor must establish a climate of trust, by speaking directly to the patient whenever his condition allows. The physician must ensure that the patient hears, sees and speaks clearly (wearing glasses, hearing aids and dental appliances). The office in which the interview takes place should be quiet and well lit. Questioning of a relative is necessary if the patient has problems communicating. The doctor must nevertheless continue to question the patient, interpreting his words.

    The anamnesis consists of questioning the patient to collect as much information as possible:

    • What is the personal history provided by the subject and corroborated by those around him: does he have a medical history, has he stayed in hospital, does he have a family history of illness (for example Does a close relative have Alzheimer’s disease A medical history may be important if a late-onset genetic disease such as Alzheimer’s disease is suspected.
    • Does he take any prescribed or over-the-counter medications? Certain medications (anxiolytics, hypnotics, certain antidepressants) are likely to cause cognitive disorders.
    • What are the symptoms frequently reported by the patient?
    • Is the patient still independent (eg does he take the bus alone?, does he dress himself)? A test is carried out to assess the subject’s ability to perform tasks of daily living (using the questionnaire on instrumental activities of daily living) and self-care (questionnaire on functional activities).
    • Has he lost weight, does he feel listless, depressed or confused, does he have memory loss, has he recently had falls, does he suffer from gait disturbances and posture, sleep (nightmares)? The observations made by the patient’s entourage describing, for example, the patient’s cognitive decline, are taken seriously into account by the doctor.

    B. Physical examination

    The doctor assesses mental and functional abilities (that is, their ability to perform physical activities of daily living).

    B1. Examination of cognitive functions

    It is done using the following assessment tests:

    1. The Mini-Mental State Examination
    2. The clock test
    3. The five-word test
    4. Grober and Buschke’s free and cued recall tests

    B2. Neurological examination

    The neurological examination includes examination of motor skills, tone and posture. The search for a parkinsonian syndrome (tremor at rest, akinesia, parkinsonian hypertonia) or frontal syndrome (reduction of the capacity to carry out a simple movement up to akinesia) must be sought systematically. The tremors at rest – at the rate of 5 per second – appear for a certain degree of muscular relaxation, and disappear during the execution of a voluntary movement.

    It is at the end of the upper limb that it begins and is most characteristic. Akinesia is characterized for example by a rarity of blinking and the reduction of mimicry, giving the patient a frozen appearance, and a reduction in the associated swinging of the arms when walking. The examination highlights a difficulty in executing alternating movements quickly. For example, in strumming movements, there is a rapid decrease in the amplitude of the movements which can lead to a real blockage. Akinesia can disappear temporarily under the influence of an emotion.

    The examination of reflexes is not only an exploration of the afferent and efferent elements of the reflex arc. It is also a test that evaluates the responsiveness of the nervous system as a whole at a specific time. Inhibition of Achilles tendon reflexes, caused by stimulation of the Achilles tendon, is frequently observed in very old people. It does not necessarily indicate peripheral neuropathy.

    B3. Autonomy Review

    The most widely used tool for assessing autonomy is the Activities of Daily Living (ADL) scale , which explores the basic activities of daily living: continence, eating, dressing , hygiene care, mobility, grooming.

    If the subject appears to be autonomous, the doctor pursues the evaluation further using the scale of instrumental activities of daily living (AIVQ, in English Instrumental Activities of Daily Living or AIDL).

    In France, the AGGIR grid (gerontological autonomy, isoresource groups) gives an overall score of autonomy that includes the patient’s ability to carry out the various acts of daily living independently. Patients are thus divided into six ‘iso-resource’ groups (GIR), which allows them to receive a social benefit for autonomy. The AGIR grid does not make it possible to accurately assess the specific needs of the patient.

    The presence of a loss of functional autonomy must evoke the existence of dementia because these daily utilitarian tasks (for example managing one’s finances, using one’s telephone, driving a car, making purchases, etc.) are essentially governed by functions cognitive (judgment, language, orientation, calculation, memory, praxis, planning).

    B4. Mental examination

    The doctor must detect the signs reflecting a mood disorder or anxiety, corroborated by the patient’s entourage.

    Psychiatric disorders are also important to identify because they are often inaugural in certain dementias such as frontotemporal dementia, Alzheimer’s disease and vascular dementia.

    For example, anosognosia (the individual’s lack of knowledge of his disease) appears in certain Alzheimer’s patients (it is detected by the Cornell scale) and in other dementias.

    Depression is considered a differential diagnosis of dementia (a condition called pseudodementia). It is often difficult to differentiate the two pathologies (dementia and pseudodementia) characterized by the presence of depressive symptoms. The diagnosis is made by prescribing the patient an antidepressant (if the antidepressant has no effect on cognitive disorders, this means that the patient suffers from dementia).

    The existence of behavioral disorders should prompt the physician to assess cognitive functions and make a diagnosis of dementia. But he must avoid mistakenly evoking dementia. Indeed, some disorders such as hallucinations can be caused by drugs or delusional manifestations (eg Charles Bonnet syndrome with visual hallucinations).

    The rating scales are:

    • Penn State Questionnaire
    • Geriatric depression scale
    • Hamilton Depression Scale
    • The Neuropsychiatric Inventory

    Dementia diagnostic criteria

    The diagnostic criteria of the Diagnostic and Statistical Manual of Mental Disorders 4th Edition (DSM IV) will be used to make the diagnosis dementia, or to make a differential diagnosis, that is to say find another cause at the origin of these cognitive disorders /behavioural; mental confusion may be one such cause.

    A. Appearance of multiple cognitive deficits, as evidenced by both:

    • Memory impairment (impaired ability to learn new information and/or recall previously learned information).
    • One (or more) of the following cognitive disturbances:
    • Aphasia: language disturbance (difficulty naming objects or people, vague speech with long convolutions, and excessive use of imprecise words like “thing” and “it.
    • Apraxia: Impaired ability to perform motor activity despite intact motor functions (subjects cannot imitate gestures such as combing their hair or correctly perform symbolic gestures such as waving their hands. Apraxia can lead to impossibility of essential independent tasks dressing, etc.).
    • Agnosia: inability to recognize or identify objects despite intact sensory functions (objects, family members or even their own image in the mirror).
    • Disturbance of executive functions (making plans, organizing, ordering in time, thinking abstractly).
    • Both criteria A1 and A2 cognitive deficits cause significant impairment in social or occupational functioning and represent a significant decline from the previous level of functioning.
    • Demonstration from the history of the disease, physical examination or complementary investigations that the disturbance is the direct physiological consequence of one of the general medical conditions listed below.
    • Deficits do not occur exclusively during the course of delirium.

    Reference: American Psychiatric Association, DSM-IV, Diagnostic and Statistical Manual of Mental Disorders. French translation, Paris, Masson, 1996.


    The etiology of dementia

    When the diagnosis of dementia is made, it is necessary to seek the etiology, that is to say the causes and factors at the origin of the disease.

    The doctor studies the way in which the disorders have settled, their evolution since the appearance of the first signs, the existence of accompanying signs (motor, psychological and behavioral disorders such as hallucinations), the profile of the neuropsychological disorders, the detection of cerebral abnormalities by neuroimaging (in particular cerebrovascular lesions characteristic of vascular dementia). Other complementary examinations can be useful for the etiological diagnosis.


    Dementia Diagnosis Reliability

    If the doctor is in doubt about the diagnosis of dementia, another diagnosis can be made within 6 months.

    However, and despite a rigorous clinical approach, a quarter of the diagnoses made are invalidated by the post-mortem study of the patient’s brain, which ultimately determines the diagnosis.


    Other possible causes of memory problems

    If the patient complains of isolated and unproven memory problems (i.e. not validated by neuropsychological tests), the doctor must screen for the existence of anxiety and/or depressive disorders, or ask the patient about the taking harmful drugs.

    In those suffering from mild cognitive decline with memory impairment validated by neuropsychological tests, the patient must be followed regularly because the evolution towards dementia is frequent (about 15% of patients suffering from mild cognitive impairment develop
    dementia per year). In some cases, these memory disorders can also be caused by drugs with side effects by a mood disorder.

    Here is a list of drugs that can cause cognitive and behavioral disorders:

    • Medicines with anticholinergic effects such as antiparkinsonians (e.g. amantadine).
    • Anti-epileptics (eg phenobarbital).
    • Tricyclic antidepressants (confusion, disorientation, delirium).
    • Hypnotics (or sleeping pills).
    • Antihistamines.
    • Central antihypertensives.
    • Benzodiazepines (treatment longer than one month).
    • Benzodiazepine withdrawal.
    • Cimetidine (an antihistamine which can cause confusion, especially in the elderly and in cases of severe renal insufficiency).
    • Corticosteroids.
    • Isoniazid (antibiotic that can cause confusion).
    • Lithium (mood stabilizer that can cause confusion and memory loss).
    • Muscle relaxants (e.g. baclofen; cause rare disturbances such as hallucinations, euphoria and mental confusion).
    • Antipsychotics (confusion, memory problems).
    • Opiates (morphine).
    • Quinidine (visual or auditory disturbances).
    • Theophylline.
    • Alcohol abuse (or alcohol withdrawal).

    Laboratory tests and neuroimaging

    Neuroimaging and laboratory examinations are then carried out when the diagnosis of dementia is probable, in order to exclude any reversible form of cognitive decline and to refine the diagnosis.

    The laboratory tests thus are intended to identify the reversible causes, the focal (localized) lesions affecting the white matter observed in vascular dementia, as well as atrophy of the medial temporal lobe characteristic of Alzheimer’s disease.

    MRI (magnetic resonance imaging) makes it possible to observe cerebral atrophy whose topography points to the etiology of dementia:

    • Alzheimer’s disease: predominantly medial temporal atrophy.
    • Frontotemporal dementia: Marked frontal and anterior temporal atrophy, as well as less medial temporal atrophy than seen in Alzheimer’s disease.
    • Vascular dementia: presence of focal lesions (lacunae), small bleeding (infarction) and white matter signal abnormalities.

    Positron emission tomography (PET) or single photon emission tomography (SPECT) are useful in differentiating Alzheimer’s disease (marked functional abnormalities of the bilateral parietal and temporal lobes) from normal aging or degeneration fronto-temporal (Figure 3), but they are not necessary in the assessment of dementia. Single-photon emission tomography (SPECT) and PET are also used to distinguish dementia with Lewy bodies from Alzheimer’s disease, using the dopamine transporter (DATscan®).

  4. Dementia: behavioral and psychological symptoms

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    Behavioral and psychological symptoms of dementia (BPSD) are defined as the signs and symptoms suggestive of disturbances in perception, thought content, mood and behavior.

    These behavioral and psychological symptoms have been divided into two groups:

    • symptoms assessed usually and primarily by patient and family interviews. These symptoms are: anxiety, depressed mood, hallucinations and delusions and
    • symptoms usually detected by observation of the patient’s behavior: aggression, shouting, restlessness, restlessness, wandering, culturally inappropriate behavior, sexual disinhibition, hoarding, cursing.

    In addition to suffering, behavioral disorders aggravate the loss of functional autonomy, disturb those around them and are often the cause of hospitalization and permanent institutionalization.

    They increase health care costs and greatly affect the quality of life of the patient, their family and other health care providers.

    In institutions, the appearance of these disorders represents a real challenge for the medical team who must diagnose them in time in order to better treat them with a dual therapeutic and behavioral approach.

    Finding the cause is important because it allows you to choose the most appropriate treatment (antidepressant, antipsychotic). The doctor will look for the existence of triggering factors.


    Type and frequency of behavioral and psychological symptoms

    These symptoms can be categorized according to the type of symptoms:

    CategoriesSymptoms
    Affective disordersDepression/dysphoria, anxiety
    , mood elevation/euphoria, irritability/mood instability
    Emotional and motivational disordersEmotional and motivational disorders
    : emotional disturbances, apathy/indifference, regressive behavior
    Behavioral disordersPsychomotor instability, compulsion,
     
    disinhibition, agitation/aggressiveness.

     
    Psychotic manifestations
    Delusions (e.g. theft, harm,
     
    persecution), hallucinations
    Identification disorders
    Basic
    conduct   disorders

    The behavioral and psychological symptoms of dementia can be classified according to their frequency and difficulties in management:

    SymptomsFrequency and support
    Delusions
    Hallucinations
     depression and anxiety
     insomnia
     physical aggression
    wandering and restlessness
    The most frequent and the most difficult to manage
    The problems of identification
    Restlessness, inappropriate behavior and sexual disinhibition
    The tendency to pace
    Screams
    Relatively frequent which can also be stressful
    The cries
     swear words
     The lack of enthusiasm
     Repetitive questions
     The relentless pursuit of a loved one
    Less common and for which treatment remains possible

    About 60-90% of patients with dementia related to Alzheimer’s disease show behavioral problems during the course of the disease. According to the REAL study, the frequency of behavioral and psychological symptoms is very high ranging from 84% for people with an MMSE test score of 21 to 30 to 92.5% of patients when the MMSE test score is between 11 and 20 .

    Behavioral and psychological symptoms occur at different stages of the disease. Affective symptoms are more likely to appear at an early stage of the disease. Agitated and psychotic behaviors are common in patients with moderate cognitive impairment; however, they become less apparent in advanced stages of dementia, most likely due to deterioration in the patient’s physical condition.

    It is often the nurses and caregivers who generally notice them first. The earliest are signs of depression, anxiety, apathy, disinterest, social withdrawal. Then follow the noisiest: agitation, aggressiveness, disinhibition.


    Symptoms depend on the type of dementia

    Psychological behavioral symptoms are not the same in all dementias: emotional disturbances and apathy often dominate in Alzheimer’s disease, while hallucinations are present in 80% of people with Lewy body dementia; agitation, aggressiveness, apathy dominate in vascular dementias, and impulsive behaviors, agitation, disinhibition characterize frontotemporal dementias.

    Some psychological behavioral symptoms are more persistent than others. For example, over a 2-year observation period, one study demonstrated that wandering and restlessness are the longest-lasting behavioral symptoms in patients with Alzheimer’s disease.

    Similar profiles have been found in patients with Alzheimer’s disease and vascular dementia. All symptom levels were high (30% of all patients had three or more psychiatric symptoms) and increased with the severity of dementia. Agitation was the most frequent symptom, followed by symptoms of depression, apathy and aberrant behavior.

    Other studies have also reported that there was no difference in behavioral profile between patients with Alzheimer’s disease and those with vascular dementia.

    Visual hallucinations are more commonly seen in patients with dementia with Lewy bodies than in those with Alzheimer’s or Parkinson’s disease.

    These hallucinations occur in nearly 80% of patients with dementia with Lewy bodies, compared to nearly 20% in those with Alzheimer’s disease.


    Frequency and evolution of psychological behavioral symptoms in Alzheimer’s disease

    SymptomsFrequency
    Depression5 to 25%
    Anxiety50%
    Psychosis50%
    Agitation/aggressiveness50 to 75%
    Apathy100%

    Psychological behavioral symptoms in frontotemporal and Lewy body dementia

    Frontotemporal dementiasDementia with Lewy bodies
    physical neglectVisual hallucinations
    DisinhibitionSleep disorder
    Psychic rigidityDepression and apathy
    HyperoralityPsychomotor restlessness
    StereotypyDelusions, often elaborate
    Usage behavior 
    Distractibility 
    Frontotemporal dementiasDementia with Lewy bodies
    Impulsiveness 
    Anosognosia 
    Depression 
    Anxiety 
    Ideal fixation 
    Delirium 
    Hypochondria 
    Somatic complaints 
    emotional indifference 
    Apathy 
    Inertia 

    Depression and apathy

    Depression represents a differential diagnosis of dementia but it can also be part of the clinical picture of Alzheimer’s disease (early stage) .

    Depressive symptoms affect a sizable minority of patients with dementia at some stage of development. Most studies, conducted with patients with Alzheimer’s disease, have shown that depressed mood is found more frequently (40-50% of patients), while depressive disorders are less common (10-20%) . A 5-year longitudinal study of patients with Alzheimer’s disease found relapse rates of 85% for depressive symptoms over a one-year period.

    The diagnosis of depression can be difficult to establish, particularly in patients with moderate or severe dementia. In the early stage of dementia, depressed mood and its symptoms can usually be determined during the medical consultation.

    As dementia progresses, it becomes more difficult to establish the diagnosis of depression due to the increasing presence of speech and communication difficulties, apathy, weight loss, sleepiness and restlessness that accompany dementia.

    A depressive disorder should therefore be considered if:

    • pervasive depressed mood and anhedonia (inability to feel positive emotions caused by a feeling of disinterest);
    • self-devaluation and desire to die;
    • personal or family history of depression prior to the onset of dementia.

    The prescription of an antidepressant -without anticholinergic properties- is justified.

    Apathy and its associated symptoms affect up to 50% of patients in the early and middle stages of Alzheimer’s disease and other forms of dementia. Patients with apathy present with:

    • lack of interest in activities of daily living and self-care;
    • decreased social interaction;
    • a decrease in facial expressiveness;
    • a more monotonous voice;
    • decreased emotional reactivity;
    • loss of initiative.

    Symptoms of apathy can be confused with those of major depression. Both states can manifest as a decline in general interest, psychomotor retardation, lack of energy and insight.

    Although a lack of motivation also accompanies the states of apathy and depression, the apathy syndrome denotes a lack of motivation without the vegetative symptoms of depression being present.

    The drug treatment of apathy is different from that of depression (the doctor will prescribe an antidepressant to a depressed patient, and a psychostimulant in case of apathy).


    Anxiety

    Anxiety is with depression the affective disturbance most frequently found (50% of cases) in demented patients. It can precede cognitive disorders to the point that its recent appearance in an individual should lead to the evaluation of his cognitive functions. Demented patients with anxiety will express previously unmanifest concerns and fears about their finances, future, and health (including memory), and fears about events and activities, like being away from home.

    The patient may incessantly repeat questions relating to an upcoming event (this is Godot’s syndrome). Another symptom of anxiety characteristic of the demented patient is the fear of being left alone. This form of phobia can manifest itself as soon as the carer goes to another room in the home (the patient follows the carer in his movements) and can be expressed by the patient’s repeated requests not to be left alone. Other phobias may also appear, such as a fear of travelling, being left in the dark, or taking a bath.

    It is often difficult to spot anxiety in a person with dementia. Indeed, aphasia can prevent the verbal communication of affects and transform the expression of emotional disorders. Similarly, emotional responses may be maladaptive due to misinterpretation of a stimulus.

    Apraxia can also impair nonverbal emotional expression abilities.

    Sometimes, the demented subject adopts defense mechanisms against anxiety: for example, he will invoke a relative as if he were still alive. When the dementia is more pronounced, the anxiety presents itself in a more physical form: aggressiveness, running away, incessant wanderings…


    Agitation and aggression

    They are relatively infrequent but can create a climate of disorganization in an institution. Agitation is defined as inappropriate verbal, vocal or motor activity that is not the result of an immediate need or a state of confusion. Interventions must be immediate and based on the intensity of the crisis.

    Aggression is a feared behavioral disorder because it is difficult to control. A distinction must be made between verbal aggression (anger, insults, shouting, etc.) and physical aggression (violent gestures). This type of behavior generally takes shape during exchanges between the patient and the carer (toilet, dressing, meals, bedtime).

    There are four forms of agitation/aggressiveness:

    Non-aggressive physical behavior :

    • repetitive gestures (eg hoarding objects – pencils, cups, toiletries, clothes – that are in the room of other patients;
    • comings and goings;
    • wandering around, entering other patients’ rooms or bathrooms, lying in their beds;
    • attempts to travel to another location;
    • hiding objects, tearing things up, throwing them in the toilet;
    • inappropriate urination or defecation, including handling stool;
    • wearing inappropriate clothing;
    • knocking over food trays, eating from other patients’ trays;
    • take objects belonging to other patients and staff members (glasses, teeth, pants).

    Non-aggressive verbal behavior :

    • negative attitude;
    • to love nothing;
    • constant attention seeking;
    • give orders;
    • whining complaints or grievances;
    • relevant interruptions;
    • repetition of sentences.

    Aggressive physical behavior :

    • to kick;
    • jostle;
    • scratch;
    • seize objects;
    • grabbing people;
    • kicking and biting;
    • pull out restraints or catheters.

    Aggressive verbal behavior :

    • to yell;
    • display inappropriate hostility (insults; calls, swearing, shouting* etc.);
    • surge of anger;
    • make strange sounds.

    * Cries most often occur when the person is alone in their room, in the evening or at night. Their appearance is more important at the time of interventions carried out in a situation of constraint for the person (toilet, dressing). It is necessary to determine whether these cries come from pain or are the cause of a manifestation of fear, a depressive state or moral suffering that cannot be expressed in words. The installation of bed rails generally increases the intensity and duration of these cries in some patients. It is therefore important to stimulate the patient as much as possible by providing him with activities adapted to his condition (playing of musical tapes, video-cassettes evoking family memories).

    Dementia by itself does not completely explain the agitation phenomenon. Indeed, other factors – medical, psychological and environmental – are involved in agitation.

    It is important to have a calm attitude and voice, to try to appease the patient by word and gesture, not to be more than three people involved (the patient may feel threatened). It is sometimes necessary to isolate the patient in his room, knowing that there is a risk of a panic attack. Restraints are to be avoided, as they often increase the intensity of the crisis.

    The causes and triggering factors depend on the personality of the patient and his situation: it may be, for example, a reaction to pain, an annoyance (loss of a life habit), a reaction to an over -stimulation (sensory or cognitive) for the patient who no longer has the ability to respond.

    For example, a patient may be aggressive or even violent if the nursing staff refuses her access to her bathroom after her meal. An interview with one of her children will make it possible to understand the reasons for her anger: she had the habit of brushing her teeth after each meal, a habit which had not been followed when she entered an institution (this is an annoyance relating to that of care which must take place in an institution at specific times).


    Delusional Disorders

    The frequency of delusions in people with dementia is between 10% and 73% depending on the population studied. About a third of patients with probable Alzheimer’s disease suffer from delusions, and are considered to be at risk for physical aggression. According to one study, 80% of participants with high levels of physical aggression (>1 episode/month) also suffered from delusions. Patients with Lewy body dementia very often present with delusional pathology (about 80%).

    Delusional disorders at the beginning of the dementia stage revolve mainly around forgetfulness. They lead to ideas of displacement and theft of objects, intrusion into the home…

    They may be accompanied by aggressiveness in a person with a psychiatric history. As the disease worsens, the delusions aim to fill the growing void caused by the memory loss, and draw on the remnants of memories still intact in the patient. The most frequent delusional themes are theft, prejudice and infidelity and jealousy (15% of cases).

    The Behavioral Pathologic Rating Scale for Alzheimer’s disease is a behavioral disorder rating scale that describes the different forms of delirium in Alzheimer’s disease. These forms are classified by theme (theft, impostor syndrome, etc.):

    The patient believes that he has had things stolen (frequency = 18% to 43%)

    Likely explanation: the patient does not remember the location of their personal items. He will therefore be led to blame a third party for their disappearance. In serious forms, he is convinced that people break into his home with the aim of hiding or stealing objects.

    The patient believes he is living in a home that is not his

    The patient does not remember or recognize his home. He may end up leaving it to return « home » (this is the phenomenon of wandering).

    The spouse (or the relative in charge of the patient) is perceived as an impostor

    The patient no longer recognizes his loved one. He can also consider the family caregiver or his doctor as an impostor, leading to a reaction of mistrust, even of great violence. This may be similar to an identification disorder (this is Capgras syndrome).

    A feeling of abandonment (frequency = 3% to 18%)

    The patient is convinced that he has been abandoned, that he will be placed in an institute, and that a plot is being organized for this purpose. This feeling stems from the fact that he realizes the burden he represents for those around him because he retains a certain awareness of his condition. Relatives feel guilty for this feeling of abandonment experienced by the patient.

    A feeling of infidelity (frequency = 1% to 9%)

    This feeling mainly concerns the spouse or caregivers.

    Although the diagnosis of delirium is sometimes difficult in a person with dementia (indeed people with dementia already have a disorder of ideation and confusion), it is possible, with some experience, to tell the difference between delirium and dementia.

    Indeed, delirium is usually accompanied by:

    • a sudden onset of symptoms;
    • a decrease or increase in alertness in the patient already presenting with dementia, or a marked fluctuation in symptoms;
    • visual hallucinations accompanied by agitation;
    • impaired psychomotor activity;
    • language disorders (slurred speech, slowing or speeding up of speech);
    • of tremors.

    Once the diagnosis of delirium is made, the choice of treatment will depend on identifying the cause. These causes are many and include:

    • medication side effects;
    • malnutrition;
    • an infection;
    • cerebral pathologies (e.g. subdural hematomas);
    • endocrine disorders (eg hyperthyroidism);
    • metabolic diseases (eg certain kidney or liver conditions);
    • patient environmental factors;
    • Hypoxia caused by pneumonia, congestive heart failure or sleep apnea;
    • Urinary retention or fecal impaction (accumulation of feces).

    Hallucinations

    Hallucinations interfere with the patient’s ability to understand the outside world. This phenomenon can alter their ability to perform activities of daily living and can affect their relationship with caregivers. The frequency of hallucinations in people with dementia ranges from 12 to 49%.

    Visual hallucinations are the most common (up to 30% of patients with dementia), and they are more common in moderate dementia than in mild or severe dementia. Auditory hallucinations are present in 10% of dementia cases. Other forms of hallucinations – tactile and olfactory – are rare.

    A common type of visual hallucination involves observing the presence of certain people in one’s home, when in fact they are not there. In the case of Lewy’s dementia, the interpretation disorders are based above all on gnosic deficits, and to a lesser extent on mnesic disorders and sensory perception defects.

    The most frequently observed gnosic deficits are prosopagnosia (the patient does not recognize his relatives; 12% of cases), self-agnosia (4% of cases), intrusion of people into the patient’s life ( 6% of cases), or the ghost companion syndrome (the patient is convinced that a person is hiding in his home (17% of cases). These hallucinations sometimes require treatment when they are a source of stress. This treatment depends on the etiology.

    There seems to be a relationship between a decrease in visual acuity and hallucinations (Bonnet syndrome is quite common). Indeed, a significant percentage of people with dementia have visual impairment (e.g. visual agnosia characterized by difficulty recognizing faces or objects), and many experience difficulty in contrast perception, especially at low frequencies. In these patients, the line of demarcation between the areas of shadow and light appears blurred, which partly explains the high rate of identification disorders and visual hallucinations. It is therefore important to assess the visual perception functions of patients with dementia and suffering from hallucinations. From a practical point of view,

    An attitude of empathy from the nursing staff is often the most effective approach when dealing with a patient suffering from delusion of flight. The nurse can then look with him for the objects supposed to have disappeared, which has the effect of reassuring him.


    Wandering

    Wandering (also called motor hyperactivity) describes a set of manifestations during which the patient follows and seeks caregivers throughout the day. This wandering can be aimless or will be characterized on the contrary by comings and goings between two very specific places. These manifestations, specific to demented states but whose causes are complex, would be the expression of boredom, sadness or anxiety. Here are some causes that would be at the origin of this type of behavior: hyperactivity, orientation disorders leading to seek new landmarks, attempt to escape or escape isolation,

    These problems are the most delicate to manage at home, which obliges the relative to hospitalize the patient.

    It should be noted that the ambulation associated with akathisia can be caused by the side effects of antipsychotics, effects which persist for several months after stopping treatment.

    The management of ambulation primarily involves non-drug treatments. Physical restraints should be avoided because on the one hand they have no effect and on the other hand they raise an ethical problem. The architects have provided spaces in the institutions allowing unrestricted walking. These spaces should be bright, spacious, attractive, risk-free and create a sense of security.

    The planning of physical activities (gymnastics, walks) must complete the care program, with dance and singing programs as well. It is strongly advised to monitor the nutritional status of these people, whose energy expenditure and water loss are significant. The room must be arranged so that the patient can find familiar landmarks (small pieces of furniture, family and home photographs, etc.).


    Repetitive behaviors

    Repetitive behaviors are, like wandering, specific to demented states and often concern the same people. There are two forms of repetitive behavior:

    1. Risk-free behaviors

    These people are constantly doing and undoing (eg emptying and filling a cupboard, making and undoing a bed, etc.). These activities are favored by boredom and the absence of activities (which is somewhat paradoxical…). The programs proposed to reduce ambulation are quite suitable in this case.

    2. Risky behaviors

    These are often behaviors of self-mutilation (eg repeated scratching of the face with the fingernails) whose intention is difficult to understand. This behavior can temporarily stop if an affective derivative is offered: caresses, massages or animal therapy.

    Runaways are behavioral problems feared by health professionals. They occur most often in the weeks following entry into an institution and tend to subside after a period of adaptation. It would seem that the patient wants to flee a place because it is inhospitable to him, even hostile. However, it is difficult to offer closed structures for security reasons (risk of fire) and psychological reasons (feelings of being in a prison). Some institutions suggest placing exits in dark areas or concealing them. We can also prevent the risk of running away by arranging the environment with familiar objects to familiarize the patient with his environment and improve his well-being.


    Disinhibition

    It results in impulsive and inappropriate behavior. The patient cannot maintain the type of social behavior he had before. Symptoms include:

    • the cries;
    • euphoria;
    • verbal abuse;
    • physical violence directed at others or objects;
    • self-destructive behaviors;
    • sexual disinhibition;
    • motor restlessness;
    • intrusive behaviors;
    • impulsiveness;
    • wandering.

    Shoplifting, gambling addiction, compulsive shopping can lead to financial and social problems in patients with disinhibition. Patients with impaired judgment are more likely to consume alcohol or drugs excessively.


    Intrusive behaviors

    The intrusive behavior manifests itself in gestures of protest, impatience, clinging or jostling. These behaviors have a prevalence of about 40% in dementia, and do not seem to depend on the severity of the cognitive and functional deficit.


    Sleep disorders

    These disorders end up exhausting the family caregivers, leading them to place the patient in a medical institution. The doctor must inform the relative of the physiological changes in sleep (lengthened sleep onset, jerky sleep, reduced quality of sleep, etc.) that accompany dementia. Difficulties falling asleep are caused by anxiety disorders, while early awakenings evoke depression.

    The use of sleeping pills should be temporary and of short duration. Some non-drug measures can improve sleep disturbances.


    Vocalization behaviors

    These verbal expressions, often brief but repetitive, are more frequent when the patient is isolated, in the evening between meals and going to bed, or in the morning between waking up and getting up. It is difficult for caregivers to determine the causes and reasons for these cries. In the absence of specific causes (pain, hallucinations, etc.), the cries are attributed to dementia.

    Treating these symptoms is difficult. Certain non-drug approaches sometimes prove effective: correction of sensory deficits, reduction of sensory stimulation (noise, light, cognitive activity), getting the patient to talk about the difficulties he is experiencing in the institution (his daily life, his isolation) , adopt a calm and reassuring attitude, communicate non-verbally (caress the patient’s hands and face), offer massage sessions.

    Atypical antipsychotics present but seem, according to some doctors, to be less well tolerated than selective serotonin reuptake inhibitor type antidepressants (eg Paxil).


    The problems of identification

    Unlike hallucinations (which occur in the absence of external stimuli), identification disorders are due to errors in the perception of external stimuli. There are four forms:

    • ‘ghost boarder’ syndrome: presence of people inside the patient’s home (about 5% are convinced that people appearing on television are present in the room);
    • self-identification disorder: it is often manifested by the fact that the subject does not recognize himself in a mirror; (about 4% of patients);
    • other people’s identification disorder: the patient takes people for other people (about 12%);
    • misidentification of events.

    In 1990, Ellis and Young distinguished three forms of delusional identification disorder: Capgras syndrome .

    Fregoli syndrome is a type of hyperidentification characterized by the fact that patients are convinced that individuals wishing to harm or influence them disguise themselves to assume the identity of other people. In many ways, Fregoli syndrome can be like the normal experience.

    When a non-demented subject expects to meet a person, he may, for a brief moment, take a stranger for the person he was expecting, but this perception is quickly corrected by noting divergent facts. A patient with Fregoli syndrome will attribute these divergent facts to the notion of a disguise.

    Intermetamorphosis delusion describes a situation in which one person’s physical appearance is perceived as that of another.

    Many parents and caregivers find their own ways to cope with the difficulties of identification. It is important to understand that what works well with one person may not be as effective with another. In some cases, humor will be preferred while in others, comfort or diversion will lead to greater success.


    Care

    What are the actions to take when faced with a person suffering from dementia accompanied by psychological and behavioral disorders?

    Anxiety

    Anxiety often causes physical manifestations related to anxiety. In some cases, it can result in delusional states during which the elder will accuse those around them of theft, for example.

    In the patient, anxiety results in momentary disturbances which concern both the body and the consciousness. It becomes abnormal when it occurs for no apparent reason and permanently.

    At the psychological level, it results in a feeling of inner malaise, internal tensions, difficulty concentrating, threat or depersonalization. At the physical level, anxiety results in an increase in heart rate, respiratory rate and sweating. From the behavioral point of view, we observe agitation, incessant movements, clenching of the hands and aggressiveness.

    How to deal with this type of problem?
    – Prescribe a short-lived anxiolytic.
    – Use relaxation techniques to relax the muscles and the mind.
    – Identify the triggering factor.
    – Reassure the person by speaking calmly.
    – Try to determine the origin of the agitation, taking into account the person’s biography.

    Agitation and aggression

    Agitation is manifested above all by incessant wanderings, diurnal or nocturnal, messy activities, akathisia, running away caused by temporal and spatial disorientation, repeated manual movements (eg scratching, folding of clothes). Two-thirds of patients show signs of institutional agitation. This percentage reaches 90% in those suffering from dementia.

    Aggression, whether verbal or physical, often has an unusual character that surprises those around you. The latter dreads it, because it is often unpredictable and difficult to control. Aggression refers to all activities aimed at harming an individual or an object directly or indirectly. This behavioral disorder generally takes place during a relational exchange, in particular when washing, dressing, eating or going to bed.

    A distinction must be made between aggressive and non-aggressive behaviors, which are expressed verbally and non-verbally (physically): – motor agitation: aimless walk, nocturnal wandering;
    – physical aggression: throwing or destroying objects, making inappropriate gestures, biting, spitting, scratching, kicking, beating another person;
    – verbal aggression: speaking loudly, shouting, swearing, using rude words, threatening, accusing, making unusual noises, complaining, whining, making repeated demands;
    – passive aggression: delaying, avoiding or refusing help.

    How to prevent or mitigate this type of behavior?
    – Prescribe pharmacological treatment (neuroleptics, lithium, carbamazepine, buspirone, antidepressants, short-lived benzodiazepines), particularly in the event of an acute situation of agitation and/or aggressiveness accompanying dementia.
    – Try to restore an activity during the day (in case of nocturnal restlessness).
    – Adopt a serene attitude and a soothing tone of voice.
    – Stand facing the person and at the same height.
    – Express yourself in simple words.
    – Establish physical contact by staying close to the patient or holding their hand, especially when there are visitors in the house.
    – Listen and decode non-verbal language.
    – Name yourself and name the person.
    – Give a snack at the time of the crisis of nocturnal agitation.
    – Leave a little light in the room in case of nocturnal agitation.
    – Install the person in a room for two to reduce anxiety in the event of nocturnal restlessness in an institution.
    – Propose a relaxing activity (walking, listening to music, isolation for some time in the room).
    – Try to establish routines in the activities of daily living (bathing, meals).
    – Avoid placing the patient near a source of noise (washing machine, washing machine) which could cause agitation.
    – De-dramatize situations that could humiliate or make the patient feel guilty (in the event of aggressive behaviour).

    Don’ts:
    – Do not insist if the person refuses to cooperate.
    – Avoid using the subject “on”.
    – Do not respond to aggression with aggression.
    – Do not adopt an infantilizing attitude.
    – Do not try to reason with the patient with arguments that go beyond the possibilities of understanding.
    – Do not argue with her by contradicting her.
    – Do not offer him things that are too difficult for his remaining abilities.
    – Do not express your frustration.
    – Do not re-discuss events that led to aggressive behavior.

    After having tackled the problem, you must try to determine the origin of the conflict: look for the triggering elements showing significant frustration (agitation and/or aggressiveness in a demented state). Look for bodily, psychological or psychosocial causes and then treat them.

    Here are some questions to ask yourself in order to identify the factors if possible:
    – Does the patient have a headache? 
    – Is he particularly tired?
    – Is he constipated?
    – Does he sleep badly?
    – Are his clothes inappropriate (too warm, tight)? 
    – Is he too stimulated by the environment (continuous television, radio at too high a volume)? 
    – Is he upset by a new environment (bedroom, kitchen) in which he has lost his bearings?
    – Is he more restless when he is alone or, on the contrary, when there are people around?
    – Does he feel compelled to perform an activity against his will?

    Agitation, confusional states and end of life

    Agitation is common in elderly subjects at the end of life. The causes come from several factors, hence the need to seek a curable cause or poorly relieved pain, or to remove drugs that are not essential.

    Elements to look for in a patient at the end of life: 
    – Unrelieved pain.
    – Urinary retention.
    – Dry mouth, dehydration.
    – Confusion caused by medication (neuroleptics, morphine, antiemetic, anticholinergic).
    – Metabolic disorders (hypoglycaemia).
    – Neurological origin (eg brain metastasis).
    – Psychological origin (anxiety, conflict).


    Psychological Behavioral Symptoms References

    Pancrazi MP, Métais P. Alzheimer’s disease, diagnosis of psychological and behavioral disorders. Medical Press 2005; 34(9): 661-6.

    Brocker P et al. Psychological and behavioral symptoms of dementia: description and management. The Journal of Geriatrics, Volume 30, N°4 April 2005

    Cummings JL, Mega MS, Gray K, Rosemberg-Thompson S, Gornbein T. The Neuropsychiatric Inventory: comprehensive assessment of psychopathology in dementia. Neurology 1994;44:2308-14.

    Conn D, Thorpe L. Assessment of behavioral and psychological symptoms associated with dementia. Can J Neurol Sci. 2007 Mar;34 Suppl 1:S67-71.

    Benoit M, Staccini P, Brocker P, Benhamidat T, Bertogliati C, Lechowski L, Tortrat D, Robert PH. Behavioral and psychological symptoms in Alzheimer’s disease: results of the REAL.FR study Rev Med Interne. 2003 Oct;24 Suppl 3:319s-324s.

  5. Confusional syndrome

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    Delirium – a confusional syndrome or state – is characterized by changes in the level of consciousness, disorientation and behavioral problems.

    It is common after surgery.

    Do not confuse delirium (literally translated from Latin as outside the groove) and delirium, which is a disturbance of logical reasoning.

    History of delirium

    1881: Lasègue describes for the first time delirium tremens in alcoholics.

    1892: Chaslin describes mental confusion and already notes clinical heterogeneity.

    1911: Regis describes secondary post-dream delusions.

    1935: Wolff and Curran describe it as a mental condition caused by malnutrition and poor blood supply in the brain.

    Epidemiology of delirium

    The highest incidence rates were observed in intensive care, postoperative and palliative care units. Since many of these studies excluded patients with cognitive impairment or dementia at baseline, these rates are likely underestimated.

    In general medicine and geriatrics departments, the prevalence of delirium (present on admission) varies from 18 to 35%. More specifically, the prevalence of delirium in hospitalized elderly patients varies from 15 to 25% after major surgery and is estimated at 50% after high-risk surgery in the elderly, such as a hip fracture or heart surgery. Confusional state is therefore common after surgery.

    The prevalence of delirium in the community setting is relatively low (1–2%), but its onset usually brings the patient to urgent care. It is present in 8 to 1% of elderly people admitted to the emergency room. Its prevalence at the end of life is around 85% in palliative care.

    In intensive care units, delirium usually begins within the first few days of hospitalization and usually lasts 24 to 48 hours. The prevalence is 70%.

    Delirium is consistently associated with an increased mortality rate in all non-surgical patient populations (e.g. medical, geriatric, and intensive care units). 15-18% of those who develop delirium in general or geriatric medicine wards are 1.5 times more likely to die within a year. In older patients with dementia, delirium is associated with increased rates of cognitive decline, institutionalization, and mortality.

    The causes of delirium

    While a single factor can lead to delirium, most often delirium is multifactorial. There are predisposing factors that are associated with etiological factors: advanced age, male sex, presence of dementia or psychiatric illness, consumption of drugs (eg benzodiazepines, sedatives, hypnotics) , alcohol dependence and decreased visual acuity.

    In patients who are highly vulnerable to delirium, such as those with underlying dementia and several other disorders, a simple intake of medication – such as a single dose of sleeping pills – may be enough to precipitate delirium.

    Conversely, in a healthy young patient, delirium will only develop after exposure to a series of major events, such as general anesthesia, major surgery, taking multiple psychotropic drugs, a stay in intensive care and sleep deprivation. 

    Clinically, the implication of multiple causative factors is that treatment of a single risk factor is unlikely to resolve delirium, and that multiple approaches will be most effective in both preventing and treating delirium. .

    The causes can be:

    • metabolic disorders;
    • infections (pneumonia, urinary tract infection, sepsis, etc.);
    • neurological diseases or accidents (stroke, depression, epilepsy);
    • surgical operations (operative shock, immobilization, general anesthesia );
    • heart problems (heart failure, heart attack, heart rhythm disorder);
    • trauma;
    • autoimmune diseases (lupus);
    • somatic ailments (retention of urine, fecal impaction);
    • psychological causes;
    • neoplasms;
    • taking multiple medications or using psychoactive drugs (risk increased by 4.5 times).
    • Withdrawal from a substance or medication (benzodiazepines, opiates, psychostimulants, alcohol).

    Dementia is, along with mental confusion and depression, one of the etiological factors of delirium. Confusional episodes are common after an operation caused, for example, by postoperative hypoxia or hypotension. Tricyclic  antidepressants , antipsychotics and antiparkinsonens (which have anticholinergic properties), benzodiazepines and barbiturates, drug withdrawals (benzodiazepines, barbiturates) also cause delirium, as do morphine-type analgesics, some antihypertensives (beta-blockers, calcium channel blockers, etc.).

    Pathophysiology

    Delirium is undoubtedly the consequence of the involvement of several causal factors which, taken one by one, seem minor but which, when accumulated, trigger the disease.

    It is likely that several sets of interacting biological factors lead to disruption of neural networks and decreased metabolism in certain regions of the brain, leading to cognitive dysfunction. Other causal mechanisms interfere more indirectly with neurotransmission. For example, the inflammatory response seen in sepsis can lead to a cascade of local neuroinflammation in the brain triggered by cytokines, leading to decreased blood flow and neuronal death. Neuroinflammation can lead to glial cell activation, which in turn leads to neuron death.

    Changes in the sleep-wake cycle have been reported in patients with  sleep disturbances and sundowning syndrome. The cholinergic system is affected in delirium, a hypothesis supported by the fact that drugs with anticholinergic properties (ie, which cause a drop in acetylcholine levels) cause acute confusional episodes. Other neurotransmitters (GABA, dopamine) may also be involved.

    The risk factors are:

    • age
    • Madness
    • The male gender
    • Previous history of delirium
    • Vitamin deficiencies
    • Depression, anxiety
    • Pain, fractures. dehydration.

    Diagnostic criteria  for delirium

    Delirium is a clinical diagnosis, often misunderstood and easily overlooked. Recognition requires a brief cognitive screening and clinical observation.

    Key diagnostic features include sudden and fluctuating onset of symptoms, inattention, altered level of consciousness, and impaired cognition (eg, disorientation, memory impairment, impaired language).

    Perceptual disturbances (hallucinations or illusions), delusions, psychomotor disorders (hypo- or hyper-activity), inappropriate behaviors and emotional lability. The current reference standard diagnostic criteria are the American Psychiatric Association’s Diagnostic and Statistical Manual (DSM-IV) and the World Health Organization’s International Classification of Diseases (ICD-10).

    The DSM-IV defines delirium as a mental disorder due to a general medical condition consisting of the combination of the following diagnostic criteria:

    • disturbance of attention and consciousness;
    • modification, impairment of cognitive performance (memory, orientation, language, perception disorders);
    • alteration of sensory perceptions manifested by visual or auditory illusions or hallucinations that affect the patient’s behavior, with the possibility of panic reactions (fugue, aggression, etc.);
    • the disturbance sets in in a short time (a few hours to a few days), with a fluctuating course throughout the day;
    • evidence from the anamnesis, clinical and paraclinical examinations, that the disturbance is due to the direct physiological consequences of a general medical condition.

    For the CIM-10 , the criteria are substantially the same, except that according to the CIM-10, the onset is usually sudden, the evolution is fluctuating during the day and the total duration of the episode is less than six month. In addition to these main criteria, there are:

    • psychomotor disorders (hypo- or hyperactivity, prolonged reaction time, increased or decreased verbal flow, exaggerated startle reaction);
    • a disturbance of the sleep-wake rhythm;
    • emotional disturbances,  depression ,  anxiety , irritability,  apathy
    • sometimes vegetative disorders (tachycardia, sweats, fever…);
    • incoherent, logorrheic language.

    More than 24 instruments have been used in scientific studies to identify delirium. The most widely used is the Confusion Assessment Method (CAM), with a sensitivity of 94% and a specificity of 89%. Cognitive testing is recommended for optimal use of the CAM. The CAM has been adapted for use in intensive care units, emergency rooms and nursing homes.

    Clinical forms

    Perceptual abnormalities include hallucinations, delusions, and misinterpretations. They are mostly visual and accompanied by emotional reactions. A sudden onset and a short and limited duration are necessary criteria for the diagnosis of the confusional episode, but the ICD-10 admits a maximum duration of the table over six months. The confusional episode can either reveal the presence of an undiagnosed dementia, or aggravate an already installed dementia.

    Differential diagnosis

    One `two-thirds of delirium diagnoses are missed due to the fluctuation of the clinical picture throughout the day.

    Acute confusional state can be confused with the following diseases:

    1. Dementia. Unlike delirium, the onset of  dementia  is insidious, vigilance is intact, hallucinations are rare, psychomotor activity is normal, mood is little altered, delusions are infrequent, speech is most often normal during early disease and neurological signs are often absent.

    2. Wernicke’s aphasia. This disorder is marked by disorders of oral comprehension, verbal productions characterized by jargon or paraphasias. In some cases, the patient is difficult to channel, which can lead to a confusing diagnosis. A CT scan will help differentiate Wernicke’s aphasia from  delirium.

    3. Amnesic stroke. The patient suffers from isolated amnesia, of sudden and transient installation (a few hours). The other cognitive functions are intact.

    4. Gayet-Wernicke encephalopathy. This vitamin B1 deficiency results in a confusional syndrome with hypersomnia and hallucinations, and concerns people who are undernourished. Early treatment, before neurological signs appear, is critical.

    Clinical evaluation of delirium

    The most important step in the assessment is to learn the history from an informed observer (eg, a family member or caregiver) and perform a brief cognitive assessment.

    A brief cognitive screening should be done using cognitive screening tests such as the short MMSE or the Montreal Cognitive Assessment. If time is extremely limited, orientation assessment with an attention task provides a baseline screening.

    The electroencephalogram (EEG) has limited sensitivity and specificity in the diagnosis of delirium. However, delirium is characterized by increased theta and delta activity.

    The tools for assessing the severity of delirium are the Delirium index  and the Confusional State Evaluation, while the main screening tool is the Confusion Assessment Method. Other neuropsychological tests are also useful:  the mini-mental exam,  the clock test, and the  tracing test.

    Given the high mortality rates, any suspicious or uncertain cases (including those with lethargy or unable to complete an interview) should be treated as delirium until proven otherwise. Initial management focuses on three concurrent priorities: (1) maintaining patient safety; (2) investigate causes; and (3) management of symptoms of delirium.

    To maintain patient safety, efforts should focus on protecting the airway, maintaining hydration and nutrition, preventing falls, and avoiding restraints that increase the risk and persistence of delirium.

    A complete medical check-up is necessary: ​​blood sugar, drug dosage, vitamin B12, thyroid function test, albumin, sodium, potassium, magnesium, etc.

    Treatments

    Delirium must be treated because it increases morbidity and the risk of institutionalization and length of hospitalization.

    1. Stimulation of the patient during the day, by encouraging him and facilitating references to his natural living environment. Avoid isolation which promotes sensory deprivation. Reassure the patient by speaking calmly. Avoid noise and commotion.

    2. Pharmacological treatment with psychotropic drugs with sedative effects: Clometiazole, carbamates, antipsychotics without anticholinergic effects (haloperidol, risperidone, clozapine, quetiapine, benzamides). It is absolutely necessary to avoid barbiturates and benzodiazepines, drugs which are often the cause of delirium, except in the case of delirium due to withdrawal from alcohol or benzodiazepines.

    It is preferable to prescribe psychotropic drugs in a single evening dose, in order to restore the sleep-wake cycle. Repeated treatment during the day can cause a paradoxical on-off phenomenon with sudden aggravation of symptoms.

    3. Parental treatment with vitamins B1, B6 and PP in alcoholics.

    4. Sleep a lot, stay well hydrated and eat well.

    5. Ensure that the patient sees and hears well.

    6. Make sure loved ones are present. They must be well informed about the disease.

    7. Communicate succinctly.

    Does delirium lead to dementia?

    A major area of ​​controversy is whether delirium is simply a factor in dementia vulnerability, or whether delirium itself leads to dementia. It is likely that both hypotheses are true. There is little doubt that the occurrence of an episode of delirium may reflect brain vulnerability and an increased risk of future dementia. In some cases, delirium can cause previously undiagnosed cognitive disorders to be treated. Delirium and dementia usually coexist, with dementia being a major risk factor for delirium, i.e. increasing the risk of delirium by 2-5 times.

    A meta-analysis involving two studies with a total of 241 patients demonstrated that delirium was associated with an increased rate of dementia (+457%). In a sample of 225 cardiac surgery patients, delirium caused a severe one-time decline in cognitive functioning, followed by recovery over 6 to 12 months in most patients. However, a significant proportion, particularly those with prolonged delirium, never return to their original functioning. In 263 patients with Alzheimer’s disease, delirium caused an accelerated rate of cognitive decline after hospitalization. The decline is estimated to occur three times faster.

    In summary

    The confusional state (or delirium) is easy to overlook without a formal cognitive assessment. A brief cognitive examination can help identify delirium, with appropriate management. Additionally, older adults often take multiple psychoactive medications that increase the risk of delirium. Falling and loss of appetite are often warning signs.

    1. Assess delirium in all older hospitalized patients: using a simple cognitive screening and confusional state rating scale. Be sure to get the history from someone close to the patient.
    2. Reduce psychoactive drugs.
    3. Use non-pharmacological approaches to manage sleep, anxiety, and restlessness.
    4. Have pharmacological approaches for patients with severe agitation, who are at risk for self-harm, or who have psychotic symptoms (eg, hallucinations, delusional states).
    5. Invite family members to care, especially for redirection and prevention of self-harm.
    6. Encourage mobility.
    7. Make sure patients wear their glasses, hearing aids and dentures. Being able to see, hear and eat is important.
    8. Let patients know their schedule and keep them involved in their care. Communicate regularly with patients and their families.

    Source: Sharon K et al. Delirium in elderly people. Lancet. 2014 March 8; 383(9920): 911–922.

    Clinical case #1

    Mrs. M, 71 years old, was diagnosed with Alzheimer’s disease (mild stage) after a physical examination and a cognitive performance evaluation (her Mini-Mental State Examination score is 22). In addition to medication for high blood pressure, Ms. M has been taking lorazepam 1 mg, 3 times a day, for more than 15 years to treat anxiety.
    Mrs. M has been getting more confused at home for a few days, and her daughter is taking her to her doctor for an evaluation. Recognizing that benzodiazepines can contribute to acute confusional state  (delirium), the doctor stops the lorazepam. Three days later, Mrs. M’s confusion worsens and she develops nausea and tremors.

    She is taken to the emergency room where she is admitted for benzodiazepine withdrawal, to find out if the delirium is caused by Alzheimer’s disease or the medication.

    Although delirium is caused by several factors, drugs are frequent predisposing and aggravating factors and contribute to approximately 12% to 39% of cases of delirium.

    Benzodiazepines and opioids are the drugs most often associated with an increased risk of delirium, as are drugs with strong anticholinergic properties (i.e. lowering acetylcholine in the brain).

    In general, there are no strict rules on how to reduce and discontinue potentially risky medications. The steps to consider are:

    • Consider tapering and discontinuing benzodiazepines in a patient taking more than the minimum expected doses for at least two weeks, especially after eight weeks of treatment.
    • In the case of opioids, consider reducing them in a patient taking more than the minimum expected dose for more than a few days. When trying to eliminate symptoms of delirium, reduce opioids as quickly and as safely as possible, with a recommended reduction of less than 20% per day to prevent withdrawal symptoms.
    • The onset and duration of withdrawal symptoms depend on the half-life of a drug. Withdrawal occurs earlier when one stops taking drugs with short elimination half-lives (usually within 1-2 days), while it may not appear until 3-8 days after stopping drugs with a half-life greater than 24 hours.

    Abruptly stopping a sedative – both hypnotic and opioid – can lead to intolerable withdrawal symptoms.

    Benzodiazepine withdrawal should be avoided because of the risk of severe complications, such as seizures and delirium.

    Withdrawal seizures are particularly common with alprazolam due to its short half-life.

    Therefore, greater caution should be exercised when phasing out this drug.

    In general, withdrawal from opioids or anticholinergics is not life-threatening, but should be done with caution.

    Key points

    • Medications strongly implicated in delirium should be withdrawn or changed.
    • Consider the dosage and duration of treatment, the half-life of the drug, and the nature of withdrawal symptoms when determining how quickly the dose of a drug should be tapered.
    • A gradual reduction in activity over 2 or 3 days may be considered in hospitalized patients.

    Clinical case #2

    An octogenarian woman arrives at the emergency room for behavioral problems (agitation and visual and auditory hallucinations) accompanied by falls.

    She is being treated for high blood pressure and has no psychiatric history. She is being treated with Plavix .

    She has no confusion during the examination because she is aware of her hallucinations, which is the source of her anxieties.

    Two diagnostic hypotheses are proposed:

    • A confusional state  that occurs during dementia;
    • A confusional state with a transient organic cause.

    The following additional examinations were requested:

    • A scanner having reported neither signs of hemorrhage or cerebral ischemia, nor of cerebral atrophy.
    • An electrocardiogram.
    • An electroencephalogram, which revealed heart rhythm disorders, with fluctuation of alertness.
    • A mini-mental exam score of 24 out of 30, suggesting cognitive decline.
    • No chronic mental illness according to the psychiatrist.

    1st diagnosis _

    A diagnosis of confusional state with hallucinations is made. Treatment with seresta (benzodiazepine) is provided.

    The low MMSE score suggests the presence of mild cognitive decline .

    An anomaly on the ECG suggests a heart problem, a hypothesis supported by the observation of an irregular heartbeat on the electroencephalogram.

    A second, more in-depth electrocardiogram is undertaken.

    2nd diagnosis

    Medical staff diagnose:

    • Atrial fibrillation treated in particular with anti-vitamin K (anticoagulant) and an antiarrhythmic.
    • An enlarged left ventricle, characteristic of heart disease (heart disease is present in 70% of cases of atrial fibrillation)

    This so-called paroxysmal atrial fibrillation (that is to say that it manifests itself in the form of an acute crisis for about a week and then ends spontaneously) leads to an acute confusional syndrome with a decrease in cerebral blood flow.

    • Onset of very moderate cognitive impairment with preserved autonomy.

    Following the implementation of the treatments, no recurrence was observed.

  6. Delusional disorder

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    Delusional disorders are clinical manifestations during which the patient does not control the reality of things and has the conviction to hold the truth.

    Previously, we used the term paranoia (Greek origin which means “side thinking”).

    This misinterpretation of reality is confirmed by the patient’s entourage during the medical examination.

    Despite the coherence of the ideas and the unreality of the facts, it is impossible to reason with the patient.

    Delusional disorders should not be confused with:

    • hallucinations found in schizophrenic patients (psychiatric illness characterized by psychoses).
    • delirium (also called acute confusional episode) which is characterized by an incoherence of ideas, and an alteration of consciousness.

    Historical

    In the late 19th century, German psychiatrists such as Kraepelin included delusional disorder in the definition of paraphrenia, a mental disorder characterized by paranoid delusion without hallucinations.

    While Kraepelin excludes hallucinations from the criteria, Bleuer considers schizophrenia to be a paranoid form of dementia praecox associated with hallucinations.

    Over the years, Canadian psychiatrists have proposed a paranoid spectrum with several profiles: personality disorders (borderline, avoidant), delusional disorders (persecution, megalomaniac, jealousy, etc.), psychotic disorders, paraphrenia (paranoia, paranoid psychosis), organic disorders ( substance abuse, Alzheimer’s, delirium)


    Is delirium common in the elderly?

    The lifetime prevalence is 0.03% (1% for schizophrenia), with a majority of men suffering from paranoid delusional disorder.

    Delusional disorder usually occurs between the ages of 35 and 45.

    It is difficult to assess the frequency in the elderly because, on the one hand, the number of studies is limited and, on the other hand, the concept of an elderly person varies from one study to another.

    However, it is estimated that 4% of individuals aged 65 and over living in the community have ideas of persecution (see below the different themes of delirium).

    The prevalence would be 10% in individuals aged 65 and over admitted to hospital.

    Another study reports a 7% frequency of delusions among people aged 85 and over.


    What are the recurring themes of delusional disorder?

    Delusional themes represent the basis on which delusions develop.

    These themes are those of persecution, prejudice, intrusion, jealousy, megalomania… They are centred on his person, his body, his family, his neighbours and his possessions.

    Persecution

    This theme is the most common. The subject is convinced of being persecuted, watched or threatened, convinced of the existence of a conspiracy. Ideas of persecution may be accompanied by attacks of death anxiety with fear of imminent danger or annihilation. Unlike the delusion of schizophrenia, the persecutory delusional theme is clear, with some logic.

    Injury

    The patient is afraid of losing his property, his health and his reputation. The patient is sad and worried. He criticizes those around him. He thinks that someone is breaking into his house and that he risks losing his property. He isolates himself and flees his neighborhood.

    ruin, theft

    The patient is convinced of being ruined, robbed, abandoned by his loved one.

    Jealousy

    The theme relates to the conviction of his wife’s infidelities . Delirium develops from the misinterpretation and amplification of trivial facts. The jealous person can hire a detective to follow them. This type of delirium is often linked to alcohol consumption.

    hypochondria

    The patient thinks he is being ‘persecuted’ by his organs or living organisms. This is the case, for example, of Eckbom syndrome, a condition during which the patient is convinced that he is infested by small animals (insects, parasites) which develop on or in the skin. Many of these patients suffer from manic depression or paranoid delirium. The patient is therefore convinced that he is suffering from a serious illness, but he can also be convinced that he is giving off bad smells.

    Megalomania

    The patient has an exaggerated idea of ​​his own worth, power and knowledge. He thinks he has an exceptional relationship with a famous person. He thinks he has been appointed to accomplish a great mission. This theme is frequent in delusional manias. This megalomania is distinct from paranoid schizophrenia, where megalomania is associated with schizophrenic symptoms.

    erotomaniac

    The patient believes he is loved by someone, usually on a higher level. It is above all an idealized and romantic love.

    Charles Bonnet Syndrome

    It occurs after an ophthalmological intervention (caused for example by a sudden ocular occlusion), or in patients suffering from retinopathy, cataracts, or when the associative visual area is affected (in the case of dementia). It is characterized by visual, colorful hallucinations rich in detail depicting characters or animals that are not threatening. The triggering factors are a drop in the level of consciousness or low ambient light.

    Madness for two

    Delusional syndrome involving a couple (husband-wife; father-daughter, mother-daughter) during which one of the two partners, schizophrenic and of a dominant character, transmits his delirium to his partner with a physical (or intellectual) handicap and a passive personality -dependent. Sometimes the passive-dependent partner is also psychotic (this is called simultaneous insanity). The separation of the two people is generally necessary, which can lead to the disappearance of the delirium in the second person, while the first will be treated with antipsychotics.

    How does the doctor diagnose delirium?

    The physician relies on diagnostic criteria from the American psychiatry manual DSM IV (used in North America) and the International Statistical Classification of Diseases and Related Health Problems, 10th revision (ICD-10, World Health Organization). Health), mostly used in Europe.


    Factors that increase the risk of delirium

    Cognitive decline appears to be the primary risk factor.

    There are also biographical, social or psychological factors that favor the appearance of delirium:

    • Family history of schizophrenia
    • Avoidant personality disorder, borderline, paranoid.
    • Paranoid or schizoid personality (personality that tends to withdraw into itself).
    • Isolation and loneliness (single, widowhood).
    • The lack of social fabric and withdrawal into oneself (schizoid personality).
    • The attitude of those around you.
    • The feeling of insecurity.
    • A low socio-economic level.
    • A low level of education.
    • Sensory deficits (auditory and visual) that lead to misinterpretations
    • Alterations associated with physical illnesses (hypoglycemia due to diabetes, high fever, electrolyte disturbances, lupus, cerebrovascular disorders)

    Aging delirium versus late-onset delirium

    There are two forms of delirium:

    1. Delirium diagnosed in adulthood and persisting into old age. The intensity of the delirium tends to fade.

    2. Delirium that appears in old age (or late-onset delirium), i.e. after 65 years. The onset is insidious and is sometimes accompanied by hallucinations. This form may or may not be associated with a brain condition such as  Alzheimer’s disease,  vascular dementia, depression,  bipolar disorder.

    At advanced age, doctors therefore distinguish functional delusions from delusions caused by a neurological disease.

    In summary , delusional disorders are classified with the psychotic disorders seen in schizophrenia:

    – Paranoid, disorganized, catatonic, undifferentiated schizophrenia…

    – Brief psychotic disorder.

    – Shared psychotic disorder (madness for two).

    – Psychotic disorder secondary to a general medical condition.

    – Delusional disorders.

    – Persistent delusional disorders (late paraphrenia*, involutional paranoia**): this encompasses all conditions involving delirium accompanied by hallucinations, in particular auditory.

    Paraphrenia*: imaginative delirium organized around themes of greatness, persecution, melancholy, mysticism…

    Paranoia of involution**: delusion of claim appearing late.

    The doctor must take into account the personality of the patient, his past, his social and affective environment and somatic factors.

    The doctor questions the patient and his entourage in order to determine the age at which the symptoms appeared.

    It captures the patient’s personality, mood, medical history, and identifies delusional themes.

    Neurological examination can determine if a brain condition is causing the delirium.


    Delirium Assessment

    Various symptoms can be associated with delirium;

    • Hypervigilance. The person has a misinterpretation of the observed facts that he observes in detail.
    • Personal interpretation. He systematically interprets his observations in an unambiguous sense that confirms his delusional theory.
    • Mistrust. He responds in an irritated manner when asked about his delirious themes.
    • Auditory or visual hallucinations. They are rare in delusional disorders.
    • Unwanted behaviors. The patient who feels provoked may respond defensively, fearfully, or aggressively.
    • Grandiosity. The patient places excessive personal importance on herself. He becomes easily hostile, feeling persecuted by envious people who want to discredit him.
    • Depressive affect. Some patients burst into tears when they meet a person receptive to their sufferings.

    Diagnostic tools

    There is no instrument that specifically assesses delirium in the elderly. There is, for example, the scale for evaluating psychoses in adults (example PDI) or the psychological and behavioral disorders of dementia (example:  the neuropsychiatric inventory of dementia).

    Finally, the Behavioral Pathologic Rating Scale for Alzheimer’s disease is a behavioral disorder rating scale that describes the different forms of delirium in Alzheimer’s disease.

    In the Behavioral Pathologic Rating Scale for Alzheimer’s disease, the different forms of delirium are classified by theme (theft, imposter syndrome, etc.):

    1. The patient believes that he has had things stolen (frequency = 18% to 43%).

    Probable explanation: the patient no longer remembers the location of his personal objects, and will blame a loved one for their disappearance. In serious forms, he is convinced that someone is entering his home with the aim of hiding or stealing objects.

    2. The patient believes he is living in a home that is not his.

    The patient does not remember or recognize his home. He may end up leaving it to return « home » (this is the phenomenon of wandering).

    3. The spouse (or the relative in charge of the patient) is perceived as an impostor.

    The patient no longer recognizes his loved one. He may also consider his caregiver as an impostor, which results in a reaction of mistrust, even violence. In some cases, the patient is convinced that familiar people have been replaced by identical look-alikes: this is Capgras syndrome. These identification disorders are stressful for those around them because they are difficult to manage.

    4. A feeling of abandonment (frequency = 3% to 18%).

    The patient is convinced that he has been abandoned, that he will be placed in an institute, and that a plot is being organized for this purpose. This feeling stems from the fact that he realizes the burden he represents for those around him because he retains a certain awareness of his condition. Relatives feel guilty for this feeling of abandonment experienced by the patient.

    5. A feeling of infidelity (frequency = 1% to 9%).

    This feeling mainly concerns the spouse or caregivers.

    Although the diagnosis of delirium is sometimes difficult in a person with dementia  (indeed people with dementia already have a disorder of ideation and confusion), it is possible with some experience to tell the difference between delirium and dementia. Indeed, delirium is usually accompanied by:

    • a sudden onset of symptoms;
    • a decrease or increase in alertness in the patient already presenting with dementia, or a marked fluctuation in symptoms;
    • visual hallucinations accompanied by agitation;
    • impaired psychomotor activity;
    • language disorders (slurred speech, slowing or speeding up of speech);
    • of tremors.

    Once the diagnosis of delirium is made, the choice of treatment will depend on identifying the cause. These causes are many and include:

    • medication side effects;
    • malnutrition;
    • an infection;
    • cerebral pathologies (eg, subdural hematomas);
    • endocrine disorders (eg hyperthyroidism);
    • metabolic diseases (eg certain kidney or liver conditions);
    • patient environmental factors;
    • hypoxia caused by pneumonia, congestive heart failure or sleep apnea;
    • urinary retention or fecal impaction (accumulation of feces).

    Delirium occurring in adulthood (before age 65)

    It encompasses paranoid states and psychotic disorders diagnosed in adults with schizophrenia and which persist into old age. These disorders become less intense as the person ages. An estimated 13% of people with schizophrenia (usually diagnosed in their 20s) show initial symptoms after their 40s, and only 3% after their 60s. In this category of patients, the negative symptoms (eg withdrawal, indifference) tend to persist while the delusional manifestations and hallucinations, mainly auditory, considered as positive symptoms, tend to diminish.


    Late-onset delirium (after age 65)

    Late-onset delusions are delusions appearing after age 65.

    These delusions are caused, for example, by a sensory deficit (we then speak of functional delirium), a mental illness (depression, dementia) or cerebrovascular disease.

    Evaluation of cognitive functions, questioning of the family and a brain examination (MRI) make it possible to know if a dementia (dementia of the Alzheimer type,  vascular dementia,  dementia with Lewy bodies) is at the origin of a delirium.


    Functional delusions

    They develop in a lasting mode and are caused by:
    – a stressful situation (death, move, entry into a medical institution, etc.);
    – a sensory, cognitive deficit, affecting communication and relational life. This is the Charles Bonnet syndrome (see above), the Eckbom syndrome (see above), the paranoia of the deaf (the patient, suffering from severe hearing loss, is wary and withdraws into himself. He has auditory hallucinations).


    Delirium associated with depression

    Depression in old age is often accompanied by delirium: this is called delusional depression. 40% of hospitalized patients suffer from delusional depression. The themes of the delirium relate to ruin, guilt and persecution.

    Delusional depression may or may not be melancholic. In cases of melancholy, patients close themselves in the past, with representations or apparitions.

    In certain cases of delusional depression, the patient, hypochondriacal, feels his organs putrefying and destroying himself, thinks he has an incurable disease: this is Cotard’s syndrome.


    Delusional disorders associated with Alzheimer’s disease

    Delusional disorders at the beginning of the dementia stage revolve mainly around forgetfulness.

    The frequency of delusions in people with dementia is between 10% and 73% depending on the population studied. About a third of patients with probable Alzheimer’s disease suffer from delusions, and are considered to be at risk for physical aggression. According to one study, 80% of participants with high levels of physical aggression (>1 episode/month) also suffered from delusions.

    Delusions in the early stage are linked to memory loss. They lead to ideas of displacement and theft of objects, intrusion into the home, spoliation, infidelity and jealousy (15% of cases). They may be accompanied by aggressiveness in a person with a psychiatric history. Late companion delirium is typical of dementia. The subject reconstructs a new reality where people from the past or fantasy come to keep him company.

    As the disease progresses, the delusions aim to fill the growing void caused by the memory loss, and draw on the remnants of memories still intact in the patient.

    We observe delusions of identification during which the patient, suffering from gnosic, mnesic and judgment disorders, perceives people or objects in a distorted way, resulting in situations that are poorly experienced by those around him.

    Thus, the spouse can be taken for example for an impostor (this is Capgras syndrome), or the patient is convinced that people take on the appearance of others (this is Fregoli syndrome), suffers from ‘a disorder of self-identification in the mirror (prosopagnosia), has the conviction of the presence of people in the house, the certainty that the television characters are in the room and steal thoughts, etc. These disorders cause anxiety and/or behavioral disorders (agitation, wandering).


    Dementia secondary to Parkinson’s disease

    Dementia secondary to Parkinson’s disease occurs after at least 5 years of evolution. Hallucinations are found in three quarters of cases, and are essentially visual.


    Delusions associated with cerebrovascular  disease

    Mini-lesions increase the risk of delusional disorders, accompanied by hallucinations evoking the presence of animals and people.


    Delirium and hallucinations

    Although delirium should not be confused with hallucinations, a person suffering from delirium can have hallucinations, but these are not predominant.

    Hallucinations interfere with the patient’s ability to understand the outside world. This phenomenon can alter their ability to perform activities of daily living and can affect their relationship with caregivers. The frequency of hallucinations in people with dementia ranges from 12 to 49%.

    Visual hallucinations are the most common (up to 30% of patients with dementia), and they are more common in moderate dementia than in mild or severe dementia.

    Auditory hallucinations are present in 10% of dementia cases.

    Other forms of hallucinations, tactile and olfactory, are rare.

    A common type of visual hallucination involves observing the presence of certain people in one’s home, when in fact they are not there. In the case of Lewy* dementia, the interpretation disorders are based above all on gnosic deficits, and to a lesser extent on mnesic disorders and sensory perception defects. The most frequently observed gnosic deficits are prosopagnosia (the patient does not recognize his relatives; 12% of cases), self-agnosia (4% of cases), intrusion of people into the patient’s life ( 6% of cases), or the ghost companion syndrome (the patient is convinced that a person is hiding in his home (17% of cases). These hallucinations sometimes require treatment when they are a source of stress. This treatment depends on the etiology.

    Dementia with Lewy bodies* is characterized by the presence of hallucinations in 60% of cases and this at an early stage (living or deceased pets or familiar characters.

    There is an association between decreased visual acuity and hallucinations (see Bonnet syndrome above). Indeed, a significant percentage of people with dementia have a visual deficit (eg visual agnosia characterized by difficulty recognizing faces or objects), and many experience difficulty in contrast perception, especially in low frequencies. Indeed, the line of demarcation between the areas of shadow and light is blurred in demented patients, which partly explains the high rate of identification disorders and visual hallucinations.

    To prevent these hallucinations, the eyesight of patients with dementia must be assessed and home lighting improved.


    The differential diagnosis

    The doctor will have to rule out the diagnosis of mental confusion which can a priori be confused with delirium.

    Indeed, during a confusional episode, the patient has convictions that are erroneous and persistent.

    In mental confusion, the mode of onset is abrupt, the disturbances are fluctuating and alertness is impaired.

    To eliminate any doubt, the doctor will have to determine a somatic, iatrogenic or toxic cause.

    Delusional states can be the consequence of Lewy body dementia. In this case, they precede cognitive decline, which can lead the doctor to misdiagnose.

    The presence of motor disorders (akinesia), the occurrence of falls, a cerebral examination and hypersensitivity to antipsychotics*, will guide the doctor towards the diagnosis of this form of dementia. * The doctor usually prescribes an  antipsychotic (or neuroleptic)  to patients with psychosis. If this psychosis is caused by dementia with Lewy bodies, the drug will cause side effects that will aggravate motor disorders, one of the main symptoms of this form of dementia.


    Therapy

    If the delirium is associated with another mental disorder, it must be treated first.

    The ideal treatment includes:

    • an antidepressant (of the selective serotonin reuptake inhibitor type) in the case of major depression with psychotic symptoms.
    • an antipsychotic (eg risperidone or olanzapine) to reduce anxiety, restlessness and sleep disturbance caused by delirium if the latter is part of schizophrenia.
    • valproic acid or lithium in the case of a manic episode, with a benzodiazepine.

    In the case of delusions associated with dementia (Alzheimer’s disease or dementia with Lewy bodies), acetylcholinesterase inhibitors (i.e. donepezil, rivastigmine or galantamine) would reduce the agitations related to delirium . The use of antipsychotics is possible, provided that they are prescribed at low doses (1 mg/day for risperidone, 5 mg/day for olanzapine) and over a short period (two weeks maximum). Indeed, elderly patients suffering from dementia and receiving an antipsychotic have an increased risk of stroke. Antipsychotics are not recommended in dementia with Lewy bodies because they aggravate motor disorders.

    A non-pharmacological approach will be combined with drug treatment.

    Thus psychotherapy sessions will be offered to gain the patient’s trust, so that he can express without hesitation what worries him.

    The psychotherapist will have to accept the delusional comments of the patient, without adhering to them.

    The care team can also improve the relationship between the patient and the family and correct any factors that promote these disorders (correction of a sensory handicap, promote social relations, reduce the feeling of insecurity, etc.).

    A non-pharmacological approach will be combined with drug treatment.

    Thus psychotherapy sessions will be offered to gain the patient’s trust, so that he can express without hesitation what worries him.

    The psychotherapist will have to accept the delusional comments of the patient, without adhering to them.

    The healthcare team can also improve the relationship between the patient and the family and correct any factors that favor these disorders (sensory handicap, lack of social relationships, feeling of insecurity, etc.).


    Clinical case

    A woman was treated for decades for bipolar 1 disorder with lithium. His treatment was stopped because relapses were frequent. In addition, lithium caused hypothyroidism in her.

    Around the age of 70, she presented significant depressive symptoms accompanied by delusional thoughts (notably delusion of persecution).

    Doctors diagnose delirious melancholy.

    She is being treated with an antidepressant combined with an antipsychotic.

    Her treatment is difficult because, on the one hand, she is convinced that the drugs are prescribed to aggravate her physical condition and, on the other hand, the food is « poisoned » by drugs.

    His mental and physical condition deteriorated: social withdrawal, repeated falls, incontinence. She refuses to take her antidepressant.

    Delusional disorders with hypochondria develop: the patient thinks that her liver is no longer in her body and that she cannot therefore absorb the drugs that the doctors want to give her.

    Treatment with electroconvulsive therapy (ECT) is indicated by doctors given his poor nutritional status. The doctors obtain the written consent of one of the children as required by French law (in this case, the doctors could not obtain the patient’s consent because of her condition).

    After about ten sessions, the patient shows signs of improvement: improvement in contacts, reduction in the delirium of persecution.

    An anti-depressant and a mood modulator are prescribed.

    This time the patient agrees to these treatments.

    Her delusional disorders decrease in intensity, and her condition improves: she talks with the nursing staff, reads, washes herself, moves, etc. Her mood is stable.

    She will go home and get help at home.

  7. Macular degeneration

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    Age-related macular degeneration (AMD) is an eye disease that can get worse over time. It is the leading cause of severe and permanent vision loss among people over the age of 60.

    It is caused when the small central part of your retina, called the macula, wears down. The retina is the light-sensitive nervous tissue located at the back of the eye.

    Because the disease occurs with age, it is often called age-related macular degeneration. It is usually not the cause of blindness, but it can cause serious vision problems.

    Similarly, another form of macular degeneration, called Stargardt disease, affects children and young adults.

    Wet or dry macular degeneration

    There are two main types of degeneration:

    • Dry form. The affected individuals may have deposits of yellow in their macula. As they get larger and more numerous, they can cloud or distort your vision, especially when reading. As the condition worsens, the light-sensitive cells in your macula thin out and eventually die. 
    • Wet form. Blood vessels grow under your macula and send blood and fluid to your retina. Your vision is distorted so that straight lines appear wavy. You may also have blind spots and loss of central vision. These blood vessels and their bleeding can eventually scar, leading to permanent loss of central vision.

    Most people with degeneration have the dry form, but the dry form can lead to the wet form. Only about 10% of sufferers have the wet form.

    Macular Degeneration Symptoms

    At first, you may not have any noticeable signs of macular degeneration. It is possible that it will not be diagnosed until it gets worse or affects both eyes.

    Symptoms of macular degeneration can include:

    • Worse or less clear vision. Your vision may be blurry and it may be difficult to read fine print.
    • Dark, blurry areas in the center of your vision
    • Difficult or different perception of colors (rare phenomenon)

    Possible causes

    Age-related macular degeneration is more common in older people. It is the leading cause of severe vision loss in adults over 60.

    It may be of genetic origin. If someone in your family has it, your risk could be higher.

    Smoking, hypertension or high cholesterol, obesity, saturated fat consumption, fair skin, being female, and having a light eye color are also risk factors.

    How is macular degeneration diagnosed?

    A routine eye exam can detect age-related macular degeneration. One of the most common early signs is the presence of yellow spots under the retina. Your doctor can see them when they examine your eyes.

    Your doctor may also ask you to look at an Amsler grid, a pattern of straight lines that looks like a checkerboard. Certain lines may appear wavy or you may notice that some lines are missing, which could be a sign of the disease.

    If your doctor discovers age-related macular degeneration, you may need to undergo a procedure called angiography. The doctor injects a dye into a vein in your arm. They take photographs as the dye travels through the blood vessels in your retina. If there are vessels that send fluid or blood to your macula, the photos will show their exact location and type. 

    What treatments are available for macular degeneration?

    There is no cure for macular degeneration. Treatment can slow it down or prevent you from losing your sight too quickly. Your options may include:

    • Anti-angiogenesis drugs. These drugs block the creation of blood vessels.
    • Laser therapy. High-energy laser light can destroy abnormal blood vessels growing in your eye.
    • Photodynamic laser therapy. Your doctor injects a light-sensitive drug into your bloodstream, which is absorbed by abnormal blood vessels. Your doctor then sends a laser into your eye to trigger the drug and damage those blood vessels.
    • Low vision aids. These are devices that help people make the most of their remaining vision.

    Prevention

    A large study found that some people with dry AMD could slow the disease by taking supplements of  vitamins C and E , lutein, zeaxanthin, zinc, and copper.

    Outlook for people with macular degeneration?

    People rarely lose all their vision due to age-related macular degeneration. Their central vision may be poor, but they are still able to do many normal daily activities.

    The dry form tends to get worse slowly, so you can keep most of your vision.

    The wet form is one of the main causes of permanent vision loss. If it’s in both eyes, it can affect your quality of life.

    Wet macular degeneration may require repeated treatments. 

    Underdiagnosed age-related macular degeneration

    One in four cases of age-related macular degeneration is not identified early, according to a study published in 2017. Stricter detection standards must be put in place.

    644 60-year-olds participating in a study had an eye exam during which no abnormalities were detected.

    However, when they were re-examined by a research team from the University of Alabama at Birmingham (USA), about 25% of them showed signs of age-related macular degeneration.

    « It is imperative that tougher standards are put in place to detect this disease. » Careful inspection of the macula of the eye (the center of the retina) is necessary to determine if signs of this disease are present in the patient”.

    If age-related macular degeneration is suspected, many things can be done. Dietary change and the use of nutritional supplements can significantly slow the progression of the disease. Source: Mark Fromer et al. JAMA Ophthalmology, April 2017.

  8. Corticobasal degeneration

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    Corticobasal degeneration is a neurodegenerative disease characterized by progressive death of neurons located in the central gray nuclei  and part of the cerebral cortex (cerebral area located on the surface of the brain).

    It is a rare disease (less than 1000 cases in France) described for the first time in 1968.

    It begins, generally after the age of 60, with asymmetric apraxia of the upper limb (clumsy hand gestures) and gait disturbance (impression of stiffness, postural instability).

    Corticobasal degeneration is caused by the progressive death of neurons located in the basal ganglia (mauve area)

    Neurons, dying, secrete less and less dopamine, which explains the appearance of motor disorders.

    Corticobasal degeneration belongs to the “primary” atypical parkinsonian syndromes, a group of sporadic neurodegenerative conditions that also include multiple system atrophy and progressive supranuclear palsy.

    Causes of corticobasal degeneration

    The causes are not known at this time. We know, however, that the cases are overwhelmingly sporadic (the genetic component is almost non-existent).

    Symptoms of corticobasal degeneration

    Symptoms are similar to those seen in Parkinson’s disease. They begin from the age of 55 and worsen quickly, so that the cases of elderly patients are infrequent:
    – clumsiness of a limb (more often an upper limb) with often bilateral and inaugural rigidity.
    – Dystonia (involuntary muscle contractions) in a hand or arm that freezes part or all of the body in an abnormal attitude.
    – Akinesia (slow initiation of movements with a tendency to immobility).
    – Apraxia (loss of ability to perform movements or use objects, without any paralysis).
    – Dysarthria (speech disorder. The patient has difficulty speaking and making sounds. The voice appears too deep or too high-pitched, hoarse and occasionally the patient is speechless).
    – Disorders of executive functions.
    – Aphasia (partial or total impairment of the ability to express oneself and understand spoken or written language).
    – Agnosia (loss of the ability to recognize objects that we see or noises that we hear, while the sensory functions (vision, hearing, touch, etc.) are normal.

    Treatment consists of prescribing the drugs used in Parkinson’s disease. Their therapeutic efficacy is low.

    After three years of progression, almost all patients with corticobasal degeneration present with a motor syndrome of the parkinsonian type accompanied by significant rigidity, apraxia and gait disturbance.

    Clinical case

    Mrs. A., aged 75, admitted to a long-term care center (CHSLD, long-term care center in Quebec) after having suffered several falls.

    Upon her arrival at the CHSLD (HEPAD in France), Mrs A. underwent a neurological examination and neuropsychological tests.

    Neurological and neuropsychological assessment

    – Extrapyramidal syndrome (parkinsonian type motor disorders) responsible for falls.
    – The score on the mini-mental state examination (MMSE) 1  is 12/30, reflecting a moderate deficit.
    – Spatial (but not temporal) disorientation.
    – Language disorders.
    – Very significant ideomotor apraxia (predominant in the right hemibody).
    – Visuoconstructive apraxia.
    – Disorders of  executive functions.
    – Attention disorders with psychomotor slowing.
    – Difficulties performing mental calculations.
    – Preservation of   visual episodic memory.
    – Preservation of visual gnosis.
    – Preservation of verbal naming capabilities.

    Neuroimaging examination

    – Exclusion of a cerebrovascular accident.
    – Brain scan reveals hypoperfusion (slow blood flow) of the parietal lobe.

    The cerebral scintigraph is a medical examination consisting of injecting a radioactive molecule in order to highlight the shape and activity of areas of the brain.

    Diagnosis: The patient probably has corticobasal degeneration.

  9. 8 choses que vous devez savoir sur les clubs de cannabis de Barcelone

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    Les clubs de cannabis à Barcelone sont privés, pas publics. Ne confondez pas un club de cannabis à Barcelone avec un café à Amsterdam; ce ne sont absolument pas les mêmes. Les coffee shops d’Amsterdam sont publics et ouverts à tous à tout moment. Les clubs de cannabis de Barcelone, en revanche, ne sont ouverts aux nouveaux membres que par le biais de recommandations de membres existants. Cette politique se traduit par des différences frappantes entre les deux :

    • les meilleurs coffee shops d’Amsterdam ont l’impression de traîner dans un pub ou un bar
    • Les meilleurs clubs de cannabis de Barcelone dans leur propre salon

    Lorsque vous rejoignez un club de cannabis social à Barcelone, vous pouvez être sûr que vos informations personnelles resteront privées. Vous ne recevrez pas d’e-mails marqués du club, le club ne vendra, ne donnera ou ne donnera vos informations à personne d’autre, le club ne divulguera pas ou ne mettra pas vos informations à la disposition du gouvernement ou d’autres autorités, et le club ne vous spammer avec des publicités ou des offres. Pourquoi? Parce que tout est privé, pas public.

    Vous n’ “achetez“ as d’herbe aux Cannabis Clubs de Barcelone

    Lorsque vous devenez membre d’un club de cannabis à Barcelone, vous faites essentiellement partie d’une coalition qui cultive et distribue de la marijuana parmi ses membres. Par conséquent, la marijuana qui a été cultivée appartient à tous les membres, y compris vous. Vous devez payer votre part de ce qu’il en coûte pour cultiver la marijuana et pour l’espace du bâtiment et d’autres installations, services publics, etc. Ces coûts sont récupérés de plusieurs façons et les membres partagent généralement les coûts.

    Cela signifie que vous n’achetez pas de marijuana lorsque vous allez dans un club fumeur à Barcelone. Vous obtenez simplement votre part de ce que vous et les autres membres avez collectivement cultivé. C’est pourquoi il est considéré comme impoli de parler « d’acheter de l’herbe », et si vous le faites dans un club, vous pourriez vous faire gronder. Demandez plutôt à combien s’élève la part du membre, ou quelle est la contribution requise pour X grammes de cannabis. De plus, vous devez considérer que les cafés en Espagne ne sont pas autorisés à faire de la publicité pour leurs établissements car cela est interdit par la loi.

    Vous avez besoin d’une pièce d’identité avec photo et d’une adresse en Espagne pour devenir membre d’un club de cannabis

    de Barcelone présenter une carte ou un autre visa avec photo. Vous devez également vous inscrire avec une adresse résidentielle régulière en Espagne ; dans la plupart des cas, l’adresse d’un hôtel ou d’une auberge de jeunesse ne fonctionnera pas, vous devez donc fournir une adresse résidentielle. Aucun courrier ne sera jamais envoyé à l’adresse que vous fournissez, les informations sont strictement confidentielles et dans la plupart des cas, vous n’êtes pas tenu de « prouver » votre adresse. La résidence espagnole n’est PAS nécessaire pour rejoindre un club de cannabis à Barcelone ou dans une autre ville ; il vous suffit de fournir une adresse résidentielle au moment de votre inscription. AirBnB et les adresses similaires sont parfaitement acceptables à utiliser lors de l’inscription.

    De plus, certains clubs exigent que les membres aient 21 ans ou plus, tandis que d’autres acceptent de nouveaux membres dès l’âge de 18 ans. Si vous essayez d’en attirer un rapidement parce que vous êtes mineur, vous ne vous inquiétez pas ; votre identité sera strictement vérifiée par le personnel du club avant que vous ne soyez autorisé à entrer.

    Vous pouvez toujours avoir des ennuis pour avoir fumé de la marijuana à Barcelone

    Juste parce que vous pouvez obtenir de l’herbe légalement à Barcelone, La loi espagnole est très libérale dans les espaces privés. C’est pourquoi il est bon d’avoir de la marijuana chez soi ou dans un club de cannabis privé à Barcelone. Mais si vous affichez ou utilisez de la marijuana dans un lieu public et que vous êtes pris, vous serez presque certainement condamné à une amende, la marijuana sera confisquée et, selon les circonstances, vous pourriez être arrêté et emprisonné.

    Soyez intelligent. Ce n’est pas parce que vous voyez des gens fumer des joints sur Las Ramblas que vous devriez le faire aussi. En fait, la vérité est que vous pouvez être harcelé et verbalisé par la police en dehors d’une résidence privée ou d’un club de cannabis légitime. Si vous sortez du cannabis d’un club (la plupart des gens le font), n’oubliez pas de le transporter dans vos sous-vêtements. Les autorités espagnoles ne peuvent y perquisitionner sans mandat. Si vous êtes pris avec de l’herbe en public, vous recevrez une contravention et paierez une amende, mais il n’y a pas de crime à moins que vous ne dépassiez un seuil que la plupart des membres du cannabis club ne dépassent jamais.

    La meilleure politique si vous êtes arrêté par la police et trouvé avec du cannabis est d’en dire le moins possible et de ne pas dire à la police où vous avez acheté le cannabis.

    Toute la marijuana dans les Cannabis Clubs de Barcelone n’est pas cultivée par le Club

    Certains clubs de fumeurs de Barcelone ne peuvent pas se permettre l’espace, l’équipement, les risques ou les services nécessaires pour cultiver de la marijuana de bonne qualité. Au lieu de cela, ils recourent à l’obtenir par d’autres moyens. Dans certains cas, cela peut impliquer d’obtenir de l’herbe auprès d’autres clubs de cannabis à Barcelone, ou cela peut nécessiter une collaboration avec de grands producteurs de la campagne espagnole. Il y a aussi des clubs qui obtiennent leur marijuana des gars qui la vendent sur la plage.

    Vous ne vous souciez pas d’où le club obtient son cannabis, mais pour moi, c’est définitivement le cas. Après tout, si je voulais de la marijuana dans la rue, je l’obtiendrais directement des gars de la rue, et à un bien meilleur prix. Le problème est que, comme la culture du cannabis à grande échelle n’est pas légale en Espagne, de nombreux clubs ont été perquisitionnés à plusieurs reprises, et à grands frais. Par conséquent, de nombreux clubs choisissent d’acheter du cannabis via des réseaux de fournisseurs locaux, qui desservent souvent un grand nombre de clubs. Souvent, le cannabis acheté auprès de ces réseaux est excellent, mais dans certains cas, il est inférieur aux normes, alors assurez-vous de ne rejoindre qu’un club de cannabis de Barcelone avec une réputation supérieure pour la qualité de leur marijuana.

    Tous les Barcelona Smoking Clubs ne sont pas créés égaux

    Les différences d’un cannabis club à Barcelone à l’autre sont surprenantes. Il y a d’énormes clubs qui s’étendent sur trois étages d’un grand bâtiment, et il y a des clubs qui ne sont qu’une petite pièce avec quelques chaises bon marché. Il y a des clubs qui sont situés dans des sous-sols sombres et des clubs qui se trouvent dans de nouveaux espaces lumineux. Certains sont thématiques, d’autres non. Certains sont fantaisistes, d’autres ternes.

    Quel que soit le type d’environnement que vous recherchez, il y a de fortes chances que vous puissiez le trouver dans un club de cannabis à Barcelone. En fait, il y a même un club de cannabis gay en ville qui s’appelle Berry Boi, mais je n’ai jamais eu beaucoup d’informations à ce sujet. Si vous connaissez ce club ou si vous en êtes membre, veuillez me contacter : russ@marijuanagames.org

    Ce que j’ai trouvé, c’est que la plupart des gens qui sont des habitués des clubs de cannabis de Barcelone sont membres de plusieurs clubs – généralement au moins 5 ou 6 – et souvent pour diverses raisons ; différentes souches de cannabis, différentes personnes, différents environnements, différents endroits de la ville, etc.

    La plupart des clubs de cannabis facturent des frais d’adhésion annuels.Vous

    paierez votre juste part pour l’effort requis pour cultiver votre marijuana et vous accommoder de plusieurs façons. Premièrement, presque tous les clubs exigent le paiement d’une cotisation annuelle. Ceci est généralement de 25 à 50 euros, mais peut être aussi bas que 20 euros et aussi élevé que 100 euros. Certains clubs offrent une adhésion gratuite, mais cela est rare et a souvent un prix – service médiocre, environnement sale, mauvaise herbe, etc.

    Il n’est pas approprié de négocier ou de tenter de renoncer aux frais d’adhésion. Nous sommes tous membres; nous devons tous nous soutenir les uns les autres, et ces petites allocations nous permettent de nous unir pour y parvenir. Vous contribuerez également un montant fixe par gramme pour diverses souches de marijuana et de hachage, et pour tout autre produit ou service offert par le club.

    De plus, vous pouvez emmener un ami ou un membre de la famille au club qui ne fume pas, mais qui veut quand même voir à quoi ça ressemble. C’est tout à fait acceptable, mais cette personne doit tout de même s’inscrire pour adhérer au club, compte tenu du caractère privé des clubs nécessaire à leur existence. Rappelles toi; si une personne pouvait simplement entrer dans un club depuis la rue, sans devenir membre, alors le club ne peut pas être considéré comme «privé» et n’aura donc aucune protection en vertu de la loi. La meilleure chose à faire est d’amener votre ami avec vous, même s’il ne consomme pas de cannabis ; la plupart des clubs proposent de la bière et du vin, des collations et des bonbons, des films, des jeux, des vidéos, de la musique en direct, des événements spéciaux et bien plus encore pour que tout le monde soit heureux ; même les non-fumeurs.

    Il existe des limites légales à la quantité de marijuana que vous pouvez obtenir

    . C’est important; il y a des limites à la quantité d’herbe que vous pouvez acheter par mois dans un club de cannabis à Barcelone. Je pense que les limites sont d’environ 98 grammes, selon le club, ce qui signifie que si vous obtenez beaucoup d’herbe dans plusieurs clubs, vous pourriez faire l’objet d’une enquête. Probablement pas, mais vous devriez le savoir. Lorsque vous vous inscrivez dans un club de cannabis de Barcelone, vous recevez des informations sur les limites et vous signez un formulaire indiquant que vous avez lu ces informations.

    On vous demandera sur les formulaires combien de grammes par semaine vous recevez du club. Ce n’est pas un engagement; il ne s’agit que d’une estimation, vous n’êtes donc pas obligé de percevoir ce montant chaque semaine. Les clubs ne vous permettront d’obtenir que 5 grammes par jour maximum, bien que certains clubs autorisent plus ou moins, selon le club et le membre en question. J’écris habituellement que j’obtiendrai environ 8 à 10 grammes par semaine ou jusqu’à 40 par mois, et pour moi, c’est probablement assez précis, sauf si je fais beaucoup de divertissements ce mois-ci.

    En remplissant ce formulaire, vous autorisez le club à cultiver X grammes de cannabis en votre nom. Cela protège le club en cas d’enquête sur ses opérations de culture.

  10. Cystitis

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    Cystitis is a bacterial infection of the urethra and bladder, which are normally sterile (i.e. free of germs).

    The bacteria attach themselves to the lining of the bladder, which causes the area to become inflamed.

    It affects people of both sexes and all ages. It is more common in women than in men.

    Escherichia coli is the cause of about 80% of all urinary tract infections.

    These bacteria are part of the healthy intestinal flora. However, virulent types can enter the bladder through the urethra and cause urinary tract infections (UTIs).

    A large proportion of hospitalized infections are caused by urinary tract infections, especially in patients using urinary catheters.

    Causes of cystitis

    There are many possible causes of cystitis, but most cases have an infectious cause. Most infectious cases are caused by bacterial infection from the ascending genital/urinary areas.

    Some risk factors

    • Insertion of a tampon, there is a slight risk of bacteria forming through the urethra.
    • Use of a diaphragm for contraception.
    • Incompletely emptied bladder.
    • Insufficient mucus in postmenopausal women, favoring the multiplication of bacteria.
    • Postmenopausal women on hormone replacement therapy.
    • Lower estrogen levels.

    Diagnosis of cystitis

    A doctor will ask the patient a few questions, perform an exam, and perform a urine test.

    A urine sample may be taken to determine the type of bacteria in the urine. After finding out which bacteria is causing the infection, the patient will be given an oral antibiotic.

    Most doctors will also suggest whether the patient may have a sexually transmitted infection, the symptoms of which are similar to cystitis.

    Patients who have cystitis regularly may require further testing. This could include an ultrasound, X-ray, or cystoscopy (a fiber optic camera examination) of the bladder.

    Cystitis treatments

    Cranberry juice is commonly consumed to prevent bladder infections. Cranberries contain an active ingredient that helps prevent bacteria from sticking to the bladder wall. However, cranberry juice or capsules derived from cranberries may not contain enough of this active ingredient to be beneficial in preventing symptoms. Nevertheless, cranberry juice is a common method used by people to prevent UTIs. In the vast majority of cases, mild cystitis will resolve within a few days.

    Any cystitis that lasts more than 4 days must be the subject of a medical consultation.

    Occasionally a 3-10 day antibiotic prescription is needed. Most patients will feel the beneficial effects of an antibiotic within the first day of treatment. If the symptoms do not improve after taking the antibiotics, the patient should return to the doctor.

    Older people and those with weakened immune systems, such as people with diabetes, have a higher risk of spreading infection to the kidney, as well as other complications. Vulnerable people should be treated quickly.

    Drinking plenty of fluids helps flush bacteria through the system. Avoid alcohol.

    Symptoms of cystitis

    • Traces of blood in the urine.
    • Dark or cloudy urine.
    • Strong smell of urine.
    • Pain just above the pubic bone.
    • Lower back pain.
    • Pain in the abdomen.
    • Frequent need to urinate.
    • Burning sensation when urinating.
    • Older women may feel weak and feverish but have none of the other symptoms mentioned above

    Other diseases or conditions have similar symptoms to cystitis, such as:

    • Urethritis (inflammation of the urethra).
    • Prostatitis (inflammation of the prostate).
    • Benign prostatic hyperplasia (only in men).
    • Gonorrhea.
    • Candida albicans (thrush)

    Prevention of cystitis

    Many cases of cystitis are not preventable. However, the following few steps can help:

    • Practice good hygiene (use fragrance-free around the genitals).
    • Completely help the bladder.
    • Avoid tight underwear and pants.
    • Wear cotton underwear

    If men suffer from cystitis, it is potentially more serious than in women. Male cystitis is more likely to be caused by another underlying condition, such as a prostate infection, cancer, obstruction, or a large prostate.

    In most cases of male cystitis, early treatment is effective, and the problem is resolved. However, untreated bladder infections can lead to kidney or prostate infections or damage.