Primary progressive aphasia

Aphasia

Hyperosmia

Apathy

Generalized anxiety

Anosognosia

Anosmia

Un mode de vie sédentaire est-il mauvais ?

Is a sedentary lifestyle bad for you?

Aneurysm

Author Archives: Stéphane Bastianetto

  1. Primary progressive aphasia

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

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

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

    There are different forms of progressive primary aphasia:

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

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

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

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

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

    Epidemiology

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

    Diagnostic criteria

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

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

    What is the differential diagnosis of primary progressive aphasia?

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

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

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

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

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

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

    Practical case of primary progressive aphasia

    Anamnesis

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

    Neuropsychological assessment

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

    His score is 39/50.

    Diagnostic

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

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

    Diagnosis: The patient probably suffers from progressive primary aphasia.

  2. Aphasia

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

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

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

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

    Causes

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

    Signs and symptoms

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

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

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

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

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

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

    There are mainly three forms of aphasia:

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

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

     FluencyMissing wordUnderstandingsigns
    Global aphasiavery diminishedStrong inability to find the wordvery alteredSpeech often limited to a stereotype
    Wernicke’s aphasiaNormalFairly strong inability to find the wordvery alteredParaphasias, dyssyntaxia, jargon
    Broca’s aphasiaDiminishedInability to find the wordBelow parDysprosody, agrammatism

    Other forms of aphasia are:

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

    Diagnostic

    Examination of the expression and comprehension of oral language.

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

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

    Written language exam

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

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

    Aphasia caused by stroke

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

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

    Aphasia and dementia

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

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

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

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

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

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

    Rehabilitation

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

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

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

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

    Symptoms

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

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

    Complications and associated diseases

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

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

    The causes of hyperosmia

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

    Pregnancy

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

    Migraines

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

    Lyme disease

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

    Autoimmune diseases

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

    Neurological diseases

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

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

    Other possible causes include:

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

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

    Treatment of hyperosmia

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

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

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

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

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

    Prognosis

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

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

  4. Apathy

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

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

    How to differentiate apathy from depression?

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

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

    Apathy and Alzheimer’s disease

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

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

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

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

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

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

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

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

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

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

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

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

    Apathy is accompanied by dysfunction of certain regions of the brain

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

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

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

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

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

    Parkinson disease

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

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

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

    Frontotemporal dementia

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

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

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

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

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

    Apathy and vascular disease

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

    Evaluation

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

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

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

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

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

    Apathy would increase the risk of cognitive impairment

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

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

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

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

  5. Generalized anxiety

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

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

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

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

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

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

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

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

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

    Historical

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

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

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

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

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

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

    Prevalence

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

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

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

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

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

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

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

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

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

    Diagnostic criteria for generalized anxiety disorder

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

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

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

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

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

    5. Suffering and impairment of significant social, professional activities

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

    Signs and symptoms of generalized anxiety disorder

    Here are the main symptoms:

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

    Comorbidity

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

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

    Etiology

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

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

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

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

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

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

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

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

    What are the treatments for anxiety?

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

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

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

    Medications typically used to treat anxiety include antidepressants and benzodiazepines.

    What natural remedies are used to treat generalized anxiety disorder?

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

    These include:

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

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    Anosognosia is a neuropsychological disorder defined by an individual’s lack of awareness of his own disease or the loss of functional capacity from which he suffers. The term is derived from Greek and associates nosos (disease) and gnosia (knowledge), described by Babinski in 1914.

    It was associated in the 1980s with dementia in general and Alzheimer’s disease in particular. In this case, anosognosia is the inability to recognize the presence of a deficit or to appreciate its severity.

    Anosognosia is therefore common in patients with Alzheimer’s disease or other types of dementia.

    It is a cause of difficulty in taking care of and increasing the caregiver’s burden.

    It is mainly reflected by a loss of awareness of their deficit in instrumental activities of daily life, depressive disorders, and behavioral disorders (hallucinations, delusions)

    Patients with anosognosia are more often apathetic.

    Anosognosia: a harbinger of Alzheimer’s disease?

    Patients who are unaware that they have memory problems are more likely to see their condition worsen in a short period of time and develop Alzheimer’s disease.

    Certain brain conditions can interfere with a patient’s ability to understand that they have a health condition. Anosognosia, which is often associated with Alzheimer’s disease, is a neurological disorder that affects a patient’s ability to realize they have a health condition.

    A study published by a Canadian team (McGill University) found that people who were unaware of their condition had almost three times the likelihood of developing dementia within two years.

    Anosognosia would therefore be a new identified precursor sign of Alzheimer’s disease.

    The researchers analyzed 450 patients who had mild memory deficits but were still able to take care of themselves.

    The researchers asked them and their relatives to assess their cognitive abilities.

    When a patient self-reported no cognitive issues but a family member reported significant difficulties, the patient was considered unaware of their condition.

    The researchers then compared the anosognosia group to those who had no problems with consciousness and found that the anosognosia group had impaired brain metabolic function (neurons were less active) and increased amyloid deposits.

    Two years later, a follow-up showed that patients who were unaware of their memory problems were more likely to have developed dementia, even when controlling for other factors such as genetic risk, age, sex and gender, and education.

    The increased progression to dementia coincides with a decline in brain metabolism in regions affected by Alzheimer’s disease (particularly the hippocampus)

    This discovery highlights the importance of consulting the patient’s close family members during medical visits.

    “According to Dr. Serge Gauthier, professor of neurology at McGill University, people with mild memory impairment should have an assessment that takes into account information gathered from reliable informants, such as family members or close friends.

    Source J. Therriault et al. Anosognosia predicts default mode network hypometabolism and clinical progression to dementia. Neurology, 2018.

  7. Anosmia

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    Anosmia is the complete absence of the sense of smell. Without your sense of smell, food doesn’t taste the same, you can’t smell a flower, and you could find yourself in a dangerous situation without knowing it. For example, you would not be able to detect smells like gas leaks, smoke from a fire, or curdled milk without the ability to detect odors.

    The basics of smell

    A person’s sense of smell is influenced by certain processes. First, a molecule released by a substance (such as the scent of a flower) must stimulate special nerve cells known as olfactory cells that are located in the nose. 

    Nerve cells then send information to the brain, where the specific smell is identified. Anything that interferes with these processes, such as nasal congestion or nasal blockage, can lead to loss of smell. Damage to the nerve cells themselves can also lead to loss of smell.

    The ability to smell also affects our ability to taste. Without a sense of smell, our taste buds are only able to detect a few flavors, which can impact your quality of life.

    Causes of Anosmia

    Nasal congestion caused by a cold, allergy, sinus infection, or poor air quality is the most common cause of anosmia. Other causes of anosmia include:

    • Nasal polyps – small, non-cancerous growths in the nose and sinuses that block the nasal passage.
    • Nose injury and nerve odour from surgery or head trauma.
    • Exposure to toxic chemicals, such as pesticides or solvents.
    • Certain medications, including antibiotics,  antidepressants, anti-inflammatories, and heart medications.
    • Cocaine abuse.
    • Old age. Like vision and hearing, your sense of smell can weaken as you age. In fact, the sense of smell is most pronounced between the ages of 30 and 60 and begins to decline after age 60.
    • Certain neurological diseases, such as Alzheimer’s disease, Parkinson’s disease, multiple sclerosis, nutritional deficiencies, congenital conditions, and hormonal disorders.
    • Radiological treatment of head and neck cancers.

    The effect of aging on olfaction

    The olfactory functions begin a decline beginning around the age of 60. The decline appears earlier in men than it does in women. Around the age of 80, more than half of the elderly have olfactory disorders.

    The causes that lead to a poorer perception of odours are multiple: slow regeneration of the tissues of the olfactory system, alteration of the nasal mucosa which produces mucus-producing glands, etc.

    Anosmia and other smell disorders

    The doctor takes note of the complaints of the patient who smells badly or who no longer smells odours. Hyposmia (loss of sensitivity to odours) is the most common smell disorder, while anosmia is a smell disorder frequently caused by damage to the olfactory nerve. 

    Parosmias are characterized by a diminished ability to perceive smells, while dysosmias (total loss of smell) are even more rare.

    These complaints may be due to head trauma or “whiplash” or sinusitis (transmission anosmia), the latter being treated with corticosteroids.

    Anosmia and Alzheimer’s disease

    Disorders of smell can occur before the first cognitive symptoms appear. Researchers have actually noticed that there is a link between memory complaints reported by an individual and the presence of olfactory disorders detected using specific tests.

    These observations are confirmed by a team of researchers from the University of Montreal. It would seem that 80% of people with Alzheimer’s disease first present with smell disorders. In particular, people would have difficulty distinguishing and memorizing an odour.

    In a study published in 2009, it was shown that olfactory disorders are often present at the onset of  Alzheimer’s disease, and even before the first cognitive symptoms appear.

    From a cohort of 144 people aged 50 to 86, the authors of this longitudinal study observed a correlation between subjective memory complaints (i.e. not validated by tests) and the presence of mental disorders. Olfaction was detected using qualitative discrimination and identification tests.

    These results suggest that olfaction can be a good indicator for identifying subjects at risk of memory disorders.

    Source:  Sohrabi HR et coll. Olfactory dysfunction is associated with subjective memory complaints in community-dwelling elderly individuals. J Alzheimers Dis. 2009;17(1):135-42.

    Parkinson disease

    People with Parkinson’s disease also have olfaction disorders, which are characterized by a loss of sensitivity in the perception of odors. The presence of olfactory disorders predicts cognitive impairment in the disease.

    Researchers hope to diagnose Parkinson’s disease based on body odor.

    How can these observations be explained?

    Neurons send information via the olfactory nerve to the olfactory bulb, which in turn sends it to the olfactory cortex. Most regions of the olfactory cortex are part of the limbic system, responsible for processing emotions and memory (hippocampus, entorhinal cortex, amygdala). This explains why the memory of a smell is all the more pregnant as it arouses emotion.

    The olfactory bulb is notably modulated by neurons which produce a neurotransmitter called acetylcholine. This neurotransmitter is involved in memory and learning. These neurons project to regions of the structural system of the limbic system (hippocampus and amygdala) involved in the perception of odors.

    In Alzheimer’s and Parkinson’s diseases, these neurons are damaged early by lesions characteristic of these diseases, namely neurofibrillary tangles and alpha-synuclein deposits respectively.

  8. Un mode de vie sédentaire est-il mauvais ?

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    Mener une vie sédentaire devient un problème de santé publique important. Il semble que les modes de vie sédentaires soient de plus en plus répandus dans de nombreux pays, et sont liés à un éventail de problèmes de santé chroniques.

    On suppose qu’une faible participation à l’activité physique est influencée par de multiples facteurs. Certains facteurs environnementaux comprennent la congestion routière, la pollution atmosphérique, le manque de parcs ou de sentiers piétonniers et le manque d’installations sportives ou récréatives. La télévision, regarder des vidéos et utiliser des téléphones mobiles sont corrélés à un mode de vie de plus en plus sédentaire.

    Il est peu probable que la plupart des personnes qui mènent une vie sédentaire respectent les directives en matière d’activité physique.

    Environ 31% de la population mondiale âgée ≥ 15 ans est insuffisamment active, ce qui contribue à la mort d’environ 3,2 millions de personnes chaque année. L’inactivité physique n’est pas le seul problème grave: le comportement sédentaire est également une préoccupation sérieuse, et un nombre important de personnes s’y engagent pendant de longues périodes. Par exemple, les Américains consacrent 55% de leur temps d’éveil (7,7 heures par jour) à des activités sédentaires, tandis que les Européens passent 40% de leur temps libre (2,7 heures par jour) à regarder la télévision.

    Selon les médecins, les adultes devraient faire au moins 150 minutes d’activité physique d’intensité modérée chaque semaine.

    Le comportement sédentaire est généralement défini comme toute activité impliquant de s’asseoir, de s’allonger ou de s’allonger et qui a une très faible dépense énergétique. La mesure de la dépense énergétique est constituée d’équivalents métaboliques (MET), et les auteurs considèrent que les activités qui dépensent 1,5 MET ou moins d’énergie sont sédentaires.

    MET est défini comme le rapport entre le taux métabolique de travail et le taux métabolique standard au repos (RMR) de 1 kcal / (kg / h). Un MET est le coût énergétique pour une personne au repos. Lorsqu’elles sont classées quantitativement en fonction de leur intensité, les activités physiques peuvent être classées en 1,0 à 1,5 MET (comportement sédentaire), 1,6 à 2,9 MET (intensité légère), 3 à 5,9 (intensité modérée) et ≥ 6 MET (intensité vigoureuse).

    La recherche suggère que seulement 21% des adultes respectent les directives en matière d’activité physique, tandis que seulement 5% effectuent 30 minutes d’activité physique par jour.

    Les risques pour la santé sont nombreux

    Un mode de vie sédentaire peut contribuer à l’obésité, au diabète et à certains types de cancer.

    Des recherches récentes commencent à confirmer les risques pour la santé associés à un mode de vie sédentaire.

    Des études ont maintenant démontré de manière constante que mener une vie sédentaire peut contribuer à:

    • obésité
    • diabète de type 2
    • certains cancers
    • maladie cardiovasculaire
    • Mort prématurée

    Des périodes prolongées d’inactivité peuvent réduire le métabolisme et nuire à la capacité du corps à contrôler le taux de sucre dans le sang, à réguler la pression artérielle et à décomposer les graisses.

    Une étude a analysé les données recueillies sur 15 ans et a révélé qu’un mode de vie sédentaire était associé à un risque accru de décès prématuré, quel que soit le niveau d’activité physique.

    Cela montre qu’il est essentiel de réduire le temps passé à être sédentaire en plus de faire plus d’exercice.

    Santé mentale

    Un mode de vie sédentaire semble également avoir un impact négatif sur le bien-être mental.

    La combinaison de l’impact physique et mental sur la santé rend un mode de vie sédentaire particulièrement problématique.

    Une étude portant sur 10 381 participants a établi un lien entre un mode de vie sédentaire et un manque d’activité physique et un risque plus élevé de développer un trouble de santé mentale.

    Une revue qui comprenait des données de 110 152 participants a trouvé un lien entre le comportement sédentaire et un risque accru de dépression.

    Solutions pour réduire le mode de vie sédentaire

    Un mode de vie plus actif peut réduire considérablement les risques de problèmes de santé chroniques, de troubles de santé mentale et de décès prématuré.

    Augmenter la période d’activité physique

    La recherche a démontré que l’activité physique, y compris l’exercice et les sports, peut réduire le risque de maladie cardiovasculaire, de diabète de type 2, d’obésité et de décès prématuré.

    Les preuves montrent également que l’exercice peut améliorer la santé mentale. Une étude portant sur 1 237 194 personnes a révélé que ceux qui faisaient de l’exercice signalaient moins de problèmes de santé mentale que ceux qui ne le faisaient pas.

    Il est préférable de combiner une variété d’exercices cardiovasculaires, tels que la course à pied ou le vélo, avec des exercices de musculation, qui peuvent inclure des exercices de musculation ou de poids corporel. Faire au moins trois courses de 30 minutes et faire deux séances de 30 minutes d’exercices de musculation par semaine serait suffisant pour respecter les directives minimales en matière d’activité physique.

    Réduire le temps passé à être sédentaire

    L’activité physique est importante, mais passer la majeure partie de la journée à être sédentaire est toujours dangereux.

    Les gens peuvent réduire le temps qu’ils passent à être sédentaires en:

    • debout plutôt que assis dans les transports en commun
    • Se rendre au travail à pied
    • faire des promenades pendant les pauses déjeuner
    • Définir des rappels pour se lever toutes les 30 minutes lorsque vous travaillez à un bureau
    • investir dans un bureau debout ou demander au lieu de travail d’en fournir un
    • faire une promenade ou se lever pendant  les pauses café ou thé
    • passer plus de temps à faire des tâches ménagères, en particulier le bricolage ou le jardinage
    • trouver des excuses pour quitter le bureau ou se déplacer dans l’immeuble
    • prendre des appels téléphoniques à l’extérieur et se promener en même temps
    • passer du temps libre à être actif plutôt que de regarder la télévision ou de jouer à des jeux vidéo
    • se lever et se promener pendant les publicités télévisées
    • prendre les escaliers au lieu d’utiliser l’ascenseur
  9. Is a sedentary lifestyle bad for you?

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    Lifestyle refers to the way we live our lives. It includes how we spend our time, where we go, who we hang out with, and what we do. The term lifestyle is often used interchangeably with terms like ‘culture’ and ‘social life’.

    Leading a sedentary lifestyle is becoming a significant public health issue. It appears that sedentary lifestyles are becoming increasingly widespread in many nations, even though they are linked to various chronic health conditions.

    It is assumed that low participation in physical activity is influenced by multiple factors. Some environmental factors include traffic congestion, air pollution, lack of parks or pedestrian pathways, and lack of sports or recreational facilities. Television, watching videos, and using mobile phones are correlated with an increasingly sedentary lifestyle.

    Most people living a sedentary lifestyle are unlikely to meet the physical activity guidelines. 

    Approximately 31% of the world’s population aged ≥ 15 years is insufficiently active, and this is known to contribute to the deaths of approximately 3.2 million people each year. Physical inactivity is not the only serious problem: sedentary behavior is also a serious concern, and a significant number of people engage in it for prolonged periods of time. For example, Americans spend 55% of their waking time (7.7 hours per day) on sedentary activities, while Europeans spend 40% of their free time (2.7 hours per day) watching television.

    According to physicians, adults should get at least 150 minutes of moderate-intensity physical activity each week.

    Sedentary behavior is usually defined as any activity involving sitting, reclining, or lying down that has a very low energy expenditure. The measurement for energy expenditure is metabolic equivalents (METs), and the authors consider activities that expend 1.5 or less METs of energy to be sedentary.

    MET is defined as the ratio of the working metabolic rate to the resting standard metabolic rate (RMR) of 1 kcal/(kg/h). A MET is the energy cost for a person at rest. When quantitatively classified according to their intensity, physical activities can be classified into 1.0 to 1.5 MET (sedentary behaviour), 1.6 to 2.9 MET (mild intensity), 3 to 5.9 (moderate intensity) and ≥ 6 MET (vigorous intensity).

    Research suggests that only 21 percent of adults meet the physical activity guidelines, while only 5 percent perform 30 minutes of physical activity per day.

    The health risks of a sedentary lifestyle are numerous

    A sedentary lifestyle can contribute to obesity, diabetes, and some types of cancer.

    Recent research is starting to confirm the health risks of a sedentary lifestyle.

    Studies have now consistently demonstrated that leading a sedentary lifestyle can contribute to:

    • obesity
    • type 2 diabetes
    • some types of cancer
    • cardiovascular disease
    • early death

    Prolonged periods of inactivity can reduce metabolism and impair the body’s ability to control blood sugar levels, regulate blood pressure, and break down fat.

    One study analyzed data collected over 15 years and found that a sedentary lifestyle was associated with an increased risk of early death, regardless of physical activity levels.

    This shows that it is essential to reduce the amount of time spent being sedentary in addition to doing more exercise.

    Mental well-being

    A sedentary lifestyle also appears to have a negative impact on mental well-being.

    The combination of the physical and mental impact on health makes a sedentary lifestyle particularly problematic.

    One study with 10,381 participants linked a sedentary lifestyle and lack of physical activity with a higher risk of developing a mental health disorder.

    A recent review that included data from 110,152 participants found a link between sedentary behavior and an increased risk of depression.

    How to change your sedentary lifestyle

    A more active lifestyle can significantly reduce the chances of chronic health conditions, mental health disorders, and premature death.

    Increasing physical activity

    Research has demonstrated that physical activity, including exercise and sports, can reduce the risk of cardiovascular disease, type 2 diabetes, obesity, and early death.

    Evidence also consistently shows that exercise can improve mental health. A study of 1,237,194 people found that those who exercised reported fewer mental health problems than those who did not.

    It is best to combine various cardiovascular exercises, such as running or cycling, with strength-training exercises, including weight training or body-weight exercises. Going for at least three 30-minute runs and doing two 30-minute sessions of strength-training exercises per week would be sufficient to meet the minimum physical activity guidelines.

    Change your daily habit

    Physical activity is important, but spending most of the day being sedentary is still dangerous.

    People can reduce the amount of time they spend being sedentary by:

    • standing rather than sitting on public transport
    • walking to work
    • taking walks during lunch breaks
    • setting reminders to stand up every 30 minutes when working at a desk
    • investing in a standing desk or asking the workplace to provide one
    • taking a walk or standing up during coffee or tea breaks
    • spending more time doing chores around the house, especially DIY or gardening
    • making excuses to leave the office or move around the building
    • taking phone calls outside and walking around at the same time
    • spending some leisure time being active rather than watching television or playing video games
    • getting up and walking around during television commercials
    • taking the stairs instead of using the elevator

  10. Aneurysm

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    An aneurysm is a widening of an artery, which can weaken the arterial wall and lead to a tear or rupture. 

    The ruptured aneurysm can cause severe bleeding (hemorrhage), stroke, or death. An aneurysm usually develops in the aorta, but can also occur in the brain, carotid arteries in the neck, groin, or back of the legs.

    Aneurysms usually develop in your abdomen and chest in the aorta (the main artery that starts from your heart and runs through your chest). They are known as abdominal and thoracic aortic aneurysms. 

    Aneurysms can also occur in the brain. This is called a cerebral or intracranial aneurysm. Aneurysms that form in the carotid arteries in the neck, groin, or back of the legs are called peripheral aneurysms.

    The causes of aneurysm

    Risk factors for aneurysms include:

    • Some types of aneurysm, such as those in the abdomen, are more common in older men. Brain aneurysms are more common in women after age 45.
    • Research suggests that genetic mutations may contribute to the development of aneurysms.
    • Smoking: former and current smokers
    • High blood pressure
    • Atherosclerosis and high cholesterol
    • Obesity
    • Alcoholism
    • car accidents
    • Chest trauma 
    • Previous aneurysms

    A decreased risk of abdominal aneurysm is associated with:

    • female gender
    • non-white race
    • Diabetes

    Symptoms

    Small aneurysms usually cause no symptoms. However, depending on the location and size of the aneurysm, it can also cause pain in the groin, lower back, lower abdomen, chest, or above or behind the eye.

    Larger aneurysms can also lead to:  

    • fainting spells
    • vision changes
    • a droopy eyelid
    • numbness or weakness on one side of your face or body
    • heart failure symptoms (shortness of breath, swelling)
    • abdominal pulsation

    Diagnosis and tests

    There are several tests available that can help diagnose an aneurysm.

    Physical examination

    When your healthcare professional presses on your abdomen during a physical exam, they may be able to detect an abdominal aortic aneurysm. 

    However, aneurysms often do not cause symptoms and cannot be found during a physical exam. « Silent » aneurysms are sometimes discovered during surgery or when an X-ray, ultrasound, CT scan, MRI, or echocardiogram is done for another reason.

    There is currently insufficient evidence to recommend that women undergo a screening abdominal ultrasound, regardless of their smoking history.

    Ultrasound

    This procedure uses sound waves to create an image of the inside of your body and can reveal an aneurysm and its size. 

    Depending on your symptoms, your doctor may recommend other tests, including:

    CT-scan

    These use x-rays to take pictures of your internal organs. The technician will inject a dye into your vein, which will appear on x-ray images, revealing the size and shape of the aneurysm. A CT scan provides a more detailed image than an ultrasound.

    MRI

    This test is very accurate in detecting aneurysms and identifying their exact size and location.

    Angiography

    During an angiogram, a special dye is injected into a blood vessel so that it can be seen and examined for problems.

    Aneurysm care and treatment

    If an aneurysm is found, your healthcare provider can monitor it closely to see if it gets bigger over time. This is called “watchful waiting”. Your provider will order regular ultrasounds every 3 to 12 months, depending on the size and location of the aneurysm. If the aneurysm is large, it may need to be repaired immediately before it ruptures or leaks.

    Medications

    During watchful waiting, your healthcare professional may prescribe high blood pressure medication to keep your aneurysm from growing. The drugs will decrease the force of the blood flowing against the walls of the arteries. These drugs include those that help relax blood vessels, such as:

    • Vasodilators
    • Angiotensin converting enzyme inhibitors
    • Angiotensin II receptor blockers
    • Calcium channel blockers

    Your healthcare professional may also prescribe blood thinners (sometimes called “blood thinners”) to help prevent blood clots from forming in the affected part of the artery.

    Surgery

    If an aneurysm grows too large, or if it grows too quickly, or if it puts pressure on other important parts of your body and causes symptoms, your doctor may recommend surgery to repair the aneurysm and prevent it from rupturing. Several new, less invasive techniques have been developed to repair aneurysms.

    Surgery involves removing the damaged part of your artery and replacing it with a synthetic (artificial) tube called a graft. This can be achieved through open surgery or by threading the graft through a small incision in your artery and securing it over the site of the aneurysm (this is called endovascular surgery).

    The type of surgery recommended by your healthcare professional will depend on:

    • The location and size of the aneurysm
    • Other illnesses that may affect your tolerance to surgery and any complications that may arise during or after surgery

    Your healthcare professional can perform emergency surgery in the event of a ruptured aneurysm, but the surgical risks are much higher and the survival rate is lower.

    Aneurysm lifestyle and management

    You can reduce your risk of developing an aneurysm by making sensible lifestyle changes, including:

    • Quitting smoking or using tobacco products
    • Lose weight if necessary
    • Reduce cholesterol and fats in your diet
    • Get screened by ultrasound, if appropriate for your age and gender