Dysarthria is a speech disorder that is caused by the degeneration of a muscle or certain brain structures.
These affected structures are the medulla oblongata or the cortex in the latter case.
Multiple sclerosis (a neurological disease) or a stroke can cause dysrathrias.
Parkinson’s disease and Huntington’s disease are some of the neurological diseases that lead to dysarthria. Only the expression is altered.
It is not caused by damage to the organs of phonation (tongue, lips, palate) and must be differentiated from aphasia, which is an oral and/or written language disorder affecting the expression and understanding of speech. language (aphasia is found in particular in Alzheimer’s disease).
Patients have weakness, slowness, or incoordination in breathing, articulation, phonation, rate, and/or prosody (loudness and duration of sound).
The condition is often characterized by slurred or slow speech that can be difficult to understand.
The different forms of dysarthria
Here is the classification of dysarthria with the pathologies in parentheses. 1. Spastic dysarthria (stroke). 2. Flaccid dysarthria (neuropathy innervating the effector muscles of the face, for example). 3. Ataxic dysarthria (involvement of the cerebellum). 4. Hypokinetic (Parkinson’s disease) and hyperkinetic dysarthria (Huntington’s disease). 5. Mixed dysarthria (head trauma, multiple sclerosis, amyotrophic lateral sclerosis).
How are dysarthria assessed?
GBRAS scale
GRBAS stands for Grade, Breathness, Roughness, Asthenicity and Strain.
G (for Grade): what is the general impression of the quality of the voice? R (for Roughness): is the voice hoarse?. B (for Breathness): is a breath audible when the patient speaks? A (asthenicity): is there a feeling of asthenia? S (strain): is there an impression of the patient?
These five parameters are rated from 0 (normal voice) to 3 (maximum alteration of the voice). Scoring is relatively easy for hoarseness and breath, but it is difficult for asthenia and forcing.
Perceptual assessment of dysarthria
It consists of 32 criteria related to the volume and timbre of the voice, breathing, etc. A scale notes the severity of the criterion (0: no anomaly, 4: severe anomaly).
Intelligibility measurement
Several tests translated from English have been developed including the Assessment of Intelligibility in Dysarthric Speakers.
Additional tests
There are instruments that perform acoustic and aerodynamic measurements of speech. For example, the Assisted Voice Assessment device records certain physiological parameters of voice and speech (intensity, pitch, airflow, pressure). .
Chronic pain is one of the costliest health problems. The economic consequences of chronic pain include increased medical expenses, loss of income, loss of productivity, compensation payments, and legal fees.
Low back pain is one of the most important health problems. It is a common cause of activity limitation in adults, especially back pain.
Cancer pain affects most people with advanced cancer.
Approximately 15-20% of the population is affected by arthritis.
Headaches affect millions of adults. Migraines and tension headaches are some of the most common types of chronic headache.
Neuropathy and other pain disorders affect nerves throughout the body.
Pain caused by damage to the central nervous system (the brain and spinal cord) as well as pain without a physical cause.
What is the source of the pain?
The pain begins in the receptor nerve cells located under the skin and in the organs of the body. The message is sent along nerve pathways to the spinal cord, which then transmits the message to the brain when you are sick, injured or have a problem. These messages are reduced or blocked by painkillers before they reach the brain.
The pain can be something bothersome, like a mild headache, or very intense, like chest pain that accompanies a heart attack, or pain due to kidney stones. The pain can be acute, that is to say new, subacute, lasting a few weeks or a few months, and chronic, when it lasts more than 3 months.
Are there different types of pain?
Two types of pain include the following:
Acute pain. This pain can be from inflammation, tissue damage, injury, disease, or recent surgery. This usually lasts less than a week or two. The pain usually ends after the underlying cause is treated.
Chronic pain. Pain that persists for months or even years.
What is chronic pain?
Chronic pain is persistent pain that persists beyond the usual recovery period or occurs alongside a chronic health condition, such as arthritis, Chronic pain can be “on” and “off” or continuous. It can affect people to the point that they can no longer work, eat properly, exercise, or enjoy life.
Chronic pain is a major medical condition that can and should be treated.
What is the cause of chronic pain
There are many causes of chronic pain. You may have experienced an illness or injury that you have recovered from for a long time, but the pain remained. Or there may be an ongoing cause of pain, such as arthritis or cancer. Despite a previous injury or signs of illness, many people experience chronic pain.
There are usually three causes of chronic pain:
Inflammatory causes: example of rheumatoid arthritis. Peripheral nerve fibers are abnormally sensitive to pain.
Neuropathic causes: Neuropathic pain is the consequence of damage to the nerves and nervous system.
Central pain due to a central abnormality in the pain control system. This includes, for example, tension headaches, fibromyalgia, somatic chest pain or irritable bowel syndrome.
Pain, sleep and psychological disorders form a triad
When pain becomes such a problem that it interferes with work and normal life activities, you can become the victim of a vicious cycle. Pain can worry you, depress you, and irritate you. Depression and irritability often lead to insomnia and lassitude, resulting in more irritability, depression, and pain. The urge to stop the pain can lead some people to become addicted to drugs and can lead others to undergo repeated surgeries or resort to questionable treatments. Family members may find the situation as difficult as the sufferer is.
How is chronic pain treated?
The most effective treatment includes symptom relief and support. A multidisciplinary approach is often needed to provide the resources to manage pain.
Neurologists and Neurosurgeons
Orthopedists and orthopedic surgeons
Anesthesiologists
Oncologists
Nurses
Physiotherapists
Occupational therapists
Psychologists/psychiatrists
Special pain programs are offered in many hospitals, rehabilitation centers and pain clinics.
Rehabilitation program to manage pain
A rehabilitation program for pain management is designed to meet your needs. The schedule will depend on the specific type of pain and disease. Your active participation and that of your family is essential to the success of the program.
Pain management programs are designed to help you achieve the highest level of functioning and independence possible, while improving your overall quality of life – physically, emotionally and socially. Pain management techniques help reduce your suffering.
To help achieve these goals, pain management programs may include:
Medical management of chronic pain, including drug management:
Over-the-counter medications may include nonsteroidal anti-inflammatory drugs, aspirin, or acetaminophen.
Prescription painkillers, including opioids, may be needed to relieve pain more strongly than aspirin. However, these drugs are reserved for more severe types of pain, as they have some potential for abuse and can have unpleasant and potentially very dangerous side effects.
Prescription antidepressants can help some people. These medications increase the supply of the naturally produced neurotransmitters serotonin and norepinephrine. Serotonin is an important part of a pain control pathway in the brain.
Heat and cold treatments to reduce stiffness and pain, especially with joint problems such as arthritis
Physiotherapy and occupational therapy such as massages and whirlpool baths
Exercise to reduce spasticity, joint contractures, joint inflammation, spinal alignment problems, or weakening and shrinking of muscles to prevent other problems
Local electrical stimulation involving the application(s) of brief electrical pulses to nerve endings under the skin to relieve pain
Injection therapies, such as epidural steroid injection
Emotional and psychological support for pain, which may include the following:
Psychotherapy and group therapy
Stress management
Training on relaxation methods
Meditation
Hypnosis
Biofeedback
The philosophy common to all of these varied psychological approaches is the belief that you can do something on your own to control pain. This includes changing your attitudes, perception of being a victim, feelings or behaviors associated with pain, or understanding how unconscious forces and past events have contributed to the pain.
Additionally, treatment may include:
Operation. Surgery may be considered for chronic pain. Surgery can relieve pain, but can also destroy other sensations or become the source of new pain. The relief is not necessarily permanent and the pain may return. There are a variety of operations to relieve pain.
Acupuncture. Acupuncture is a 2000-year-old Chinese technique of inserting thin needles under the skin at selected points on the body and has shown promise in treating chronic pain. The needles are manipulated by the practitioner to produce pain relief.
Common dysfunctional beliefs
Pain is synonymous with progressive tissue damage rather than the result of a stable problem. This belief leads to more suffering.
Chronic pain decreases with prolonged rest. This belief encourages passivity
The pain is inexplicable. This belief leads the patient to minimize his ability to reduce pain.
La perte de cheveux chez les hommes est la forme la plus courante de perte de cheveux chez les hommes, affectant environ 30 à 50% à l’âge de 50 ans.
La recherche montre que la nutrition joue un rôle important dans la perte de cheveux chez les hommes. Certaines études montrent que le métabolisme du glucose peut causer la perte de cheveux.
Récemment, des chercheurs de l’Université Tsinghua, à Beijing, en Chine, ont examiné le lien entre la consommation de boissons sucrées et la perte de cheveux.
Ils ont constaté qu’une consommation plus élevée de BSR est corrélée à un risque plus élevé de perte de cheveux.
« Traditionnellement, la plupart des médecins ou des chirurgiens de restauration capillaire comprennent que les nutriments et l’alimentation jouent un rôle clé dans la santé et le bien-être globaux de nos patients », a noté le Dr Williams. « L’exercice, l’évitement des produits du tabac et des drogues illicites, une bonne nutrition et une alimentation équilibrée sont essentiels à la santé et à la longévité de nos patients. »
Boissons sucrées et perte de cheveux
Les chercheurs ont recruté 1028 étudiants et enseignants âgés en moyenne de 27,8 ans dans 31 provinces de Chine.
Les participants ont reçu un sondage dans lequel ils ont rempli des informations sur :
Informations sociodémographiques de base
État des cheveux
Apport alimentaire
mode de vie
l’état psychologique;
La consommation de boissons sucrées a été déterminée à partir des réponses à un questionnaire de consommation de boissons de 15 questions, qui examinait leur consommation de boissons au cours du dernier mois. Les boissons sucrées comprenaient :
boissons de jus sucrées
boissons gazeuses
Boissons énergisantes et pour sportifs
lait sucré
thé et café sucrés
Dans l’ensemble, 57,6 % des participants ont déclaré une perte de cheveux, alors que les autres n’en ont pas déclaré.
Les chercheurs ont constaté que les personnes atteintes de perte de cheveux étaient plus susceptibles de :
être plus âgé
être fumeur actuel ou ancien
avoir un niveau d’éducation inférieur
faire moins d’activité physique
avoir une durée de sommeil plus courte
souffrir d’anxiété sévère ou de TSPT
avoir des antécédents familiaux positifs de perte de cheveux
avoir des maladies liées à la perte de cheveux
d’avoir des cheveux teints, décolorés
Ils ont également constaté que les personnes atteintes de perte de cheveux consommaient plus d’aliments frits, de sucre et de miel, de bonbons et de crème glacée, et moins de légumes que ceux sans la condition.
Par rapport à ceux qui ne sont pas atteints de la maladie, les personnes atteintes de perte de cheveux chez les hommes consomment en moyenne 4,3 litres de boissons sucrées par semaine.
Ils ont également constaté que les antécédents de la maladie influençaient le lien entre la prise de boisson sucrée et la perte de cheveux. Ils ont par ailleurs noté un lien entre la fréquence de la consommation de boissons sucrées et du trouble anxieux, et le trouble anxieux et la perte de cheveux chez les hommes.
Les chercheurs ont noté que l’association entre la consommation de boissons sucrées et la perte de cheveux existait même après la prise en compte des facteurs sociodémographiques, l’apport alimentaire et l’état psychologique.
L’effet de la consommation de sucre sur les cheveux.
Les scientifiques suggèrent qu’une consommation plus élevée de sucre augmente la concentration de sucre dans le sang, ce qui déclenche des voies de polyol, qui convertissent le glucose en d’autres sucres.
Des études montrent que ce processus réduit la quantité de sucre dans les follicules pileux, ce qui peut conduire à une perte de cheveux. Elle a ajouté que la consommation de sucre s’accompagne souvent d’un apport excessif en lipides, qui est également lié à la perte de cheveux.
Le Dr Zhao a mentionné que des études antérieures ont montré qu’une consommation élevée de sucre est liée à des problèmes de santé mentale. Selon une méta-analyse, ceux qui boivent l’équivalent de trois canettes de cola par jour ont un risque de dépression 25% plus élevé que ceux qui ne le font pas.
Limites de l’étude
Comme l’a noté le Dr Zhao, leurs résultats sont limités, car ils se sont appuyés sur des données autodéclarées plutôt que sur des diagnostics cliniques. Les chercheurs ont également noté qu’ils n’avaient pas recueilli de données sur la consommation d’autres produits sucrés et qu’ils ne pouvaient pas distinguer la gravité de la perte de cheveux.
Le Dr George Cotsarelis, professeur de dermatologie à l’Université de Pennsylvanie et directeur des cliniques capillaires et du cuir chevelu de l’Université de Pennsylvanie, non impliqué dans l’étude, a déclaré :
« L’étude ne montre qu’une corrélation entre les boissons sucrées et la calvitie. Je doute qu’il s’agisse d’une corrélation réelle, car il est difficile d’imaginer comment les boissons sucrées pourraient avoir un impact sur la calvitie. De plus, parmi les hommes qu’ils ont étudiés, le groupe chauve avait un pourcentage plus élevé d’hommes ayant des antécédents familiaux de calvitie.
Le Dr Williams a noté que l’étude est détaillée et bien conçue. Cependant, il a ajouté qu’il ne recommande pas nécessairement d’éliminer toutes les boissons contenant du sucre.
Je recommande de toujours avoir une alimentation équilibrée et de consommer des groupes d’aliments sains et des sources nutritionnelles. Évitez les produits du tabac, les drogues et la consommation excessive d’alcool, a-t-il conclu.
Diabetes has detrimental consequences on brain function and mental state in the elderly, since it accelerates cognitive decline and increases the risk of the onset of depressive symptoms and cerebrovascular accidents (CVA) of ischemic origin in the elderly.
In the general population, diabetes prevalence is around 5% and 10% in subjects over 65, with an increasing proportion as the population ages (25% in those over 75 ).
However, with the improvement of our lifestyle and the existence of effective preventive measures against stroke, diabetics are able to live longer with fewer major complications.
Diabetes decreases the faculties of the brain
There is growing evidence that diabetes impairs brain function.
Diabetes increases the risk (by about 100%) of seeing decline in cognitive functions, compared to non-diabetics.
The association between diabetes and arterial hypertension – which is associated with a more pronounced decline in cognitive abilities – being very frequent, it is difficult to assess the exact role of diabetes.
In 2014, researchers found that people who develop diabetes or hypertension between the ages of 40 and 64 are more likely to have neuronal loss and/or cognitive disorders (memory problems, thought disorders)
According to one of the study authors (Mayo Clinic), « if we prevent diabetes and hypertension, we can prevent or delay brain damage that occurs decades later ».
To reach this conclusion, the researchers recruited 1,437 people with an average age of 80 who underwent neuroimaging examinations to detect markers associated with brain damage.
Results: people with diabetes have an average brain volume 3% smaller than that of non-diabetic subjects. Such a reduction in volume is also observed in patients who suffer from hypertension.
The researchers conclude that these diseases take decades to produce their deleterious effects on the brain, leading to cognitive impairments that affect memory and thinking.
In the same year, another group showed that type two diabetes could be associated with premature brain aging, according to a study carried out on 614 patients (average age = 62 years) followed for an average of 10 years.
This conclusion is in line with previous studies that reported a link between type 2 diabetes and ischemia affecting small vessels, a disease during which the brain does not receive enough oxygenated blood.
« These patients show less brain tissue, suggesting the presence of cerebral atrophy, » said one of the study’s authors.
The authors used the magnetic resonance imaging technique to assess the patients’ brain volume. The results further reported a positive association between duration of diabetes and loss of brain volume, particularly in gray matter. More specifically, the results suggest that a person with diabetes for 10 years exhibits premature brain aging (of a period of 2 years) compared to a non-diabetic patient.
These results are in line with those of previous longitudinal studies, confirming that the cognitive functions of diabetics deteriorate more rapidly.
In a six-year follow-up study of a group of 9679 women over the age of 65, diabetics whose disease had been evolving for more than 15 years had a 57 to 114% increased risk of presenting with cognitive decline.
Several hypotheses have been put forward to explain this link:
Hyperglycemia affects neurons in the hippocampus, a key brain region involved in learning and remembering events.
Diabetes is accompanied by inflammation in the brain – called neuroinflammation – which also damages neurons.
Dysregulation of glucose levels affects neurons in the brain that produce a neurotransmitter called acetylcholine. This neurotransmitter is necessary to obtain a memory.
The microalbuminuria (low amounts of albumin in the urine) present in diabetics reflects a dysfunction of the vascular system which prevents poor oxygenation of the brain.
Research is investigating the possible beneficial effects of treating diabetes with insulin in preventing cognitive decline. This is particularly the case of intranasal insulin injections which would provide protection to the brain.
Watch out for hypoglycaemia
The brain is particularly sensitive to changes in blood sugar – especially hypoglycemia. The consequences of hypoglycaemia can be serious in elderly diabetics. Thus, elderly people with diabetes are five times more likely to be hospitalized than younger people due to a greater risk of hypoglycaemia.
A study suggests that hypoglycemia, which occurs frequently in patients with diabetes, can negatively influence cognitive performance. These cognitive disorders will in turn compromise the management of diabetes and lead to hypoglycemia.
These are the conclusions of an American study (University of California, San Francisco) involving 783 adults (average age 74 years) with diabetes. After 12 years of follow-up, 8% had a reported episode of hypoglycaemia and 19% developed dementia.
Patients who had a hypoglycemic event had a twice as high risk of developing dementia compared to those who did not (34% versus 17%).
In addition, elderly diabetics who have developed dementia have a greater risk of subsequently having an episode of hypoglycemia compared to patients who have not developed dementia (14% versus 6%).
Obtaining a normal blood sugar level would improve – or at least maintain – his cognitive performance.
Dementias
Diabetes: arisk factor for vascular dementia?
Diabetes is a risk factor for cerebrovascular accident (CVA) which promotes the development of vascular dementia, with a risk multiplied by 2 to 2.6 according to studies. If the individual has suffered a stroke, this risk can be multiplied by eight. The presence of hypertension in diabetics plays an important role in this increase.
Alzheimer’s disease
Diabetes could also be a cardiovascular risk factor in the onset of Alzheimer’s dementia, with an estimated increased risk of between 45% and 90% depending on the studies.
However, this link is questioned by other studies.
Better prevention of dementia would be possible thanks to a normalization of blood sugar, in the same way as arterial hypertension.
The Depression
Depression can be mistaken for dementia or, conversely, can be one of the first symptoms of Alzheimer’s disease. It is therefore important to detect it, which is often difficult.
According to scientific data, about 20 to 30% of elderly diabetics suffer from depression, including 10% from major depression. There would be at least one depressive symptom in half of elderly diabetics.
According to a study conducted in 2015 on people with diabetes (average age = 54 years), they have difficulties with family functioning and a lower quality of life.
Stroke
Diabetes is usually considered one of the major risk factors for stroke, with an increased risk of 50% to 100%. The risk of stroke is all the higher when the subject is hypertensive, has atrial fibrillation, carotid stenosis or a history of stroke. In addition, the occurrence of a stroke in a diabetic is strongly associated with a high risk of disability and higher mortality.
In 2016, researchers showed that type 2 diabetics have a greater risk (+60%) of developing dementia, compared to those without diabetes. Additionally, women with type 2 diabetes have a much higher risk of developing vascular dementia than men with diabetes. Indeed, the risk of vascular dementia is multiplied by 2.3 in women and by 1.7 times in men, compared to those who do not have diabetes. The analysis included data from 14 studies with more than 2.3 million people and more than 100,000 cases of dementia.
These results suggest that diabetes increases the risk of developing vascular dementia and that women with diabetes are particularly vulnerable. A previous study reported that people with diabetes had a 70% increased risk of dementia. However, these results are limited by the fact that most cases of dementia were reported in people of Asian origin.
The researchers were unable to analyze the links between the duration of diabetes, glycemic control and dementia. They suggest, however, that treatment differences in diabetes management – particularly poor care for women – may play a role in these results.
Further physiological studies are needed to examine how blood sugar interacts with the vasculature and whether there are notable gender differences.
On the other hand, diabetes seems to protect against the occurrence of hemorrhagic strokes, with a risk of stroke of hemorrhagic origin reduced by a factor of 4 to 10.
Prevention
Stroke prevention is possible through risk factor control and better blood sugar control. Controlling blood pressure is an essential part of stroke prevention. However, too great a decrease in blood pressure can lead to a stroke through a drop in cerebral circulation.
The use of statins is also found to be very beneficial. Thus, simvastatin (40 mg) or atorvastatin (10 mg) can reduce strokes by 25% to 50%.
In addition, antiplatelet drugs are recommended to reduce the risk of stroke. Aspirin is very frequently used in elderly diabetics at high risk of stroke.
The surgical management of carotid stenosis does not differ from that of non-diabetic subjects. The occurrence of a stroke and the operative risk are higher, but the benefit of an intervention is greater in diabetics. The indication for surgery must therefore be established according to the general condition of the elderly subject and the severity of the stenosis.
Diabetes increases the risk of heart and brain disease
The risk of developing cardiovascular disease is almost twice as high in patients who develop type 2 diabetes before age 40, compared to those who develop the disease later. The age of diagnosis of type 2 diabetes is getting younger around the world, mainly due to rising rates of obesity.
“Given the increasingly frequent onset of type 2 diabetes at an early age, it is hardly surprising that cardiovascular complications also appear earlier and earlier due to an increasingly unfavorable environment. a long time,” explains the lead author of the study.
The researchers used a large diabetes database, with participation from 630 hospitals and 222,773 patients. The average age of the cohort is 58.3 years. Patients who had early-onset diabetes were on average 34 years old, compared to 55 for those who developed diabetes later in life.
Early-onset type 2 diabetes was associated with a greater risk (+91%) of diseases associated with the brain and heart system (coronary heart disease and stroke), compared to late-onset diabetes.
According to some experts, the best way to measure risk in young patients with type 2 diabetes is to identify and treat cardiovascular risk factors. A very high proportion – around 80% – of young people with type 2 diabetes have at least two cardiovascular risk factors.
Septuagenarians are healthier than their elders
Americans with diabetes born in the 1940s live longer without major complications and with fewer disabilities than those born 10 years earlier.
These major complications are heart attack, stroke and amputations.
The three types of disability were reduced mobility, inability to carry out activities of daily living and total or partial inability to carry out essential activities (use of the telephone, shopping, meal preparation, etc.).
The messages of the medical authorities aiming to sensitize the individuals to have a better hygiene of life are undoubtedly for something.
This health improvement also concerns people who are not necessarily diabetic. The data analysis focused on Americans born in the 1930s and 1940s, more than 10% of whom had diabetes.
However, this improvement may not last in the United States due to rising obesity rates and poorer lifestyles. In this country, the incidence of type 2 diabetes has more than doubled in the last 20 years
Diabetes and brain disease article references
Barbagallo M and Dominguez LJ. Type 2 diabetes mellitus and Alzheimer’s disease. World J Diabetes 2014 December 15; 5(6): 889-893
Bardenheier BH et al. Compression of disability between two birth cohorts of US adults with diabetes, 1992–2012: a prospective longitudinal analysis. The Lancet Diabetes and Endorinology, June, 2016.
Bryan RN et al. Effect of diabetes on brain structure: the action to control cardiovascular risk in diabetes MR imaging baseline data. Radiology. July 2014: 210-6.
Chatterjee S et al. Type 2 Diabetes as a Risk Factor for Dementia in Women Compared With Men: A Pooled Analysis of 2.3 Million People Comprising More Than 100,000 Cases of Dementia. Diabetes care, December 2015.
Huo X et al. Risk of non-fatal cardiovascular diseases in early-onset versus late-onset type 2 diabetes in China: a cross-sectional study. The Lancet Diabetes & Endocrinology, Volume 4, No. 2, p115–124, February 2016.
Roberts RO et al. Association of type 2 diabetes with brain atrophy and cognitive impairment. Neurology, 2014.
Saedi E et al. Diabetes mellitus and cognitive impairments. World J Diabetes 2016 September 15; 7(17): 412-422.
Wang J et al. Depressive Symptoms, Family Functioning and Quality of Life in Chinese Patients with Type 2 Diabetes. Can J Diabetes 39 (2015).
Yaffe K et al. Association Between Hypoglycemia and Dementia in a Biracial Cohort of Older Adults With Diabetes Mellitus, Hypoglycemia and Dementia in Older Adults With DM. JAMA Internal Medicine, June 2013.
Depression in the elderly is different from depression in a young person. Older people have more somatic complaints and minimize their state of sadness. They are often hypochondriac and have an increased risk of chronic diseases.
Depression is one of the forms of mood disorders that are generally classified as follows:
major depression which causes the individual to work normally, sleep well and eat well, concentrate and enjoy the pleasures of life. A person usually has several episodes of major depression;
dysthymia, with less severe symptoms but lasting longer (at least two years);
minor depression, with symptoms of less severe intensity than in the two previous cases and which are temporary.
Mood disorders are the most common mental disorders in the elderly. Indeed, old age is a period of vulnerability conducive to the onset of mood disorders.
Here are some risk factors that may trigger depression in the elderly:
Loneliness (or feelings of loneliness) and social isolation.
Consequences of retirement (e.g. feeling useless, loss of activity).
Interpersonal conflicts.
Death of close friends.
Anniversary date of the bereavement.
Loss of autonomy due to physical illnesses.
Hormonal disruption due to dysregulation of melanin or thyroid hormones.
To be female.
Suffer from a chronic disease (cancer, diabetes, heart disease).
Restless sleep.
Have a family history of depression.
Take certain medications.
Consuming too much alcohol.
Leading a stressful life (caring for someone with a chronic illness).
Major depression in the elderly is not properly taken care of because those around you mistakenly believe that it is normal to be sad because you have lost a loved one or because you are losing your autonomy. However, in the case of depression, the sadness persists.
Prevalence of depression
The prevalence of depression in people aged 65 and over is estimated at around 1%, while 5% of people over 65 suffer from depressed mood. Here are the prevalence percentages according to age categories.
Population
Percentage
Male (55-75 years old)
2.6
Female (55-75 years old)
6.6
All 15-75 years old
7.8
Etiologies
Genetic causes : Having a first-degree relative who suffers from recurrent depression increases the risk of suffering from depression by two to four. Studies with homozygous twins confirm the role of heredity, with an increased risk of around 40%.
Physiological causes : activation of the hypothalamic-pituitary axis associated with an abnormally high level of cortisol is observed in patients with major depression, leading to inhibition of growth factors (including BDNF) and dysregulation of monoaminergic neurotransmitters (noradrenaline, serotonin, and dopamine).
Psychological causes : A certain view of life (tendency to a negative view of oneself, events and a pessimistic approach to the future)
Social causes : acute stress caused by different events: job loss, poverty, social exclusion, family conflicts, excessive demands, physical health problems, death of a loved one can be the cause of depression, as well than harmful experiences during childhood or adolescence.
Diagnostic criteria
The diagnostic criteria are those taken from the American psychiatry manual DSM IV and the International Statistical Classification of Diseases and Related Health Problems, 10th revision (ICD-10, World Health Organization). However, classifications of depression are not entirely suitable for older people because they tend not to express their sadness verbally.
DSM V Criteria
A: at least 5 symptoms during the same 2-week period and represent a change from normal functioning; at least one of the following symptoms: One of the following symptoms:
depressed mood;
anhedonia (loss of interest or pleasure)
significant weight loss or gain (5%) or increased or decreased appetite almost daily;
insomnia or hypersomnia;
psychomotor agitation or retardation;
fatigue or loss of energy;
feeling of worthlessness or excessive or inappropriate guilt;
loss of concentration;
recurrent thoughts of death, suicidal ideation or attempted suicide.
B: Symptoms cause significant distress and impairment of daily functioning.
C: The symptomatology is not attributable to the physiological effects of a substance or a medical condition.
D: the onset of the depressive episode is not explained by schizophrenia or delusional disorder.
E: no previous manic or hypomanic episode.
ICD-10 criteria
In the ICD-10 manual (2003), mood disorders are divided into seven parts. Most of these disorders tend to be recurrent. The onset of individual episodes can often be related to stressful situations or events. The change in mood is usually accompanied by a change in overall activity level.
1. Manic episode 1.a Hypomania. 1.b Mania without psychotic symptoms. 1.c Mania with psychotic symptoms (delusions, hallucinations, agitation, or hyperactivity).
2. Bipolar affective disorder The mood and level of activity of the subject are profoundly disturbed, sometimes in the sense of elevation (hypomania or mania), sometimes in the direction of depression (depression). 2.a Subject is currently hypomanic, and has had at least one other affective episode in the past. 2.b Subject is currently manic with no psychotic symptoms. 2.c Subject is currently manic, with psychotic symptoms. 2.d The subject is currently depressed, such as during a depressive episode of mild or moderate intensity. 2.e The subject is currently depressed, such as during a depressive episode of severe intensity without psychotic symptoms. 2.f Subject is currently depressed, such as during a depressive episode of severe intensity with psychotic symptoms. 2.g Simultaneous or alternating presence of manic and depressive symptoms. 2.h Bipolar affective disorder, currently in remission.
3. Depressive episodes 3.a Mild depressive episode. The subject remains, most often, able to continue most of its activities. 3.b Moderate depressive episode. The subject experiences considerable difficulty in continuing his or her usual activities. 3.c Severe depressive episode without psychotic symptoms. Suicidal thoughts and acts are common, and several “somatic” symptoms are usually present. 3.d Severe depressive episode with psychotic symptoms (hallucinations, delusions) or psychomotor retardation or stupor. Usual social activities are impossible. Risk of suicide, dehydration, or malnutrition.
4. Recurrent Depressive Disorder 4.a A disorder characterized by the repeated occurrence of depressive episodes, the current episode being mild, moderate, or severe in intensity, in the absence of any history of mania and without psychotic symptoms. 4.b Disorder characterized by the repeated occurrence of depressive episodes, the current episode of severe intensity with psychotic symptoms. 4.c Recurrent depressive disorder, currently in remission (F33-4)
5. Persistent Mood Disorders 5.a Persistent and usually fluctuating mood disorders in which most individual episodes are not severe enough to warrant a diagnosis of hypomanic episode or mild depressive episode. 5.b Cyclothymia: Persistent instability of mood, including numerous periods of depression or slight elation (F34-0). 5.c Dysthymia : chronic low mood.
6. Other mood disorders
7. Mood disorder, unspecified
Depression in the elderly is different from depression in a young person. Older people have more somatic complaints and minimize their state of sadness. They are often hypochondriac and have an increased risk of chronic diseases.
Depression is one of the forms of mood disorders that are generally classified as follows:
major depression which causes the individual to work normally, sleep well and eat well, concentrate and enjoy the pleasures of life. A person usually has several episodes of major depression;
dysthymia, with less severe symptoms but lasting longer (at least two years);
minor depression, with symptoms of less severe intensity than in the two previous cases and which are temporary.
Mood disorders are the most common mental disorders in the elderly. Indeed, old age is a period of vulnerability conducive to the onset of mood disorders.
Here are some risk factors that may trigger depression in the elderly:
Loneliness (or feelings of loneliness) and social isolation.
Consequences of retirement (e.g. feeling useless, loss of activity).
Interpersonal conflicts.
Death of close friends.
Anniversary date of the bereavement.
Loss of autonomy due to physical illnesses.
Hormonal disruption due to dysregulation of melanin or thyroid hormones.
To be female.
Suffer from a chronic disease (cancer, diabetes, heart disease).
Restless sleep.
Have a family history of depression.
Take certain medications.
Consuming too much alcohol.
Leading a stressful life (caring for someone with a chronic illness).
Major depression in the elderly is not properly taken care of because those around you mistakenly believe that it is normal to be sad because you have lost a loved one or because you are losing your autonomy. However, in the case of depression, the sadness persists.
Here are some clinical features of depression in the elderly that are sometimes the same as in younger subjects:
persistent feelings of sadness and hopelessness.
Pessimism.
Inability to find a pleasant life as before.
Disturbed sleep (sleeps little or not enough).
Unexplained crying spells.
Change in appetite and weight.
Disinterest in sexuality.
Fatigue, lack of energy.
Clothing or bodily negligence.
Feelings of worthlessness and guilt.
Psychomotor restlessness or retardation.
Loss of interest in things.
Suicidal thoughts.
Loss of self-esteem.
Anxiety which is often the mask of depression.
Hypochondriacal and delusional symptoms.
Irritability and hostility.
Inability to take pleasure in doing an activity, eating, etc. (anhedonia)
Difficulty concentrating and remembering.
Difficulties making decisions.
Diagnosis and assessment of severity
The Geriatric Depression Scale (or GDS): This is a test to diagnose depression in an older person.
The Hamilton Depression Scale : This is the most widely used test to assess the intensity of depressive symptoms.
Before starting treatment with an antidepressant, it is important to pay attention to the symptoms, with particular attention to the following:
Dysphoric restlessness
Suicidal risk
Psychotic symptoms
Possible comorbidity
Depression in the elderly associated with certain chronic diseases
Older people with depression have an increased risk of cardiovascular disease, Parkinson’s disease and Alzheimer’s disease. On the other hand, elderly people suffering from a chronic illness (diabetes, high blood pressure, heart problem) are two to four times more likely to have major depression than others of the same age and in good health.
Depression and somatic complaints
Somatic complaints are an integral part of depression in the elderly. Indeed, a depressed person can express his suffering through pain in his body. It is estimated that half to three quarters of depressed people who consult have somatic symptoms such as gastrointestinal disorders, joint pain or cardiovascular symptoms.
Treatment
Antidepressants. When the diagnosis of major depression is made in the elderly, studies report that the effectiveness of an antidepressant is recognized compared to a placebo, which is not the case if the depression is minor.
It is common for older people to try several antidepressants before finding the right drug, leading to a remission rate of over 80%. Combinations of antidepressants are not recommended.
It is important not to stop treatment without the advice of your doctor. Treatment should be continued for several months even if the beneficial effects are felt.
Electroconvulsive therapy (ECT) is sometimes used in severe depression in subjects refractory to antidepressants, at the rate of two to three sessions per week under general anesthesia for about a month. ECT is a therapy that involves stimulating the brain directly with electricity, magnets or implants. Some of these treatments are still in the experimental stage. If the depression persists despite medication, or if the depression is so severe that the individual is unable to eat or develops false beliefs (delusions) about their illness, the doctor may recommend ECT as the best option. Although it has been used for almost 80 years, the electroconvulsive therapy remains the most powerful and fastest treatment in severe depression.
Although ECT is effective and safe in the elderly, many misconceptions remain among patients and healthcare professionals. Admittedly, ECT can cause side effects such as confusion and memory loss that are usually temporary.
Malnutrition that occurs when the body does not receive enough food.
Malnutrition results in progressive weight loss. It is common in older people, especially those with Alzheimer’s disease. Depending on whether the person is at home (10%), in an institution (30%), or in the hospital (70%), its prevalence differs.
A person suffering from undernutrition may be deficient in vitamins, minerals, and other essential substances that the body needs to function.
Malnutrition can lead to:
short-term and long-term health problems
slow recovery from injury and illness
a higher risk of infection
difficulty concentrating at work or school
Certain deficiencies can trigger specific health problems.
For example a lack of vitamin C can lead to scurvy. Although rare in developed countries, it can develop if a person does not eat a varied diet with plenty of fresh fruits and vegetables.
Older people who drink heavily and people with certain mental health conditions may be particularly at risk. Undernutrition is particularly common in people over 60 years of age. Weight loss in this category approximately doubles the risk of dying.
Malnutrition symptoms
Some signs and symptoms of malnutrition include:
a lack of appetite or interest in food or drink
tiredness and irritability
an inability to concentrate
always be cold
the Depression
loss of fat, muscle mass, and body tissue
a higher risk of getting sick and taking longer to heal
longer healing time
a higher risk of complications after surgery
Eventually, a person may also experience difficulty breathing and heart failure.
The causes
Undernutrition can occur for a variety of reasons.
Low food intake
Some people are undernourished because there is not enough food available or because they have difficulty eating or absorbing vitamins and minerals.
This can happen as a result of:
cancer
liver disease
disorders that cause nausea or make it difficult to eat or swallow
taking medications that make it difficult to eat – for example due to nausea
Mental health problems
Undernutrition or malnutrition can affect people with:
depression
dementia
schizophrenia
anorexia nervosa
Social and mobility issues
Factors that can affect a person’s eating habits and potentially lead to undernutrition include:
being unable to leave the house or go to a store to buy food
find it physically difficult to prepare meals
living alone, which can affect a person’s motivation to cook and eat
have limited cooking skills
not having enough money to buy food
Digestive disorders
If the body does not absorb nutrients efficiently, even a healthy diet may not prevent undernutrition.
Here are examples of digestive and gastric conditions that can cause it:
Crohn’s disease
celiac disease
persistent diarrhea, vomiting, or both
Alcohol use disorder
Consuming a lot of alcohol can lead to gastritis or long-term damage to the pancreas. This can make it difficult to digest food, absorb vitamins, and produce hormones that regulate metabolism.
Alcohol also contains calories, so a person may not feel hungry after drinking. She may therefore not be eating enough healthy foods to provide the body with essential nutrients.
Malnutrition and Alzheimer’s disease
Between 20 and 45% of patients with dementia are undernourished and lose weight in the year following the onset of their disease, according to the report entitled “Nutrition and dementia”, from Alzheimer’s Disease International (ADI, February 11, 2014) .
Energy malnutrition results from an imbalance between the body’s intake and needs, leading to tissue loss (including muscle), which has deleterious functional consequences.
In addition, 10% of elderly people at home suffer from undernutrition, and this percentage rises to 30% when they are placed in a retirement home. Finally, this is the case for 70% of hospitalized elderly people.
In people with dementia, malnutrition can be the cause of falls or worsening cognitive impairment.
The Association even suggests that undernutrition is a triggering factor for certain forms of dementia.
The report says that certain measures can be taken to improve the nutrition of patients with dementia. These measures include setting nutritional standards, better monitoring the weight of patients, looking at diet and eating habits regularly, and training the family and professional environment.
This malnutrition may be due to cognitive deficits and loss of autonomy or to an increase in energy expenditure (wandering, hyperactivity).
Protein-energy malnutrition
A disorder characterized by a negative balance of protein and energy, leading to loss of weight and muscle mass. Malnutrition can have several causes:
– Diet that does not meet nutritional needs in protein and energy.
– Poor intestinal absorption.
– Increased nutritional needs following an acute or chronic illness.
– Abnormally large losses caused for example by a nephrotic syndrome or a wound.
It is often observed in elderly people of fragile constitution, living or not in an institution or hospitalized.
Protein-energy malnutrition is retained when, among other things, the elderly person:
– involuntarily loses more than 5 kg.
– Has a body mass index of less than 21 kg/m2.
– Has a Mini Nutritional Assessment test result of less than 17.
The consequences of undernutrition
The consequences are as follows:
weightloss;
appearance of bedsores;
falls and fractures;
lowered immune system;
bacterial infections (urinary, bronchopulmonary);
hospitalization.
Evaluation
It requires:
a weight curve;
an assessment scale such as the Mini Nutritional Assessment or the Mini Nutritional Assessment Short Form.
Some patients affected by advanced Parkinson’s disease may suffer from cognitive disorders and more generally from a specific form of dementia.
There are other neurodegenerative diseases that can cause both motor and cognitive impairment: dementia with Lewy bodies, progressive supranuclear palsy, multiple system atrophy and corticobasal degeneration.
Lewy body dementia
It is characterized by the existence of lesions called Lewy bodies.
Progressive supranuclear palsy
This disease, also called Steele-Richardson-Olszewski disease, usually begins after the age of 40. Its prevalence is 1.4/100,000 versus 100 to 170/100,000. It is characterized by a decline in ocular motor skills (especially vertical gaze), postural instability with frequent falls and akinesia.
There are differences with Parkinson’s disease: – Significant axial stiffness in the neck. – Dysarthria (speech disorder linked to neurological impairment). – Dysphagia (discomfort in swallowing). – Minor tremor. – Significant postural problems. – Motor disorders do not improve after treatment with L-dopa or a dopaminergic agonist. – Cognitive disorders of the frontal type appear during the evolution.
These disorders are caused by damage to the basal ganglia and brainstem, with the presence of neurofibrillary tangles including the abnormal form of tau protein.
Multiple system (or multiple system) atrophy
It is a set of neurodegenerative diseases including: – degeneration of the nigrostriatal pathway, with an extrapyramidal syndrome characterized by rigidity and akinesia. The damaged cerebral structures are the substantia nigra and striatum and involved in motricity are affected. – Shy-Drager syndrome, with dysautonomia (dysfunction of the autonomic nervous system. – Olivo-pontocerebellar atrophy with cerebellar syndrome. The cerebral structures called pons nuclei and the cerebellum are affected.
The occurrence of cognitive disorders can be observed in advanced forms. Levodopa (reference treatment for Parkinson’s disease) only partially responds to the extrapyramidal syndrome.
Corticobasal degeneration
It is caused by damage to the frontal and temporal cortex, as well as damage to the basal ganglia. The neurons are said to be ballooned (ie swollen) and surrounded by glial cells which proliferate (we speak of a phenomenon of gliosis).
Clinically, the disease is characterized by apraxia and extrapyramidal syndrome.
Apraxia often begins in one part of the body, causing the inability to perform elaborate movement, despite good understanding and normal muscle strength.
The extrapyramidal syndrome is asymmetrical, even unilateral and is limited to akinesia and rigidity. However, there may be postural tremor, dystonic disorders usually beginning in the upper limb, myoclonus (rapid, involuntary, low-amplitude muscle contraction) and apraxic disorders.
The cognitive impairment appears during the evolution with behavioral disorders and signs of frontal dementia. Treatment with levodopa (or L-Dopa) has no effect. Myoclonus can be treated with clonazepam (a benzodiazepine).
The signs of dementia – a syndrome whose term appeared at the beginning of the 19th century – are characterized by different disorders:
memory ( these are early disorders);
other higher functions: orientation, attention, judgment, reasoning;
phasic (difficulties reading, speaking, reading, writing or repeating a sentence;
praxis (inability to perform motor tasks despite intact motor skills);
gnostic (lack of recognition of familiar objects despite intact sensory functions);
executive functions (loss of sense of abstraction, planning, initiation and organization of tasks).
These cognitive disorders are generally accompanied by psychological and behavioral signs and symptoms (apathy, depression, agitation, aggressiveness, irritability, wandering, insomnia, delusions, etc.) that can affect activities of daily living.
The symptoms of dementia have two main characteristics:
Symptoms appear in adulthood (mental retardation is not one of them).
The symptoms are in most cases progressive and irreversible (confusions and depressive states of the elderly are not included).
Signs of cognitive impairment in dementia
Cognitive disorders
Examples
Inability to learn recent information and events
• The subject involuntarily makes the same purchase several times during the day. • The subject repeats the same question.
Loss of orientation (especially temporal)
• The subject wanders for several hours in his neighborhood and no longer knows how to get home. • He cannot name today’s date.
Difficulties performing an abstract task
• The subject becomes distraught in front of a tax form because he has difficulty performing simple calculations or recognizing numbers. • Subject cannot plan a subway trip requiring one or more connections.
Difficulties finding words
• The subject compensates for the omission of words by using other words such as “trick, thing, contraption”. • The subject uses phonemic verbal paraphasias (says lion instead of violin). • The subject uses sentences that are difficult to understand.
Misplaced objects
Subject puts dirty clothes in a closet and does not remember where they have been stored.
Difficulties understanding symbols
Subject no longer recognizes a road sign.
Forgetting old facts
The subject forgets the name of a famous person, a birthday.
Poor or impaired judgment
The subject dresses warmly on a very hot summer day, or goes shopping in a dressing gown
Difficulty performing familiar tasks
• The subject has difficulty using household appliances. • Subject has difficulty preparing a meal. He forgets to serve it or to have prepared it.
Is memory the only one affected in dementia?
No, these cognitive disorders are accompanied by changes in mood, behavior and a loss of initiative.
Here are some signs of behavioral dementia:
Asocial behavior For example: the subject is apathetic, sits idle, remains indifferent, has little interest in others, cuts off all contact with friends, abandons leisure activities.
Sadness
emotional lability
Irascibility or even verbal and physical aggression
Suspicion
Fearful behaviors
Social disinhibition
Appearance of excessive familiarity
Noisy behaviors
Euphoria, boundless energy
Episodes of depression and anxiety (the subject becomes aware of his cognitive disorders)
Insomnia
Paranoia
Hallucinations visual, auditory (rare)
Slower movement speed
Signs of dementia that affect daily life
Difficulty driving
Wandering
Forgetting to serve a dish cooked in the oven
Negligence (housework, toilets, etc.) or carelessness
Difficulties managing expenses
Professional errors
Difficulties making purchases
Why does the subject or his entourage ask to be consulted?
At an early stage, it is usually for memory disorders (appearing gradually) that the subject or most often a member of his or her entourage asks to be consulted (in 75% of cases, memory disorders presage dementia of the Alzheimer type ). Studies have shown that, in 30% to 50% of cases, the cognitive deficit is ignored by the person concerned.
Rarer are dementias of the Alzheimer type beginning with behavioral disorders. In the case of disorders that are already visible and seem to be getting worse, the request comes from the family and medical environment. It is then a question of behavioral disorders whose appearance or aggravation provoke a crisis in the family care.
What are the different stages during the consultation?
Whether or not the doctor makes a diagnosis following:
An anamnesis which is a series of information provided by the subject (eg medical history) and confirmed if necessary by those around him. The doctor assesses the subject’s functional abilities (eg ability to carry out physical activities of daily living).
Basic exams.
A clinical physical examination which assesses in particular the mental faculties of the patient, in particular with the mini-mental state examination, which is the test used.
If a diagnosis of dementia is made, the next step is to determine the underlying cause.
The causes may be reversible (depression, delirium, ‘toxic’ side effects of medication, infections, etc.) or irreversible (Alzheimer’s type dementia, vascular dementia, frontotemporal dementia, Lewy body dementia, dementia associated with Parkinson’s disease, etc.).
Alzheimer’s disease is the most common cause of dementia (about 60% of dementia cases).
In summary
Cognitive disorders + emotional and behavioral disorders + disturbances in daily activities:
=> suspected dementia.
=> medical visit.
=> if dementia, search for the reversible or irreversible cause.
Vascular dementia is recognized as multiple infarct dementia resulting from successive strokes.
It was described at the end of the 19th century by doctors Binswanger and Alzheimer.
Vascular dementia includes heterogeneous categories of vascular diseases, excluding those caused by asphyxia, respiratory failure or carbon monoxide poisoning.
It varies depending on the location and type of lesions associated with it. In nearly 70% of cases, these lesions affect the small vessels and the white matter in the regions below the cortex (eg the amygdala).
Most studies indicate that vascular dementia is the second leading cause of dementia after Alzheimer’s disease, accounting for between 10 out of 20% of cases.
The prevalence of the disease varies from 1.2 to 4.2% in people aged 65 and over.
These figures should be taken with caution because unlike Alzheimer’s disease, there is no consensual definition and valid diagnostic criteria for vascular dementia. In addition, brain imaging is generally not performed in population studies.
The differential diagnosis between Alzheimer’s disease and vascular dementia is sometimes difficult because, on the one hand, the latter is not always associated with a vascular event and, on the other hand, its clinical evolution is gradual as in Alzheimer’s disease.
The causes of vascular dementia
There are several forms of lesions that cause the different forms of vascular dementia. These diseases are divided according to the regions of the brain affected, their frequency, and the size of the arteries and vessels affected. There is no official classification of vascular dementias, but they can be classified as follows, inspired by the classification proposed by the clinician Roman.
Dementia caused by multiple and extensive cerebral infarctions (or strokes), affecting cortical and subcortical regions that play a role in cognitive functions. These infarctions are often accompanied by mini-lesions damaging the white matter. Although this form reflects the classic view of vascular dementia, it is not the most common.
Clinical signs: focal neurological signs, cognitive disorders such as aphasia, apraxia, agnosia.
Its evolutionary course describes either a sudden onset and a stepwise worsening (one-third of cases), or an insidious onset and gradual evolution (one-third of cases).
2. Dementia caused by single lacuna-sized brain infarctions affecting a specific cortical and subcortical region that plays an important functional role. Cortical regions affected are the medial temporal lobe, angular and cingulate gyrus, while subcortical regions affected are the thalamus, caudate nucleus, internal capsule and anterior cerebral artery. These infarcts generally affect both hemispheres.
3. Dementia caused by damage to small vessels (also called subcortical ischemic vascular dementia). These small vessels are either obstructed by atherosclerosis leading to the formation of several gaps, or narrowed (phenomenon of stenosis) leading to partial infarctions of the white matter . This dementia affects subcortical regions (as seen in Binswanger’s disease, rare CADASIL, multiple lacunae), or cortical and subcortical regions (arteriolosclerotic and hypertensive angiopathy, amyloid angiopathy). This form of dementia presents with mini-lesions or multiple white matter lacunae, located particularly in the frontal regions.
Clinical signs: psychomotor and balance disorders, urinary incontinence, cognitive disorders (executive functions and to a lesser extent memory) and behavior (mood). Balance disorders worsen as the disease progresses. Patients become increasingly apathetic, exhibit rapid and significant changes in mood (emotional lability), loss of attention, perseverations (stereotypical behavior of repeating the same word, performing the same movement, in response to various questions or tasks requested).
4. Dementia caused by hypoperfusion:
• Diffuse anoxic encephalopathy (anoxic: decrease in the amount of oxygen). • Incomplete white matter infarction.
5. Hemorrhagic dementia, caused by subdural hematoma (hematoma of the meningeal spaces, between the arachnoid and the dura mater), subarachnoid hemorrhage, or venous thrombosis. MRI has identified chronic hemorrhagic lesions characterized by the presence of hemosiderin deposits (iron deposits impregnating the tissues).
Lacunae affecting the thalamus (arrow), cerebral region located below the motor regions of the basal ganglia.
Diagnostic criteria
There are at least eight diagnostic criteria for vascular dementia, reflecting the lack of consensus among the medical community. The main ones are: Hachinski ischemic score, DSM-IV, NINDS-AIREN criteria, ICD 10, ADDTC criteria (State of California Alzheimer’s Disease Diagnostic and Treatment Center).
NINCDS–AIREN Criteria
These criteria divide the patient into three stages: probable, possible and definite vascular dementia. The three criteria for probable vascular dementia:
Presence of dementia characterized by impairment of episodic memory and at least two other cognitive domains: orientation, attention, language, visual and spatial abilities, executive functions, motor control and praxis. They are significant enough to interfere with activities of daily living. Exclusion criteria: impaired consciousness, confusion, psychotic symptoms, severe aphasia, major sensorimotor disorder preventing neuropsychological assessment, other brain diseases (such as Alzheimer’s disease).
Presence of cerebrovascular disease defined by focal neurological signs (hemiparesis, central facial paralysis, Babinski’s sign, sensory deficit, hemianopsia, dysarthria on neurological examination, and the presence of cerebrovascular disease demonstrated by brain imaging.
A relationship between dementia and cerebrovascular disease manifested by the presence of at least one of the following three points:
onset of dementia within 3 months of stroke
sudden deterioration of cognitive functions;
a fluctuating or stair-stepping course of cognitive impairment;
Elements supporting the diagnosis of vascular dementia:
presence of an early gait disorder (walking with small steps);
a history of instability or frequent unprovoked falls;
urinary disorders unexplained by a urological condition;
pseudobulbar palsy;
personality or mood changes, abulia, depression, emotional lability, psychomotor retardation and executive function abnormalities.
The diagnosis of vascular dementia is questioned if the progressive deterioration of cognitive functions is not accompanied by vascular lesions (validated by scanner or MRI) or neurological signs.
The criteria for possible vascular dementia are:
presence of dementia and neurological signs when no neuroimaging study is available or;
no clear temporal relationship between dementia and stroke or;
insidious onset and variable fluctuating course of cognitive deficits.
The criteria for definite vascular dementia are:
a clinical history of probable vascular dementia;
anatomical evidence of cerebrovascular disease (e.g. after autopsy);
absence of neurofibrillary tangles and abnormally high amyloid plaques for age;
the absence of other clinical or pathological signs capable of causing dementia.
Magnetic resonance imaging of a brain of a person with vascular dementia. In the region of the frontal lobe (arrow), a decrease in cerebral blood flow significant of a severe lesion is observed. This decrease is characterized by a yellow color, while the red color reflects a normal flow. The lesion is characteristic of neuronal death leading to a decrease in oxygen consumption by the neurons.
Brain imaging techniques
The different cerebral imaging techniques make it possible to determine the presence of significant anomalies responsible for the different types of vascular dementia. They complete the diagnostic criteria.
Forms of brain imaging are:
Magnetic resonance imaging, the most widely used method to assess cerebrovascular pathology.
Functional magnetic resonance imaging. It assesses how the functions of different brain regions are reorganized following vascular dementia.
Positron emission tomography (PET) imaging. It is a technique that measures the metabolic activity of brain regions by injecting the radioactive tracer called 18-fluorodeoxy-D-glucose. In vascular dementia, decreased metabolism is seen in the association cortex (as in Alzheimer’s disease), primary cortices, basal ganglia, thalamus, and cerebellum.
Single photon emission tomography (SPECT). Unlike PET, SPECT only detects a single photon (while PET detects two), which decreases the spatial resolution of the images. However, it is a much more accessible method, because on the one hand the radiotracers are more available (they do not require emitting positrons) and on the other hand the imaging system is simpler.
Despite the usefulness of these techniques, functional neuroimaging cannot distinguish the lesions associated with Alzheimer’s disease from those observed in vascular dementia.
Blood tests
Doctors may need to order lab tests to check for health indicators that aren’t apparent in a person’s recent medical history. This may include tests to check their cholesterol or blood sugar levels.
They may also order additional tests to help rule out other issues that may be causing similar symptoms, such as vitamin deficiencies, anemia, and thyroid disorders.
The signs and symptoms
Cognitive functions
Vascular dementia is characterized by:
early impairment of executive functions (planning, abstract thoughts),
attention deficit, decreased verbal fluency (semantic memory disorder) and
deterioration of visual-spatial functions.
These 3 types of cognitive disorders are more marked than in Alzheimer’s disease.
On the other hand, episodic memory is less affected in vascular dementia than in Alzheimer’s disease.
There is a correlation between the location of brain damage and the type of cognitive impairment patients suffer from.
With regard to vascular accidents of small vessels, characterized by lesional damage limited to the subcortical regions, cognitive deficits are quite frequently limited to impaired executive functions (flexibility, inhibition, working memory). Memory damage, characterized by a deficit in retrieving a memory, makes it possible to differentiate these disorders from those observed in Alzheimer’s disease.
With regard to vascular accidents of the large vessels (lesional damage affecting both the cortical and subcortical regions), establishing a differential diagnosis proves to be much more difficult. In general, episodic memory (measured by the word recall test) is better preserved in vascular dementia than in Alzheimer’s disease. Degradation of working memory (characterized for example by the ability to repeat a series of numbers) is also very common in this type of lesion.
Some clinicians suggest removing the notion of memory decline as a diagnostic criterion.
Functional autonomy
Functional decline in basic activities of daily living appears to be identical in vascular dementia and Alzheimer’s disease, whereas decline in instrumental activities of daily living (eg managing money) appears slower in vascular dementia.
Behaviour
Behavioral disorders are generally similar to those observed in Alzheimer’s disease. Depressive symptoms, emotional behavioral disturbances, and apathy appear to be more common in vascular dementia than in Alzheimer’s disease.
Risk factors for vascular dementia
Risk factors for vascular dementia can include smoking, obesity, and high blood pressure.
The risk of vascular dementia tends to increase as a person ages. The National Heart, Lung, and Blood Institute states that the disease affects nearly a third of people over the age of 70.
Additionally, a number of other factors and conditions can increase the risk of damaged blood vessels and vascular dementia, including:
smoking
obesity
abnormal heart rhythms
high cholesterol
high blood pressure
atherosclerosis
diabetes
a history of heart attack or stroke
Evaluation of vascular dementia
Cognitive functions
The Alzheimer’s Disease Assessment Scale (ADAS-cog), a scale used in Alzheimer’s disease, explores numerous functions (memory, comprehension, temporal-spatial orientation and spontaneous language) altered in vascular dementia. The Trail Making B (tracing test) or the EXIT-25 are used in addition to assess executive functions.
Functional autonomy
Functional decline in basic activities of daily living appears to be identical in vascular dementia and Alzheimer’s disease, whereas decline in instrumental activities of daily living appears to be slower in vascular dementia.
The Disability Assessment in Dementia Scale (DAD) and the Interview for Deterioration in Daily Living Activities in Dementia (IDDD) are functional scales taking into account the consequences of executive function disorders in dementia. These scales make it possible to determine whether the functional incapacity originates from a cognitive deficit (for example difficulty handling money) or a motor deficit (difficulty walking).
Behaviour
The Neuropsychiatric Inventory is, together with the Behave-AD, an appropriate rating scale.
Vascular dementia and Alzheimer’s disease: the differences
There are many differences between vascular dementia and Alzheimer’s disease: prevalence, causes, clinical signs.
Prevalence
Alzheimer ‘s disease is by far the most common type of dementia. It accounts for about two-thirds of dementia cases.
It is estimated that vascular dementia accounts for 10% to 20% of dementia cases.
About 50% of older people with dementia (especially Alzheimer’s type) show signs of vascular dementia. We then speak of mixed dementia if the vascular dementia is associated with dementia of the Alzheimer type.
The causes
Vascular dementia is often caused by a specific acute event, such as a stroke or a transient ischemic attack in which blood flow to the brain has been interrupted. It can also develop more gradually over time as a result of slow blood flow.
The causes of Alzheimer’s disease are not understood, although it is known to be characterized by a buildup of proteins in the brain called amyloid and tau. There seem to be many components, such as genetics, lifestyle, and other environmental factors.
Diagnostic criteria
Alzheimer’s disease
Vascular dementia
1. Presence of dementia 2. Onset between 40 and 90 years of age 3. Deficits in at least 2 cognitive domains 4. Progression of deficits lasting longer than 6 months 5. Unimpaired state of consciousness 6. No other diagnosis made .
1. Presence of dementia 2a. Focal neurological signs 2b. Vascular lesions observed by cerebral imaging 3. Association of 1 and 2 with either: – the existence in the previous 3 months of a cerebrovascular accident or; – sudden cognitive deterioration.
Clinical profiles
The differences between vascular dementia and Alzheimer’s disease also concern the clinical signs.
In the case of vascular dementia: cognitive abilities often seem to decrease sharply in relation to an event such as a stroke or transient ischemic attack (TIA), then remain stable for a period of time.
In the case of Alzheimer’s disease, cognitive functions gradually decline over time. There are usually no sudden, large changes from one day to the next.
Alzheimer’s disease
Vascular dementia
Attention intact
Attention intact
Impaired short and long term memory, amnesia
Failing short-term memory , difficulty in retrieving information. Long-term memory is normally intact.
Poor speech
Poor language
Impaired visual and spatial function
Impaired visual and spatial function
Absence of localized lesions
Presence of localized lesions
Personality change with predominant apathy
Psychosis and agitation in the late phase of the disease
Motor disorders appear only in the severe stage of the disease
Neurological disturbances may be subtle (eg, decreased arm swing when patient is asked to walk on heels or tiptoes). Other neurological disorders are dysarthria, parkinsonism, incontinence and a change in gait.
Poor speech, loss of meaning of words
Poor language, loss of meaning of words
Impaired executive functions
Faulty executive functions
Predominant apathy followed by a psychotic state and agitation in the late phase of the disease
Predominant apathy rarely accompanied by a psychotic state
Absence of localized lesions
Presence of localized lesions
Treatments
There is currently no cure for vascular dementia because there is no way to reverse brain damage. However, it may be possible to slow or sometimes stop the progression of the disease by controlling certain risk factors, for example.
Antihypertensives
Antihypertensives are recommended in hypertensive individuals to reduce the risk of cardiovascular disease. However, there is no consensus regarding the effectiveness of these drugs in reducing the risk of dementia. A study published in 2013 reports this fact, but points out that calcium channel blockers (e.g. lercanidipine, nitrendipine) seem more effective. Some clinicians point out that lowering blood pressure can have deleterious effects in people with cerebrovascular disease. Further studies are needed to determine optimal blood pressure in individuals at risk for vascular dementia.
Antidiabetics
Blood sugar management is recommended in the prevention of diabetes-related complications. The studies that have analyzed the association between diabetes and dementia are not of good enough quality to draw a conclusion.
Statins
Taking statices reduces the risk of dementia in people with high cholesterol. However, if we look at the different forms of dementia, there is no association between taking statins and the risk of vascular dementia.
Antiplatelets
To date, there is no evidence that regular aspirin consumption reduces the risk of developing vascular dementia and slows its progression.
The results of a phase III clinical trial have shown that the combination of anticoagulant drugs (clopidogrel (Plavix) and aspirin) – decreases the risk of recurrence by about a third in patients who have suffered a transient ischemic attack . This decrease is compared to the group of patients who received only aspirin. 8.2% of patients taking both drugs relapsed within three months compared to 11.7% in those taking only aspirin (Source: Clopidogrel with Aspirin in Acute Minor Stroke or Transient Ischemic Attack. New England Journal of Medicine, 2013).
Vitamin B
B vitamins are prescribed to lower blood homocysteine, new highs of which are a cardiovascular risk factor. Several studies have shown the effectiveness of a combination of vitamins B2, B6 and B12 in elderly people suffering from vascular diseases. However, although homocysteine levels were reduced, this treatment was not accompanied by an improvement in cognition.
Lifestyle
It is recognized that the adoption of a healthier lifestyle (stopping smoking, moderate alcohol consumption, physical activity and healthy eating) is associated with better cognitive performance towards old age. Observational studies indicate that intellectual activity (eg bridge) is associated with a reduced risk of mixed and vascular dementia, as well as cognitive impairment of vascular origin.
In addition, such a reduction in risk is observed in those who practice physical activity frequently, compared to inactive people.
Acetylcholinesterase inhibitors
Lack of acetylcholine – the memory neurotransmitter – in the brain is not only seen in Alzheimer’s disease, but also in vascular dementia.
The three acetylcholinesterase inhibitors, aimed at increasing the level of this neurotransmitter in the brain, are also prescribed in the treatment of vascular dementia.
Calcium channel blockers
A meta-analysis concludes that nimodipine (90 mg/day) improves some aspects of cognition, but has no positive effects on activities of daily living. Clinical studies over longer periods (one to two years) are needed to confirm these results. No beneficial effects have been reported with nicardipine and cyclandelate.
Clinical case
A 75-year-old patient is undergoing abdominal surgery. Following this operation, she was again hospitalized for incoherent speech and occasional hallucinations. He was diagnosed with postoperative confusion, cognitive impairment (his mini-mental state exam score was 16/30), and mood disorders.
The doctor prescribed him an antidepressant and an antipsychotic. She then returned to her nursing home. A year later, the patient presented with Parkinsonian-like symptoms (tremor, rigidity) which, together with a cognitive deficit, suggested dementia with Lewy bodies. The doctor prescribed Aricept (a drug used in the treatment of Alzheimer’s disease) and piripedil.
Four years later, the patient entered a long-term care center because she frequently fell due to severe limb rigidity and psychomotor retardation. The treatment with the neuroleptic (known to cause motor disorders) is then stopped. His cognitive performance stabilized with an MMSE score identical to that obtained four years previously. However, she suffers from temporal disorientation, moderate executive function disorders, difficulty memorizing information and retrieving it.
The medical staff suggested the existence of subcortical frontal dementia. However, the neuroimaging examination (magnetic resonance imaging) reveals the presence of ischemic-type vascular lesions as well as diffuse leucoaraiosis.
Diagnosis of this clinical case: the patient probably suffers from vascular dementia.
1 Piripédil (trade name: Trivastal®, France): medicinal product used in particular in the adjunctive treatment of chronic pathological cognitive and neurosensory deficit in the elderly (excluding Alzheimer’s disease and other dementias).
Frontal subcortical dementia is a form of dementia characterized by attention disorders, slowed cognitive performance, severe dysexecutive syndrome, decreased verbal fluency and elaborate language, constructive apraxia (loss of ability to executing gestures or using objects, without any paralysis).
Practical case of frontal subcortical dementia
Mr. A. was diagnosed with Alzheimer’s disease upon entering a long-term care facility with a Mini-Mental State Examination (MMSE) score of 16/30.
His GMP is 850, which means he is very addictive. GMP stands for Weighted Average GIR. It corresponds to the average level of dependency of residents of a long-term care facility in France. The higher the GMP, the greater the level of resident dependency. Generally speaking, a GMP greater than 300 corresponds to a medical establishment. An establishment with a GMP greater than 700 corresponds to a geriatric hospital.
Long-term care takes care of elderly patients, the vast majority of whom have memory problems which are often the reason for their placement.
The medical staff suspected that the diagnosis made before the patient arrived at the facility was incorrect because his cognitive state was not deteriorating.
He continued to memorize names well, to orient himself well in space and to remember past events concerning him (autobiographical memory). In addition, he obtained a score of 20/30 on the MMSE five years after entering the establishment, an increase of 4 points.
A neuropsychometric assessment and a neuroimaging examination (magnetic resonance imaging) indicate that the pathology from which Mr. A. suffers is not characteristic of Alzheimer’s disease.
Neuropsychometric assessment
The patient’s cognitive performance declines only slightly, with mild time orientation disorder , episodic memory encoding and retrieval disorder, dysexecutive syndrome, mild selective attention deficit, mild apraxia ideomotor, as well as difficulties in performing mental calculations.
Neuroimaging examination: the diagnosis of subcortical frontal dementia is made
Presence of vascular lesions and atrophy of the hippocampus.
Presence of a decrease in volume (atrophy) in the hippocampus in a patient with subcortical frontal dementia.
The diagnosis of Alzheimer’s disease remains therefore uncertain.
Symptoms are those seen in subcortical frontal dementia.
The patient continues to receive an acetylcholinesterase inhibitor type medicine (e.g. Aricept) and a platelet aggregation inhibitor.
