DEMENTIA
I Introduction / General
Among the neurological and psychiatric clinical problems related to brain aging, Alzheimer’s disease occupies a central position. Of all neurodegenerative diseases, it is the most common form of senile dementia; it is primarily characterized by a deterioration in memory abilities, secondarily associated with a decline in other cognitive domains, responsible for a decrease in the ability to be independent in daily life, with a reduction in life expectancy.
II Epidemiology:
Dementia affects 5% of those over 65 and 20% of those over 80.
Early-onset forms occur before age 65.
Alzheimer’s disease accounts for half of all dementias, followed by vascular dementias which account for a third.
The disorder is slightly more common in women than in men.
- Risk factors:
– The main risk factor is age.
– Other risk factors: Hypertension, diabetes, arteriosclerosis and smoking double or triple the risk of suffering from Alzheimer’s disease.
– Low level of education / Head injuries / Certain illnesses “Down syndrome, trisomy 21, arthritis”
– Lifestyle “diet, exercise, consumption of alcohol, coffee or tobacco”
– Exposure to substances in the environment or in the context of professional activities “aluminium, lead, etc.”
– Compared to the general population, first-degree biological relatives of people with Alzheimer’s disease are at greater risk of having the same disorder.
III Pathophysiology of Alzheimer’s disease:
The 2 pathological characteristics of Alzheimer’s disease are:
Extracellular deposits of beta-amyloid (in senile plaques)
Intracellular neurofibrillary tangles (paired helical filaments)
Deposits and neurofibrillary tangles of beta-amyloid cause loss of synapses and neurons, resulting in massive atrophy of affected areas of the brain, usually beginning in the mesial temporal lobe.
The mechanism by which beta-amyloid and neurofibrillary tangles cause such damage is not fully understood.
There are several hypotheses:
1. Viral hypothesis: Hypothesis raised by analogy with Creutzfeldt-Jacob disease, but no infectious agent has been isolated.
2. Autoimmune hypothesis: presence of autoimmune antibodies directed against prolactin cells; appears for some to present the reliable serum marker because their presence has been found in 90% of cases.
3. Toxic hypothesis: intra-neuronal concentration of Aluminum; On the other hand, Zinc deficits have been observed.
4. Vascular and metabolic hypothesis: AD is accompanied by hypometabolism in the temporo-parietal cortex, and a significant decrease in perfusion flow in these regions.
5. Genetic hypothesis: abnormal expression of a gene (located in chromosomes 19 and 21) coding for beta-amyloid protein, which accumulates in the brain.
DEMENTIA
IV Clinical study of Alzheimer’s disease:
Alzheimer’s disease has a slow onset and progressive development. Progression takes an average of ten years.
A. Early phase : The signs of the disease develop gradually and are characterized above all by cognitive deterioration that follows the progression of histological lesions.
The patient is more or less aware of his disorders, hides his intellectual deterioration behind automatic behaviors.
1. Memory disorders: Constant, necessary for diagnosis and indicative of the disease in more than 75% of cases. These are episodic memory disorders “ability to form new memories”.
A deficit in delayed recall of a list of words, sentences, or series of objects is the most reliable predictor of AD.
Recent memories fade “fixation amnesia”.
Old facts are better preserved.
2. Character and behavioral disorders: Lack of interest in surroundings and/or work, apragmatism, difficulty adapting to a new situation, irritability, angry outbursts, nocturnal turbulence, running away and wandering, oppositional attitude or suggestibility.
3. Language disorders “Aphasia”: Aphasia appears after memory disorders and is manifested by a lack of words in spontaneous language and in naming, often compensated by boilerplate words and circumlocutions.
4. Depressive syndrome: insidious onset with apathy, despair and sadness, psychomotor retardation, anorexia, insomnia, hypochondriacal complaints, with morning worsening of symptoms.
5. Delusional syndrome: Absurd, mobile and incoherent delusional ideas of persecution, of “financial” harm, or sometimes ideas of grandeur.
6. Confusional syndrome: Abrupt onset with impaired vigilance, temporal-spatial disorientation, dreaminess
B. State phase : this is the typical dementia syndrome
** Presentation with carelessness, unkempt dress, lost face, amimic
** Decreased spontaneous attention and ineffectiveness of voluntary attention, distractibility; the patient is distracted by the surrounding environment; difficulty concentrating and understanding.
** Memory disorders predominate over recent events “anterograde amnesia”: At first the idea is evoked with precision but the word to express it does not come immediately. Proper names, especially recently acquired ones, are the first to be affected. Memories are imprecise, vague and inexact.
The patient no longer remembers where the objects are stored, having gone out to do the shopping, he returns without having bought anything. Periphrases are frequent: he uses vague words instead of naming objects “passwords”.
** Temporo-spatial disorientation : Does not know where he is or where he comes from. The disturbances first concern unfamiliar places “eg: large spaces; hospital, supermarket, city” and then small spaces; the subject ends up getting lost in his own house.
** Judgment disorders : Judgment may be disturbed in its various aspects: its openness “narrowness of points of view”, its flexibility “judgment becomes rigid, unadaptable”, its stability, its reference to a scale of values adapted to the situation.
** Impairment of instrumental and executive functions : The study of instrumental or symbolic functions concerns the perception of the body, the recognition of objects by palpation, sight or hearing, the performance of voluntary gestures and the expression and understanding of language.
- Aphasia: subtle at first (lack of words) to become massive with impoverishment of vocabulary and stereotyped responses going as far as echolalia and perseveration.
- Apraxia: inability to perform symbolic gestures (goal-oriented movements) such as: the military salute, the sign of the cross or usual daily gestures: getting dressed, doing up or undoing buttons, lighting a cigarette.
- Agnosia: Inability to recognize certain objects and shapes,
- Visual agnosia: when presenting objects or images
- Prosopagnosia: disorder of face recognition, an inability to recognize loved ones, sometimes the subject himself no longer recognizes himself in a mirror.
** Personality change : This is either an exacerbation of pre-morbid personality traits or a real personality change with frequent irritability, emotional instability, intolerance to frustration, angry reactions and egocentrism “tendency to relate everything to oneself”. The subject becomes greedy, suspicious, and sometimes expresses verbal obscenity, an invincible stubbornness “a decision once made is stubbornly maintained”.
** Behavioral disorders : The patient neglects himself with poor hygiene, dirty and disheveled clothing. Almost constant nocturnal agitation “in the dark”. Sexual behavior can manifest itself in an unusual way with disinhibition. The acts are stereotyped and repeated tirelessly, reproduced with fixity: stereotypy of scratching, rocking, rotating, etc.
** Alteration of instinctual behavior : insomnia with inversion of the nycthemeral cycle, anorexia, refusal of food or bulimia, sphincter disorders “urinary and/or fecal incontinence”.
**Thought disorders : An impoverishment of thought with slowness of ideation “bradypsychia, the patient does not finish his sentence, loses the thread of his speech, then returns to the same things; resulting in verbal perseveration.
**Delusional syndrome and mood disorders
C. Terminal phase :
- At this stage, the patient needs to be assisted in the basic actions of daily life and placement in an institution is generally necessary. Unable to walk or get up alone, difficulty getting dressed, washing, impossible communication. Progressive decline in cognitive functions: this is the picture of severe dementia. Appearance or worsening of psychological disorders: depression, anxiety, delirium and hallucinations, agitation, episodes of confusion.
Most people with this disease do not die from the disease itself, but rather from a problem caused by their cognitive or neuromotor degeneration or their inability to take care of themselves. Among others:
- Complications following a fall: fracture, serious shock to the head;
- Worsening of a urinary tract infection due to use of a urinary catheter “inserted due to incontinence”.
V Diagnosis:
1. Questioning: must be thorough and precise. Done with those around you; specifies the methods of appearance, development of the disorders, evolution, family aspects, etc.
2. Physical examination: It is “normal” in Alzheimer’s disease. Any somatic neurological sign, such as extra-pyramidal syndrome, myoclonus, epileptic seizures, should lead to the search for other etiologies.
3. Paraclinical examinations: Biological assessment, Brain imaging “scanner and/or MRI”, Microscopic examination: “Anatomo-pathological alterations”, Folstein Mini Mental Test “MMS”
VI SUPPORT
- Pharmacological means
A. Specific treatment of Alzheimer’s disease :
- Acetylcholinesterase inhibitors:
During normal functioning of a cholinergic synapse, the enzyme acetylcholinesterase “AchE” degrades acetylcholine “Ach” in the synaptic cleft. Inhibitors of this enzyme have been developed to reduce this physiological degradation and thus enhance cholinergic synaptic transmission where it is spared.
Donepezil “Aricept” : tab 5 and 10 mg
Dosage: 5 mg/day for 1 month then 10 mg/day Single dose in the evening before bedtime. Dose-dependent effectiveness
- NGF (Nerve Growth Factor) and “GM1” gangliosides are molecules that stimulate the trophic actions of neurons.
- Others: Vit E, ergot derivatives, NSAIDs, estrogen replacement therapy, Ginkgo Biloba.
B. Treatment of neuropsychiatric disorders :
- Atypical antipsychotics: Olanzapine «Zyprexa» 5 – 10 mg/day; Risperidone «Risperdal» 1 mg/day significantly reduce neuropsychiatric symptoms, mainly agitation, aggression, delusions and hallucinations.
- Serotonergic antidepressants: Well tolerated and effective in depression. But also acts on anxiety, irritability, agitation, impulsivity and hostility.
- Mood stabilizers: “carbamazepine” “tegretol”, valproate “Depakine”, Common side effects “drowsiness”. Can act on agitation, impulsivity and hostility.
- Non-pharmacological treatment:
- Psychological support for the patient is essential, encouragement to maintain social, intellectual and physical activities, we must encourage him to write, read, behave, inform him of current events, improve communication.
- Family support is essential: offering home help, childcare services, home help, nursing care.
- Body-based approaches: Stress is one possible cause of agitated behavior in people with Alzheimer’s disease. The awareness of memory loss and the difficulty in communicating that some of them experience often leads to frustration and anxiety. Anti-stress techniques such as massage therapy and therapeutic touch may prove beneficial.
- Cognitive rehabilitation: its aim is, on the one hand, to strengthen residual resources in social and family life and daily life activities, and on the other hand to strengthen self-esteem in order to preserve autonomy and quality of life.
- Speech therapy.
VII PREVENTION
- Currently, there is no strong evidence that there are ways to prevent Alzheimer’s disease . However, some avenues of research are encouraging.
- It is possible to reduce the risk of developing Alzheimer’s disease through medical intervention or efforts on lifestyle habits and certain diseases, such as high blood pressure, diabetes, arteriosclerosis or smoking.
- Hormone replacement therapy in postmenopausal women or taking nonsteroidal anti-inflammatory drugs “such as aspirin and ibuprofen” may offer some protection against Alzheimer’s disease, but this remains to be proven.
- A diet rich in vitamin E or vitamin C can reduce the risk of developing it, especially in smokers.
- Keeping an active mind throughout life helps maintain and grow connections between neurons, which may delay dementia.
- Reduced exposure to aluminum and lead.
DEMENTIA
VIII Conclusion
Dementia is a chronic, global deterioration of cognition, usually irreversible. Diagnosis is clinical; treatment is supportive. Cholinesterase inhibitors can sometimes temporarily improve cognitive status
The worsening loss of autonomy with the progression of the disease will require the intervention of home help. A cautious and reassuring approach is essential and decoding is often necessary to understand what the patient is transmitting to us through his behavior.
DEMENTIA
Wisdom teeth may need to be extracted if they are too small.
Sealing the grooves protects children’s molars from cavities.
Bad breath can be linked to dental or gum problems.
Bad breath can be linked to dental or gum problems.
Dental veneers improve the appearance of stained or damaged teeth.
Regular scaling prevents the build-up of plaque.
Sensitive teeth can be treated with specific toothpastes.
Early consultation helps detect dental problems in time.