Cognitive impairment and dementia are the clinical expression of three large groups of processes that involve a compromise of the cerebral cortex or its connections and include brain aging, brain diseases and systemic diseases. ;micas that affect the brain. Our clinic's universe of work is the study and care of all diseases that compromise cognitive functions, but places particular emphasis on the approach to degenerative dementia.
For this reason, in the last 10 years, experience has been accumulated that includes the evaluation of more than 600 patients with dementia of this type, where Alzheimer's disease, the dementia associated with parkinsonism, tauopathy and other variables of fronto-temporal dementia.
In 1990 there was no alternative for pharmacological treatment or surgical treatment for Alzheimer's disease, which forced the creation and development of a comprehensive dementia care program, which began in 1991 with the creation of a service located in the Basic Area, where more than 100 patients with Alzheimer's disease were admitted and a cognitive training and behavioral rehabilitation program was developed in more of 40 patients. It was verified This type of multidisciplinary approach benefited patients by increasing their functional capacity, improving some particular processes such as attention and memory, and reducing the intensity of the cognitive deficit by up to 30%.
Towards 1993 this hypothesis, supported by Stanley and Cols, gained popularity. Evidence was demonstrated in biomodels due to lesion of the fimbria fornix and excitotoxic lesion of the basal nucleus of Meyner in which training through learning techniques promoted an increase in synaptic activities in rodents. optics in cortical areas and in the denervated hippocampus.
In 1994, studies were published that demonstrated the lower incidence of the disease in people with a higher intellectual level or with a higher degree of education, experiences that were reproduced later that year and in 1995 by Rosemberg and Cols, who reestablished a negative risk factor for developing the disease in university professionals practicing their work for more than 30 years, without differences in sex. A bibliographic review of the state of knowledge on the subject resulted in in the acquisition of information that allowed us to speculate that an option to oppose the cognitive deterioration induced by these diseases could be based on the stimulation of the brain reserve.
With the advent of new techniques for functional exploration of higher nervous activity, including neurophysiological and psychophysiological studies, positron emission tomography and functional magnetic resonance imaging, demonstrated that the modifications observed in the range of decline of cognitive functions in Alzheimer's patients when comparing intellectuals with manual workers are related to a greater preservation of the inhibitory mechanisms of the brain and a greater facilitation for the activation of temporoparietal cortical areas in the former. These findings allow us to assume that prolonged mental training can stimulate neuroplastic mechanisms linked to learning and/or recovery of functions (use-dependent plasticity).
More recent studies in models of chemical lesion of the basal nucleus of Meynert and a transgenic model of Alzheimer's, as well as As a study of human brains obtained from patients with Alzheimer's disease and healthy subjects have shown that synaptic loss and the consequent retrograde axonal alteration are the first changes observed anatomopathologically in the disease and that they occur long before appearing of neuronal population and/or abnormal accumulation of proteins (senile plaques with amyloma deposits, fibrillar rings, Irano bodies, etc.).
It has also been shown that this synaptic loss directly correlates with the degree of cognitive deterioration in subjects affected by Alzheimer's disease, which makes it clear that one of the main etiopathogenic events of The genesis of age-related cognitive decline is synaptic lossa, more than the neuronal loss itself.
Two articles have recently been published that demonstrate that in the brain of patients with Alzheimer's there is evidence of neuroplastic changes and the expression of molecular mechanisms linked to neuronal plasticity, specifically an increase in synaptogenesis. reactive nesis (increased concentration of cinapophysin, synaptobremin and other synaptic contact proteins), all these elements argue that synaptic loss is the cause of a large part of cognitive disorders and that it spontaneously occurs. There are clearly compensatory increases in neuroplastic mechanisms that, for reasons that are not very clear, abort or are insufficient in the advanced stages of the disease. This, together with the fact that the greater the brain reserve, or in other words, the greater the synaptic density and efficiency, the slower the speed of progression in sick subjects, so the stimulation of this brain reserve in the early stages of the disease and complaints of other dementias could be beneficial in the evolutionary periods of the disease. Although this is not Our initial results and 10 years of experience have clearly demonstrated that this is possible.
With the approval of the Federal Drug Administration in 1995 of the THA, the the history and prognosis of the disease. In fact, for the first time there is a therapeutic agent capable of reversing the cognitive deficit and memory loss of these patients.
Since then, new drugs based on blocking the degradation of acetylcholone through the inhibition of the acetylcholinesterase enzyme or cholinergic receptor agonists (nicotinic or muscari) have been introduced. unique that together improve the synaptic concentration of the neurotransmitter acetylcholine, have demonstrated effectiveness in the treatment of these patients in the initial mild or moderate stages. moderate impact of the disease, including long-term effects in delaying the institutionalization of patients linked to disability and dependency, by studying why Of these phenomena it has been suggested that both acetyl inhibitors and nicotinic agonists have a primary effect of stimulating the postsynaptic neuron and have a more presynaptic effect on neurotransmitter reception and energy balance of said synaptic terminal.
In this way, chemical stimulation now repeats the fact that synaptic preservation is a strategic point in the regression of symptoms and in the protection of the neuron against degeneration.
On the other hand, the fact that there is a specific treatment that stops cognitive deterioration and increases the functional capacity of the individual should modify the conception of patient care since it is now possible to extend life expectancy. maintaining quality of life, independence and self-worth for longer than before.
The hypothetical double capacity of cognitive training to train the brain reserve through neuroplastic mechanisms and to act cynergically with drugs to improve the functional capacity of these patients, allows us to assume that its rational use with a Appropriate design could improve the cognitive and functional capacity of patients with Alzheimer's disease more than the isolated use of drugs. Simultaneously, the cognitive rehabilitation activity can avoid, at least temporarily, the sensory and social deprivation that these patients usually suffer in relation to the social, family and emotional isolation to which they are subjected by virtue of the dogma of the irremediable cognitive deterioration.
Based on the evidence and hypotheses previously raised, we have decided to propose a revised and improved cognitive training PROGRAM for the treatment of light and moderate stages of dementia.
Specialized training of the main cognitive domains, especially memory and attention, can reduce the intensity of cognitive deterioration, the speed of the progression of said deterioration and favorably enhance the effect of acetylcholinesterase inhibitors.
The Neurological Restoration or Rehabilitation program includes a week of evaluation duringin which a specialized clinical evaluation of the dementia syndrome is carried out, a general clinical evaluation of the patient's health status, a quantification by international scales to measure neurological condition, ability cognitive ability, functional capacity and quality of life, neurophysiological studies specialized in the exploration of higher nervous activity, structural and functional imaging studies using Computed Axial Tomography techniques, Nuclear Magnetic Resonance, Emission. n Simple photonics and biochemical and molecular studies.
This evaluation is complemented by a specialized neuropsychological evaluation and the application of international instruments to determine the degree of disability or objectify the neurological defect to be modified.
The information obtained by this comprehensive evaluation is analyzed collectively by specialists from various disciplines and a unique program is designed in stages, with specific objectives that are set according to the patient's possibilities and the previously accumulated experience.
The Neurological Restoration or Rehabilitation program is executed by therapeutic cycles of 4 weeks (28 days) that include hygienic-dietary measures to improve general condition, and pharmacological adjustment. logical to control as much as possible the manifestations of loss of memory and attention and improve the trophic and nutritional support of the nervous system. At the same time, sleep disorders, appetite disorders, blood pressure disorders and other autonomic or mental alterations that usually coexist with the progression of the disease are controlled.
A comprehensive rehabilitation program is also developed that includes cognitive training using an automated system designed at the CNC and adapted at the CIREN for such purposes, complemented by physical conditioning techniques. and functional and behavioral adjustment techniques.
It has been determined in an open clinical trial that the effectiveness of the comprehensive care program is 83% and the ranges of improvement obtained for cognitive capacity are approximately 7% and for functional capacity of approximately 33%. In more than 200 patients treated to date, no complications, accidents or adverse events that compromise life or leave sequelae have been observed. The rate of adverse effects or transient complications is less than 10%.
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