The aim of this article is to describe the available measures of preventing post-stroke depression and their efficacy with regard to psychological interventions. The said affective disorder is often poorly diagnosed for a number of reasons. Also the treatment itself turns sometimes to be inappropriate. It is worth highlighting that post-stroke depression affects the process of recovery of the patient, thus its harmful effect is not limited to a mere depressed mood. Studies describing the measures of prophylaxis of depression after stroke are dominated by those assessing the efficiency of pharmacotherapy. Meta-analyses point to a low efficiency of this type of therapeutic effects as well as to the inconsistency of their outcomes. Other methods of prevention efforts include those of psychological nature which should be divided into different categories, such as: psychotherapy, other unstructured interactions (for example: education, emotional and instrumental support, service of multidisciplinary team, physical exercises) or motivational interviewing. The results show that motivational interviewing is the most effective of all methods. Problem-solving therapy appears to be another effective intervention within the prevention of post-stroke depression. Also a short-term psychosocial-behavioral therapy produces good results. There is a definite and urgent need for more research on this subject that would enable the recommendation of an appropriate form of prophylaxis. The majority of the described studies are characterized by a small number of patients. It seems that different psychotherapeutic approaches that place the individual needs of the patient in the first place are worth further research. Those related to the behavioral approach seems to bring hope for greater efficacy.
Aging of the population increases the number of people with dementia. Because of the lack of effective causal treatment, prevention of the conversion to the full-blown dementia becomes a priority. Researchers have focused on the identification of dementia risk factors, especially those which are susceptible to modification. Apart from the prevention of cardiovascular diseases, the most important are education, along with other components of cognitive reserve, and maintaining activity in old age. Of particular relevance is cognitive and social activity, the combination of which may significantly increase the effects of dementia prevention. Actions leading to the delay of the full manifestation of dementia should become widespread and promoted by specialists involved in care over dementia patients. They should become a part of the national programs in which attention to cognitive and social dementia preventive factors should be equal to general health factors. The paper discusses the importance of education, cognitive reserve as well as social and mental activity in delaying the manifestation of dementia clinical symptoms.
For years, predictions concerning the epidemiology of dementia, particularly Alzheimer’s disease, have been sinister. The commonness of dementia at present and prognoses saying that the number of demented patients will triple in the next decades prompts the search for effective treatment methods. Unfortunately, despite long studies, no effective therapy for neurodegenerative syndromes has been developed. Therefore, simultaneously conducted studies aim at establishing effective prevention. Apart from physical and mental activity, diet is another field explored in the preventive investigations. More and more correlations between nutritional status, diet and cognitive functions are observed. The investigations in this area may be divided into three basic fields. First, basic examinations are used to analyse the impact of nutrients on the functioning of the nervous system. Second, there are ongoing observation projects and population-based studies. A long observation of behaviours and nutritional habits in large cohorts as well as rates indicating compliance to given dietary guidelines enable researchers to draw conclusions concerning protective effects of diet. Third, it is attempted to conduct prospective preventive studies (with dietary interventions and recommendations concerning mental and physical activity) as well as clinical trials evaluating the effects of specific diets or impact of some food products (e.g. foods for special medical purposes). The current knowledge suggests that dietary interventions, particularly when combined with physical and mental activity, may be the most advantageous if implemented early enough and observed nearly for the entire life.
Regular physical activity induces a range of adjustment changes, particularly in the circulatory system and metabolism. Numerous publications on single exertion and increased physical activity more and more frequently confirm their positive influence on the shaping of cognitive functions. Anatomic and functional changes, such as increased cerebral blood flow, angiogenesis and neurogenesis as well as increased volume of the grey matter in the frontal and temporal cortices, are the basis of this positive influence. Physical exertion stimulates the production of trophic factors, among which the brain-derived neurotrophic factors and insulin-like growth factors are crucial for cognitive processes, synaptic plasticity as well as for the improvement of the neurogenesis signalling pathways and vascular functioning. Physical activity induces enhanced expansion of the brain-derived neurotrophic factor. This has a positive influence on energy processes and activates numerous cerebral energy centres which positively modify the synaptic potential for processing information that is important for developing cognitive functions. Exertion reduces inflammation by decreasing the blood concentration of proinflammatory cytokines that can contribute to the development of neurodegenerative processes. Moreover, it reduces metabolic syndrome risk factors, particularly hypertension and insulin resistance thus decreasing the risk of cognitive dysfunctions, improving brain functioning, delaying the onset and decelerating the development of disorders in neurodegenerative syndromes, including Alzheimer’s and Parkinson’s diseases. Taking these mechanisms into consideration, it seems that physical activity is indispensable for maintaining normal cognitive functions at any age.
Posterior cortical atrophy is a rare form of an early-onset dementia syndrome (usually affecting people below 65 years of age) with predominant deficits in visual perception and visuospatial functions. This form of disease is often considered as atypical manifestation of Alzheimer’s disease, also known as its visual variant. Reading difficulties, face and object recognition problems, topographical disorientation, inability to perceive more than one object at a time and misreaching objects under visual control are frequently observed. These deficits lead to progressive loss of independence in the activities of daily living, that occurs earlier than observed in patients with Alzheimer’s disease. Cognitive dysfunction is caused by a dysfunction of one or two main visual pathways (dorsal – enabling the localization of stimuli, or ventral – enabling stimulus recognition) and subsequent parietal and/or occipital atrophy. Posterior cortical atrophy may be also associated with other, more complex neurological and psychiatric symptoms. In this paper, clinical presentation and diagnostic criteria of posterior cortical atrophy as well as neuropsychological assessment tools useful in the differential diagnosis and management options, both pharmacological and non-pharmacological, are presented.
Disorders of consciousness are among the main consequences of severe brain injury. They are characterised by the disruption of the relationship between the quantitative (arousal, wakefulness) and the qualitative (awareness of the self and environment) aspects of consciousness. This includes conditions where a high level of arousal is not accompanied with retained awareness (and vice versa). An accurate diagnosis of patients with severe brain injuries who present with various forms of disorders of consciousness still poses a real clinical, scientific and ethical challenge. This paper describes those conditions as well as diagnostic criteria and behavioural tools commonly used for their discrimination. The authors discuss brain death, coma, vegetative state, minimally conscious state and locked-in syndrome. Ethical and prognostic issues associated with the diagnosis and treatment of such patients are also discussed. Moreover, a clear classification of disorders of consciousness is proposed, which is intended to eliminate some ambiguities in Polish nomenclature concerning this type of neurological disorders. Behavioural scales are standard clinical tools for bedside assessment of patients with disorders of consciousness. In this paper, we review several behavioural scales, and describe their diagnostic advantages and shortcomings. The JFK Coma Recovery Scale–Revised (CRS-R) appears to present high sensitivity and specificity of diagnosing disorders of consciousness. The use of scales, such as the CRS-R, along with neuroimaging approaches (which have been developing intensively in the recent years) may provide a way to obtain a complete and accurate diagnosis of disorders of consciousness. That is why translation of the CRS-R and its validation in Polish conditions might play an important role in the diagnosis of such patients in our country.
The case of a 43-year-old patient with botulism is described in order to draw attention to a rare disease, but still quite common in Poland, caused by Clostridium botulinum. Botulinum toxin is produced by anaerobic Gram-positive bacteria and considered as one of the strongest poisons. The authors describe a case of foodborne botulism, the oldest and the best understood form of intoxication. A characteristic sequence of clinical symptoms, in combination with a positive history of stale food consumption (particularly pickled meat), makes it possible to diagnose the disease accurately even in an outpatient clinic. The symptoms in the hospitalised patient were typical: symmetric paresis of the cranial nerves followed by flaccid paralysis consequently resulting in respiratory failure. The patient denied the possibility of stale food consumption, none of his entourage fell sick, which resulted in extensive differential diagnosis thus delaying the final recognition. Treatment of botulism is not only based on symptomatic management, but also involves the neutralization of the circulating neurotoxin. The detection of the presence of type B botulinum toxin in the blood after 10 days from poisoning and the administration of an antitoxin resulted in a very good therapeutic effect thus confirming the validity of the selective treatment implemented in the presented case.
Introduction: Encephalitis is the most severe form of neuroborreliosis. The incidence rate is estimated to be 0.1% of those infected with Borrelia burgdorferi. Material and method: The presented case study is based on the medical documentation of the patient. Case study: This report describes the case of a 67-year-old female patient with multilevel degenerative disc disease (C and L–S levels), spinal pain syndrome (L–S level), recurring bilateral sciatic pain for many years, arterial hypertension, with an implanted DDD-R artificial pacemaker, and mixed anxiety-depressive disorder, who was admitted to the Department of Neurology in Biskupiec due to the symptoms suggesting the exacerbation of chronic sciatica. During hospitalization, spinal pain at the Th and L–S levels exacerbated. The patient experienced rib cage, stomach and the pubic symphysis pain, and then she developed psychotic symptoms. In the course of the disease, apart from tension myositis syndrome, neurological examination did not detect neurological deficits, focal symptoms or meningeal signs. Results: When the patient developed symptoms of psychiatric disorders, a lumbar puncture was carried out and encephalomeningitis was diagnosed. Conclusions: The presented case confirms the difficulties inherent in diagnosing neuroborreliosis that can mimic other diseases.