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Encephalopathy caused by manganese compounds used for illicit production of ephedrone (methcathinone) is described. The onset of disease could be observed after some months of regular intravenous use of ephedrone contaminated with manganese. In clinical picture dominate neurological signs and symptoms, mainly extrapyramidal syndromes: parkinsonism, tremor, muscle distonia, pro- and retropulsion. Some other symptoms may be observed: hypophonia or dysarthria, gain disturbances, impairment of precise movement, and micrographia. In cranial NMR often appears bilaterally an increase of an intensity of T1 signal in globus pallidus and in some other brain structures. Elimination of manganese with the use of chelating therapy as well as symptomatic treatment, mainly with the antyparkinsonic drugs, seems to be ineffective.

Cigarette smoking is a major modifiable risk factor for stroke. Smoking dose dependently increases the risk of stroke, especially in patients below 75 years of age. Although smoking cessation is considered as one of the most effective methods of secondary stroke prevention, little is known about nicotine dependence and predictors of smoking cessation after stroke. Identification of such predictors could facilitate the development of anti-smoking interventions in post-stroke patients. Results of previous studies showed that smoking cessation is determined by the interplay of multiple factors, including sociodemographic (gender, age, race, living conditions, employment), clinical (functional status), psychobiological (nicotine dependence, depressed mood) and environmental (smoking household members) factors. Limitations of most studies were relatively small sample sizes and lack of verification of smoking status with a biochemical marker (e.g. expired CO). The aim of this article is to summarize current knowledge about predictors of smoking cessation after stroke.

Introduction: Esthesioneuroblastoma is a malignant tumour arising from the olfactory epithelium located in the upper part of the nasal cavities. Recent clinical and preclinical studies shed more light on etiopathogenesis, diagnosis, and treatment of this rare malignancy., Material and Methods: A systematic review of PubMed/Medline and available Polish literature., Results: Molecular studies indicate basal progenitor cells of the olfactory epithelium as the origin of esthesioneuroblastoma. Tumour symptoms are related to its location and typically include: epistaxis, nasal obstruction, olfactory and ophtalmic disturbances as well as craniofacial pain. Esthesioneuroblastoma should be differentiated from embryonic rhabdomyosarcoma, Ewing's sarcoma, melanoma, lymphoma, and pericytoma. A combination of surgery and radiotherapy seems to be the optimum approach to treatment. More aggressive treatment regimens are promising but require further studies., Conclusions: Esthesioneuroblastoma is a rare malignant tumour arising from the olfactory epithelium. Early diagnosis and interdisciplinary approach to treatment is vital in the management of the tumour.

Background and Purpose: The aim of the work was to investigate the effect of treatment with rivastigmine, one of the inhibitors of acetylcholinesterase (AChE-I) on the regional cerebral perfusion (rCBF) and the cognitive functions of the brain in patients with Alzheimer's Disease (AD) and Vascular Dementia (VaD)., Material and Methods: The investigations of rCBF were carried out using SPECT (Single Photon Emission Computed Tomography). The results given concern investigations of patients carried out at the onset of the investigation, after 12 months, and 24 months of rivastigmine treatment., Results: In patients with AD it was found that treatment with rivastigmine increases rCBF by 5-7% in the temporal areas during the first 12 months. In the frontal areas the increase was by 3-5%. During the next 12 months rCBF with an accuracy of 2% returned to the initial level, with the exception of the motor cortex, where it remained on the level increased by 5-6%. However, the cognitive functions remained constant during the first 12 months of treatment and decreased significantly during the next 12 months. In patients with VaD rCBF increased in all the regions of the brain except for the temporal posterior regions, and remained at an elevated level for the next 12 months. The cognitive functions deteriorated slowly, but to a much lesser degree than in the case of AD., Conclusions: From the investigations carried out it follows that treatment with rivastigmine during 24 months prevents a decrease of rCBF in patients with AD. However, the cognitive functions deteriorate after 24 months.

The Creutzfeldt-Jakob disease (CJD) is rare spongiform encephalopathy. Its main symptoms are rapidly progressing dementia, myoclonic jerks, visual disturbances, ataxia, and pyramidal and extrapyramidal signs. A case of sporadic form of the CJD is reported, with blurred vision as one of the first symptoms. This symptom occurred shortly after vaccination against influenza, and was accompanied by other signs suggesting postvaccinal encephalitis. However, at a later stage of the disease typical changes were found in EEG recording and in magnetic resonance imaging (MRI). The presence of the 14-3-3 protein was detected in the patient's cerebrospinal fluid. The diagnosis of sporadic Creutzfeldt-Jakob disease was verified neuropathologically.

Alzheimer's disease is the most common cause of memory disruption in elderly people. The main pathogenic factor of the disease is beta-amyloid protein, which may cause toxic damage of neurones. Other suggested pathogenic factors include an inflammatory process around the senile plaques, apoptosis and necrotic death of neurones, and, in consequence, changes in functioning of neurotransmitter systems. In this article the authors present the main directions in pharmacotherapy of Alzheimer's disease: causal therapy, which prevents the neurodegenerative changes and slows down the pathogenetic process, and symptomatic therapy. The aim of symptomatic therapy is to reduce memory disruption and psychiatric symptoms associated with the disease. Positive influence on cognitive processes is exerted by cholinergic drugs, e.g. the actually used inhibitors of acetylcholinesterase (rivastigmine, donepezil), the nootropic agents (piracetam, nefiracetam) and extracts of Gingko biloba. For treatment of the disease accompanying psychiatric symptoms (anxiety, depression, hallucinations, sleepness) the drugs with minimal influence on cognitive processes are recommended. Attempts at causal therapy are focussed on searching for the substances that can prevent the formation and toxicity of beta-amyloid (droloksifen, estrogens, agonists of muscarinic receptors M1), the cytotoxic influence of excitatory aminoacids (memantine, lamotrigine), calcium (nimodipine) and free radicals (selegiline, alpha-tocoferol), and the development of inflammatory process (non-steroidal antiinflammatory drugs). The new target of research is correction of deficits of nerve growth factor and neurotransmitters by intracerebral implantation of modified fibroblasts. Another way is prevention of the formation of amyloid plaques using appropriate antisense oligonucleotides.