Limbic encephalitis (LE) is a condition affecting the limbic system that typically presents with memory disorders, with recent memory being most affected; concurrently, epileptic seizures and psychiatric symptoms can occur. Paraneoplastic limbic encephalitis (PLE) and non-paraneoplastic limbic encephalitis (NLE) are distinguished. Recently, an association of NLE with anti-LGI1 antibodies has been described. We report a case of a 45-year-old female patient with LE and positivity of anti-LGI1 antibodies. The differential diagnosis and treatment of this disease are also discussed.

Polymorbid patient with pain is a difficult problem for physicians. It is usually more of the diseases that are accompanied by various types of pain, and is treated with medicaments which have different pharmacologic properties and adverse effects (Slíva, 2011). In these cases it is very important detailed examination of pain etiology and rational use of analgesic treatment (Ambler, 2012). In our case report, we present example of polymorbid middle-aged patient who suffers from serious illnesses, underwents radical surgery on the musculoskeletal system and has a long-term chronic medication therapy, including corticosteroids. Patient is treated with several analgesics, despite its multiple pain are not sufficiently covered. Etiology of pain is mixed. Nociceptive component dominates, but is combined with a neuropathic component. In our department was adjusted pharmacotherapy emphasizing the influence component of neuropathic pain. At the control examination, we noticed reduce pain, lower incidence of adverse events of drugs and signs of improvement in quality of life.

Lumbar spinal stenosis (LSS) is a frequent disease of older age that contributes to impaired mobility of patients, but that is often underdiagnosed. Diagnostics and therapy of patients with LSS are multidisciplinary issue with contribution of neurologist, spine surgeon and radiologist. This article summarizes recent findings about clinical manifestation, diagnostics, differential diagnostics and choice of optimal therapy for patients with LSS.

Huntington’s disease is a hereditary neurodegenerative disease primarily affecting striatal neurons, manifested mostly in adulthood by a combination of neurological and psychiatric symptoms, most typically by choreatic hyperkinesias and development of dementia. We report a case of a female patient with Huntington’s disease presenting as multisystem atrophy (MSA) with delayed manifestation of chorea. Unlike a typical MSA presentation, asymmetry in manifestations of Parkinson’s syndrome and responsiveness to levodopa were evident.

The risk of the central nervous system damage in terms of a chronic toxic encephalopathy caused by long-term low-level exposure to organic solvents is constantly in the focus of interest of the occupational neurology. Clinical manifestation of such a disease involves subjective neurasthenic complaints and subtle non-focal signs in the physical neurological examination. To assess the severity of impairment, two international classification systems are available. The boom of interest in the issue culminated in the 1970s, especially in the Scandinavian countries. Currently, it experiences a revival in connection with reports on findings in the neuroimaging methods, documenting some structural brain changes in the patients, such as the multifocal toxic leukoencephalopathy on MRI. Attempts at the international standardization of diagnosis based mainly on the results of a neuropsychological examination are in progress, to be used especially in the framework of recognition as an occupational disease. However, the number of such cases reported in the Czech Republic is quite low.

Therapy of myasthenia gravis is based on two parts: symptomatic and disease modifying procedures. Among cholinestrase inhibitors (symptomatic therapy) pyridostigmine is widely used. This medication is administered in patients with the ocular or very mild form of myasthenia. In other patients immunosuppressive medication should be introduced. The key role plays prednisone and/or other steroid sparing drugs as azathioprine, cyclosporine, or mycophenolate mophetil. Plasma exchange or intravenous immunoglobulin is indicated in patients with myasthenic crisis or other severe resistant symptoms.

Painful diabetic neuropathy developes in 16 % of all diabetics and in 40–50 % of diabetics with previously diagnosed diabetic neuropathy. Various medicaments are used in treatment of neuropatic pain in painful diabetic neuropathy: antidepressants, anticonvulsants, opioids, topically administered drugs, other medicaments and non-pharmacological procedures. According to evidence of pain-relieving effects in painful diabetic neuropathy there were evaluted more than 2000 citations, the titles and abstracts of which 79 were chosen, that fulfilled all the criteria of evaluating panel (from AAN – American Academy of Neurology). The highest level of recommendation (level A) reached pregabalin, then duloxetine (with respect to its adverse events, level B), then venlafaxine, tricyclic antidepressants, gabapentin, opioids, capsaicin. The combination of drugs is successful (e.g. with opioids).

In the introduction, the author describes the history of the Czech Headache Society which has played an important role in developing the knowledge of headaches in the Czech Republic. Next, the IHS headache classification is briefly mentioned and an overview is given of the most commonly occurring primary as well as secondary headaches – migraine, tension headache, cluster headache syndrome, headaches related to head and/or neck injury, headaches related to cerebrovascular disease, headaches related to intracranial involvement of other than vascular aetiology, headaches related to the use or discontinuation of a pharmacologically active substance, and cervicogenic headaches. For each type of headache, the clinical presentation and therapy are described.

Diabetic neuropathy, a common complication of diabetes mellitus type 1 and type 2, represents clinically heterogeneous syndrome with various involvement of peripheral, cranial and autonomic nerves. The progression is usually slow and patients may stay for a long time asymptomatic. Prevalence of diabetic neuropathy is estimated between 13 and 54 % according to the duration of the disease. Two main clinical types of diabetic neuropathy – generalized and focal – can be distinguished by clinical examination. The basic diagnostic tool is electromyography. The symptomatic treatment is focused on neuropathic pain. As the effective treatment is still unavailable diabetic neuropathy represents a high risk for development of diabetic foot. It is very important to differentiate other causes leading to neuropathy in diabetic patient as this may lead to causative and usually more effective therapy.

Clinical picture of serious central nervous infections include disturbance of consciousness, seizures or local neurological signs. Purulent meningitis, encephalitis and brain abscesses are the most frequent etiology. Rapid diagnostic and empiric therapy is necessary especially in patients with purulent meningitis and herpetic encephalitis. Delay of causal therapy increase risk of serious course or death of the patient.

Painful diabetic neuropathy is common and is associated with significant reduction in quality of life. A distal and symmetric peripheral neuropathy is the most frequent form, and small fiber damage is thought to result in painful symptoms. The much less common though well recognized are acute painful and atypical neuropathies. Management of the patient with painful neuropathy is difficult, must be tailored to individual requirements, taking into consideration comorbidities and other factors. Pharmacological management represents the most important therapeutic option for chronic neuropathic pain. Current first-line agents with proven efficacy for painful neuropathies are tricyclic antidepressants (amitriptyline, nortriptyline), serotonin-norepinephrine reuptake inhibitors (SNRI – duloxetine and venlafaxine) and the anticonvulsants pregabalin and gabapentin. Second line approaches include use of opioids, thioctic acid and sodium valproate.

The author discusses the pitfalls of differential diagnosis between migraines, particularly those with aura, and idiopathic focal (partial) epilepsies, particularly benign, age-related ones. These diagnoses are among the most common in the outpatient practice of a paediatric neurologist. The author points out to the similarity of both entities in terms of medical history data, clinical presentations, and normal results of auxiliary examinations, including structural brain imaging, and highlights the similar therapeutic strategies and prognostic aspects. EEG remains a decisive examination tool for distinction; nevertheless, correct interpretation of findings in terms of electroclinical correlation may not always be unequivocal. The author also emphasizes that diagnostic considerations may be greatly complicated by their concurrent presence or mutual transitions over time in the same patient, or by possible combinations with other non-epileptic seizures, which is not an uncommon occurrence in paediatric age. The above applies not only to clinical presentations that, particularly in the lowest age groups, are often atypical, with children being frequently unable to describe their complaints in a relevant way, but also to EEG patterns.

The most important changes in the Guidelines for management of ischaemic stroke and transient ischaemic attack (ESO 2008–2009) include changes in antiplatelet (preferential administration of ASA and dipyridamole or clopidogrel alone rather than administration of ASA alone), thrombolytic (prolongation of IVT time window to 4.5 h, implementation of intra-arterial treatment as an option in acute MCA occlusion within 6 h, treatment options of acute basilar artery occlusion using IAT or IVT even after 3 h since symptom onset), surgical (recommendation to perform the CEA as soon as possible, ideally within 2 weeks after the last ischaemic event and recommendation of surgical decompressive therapy in patients up to 60 years of age with evolving malignant MCA infarcts within 48 h after symptom onset) and endovascular (option to consider endovascular treatment in patients with symptomatic intracranial stenosis) therapy.

Low back pain (LBP) is defined as pain, muscle tension or stiffness localized below the low costal margin and above the gluteal folds, with or without leg pain. LBP is currently a tremendous medical and socio-economic problem and it has a lifetime prevalence of 60–85 %. The article is focused on non-specific low back pain. There is a syndrome, which mostly is not in the preference of neurologists. The basic division of LBP is to acute and chronic, but more important division is to specific cause and just non-specific one (without clear cause – up to 90 % cases). But now, it seems, the most important is a division into a diagnostic triage (very serious illness, radicular pain, simple LBP). Numerous randomized controlled trials and systematic reviews show strong evidence for advice to stay active and fitness programmes. Treatment targets are reduction of pain, bettter activity and participation, including disability prevention as well as maintenance of work capacity. Maintenance of activity, simple analgesics and non-steroidal anti-inflammatory drugs are effective in treatment of acute LBP. Exercise therapy (aerobic fitness), behavioural therapy and multidisciplinary pain treatment programmes are effective in treatment of chronic LBP.

Introduction: Lumbar spinal stenosis is a relatively common disorder in patients of higher age groups. Opinions on treatment options vary. Material and methods: Sixty-seven patients were operated on for central spinal stenosis at L2–L5 at our department between 2004 and 2008. All were over 60 years of age and 75 % of them had one-level stenosis mostly at L4–L5 or L3–L4. The length of the stenotic segment was 4–9 mm at the site of maximal involvement. The major symptoms included claudications, nocturnal pain, and/or complete chronic cauda equina syndrome. All patients underwent MRI and functional imaging of the lumbar spine. Given their age and the typical finding of osteophytes that had a stabilizing effect, no shift or instability of the lumbar vertebrae were present concurrently. In the case of failure of conservative treatment (rehabilitation, oxygen therapy, staying at a health resort), surgery was usually performed which, in this age group, i. e. the elderly, involved laminectomy with sparing the facets of the intervertebral joints. Results: In the early postoperative period (six weeks), 56 (84 %) patients were improved showing disappearance of paraesthesias and improved ambulation and life comfort. Out of them, 13 (15 %) reported a feeling of weakness in the lumbar area when working. Fifty (75 %) patients were still improved at two years postoperatively. Conclusion: Laminectomy without stabilization is usually an adequate and effective management strategy in patients with lumbar spinal stenosis in this age group. Postoperatively, many patients return to their previous recreational, sports, or work activities.

In the synoptic article the authoress presents the results of scientific studies which she reached together with her team while dealing with the grant project IGA MZ ČR 1A862-5/2005 ´The Use of Plasticity of the Central Nervous System in Neurorehabilitation of MS Patients´. She tried to interpret and generalize the results in the way they were applicable in the current clinical practice on two levels: firstly in the evaluation of the therapy effect (she has worked out and validated a set of clinical functions which enables a complex evaluation of the rehabilitation effect, or physiotherapy effect, in people with central impairment, especially in patients with MS), secondly in producing evidence of the effectiveness of physiotherapy in MS patients (by means of chosen clinical test, immunologic examinations, tractography and functional magnetic resonance imaging). set, examination of immune parameters diffusion tensor imaging, functional magnetic resonance imaging.

Tumors of central nervous system are the most frequent solid tumors in children and represent an important part of cancer related morbidity and mortality. Prognosis for many high risk tumors remains unsatisfactory. A progress in molecular biology enables to establish biological markers to predict the course of disease. The modern therapeutic approaches should be utilized in conjuction with standard therapy to improve the outcome.

We report a case of rapidly progressive dementia and Parkinsonism; the clinical diagnosis concluded to mixed dementia (Alzheimer’s disease and vascular dementia). Neuropathologic findings, however, showed surprisingly a diffuse anaplastic astrocytoma with areas of glioblastoma. We discuss the principal atypical clinical features in our patient and suggest possible reasons that might have been involved into the discrepancies between clinical conclusions and the definite histopathological diagnosis. Our observation underlines the need for confrontations of clinical signs and neuroimaging findings and strengthens the importance of neuropathological verification of clinical diagnoses in receiving valuable feedback and lessons for the future.

The term acute symptomatic seizure describes a seizure occurring in close temporal relationship with various CNS insults. In contrast to unprovoked seizures, early mortality of acute symptomatic seizures is higher and largely aetiology-dependent. On the other hand, the risk of developing epilepsy following acute symptomatic seizure is lower than in unprovoked seizure. Apart from different pathogenesis, different mechanisms of ictogenesis are implied as well. Acute symptomatic seizures represent approximately 40% of all first seizures. Their aetiology is clearly identifiable – most common causes include cerebrovascular events, CNS injuries, inflammatory disorders of the CNS, metabolic derangements and drug-related and toxic causes, especially alcohol abuse. The most severe form of acute symptomatic seizure is acute symptomatic status epilepticus. Therapy is focused not only on seizure termination, but, more importantly, on treating the underlying aetiology. Therefore, timely ascertainment of the cause is a crucial factor determining the patients´ outcome.

Multiple sclerosis is an inflammatory disease of the central nervous system that, without treatment, causes significant disability in most patients. At present, the only prevention is early antiinflammatory treatment. Unfortunately, currently used drugs are only partially effective, and, in most patients clinical activity persists. Accurately assessing the treatment response to disease-modifying agents enables non-responder patients to be identified at an early stage of therapy. Patients can then be switched to another, potentially more effective treatment. The follow up must be comprehensive and involve clinical and modern paraclinical examinations with objective evaluation of underlying pathological processes in the central nervous system.

Reduced cognitive ability and dementia significantly affect the quality of life in elderly people, including their carers. Therapeutic options have been limited so far; therefore, preventive strategies reducing the risk of developing dementia are being intensively sought. In this regard, healthy lifestyle has been increasingly discussed. This paper summarizes the current knowledge on the lifestyle components most commonly investigated in association with dementia; in particular, eating habits, alcohol, smoking, physical activity, education and cognitive stimulation, spirituality, and social involvement. The effect as well as the potential mechanisms of action on the cognitive status are assessed. From available evidence, it can be concluded that lifestyle modifications are an important tool in preventing the development of dementia; however, more sophisticated intervention studies are required to elucidate their physiological effect and find an optimal strategy.

Subcortical laminar heterotopia of the cerebral cortex, also referred to as band heterotopia (BH) or double cortex, is a rather rare developmental defect of the cerebral cortex characterized by the presence of large bands of grey matter below the surface of the cortex. This malformation occurs mostly in women and is manifested as sporadic or familial cases with epilepsy and varying degrees of mental retardation. The most common cause of the disease is a mutation in the doublecortin gene, resulting in BH in females and, predominantly, in agyria-pachygyria and, only sporadically, in BH in males. Two female patients were followed for delayed psychomotor development and pharmacoresistant epilepsy with partial seizures with occasional secondary generalizations. Magnetic resonance imaging of the brain showed a typical presentation of BH. Multiregional epileptiform activity with an occasional generalized epileptiform pattern was recorded on electroencephalography (EEG). An ictal pattern with secondary generalized epileptiform activity was repeatedly detected during video-EEG monitoring. During many years of follow-up of the patients, a number of antiepileptic drugs and their combinations have been tried. Due to comprehensive evaluation, including video-EEG monitoring and an analysis of drug history, it has been possible to optimize the treatment with antiepileptic drugs and even to discontinue some of them. In one of the patients, treatment with vagus nerve stimulation was indicated, which resulted in a significant reduction in atonic and in myoclonic seizures. In terms of pharmacotherapy, BH is a very challenging area for an epileptologist, with a need for combined therapy using antiepileptic drugs with their potential interactions and side effects; the possibilities for successful epilepsy surgery are largely limited in this case. With that said, a certain hope of at least some improvement for these patients remains in VNS treatment or palliative anterior callosotomy.

Both the epidemiological data and results of experimental works have shown tight relations of the insulin resistance, type 2 diabetes mellitus (DM2), cognitive disturbances and sporadic form of Alzheimer´s disease. Plethora of events, standing behind these relations, is associated with an abnormal brain glucose metabolism. Some authors call Alzheimer‘s disease, „type 3 diabetes mellitus“. In the article, an outline is given on the mechanisms, connecting both the insulin resistance and DM2 with the cognitive disturbances or dementia. Some new potential possibilities of the favourable influencing of the sporadic form of Alzheimer´s disease are also mentioned. The research in the field could help to find new biological markers of the Alzheimer´s disease, recognition of the new treatment targets and of new preventive and treatment modalities of this serious disorder.