Sleep-related movement disorders are simple, non-purposeful and usually stereotyped movements that occur at sleep onset orduring sleep. In some cases they represent transient or insignificant symptom without any health consequences. But they can alsocause insomnia, worsening of sleep quality or lead to injury. Bruxism and sleep-related leg cramps are very frequent. Sleep-relatedrhythmic movement disorder, propriospinal myoclonus at sleep onset and benign sleep myoclonus of infancy are less common.The definition of these disorders, clinical picture, diagnostics and therapy are summarized in the article.

Isolated sleep paralysis occurs in up to 7,6 % of general population, which makes it to be a common sleep disorder. Recurrent isolated sleep paralysis (RISP) means REM (rapid eye movement) related parasomnia, which occurs recurrently during the transition between sleep and wake that means during falling asleep or awakening. It is a transient loss of speech and voluntary movement that affects limbs and trunk muscles, which is especially at the beginning of the accompanied by an intensive fear. This burdensome experience can be elevated by accompanying fearful dreamy delusions, so called hypnagogic/hypnopompic hallucinations. Pathophysiological background of sleep paralysis is the continuing muscle atonia of REM sleep that persists until the full awakening. Current sleep medicine offers psychoterapeutic as well as farmacological treatment options.

Duchenne/Becker muscular dystrophy, caused by mutations in dystrophin gene,is one of the most frequent muscular dystrophies. First
symptoms of DMD include delayed motor milestones, difficult running or climbing stairs. Boys with DMD use the Gower´s maneuver to
arise from floor. Cardiomyopathy and respiratory failure most often occur in the third decade. Diagnostical process is based on clinical
picture, blood tests results (esp. elevated CK) and confirmation on molecular genetic base. Treatment aims to control symptoms. New drugs
in clinical practice as well as in clinical trials together with better multidisciplinary care can prolong patients life and improve its quality.

How did we improve the diagnosis since 1984 and why we don’t have a causal therapy yet? In 2011, new guidelines for the diagnosis of Alzheimer’s disease (AD) based on biomarker assessment were published. They define AD as a neuropathological continuum independently of the clinical symptoms of the patient. They describe three clinical stages – preclinical with AD pathology only, prodromal with AD pathology and mild cognitive impairment and dementia stage. We evaluate the benefits and pitfalls of particular biomarker examinations, their availability and benefits for clinical practice and the ethical impact of early diagnosis in the light of so far unavailable causal therapy. We present recommendations for clinical practice emanating from the international harmonized guidelines from 2014.

The reason for introduction of novel therapies in epilepsy surgery is invasiveness and adverse effects of existing therapies. Inclinical epileptology, radiosurgical, radiofrequency, laser, and ultrasound ablations have been used. The article summarizescontemporary literary data and, in case of radiosurgery and radiofrequency ablations, personal experience with these methods.

Progress in developing new monoclonal antibodies allows us to affect pathological immune processes on many different levels.For treating MS, we now have available monoclonal antibodies capable of influencing the lymphocytes migration or inducingtheir depletion. Also, the development of new humanized and human antibodies caused significant improvement of their safetyprofile. Currently there are four types of monoclonal antibodies available in Europe for treating MS: natalizumab, alemtuzumab,daclizumab and ocrelizumab. The last one has also shown effectivity on suppressing progression of primary progressive form of MS.

Multiple sclerosis is a chronic inflammatory autoimmune disease which affect central nervous system. Treatment initiation ofearly multiple sclerosis may postpone thie development of disease progression and disablement. Goal of MS treatment is statewithout cninical and sublinical markers of diseasety aktivity, state known as NEDA (No Evidence of Disease Activity). This work isconcerned with treatment of MS, monitoring and predictors of treatment.

Ocrelizumab (Ocrevus) is a humanized monoclonal antibody that was approved by the US Food and Drug Administration (FDA)on 28th March 2017 for the treatment of relapsing remitting multiple sclerosis (RRMS) and primarily progressive multiple sclerosis(PPMS) approved immunomodulatory treatment. European Medicines Agency (EMA) has recommended 10th November 2017OCR for the treatment of adult RRMS patients and early primary progressive MS patients in the European Union (EU) countries.In the Czech Republic, OCR was registered on 8th January 2017. The treatment is focused on mature B lymphocytes, immune cellsexpressing the protein CD20 molecule on their surface. It is believed that these CD20-positive B-lymphocytes are directed againstthe axons and myelin of healthy neurons, initiating a cascade of immune responses that lead to their damage and consequentlyto the disability in MS patients. This new view on MS pathogenesis was supported by evidence from a phase III, OPERA I, OPERAII and ORATORIO clinical trial.

Iatrogenic cause of disease is defined as a harmful response to medicamentous or surgical therapy. Iatrogenic peripheral nerve
lesions can be brought about with a surgical instrument in an operational field, but also with compression, traction, catching the
nerve by splint, damage of nerve by bleeding or radiation. In the paper there is given an overview of the most frequently injured
peripheral nerves and situations, in which a iatrogenic lesion developes.

The Lennox-Gastaut syndrome (LGS) is one of the most severe epileptic encephalopathies of childhood onset. LGS is characterised by occurence of multiple type of epileptic seizures (tonic, atonic, atypical absences), an EEG finding, psychomotor delay and behaviour disorders. The optimum treatment for LGS remains uncertain. This paper summarizes the therapeutical options of LGS including pharmacological therapy, diet and surgery. No study has shown any one drug to be highly efficacious; rufinamide, lamotrigine, topiramate and felbamate may be helpful as add-on therapy. Until further research has been undertaken, clinicians will need to continue to consider each patient individually, taking into account the potential benefit of each therapy weighed against the risk of adverse effects.

The aim of therapeutic plasma exchange (TPE) is to remove pathological (autoantibodies, monoclonal proteins, toxins bound to plasma proteins) or increased physiological plasma components (cytokins, kinins). Among neurological diseases, TPE is the accepted first-line therapy (according to American Society for Apheresis [ASFA] – category I) in PANDAS („Pediatric Autoimmune Neuropsychiatric Disorders Associated with streptoccal infections and Sydenham’s chorea“), and the second-line therapy (category II) in acute disseminated encephalomyelitis, multiple sclerosis, Devic disease and some paraneoplastic neurological syndromes with autoantibodies. Autoimmune neuromuscular disorders, however, are the most frequent indications for TPE in neurology: myasthenia gravis (MG), Guillain- Barré syndrome (GBS), chronic inflammatory demyelinating polyneuropathy (CIDP) and paraproteinaemic polyneuropathy IgG/IgA are classified as category I (acc. to ASFA), and Lambert-Eaton myastenic syndrome (LEMS) and acquired neuromyotonia as category II. Guidelines of the European Federation of Neurology, the American Academy of Neurology and the Czech Neurological Society, however, consider TPE as the first-line therapy in GBS and MG only (as the alternative method to intravenous humane immunoglobulin [IVIG] that has more favourable safety profile), while TPF is recommended as the second-line therapy in CIDP, and the evidence of the TPE effect in paraproteinaemic polyneuropathies and LEMS is lacking.

This systematic review summarizes the clinical manifestations and the existing knowledge about the treatment of the most frequentprimary headaches – migraine, tension type headache and cluster headache. The acute treatment of migraine attacks consists inthe use of simple analgesics, non-steroidal anti-inflammatory drugs, ergotamines and triptans. Patients with frequent or long lastingattacks require the prophylactic treatment. So far beta-blockers, antiepileptic drugs, calcium channel blockers and antidepressantsare used. Injections of onabotulinumtoxin A reduce the frequency of attacks in chronic migraine. The most promising new approachin the prophylactic treatment are monoclonal antibodies able to block either CGRP or its receptor, such as erenumab, fremanezumab,galcanezumab, and eptinezumab. Tension type headache is the most frequent type of headache. The treatment of acute attacks andprophylactic treatment in frequent episodic and chronic forms are described. Cluster headache (CH) is a primary headache from theTACs group. The clinical manifestation and the existing knowledge about the acute, bridging and prophylactic treatment are described.

Multiple sclerosis is a chronic inflammatory autoimmune disease which affect central nervous system. Treatment initiation ofearly multiple sclerosis may postpone the development of disease progression and clinical activity, including magnetic resonancefindings and disablement. The aims of this paper is to describe options for treating multiple sclerosis and risks.

Prophylactic treatment of frequent episodic and chronic migraine is often unsuccessful. In recent years, the therapeutic procedures
have focused on the particular segments of the pathophysiological chain of migraine. Calcitonin Gene-Related Peptide (CGRP) is
a key peripheral and central agent. Data emerging from trials with monoclonal antibodies (mAb) suggest that this specific blockade
of the CGRP pathway may provide an effective and safe novel preventive therapeutical approach in migraine.

Brain abscess is defined as purulent and inflammation region within brain parenchyma. We present a case report of a 44-yearsoldman who was urgently received at the Neurological Clinic of University Hospital Ostrava for acute headache. This headachebegan after coughing. CT scan including angiography excludes the diagnosis of subarachnoid hemorrhage. Episode of epilepticseizure appeared quickly after admission to the hospital. We made lumbar puncture, where was typical cytological picture ofacute inflammation. We thinking about possible meningoencephalitis, so broad-spectrum antibiotics was used. Deteriorationof the condition appeared in the further course of hospitalization, right lateral and expressive aphasia developed. Consequently,magnetic resonance was realised and brain abscess and subdural empyema parieto-occipital was demonstated.

Muscle dystrophies are progressive, hereditary diseases which are characterized by not fluctuating, chronic and (mostly) painless weakness of groups of muscles and their atrophies. They can manifest in childhood or in adult age. These diseases are rare with overlapping clinical pictures and similar phenotypes and their diagnostics is complicated, mostly performed in the neuromuscular centers. The most common muscular dystrophies should be recognized by each neurologist. Dystrophinopathies, myotonic dystrophies, facioscapulohumeral muscular dystrophy and limb girdle dystrophies are the most common dystrophies of adult age. Some dystrophies with characteristic phenotypes can be quite easily diagnosed (facioscapulohumeral muscular dystrophy, myotonic dystrophy type 1), the issue of the most common dystrophies is described in this article. Not only appointment of diagnosis is important, but also – monitoring of disability of associated systems (heart, eyes, endocrine system, lungs), genetic consultations and solutions of social problems associated with the disease – this is a common care of each neurologist.

Migraine is one of the most frequent neurological diseases. The differential diagnosis of migraine is rather extensive comprising
the whole spectre of primary headaches, i.e. various migraine types, trigeminal autonomic cephalalgias, tension-type headaches,
migraine with autonomic displays and other primary headaches including migraine complications. The problems of secondary
headaches are very comprehensive. However, the essential for diagnosis is to carry out a thorough anamnesis, clinical picture
and neuroimaging methods.

Paroxysmal atrial fibrillation is frequently undetected by standard examination procedures in patients with acute ischaemic stroke. However, its detection is crucial for choosing appropriate secondary stroke prevention. In this review article, the relation of particular forms of atrial fibrillation and ischaemic stroke is firstly characterized. All available means of heart rhythm monitoring are then compared. Particular aspects of optimal monitoring strategy are assessed – the length of monitoring, the choice of monitoring method, the appropriate time interval of monitoring commencing after stroke event and the use of biomarkers in atrial fibrillation prediction after stroke.

Nowadays we should suppose that epileptology come in the period of DNA and the genetics has become one of main trend of research in epileptology over the world. Epilepsies in which genetic background is predicted are called “idiopathic”. In recent years genetic discoveries have shown the central role of ion channels in the pathophysiology of idiopathic epilepsies. Ion channels are divided to voltage-gated and ligand-gated ion channels. For voltage-gated ion channels, mutation of Na+, K+ and Cl- channels are associated with forms of generalized epilepsy and infantile seizures syndromes. Mutations in ligand-gated ion channels, such as nicotinic acetylcholine receptors and GABA receptors, are associated with specific syndromes of frontal and generalized epilepsies, respectively. Mutations in few genes that do not encode ion channels have been identified in the idiopathic human epilepsies. In children and young adults are idiopathic epilepsies often, that´ s way identification of the genetic-biological ethiopatogenesy can perspectively lead to individualization and selection of farmacotherapy in clinical practice. The article suggests the summary of up-todate discoveries in the field of genetic epilepsy research.

Autoimmune involvement of CNS can accompany systemic or organ specific autoimmune diseases or is a primary CNS affection. Clinically, autoimmune CNS disorders present with a variety of symptoms and there are distinctive neurological syndromes where autoimmune etiology should be suspected like limbic and NMDAR encephalitis, opsoclonus-myoclonus or stiff person syndrome. In other CNS disorders (myelitis, cerebellar ataxia, acute/subacute encephalopathy, status epilepticus and some types of epilepsy), autoimmune etiology should be considered if no other cause has been identified. Autoimmune etiology can be suggested by results of some investigations – autoantibodies, cerebrospinal fluid pleocytosis, specific brain or spinal cord MR findings, which should by always interpreted within the clinical context of an individual patient.

Spontaneous intracranial hypotension is a remarkable but often misdiagnosed cause of new daily persistent headaches. The syndrome is characterised by headache that occurs shortly after assuming an upright position, low cerebrospinal fluid pressure, and magnetic resonance imaging findings diffuse pachymeningeal enhancement after gadolinium administration. We describe a 39-year-old man, with history of an operation of lumbar spine for radiculopathy, who presented 6-weeks after the operation orthostatic headache with photophobia, osmophobia and tinnitus. He was primary diagnose as aseptic meningitis syndrome. Soon after the patient´s history was carefully reviewed, he was treated successfully with epidural autologous blood patch.

Intraparenchymal hemorrhage (ICH) accounts for 10–20 % of all strokes, its mortality is much higher compared to ischemic strokes. 55 % of hematomas are localised deeply in brain hemisphere, 30 % in lobes and 15 % in the brain stem. The most frequent causes of ICH are hypertensive vasculopathy, amyloid angiopathy, vessel malformation or tumors. ICH patients should be admited to an ICU, the goal of therapy is blood pressure normalisation using intravenous drugs, coagulopathy treatment in patients on anticoagulation therapy and cerebral edema treatment. Prophylactic antiseizure medication is not recommended. Surgical treatment is effective in cerebellar or superficial hemorrhages. Anticoagulation after ICH is possible in carefully selected patients, an alternative approach in atrial fibrilation patients is left appendage closure.

The treatment of the inherited metabolic disorders with primary biochemical defects in the CNS has undergone a considerableprogress, recently. Our work brings a brief summary of currently available therapeutic possibilities including intrathecal applicationof enzyme replacement therapy, small molecules treatment, hematopoietic stem cells transplantation and the gene therapy. Theearly diagnosis and introduction to the therapy are crucial for the therapeutic success.