Mononeuropathies (entrapment syndromes and compressions of peripheral nerves) and polyneuropathies develop during occupational exposition on the ground of physical reasons. The most common physical impact is overload, followed by exposition to vibrations transmitted to upper extremities, then cold, humidity, unfavorable position in work, and pressure on the nerve against a hard structure. Entrapment syndromes and outer compressions of peripheral nerves lead to the ischemic changes of fascicles and single axons, to development of oedema, to failure of the venous outflow, to the increase of pressure in entrapment and lastly to the focal demyelinization or axonal lesion. Over-limit vibration transferred via the upper extremity cause spasms of arteriols, leading to the tissue ischemia at the terminal structures of hand and fingers, to lesion of sensitive and later of motor nerve fibres and to the development of vibration neuropathy. Clinical and electrophysiological evaluation of these disorders is important. Treatment and the complex prophylactic measures follow.

Pain is a common symptom accompanying the coronavirus disease COVID-19 caused by coronavirus SARS-CoV-2. In addition to acute headache, myalgia and arthralgia or neuropathic pain in context of acute viral illness, chronic pain can be worsened as well. This can be due to post-viral syndrome, direct affection of nervous system by viral penetration, or as a consequence of psychological distress due to limited health care, social isolation, fear of infection and so on. When proceeding of the interventional procedures in patients with COVID-19 disease we should take general precautions for personal protection and consider a dose of corticoids and undergoing anticoagulation therapy. We can anticipate a higher incidence of chronic fatigue syndrome in patients with COVID-19. We found 82 patients with chronic pain of locomotive systems in our clinical praxis who suffered Covid-19, 23% with severe form and 77% light to moderate form of Covid-19. A similar worsening of chronic pain was reported in 68% cases in both groups, whilst the same degree of chronic pain was reported in 32% cases.

Ravulizumab is a humanized monoclonal antibody targeting the complement C5 protein. This drug has been approved by different regulatory agencies worldwide for the treatment of AQP-4 seropositive NMOSD based on the results of the CHAMPION-NMOSD trial. Similar to eculizumab, ravulizumab offers highly effective prevention of NMOSD relapses. Both molecules demonstrated more than 90% reduction in relapse risk compared to the placebo group. Ravulizumab has a longer half-life allowing extending interval dosing from two to eight weeks compared to eculizumab. Patients taking C5 complement inhibitors have an increased risk of serious meningococcal infections, therefore vaccination is mandatory before treatment initiation.

New-onset refraktory status epilepticus (NORSE) is a rare severe condition with possible fatal consequences. Etiology of the syndrome often remains unclear. The term NORSE describes the clinical condition according to patient's symptoms and history but has no connection with a specific etiology. Achievement of the control of seizures is our main priority in management of every status epilepticus (SE), however finding the etiology of SE has both therapeutic and prognostic implications. Aim of this article is to suggest diagnostic and therapeutic processes based on the considered/confirmed underlying cause of NORSE.

More effective treatment strategies have been appearing in the treatment of cancer, but they also bring new unpleasant side effects with them. A breakthrough is the use of immuno-oncology therapy, which includes checkpoint inhibitors. Unfortunately, this treatment relates to number of immune-mediated adverse effects, which may affect also the nervous system. Myasthenia gravis, Guillain-Barré syndrome, neuropathy, aseptic meningitis, mononeuritis multiplex, encephalitis and transverse myelitis are the most common neurotoxic side effects. Other drugs that can lead to damage to the nervous system are BRAF and MEK inhibitors, for example used in the treatment of metastatic melanoma. Knowledge of these immune-related side effects is necessary for prompt diagnosis and treatment. Immediate discontinuation of oncology therapy, administration of high doses of corticosteroids, intravenous immunoglobulins or exchange plasmapheresis is recommended.

Progressive multifocal leukoencephalopathy is a rare demyelinating disorder of the central nervous system, which is found almost entirely in immunocompromised persons - mostly as late complication of HIV infection. We present a case report of rare situation, in which the diagnosis of PML preceded the diagnosis of long-lasting HIV infection. This patient was also the first patient with this diagnosis in Neurology department of The University Hospital Olomouc.

From a historical definition, congenital muscular dystrophies are a heterogenous group of muscle disorders characterized by early-onset muscle disease with histopathological evidence of a dystrophic process. Recent progress of molecular genetics has changed the perspective of the entire group. Continuous deciphering of the genetic background and increasing number of genetically confirmed cases highlights a significant genetic and clinical heterogenicity and makes former clinico-histopathological classifications less useful. It also blurs the classification barriers between congenital muscular dystrophies, limb girdle muscular dystrophies and congenital myopathies groups as they share and overlap at clinical, morphological and genetic level. This text provides a brief summary of the current knowledge accompanied by clinical vignettes from the clinical practice.

Posttraumatic hydrocephalus is an active and progressive process of excessive accumulation of cerebrospinal fluid due to impaired dynamics of cerebrospinal fluid caused by traumatic brain injury. The incidence of posttraumatic hydrocephalus is given in the literature in a very wide range of 0.7-86 %, which is the result of differences in the diagnostic criteria and classification. A 32-year-old patient was admitted after a fall on inline skates at the nape area. His entering condition was assessed as Glasgow Coma Scale 4 with right-sided mydriasis. Brain computed tomography revealed acute subdural hematoma frontotemporoparietally above right hemisphere with midline structures being shifted to the left side and diffuse cerebral edema. The hematoma was evacuated from decompressive craniectomy. One month later the patient developed severe left-sided hemiparesis, somnolence and slowing down of psychomotor speed. Brain computed tomography revealed four-ventricles communicating posttraumatic hydrocephalus. The patient was introduced ventriculoperitoneal shunt and he was treated with cranioplasty of the skull defect after decompressive craniectomy because of sinking skin flap. Despite primarily disappointingly evolving clinical condition with the need to repeatedly adjust the opening pressure in the valve of ventriculoperitoneal shunt and once to replace the entire shunt system, five years after craniotrauma the patient was in very good condition - lucid, oriented across all aspects, communicating and without movement disorders, modified Rankin Scale 2.

Hypertension, defined as an increase in blood pressure above 140/90 mmHg, is associa­ted with damage to a number of organs, including the brain. Clinical manifestations include hypertensive encephalopathy, posterior reversible encephalopathy syndrome, and cerebrovascular accidents. Chronic hypertension contributes to structural and functional changes in brain tissue, which can lead to clinically manifest impairment of cognitive functions and the development of dementia. The pathophysiological basis of brain damage induced by hypertension is complex. Early detection of hypertension and its adequate treatment are crucial for reducing the risk of neurological complications.

The article provides an overview of the pathophysiological mechanisms responsible for the development of chronic pain after nerve injury and especially of the strategies for its treatment. Special attention is given to the complex regional pain syndrome (CRPS) and phantom pain. Chronic pain is a very unpleasant consequence of peripheral nerve injury. The pain is not only the result of the injury itself but is maintained and even augmented by the mechanisms of peripheral and central sensitization. Therefore, adequate pain therapy must be started already in the acute stage of the injury. Correctly indicated and performed surgical procedure is essential for the treatment of nerve injuries. In the management of pain, various methods are combined, from pharmacotherapy - following the guidelines for the treatment of neuropathic pain - through rehabilitation to invasive methods including neurostimulation.

Pituitary tumors are common intracranial tumors in adults. Pituitary neuroendocrine tumors (PitNETs, formerly adenomas) represent a vast majority of pituitary lesions. These tumors can be classified according to the lineage of differentiation in tumor cells that corresponds to cellular subpopulations of normal pituitary. These cell lineages are determined by one or more transcription factors (Pit1, Tpit, SF1 and GATA3) that also regulate hormonal production in both normal pituitary cells and their neoplastic counterparts. This review article summarizes briefly current approach in histopathological diagnosis of PitNETs according to the latest WHO classification. Furthermore, rarer entities, including pituictyomas and craniopharyngiomas are discussed, as well as secondary tumors of sellar region.

Transcranial sonography (TCS) is a quick, inexpensive, widely available and well applicable examination in the diagnosis of Parkinson's disease (PD) and Lewy body dementia (LBD), especially for screening in the early and prodromal stages of these diseases. Patients with PD and DLB reveal increased echogenicity of substantia nigra (SN). The SN hyperechogenicity particularly reflects excessive iron accumulation and tissue degeneration. The aim of this review is to describe the role and utility of TCS in the diagnosis of patients with PD and LBD, including a focus on their prodromal stages and differential diagnosis. In the asymptomatic period, the finding of SN hyperechogenicity is considered to be one of the risk factors for the development of synucleinopathies, especially PD. The results of TCS studies are placed in the context of diagnostic criteria for PD and LBD.

This review summarizes current options for both disease-modifying and symptomatic treatment of degenerative cerebellar ataxias, with a particular focus on two conditions that are significantly reshaping everyday neurological practice: Friedreich's ataxia (FA), with the recent availability of the targeted therapy omaveloxolone, and spinocerebellar ataxia type 27B (SCA27B), for which accumulating evidence supports the efficacy of 4-aminopyridine (4-AP).

Constantin Economo was born in 1876, into a rich Greek patrician family in the city of Brãila, Romania. His father was a merchant with extensive properties in Thessaly and Macedonia, where in the city of Edessa his family was rooted; Economo's ancestors included several bishops of the Greek Orthodox Church. In 1877, the family moved to Trieste where Economo spent his childhood and youth. After his school-leaving exam in 1893, he started to study at the Polytechnic University of Vienna at the request of his father, but switched to medicine after two years. While still studying, he published his first scientific paper on the development of the pituitary gland in birds. He graduated in 1901, by which time he had already worked in professor Exner's laboratory for one year, where he stayed until 1903. He spent the following year as a resident at the Clinic of Internal Medicine under professor Nothnagel; subsequently, he travelled for two years visiting European clinics and laboratories, where he worked with Joffroy, Magnan, Marie, Bernheim, Kraepelin, Ziehen, and Oppenheim, to name only a few. In 1906, Economo's father was ennobled by the Emperor Franz Joseph I and received the hereditary title "Freiherr", making Constantin a baron, too. Since 1907 he worked as an assistant at the Clinic for Psychiatry and Nervous Diseases headed by professor Wagner-Jauregg at Vienna's General Hospital. He obtained his habilitation in 1913 with a thesis on sensory disorders accompanying pontine tumours. He was appointed professor of neurology and psychiatry in 1921. In 1931, he was made head of a newly established department of brain research (nowadays known as Neurologische Institut) at Vienna University which he headed for six months only. During his career in neuroscience, he mainly dealt with three topics which became his lasting professional legacy: epidemic encephalitis which was later called by his name; sleep disorders and localization of the sleep centres; and cytoarchitectonics of the cerebral cortex. Another one of Constantin von Economo's passions (apparently as great as medicine) was aeronautics. While in Paris, he learned how to fly a balloon. After returning to Vienna, he started flying frequently at the old Viennese airfield in Aspern. He was a holder of the first official Austro-Hungarian international pilot licence, and since 1910 the president of the Austrian Aeroclub, remaining in office until 1926. During the First World War, he was a fighter pilot for the Austro-Hungarian air force during two campaigns in the years 1915 and 1916 on the Dolomite front. At the request of his parents with the Ministry of Aviation, he was demobilized in late 1916 and summoned back to the Vienna Military Hospital to care for patients with head injuries. In 1919, at the age of 43, he married Karoline, a daughter of prince Alois von Schönburg-Hartenstein; the couple had no children of the marriage. Constantin von Economo died in 1931, aged 55, of the sequelae of a heart attack.

Introduction and aim: Subacute cerebellar degeneration is one of the paraneoplastic neurological syndromes that occur in cancer diseases in which tumour cells express neuronal proteins, causing an immune response not only against the tumour, but also against the nervous system. Patient-produced onconeural antibodies attack and damage various parts of the nervous system, resulting in the development of a broad spectrum of neurological symptoms.  Methods: We report the case of a 62-year-old woman with a history of cancer and advanced neurological cerebellar signs. Accordingly, after the exclusion of the most common causes of cerebellar syndrome (stroke, neurological infection), the diagnostic workup was aimed at identifying a paraneoplastic process that was confirmed by a high seropositivity of paraneoplastic anti-Yo antibodies (highly specific antibodies attacking the Purkinje cells of the cerebellum). Conclusion: The development of neurological symptoms in cancer patients should raise suspicion of a paraneoplastic process. Current treatment strategies allow to only minimally slow down the paraneoplastic process, and it is the treatment of the underlying cancer disease that remains essential.

Musculoskeletal (MSK) ultrasound is very useful tool for imaging musculoskeletal body structures- muscles, tendons, joints, bones, peripheral nerves and vessels. In last decade becoming MSK ultrasound common diagnostic tool in neurological practices and amount of publications and studies which prove ultrasound as a useful diagnostic tool in neurological diseases increase. Other important field for ultrasound application are interventional procedures in neurology- peripheral nerve injection, nerve block, vessel puncture, lumbar puncture, muscle biopsy. Ultrasound diagnosing is quick, widely available, relatively cheap, non-invasive and for patient comfortable diagnosing method applicable in musculoskeletal diseases including peripheral nerves. Ultrasond in addition enable dynamic investigation. Ultrasound is eligible method of first choice, current MSK ultrasound probes can provided higher quality structure imaging than magnetic resonance.

The article introduces the options of rehabilitation interventions that can be used to restore function and fitness after Covid-19 disease in patients with a chronic neurological disease - multiple sclerosis. Two individual case reports of patients are included to discuss the use of respiratory physiotherapy as well as the issue of restoring mobility and increasing fitness in post-Covid-19 patients.

Multiple sclerosis is the most common acquired chronic inflammatory demyelinating disease of the central nervous system. The diffferential diagnosis of multiple sclerosis includes acute disseminated encephalomyelitis, which is a monophasic autoimmune demyelinating disease. Clinically, acute disseminated encephalomyelitis is manifested by encephalopathy and multifocal involvement. In addition to clinical findings, magnetic resonance imaging and cerebrospinal fluid examination can hepl us to differentiate these two entities. This case report describes a rare variant of tumefactive multiple sclerosis, which was initially presented with epileptic seizure and encephalopathy.

We are presenting a rare case-report of a patient with two succesive hemorrhagic strokes in the area of both posterior cerebral arteries. She has suffered bilateral lesions of occipital lobes. However, due to the size of the lesions, the neighbouring structures of temporal and parietal lobes have been affected too, more severly on the left side. Clinically we found Anton-Babinski syndrome (cortical blindness, anosognozia, state of confusion, confabulations). We also could notice a cognitive impairment of the patient and Gerstmann syndrome (acalculia, agraphia, right-left disorientation, finger agnosia). We consider the cause of hemorrhagic strokes an amyloid angiopathy, as no other vessel pathology has been revealed.

Hereditary neuromuscular disorders (NMD) are a broad group of diseases affecting peripheral nerves, muscles, or neuromuscular transmission. They are considered rare diseases with variable clinical presentation. A common feature of NMD is muscle weakness, which is progressive and can lead to respiratory failure in some patients. In the past, therapy for genetically conditioned NMD consisted only of symptomatic care without the possibility of influencing the natural course of the disease. A breakthrough occurred with the advent of gene therapy for spinal muscular atrophy (SMA). Progress has also been made in the treatment of muscular dystrophies. The effectiveness of gene therapy goes hand in hand with the availability of modern diagnostic methods such as next-generation sequencing or the use of newborn screening to detect asymptomatic patients.

Cerebrospinal fluid analysis represents a key diagnostic instrument in confirming and differentiating various forms of CNS infections due to its ability to reveal specific cytologic, biochemical and microbiological changes. In cases where CNS infection is suspected, a basic cerebrospinal fluid examination includes the enumeration of nucleated cells and erythrocytes, the differentiation of nucleated cells into mononuclear and polymorphonuclear cells, and, if applicable, a detailed qualitative analysis from a permanent cytological slide. Furthermore, the determination of total protein, glucose and lactate concentrations and the coefficient of energy balance (KEB) is essential. In cases where the differential diagnosis is subarachnoid haemorrhage, an additional spectrophotometric examination is recommended. Multiplex PCR is a useful technique for identifying the causative agent in both serous and purulent inflammation. In cases of bacterial or mycotic infections, microscopic and culture examinations are also ne­cessary. Other examinations of the CSF include indirect diagnostics, such as the detection of an antibody response (e. g. in Central European tick-borne encephalitis) or, in selected diseases, the demonstration of intrathecal (IT) synthesis of specific antibodies. This test is particularly useful in the diagnosis of neuroborreliosis and neurosyphilis, and can also be used in suspected herpetic infections with EBV, HSV, VZV and CMV. However, it is important to note that confirmation of IT synthesis does not always indicate acute disease. Indeed, it may persist after a previous illness or be seen in a chronic inflammatory autoimmune process in the CNS. In the case of Lyme disease, the detection of the chemokine CXCL13 is also useful to support the diagnosis in cases where there is a negative IT synthesis at an early stage.

Migraine is a condition that occurs across all age groups. In the pediatric population, it is underdiagnosed compared to adults. Pediatric migraine has specific neurodevelopmental and clinical characteristics, and its diagnostic and therapeutic approaches differ partially from those used in adults. In this article, we aim to highlight these issues.We present some epidemiological data on migraine occurrence, migraine phenotypes in the pediatric population, diagnostic and treatment approaches, and practical insights, with a broader focus on treatment.

Laboratory biomarkers play a crucial role in the diagnosis, prediction, and monitoring of treatment efficacy in patients with multiple sclerosis (MS). Their use enables better individualization of therapy, increasing the chances of slowing disease progression and improving patients' quality of life. The most important diagnostic laboratory biomarkers in MS are oligoclonal IgG bands and free kappa light chains, while neurofilament light chains are essential for disease prediction and monitoring treatment efficacy. Research in this area is continuously evolving with the aim of discovering new indicators that further improve diagnostic accuracy and enable more detailed monitoring of disease progression.

Hereditary spastic paraplegias (HSP) are a group of genetic disorders causing central motor neuron degeneration, while amyotrophic lateral sclerosis (ALS) affects both central and peripheral motor neurons, progressing more rapidly with a poorer prognosis. In this study, we present a case of spastic paraplegia type 6 (SPG6), a rare form of HSP caused by mutations in the NIPA1 gene, that progressed to ALS. Similar phenotypic conversions have also been reported in other HSP types, such as SPG5 and SPG18. This case suggests that there may be a pathophysiological link between these two disorders, but its mechanisms remain unclear and warrant further investigation.