Ofatumumab is a subcutaneously administered, fully human anti-CD20 monoclonal antibody, approved for the treatment of relapsing multiple sclerosis. It is considered a highly effective therapy, and at the same time has a good safety and tolerability profile. This review presents up-to-date information regarding the general safety profile of ofatumumab, including the incidence of serious infections, injection-related reactions, malignancies, and effects on laboratory parameters, such as immunoglobulins M and G, and lymphocyte and neutrophil counts. Currently available data show that the most common adverse effects of ofatumumab include upper respiratory tract infections (mild to moderate), injection-related reactions (mild to moderate, and very rare beyond the first injection), and urinary tract infections. The depletion of CD20+ lymphocytes causes a decrease in immunoglobulin M levels, which does not correlate with the risk of serious infections. The drop in absolute lymphocyte count is temporary, and neutropaenia risk is very low (<1%). So far, no increased risk of associated malignancies has been identified for ofatumumab. All disease-modifying therapies approved for multiple sclerosis exert complex effects on immune system function; thus, potential adverse events may be unpredictable. Therefore, active monitoring of multiple sclerosis patients subject to immune therapies, including ofatumumab, remains essential. This applies to patients in open-label extension studies, as well as patients in real-world clinical settings.
Neurosarcoidosis is an inflammatory disease of unknown aetiology, characterised by the presence of non-caseating granulomas within the nervous system. Its prevalence in patients diagnosed with sarcoidosis is estimated to be approximately 10%. The clinical presentation is ambiguous, with symptoms that may manifest acutely or progress gradually over time. Many of these symptoms mimic those of other diseases, making neurosarcoidosis a diagnostic challenge. No sufficiently sensitive or specific biomarkers are available to enable an accurate diagnosis. A range of diagnostic tests must be performed to exclude other conditions. Histopathological confirmation via biopsy is necessary to make a definitive diagnosis, which is not always possible due to the location of lesions and the potential risk of complications associated with performing a biopsy. Once a diagnosis is established, regular follow-up examinations are necessary to monitor disease activity and assess the progression of changes. The optimal treatment strategy depends on the patient’s current clinical status and the potential risk of side effects. Three main lines of treatment for neurosarcoidosis have been described. Treatment selection should also take into account the ability of medications to cross the blood–brain barrier. Treatment response, severity of the disease at the time of diagnosis, and lesion location within the nervous system all influence the prognosis. With appropriate treatment, the majority of patients achieve either complete or partial remission. Therefore, neurosarcoidosis requires multidisciplinary specialist care and a comprehensive approach to each patient.
Sciatica is a common pain syndrome caused by compression of nerve roots at the L4/L5 or L5/S1 vertebral levels, most frequently due to intervertebral disc herniation. Symptoms include sharp pain radiating from the lumbar region through the buttock, the posterior and lateral thigh and lower leg, and down to the toes, along with sensory disturbances and muscle weakness. Treatment typically begins with conservative methods, primarily pharmacotherapy. Depending on pain severity, physical therapy is also recommended. In most cases, these approaches are sufficient. Epidural administration of glucocorticoids is one treatment option that has been shown to be effective for pain relief, particularly in the short-term. If there is no improvement, surgical intervention is considered. In Poland, single intramuscular or intravenous injections of dexamethasone are commonly used; however, the lack of scientific consensus prevents this method from being recognised as a standard treatment. The aim of this article is to evaluate the efficacy and rationale for the use of systemic use of glucocorticoids in the conservative treatment of sciatica. Studies on systemic glucocorticoid treatment show improvement in some patients, but the results remain inconclusive. Limitations include low statistical power due to small patient groups, inconsistent therapy protocols, and short follow-up periods. Systematic reviews and guidelines from international medical organisations suggest alternative therapeutic approaches, and systemic glucocorticoid use is generally not recommended for the treatment of sciatica. Therefore, continued research into this treatment method is necessary. Until more reliable data become available, it is advisable to follow current guidelines and the conclusions of meta-analyses.
Epilepsy is a common chronic neurological disorder that causes recurrent seizures, reduces quality of life, and increases the risk of unexpected death. The development of seizure-detection systems through mobile health technology has become possible due to rapid progress in wearable sensor technology and portable electroencephalography devices, and smartphonebased applications. This review examines existing research on these tools, which help treat epilepsy in both adult and paediatric patients. A medical literature search from 2015 to 2025 included systematic reviews and meta-analyses, randomised controlled trials, and clinical guidelines evaluating seizure-detection precision, self-management tools, telemonitoring functions, and patient-reported outcomes. Mobile applications which allow users to track seizures, send medication alerts, and access educational content show potential to enhance treatment compliance, although more research is needed to confirm their effectiveness. The combination of wearable devices with portable electroencephalography technology allows extended surveillance which successfully identifies generalised tonic-clonic seizures in clinical tests; however, their performance decreases when used in home environments because of increased false alerts. Telemedicine systems that combine application data with detector information allow healthcare providers to track patients remotely, which results in enhanced safety results for patients who have recurring seizures or nocturnal events. Future research should evaluate the medical value and deployment methods of mobile applications, wearable devices, and portable electroencephalography
Multiple sclerosis is an autoimmune disease of the central nervous system associated with abnormal activation of both cellular and humoral immune responses. B lymphocytes play a key role by crossing the damaged blood-brain barrier and releasing antibodies that contribute to inflammation within the central nervous system. The presence of oligoclonal bands in the cerebrospinal fluid is evidence of intrathecal immunoglobulin synthesis and serves as a recognised biochemical marker of multiple sclerosis. Despite their high sensitivity and specificity, oligoclonal bands have certain limitations. As a qualitative test, they do not reflect the severity of inflammation, are time-consuming and costly, and their interpretation may be subjective and dependent on the experience of the diagnostician. The 2024 revision of the McDonald criteria allows the use of the kappa free light chain index as an equivalent or alternative to oligoclonal band detection. Free kappa light chains, produced in excess by plasma cells, are components of immunoglobulins. Their measurement offers a simpler, faster, and more affordable quantitative method with diagnostic value similar to oligoclonal bands. When present at appropriate levels, they fulfil the criterion of dissemination in time and enable the diagnosis of multiple sclerosis, including in patients with radiologically isolated syndrome, clinically isolated syndrome, and primary progressive multiple sclerosis. Additionally, they may provide prognostic insight. It is suggested that their concentration may help estimate the time to radiological progression, disease relapse, or worsening of disability. Kappa free light chains, especially the calculated index reflecting intrathecal immunoglobulin synthesis within the central nervous system, represent a new and promising diagnostic option in multiple sclerosis, particularly in therapies targeting B lymphocytes.
Identifying risk factors for rapid progression of multiple sclerosis and initiating effective treatment are crucial for preventing disability, particularly in patients with relapsing remitting disease who develop a severe, rapidly progressive form. A 21 year old man presented with progressive lower limb weakness and gait disturbance, preceded by transient symptoms. Physical examination revealed pyramidal weakness, sensory impairment, and dysmetria (Expanded Disability Status Scale, EDSS 6.0). Magnetic resonance imaging showed more than 20 contrast enhancing T2/FLAIR lesions located cortically, periventricularly, in the corpus callosum, infratentorially, and within the spinal cord. Oligoclonal bands were present in cerebrospinal fluid. Steroid therapy led to improvement, but a relapse occurred one week later (EDSS 4.0), accompanied by new magnetic resonance imaging lesions. After initiation of natalizumab, remission was achieved at 12 months (EDSS 2.0). Risk factors for rapid progression include male sex, high early disease activity, motor or cerebellar symptoms, and extensive spinal cord involvement. Early recognition of a severe, rapidly progressive form of multiple sclerosis and timely initiation of high efficacy disease modifying therapy are essential to prevent disability.
This review article addresses the topic of central nervous system infections, specifically meningitis and encephalitis of infectious aetiology. It discusses the epidemiology (including the prevalence of individual pathogens and their geographic distribution) as well as currently recommended diagnostic methods, such as cultures of cerebrospinal fluid and other clinical materials, latex agglutination tests, polymerase chain reaction, serology, histopathology, antigen testing, fluorescence hybridisation, spectrometry, next-generation sequencing, imaging studies including computed tomography and nuclear magnetic resonance, and both conventional and electron microscopy. The article also describes treatment recommendations organised according to the etiological factor (bacteria, viruses, fungal pathogens, and parasites) and patient age. Other recommended interventions, such as reversal of immunosuppression and surgery, are also addressed. Diagnostic protocols for specific diseases are discussed in detail. Furthermore, the anatomy of the central nervous system is described, and other types of neuroinfections are listed, along with a discussion of their potential co-occurrence, and non-infectious factors causing meningitis, such as neoplastic diseases, systemic diseases, and medications. The section on meningitis describes characteristic symptoms of the disease and highlights differences between hospital-acquired (nosocomial) and community-acquired meningitis. Mollaret's disease (recurrent meningitis caused by human herpesvirus 2), post-infectious encephalomyelitis, vaccines used to prevent CNS infections, and differences in disease presentation between immunocompromised and immunocompetent patients are also discussed.
Primitive intracranial arteries, including the trigeminal, proatlantal, otic, hypoglossal, and stapedial arteries, are embryonic vascular structures that temporarily connect the anterior and posterior, or intracranial and extracranial, circulations before typically regressing during development. Their persistence into adulthood, although rare, may alter local haemodynamics, contributing to aneurysm formation, vessel stenosis, or cranial nerve dysfunction. However, given the low incidence of associated pathologies, the mere presence of a persistent primitive anastomosis is not considered a concern for aneurysm formation. The persistent trigeminal artery is the most commonly observed persistent intracranial artery, with an incidence rate of up to 0.6%. It is followed by the persistent hypoglossal artery, present in 0.02-0.09% of cases, and the persistent proatlantal artery, with an incidence of 0.03%, while others, such as the otic and stapedial arteries, are exceptionally rare. Each persistent anastomosis has distinct embryological origins, anatomical variants, and potential roles in cerebrovascular compensation. Although persistent arteries may serve as collateral pathways in cases of cerebrovascular stenosis or occlusion, they can also pose risks during neurosurgical and endovascular procedures. Given their potential association with vascular pathologies in some cases, precise recognition of these arteries via imaging is essential to prevent misdiagnosis and optimise therapeutic strategies. This study provides a comprehensive review of the embryology, anatomy, and clinical relevance of persistent primitive intracranial arteries, aiming to enhance understanding, facilitate diagnosis, and improve treatment planning in cerebrovascular interventions.
Electronic cigarette aerosols contain numerous chemicals that can affect the central nervous system through mechanisms involving oxidative stress, inflammatory processes, and blood-brain barrier dysfunction. When the liquid is heated, aldehydes, heavy metals, free radicals, and pyrolysis products of propylene glycol and glycerine are formed. These compounds lead to damage to endothelial structures, degradation of tight junction proteins, and increased blood-brain barrier permeability, which promotes the penetration of pro-inflammatory cytokines and the activation of microglia and astroglia. Preclinical studies have shown increased production of inflammatory mediators, disturbances in mitochondrial homeostasis, and changes in the functioning of transporters responsible for neuronal metabolism. Nicotine present in aerosols modulates the activity of nicotinic acetylcholine receptors, affecting dopaminergic, glutamatergic, and GABAergic transmission. These changes lead to neuroadaptation within the mesolimbic reward system and promote the reinforcement of addictive behaviours. Some aromatic compounds, including menthol and farnesol, may further exacerbate oxidative stress and enhance the effects of nicotine. Evidence from animal studies indicates that chronic exposure to electronic cigarette aerosols may lead to cognitive impairment, behavioural changes, and increased susceptibility to neurodegenerative processes, especially during developmental periods. Despite the growing number of mechanistic studies, clinical data remain limited. This paper summarises the current state of knowledge on the neurotoxic potential of electronic cigarette aerosols, with particular emphasis on molecular and cellular mechanisms, and highlights the need for further research into their long-term effects on the nervous system.
The diagnostic criteria for multiple sclerosis are constantly evolving. A single, specific and sensitive marker of the disease is still lacking; therefore, the diagnosis of multiple sclerosis remains a diagnosis of exclusion. At the same time, it is crucial to start therapy with drugs that inhibit disease progression as early as possible. The successive criteria for the diagnosis of multiple sclerosis, known as the McDonald criteria, have aimed to incorporate the need for rapid disease diagnosis without compromising high sensitivity and specificity. A subsequent version of the McDonald criteria was introduced in 2017, and after 2021 new recommendations for the diagnosis of this disease had been developed by an international committee of experts. The first full version of the proposed changes was presented at the annual ECTRIMS meeting in Copenhagen on 18 September 2024. Consequently, the newest criteria are referred to as the 2024 version, although the final set was published in 2025. The most important changes are updates of the dissemination in space criteria, such as the inclusion of the optic nerve as a typical location affected by demyelinating changes in multiple sclerosis and incorporation of new magnetic resonance imaging methods. It was also proposed that the dissemination in time criterion may no longer be necessary for diagnosis, for example with the use of new methods for detecting intrathecal immunoglobulin synthesis. The committee proposed when radiologically isolated syndrome should be considered a manifestation of multiple sclerosis. Finally, the need to clarify and unify the diagnostic criteria for multiple sclerosis in individuals over 50 and under 18 years of age, and for those with primary progressive multiple sclerosis, was addressed.
The number of older individuals with multiple sclerosis is steadily increasing, encompassing both those with late-onset multiple sclerosis and those experiencing long-term disease progression from earlier diagnoses. Late-onset multiple sclerosis (LOMS) refers to disease onset after the age of 50, while very-late-onset multiple sclerosis (VLOMS) is defined as onset after the age of 60. It is estimated that late-onset multiple sclerosis accounts for approximately 1.1-21.3% of patients, while 0.6-3.6% of multiple sclerosis cases are very-late-onset. Late-onset multiple sclerosis usually has a primary progressive course, and the first symptoms are pyramidal in 60-70% cases. The specific characteristics of multiple sclerosis in this population are influenced by immunosenescence and brain aging processes. Managing multiple sclerosis in older patients requires meticulous differential diagnosis and close monitoring, considering the impact of comorbidities and other age-related factors. Therapeutic decisions should be highly individualised, striking a balance between the efficacy and safety of available treatments. Given the limited data on optimal multiple sclerosis management in this demographic, further observational studies are essential. This review presents the current state of knowledge needed for understanding and effectively treating multiple sclerosis in older age.
Multiple sclerosis is chronic, autoimmune-mediated, demyelinating, and degenerative disease of the central nervous system that affects a broad population of patients of childbearing potential. The disease does not negatively influence pregnancy outcome or foetal health. Due to the availability of disease-modifying therapies, it is possible to individualise treatment decisions to include family planning. Certain disease-modifying therapies may impact foetal health. Decision-making in women has to take into consideration guidelines from the Food and Drug Administration and the European Medicines Agency, as well as data from clinical trials and pregnancy registries. Health care providers should discuss family planning early and frequently with patients and their partners, considering disease activity, comorbidities, wash-out periods after treatment, and the risk of discontinuation rebound. Postpartum care should focus on the health of both the patient and the newborn. Patients should be encouraged to plan a family and breastfeed. Disease-modifying treatment should be resumed in women at risk of postpartum relapse. An increasing body of data on drug transfer to breast milk helps choose safe treatment for both the patient and the newborn. Counselling around disease-modifying drugs and symptomatic medication in pregnancy should ideally take place before the woman discontinues contraception. There is a need for new updates and data to guide how to balance multiple sclerosis stability during pregnancy and postpartum with foetal and neonatal safety.
This article highlights the role of the patient in the selection of sequential therapy for multiple sclerosis through the examination of two clinical case examples. The first case presents a patient with an exacerbation of relapsing-remitting multiple sclerosis, who was irregularly taking an oral medication administered twice a day. The second case describes a patient who experienced numerous side effects of the drug, which was administered via intramuscular injections. In both patients, due to clinical indications, a change of therapy was implemented. The key factor in selecting the medication was identifying the problems and complaints related to the current therapy, determining treatment priorities for the patients, and then individually modifying the treatment. Following the change, an improvement was observed in terms of compliance, with very good clinical and radiological control of disease progression and increased patient satisfaction.
B lymphocytes are specialised leukocytes essential to the adaptive immune response, characterised by specificity and memory, in contrast to innate immunity. They mediate humoral immunity by targeting extracellular pathogens, while T lymphocytes are pivotal in intracellular antigen destruction and immune regulation. The differentiation of B cells begins with hematopoietic stem cells (HSCs), pluripotent cells in the bone marrow that generate all blood cell lineages. HSCs differentiate into myeloid and lymphoid lineages, giving rise to B and T lymphocytes. During development, B cells acquire antigen-specific receptors (B-cell receptor, BCR) and express CD20, a key surface antigen critical for their identification and therapeutic targeting. Monoclonal antibodies against CD20 are a cornerstone of multiple sclerosis treatment. They deplete B cells, modulate immune responses, and reduce disease activity. Anti-CD20 therapies, including ocrelizumab, ofatumumab, rituximab, and ublituximab, vary in binding site specificity, molecular structure, pharmacokinetics, and administration routes, impacting their efficacy and safety profiles. CD20 is also expressed in a rare subset of T cells with unique pro-inflammatory properties, highlighting its diverse immunological roles. This review explores the biology of CD20-positive lymphocytes, the mechanisms of action of anti-CD20 therapies, and their applications in multiple sclerosis. It discusses the nuances of efficacy, immunogenicity, and adverse effects, including neutropenia and secondary immune dysregulation, providing insights into personalised therapeutic strategies.
Ofatumumab is a subcutaneously administered, fully human anti-CD20 monoclonal antibody, approved for the treatment of relapsing multiple sclerosis. It is considered a highly effective therapy, and at the same time has a good safety and tolerability profile. This review presents up-to-date information regarding the general safety profile of ofatumumab, including the incidence of serious infections, injection-related reactions, malignancies, and effects on laboratory parameters, such as immunoglobulins M and G, and lymphocyte and neutrophil counts. Currently available data show that the most common adverse effects of ofatumumab include upper respiratory tract infections (mild to moderate), injection-related reactions (mild to moderate, and very rare beyond the first injection), and urinary tract infections. The depletion of CD20+ lymphocytes causes a decrease in immunoglobulin M levels, which does not correlate with the risk of serious infections. The drop in absolute lymphocyte count is temporary, and neutropaenia risk is very low (<1%). So far, no increased risk of associated malignancies has been identified for ofatumumab. All disease-modifying therapies approved for multiple sclerosis exert complex effects on immune system function; thus, potential adverse events may be unpredictable. Therefore, active monitoring of multiple sclerosis patients subject to immune therapies, including ofatumumab, remains essential. This applies to patients in open-label extension studies, as well as patients in real-world clinical settings.
Anti-CD20 monoclonal antibodies represent a particularly important class of drugs in the treatment of multiple sclerosis. This results from the discovery of the instrumental function of B cells in the initiation of multiple sclerosis autoimmunity, as well as their role in the protraction of the disease process. Ofatumumab is the first fully human anti-CD20 monoclonal antibody. Phase 2 and 3 trials demonstrated high efficacy of ofatumumab in a population of patients with the relapsing-remitting and relapsing form of multiple sclerosis. Ofatumumab very efficiently decreased number of relapses. In comparison to placebo or the active comparator, teriflunomide, the annual relapse rate was reduced by more than 50%. Even more spectacular efficacy was demonstrated in the reduction of active magnetic resonance imaging lesions. Compared to teriflunomide, the number of gadolinium-enhancing lesions was reduced by more than 90%. In the pooled population from both phase 3 studies, ofatumumab also reduced the risk for disability progression. These data allow for the classification of ofatumumab in the group of high-efficacy treatment agents for multiple sclerosis. In a protracted disorder like multiple sclerosis, it is critically important to understand long-term efficacy and safety. To date, six-year data are available on ofatumumab treatment in relapsing-remitting multiple sclerosis. These results confirm the high efficacy of ofatumumab in long-term treatment in the population of relapsing-remitting multiple sclerosis patients.
Current evidence emphasises the immunomodulatory role of vitamin D, particularly through the enhancement of immune tolerance mechanisms. Vitamin D deficiency is an established risk factor for the development of autoimmune diseases, including multiple sclerosis. Vitamin D has a range of neuroprotective properties and remyelinating potential in multiple sclerosis patients. Reduced serum vitamin D levels are associated with progression of the disease, increased cognitive impairment, and fatigue. However, the therapeutic effect of vitamin D supplementation on clinical progression (incidence of relapses and disability progression) has not been confirmed. In contrast, some findings support a beneficial effect of vitamin D supplementation on radiological activity. Despite the above data, the use of vitamin D as an adjunct therapy to multiple sclerosis treatment is currently not a standardised recommendation. According to the Polish experts' guidelines of endocrinological societies, patients with multiple sclerosis are considered a special risk group for vitamin D deficiency, which necessitates screening for vitamin D status based on the assessment of serum 25(OH)D concentration, with subsequent correction of deficiency under control of this parameter to achieve an optimal 25(OH)D concentration (>30-50 ng/mL). Prophylactic doses of cholecalciferol are 1,000-4,000 IU/day, depending on age. In contrast, the therapeutic dose of cholecalciferol is 4,000 IU/day, with 25(OH)D reassessment after 8-12 weeks of therapy. The presented principles of prophylactic and therapeutic treatment of vitamin D deficiency are associated with high efficacy and safety, and could potentially result in the enhancement of anti-inflammatory mechanisms and improved overall well-being in multiple sclerosis patients.
The ketogenic diet, a high-fat, low-carbohydrate dietary approach, is increasingly used as a therapeutic strategy for the treatment of drug-resistant epilepsy and neurodegenerative diseases such as Alzheimer’s and Parkinson’s disease. The primary mechanism of the ketogenic diet is the induction of a state of ketosis, during which the brain begins to use ketone bodies. Not only do ketones replace glucose as a fuel but also exhibit a number of neuroprotective effects, such as reducing oxidative stress, stabilising mitochondrial function, mitigating excitotoxicity, reducing neuroinflammatory signalling pathways, and stimulating autophagy. In drug-resistant epilepsy, the ketogenic diet can significantly reduce seizure frequency, especially in children with metabolic syndromes (glucose transporter type 1 deficiency syndrome, pyruvate dehydrogenase complex deficiency). In Alzheimer’s disease, the ketogenic diet improves cerebral metabolism, reduces β-amyloid deposition, and supports cognitive function, especially in the early stages of the disease. In Parkinson’s disease, a reduction in non-motor symptoms, improvement in mood and mitochondrial function, and potential modulation of the gut microbiota have been observed. However, it should be noted that the ketogenic diet is not without side effects, which include gastrointestinal disorders, hypoglycaemia, lipid abnormalities, kidney stones, micronutrient deficiencies, and possible stunted growth in children. Contraindications, on the other hand, include metabolic diseases, liver and kidney failure, type 1 diabetes, and pregnancy. In conclusion, the ketogenic diet is a promising non-pharmacological therapeutic option in neurology. However, its use requires individual assessment, specialised supervision, and further multicentre studies to confirm long-term efficacy and safety.
The issue of patients experiencing difficulty in completely voiding their bladders is well documented in the clinical setting. It is common for both urologists and family doctors to encounter neurological dysfunctions of the lower urinary tract. In numerous neurological conditions, incomplete bladder emptying and urinary retention are frequently observed. This problem predominantly manifests in cases of bladder detrusor muscle hypofunction or detrusor-sphincter dyssynergia. Urinary retention can lead to recurrent urinary tract infections and, in severe cases, kidney damage. In Poland, the most common management method remains the insertion of a permanent catheter into the bladder. Both permanent transurethral catheterisation and, to a lesser extent, suprapubic cystostomy are associated with various complications and an increased risk of urinary tract infections. The first documented use of clean intermittent self-catheterisation, or catheterisation performed by a third party, dates back to the 1970s. Since then, this approach has become increasingly widespread in clinical practice. The primary rationale for self-catheterisation is the reduced risk of urinary tract infections compared to permanent catheters. However, self-catheterisation requires greater involvement from healthcare professionals, particularly urology nurses. It is essential to provide adequate support to patients and their caregivers during the preparatory phase for self-catheterisation. Despite these efforts, a significant proportion of patients ultimately discontinue self-catheterisation.
