Neuropathic pain is generally defined as a non-physiological pain experience caused by damage to the nervous system. It can occur spontaneously, as a reaction to a given stimulus, or independently of its action, leading to unusual pain sensations usually referred to as firing, burning or throbbing. In the course of spine disorders, pain symptoms commonly occur. According to available epidemiological studies, a neuropathic component of pain is often present in patients with spinal diseases, with a frequency ranging from 36% to 55% of patients. Distinguishing between chronic nociceptive pain and neuropathic pain very often remains a challenge. Consequently, neuropathic pain is often underdiagnosed in patients with spinal diseases. In reference to current guidelines for the treatment of neuropathic pain, gabapentin, serotonin and norepinephrine reuptake inhibitors and tricyclic antidepressants constitute first-line therapeutic agents. However, long-term pharmacologic treatment often leads to developing tolerance and resistance to used medications. Therefore, in recent years, a plethora of therapeutic methods for neuropathic pain have been developed and investigated to improve clinical outcomes. In this review, we briefly summarized current knowledge about the pathophysiology and diagnosis of neuropathic pain. Moreover, we described the most effective treatment approaches for neuropathic pain and discussed their relevance in the treatment of spinal pain.

Epilepsy is a chronic disease of the central nervous system characterized by recurrent epileptic seizures. As a result of epileptic seizure or status epilepticus oxidants are excessively formed, which may be one of the causes of neuronal death. Given the role of oxidative stress in epileptogenesis, as well as the participation of this process in other neurological conditions, we decided to review the latest state of knowledge regarding the relationship between selected newer antiepileptic drugs (AEDs), also known as antiseizure drugs, and oxidative stress. The literature review indicates that drugs enhancing GABA-ergic transmission (e.g., vigabatrin, tiagabine, gabapentin, topiramate) or other antiepileptics (e.g., lamotrigine, levetiracetam) reduce neuronal oxidation markers. In particular, levetiracetam may produce ambiguous effects in this regard. However, when a GABA-enhancing drug was applied to the healthy tissue, it tended to increase oxidative stress markers in a dose-dependent manner. Studies on diazepam have shown that it exerts a neuroprotective effect in a “U-shaped” dose-dependent manner after excitotoxic or oxidative stress. Its lower concentrations are insufficient to protect against neuronal damage, while higher concentrations produce neurodegeneration. Therefore, a conclusion follows that newer AEDs, enhancing GABA-ergic neurotransmission, may act similarly to diazepam, causing neurodegeneration and oxidative stress when used in high doses.

Introduction and purpose: Migraine is a chronic condition affecting up to 10% of the adult population in Poland. Migraine pain is severe and may be accompanied by nausea or vomiting, as well as hypersensitivity to light, sounds or smells. Chronic form of migraine means the occurrence of headache a minimum of 15 days per month, for a period of at least three months, of which eight days or more of pain meet the criteria for migraine pain. The chronic form of migraine is targeted for treatment with botulinum toxin, a neurotoxin secreted by the bacteria Clostridium botulinum. Brief description of the state of knowledge: The pathogenesis of migraine is still unknown. There are many hypotheses explaining the origin of migraine pain, of which the most plausible seems to be the theory involving the trigeminal nerve system, as well as trigger points in the head and neck area. Their activation leads to the triggering of pain. Botulinum toxin has been used to treat migraine for several years. The only registered drug is Botox, the effectiveness of which has been confirmed in clinical studies. The preparation is administered by injection into the muscles of the head and neck region in cycles with an interval of 12 weeks. Botulinum toxin works by blocking the release of inflammatory and pain mediators from the trigeminal nerve endings. Summary: Chronic migraine refers to the occurrence of headache for more than half of the month, which significantly reduces the quality of life of people worldwide. Migraine headaches often refractory to pharmacological treatment may respond well to botulinum toxin type A. Therapy should be under the supervision of a neurologist, who will familiarise the patient with the expected effects of botulinum toxin treatment before starting treatment.

Along with the increasing number of reported cases, multiple sclerosis, one of the main causes of disability among young adults, is nowadays an increasingly common health problem. Considering the fact that it occurs mainly between 20 and 40 years and affects women more often, the question of the impact of the disease on pregnancy becomes obvious. In view of the wide selection of drugs for various purposes and often highly individualized forms of therapy, it seems also important to determine the safety profile of these agents in relation to the health of the pregnant woman and the fetus. All of this is a significant challenge for neurologists and obstetricians and is the subject of many research and studies. The awareness of society, especially women, in the face of the growing problem seems to be equally important. This paper summarizes the current state of knowledge on these issues.

Introduction. Acute respiratory distress syndrome is an inflammatory process that results in impaired lung function. It is predicted that by 2025, it will be the third largest cause of death. In some cases, extracorporeal membrane oxygenation may be the last option, improving patient outcome. Case report. The study presents a case of successful treatment od 47-year-old man. Due to respiratory failure following trauma, veno-venous extracorporeal membrane oxygenation therapy was initiated. Systemic anticoagulation with unfractionated heparin was not used in this case. A prophylactic dose of low molecular weight heparin was administered instead. After stabilization of the vital signs, the patient was discharged from the intensive care unit. Conclusions. Extracorporeal membrane oxygenation might be a good option for patients suffering from severe acute respiratory distress syndrome, but protective ventilation is still a method of choice. There have been studies indicating patients outcome improvement; however mortality reduction is still elusive.