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.

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.

Oxidative stress develops when there is an excess of oxidants leading to molecular and cellular damage. Seizure activity leads to oxidative stress and the resulting increased lipid peroxidation. Generally, antiseizure medications reduce oxidative stress, although the data on levetiracetam are ambiguous. Exogenous antioxidants (vitamin E, resveratrol, hesperidin, and curcumin) have been documented to exert an anticonvulsant effect in animal models of seizures and some recent clinical data point to curcumin as an affective adjuvant for the therapy of pediatric intractable epilepsy. Melatonin is an antioxidant with an ability to attenuate seizure activity induced by various convulsants in rodents. Its clinical effectiveness has been also confirmed in a number of clinical studies. Experimental studies point to a possibility that endogenous melatonin may possess proconvulsive activity. Moreover, some scarce clinical data seem to express this view; however, a limited number of patients were included. The anticonvulsant activity of exogenous melatonin may involve GABA-mediated inhibition, while endogenous melatonin may act as a proconvulsant due to a decrease in the brain dopaminergic transmission. Antioxidants, including melatonin, may be considered as adjuvants in the therapy of epilepsy and melatonin, in addition, in patients with epilepsy suffering from sleep disorders.

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Introduction and objective: Multiple sclerosis (MS) is the most common demyelinating disease. The symptoms resulting from the destruction of the myelin sheaths in the CNS are very diverse. The cause of the disease is not fully understood. Treatment can be divided into symptomatic, relapse...