Neuropathic pain (NeP) is a disorder of the nervous system resulting from altered mechanisms operating at the peripheral nervous system, spinal cord and supraspinal levels and is defined by the International Association for the Study of Pain as pain resulting from nervous system pathologies that cause changes in the function, chemistry and structure of neurons . NeP affects 2-8% of the world population and can have a significant impact on the patient's functional abilities and quality of life. NeP can be caused by spinal cord injury, brain and spinal cord tumours and other diseases affecting the nervous system. NeP can be secondary to extremely common conditions such as diabetes, stroke, cancer, herpes zoster virus infection and autoimmune disease. These recommendations were finalised in 2019 and published in April 2020. Following the GRADE system, the recommendations suggest first-line treatment options including serotonin-noradrenaline reuptake inhibitors (duloxetine and venlafaxine), gabapentin, tricyclic antidepressants, and the specialised use of topical lidocaine and transcutaneous electrical nerve stimulation for peripheral neuropathic pain. Pregabalin, tramadol and combination therapy (combining antidepressants with gabapentinoids) are recommended as second-line treatments. Highly concentrated capsaicin patches and botulinum toxin A are recommended as second-line treatments, especially for focal peripheral neuropathic pain. Third-line treatment options include high-frequency repetitive transcranial magnetic stimulation (rTMS) of the primary motor cortex (motor cotex-1/M1), spinal cord stimulation (for failed back surgery syndrome and painful diabetic polyneuropathy) and strong opioids as a last resort in the absence of alternatives. In addition, psychotherapy, including cognitive behavioural therapy and mindfulness, is recommended as second-line treatment in combination with other therapies.

Pregabalin is also used in the treatment of epilepsy by blocking and modulating the α2 δ subunit of voltage-dependent calcium channels. There are studies showing that antiepileptics cause folate and vitamin B12 deficiency in epilepsy patients. In our study, we aimed to retrospectively analyse vitamin B12 and folic acid levels before and after treatment in patients using antiepileptics (anticonvulsants) for neuropathic pain.

After the acceptance of the study (after obtaining ethics committee approval), patients who have been followed up for at least 6 months in the physical medicine and rehabilitation outpatient clinic with a diagnosis of neuropathic pain and who use pregabalin will be evaluated retrospectively (1-year records). Blood vitamin B12 and folate (folic acid) levels of the patients before and after pregabalin use will be determined. Patients will be evaluated whether there is a change in vitamin B12 and folic acid levels due to drug use.

Inclusion Criteria:

• Patients aged 18-90 years who have been diagnosed with neuropathic pain, whose vitamin B12 and folic acid levels have been analysed, who do not receive vitamin B12 and folic acid treatment, and who do not have diabetes mellitus, liver and kidney failure

Exclusion Criteria:

• Patients receiving vitamin B12 and folic acid therapy at the time of antiepileptic (anticonvulsant) drugs initiation, patients with hepatic and renal insufficiency

Patients who were followed up for 6 months in the physical medicine and rehabilitation clinic with a diagnosis of neuropathic pain and who used antiepileptic (anticonvulsant) drugs will be retrospectively evaluated for the 6 months period (June-December 2024) before the ethics committee approval was obtained. Blood vitamin B12 and folate (folic acid) levels of the patients before and after antiepileptic drug use will be determined. Patients will be evaluated whether there is a change in vitamin B12 and folic acid levels depending on drug use.