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Neurological disorders associated to long term tramadol utilization: Pathological mechanisms and future perspective.

Tramadol is a synthetic analog of codeine used to treat pain of moderate to severe intensity and is reported to have neurotoxic potential. At therapeutic dose, tramadol does not cause major side effects in comparison to other opioid analgesics, and is useful for the management of neurological problems like anxiety and depression. Long term utilization of tramadol is associated with various neurological disorders like seizures, serotonin syndrome, Alzheimer's disease and Parkinson's disease. Tramadol produces seizures through inhibition of nitric oxide, serotonin reuptake and inhibitory effects on GABA receptors. Extensive tramadol intake alters redox balance through elevating lipid peroxidation and free radical leads to neurotoxicity and produce neurobehavioral deficits. During Alzheimer's disease progression some intracellular signaling molecules like cGMP, cAMP, PKC and PKA are known to decreased and affect to both learning and memory. Pharmacologically tramadol produces actions similar to selective serotonin reuptake inhibitors (SSRIs), increases the concentration of the serotonin which produce cause serotonin syndrome. In addition tramadol also inhibit GABAA receptors in the CNS has been evidenced to interfere with dopamine synthesis and release, responsible for motor symptoms. The reduced level of dopamine may produce bradykinesia and tremors which are chief motor abnormalities in Parkinson's disease (PD).