## 1 Introduction  
Neuropathic pain is a complicated disorder that can be a long-lasting complex chronic condition characterized mainly by various sensory, cognitive, and emotional symptoms [1]. An abnormal alteration of the somatosensory system, resulting from damage to the nervous system, is the real cause of neural pain [2]. The senses of touch, pressure, pain, temperature, position, motion, and vibration are all perceived through the somatosensory system. In total, 7-10% of the general population is affected by the neuropathological pain from the somatosensory system, which includes central neurons and peripheral fibres (A\(\beta\), A\(\delta\), and C fibres). Several factors that can lead to neuropathic pain and its pervasiveness are expected to increase over time due to factors such as the ageing of the world population, the increasing prevalence of diabetes, and higher cancer survival rates after chemotherapy [3]. Neuropathatic pain is caused by nerve damage in the central and peripheral nervous systems [4]. Worldwide, peripheral neuropathic pain is becoming increasingly debilitating, with an increasing number of people suffering from it [5]. After peripheral nerve damage, a series of actions occur in the primary afferents that result in peripheral sensitization, leading to impulsive nociceptor activation, increased reactivity to suprathreshold stimuli, and lowered pain threshold [6]. The inflammatory reactions in the injured nerve trunk may cause ectopic activation of nociceptors, which would result in spontaneous pain. During overactive nociceptors, the brain and spinal cord undergo pathological changes. These changes contribute to the perception of mechanoreceptive fibres as painful sensations. A constant supply of growth factors on normal skin is essential for maintaining the neuronal phenotype [5]. It is well-established and well-supported that nerve growth factor (NGF) is associated with different pains, including visceral, inflammatory, and neuropathic [7]. In both the peripheral and central nervous systems, NGF is a vital neurotrophin that controls neuron survival and development [8]. NGF is retrogradely transported from the innervation sites of sensory neuron cell bodies, which modulate neuropeptide transmitter concentrations [9]. In the animal model, [PERSON]'s degeneration is a prerequisite for neuropathic pain after peripheral nerve injury. Activated Schwann cells produce significant amounts of NGF over many weeks during [PERSON]'s degeneration; thus, in the context of nerve diseases, NGF may play a role in neuropathic pain [10]. [PERSON] et al., in 2013, concluded that various pains and conditions had been associated with elevated levels of growth factor NGF and its involvement in enhancing pain sensation. The analgesic effects of NGF antagonism have the potential to be improved compared with currently available treatments [11]. In addition, pro-inflammatory cytokines have been found to increase pain sensations by altering neurotransmitter release, particularly substance P [12]. In the peripheral and central nervous systems, the substance P is known as a transmitter of nociception and inflammation by altering cellular signalling pathways [13]. Furthermore, the literature disclosed the contribution of inflammatory cytokines, inducible nitric oxide synthase (iNOS), cyclooxygenase, and nuclear factor kappa B (NF-kB) in the pathogenesis of neuropathic pain [12]. There are several hypotheses about peripheral neuropathic pain and its treatment, but we have to give attention to the factors that cause the condition or symptoms per se, and the processes that cause the transformation of such conditions [14]. Most research has focused on conventional non-steroidal anti-inflammatory drugs and opioid-based treatments [15]. Some conventional analgesics, such as carbamazepine, pregabalin, gabapentin, etc., have been accepted for treating neuropathic pain for the last 50 years.