Nerve growth factor (NGF) is a neurotrophic protein that has crucial roles in survival, growth and differentiation. It is expressed in neuronal and non-neuronal tissues. NGF exerts its effects via two types of receptors including the high affinity receptor, tropomyosin receptor kinase A and the low affinity receptor p75 neurotrophin receptor highlighting the complex signaling pathways that underlie the roles of NGF. In pain perception and transmission, multiple studies shed light on the effects of NGF on different types of pain including inflammatory, neuropathic, cancer and visceral pain. Also, the binding of NGF to its receptors increases the availability of many nociceptive receptors such as transient receptor potential vanilloid 1, transient receptor potential ankyrin 1, N-methyl-D-aspartic acid, and P2X purinoceptor 3 as well as nociceptive transmitters such as substance P and calcitonin gene-related peptide. The role of NGF in pain has been documented in pre-clinical and clinical studies. This review aims to shed light on the role of NGF and its signaling in different types of pain.

Chronic pain is a universal problem that directly evolves the central nervous system, altering both its structure and function. This review discusses neuroplastic alterations in critical areas in the brain like the anterior cingulate cortex, insula, prefrontal cortex, primary (S1) and secondary (S2) somatosensory cortices, and thalamus. These regions exhibit gray matter decrease and changes in connectivity during chronic pain. Several cortical networks, mainly the central executive network, the default mode network, and the salience network exhibit neuroplasticity which reallocates cognitive and emotional resources to pain processing. Thus, it was reported that sensitivity to pain enhances emotional suffering, indicating that altered connectivity and functional reorganization of these networks support maladaptive pain processing and underpin chronic pain persistence. Neuroplasticity-focused treatments such as brain stimulation, neuro-feedback, and exercise-based therapies constitute potential interventions for preventing such negative changes. Further, innovative neuroimaging biomarkers are effective in demonstrating precise neural changes and in providing information about the diagnosis of chronic pain syndromes. This review highlights neuro-plastic changes in chronically painful patients and acknowledges the brain’s plasticity as a target for chronic pain treatment. It, also, points to the diagnostic strategies and practical interventions that address these alterations.

Nerve growth factor (NGF) is a neurotrophic protein that has crucial roles in survival, growth and differentiation. It is expressed in neuronal and non-neuronal tissues. NGF exerts its effects via two types of receptors including the high affinity receptor, tropomyosin receptor kinase A and the low affinity receptor p75 neurotrophin receptor highlighting the complex signaling pathways that underlie the roles of NGF. In pain perception and transmission, multiple studies shed light on the effects of NGF on different types of pain including inflammatory, neuropathic, cancer and visceral pain. Also, the binding of NGF to its receptors increases the availability of many nociceptive receptors such as transient receptor potential vanilloid 1, transient receptor potential ankyrin 1, N-methyl-D-aspartic acid, and P2X purinoceptor 3 as well as nociceptive transmitters such as substance P and calcitonin gene-related peptide. The role of NGF in pain has been documented in pre-clinical and clinical studies. This review aims to shed light on the role of NGF and its signaling in different types of pain.

Chronic pain is a universal problem that directly evolves the central nervous system, altering both its structure and function. This review discusses neuroplastic alterations in critical areas in the brain like the anterior cingulate cortex, insula, prefrontal cortex, primary (S1) and secondary (S2) somatosensory cortices, and thalamus. These regions exhibit gray matter decrease and changes in connectivity during chronic pain. Several cortical networks, mainly the central executive network, the default mode network, and the salience network exhibit neuroplasticity which reallocates cognitive and emotional resources to pain processing. Thus, it was reported that sensitivity to pain enhances emotional suffering, indicating that altered connectivity and functional reorganization of these networks support maladaptive pain processing and underpin chronic pain persistence. Neuroplasticity-focused treatments such as brain stimulation, neuro-feedback, and exercise-based therapies constitute potential interventions for preventing such negative changes. Further, innovative neuroimaging biomarkers are effective in demonstrating precise neural changes and in providing information about the diagnosis of chronic pain syndromes. This review highlights neuro-plastic changes in chronically painful patients and acknowledges the brain’s plasticity as a target for chronic pain treatment. It, also, points to the diagnostic strategies and practical interventions that address these alterations.

Nerve growth factor (NGF) is a neurotrophic protein that has crucial roles in survival, growth and differentiation. It is expressed in neuronal and non-neuronal tissues. NGF exerts its effects via two types of receptors including the high affinity receptor, tropomyosin receptor kinase A and the low affinity receptor p75 neurotrophin receptor highlighting the complex signaling pathways that underlie the roles of NGF. In pain perception and transmission, multiple studies shed light on the effects of NGF on different types of pain including inflammatory, neuropathic, cancer and visceral pain. Also, the binding of NGF to its receptors increases the availability of many nociceptive receptors such as transient receptor potential vanilloid 1, transient receptor potential ankyrin 1, N-methyl-D-aspartic acid, and P2X purinoceptor 3 as well as nociceptive transmitters such as substance P and calcitonin gene-related peptide. The role of NGF in pain has been documented in pre-clinical and clinical studies. This review aims to shed light on the role of NGF and its signaling in different types of pain.

Chronic pain is a universal problem that directly evolves the central nervous system, altering both its structure and function. This review discusses neuroplastic alterations in critical areas in the brain like the anterior cingulate cortex, insula, prefrontal cortex, primary (S1) and secondary (S2) somatosensory cortices, and thalamus. These regions exhibit gray matter decrease and changes in connectivity during chronic pain. Several cortical networks, mainly the central executive network, the default mode network, and the salience network exhibit neuroplasticity which reallocates cognitive and emotional resources to pain processing. Thus, it was reported that sensitivity to pain enhances emotional suffering, indicating that altered connectivity and functional reorganization of these networks support maladaptive pain processing and underpin chronic pain persistence. Neuroplasticity-focused treatments such as brain stimulation, neuro-feedback, and exercise-based therapies constitute potential interventions for preventing such negative changes. Further, innovative neuroimaging biomarkers are effective in demonstrating precise neural changes and in providing information about the diagnosis of chronic pain syndromes. This review highlights neuro-plastic changes in chronically painful patients and acknowledges the brain’s plasticity as a target for chronic pain treatment. It, also, points to the diagnostic strategies and practical interventions that address these alterations.

Nerve growth factor (NGF) is a neurotrophic protein that has crucial roles in survival, growth and differentiation. It is expressed in neuronal and non-neuronal tissues. NGF exerts its effects via two types of receptors including the high affinity receptor, tropomyosin receptor kinase A and the low affinity receptor p75 neurotrophin receptor highlighting the complex signaling pathways that underlie the roles of NGF. In pain perception and transmission, multiple studies shed light on the effects of NGF on different types of pain including inflammatory, neuropathic, cancer and visceral pain. Also, the binding of NGF to its receptors increases the availability of many nociceptive receptors such as transient receptor potential vanilloid 1, transient receptor potential ankyrin 1, N-methyl-D-aspartic acid, and P2X purinoceptor 3 as well as nociceptive transmitters such as substance P and calcitonin gene-related peptide. The role of NGF in pain has been documented in pre-clinical and clinical studies. This review aims to shed light on the role of NGF and its signaling in different types of pain.

Chronic pain is a universal problem that directly evolves the central nervous system, altering both its structure and function. This review discusses neuroplastic alterations in critical areas in the brain like the anterior cingulate cortex, insula, prefrontal cortex, primary (S1) and secondary (S2) somatosensory cortices, and thalamus. These regions exhibit gray matter decrease and changes in connectivity during chronic pain. Several cortical networks, mainly the central executive network, the default mode network, and the salience network exhibit neuroplasticity which reallocates cognitive and emotional resources to pain processing. Thus, it was reported that sensitivity to pain enhances emotional suffering, indicating that altered connectivity and functional reorganization of these networks support maladaptive pain processing and underpin chronic pain persistence. Neuroplasticity-focused treatments such as brain stimulation, neuro-feedback, and exercise-based therapies constitute potential interventions for preventing such negative changes. Further, innovative neuroimaging biomarkers are effective in demonstrating precise neural changes and in providing information about the diagnosis of chronic pain syndromes. This review highlights neuro-plastic changes in chronically painful patients and acknowledges the brain’s plasticity as a target for chronic pain treatment. It, also, points to the diagnostic strategies and practical interventions that address these alterations.

Nerve growth factor (NGF) is a neurotrophic protein that has crucial roles in survival, growth and differentiation. It is expressed in neuronal and non-neuronal tissues. NGF exerts its effects via two types of receptors including the high affinity receptor, tropomyosin receptor kinase A and the low affinity receptor p75 neurotrophin receptor highlighting the complex signaling pathways that underlie the roles of NGF. In pain perception and transmission, multiple studies shed light on the effects of NGF on different types of pain including inflammatory, neuropathic, cancer and visceral pain. Also, the binding of NGF to its receptors increases the availability of many nociceptive receptors such as transient receptor potential vanilloid 1, transient receptor potential ankyrin 1, N-methyl-D-aspartic acid, and P2X purinoceptor 3 as well as nociceptive transmitters such as substance P and calcitonin gene-related peptide. The role of NGF in pain has been documented in pre-clinical and clinical studies. This review aims to shed light on the role of NGF and its signaling in different types of pain.

Chronic pain is a universal problem that directly evolves the central nervous system, altering both its structure and function. This review discusses neuroplastic alterations in critical areas in the brain like the anterior cingulate cortex, insula, prefrontal cortex, primary (S1) and secondary (S2) somatosensory cortices, and thalamus. These regions exhibit gray matter decrease and changes in connectivity during chronic pain. Several cortical networks, mainly the central executive network, the default mode network, and the salience network exhibit neuroplasticity which reallocates cognitive and emotional resources to pain processing. Thus, it was reported that sensitivity to pain enhances emotional suffering, indicating that altered connectivity and functional reorganization of these networks support maladaptive pain processing and underpin chronic pain persistence. Neuroplasticity-focused treatments such as brain stimulation, neuro-feedback, and exercise-based therapies constitute potential interventions for preventing such negative changes. Further, innovative neuroimaging biomarkers are effective in demonstrating precise neural changes and in providing information about the diagnosis of chronic pain syndromes. This review highlights neuro-plastic changes in chronically painful patients and acknowledges the brain’s plasticity as a target for chronic pain treatment. It, also, points to the diagnostic strategies and practical interventions that address these alterations.