If the sensory system becomes impacted by injury or disease, the nerves in that system can't function in the transmitting of sensation to the brain. This can lead to a sensation of numbness, or lack of sensation. In some cases when the sensory system is injured, individuals can experience pain in the affected region. Neuropathic pain does not start quickly or ends quickly. It's a chronic condition that leads to symptoms of persistent pain. For many, the intensity of the symptoms can come and go throughout a day. Neuropathic pain is thought to be associated with peripheral nerve problems, i.e. neuropathy caused by diabetes, spinal stenosis, injury to the brain or spinal cord can also lead to chronic neuropathic pain.
NEUROPATHIC PAIN
Objectives:
- What is it?
- What is the pathophysiology behind it?
- What are the causes
- What are some of the pathways
- How can we fix it?
NEUROPATHIC PAIN
- Pain initiated or caused by a primary lesion or dysfunction in the somatosensory nervous system.
- Neuropathic pain is usually chronic, difficult to treat and often resistant to standard analgesic management.
PATHOGENESIS OF NEUROPATHIC PAIN
- PERIPHERAL MECHANISMS
- After a peripheral nerve lesion, neurons become more sensitive and develop abnormal excitability and elevated sensitivity to stimulation
- This is known as...Peripheral Sensitization!
- CENTRAL MECHANISMS
- As a consequence of ongoing spontaneous activity arising in the periphery, neurons develop an increased background activity, enlarged receptive fields and increased responses to afferent impulses, including normal tactile stimuli
- This is known as...Central Sensitization!
COMMON CAUSES
Lesions or diseases of the somatosensory nervous system can lead to altered and disordered transmission of sensory signals into the spinal cord and the brain; common conditions associated with neuropathic pain include:- Postherpetic neuralgia
- Trigeminal neuralgia
- Painful radiculopathy
- Diabetic neuropathy
- HIV infection
- Leprosy
- Amputation
- Peripheral nerve injury pain
- Stroke (in the form of central post-stroke pain)
PHANTOM LIMB PAIN & AUGMENTED REALITY
- Phantom Limb Pain and AR
NEUROGENIC INFLAMMATION
Objectives:
- What is it?
- What is the pathophysiology behind it?
- What are the causes
- How can we fix it?
NEUROGENIC INFLAMMATION
- Neurogenic inflammation is a neurally elicited, local inflammatory response characterized by vasodilation, increased vascular permeability, mast cell degranulation, and the release of neuropeptides including SP and calcitonin gene-related peptide (CGRP)
- It appears to play an important role in the pathogenesis of numerous disease including migraine, psoriasis, asthma, fibromyalgia, eczema, rosacea, dystonia and multiple chemical sensitivity
COMMON CAUSES
- There are multiple pathways by which neurogenic inflammation may be initiated. It is well documented, using both animal models and isolated neurons in vitro, that capsaicin, heat, protons, bradykinin, and tryptase are upstream regulators of the intracellular calcium influx, which results in inflammatory neuropeptide release. In contrast, it is thought that prostaglandins E2 and I2, cytokines, interleukin-1, interleukin-6, and tumor necrosis factor do not cause neurotransmitter release themselves, but rather excite sensory neurons and thus lower the threshold for firing and cause augmented release of neuropeptides.
- While neurogenic inflammation has been extensively studied and well documented in peripheral tissues, until recently the concept of neurogenic inflammation within the CNS has remained largely unexplored. Given the capacity for neurogenic inflammation to influence vascular permeability and lead to the genesis of edema, it has now been widely investigated for its potential to influence BBB permeability and vasogenic edema within the brain and spinal cord under varying pathological conditions.