Therefore, we tend to give our external a lot more love than our internal. When we look into healing, although pain may manifest externally, the root cause is almost always an emotional pain that has become lodged in the subtle body unless caused by a trauma where the physical body has been damaged.
These emotional blocks store inside the body until they start to cause pain. Facing our emotions and tracing them back to the trigger helps to remove such blockages from within our present day; it is when the healing begins.
This journey is not as straightforward as a physical examination, some tablets or rest though, it needs emotional healing. When we suffer from physical pain, a short-term improvement can be sought.
We take an aspirin. We have a massage. There might be an operation. But more often than not the pain returns, and it returns time and time again.
Emotional healing: releasing trapped emotions to heal physical pain
When the pain has been gradual, arising over time, and not the result of a sudden injury or break, it is likely to be an energetic block in the body that is showing itself as physical pain. Satyatma is a Spiritual Channel, sharing words of truth from our non-physical Spiritual Guides. He began his spiritual path with a spontaneous and extremely powerful Kundalini Awakening in and ever since this life-affirming moment, he has been a student of his Guides, Yoga, Eastern Philosophy, Meditation and Metaphysics.
Through his work, Satyatma helps to guide people back to themselves, to the truth. To reconnect with our truth requires space, stillness and some slowing-down of the mind in order to be honest with how and who we are.
But, in our busy lives this rarely happens, so the power of the mind can easily mislead us into a false sense of happiness, hiding our truth through external distraction. Our mind attaches to glimmers of happiness from external sources to mask a trapped emotion. Remedying our suffering by doing things which provide temporary relief from emotional pain through sex, games, drugs, alcohol, TV, films and life on social media, to make us forget about a past experience, a current relationship or present life situation that is the cause of our emotional blocks.
But, when physical pain arises, it is the body crying out to tell us that something is wrong. Meaning that if external factors only provide us with a temporary state of relief or a false sense of happiness, we need to start looking inside rather than outside for true healing. With an authentic manner and honest style that gets to the "heart of the matter", Satyatma told us that the goal of any session he conducts is to understand the root cause of pain a nd start his clients on the path to the truth: identifying with the Self.
Not even the person they have the problem with. When a painful truth is left unsaid, the emotional energy attached to this pain festers inside the body causing emotional blocks — this is when the physical pain appears. It might be easier but, if we continue to hide away then we will never heal. Following injury, however, the channels are relocated to the paranode, where they can suppress hyperexcitability see figure below.
In the current paper, the authors found that both CASPR2 and Kv1 are also expressed in the cell bodies of sensory neurons.
When Bennett first moved to the University of Oxford, he had a conversation with coauthor Angela Vincent about a unique observation she made in her patients. This led the two to wonder if these patients experienced neuropathic pain because the CASPR2 autoantibodies caused mislocalization of Kv1 channels, resulting in hyperexcitability of sensory neurons.
The researchers isolated antibodies from two patients who had high serum levels of CASPR2-Abs and were experiencing neuropathic pain. First author John Dawes and colleagues treated wild-type mice daily with purified CASPR2-Abs from either patient 1 for 14 days or from patient 2 for 22 days, while assessing mechanical sensitivity with von Frey hairs. To control for nonspecific effects, the investigators treated other sets of mice with antibodies from healthy donors who lacked CASPR2-Abs and confirmed that no hypersensitivity was present.
These experiments showed that an autoimmune, peripheral neuropathic pain disorder could be passively transferred. To rule this out, the team examined the peripheral and central nervous systems for signs of inflammation. There was no increase in markers for neutrophils, macrophages, lymphocytes, or inflammatory cytokines within the dorsal root ganglion DRG , and no elevation in markers for neutrophils, lymphocytes, or activated astrocytes in the spinal cord.
Using intra-epidermal nerve fiber density in the paw as a measure of nerve damage and examining peripheral nerve structure with electron microscopy, they found no abnormalities in the nerves of antibody-treated mice. However, what they did see in these animals, here with immunostaining, was a decrease in both CASPR2 protein and Kv1 along the sciatic nerve. Instead, these mice only expressed a version of the protein missing most of its extracellular portion, a modification that would interfere with its ability to interact with Kv1 channels.
Similar to the mice treated with patient-derived CASPR2-Abs, these animals were hypersensitive to mechanical stimulation. They also featured enhanced pain behaviors in response to hind paw injection of either capsaicin or formalin, chemicals that result in inflammation and activate pain neurons. The team also looked at how the loss of full-length CASPR2 and a decrease in Kv1 expression affected sensory neuron excitability in a series of electrophysiological and imaging experiments.
Using in vivo calcium imaging to directly observe cell body activity of sensory neurons in anesthetized animals while mechanically stimulating the hind paw, they found hyperexcitability in small- and medium-diameter neurons, which transmit nociceptive signals. The researchers explored physiological changes in the cell bodies of cultured DRG neurons from mice lacking full-length CASPR2 using patch-clamp electrophysiology.versinscompcer.tk
Here, too, small- and medium-diameter neurons showed increased excitability. Use of a potassium channel blocker revealed that this hyper-responsiveness was likely due to the loss of potassium channel function. The group then turned to in vivo extracellular recordings of spinal cord neurons in anesthetized mice to examine changes of sensory neuron integration into the spinal cord. This, too, revealed hyperexcitability in response to mechanical stimulation of the paw with von Frey hairs. Next, use of a tibial nerve-skin ex vivo preparation allowed for recording from the axons of tibial nerve fibers during mechanical stimulation of the paw.
Considering known electrophysiological properties and using various mechanical stimulation parameters to categorize sensory neuron subtypes, the authors found that only D-hair afferents were hyperexcitable when recording at the axon; these afferents are a type of low-threshold, A-delta mechanoreceptor that forms lanceolate endings around hair follicles in the skin and play a role in pain under pathological conditions. Patch-clamp electrophysiology at the level of the cell body showed that treating cultured sensory neurons from normal mice with patient-derived, CASPR2-Ab-containing plasma for 24 hours also increased neuronal excitability and decreased Kv1 expression.
From a mechanistic perspective, the current study lays the foundation for using immune therapy to treat patients who have CASPR2-Abs and neuropathic pain. However, the patients in the new work had very high levels of CASPR2-Abs and were already going to be treated for their other neurological signs with immune therapy in order to decrease systemic levels of the antibodies. For the wider population of people with chronic pain, the research also casts CASPR2 itself as an interesting therapeutic target.
By increasing expression of this protein, it may be possible to decrease neuronal excitability. Ultimately, Bennett hopes the findings encourage researchers to pay more attention to antibody-induced pain. Additional permissions for appropriate reuse available on request.