Tampilkan postingan dengan label Nerves. Tampilkan semua postingan
Tampilkan postingan dengan label Nerves. Tampilkan semua postingan

Kamis, 16 Februari 2017

Low Level Laser Repair Of Insulation Around Damaged Nerves


Today's post from thediabeticnews.com (see link below) brings us back to the use of light (or more specifically here...lasers) to treat nerve damage. In this case, it's refreshing to see that the therapy is aimed at repair rather than simply lessening symptoms, although if the treatment works, symptoms are automatically lessened. The theory is that laser treatment has been found to activate repair of the myelin sheaths around nerves. As you probably know, myelin sheaths are the insulation around nerves that prevent 'short-circuiting'. Just as in a household wiring system, short circuits (and therefore pain) occur when insulation is damaged and the wires come into contact with outside influences. It's more or less the same with the nervous system. Apparently. laser treatment also positively affects mitochondria (the energy packs that drive cellular activity) which in turn, stimulates repair of the myelin. It's another lab study unfortunately but the rats are proving the theories to be true and if this translates to humans, then neuropathy patients will be on the verge of a major breakthrough in the treatment of their pain. A fascinating article...well worth a read.



Phototherapy Used to Combat Neuropathic Pain
April 7, 2017 Source: Fundação de Amparo à Pesquisa do Estado de São Paulo

As diabetes progresses, the structure of the sciatic nerve’s myelin sheath changes – but after four sessions of laser therapy treatment, researchers found that the myelin had almost completely recovered.

Low-level laser therapy has been shown by recent studies to be a non-invasive and effective alternative for treating neuropathic pain, a chronic condition caused by nerve damage, spinal cord injury or diseases such as diabetes.

Recent studies performed at the University of São Paulo’s Biomedical Science Institute (ICB-USP) in Brazil helped elucidate the mechanisms behind the effect of low-level laser therapy.

This research has been conducted as part of a project supported by FAPESP, with Professor Marucia Chacur as the principal investigator.

“We tested laser therapy in different rat neuropathy models, and behavioral responses improved in all of them,” Chacur told. “One of the beneficial effects observed was myelin sheath recovery. The myelin sheath is a lipid layer that covers the axon and acts as electrical insulation to assist nerve impulse propagation.”

The treatment in a model of diabetic neuropathy, one of the most common chronic and incapacitating complications of diabetes was tested.

The problem occurs when the disease is not properly controlled and excessive amounts of blood sugar cause oxidation of the myelin sheath, damaging the structure of peripheral nerves. As well as causing pain, this degenerative process impairs communication among neurons and can even lead to amputation of the lower limbs.

To induce a condition similar to type 1 diabetes, the researchers injected the rats with streptozotocin (STZ), a chemical that destroys the insulin-producing beta cells of the pancreas. In this model, the animals became diabetic approximately one week later.

“We began the treatment after 45 days, when the neuropathic condition was well-established and had become chronic,” Chacur said. “We used a 904-nanometer laser, which can penetrate deep into tissue.”

The degree of pain was evaluated before and after the start of treatment by behavioral tests such as the von Frey hair test, in which nylon filaments of different thicknesses are pressed against the rat’s paw. Each filament represents a force in grams and indicates the pressure tolerated without signs of discomfort. There are similar tests that use thermal and mechanical stimulation.

“We plan to apply the technique to humans, so we used similar therapeutic protocols,” Chacur said. “We initially scheduled ten sessions of phototherapy applied to the thigh every ten days, each lasting one minute, but we observed an improvement shortly after the fourth session and sacrificed the rats to analyze their sciatic nerves.”

With the aid of a transmission electron microscope, the researchers found that as diabetes progressed, the structure of the sciatic nerve’s myelin sheath changed. After four sessions of the treatment, however, the myelin had almost completely recovered.

“The condition of the nerve practically returned to baseline levels after treatment. We’re now continuing the study by analyzing protein expression and the release of inflammatory cytokines to understand exactly what’s happening,” Chacur said.

In another study, treatment again focused on the sciatic nerve, but the injury was induced by compression to simulate what happens in patients with spinal stenosis or disc herniation.

“The nerve was ligated and kept compressed for two weeks until the injury became chronic. Phototherapy began on the 14th day,” Chacur explained. “Shortly after the second session, we observed a behavioral improvement, which persisted until the end of the treatment.”

After the tenth session of phototherapy, the animals were sacrificed for analysis of the dorsal root ganglion, a cluster of nerve cell bodies located in the posterior region of the vertebrae along the spinal cord and conveying sensory and motor information.


This News Story Continues Below

The researchers used immunoblotting to scan the dorsal root ganglion for the presence of astrocytes, star-shaped cells that play an active role in brain function and inflammatory responses.

“Astrocytes are the first type of cell to migrate to the site of a nerve injury or inflammatory process,” Chacur said. “They’re like a sort of macrophage for the central nervous system, the first line of defense.”

The analysis showed smaller numbers of astrocytes in rats treated with laser therapy than in untreated rats.

“These cells release several inflammatory mediators, including interleukin-1 (IL1), tumor necrosis factor alpha (TNF-α) and glutamate. These mediators in turn trigger the release of other inflammatory substances. We believe the laser curtails this chain reaction as if it were anti-inflammatory medication, by reducing the migration of astrocytes to the site of the injury,” Chacur said.

The next step is to measure the concentration of each inflammatory substance separately, she added. The third model used to test low-level laser therapy focused on orofacial pain. In this model, a lesion was induced by crushing the inferior alveolar nerve, one of the branches of the trigeminal nerve responsible for innervating the face.

“This type of injury can occur during extraction of a wisdom tooth, for example. Many dentists are using low-level laser therapy for patient pain relief,” Chacur said.

Phototherapy began two days after the nerve was injured. An improvement in pain-related behavior was observed after two sessions and persisted throughout the treatment, which comprised ten sessions (one every two days).

The animals were sacrificed, and then Western blotting was used to analyze the treated tissue for the presence of certain proteins.

“We set out to understand the mechanisms and mediators involved because we believed phototherapy could be used in association with pharmacological treatment because it acts via a different pathway. In this way, it may be possible to reduce the drug dose and mitigate the systemic effects of the treatment,” Chacur said.

The results suggest that all three models of neuropathic pain studied share a common mechanism involving myelin sheath regeneration and reduced astrocyte migration to the site of the lesion, she added.

“Evidence in the literature also suggests an effect on mitochondria. The laser apparently facilitates the flow of calcium in these organelles, boosting production of ATP [adenosine triphosphate, the body’s cellular fuel] and leading to enhanced healing as well as the release of mediators that assist remodeling. In future studies, we plan to investigate this effect on mitochondria more thoroughly,” Chacur concluded.


Photo credit: OpenStax Anatomy and Physiology

Journal: Lasers in Medical Science

Funder: São Paulo Research Foundation

http://thediabeticnews.com/phototherapy-used-to-combat-neuropathic-pain/

Rabu, 04 Januari 2017

Immune Neuropathy Is Your Immune System Attacking Your Nerves


Today's post from health-innovations.org (see link below) is an interesting one for neuropathy patients whose neuropathy has been diagnosed as, or is suspected of having an auto-immune cause. This especially applies to people with HIV and other auto-immune conditions where the immune system itself attacks the nervous system, causing the symptoms we're all aware of. This article looks at new findings regarding what's causing this and where in the nervous system it's happening. It's technical and goes deeper into the structure of nerves and nerve cells than the average reader will be comfortable with but it's fairly easy to follow and to be honest, you don't need to know all the facts to be able to identify with its conclusions. May be better to talk it over with your neurologist rather than your home doctor, (who may be just as much in the dark as you) but it does give us a reason why certain labels are attached to our version of nerve damage.

Study identifies previously unknown cause of immune neuropathy.
Posted on August 5, 2016 by Healthinnovations 




Patients suffering from so-called immune-mediated neuropathies frequently have a long medical record. As there are no diagnostic tests available to reliably diagnose the disease, the diagnosis is frequently made belatedly and patients can be misdiagnosed. Accordingly, many years often pass before an effective therapy is started. However, not all patients respond to first-choice drugs even when treated immediately. Therefore, identifying biomarkers for this disease is key to early-diagnosis and optimal treatment. Now, a study from researchers at the University of Wuerzburg identifies a new potential trigger of these neuropathies. The team state that they were able to show in patients with antibodies against Caspr, a protein involved in building the myelin sheath, the structure of the Nodes of Ranvier is destroyed and nerve function severely impaired. The study is published in the journal Brain.

Previous studies show that an autoimmune process is believed to cause this neuropathy in which the immune system attacks and destroys components of the nerve fibres. However, exactly how this mechanism works is largely unknown, a fact which makes it more difficult to develop targeted drugs. In the past years, researchers from Spain and Japan have identified autoantibodies against Nodes of Ranvier proteins, such as Contactin-1 and Neurofascin-155, in patients with immune-mediated neuropathies. Caspr is also involved in building the Nodes of Ranvier, therefore, the group decided to investigate this protein. The current study shows that some patients with immune-mediated neuropathies have antibodies against the protein Caspr, which causes the destruction of the Nodes of Ranvier.

The current study examined 35 patients with chronic inflammatory demyelinating polyneuropathy (CIDP), a chronic form of inflammatory nerve disorder, and 22 patients suffering from Guillain-Barré syndrome, an acute form. Results show that in one patient each with CIDP and Guillain-Barré syndrome, antibodies against the protein Caspr were detected in the blood. Data findings show that antibody production in these patients can be inhibited by the drug Rituximab which reverses the symptoms.

Results show that the disease develops rapidly, causes severe paralysis and responds poorly to standard therapy, and responds excellently to Rituximab treatment. Data findings show that strong neuralgia is another typical symptom in patients with Caspr antibodies, as opposed to patients with antibodies against the two other proteins, Neurofascin-155 and Contactin-1, who typically exhibit a distinct tremor in targeted movements.

The team surmise that their findings verify previous studies which show patients who have antibodies against proteins of Nodes of Ranvier exhibit characteristic features. For the future, the researchers state that their study raises hopes for identifying the cause of inflammatory neuropathies in a select subset of patients and that a simple blood test for autoantibodies could provide a targeted treatment.

Source: University of Würzburg




Nodes of Ranvier. Each Schwann cell myelinates about 100 µm of an axon. Gaps between neighboring Schwann cells are called nodes of Ranvier. Action potentials jump from node to node while traversing an axon. Credit: Yale Histology

https://health-innovations.org/2016/08/05/study-identifies-previously-unknown-cause-of-immune-neuropathy/