Neuropathies – Inpha2000

Neuropathies - Inpha2000

Doctors call it postherpetic neuralgia or PHN. Some people, though never get cold sores. The peripheral nervous system is the term used for all of the nerves outside the brain and spinal cord. Vitamin problems are another cause of neuropathy, especially with respect to vitamins B-1, B-6 and B-12. Symptoms depend on the type of involved nervous fibers (motor, sensory, vegetative) and their location, but in most cases they appear with weakness, tingling and pain. But for 12% to 15% of people the pain remains. removing the cause of the disease.

Nerves that help you move your muscles are called motor nerves. The first is by direct toxicity to the nerves. The recovery degree depends on how severe was the damage. The findings appear in the July issue of the free-access online journal PloS Medicine. A precocious diagnosis is therefore extremely important, so that it can allow a speedy therapy start; reducing the neuropathy symptoms. The nerves controlling internal organs are called autonomic nerves. In other autoimmune disorders, multiple body tissues are affected.

Physiotherapy and physioterapeutic aids may help keeping muscle strenght and better motor performance. The therapy involves the use of neuroprotecting substances, such as alpha lipoic acid, that work as antioxidizing agents, so that they increase the nerve conduction speed and the endoneural hematic flow, so reducing pain and hypodistesis(sensitivity weakening). The DHA is the optimal integration for the reconstitution of the integrity of the neuronal cell membrane, indeed constituing 85% of it. You may have a nerve conduction test. Some sports drinks contain megavitamins and have been reported to cause vitamin B-6 toxicity. The nervous impulse passes from one cell to another through the synapsis. The axons are wrapped in neurolemma, a sort of isolating that allows the nervous impulse to be conducted along the nerve fiber.

Neurolemma is not a continuous casing but it is interrupted in spots called nodes. If the neuropathy is caused by a disease such as diabetes or lupus, you may need treatment that controls the disease better. Trauma or compression: A common cause of nerve injury is physical trauma to the nerves, such as by injuries, falls, sports activities or surgery. The peripheral nervous system is the damaged part during neuropathy. Neuropathy is, therefore, the term used to describe disorders following a damage to the peripheral nerves. motor nerves are responsible for voluntary movements. In high doses they may cause trouble breathing and even cause death.

Tumors, scars or bone spurs can also press on nerves and cause damage. Although many neuropathies involve, in a different way, all three kinds of nervous fibers, in some cases just one or two types of fibers are involved and, therefore, we talk of purely or mostly motor, sensory or vegetative neuropathies. With the term neuropathy we identify a functional disorder or pathological alteration of the peripheral nervous tissue. It may be limited to just one nerve (mononeuropathy), or several nerves (multiple mononeuropathy) or acquire a symmetrical and bilateral allocation (polineuropathy). It may or may not go away with time. Many are due to lack of a protein necessary for the production of the myelin sheath. **The Bell’s paralysis is a disorder of the VII cranial nerve (facial nerve) that contains motor fiber for the face and vegetative fibers’ mimicry muscles.

In most cases the cause of the disorder is unknown, that is displayed by the lips asymmetry (you may notice having a ‘crooked mouth’) and the difficulty with closing the eye on the same side. They may sometimes be associated with hearing disorders (hyperacusis) and taste disorders. In most cases the deficit recovers spontaneously in longer or shorter periods of time (one to 5 or more months) whether the damage has involved only the neurolemma (better prognosis) or the axon as well (less favourable prognosis). Genetic testing may be appropriate for some patients, if their symptoms or test results suggest they may have an inherited/genetic basis for their neuropathy. Some neuropathies have a sudden beginning, some gradual throughout the years. Symptoms depend on the type of involved nervous fibers (motor, sensory, vegetative) and their location, but in most cases they appear with weakness, tingling and pain, as briefly listed. Arm or leg weakness: muscle weakness, exhaustion are symptoms caused by the motor nerve compression.

If lower limbs are involved, easy weakening and legs ‘heaviness’ may appear, difficulty   climbing up the stairs, walking or running. If upper limbs are involved, a sense of fatigue may be felt when carrying grocery bags, unscrewing jars, opening doors, hair brushing. Numbness, tingling, pain: a damage to the sensory nerves may cause different symptoms. It may cause spontaneous sensations (paresthesias), that may induce numbness, tingling, a sensation of ‘pins’ or needles or pinches, itches, burning sensations, cold, painful pangs, electric shocks. These disorders often worsen at night. Furthermore, unpleasant sensations may occur caused by tactile stimuli (dysesthesias), or reduction (hypoesthesia) or disappearing (anesthesia) of the sensation, that may cause cutting or burning themselves without knowing it. Absence of position sense: when this disorder occurs, it is not sure of where exactly feet are and incoordination and walking insecurity may occur.

Or you may notice that the way of walking has changed, without knowing exactly how and why. It is possible to ‘drag’ your feet, or steps widen in the unconscious attempt of keeping a balance. Autonomic fibers damage symptoms: a lesion to the autonomic fibers (of those nerves controlling involuntary actions) may cause a sense of instability and/or vertigo when standing up, constipation, diarrhea, sexual disfunction or skin thinning, facilitation of developing of bruises and difficulty with wound healing. Acquired neuropathies Trauma or compression (mechanical neuropathy): localized neuropathies may be caused by an external trauma or sinew or other surrounding tissues compression. The most know are the carpal tunnel syndrome, that is caused by the compression of the wrist’s median nerve; cervical and lumbosacral radiculopathies (the latter known as ‘sciatica’) caused by the compression of the nerves roots at their exit point at the spinal cord level. Other areas of frequent compressions are the elbow, armpit and knee back nerves. Diabetes: it is one of the most common neuropathies.

It appears during the course of the disease, but may sometimes be precociously present. It’s a mostly sensory neuropathy (paresthesias, pain), to which autonomic disorders and cranial nerves deficit may be associated. In diabetic patients glucose levels in their blood may cause the formation of free radicals. In these cases oxidative stress lowers the blood flow and takes to a condition of hypoxia at the nervous level with resulting disfunction, pain, numbness, limb tingling, especially in the lower limbs. Alcohol and other toxic substances: alcohol abuses is a frequent cause of neuropathy. Other toxic substances that may damage the nerves are: lead (motor neuropathy); arsenic, mercury (sensory neuropathy); organic solvents or insecticides. Nutritional deficit: deficit neuropathies: B12, B1 (thiamine) vitamin deficit, B6 (pyrodixine) and E vitamin deficit and may cause polineuropathies with axon degeneration.

Vitamin deficit may be caused by an insufficient diet or gastric or intestinal malabsorption problems. Even B6 vitamin excess may cause a neuropathy. It is unclear whether these deficits are a factor predisposing to neuropathy or they are its consequence. Neuropathies during systemic diseases: other than diabetes, several systemic conditions may associate to neuropathy. Among those, chronic kidney insufficiency, liver diseases, endocrinal alterations (i.e. Hypothyroidism). Neuropathies may occur even in patients in intensive cure unit.

Immuni-mediated neuropathies: the role of the immune defence system is to protect the organism against external infective agents. Sometimes, however, for unknown reasons, the immune system attacks part of our organism causing the insurgency of autoimmune diseases. If it’s the peripheral nerves to get ‘attacked’, this may cause immuno-mediated neuropathies.Guillain-Barre Syndrome: it is an acute poliradicolonevritis, with sudden beginning, that may evolve into a total paralysis or respiratory insufficiency within days after the onset. It is often preceded by infections or vaccinations that are considered “triggering” factors. The disease is autolimiting, with spontaneous recovery within 6-8 weeks, but sometimes consequences remain. The prematurity of the therapeutic intervention is crucial, that uses intravenous immunoglobulin or plasmapherasis. A variation of the Guillain-Barre is the Miller-Fisher syndrome, that appears with the ‘falling’ of the eyelids (eyelid ptosis) or unstable march (ataxic).Chronic inflammatory demyelinizing poliradicolonevritis.

It is considered the chronic variation of the Guillain-Barre and it may present with repeated attacks or with a slowly progressive walk.Chronic neuropathies with auto antibodies toward the peripheral nerves. In some neuropathies antibodies have been identified directed against specific peripheral nerve components, such as the Myelin Associated Glycoprotein (MAG), gangliosides (GM1, GD1a, GD1b), sulfatides. Vasculitis associated neuropathies. The term vasculites concerns an inflammation of the blood vessels that may involve both the vessels directed to the peripheral nerves and those headed to other organs. If the inflammatory process involves the vases directed to the peripheral nerves it may cause little ‘heart attacks’ of the nerves causing a vasculatic neuropathy. Several rheumatologic conditions, such as the rheumatoid arthritis, the systemic lupus erythematosus, the panarteritis nodosa or the Sjogren syndrome are associated with the generalized vasculitis, that may involve the peripheral nerves. Vasculitis may cause neuropathies, or multiple mononeurites, according to the distribution and severity of the lesion.

Neuropathies - Inpha2000
Neuopathies associated with monoclonal gammopathies. In monoclonal gammopathies, single lymphocyte B bones or bone marrow plasmacell or lymphoid organs expand forming tumors, benign or malignant, that secrete antibodies. Each single Lymphocyte B clones produces only one kind (monoclonal) of antibody (or gamma-globuline), hence the name monoclonal gammopathy. In some cases the antibodies react against peripheral nerves’ components, in other case antibodies’ fragments settle in the tissues forming ‘amyloid’. HSMN (Hereditary Sensory Motor Neuropathy) or Charcot-Marie-Tooth disease (CMT). These are the most common hereditary neuropathies. Once called Charcot-Marie-Tooth disease, they have been recently reclassified as HSMN (Hereditary sensor motor neuropathies).

Several subgroups can be identified based on their clinical characteristics and underlying genetic alterations. The type 1 HSMN is the most common. It is a slow evolving, demielinizing neuropathy, often associated with the foot (hollow foot). Family Amyloidotic neuropathy is displayed with vegetative nervous system and sensory alterations (diarrhea, impotence, etc.). It is caused by a mutation of a protein called transthyretin. The abnormal protein sediments as an amyloid in the peripheral nerves, causing pain. A correct diagnosis begins with the detailed gathering of symptoms, previous and concurrent diseases of the patient, a research of possible causal factors (exposition to toxic elements, drugs, etc.).

After carefully visiting the patient, the physician recommends some lab tests that may help identifying the cause of the neuropathy. The Electromyogram or electromyography (EMG) and the study of the nerve fibers conduction speed is important to study the electrical properties of the nerves. These investigations help identifying which nerves are involved and the damage distribution. A nerve biopsy may sometimes reveal important information on the kind and cause of the neuropathy. You can see, in fact, if the nerve shows signs of vasculitis, inflammation or amyloid deposit. A spinal tap may be helpful for showing the presence of infections or inflammations, whereas focused blood and urine analysis may help identifying underlying diseases or genetic defects that cause the neuropathy. For instance, a vitamin deficit may be corrected with oral or parenteral administration of the deficiting vitamin.

Potential infections are treated with antibiotics or anti-viral agents. Autoimmune diseases often respond to plasmapheresis, immunosuppressive or immunomodulatory therapies (corticosteroids, intravenous immunoglobulin or chemotherapy). In paraneoplastic neuropathies (namely associated and sometimes precede the appearance of a tumor) the treatment is directed to removing the underlying tumor. Toxic or drug induced neuropathies are treated by removing the causal agent. In case of diabetes, a careful control of the hyperglycemia helps slowing down the neuropathy progression. According to the cause of the neuropathy, the therapy may alleviate, slow down or heal the neuropathy. Once the damage has been stopped, the nerve can regenerate.

The recovery degree depends on how severe was the damage. The lesser the damage, the better the recovery. A precocious diagnosis is therefore extremely important, so that it can allow a speedy therapy start. B. Reducing the symptoms of the neuropathy. The main symptoms of neuropathies are pain and muscle weakness. The pain may be mitigated with analgesic medications.

Physiotherapy and physioterapeutic aids may help keeping muscle strength and better motoric performance. BIBLIOGRAFY AINP – Associazione Italiana Neuropatie Periferiche – www.neuropatia.it; http://www.ilmedicosportivo.it/magaz/n1a10/indice.htm. Barbiroli B. et al. (1995): Lipoic (thioctic) acid increases brain energy and availability and skeletal muscle performance as shown by in vivo 31P-MRS in a patient with mitochondrial cytopathy. J. Neurol.

242:472.Changyuan Lu and Yanyun Liu. Interactions of lipoic acid radical cations with vitamins C and E analogue and hydroxycinnamic acid derivatives. Archives of Biochemistry and Biophysics 406 (2002) 78–84.Coste Thierry C. (2003): Neuroprotective Effect of Docosahexaenoic Acid–Enriched Phospholipids in Experimental Diabetic Neuropathy DIABETES, VOL. 52, OCTOBER.Garrett N. E. et al.

(1997): Alpha-lipoic acid corrects neuropeptide deficits in diabetic rats via induction oftrophic support. Neurosci. Lett. 222:191.Gries F. A. et al. (1995): Alternative therapeutic principles in the prevention of microvascular and neuropathic complications.

Diabetics Research and Clinical Practice, 28 Suppl.:S201-S207.Head Richard J., (2000): Prevention of nerve conduction deficit in diabetic rats by polyunsaturated fatty acids Am J Clin Nutr; 71(suppl): 386S–92S.Innis Sheila M. Dietary (n-3) Fatty Acids and Brain Development. American Society for Nutrition. J. Nutr. 137: 855–859, 2007.Jameel Noor Mohamed at al.(2006): a-lipoic acid: An inhibitor of secretory phospholipase A2 with anti-inflammatory activity. LFS-11506; No of Pages 8.Mitsui Y.

et al. (1999): Alpha-Lipoic acid provides neuroprotection from ischemia-reperfusion injury of peripheral nerve. Journal of the Neurological Sciences, 163:11-16.Murase K. et al. (1993): Stimulation of NGF syntesis/secretion in mouse astroglial cells by coenzymes. Biochem. Mol.

Biol. Intnl. 30:615.Packer L, Witt EH, Tritschler HJ. alpha-Lipoic acid as a biological antioxidant. Free Radic Biol Med. 1995 Aug;19(2):227-50.Packer L. et al.

(1997): Neuroprotection by the metabolic antioxidant a-Lipoic acid. Free Rad. Biol. Med. 22:359.Srikanth Sola et al. (2005): Irbesartan and Lipoic Acid Improve Endothelial Function and Reduce Markers of Inflammation in the Metabolic Syndrome. Results of the Irbesartan and Lipoic Acid in Endothelial Dysfunction (ISLAND) Study.

(Circulation;111:343-348).Suh Jung H. at al. Decline in transcriptional activity of Nrf2 causes age-related loss of glutathione synthesis, which is reversible with lipoic acid. PNAS March 9, 2004 vol. 101 no. 10 3381–3386.Van der Goes et al. (1998): Reactive oxygen species are required for the phagocytosis of myelin by macrophages.

J. Neurol. 242:472Ziegler Dan et al. Oral Treatment With _-Lipoic Acid Improves Symptomatic Diabetic Polyneuropathy. Diabetes Care, Volume 29, Number 11, November 2006.

You may also like