has anyone had peripheral neuropathy/GBS after surgery??I am trying to find out for myself not just from what the doctors have told me.

Since surgey on april 11 i have been ill and finally hospitalized from june until now. I was just diagnosed with peripheral neuropathy/GBS. I am just trying to get some input from you here on OH.

Thanks

You made me curious as to what this was.  Did the doctor tell you why you have developed this?

Peripheral neuropathy

Last reviewed: April 26, 2011.

Peripheral nerves carry information to and from the brain. They also carry signals to and from the spinal cord to the rest of the body.

Peripheral neuropathy means these nerves don't work properly. Peripheral neuropathy may be damage to a single nerve. It may be damage to a nerve group. It may also affect nerves in the whole body.

Causes, incidence, and risk factors

Nerve damage is very common. There are many types and causes. Often, no cause can be found. Some nerves diseases run in families.

Diabetes is the most common cause of this type of nerve problem. It happens when you have high blood sugar levels over a long time.

Other medical problems that may cause neuropathy are:

• Autoimmune disorders rheumatoid arthritis or lupus

• Chronic kidney disease

• Infections such as HIV and liver infections

• Low levels of vitamin B12 or other problems with your diet

• Poor blood flow to the legs

• Underactive thyroid gland

Drugs and toxins may damage nerves. One example is heavy alcohol use. Glue, lead, mercury, and solvents may damage nerves. Drugs that treat infections, cancer, seizures, and high blood pressure may cause nerve damage.

Pressure on a nerve near a body part may be a cause. An example is carpal tunnel syndrome.

A bone fracture or other trauma may damage a nerve. Being exposed to cold temperatures for a long period of time may too. Pressure from bad-fitting casts, splints, a brace, or crutches can damage a nerve.

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Guillain-Barré Syndrome / Acute Inflammatory Demyelinating Polyneuropathy (AIDP)

Guillain-Barré (ghee-yan bah-ray) syndrome (GBS) is a rare inflammatory disorder in which the body's immune system attacks the protective covering of the peripheral nerves (myelin sheath), preventing the nerves from sending signals to the muscles. It can develop over the course of several hours or days, or it may take up to 3 or 4 weeks. It is the most common cause of rapidly acquired paralysis and should be treated as a condition requiring urgent diagnosis and treatment.

The first symptoms of GBS usually include varying degrees of weakness or tingling sensations in the legs. In many instances, the weakness and abnormal sensations ascend and spread to the arms and upper body. Although many cases are mild, these symptoms can increase in intensity until the muscles cannot be used at all and the patient is almost totally paralyzed. In extreme cases, the patient has difficulty breathing and must be placed on a ventilator. If the throat and face are affected, a feeding tube may be required. In some cases, peripheral neuropathy may develop.

GBS improves spontaneously, but the recovery period may take from several weeks to more than a year. Most patients make a total recovery, from even the most severe cases of GBS, although some continue to have a certain degree of weakness, numbness or occasional pain.

Because of its sudden and unexpected onset, GBS can be a devastating disorder. It is called a syndrome rather than a disease because it is not clear that a specific disease-causing agent is involved. No one yet knows why GBS strikes some people and not others, or what sets the disease in motion. There is no known cure for GBS, but therapies can lessen the severity of the illness and speed up recovery in most patients.

GBS can strike anyone, regardless of age or sex. GBS is not contagious, but it may follow a bacterial or viral infection, such as campylobacterial infection (caused by a bacteria found in undercooked food, especially poultry) or Epstein-Barr virus (EBV). Although GBS is not inherited, there may be a genetic predisposition to the disease. Some patients have a similar but longer-lasting illness called chronic inflammatory demyelinating polyneuropathy (CIDP). Once called 'chronic GBS,' CIDP is now considered a related, but distinct condition. GBS is also sometimes known as acute inflammatory demyelinating polyneuropathy (AIDP).

SYMPTOMS AND SIGNS

(Not all symptoms and signs may be present.)

• Acute or sub acute onset
  • 50 - 60% of cases occur days or weeks after a viral or bacterial infection, such as a sore throat, the flu, or diarrhea.
  • Surgery, childbirth or vaccinations may also trigger the syndrome
• Full recovery (even from extreme cases) probable for most patients
• Pain in spine and limbs
• Reflexes such as knee jerks are lost
• Weakness and tingling sensation in legs, possibly spreading to upper body and arms
• Weakness in breathing, swallowing and the muscles used to cough
• In extreme cases, paralysis

Wow, Nikki I know nothing about this, but, man in the hospital since June!  So sorry to hear his and I hope they can find a resolution for you soon!

I know two women that have had GBS neither had WLS one was very ill for a full year the other was impacted for four months both are okay now. I hope you are well soon

I developed foot drop due to a Thiamine deficiency (B1) about 7 months out from surgery.  Massive doses of B100 complex fixed the problem within a few weeks.

http://usmlepathslides.tumblr.com/post/18142623924/patient-w ith-thiamine-deficiency-and-foot-drop

Patient with thiamine deficiency and foot drop: 
Note how the foot drops. This is due to a peripheral neuropathy involving the common peroneal nerve. Recall that thiamine catalyzes reactions that are important in the synthesis of ATP. ATP depletion leads to wet and dry beriberi. In addition to Wernicke’s encephalopathy, peripheral neuropathy is a manifestation of dry beriberi.

There is more information on Nutritional Neuropathy's on the following link.

http://emedicine.medscape.com/article/1171558-clinical

History

Peripheral neuropathies due to nutritional deficiencies have few individually characteristic signs but can be differentiated by observing other symptoms of the patient's underlying systemic disease. Neuropathies mostly affect the long fibers first, starting in the feet and progressing upward. Once they have progressed to the calf, symptoms may appear in the hands. Cyanocobalamin (vitamin B₁₂) deficiency occasionally manifests in the upper extremities.

• Alcohol neuropathy
  • This disease is characterized by paresthesias (decreased pain and temperature sensation in a stocking-glove distribution), pain, and weakness, especially in the feet but extending proximally to the arms, causing difficulty in climbing stairs and walking.
  • Autonomic symptoms are less common than those listed above, but include GI dysmotility, urinary or fecal incontinence, and abnormal sweat patterns.
  • The neuropathy may be seen in conjunction with Wernicke encephalopathy (ie, ophthalmoplegia, ataxia, encephalopathy) or Korsakoff syndrome (ie, amnestic dementia).
• Thiamine (vitamin B1) deficiency
  • Dry beriberi is characterized by severe burning dysesthesias (feet more than hands), weakness and wasting (distal more than proximal), trophic changes (shiny skin, hair loss), and acrodistal sensory loss in a graded fashion typical of dying-back polyneuropathies.
  • Some patients do not become symptomatic, possibly because they are absorbing thiamine produced by bacteria in the large intestine. However, one half become symptomatic by 7 weeks; by 15 weeks, axonal changes start to appear histologically.
  • The neuropathy begins with fatigue and loss of sensation, pain, and heaviness in the legs. Then, pretibial edema develops, along with glove-and-stocking paresthesias and difficulty with tasks such as climbing stairs and standing on one leg.
  • If the thiamine deficiency is long standing, muscles on the dorsum of the feet atrophy and paralysis can ensue.
  • Difficulty with talking or swallowing may also be noted.
• Niacin (vitamin B₃) deficiency
  • Pellagra is characterized by the 3 D s, which are (1) dermatitis, ie, hyperkeratotic skin lesions, particularly on hands, feet, face, and neck (sun-exposed regions); (2) diarrhea; and (3) dementia. In addition, patients may exhibit peripheral neuropathy and other CNS signs, such as depression, excitation, seizures, insomnia, dizziness, cog-wheeling of the extremities, tremor, loss of hearing, tingling fingers, muscle tenderness, and bilateral symmetric glove-and-stocking numbness.
  • Polyneuropathy is not always associated with pellagra and may be related to accompanying thiamine or pyridoxine deficiency. Therefore, it should be considered an accompanying rather than guiding symptom. It is characterized by acrodistal sensory excitation, the itching and burning in the hands, feet, and trunk, and it sometimes manifests as hydromania, or the compulsion to immerse oneself in cold water.
  • The dysesthesias progress proximally to the knees, thighs, and hips, after which weakness in the legs becomes manifest.
  • Paresis is rare, but bulbopontine symptoms can ensue, with abnormalities of the cranial nerves, especially the vestibular, acoustic, and ocular nerves (where symptoms manifest as optic atrophy or amblyopia), as well as seizures.
  • Eventually, the initial peripheral excitation, erythema, and GI distress progress to cerebral and spinal defects.
  • Finally, marasmus, cachexia, macrocytic anemia, and coma develop.
• Pyridoxine (vitamin B 6) deficiency or excess
  • This deficiency must be suspected any time a sensory polyneuropathy occurs after hyperesthesia-causalgia syndrome.
  • First, bilateral numbness and tingling begin in the distal feet. This proceeds proximally up the feet and legs, occasionally appearing in the fingers and hands. Then pain becomes prevalent in these areas, and symptoms can include a burning sensation in the feet.
  • In rare cases, patients experience loss of power in the legs, in which sensory loss is greater than motor loss; the etiology is axonal loss.
  • One week after the removal of vitamin B₆ from the diet, levels of xanthurenic acid increase and levels of pyridoxine decrease in the urine. At 3 weeks, EEG abnormalities manifest, and tonic-clonic seizures refractory to anticonvulsants may follow.
  • The 4 main symptoms and signs are as follows:
    • Cutaneous mucosal symptoms - Glossitis, conjunctivitis, cheilosis
    • CNS symptoms - Lethargy, decreased level of consciousness, anorexia, vomiting, seizures
    • Ascending sensory polyneuropathy
    • Anemia - Lymphopenia with eosinophilia
  • Neuropathy due to toxicity occurs 1 month to 3 years after the individual starts excessive consumption.
• Cyanocobalamin (vitamin B₁₂) deficiency
  • About 80% of all cases are due to pernicious anemia, and another 10% are due to achlorhydria. Exposure to nitrous oxide can suddenly precipitate the deficiency, which should be considered in any patient who develops postoperative paresthesias.
  • The disease predominantly affects the spinal cord; therefore, separating the painful sensory and sensorimotor paresthesias of the peripheral neuropathy from the symptoms of spinal cord involvement is difficult.
  • Presentations vary greatly among patients.
  • The symmetric glove-and-stocking paresthesias, or tingling in the distal aspect of the toes, numbness, coldness, a pins-and-needles feeling, and occasional feelings of swelling or constriction, are slowly progressive and insidious. Symptoms progress up the legs, occasionally affect the fingers, and culminate in weakness and spasticity.
  • In late stages, manifestations include moderate muscular wasting, optic atrophy, sphincter dysfunction, and mental disturbances. Examples of these disturbances are mild dementia (which is often the first symptom and clinically indistinguishable from other dementias), disorientation, depression, psychosis, and persecutory delusions.
  • The hematologic manifestation of anemia, if present, can cause weakness, light-headedness, vertigo, tinnitus, palpitations, angina, heart failure, cardiomegaly, pallor, tachycardia, and hepatosplenomegaly.
  • GI symptoms include a sore, beefy red tongue and anorexia.
  • If left untreated, the gait becomes ataxic, followed by paraplegia with spasticity and contractures.
  • The subacute combined degeneration that develops results in a severe myelopathy, involving posterior columns and lateral corticospinal tracts, with other manifestations including optic (retrobulbar) neuropathy^[13] , sensorimotor polyneuropathy, and dementia.
• Pantothenic acid deficiency: This manifests as painful burning paresthesias in the feet, ataxia, and hyperreflexia, followed by weakness, fatigue, apathy, and psychiatric disturbances 5-8 weeks later.
• Alpha-tocopherol (vitamin E) deficiency^{[14, 15]}
  • This syndrome resembles Friedreich ataxia. Symptoms include hyporeflexia progressing to areflexia, decreased proprioception and vibration sense with preserved pain and temperature senses, distal muscular weakness progressing to ataxia, dysphagia, and cardiac problems, and nyctalopia (night blindness). Nystagmus, ophthalmoplegia, and blindness, and dementia follow.
  • Symptoms vary with etiology. Patients with isolated vitamin E deficiency syndrome tend to present without the hyporeflexia, and deficiency from abetalipoproteinemia manifests as increased eye problems, in contrast with deficiency from cholestatic disease, which tends to spare the eye but causes increased psychiatric and behavioral problems.
• Folate deficiency: The symptoms of folate deficiency are indistinguishable from those of cobalamin (vitamin B₁₂) deficiency, though the dementia tends to be more prominent.
• Hypophosphatemia
  • Invariably found in patients on total parenteral nutrition, this deficiency causes tingling paresthesias in the tongue, fingers, and toes but can progress to severe weakness and areflexia, sensory loss, and cranial neuropathies.
  • It can resemble Guillain-Barré syndrome.
  • Patients may have gluten sensitivity.
  • Neurologic manifestations can include ataxia, myoclonus, myopathy, myelopathy, dementia, and a peripheral neuropathy that can include sensorimotor axonal neuropathy, axonal motor and mononeuropathy multiplex.
• Copper deficiency (usually following bariatric surgery) is commonly associated with myelopathy and spastic gait. Other features can include peripheral neuropathy, myeloneuropathy, optic neuropathy^[16] , CNS demyelination, myopathy, myelo-opticoneuropathy, and motor neuron disease. Clinically and radiologically it can appear similar to B₁₂deficiency.^[2]
• Bariatric surgery
  • History is generally sufficient to establish the diagnosis. Three distinctive patterns are most common: sensory polyneuropathy, mononeuropathies, and radiculoplexopathy.
  • Sensory neuropathies tend to present with symmetrical numbness, burning, sharp pain, and tingling. Some also have distal motor weakness, commonly foot drop. Cramping, autonomic and bulbar symptoms, and involvement of trunk nerves may also occur.
  • Mononeuropathies are usually asymmetric and have been described in the radial, sensory radial, ulnar, greater occipital, and fibular nerves, as well as carpal tunnel syndrome, and meralgia paresthetica. The last 2 are the most common, and the carpal tunnel syndrome is usually symmetrical.
  • Radiculoplexopathies affect the cervical and lumbosacral regions, and are usually unilateral, causing pain and numbness followed by limb weakness but usually no autonomic or bulbar symptoms.
• Multifactorial disease
  • This paresthesia-causalgia syndrome (ie, acrodynia or burning-foot syndrome) escalates from a mild paresthesia to painful burning and freezing sensations in the feet, prominent at night, relieved with exercise. This disease may mask sensory deficits, especially those on the soles of the feet.
  • Tobacco-alcohol amblyopia is a slowly progressive symmetrical visual field loss often described as a central haze or cloud. There is no pain, photopsia, or other positive symptoms, but loss of color vision (especially red) is more profound than the loss of visual acuity. It presents clinically as a characteristic retrobulbar optic neuropathy with slow evolution and a classical cecocentral scotoma with an appearance of "champagne cork" and red-green dyschromatopsia.
  • Less common is mild-to-moderate unilateral or bilateral hearing loss with tinnitus or vertigo.
  • Hoarseness and other laryngeal symptoms are equally rare.

I have been a few cases on this board and others I participate on. The cause is usually a B vitamin or other deficiency. Have you had a complete nutritional blood work-up done?

I am also interested in the Nutritional Blood Work... But on top of that... Your CBC... Complete Blood Count. Is there anything out of whack? What was the diagnostic criteria they used to determine GBS with? What is the treatment plan?

I can't offer personal experience with post WLS GBS but this may help a bit:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3015935/

and searching Barre here got me:

http://www.obesityhelp.com/forums/rny/4490926/Guillain-Barre -Syndrome/

http://www.obesityhelp.com/forums/vsg/4477882/Anyone-ever-he ard-of-Guillian-Barre/

In other words... It happens. Rarely... But it happens.

FYI... That show... My 600lb life or whatever it was... Donald. He had this happen in one of the more extreme cases (affected his lungs). I never watched the show but found that on googling.