Nerve root hypertrophy as the cause of lumbar stenosis in chronic inflammatory demyelinating polyradiculoneuropathy

Goldstein, Jonathan; Parks, Becky; Mayer, Peter L.; Kim, Jung Ho; Sze, Gordon; Miller, Robert G.

doi:10.1002/(sici)1097-4598(199607)19:7<892::aid-mus12>3.0.co;2-l

Cited by 46 publications

(26 citation statements)

References 8 publications

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“…It has been suggested that axonal narrowing such as that occurring in the lysolecithin model may be a response to the loss of myelin or may be due to some interference with the normal Schwann cell/axon relationship (11). Such interference, if it really existed, did not lead to the formation of the onion bulbs observed in progressive or recurrent polyneuropathies (16,17) or to the occurrence of hypoor dysmyelination similar to that reported in the quaking and Trembler mouse mutants in which the communication between Schwann cells and axons is genetically disturbed (18,19).…”

mentioning

confidence: 99%

Ethidium bromide-induced demyelination of the sciatic nerve of adult Wistar rats

Riet-Correa

Fernandes

Graça

2002

Braz J Med Biol Res

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Peripheral nerve ultrastructure was assessed after single or multiple local injections of the intercalating dye ethidium bromide. Thirty-four adult Wistar rats of both sexes were divided into five groups and maintained in a controlled environment with rat chow and water ad libitum throughout the experiment. The experimental animals were injected with 1 µl of 0.1% ethidium bromide in 0.9% saline into the central third of the left sciatic nerve 1 (group 1), 2 (group 2), 4 (group 3), 6 (group 4) or 8 (group 5) times. In groups 2 to 5 the injections were made at 28-day intervals. Control animals received the same amount of 0.9% saline. The animals were killed at different times after injection: group 1 at 7 days (2 rats) and 15 days (2 rats); for groups 2, 3, 4 and 5, all rats were killed 10 days after the last injection and the lesions were investigated by light and transmission electron microscopy. In the acute lesions, intoxicated Schwann cells showed a vacuolated cytoplasm and separation of the sheaths from the axon. Myelin sheaths underwent progressive vesiculation and subsequent segmental demyelination. Myelin debris were withdrawn by macrophages and remyelination by Schwann cells was prominent. With the increase in the number of injections collagen fibers also increased in number and progressively enveloped smaller numbers of remyelinated axons composing new fascicles. Wallerian degeneration of fibers apparently not affected by ethidium bromide was more intense in the nerves from groups 4 and 5. The peripheral nerve repairs itself after demyelinating challenges with a profusion of collagen fibers and new fasciculations. This experimental model is valid to mimic recurrent demyelinating neuropathies.

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mentioning

confidence: 99%

Ethidium bromide-induced demyelination of the sciatic nerve of adult Wistar rats

Riet-Correa

Fernandes

Graça

2002

Braz J Med Biol Res

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“…In our patient, the initial diagnosis was multiple sclerosis because of progressive weakness that developed severe in the lower extremities, increased tonus and brisk deep tendon reflexes. MRI may be helpful in the diagnosis of CIDP by excluding the compressive or structural lesions that may lead to polyradiculopathy and MRI may also show hypertrophy of nerve roots and inflammatory processes in CIDP (Crino et al, 1993;Morgan et al, 1993;Goldstein et al, 1996;Midroni and Dyck, 1996;Mizuno et al, 1998). Duggins et al (1999) demonstrated that all patients with spinal root and plexus hypertrophy had a relapsing-remitting course and a significantly longer duration of disease than those without hypertrophy.…”

Section: Discussionmentioning

confidence: 99%

“…The reported prevalence of CIDP ranges from 1 to 2 per 100.000 population and is equal in both sexes (Rentzos et al, 2007). Demyelinating neuropathy predominantly affects spinal roots, plexuses and proximal nerve trunks and thickened nerves can be palpable in about 10% of the patients (Crino et al, 1993;Morgan et al, 1993;Matsuda et al, 1996;Goldstein et al, 1996;Mizuno et al, 1998). When ranked by the descending frequency, postural tremor in the arms, peripheral nerve thickening, papilledema and facial or bulbar weakness, respiratory failure and autonomic dysfunction can be seen in patients with CIDP (Rotta et al, 2000;Pollard, 2002).…”

Section: Introductionmentioning

confidence: 99%

An Atypical Chronic Inflammatory Demyelinating Polyradiculoneuropathy that Radiologically Mimicking Neurofibromatosis: Case Report

Akpınar¹,

Doğru²,

Balcı³

et al. 2014

jecm

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Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is an uncommon demyelinating disorder with a relapsing and remitting or continuously progressive course. Patients may have motor and sensory involvement, but generally motor involvement may be more prominent and more severe in lower extremities. CIDP is a treatable neuropathy that is challenging to diagnose and has a broad spectrum of presentations. When ranked by the descending frequency, postural tremor in the arms, peripheral nerve thickening, papilledema and facial or bulbar weakness, respiratory failure and autonomic dysfunction can be seen in patients with CIDP. Demyelinating neuropathy predominantly affects spinal roots, plexuses and proximal nerve trunks and thickened nerves can be palpable in about 10% of the patients. In patients with atypical presentation, the diagnosis of CIDP may be delayed and hypertrophic nerve roots have been reported in CIDP patients with delayed diagnosis. Magnetic Resonance Imaging (MRI) may be helpful in the diagnosis of CIDP by excluding the compressive or structural lesions that may lead to polyradiculopathy and MRI may also show hypertrophy of nerve roots and inflammatory processes in CIDP. We presented a patient with CIDP who had MRI findings of diffuse enlargement and mild enhancement of roots and extraforaminal segments of nerves in all segments.

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“…Known causes of hypertrophic spinal roots of the cauda equina include hereditary neuropathies (Charcot-Marie-Tooth disease 1A, Dejerine-Sottas syndrome, Refsum disease, neurofibromatosis), chronic inflammatory demyelinating neuropathies, other inflammatory neuropathies (sarcoidosis), redundant nerve root syndrome, peripheral nerve sheath tumors, lymphoma, and amyloidoma. [7][8][9][10][11][12] In our patient, there was no clinical or electrophysiologic evidence for a generalized hypertrophic neuropathy, as the process seemed to be confined to the cauda equina. The normal lumbar roots seen on an MRI study years before the intrathecal stem cell injection suggests an acquired process.…”

Section: Discussionmentioning

confidence: 99%

Erratum: Inflammatory hypertrophic cauda equina following intrathecal neural stem cell injection

2013

Muscle and Nerve

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Introduction: Potential benefit from stem cell treatments has more patients seeking treatment without understanding possible risks. Methods: We describe a woman who presented with progressive bilateral leg pain, numbness, and gait difficulties. A prior stroke, macular degeneration, osteoarthritis, and depression, led her to receive intrathecal neural stem cell therapy overseas 1 year before onset of symptoms. Results: Imaging showed marked enlargement of lumbosacral roots of the cauda equina, which was not seen before stem cell treatment. Electrodiagnostic studies confirmed chronic multiple lumbosacral radiculopathies. Biopsy of a lumbar dorsal sensory root showed myelinated fiber degeneration and loss, with endoneurial inflammation. The hypertrophic inflammatory cauda equina syndrome was potentially triggered by the prior intrathecal neural stem cell injection. Conclusions: Safety of intrathecal stem cell treatments is not regulated routinely in overseas stem cell facilities. We wish to bring this potential complication to the attention of health care providers. 48: 831-835, 2013 The potential benefit for stem cell therapy to repair, restore, replace, and regenerate damaged tissues has many patients with chronic neurological conditions excited about possible treatments. Research in this area continues to grow throughout the world. The U.S. National Institute of Health reports over 45 registered trials world-wide that relate to stem cell therapy and spinal cord injury alone. Muscle Nerve1 There is no way to know how many unregistered and uncontrolled treatments are offered in "notorious" stem cell clinics for chronic conditions that range from rejuvenation to cerebral palsy, stroke, Parkinson disease, traumatic brain and spinal cord injury, multiple sclerosis, and amyotrophic lateral sclerosis.2-5 Along with increased research, more and more patients are seeking stem cell therapy before the safety and efficacy of such treatments have been established. Some experts have concerns that the hope and expectations patients have for cures cannot be met. This may leave patients vulnerable to nonregulated providers of stem cell treatments that are potentially harmful. 3,6 Stem cells have 3 fundamental properties. First, they have a high proliferative potential. Second, they are capable of self-renewal. Third, they have the ability to differentiate into multiple cell types.These properties are what make stem cell therapy so attractive, especially in the setting of central nervous system injury, such as acute spinal cord injury, prior stroke, multiple sclerosis, and amyotrophic lateral sclerosis. However, these same properties, without a full understanding or control of their subsequent activities, are what potentially make stem cell therapy dangerous. Cells in a different environment may multiply, form tumors, or leave the site of origin and migrate somewhere else in the body. 4,5 In this case report, we postulate that intrathecal administration of neural stem cells may have induced inflammatory hypertroph...

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Nerve root hypertrophy as the cause of lumbar stenosis in chronic inflammatory demyelinating polyradiculoneuropathy

Cited by 46 publications

References 8 publications

Ethidium bromide-induced demyelination of the sciatic nerve of adult Wistar rats

Ethidium bromide-induced demyelination of the sciatic nerve of adult Wistar rats

An Atypical Chronic Inflammatory Demyelinating Polyradiculoneuropathy that Radiologically Mimicking Neurofibromatosis: Case Report

Erratum: Inflammatory hypertrophic cauda equina following intrathecal neural stem cell injection

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