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PubMed2003

Celiac neuropathy.

BACKGROUND: Celiac disease (CD) is a chronic inflammatory enteropathy resulting from sensitivity to ingested gluten. Neurologic complications are estimated to occur in 10% of affected patients, with ataxia and peripheral neuropathy being the most common problems. The incidence and clinical presentation of patients with CD-associated peripheral neuropathy have not previously been investigated. OBJECTIVE: To determine the incidence of CD in patients with neuropathy and to characterize the clinical presentation. METHODS: The records of 20 patients with neuropathy and biopsy-confirmed CD were reviewed. RESULTS: Six of the 20 patients had neuropathic symptoms alone without gastrointestinal involvement, and neuropathic symptoms preceded other CD symptoms in another 3 patients. All patients had burning, tingling, and numbness in their hands and feet, with distal sensory loss, and nine had diffuse paresthesias involving the face, trunk, or lumbosacral region. Only two had weakness. Results of electrophysiologic studies were normal or mildly abnormal in 18 (90%) of the patients. Sural nerve biopsies, obtained from three patients, revealed mild to severe axonopathy. Using the agglutination assay, 13 (65%) of the patients were positive for ganglioside antibodies. Excluding patients who were referred with the diagnosis of celiac neuropathy, CD was seen in approximately 2.5% of all neuropathy patients and in 8% of patients with neuropathy and normal electrophysiologic studies seen at our center. CONCLUSION: CD is commonly associated with sensory neuropathy and should be considered even in the absence of gastrointestinal symptoms.

Adult↗
PubMed2005

Reliability and validity of the CMT neuropathy score as a measure of disability.

OBJECTIVE: To determine the validity and reliability of the Charcot-Marie-Tooth disease (CMT) neuropathy score (CMTNS) in patients with inherited neuropathy. BACKGROUND: Natural history studies and potential treatment trials for patients with various forms of CMT are limited by the lack of quantitative methodologies to monitor disease progression. Most cases of CMT can be considered length-dependent axonal neuropathies because disability for even the demyelinating forms correlates with length-dependent axonal degeneration. The total neuropathy score (TNS) is a validated composite measure of disability in length-dependent axonal neuropathies but is weighted toward predominantly sensory neuropathies. Thus, the authors have devised a CMTNS, modified from the TNS, to provide a single measure to quantify CMT disability. METHODS: The authors measured inter- and intrainvestigator reliability of the CMTNS and performed a validation of the score with the Neuropathy Impairment Score (NIS), patient self-assessment scores, an ambulation index, and other measures of disability. RESULTS: Inter- and intrainvestigator reliability was more than 95% in the 60 patients evaluated. Patients could be divided into mild (CMTNS, < or =10), moderate (CMTNS, 11 to 20), and severe (CMTNS, > or =21) categories and demonstrated excellent correlations among all measures of disability. CONCLUSION: The Charcot-Marie-Tooth disease (CMT) neuropathy score is a validated measure of length-dependent axonal and demyelinating CMT disability and can be investigated as an end point for longitudinal studies and clinical trials of CMT.

Action Potentials↗
PubMed1988

Predominantly sensory neuropathy in patients with AIDS and AIDS-related complex.

The most common type of peripheral neuropathy associated with human immunodeficiency virus (HIV) infection, predominantly sensory neuropathy, affects 10-30% of patients with acquired immunodeficiency syndrome (AIDS). From 40 individuals with peripheral neuropathy and HIV infection, we have identified 26 patients with this syndrome. All had constitutional symptoms when neuropathic symptoms developed; 20 had AIDS and six had AIDS-related complex. The most common complaint was pain on the soles. Paresthesias were frequent and usually involved the entire foot. Signs of peripheral neuropathy were present in all; the most frequent finding was absent or reduced ankle reflexes. Electrophysiologic studies revealed abnormal sensory and motor conduction, studies suggesting a dying-back axonopathy. Over time, the neuropathy progressed in all except one patient with ARC, who had spontaneous subjective improvement. Tricyclic antidepressants provided partial symptomatic relief. In three patients, the neuropathy did not change during azidothymidine treatment. Predominantly sensory neuropathy in HIV infection appears to be a distal axonal degeneration primarily involving sensory neurons. The mechanism is unknown, but the neuropathy is associated with the late manifestations of HIV infection.

AIDS-Related Complex↗
PubMed1995

Cutaneous innervation in sensory neuropathies: evaluation by skin biopsy.

OBJECTIVE: To use punch skin biopsies to evaluate the loss of intra-epidermal nerve fibers in sensory neuropathies. BACKGROUND: Previous assessments of epidermal nerve fibers have been constrained by relatively insensitive staining techniques and variability in quantification. METHODS: Punch skin biopsies were performed on the heel and leg of HIV-seronegative controls, HIV-seropositive individuals without neuropathy, and patients with sensory neuropathies, including HIV-seronegative and HIV-positive individuals. After formalin fixation, 50-microns free-floating sections were stained with a monoclonal antibody to neuron-specific ubiquitin hydrolase, PGP9.5. The number of intraepidermal fibers/mm in at least three sections from each patient was counted by one observer blinded to site and clinical status. RESULTS: Dermal and epidermal nerve fibers were readily identified and quantified. The immunostaining technique reliably demonstrated a dermal plexus of myelinated and unmyelinated fibers parallel to the surface of the skin. In the epidermis, unmyelinated fibers ascended vertically between the keratinocytes to reach the stratum corneum. The number of intra-epidermal fibers/mm in the distal leg (mean +/- SEM) was 17.84 +/- 3.03 in seven HIV-seronegative controls. Epidermal fiber number was significantly reduced (p = 0.01) in five HIV-infected patients with sensory neuropathies associated with didanosine or zalcitabine therapy (1.07 +/- 0.40) and in eight HIV-seronegative patients with sensory neuropathies (3.1 +/- 3.1). Four of five neurologically normal HIV-seropositive subjects had reduced numbers of epidermal fibers, suggesting a subclinical neuropathy. Serial biopsies in one individual demonstrated the evolution of degenerating epidermal fibers after development of zalcitabine-induced sensory neuropathy. CONCLUSION: Skin biopsies stained with the sensitive panaxonal marker anti-PGP9.5 demonstrated significant reduction in intraepidermal fibers in sensory neuropathies. This simple and repeatable technique is a reliable method for quantitation of small cutaneous sensory fibers. In addition, skin biopsies may be useful in assessing the course and spatial distribution of involvement in peripheral nerve disease.

Adult↗
PubMed1997

Peripheral neuropathy associated with sicca complex.

Peripheral neuropathy occurs in Sjögren's syndrome, a disorder in which systemic immunologic phenomena, including vasculitis, are common. Neuropathy also occurs with isolated sicca complex (keratoconjunctivits sicca and xerostomia); whether this represents a distinct syndrome is unclear. We retrospectively studied 54 patients with sicca complex and peripheral neuropathy to determine mode of presentation, neuropathic patterns, frequency and pattern of serologic abnormalities, and frequency of systemic disease, including necrotizing vasculitis. Peripheral neuropathy was the presenting problem in 87%. Although sicca symptoms occurred in 93%, they were a presenting complaint in only 11% and were usually mild, reported only after specific inquiry. Minor salivary gland biopsy was positive in 73%. Sensory neuropathies strongly predominated; 61% of patients manifested either sensory polyneuropathy or polyganglionopathy. Less common patterns included sensorimotor polyneuropathy (17%) and polyradiculoneuropathy (11%). Vasculitic neuropathy was demonstrated in only two patients, but nonspecific epineurial inflammation was present in 70% of nerve biopsies. Clinical evidence of systemic disease was uncommon, particularly in the sensory polyganglionopathy group, in whom extraglandular features other than weight loss occurred in only 1 of 12 patients. Antibodies to extractable nuclear antigens, the most specific serologic marker of Sjögren's syndrome, were present in 10.4%. We conclude that peripheral neuropathy and isolated sicca complex form a distinctive syndrome in which neuropathy is the presenting feature and sicca is easily overlooked; sensory polyneuropathy and polyganglionopathy predominate; serology is confirmatory but very insensitive; and extraglandular disease, including vasculitis, is uncommon compared with typical Sjögren's syndrome. Tests of ocular or salivary involvement are needed for diagnosis, and demonstration of inflammation in biopsied nerve is supportive. Improved definition of this disorder should permit further studies of natural history and efficacy of immunotherapy.

Adult↗
PubMed1999

Painful sensory neuropathy: prospective evaluation using skin biopsy.

OBJECTIVE: In patients presenting with painful, burning feet with minimal signs of neuropathy, the following questions were addressed: 1) How many of these patients have a peripheral neuropathy? 2) What is the role of skin biopsy in establishing a diagnosis of neuropathy? 3) What conditions are associated with the neuropathy? and 4) What laboratory studies are useful in this patient population? METHODS: A total of 117 consecutive patients referred for evaluation were prospectively studied. All underwent nerve conduction studies (NCS) and a battery of blood tests, including antinerve antibodies. If NCS were normal, a punch biopsy of the skin of the distal leg was performed to ascertain the intraepidermal nerve fiber (IENF) density. In a subset of 32 patients, the sensitivity of skin biopsy was compared to quantitative sudomotor axon test (QSART) and quantitative sensory tests (QST). RESULTS: Three groups emerged. Group 1, with abnormal NCS (n = 60, 34 F/26 M, mean age 60 +/- 14 years), represented 51% of the cohort. The majority had neuropathies of undetermined cause, but 18 (30%) had associated conditions. Group 2, with normal NCS and reduced IENF density (n = 44, 29 F/15 M, mean age 57 +/- 14 years), represented 38% of the cohort. Three in this group had associated conditions. Group 3, with normal NCS and IENF density (n = 13, 6 F/7 M, mean age 53 +/- 13 years), represented 11% of the cohort; most had no diagnoses but two had MS. In a comparative subset analysis, skin biopsy was more sensitive than QSART or QST in diagnosing a neuropathy. CONCLUSIONS: Patients presenting with painful feet are heterogeneous, consisting of both large and small fiber sensory neuropathies. In rare cases, a central cause for pain can be found. Over one-third of patients required a skin biopsy to diagnose a small fiber sensory neuropathy. A limited battery of blood tests facilitated diagnosis, but serum antinerve antibodies were not helpful.

Aged↗
PubMed2000

Antisulfatide antibodies in neuropathy: clinical and electrophysiologic correlates.

OBJECTIVE: To investigate the clinical and electrophysiologic characteristics of the neuropathy associated with elevated serum antisulfatide antibodies. METHODS: Clinical, electrophysiologic, morphologic, and laboratory data of 25 patients with significantly elevated (>25,600) antisulfatide antibodies were reviewed. RESULTS: Four groups were distinguished based on clinical and electrophysiologic data: Group 1, eight patients with predominantly small fiber sensory neuropathy (32%); Group 2, five patients with mixed large and small fiber sensory neuropathy (20%); Group 3, seven patients with axonal sensorimotor neuropathy (28%); and Group 4, three patients with demyelinating sensorimotor neuropathy (12%). One additional patient had mononeuritis multiplex and one had ALS. An immunoglobulin M (IgM) monoclonal gammopathy was found in 30% of the patients tested, but not in any of the Group 1 patients with small fiber sensory neuropathy. Serum IgM level was elevated in 12 patients, of whom six had a concomitant monoclonal gammopathy. Morphologic studies in five patients showed predominantly axonal degeneration, with three of the patients also exhibiting additional features of demyelination. CONCLUSIONS: Antisulfatide antibodies are associated with several subtypes of peripheral neuropathy. Predominantly sensory or sensorimotor axonal neuropathies are most common in this series, with the sensory component either small fiber or mixed fiber type. A smaller demyelinating group indistinguishable from patients with chronic inflammatory demyelinating polyradiculopathy was also seen. One third of patients had a concomitant IgM monoclonal gammopathy, and approximately one half had elevated serum IgM.

Adult↗
PubMed2000

Glycosphingolipid antibodies and blood-nerve barrier in autoimmune demyelinative neuropathy.

OBJECTIVE: To evaluate morphologic changes in small endoneurial vessels in patients with autoimmune demyelinative neuropathy and antiglycosphyngolipid antibodies. BACKGROUND: Although a humoral immune cause has been postulated for various demyelinating neuropathies, the mechanism by which large molecules like immunoglobulins can traverse the blood-nerve barrier (BNB) to enter the endoneurium is not understood. METHODS: We examined histologic and ultrastructural changes in small endoneurial vessels in sural nerve biopsy specimens from autoimmune demyelinative neuropathy patients, with or without anti-glycosphingolipid (GSL) antibodies. Density of small endoneurial vessels, mean endothelial area, mean luminal area, and the percentage of endothelial cell junctions (that make up the BNB) that showed evidence of disruption were evaluated. RESULTS: Only junctional disruption showed a significant difference: autoimmune demyelinative neuropathy patients with anti-GSL antibodies showed more BNB disruption than autoimmune demyelinative neuropathy patients without antibodies or control patients with nonautoimmune neuropathies. The most commonly observed endoneurial change in antibody-positive autoimmune demyelinative neuropathy patients was the finding of continuous, patent spaces lacking tight junctions between endothelial cells. CONCLUSIONS: Brain endothelial cells and endoneurial endothelial cells share various GSL antigens, including GM1 and GD1b gangliosides, with peripheral nerve tissues. Circulating anti-GSL antibodies could damage cell-to-cell attachments in endoneurial endothelium. This barrier disruption may permit the large molecules like immunoglobulins to enter the endoneurial space, contributing to development of autoimmune demyelinative neuropathy.

Adolescent↗
PubMed2002

Therapy of CIDP and related immune-mediated neuropathies.

This study assesses the data supporting the current use of immunotherapy for management of neuropathies with a presumed autoimmune basis. Immune or inflammatory mechanisms are implicated in an increasing number of disorders that involve damage to peripheral nerves and sensory ganglia. The most prevalent of these is chronic inflammatory demyelinating polyradiculoneuritis (CIDP). CIDP is clinically distinguishable from a series of other immune- or inflammation-mediated neuropathies. These include the following: multifocal acquired demyelinating sensory and motor (MADSAM) neuropathy associated with conduction block; brachial or lumbar plexitis; multifocal motor neuropathy, a distal demyelinating neuropathy associated with antibodies to the myelin-associated glycoprotein (MAG); and sensory neuronopathy. We reviewed the literature of the National Library of Medicine using the above terms and their variations. The results from short-term, randomized, controlled trials support the efficacy of intravenous immunoglobulin (IVIg), plasma exchange, and corticosteroids in the treatment of CIDP, and the efficacy of IVIg in the treatment of MMN. Only anecdotal experience is available for assessing the treatment of MADSAM neuropathy, lumbar and brachial plexitis, MAG neuropathy, and sensory neuronopathy. Cytotoxic and immunosuppressive drugs are frequently used to treat patients with many of these disorders when they are refractory to standard treatments, but no controlled trials have been done to support their use. This review discusses the complications and criteria for use of these therapies. Selecting the best immunotherapy for an individual patient should be based on the proven efficacy of a given regimen in modulating the pathophysiology underlying the neuropathy, the anticipated duration of disease, and the patient's age, reproductive status, and coexisting metabolic derangement.

Humans↗
PubMed2004

Prevalence of peripheral neuropathy in type 2 diabetic patients attending a diabetes center in Turkey.

The aim of this study was to determine the prevalence and risk factors for neuropathy in type 2 diabetic patients attending a major Turkish diabetes center. Eight hundred and sixty-six consecutive type 2 diabetic patients were included in the study. A single observer performed biothesiometry studies on these patients. The presence of diabetic neuropathy was investigated using neurological symptom scale (NSS) and neurological disability score (NDS) performed. Neuropathy was determined with standardized neurological examinations and defined as the presence of abnormal NSS and NDS together with abnormal sensory or motor signs and symptoms as well as decreased great toe vibration perception. Overall, 60% (n = 520) of the patients were diagnosed as having neuropathy. The prevalence of neuropathy increased with age (p < 0.001) and duration of diabetes (p < 0.001). Multiple logistic regression analysis revealed the duration of diabetes (p < 0.001) and HbA1c levels (p < 0.001) as the risk factors for neuropathy. The overall prevalence of neuropathy in Turkish type 2 diabetic population was 60%. Age, duration of diabetes, and poor glycemic control were considered to be the risk factors for neuropathy.

Adult↗
PubMedDate not supplied

Prevention and management of drug-induced peripheral neuropathy.

When symptoms of peripheral neuropathy appear, the possibility that they have been induced by drugs should be considered. A large number of drugs of all kinds, several of which are considered indispensable, have been implicated in peripheral neuropathy. A list of some of these drugs is provided. Neuropathy is a universal and dose-limiting factor during treatment with vinca alkaloids, but is otherwise a rare complication of drug therapy. Drug-induced peripheral neuropathy is almost always due to a dose-dependent primary axonal degeneration caused either by toxic reactions or by metabolic changes in neurons or their surroundings. The use of drugs should be restricted, especially in patients with a risk for development of neuropathy or with already existing neuropathy, e.g. patients with hepatic or renal failure, diabetes mellitus, or malnutrition. Patients should be given vitamins, prophylactically or therapeutically, which will sometimes allow a treatment to be continued. In other cases of drug-induced neuropathy the drug should be stopped. Reversal depends on the severity of the neuropathy, intensity and duration of the treatment and existence of causative cofactors, but generally the prognosis is good. While waiting for recovery physiotherapy is of importance, and when paraesthesia and pain are troublesome the patient should be treated with carbamazepine, imipramine or lidocaine (lignocaine).

Humans↗
PubMed2003

Peripheral neuropathy in Japanese patients with hepatitis C virus infection.

OBJECTIVE: The aim of this study was to report a series of Japanese patients with neuropathic symptoms following HCV infection. PATIENTS AND METHODS: Fifteen patients with neuropathic symptoms and HCV infection were studied retrospectively (neuropathy group). We evaluated clinical and electrophysiologic findings. As a control group, we investigated prospectively 11 patients with chronic HCV hepatitis without neuropathic symptoms. RESULTS: In the neuropathy group, the peripheral neuropathy was a multiple mononeuropathy (MM) in 8 patients, a polyneuropathy in 4 patients, a single cranial neuropathy in 2 patients, and a cervical radiculopathy in one patient. Five patients with MM had relapsing symptoms. Two patients showed a progression of neurologic symptoms following varicella zoster virus infection. Mixed cryoglobulinemia was noted in 4 of 13 tested patients. Circulating immunocomplexes were detected in 3 of 10 tested patients, and low complement (C3, C4, or CH50) levels were noted in 10 of 13 tested patients. Nerve conduction study (NCS) showed abnormal findings in 10 of 13 investigated patients. In the control group, only the frequency of low CH50 was significantly lower than that in the neuropathy group. Abnormal findings of NCS were found in 3 of 11 patients. CONCLUSION: We showed the presence of various types of neuropathies in patients with HCV infection. Our results suggest that relapsing MM is common in HCV positive neuropathy with or without cryoglobulinemia, and that the virus may modulate neurologic manifestations of other viral infections. Subclinical neuropathy may be present in some patients with HCV infection without neurologic symptoms.

Adult↗
PubMedDate not supplied

[Chronic inflammatory neuropathies].

INTRODUCTION: The group of chronic inflammatory neuropathies is made up of a variety of neuropathies of autoimmune or infectious origin. DEVELOPMENT: We describe three types of neuropathies and their treatment: demyelinating chronic neuropathy, motor multifocal neuropathy and demyelinating neuropathy associated with monoclonal gammapathy. These three types of neuropathy have uniform characteristics and features, which permit precise identification and suggest that they are separate entities. CONCLUSIONS: In the management of any type of neuropathy it is essential to make the correct diagnosis. Initial investigations should include detailed electrophysiological examination to detect the presence of demyelination, lumbar puncture and, if pleocytosis is found, the possibility of associated acquired immunodeficiency syndrome should be investigated. Also, before immunosuppressive treatment is begun, a systematic medical examination should be done to detect any other coexisting illness which might affect use of the different drugs involved.

Demyelinating Diseases↗
PubMedDate not supplied

[Autonomic and somatic neuropathy in the diabetic patient: electric clinical analysis].

INTRODUCTION AND OBJECTIVE: Neuropathy is the more often complication in the diabetic patients. The relationship between somatic and autonomic neuropathy has not been studied on these patients, so we decided to compare both situations. PATIENTS AND METHODS: We have performed a comparative study among clinical elements, the nerve conduction study (NCS) and the autonomic cardiovascular function in 120 insulin dependent diabetics patients. We use clinical scales, the NCS and the heart rate variability study (HRVS) to know de autonomic cardiovascular function. RESULTS: Sensation was the clinical manifestation more compromised and there was not correlation between clinical manifestation and the HRVS. In the NCS the nerve conduction velocity was the element more affected and the nerve more compromised was the sural; there was good correlation between NCS and HRVS. Fifty per cent of patients had some degree of neuropathy, and the duration of the disease was an important factor on this damage. The clinical elements, the NCS and the HRVS together let us classified patients in: patients without neuropathy (10 cases), patients with somatic neuropathy (31 cases), patients with autonomic neuropathy (7 cases), patients with somatic-autonomic neuropathy (72 cases). CONCLUSIONS: To defined the diagnosis of cardiovascular autonomic neuropathy (CAN) is necessary the HRVS, the subclinical presentations of CAN are often without manifestation. There is a close relationship between the somatic and autonomic nerve damage, influenced by the duration of the disease.

Adult↗
PubMed2000

[Infectious neuropathies].

Infective neuropathies constitute a leading cause of neuropathies in the world. The number of patients with nerve lesions related to leprosy remains high despite decreasing number of new cases requiring multidrug regimens. Peripheral neuropathies associated with HIV infection may be found in up to 50% of patients. Neuropathies may be related to the inflammatory reaction against viral antigens, immunodepression, opportunistic infections, and iatrogenic complications of anti-viral drugs. Hepatitis C virus infection has been found in cryoglobulinemic neuropathies. This virus should be screened for exploration of all neuropathies. Rare causes of neuropathy, such as poliomyelitis and diphtheria, and treatable neuropathies such as Lyme disease, should not be forgotten.

Antiviral Agents↗
PubMed2001

Acquired inflammatory demyelinating neuropathies.

The acquired demyelinating neuropathies can be divided into those with an acute onset and course and those with a more chronic course. The acute neuropathies present as Guillain-Barré syndrome and include acute inflammatory demyelinating polyradiculoneuropathy (AIDP), Miller Fisher syndrome, acute motor axonal neuropathy (AMAN), acute motor and sensory axonal neuropathy (AMSAN), and acute pandysautonomia. The chronic neuropathies are collectively known as chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) and include MADSAM (multifocal acquired demyelinating sensory and motor neuropathy, also know as Lewis-Sumner syndrome) and DADS (distal acquired demyelinating symmetric neuropathy) as variants. The clinical features, pathology, pathogenesis, diagnosis, treatment, rehabilitation, and prognosis of these neuropathies are discussed.

Acute Disease↗
PubMed2002

[Neuropathy in nearby cranial nerves after acoustic schwannoma gamma knife radiosurgery, a follow-up study].

OBJECTIVE: To investigate the risks of facial, trigeminal and acoustic neuropathies after acoustic schwannoma gamma knife radiosurgery. METHODS: The clinical data of forty-three patients with 46 masses of acoustic schwannoma who underwent gamma knife radiosurgery with the dose of 12 approximately 15 Gy to the tumor margin between January 1997 and October 2000 and were followed up for 6 approximately 24 months (on average 16.9 months) were studied. The tumor diameter was 10 approximately 20 mm in 12 cases, 21 approximately 30 mm in 23 cases, >/= 31 mm in 11 cases, with the average value of 28 mm. RESULTS: The general tumor control rate was 91.3%. The useful hearing preservation rate was 100% immediately after radiosurgery, 87% 6 months later and 78% 2 years later. The hearing preservation rate was high for small tumors. The facial and trigeminal neuropathies began to appear after 6 months. The incidence rates of facial neuropathy was 15.3%, 7.6%, and 3.8% 6 months, 1 year and 2 years after radiosurgery respectively. The incidence rates of trigeminal neuropathy was 11.4%, 3.8%, and 3.8% respectively 6 months, 1 year, and 2 years after radiosurgery. The incidence of neuropathy was 3.8% for tumors with a diameter < 30 mm for both facial and trigeminal nerves. The hearing in 2 out of 15 cases with dysaudia began to improve 6 months after radiosurgery. The incidence of neuropathy for tumors with the diameter > 30 mm was 3.8% for both nerves 2 years after raadiosurgery. The preservation rate of useful hearing for tumors with the diameter < 20 mm was 100% after radiosurgery. CONCLUSION: Stereotactic radiosurgery using gamma knife with a dose of 12 approximately 15 Gy to the tumor margin succeeds in controlling acoustic schwannoma and preserving useful hearing. The incidence of facial and trigeminal neuropathies are low. The neuropathy caused by gamma knife radiosurgery is sub-lethal and can be recovered gradually.

Adolescent↗
PubMed2003

[Treatment of peripheral neuropathies with neutrotrophic factors: animal models and clinical trials].

In vitro experiments and works with knock-out mice have demonstrated the physiological importance of neurotrophic factors (NF) in the development and the survival of peripheral nervous system neurons. Therefore, NF may be useful in the treatment of peripheral neuropathies. These pathologies may be more amenable than central nervous diseases to the systemic delivery of NF. Indeed, NF can readily access peripheral nerves from blood whereas penetration into the central nervous system is limited by the blood-brain barrier. The objectives of NF treatment are: 1) to compensate a putative deficiency of NF associated with the pathogenesis of some neuropathies, such as diabetic neuropathy; 2) to stop or slow disease progression by acting on the biochemical pathways involved in the neurodegenerative cascade; and 3) to enhance the physiological compensatory mechanism of axonal sprouting. The efficacy of treatment with NF has been demonstrated in animal models mimicking various neuropathies, such as neuropathies related to diabetes or treatment with chemotherapeutic agents. However, a phase 3 trial in diabetic neuropathy and a phase 2 trial in HIV-related neuropathy have failed to demonstrate any substantial effect of treatment with NGF. In this review, we discuss the factors that may explain these negative results. A major limitation of systemic administration is the poor bioavailability of NF due to their short half-life. Alternative modes of delivery may be more appropriate than systemic administration of the recombinant protein. In particular, muscular-based gene therapy allows the delivery of sustained levels of neurotrophic factor into the circulation. This strategy has shown to be effective in animal models of motor and sensory neuropathies. Another promising treatment is the use of small molecules that induce the endogenous synthesis of NF, such as xaliprodene or 4-methylcathecol.

Animals↗