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At least 631 records · Page 35Linked to original sources
PubMed2007

Therapeutic angiogenesis inhibits or rescues chemotherapy-induced peripheral neuropathy: taxol- and thalidomide-induced injury of vasa nervorum is ameliorated by VEGF.

Toxic neuropathy represents an important clinical problem in the use of the chemotherapeutic substances Taxol and thalidomide. Sensory neuropathy has a high incidence, lacks an effective treatment and is the dose-limiting factor for these drugs. The pathogenic basis of these neuropathies is unknown. We investigated the hypothesis that the experimental toxic neuropathies from Taxol and thalidomide results from destruction of vasa nervorum and can be reversed by the administration of an angiogenic cytokine. In animal models of Taxol- and thalidomide-induced neuropathy, nerve blood flow has been attenuated and the number of vasa nervorum has been reduced. Intramuscular gene transfer of naked plasmid DNA encoding VEGF-1 administered in parallel with Taxol injections completely inhibited deterioration of nerve function and diminution of the peripheral nerve vasculature. Gene therapy in animals with established Taxol- or thalidomide-induced neuropathies resulted in recovery of vascularity and improved nerve electrophysiology. These findings implicate microvascular damage as the basis for toxic neuropathy and suggest that angiogenic growth factors may constitute a novel treatment for this disorder.

Animals↗
PubMed2002

Cryoglobulinemia is a frequent cause of peripheral neuropathy in undiagnosed referral patients.

Cryoglobulinemia represents an emerging cause of peripheral neuropathy, especially in Southern Europe, in view of its relationship with hepatitis C virus infection. In a series of 100 consecutive referral patients with uncharacterized peripheral neuropathies, we systematically investigated cryoglobulinemia to assess its diagnostic yield. The most frequent diagnosis was hereditary neuropathy (33%), 29% were acquired neuropathies of different types, and no cause could be identified in 27%. Cryoglobulinemic neuropathy was diagnosed in 11 patients (7 women and 4 men), aged 54-77 (mean = 63.5 years), most presenting with sensory polyneuropathy, often asymmetrical. Cryoglobulin was also detected in 2 additional patients in whom a final diagnosis of non-Hodgkin lymphoma was made. Purpura was absent in 4 patients (and in 2 with lymphoma), or restricted to discrete manifestations in the remaining patients, which did not provide a clue to the diagnosis. Thus, search for cryoglobulin proves useful in a substantial number of undiagnosed peripheral neuropathies (11% to 13% in our series), even in the absence of typical skin lesions, and it is recommended as a first-line investigation in patients with unexplained neuropathy presenting in middle to older age.

Aged↗
PubMed2003

Other autonomic neuropathies.

Acquired forms of autonomic neuropathy may be isolated or may coexist with somatic neuropathy. Clinical identification of symptoms and signs in the patient with autonomic dysfunction is crucial in the diagnosis of autonomic neuropathy and its separation from pure autonomic failure or multiple system atrophy. Once an autonomic neuropathy has been identified, several clinical features can be useful in the diagnosis of a specific form of autonomic neuropathy. Other factors, such as the presence of somatic neuropathy and systemic disease, are critical for diagnosis. This article reviews the clinical presentation, diagnosis, pathogenesis, and management of the acquired forms of autonomic neuropathy.

Animals↗
PubMed2002

Metabolic optic neuropathies.

Metabolic optic neuropathies form a rubric of disease characterized by bilaterally symmetrical visual impairment with loss of central visual acuity, dyschromatopsia, centrocecal visual field defects, temporal optic disc atrophy, and specific loss of the nerve fiber layer in the papillomacular bundle. The three subcategories of metabolic optic neuropathies are heredodegenerative (such as Leber's hereditary optic neuropathy), nutritional deficiencies (such as vitamins B12 or folic acid), or toxicities (such as ethambutol or cyanide). It's interesting to note that the first of these three is a congenital cause of mitochondrial impairment, whereas the latter two are acquired injuries to mitochondria. Hence, most if not all causes of metabolic optic neuropathies are, in fact, related to mitochondrial impairment. At the present time there is no effective treatment for heredodegenerative optic neuropathy. Nutritional deficiency metabolic optic neuropathies are treated by giving supplements of the appropriate nutrient or vitamin, whereas toxic metabolic optic neuropathies are treated by removing or preventing exposure to the toxin in question.

Humans↗
PubMed1998

Neuropathy as an extrahepatic manifestation of chronic liver diseases.

Gastrointestinal motor disturbances and various cardiovascular symptoms are the characteristic features of autonomic neuropathy. Autonomic and sensory neuropathy has been described in chronic alcoholic liver diseases. Cardiovascular autonomic reflex tests as the gold standard for autonomic neuropathy and measuring of thresholds for constant current electric sine wave stimulation by neurometer were used for measuring sensory neuropathy in patients with chronic liver diseases of different etiology. Autonomic and sensory neuropathy was also observed in non-alcoholic liver diseases. We proved that there is a correlation between autonomic neuropathy and prolongation of corrected QT interval in chronic liver diseases. We claim that autonomic neuropathy may have a role to play in the development of hyperdynamic circulation and portal hypertension in chronic liver diseases.

Autonomic Nervous System Diseases↗
PubMed1995

Upper extremity neuropathies in patients with spinal cord injuries.

We present a cross-sectional study designed to screen and evaluate 19 male patients with acute or chronic spinal cord injury for the presence of carpal tunnel syndrome (CTS) and radial neuropathies (RNP) in order to establish the prevalence of CTS and RNP, to compare characteristics of persons with spinal cord injury who do not have these neuropathies, to evaluate the effects of their activities and to define the causation of these neuropathies in order to prevent their occurrence during and after the rehabilitation process. Patients admitted to the Spinal Cord Injury Service with acute and chronic spinal injury (below C3) were included in the study. The level of activity was determined with the Functional Independence Measure (FIM) Score. Patients underwent neurological examination. Neurophysiological studies were done in all cases to determine the presence, nature and duration of CTS and RNP. As longevity of the spinal cord injured population is increasing, heightened awareness of the prevalence of CTS and RNP are necessary to develop strategies to prevent and manage these neuropathies which may adversely affect the patient's quality of life. Of 19 patients studied, three had clinical CTS, confirmed by neurophysiological had no neuropathies and five had non-CTS neuropathies. No RNP was found, but one patient in the non-CTS group had symptomatic left ulnar neuropathy also confirmed by neurophysiological exam.

Carpal Tunnel Syndrome↗
PubMed2003

Coexistent hereditary and inflammatory neuropathy.

Classically, the course of Charcot-Marie-Tooth (CMT) disease is gradually progressive. We describe eight atypical patients who developed acute or subacute deterioration. Seven of these had genetically proven CMT disease type 1A (CMT1A) due to chromosome 17p11.2-12 duplication, and one had X-linked disease (CMTX) due to a mutation in the GJB1 gene. In this group there was sufficient clinical, electrophysiological and neuropathological information to indicate a diagnosis of a superimposed inflammatory polyneuropathy. The age range of the patients was 18-69 years, with a mean of 39 years. A family history of a similar neuropathic condition was present in only four patients. All eight had an acute or subacute deterioration following a long asymptomatic or stable period. Seven had neuropathic pain or prominent positive sensory symptoms. Nerve biopsy demonstrated excess lymphocytic infiltration in all eight patients. Five patients were treated with steroids and/or intravenous immunoglobulin, with variable positive response; three patients received no immunomodulatory treatment. Inflammatory neuropathy has previously been recognized in patients with hereditary neuropathy, with uncharacterized genetic defects and with CMT1B. We present detailed assessments of patients with CMT1A and CMTX, including nerve biopsy, and conclude that coexistent inflammatory neuropathy is not genotype-specific in hereditary motor and sensory neuropathy. Although this was not a formal epidemiological study, estimates of the prevalence of CMT disease and chronic inflammatory demyelinating polyneuropathy indicate that the association is more frequent than would be expected by chance. This has implications for understanding the pathogenesis of inflammatory neuropathies and raises important considerations in the management of patients with hereditary neuropathies. If a patient with CMT disease experiences an acute or subacute deterioration in clinical condition, treatment of a coexistent inflammatory neuropathy with steroids or immunoglobulin should be considered.

Acute Disease↗
PubMed1994

Molecular genetics of Charcot-Marie-Tooth disease and related neuropathies.

Collectively, the inherited disorders of peripheral nerves represent a common group of neurologic diseases. Charcot-Marie-Tooth neuropathy type 1 (CMT1) is a genetically heterogeneous group of chronic demyelinating polyneuropathies with loci mapping to chromosome 17 (CMT1A), chromosome 1 (CMT1B), the X chromosome (CMTX) and to another unknown autosome (CMT1C). CMT1A is most often associated with a tandem 1.5 megabase (Mb) duplication in chromosome 17p11.2-12, or in rare patients may result from a point mutation in the peripheral myelin protein-22 (PMP22) gene. CMT1B is associated with point mutations in the myelin protein zero (P0) gene. The molecular defect in CMT1C is unknown. X-linked Charcot-Marie-Tooth neuropathy (CMTX) is associated with mutations in the connexin32 gene. Charcot-Marie-Tooth neuropathy type II (CMT2) is an axonal neuropathy, also of undetermined cause. One form of CMT2 maps to chromosome 1p36 (CMT2A). Dejerine-Sottas disease, also called hereditary motor and sensory neuropathy type III (HMSNIII), is a severe, infantile onset demyelinating polyneuropathy syndrome that may be associated with point mutations in either the PMP22 gene of the P0 gene. Hereditary neuropathy with liability to pressure palsies (HNPP) is an autosomal dominant disorder that results in a recurrent, episodic demyelinating neuropathy. HNPP is associated with a 1.5 Mb deletion in chromosome 17p11.2-12 and may result from reduced expression of the PMP22 gene. CMT1A and HNPP are apparent reciprocal duplication/deletion syndromes originating from unequal crossover during germ cell meiosis.

Charcot-Marie-Tooth Disease↗
PubMed1999

Ulnar neuropathy in surgical patients.

BACKGROUND: The goal of this project was to study the frequency and natural history of perioperative ulnar neuropathy. METHODS: A prospective evaluation of ulnar neuropathy in 1,502 adult patients undergoing noncardiac surgical procedures was performed. Patients were assessed with a standard questionnaire and neurologic examination before surgery, daily during hospitalization in the first week after surgery, and by telephone if they were discharged before 1 postoperative week. Patients in whom ulnar neuropathy developed were followed for 2 yr. RESULTS: Ulnar neuropathy developed in seven patients (0.5%; 95% confidence interval, 0.2% to 1.0%). Six of the seven patients were men. Symptoms of ulnar neuropathy began 2-7 days after surgery. Manifestations were mild and confined to sensory deficits in six patients. Symptoms resolved in four patients within 6 weeks. The remaining three patients had residual symptoms 2 yr later. CONCLUSIONS: In this surgical population, ulnar neuropathy was an infrequent complication. It occurred primarily in men who were 50-75 yr old and was not symptomatic until several days after surgery. Gender-dependent differences in the anatomy of the ulnar nerve and related structures at the elbow may serve as risk factors for ulnar neuropathy in patients having surgery.

Aged↗
PubMed2000

Lower extremity neuropathies associated with lithotomy positions.

BACKGROUND: The goal of this project was to study the frequency and natural history of perioperative lower extremity neuropathies. METHODS: A prospective evaluation of lower extremity neuropathies in 991 adult patients undergoing general anesthetics and surgical procedures while positioned in lithotomy was performed. Patients were assessed with use of a standard questionnaire and neurologic examination before surgery, daily during hospital stay in the first week after surgery, and by phone if discharged before 1 postoperative week. Patients in whom lower extremity neuropathies developed were observed for 6 months. RESULTS: Lower extremity neuropathies developed in 15 patients (1.5%; 95% confidence interval, 0.8-2.5%). Unilateral or bilateral nerves were affected in patients as follows: obturator (five patients), lateral femoral cutaneous (four patients), sciatic (three patients), and peroneal (three patients). Paresthesia occurred in 14 of 15 patients, and 4 patients had burning or aching pain. No patient had weakness. Symptoms were noted within 4 h of completion of the anesthetic in all 15 patients. These symptoms resolved within 6 months in 14 of 15 patients. Prolonged positioning in a lithotomy position, especially for more than 2 h, was a major risk factor for this complication (P = 0.006). CONCLUSIONS: In this surgical population, lower extremity neuropathies were infrequent complications that were noted very soon after surgery and anesthesia. None resulted in prolonged disability. The longer patients were positioned in lithotomy positions, the greater the chance of development of a neuropathy. These findings suggest that a reduction of duration of time in lithotomy positions may reduce the risk of lower extremity neuropathies.

Adult↗
PubMed2002

CT scan evidence of dysthyroid optic neuropathy.

PURPOSE: To determine the utility of CT imaging in identifying patients with dysthyroid optic neuropathy. METHODS: Orbital CT scans of 12 randomly selected patients with dysthyroid optic neuropathy and 15 control subjects with Graves orbitopathy were retrospectively reviewed by two investigators blinded to the clinical data. The clinical diagnosis of optic neuropathy was made by one author before obtaining CT images and was based on clinical features. RESULTS: Optic nerve crowding (P<0.001) and intracranial fat prolapse (P<0.05) were the imaging features independently related to optic neuropathy. A muscle index greater than 50% had excellent sensitivity (100%) but did not have high specificity (47%) for dysthyroid optic neuropathy. Superior ophthalmic vein dilation and proptosis did not show significant relations with optic neuropathy. CONCLUSIONS: This study suggests that patients with Graves orbitopathy who have severe optic nerve crowding, intracranial fat prolapse, and/or muscle index greater than 50% present on orbital CT scans are more likely to have coexisting optic neuropathy.

Adult↗
PubMed1994

Causes and diagnosis of sensory neuropathies: a review.

Sensory neuropathies are rare but unique peripheral neuropathies that involve only the peripheral sensory system. The diagnosis is made by both clinical and electrophysiological findings. Sensory neuropathies occur predominantly in women. The symptoms begin in the arms more often than the legs and occur asymmetrically. Pain and severe sensory ataxia in varying degrees are the main presenting symptoms. Definable causes of sensory neuropathies are hereditary, paraneoplastic, immunological, metabolic, infectious, and drug-induced disorders. In our experience, however, nearly half of all sensory neuropathies have been idiopathic. The clinical course of these sensory neuropathies is variable. The symptoms clearly worsened in 25% of our patients, but in the rest remained unchanged for many years, resulting in a poor functional prognosis because of intractable pain and ataxia. Most sensory neuropathies are resistant to any treatment. We review the electrophysiological features, laboratory findings, and nerve biopsy results in our patients and discuss in detail the potential underlying diseases included in the differential diagnosis.

Adult↗
PubMed1994

Autonomic neuropathies.

There is a spectrum of acute autonomic neuropathies. Acute panautonomic neuropathy (pandysautonomia), characterized by severe widespread sympathetic and parasympathetic failure, is at one extreme. Guillain-Barré syndrome is at the other end of the spectrum, where the brunt of the disorder falls on the somatic nervous system. Pure acute panautonomic neuropathies are relatively rare. The majority of acute autonomic neuropathies have some minor somatic features. Dysautonomia may be restricted to the cholinergic system (acute cholinergic neuropathy), adrenergic system, or other organ systems (eg, motility disorders). Recently, an important gap in the clinical description of idiopathic autonomic neuropathies and their course was filled, with neurologic and autonomic testing end-points. About one in four to one in three patients will improve substantially. Two other manifestations of autonomic neuropathy are the pseudoobstruction and postural tachycardia syndromes. Loss of the baroreceptors and consequent impairment of buffering of blood pressure results in wild swings in blood pressure that are treatable. Correcting anemia improves orthostatic tolerance, if necessary by hemopoietin. Improved evaluation of neural structure, in skin and in the laboratory, has led to better quantitation of autonomic failure and mechanisms of syncope. This understanding has been extended to the frequency domain and to a study of cerebral vasoregulation.

Autonomic Nervous System Diseases↗
PubMed2002

Secondary axon atrophy and neurological dysfunction in demyelinating neuropathies.

PURPOSE OF THE REVIEW: Secondary axonal atrophy is common in most if not all demyelinating neuropathies and is likely responsible for the majority of clinical symptoms. We review clinical, electrophysiological and morphological evidence for secondary axonal atrophy in demyelinating neuropathies and summarize recent hypotheses on possible pathomechanisms. RECENT FINDINGS: Elucidation of genetic defects responsible for hereditary demyelinating neuropathies and insights into axon-Schwann cell interactions have allowed longitudinal studies of genetically defined demyelinating neuropathies and research into the pathomechanism of secondary axonal atrophy. SUMMARY: There is ample clinical electrophysiological and electropathological evidence that secondary axonal atrophy is found in hereditary and demyelinating neuropathies. Recognizing secondary axonal atrophy as a main cause for clinical disability in demyelinating neuropathies is important for the clinician and may reveal a therapeutic target common to all different forms of demyelinating neuropathies.

Atrophy↗
PubMed2000

New therapies for optic neuropathies: development in experimental models.

Experimental models of human diseases have affected the design and direction of both basic and clinical research into understanding the pathogenesis and treatments of demyelinating disease, stroke, and hereditary disorders of the central nervous system. However, in spite of major advances in molecular research that have linked Leber Hereditary Optic Neuropathy to mutations in mitochondrial DNA, there has been relatively little focus in applying basic scientific methodologies to optic neuropathies other than glaucoma. The relative absence of detailed scientific knowledge about the basic mechanisms involved in the pathogenesis of optic nerve injury has contributed to the use of empiric therapies for neuro-ophthalmic optic neuropathies. Over the past decade major clinical trials, such as the Optic Neuritis Treatment Trial and Ischemic Optic Neuropathy Decompression Trial, have proven that currently available treatment options for demyelinating and ischemic optic neuropathies are ineffective and can even be harmful. Although the pathogenesis of visual failure in demyelinating, ischemic, and hereditary optic neuropathies appears diverse, a final common pathway for irreparable optic nerve injury may exist. This article reviews several models of experimental optic neuropathies that may aid in the development of novel treatments for neuro-ophthalmic disorders of the optic nerve during the 21st century.

Animals↗
PubMed2002

Ciprofloxacin-related acute peripheral neuropathy in a patient with lupus nephritis.

Ciprofloxacin is a commonly prescribed antibiotic, and drug-related peripheral neuropathy is a rare side effect. A woman with lupus nephritis on high-dose prednisone presented with acute peripheral neuropathy within 2 days of starting ciprofloxacin for a urinary tract infection. Nerve conduction and electromyographic studies confirmed a predominantly sensory, bilateral, lower extremity neuropathy with mild motor nerve involvement. At initial presentation, it could not be determined whether neuropathy was secondary to lupus or related to ciprofloxacin. Based on the temporal association of drug initiation and the onset of neuropathy, ciprofloxacin was discontinued. Her symptoms resolved within 2 weeks of ciprofloxacin discontinuation despite a simultaneous reduction in prednisone. The short duration of the peripheral neuropathy, the absence of lupus flare at the time of presentation, and the remission of symptoms during the prednisone taper all strongly suggest a rare but serious neuropathic adverse effect from ciprofloxacin. Ciprofloxacin neuropathy must be considered in patients with lupus who present with neuropathic symptoms after initiation of this commonly used antibiotic.

Journal Article↗
PubMed2006

Oxidant stress and peripheral neuropathy during antiretroviral therapy: an AIDS clinical trials group study.

BACKGROUND: Peripheral neuropathy that complicates HIV nucleoside reverse transcriptase inhibitor (NRTI) therapy is likely caused by mitochondrial injury. Mitochondria play a central role in regulating oxidant stress. We explored the relationships between oxidant stress and NRTI-induced peripheral neuropathy. METHODS: The AIDS Clinical Trials Group (ACTG) studied the cases of 384 antiretroviral-naive individuals randomized to receive didanosine/stavudine or zidovudine/lamivudine, plus efavirenz, nelfinavir, or both. The participants were followed for up to 3 years. Peripheral neuropathy was ascertained by signs and symptoms. We performed a case-control study of ACTG 384 participants. Peripheral neuropathy cases and nonneuropathy control subjects were selected from didanosine/stavudine recipients. Alternate control subjects were selected from zidovudine/lamivudine recipients who developed peripheral neuropathy. Oxidant stress was assessed by quantifying F2-isoprostanes (F2-IsoPs) in cryopreserved plasma. RESULTS: Seventy-five cases, 71 control subjects, and 18 alternate control subjects were identified. The median baseline F2-IsoP values were 53 (interquartile range [IQR], 40-85), 57 (IQR, 41-77), and 53 (IQR, 47-101) pg/mL, respectively, and did not differ between cases and control subjects (P = 0.78) or alternate control subjects (P = 0.60). Changes in F2-IsoPs from baseline to time of peripheral neuropathy did not differ significantly between cases (median, 10 [IQR, -17 to 26] pg/mL) and control subjects (median, 4 [IQR, -11 to 17] pg/mL; P = 0.48) or alternate control subjects (median, 1 [IQR, -48 to 10] pg/mL; P = 0.21). CONCLUSIONS: Peripheral neuropathy that complicates antiretroviral therapy with NRTIs was not associated with increased systemic oxidant stress assessed by plasma F2-IsoPs.

Adult↗
PubMed2006

Peripheral neuropathy associated with nodular prurigo.

Nodular prurigo is characterized by nodules and papules that are intensely pruritic. Thalidomide is used to treat patients with recalcitrant disease. Because thalidomide may cause peripheral neuropathy, it is current practice to perform nerve conduction studies to exclude subclinical neuropathy before treatment. The clinical record of eight patients with nodular prurigo, in whom thalidomide treatment was proposed, were looked at. Five of them showed evidence of subclinical neuropathy, thereby contraindicating the use of thalidomide. None of the patients had any symptoms of a peripheral neuropathy and none was taking any medications with a recognized potential to cause peripheral neuropathy. We propose that nodular prurigo may be associated with an underlying peripheral neuropathy in a subset of patients. In patients with nodular prurigo and demonstrable peripheral neuropathy, there may be a role for treatment with agents such as amitryptiline and gabapentin, which are normally used for neuropathic pain.

Adult↗