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At least 865 records · Page 48Linked to original sources
PubMed1998

Demyelinating neuropathy in a patient with multiple sclerosis and genotypical HMSN-1.

Patients with multiple sclerosis (MS) may develop a peripheral neuropathy, sometimes attributed to nutritional deficiency. Other patients present with a demyelinating neuropathy which is presumed to be the result of an autoimmune process that affects both the central and peripheral nervous systems. We report a case of concurring MS and demyelinating neuropathy, without a positive family history, in whom genetic testing proved the neuropathy to be hereditary and not autoimmune. Hereditary neuropathy should be a consideration in sporadic cases of peripheral neuropathy and MS.

Adult↗
PubMed1999

Longstanding trigeminal sensory neuropathy of nontraumatic cause.

OBJECTIVE: Trigeminal sensory neuropathy is an uncommon but often significant orofacial symptom. There are few detailed descriptions of the problem in the dental literature. The aim of this study was to evaluate the clinical presentation and management of a cohort of patients presenting with anesthesia/paresthesia affecting one or more divisions of the trigeminal nerve unrelated to any identifiable traumatic cause. STUDY DESIGN: Nine patients with trigeminal neuropathy were examined. Each patient underwent a standard protocol of examination and hematologic, serologic, radiologic, and histopathologic investigations, as appropriate. RESULTS: Trigeminal neuropathy was found to be secondary to distant malignancy in 4 patients and to connective tissue disease in 2 patients. In each of 3 other patients, there was no obvious cause for the neuropathy. Patients with malignancy as the cause of their neuropathy tended to have involvement of more than one division of the trigeminal nerve and/or other neurologic features. CONCLUSIONS: Trigeminal sensory neuropathy may herald underlying distant malignancy or connective tissue disease. Anesthesia and paresthesia of the orofacial region are therefore serious clinical symptoms that must be carefully investigated before a diagnosis of idiopathic disease is made.

Adenocarcinoma↗
PubMed1999

Trigeminal sensory neuropathy: a study of 35 cases.

OBJECTIVE: Trigeminal sensory neuropathy includes a wide variety of conditions sharing a common symptom described as sensory disturbance of the face--usually numbness. STUDY DESIGN: This 10-year retrospective study included 35 patients referred for investigation of trigeminal sensory neuropathy. RESULTS: The most common causes of trigeminal sensory neuropathy were nonneoplastic cerebral disorders, mainly represented by multiple sclerosis and idiopathic trigeminal sensory neuropathy. Furthermore, when only mandibular trigeminal sensory neuropathy was considered, metastatic neoplasia was the most frequent cause, often afflicting men over the age of 60 years. CONCLUSIONS: This overview will orient clinicians in their diagnosis when they are faced with patients consulting for trigeminal sensory neuropathy.

Adolescent↗
PubMed2003

Peripheral neuropathies of infancy.

Over a 33-year period, 260 patients (< 17 years of age; 119 males, 141 females) from New South Wales, Australia who had peripheral neuropathies confirmed by nerve biopsy, were studied. Of these, 50 infants presented with symptoms or signs of neuropathy under 1 year of age: including 24 patients with demyelinating neuropathies and 21 axonal neuropathies; a further five patients had spinal muscular atrophy with associated secondary sensory axonopathy. Nineteen infants had hereditary motor sensory neuropathy, of whom 13 had myelin protein mutations confirmed by molecular genetic studies. Peripheral neuropathy is not an unusual diagnosis in infancy. Awareness of this association will aid early diagnosis and prognosis as well as facilitate interventional patient management.

Adolescent↗
PubMed2004

Risk modifiers for peripheral sensory neuropathy in HIV infection/AIDS.

The objective of this study is to examine the risk factors associated with the development of sensory neuropathy in human immunodeficiency virus (HIV)-infected patients in 292 HIV+ patients recruited through a community-based sentinel survey. We determined the clinical and treatment factors associated with the presence of peripheral sensory neuropathy in HIV+ subjects at baseline examination, and at 1-year follow-up. Baseline examination was assessed with a logistic regression analysis controlling for age, education level, history of drug/alcohol use, and anti-retroviral treatment. The risk of developing new peripheral neuropathy at follow-up was determined using a Cox proportional hazard model analysis. At study entry, neuropathy (n=64) was associated with acquired immunodeficiency syndrome (AIDS), nucleoside analogue reverse transcriptase inhibitors (NRTI) (i.e. ddC), and history of alcohol abuse. After 1-year follow-up, the development of neuropathy was predicted by AIDS, age (older subjects), and NRTI use. These findings indicated that AIDS, age, alcohol abuse/dependence, and anti-retroviral medication use are important predictors of motor/sensory peripheral neuropathy in the HIV infection. The peripheral neurotoxic effect of anti-retroviral medication should be taken into account in the design of long-term therapies.

Acquired Immunodeficiency Syndrome↗
PubMed2001

Diagnosis of motor neuropathy.

Motor neuropathy is a clinical entity which leads to consideration of a wide spectrum of peripheral nerve disorders. Firstly, it may be distinguished from other causes of peripheral motor involvement such as muscle diseases and disorders of the neuromuscular junction. Secondly, it may be discussed in two different forms: acute and chronic. Acute chronic neuropathies are mainly observed in Guillain-Barré syndrome, in which electrophysiological studies allow us to recognize the classical demyelinating form and the axonal form. The other causes of acute motor neuropathy are mainly poliomyelitis and porphyrias. Chronic motor neuropathies are mainly observed in motor neuron diseases, mainly amyotrophic lateral sclerosis, but also Kennedy's disease and other lower motor neuron diseases which may be inherited or acquired. The other causes are multifocal motor neuropathy and the predominantly motor forms of chronic inflammatory demyelinating polyneuropathy. The characterization of these different types of chronic neuropathy is of major importance because of the therapeutic consequences which may lead to the proposal of specific treatments.

Acute Disease↗
PubMed2001

Peripheral neuropathy and antiretroviral drugs.

Patients treated with nucleoside analogue reverse transcriptase inhibitors (NRTIs) develop a varying degree of myopathy or neuropathy after long-term therapy. Zidovudine (AZT) causes myopathy; zalcitabine (ddC), didanosine (ddl) and lamuvidine (3TC) cause neuropathy; stavudine (d4T) and fialuridine (FIAU) cause neuropathy or myopathy and lactic acidosis. The tissue distribution of phosphorylases responsible for phosphorylation of NRTIs relates to their selective tissue toxicity. The myopathy is characterized by muscle wasting, myalgia, fatigue, weakness and elevation of CK. The neuropathy is painful, sensory and axonal. In vitro, NRTIs inhibit the gamma-DNA polymerase, responsible for replication of mtDNA, and cause mtDNA dysfunction. In vivo, patients treated with AZT, the best studied NRTI, develop a mitochondrial myopathy with mtDNA depletion, deficiency of COX (complex IV), intracellular fat accumulation, high lactate production and marked phosphocreatine depletion, as determined with in vivo MRS spectroscopy, due to impaired oxidative phosphorylation. Animals or cultured cells treated with NRTIs develop neuropathy, myopathy, or cell destruction with similar changes in the mitochondria. There is evidence that the NRTI-related neuropathy is also due to mitochondrial toxicity. The NRTIs (AZT, ddC, ddl, d4T, 3TC) contain azido groups that compete with natural thymidine triphosphate as substrates of DNA pol-gamma and terminate mtDNA synthesis. In contrast, FIAU that contains 3'-OH groups serves as an alternate substrate for thymidine triphosphate with DNA pol-gamma and is incorporated into the DNA causing permanent mtDNA dysfunction. The NRTI-induced mitochondrial dysfunction has an influence on the clinical application of these agents, especially at high doses and when combined. They have produced in humans a new category of acquired mitochondrial toxins that cause clinical manifestations resembling the genetic mitochondrial disorders.

Acquired Immunodeficiency Syndrome↗
PubMed2003

[Diagnosis and therapy of vasculitic neuropathy. Consensus statement of the German Centers for Neuromuscular Disease].

Vasculitic neuropathies are immune mediated diseases of the peripheral nervous system, in which inflammation of the blood vessels causes damage to the nerves. We distinguish neuropathies associated with primary and secondary systemic vasculitis, with rheumatic diseases, with malignant disorders, drug-induced vasculitis and the non-systemic vasculitic neuropathies (NSVN). The typical clinical picture consists in an asymmetric or multifocal, painful sensorimotor neuropathy with an acute, subacute or chronic course and acute relapses. Neurophysiology reveals an active, asymmetric, axonal sensorimotor neuropathy. The disorders usually respond to immunosuppressive treatment. A diagnosis of definite vasculitis can be made with evidence of vasculitis in a biopsy specimen. The absence of positive morphological evidence, however, does not exclude the diagnosis. There is no single laboratory test that can prove or exclude vasculitis, in NSVN even an elaborate panel of blood tests can show normal findings. Systemic vasculitis has an incidence of 4/100,000 per year and, untreated, has a poor prognosis, which is greatly improved by the use of immunosuppressive treatment. The prognosis of NSVN is generally better, although many patients need long term immunosuppression. Current treatment recommendations for vasculitic neuropathies are presented.

Humans↗
PubMed1998

Neuropathies associated with connective tissue disease.

Neuropathies are a common neurologic manifestation of diffuse connective tissue disease. Vasculitic neuropathy requires prompt diagnosis and treatment to improve its outcome. It is commonly multifocal but may be confluent and symmetrical. Vasculitic neuropathy needs to be distinguished from the more common syndromes of compression neuropathy, which may also be multifocal, and nonvasculitic distal axonal polyneuropathy. Sensory neuronopathy is a distinctive syndrome unique to Sjögren's syndrome among the connective tissue diseases. Trigeminal sensory neuropathy may be the presenting feature of systemic sclerosis or may develop during the course of other connective tissue diseases. This article reviews the clinical and diagnostic features of neuropathies associated with the common diffuse connective tissue diseases.

Connective Tissue Diseases↗
PubMed1998

Neuropathies associated with malignancy.

Patients with malignancy can develop peripheral neuropathies as (1) a direct effect of the cancer by invasion or compression of nerves, (2) a remote or paraneoplastic effect, or (3) an iatrogenic effect of treatment. Focal or multifocal cranial neuropathies, radiculopathies, and plexopathies typically result from tumor infiltration, herpes zoster infection, or radiation-induced injury. Sensorimotor polyneuropathies are the most frequently encountered peripheral nerve syndromes, but motor neuropathies, sensory neuronopathies, polyradiculoneuropathies, and autonomic neuropathies can also occur. Although uncommon, paraneoplastic mechanisms should be considered in a patient with malignancy and an associated peripheral nerve disorder, especially in the setting of small-cell lung cancer or lymphoproliferative cancer. Toxic neuropathies occur with exposure to several chemotherapeutic agents, including the vinca alkaloids, cisplatin, taxanes, and suramin. These neuropathies are usually dose-related, sensory-predominant, and at least partially reversible, with an axonopathic or ganglionopathic mechanism. Suramin is unique in causing subacute, demyelinating polyradiculoneuropathy.

Antineoplastic Agents↗
PubMed2000

Central nervous system toxicity and early peripheral neuropathy following dermal exposure to methyl bromide.

CASE REPORT: We describe a case of early peripheral neuropathy and central nervous system toxicity as a result of acute predominantly dermal exposure to methyl bromide. A 32-year-old male was admitted after an accidental predominantly dermal exposure to methyl bromide while fumigating soil for pest control. The patient suffered dermal burns and vesicles on the upper and lower limbs. One week following exposure, he developed progressive weakness of the lower limbs, ataxia, paresthesiae of both legs and the left arm, hyperactive tendon reflexes in the lower limbs, and left Babinski sign. Nerve conduction velocity testing was compatible with axonal neuropathy. The patient recovered gradually from his burns. Three months postexposure he showed no signs of central nervous system toxicity, but the peripheral neuropathy was still present. DISCUSSION: Neurological effects primarily referable to the central nervous system following severe inhalation of methyl bromide have frequently been reported. The patient described in this study developed an unusual early peripheral neuropathy following dermal exposure. Peripheral neuropathy can be an outcome of methyl bromide intoxication, but is usually a late sequela of acute central nervous system toxicity or an aftereffect of repetitively inhaled chronic exposure. In this case, exposure to methyl bromide through abraded skin caused early peripheral neuropathy and central nervous system toxicity.

Administration, Cutaneous↗
PubMed1995

Postoperative brachial plexus neuropathy after total knee replacement under spinal anaesthesia.

We describe a case of idiopathic postoperative brachial plexus neuropathy. A 68-yr-old man underwent elective total knee replacement under spinal anaesthesia. Two days after surgery, there was sensory loss and weakness in the right forearm and hand, which suggested an ulnar nerve neuropathy. Two weeks later the patient complained of a dull ache between the scapulae, followed by a burning sensation in the forearm and severe pain in the elbow. A diagnosis of brachial plexus neuropathy was made based on clinical examination and nerve conduction studies. The pain disappeared after a few months, although weakness of the right arm persisted 9 months later. The differential diagnosis between brachial plexus neuropathy and ulnar nerve neuropathy is important, as the prognosis of brachial plexus neuropathy is generally good.

Aged↗
PubMed1975

Recurrent brachial plexus neuropathy.

The clinical, electrophysiological and pathological changes in 3 patients with recurrent attacks of non-traumatic brachial plexus neuropathy have been described. Two had recurrent attacks and a dominant family history of similar attacks, together with evidence of lesser degrees of nerve involvement outside the brachial plexus. In one patient the attacks were moderately painful, while in the other there was little or no pain. Only one showed undue slowing of motor nerve conduction during ischaemia, but in both cases the sural nerves had the changes of tomaculous neuropathy, with many sausage-shaped swellings of the myelin sheaths, and extensive segmental demyelination and remyelination. The third patient had two attacks of acute brachial plexus neuropathy which were both extremely painful. The clinical features were compatible with a diagnosis of neuralgic amuotrophy. In the second attack, there was vagus nerve involvement and the sural nerve showed evidence of healed extensive segmental demyelination. The various syndromes presenting with acute non-traumatic brachial plexus neuropathy are reviewed, and a tentative nonsological classification advanced. Most patients fall into the category of acute, painful paralysis with amyotrophy, with no family history and no evidence of lesions outside the brachial plexus. It is suggested that the term "neuralgic amyotrophy" be restricted to this group. Patients with features outside this clinical picture probably suffer from other disease entities presenting with brachial plexus neuropathy. The familial cases constitute one or more aetioliogical subgroups, differing from neuralgic amyotrophy in the frequency of recurrences, the relative freedom from pain in the attacks, the frequency of nerve lesions outside the brachial plexus, and of hypotelorism. Individual attacks of acute brachial plexus neuropathy, however, may be identical in patients with the different diseases, and further pathological and biochemical studies are awaited to aid in nosology.

Acute Disease↗
PubMed2002

Nerve granulomas and vasculitis in sarcoid peripheral neuropathy: a clinicopathological study of 11 patients.

Peripheral neuropathy is a rare, yet treatable manifestation of sarcoidosis, a multisystem disorder characterized by the presence of non-caseating granulomas that are seldom found in nerve biopsy specimens. In order to learn more about the subject, we reviewed our clinical and pathological findings in a series of 11 patients (six men and five women aged 26-83 years) with symptomatic neuropathy associated with characteristic granulomas in nerve biopsy specimens. Only two patients were known to have sarcoidosis before the occurrence of the neuropathy. The neuropathy was focal or multifocal in six patients, including one with a multifocal neuropathy associated with conduction blocks, and one with a multifocal axonal motor deficit. Four patients had a distal symmetrical deficit and one patient had a Guillain-Barré-like syndrome with facial diplegia and respiratory failure. Serum angiotensin-converting enzyme concentration was elevated in only two patients. Epineurial granulomas and perineuritis were present in all nerve specimens. The inflammatory infiltrates invaded the endoneurium, following connective tissue septae and blood vessels, in five patients. Multinucleated giant cells were found in eight patients and necrotizing vasculitis in seven. Inflammatory lesions were associated with variable, asymmetrical involvement of nerve fascicles and axon loss. A muscle specimen was sampled during the same procedure in 10 patients. It showed inflammatory infiltrates and granulomas in nine patients and necrotizing vasculitis in two. Immunolabelling showed a mixed inflammatory infiltrate of T cells (predominantly CD4+ cells) and macrophages, in keeping with a delayed hypersensitivity reaction. In addition to nerve involvement, all patients had at least one other tissue or organ affected, including muscle in nine patients, lungs and/or intrathoracic lymph nodes in eight, skin in three, arthritis in two, and peripheral lymph nodes, stomach and eye in one patient each. Most patients improved on corticosteroids. Two patients remain free of symptoms after 7 years. Severe side-effects of long-term treatment with corticosteroids occurred in two patients, leading to death in one. This study illustrates the wide range of clinical manifestations of sarcoid neuropathy and the frequent association of granulomatous inflammatory infiltrates with necrotizing vasculitis and with silent or symptomatic involvement of other organs.

Adult↗
PubMed2002

Peripheral neuropathies and anti-glycolipid antibodies.

This review charts the progress of anti-glycolipid antibodies in neuropathy, from their original discovery 20 years ago in immunoglobulin M paraproteinaemic neuropathy through to current discoveries mapping their relationship to subtypes of Guillain-Barré syndrome. Antibodies to >20 different glycolipids have now been associated with a wide range of clinically identifiable acute and chronic neuropathy syndromes. Particular progress has been achieved in understanding the link between acute motor axonal neuropathy and antibodies to GM1, GD1a, GM1b and GalNAc-GD1a, and between the cranial, bulbar and sensory variants of GBS and antibodies to the disialylated gangliosides GQ1b, GT1a, GD1b and GD3. In addition to clinical and serological studies, the origins and measurement of anti-glycolipid antibodies and their relationships to similar carbohydrate structures on infectious organisms, particularly Campylobacter jejuni, are discussed in the context of a molecular mimicry hypothesis. The structure and nomenclature of relevant glycolipids are outlined, along with information on their localization in nerve, and the influence this has on clinical phenotypes. Major advances have been made in animal modelling of anti-glycolipid antibody-associated diseases, both in vitro and in vivo. This has advanced our understanding of the role of anti-GQ1b antibodies in Miller Fisher syndrome with particular respect to the motor nerve terminal as a potential site of injury, and led to the creation of rabbit models of anti-GD1b and anti-GM1 antibody-mediated sensory and motor neuropathy, respectively. With such information in place, it will now be possible to determine the precise mechanisms by which antibodies injure the different compartments of peripheral nerve and establish how a range of immunomodulating therapies, including current treatments, exert their therapeutic effects. Despite these very significant advances, considerable gaps in our knowledge persist, and it is likely that other pathogenic pathways operate in inflammatory neuropathy that are unrelated to glycolipid antibodies, although these are outside the scope of this review.

Animals↗
PubMed2003

Cochlear implantation in patients with auditory neuropathy of varied etiologies.

OBJECTIVES/HYPOTHESIS: Auditory neuropathy is a relatively recently described pattern of hearing loss characterized by preservation of outer hair cell function despite absent brainstem auditory evoked responses. Intact outer hair cell function is demonstrated by the presence of otoacoustic emissions and/or a measurable cochlear microphonic on electrocochleography, whereas no synchronous neural activity (absent action potentials) is seen on acoustically evoked brainstem auditory evoked response testing. The study reviews the authors' experience with six patients diagnosed with auditory neuropathy, four of whom have undergone cochlear implantation. MATERIALS AND METHODS: A retrospective review of all medical and audiological charts at the University of Virginia Hospitals (Charlottesville, VA) was performed to identify patients who have undergone cochlear implantation or have been diagnosed with auditory neuropathy, or both. RESULTS: Six patients with hearing loss attributable to auditory neuropathy were identified, four of whom have undergone cochlear implantation. Causes varied, including congenital, infectious, and idiopathic origins. Adults demonstrated subjective auditory perception on promontory stimulation, whereas no repeatable brainstem auditory evoked response waveforms could be demonstrated on pediatric promontory stimulation testing. Patients with implants demonstrated implant-evoked brainstem auditory evoked responses and improved audiological performance. CONCLUSIONS: The six cases presented in the study represent varied causes and, probably, varied sites of lesions of auditory neuropathy. Promontory stimulation has been valuable, particularly in adults. Cochlear implantation allows the opportunity to provide a supraphysiological electrical stimulation to the auditory nerve, with the hope of reintroducing synchronous neural activity. Greater confidence and enthusiasm for cochlear implantation in appropriately selected patients with auditory neuropathy are gained through experience with such diverse cases.

Adult↗
PubMed2003

Vincristine-induced neuropathy as the initial presentation of charcot-marie-tooth disease in acute lymphoblastic leukemia: a Pediatric Oncology Group study.

PURPOSE: After profound peripheral neurotoxicity during induction chemotherapy for acute lymphoblastic leukemia (ALL) in the index patient with Charcot-Marie-Tooth hereditary neuropathy (CMT), study coordinators of the Pediatric Oncology Group (POG) front-line ALL protocols reviewed patient registrations to identify any other patients with possible CMT. The goal was to provide preliminary information about patients with undiagnosed CMT who develop ALL. PATIENTS AND METHODS: Five children with ALL who were enrolled in POG B-precursor or T-cell ALL protocols from 1994 to 1999 subsequently were determined to have CMT hereditary neuropathy. Their clinical presentations and treatment records were reviewed in detail. Records of all patients entered on POG 9201 (lesser-risk ALL) were reviewed to identify all cases of significant vincristine toxicity noted in the first 6 months of treatment. RESULTS: The five identified patients all had substantial peripheral neurotoxicity that required alteration in treatment and/or orthopedic/physical therapy evaluation and follow-up. The POG 9201 review identified 25 of 686 patients (3.6%) with significant peripheral neuropathy. Three of 25 were diagnosed with CMT; the others have had no testing reported. CONCLUSIONS: A family history of CMT or other peripheral neuropathy should be sought at the time of diagnosis of ALL. Testing for CMT should be considered in any child with substantial vincristine-induced peripheral neurotoxicity. Treatment of such patients must be individualized. Testing of all patients with significant peripheral neuropathy would be necessary to determine the percentage of such neuropathy explained by underlying CMT.

Adolescent↗
PubMedDate not supplied

Diagnosis and treatment of multiple sclerosis and amyotrophic lateral sclerosis: neuropathies from Bordetella pertussis.

Having found positive the research for anti-Bordetella antibodies in the 95.47% of 92 patients affected by defined multiple sclerosis and in the 100% of 55 patients affected by non-patched neuropathies (amyotrophic lateral sclerosis and correlated neuropathies), I reassessed the pathogenesis of the neuropathies from Bordetella pertussis. In the two categories of neuropathies (with and without patches), the beginning pathogenetic mechanisms are the same: 1) pertussis re-infection in patients with mucociliary barrier defect; 2) pertussis toxins passage in the blood; and 3) formation of circulating immune complexes. In multiple sclerosis, astrocytes produce class II human leukocyte antigens, the endothelia of the small brain vessels show the "adhesion molecules," and the immune complexes fall in the central nervous system (patches are formed). In amyotrophic lateral sclerosis and in the other non-patched neuropathies, the astrocytes do not produce the class II human leukocyte antigens, the endothelia do not show adhesion molecules, and immune complexes do not fall in the central nervous system; but they increase in blood until they inhibit the ulterior antibodies production. For relative antibodies lack, pertussis toxins fix directly on neuro-epithelia; their pathogenic power and physiopathologic astrocytes role in the central nervous system produce the damage. With a blood sample, we can assess Bordetella etiology. In all these neuropathies, an extended antibiotic therapy to clear mucosae and to prevent reinfections is necessary.

Adult↗