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Biomedical subjects

K Viala

Publications and source records attributed to K Viala.

9 recordsLinked to original sources
PubMed2006

[Neurological complications of lymphomas].

Peripheral neurological complications of lymphomas are rare, but all types of neuropathy can be observed in the context of lymphoma. This great clinical heterogeneity can be related to the variety of pathological processes that can affect the peripheral nerve or be linked to the different subtypes of lymphoma. In addition to the common causes of peripheral nerve involvement, such as iatrogenic toxicity, there are mechanisms that are more specifically related to lymphomas, such as nerve tumor infiltration, or dysimmune perturbations induced by the hemopathy. These dysimmune processes can result in various neuropathies, such as inflammatory demyelinating polyradiculoneuropathy, or neuropathies secondary to the secretion of a monoclonal immunoglobulin. Identifying the mechanism of the neuropathy is necessary in order to determine the therapeutic options and to improve the prognosis.

Antibodies, Monoclonal↗
PubMed2005

[Idiopathic lumbosacral plexopathy].

INTRODUCTION: Lumbosacral plexopathy is the equivalent in the lower limbs of neuralgic amyotrophy (also known as Parsonage-Turner syndrome) in the upper limbs. It is well-known in patients with diabetes mellitus, when it is known as Bruns-Garland syndrome. CASE: We report the case of a 47-year-old woman who developed a unilateral neuropathy of the leg, neither radicular nor truncal in origin. The slow continuous improvement was not affected by any of the treatments administered. DISCUSSION: Lumbosacral plexopathy is characterized by intense pain in one or both legs, associated with motor and sensory deficits. Recovery is usually slow (6 to 36 months) and often incomplete. The electrodiagnostic examination shows important acute motor and sensory axonal loss, characterized by denervation and low-amplitude sensory action potential. Treatment generally combines analgesics with narcotic agents, neuropathic pain medication, short-term corticosteroids, and rehabilitation. In the most severe cases, long-term corticosteroids and other immunosuppressive agents may be required. This diagnosis cannot be reached until all other radicular, plexal and truncal origins have been ruled out.

Female↗
PubMed2005

[Chronic inflammatory demyelinating polyradiculoneuropathy: diagnostic strategy. Guidelines of the French CIDP study group].

Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) comprises a group of dysimmune neuropathies easily diagnosed in more than half of the patients. Diagnosis is based on clinical, electrophysiological and biological clues. In some patients, diagnosis is unclear because of the debated value of the available clues. In such circumstances, dysimmune neuropathies may not be diagnosed, leading to insufficient treatment. This is an important category of patients because immunomodulatory drugs have proven efficacy. The CIDP spectrum includes a relatively wide range of diseases. Besides the easily recognized classic forms, there are many clinical variants, sometimes with a paucisymptomatic presentation leading to uncertain diagnosis. The French CIDP study group has established guidelines for diagnostic strategy in CIDP patients. The first part of this paper is devoted to the clinical aspects of the disease, classical forms and variants. In the second part, the results of electrophysiological studies are reported. In a third chapter, complementary examinations useful for diagnosis are discussed. The fourth chapter deals with the diagnostic strategy, discussed in relation to the different situations which may be encountered in clinical practice. details the technical modalities of appropriate electrophysiological studies and presents normal results together with those indicating demyelinating neuropathy. Nerve biopsy technique and results are given in appendix II.

Humans↗
PubMed2004

Follow-up study and response to treatment in 23 patients with Lewis-Sumner syndrome.

Lewis-Sumner syndrome (LSS) is a dysimmune peripheral nerve disorder, characterized by a predominantly distal, asymmetric weakness mostly affecting the upper limbs with sensory impairment, and by the presence of multifocal persistent conduction blocks. The nosological position of this neuropathy in relation to multifocal motor neuropathy (MMN) and chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is still debated. We report the clinical, biological and electrophysiological features, the course and the response to treatment in 23 LSS patients. The initial symptoms started in the distal part of an upper limb in 70% of patients. They were sensorimotor in 65% and purely sensory in 35% of patients. A cranial nerve involvement was observed in 26% of patients and a distal limb amyotrophy in 52%. The CSF protein level was normal in 67% of patients and mildly elevated in the remainder. None had serum anti-GM1 antibodies. There were multiple motor conduction blocks (average of 2.87/patient), predominantly located in the forearm, whereas demyelinating features outside the blocked nerves were rare. Abnormal distal sensory potentials were found in 87% of patients. The electrophysiological pattern suggests a very focal motor fibre demyelination sparing the nerve endings, whereas sensory fibre involvement was widespread. The course was chronic progressive in 71% of patients and relapsing-remitting in the others. During the follow-up study (median duration of 4 years), half of the patients progressed with a multifocal pattern and the distribution of the motor deficit remained similar to the initial presentation. The other patients showed a progression to the other limbs, suggesting a more diffuse process. Fifty-four percent of the patients treated with intravenous immunoglobulin showed an improvement, compared with 33% of the patients treated with oral steroids. Overall, 73% of patients had a positive response to immune-mediated therapy. LSS may be distinguished from MMN by the presence of sensory involvement, the absence of serum anti-GM1 antibodies and, in some cases, a positive response to steroids. In some of the patients in our study, LSS evolved into a more diffuse neuropathy sharing similarities with CIDP. Others had a clinical course characterized by a striking multifocal neuropathy, which suggests underlying mechanisms different from CIDP. Overall, whatever the clinical course, LSS responded to immune-mediated treatment in a manner similar to CIDP.

Action Potentials↗
PubMed2004

[Recent acquisitions in the treatment of chronic immune-mediated polyneuropathies].

Chronic immune-mediated polyneuropathies encompass chronic inflammatory demyelinating polyneuropathies, polyneuropathies associated with monoclonal gammopathy and multifocal motor neuropathy with persistent conduction blocks. Their diagnosis is made on clinical, electrophysiological and sometimes immunochemical and pathological criteria. The efficacy of intravenous immunoglobulins has been reported in the short-term treatment of these neuropathies in the same way than corticosteroids and plasma exchanges, depending on the type of the polyneuropathy. The efficacy of long-term treatments needs further evaluation.

Autoimmune Diseases of the Nervous System↗
PubMed2001

[Study with localized proton magnetic resonance spectroscopy of 31 multiple sclerosis lesions: correlations with clinical and MRI features].

We have analyzed with localized proton magnetic resonance spectroscopy (MRS) 31 lesions in 28 patients with multiple sclerosis (MS). The course of the disease was either relapsing remitting, secondary progressive, or primary progressive. Four patients had an isolated neurological syndrome suggestive of MS. The decrease in the NAA/Cre ratio and the raise of the Cho/Cre ratio were more pronounced in patients with an acute isolated neurological syndrome, suggesting the predominance of an inflammatory process, and the presence of an axonal dysfunction in the initial course of the lesion. The NAA/Cre ratio was negatively correlated with clinical disability and thus could be used as an index of disease activity. Patients with a secondary progressive course exhibited a significant increase in the Myo/Cre ratio compared to those with a relapsing remitting course. Thus, there may be an association between the evolution towards a progressive disease and axonal loss or the development of gliosis. The isointense lesions to the cerebrospinal fluid on MRI T1 weighted sequences were characterized by a sharp raise in the Cho/Cre ratio suggesting demyelination and/or intense inflammation. Gadolinium enhanced lesions were not characterized by a specific neurochemical profile.

Adolescent↗
PubMed2000

[Magnetic resonance spectroscopy in multiple sclerosis].

Magnetic resonance spectroscopy allows in vivo neurochemical exploration of multiple sclerosis (MS) lesions and normal appearing white matter on MRI. It gives insights into pathophysiology: inflammation (increase of choline), recent demyelination (increase in lipids and choline), axonal dysfunction (decrease of NAA), gliosis (increase of myoinositol). The spectroscopic profile of lesions is not specific to MS. Therefore MRI remains the first investigation to perform when MS is suspected. However, spectroscopy is a sensitive, reproducible, non invasive tool which may provide an index of activity. In the future, spectroscopy may contribute in homogenizing patient selection for clinical trials and might be used, in association with MRI, to evaluate therapeutic efficiency. Spectroscopy might also influence therapeutic choices by identifying the prevailing lesional mechanism: inflammation, demyelination, axonal destruction, or gliosis.

Brain↗
PubMed1998

[Hemicerebral atrophy and epilepsy in an adult].

We report the case of a 49 year-old man who presented a partial status epilepticus with left-sided clonic seizures after the occurrence of a left cerebral hematoma. The patient had left-side hemiplegia that progressively recovered in 3 months. Neuroimaging studies revealed a moderate cerebral atrophy on the right side and crossed cerebellar atrophy. Six years later, he had a partial status epilepticus with left hamiconvulsions leading to permanent left hemiplegia. The right cerebral and the left cerebellar atrophy observed one year later were significantly increased. Cerebral hemiatrophy associated with epilepsy in adulthood is exceptional. Our case suggests that the occurrence of partial status epilepticus, even during adulthood, may aggravate cerebral hemiatrophy formally silent.

Atrophy↗