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Clinical Neuroscience

MAY 25, 2014

[Temperature sensitivity of some nerve conduction parameters in diabetic polyneuropathy]

HIDASI Eszter, DIÓSZEGHY Péter, KÁPLÁR Miklós, MECHLER Ferenc, BERECZKI Dániel

[Background - We tested whether in diabetic polyneuropathy the temperature dependence of the median nerve conduction parameters reflects the severity of neuropathy. Methods - We validated an electrophysiological score against clinical signs of polyneuropathy. Electroneurography was performed at temperatures from 20-40 °C in diabetic patients with mild, moderate and severe neuropathy and controls. Results - The electrophysiological score reflected the clinical severity of polyneuropathy. At room temperature there were significant differences among groups in almost all parameters. In thermal sensitivity studies were significant differences in distal and proximal motor and sensory areas and in sensory conduction velocities. These four parameters normalized to 1 °C change in temperature also significantly differed among the four groups and were largest in controls and smallest in severe polyneuropathy. Conclusions - The use of an integral parameter - areas are essentially amplitudes integrated over time - increases the probability of detecting decreased thermal sensitivity of peripheral nerves in diabetes.]

Journal of Nursing Theory and Practice

OCTOBER 30, 2013

[Causes of leg problems in chronic kidney failure, and opportunities for prevention]

KRIMMER-S. Tünde

[In patients with chronic kidney failure, especially diabetic haemodialysis patients, the risk of lower-limb complications increases. Through the early recognition of changes in the leg, the definition of risk factors and timely intervention, the prevalence of ulcers and amputations can be reduced. The author aims, through a review of the specialist literature, to provide skills for the recognition of lower-limb complications occurring in chronic kidney patients, and to summarise the most common factors leading to amputation, and the opportunities for prevention. It gives guidance for the definition of risk factors, briefly describes the procedure for assessing the condition of the leg, and the basic principles and options relating to patient education. ]

Clinical Neuroscience

MAY 30, 2013

[Benign-onset acute disseminated encephalomyelitis: A report on two cases]

DEGIRMENCI Eylem, ERDOGAN Cagdas, OGUZHANOGLU Attila, BIR Sinan Levent

[The signs and symptoms of acute disseminated encephalomyelitis are heterogeneous and dependent on the location and severity of the inflammatory process. The meningoencephalitic presentation may include meningism, impaired consciousness (occasionally leading to coma), seizures and confusion, or behavioral disturbances. Multifocal neurological features include a combination of optic neuritis, visual field defects, cranial neuropathy, sensorimotor impairment, ataxia, aphasia, and involuntary movements. One definition of acute disseminated encephalomyelitis is “an initial clinical event with a presumed inflammatory and demyelinating cause, with acute or sub-acute onset affecting multifocal areas of the central nervous system”. Patients with acute disseminated encephalomyelitis frequently suffer from seizures, disturbances of consciousness, fever, and headaches, and occasionally there are focal signs and symptoms. Here, we report on two cases who presented with different symptoms, but the clinical findings that the patients showed were benign.]

LAM Extra for General Practicioners

JUNE 20, 2012

[THE DIABETIC FOOT SYNDROME: PATHOMECHANISM, CLINICAL PICTURE, CURRENT TREATMENT AND PREVENTION]

JERMENDY György

[Diabetic foot syndrome is a characteristic late complication of diabetes mellitus. It can develop in patients with type 1 as well as type 2 diabetes mellitus, especially in case of a long duration of diabetes and sustained poor metabolic state. Diabetic neuropathy plays a pivotal role in the pathomechanism, but vascular symptoms might also contribute to the complex clinical picture. For making the diagnosis, evaluation of complaints, performing physical examination and using simple tests for identifying both distal, somatosensory neuropathy and potential angiopathy are of great importance. Therapeutic approaches aim to achieve proper glycaemic control, as well as to ameliorate symptoms of neuropathy, improve peripheral blood supply by medicines, angioplasty or intervention radiological methods, fight against infections and off-load the foot. Surgical intervention might also be necessary, and in severe cases, amputation might be needed. The diabetic foot syndrome increases mortality risk in patients with diabetes. Complaints related to diabetic foot syndrome are often resistant to treatment and tend to recur. Thus, prevention with long-term, good metabolic control and protection of the foot are of particular importance.]

Lege Artis Medicinae

APRIL 20, 2012

[The diabetic foot syndrome: pathomechanism, clinical picture, current treatment and prevention]

JERMENDY György

[Diabetic foot syndrome is a characteristic late complication of diabetes mellitus. It can develop in patients with type 1 as well as type 2 diabetes mellitus, especially in case of a long duration of diabetes and sustained poor metabolic state. Diabetic neuropathy plays a pivotal role in the pathomechanism, but vascular symptoms might also contribute to the complex clinical picture. For making the diagnosis, evaluation of complaints, performing physical examination and using simple tests for identifying both distal, somatosensory neuropathy and potential angiopathy are of great importance. Therapeutic approaches aim to achieve proper glycaemic control, as well as to ameliorate symptoms of neuropathy, improve peripheral blood supply by medicines, angioplasty or intervention radiological methods, fight against infections and off-load the foot. Surgical intervention might also be necessary, and in severe cases, amputation might be needed. The diabetic foot syndrome increases mortality risk in patients with diabetes. Complaints related to diabetic foot syndrome are often resistant to treatment and tend to recur. Thus, prevention with long-term, good metabolic control and protection of the foot are of particular importance.]

Clinical Neuroscience

JANUARY 30, 2011

[ULCERATIVE CARPAL TUNNEL SYNDROME]

KAMONDI Anita, TEIXEIRA Jose Maria, SZIRMAI Imre

[The carpal tunnel syndrome is the most frequent compression- induced neuropathy. A severe but rare clinical manifestation of this disorder associates with ulceration, acral osteolysis and mutilation of the terminal phalanges of the second and third fingers. Recognition of this disorder is difficult, because various dermatological and internal diseases might lead to acral ulcerative lesions, and these patients are seldom referred to neurological and/or electrodiagnostic examination. In this article, we present three cases of this rare clinical form of carpal tunnel syndrome and discuss the electrodiagnostic findings. The early diagnosis is important since decompression of the median nerve in due time might prevent mutilation and could significantly improve the patients’ quality of life.]

Clinical Neuroscience

SEPTEMBER 30, 2008

[Paraneoplastic chronic demyelinating neuropathy and lambert-eaton myasthenic syndrome associated with multiple anti-neural antibodies and small-cell lung cancer]

RÓZSA Csilla, VINCENT Angela, ARÁNYI Zsuzsanna, KOVÁCS G. Gábor, KOMOLY Sámuel, ILLÉS Zsolt

[Lambert-Eaton myasthenic syndrome (LEMS) developed in a patient with presumed chronic inflammatory demyelinating polyneuropathy (CIDP) and negative chest CT. Since antibodies against both Hu and voltage-gated calcium channel (VGCC) were detected, repeated chest CT was performed, which eventually showed a pulmonary mass lesion. Biopsy revealed small cell lung cancer (SCLC) indicating the importance of repeated chest CT in LEMS even when an existing autoimmune-like disease and negative CT may suggest an autoimmune origin. This is the first report of paraneoplastic CIDP and LEMS associated with anti-Hu, anti-VGCC and SCLC.]

Clinical Neuroscience

NOVEMBER 30, 2009

[Guillain–Barré syndrome in childhood]

KOLLÁR Katalin, LIPTAI Zoltán, ROSDY Beáta, MÓSER Judit

[Background - Guillain-Barré syndrome (GBS) is clinically well known since 1916. It can occur at any age. Its main characteristic is acute rapidly ascending flaccid paresis. It is a neuro-immunologic disorder with heterogeneous background. In Hungary we could not find reports about big paediatric population with GBS. Patient and method - We analysed retrospectively the data of 38 children diagnosed and treated with GBS at the Neurological Department of Paul Heim Children’s Hospital or at the Paediatric Department of St. László Hospital from January 2000 till April 2008. We analysed the clinical characteristics, seriousness of clinical signs, laboratory results, and electrophysiological features of them as well documented the preceding illness. We observed the effectiveness of our treatment; we measured the speed and time of the healing process and documented the residual clinical signs. Results - 35 children could be classified as having acute inflammatory demyelinating polyneuropathy (AIDP), 2 as having acute motor axonal neuropathy (AMAN) and 1 as Miller-Fisher syndrome. By those patients who at the very beginning did not show the characteristic clinical signs, electrophysiology helped in establishing the diagnosis. By one child spinal MRI with gadolinium supported our diagnosis. Those children, who lost their ambulation, got immunotherapy: intravenous immunoglobulin (IVIG) or plasmapheresis (PEX). Both method seemed to be effective. None of our patients died. All were cured. By five patients residual clinical symptoms could be found. Conclusion - The disease process, the relative incidence of each subtype of GBS is nearly similar to that in Western Europe and North America according to the literature. By the currently used immune therapy most of the pediatric patients recover fully within a short time.]

Clinical Neuroscience

DECEMBER 20, 2008

[Screening of hereditary neuromuscular disorders in the roma population living in Hungary]

HERCZEGFALVI Ágnes, PIKÓ Henriett, KARCAGI Veronika

[Recent medical genetic research has identified a number of novel, or previously known, but rare conditions, caused by private founder mutations. The Finnish and Ashkenazi Jew populations provide the best examples for identifying genes in unique genetic disorders. In these populations, research efforts and high-level medical services resulted in intense improvements of medical care and in organization of population- based screening programs. Hereditary disorders of the Roma populations are known for a long time. The genetic background of these diseases has been established by extensive molecular genetic studies. The Romas represent 6% of the Hungarian population and live under extremely bad health conditions. Therefore, our aim was to map the incidence of the hereditary neuromuscular disorders among the Hungarian Roma population. Moreover, we intended to provide proper information, genetic counseling and possible prevention strategies for the families at risk, which should represent a primer task in public health. Because of our experience in neuromuscular disorders, we choose six, frequent, autosomal recessive disorders for these clinical and genetic studies: hereditary motor and sensory neuropathy type Lom (HMSNL), hereditary motor and sensory neuropathy type Russe (HMSNR), congenital cataracts facial dysmorphism syndrome (CCFDN), Limb- Girdle muscular dystrophy 2C (LGMD2C), congenital myasthenic syndrome (CMS) and spinal muscular atrophy (SMA). Following identification of the founder mutations, the possibility of prenatal diagnosis and carrier screening for family members will contribute to the decrease of the recurrence risk for these severe, mostly untreatable disorders.]

Clinical Neuroscience

MAY 10, 2005

[Pathophysiology of restless leg syndrome and periodic leg movement disorder in view of the latest research findings]

KÖVES Péter, SZAKÁCS ZOLTÁN

[Both restless leg syndrome and periodic leg movement disorder have been classified as primary sleep disorders by the International Classification of Sleep Disorders. Considering the characteristic clinical symptoms, it is supposed that their pathomechanism involves the peripheral and central stimulusprocessing mechanisms of the nervous system as well as several elements of the motor system. During the last couple of years many new elements of the pathomechanism have been discovered, in particular the dysfunction of the postsynaptic dopamin receptors related to the iron metabolism of the central nervous system, the role of opiate receptors, and the involvement of subclinical small fiber neuropathy. Many of these findings have been incorporated into the diagnostic and treatment protocols used in the management of patients with restless leg syndrome or periodic leg movement disorder. Considering the rapidly increasing number of publications on their pathomechanism and the various fields it involves, the authors found it necessary to evaluate these data and to interpret their relationships within the frame of sleep-wake regulation.]