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System Lesions (system + lesion)

Distribution by Scientific Domains
Medical Sciences88%

Kinds of System Lesions

  • central nervous system lesion
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  • nervous system lesion
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    Selected Abstracts

    Critical reappraisal of referrals to electromyography and nerve conduction studies,

    EUROPEAN JOURNAL OF NEUROLOGY, Issue 2 2005
    S. Podnar
    A large number of examinees referred to electromyographic (EMG) laboratories do not have symptoms or signs suggestive of a peripheral nervous system disorder, and the aim of the present study was to check this. All examinees evaluated by the author in a ,general' EMG laboratory in the first 4 months of 2002 were included. Data on examinees, referral physicians and diagnoses, clinical symptoms and signs, and electrodiagnostic findings were statistically evaluated. Three hundred examinees, 42% men, were included. A neurological diagnosis was provided in 55% of referrals. Electrodiagnostic abnormalities were found in 45% of examinees. Using multivariate statistics, a positive effect of neurological referral diagnosis, history of paraesthesias and of weakness and sensory loss on examination, and a negative effect of history of pain on pathological electrodiagnostic findings were found. Except 20 patients with carpal tunnel syndrome, no patient with normal clinical examination had abnormal electrodiagnostic findings. Our study confirmed the inappropriateness of referrals to electrodiagnostic examination to screen patients for peripheral nervous disorders. We propose electrodiagnostic examination mainly of patients with unequivocal clinical signs of a peripheral nervous system lesion and of patients with typical symptoms of the carpal tunnel syndrome. [source]

    Altered neuronal responses and regulation of neurotrophic proteins in the medial septum following fimbria-fornix transection in CNTF- and leukaemia inhibitory factor-deficient mice

    EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 8 2006
    Thomas Naumann
    Abstract Degeneration of axotomized GABAergic septohippocampal neurones has been shown to be enhanced in ciliary neurotrophic factor (CNTF)-deficient mice following fimbria-fornix transection (FFT), indicating a neuroprotective function of endogenous CNTF. Paradoxically, however, the cholinergic population of septohippocampal neurones was more resistant to axotomy in these mutants. As leukaemia inhibitory factor (LIF) has been identified as a potential neuroprotective factor for the cholinergic medial septum (MS) neurones, FFT-induced responses were compared in CNTF,/,, LIF,/, and CNTF/LIF double knockout mice. In CNTF,/, mice, FFT-induced cholinergic degeneration was confirmed to be attenuated as compared with wildtype mice. The expression of both LIF and LIF receptor , was increased in the MS providing a possible explanation for the enhanced neuronal resistance to FFT in these animals. However, ablation of the LIF gene also produced paradoxical effects; following FFT in LIF,/, mice no loss of GABAergic or cholinergic MS neurones was detectable during the first postlesional week, suggesting that other efficient neuroprotective mechanisms are activated in these animals. In fact, enhanced activation of astrocytes, a source of neurotrophic proteins, was indicated by increased up-regulation of glial fibrillary acidic protein and vimentin expression. In addition, mRNA levels for neurotrophin signalling components (e.g. nerve growth factor, p75NTR) were differentially regulated. The positive effect on axotomized cholinergic neurones seen in CNTF,/, and LIF,/, mice as well as the increased up-regulation of astrogliose markers was abolished in CNTF/LIF double knockout animals. Our results indicate that endogenous CNTF and LIF are involved in the regulation of neuronal survival following central nervous system lesion and are integrated into a network of neurotrophic signals that mutually influence their expression and function. [source]

    Painless legs moving toes in a patient with Wilson's disease

    MOVEMENT DISORDERS, Issue 4 2006
    Spiridon Papapetropoulos MD
    Abstract We describe and present a video of a 20-year-old woman with Wilson's disease (WD) who developed the painless variant of painful legs and moving toes (PLMT) syndrome. The symptoms appeared during a subsequent minor exacerbation of her extrapyramidal symptomatology, only to gradually disappear 3 to 4 months later. We suggest that, in our case, a structural central nervous system lesion caused by WD may have been associated with the development of PLMT. © 2006 Movement Disorder Society [source]

    Hereditary neuropathy with liability to pressure palsies associated with central nervous system myelin lesions

    EUROPEAN JOURNAL OF NEUROLOGY, Issue 6 2001
    J. Dac
    Hereditary neuropathy with liability to pressure palsies (HNPP) is an autosomal dominant disorder most commonly caused by a 1.5-Mb deletion in chromosome 17p11.2 which contains the peripheral myelin protein-22 (PMP22) gene. Mutations resulting in functional loss of one PMP22 gene copy are less frequent. We present a 51-year-old patient with a l.5-Mb deletion in chromosome 17p11.2 who exhibited signs of peripheral as well as central nervous system lesions. He gave a history of recurrent episodes of limb numbness and weakness with spontaneous but incomplete recovery since age 20. His father and two brothers had similar symptoms. Neurological examination revealed signs of multiple mononeuropathy associated with frontal lobe, corticospinal tract and cerebellar dysfunction, as well as signs of initial cognitive impairment. Electrophysiological investigations showed a demyelinating peripheral nerve disease with multiple conduction blocks and conduction disturbances in both optic nerves. Magnetic resonance imaging of the brain revealed multiple subcortical and periventricular foci of myelin lesions. The association of central and peripheral nervous system lesions in this patient indicates a possible role of PMP22 not only in peripheral but also in central nervous system myelin structure. [source]

    Postnatal glutamate-induced central nervous system lesions alter periodontal disease susceptibility in adult Wistar rats

    JOURNAL OF CLINICAL PERIODONTOLOGY, Issue 10 2001
    Torbjørn Breivik
    Abstract Background: Inability to mount a suitable brain-neuroendocrine response to bacterial or other antigenic challenges has been found to play an important rôle in infectious and inflammatory disease susceptibility and progression, including periodontal disease. Objective: The present study was designed to determine the effects of glutamate administration to new-born Wistar rats on the development and progression of naturally occurring and ligature-induced periodontal disease in the rats as adults. Postnatal glutamate administration is known to permanently damage neurones in the hypothalamic arcuate nucleus. Method: New-born rats were treated 1× daily subcutaniously with 2 mg/g of monosodium-L-glutamate (MSG) for 5 days from day 3 to 6. Control animals were injected with similar amounts of saline. Experimental ligature-induced periodontal disease was induced in the rats at the age of 12 weeks at maxillary right 2nd molar teeth. The contralateral maxillary left 2nd molars served as control teeth, and for assessment of naturally occurring periodontal disease. Disease progression was evaluated histometrically. Results: The results revealed that the glutamate-lesioned rats developed significantly more periodontal tissue destruction compared to sham-lesioned control rats in both the ligated and non-ligated teeth. Conclusions: This study supports our resent findings indicating that inappropriate brain-neuroendocrine-immune regulation may play a rôle in periodontal disease susceptibility and progression. Zusammenfassung Hintergrund: Es hatte gezeigt werden können, dass die Unfähigkeit des Gehirns auf einen bakteriellen oder antigenen Reiz mit einer angemessenen neuroendokrinen Antwort zu reagieren, eine wichtige Rolle für die Empfänglichkeit für infektiöse und entzündliche Erkrankungen einschliesslich Parodontitis spielt. Die Gabe von Glutamat nach der Geburt führt zu irreversiblen Schäden der Neurone des Nucleus arcuatus des Hypothalamus. Zielzetzung: Untersuchung der Auswirkungen von Glutamatgaben bei neugeborenen Wistar-Ratten auf die Entstehung und das Fortschreiten natürlich vorkommender und ligaturinduzierter Parodontitis im Erwachsenenalter. Material und Methoden: Bei 24 neugeborenen Wistar-Ratten wurden einmal täglich 2 mg/g L-Mononatriumglutamat und bei 20 Kontrolltieren statt dessen Kochsaltzlösung vom 4. Lebenstag an 4 Tage lang subkutan injiziert. Am rechten zweiten Oberkiefermolaren wurden bei den 12 Wochen alten Ratten eine experimentelle ligaturinduzierte Parodontitis ausgelöst. Der kontralaterale 2. Molar des Oberkiefers diente als Kontrolle und um natürlich vorkommende Parodontitis zu untersuchen. Das Fortschreiten der parodontalen Zerstörung wurde histometrisch erfasst. Ergebnisse: Die Ergebnisse zeigten, dass die Ratten mit den glutamatinduzierten Läsionen statistisch signifikant stärkere parodontale Zerstörungen sowohl an den Zähnen mit wie auch an denen ohne Ligaturen im Vergleich zur Kontrollgruppe aufwiesen. Schlussfolgerungen: Eine unangemessene neuroendokrinoimmunologische Regulation des Gehirns scheint eine Rolle bei der Empfänglichkeit für und das Fortschreiten von Parodontitis zu haben. Résumé Origine: L'incapacitéàétablir une réponse neuroendocrinienne cervicale efficace pour des défis bactériens ou antigèniques joue un rôle important dans la susceptibilité et la progression des maladies infectieuses et inflammatoires, dont les parodontites. But: Cette étude a été imaginée pour déterminer les effets de l'administration de glutamate à des rats Wistar nouveau-nés sur le développement et la progression de maladies parodontales naturelles et induites par des ligatures chez le rat adulte. On sait que l'administration de glutamate en postnatal endommage de façon permanente les neurones du noyau d'arc hypothalamique. Méthodes: Les rats nouveaus-nés furent traités une fois par jour par administration sous cutanée de 2 mg/g de monosodium-L-glutamate (MSG) pendant 5 jours. Les animaux contrôles recevaient une dose similaire de sérum physiologique. La parodontite expérimentale par ligature était réalisée à l'âge de 12 semaines, sur la deuxième molaire supérieure droite. La dent controlatérale servait de contrôle et à la mise en évidence de maladie parodontale naturelle. La progression de la maladie fut évaluée par histométrie. Résultats: Les résultats montrent que les rats atteints de lésions dues au glutamate développent plus de destructions parodontales (par ligatures ou sans ligatures) par rapport aux rats contrôles atteints de lésions simulées. Conclusion: Cette étude supporte nos récentes découvertes qui indiquent qu'une régulation immunitaire neuroendocrinienne cervicale inappropriée peut jouer un rôle dans la susceptibilité et la progression des maladies parodontales. [source]

    Biliary fascioliasis: Sonographic appearance patterns

    JOURNAL OF CLINICAL ULTRASOUND, Issue 1 2009
    Ahmet Yesildag
    Abstract Purpose. To describe the sonographic findings of biliary fascioliasis. Method. The study included 27 patients with fascioliasis and abdominal sonographic findings in biliary system. All diagnoses were confirmed via serologic enzyme-linked immunosorbent assay, and 5 patients underwent cholecystectomy. Sonographic findings in the biliary system were defined as primary and secondary. Results. Primary findings included spontaneously moving echogenic structures, linear echoes, curvilinear echoes, oval-shaped echogenic structure, matted echogenic particle, echogenic particle adherent to the gallbladder wall, motionless freely floating round echogenic foci, and leaf-like echogenic structures. Secondary findings were dilatation or wall thickening of the biliary system. In the liver, multiple confluent subcapsular nodules were also noted on sonography and CT in 14 of 27 patients. Conclusion. Sonography can detect biliary system lesions in fascioliasis and can aid diagnosis of the disease. However, the radiologist should be familiar with the different sonographic appearances of biliary fascioliasis. © 2008 Wiley Periodicals, Inc. J Clin Ultrasound, 2009 [source]

    Clinical entity of frontotemporal dementia with motor neuron disease

    NEUROPATHOLOGY, Issue 6 2009
    Yoshio Mitsuyama
    Non-Alzheimer-type dementias occur in association with a variety of pathological conditions that include a group of diseases characterized by atrophy of the frontal and temporal lobes. Frontotemporal dementia (FTD) is a clinical entity that comprises at least two distinct diseases: Pick's disease with Pick bodies and frontotemporal lobar degeneration with ubiquitin-positive inclusions (FTLD-U). The vast majority of FTLD-U is now referred to as FTLD-TDP, following the recent discovery of TAR DNA-binding protein of 43 kDa (TDP-43) as the major constituent of the ubiquitin-positive inclusions. FTLD-TDP, but not Pick's disease with Pick bodies, is often associated with motor neuron disease (MND). MND is a group of diseases in which the central nervous system lesions were long believed to be confined to the motor neuron system. In other words, MND was not considered to be associated with other neurological symptoms such as dementia. Nevertheless, more than 200 FTD cases associated with clinical MND have been reported in Japan since 1964. Neuropathologically, MND in such FTD cases was essentially similar to MND in cases without dementia. The combination of FTD and MND was so characteristic that we considered these cases comprise a unique clinicopathological subgroup of FTD. FTD with MND and the classical MND without dementia share the occurrence of ubiquitinated TDP-43-positive inclusions, a finding that could be a key to unlock the pathological backgrounds of both diseases. [source]

    Tissue culture methods to study neurological disorders: Establishment of immortalized Schwann cells from murine disease models

    NEUROPATHOLOGY, Issue 1 2003
    Kazuhiko Watabe
    Previously, the authors have established spontaneously immortalized cell lines from long-term cultures of normal adult mouse Schwann cells. Establishment of such Schwann cell lines derived from murine disease models may greatly facilitate studies of the cellular mechanisms of their peripheral nervous system lesions in the relevant diseases. Recently, the authors have established immortalized Schwann cell lines derived from Niemann,Pick disease type C mice (NPC; spm/spm) and globoid cell leukodystrophy mice (twitcher). In the present study, long-term cultures were maintained of Schwann cells derived from dorsal root ganglia and consecutive peripheral nerves of another NPC mouse (npcnih/npcnih, npcnih/+), myelin P0 protein-deficient mice (P0,/,, P0+/,) with their wild-type littermates (P0+/+), and neurofibromatosis type 1 gene (NF1)-deficient mice (Nf1Fcr/+) for 8,10 months, and immortalized cell lines from all these animals established spontaneously. These cell lines had spindle-shaped Schwann cell morphology and distinct Schwann cell phenotypes and retained genomic and biochemical abnormalities, sufficiently representing the in vivo pathological features of the mutant mice. These immortalized Schwann cell lines can be useful in studies of nervous system lesions in these mutant mice and relevant human disorders. [source]

    Laryngeal and diaphragmatic muscle activities after central nervous system lesions in cats

    ACTA PAEDIATRICA, Issue 11 2003
    AA Hutchison
    Aim: To examine the central control and coordination of respiratory pump muscles and laryngeal valve muscles by systematic decerebration (DECER), cerebellectomy (CBELL), pontine respiratory group lesioning (PRG) and pontomedullary section (PMED). Methods: Activities of posterior cricoarytenoid (PCA), thyroarytenoid (TA) and diaphragm (D) muscles and their responses to inspiratory (I) and expiratory (E) total occlusions were determined in 10 adult cats. Results: INTACT anesthetized cats (n= 6) exhibited inspiratory PCA (PCAI) and D activities. Expiratory PCA (PCAE) was present but TA activity was absent. It was found that successive DECER, CBELL and PRG lesions attenuated PCAE, the intact pattern being noted in 7/10, 4/10 and 0/6 cats, respectively. After PMED, variable PCA, TA and continuous D activities occurred only with blood gas abnormalities. Augmented PCA and D responses to I- and E-loads occurred after PRG lesions: the I-load PCAI and D responses resembled apneusis and the E-load PCAE and D responses resembled central apnea. Conclusion: The decreasing PCAE activity observed with successive DECER, CBELL and PRG lesions suggests that these areas influence laryngeal abductor control of glottic size. The synchronous activities after PMED transection suggest a role for more rostral structures in coordinating laryngeal and diaphragmatic muscle activities. [source]