Log in

Relevant bibliographies by topics / Upper motor neuron syndrome / Journal articles

To see the other types of publications on this topic, follow the link: Upper motor neuron syndrome.

Journal articles on the topic 'Upper motor neuron syndrome'

Author: Grafiati

Published: 4 June 2021

Last updated: 24 April 2022

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the top 50 journal articles for your research on the topic 'Upper motor neuron syndrome.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.

1

Hagiwara, Koichi, Hiroyuki Murai, Hirofumi Ochi, Manabu Osoegawa, Hiroshi Shigeto, Yasumasa Ohyagi, and Jun-ichi Kira. "Upper Motor Neuron Syndrome Associated with Subclinical Sjögren's Syndrome." Internal Medicine 47, no. 11 (2008): 1047–51. http://dx.doi.org/10.2169/internalmedicine.47.0846.

Full text

APA, Harvard, Vancouver, ISO, and other styles

2

H Mayer, Nathaniel. "Upper Limb After Effects of an Upper Motor Neuron Syndrome." Journal of Physical Medicine, Rehabilitation and Disabilities 4, no. 1 (August 22, 2018): 1–8. http://dx.doi.org/10.24966/pmrd-8670/100027.

Full text

APA, Harvard, Vancouver, ISO, and other styles

3

Ambrose, Anne Felicia, Tanya Verghese, Carolin Dohle, and Jennifer Russo. "Muscle Overactivity in the Upper Motor Neuron Syndrome." Physical Medicine and Rehabilitation Clinics of North America 29, no. 3 (August 2018): 483–500. http://dx.doi.org/10.1016/j.pmr.2018.03.004.

Full text

APA, Harvard, Vancouver, ISO, and other styles

4

Miczak, Kimberly, and Joseph Padova. "Muscle Overactivity in the Upper Motor Neuron Syndrome." Physical Medicine and Rehabilitation Clinics of North America 29, no. 3 (August 2018): 529–36. http://dx.doi.org/10.1016/j.pmr.2018.03.006.

Full text

APA, Harvard, Vancouver, ISO, and other styles

5

Segal, Miriam. "Muscle Overactivity in the Upper Motor Neuron Syndrome." Physical Medicine and Rehabilitation Clinics of North America 29, no. 3 (August 2018): 427–36. http://dx.doi.org/10.1016/j.pmr.2018.04.005.

Full text

APA, Harvard, Vancouver, ISO, and other styles

6

Fullam, Timothy, and Jeffrey Statland. "Upper Motor Neuron Disorders: Primary Lateral Sclerosis, Upper Motor Neuron Dominant Amyotrophic Lateral Sclerosis, and Hereditary Spastic Paraplegia." Brain Sciences 11, no. 5 (May 11, 2021): 611. http://dx.doi.org/10.3390/brainsci11050611.

Full text

Abstract:

Following the exclusion of potentially reversible causes, the differential for those patients presenting with a predominant upper motor neuron syndrome includes primary lateral sclerosis (PLS), hereditary spastic paraplegia (HSP), or upper motor neuron dominant ALS (UMNdALS). Differentiation of these disorders in the early phases of disease remains challenging. While no single clinical or diagnostic tests is specific, there are several developing biomarkers and neuroimaging technologies which may help distinguish PLS from HSP and UMNdALS. Recent consensus diagnostic criteria and use of evolving technologies will allow more precise delineation of PLS from other upper motor neuron disorders and aid in the targeting of potentially disease-modifying therapeutics.

APA, Harvard, Vancouver, ISO, and other styles

7

Shahani, Bhagwan T., Margaret M. Wierzbicka, and Stephen W. Parker. "Abnormal single motor unit behavior in the upper motor neuron syndrome." Muscle & Nerve 14, no. 1 (January 1991): 64–69. http://dx.doi.org/10.1002/mus.880140111.

Full text

APA, Harvard, Vancouver, ISO, and other styles

8

Corcia, Philippe, Peter Bede, Pierre-François Pradat, Philippe Couratier, Steve Vucic, and Mamede de Carvalho. "Split-hand and split-limb phenomena in amyotrophic lateral sclerosis: pathophysiology, electrophysiology and clinical manifestations." Journal of Neurology, Neurosurgery & Psychiatry 92, no. 10 (July 20, 2021): 1126–30. http://dx.doi.org/10.1136/jnnp-2021-326266.

Full text

Abstract:

Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disorder affecting the upper and lower motor neurons. A key clinical feature of ALS is the absence of accurate, early-stage diagnostic indicators. ‘Split-hand syndrome’ was first described in ALS at the end of the last century and a considerable body of literature suggests that the split-hand phenomenon may be an important clinical feature of ALS. Considering the published investigations, it is conceivable that the ‘split-hand syndrome’ results from the associated upper and lower motor neuron degeneration, whose interaction remains to be fully clarified. Additionally, other split syndromes have been described in ALS involving upper or lower limbs, with a nuanced description of clinical and neurophysiological manifestations that may further aid ALS diagnosis. In this review, we endeavour to systematically present the spectrum of the ‘split syndromes’ in ALS from a clinical and neurophysiology perspective and discuss their diagnostic and pathogenic utility.

APA, Harvard, Vancouver, ISO, and other styles

9

Riggs, Jack E., Sydney S. Schochet, and Jeffery P. Hogg. "Delayed Diffuse Upper Motor Neuron Syndrome after Compressive Thoracic Myelopathy." Military Medicine 164, no. 9 (September 1, 1999): 666–68. http://dx.doi.org/10.1093/milmed/164.9.666.

Full text

APA, Harvard, Vancouver, ISO, and other styles

10

Swash, Michael, David Burke, Martin R. Turner, Julian Grosskreutz, P. Nigel Leigh, Mamede deCarvalho, and Matthew C. Kiernan. "Occasional essay: Upper motor neuron syndrome in amyotrophic lateral sclerosis." Journal of Neurology, Neurosurgery & Psychiatry 91, no. 3 (February 13, 2020): 227–34. http://dx.doi.org/10.1136/jnnp-2019-321938.

Full text

APA, Harvard, Vancouver, ISO, and other styles

11

Andrews, J. A., Sabrina Paganoni, Corey Braastad, Merit Cudkowicz, and Nazem Atassi. "Disease Burden in Upper Motor Neuron Syndromes." Journal of Clinical Neuromuscular Disease 16, no. 2 (December 2014): 104–5. http://dx.doi.org/10.1097/cnd.0000000000000051.

Full text

APA, Harvard, Vancouver, ISO, and other styles

12

Rhee, Peter Charles. "Surgical Management of Upper Extremity Deformities in Patients With Upper Motor Neuron Syndrome." Journal of Hand Surgery 44, no. 3 (March 2019): 223–35. http://dx.doi.org/10.1016/j.jhsa.2018.07.019.

Full text

APA, Harvard, Vancouver, ISO, and other styles

13

Turner, Martin R., Richard J. Barohn, Philippe Corcia, John K. Fink, Matthew B. Harms, Matthew C. Kiernan, John Ravits, et al. "Primary lateral sclerosis: consensus diagnostic criteria." Journal of Neurology, Neurosurgery & Psychiatry 91, no. 4 (February 6, 2020): 373–77. http://dx.doi.org/10.1136/jnnp-2019-322541.

Full text

Abstract:

Primary lateral sclerosis (PLS) is a neurodegenerative disorder of the adult motor system. Characterised by a slowly progressive upper motor neuron syndrome, the diagnosis is clinical, after exclusion of structural, neurodegenerative and metabolic mimics. Differentiation of PLS from upper motor neuron-predominant forms of amyotrophic lateral sclerosis remains a significant challenge in the early symptomatic phase of both disorders, with ongoing debate as to whether they form a clinical and histopathological continuum. Current diagnostic criteria for PLS may be a barrier to therapeutic development, requiring long delays between symptom onset and formal diagnosis. While new technologies sensitive to both upper and lower motor neuron involvement may ultimately resolve controversies in the diagnosis of PLS, we present updated consensus diagnostic criteria with the aim of reducing diagnostic delay, optimising therapeutic trial design and catalysing the development of disease-modifying therapy.

APA, Harvard, Vancouver, ISO, and other styles

14

Campanini, Isabella, Andrea Merlo, and Dario Farina. "Motor unit discharge pattern and conduction velocity in patients with upper motor neuron syndrome." Journal of Electromyography and Kinesiology 19, no. 1 (February 2009): 22–29. http://dx.doi.org/10.1016/j.jelekin.2007.06.018.

Full text

APA, Harvard, Vancouver, ISO, and other styles

15

Yang, Huijia, Xiaozhong Jing, Jinhua Yan, and Dihui Ma. "Sjögren’s syndrome with rapidly progressive motor neuron disease: a case report." Journal of International Medical Research 48, no. 11 (November 2020): 030006052097446. http://dx.doi.org/10.1177/0300060520974465.

Full text

Abstract:

Sjögren’s syndrome is an autoimmune disease that can affect multiple systems. Sjögren’s syndrome with motor neuron disease is rarely reported. Herein, we describe a patient with rapidly progressive motor neuron disease secondary to Sjögren’s syndrome. A 42-year-old woman was admitted to our hospital with a 2-month history of progressive limb weakness. Neurological assessment revealed fasciculation in the lower limbs and amyotrophy in the bilateral supraspinatus, interosseous, and thenar muscles. Serological examination and labial gland biopsy revealed Sjögren’s syndrome. In addition, electromyography demonstrated neurogenic damage to the upper and lower limbs. The patient received a short course of high-dose corticosteroids, intravenous immunoglobulins, and immunosuppressant treatment, including a weekly dose of 0.4 g cyclophosphamide and a daily dose of 0.2 g hydroxychloroquine. However, the patient’s limb weakness was further aggravated and her respiratory function was compromised. Electromyography re-examination demonstrated extensive neurogenic damage, and she was diagnosed with Sjögren’s syndrome with motor neuron disease. The patient died of respiratory failure after 2 months. We suggest that more effective maintenance treatments should be sought. Further investigation is required to elucidate the association between autoimmune motor neuron disease and Sjögren’s syndrome.

APA, Harvard, Vancouver, ISO, and other styles

16

Esquenazi, Alberto. "Upper motor neurone syndrome and spasticity." Lancet Neurology 8, no. 6 (June 2009): 517. http://dx.doi.org/10.1016/s1474-4422(09)70124-3.

Full text

APA, Harvard, Vancouver, ISO, and other styles

17

Jellinger, K. A. "Upper Motor Neuron Syndrome and Spasticity: Clinical Management and Neurophysiology, 2nd edn." European Journal of Neurology 16, no. 4 (April 2009): e93-e93. http://dx.doi.org/10.1111/j.1468-1331.2008.02483.x.

Full text

APA, Harvard, Vancouver, ISO, and other styles

18

Jain, Pallav, and Vijay Sardana. "Wallenberg syndrome with ipsilateral upper motor neuron facial palsy: A rare manifestation." APIK Journal of Internal Medicine 10, no. 1 (2022): 48. http://dx.doi.org/10.4103/ajim.ajim_57_20.

Full text

APA, Harvard, Vancouver, ISO, and other styles

19

Primdahl, Ditte, Brad Beinlich, and Megan Albertson. "NCMP-21. REVERSIBLE MOTOR NEURON SYNDROME IN THE SETTING OF CANCER." Neuro-Oncology 22, Supplement_2 (November 2020): ii127. http://dx.doi.org/10.1093/neuonc/noaa215.532.

Full text

Abstract:

Abstract 60 year old female was admitted with difficulty swallowing, slurred speech and gait instability resulting in multiple falls worsening over 2-3 weeks. Her exam revealed subtle spastic dysarthric speech, spasticity in all four extremities (lower > upper and right > left), hyperreflexia, and bilateral Babinksi and Hoffman signs consistent with pure upper motor neuron syndrome. An MRI brain and total spine were without evidence of neurological pathology but revealed an incidental finding of lymphadenopathy concerning for neoplastic process. Her symptoms continued to worsen over the next few weeks and she developed severe, nearly continuous, extensor spasms of BLE (right > left) with stimulus sensitivity causing inability to walk. She was started on baclofen, tizanidine and diazepam for spasticity with only mild improvement. An MRI cervical spine was repeated (please see below) and revealed hyperintense T2 signal in lateral corticospinal tract (right > left) without enhancement and no cord compression. Given strong clinical concern for paraneoplastic process patient received 0.4 g/kg IVIG for 5 days and concurrent 1000 mg methylprednisolone for 3 days with dramatic improvement within days. Cervical lymph node biopsy lead to diagnosis of nodal marginal zone lymphoma. A CT abdomen revealed an ovarian mass concerning for teratoma vs dermoid cyst (pending resection and final pathology). She was treated with weekly boosters of IVIG and IV methylprednisolone and was started on Rituximab for her Lymphoma. When seen in clinic a month post discharge nearly all of her symptoms had resolved. Neurological exam showed subtle residual spasticity making this presentation most consistent with a reversible pure upper motor neuron syndrome.

APA, Harvard, Vancouver, ISO, and other styles

20

Simonini, Cecilia, Elisabetta Zucchi, Roberta Bedin, Ilaria Martinelli, Giulia Gianferrari, Nicola Fini, Gianni Sorarù, Rocco Liguori, Veria Vacchiano, and Jessica Mandrioli. "CSF Heavy Neurofilament May Discriminate and Predict Motor Neuron Diseases with Upper Motor Neuron Involvement." Biomedicines 9, no. 11 (November 5, 2021): 1623. http://dx.doi.org/10.3390/biomedicines9111623.

Full text

Abstract:

Objective: To assess whether phosphorylated neurofilament heavy chain (pNfH) can discriminate different upper motor neuron (UMN) syndromes, namely, ALS, UMN-predominant ALS, primary lateral sclerosis (PLS) and hereditary spastic paraparesis (hSP) and to test the prognostic value of pNfH in UMN diseases. Methods: CSF and serum pNfH were measured in 143 patients presenting with signs of UMN and later diagnosed with classic/bulbar ALS, UMNp-ALS, hSP, and PLS. Between-group comparisons were drawn by ANOVA and receiver operating characteristic (ROC) analysis was performed. The prognostic value of pNfH was tested by the Cox regression model. Results: ALS and UMNp-ALS patients had higher CSF pNfH compared to PLS and hSP (p < 0.001). ROC analysis showed that CSF pNfH could differentiate ALS, UMNp-ALS included, from PLS and hSP (AUC = 0.75 and 0.95, respectively), while serum did not perform as well. In multivariable survival analysis among the totality of UMN patients and classic/bulbar ALS, CSF pNfH independently predicted survival. Among UMNp-ALS patients, only the progression rate (HR4.71, p = 0.01) and presence of multifocal fasciculations (HR 15.69, p = 0.02) were independent prognostic factors. Conclusions: CSF pNfH is significantly higher in classic and UMNp-ALS compared to UMN diseases with a better prognosis such as PLS and hSP. Its prognostic role is confirmed in classic and bulbar ALS, but not among UMNp, where clinical signs remained the only independent prognostic factors.

APA, Harvard, Vancouver, ISO, and other styles

21

De Gobbi Porto, Fábio Henrique, Marco Orsini, Marco Antônio Araújo Leite, José Moreira dos Santos, Soraia Pulier, Mariana Mello, and Osvaldo J. M. Nascimento. "Mills’ syndrome: a case report." Neurology International 1, no. 1 (November 3, 2009): 15. http://dx.doi.org/10.4081/ni.2009.e15.

Full text

Abstract:

The syndrome of progressive, ascending or descending hemiplegia, with no significant sensory impairment was first describes by Mills in 1900, which several cases were reported later. However after diagnostic tests and image improvements, the number of reports has shortened. A possible explanation for this shortage is the identification of other diseases that could mimic the clinical picture. Currently, the syndrome has an uncertain nosological status, since it was described based on clinical examination only. We can find this clinical presentation (Mills syndrome) in cases of amyotrophic lateral sclerosis (ALS), predominant upper motor neuron amyotrophic lateral sclerosis (UMN-ALS) and primary lateral sclerosis (PLS), besides its symptomatic (secondary) forms. We describe a case (initial presentation and one year follow-up) of progressive ascending hemiplegia with clinical isolated upper neuron signs and normal sensory examination, discussing its nosological status, electromyographic findings, differential diagnosis and prognosis.

APA, Harvard, Vancouver, ISO, and other styles

22

Caimmi, M., A. Chiavenna, C. Giovanzana, M. Malosio, F. Molteni, and L. Molinari Tosatti. "A robotic device for ankle motor evaluation and rehabilitation in patients with upper motor neuron syndrome." Gait & Posture 42 (December 2015): S49—S50. http://dx.doi.org/10.1016/j.gaitpost.2015.03.089.

Full text

APA, Harvard, Vancouver, ISO, and other styles

23

Pinto, Wladimir B. V. R., Igor Braga Farias, Bruno de Mattos Lombardi Badia, Luiz Henrique Libardi Silva, Mario Teruo Yanagiura, Marco Antônio Troccoli Chieia, Paulo Victor Sgobbi de Souza, and Acary Souza Bulle Oliveira. "Finger extension weakness and downbeat nystagmus motor neurone disease (FEWDON-MND)." Practical Neurology 19, no. 5 (April 24, 2019): 424–26. http://dx.doi.org/10.1136/practneurol-2018-002188.

Full text

Abstract:

Atypical motor neurone disease (MND) represents a challenging and expanding group of neurodegenerative disorders involving the upper or lower motor neurones, and rarely both. Neuro-ophthalmological disturbances such as gaze-evoked downbeat nystagmus are extremely rare in the context of typical and atypical MND. Finger extension weakness and downbeat nystagmus motor neurone disease (FEWDON-MND) syndrome has been recently recognised as a distinct syndromic phenotype of MND, with a characteristic clinical picture. We describe a 63-year-old woman with long-standing lower motor neurone involvement of the upper limbs, who on examination had gaze-evoked downbeat nystagmus. After extensive negative investigation for secondary causes of MND and downbeat nystagmus, we diagnosed FEWDON-MND syndrome.

APA, Harvard, Vancouver, ISO, and other styles

24

Greiffenstein, Manfred F., W. John Baker, and Thomas Gola. "Motor dysfunction profiles in traumatic brain injury and postconcussion syndrome." Journal of the International Neuropsychological Society 2, no. 6 (November 1996): 477–85. http://dx.doi.org/10.1017/s1355617700001648.

Full text

Abstract:

AbstractMotor measures are sensitive to central lesions, but they are also affected by peripheral injury and motivation. The motor skills profiles of proven brain injury clients were compared with the profiles of healthy postconcussion patients. The chief result was a double dissociation: The traumatic brain injury (TBI) group produced a motor dysfunction gradient consistent with upper motor neuron disease, while the compensation-seeking postconcussion group produced a nonphysiologic pattern. Objective measures of behavioral pain and emotional distress did not correlate with the findings. Motor skill deficiencies in postconcussion syndrome (PCS) are probably functional in nature. (JINS, 1996, 2, 477–485.)

APA, Harvard, Vancouver, ISO, and other styles

25

Messina, M. F., M. Autunno, K. Koehler, M. Russo, T. Arrigo, G. Crisafulli, A. Huebner, and F. De Luca. "Upper and lower motor neuron involvement as presenting manifestation of Triple A syndrome." Journal of Endocrinological Investigation 32, no. 5 (May 2009): 482–83. http://dx.doi.org/10.1007/bf03346490.

Full text

APA, Harvard, Vancouver, ISO, and other styles

26

Farníková, Kateřina, Petr Kaňovský, Igor Nestrašil, and Pavel Otruba. "Coexistence of parkinsonism, dementia and upper motor neuron syndrome in four Czech patients." Journal of the Neurological Sciences 296, no. 1-2 (September 2010): 47–54. http://dx.doi.org/10.1016/j.jns.2010.06.011.

Full text

APA, Harvard, Vancouver, ISO, and other styles

27

Esquenazi, Alberto, Nathaniel H. Mayer, Antonio E. Elia, and Alberto Albanese. "Botulinum toxin for the management of adult patients with upper motor neuron syndrome." Toxicon 54, no. 5 (October 2009): 634–38. http://dx.doi.org/10.1016/j.toxicon.2009.01.022.

Full text

APA, Harvard, Vancouver, ISO, and other styles

28

Koelman, J. H., L. J. Bour, A. A. Hilgevoord, G. J. van Bruggen, and B. W. Ongerboer de Visser. "Soleus H-reflex tests and clinical signs of the upper motor neuron syndrome." Journal of Neurology, Neurosurgery & Psychiatry 56, no. 7 (July 1, 1993): 776–81. http://dx.doi.org/10.1136/jnnp.56.7.776.

Full text

APA, Harvard, Vancouver, ISO, and other styles

29

Pohl, Marcus. "Messmethoden zur Objektivierung der Plussymptome des Upper-Motor-Neuron-Syndroms." neuroreha 2, no. 03 (September 2010): 111–17. http://dx.doi.org/10.1055/s-0030-1265122.

Full text

APA, Harvard, Vancouver, ISO, and other styles

30

Brugman, Frans, John H. J. Wokke, Hans Scheffer, Martina H. A. Versteeg, Erik A. Sistermans, and Leonard H. van den Berg. "Spastin mutations in sporadic adult-onset upper motor neuron syndromes." Annals of Neurology 58, no. 6 (2005): 865–69. http://dx.doi.org/10.1002/ana.20652.

Full text

APA, Harvard, Vancouver, ISO, and other styles

31

Brugman, F., H. Scheffer, J. H. J. Wokke, W. M. Nillesen, M. de Visser, E. Aronica, J. H. Veldink, and L. H. van den Berg. "Paraplegin mutations in sporadic adult-onset upper motor neuron syndromes." Neurology 71, no. 19 (September 17, 2008): 1500–1505. http://dx.doi.org/10.1212/01.wnl.0000319700.11606.21.

Full text

APA, Harvard, Vancouver, ISO, and other styles

32

Ricci, Claudia, Fabio Giannini, Giulia Riolo, Silvia Bocci, Stefania Casali, and Stefania Battistini. "A Novel Variant in Superoxide Dismutase 1 Gene (p.V119M) in Als Patients with Pure Lower Motor Neuron Presentation." Genes 12, no. 10 (September 29, 2021): 1544. http://dx.doi.org/10.3390/genes12101544.

Full text

Abstract:

Amyotrophic lateral sclerosis (ALS) is a progressive and fatal disorder characterized by degeneration of motor neurons in the cerebral cortex, brain stem, and spinal cord. Most cases of ALS appear sporadically, but 5–10% of patients have a family history of disease. Mutations in the superoxide dismutase 1 gene (SOD1) have been found in 12–23% of familial cases and in 1–2% of sporadic cases. Currently, more than 180 different SOD1 gene variants have been identified in ALS patients. Here, we describe two apparently sporadic ALS patients carrying the same SOD1 c.355G>A variant, leading to the p.V119M substitution, not previously described. Both the patients showed pure lower motor neuron phenotype. The former presented with the flail leg syndrome, a rare ALS variant, characterized by progressive distal onset weakness and atrophy of lower limbs, slow progression and better survival than typical ALS. The latter exhibited rapidly progressive weakness of upper and lower limbs, neither upper motor neuron nor bulbar involvement, and shorter survival than typical ALS. We provide an accurate description of the phenotype, and a bioinformatics analysis of the p.V119M variant on protein structure. This study may increase the knowledge about genotype-phenotype correlations in ALS and improve the approach to ALS patients.

APA, Harvard, Vancouver, ISO, and other styles

33

Sengupta, Poly, Rama Biswas, Hasan Shahrear Ahmed, and Kaniz Fatema. "Guillain Barrè Syndrome following Hepatitis E." Bangladesh Critical Care Journal 2, no. 1 (August 11, 2014): 48–49. http://dx.doi.org/10.3329/bccj.v2i1.19973.

Full text

Abstract:

Guillain- Barrè Syndrome is characterized by acute progressive symmetric limb weakness and areflexia. A 32 year old female presented with progressive ascending areflexic muscular weakness and bilateral lower motor neuron type of facial palsy. She had anorexia, nausea and upper abdominal pain for 2 weeks. The findings of motor nerve conduction study are consistent with acute inflammatory demyelinating polyradiculoneuropathy. She had elevated liver enzyme and positive immunoglobulin M antibody against hepatitis E in blood. Based on clinical features, laboratory findings and electrophysiological study, she was diagnosed as Guillain- Barrè Syndrome following hepatitis E. She was treated with intravenous immunoglobulin and recovered fully. DOI: http://dx.doi.org/10.3329/bccj.v2i1.19973 Bangladesh Crit Care J March 2014; 2 (1): 48-49

APA, Harvard, Vancouver, ISO, and other styles

34

Fagioli, S., A. Berardelli, M. Hallett, N. Accornero, and M. Manfredi. "The first agonist and antagonist burst in patients with an upper motor neuron syndrome." Movement Disorders 3, no. 2 (1988): 126–32. http://dx.doi.org/10.1002/mds.870030204.

Full text

APA, Harvard, Vancouver, ISO, and other styles

35

Chen, Chia-Ling, May-Kuen Wong, Hsieh-Ching Chen, Pao-Tsai Cheng, and Fuk-Tan Tang. "Correlation of polyelectromyographic patterns and clinical upper motor neuron syndrome in hemiplegic stroke patients." Archives of Physical Medicine and Rehabilitation 81, no. 7 (July 2000): 869–75. http://dx.doi.org/10.1053/apmr.2000.6284.

Full text

APA, Harvard, Vancouver, ISO, and other styles

36

Kok, Chin Yong, Hoskote Chandrashekar, Christopher Turner, Hadi Manji, and Alexander M. Rossor. "Can compressive thoracic cord lesions cause a pure lower motor neurone syndrome?" Practical Neurology 19, no. 1 (October 3, 2018): 72–74. http://dx.doi.org/10.1136/practneurol-2018-002016.

Full text

Abstract:

Compressive lesions of the spinal cord usually cause a syndrome of upper motor neurone weakness, spasticity and sensory loss below the level of the lesion. It has long been recognised that compressive cervical cord lesions may present as isolated lower motor neurone weakness of the upper limbs, a syndrome termed cervical spondylotic amyotrophy. We describe two patients presenting with isolated lower motor neurone weakness of the lower limbs in association with a compressive cord lesion at T11/12, a condition we have termed thoracic spondylotic amyotrophy.

APA, Harvard, Vancouver, ISO, and other styles

37

Segal, Miriam. "Muscle Over-Activity in Upper Motor Neuron Syndrome: Assessment and Problem Solving for Complex Cases." Physical Medicine and Rehabilitation Clinics of North America 29, no. 3 (August 2018): i. http://dx.doi.org/10.1016/s1047-9651(18)30781-2.

Full text

APA, Harvard, Vancouver, ISO, and other styles

38

Segal, Miriam. "Muscle Over-Activity in Upper Motor Neuron Syndrome: Assessment and Problem Solving for Complex Cases." Physical Medicine and Rehabilitation Clinics of North America 29, no. 3 (August 2018): xvii—xviii. http://dx.doi.org/10.1016/j.pmr.2018.05.001.

Full text

APA, Harvard, Vancouver, ISO, and other styles

39

Barlow, Steven M., and James H. Abbs. "Fine force and position control of select orofacial structures in the upper motor neuron syndrome." Experimental Neurology 94, no. 3 (December 1986): 699–713. http://dx.doi.org/10.1016/0014-4886(86)90248-7.

Full text

APA, Harvard, Vancouver, ISO, and other styles

40

Hansel, Anna, Johannes Dorst, Angela Rosenbohm, Annemarie Hübers, and Albert Ludolph. "ALS Mimics." Neurology International Open 02, no. 01 (January 2018): E60—E71. http://dx.doi.org/10.1055/s-0043-119960.

Full text

Abstract:

AbstractAmyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease. Most patients die within 2–5 years of symptom onset due to the lack of effective therapy options. A diagnostic delay is encountered quite often, since disease progression as well as site and speed of onset may vary significantly. Some diseases can mimic features of ALS, especially in early stages. It is very important to differentiate those mimics from ALS as potentially treatable conditions might be missed otherwise. ALS typically affects the upper as well as the lower motor neuron, which implies that diseases sharing at least one of these clinical features have to be considered in the differential diagnosis. The following conditions should be taken into account as a differential diagnosis for ALS with predominant affection of the lower motor neuron: Immune mediated neuropathies such as multifocal motor neuropathy (MMN) with pronounced distal paresis without striking atrophy signs and conduction blocks in electroneurography, and chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) with common signs of sensibility disturbances, areflexia and cytoalbuminologic dissociation in the cerebrospinal fluid (CSF). Sporadic inclusion body myositis (sIBM) with typical biopsy findings and clinically predominant affection of the finger flexors. Spinal and bulbar muscular atrophy (SBMA), in which androgen receptor (AR-)gene testing and clinical signs of androgen insensitivity will help to differentiate the disease from ALS. Hirayama disease shows cold paresis; a cervical MRI scan and a normal neurography will help to confirm the diagnosis. In benign fasciculation syndrome, there is no muscle paresis or atrophy, and acute denervation cannot be detected in the EMG. In spinal muscular atrophy (SMA), testing for the SMN gene will help to differentiate the condition from ALS; furthermore, SMA is a very rare disease in adults. As a differential diagnosis for ALS with both clinical affection of the upper and lower motor neuron e. g. metabolic diseases such as adrenoleukodystrophy, metachromatic leukodystrophy and Tay-Sachs disease should be taken into account. Here, laboratory tests are the most important steps for a correct diagnosis. Cervical myelopathy is also capable of affecting the upper and lower motor neuron, but can easily be differentiated by a cervical MRI scan. As a differential diagnosis of ALS with predominant affection of the upper motor neuron, we discuss hereditary spastic paraparesis (HSP) which presents with a symmetric spasticity of the legs. The MRI often shows atrophy of the spinal cord, and SPG gene testing is done to differentiate HSP from ALS.

APA, Harvard, Vancouver, ISO, and other styles

41

Sämann, P. G., H. Himmerich, T. Merl, C. Erös, M. B. Müller, J. C. Tonn, and B. Buchwald. "Cervicothoracic Intradural Arachnoid Cyst Misdiagnosed as Motor Neuron Disease." Case Reports in Medicine 2010 (2010): 1–4. http://dx.doi.org/10.1155/2010/261657.

Full text

Abstract:

Recognizing syndromes which mimic ALS is crucial both to avoid giving this diagnosis erroneously and since there may be appropriate treatments. We report a 63-year-old woman diagnosed with possible ALS five years ago based on upper and lower motor neuron signs with typical electrophysiology and normal cranial MRI. At reassessment, spinal MRI revealed a cervicothoracic cyst with cord compression that was successfully treated neurosurgically. Histopathology confirmed an arachnoid origin as suspected from MRI. Spinal cysts may mimic ALS and need to be thoroughly excluded by appropriate imaging.

APA, Harvard, Vancouver, ISO, and other styles

42

Zucchi, Elisabetta, Roberta Bedin, Antonio Fasano, Nicola Fini, Annalisa Gessani, Marco Vinceti, and Jessica Mandrioli. "Cerebrospinal Fluid Neurofilaments May Discriminate Upper Motor Neuron Syndromes: A Pilot Study." Neurodegenerative Diseases 18, no. 5-6 (2018): 255–61. http://dx.doi.org/10.1159/000493986.

Full text

Abstract:

Background: Patients presenting with upper motor neuron (UMN) signs may widely diverge in prognosis, ranging from amyotrophic lateral sclerosis (ALS) to primary lateral sclerosis (PLS) and hereditary spastic paraplegia (hSP). Neurofilaments are emerging as potential diagnostic and prognostic biomarkers for ALS, but the diagnosis of UMN syndromes still relies mostly on clinical long-term observation and on familiarity or genetic confirmation. Objectives: To test whether phosphorylated neurofilament heavy chain (pNfH) may discriminate different UMN syndromes at diagnosis and to test their prognostic role among these diseases. Methods: We measured the cerebrospinal fluid (CSF) and serum pNfH of 30 patients presenting with UMN signs and diagnosed with ALS, hSP, and PLS, plus 9 healthy controls (HC). Results: ALS patients had higher levels of pNfH in CSF and serum compared to HC (p < 0.001 and p < 0.001 in CSF and serum, respectively) and PLS (p = 0.015 and p = 0.038) and hSP (p = 0.003 and p = 0.001) patients. PLS and hSP patients had similar CSF and serum pNfH concentrations, but a higher CSF pNfH concentration, compared to HC (p = 0.002 and p = 0.003 for PLS and hSP, respectively). Receiver operating characteristic curves for discriminating ALS from PLS and hSP showed an area under the curve of 0.79 for CSF and 0.81 for serum. In multivariable survival analysis including relevant clinical factors CSF pNfH represented the strongest variable predicting survival (HR 40.43; 95% CI 3.49–467.79, p = 0.003) independently of clinical group. Conclusions: Despite some statistical instability of the results due to limitations in sample size, our study supports the role of CSF pNfH as a prognostic biomarker for motor neuron diseases presenting with UMN signs. A potential power to discriminate between ALS and other UMN syndromes at presentation, and between all of the examined MND and HC, has been detected for both CSF and serum pNfH.

APA, Harvard, Vancouver, ISO, and other styles

43

Xie, Nina, Guang Yang, Weiru Zhang, Hongwei Xu, and Qiying Sun. "Clinical Reasoning: A 50-Year-Old Man With Progressive Limb Weakness and Slurred Speech." Neurology 98, no. 14 (February 10, 2022): 592–96. http://dx.doi.org/10.1212/wnl.0000000000200008.

Full text

Abstract:

A 50-year-old man presented with a 9-month history of progressive left arm weakness and dysarthria. Family history showed that his parents are cousins, and one of his siblings died of motor neuron disease. Brain MRI showed T2-weighted white matter hyperintensities along the course of pyramidal tracts. Neurologic examination and EMG revealed upper and lower motor neuron signs involving the bulbar, cervical, thoracic, and lumbosacral segments, which meets the criteria of a definite amyotrophic lateral sclerosis (ALS), according to the revised EI Escorial criteria. Whole-exome genetic sequencing found 2 novel LYST missense variations, confirming the diagnosis of Chediak-Higashi syndrome (CHS), a rare autosomal recessive hematologic disorder. Our case indicates that CHS can present as ALS phenotype, and the LYST might be a novel causative gene for ALS.

APA, Harvard, Vancouver, ISO, and other styles

44

Brugman, Frans, Hans Scheffer, H. Jurgen Schelhaas, Willy M. Nillesen, John H. J. Wokke, Bart P. C. van de Warrenburg, and Leonard H. van den Berg. "Seipin/BSCL2 mutation screening in sporadic adult-onset upper motor neuron syndromes." Journal of Neurology 256, no. 5 (March 1, 2009): 824–26. http://dx.doi.org/10.1007/s00415-009-5009-6.

Full text

APA, Harvard, Vancouver, ISO, and other styles

45

Bot, S. T., J. H. Veldink, S. Vermeer, A. R. Mensenkamp, F. Brugman, H. Scheffer, L. H. den Berg, H. P. H. Kremer, E. J. Kamsteeg, and B. P. Warrenburg. "ATL1 and REEP1 mutations in hereditary and sporadic upper motor neuron syndromes." Journal of Neurology 260, no. 3 (October 30, 2012): 869–75. http://dx.doi.org/10.1007/s00415-012-6723-z.

Full text

APA, Harvard, Vancouver, ISO, and other styles

46

MAYUSUMI, Taisuke, Akira HARADA, and Shigeru USUDA. "Gait-related Changes in Ankle Plantar Flexor Muscle Tone during Movement in Upper Motor Neuron Syndrome." Rigakuryoho Kagaku 35, no. 6 (2020): 819–24. http://dx.doi.org/10.1589/rika.35.819.

Full text

APA, Harvard, Vancouver, ISO, and other styles

47

Goldberg, Gary, and Nathaniel H. Mayer. "The goal of treatment for motor impairment is not to “normalize” but to “functionalize” through facilitative modulation and enabling context." Behavioral and Brain Sciences 19, no. 1 (March 1996): 75–76. http://dx.doi.org/10.1017/s0140525x00041558.

Full text

Abstract:

AbstractAdaptations occurring in the central nervous system (CNS) in the presence of pathology are not uniformly “good” for the organism when viewed in a functional context. A functional reordering of CNS priorities can be produced by allowing restructuring of the external context or through modification of neuromuscular physiology or anatomy designed to reduce the inherent restriction of functional movement in upper motor neuron syndrome. In fact, volitional control can often be “unmasked” through such interventions. Therapeutic interventions should not be directed toward “normalization” of motor patterns but should permit a functional reordering of CNS priorities that would otherwise not be possible.

APA, Harvard, Vancouver, ISO, and other styles

48

White, Steven. "Upper Motor Neurone Syndrome and Spasticity: Clinical Management and Neurophysiology." Early Human Development 65, no. 2 (December 2001): 165–66. http://dx.doi.org/10.1016/s0378-3782(01)00198-0.

Full text

APA, Harvard, Vancouver, ISO, and other styles

49

Greaves, Andrea. "Upper Motor Neurone Syndrome and Spasticity. Clinical Management and Neurophysiology." Journal of Applied Research in Intellectual Disabilities 17, no. 2 (June 2004): 135–36. http://dx.doi.org/10.1111/j.1360-2322.2004.0182b.x.

Full text

APA, Harvard, Vancouver, ISO, and other styles

50

WADE, D. "Upper motor neurone syndrome and spasticity. Clinical management and neurophysiology." Journal of Neurology, Neurosurgery & Psychiatry 71, no. 6 (December 1, 2001): 822d—822. http://dx.doi.org/10.1136/jnnp.71.6.822d.

Full text

APA, Harvard, Vancouver, ISO, and other styles

We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!