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Journal articles on the topic 'Upper motor neuron lesion'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

Hartman, David E., and James H. Abbs. "Dysarthria associated with focal unilateral upper motor neuron lesion." International Journal of Language & Communication Disorders 27, no. 3 (1992): 187–96. http://dx.doi.org/10.3109/13682829209029419.

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2

Kim, Jiyoung, and Kyoung Jin Hwang. "Isolated unilateral lingual paralysis in a supranuclear infarction." Neurology Asia 26, no. 3 (2021): 621–22. http://dx.doi.org/10.54029/2021urm.

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Lingual paralysis can result from damage to both upper and lower motor neurons. However, since the hypoglossal nucleus is innervated from both hemispheres simultaneously, unilateral lingual paralysis caused by upper motor neuron has rarely been reported. We report a case which a patient isolated unilateral lingual paralysis due to supranuclear infarction. A 50-year-old right-handed woman was admitted to our hospital due to suddenly developed dysarthria. Her tongue deviated to the right on protrusion without fasciculation or atrophy. A brain MRI showed focal lesion in the left corona radiate and basal ganglia.

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3

Nowak, Dennis A. "The Thumb Rolling Test: A Novel Variant of the Forearm Rolling Test." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 38, no. 1 (2011): 129–32. http://dx.doi.org/10.1017/s0317167100011173.

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Abstract:Background:Neurologists use a variety of tests to detect subtle upper motor neuron lesion causing a mild motor impairment of the upper limb. The forearm and index finger rolling tests are some of these. Their sensitivity varies, but in general these tests appear to be more likely to be abnormal in mild motor impairment of the arm and hand due to a cortico-spinal tract lesion than tests of power, muscle tone or reflexes. Thumb rolling involves more distal limb segments than forearm rolling and distal limb segments are typically more affected than proximal limb segments after cerebral lesions to the cortico-spinal tract.Methods:Thumb rolling was tested, in comparison to pronator drift, forearm rolling and index finger rolling, for its sensitivity to detect a cerebral lesion of the cortico-spinal tract in 17 consecutive patients with mild pure motor stroke affecting only one arm and hand.Results:Thumb rolling is more sensitive (88%) than pronator drift (47%), forearm rolling (65%) and index finger rolling (65%) to detect a cerebral lesion of the cortico-spinal tract in mild pure motor stroke of the upper limb.Conclusion:The thumb rolling test may be a valuable adjunct clinical test to detect a subtle lesion of the cortico-spinal tract causing mild pure motor stroke of the arm and hand when the remainder of routine neurological examination is unremarkable.

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4

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 (2018): 72–74. http://dx.doi.org/10.1136/practneurol-2018-002016.

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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.

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5

Bersch, Ines, and Jan Fridén. "Upper and lower motor neuron lesions in tetraplegia: implications for surgical nerve transfer to restore hand function." Journal of Applied Physiology 129, no. 5 (2020): 1214–19. http://dx.doi.org/10.1152/japplphysiol.00529.2020.

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Nerve transfers (neurotizations) performed under optimal conditions can restore some voluntary control in muscles of the upper extremities in patients with tetraplegia. However, the type of motoneuron lesions in target muscles for nerve transfers influences the functional outcome. Using standardized maps of motor point topography, surface electrical stimulation reliably defines the kind and extent of motoneuron lesion in the selected muscles. In a muscle with an intact lower motor motoneuron, nerve transfers can often successfully reinnervate the chosen key muscle. Conversely, in a lower motoneuron lesion, the nerve transfer outcome is less predictable. However, direct muscle stimulation appears to ameliorate the morphological precondition, a finding that necessitates new preoperative approaches to optimize reinnervation in denervated/partially denervated muscles. Therefore, understanding the impact of electrical stimulation in diagnostics, prognostics, and treatments of upper limbs in tetraplegia is critical for neurotization procedures.

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6

Keegan, B. Mark, Timothy J. Kaufmann, Brian G. Weinshenker, et al. "Progressive motor impairment from a critically located lesion in highly restricted CNS-demyelinating disease." Multiple Sclerosis Journal 24, no. 11 (2018): 1445–52. http://dx.doi.org/10.1177/1352458518781979.

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Objective: To report progressive motor impairment from a critically located central nervous system (CNS) demyelinating lesion in patients with restricted magnetic resonance imaging (MRI)-lesion burden. Methods: We identified 38 patients with progressive upper motor-neuron impairment for >1 year, 2–5 MRI CNS-demyelinating lesions, with one seemingly anatomically responsible for progressive motor impairment. Patients with any alternative etiology for progressive motor impairment were excluded. A neuroradiologist blinded to clinical evaluation reviewed multiple brain and spinal-cord MRI, selecting a candidate critically located demyelinating lesion. Lesion characteristics were determined and subsequently compared with clinical course. Results: Median onset age was 47.5 years (24–64); 23 (61%) women. Median follow-up was 94 months (18–442); median Expanded Disability Status Scale Score (EDSS) at last follow-up was 4.5 (2–10). Clinical presentations were progressive: hemiparesis/monoparesis 31; quadriparesis 5; and paraparesis 2; 27 patients had progression from onset; 11 progression post-relapse. Total MRI lesions were 2 ( n = 8), 3 ( n = 12), 4 ( n = 12), and 5 ( n = 6). Critical lesions were located on corticospinal tracts, chronically atrophic in 26/38 (68%) and involved cervical spinal cord in 27, cervicomedullary/brainstem region in 6, thoracic spinal cord in 4, and subcortical white matter in 1. Conclusion: Progressive motor impairment may ascribe to a critically located CNS-demyelinating lesion in patients with highly restricted MRI burden. Motor progression from a specific demyelinating lesion has implications for understanding multiple sclerosis (MS) progression.

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7

Adams, SE, and AF Hoffman. "Multi-beat clonus in a patient without an upper motor neuron lesion. A case report." Journal of the American Podiatric Medical Association 79, no. 4 (1989): 194–96. http://dx.doi.org/10.7547/87507315-79-4-194.

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The authors present a case of five-beat clonus in the absence of a central nervous system pathologic condition. As data obtained from the literature demonstrate, clinicians should be aware that multi-beat clonus is not always associated with upper motor neuron lesions.

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8

Cengiz, Bulent, Zeki Odabasi, and Okay Vural. "Clonus is a sign of upper motor neuron lesion, not a different neurological complication." Burns 28, no. 6 (2002): 618. http://dx.doi.org/10.1016/s0305-4179(02)00102-x.

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9

Svantesson, Ulla, Hidetoshi Takahashi, Ulrika Carlsson, Anna Danielsson, and Katharina Stibrant Sunnerhagen. "Muscle and tendon stiffness in patients with upper motor neuron lesion following a stroke." European Journal of Applied Physiology 82, no. 4 (2000): 275–79. http://dx.doi.org/10.1007/s004210000216.

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10

Tomita, Yosuke, and Shigeru Usuda. "Temporal Motor Coordination in the Ankle Joint Following Upper Motor Neuron Lesions." Journal of Physical Therapy Science 25, no. 5 (2013): 539–44. http://dx.doi.org/10.1589/jpts.25.

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11

Uncini, A., R. Cutarella, A. Di Muzio, M. Assetta, A. Lugaresi, and D. Gambi. "F response in vascular and degenerative upper motor neuron lesions." Neurophysiologie Clinique/Clinical Neurophysiology 20, no. 4 (1990): 259–68. http://dx.doi.org/10.1016/s0987-7053(05)80116-9.

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12

Marcus, J. C. "Flexor Plantar Responses in Children With Upper Motor Neuron Lesions." Archives of Neurology 49, no. 11 (1992): 1198–99. http://dx.doi.org/10.1001/archneur.1992.00530350120027.

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13

Pilut, Elżbieta Szczygieł, Agata Stenwak, and Monika Rudzińska Bar. "MPAN – Does Upper and Lower Motor Neuron Lesion Correspond with the C19orf12 Phenotype? - Case Report." Neurology - Research & Surgery 1, no. 1 (2018): 1–3. http://dx.doi.org/10.33425/2641-4333.1005.

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14

Svantesson, Ulrika Österber, Ulla. "THE STANDING HEEL-RISE TEST IN PATIENTS WITH UPPER MOTOR NEURON LESION DUE TO STROKE." Scandinavian Journal of Rehabilitation Medicine 30, no. 2 (1998): 73–80. http://dx.doi.org/10.1080/003655098444165.

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15

Nonnekes, Jorik, Nathalie Benda, Hanneke van Duijnhoven, et al. "Management of Gait Impairments in Chronic Unilateral Upper Motor Neuron Lesions." JAMA Neurology 75, no. 6 (2018): 751. http://dx.doi.org/10.1001/jamaneurol.2017.5041.

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16

Doherty, Jeanne G., Anthony S. Burns, Dermot More O'Ferrall, and John F. Ditunno. "Prevalence Of Upper Motor Neuron Vs Lower Motor Neuron Lesions In Complete Lower Thoracic And Lumbar Spinal Cord Injuries." Journal of Spinal Cord Medicine 25, no. 4 (2002): 289–92. http://dx.doi.org/10.1080/10790268.2002.11753630.

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17

Jangra, Kiran, Hemant Bhagat, and Aastha Takkar. "Acute Nontraumatic Muscle Weakness." Journal of Neuroanaesthesiology and Critical Care 06, no. 03 (2019): 236–56. http://dx.doi.org/10.1055/s-0039-1696061.

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AbstractAcute nontraumatic weakness (ANTW) is defined as acute onset of weakness in any part of the body. The weakness occurs due to interruption at any point along the motor pathway. The motor pathway originates from upper motor neuron cells in the cerebral cortex and traverses through the brainstem till lower motor neurons in the spinal cord. The axon of a lower motor neuron is known as the peripheral motor nerve that synapses with muscle. ANTW is of varied etiology and presentation that may be immediately life-threatening if respiratory muscles or autonomic nervous system is involved. Involvement of respiratory muscles may be associated with respiratory failure that may require mechanical ventilation. The weakness may be localized to one limb or generalized involving several muscle groups. When bulbar muscles are involved, weakness leads to problem in swallowing and coughing that endangers the patient's airway. Similarly, the course of the disease also varies, and these patients may worsen rapidly. Hence, a comprehensive history, systematic evaluation, and a detailed neurological examination are performed to localize the disorder. There are specific clinical features peculiar to the particular location of the lesion in the body. Hence, it is possible to anatomically localize these lesions based on the clinical features. Initial laboratory tests and appropriate neuroimaging should be obtained as indicated by history and examination. The time-sensitive emergencies should be addressed immediately, as the delay in management may lead to either permanent neurological damage or may worsen the overall outcome in such conditions. The initial management should always include care of airway, breathing, and circulation (ABC). The imaging should be obtained only after initial stabilization of ABC. The definitive treatment should be done as per the etiology.

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18

Wang, Y., L. Y. Cui, and H. Wang. "P11-13 Assessment of the upper motor neuron lesion in amyotrophic lateral sclerosis with triple stimulation technique." Clinical Neurophysiology 121 (October 2010): S168. http://dx.doi.org/10.1016/s1388-2457(10)60690-6.

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19

Catania, Quyen, Marjorie Morgan, and Rebecca Martin. "Trends in Pressure Injury Development in Patients With Lower Motor Neuron and Upper Motor Neuron Lesions: A Retrospective Descriptive Study." Wound Management & Prevention 67, no. 7 (2021): 16–21. http://dx.doi.org/10.25270/wmp.2021.7.1621.

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BACKGROUND: Persons with spinal cord injury (SCI) are at high risk of pressure injury (PrI) development, but there is limited information about the effect of injury patterns (ie, upper motor neuron [UMN] or lower motor neuron [LMN] presentations) on PrI risk. PURPOSE: This study was conducted to explore the rate of PrI development in patients with LMN and UMN lesions. METHODS: A retrospective descriptive review of data from patients who were treated at a specialized outpatient SCI rehabilitation center in Baltimore, MD, between January 1, 2013, and December 31, 2019. Patients with neurological levels T8 and below, any type of SCI motor ability, and whose records were complete were included in the study. Data extracted included age, sex, date of injury, injury type, modified Ashworth Scale (MAS) score (ie, scale representing resistance to passive movement), date MAS was performed, body mass index, Spinal Cord Independent Measures-III, Braden Scale scores, ambulatory status, antispasticity medication, presence or history of PrI, and method of closure. Patients with a score of 0 on the MAS and without pharmacological management for spasticity were included in the LMN group, and patients with a score greater than 0 on the MAS with or without pharmacological management were included in the UMN group. Variables were compared using mean ± standard deviations, range, t-test, and Pearson’s chi-squared and Fisher exact tests where appropriate. P values < .05 were considered statistically significant. RESULTS: Of the 602 records examined, 194 were complete and met inclusion criteria. Most patients (119, 61.34%) were male and classified in the UMN group (162, 84%). Mean age and time since injury were 35.20 ± 18.78 and 6.20 ± 7.62 years, respectively. Seventy-three (73) of 194 patients (37.6%) had, or had a history of, a PrI; 21 (66%) in the LMN and 52 (32%) in the UMN group (X21 = 12.8; P < .001). Statistically significant differences were noted between persons with LMN and UMN in terms of Braden Scale scores, age, body mass index, Spinal Cord Independent Measures-III, and time since injury. Compared with the UMN group, more patients in the LMN group had motor complete injuries with ISNCSCI levels A/B (P < .001) and were nonambulatory (P < .001). CONCLUSION: The results of this study confirm that patients with SCI have a high rate of PrI development. The percentage of PrIs was significantly higher in the LMN than in the UMN group. Additional studies to examine the other variables that were significantly different between groups and their effect on PrI risk are needed.

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Keller, Jeffrey W., Annina Fahr, Julia Balzer, Jan Lieber, and Hubertus JA van Hedel. "Validity and reliability of an electromyography-based upper limb assessment quantifying selective voluntary motor control in children with upper motor neuron lesions." Science Progress 104, no. 2 (2021): 003685042110080. http://dx.doi.org/10.1177/00368504211008058.

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Current clinical assessments evaluating selective voluntary motor control are measured on an ordinal scale. We combined the Selective Control of the Upper Extremity Scale (SCUES) with surface electromyography to develop a more objective and interval-scaled assessment of selective voluntary motor control. The resulting Similarity Index (SI) quantifies the similarity of muscle activation patterns. We aimed to evaluate the validity and reliability of this new assessment named SISCUES (Similarity Index of the SCUES) in children with upper motor neuron lesions. Thirty-three patients (12.2 years [8.8;14.9]) affected by upper motor neuron lesions with mild to moderate impairments and 31 typically developing children (11.6 years [8.5;13.9]) participated. We calculated reference muscle activation patterns for the SISCUES using data of 33 neurologically healthy adults (median [1st; 3rd quantile]: 32.5 [27.9; 38.3]). We calculated Spearman correlations (ρ) between the SISCUES and the SCUES and the Manual Ability Classification System (MACS) to establish concurrent validity. Discriminative validity was tested by comparing scores of patients and healthy peers with a robust ANCOVA. Intraclass correlation coefficients2,1 and minimal detectable changes indicated relative and absolute reliability. The SISCUES correlates strongly with SCUES (ρ = 0.76, p < 0.001) and moderately with the MACS (ρ = −0.58, p < 0.001). The average SISCUES can discriminate between patients and peers. The intraclass correlation coefficient2,1 was 0.90 and the minimal detectable change was 0.07 (8% of patients’ median score). Concurrent validity, discriminative validity, and reliability of the SISCUES were established. Further studies are needed to evaluate whether it is responsive enough to detect changes from therapeutic interventions.

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Fahr, Annina, Andrina Kläy, Jeffrey W. Keller, and Hubertus J. A. van Hedel. "An Interactive Computer Game for Improving Selective Voluntary Motor Control in Children With Upper Motor Neuron Lesions: Development and Preliminary Feasibility Study." JMIR Serious Games 9, no. 3 (2021): e26028. http://dx.doi.org/10.2196/26028.

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Background Computer game–based interventions are emerging in pediatric neurorehabilitation, as they can provide two key elements for motor learning—motivating environments that enable long-term compliance, which is particularly relevant for children, and augmented feedback for improving movement performance. Objective The overall aim of this study is to develop an interactive computer play for children with upper motor neuron lesions to train selective voluntary motor control and give particular attention to motivation and feedback. We also aim to determine features that make games engaging, investigate which sensory feedback modality is noticed the fastest during play, develop an interactive game, and evaluate its feasibility. Methods We identified engaging game features by interviewing 19 children and adolescents undergoing rehabilitation. By using a test version of the game, we determined the response times of 10 patients who had to react to visual, auditory, or combined feedback signals. On the basis of the results of these two subprojects, we developed and designed a game environment. Feasibility was studied in terms of the practicability and acceptability of the intervention among 5 children with upper motor neuron lesions. Results The game features deemed the most important by pediatric patients were strategic gameplay (13/29, 45% of answers) and choice (6/29, 21%). While playing the game, an acoustic alarm signal (reaction time: median 2.8 seconds) was detected significantly faster (P=.01) than conditions with other feedback modalities (avatar velocity reduction: median 7.8 seconds; color desaturation: median 5.7 seconds). Most children enjoyed playing the game, despite some technical issues. Conclusions The careful identification of game features that increase motivation and feedback modalities that inform children quickly led to the development of an interactive computer play for training selective voluntary motor control in children and adolescents with upper motor neuron lesions.

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Ashby, P., A. Mailis, and J. Hunter. "The Evaluation of “Spasticity”." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 14, S3 (1987): 497–500. http://dx.doi.org/10.1017/s0317167100037987.

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ABSTRACT:Lesions of the upper motor neuron cause: 1. Alterations in segmental reflex activity. For example increased tendon jerks and velocity dependent stretch reflexes ("spasticity"), clonus, the clasp knife response, release of flexion reflexes and extensor plantar reflexes. 2. Impaired ability to activate motoneurons rapidly and selectively. Voluntary movements may also be restrained by co-contraction of antagonists muscles, by segmental reflexes (enhanced during voluntary effort) or by contractures. A combination of these factors may impair overall functional ability. Segmental reflexes, voluntary power and overall functional abilities can be assessed using clinical scoring systems. Recordings of muscle length, tension andEMG offer more objective measures of reflex and voluntary activity and of overall functions such as locomotion, and can separate weakness from co-contraction, spasticity from contracture. Methods are now available for exploring individual (transmitter specific) segmental reflex pathways and descending pathways in man. Lesions of the upper motor neuron are complicated by secondary changes in segmental neurons. Segmental reflex activity and muscle mechanics depend on the immediate past history of events. These factors must be taken into account.

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Shahani, Bhagwan T. "WS-24-1 Single motor unit (SMU) studies in patients with upper motor neuron lesions (UMNL)." Electroencephalography and Clinical Neurophysiology/Electromyography and Motor Control 97, no. 4 (1995): S48—S49. http://dx.doi.org/10.1016/0924-980x(95)92590-i.

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Alves, Ivânia, Vítor Tedim Cruz, and Hans Peter Grebe. "Spasticity as the First Manifestation of Ischaemic Lesions Involving the Cingulum." Case Reports in Neurological Medicine 2013 (2013): 1–3. http://dx.doi.org/10.1155/2013/534243.

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Background and Purpose. Spasticity is a positive sign of upper motor neuron syndrome that usually develops weeks after a stroke. The mechanisms that lead to its appearance are not completely understood, namely, the cortical regions whose lesion may induce spasticity.Summary of Cases. We report two patients with an ischaemic stroke entailing the anterior cingulate gyrus (pericallosal artery territory), who presented with acute hemiplegia and spasticity since symptom onset. Spasticity resolved within days after onset.Conclusions. The acute destruction of the anterior cingulate region, interrupting inhibitory projections towards lower motor centres, probably explains the acute onset of spasticity that occurred in these two patients. Further studies addressing the role of this region in acute and chronic disturbances of muscular tone are necessary.

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Merlo, Andrea, Maria Giulia Montecchi, Francesco Lombardi, et al. "Monitoring Involuntary Muscle Activity in Acute Patients with Upper Motor Neuron Lesion by Wearable Sensors: A Feasibility Study." Sensors 21, no. 9 (2021): 3120. http://dx.doi.org/10.3390/s21093120.

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Sustained involuntary muscle activity (IMA) is a highly disabling and not completely understood phenomenon that occurs after a central nervous system lesion. We tested the feasibility of in-field IMA measuring at an acute rehabilitation ward. We used wearable probes for single differential surface EMG (sEMG), inclusive of a 3D accelerometer, onboard memory and remote control. We collected 429 h of data from the biceps brachii of 10 patients with arm plegia. Data quality was first verified in the time and frequency domains. Next, IMA was automatically identified based on the steady presence of motor unit action potential (MUAP) trains at rest. Feasibility was excellent in terms of prep time and burden to the clinical staff. A total of 350.5 h of data (81.7%) were reliable. IMA was found in 85.9 h (25%). This was often present in the form of exceedingly long-lasting trains of one or a few MUAPs, with differences among patients and variability, both within and between days in terms of IMA duration, root mean square (RMS) and peak-to-peak amplitude. Our results proved the feasibility of using wearable probes for single differential sEMG to identify and quantify IMA in plegic muscles of bedridden acute neurological patients. Our results also suggest the need for long-lasting acquisitions to properly characterize IMA. The possibility of easily assessing IMA in acute inpatients can have a huge impact on the management of their postures, physiotherapy and treatments.

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Cengiz, B., and H. R. Kuruoglu. "Turns-amplitude analysis of the electromyographic recruitment pattern following upper motor neuron lesions." Acta Neurologica Scandinavica 110, no. 6 (2004): 403–7. http://dx.doi.org/10.1111/j.1600-0404.2004.00322.x.

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COLEBATCH, J. G., and S. C. GANDEVIA. "THE DISTRIBUTION OF MUSCULAR WEAKNESS IN UPPER MOTOR NEURON LESIONS AFFECTING THE ARM." Brain 112, no. 3 (1989): 749–63. http://dx.doi.org/10.1093/brain/112.3.749.

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Svantesson, U., and K. Stibrant Sunnerhagen. "Stretch-shortening cycle in patients with upper motor neuron lesions due to stroke." European Journal of Applied Physiology 75, no. 4 (1997): 312–18. http://dx.doi.org/10.1007/s004210050166.

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Anuradha, S., and Vanlalmalsawmdawngliana Fanai. "Hirayama Disease: A Rare Disease with Unusual Features." Case Reports in Neurological Medicine 2016 (2016): 1–4. http://dx.doi.org/10.1155/2016/5839761.

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Hirayama disease, also known as monomelic amyotrophy (MMA), is a rare cervical myelopathy that manifests itself as a self-limited, asymmetrical, slowly progressive atrophic weakness of the forearms and hands predominantly in young males. The forward displacement of the posterior dura of the lower cervical dural canal during neck flexion has been postulated to lead to lower cervical cord atrophy with asymmetric flattening. We report a case of Hirayama disease in a 25-year-old Indian man presenting with gradually progressive asymmetrical weakness and wasting of both hands and forearms along with unusual features of autonomic dysfunction and upper motor neuron lesion.

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Lee, Seung-Jae, Dong-Geun Lee, Hye-Jin Moon, and Tae-Kyeong Lee. "Lesion Pattern, Mechanisms, and Long-Term Prognosis in Patients with Monoparetic Stroke: A Comparison with Nonmonoparetic Stroke." BioMed Research International 2017 (2017): 1–7. http://dx.doi.org/10.1155/2017/9373817.

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Background. Monoparetic stroke is rare but could be misdiagnosed as peripheral neuropathy. We investigated the prevalence, lesion pattern, stroke mechanism, and long-term prognosis in patients with monoparetic stroke.Methods. 586 acute ischemic stroke patients (including 31 with monoparesis) were studied. Monoparetic stroke was defined as a motor deficit in either an arm or a leg but without facial weakness or speech disturbance. Median follow-up period was 32.0 months. Kaplan-Meier survival curves, log-rank tests, logistic regressions, and Cox proportional hazards models were used for clinical outcome analyses.Results. The mean age (313 men and 273 women) was 67.6 years. Among monoparetic patients, most had cortical (80.6%) and multiple (64.5%) lesions. The main stroke mechanisms were cardioembolism (38.7%) and large artery atherosclerosis (29.0%). Precentral gyrus with additional regions was most frequently involved in monoparesis (45.2%). Upper motor neuron signs were found in only 11 patients (35.5%). Compared with the nonmonoparetic group, these patients had better functional outcomes (6-month modified Rankin scale ≤2) and long-term survival but had comparable risks for further vascular events, including stroke recurrences.Conclusions. Although monoparetic stroke may have a better functional outcome, the risk of the further vascular event seems similar to nonmonoparetic stroke.

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Carlsson, U., G. B. Henning, U. Svantesson, and K. S. Sunnerhagen. "Plantar flexor muscle action while sitting, standing and prone in patients with upper motor neuron lesion due to stroke." Isokinetics and Exercise Science 11, no. 4 (2003): 205–11. http://dx.doi.org/10.3233/ies-2003-0148.

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Kern, H., C. Hofer, M. Mödlin, et al. "Stable muscle atrophy in long-term paraplegics with complete upper motor neuron lesion from 3- to 20-year SCI." Spinal Cord 46, no. 4 (2007): 293–304. http://dx.doi.org/10.1038/sj.sc.3102131.

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Campanini, Isabella, Andrea Merlo, Maria Giulia Montecchi, and Francesco Lombardi. "Muscle overactivity (MO) monitoring in sub-acute patients with upper motor neuron lesion (UMNL) by sEMG long-lasting acquisitions." Gait & Posture 42 (September 2015): S6. http://dx.doi.org/10.1016/j.gaitpost.2015.07.022.

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Ghosh, Ritwik, Souvik Dubey, Subhankar Chatterjee, Biman Kanti Ray, and Julián Benito-León. "Mixed Upper and Lower Motor Neuron Damage in Japanese Encephalitis Virus Infection." Case Reports in Neurology 12, no. 3 (2020): 482–88. http://dx.doi.org/10.1159/000510711.

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Cerebral manifestations in Japanese B encephalitis are well known. However, there are very few studies focusing on extra-cerebral manifestations, among which focal anterior horn cell involvement is exceedingly rare. We herein report a case of Japanese B encephalitis with focal anterior horn cell involvement and unfurl how stepwise clinical approach and targeted investigations helped to solve the diagnostic conundrum. A 27-year-old female was admitted with fever, headache, altered sensorium, and convulsions. She tested positive for Japanese B encephalitis-IgM. Following conservative management, she regained consciousness after 5 days when neurological examination revealed marked cognitive impairment, medial convergence of eyeballs, upward gaze restriction, upper limbs dystonia with brisk tendon jerks, and flaccid paraparesis. A repeat neurological examination, on day 15 of admission, showed marked wasting and intermittent fasciculation in both lower limbs. Brain magnetic resonance imaging showed asymmetrical (right &#x3e; left) bilateral thalamic and midbrain lesions, hyperintense on T2 and T2-fluid-attenuated inversion recovery (FLAIR)-weighted imaging with mild diffusion restriction on diffusion-weighted imaging and apparent diffusion coefficient map, suggestive of encephalitis . Nerve conduction study revealed decreased compound muscle action potentials exclusively in lower limbs with intact sensory nerve action potentials. Electromyogram showed chronic denervation potentials and presence of spontaneous activity in lower limbs, but not in upper limbs, indicative of focal anterior horn cell involvement. Prognosis of Japanese B encephalitis does not only depend on cerebral sequelae. Anterior horn cell involvement can dictate poor outcome and can easily be missed if not carefully dealt with.

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Dimitrijević, M. R. "Neurocontrol of upper motor neuron deficits in patients with brain and spinal cord lesions." Electroencephalography and Clinical Neurophysiology 75 (January 1990): S37—S38. http://dx.doi.org/10.1016/0013-4694(90)91852-g.

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Sunnerhagen, Katharina Stibrant, Ulla Svantesson, Lars Lönn, Marcin Krotkiewski, and Gunnar Grimby. "Upper motor neuron lesions: Their effect on muscle performance and appearance in stroke patients with minor motor impairment." Archives of Physical Medicine and Rehabilitation 80, no. 2 (1999): 155–61. http://dx.doi.org/10.1016/s0003-9993(99)90113-2.

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Mazzoli, D., A. Merlo, P. Zerbinati, et al. "Is there a role for functional surgery in the management of quadriceps spasticity in adults with upper motor neuron lesion?" Gait & Posture 66 (October 2018): S27. http://dx.doi.org/10.1016/j.gaitpost.2018.07.142.

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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 (1996): 477–85. http://dx.doi.org/10.1017/s1355617700001648.

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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.)

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Varyani, Neeraj, Anubhav Thukral, Sunny Garg, Kailash Kumar Gupta, Ravi Tandon, and Kamlakar Tripathi. "Atypical Neurofibroma and Osteosclerotic Metastasis." Case Reports in Oncological Medicine 2012 (2012): 1–4. http://dx.doi.org/10.1155/2012/301437.

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35-year-old male presented with multiple swellings in left leg, headache, weakness of limbs for 4 months, and blurring of vision for the last 15 days. On examination, he was pale, cachexic with generalized lymphadenopathy and lower motor neuron type weakness of limbs sparing right upper limb. Blood investigations showed anemia with high alkaline phosphatase. Chest radiograph revealed osteosclerotic metastatic lesion in humerus. Biopsy of leg lesion revealed atypical neurofibroma. Computed tomography (CT) of thorax revealed osteoblastic metastasis. Bone marrow aspiration showed cells with round to oval nuclei, fine granular chromatin with large central prominent nucleoli and eosinophilic cytoplasm with acini formation. Magnetic resonance imaging (MRI) of brain and spinal cord defined metastatic leptomeningeal deposits. Cerebrospinal fluid (CSF) cytology was positive for malignant cells. Gastroscopy showed an ulceroinfiltrative growth from stomach which on histopathology revealed diffuse adenocarcinoma. Palliative treatment was given with intrathecal methotrexate and systemic corticosteroid with chemotherapy. Patient’s symptom improved drastically, but we lost him to followup.

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Páscoa Pinheiro, João, Joana Rato, Olinda Rebelo, and Gonçalo Costa. "Primary spinal epidural lymphoma: a rare entity with an ambiguous management." BMJ Case Reports 13, no. 1 (2020): e233442. http://dx.doi.org/10.1136/bcr-2019-233442.

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Lymphomas are malignant lymphoid tumours arising from lymphocytic cells. They usually develop in the lymphoid tissues and can spread to other organs; however, primary extra-nodal locations such as the spinal epidural space are less common. The authors report the case of a primary diffuse large B-cell lymphoma of the thoracic spine in a 65-year-old man, who presented to the emergency department with signs of upper motor neuron lesion. The patient underwent surgery in order to decompress the spinal cord. The treatment was concluded with six cycles of chemotherapy with methotrexate, rituximab, cyclophosphamide, vincristine and prednisone followed by radiotherapy. At the 24-month follow-up, no signs of epidural lesion or bone contrast enhancement were observed in thoracic spine MRI. Surgical decompression is recommended in patients with signs of spinal cord injury in order to prevent irreversible neurological damage and is related to high rates of disease-free survival.

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Balzer, Julia, Marietta L. van der Linden, Thomas H. Mercer, and Hubertus J. A. van Hedel. "Selective voluntary motor control measures of the lower extremity in children with upper motor neuron lesions: a systematic review." Developmental Medicine & Child Neurology 59, no. 7 (2017): 699–705. http://dx.doi.org/10.1111/dmcn.13417.

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Bakulin, I. S., A. V. Chervyakov, M. N. Zakharova, N. A. Suponeva, and M. A. Piradov. "NAVIGATED TRANSCRANIAL MAGNETIC STIMULATION POSSIBILITIES IN DIFFICULT DIAGNOSTIC CASES UPPER MOTOR NEURON LESIONS – CASE REPORT." Neuromuscular Diseases 5, no. 2 (2015): 32. http://dx.doi.org/10.17650/2222-8721-2015-5-2-32-37.

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Sethi, Rajesh K., Stuart B. Bauer, Frances M. Dyro, and Christian Krarup. "Modulation of the bulbocavernosus reflex during voiding: Loss of inhibition in upper motor neuron lesions." Muscle & Nerve 12, no. 11 (1989): 892–97. http://dx.doi.org/10.1002/mus.880121104.

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Becher, Meni, Shmuel Springer, Orit Braun-Benyamin, and Yocheved Laufer. "The Effect of an Interphase Interval on Electrically Induced Dorsiflexion Force and Fatigue in Subjects With an Upper Motor Neuron Lesion." Artificial Organs 40, no. 8 (2016): 778–85. http://dx.doi.org/10.1111/aor.12698.

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Memarpour, Roya, Basheer Tashtoush, Lydia Issac, and Fernando Gonzalez-Ibarra. "Syringomyelia with Chiari I Malformation Presenting as Hip Charcot Arthropathy: A Case Report and Literature Review." Case Reports in Neurological Medicine 2015 (2015): 1–6. http://dx.doi.org/10.1155/2015/487931.

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Neuroarthropathy (neuropathic osteoarthropathy), also known as Charcot joint, is a condition characterized by a progressive articular surface destruction in the setting of impaired nociceptive and proprioceptive innervation of the involved joint. It is seen most commonly in the foot and ankle secondary to peripheral neuropathy associated with diabetes mellitus. Cases of hip (Charcot) neuroarthropathy are rare and almost exclusively reported in patients with neurosyphilis (tabes dorsalis). We report a case of a 36-year-old man who presented to the emergency department complaining of right hip pain. On physical examination, pain and thermal sensory deficits were noted in the upper torso with a cape-like distribution, as well as signs of an upper motor neuron lesion in the left upper and lower extremities. A magnetic resonance imaging study (MRI) of the right hip showed evidence of early articular surface destruction and periarticular edema consistent with hip Charcot arthropathy. An MRI of the spine revealed an Arnold-Chiari type I malformation with extensive syringohydromyelia of the cervical and thoracic spine.

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Shibuya, Kazumoto, Sonoko Misawa, Akiyuki Uzawa, et al. "Split hand and motor axonal hyperexcitability in spinal and bulbar muscular atrophy." Journal of Neurology, Neurosurgery & Psychiatry 91, no. 11 (2020): 1189–94. http://dx.doi.org/10.1136/jnnp-2020-324026.

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ObjectiveThe ‘split hand’ sign refers to preferential wasting of the thenar and first dorsal interosseous muscles with relatively sparing of the hypothenar muscles in amyotrophic lateral sclerosis (ALS) and both cortical and spinal/peripheral excitotoxic mechanisms have been proposed. We aimed to study split hand and axonal excitability in spinal and bulbar muscular atrophy (SBMA) in which cortical motor neurons are intact.MethodsIn 35 patients with genetically confirmed SBMA, 55 with ALS, 158 with other neuromuscular diseases and 90 normal controls; split hand was strictly determined by amplitudes of compound muscle action potentials. Nerve excitability testing of median motor axons was performed in 35 SBMA and 55 patients with ALS and 45 normal controls.ResultsSplit hand was as frequently found for patients with SBMA (57%) and ALS (62%), compared with disease (20%) and normal (0%) controls. Excitability testing showed that in both SBMA and ALS, strength-duration time constant was longer, and threshold changes in depolarising threshold electrotonus and superexcitability in the recovery cycle were greater than in normal controls (p<0.01).ConclusionsSplit hand is not specific to ALS and can be caused by the peripheral mechanism alone in SBMA, whereas the effect of upper motor neuron lesion cannot be excluded in ALS. Our results also suggest that SBMA and ALS share common axonal excitability changes; increased nodal persistent sodium and reduced potassium currents that may accelerate motor neuronal death and differently affect axons-innervating different muscles. Ion channel modulators could be a therapeutic option for both SBMA and ALS.

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Plattner, Brandon L., Marc Kent, Brian Summers, et al. "Gliomatosis Cerebri in Two Dogs." Journal of the American Animal Hospital Association 48, no. 5 (2012): 359–65. http://dx.doi.org/10.5326/jaaha-ms-5796.

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A 3.5 yr old Saint Bernard was evaluated for nonambulatory tetraparesis and cranial nerve dysfunction, and a 7 yr old rottweiler was evaluated for progressive paraparesis. Clinical signs of left-sided vestibular and general proprioceptive ataxia and cranial nerve VII dysfunction in the Saint Bernard suggested a lesion affecting the brain stem. Signs in the rottweiler consisted of general proprioceptive/upper motor neuron paraparesis, suggesting a lesion involving the third thoracic (T3) to third lumbar (L3) spinal cord segments. MRI was normal in the Saint Bernard, but an intra-axial lesion involving the T13–L2 spinal cord segments was observed in the rottweiler. In both dogs, the central nervous system (CNS) contained neoplastic cells with features consistent with gliomatosis cerebri (GC). In the Saint Bernard, neoplastic cells were present in the medulla oblongata and cranial cervical spinal cord. In the rottweiler, neoplastic cells were only present in the spinal cord. Immunohistochemistry disclosed two distinct patterns of CD18, nestin, and vimentin staining. GC is a rarely reported tumor of the CNS. Although GC typically involves the cerebrum, clinical signs in these two dogs reflected caudal brainstem and spinal cord involvement.

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Allett, Brian, Michael R. Broome, and David Hager. "MRI of a Split Cord Malformation in a German Shepherd Dog." Journal of the American Animal Hospital Association 48, no. 5 (2012): 344–51. http://dx.doi.org/10.5326/jaaha-ms-5780.

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A 9 yr old spayed female German shepherd dog was referred for MRI of the thoracic and lumbar spine because she had clinical signs of chronic neurogenic bladder dysfunction of an unknown cause. Transverse T2-weighted images identified a type II split cord malformation (i.e., diastematomyelia) in the thoracic spine. Split cord malformations are forms of spinal dysraphism where the abnormal development of spinal cord results in sagittal splitting of a portion of the cord into two hemicords. The location of the lesion in the thoracic spine was consistent with the dog’s clinical signs of an upper motor neuron bladder. Split cord malformations that occur in humans have similar MRI characteristics and can result in similar clinical signs as those identified in the dog described in this report.

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Kerwin, SC, RJ McCarthy, JL VanSteenhouse, BP Partington, and J. Taboada. "Cervical spinal cord compression caused by cryptococcosis in a dog: successful treatment with surgery and fluconazole." Journal of the American Animal Hospital Association 34, no. 6 (1998): 523–26. http://dx.doi.org/10.5326/15473317-34-6-523.

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A six-year-old, male Doberman pinscher was presented for acute onset of upper motor neuron tetraparesis. An extradural compressive lesion compatible with intervertebral disk rupture at the sixth to seventh cervical (C6-C7) disk space was evident on myelography. A large, gelatinous mass of pure cryptococcal organisms causing spinal cord compression was identified upon exploratory surgery. Removal of the mass caused relief of clinical signs. No evidence of involvement of other organ systems was found; however, serum and cerebrospinal fluid titers were positive for cryptococcal infection. The dog was treated with fluconazole (5.5 mg/kg body weight, per os sid) until serum titers for cryptococcal infection were negative at seven months postsurgery. To the authors' knowledge, this is the only report of a dog with cryptococcosis treated successfully using fluconazole as a sole agent.

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Furmann, Meiriélly, Juliana Aparecida Wosch Pires, Andersom Ricardo Fréz, et al. "Influence of autonomic nervous system in muscle activity of individual with sequelae af ter stroke." Manual Therapy, Posturology & Rehabilitation Journal 12 (June 11, 2014): 184. http://dx.doi.org/10.17784/mtprehabjournal.2014.12.184.

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Introduction: The stroke is a lesion of the Central Nervous System inducing spasticity, caused by a lesion of the upper motor neuron. The presence of spasticity limits the patient in achieving the necessary adjustments for the execution of required functional movements, causing limitations in daily life activities, interfering in our quality of life. Objective: To analyze the influence of the Autonomic Nervous System (ANS) in spastic patient consequential of stroke and decrease spasticity resulting of stimulus in the ANS. Method: It is a case study, where the spasticity was analyzed by means of Electromyography record (RMS), Ashowrth Scale modified and goniometry. The intervention consisted in 10 visits by performing Parasympathetic Laringe-Faringe Maneuvers, Plantar Arch and inhibition of Gastrocnemius. Results: The ANS has influence on the muscular activity, seen that there was a reduction of spasticity with decrease of the RMS values, increase in the amplitude of movement quantified by degrees and by means of the Modified Ashworth Scale. Conclusion: However, the mobilization of the autonomic nervous system through parasympathetic maneuvers are effective in decreasing spasticity due to stroke.

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