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Relevant bibliographies by topics / Upper motor neuron lesion

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Academic literature on the topic 'Upper motor neuron lesion'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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Journal articles on the topic "Upper motor neuron lesion"

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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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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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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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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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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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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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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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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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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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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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Dissertations / Theses on the topic "Upper motor neuron lesion"

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Carruth, Elaine M. "The effects of non-noxious cutaneous stimulation on reflex excitability in neurological intact individuals and patients with spasticity following an upper motor neurone lesion." Thesis, Glasgow Caledonian University, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.547420.

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Luhmann, Ole. "Development of a Novel Hand Exoskeleton for the Rehabilitation and Assistance of Upper Motor Neuron Syndrome Patients." Thesis, KTH, Maskinkonstruktion (Inst.), 2020. http://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-281248.

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Hand exoskeletons are wearable robotic devices which are used to compensate for impaired handmovements in patientswith impaired upper-limbs. These devices can either help patients to grasp objects for a therapeutic purpose or to performactivities of daily living. This Thesis describes the development of a novel hand exoskeleton, with a focus on the user, based on the product development methodology "the V-Model". Therefore, user needs are identified through interviews and a thorough literature review. Three potential concepts are developed and sub-sequential a concept is selected based on a logical decision process. A mathematical model of the selected concept is generated and then used for dimensioning the hand exoskeleton. Moreover, three variants of the hand exoskeleton are built as prototypes. Finally, the variants of the device are tested on a bench top. The result of the development process is a novel hand exoskeleton for the rehabilitation of upper motor neuron syndrome patients. Force and range of motion tests revealed, that a design with a higher level of underactuation is favourable. The design presented in this thesis does not reach the defined range of motion and force augmentation. However, the defined target values are the results of a conservative approach, thus are a challenge to reach. The augmented closing force and range of motion surpass other state of the art hand exoskeletons. Nevertheless, the augmented opening force under-performs in comparison with other designs. Decisively, a validation with users is needed for a usability assessment.<br>Exoskelett för händer är robotiska hjälpmedel som kan användas för att kompensera nedsatt muskelstyrka och rörlighet hos patienter med nedsatt muskelfunktion i armarna. Dessa hjälpmedel kan hjälpa patienter att greppa föremål i ett terapeutiskt syfte eller för att utföra vardagliga sysslor. Examensarbetet beskriver utvecklingsarbetet av ett nytt exoskelett med fokus på användaren genom att tillämpa produktutvecklingsmotodikens V-modell. Användarens krav och behov identifieras genom intervjuer och en gedigen litteraturstudie. Tre koncept utvecklas och ett vidareutvecklat koncept väljs slutligen baserat på en logisk beslutsprocess. En matematisk modell genereras och används för att dimensionera exoskelettet. Dessutom tillverkas tre prototyper av exoskelettet i olika utföranden för att slutligen utvärderas i en testrigg. Resultatet av utvecklingsprocessen är ett nytt handexoskelett ämnat för rehabilitering av patienter med övre motorneuronsjukdom. Tester som genomfördes för att mäta Kraft och rörlighet visade att en design med en högre grad av underaktuering är gynnsamt. Designen som presenteras här når inte upp till de krav som ställs på kraft och rörlighet, de målvärden som definieras är dock baserade på ett konservativt synsätt och är därmed svåra att uppnå. Exoskelettet producerar en högre stängningskraft och uppvisar bättre rörlighet än andra toppmoderna exoskelett. Exoskelettet underpresterar dock vad gäller den producerade öppningskraften jämfört med andra modeller och designen behöver valideras hos användarna för att användarbarheten ska kunna bestämmas.

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Rajagopalan, Venkateswaran. "Evaluation of Upper Motor Neuron Pathology in Amyotrophic Lateral Sclerosis by MRI: Towards Identifying Noninvasive Biomarkers of the Disease." Cleveland State University / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=csu1288020485.

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Nycz, Christopher Julius. "Modeling & Analysis of Design Parameters for Portable Hand Orthoses to Assist Upper Motor Neuron Syndrome Impairments and Prototype Design." Digital WPI, 2018. https://digitalcommons.wpi.edu/etd-dissertations/501.

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Wearable assistive robotics have the potential to address an unmet medical need of reducing disability in individuals with chronic hand impairments due to neurological trauma. Despite myriad prior works, few patients have seen the benefits of such devices. Following application experience with tendon-actuated soft robotic gloves and a collaborator's orthosis with novel flat-spring actuators, we identified two common assumptions regarding hand orthosis design. The first was reliance on incomplete studies of grasping forces during activities of daily living as a basis for design criteria, leading to poor optimization. The second was a neglect of increases in muscle tone following neurological trauma, rendering most devices non-applicable to a large subset of the population. To address these gaps, we measured joint torques during activities of daily living with able-bodied subjects using dexterity representative of orthosis-aided motion. Next, we measured assistive torques needed to extend the fingers of individuals with increased flexor tone following TBI. Finally, we applied this knowledge to design a cable actuated orthosis for assisting finger extension, providing a basis for future work focused on an under-represented subgroup of patients.

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Kapelner, Tamás [Verfasser], Dario [Akademischer Betreuer] Farina, Dario [Gutachter] Farina, and David [Gutachter] Liebetanz. "Decoding motor neuron behavior for advanced control of upper limb prostheses / Tamás Kapelner ; Gutachter: Dario Farina, David Liebetanz ; Betreuer: Dario Farina." Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2016. http://d-nb.info/1149958413/34.

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Tiwari, Ekta. "ASSESSMENT OF CANINE BLADDER FUNCTION RESTORATION USING BEHAVIORAL MONITORING AND IN-VIVO ELECTROPHYSIOLOGICAL TECHNIQUES." Diss., Temple University Libraries, 2019. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/590674.

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Electrical and Computer Engineering<br>Ph.D.<br>Spinal cord injuries and other neurological disorders can disturb the regulation of normal bladder function including continence and micturition. Developing new neuronal pathways by surgically rerouting nerves is a potential approach for restoring bladder function. Our laboratory successfully rerouted somatic nerves to the anterior vesical branch of the pelvic nerve to reinnervate the bladder muscle in canines. Electrical stimulation of these transferred nerves induced detrusor pressure and bladder emptying and we confirmed regrowth of these rerouted nerves using retrograde neurotracing methods. In these studies, reinnervation was proved at 1st and 3rd months after decentralization. We believe that our aim of developing an approach to surgically reinnervate the bladder after long-term decentralization is critical to the success of the reinnervation surgery due to the possibility that patients would delay having a surgery until they try other non-surgical approaches or therapies. We also demonstrated the reinnervation of urethral and anal sphincters by femoral to pudendal nerve transfer after sacral ventral root transection to restore continence. However, these studies did not demonstrate the reinnervation of bladder, urethra and anal sphincter, all in same animal that would be helpful to human patients with lower motor neuron lesioned bladders to restore both continence and emptying. Therefore, prior to applying these surgical procedures to human patients, further investigation is required to prove the effectiveness of nerve transfer strategies in this canine model using multiple experimental techniques. This dissertation is a part of a larger project in canines examining whether surgical rerouting of obturator to pelvic nerve and sciatic to pudendal nerve allows restoration of bladder, urethral and anal sphincter functions, including continence (storage) and emptying (voiding and defecation) functions, in lower motor neuron lesioned bladders. In this study, it was aimed to explore bladder and urethral reinnervation using behavioral observation and in-vivo electrophysiological techniques. In order to completely prove that the reinnervation surgeries are responsible for restoration of bladder and urethral functions, it was first necessary to demonstrate the absence of these functions in animals with long term decentralized bladders and to determine whether the same animals were able to recover functions after reinnervation. In specific aim 1, we addressed this goal by tracking squat-and-void behaviors at monthly intervals after decentralization and reinnervation, using home cage video recordings and evaluation of bladder sensation and emptying after bladder filling. Immediately prior to euthanasia, reinnervation was also explored by electrical stimulation of transferred nerves to evaluate motor function. Retrograde neuronal tracing was also performed to explore sensory reinnervation. Results showed evidence of functional restoration of bladder and urethral function in reinnervated animals based on behavior observation and electrical stimulation of transferred nerves. Also, regrowth of neuronal cells in the new neuronal pathways was observed that were developed by the nerve transfer surgeries. This study also aimed to establish an electroneurogram recording method (part of in-vivo electrophysiological experiments) to explore afferent (sensory) neuronal activity in transferred nerves induced by bladder filling. However, the extraction of neuronal activity from the peripheral nerves is a challenging task. Several factors including noise, interference from surrounding muscle activities and the electronic components can affect these microvolts level recordings. Choice of recording electrode in configuration with the whole recording setup also plays a significant role while performing these low amplitude signal recordings. In specific aim 2, we addressed this issue by refining electroneurogram recording techniques to obtain high strength signal during multifiber recording. We first developed custom electrodes, suitable for varying nerve diameters and available implantation sites, were tested for functionality. Then, we performed multiple testing using these electrodes with different amplifiers to calibrate noise in saline. Testing results helped to establish the recording setup suitable for in-vivo experimental environment. Later, these refined techniques were applied to record afferent (sensory) activity of sciatic nerves and afferent (sensory) and efferent (motor) activity of hypogastric nerves in rats. Based on the recording results, it was aimed to employ similar techniques in order to record nerve activity in the canine model. Prior to applying these refined techniques to explore sensory reinnervation from new neuronal pathways after nerve transfer surgeries, in specific aim 3, we aimed to assess the hypogastric nerve activity in normal intact and acutely lumbosacral decentralized bladders using these refined techniques. The effects of electrical stimulation of hypogastric nerves or lumbar roots on detrusor pressure were determined, as were effects of isoflurane versus propofol anesthetics on hypogastric nerve stimulation evoked pressure. Hypogastric nerve activity was recorded using custom-made bipolar cuff electrodes during bladder filling. To confirm or refute that any increase in electroneurogram during bladder filling is due to afferent activity from the end organ, the hypogastric nerve was transected between the recording electrode and the spinal cord and the effects of bladder filling on afferent but not efferent activity were recorded. Results showed that electrical stimulation of hypogastric nerves evoked low amplitude detrusor pressures that did not differ between the two anesthetics. Upper lumbar (L2) ventral root stimulation evoked detrusor pressures were suppressed, yet not eliminated after transection of hypogastric nerves and all spinal roots below L5. Afferent and efferent hypogastric nerve activity did not change with bladder filling in neuronally intact bladders but decreased in decentralized bladders. No change in afferent activity were observed during bladder filling in normal intact and decentralized bladders. Overall findings in this research indicate that the new neuronal pathways created by nerve transfer can restore bladder sensation and emptying function in lower motor neuron-lesioned canines. A more complete decentralized bladder model needs to include transection of both the lumbosacral spinal roots innervating the bladder and the hypogastric nerves prior to performing nerve transfer surgeries. The refined electroneurogram recording methods may be suitable for evaluating the effectiveness of nerve transfer surgeries by monitoring the sensory activities of the transferred nerve.<br>Temple University--Theses

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Lundström, Erik. "Spasticity after first-ever stroke." Doctoral thesis, Uppsala universitet, Neurologi, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-107134.

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The prevalence of spasticity after first-ever stroke is approximately 20%, but there are no data on the prevalence of disabling spasticity.The reported prevalence of pain after stroke varies between 19% and 74%, whether pain is associated with spasticity is not known. Until now, there is no health economic analysis of patients with spasticity after stroke. Methods: Two groups of patients were studied. Cohort I was a cross-sectional survey. A representative sample of 140 patients was investigated 1 year after their first-ever stroke. Spasticity was defined as ≥ 1 score on the modified Ashworth scale, disabling spasticity was defined as spasticity having such an impact that intervention, e.g. intensive physiotherapy, orthoses or pharmacological treatment, should be offered. Pain was assesed with the Visual Analogue Scale. All direct costs during one year were identified and converted into Purchasing Power Parities US dollar (PPP$). Cohort II was a prospective cohort study. Forty-nine patients were examined at day 2–10, at one month, and at six months after their first-ever stroke. Assessment and definitions were similar as for cohort I. Results: Spasticity occurs within 1 month and disabling spasticity occur within 6 months. After one year, the prevalence of spasticity was 17% and that of disabling spasticity 4%. Disabling spasticity was more frequent in the upper extremity. There was an independent effect of severe upper extremity paresis (OR 22, CI 3.9–125) and age below 65 years (OR 9.5, CI 1.5–60). The prevalence of stroke-related pain was 21% after one year. Stroke-related pain was associated with paresis (OR 3.1, 95% CI 1.2–7.7), sensory disturbance (OR 3.1, 95% CI 1.1–8.9) and depression (OR 4.1, 95% CI 1.4–13), but not with spasticity as an independent variable. The majority of the direct costs for one year (78%) were associated with hospitalization, whereas 20% was associated with municipality services. Only 1% of all direct costs were related to primary health care and 1% to medication. The mean (median, inter-quartile range) direct cost for stroke patients with spasticity was PPP$ 84 195 (72 116, 53 707) compared to PPP$ 21 842 (12 385, 17 484) for stroke patients without spasticity (P < 0.001).

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Takeno, Katsumi. "Neuromuscular Function of the Shoulder Girdle and Upper Extremity Muscles in Individuals with Glenohumeral Labral Repair." University of Toledo / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=toledo1596111099423871.

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Parodi, Livia. "Identification of genetic modifiers in Hereditary Spastic Paraplegias due to SPAST/SPG4 mutations Spastic paraplegia due to SPAST mutations is modified by the underlying mutation and sex Hereditary spastic paraplegia: More than an upper motor neuron disease." Thesis, Sorbonne université, 2019. http://www.theses.fr/2019SORUS317.

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Les Paraplégies Spastiques Héréditaires (PSHs) sont un groupe de maladies neurodégénératives rares qui surviennent suite à la dégénérescence progressive des voies corticospinales, entraînant une spasticité des membres inférieurs, signe distinctif de la pathologie. Elles se caractérisent par une extrême hétérogénéité qui concerne à la fois les facteurs génétiques et cliniques, ainsi que d’autres aspects de la maladie, tels que l’âge d’apparition et la sévérité des signes. Cette variabilité est typiquement observée chez les patients porteurs de mutations pathogènes dans SPAST, le gène le plus fréquemment muté dans les PSHs. Après avoir réuni une cohorte de 842 patients mutés dans SPAST, nous avons utilisé une combinaison de différentes approches de Séquençage de Nouvelle Génération (NGS) afin de mieux comprendre les causes de l’hétérogénéité observée chez les patients, afin d’identifier des facteurs génétiques responsables de variations de l’âge au début de la maladie. Les données résultantes du génotypage de l’ensemble du génome ont ainsi été utilisées pour effectuer des analyses d’association et de liaison qui, combinées aux données de séquençage de l’ARN, ont permis d’identifier différents variantes/gènes candidats, potentiellement impliqués comme facteurs modificateurs de l’âge de début des SPAST-PSHs<br>Hereditary Spastic Paraplegias (HSPs) are a group of rare, inherited, neurodegenerative disorders that arise following the progressive degeneration of the corticospinal tracts, leading to lower limbs spasticity, the disorder hallmark. HSPs are characterized by an extreme heterogeneity that encompasses both genetic and clinical features, extending to additional disorder’s features, such as age of onset and severity. This phenotypic variability is typically observed among HSP patients carrying pathogenic mutations in SPAST, the most frequently mutated HSP causative gene. After assembling a cohort of 842 SPAST-HSP patients, a combination of different Next Generation Sequencing approaches was used to dig deeper into the causes of the observed heterogeneity, especially focusing on the identification of age of onset genetic modifiers. Sequencing data resulting from Whole Genome Genotyping were used to perform both association and linkage analysis that, combined with RNA sequencing expression data, allowed to identify different candidate variants/genes, potentially acting as SPAST-HSP age of onset modifiers

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Stewart, Heather G. "Amyotrophic lateral sclerosis (ALS) associated with superoxide dismutase 1 (SOD1) mutations in British Columbia, Canada : clinical, neurophysiological and neuropathological features." Doctoral thesis, Umeå : Dept. of Pharmacology and Clinical Neurosciences, Umeå University, 2005. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-638.

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Books on the topic "Upper motor neuron lesion"

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Shaibani, Aziz. Hyperreflexia. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199898152.003.0018.

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Hyperactive deep tendon reflexes area sign of upper motor neuron lesion. They are also commonly seen in normal but tense people. Proper technique of reflexes examination and experience play a major role in eliciting and categorizing deep tendon reflexes. Clonus is the highest degree of hyperreflexia. The most important neuromuscular disease associated with hyperreflexia is ALS due to degeneration of the cortical motor neurons. Diagnostic difficulty occurs when hyperreflexia and spasticity are the only findings. In these cases, PLS, HSP, and other causes of myelopathies should be entertained. Jaw clonus often indicates a lesion above the midpontine level. When hyperreflexia is found, it is wise to look for other features of upper motor neuron dysfunction such as positive Babiniski signs and hypertonia.

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Sandbrink, Friedhelm. The MEP in clinical neurodiagnosis. Edited by Charles M. Epstein, Eric M. Wassermann, and Ulf Ziemann. Oxford University Press, 2012. http://dx.doi.org/10.1093/oxfordhb/9780198568926.013.0019.

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This article gives information on the clinical application of motor-evoked potential (MEP). Transcranial stimulation of the cerebral cortex to elicit MEPs is a noninvasive method for assessing the integrity of the central motor pathway function. Transcranial magnetic stimulation (TMS) is used in diagnosing and monitoring neurological disorders. This article highlights the neurophysiological differences between TMS and transcranial electric stimulation. All the different MEP parameters that can be measured by TMS, the latency of the MEP is generally regarded as the most reliable and useful. TMS studies have been described in many neurological disorders. The sensitivity of TMS in detecting subclinical upper motor neuron lesion varies in different disorders, depending on number of muscles and different parameters used. This article talks about the application of MEP in pathophysiology, multiple sclerosis, motor neuron diseases, meyloptahy, cerebral infarction, movement disorders, epilepsy, Lumbar spinal stenosis and radiculopathies, peripheral nerve disorders etc.

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Katumbay, Desire Tshala. On the Site of the Lesion in Konzo: Clinical and Neurophysiological Studies on a Non-Progressive Upper Motor Neuron Disorder (Comprehensive Summaries of ... from the Faculty of Medicine, 1092). Uppsala Universitet, 2001.

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Shaibani, Aziz. Hyperreflexia. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190661304.003.0018.

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Hyperactive deep tendon reflexes (DTRs) is a sign of upper motor neuron (UMN) lesions. It is also commonly seen in normal but anxious people. The proper technique of deep tendon reflex examination and experience play a major role in eliciting and categorizing DTRs. Sustained clonus is the highest degree of hyperreflexia. The most important neuromuscular disease associated with hyperreflexia is amyotrophic lateral sclerosis (ALS) due to degeneration of the cortical motor neurons. Diagnostic difficulty occurs when hyperreflexia and spasticity are the only findings. In these cases, primary lateral sclerosis (PLS), hereditary spastic paraplegia (HSP), and other causes of myelopathies should be entertained. Compressive myelopathies are easily excludable by neuroimaging.

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Fink, John K. Upper Motor Neuron Disorders. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0031.

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Symptomatic disturbance of corticospinal and corticobulbar tracts (collectively, the upper motor neuron UMN) occurs in innumerable acquired central nervous system disorders including the consequences of trauma, hypoxia-ischemia, inflammation (e.g. multiple sclerosis), toxins (e.g. thiocyanate1 and specific organophosphorus compound toxicity2) and deficiencies (e.g. hypocupremia3 and vitamin B12 deficiency). Variable degrees of UMN disturbance frequently accompany degenerative disorders in which disturbance of another neurologic system results in the primary clinical. Neuropathologic studies have shown prominent axon degeneration involving corticospinal tracts (HSP and PLS) and corticobulbar tracts (PLS); and mildly affecting dorsal columns (HSP and PLS to some degree). Myelin loss is considered secondary to axon degeneration. Loss of cortical motor neurons is observed in PLS. Anterior horn cells are typically spared in both HSP and PLS. Presently, treatment for HSP and PLS is symptomatic and includes physical therapy and spasticity reducing medications.

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Shaibani, Aziz. Muscle Stiffness and Cramps. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199898152.003.0020.

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Muscle stiffness is a nonspecific term meaning limited muscle mobility that is not due to weakness. It is opposite to flexibility. Muscle and joint pain may be described as stiffness. Painful sustained muscle cramps are usually associated with muscle stiffness. A careful history is paramount. Exercise-induced muscle cramps are usually myopathic (metabolic or mitochondrial myopathy), while resting and nocturnal cramps are neurogenic (neuropathy, motor neuron disease, etc). Metabolic cramps are electrically silent. Focal or generalized stiffness is typically seen in stiff person syndrome. Upper motor neuron lesions are associated with spasticity and stiffness (HSP, PLS, myelopathies, etc.). Painful cramps and fasciculations are important clues to peripheral nerve hyperexcitability disorder, which may also present with neuromyotonia. Not unusually, no cause is found for muscle cramps and stiffness. Symptomatic treatment frequently helps.

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Shaibani, Aziz. Muscle Stiffness and Cramps. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190661304.003.0020.

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Muscle stiffness as a nonspecific term means limited muscle mobility. Muscle and joint pain may be described as stiffness. Painful, sustained muscle cramps are usually associated with muscle stiffness. A careful history is paramount. Exercise-induced muscle cramps are usually myopathic (metabolic or mitochondrial myopathy) while resting, and nocturnal cramps are neurogenic [neuropathy, motor neuron disease (MND), etc.]. Metabolic cramps are electrically silent. Focal or generalized stiffness is typically seen in stiff person syndrome (SPS). Upper motor neuron (UMN) lesions are associated with spasticity and stiffness [hereditary spastic paraplegia (HSP), primary lateral sclerosis (PLS), myelopathies, etc.]. Painful cramps and fasciculation are important clues to peripheral nerve hyperexcitability disorder, which may also present with neuromyotonia. Not unusually, no cause is found for muscle cramps and stiffness. Symptomatic treatment frequently helps.

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R, Dimitrijevic Milan, and Eccles, John C. Sir, 1903-, eds. Upper motor neuron functions and dysfunctions. Karger, 1985.

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(Editor), John Eccles, and Milan R. Dimitrijevic (Editor), eds. Upper Motor Neuron Functions and Dysfunctions. S. Karger AG (Switzerland), 1985.

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Turner, Martin R. Motor neuron disease. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0232.

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Motor neuron disease (MND) is characterized by progressive muscular weakness due to simultaneous degeneration of lower and upper motor neurons (L/UMNs). Involvement of LMNs, arising from the anterior horns of the spinal cord and brainstem, leads to secondary wasting as a result of muscle denervation. Involvement of the UMNs of the motor cortex and corticospinal tract results in spasticity. In ~85% of cases, there is clear clinical involvement of both, and the condition is termed ‘amyotrophic lateral sclerosis’ (ALS; a term often used synonymously with MND). In ~13% of cases, there may be only LMN signs apparent, in which case the condition is termed ‘progressive muscular atrophy’, although such cases have a natural history that is to largely identical to that of ALS. In a very small group of patients (~2%), there are only UMN signs for at least the first 4 years, in which case the condition is termed ‘primary lateral sclerosis’; such cases have a uniformly slower progression. There is clinical, neuropathological, and genetic overlap between MND and some forms of frontotemporal dementia.

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Book chapters on the topic "Upper motor neuron lesion"

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van der Linden, Marietta L., and Thomas H. Mercer. "Functional Electrical Stimulation to Treat Foot Drop as a Result of an Upper Motor Neuron Lesion." In Electroceuticals. Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-28612-9_11.

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Murdoch, B. E. "Dysarthria associated with upper and lower motor neurone lesions." In Acquired Speech and Language Disorders. Springer US, 1990. http://dx.doi.org/10.1007/978-1-4899-3458-1_8.

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Truong, Hong, and Ahmad H. Bani Hani. "Neurogenic Bladder in Cerebral Palsy: Upper Motor Neuron." In Cerebral Palsy. Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-319-74558-9_57.

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Truong, Hong, and Ahmad H. Bani Hani. "Neurogenic Bladder in Cerebral Palsy: Upper Motor Neuron." In Cerebral Palsy. Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-50592-3_57-1.

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Trontelj, J. V., J. M. Fernandez, M. Mihelin, and D. Rugelj. "The Function of Neuromuscular Junction in Upper Motor Neuron Weakness." In Neuroprosthetics: from Basic Research to Clinical Applications. Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-80211-9_16.

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Vieira, Andre Schwambach, Alexandre Cesar Santos de Rezende, and Fabio Rogerio. "Evaluating Motor Neuron Death in Neonatal Rats Subjected to Sciatic Nerve Lesion." In Neurotrophic Factors. Humana Press, 2012. http://dx.doi.org/10.1007/978-1-61779-536-7_32.

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Khanorkar, Sudha. "Upper Motor Neuron Lesion, Lower Motor Neuron Lesion and Internal Capsule." In Insights in Physiology. Jaypee Brothers Medical Publishers (P) Ltd., 2012. http://dx.doi.org/10.5005/jp/books/11552_105.

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Devereaux, M., B. Katirji, and R. Daroff. "Upper Motor Neuron Lesions." In Encyclopedia of the Neurological Sciences. Elsevier, 2014. http://dx.doi.org/10.1016/b978-0-12-385157-4.01183-0.

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Daroff, Robert B. "Upper Motor Neuron Lesions." In Encyclopedia of the Neurological Sciences. Elsevier, 2003. http://dx.doi.org/10.1016/b0-12-226870-9/00774-7.

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Christofi, Gerry, and Guy Leschziner. "Neurology." In The Pocketbook for PACES. Oxford University Press, 2012. http://dx.doi.org/10.1093/oso/9780199574186.003.0014.

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The neurology section of the PACES examination is often the major cause of (unnecessary!) anxiety for MRCP candidates. The key is to approach the patient in a logical fashion. Some neurology cases are simply an exercise in pattern recognition – noticing the frontal balding and ptosis of myotonic dystrophy, the distal wasting and pes cavus of Charcot–Marie–Tooth disease, for example. However, in those cases without obvious clues to the underlying diagnosis, a clear systematic approach will usually pay dividends. When faced with a neurological problem, the first question that should be posed is the site of the lesion. During the course of the examination, identify signs that might help in localization: • Cortex: signs of dysfunction of higher cognitive function. • Subcortical: upper motor neuron (UMN) signs (hypertonia, pyramidal pattern of weakness, hyper-reflexia, extensor plantars), slowness of thought. • Basal ganglia: cogwheel rigidity, resting tremor, bradykinesia, postural instability, dyskinesias, dystonias. • Brainstem: cranial nerve abnormalities with contralateral UMN signs. • Cerebellum: gait ataxia, nystagmus, finger-nose ataxia, past-pointing. • Spinal cord: bilateral UMN signs, presence of a sensory level. • Nerve root: lower motor neuron (LMN) signs (wasting, weakness, hyporeflexia, sensory loss) in a myotomal or dermatomal distribution. • Single or multiple nerve/plexus: LMN signs that are focal, and are not consistent with a nerve root lesion. • Polyneuropathy: LMN signs, more pronounced distally, affecting the legs more than the hands, diminished reflexes, sensory signs. • Neuromuscular junction: weakness without sensory involvement or significant wasting, usually but not invariably proximal, which fluctuates (either with time of day or during the course of the examination). • Muscle: wasting and weakness with normal reflexes and sensation. Once the lesion has been localized, consider the disease processes that commonly affect that site. Clues may be obtained from the history, if you are permitted to ask questions. The most helpful aspect of the history is usually the speed of onset: • Seconds: electrical disturbance (i.e. epilepsy), trauma. • <5 minutes: infarction. • > 5 minutes: migraine, haemorrhage. • Minutes–hours: infection, inflammation, drugs. • Hours–days: infection, inflammation, nutritional, drugs.

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Conference papers on the topic "Upper motor neuron lesion"

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Song, Seung Yun, Yinan Pei, Jiahui Liang, and Elizabeth T. Hsiao-Wecksler. "Design of a Portable Position, Velocity, and Resistance Meter (PVRM) for Convenient Clinical Evaluation of Spasticity or Rigidity." In 2017 Design of Medical Devices Conference. American Society of Mechanical Engineers, 2017. http://dx.doi.org/10.1115/dmd2017-3503.

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Spasticity is a common consequence of the upper motor neuron syndrome and usually associated with brain lesion, stroke, cerebral palsy, spinal cord injury, and etc. On the other hand, rigidity is a neuromuscular disorder often found in Parkinson’s disease patients. Both of spasticity and rigidity are characterized by abnormal hypertonic muscle behaviors that will cause discomfort and hinder daily activities. Worldwide, the estimated affected population of spasticity is around 12 million [1], and rigidity affects more than 10 million people [2]. Clinical evaluation of spasticity or rigidity involves personal assessment using qualitative scales, such as the Modified Ashworth Scale (MAS) or Modified Tardieu Scale (MTS) for spasticity and Unified Parkinson’s Disease Rating Scale (UPDRS) for rigidity. However, this evaluation method heavily relies on the rater’s personal experience/interpretation and usually results in poor consistency and low reliability. The goal of this design was to develop a quantitative measurement device that can be used to assist clinical evaluation of spasticity or rigidity. This portable device, the Position, Velocity, and Resistance Meter (PVRM), can be strapped around a patient’s limb to measure angular position, angular velocity and muscle resistance of a given joint while the patient’s limb is passively stretched by the clinician. Acquiring this quantitative data from patients will not only allow clinicians to make more reliable assessments but also help researchers gain additional insights into the quantification of spasticity and rigidity.

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Hasselholt, Stine. "Upper motor neuron effects in a genetic model of amyotrophic lateral sclerosis." In European Microscopy Congress 2020. Royal Microscopical Society, 2021. http://dx.doi.org/10.22443/rms.emc2020.932.

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McGee, Michael, and Said Shakerin. "Leg Stretcher for Rehabilitation." In ASME 2004 International Mechanical Engineering Congress and Exposition. ASMEDC, 2004. http://dx.doi.org/10.1115/imece2004-60258.

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To alleviate some of the problems associated with upper motor neuron diseases, passive movement and stretching are often prescribed. However, the patient has to make continual and frequent visits to a physical therapist, which is expensive and inconvenient. Therefore, there is a need for devices by which the patient can self-administer some of the prescribed exercise(s) at home. In this paper, the design of a portable unit for self-administered stretching of thigh muscles is presented.

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Viscuso, Stefano, Lorenzo Garavaglia, and Simone Pittaccio. "A Neuro-Mechanical Model Comparing Traditional and Pseudoelastic Splinting of Spastic Joints." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80240.

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Neuromuscular rehabilitation of patients with upper motor neuron syndromes (traumatic brain injury - TBI, stroke, cerebral palsy…) is based on multidisciplinary approaches aiming at preventing or contrasting the detrimental sequelae of paresis, contracture and spasticity. Due to the large individual variability of patients’ conditions and impairments it is generally difficult to have a quantitative grasp of the appropriate line of action to prescribe bracing in the most effective manner. This is an even more complex task when testing new therapeutic principles and using non-standardized devices. To this end, it is important to evaluate both instantaneous interaction (orthosis compliance to patient’s movement, localized pressure on the skin, reflex responses, etc.) and mid-long term evolution of the ill-posture (resting angle, reflex adaptation, range of motion, etc.). Accordingly, the current paper presents a model devised to investigate the interaction between the human body and two main types of othotic devices: traditional and pseudoelastic Ni-Ti based orthoses. The two devices represent different approaches to repositioning: traditional braces impose a joint angle and expect plastic relaxation, while pseudoelastic splints promote a plastic creep of tissues towards a more physiological posture without forcing the joints into any particular position. This idea has already been described in previous work [1] and ad-hoc devices have been constructed [2]. The focus here is on possible application scenarios.

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