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Motor Neurological Examination of the Hand and Upper Limb
Published in J. Terrence Jose Jerome, Clinical Examination of the Hand, 2022
This ability of the muscles to function, based on their neurological supply, can be compromised in two situations: Upper motor neuron lesions and the lower motor neuron lesions. The upper motor neuron lesion involves any part of the upper motor neuronal pathway and the lower motor neuron lesion involves any part of the lower motor neuronal pathway.
Diseases of the Peripheral Nerve and Mononeuropathies
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Diana Mnatsakanova, Charles K. Abrams
Neurogenic: Upper motor neuron lesion.Spinal muscular atrophy: often have weakness in intrinsic hand muscles as well.C7 radiculopathy.
7th Cranial Nerve (Facial) Palsy
Published in K. Gupta, P. Carmichael, A. Zumla, 100 Short Cases for the MRCP, 2020
K. Gupta, P. Carmichael, A. Zumla
The facial nerve (7th cranial nerve) supplies the muscles of facial expression, the stapedius muscle, and is responsible for the taste sensation from the anterior two-thirds of the tongue. Parasympathetic motor fibres to the salivary glands and chorda tympani are also carried with the facial nerve. Since a minor degree of facial asymmetry is not uncommon, one should not jump into making a diagnosis of facial nerve palsy without a thorough examination revealing the presence of definitive physical signs. The most common cause for an upper motor neurone lesion is a stroke that is characterized by weakness of the lower face contralateral to the lesion. The upper face is spared because of the bilateral innervation.
Prevalence of upper-limb spasticity and its impact on care among nursing home residents with prior stroke
Published in Disability and Rehabilitation, 2020
Christine T. Shiner, Angela Vratsistas-Curto, Valerie Bramah, Steven G. Faux, Yuriko Watanabe
Spasticity is a well-known consequence of upper motor neuron lesions such as stroke. It is defined as a “motor disorder characterised by a velocity-dependent increase in tonic stretch reflexes (muscle tone) with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex” [1]. Typically this manifests as hypertonia and increased resistance to passive movement [2]. Spasticity can contribute to post-stroke disability by impairing motor performance and complicating the performance of functional tasks, such as dressing, eating, grooming and maintaining limb hygiene [2,3]. It can also cause pain [4] and result in secondary complications including contracture, joint deformity, and pressure injuries [2,3]. Stroke survivors with spasticity report lower health-related quality of life than those unaffected by spasticity [5,6]. Economic evaluations have suggested that the direct costs of stroke are four-fold higher for stroke survivors with spasticity compared to those without [7]. Substantial indirect costs associated with productivity losses and a high caregiver burden have also been identified [8,9]. Disabling spasticity appears to be more common in the upper versus lower limb following stroke [3,10].
Effect of oral baclofen on spasticity poststroke: responders versus non-responders
Published in Topics in Stroke Rehabilitation, 2018
Shiho Mizuno, Kotaro Takeda, Shinichiro Maeshima, Sonoda Shigeru
Clonus and increased muscle tone during fast stretch are both positive signs for an upper motor neuron lesion. The mechanism of increased muscle tone during fast stretch is summarized below. Stretch of the extrafusal muscle fiber is detected by the muscle spindle and transmitted to the central nervous system by Ia afferents that project through the dorsal roots and make connections with the α motor neurons in the spinal cord. The α-motor neurons also receive input from the upper motor neurons. After upper motor neuron lesion, a net loss of inhibition impairs the descending control over the attached α-motor neurons. Additionally, loss of inhibitory control over the interneuronal pathways in the spinal cord also occurs. Thus, increased signals are passed to the α-motor neuron, leading to excessive muscle contraction.22
Potential contributing factors to upper limb associated reactions in people with acquired brain injury: an exploratory study
Published in Disability and Rehabilitation, 2022
Michelle B. Kahn, Ross A. Clark, Benjamin F. Mentiplay, Kelly J. Bower, John Olver, Gavin Williams
The demographic data for the 42 participants are presented in Table 1. All participants had a stable non-progressive upper motor neuron lesion with an apparent hemiplegia. Where any bilateral deficits were present, the hemiplegic upper limb was evaluated. Most data were normally distributed, except for the outcome measure scales (Arm Activity Measures A and B, Short Form Berg Balance Scale, Short Falls Efficacy Scale International, Hospital Anxiety and Depression Scale) which therefore underwent non-parametric correlation analyses. All KDSw scores were normally distributed, therefore, parametric analyses were used for between-group differences.