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Stroke
Published in Henry J. Woodford, Essential Geriatrics, 2022
‘Spasticity' is a term for inappropriate increases in muscular tone caused by an upper motor neuron lesion. Not only can this reduce the function of the affected area but also it may result in contracture formation and pain. Additionally, it may make dressing and personal hygiene more difficult (e.g. adequate cleaning of the palmar skin fold of a hand closed by spasticity). Appropriate joint positioning, movement and exercise, and splints or orthoses are important for limiting its development.105 It may be made worse by intercurrent illness, stress/anxiety or medication effects. Contractures are caused by shorting of the connective tissues around joints with reduced mobility. Splinting of joints, for selected people and fitted by someone appropriately trained, can reduce the formation of contractures (but won't improve function).6
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.
Modelling human neurodegeneration using induced pluripotent stem cells
Published in Christine Hauskeller, Arne Manzeschke, Anja Pichl, The Matrix of Stem Cell Research, 2019
Iryna Prots, Beate Winner, Jürgen Winkler
MND is a heterogeneous group of neurological disorders that causes rapidly progressive muscle weakness, affecting a person’s ability to walk, speak, swallow, and breathe (Worms, 2001). MND typically affects people in their mid-fifties. MND primarily attacks motor neurons, the neurons that control essential voluntary muscles of the body. Motor neurons consist of two types: the corticospinal motor neurons (or upper motor neurons) and the alpha motor neurons (or lower motor neurons). Motor neurons are responsible for the transmission of the movement commands from the motor cortex in the brain to the spinal cord (upper motor neurons), and from the spinal cord to the muscle fibres (lower motor neurons). The activation of muscle fibres by lower motor neurons leads to the contraction of the muscle, resulting in the voluntary movement of the body.
Transcranial Direct Current Stimulation of Motor Cortex Enhances Spike Performances of Professional Female Volleyball Players
Published in Journal of Motor Behavior, 2023
Seung-Bo Park, Doug Hyun Han, Junggi Hong, Jea-Woog Lee
In another aspect, although electrical stimulation was applied to the specific cortical area of M1 induced by tDCS in the present study, it might have affected adjacent areas, resulting in a somewhat more widespread area of target stimulation. This means that the premotor cortex, complex system of interconnected frontal lobe areas anterior to the primary motor cortex, s mainly responsible for motor functions. The upper motor neurons in the premotor cortex regulates motor behavior via extensive reciprocal connections with the primary motor cortex and axons projecting through the corticobulbar and corticospinal pathways that affect local circuit and lower motor neurons of the spinal cord and brainstem (Purves et al., 2001). In particular, the left dorsal premotor cortex activity is associated with complex motor coordination performance, meaning that tDCS has potential to improve visuomotor coordination (Pavlova et al., 2014). According to Tzvi et al. (2022), the cerebellum plays an essential role in the process of visuomotor adaptation. They noted that interaction with cortical structures, especially the premotor cortex, contributed mainly to this process. The cerebellum plays a central role in coordinating voluntary movements and motor skills including balance, coordination, and posture (Manto et al., 2012). These relationships suggest that activation of the premotor cortex and its interactions with the cerebellum could enhance the process of motor coordination by tDCS (Kwon et al., 2015; Tzvi et al., 2022).
A case of vertebral artery compression syndrome mimicking primary lateral sclerosis
Published in International Journal of Neuroscience, 2022
Huimin Cai, Bin Zhang, Biao Huang, Lijuan Wang, Limin Wang
A 65-year-old right-handed man with a history of hypertension was referred to our neurology department in the suspect of possible PLS by the referring neurologist. The patient presented with a 10-year history of involuntary jerk characterised by brisk extension of the left lower extremity while he was sitting. Seven years after onset, he developed intermittent painful spasms with a tendency to drag his left leg. In the preceding year, his symptoms progressed to the left upper extremity marked by brisk flexion of the elbow, causing difficulty holding objects occasionally. He reported the symptoms aggravated with higher blood pressure and attenuated with optimal blood pressure. He also noticed the symptoms were worse when he lied down. He was able to walk independently without any assistance. There was no family history of neurodegenerative diseases. Neurological examination revealed upper motor neuron signs. The patient had generalized bilateral hyperreflexia and sustained left-sided ankle myoclonus. Jaw jerk reflex and Hoffman’s sign were absent. Babinski’s sign and Chaddock’s sign were positive in the left lower limb. He had increased muscle tone in the left extremities with spasticity, but normal muscle tone in the right extremities. Subtle pyramidal weakness (Medical Research Council (MRC) grade 4+) was noted in the left extremities. Muscle atrophy, fasciculation, sensory deficits, and cerebellar signs were not detected.
Juvenile amyotrophic lateral sclerosis with complex phenotypes associated with novel SYNE1 mutations
Published in Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration, 2021
Hiroya Naruse, Hiroyuki Ishiura, Jun Mitsui, Yuji Takahashi, Takashi Matsukawa, Tatsushi Toda, Shoji Tsuji
The proband, a 15-year-old man, first visited the Department of Neurology of the University of Tokyo Hospital for the evaluation of his decreased ability to exercise. His clinical information is described in detail in the Supplemental Material. There was no apparent relationship between his parents, and his family history indicated no similar diseases. In his follow-up examination, gait disturbance gradually worsened. Neurological examinations at the age of 30 revealed upper motor neuron signs including spasticity in the lower extremities, clonic jaw reflexes, hyperreflexia in the extremities except for the ankles, bilateral patellar clonus, and Babinski and Chaddock signs, and lower motor neuron signs including distal-dominant muscle weakness in extremities and atrophy of intrinsic muscles of the hands. Dysarthria, dysphagia, limb ataxia, fine tremor in hands, and pes cavus were also noted as observed earlier. Notably, mild cognitive decline was additionally revealed. He was diagnosed with juvenile ALS, and weakness of extremities, limb ataxia, dysarthria, and respiratory disturbance due to restrictive ventilation impairment gradually worsened. He died of respiratory failure at the age of 39.