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Neuroanatomy
Published in Helen Butler, Neel Sharma, Tiago Villanueva, Student Success in Anatomy - SBAs and EMQs, 2022
26 The following are all signs of a lower motor neuron lesion EXCEPT: WastingHypotoniaHyperreflexiaWeaknessFasciculations
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
If the lesion is of the lower motor neurone type, there is total involvement of the ipsilateral facial muscles. A lower motor neurone lesion may result from lesions at any point between the origin of the nerve from the nucleus right through to the site of supply, i.e. facial muscles (see above). Bilateral symmetrical weakness of the facial muscles is produced by muscle dystrophies such as myasthaenia gravis and myotonic dystrophy.
The neurological examination
Published in Michael Y. Wang, Andrea L. Strayer, Odette A. Harris, Cathy M. Rosenberg, Praveen V. Mummaneni, Handbook of Neurosurgery, Neurology, and Spinal Medicine for Nurses and Advanced Practice Health Professionals, 2017
Power: Assessed by testing the strength of movement at a single joint. Movements chosen should be able to help differentiate upper from lower motor neuron lesions. They should be innervated by a single spinal root and peripheral nerve, in order to identify the affected nerve and the site of the injury.
Split phenomenon of antagonistic muscle groups in amyotrophic lateral sclerosis: relative preservation of flexor muscles
Published in Neurological Research, 2021
Jingwen Liu, Zhili Wang, Dongchao Shen, Xunzhe Yang, Mingsheng Liu, Liying Cui
In the present study, we analyzed the correlation between multiple clinical factors and split phenomena, including the pyramidal tract. However, this pattern was not associated with pyramidal tract lesions. Notably, upper and lower motor neuron lesions exist simultaneously in ALS patients, leading to UMN lesions that are masked by LMN symptoms, resulting in UMN signs that are difficult to identify. However, these patients probably still have pyramidal tract impairment occurring, pathologically. Undoubtedly, this condition confuses the ability to discern the relevance of pyramidal tract lesions and split phenomena. Also, we observed that age-at-onset, gender, disease duration, and the region of onset did not present any definitive and consistent influence on the split phenomena in any of the antagonistic muscle groups.
Clinical utility of the modified trunk impairment scale for stroke survivors
Published in Disability and Rehabilitation, 2018
YunBok Lee, SeungHeon An, GyuChang Lee
This was a cross-sectional study of chronic stroke survivors and healthy adults. Inpatient stroke survivors were recruited through advertisements in a rehabilitation hospital and screened according to their ability to stand up independently from a chair, without using both hands and their ability to walk 10 m without assistance. Patients with musculoskeletal, neurological, or upper or lower motor neuron lesions, except those patients where the conditions were associated with stroke, were excluded to minimize the variability that can influence trunk control examinations. In total, 67 stroke survivors participated; of them, the data of 55 subjects were collected since seven subjects were excluded owing to inappropriate criteria and five were excluded because of hospital discharge or worsening health during the experiment. The mean age of the stroke survivors was 60 years (standard deviation: 2.52 years; range, 57–65 years). Healthy adults were also recruited through advertisements in a rehabilitation hospital and age- and sex-matched with the stroke subjects. Each met the criterion of being a healthy subject without musculoskeletal or lower motor neuron lesions. The data of 29 healthy adults were collected. The mean age of the healthy adults was 61 years (standard deviation, 2.73 years; range, 57–67 years).
Paraneoplastic Ophthalmoplegia as the Presenting Sign of Paediatric Glioblastoma Multiforme: A Case Report
Published in Neuro-Ophthalmology, 2021
Arjan S. Dhoot, Caroline Just, Lulu LCD Bursztyn
Our patient presented with lid retraction and bilateral ophthalmoplegia without significant ptosis that could not be localised. Only 7 months later was the diagnosis of GBM discovered. We propose that the aetiology for the abnormal eye movements was a paraneoplastic phenomenon, despite the absence of known paraneoplastic antibodies. Paraneoplastic syndromes have rarely been described in primary brain tumours,1,9 including a case report of Guillain-Barré syndrome (GBS) in a patient undergoing chemotherapy for GBM.11 As well, in a study of 33 patients with primary brain tumours, including 15 with GBM, abnormalities were detected in both sensory and motor peripheral nerves compared with controls, but no antineuronal antibodies were found.9 Our patient’s extra-ocular movement abnormalities were consistent with patchy involvement of his cranial nerves, suggestive of an inflammatory aetiology rather than neoplastic invasion. Furthermore, he presented with signs and symptoms consistent with lower motor neuron lesions, including facial weakness, limb weakness, and sensory ataxia. This diffuse and patchy constellation of findings is reminiscent of a GBS-type syndrome,19 which has previously been reported to occur in the context of GBM. We therefore propose that our patient developed ophthalmoplegia as the result of a yet uncharacterised antibody against peripheral motor nerves. This case illustrates that ophthalmoplegia, as a paraneoplastic phenomenon, may present prior to radiological evidence of GBM and this presentation should prompt a clinician to consider GBM in their differential diagnosis.