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Neurological Disease
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
Mononeuropathy (dysfunction of a single peripheral nerve) is usually caused by local compression or trauma, but there may be increased vulnerability to such lesions because of an otherwise subclinical generalized neuropathy. Most commonly involved sites are the median nerve at the wrist (carpal tunnel syndrome); the ulnar nerve at the elbow; the common peroneal nerve at the fibular head; and the lateral cutaneous nerve of the thigh (meralgia paraesthetica). Carpal tunnel syndrome is common, and causes pain in the hand, especially at night, which may be relieved by rubbing or shaking the hand. There can be sensory loss in the lateral side of the hand and weakness and wasting of the thenar eminence muscles (abductor pollicis brevis, opponens pollicis, flexor pollicis brevis). Carpal tunnel syndrome is more common in pregnancy, hypothyroidism, rheumatoid arthritis and acromegaly.
The nervous system and the eye
Published in C. Simon Herrington, Muir's Textbook of Pathology, 2020
James A.R. Nicoll, William Stewart, Fiona Roberts
Trauma with fractures, compression, and entrapment are common causes of a mononeuropathy. There is also an association with certain systemic diseases, including diabetes mellitus, vasculitis, sarcoidosis and leprosy. Commonly affected sites are the nerve roots compressed in intervertebral foramina of the spine by intervertebral disc prolapse or osteophytes, the median nerve in the carpal tunnel at the wrist, the ulnar nerve in the flexor carpal tunnel at the elbow, and the common peroneal nerve at the neck of the fibula. The nerve distal to the site of injury undergoes axonal (Wallerian) degeneration.
Nerve and Retinal Changes in Experimental Diabetes
Published in John H. McNeill, Experimental Models of Diabetes, 2018
Diabetic neuropathy can be broadly classfied as mononeuropathy or polyneuropathy. Mononeuropathies can involve isolated single nerves or may affect multiple nerves (mononeuritis multiplex). These neuropathies may affect peripheral or cranial nerves.5,6
Systemic Lupus Erythematosus and Third Nerve Palsy: Unusual Presentation and Review of the Literature
Published in Neuro-Ophthalmology, 2022
Divya Natarajan, Mohan Kannam, M Vishnu Vardhan Reddy, Virender Sachdeva
SLE is known to have various ocular manifestations, either because of an inflammatory process or as a complication of medical therapy (corticosteroids, hydroxychloroquine).1 Fortunately, Neuro-ophthalmological manifestations are less common. Prior reports suggest eye movement abnormalities are reported in 7% to 37% of patients with established SLE.2,3 Like our report, a few authors have described mononeuropathy i.e., isolated cranial nerve palsy, either as the presenting manifestation or during the course of SLE (Table 2). All cases of isolated third nerve palsy reported were complete palsies, unlike our case which had an incomplete third nerve palsy. Our case is also unique in that the mononeuropathy was the one of her early symptoms and the diagnosis of SLE was still unestablished. Further, our patient had otherwise normal neurological examination and neuroimaging. Careful clinical examination with attention to laboratory parameters, pancytopaenia, elevated ESR, and normal neuroimaging suggested an immunological cause and prompted us to seek an immunology consultation. Further work-up established the diagnosis.
Clinical manifestations and genetic analysis of a family with neurofibromatosis type 2
Published in Acta Oto-Laryngologica, 2022
Victoria Y. Wang, Te-Yi Liu, Te-Yung Fang, Ya-Hui Chen, Chi-Jung Huang, Pa-Chun Wang
Patients with NF2 often remain asymptomatic until the second or third decades of their lives, with tinnitus, hearing impairment, and imbalance being the most common clinical manifestations (involving the eighth cranial nerve). Mononeuropathy can involve the facial nerve and 3–5% of patients can develop severe polyneuropathy [2]. Members with disease from the participating family exhibited classic otological symptoms such as hearing impairment, tinnitus, dizziness, and cataracts (Table 1), but their medical histories could only be traced back 20 years – the actual times of symptom onsets were unknown (Table 2). Lesions such as cafe-au-lait spots, cutaneous neurofibroma, axillary freckling, optic glioma, and Lisch nodules are not frequent symptoms in NF2 (as they are in NF1) [9,10], which could not be observed from this studied family. No neurogenic spinal tumor or muscle wasting was discovered in this cohort either.
Two cases of refractory eosinophilic granulomatosis with polyangiitis wherein mepolizumab was effective against pulmonary and ear lesions
Published in Modern Rheumatology Case Reports, 2021
Yusuke Ushio, Risa Wakiya, Mikiya Kato, Tomohiro Kameda, Shusaku Nakashima, Hiromi Shimada, Mai Mahmoud Fahmy Mansour, Koichi Sugihara, Takenori Miyashita, Norimitsu Kadowaki, Hiroaki Dobashi
A 49-year-old woman developed bronchial asthma at 18 years of age and sinusitis and eosinophilic otitis media (EOM) at 23 years of age. Myringotomy and tympanostomy were performed for the management of EOM. However, the patient presented repeated remissions and exacerbations of EOM. At 36 years of age, the patient presented with purpura on the forearm and lower leg. Then, she experienced numbness from the left forearm to the fingertips and from both lower legs to the toes. Hence, multiple mononeuropathy was diagnosed. Laboratory tests revealed elevated leukocyte count at 22,370/μL (eosinophil count: 12,300/μL), and the patient’s MPO-ANCA level was 190 U/mL; normal range was <3.5 U/mL). A skin biopsy for the purpura revealed necrotising vasculitis and eosinophil infiltration. Based on these findings, the patient was diagnosed with EGPA and otitis media with AAV (OMAAV) by the Japanese diagnostic criteria for AGA/CSS [3] and for OMAAV [5]. Thereafter, despite the concomitant use of various immunosuppressive drugs (CY, azathioprine, methotrexate, mycophenolate mofetil and tacrolimus) in addition to glucocorticoids, repeated remissions and relapses of OMAAV were observed. Thus, at 48 years of age, mepolizumab was initiated for managing the relapse of refractory OMAAV (Figure 3).