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Neurological Disease
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
The diagnostic criteria for MS are established by a committee of experts and are subject to change. Diagnosis is based on history of typical demyelinating events, objective clinical evidence of impairment, and MRI and CSF findings. Confusingly, they come with the caveat that they are not intended to discriminate between MS and other conditions, but rather to stratify patients into those at high or low risk of recurrence, once other diagnoses have been considered unlikely.
Reconstruction
Published in Karl H. Pang, Nadir I. Osman, James W.F. Catto, Christopher R. Chapple, Basic Urological Sciences, 2021
Nadir I. Osman, Karl H. Pang, Christopher R. Chapple
Ileal resection results in:Malabsorption of bile salts (diarrhoea and reduced absorption of vitamins A, D, E, K), fat, vitamin B12.Vitamin B12 deficiency takes >5 years to manifest:Increased risk if >50 cm of terminal ileum is resected.Macrocytic anaemia.Demyelination − neurological complications.Hyperpigmentation.Tongue/mouth inflammation.Gastrointestinal symptoms.Cholesterol gallstones.
The patient with acute neurological problems
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
Demyelination describes the loss or destruction of myelin. Rapid shifts in serum sodium can cause CNS demyelination and neurological injury with symptoms similar to hypoxic brain injury. Abnormal serum sodium levels must be corrected slowly, at a rate not exceeding 5mmol/L per day. CNS demyelination is a side effect of some chemotherapy regimens. Inflammatory demyelinating diseases also occur and form part of a group of diseases called polyneuropathies, for example multiple sclerosis (MS) and Guillain-Barré syndrome (GBS).
Neuro-Ophthalmic Literature Review
Published in Neuro-Ophthalmology, 2022
David A. Bellows, John J. Chen, Hui-Chen Cheng, Panitha Jindahra, Peter W. MacIntosh, Collin McClelland, Michael S. Vaphiades, Xiaojun Zhang
Tumour necrosis factor (TNF)-alpha inhibitors are biological agents which are Federal Drug Administration-approved to treat ankylosing spondylitis, Crohn’s disease, hidradenitis suppurativa, juvenile idiopathic arthritis, plaque psoriasis, polyarticular juvenile idiopathic arthritis, psoriatic arthritis, rheumatoid arthritis, ulcerative colitis, and uveitis. There are also several off-label indications. Testing for active/latent tuberculosis and viral hepatitis B and C should occur before initiating anti-TNF agents. Serious infections are significant and concerning adverse effects, including bacterial, fungal, viral, or atypical infections. The risk of malignancies, especially lymphomas, has been an area of concern because anti-TNF agents may decrease the host defence mechanisms against malignancy by inhibiting TNF. Clinicians should monitor patients for signs of infection before, during, and after treatment. Complete blood counts and liver function tests are necessary at baseline and should be monitored closely at least every 3 to 6 months. There are several reported cases of demyelinating disorders, including optic neuritis, multiple sclerosis (including exacerbation of underlying multiple sclerosis), myelitis, encephalitis, Guillain-Barré syndrome, transverse myelitis, and chronic inflammatory demyelinating polyradiculoneuropathy, in patients taking anti-TNF agents. Anti-TNF agents should be avoided or used with extreme caution in patients with an underlying demyelinating disorder.
Miller Fisher syndrome and Guillain-Barré syndrome: dual intervention rehabilitation of a complex patient case
Published in Physiotherapy Theory and Practice, 2022
Jill E. Mayer, Christine A. McNamara, John Mayer
Written patient consent was received by the authors to present his case and findings. The patient was a 57-year-old male, 1.98-m tall and approximately 105 kg in good physical health who exercised 5 days per week. He was married, had 3 children in college and worked full time as an emergency room physician. Past medical history was significant for migraines, borderline hypertension, shingles, and Gilbert’s syndrome. He sustained a traumatic left quadriceps tear from a fall and subsequently developed complex regional pain syndrome (CRPS). Over the next 5 weeks, he experienced evolving sensory, motor and CN dysfunction with reports of ataxia, difficulty swallowing, repeated falls, diplopia, areflexia, and respiratory distress. The rapid symptom progression, along with abnormal nerve conduction studies, raised concern for possible demyelination and required emergent hospital admission. Subsequently, he was diagnosed with a complex presentation consisting of GBS with overlapping MFS, mild traumatic brain injury (TBI) and CRPS. Testing was not performed for the presence of anti-ganglioside antibodies which may be present in up to 58% of patients with MFS (Kaida et al, 2006). Following diagnosis, he underwent a 5-day course of IVIg treatment with minimal improvement in respiratory function and muscle strength. See Table 2 for a detailed timeline of inpatient medical events.
Regenerative replacement of neural cells for treatment of spinal cord injury
Published in Expert Opinion on Biological Therapy, 2021
William Brett McIntyre, Katarzyna Pieczonka, Mohamad Khazaei, Michael G. Fehlings
Damage and loss of oligodendrocytes after SCI leads to demyelination and disrupted saltatory conduction, which contribute to a proportion of functional deficits that are seen in individuals with SCI [126]. In order to reverse the functional consequences of demyelination, regenerative approaches have been investigated. After SCI, a degree of myelin remodeling occurs through the recruitment of endogenous progenitors such as oligodendrocyte progenitor cells (OPCs) and injury–activated ependymal cells [56,127–129]. These endogenous precursors can further be experimentally stimulated to strengthen the spontaneous response [130–133]. Notably, some studies suggest that the inherent, non-stimulated response may be sufficient. In this regard, the Tetzlaff lab has demonstrated the importance of distinguishing which axons become remyelinated during regenerative mechanisms [134]. Specifically, they have shown that the intact, functional axons that remain post-SCI become remyelinated by endogenous cells, whereas the demyelination that is seen can be attributed to the severed axons, which are no longer functional. Therefore, they suggest that the injured spinal cord does not have a population of axons remaining that would benefit from transplant-mediated remyelination [134]. Future studies should elaborate on this work by distinguishing which axons (healthy vs. nonfunctional) become remyelinated by transplanted cells.