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Definition, Classification, Activity and Damage Indices in Systemic Lupus Erythematosus
Published in Richard K. Burt, Alberto M. Marmont, Stem Cell Therapy for Autoimmune Disease, 2019
Jennifer M. Grossman, Kenneth C. Kalunian
SELENA-SLEDAI was adapted from the SLEDAI for use in a multicenter safety study of estrogens in women with SLE; it has been validated through its prospective use in the ongoing study.27 SELENA-SLEDAI differs from SLEDAI in the definitions of some descriptors for clarification and attribution. The definition of the seizure descriptor has been expanded to exclude seizures resulting from past, irreversible central nervous system damage. Scleritis and episcleritis have been added to the definition of the visual disturbance descriptor, and vertigo has been added to the cranial nerve disorder descriptor. The cerebrovascular accident descriptor excludes hypertensive causes in SELENA-SLEDAI. The rash, alopecia, and mucosal ulcer descriptors have been modified to include ongoing presence of the descriptors, rather than the SLEDAI definitions of new or recurrent activity. The alopecia and mucosal ulcer descriptors also have been modified in SELENA-SLEDAI to attribute the manifestations to active lupus; attribution is meant to be a clinical decision. The pleurisy and pericarditis descriptors have been modified as well; rather than defining pleurisy as pleuritic chest pain with pleural rub or effusion or pleural thickening, SELENA-SLEDAI defines this descriptor as classic and severe pleuritic chest pain, pleural rub, effusion, or new pleural thickening with attribution to lupus. Pericarditis is similarly redefined; instead of pericardial pain with rub, effusion, ECG, or echocardiographic confirmation, SELENA-SLEDAI defines this descriptor as classic and severe pericardial pain, rub, effusion, or ECG confirmation. In addition, the proteinuria descriptor in SELENA-SLEDAI simplifies the SLEDAI descriptor. The SELENA-SLEDAI definition of proteinuria is the new onset or recent increase of more than 0.5 g per 24 hour, whereas the SLEDAI definition can be interpretated to include all patients with proteinuria of greater than 0.5 g per 24 hours.
Long-term pain relief at five years after medical, repeat surgical procedures or no management for recurrence of trigeminal neuralgia after microvascular decompression: analysis of a historical cohort
Published in British Journal of Neurosurgery, 2019
Daniyal J. Jafree, Joanna M. Zakrzewska
Ethical approval was given by Frenchay Hospital Bristol LREC (Project Number: 2001/60). Patients were drawn from one neurosurgeon’s entire posterior fossa surgery practice from 1982 – 2002, reported in terms of satisfaction, quality of life and used to validate and design a patient-experience assessment set.15,17 All patients who underwent MVD for primary idiopathic TN, diagnosed using the second iteration of the International Classification for Headache Disorders, were included.18 Patients were excluded: with a secondary cause of trigeminal neuralgia including malignancy or multiple sclerosis, with a concurrent cranial nerve disorder, or with a failure of their MVD. Failure was defined as incomplete pain relief after MVD, requiring medication to obtain pain relief or surgery within 3 months after initial operation. Patients who had undergone prior procedures for TN were separated from the cohort and analysed independently.
IL-6 contributes to Nav1.3 up-regulation in trigeminal nerve following chronic constriction injury
Published in Neurological Research, 2020
Ming-Xing Liu, Jun Zhong, Lei Xia, Ning-Ning Dou, Shi-Ting Li
Trigeminal neuralgia (TN) is a common hyperactive cranial nerve disorder attributable to vascular loops compression [1–3]. This etiology has been proved by the major pathological findings of axonal loss or demyelination in the compressed cranial nerve root and verified by successful microvascular decompression surgery [3–7]. However, its underlying pathogenesis has been still unclear today [8–10]. So far, it has been acceptable that the substantiality of this disorder is a sort of hyperexcitability manifested by abnormal discharges or ectopic action potentials emerged from the demyelinated trigeminal nerve following vascular compression [11–15].
Current perspectives on the diagnosis, assessment, and management of vasculitic neuropathy
Published in Expert Review of Neurotherapeutics, 2022
Yuki Fukami, Haruki Koike, Masahisa Katsuno
Mononeuritis multiplex is present in approximately 70–90% of patients with vasculitic neuropathy, while others present with symmetric or asymmetric polyneuritis [27]. Approximately 30% of patients with vasculitic neuropathy show a slow progressive course [53,54]. Muscle weakness on the affected nerves may be pronounced and may cause muscle atrophy. Deep tendon reflexes are diminished or eliminated by the affected nerves. There is a low incidence of cranial nerve disorder in systemic vasculitis, except that GPA often forms granulomas in the cranial region [43,55].