Myasthenia gravis is an autoimmune neurological disorder caused by autoantibodies against the acetylcholine receptor or against a receptor-associated protein, muscle-specific tyrosine kinase (MuSK-Ab).
The autoimmune attack at the muscle endplate leads to failure of neuromuscular transmission and eventually muscle weakness.
In the active phase of the disease, symptoms typically fluctuates and then become severe; myasthenic crisis occur in this phase.
In the stable/inactive phase, symptoms are stable but still persist; it usually worsen attributable to infection, fatigue, tapering of medications or other identifiable factors.
In the burnt-out phase, remission may occur wherein patients are on immunotherapy and symptom-free, or may even be off medications.
In 15-20 years, if the symptoms left untreated, patient's weakness becomes fixed wherein the most severely affected muscles become atrophic.
Combination therapy with alendronate plus alfacalcidol appears to produce significant increases in bone mineral density (BMD) and reductions in bone turnover biomarker levels, and to lower the rate of hypercalciuria in myasthenia gravis patients who initiated treatment with glucocorticoids, according to a study.
Long‐term treatment with perampanel in the adjunctive setting appears to provide improved seizure control without raising new safety/tolerability signals in patients with epilepsy, particularly those with secondarily generalized seizures at baseline, according to the results of an open-label extension of phase III trials.
High rather than low levels of neonatal 25(OH)D3 pose an increased risk of incident epilepsy in early childhood, a finding that may be attributed to chance, confounding, or late gestational vitamin D exposure, according to a study.
In the treatment of idiopathic generalized epilepsy, switching from valproate to other antiepileptic drugs due to potential childbearing issues may prove detrimental, heightening the risk of poor seizure control, as shown in a recent study.