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Fibromuscular dysplasia (FMD) is a non-atherosclerotic, non-inflammatory disease of the blood vessels that causes abnormal growth within the wall of an artery. [1] FMD has been found in nearly every arterial bed in the body, although the most commonly affected are the renal and carotid arteries.
Secondary hyperaldosteronism (also hyperreninism, or hyperreninemic hyperaldosteronism) is due to overactivity of the renin–angiotensin–aldosterone system (RAAS).. The causes of secondary hyperaldosteronism are accessory renal veins, fibromuscular dysplasia, reninoma, renal tubular acidosis, nutcracker syndrome, ectopic tumors, massive ascites, left ventricular failure, and cor pulmonale.
The most common cause of arterial stenosis is atherosclerosis, however other pathologies such as fibromuscular dysplasia, dissection, trauma or external compression may occur. [2] Atherosclerotic plaque can rupture, resulting in a source of emboli. These emboli can cause TIAs or strokes in the areas of the brain supplied by the affected artery.
Symptoms of neuromuscular disease may include numbness, paresthesia, muscle atrophy, a pseudoathletic appearance, exercise intolerance, myalgia (muscle pain), fasciculations (muscle twitches), myotonia (delayed muscle relaxation), hypotonia (lack of resistance to passive movement), fixed muscle weakness (a static symptom), or premature muscle ...
Segmental Arterial Mediolysis must be differentiated from fibromuscular dysplasia, atherosclerosis, and other systemic vasculidites including polyarteritis nodosa, Takayasu's arteritis, Behcet's disease, cystic medial necrosis, and cystic adventitial artery disease. [4]
It may imitate, and is in turn imitated by, a number of other diseases that affect the blood vessels of the brain diffusely such as fibromuscular dysplasia and thrombotic thrombocytopenic purpura. [3] Primary CNS vasculitis has an incidence of 2.4 cases per 1 million people, with an associated mortality of 8-23% and a 25% risk of severe ...
Currently, while there is no cure for angiopathy, there are ways through which the symptoms can be managed. For example, therapies. Treatment options for situations of muscle weakness may include speech, occupational, or physical therapy. Medication can be used for potential seizures and memory loss. [3]
A more recent treatment for severe Raynaud's is the use of botulinum toxin. The 2009 article [37] studied 19 patients ranging in age from 15 to 72 years with severe Raynaud's phenomenon of which 16 patients (84%) reported pain reduction at rest; 13 patients reported immediate pain relief, three more had gradual pain reduction over 1–2 months ...