Those who are considered at high risk following investigation may be admitted to hospital for further monitoring of the heart.Syncope affects about three to six out of every thousand people each year. It is more common in older people and females. It is the reason for one to three percent of visits to emergency departments and admissions to hospital. Up to half of women over the age of 80 and a third of medical students describe at least one event at some point in their lives. Of those presenting with syncope to an emergency department, about 4% died in the next 30 days. The risk of a poor outcome, however, depends very much on the underlying cause. Causes
Causes range from non-serious to potentially fatal. There are three broad categories of causes: heart or blood vessel related; reflex, also known as neurally mediated; and orthostatic hypotension. Issues with the heart and blood vessels are the cause in about 10% and typically the most serious while neurally mediated is the most common. There also seems to be a genetic component to syncope. A recent genetic study has identified first risk locus for syncope and collapse. The lead genetic variant, residing at chromosome 2q31.1, is an intergenic variant approximately 250 kb downstream of the ZNF804A gene. The variant effected the expression of ZNF804A, making this gene the strongest driver of the association. Neurally mediated syncope
Reflex syncope or neurally mediated syncope occurs when blood vessels expand and heart rate decreases inappropriately leading to poor blood flow to the brain.
Other tests/analysis are:
High CK levels(x10-150 times normal)
MRI can indicate different types of LGMD. EMG can confirm the myopathic characteristic of the disease. Electrocardiography (cardiac arrhythmias in LGMD1B can occur)

Types
The "LGMD D" family is autosomal dominant, and the "LGMD R" family is autosomal recessive. Limb–girdle muscular dystrophy is explained in terms of gene, locus, OMIM and type as follows:

LGMD criteria
For a disease entity to be classified as an LGMD, the following criteria must be met:
genetic, with an identifiable inheritance pattern such as autosomal dominant, autosomal recessive, digenic, or polygenic. relatively selective to skeletal muscle
predominantly proximal muscle involvement
independent walking is achieved at one point in life
elevated serum creatine kinase
muscle fiber loss
dystrophic changes in muscle histology
degenerative changes on medical imaging
end-stage pathology seen in the most affected muscles
described in at least two unrelated families

Differential
Many diseases can manifest similarly to LGMD. Dystrophinopathies, including Duchenne muscular dystrophy, Becker muscular dystrophy, and manifesting dystrophinopathy in female carriers, can present similarly to LGMD. Facioscapulohumeral muscular dystrophy can appear similarly, especially when it spares the facial muscles. Also in the differential are Emery-Dreifuss muscular dystrophies, Pompe disease, later-onset congenital myasthenic syndromes, and proximal-predominant hereditary motor neuropathies. Treatment
There are few studies corroborating the effectiveness of exercise for limb–girdle muscular dystrophy. However studies have shown that exercise can, in fact, damage muscles permanently due to intense muscle contraction. Physical therapy may be required to maintain as much muscle strength and joint flexibility as possible. Calipers may be used to maintain mobility and quality of life.