The diagnosis of PLMD requires a visible cause-effect relationship between PLMS and an observed sleep disturbance or daytime impairment (both disturbance and impairment have to be clinically significant).Other relevant causes of Insomnia and Hypersomnia have to be ruled out before diagnosing PLMD (most importantly anxiety, obstructive sleep apnea, and narcolepsy). Furthermore, symptoms can not be better explained by any other conditions.For the differential diagnosis it is important to differentiate PLMD from other leg movements during sleep, which are high-frequency:
alternating leg movement activity (ALMA) are very similar events and could be mistaken for PLMS
hypnagogic foot tremor (HFT) events are also very similar to PLMS and could be misdiagnosed
excessive fragmentary myoclonus (EFM) events are shorter than PLMS

Classification
PLMD is classified in the third edition of the International Classification of Sleep Disorders (ICSD-3) which presents current sleep disorders nosology. ICSD-3 is divided in 7 sections and PLMD is classified in the Sleep-Related Movement Disorders section. There are some updates from ICSD-2. The diagnosis is more strict. A simple complaint is no longer enough: a significant clinical impairment is needed. Sleep impairments need to be clearly caused by PLMS and the symptoms also need to be explained solely by the PLMS. Treatment
PLMD can be effectively treated with dopaminergic agents (pramipexole, ropinirole, cabergoline, and rotigotine) and it has been found that patients with a low ferritin level respond well to oral iron supplements.
Central core disease (CCD), also known as central core myopathy, is an autosomal dominantly inherited muscle disorder present from birth that negatively affects the skeletal muscles. It was first described by Shy and Magee in 1956. It is characterized by the appearance of the myofibril under the microscope. Signs and symptoms
The symptoms of CCD are variable, but usually involve hypotonia (decreased muscle tone) at birth, mild delay in child development (highly variable between cases), weakness of the facial muscles, and skeletal malformations such as scoliosis and hip dislocation.CCD is usually diagnosed in infancy or childhood, but some patients remain asymptomatic until adulthood to middle age. While generally not progressive, there appears to be a growing number of people who do experience a slow clinically significant progression of symptomatology. These cases may be due to the large number of mutations of ryanodine receptor malfunction, and with continued research may be found to be clinical variants. Pathophysiology
Central core disease is inherited in an autosomal dominant fashion. Most cases have demonstrable mutations in the ryanodine receptor type 1 (RYR1) gene, which are often de novo (newly developed). People with CCD are at increased risk for developing malignant hyperthermia (MH) when receiving general anesthesia. Diagnosis
The diagnosis is made based on the combination of typical symptoms and the appearance on biopsy (tissue sample) from muscle. The name derives from the typical appearance of the biopsy on light microscopy, where the muscle cells have cores that are devoid of mitochondria and specific enzymes.Respiratory insufficiency develops in a small proportion of cases.