Thus, PD is often under reported and misdiagnosed, making it difficult to accurately study its prevalence in human populations.
These movement disorders are classified into three main types based on their triggers and the duration and frequency of the attacks.
[2] Attacks last from seconds to minutes and are known to be at higher risk of occurring during stress, fear, cold, heat, or menstruation.
This is an extremely rare type of paroxysmal dyskinesia characterized by sudden, involuntary, dystonic movements, often including repetitive twisting motions and painful posturing.
Despite retaining consciousness, patients are usually incapable of speech during the attack and may experience great pain in the affected area.
Another frequently noted aura is dizziness [3] PNKD patients experience attacks that last much longer than those of PKD.
One distinguishing characteristic of PED patients is that they typically experience longer durations of dystonia during their attacks.
Mutations of identified genes have been leading areas of research in the study and treatment of paroxysmal dyskinesia.
[4] Utilizing new knowledge about pathologies of related and similar disease can shed insight on the causal relationships in paroxysmal dyskinesia.
Numerous causes have been proposed for PKD, such as genetic mutations, multiple sclerosis, brain trauma, and endocrine dysfunction.
Individuals with a mutation in the MR-1 gene sequence may have problems detoxifying the body when alcohol or caffeine is ingested, perhaps resulting in the onset of PNKD.
This specific mutation leads to increased excitability of the neuron, often inducing rapid depolarization eliciting numerous action potentials.
The pathogenesis of PKND is partially defined by the identification of mutations in the myofibrillogenesis regulator 1 (MR-1), whose gene product is an enzyme involved in the detoxification of methylglyoxal (a compound present in coffee, cola, and alcoholic beverages).
[2] Long periods of continuous physical exercise is often considered the causal factor involved in a PED diagnosis.
Correlations between the causes of young-onset Parkinson's disease and PED may be due to a similar problem, specifically a mutation of a potassium channel gene on chromosome 1.
[4] The pathogenesis of PED has also been linked to mutations in the GLUT1 glucose transporter which can result in transient energy deficits in the basal ganglia.
However, the negative synchronous EEG results can be used to prove that PKD is not a sort of reflex epilepsy, but a different disease.
[4] PED has a set guideline for diagnosis that is similar, but slightly different from both PKD and PNKD.
PED patients do not feel an aura-like sensation before an attack occurs, unlike PKD and PNKD.
During a drug-testing study, patients reported a decreasing response to the latter use of anticonvulsants and switched to carbamazepine or phenytoin.
The majority of patients experience some relief from low dosages of clonazepam, a muscle relaxant and anticonvulsant.
Similar to PKD, avoidance of stress, excitement, and fatigue will lower the frequency of PNKD attacks.
A new approach to managing PED is the ketogenic diet, which alters the primary cerebral energy metabolism from glucose to ketone bodies.
The attacks for PKD can be reduced and managed with proper anticonvulsants, but there is no particular end in sight for any of the PD diseases.