Since the age of onset is relatively young of PED it is important to correctly diagnose this disease. The limited cases and limited knowledge of the disease makes this difficult but a few characteristics seem to be consistent. It appears that patients with PED would have normal neurological examinations and MRI but the noticeable characteristic would be in low levels of glucose in the cerebral spinal fluid due to the GLUT1 mutations. Related disorders PED differs from two closely related disorders, for example<unk>  kinesogenic dyskinesia (PKD) and<unk>  nonkinesigenic dyskinesia (PNKD), based on what brings on the symptoms, namely prolonged<unk> , such as brisk walking or running for at least 10 minutes. This is in contrast to PKD where the symptoms are brought about by sudden movements, and PNKD where the symptoms are spontaneous in nature and prolonged. PED is usually affects muscles on both sides of the body (bilateral), it has also been observed to have unilateral effects. PED has also been shown to be a precursor to Parkinson's disease. In two observed cases, PED preceded any symptoms of Parkinson's Disease by 1.5 and 5 years. Although a rare indicator, PED can be an early sign of the disorder, suggesting they are related. In one case a patient with PED showed evidence of dopamine depletion revealed by a dopamine transporter SPECT scan. This is typical of Parkinson's disease, further showing the linkage between the diseases. A correlation between epilepsy and PED has been observed in several families across multiple generations, demonstrating an autosomal dominant heritability of symptoms. The occurrence of coexistent seizures and PED symptoms are observed mainly during infancy and childhood, with symptoms of PED continuing throughout a lifetime. Epileptic seizures vary in type and have been observed as absence and generalized seizures. Simultaneous seizure and PED attacks are often premeditated by bouts of dizziness. Attacks have been shown to be reduced or prevented with food ingestion, although the reasons for this are unclear. Various evidence shows that the disorders are likely caused by dysfunction in voltage-gated ion channels, which may lead to abnormal excitability in different brain regions, specifically the cerebral cortex and basal ganglia.
Paroxysmal exercise-induced dystonia
Dopamine-responsive dystonia
Paroxysmal kinesigenic choreoathetosis
Potassium-aggravated myotonia
Post-encephalitic parkinsonism
Benign fasciculation syndrome
Levodopa-induced dyskinesia
Myotonia congenita