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Parkinsonism in GNDs452and treatment strategies, may reduce the burden on patients and their families searching for answers (sometimes referred to as the “Diagnostic Odyssey”), inform disease risks for family members, and help patients and their families connecting with patient organizations for peer support.113 It is important to realize that patients with GNDs may develop multiple earlyand late-onset comorbidities that require proactive attention depending on the condition, that are typically not restricted to neurological problems, but may involve all body systems.114, 115 Increasingly, expert clinics specializing in specific GNDs are available, typically providing multidisciplinary care to improve patient outcomes and quality of life.Next generation sequencing techniques, such as whole exome sequencing (WES), that may reveal a monogenic disorder,113 or chromosomal microarray analysis, that identifies genome wide CNVs,116 may be used as first line diagnostic tests. Certain features, including congenital anomalies and ‘dysmorphic facial features’, may point to the presence of a specific syndrome, but are absent in many patients. Here, it should also be noted that conventional karyotyping will not detect CNVs or monogenic disorders and that most currently available Parkinson’s disease genetic diagnostic panels do typically not include GNDs. Therefore, an additional panel for intellectual disability may need to be ordered. It should also be realized that family history is often not a good predictor; many patients with a GND have a de novo mutation. Selecting the most appropriate genetic test can however be difficult; choosing the right test can require consultation with a clinical geneticist. Limitations of most genetic tests include the high costs; these tests are not readily available for many people, or inaccessible.With recent advances in diagnosis and treatment of GNDs, targeted disease-modifying therapies have become available for an increasing number of patients diagnosed with a GND, i.e., for those with an inborn error of metabolism or tuberous sclerosis complex.117-119 Early detection of such disorders allows for timely interventions to prevent further brain damage and/or disease progression. Prominent examples of treatable inborn errors of metabolism in this review include phenylketonuria and other conditions that lead to disruptions in monoaminergic neurotransmitter metabolism (e.g., TH, and DNAJC12).117 These patients may have great benefit from