Post-nasal drip (PND), also known as upper airway cough syndrome (UACS), occurs when excessive mucus is produced by the nasal mucosa. The excess mucus accumulates in the back of the nose, and eventually in the throat once it drips down the back of the throat. It can be caused by rhinitis, sinusitis, gastroesophageal reflux disease (GERD), or by a disorder of swallowing (such as an esophageal motility disorder). Other causes can be allergy, cold, flu, and side effects from medications. However, some researchers argue that the flow of mucus down the back of the throat from the nasal cavity is a normal physiologic process that occurs in all healthy individuals. Some researchers challenge post-nasal drip as a syndrome and instead view it as a symptom, also taking into account variation across different societies. Furthermore, this rebuttal is reinforced because of the lack of an accepted definition, pathologic tissue changes, and available biochemical tests. Signs and symptoms
PND may present itself through the constant presence of discomfort in the upper airways. It is classically described as the sensation of a substance "dripping down the throat" and may also present with rhinorrhea, constant throat clearing, and cough, although its symptoms can be very nonspecific. PND is one of the most common etiologies for chronic cough, defined as a cough persisting beyond 8 weeks.GERD is often associated with a high prevalence of upper-respiratory symptoms similar to those of PND, such as coughing, throat clearing, hoarseness and change in voice.
Dopamine transporter deficiency syndrome (DTDS), also known as infantile parkinsonism-dystonia, is a rare movement disorder that causes progressively worsening dystonia and parkinsonism. It is the first known inherited dopamine transportophathy. DTDS is an extremely rare disease; only about 20 affected individuals have been described in the medical literature. Researchers believe this condition is likely underdiagnosed because its signs and symptoms overlap with other movement disorders, including cerebral palsy.The onset of DTDS is a continuum that ranges from early-onset DTDS (in the first 6 months) to atypical later-onset DTDS (in childhood, adolescence, or adulthood). Signs and symptoms
The main symptom of DTDS, presenting in 80-99% of DTDS patients, is Parkinsonism. This is a neurological anomaly resulting from degeneration of dopamine-generating cells in the substantia nigra, and is characterized by shaking and tremors, rigidity, slowness of movement, and difficulty with walking and gait.Various other symptoms present less commonly (30-79%), including bradykinesia (slowness of movement), acid reflux, muscular hypertonia, and chorea. Causes
DTDS is caused by mutations in the SLC6A3 gene, which codes for the dopamine transporter protein DAT. In contrast to various mutations that up-regulate DAT activity, which is implicated in clinical depression, this mutation results in DAT down-regulation and, consequently, DTDS. Known DTDS-related SLC6A3 mutations include:

R85L
A314V
G386R
R445C
Y470SIn vitro replication of SLC6A3 mutations like those present in DTDS demonstrate multifaceted loss of dopamine transporter functions. Dopamine intake is universally impaired.