[4][5] LPR causes respiratory symptoms such as cough and wheezing[6] and is often associated with head and neck complaints such as dysphonia, globus pharyngis, and dysphagia.

This causes a variety of symptoms, including hoarseness, postnasal drip, sore throat, difficulty swallowing, indigestion, wheezing, globus pharyngeus, and chronic throat-clearing.

[10] Individuals with more severe forms of LPR may experience abrasion of tooth enamel due to intermittent presence of gastric contents in the oral cavity.

Hoarseness is considered to be one of the primary symptoms of LPR and is associated with complaints such as strain, vocal fatigue, musculoskeletal tension, and hard glottal attacks,[12] all of which can reduce a person's ability to communicate effectively.

[14] Symptoms seen in children with LPR include a cough, hoarseness, stridor, sore throat, asthma, vomiting, globus sensation, wheezing, aspiration and recurrent pneumonia.

[14] Common symptoms of LPR in infants include wheezing, stridor, persistent or recurrent cough, apnea, feeding difficulties, aspiration, regurgitation, and failure to thrive.

[4] LPR is often regarded as a subtype of gastroesophageal reflux disease (GERD that occurs when stomach contents flow upward through the esophagus and reach the level of the larynx and pharynx.

[9] Unlike GERD, LPR also poses a risk for bronchitis or pneumonitis as reflux of stomach acid to the level of the larynx can result in aspiration.

[11] In contrast, most cases of GERD are nonerosive, with no apparent injury to the mucosal lining of the esophageal tissue exposed to the refluxed material.

While the epithelium lining the esophagus is capable of withstanding as many as 50 instances of exposure to gastric contents each day, which is the uppermost estimate considered to be within the range of normal physiologic functioning, injury to laryngeal epithelium can occur following exposure to only small amounts of acidic gastric contents.

[26] Pepsin has implications on cellular transcription and therefore, gene expression, which subsequently leads to the recruitment of inflammatory cells, but inhibition of protective mechanisms such as growth factors.

[26] These morphological changes result in decreased vibratory amplitude, increasing demands for initiating vibration and ultimately, impacting voice quality.

A scope with a specialized camera lens made of fiber optic strands is gently fed down the throat and feeds back images to a monitor.

[4] Of the debated diagnostic tools, multichannel intraluminal impedance with pH monitoring (MII-pH) is used as it recognizes both acid and non-acid reflux.

[22][27] Behavioral changes may include weight loss, cessation of smoking, limiting alcohol consumption and avoiding the ingestion of food shortly before bed.

[14] Proton-pump inhibitors (PPIs) are the leading pharmaceutical intervention chosen for the relief and reduction of LPR and are typically recommended for ongoing use twice a day for a period of 3–6 months.

[29] [dubious – discuss] While PPIs may provide limited clinical benefits in some adults, there is insufficient evidence to support routine use.

[31][32] Alginate products can form a temporary foam barrier at the lower oesophageal sphincter to block acid and pepsin from refluxing.