Because of this, a means for measuring the degree of velopharyngeal closure in consonants is also needed. A commercially available device for making such measurements is the Perci-Sar system from Microtronics. The Nasality Visualization System from Glottal Enterprises allows both the measurement of Nasal Emission and Nasalance. In the presence of a cleft palate, either of these systems can be helpful in evaluating the need for an appliance or surgical intervention to close the cleft or the success of an appliance or a surgical attempt to close the cleft. Exercises
If a child finds it difficult to blow, pinching the nose can help regulate airflow. The child should then practice speech sounds without pinching the nose. These exercises only work as treatments if hypernasality is small. Severe deviations should be treated surgically. CPAP
There is insufficient evidence to support the use of traditional non-speech oral motor exercises can reduce hypernasality. Velopharyngeal closure patterns and their underlying neuromotor control may differ for speech and nonspeech activities. Therefore, the increase in velar movement through blowing, sucking, and swallowing may not transfer to speech tasks. Thus, hypernasality remains while individual speak. Kuehn proposed a new way of treatment by using a CPAP machine during speech tasks. The positive pressure provided by a CPAP machine provides resistance to strengthen velopharyngeal muscles. With nasal mask in place, an individual is asked to produce VNCV syllables and short sentences.
DNA mutational analysis revealed that the child was homozygous for a novel E64K mutation and that his mother and father were heterozygous for the novel E64K mutation. Potential causes
Smoking: Recent studies suggest that smoking can lead to marginal biotin deficiency because it speeds up biotin catabolism (especially in women). Excessive alcohol consumption
Excessive consumption of antidiuretics or inadequate levels of antidiuretic hormone
Intestinal malabsorption caused by short bowel syndrome

Biochemistry
Biotin is a coenzyme for five carboxylases in the human body (propionyl-CoA carboxylase, methylcrotonyl-CoA carboxylase, pyruvate carboxylase, and 2 forms of acetyl-CoA carboxylase.) Therefore, biotin is essential for amino acid catabolism, gluconeogenesis, and fatty acid metabolism. Biotin is also necessary for gene stability because it is covalently attached to histones. Biotinylated histones play a role in repression of transposable elements and some genes. Normally, the amount of biotin in the body is regulated by dietary intake, biotin transporters (monocarboxylate transporter 1 and sodium-dependent multivitamin transporter), peptidyl hydrolase biotinidase (BTD), and the protein ligase holocarboxylase synthetase. When any of these regulatory factors are inhibited, biotin deficiency could occur. Diagnosis
The most reliable and commonly used methods for determining biotin status in the body are:

excretion of 3-hydroxyisovaleric acid and biotin in urine
activity of propionyl-CoA carboxylase in lymphocytes

Treatment
In the United States, biotin supplements are readily available without a prescription in amounts ranging from 300 to 10,000 micrograms (30 micrograms is identified as Adequate Intake). Epidemiology
Since biotin is present in many foods at low concentrations, deficiency is rare except in locations where malnourishment is very common.