Pain is the defining feature of TMD and is usually aggravated by manipulation or function, such as when chewing, clenching, or yawning, and is often worse upon waking. The character of the pain is usually dull or aching, poorly localized, and intermittent, although it can sometimes be constant. The pain is more usually unilateral (located on one side) rather than bilateral. It is rarely severe. Limited range of mandibular movement, which may cause difficulty eating or even talking. There may be locking of the jaw, or stiffness in the jaw muscles and the joints, especially present upon waking. There may also be incoordination, asymmetry or deviation of mandibular movement. Noises from the joint during mandibular movement, which may be intermittent. Joint noises may be described as clicking, popping, or crepitus (grating).TMJ dysfunction is commonly associated with symptoms affecting cervical spine dysfunction and altered head and cervical spine posture.Other signs and symptoms have also been described, although these are less common and less significant than the cardinal signs and symptoms listed above. Examples include:

Headache (possibly), e.g. pain in the occipital region (the back of the head), or the forehead; or other types of facial pain including migraine, tension headache. or myofascial pain. Pain elsewhere, such as the teeth or neck. Diminished auditory acuity (hearing loss). Tinnitus (occasionally). Dizziness. Sensation of malocclusion (feeling that the teeth do not meet together properly). Causes
TMD is a symptom complex (i.e.
He has worked in behavioral and developmental pediatrics for many years prior to the discovery of this new syndrome.In 1961, Dr. Hooshang Taybi, an Iranian-American pediatric radiologist, reported having assessed a three-year-old boy that appeared to have the same syndrome as described by Rubinstein. During the summer of 1963 Dr. Taybi reported having evaluated seven children with characteristics such as broad thumbs and great toes, "unusual" facial features, and intellectual disabilities – these findings went on to appear in the American Journal of Diseases of Children documenting these characteristics as a syndrome. Dr. Hooshang Taybi graduated from Tehran University School of Medicine and worked for the Ministry of Health. Later in his career he taught and practiced pediatric radiology in Oklahoma and Indiana. He had identified three new syndromes with his colleagues, among them is Rubinstein–Taybi syndrome.In 1992 the first genetic abnormalities that act as markers for Rubinstein-Taybi syndrome were identified. These abnormalities are said to affect either chromosome 16 or chromosome 22. The specific chromosome impacted by a mutation determines the type of Rubinstein–Taybi syndrome that may occur. A mutation of the CREBP gene on chromosome 16 gives rise to the first form of RTS (most common). While a mutation of the EP300 gene on chromosome 22 is characteristic of the second form of RTS. See also
Nasodigitoacoustic syndrome
List of cutaneous conditions

References
External links

GeneReview/UW/NIH entry on Rubinstein-Taybi syndrome
Rubinstein-Taybi syndrome due to 16p13.3 microdeletion on ORPHAnet