"Friction massage" uses surface pressure to causes temporary ischemia and subsequent hyperemia in the muscles, and this is hypothesized to inactivate trigger points and disrupt small fibrous adhesions within the muscle that have formed following surgery or muscular shortening due to restricted movement.Occasionally physiotherapy for TMD may include the use of transcutaneous electrical nerve stimulation (TENS), which may override pain by stimulation of superficial nerve fibers and lead to pain reduction which extends after the time where the TENS is being actually being applied, possibly due to release of endorphins. Others recommend the use of ultrasound, theorized to produce tissue heating, alter blood flow and metabolic activity at a level that is deeper than possible with surface heat applications. There is tentative evidence that low level laser therapy may help with pain.The goals of a PT in reference to treatment of TMD should be to decrease pain, enable muscle relaxation, reduce muscular hyperactivity, and reestablish muscle function and joint mobility. PT treatment is non-invasive and includes self-care management in an environment to create patient responsibility for their own health.Therapeutic exercise and Manual Therapy (MT) are used to improve strength, coordination and mobility and to reduce pain. Treatment may focus on poor posture, cervical muscle spasms and treatment for referred cervical origin (pain referred from upper levels of the cervical spine) or orofacial pain . MT has been used to restore normal range of motion, promoting circulation, stimulate proprioception, break fibrous adhesions, stimulate synovial fluid production and reduce pain.
The doctor may order any or all of the following tests to ascertain if a person has IBM2:

Blood test for serum Creatine Kinase (CK or CPK);
Nerve Conduction Study (NCS) / Electomyography (EMG);
Muscle Biopsy;
Magnetic Resonance Imaging (MRI) or Computer Tomography (CT) Scan to determine true sparing of quadriceps;
Blood Test or Buccal swab for genetic testing;

Classification
Types of hereditary inclusion body myopathy:

IBM2 is the most common form, and is an autosomal recessive form, caused by mutations in the GNE gene; this form mainly affects leg muscles, but with an unusual distribution that spares the quadriceps. The incidence of this form is about 10 per million per year. There are two forms: a quadriceps sparing myopathy (autosomal recessive form of inclusion body myopathy) and Nonaka type distal myopathy (distal myopathy with rimmed vacuoles). While occurring worldside it is most common in Jews of Persian origin. The GNE gene ecodes the rate-limiting, bifunctional enzyme of sialic acid biosynthesis, uridine diphosphate-N-acetylglucosamine 2-epimerase/N-acetylmannosamine kinase. Disease occurs when both copies in the genome are non functional. The pathophysiology is still unclear. Cardiac involvement may occur. IBM3 is a sometimes autosomal dominant and sometimes autosomal recessive form caused by mutations in MYHC2A;  it is relatively mild muscle disorder.