Testing the DTR is quick and easy. Proper technique is essential to achieve a reliable response. The examiner taps the muscle's tendon with an examination hammer, and the response is observed and graded. For effective and reliable results, the patient should be as relaxed as possible. If the patient is thinking about the test or has a rigid posture, its integrity is limited.

There are many types of examination hammers, each with its owns quality.[6] The Taylor hammer, also known as the tomahawk hammer, was designed by John M. Taylor in 1888.[7] The Taylor hammer is the best known in the US but has proven to be less reliable in eliciting an accurate response as it tends to evoke an hyporeflexic reaction.[8] The Buck hammer, Babinski hammer, Queen square hammer are other commonly used hammers to test DTR.

When testing lower extremity reflexes such as the patellar or ankle reflex, the Jendrassik maneuver is used to elicit the response if it is initially not obtained.[9][10][11][12] It consists of holding both hands together with the fingers flex and with elbows flex and pull apart the hands. Sometimes, the clinician can have the patient add teeth clenching to this reinforcement maneuver. For upper extremity reflexes, contracting a contralateral muscle or the patient looking the other way may help obtain an adequate response.

For the biceps reflex, the examiner places his thumb on the distal bicep tendon and let the hammer fall by gravity over the thumb. Sometimes additional force may be required to produce an effect. For the tricep reflex, the patient's arm should be held and suspended by the examiner at 90 degrees. Gravitational force is usually sufficient. The patellar reflex is performed with the patient sitting and legs hanging free over the chair's edge. If no visible response occurs, the examiner places his hand over the patient's ipsilateral quadriceps muscle and tries to feel a contraction; the Jendrassik maneuver helps elicit this reflex. The same position is used for the ankle reflex. Tapping the Achilles tendon will elicit a response.

The DTR is a monosynaptic reflex arc. It is monosynaptic because only two neurons are involved: a sensory and a motor neuron, with a single synapse.

After the examiner taps the muscle's tendon, the muscle fibers' stretch is detected at the muscle spindle located within the muscle fibers. The muscle spindle is a sensory proprioceptor that is responsible for identifying the length of the muscle fibers. It is composed of a few intrafusal fibers that do not contract. The Ia afferent sensory fibers in the muscle spindles will produce action potentials in response to the stretch. These Ia afferent fibers go to the spinal cord at the dorsal root and monosynaptically stimulate the alpha motor neuron that goes to the homonymous muscle extrafusal fibers. Glutamate is the neurotransmitter at the central synapse. The extrafusal muscle fibers generate a contraction to resist the stretch. When the muscle contraction occurs, the muscle spindle decreases the action potential firing frequency, and the reflex is extinguished.

The DTR is sometimes called stretch reflex or myotatic reflex because of the stretch action and the muscle response involved. Some authors argue that they are not the same reflex.[13][14][15][16] They think that the tendon reflex occurs after the tendon's active stretching when it is tapped with the hammer. In contrast, the stretch reflex occurs after the passive stretching of the muscle spindle during posture and ambulation. The tendon reflex is a short-latency reflex, while the stretch reflex is a long-latency reflex.

During the reflex, the antagonistic muscle is inhibited while the agonist muscle contracts.[17] This action occurs polysynaptically through the Ia inhibitory interneuron, which inhibits alpha motor neuron to the antagonist muscle. During the knee jerk reflex, the hamstring muscles are inhibited and relax while the quadriceps muscles are stimulated and contract. Within the muscle spindle, the gamma motor neuron cause tightening or relaxing of intrafusal muscle fibers to regulate the sensitivity of the muscle spindle and the reflex's response. It is mediated by acetylcholine.

The function of the Ia afferent fibers of the muscle spindle is different from the Ib afferent fibers of the Golgi tendon organ, which detects the tension in the muscle fiber and sends the information to the spinal cord, but also the cerebellum and cerebral cortex. The Ib fibers regulate muscle contraction and are very important for locomotion.

It is a debated topic whether the stretch reflex has some central feedback.[14][18] It probably plays an important role in maintaining muscle tone and upright posture. The cerebral cortex and possible brainstem nuclei produce influence in the muscle spindle through the gamma motor neurons.[13][15][17][19] Dorsal spinocerebellar tracts carry the information from the spinal cord to the cerebellum.

The DTR is used to assess the integrity of the motor system. They also provide information on the condition of upper and lower motor neurons. The DTR depends on the integrity of both the upper motor neuron and the lower motor neuron. If a patient has an injury or a disease involving a lower motor neuron (nerve roots or peripheral nerves), a decrease or loss of the reflex will be noted. If the lesion or injury involves the upper motor neuron (brain, brainstem, or spinal cord), an increased reflex will be present. In severe chronic cases, usually associated with spasticity, clonus can be seen. It is common in stroke, spinal cord injury, cerebral palsy, and multiple sclerosis.[20] It can also occur after ingesting a large amount of serotonergic drugs.

Although the DTR has a sensory component, it does no assess the integrity of the sensory system and is not useful for lesions involving this system. It is always essential to compare the reflex on one side to the opposite side. The DTR of the upper extremities can provide clues to the level of injury in the spinal cord.

Increased reflexes can be normal, especially if bilateral. Children frequently have exaggerated reflexes (more prominent in upper extremities). Enhanced reflexes can be associated with an upper motor neuron lesion. Clonus, if present, is never a normal finding.

Decreased reflexes present in lower motor neuron lesions, including nerve root lesions with radiculopathy and peripheral nerve lesions. Diabetes and hypothyroidism slow down the response of the DTR.  If absent when initially tested, the response can be elicited with repetitive tapping of the tendon; however, this maneuver sometimes causes extinguishment of the reflex. Muscle disease may cause the reflex to become diminished as the muscle fiber can not respond adequately. A patient with a spinal cord injury presenting spinal shock can have hyporeflexia. Cerebellar disease can also produce hyporeflexia. If the reflexes decrease bilaterally, it is often a normal finding.

If the reflex is absent, other findings are usually present secondary to the lower motor neuron disease. They include muscle atrophy, weakness, and sometimes fasciculations. If it is an isolated reflex deficit, it is most commonly the result of a root lesion, a peripheral nerve injury or entrapment, or a mononeuropathy.[21] If several reflexes are involved, peripheral neuropathy is the probable etiology. Bilateral absent ankle jerk usually indicates a peripheral neuropathy, but a cauda equina syndrome can also produce it.[21]

Specific peripheral nerve injuries can produce decreased or absent DTR. Musculocutaneous nerve injury will have the biceps reflex affected. A radial nerve injury can have the triceps or the brachioradialis reflex affected depending on the anatomical area of damage in the nerve. Femoral nerve lesions will affect the patellar reflex, and tibial nerve lesions will affect the ankle reflex.