Triceps reflex

The triceps reflex, also known as the triceps tendon reflex, is a deep tendon reflex (DTR) that involves the contraction of the triceps brachii muscle in response to a sudden stretch of its tendon, leading to extension of the forearm at the elbow joint.^[1] This monosynaptic stretch reflex arc is a fundamental component of the neuromuscular system, testing the integrity of sensory and motor pathways in the upper limb.^[2] It primarily assesses the C7 spinal nerve root, with involvement of C6 and C8, via the radial nerve.^[3] Anatomically, the triceps brachii muscle, located in the posterior compartment of the arm, consists of three heads—long, lateral, and medial—that converge into a common tendon inserting at the olecranon process of the ulna.^[3] The reflex is initiated when muscle spindles within the triceps detect the stretch caused by tapping the tendon just proximal to the olecranon, activating Ia afferent fibers that synapse directly with alpha motor neurons in the spinal cord, bypassing higher brain centers for rapid response.^[1] This physiological mechanism helps maintain muscle tone and posture by compensating for passive stretches.^[2] To elicit the triceps reflex clinically, the patient's arm is positioned with the shoulder and elbow flexed to approximately 90 degrees, and the forearm supported; a reflex hammer then delivers a quick tap to the triceps tendon above the olecranon.^[3] The normal response is a brisk extension of the forearm, graded as 2+ on the NINDS deep tendon reflex scale from 0 (absent) to 4+ (hyperactive, possibly with clonus).^[1] Abnormal findings, such as hypoactive or absent reflexes, may indicate lower motor neuron lesions like radial neuropathy or C7 radiculopathy, while hyperreflexia suggests upper motor neuron pathology, including stroke or multiple sclerosis.^[2] Symmetry between sides is essential for accurate interpretation, as asymmetry often signals unilateral neurologic dysfunction.^[1]

Anatomy

Triceps brachii muscle

The triceps brachii is a large, thick muscle located on the posterior aspect of the upper arm, forming a distinctive horseshoe shape as it occupies the entire posterior compartment of the arm. It consists of three distinct heads: the long head, which originates from the infraglenoid tubercle of the scapula; the lateral head, arising from the posterior surface of the humerus superior to the radial groove; and the medial head, which originates from the posterior humerus inferior to the radial groove. These heads converge distally to form a common tendon that inserts primarily onto the posterior surface of the olecranon process of the ulna, with additional attachments to the elbow joint capsule and antebrachial fascia.^[3]^[4]^[5] The primary function of the triceps brachii is the extension of the elbow joint, achieved through the coordinated contraction of all three heads, which straightens the forearm from a flexed position. This action is essential for movements such as pushing or pressing, and in the context of the triceps reflex, the muscle's contraction results in rapid forearm extension in response to stimulation. The long head also contributes to adduction and extension at the shoulder joint, providing additional stability to the glenohumeral joint, while the lateral head generates the greatest force during high-intensity activities, and the medial head supports finer, low-force extensions.^[3]^[4]^[5] For reflex testing, key anatomical landmarks include the triceps tendon, which is palpated just proximal to the olecranon process of the ulna when the elbow is flexed at approximately 90 degrees, allowing precise tapping to elicit the reflex response. The muscle's innervation arises from the radial nerve, primarily involving spinal segments C6 through C8, though detailed neural contributions are addressed elsewhere.^[3]^[5]

Innervation and spinal segments

The triceps brachii muscle is primarily innervated by the radial nerve, which originates from the posterior cord of the brachial plexus and carries nerve fibers from the C6, C7, and C8 spinal roots. This innervation supplies motor function to the three heads of the triceps—long, lateral, and medial—enabling elbow extension. The radial nerve emerges from the brachial plexus in the axilla, descending posteriorly along the humerus within the spiral groove before piercing the lateral intermuscular septum to reach the anterior compartment near the elbow. Along its path, it gives off branches to the triceps brachii: the long head receives innervation proximally in the axilla, while the lateral and medial heads are supplied by branches in the spiral groove and lower arm, respectively. In the context of the triceps reflex, the C7 spinal segment is the dominant level, as it provides the primary efferent and afferent fibers responsible for the reflex arc's integrity. Contributions from C6 and C8 segments support synergistic muscle activation and overall upper limb coordination, but impairment at C7 most directly affects the reflex response.

Physiology

Reflex arc components

The triceps reflex arc is a classic example of a monosynaptic stretch reflex, comprising sensory and motor components that enable rapid correction of muscle length changes in the triceps brachii. The afferent limb begins with Ia sensory fibers from primary endings (annulospiral) of muscle spindles embedded within the triceps muscle, which detect the velocity and extent of stretch. These Ia afferents, with cell bodies in the dorsal root ganglia, convey action potentials via the radial nerve through the dorsal roots of the spinal cord primarily at the C7 segment.^[6] At the spinal cord level, the Ia afferents form excitatory monosynaptic synapses directly onto alpha motor neurons in the ventral horn of the C7 spinal segment, bypassing interneurons for swift transmission. This direct glutamatergic synapse excites the alpha motor neurons, which innervate the extrafusal muscle fibers of the triceps brachii. The efferent signals travel via the ventral roots and the radial nerve back to the muscle, triggering contraction to resist the initial stretch. The radial nerve's role highlights the integrated innervation of the triceps at C7.^[7]^[6] The monosynaptic organization ensures a low-latency response, with electromyographic onset typically occurring at 10-13 ms after tendon tap in healthy adults, reflecting the short neural pathway in the upper limb.^[8]

Mechanism of response

The triceps reflex is initiated by a brisk tap on the triceps tendon, which rapidly stretches the triceps brachii muscle and activates specialized sensory receptors known as muscle spindles embedded within the muscle fibers. These spindles detect the change in muscle length and velocity through their intrafusal fibers, leading to an increased discharge rate in primary afferent Ia fibers that innervate the annulospiral endings around the central regions of these fibers. The Ia afferents transmit this sensory information directly to the spinal cord via the radial nerve, where they synapse monosynaptically onto alpha motor neurons in the anterior horn, producing excitatory postsynaptic potentials that depolarize the motor neurons and trigger a rapid contraction of the triceps muscle to counteract the stretch.^[6] Accompanying this excitatory pathway is a disynaptic reciprocal inhibition of the antagonist biceps brachii muscle, mediated by Ia afferent collaterals that activate inhibitory interneurons using glycine as the neurotransmitter. These interneurons suppress the activity of alpha motor neurons innervating the biceps, preventing opposing contraction and allowing unimpeded triceps extension; however, this inhibition is characteristically brief and minimal in amplitude during the triceps reflex, lasting only about 30 milliseconds and contributing less prominently than in lower limb reflexes.^[9] The overall magnitude and sensitivity of the triceps reflex response are finely modulated by gamma motor neurons, which originate in the spinal cord and innervate the intrafusal fibers of muscle spindles to adjust their baseline tension and responsiveness to stretch, ensuring consistent afferent feedback across different muscle lengths via alpha-gamma coactivation during voluntary movements. Additionally, supraspinal descending pathways from the brainstem (such as reticulospinal tracts) and cerebral cortex provide facilitatory or inhibitory inputs to the spinal reflex circuitry, regulating reflex gain to adapt muscle tone for posture, locomotion, and voluntary actions.^[10]^[11]

Clinical Examination

Testing procedure

The triceps reflex test is performed to assess the integrity of the C7 spinal segment and related neural pathways by eliciting a stretch reflex in the triceps brachii muscle.^[1] To begin, the patient should be positioned either seated on the edge of an examination table or supine, with the arm relaxed and supported to ensure comfort and minimize voluntary muscle contraction. The examiner cradles or supports the patient's forearm, positioning the elbow at approximately 90 degrees of flexion (midway between full flexion and extension) and the forearm in a pronated or neutral position to expose the triceps tendon.^[2]^[12] Next, locate the triceps tendon insertion on the olecranon process of the ulna at the posterior elbow, then deliver a quick, firm tap with a reflex hammer to the tendon approximately 2-3 cm proximal to the olecranon.^[1] The strike should be brisk but not painful, using a wrist motion to generate the appropriate force (typically with a hammer weighing 80-140 grams), which stretches the triceps muscle and triggers a brief contraction resulting in observable elbow extension.^[2]^[1] If the initial response is absent or unclear, the test may be repeated with slight variations in arm position or increased tap force while maintaining patient relaxation.^[2] Precautions are essential to obtain reliable results: the patient must be fully relaxed, as tension in the triceps can suppress the reflex and lead to false negatives.^[12]^[1] If relaxation is difficult, employ the Jendrassik maneuver by having the patient interlock their fingers and pull the hands apart isometrically to facilitate the response.^[2] Always compare the response bilaterally, testing both arms sequentially to identify asymmetries, and perform the examination in a quiet environment to avoid distractions that could influence muscle tone.^[2]

Grading the response

The triceps reflex is graded using a standardized scale from 0 to 4+, which evaluates the presence, strength, and quality of the muscle contraction elicited by tapping the triceps tendon with a reflex hammer.^[2] This scale, commonly employed in clinical neurology, allows for consistent documentation of reflex responses across patients.^[12] A grade of 0 indicates an absent reflex, with no visible or palpable contraction of the triceps brachii muscle.^[2] Grade 1+ denotes a diminished response, characterized by a slight but detectable movement or contraction that requires reinforcement maneuvers to elicit reliably.^[12] Grade 2+ represents the normal response in healthy individuals, featuring a visible and brisk contraction of the triceps muscle leading to elbow extension without excessive force.^[2] Grade 3+ signifies a brisk or exaggerated response, with increased amplitude and speed of contraction but without clonus.^[12] Grade 4+ indicates hyperreflexia with clonus, where the contraction is hyperactive and accompanied by sustained, rhythmic oscillations of the forearm.^[2] Clinicians compare the triceps reflex bilaterally to assess symmetry, as asymmetry between the left and right sides may suggest unilateral neurological involvement.^[2] In healthy adults, the average reflex latency—the time from stimulus to onset of contraction—is approximately 11.2 milliseconds, with typical electromyographic amplitude around 1.6 millivolts under standard conditions.^[13] These quantitative measures complement the qualitative grading for more precise evaluation in research or specialized settings.^[13]

Clinical Significance

Normal variations

In healthy adults, the triceps reflex typically elicits a brief, visible contraction of the triceps brachii muscle, resulting in slight elbow extension, and is graded as 2+ on the standard deep tendon reflex scale, indicating a normal response observed bilaterally.^[2]^[12] Normal variations in the triceps reflex response include slightly brisker reflexes (graded 3+) in young adults due to higher neuromuscular efficiency, while responses may appear subdued (graded 1+) in elderly individuals owing to age-related declines in reflex gain, slower muscle contraction, and increased stimulation threshold requirements./06:_Nervous_System/6.09:_Age_Changes_in_Reflexes)^[14] Reflexes can also be temporarily subdued in relaxed states without reinforcement, though this does not indicate pathology. No significant differences in triceps reflex responses exist between sexes, as latencies and amplitudes show no gender-based variations in healthy populations.^[15] Population norms for the triceps reflex demonstrate minor bilateral asymmetries of less than one grade difference considered acceptable in up to 17% of healthy individuals, provided no contiguous reflex asymmetries occur.^[16]

Abnormal findings and causes

Hyporeflexia or areflexia of the triceps reflex indicates disruption in the lower motor neuron pathway, including the C7 spinal segment or radial nerve, leading to diminished or absent muscle contraction upon stimulation.^[7] Common causes encompass peripheral neuropathies, such as those from diabetes or alcoholism, which impair sensory or motor components of the reflex arc.^[2] Radial nerve palsy, often due to compression at the axilla or spiral groove, results in decreased triceps reflex, particularly if the lesion affects the nerve proximal to its branching.^[17] C7 radiculopathy, frequently caused by disc herniation at C6-C7, manifests as diminished triceps reflex alongside weakness in triceps extension and wrist flexion.^[18] Myopathies, such as polymyositis or muscular dystrophy, can rarely produce hyporeflexia if severe muscle weakness prevents adequate response.^[2] Areflexia is a hallmark of Guillain-Barré syndrome, occurring in most patients at nadir due to acute inflammatory demyelination of peripheral nerves.^[19] Hyperreflexia of the triceps reflex signifies upper motor neuron dysfunction, where loss of descending inhibitory control from the corticospinal tract enhances reflex excitability.^[1] This is commonly seen in conditions like stroke, multiple sclerosis, or spinal cord injury above the C7 level, as lesions rostral to the reflex arc disinhibit segmental responses.^[7] In pyramidal tract involvement, hyperreflexia often accompanies clonus, characterized by sustained rhythmic contractions of the triceps muscle.^[1] Asymmetry in triceps reflex responses, such as unilateral hyporeflexia, points to focal lesions like a herniated disc compressing the C7 nerve root, disrupting the reflex arc on one side.^[18] Bilateral abnormalities, including symmetric hyporeflexia, suggest systemic conditions such as hypothyroidism, which slows nerve conduction and muscle relaxation across deep tendon reflexes.^[1]