stretch reflex

**Reflex arc (monosynaptic, 2-neuron):** 1. Stretch of the muscle (e.g., tendon tap) deforms intrafusal fibers of the muscle spindle (nuclear bag and nuclear chain fibers). 2. Ia afferent (large, myelinated, group Ia) fibers fire, with cell bodies in the dorsal root ganglion. 3. Ia fibers synapse directly (monosynaptic, excitatory, glutamate) on alpha motor neurons in the ventral horn of the same spinal segment. 4. Alpha motor neurons activate extrafusal fibers of the agonist muscle, causing contraction. 5. Collaterals synapse on Ia inhibitory interneurons, which inhibit alpha motor neurons of the antagonist muscle (reciprocal inhibition).

**Muscle spindle:** - It is a stretch receptor in parallel with extrafusal fibers. It detects muscle length and the rate of change in length. - Gamma motor neurons innervate the intrafusal fibers' contractile ends. They keep the spindle taut and sensitive during contraction (alpha-gamma coactivation). - Gamma motor neuron activity sets the sensitivity (gain) of the reflex.

**Contrast with the Golgi tendon reflex (inverse myotatic reflex):** - Golgi tendon organs are in series with the muscle and sense tension. They use Ib afferents and are polysynaptic with an inhibitory interneuron. - Excess tension causes relaxation of the agonist. This is the basis of the clasp-knife response in spasticity.

**Common reflexes and their roots (high-yield):** - Biceps: C5-C6 (musculocutaneous nerve) - Brachioradialis: C6 - Triceps: C7-C8 (radial nerve) - Patellar: L3-L4 (femoral nerve) - Achilles: S1-S2 (tibial nerve) - Mnemonic: "S1, S2 buckle my shoe; L3, L4 kick the door; C5, C6 pick up sticks; C7, C8 close the gate." - Grading: 0 (absent) to 4+ (hyperactive with clonus).

**Clinical significance:** - **Hyporeflexia/areflexia:** LMN lesion, peripheral neuropathy (e.g., Guillain-Barré, diabetic neuropathy), radiculopathy, anterior horn cell disease (polio, SMA), acute spinal shock, or hypothyroidism (delayed relaxation phase). The reflex arc itself is interrupted. - **Hyperreflexia:** UMN lesion (stroke, spinal cord injury, ALS with mixed UMN/LMN signs, MS). Loss of descending inhibition (corticospinal and reticulospinal) leads to spasticity, clonus, and a positive Babinski sign. Hyperthyroidism, anxiety, and serotonin syndrome can also cause brisk reflexes. - **Spinal shock:** Reflexes are initially lost below the lesion, then return as hyperreflexia over days to weeks. - **Jendrassik maneuver:** Clenching the hands or teeth increases gamma motor neuron drive and enhances a weak reflex. - **Clonus:** Sustained rhythmic oscillation from repetitive stretch reflex activation, seen in UMN disease. - **Hypermagnesemia:** Causes loss of deep tendon reflexes. Monitor this in magnesium sulfate therapy for preeclampsia, where loss of patellar reflexes is an early sign of toxicity. - **Pharmacology:** Baclofen (GABA-B agonist), tizanidine (alpha-2 agonist), and dantrolene (RyR1 blocker) reduce spasticity by acting on the reflex circuit or the muscle.

**Key point:** The stretch reflex is the only monosynaptic reflex in the body. Most other reflexes are polysynaptic.