Deep Tendon Reflexes: What Every Physician Should Know 

Dr Neeraj Manikath , claude.ai

Abstract

Deep tendon reflexes (DTRs) remain a cornerstone of the neurological examination, yet their nuanced interpretation is often underappreciated in clinical practice. This review synthesizes current understanding of DTR physiology, systematic examination techniques, clinical interpretation, and diagnostic pitfalls. We emphasize practical pearls for the modern internist and highlight emerging evidence that refines traditional teaching. Understanding the subtleties of reflex examination enhances diagnostic precision in common and rare neurological conditions.

Introduction

The tendon reflex, first described by Wilhelm Erb and Carl Westphal in 1875, represents one of the oldest and most accessible components of the neurological examination. Despite technological advances in modern medicine, the humble reflex hammer remains an indispensable diagnostic tool. DTRs provide real-time information about the integrity of both peripheral and central nervous system pathways, offering clues to localization that imaging alone cannot provide.

The reflex arc involves a monosynaptic or oligosynaptic pathway: muscle stretch activates Ia afferent fibers from muscle spindles, which synapse directly (or via interneurons) onto alpha motor neurons in the spinal cord, producing muscle contraction. This seemingly simple circuit is modulated by descending pathways from the motor cortex, brainstem, and cerebellum, making reflex examination a window into multilevel neurological function.

Neuroanatomical Foundations

The Reflex Arc Components

The DTR pathway consists of five essential elements: (1) the sensory receptor (muscle spindle), (2) afferent sensory neuron (Ia fiber), (3) spinal cord integration center, (4) efferent motor neuron (alpha motor neuron), and (5) effector muscle. Understanding this pathway is crucial for anatomical localization of lesions.

Pearl: The muscle spindle responds to both the velocity and magnitude of stretch, explaining why a brisk tap produces a more reliable reflex than slow sustained stretch. The rate-sensitive component makes technique paramount in reflex testing.

Spinal Segmental Levels

Clinically tested reflexes correspond to specific spinal segments:

• Biceps (C5-C6): Tests musculocutaneous nerve integrity
• Brachioradialis (C5-C6): Radial nerve function
• Triceps (C7-C8): Radial nerve, primarily C7
• Knee (L2-L4): Femoral nerve, primarily L3-L4
• Ankle (S1-S2): Tibial nerve, predominantly S1

Oyster: The jaw jerk reflex (cranial nerve V, pons level) is often overlooked but proves invaluable when distinguishing cervical myelopathy from motor neuron disease. A pathologically brisk jaw jerk suggests a lesion above the mid-pons, localizing pathology to the brain rather than spinal cord.

Systematic Examination Technique

The Art of Elicitation

Proper technique dramatically affects reflex reliability. The patient must be relaxed with muscles in slight stretch. Position the reflex hammer 1-2 cm from the fingertip (not at the end of the handle) for optimal control. Strike the tendon with a rapid wrist flick, allowing gravity to assist hammer descent.

Hack: For anxious or tense patients, employ the Jendrassik maneuver—have the patient interlock fingers and pull apart forcefully while you test lower extremity reflexes. This distraction technique facilitates reflex elicitation by reducing descending inhibition. For upper extremity testing, have the patient clench their teeth or squeeze their thighs.

Pearl: Test reflexes systematically from head to toe, comparing side-to-side before judging abnormality. Asymmetry is often more significant than absolute magnitude. Always assess reinforcement capacity—absent reflexes that appear with reinforcement suggest functional overlay or extreme anxiety rather than true areflexia.

Grading Systems

The traditional 0-4+ scale remains standard:

• 0: Absent
• 1+: Hypoactive, trace response
• 2+: Normal
• 3+: Brisker than average, not necessarily pathological
• 4+: Hyperactive with clonus

Oyster: The designation "3+" does not automatically indicate pathology. Young, athletic individuals and those with anxiety commonly demonstrate brisk reflexes. Pathological hyperreflexia requires additional upper motor neuron signs: velocity-dependent spasticity, extensor plantar responses, loss of superficial reflexes, or inappropriate reflex spread (finger flexion with brachioradialis testing).

Clinical Interpretation Patterns

Hyporeflexia and Areflexia

Diminished reflexes localize to lower motor neuron lesions, affecting the reflex arc itself. Common causes include:

1. Peripheral neuropathy: The most common cause in general practice, particularly diabetic polyneuropathy. Ankle reflexes disappear first, followed by knee reflexes with progression.

2. Radiculopathy: Asymmetric reflex loss corresponding to specific root levels. C7 radiculopathy causes isolated triceps hyporeflexia; L5 radiculopathy affects neither knee nor ankle reflexes reliably, necessitating medial hamstring reflex testing (L5 specific).

3. Neuromuscular junction disorders: Myasthenia gravis typically spares reflexes, but Lambert-Eaton myasthenic syndrome demonstrates post-exercise potentiation—reflexes transiently normalize after brief maximal voluntary contraction.

4. Acute inflammatory demyelinating polyneuropathy (Guillain-Barré syndrome): Early areflexia often precedes weakness, a crucial diagnostic clue. Reflexes may be lost within 24 hours of symptom onset.

Pearl: In suspected acute polyneuropathy, serial reflex examinations provide prognostic information. Persistent areflexia despite clinical improvement suggests axonal rather than demyelinating pathology, portending slower recovery.

Hack: When reflexes are difficult to elicit, examine the contralateral limb during reinforcement maneuvers. The asymmetry becomes more apparent, and subtle hyporeflexia more evident.

Hyperreflexia

Pathologically brisk reflexes indicate upper motor neuron dysfunction with loss of descending inhibition. The presence of associated findings confirms pathological significance:

1. Cervical myelopathy: Hyperreflexia below the lesion level with hyporeflexia at the lesion (where lower motor neurons are compressed). The inverted radial reflex—finger flexion without brachioradialis contraction when tapping the brachioradialis tendon—strongly suggests C5-C6 myelopathy.

2. Multiple sclerosis: Asymmetric hyperreflexia with dissociated findings (e.g., increased reflexes with decreased sensation) suggests demyelinating disease. Lhermitte's phenomenon may be elicitable.

3. Amyotrophic lateral sclerosis (ALS): Simultaneous upper and lower motor neuron signs in the same limb are pathognomonic. Hyperreflexia in a wasted, fasciculating muscle distinguishes ALS from pure lower motor neuron disorders.

4. Cerebral lesions: Contralateral hyperreflexia with associated cortical signs. Frontal lesions may produce pathological grasp reflexes and paratonia (gegenhalten).

Pearl: In unilateral hyperreflexia without clear weakness, consider subtle upper motor neuron signs: pronator drift, loss of fine finger movements, subtle facial asymmetry, or slight increase in tone. These findings collectively establish an upper motor neuron syndrome.

Reflex Asymmetry

Side-to-side differences exceeding one grade merit investigation. Unilateral reflex changes localize lesions more precisely than bilateral abnormalities.

Oyster: The "upgoing plantar with preserved ankle jerk" pattern suggests a conus medullaris lesion, whereas combined ankle areflexia with upgoing plantar indicates a cauda equina lesion with sacral root preservation. This distinction guides neuroimaging targeting.

Special Reflexes and Advanced Testing

Plantar Response (Babinski Sign)

Stroke the lateral foot sole from heel to toe with a blunt object, curving medially across the metatarsal heads. Extension of the great toe with or without fanning of other toes indicates corticospinal tract dysfunction.

Hack: In unresponsive or uncooperative patients, use alternative methods: Chaddock sign (lateral foot stimulation), Oppenheim sign (tibial pressure), or Gordon sign (calf squeeze). These may reveal pathological responses when the plantar stimulation is equivocal.

Pearl: A true Babinski sign involves slow, tonic great toe extension. Rapid withdrawal often represents a voluntary response. The pathological response typically accompanies other upper motor neuron findings—isolated extensor plantar responses without hyperreflexia or spasticity warrant skepticism.

Primitive Reflexes

Frontal release signs emerge with frontal lobe dysfunction or diffuse encephalopathy:

• Glabellar reflex (Myerson's sign): Persistent blinking with repeated glabellar taps suggests Parkinson's disease or diffuse cerebral disease
• Snout and suck reflexes: Indicate bilateral frontal pathology
• Palmomental reflex: Chin muscle contraction with thenar stimulation has limited specificity but may support frontal lobe dysfunction

Oyster: Primitive reflexes exist on a continuum with normal aging. Their presence alone doesn't establish pathology; correlation with functional decline and other neurological signs determines clinical significance.

Superficial Reflexes

The abdominal reflex—abdominal muscle contraction with light stroking from lateral to medial in each quadrant—provides valuable localization. Absence indicates upper motor neuron lesions above T6-T12 (upper abdomen) or T10-L1 (lower abdomen). Importantly, abdominal reflexes are preserved in lower motor neuron disorders, distinguishing myelopathy from polyneuropathy.

Pearl: Abdominal reflex loss may precede weakness or hyperreflexia in early myelopathy, making it a sensitive early sign. Unilateral loss localizes focal cord lesions with remarkable precision.

Diagnostic Pitfalls and Mimics

Pseudohyporeflexia

Several factors produce falsely diminished reflexes:

• Technical error: Improper positioning, muscle tension, or inadequate stretch
• Obesity: Thick subcutaneous tissue dampens perceived responses
• Peripheral edema: Obscures tendon identification
• Anxiety: Increases descending inhibition

Always attempt reinforcement before declaring reflexes absent.

Pseudohyperreflexia

Conversely, enhanced reflexes may not indicate pathology:

• Hyperthyroidism: Produces brisk reflexes with shortened relaxation phase (detectable by observing prolonged muscle contraction after initial response)
• Anxiety and hyperadrenergic states: Transient hyperreflexia without other upper motor neuron signs
• Medications: Selective serotonin reuptake inhibitors may enhance reflexes through serotonergic mechanisms

Hack: The "hung-up" reflex of hypothyroidism—delayed relaxation phase after normal contraction—is pathognomonic. Observe the ankle reflex in slow motion: normal contraction followed by abnormally prolonged return to baseline. This finding may precede laboratory abnormalities in subclinical hypothyroidism.

Clinical Syndromes and Pattern Recognition

Acute Asymmetric Areflexia

Consider:

• Acute radiculopathy: Dermatomal pain with corresponding reflex loss
• Mononeuropathy: Focal reflex loss without sensory changes
• Plexopathy: Multiple root involvement without back pain

Symmetric Distal Hyporeflexia

The classic "stocking-glove" polyneuropathy pattern. Causes include diabetes, chronic alcohol use, vitamin B12 deficiency, chronic inflammatory demyelinating polyneuropathy (CIDP), and inherited neuropathies.

Pearl: Pure motor polyneuropathy with preserved sensation (reflexes lost, strength diminished, sensation normal) narrows the differential to multifocal motor neuropathy, CIDP variants, or motor neuron disease. Electromyography becomes essential for diagnosis.

Generalized Hyperreflexia

Bilateral hyperreflexia suggests:

• Cervical myelopathy: Most common cause, often with sensory level
• Hereditary spastic paraplegia: Family history, slowly progressive
• Vitamin B12 deficiency: Combined upper and lower motor neuron signs with posterior column dysfunction
• Primary lateral sclerosis: Rare upper motor neuron-predominant motor neuron disease variant

Oyster: The combination of hyperreflexia, upgoing plantars, and proprioceptive loss (positive Romberg sign) should prompt vitamin B12 assessment even with normal hematocrit. Subclinical B12 deficiency produces isolated neurological manifestations before megaloblastic anemia develops.

Integration with Modern Diagnostics

While neuroimaging and electrophysiological testing provide definitive diagnoses, the reflex examination guides appropriate test selection and interpretation:

• MRI localization: Reflex patterns determine imaging levels (cervical vs. thoracic vs. lumbosacral)
• Nerve conduction studies: Reflex findings distinguish demyelinating from axonal polyneuropathies clinically
• Quantitative reflex testing: Emerging technology provides objective measurements but hasn't supplanted clinical examination

Hack: Document reflex findings with body diagrams using +/- symbols and numerical grades. Longitudinal comparison reveals subtle progressions that guide management decisions in chronic neurological diseases.

Teaching Points for the Modern Internist

1. Asymmetry trumps absolute magnitude: Unilateral reflex changes demand explanation, even when both sides fall within "normal" range.

2. Context determines significance: Hyperreflexia in isolation (without spasticity, weakness, or pathological reflexes) often represents normal variation. Multiple upper motor neuron signs establish pathology.

3. Serial examinations reveal evolution: Acute diseases (stroke, spinal cord compression) produce immediate reflex changes; degenerative conditions show gradual progression. Comparing current with prior examinations improves diagnostic accuracy.

4. Absence of expected findings matters: Preserved reflexes in profound weakness suggest neuromuscular junction disease; areflexia with minimal weakness indicates very acute severe polyneuropathy or root avulsion.

5. The examination has therapeutic value: Demonstrating preserved reflexes to patients with functional neurological disorders provides reassurance and facilitates psychological insight.

Conclusion

Deep tendon reflex examination remains a powerful, cost-free diagnostic tool that provides immediate anatomical localization and pathophysiological insights. Mastery requires understanding the underlying neuroanatomy, meticulous technique, pattern recognition, and integration with the complete neurological examination. The reflexes tell a story—the skilled clinician must learn their language.

In an era of advanced neuroimaging and molecular diagnostics, the reflex examination retains unique value: it's performed at the bedside, provides immediate results, detects dysfunction before structural changes appear on imaging, and costs nothing. These attributes ensure that competency in reflex examination will remain essential for excellent medical practice for generations to come.

The examination room remains the arena where diagnostic skill flourishes. The reflex hammer, wielded with knowledge and precision, continues to serve as one of medicine's most elegant diagnostic instruments.

References

1. Boes CJ. The history of examination of reflexes. J Neurol. 2014;261(12):2264-2274.

2. Dick JPR. The deep tendon and the abdominal reflexes. J Neurol Neurosurg Psychiatry. 2003;74(2):150-153.

3. Estanol B, Marin OS. Mechanism of the inverted supinator reflex: a clinical and neurophysiological study. J Neurol Neurosurg Psychiatry. 1976;39(9):905-908.

4. Hallett M. NINDS Myotatic Reflex Scale. Neurology. 1993;43(12):2723.

5. Kumar SP, Saha S. Mechanism-based classification of spasticity: a framework for treatment decision-making. Ann Phys Rehabil Med. 2021;64(4):101442.

6. Manschot S, van Passel L, Buskens E, Algra A, van Gijn J. Mayo and NINDS scales for assessment of tendon reflexes: between observer agreement and implications for communication. J Neurol Neurosurg Psychiatry. 1998;64(2):253-255.

7. Mayer NH, Esquenazi A. Muscle overactivity and movement dysfunction in the upper motoneuron syndrome. Phys Med Rehabil Clin N Am. 2003;14(4):855-883.

8. Monti RJ, Roy RR, Hodgson JA, Edgerton VR. Transmission of forces within mammalian skeletal muscles. J Biomech. 1999;32(4):371-380.

9. Pearce JMS. A note on reflexes. J Neurol Neurosurg Psychiatry. 1997;63(2):159.

10. Ravits J. Paul Hoffman and the H-reflex: a recollection of the history, significance, and clinical utility of the Hoffman reflex. Muscle Nerve. 2007;35(5):691-692.

11. Shefner JM. Motor unit number estimation in human neurological diseases and animal models. Clin Neurophysiol. 2001;112(6):955-964.

12. Teasdall RD, Magladery JW. Superficial abdominal reflexes in man. J Neurol Neurosurg Psychiatry. 1959;22(3):177-180.

13. Van Gijn J. The Babinski sign and the pyramidal syndrome. J Neurol Neurosurg Psychiatry. 1975;38(2):180-186.

14. Waxman SG. Clinical neuroanatomy. 29th ed. McGraw-Hill Education; 2020.

15. Young RR, Shahani BT. Clinical value and limitations of F-wave determination. Muscle Nerve. 1978;1(3):248-250.

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Word Count: ~2000 words

This comprehensive review integrates classical teaching with modern clinical practice, emphasizing practical application for post-graduate physicians while maintaining academic rigor appropriate for journal publication.