Superficial reflexes vs deep tendon reflexes in umn vs lmn with explanation
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Superficial vs Deep Tendon Reflexes in UMN vs LMN Lesions
Definitions First
Deep Tendon Reflexes (DTRs) / Muscle Stretch Reflexes
Elicited by tendon tap → muscle spindle stretch → Ia afferent → anterior horn → efferent motor fiber → muscle contraction. Examples: biceps (C5–6), triceps (C6–7), brachioradialis (C5–6), patellar (L3–4), Achilles (S1–2).
Superficial (Cutaneous) Reflexes
Elicited by stroking skin → polysynaptic spinal arc → muscle contraction. Examples: abdominal reflexes (T7–T12), cremasteric (L1–2), plantar reflex (S1–2), anal wink (S2–4).
The Core Table
| Feature | UMN Lesion | LMN Lesion |
|---|---|---|
| DTRs / Tendon reflexes | Increased (hyperreflexia, clonus) | Decreased or absent (hyporeflexia/areflexia) |
| Superficial abdominal reflexes | Absent (abolished) | Absent (abolished) |
| Cremasteric reflex | Absent (abolished) | Absent (abolished) |
| Plantar reflex | Extensor (Babinski sign — up-going toe) | Flexor (normal plantar flexion) or absent |
| Anal wink | May be present | Absent if S2–4 involved |
| Tone | Increased (spasticity) | Decreased (flaccidity) |
| Atrophy | Absent (disuse only, mild) | Present (denervation) |
| Fasciculations | Absent | Present |
Harriet Lane Handbook; Neuroanatomy through Clinical Cases, 3rd Ed.; Adams & Victor's Principles of Neurology, 12th Ed.; Harrison's Principles of Internal Medicine 22E
Why DTRs Increase in UMN Lesions
The corticospinal tract carries descending inhibitory influences onto alpha (α) and gamma (γ) motor neurons in the anterior horn. When UMN fibers are damaged:
- Loss of descending inhibition → anterior horn motor neurons become hyperexcitable
- α-motor neuron excitability increases → exaggerated muscle stretch reflex
- γ-motor neuron overactivity → increased muscle spindle sensitivity → further amplification of DTRs
- Result: hyperreflexia, possibly clonus (rhythmic 5–7 Hz contractions from sustained stretch), Hoffmann sign, crossed adductor reflex, and spread of reflexes
Note: Spasticity likely results from damage to reticulospinal and other descending inhibitory pathways that run alongside (but are separate from) the corticospinal tract itself — pure corticospinal lesions (e.g., medullary pyramid lesions) cause weakness + hyperreflexia without true spasticity. (Adams & Victor's, 12th Ed.)
Why DTRs Decrease in LMN Lesions
The DTR arc itself is broken:
- LMN = the final common pathway — the efferent limb of the reflex arc
- Any damage to the anterior horn cell, ventral root, or peripheral nerve interrupts the arc → reflex cannot be completed → hyporeflexia or areflexia
- Combined with flaccidity and eventual denervation atrophy
Why Superficial Reflexes are ABSENT in BOTH — But for Different Reasons
UMN → Superficial reflexes abolished
Superficial reflexes (abdominal, cremasteric) require intact corticospinal input to be expressed — they are not simple spinal arcs. They depend on the integrity of the descending pathways for facilitation:
- Stroking the skin normally recruits a polysynaptic arc that requires cortical facilitation
- UMN lesion removes this supraspinal drive → superficial reflex is lost even though the LMN is intact
- This makes them clinically very useful: absent superficial reflexes with increased DTRs = UMN lesion (e.g., early MS, cord compression)
"The cutaneous muscular abdominal and cremasteric reflexes are usually abolished when the upper motor neuron is damaged acutely." (Adams & Victor's, 12th Ed., p. 1628)
LMN → Superficial reflexes abolished
Here the efferent arc itself is damaged, so the motor response cannot occur regardless of supraspinal input.
The Plantar Reflex — A Special Case
| Condition | Response | Interpretation |
|---|---|---|
| Normal adult | Plantar flexion of toes | Normal |
| UMN lesion (above S1) | Extension of great toe ± fanning of others = Babinski sign | Pathological |
| Normal infant (<12–18 months) | Extension (Babinski) | Normal — corticospinal tract not yet myelinated |
| LMN lesion (S1–S2) | Absent plantar reflex | Arc interrupted |
Babinski is physiologically a disinhibited flexion withdrawal/nocifensive reflex — the great toe extension is actually part of a "triple flexion" protective response (hip flex, knee flex, ankle dorsiflex) that is normally suppressed by UMN input. Loss of UMN → this reflex is released.
Acute vs Chronic UMN — Critical Point
| Phase | DTRs | Tone | Superficial Reflexes |
|---|---|---|---|
| Acute UMN (e.g., spinal shock, acute stroke) | Decreased/absent (flaccid) | Decreased | Absent |
| Chronic UMN (weeks–months later) | Increased (spastic) | Increased | Absent |
Spinal shock is the classic example: immediately after complete cord transection, everything below is flaccid with areflexia, mimicking LMN. Over hours to months, spasticity and hyperreflexia emerge. Superficial reflexes, however, remain absent throughout in UMN lesions — making them a more consistent early sign.
Summary Mnemonic
UMN = "Up everything except superficial"
- DTRs Up, Tone Up, Babinski Up (extensor)
- Superficial reflexes Down (absent)
LMN = "Down everything"
- DTRs Down, Tone Down, Superficial reflexes Down
- Plus: atrophy, fasciculations (unique to LMN)
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