Neurology · MU Sofia

2. Reflexes: quantitative changes, pathological reflexes

Covers quantitative reflex changes, from areflexia and hyporeflexia to hyperreflexia and clonus, with the causes of each and the mechanism behind hyperreflexia. Goes on to pathological reflexes in the lower limb (Babinski, Chaddock, Oppenheim, Gordon and Schaefer signs, grouped as Babinski equivalents), the upper limb (Hoffmann and Trömner signs), and frontal release reflexes. Closes with a comparison of upper and lower motor neuron lesion features and includes four pictures.

Inside: 1 section · 4 labelled pictures · 14 flashcards · 2 min

Topic 2 of 88 in the MU Sofia syllabus for Neurology (Medicine, Year 4). The free AceMed note covers it in 1 section, about 344 words (2 min of reading), with 14 flashcards.

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  1. Reflexes - quantitative changes, pathological reflexes

Reflexes - quantitative changes, pathological reflexes

A. Quantitative Changes of Reflexes

Quantitative changes describe increase or decrease in reflex intensity, helping localize neurological lesions.

1. Areflexia: Complete absence of reflex

  • Causes: Lower motor neuron (LMN) lesions. Peripheral neuropathy. Radiculopathy. Acute spinal shock. Severe myopathy

2. Hyporeflexia::Reduced reflex response

  • Causes: Partial reflex arc damage. Peripheral nerve lesions. Early LMN disease. Neuromuscular junction disorders

3. Hyperreflexia: Exaggerated reflex response

  • Mechanism: Loss of inhibitory corticospinal (UMN) control → increased reflex activity
  • Causes: Upper motor neuron (UMN) lesions. Stroke. Multiple sclerosis. Spinal cord compression

4. Clonus: Rhythmic, repetitive involuntary muscle contractions after sudden stretch

  • Common sites: Ankle clonus (most important). Patellar clonus
  • Significance: Strong indicator of UMN lesion. Reflects corticospinal tract dysfunction

B. Pathological Reflexes

Pathological reflexes are abnormal reflexes due to corticospinal tract (UMN) damage, normally absent in healthy adults.

1. Lower Limb Pathological Reflexes

1. Babinski Sign (Most Important)

  • Method: Stroke lateral sole from heel → little toe → medially
  • Positive response: Dorsiflexion of great toe. Fanning of other toes

➡️ Most reliable sign of UMN lesion

2. Chaddock Sign: Stroke around lateral malleolus

  • Positive: Extension of great toe

3. Oppenheim Sign: Pressure along medial tibia

  • Positive: Extension of great toe

4. Gordon Sign: Squeeze calf muscles

  • Positive: Extension of great toe

5. Schaefer Sign: Squeeze Achilles tendon

  • Positive: Extension of great toe

All above are Babinski equivalents

2. Upper Limb Pathological Reflexes

1. Hoffmann Sign: Flick distal phalanx of middle finger downward

  • Positive: Thumb flexion/adduction. Index finger flexion

➡️ Suggests corticospinal tract lesion (often cervical cord)

2. Trömner Sign: Tap palmar side of distal middle finger

  • Positive: Finger and thumb flexion

3. Frontal Release Reflexes (Primitive Reflexes)

Normally suppressed by frontal lobes; reappear in frontal lobe dysfunction or diffuse brain disease.

Examples:

  • Grasp reflex: Involuntary grasping when palm is touched
  • Snout reflex: Lip tapping → puckering
  • Sucking reflex: Lip stimulation → sucking movement
  • Palmomental reflex: Thenar scratching → chin contraction

C. Clinical Significance

  • UMN Lesion: Hyperreflexia. Clonus. Babinski sign (+). Hoffmann sign (+). Pathological reflexes present
  • LMN Lesion: Areflexia or hyporeflexia. No Babinski sign. Reflex arc disruption. Muscle weakness + atrophy

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