What does a hyperactive (brisk) patellar reflex indicate and how should it be evaluated?

Hyperactive Patellar Reflexes: Clinical Significance and Evaluation

Hyperactive (brisk) patellar reflexes indicate upper motor neuron pathology, most commonly from spinal cord lesions, stroke, or other central nervous system disorders affecting descending inhibitory pathways. 1, 2

Pathophysiology

Hyperactive reflexes result from loss of supraspinal inhibitory control over spinal stretch reflexes, creating a state of net disinhibition at the spinal level. 1 This produces velocity-dependent hyperactivity of tonic stretch reflexes, along with other positive upper motor neuron signs including:

• Tendon hyperreflexia 1
• Clonus 1
• Clasp-knife phenomenon 1
• Extensor plantar response (Babinski sign) 1
• Spastic dystonia 2

The clinical syndrome depends more on the location, extent, and timing of the lesion than on the specific pathology. 1

Critical Distinction: Bilateral vs. Unilateral Hyperreflexia

When patellar reflexes are unequal (asymmetric), this suggests lateralizing pathology requiring immediate neurological evaluation rather than a generalized upper motor neuron syndrome. 3

Unilateral Increased Reflex

• Upper motor neuron lesion on the affected side (spinal cord lesion, stroke) 3
• Should be accompanied by abnormal plantar response (Babinski sign) 3
• Look for associated weakness, increased tone, and loss of fine motor control on the same side 3

Unilateral Decreased/Absent Reflex

• Lower motor neuron pathology: lumbar radiculopathy (L2-L4), peripheral neuropathy 3
• Test for dermatomal sensory deficits in L2-L4 distribution 3
• Assess for quadriceps weakness accompanying L3-L4 radiculopathy 3
• Look for radiating leg pain, numbness, or weakness suggesting nerve root compression 3

Specific Evaluation Approach

Clinical Examination Components

1. Reflex Testing Technique:

• Use controlled, consistent velocity of tendon tap, as reflex response is velocity-dependent 1, 4
• Angular velocity is the most stable and reliable parameter for reflex grading 4
• Compare side-to-side symmetry carefully 3

2. Associated Upper Motor Neuron Signs:

• Test for clonus (sustained rhythmic contractions with maintained stretch) 1
• Assess plantar response (Babinski sign) 1
• Evaluate for spastic co-contraction during voluntary movement 2
• Check for flexor or extensor spasms 1

3. Motor Examination:

• Assess quadriceps strength bilaterally 3
• Look for weakness patterns: upper motor neuron lesions cause weakness with preserved or increased reflexes 3
• Distinguish from lower motor neuron weakness (which has diminished reflexes) 3

4. Sensory Examination:

• Test dermatomal distribution (L2-L4 for patellar reflex) 3
• Asymmetric sensory loss suggests radiculopathy 3

5. Tone Assessment:

• Evaluate for velocity-dependent resistance (spasticity) 1
• Distinguish spasticity from rigidity (spasticity is velocity-dependent; rigidity is not) 1

Common Clinical Contexts

Bilateral Hyperactive Reflexes

• Spinal cord lesions (myelopathy, compression, demyelination) 1
• Cerebral lesions (stroke, traumatic brain injury) 1
• Multiple sclerosis 1
• Cerebral palsy (note: CP shows increased reflexes, distinguishing it from hypotonic disorders) 5

Important Pitfall: Preserved Reflexes in Hypotonia

If a patient presents with hypotonia but preserved or normal reflexes, this strongly suggests a muscle disorder (myopathy) rather than upper or lower motor neuron disease. 5 Upper motor neuron lesions increase reflexes, while lower motor neuron lesions decrease or abolish them. 3, 5

Red Flags Requiring Urgent Evaluation

• Asymmetric reflexes with progressive weakness 3
• Hyperreflexia with bowel/bladder dysfunction (suggests spinal cord compression) 6
• Acute onset hyperreflexia with sensory level (spinal cord emergency) 6
• Hyperreflexia with altered mental status (suggests cerebral pathology) 6

Quantification Considerations

While subjective grading (0-4+ scale) is standard, objective measurement shows that EMG reflex latency is significantly reduced in hyperreflexic states (e.g., 13.11 ms in cerebral palsy versus 18.11 ms in controls). 7 However, knee angular displacement may actually be reduced despite brisker reflexes. 7 This highlights that clinical assessment should focus on the speed and ease of reflex elicitation rather than amplitude alone. 4