Clinical Notes and Interpretation
Normal motor function requires proper function of muscle tissue, receptors, CNS integrating centers, the spinal cord, the cortex, the motor end plate and associated motor neurons and reflex arcs. In this framework, abnormal deep tendon reflexes may be indicative of systemic disorders, CNS dysfunction, PNS dysfunction or primary neuromuscular dysfunction. A degree of clinical differentiation of deep tendon reflexes is possible because specific patterns of dysfunction tend to predominate with different disorders. The clinician should seek to differentiate between Lower Motor Neuron Lesions (LMNL), Upper Motor Neuron Lesions (UMNL), systemic involvement and/or local neuromuscular dysfunction. Additionally, distinctions between local or global involvement and distinctions between unilateral or contralateral involvement will further aid in the clinical differentiation process.
Lower motor neuron lesions
Lower motor neurons, or second order neurons, have cell bodies in the CNS and innervate striated muscle. Lower motor neurons are present in the cranial nerves, spinal nerves, peripheral nerves and anterior horn cells. Lower motor neuron lesions present with diminished or absent reflexes; additional findings can include:
- Flaccid paralysis and weakness
- Sensory changes
- Significant atrophy
- Fasciculation and fibrillation
- Loss of vasomotor tone
Common examples of LMNL’s include direct injury to a peripheral nerve (i.e., crush injury or laceration), involvement at the level of the spinal nerve or nerve root (i.e., disc protrusion and lateral spinal stenosis with neurogenic involvement) and peripheral neuropathies (i.e., diabetic peripheral neuropathies).
