Weakness & Paralysis UMN vs LMN Lesion ( Internal Medicine ) by Dr Nishant Arya

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Weakness & Paralysis UMN vs LMN -
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Weakness and paralysis can arise from damage to either the upper motor neurons (UMNs) or lower motor neurons (LMNs), each presenting with distinct clinical features. Understanding the differences between UMN and LMN lesions is crucial for accurate diagnosis and treatment planning.
Upper Motor Neuron (UMN) Lesions

Definition: Involve damage to the motor pathways that originate in the cerebral cortex and descend to the spinal cord. These neurons influence the activity of the lower motor neurons.
Common Causes: Stroke, multiple sclerosis, cerebral palsy, traumatic brain injury, and spinal cord injury.

Clinical Features:
Weakness: Typically affects groups of muscles, often more pronounced in the upper limbs (extensors) and lower limbs (flexors).
Paralysis: Spastic paralysis, where muscles are stiff and resistant to movement.
Tone: Increased muscle tone (hypertonia), resulting in spasticity.
Reflexes: Hyperreflexia, with exaggerated deep tendon reflexes.
Babinski Sign: Positive Babinski sign (upward movement of the big toe when the sole of the foot is stimulated).
Atrophy: Muscle atrophy is minimal or absent, as the muscle itself remains innervated.
Lower Motor Neuron (LMN) Lesions
Definition: Involve damage to the motor neurons that directly innervate skeletal muscles. These neurons originate in the spinal cord or brainstem and extend to the muscles.
Common Causes: Poliomyelitis, amyotrophic lateral sclerosis (ALS), peripheral neuropathies, spinal cord injuries at the level of the LMNs, and Guillain-Barré syndrome.

Clinical Features:
Weakness: Typically affects individual muscles or specific muscle groups.
Paralysis: Flaccid paralysis, where muscles are weak and limp.
Tone: Decreased muscle tone (hypotonia), leading to flaccidity.
Reflexes: Hyporeflexia or areflexia, with diminished or absent deep tendon reflexes.
Fasciculations: Visible twitching of muscle fibers due to spontaneous firing of motor units.
Atrophy: Significant muscle atrophy occurs due to denervation and lack of stimulation.

Key Differences -
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UMN Lesion:
Spastic paralysis
Hypertonia
Hyperreflexia
Positive Babinski sign
Minimal atrophy

LMN Lesion:
Flaccid paralysis
Hypotonia
Hyporeflexia
Fasciculations
Significant atrophy

Conclusion -
Differentiating between UMN and LMN lesions is essential for clinical diagnosis and management of neurological conditions. While UMN lesions result in spasticity and hyperreflexia, LMN lesions are characterized by flaccidity, hyporeflexia, and muscle atrophy. Understanding these distinctions helps in targeting appropriate therapeutic interventions and improving patient outcomes. 🧠🩺


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