UMN vs. LMN Lesions Part 2
Conceptual Overview of Motor Neuron Differentiation
The differentiation between Upper Motor Neuron (UMN) and Lower Motor Neuron (LMN) lesions is achieved through a comprehensive neurological examination.
Understanding these distinctions is essential for localized deficit diagnosis and improving clinical outcomes in canine and feline neurology.
General Rule of Thumb:
Upper Motor Neuron (UMN): Characterized by a "loss of inhibition." These units reside within the Central Nervous System (CNS), specifically the brain and spinal cord.
Lower Motor Neuron (LMN): Characterized by a "loss of function." These units constitute the Peripheral Nervous System (PNS), including peripheral nerves, the neuromuscular junction, and the muscles themselves.
Terminology and Neurological Deficit Classification
Upper Motor Neuron (UMN) Components: Includes the brain and the spinal cord.
Lower Motor Neuron (LMN) Components: Includes peripheral nerves, the neuromuscular junction (NMJ), and the muscle.
Paresis: General term for partial loss of voluntary movement or weakness.
UMN Paresis: Manifests as abnormal gait generation.
LMN Paresis: Manifests as an inability to bear weight.
Paralysis: The complete loss of voluntary movement.
Ataxia: Characterized by disordered movement and the loss of proprioception or postural reactions.
Reflex: An immediate motor response to a specific sensory input that does not require higher-level integration from the brain. An example is the Patellar Reflex.
Reaction: A response that requires either conscious or unconscious cerebral integration. An example is the Menace Response.
Nociception: Also known as "deep pain," this refers to a conscious reaction to noxious stimuli. It is distinct from a simple withdrawal reflex.
Comparative Signs of UMN vs. LMN Dysfunction
Gait:
UMN: Characterized by delayed generation and a long-strided gait.
LMN: Characterized by weakness, a short-strided gait, and an inability to support weight.
Muscle Tone:
UMN: Results in Hypertonia (increased tone) due to the loss of inhibitory signals.
LMN: Results in Hypotonia or Atonia (decreased or absent tone).
Muscle Mass:
UMN: Typically appears normal.
LMN: Results in Neurogenic Atrophy, which occurs rapidly if the lesion persists for more than .
Spinal Reflexes:
UMN: Normal to Hyperreflexia (exaggerated reflexes).
LMN: Hyporeflexia or Areflexia (decreased or absent reflexes).
Postural Reactions/Proprioception:
UMN: Abnormal or absent.
LMN: Usually normal, though may appear abnormal if the lesion is exceptionally severe.
Anatomy of Limb Innervation
Two primary junctions facilitate the innervation of the nerves to the limbs:
Brachial Plexus:
Responsible for the movement (LMN) and sensation of the thoracic limbs.
Comprised of the ventral branches of spinal segments .
Lumbosacral Plexus:
Responsible for the movement (LMN) and sensation of the pelvic limbs.
Provides perineal and visceral innervation.
Comprised of the ventral branches of spinal segments .
Clinical Implications of Lesion Localization
UMN Lesions:
The loss of inhibition leads to increased muscle tone and hyperreflexia.
Clinical signs include Spastic Paresis or Spastic Paralysis.
LMN Lesions:
The loss of direct innervation results in decreased muscle tone and diminished or absent reflexes.
Clinical signs include Flaccid Paresis or Flaccid Paralysis.
LMN lesions are usually motor-related; sensory perception often remains normal.
These lesions may present as either focal (localized) or generalized.
Diagnostic Tools: A reflex hammer is a standard instrument used to test the presence and strength of the patellar reflex to aid in localization.
Contributors and Visual References
Clinical images and schematic representations of neurological dysfunction are credited to:
Suzy Gray, Dip ACVIM: Provided imagery of a hopping dog performing postural reaction tests.
Catherin Reiss, DVM: Provided imagery of the patellar reflex assessment.
Rcchang16: Provided schematic representations comparing the CNS vs. PNS and UMN vs. LMN units.