Overview of Upper Motor Neuron Lesions

• The central motor system primarily involves upper motor neuron lesions

• Purpose: Identify the signs/symptoms of upper motor neuron lesions and distinguish them from lower motor neuron lesions

Causes of Upper Motor Neuron Lesions

• Upper motor neuron lesions can be caused by:

  • Stroke

  • Spinal cord injury

  • Anoxic or traumatic brain injury

  • Infection

  • Tumor

  • Abnormal development

• Result from damage to motor neurons in:

  • Cerebrum

  • Brainstem

  • Termination points in spinal cord

Pathophysiology of Upper Motor Neuron Lesions

• Result in imbalance or loss of descending input:

  • Cause weakness and resistance to passive movement

  • Disrupt voluntary movement control

  • Often lead to loss of fractionated movement

• Example: Decreased inhibitory drive in the cortical spinal tract leads to:

  • Affects upper motor neuron excitability

  • Causes increased muscle contraction, especially in flexor muscles

Signs and Symptoms

• Common signs and symptoms of upper motor neuron lesions include:

  • Paresis (weakness) or full paralysis of limbs

  • Increased muscle tone (with a potential period of hypotonia shortly after injury)

  • Hyperreflexia and abnormal reflexes, such as:

  • Pispinski reflex

  • Hoffman reflex

  • Typically, deficits are contralateral to the lesion unless spinal cord injury occurs below the area of disadvantage, resulting in ipsilateral deficits.

Specific Signs

• Spasticity

  • Defined as velocity-dependent resistance to passive movement

  • Described by Bierich et al. as disordered sensorimotor control due to upper motor neuron lesions

  • Mechanism not fully understood, but involves disruption of communication between brain and spinal cord:

  • Creates net disinhibition of spinal reflexes

  • Affects feedback loop between muscle spindles and alpha motor neurons

  • Results in abnormal muscle activation

• Dystonia

  • Involuntary muscle contractions associated with upper motor neuron lesions

  • Contribute to velocity-dependent hypertonia or spasticity

Reticulospinal Tract Involvement

• In absence of corticospinal control, the reticulospinal tract provides:

  • Voluntary control of paretic limb muscles post-stroke (such as wrist and finger flexors)

  • However, lacks the ability for selective motor control, resulting in

  • Excess reticulospinal drive and abnormal synergies

Rigidity vs. Spasticity

• Rigidity

  • Increased resistance to movement across all skeletal muscles, not velocity-dependent

  • Decerebrate rigidity:

  • Rigid extension of limbs and trunk, internal rotation of upper limbs, plantar flexion

  • Results from brainstem injury between midbrain and pons

  • Loss of influence from corticospinal and rubrospinal tracts, allowing medial pathways to dominate

• Corticate rigidity:

  • Flexed upper limbs, extended neck and lower limbs, plantar flexion

  • Results from transections of superior midbrain or severe bilateral cortical lesions

  • Removal of cortical input to red nucleus while maintaining rubral spinal tract activity

Normal and Abnormal Synergies

• Normal Synergies

  • Muscle groups working together as a single unit (e.g., reaching for a coffee cup)

• Abnormal Synergies

  • Activation of muscle groups leading to ineffectiveness post-stroke

  • Example: Upon attempting to reach upward post-stroke, the reticulospinal tract activation without lateral corticospinal shaping leads to abnormal patterning

Gait Analysis and Abnormal Movements

• Post-stroke gait may exhibit:

  • Involuntary flexion of paretic upper limb fingers and elbow when walking

Differences Between Upper and Lower Motor Neuron Lesions

• Upper Motor Neuron Lesion Characteristics:

  • Hyperreflexia

  • Contralateral paresis or paralysis (if injury above lower medulla)

  • Ipsilateral (if spinal cord lesion below level of damage)

  • Disused muscle atrophy due to lack of limb use

  • Hypertonia progressing from hypotonia in acute phase to spasticity or rigidity

• Lower Motor Neuron Lesion Characteristics:

  • Hyporeflexia

  • Ipsilateral paresis or paralysis in the pattern of peripheral nerve injury

  • Neurogenic muscle atrophy due to nerve damage

  • Hypotonia and flaccidity (complete loss of tone)

Conclusion

• Upper motor neuron lesions stem from damage to motor neurons in the cerebrum, brainstem, or spinal cord, with distinct signs compared to lower motor neuron lesions.

• Key clinical manifestations include:

  • Paresis or paralysis

  • Increased muscle tone (hypertonia)

  • Hyperreflexia

  • Abnormal reflexes

  • Muscle atrophy (disused)

  • Spasticity or rigidity

  • Abnormal muscle synergies