Week 12 Lecture Notes - Motor Pathways and Spinal Cord Lesions

Focus on motor pathways, specifically efferent pathways.
Transition from sensory pathways discussed in Week 11.
Overview of descending motor pathways originating from various central nervous system (CNS) structures.
Structure of lecture and examples to follow regarding spinal cord lesions.

Sensory Pathways:
- Start in the periphery (sensory receptors).
- Move from the peripheral nervous system (PNS) to the central nervous system (CNS).
- Endpoint in the cortex.
Motor Pathways:
- Start in the CNS (motor cortex, brain stem, hypothalamus).
- Move out to the periphery.
- Focus specifically on descending motor efferent pathways.

Spinal cord lesions affect both sensory and motor pathways due to the presence of mixed fiber tracts (sensory and motor).
Nature of lesions creates a scenario to synthesize knowledge about both pathways.
Analyze real-life situations involving traumatic spinal cord damage.

No division of lecture between Tuesday and Wednesday due to practical exam on Tuesday morning.
Final lecture intended to last 1.5 hours, covering both days' syllabus in one session.
Concentration on upper and lower motor neurons, their pathways, and clinical implications.

Motor Neurons:
- Upper Motor Neurons (UMNs): Reside in the CNS and their axons travel within brain and spinal cord fibers.
- Lower Motor Neurons (LMNs): Reside in the PNS, traveling through spinal nerves to skeletal muscles.
Defined pathway structure that involves UMNs synapsing with LMNs affecting skeletal muscle ultimately.

Direct Motor Pathways: Arise from the cerebral cortex. Two main types:
1. Corticospinal Pathways:
- UMNs located in the motor cortex.
- Their axons descend through various CNS structures (corona radiata, internal capsule, etc.), eventually synapsing at the spinal cord (ventral gray horns).
- Approximately 1 million axons form these pathways.
- Name arises from their decussation in the pyramids of the medulla.
1. Corticobulbar Pathways:
- UMNs originate similarly in the motor cortex and descend through comparable CNS structures.
- End in the brain stem crusting on cranial nerves motor nuclei (represented cranially).
Indirect Motor Pathways: Originate in brain stem.
- Comprise medial and lateral upper motor neuron extrapyramidal tracts.
- They do not decussate within the pyramids but synapse with LMNs in the ventral gray horns of the spinal cord.
- Known pathways include rubrospinal, tectospinal, reticular spinal, and vestibulospinal tracts.
Hypothalamospinal Pathways:
- Begin in the hypothalamus.
- Descend to synapse at lateral gray horns of spinal cord.
- Responsible for autonomic control via sympathetic and parasympathetic lower motor neurons in the PNS.

First Order Neurons: Have nerve cell bodies in the motor cortex.
Pathway trajectory:
- Descend through corona radiata to internal capsule, then brain stem.
- In medulla, about 90% of axons decussate (form lateral corticospinal tracts).
- Remaining 10% (anterior corticospinal tracts) remain on the same side until reaching spinal cord where they decussate.
Function:
- Lateral corticospinal tracts: Control precise movements of distal limbs (more agile finger and hand skills).
- Anterior corticospinal tracts: Control proximal muscles and movement coordination of upper and lower limbs.

Comprises of UMNs:
- They synapse on cranial motor nuclei, influencing muscles for facial expression, mastication, and swallowing since they also denote general somatic and special visceral efferents.
Innervation is largely bilateral.
Understanding anatomical layout is essential for interpreting neural damage effects, particularly in the cranial nuclei control of face muscles.

Bilateral Innervation: Important for maintaining function if one part is damaged (especially facial muscles). Clinical assessments differentiate upper and lower motor neuron lesions based on presented symptoms.
Spinal Shock: Initial flaccid paralysis through spinal shock period post injury, limiting functional assessments until inflammation subsides.
Transverse Spinal Cord Lesion Trajectory: Information loss stratified by lesion location influencing sensory and motor pathway conduction ability. The higher the lesion, the more loss due to simultaneous decoupling of cranial signals.

Complete or near-complete transections lead to total loss of sensory and motor function below the injury site.
Classification of functional loss varies with anatomical area of injury: cervical (C1-C8) presents the most severe loss, including respiratory function.
Loss of sensory perception, motor function, reflex responses above the injury preserved, whereas lost below level leads to significant physical impairment.

Presents unique symptoms, such as ipsilateral weakness (spastic paralysis) along with loss of proprioception/vibration on the same side, and contralateral loss of pain and temperature sensation below the lesion.
The pattern stems from distinct crossing mechanisms of different sensory pathways:
- Dorsal columns precede in ipsilateral connectivity.
- Spinothalamic tracts decussate upon entry, leading to contralateral sensory failures.

Key focus areas should encompass neuronal pathways understanding, their clinical significance, and consequential interpretation of spinal cord injury.
Spinal lesions considerably disrupt conductance of signal transmission throughout the cord, asserting necessity for clinical diagnostics to pinpoint lesions effectively based on functional loss and preservation.

Evolution of neuroscience understanding and clinical knowledge emphasizes continued learning and application of this material.
Encouragement for students to engage with materials continuously, aiming for a comprehensive grasp of the field of neuroscience and clinical practices.