Topic 8 Motor Neuron Disorders & Spinal Cord Injury
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1 Topic 8 Motor Neuron Disorders & Spinal Cord Injury 1. Terminology 2. "Upper motor neuron" injury 3. Mechanisms of damage 4. Some disorders Motor System Disorders - Terminology Muscle Strength Paralysis / Paresis hemi-, para-, or tetra (quad)- plegia Muscle Bulk atrophy disuse or neurogenic Motor System Disorders - Terminology Upper motor neurons Originate in "higher" regions of brain such as motor cortex Corticospinal tract Lower motor neurons Directly innervate skeletal muscles
2 Motor System Disorders - Terminology Hypotonia - abnormally low resistance to stretch cerebellar disorders LMN lesions acute UMN lesions Hypertonia - abnormally strong resistance to stretch chronic UMN lesions 2 types = spastic and rigid Motor System Disorders - Terminology Spastic Hypertonia resistance to passive movement is velocity sensitive Rigidity resistance to passive movement remains constant regardless of velocity Decorticate / Decerebrate Decerebrate Rigidity
3 Decerebrate - upper brainstem or lower midbrain Source: Haines, Fundamental Neuroscience, Churchill-Livingstone, 2002 Decorticate Rigidity Decorticate - severe lesion superior to midbrain Source: Haines, Fundamental Neuroscience, Churchill-Livingstone, 2002
4 Topic 8 Motor Neuron Disorders & Spinal Cord Injury 1. Terminology 2. "Upper motor neuron" injury 3. Mechanisms of damage 4. Some disorders Overall muscle tone is determined by 1. Intrinsic elastic properties of muscle 2. Neural input Stretch reflex - - contraction in response to lengthening - receptor is muscle spindle (Ia afferent fiber) - descending pathways modify gain of reflex Source: Kandel et al., Principles of Neural Science, McGraw Hill, 2000
5 Hoffmann Reflex - stimulate Ia afferents (and motor neurons) - measure "M-wave" and "Hwave" using EMG Source: Kandel et al., Principles of Neural Science, McGraw Hill, 2000 "Spinal shock" - Complete absence of reflexes Maybe from sudden withdrawal of descending input Reflexes recover (weeks months) and become oversensitive "Hyperactive" reflexes spasm-like' muscle bursts in response to mild stimuli loss of descending inhibition Increased resistance to stretch - Velocity-dependent hypertonia tactile stim. foot Source: Latash, Neurophysiological Basis of Movement, Human Kinetics, 1998.
6 Treatment - - administration of baclofen to spinal cord - GABA B receptor agonist - inhibition of synapse between Ia fibers and motor neurons Babinski s Sign stroking across plantar surface of foot normally causes flexion of toes Upper motor neuron damage can reverse this response Source: Lundy-Ekman, Neuroscience: Fundamentals for Rehabilitation, Saunders, 2002 Summary of "UMN" Injury Effects Source: Latash, Neurophysiological Basis of Movement, Human Kinetics, 1998.
7 Topic 8 Motor Neuron Disorders & Spinal Cord Injury 1. Terminology 2. "Upper motor neuron" injury 3. Mechanisms of damage 4. Some disorders Primary Injury mechanical damage to neuronal apparatus Secondary Injury occurs over hours post-injury Glutamate - Excitotoxicity NMDA Receptor - GLU binds to R and opens Na + channels - Na +, draws water into the cell = edema - Ca ++, activates proteases, lipases that degrade components of cell, may initiate apoptosis Source: Kandel et al., Principles of Neural Science, McGraw Hill, 2000
8 Neuroprotective strategies - block glutamate receptors - antioxidants - block Na+ channels Na + Channel Blockers BBB = measure of locomotor function Riluzole Control Weeks Post-Injury Adapted from: Schwartz and Fehlings, J. Neurosurg., 2001, 94(Suppl 2): Na + Channel Blockers effects on integrity of descending spinal tracts Adapted from: Schwartz and Fehlings, J. Neurosurg., 2001, 94(Suppl 2):
9 Na + Channel Blockers Tissue Loss Riluzole Control Source: Schwartz and Fehlings, J. Neurosurg., 2001, 94(Suppl 2): Wallerian Degeneration Axotomy - transection of the axon by cutting or crushing Can result in degeneration of pre- / post-synaptic cells and glia. Source: Kandel et al., Principles of Neural Science, McGraw Hill, 2000 Wallerian Degeneration Source: Kandel et al., Principles of Neural Science, McGraw Hill, 2000
10 Possible Therapies Regeneration of damaged axons Remyelination Schwann cell transplants Cell replacement stem cells Restoring function: disruption of nerve pathway Unlike peripheral nerves, axons in the brain and spinal cord cannot regenerate Therapeutic goal: regrowth, bridge the gap Prepare graft using peripheral helper cells (schwann) Still being tested on rats. No huge success yet (but getting there!) Source: Miami Project to Cure Paralysis One problem this research is encountering is getting the graft past the bridge and onto the spinal tissue Source: Miami Project to Cure Paralysis
11 Instead of patching disruption, a second approach is to REPLACE damaged nerves Use of fetal cells successful in animal research Problem 3: Demyelination Also get with some spinal cord injuries Again, trying to trigger Remyelination using Schwann cells from the periphery Poliomyelitis Loss of lower motor neuron cell bodies poliovirus acute infection of ventral horn of spinal cord Selectively destroys lower motor neurons denervates muscle Source: Lundy-Ekman, Neuroscience: Fundamentals for Rehabilitation, Saunders, 2002 Poliomyelitis Source: Lundy-Ekman, Neuroscience: Fundamentals for Rehabilitation, Saunders, 2002
12 Amyotrophic Lateral Sclerosis (ALS) - degeneration of "upper" and "lower" motor neurons - neurogenic atrophy of muscles - correlated with mutation in chromosome 21 Multiple Sclerosis Source: Kandel et al., Principles of Neural Science, McGraw Hill, 2000 Axonal Conduction Block normally, voltage gated K + channels are present in the internodes and v-g Na+ channels are densely packed in region of node after demyelination, electrical properties of axon change Conduction slows or may become blocked
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