Term
| What are the 3 basic functional elements of the "motor system"? |
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Definition
1) Alpha-motorneuron
2) Descending pathways in spinal chord (and homologues for the head) that influence motor units monosynaptically or polysynaptically
3) Basal ganglia and Cerebellum make contacts with cells that synapse on descending spinal tract cells. |
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Term
| How do the lateral and medial descending motor pathways of the spinal cord differ? |
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Definition
Medial tracts terminate in a greater number of spinal segments and exert more influence on muscles that oppose the force of gravity (i.e biceps and quadriceps)
1) Medial tracts control proximal and axial musculature and synapse on medial anterior horn (mostly in interneurons).
- Reticulospinal (posture and tone)
- Anterior Corticospinal (Descends opposite to lateral tract, but crosses at segmental levels to innervate grey matter)
- Tectospinal (Orienting body toward stimulus)
- Vestibulospinal (Posture and balance)
2) Lateral tracts control distal musculature and synpase on lateral anterior horn.
- Lateral corticospinal (arises from contralateral cortex) for hands and fingers
- Rubrospinal (arises from contralateral red nucleus and recieves cortical and cerebellar input) for arms and hands. |
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Term
| What are Propriospinal circuits and why are they important? |
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Definition
Intrinsic pathways that link different segmental levels of spinal grey matter (Lateral in "intra-limb" muscle groups and Medial is inter-limb or limb-trunk muscle groups)
Regulate activity of different muscle groups and generate coordinated movements and whole body movements (walking) |
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Term
| What Neurological Processing (abnormal) causes Decorticate posture, with contralateral leg extension at the knee and hip, and contralateral arm flexion at the elbow and wrist) |
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Definition
Lesion to Corticobulbar projections from the cortex that normally excite the inhibitory reticular area (IRA) of the medulla and reduce extensor reflex activity and extensor muscle tone.
Remember, normally these corticobulbar projections counter the excitatory drive of the spinal chord and Vestibular nuclei of the brainstem towards these muscles. |
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Term
| What causes Decerebrate posture with leg and arm extensions? |
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Definition
| Large lesions of the upper pons and midbrain (interesting that arms extend in this case, as compared to Decorticate posture with Corticobulbar lesions- may be due to absence of rubrospinal tract) |
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Term
| What are 6 classic LMN signs? |
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Definition
Flacid paralysis, Hyporeflexia, Atrophy, Fibrillation and Fasciculations,
1) Weakness or paralysis (nerve-muscle conduction, but needs to be distinguished from primary muscle disease).
2) Hypotonia- lack of resistance to passive movement (interruption of efferent limb of spinal reflex)
Paralysis + Hypotonia = FLACCID PARALYSIS
3) Hyporeflexia
4) Atrophy (disuse or neurogenic with lack of innervation)
5) Fibrillation (by EMG)
6) Fasciculation (twitches under skin) |
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Term
| What are 3 common causes of LMN syndromes? |
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Definition
1) Viruses (poliomyelitis selective for anterior horn cells)
2) Peripheral nerve injury (damage to alpha motorneurons)
3) Lesion of SC anterior horn or brainstem efferent nuclei |
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Term
| How can you tell if UMN damage has occurred? |
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Definition
Involves descending spinal pathways that originate in cortex or brainstem
1) Inability to produce voluntary movements (mild paresis or severe paralysis)
2) Spasticity (increased reactivity to stretch)- hard to bend legs and straighten arms)- CLONUS
Paralysis + Spasticity= Spastic Paralysis
3) Diminution of superficial cutaneous reflexes (absent abdominal reflex)
4) (+) Babinski |
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Term
| What are 3 examples of UMN pathologies? |
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Definition
1) Lesion of internal capsule (loss of control of descending spinal circuitry, leading to overactivity of alpha-motorneurons)
2) Lesion of both M1 AND adjacent areas of cortex (If confined to area 4 you see flaccid and not spastic!)
3) Transection of spinal cord (caudal to level of lesion you see signs) |
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Term
| Why might you give a GABA agonist such as Baclofen? |
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Definition
To treat Upper Motor Neuron Issue.
Spasticity results from a) inappropriate modulation of activity of motor-neurons because of lack of descending control and 2) Increased excitability of alpha motor-neurons.
GABA agonist decreases excitability of the alpha motor-neurons. |
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Term
| What is the characteristic Tim course of symptoms in an Upper Motor Neurons syndrome? |
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Definition
1) Immediately following trauma you see hypoactive reflexes and flaccid muscles (absense of tonic descending drive)
2) 1-6 weeks later, reflex activity returns and tendon reflexes become hyperactive because
a) heightened sensitivity of spinal cord interneurons or motor-neurons to remaining synaptic inputs and
b) Sprouting of axon collateral to occupy synaptic sites.
** this is paralleled by preganglionic sympathetic and parasympathetic neurons (may see low BP followed by very high BP)** |
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