Session 4 - Pyramidal Tracts Flashcards Preview

Semester 5 - CNS > Session 4 - Pyramidal Tracts > Flashcards

Flashcards in Session 4 - Pyramidal Tracts Deck (23)

What are the two main classes of descending tracts?

Pyramidal tracts
Extrapyramidal tracts


What do pyramidal tracts do?

Maintain somatic control of muscle by making direct (monosynaptic) contact with LMN supplying distal muscle of extremities


What are the two mains part of the pyramidal tract?



What are the two different part of the corticospinal tract?

Lateral and anterior


Outline the path of the corticospinal tract

 Skeletal Muscle α-LMN
 Lateral decussates in Medullary Pyramids
 Anterior remains ipsilateral


Where does the corticotubular pyramid extend to?

 Cranial Nerve Nuclei


What are extrapyramidal tracts?

Indirect contact (polysynaptic) with motor neurones, via regulation of ventral horn interneurons.


What is the difference in relationships with LMN's between pyramidal and extra-pyramidal systems

Pyramidal system has direct (monosynaptic) contact with lower motor neurones supplying the distal muscles of extremities (e.g. the hand)

The extra-pyramidal system has an indirect contact with the rest of the motor neurone pool.


Give three causes of upper motor neurone lesions

 Stroke
 Spinal cord injury
 Motor neurone disease


Give three causes of LMN lesions

 Trauma
 Peripheral neuropathy
 Motor neurone disease


Give key signs of UMN lesions

 Hypertonia
 Hyerreflexia
 Clonus
 +’ve Babinski sign
 No fasiculations
 Clasp-knife reflex
 No muscle wasting
 Muscle weakness


Give key signs of LMN lesions

 Hypotonia
 Hyporeflexia
 Fasciculations
 Muscle wasting
 Muscle weakness


Where does hypertonia, hyperreflexia and spastic paralysis come from in a UMN lesion?

Loss of descending inhibition of spinal reflexes


What is clasp knife reflex?

 Increased tone gives resistance to movement, but when sufficient force is applied resistance suddenly decreases


What is clonus caused by?

 Loss of descending inhibition leads to self re-excitation of hyperactive reflexes


What is a positive Babinski sign?

 Scrape along lateral edge of foot and in towards great toe
 Dorsiflexion of hallux, extension/flaring of toes (Loss of descending inhibition means the reflex is unable to be suppressed)


What is hypotonia caused by in LMN lesions?

 Lack of LMN means muscle cannot contract to produce tone


Name the extra-pyramidal tracts

Tectospinal tract
Vestibulospinal tract
Reticulospinal tract
Rubrospinal and rubrobulbar tract


Where does the tectospinal tract arise and what does it do?

– Main inputs are from the superior and inferior colliculi in the midbrain; decussate in the midbrain
– Innervate Motor neurone pools of neck – coordinate eye-head movements, responses to visual & auditory stimuli


Where does vestibulospinal tract arise and what does it do?

– Originates from vestibular nuclei in the Pons; remain ipsilateral;
– Innervates motor-neurone pools of anti-gravity muscles - balance reflexes.


Where does reticulospinal tract arise and what does it do

– Widespread inputs, including from motor cortex, medulla oblongata, pons and midbrain
- remain ipsilateral
– Medullary (lateral tract) - Flexor reflex facilitation
- Extensor reflex inhibition
– Pontine (medial tract) - Extensor reflex facilitation
– Role in regulation of posture and rhythmic movements


Where does rubrospinal tract arise and what does it do?

– Originates from red nucleus (tegmentum of the mid-brain at superior colliculus), inputs include motor cortex
- Decussates at level of nucleus
– Control flexor tone in distal muscles, also tone of facial muscles


Where do corticospinal tracts arise from?

1/3 motor cortex
1/3 secondary motor cortex
1/3 parietal lobe

(2/3 precentral gyrus, 1/3 post-central gyrus)