Pyramydial vs. Extra pyramidal (confused about the terms)

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Can you explain a major difference between the twos to the level of USMLE? Thanks.

Here is how I understand. Please let me know if they are correct.

Pyramidal tracts = descending corticospinal tract (you have two - Lateral and Anterior - lateral for limbs and anterior for truncal)

Pyramidal signs = seen with UMN lesions.

I am confused about extrapyramidal signs/ tracts though. I saw somewhere that it means LMN signs, then in other place, it says it's of basal ganglia disorders.

Thanks again.

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Here is a Wiki explanation below that may help you.

Pyramidal signs basically mean plantar extension and hyperreflexia.

Extrapyramidal signs/symptoms are due to the side effects from dopamine blockade such as Dyskinesias (pseudoparkinsonism, dystonia, akathisia, tardive dyskinesia). Hope this helps.

In anatomy, the extrapyramidal system is a neural network that is part of the motor system that causes involuntary reflexes and movement, and modulation of movement (i.e. coordination). The system is called "extrapyramidal" to distinguish it from the tracts of the motor cortex that reach their targets by traveling through the "pyramids" of the medulla. The pyramidal pathways (corticospinal and some corticobulbar tracts) may directly innervate motor neurons of the spinal cord or brainstem (anterior (ventral) horn cells or certain cranial nerve nuclei), whereas the extrapyramidal system centers around the modulation and regulation (indirect control) of anterior (ventral) horn cells.

Extrapyramidal tracts are chiefly found in the reticular formation of the pons and medulla, and target neurons in the spinal cord involved in reflexes, locomotion, complex movements, and postural control. These tracts are in turn modulated by various parts of the central nervous system, including the nigrostriatal pathway, the basal ganglia, the cerebellum, the vestibular nuclei, and different sensory areas of the cerebral cortex. All of these regulatory components can be considered part of the extrapyramidal system, in that they modulate motor activity without directly innervating motor neurons.

The extrapyramidal system is very old and three of the four tracts of the human extrapyramidal system are clearly present in salamanders.[1][2]

The extrapyramidal tracts include parts of the following:[3]

 
Here is a Wiki explanation below that may help you.

Pyramidal signs basically mean plantar extension and hyperreflexia.

Extrapyramidal signs/symptoms are due to the side effects from dopamine blockade such as Dyskinesias (pseudoparkinsonism, dystonia, akathisia, tardive dyskinesia). Hope this helps.

In anatomy, the extrapyramidal system is a neural network that is part of the motor system that causes involuntary reflexes and movement, and modulation of movement (i.e. coordination). The system is called "extrapyramidal" to distinguish it from the tracts of the motor cortex that reach their targets by traveling through the "pyramids" of the medulla. The pyramidal pathways (corticospinal and some corticobulbar tracts) may directly innervate motor neurons of the spinal cord or brainstem (anterior (ventral) horn cells or certain cranial nerve nuclei), whereas the extrapyramidal system centers around the modulation and regulation (indirect control) of anterior (ventral) horn cells.

Extrapyramidal tracts are chiefly found in the reticular formation of the pons and medulla, and target neurons in the spinal cord involved in reflexes, locomotion, complex movements, and postural control. These tracts are in turn modulated by various parts of the central nervous system, including the nigrostriatal pathway, the basal ganglia, the cerebellum, the vestibular nuclei, and different sensory areas of the cerebral cortex. All of these regulatory components can be considered part of the extrapyramidal system, in that they modulate motor activity without directly innervating motor neurons.

The extrapyramidal system is very old and three of the four tracts of the human extrapyramidal system are clearly present in salamanders.[1][2]

The extrapyramidal tracts include parts of the following:[3]


Thanks for the wiki.

For Pyramidal signs, I think it should be dorsiflexion instead of plantar extension because Pyramidal sing indicates an UMN lesion. Let me know if I am wrong..

Yeah, I am confused about ExtraPyramidal sings - I have seen dyskinesis/akinesis as being referred to as ExtraPyramidal signs.. But, I am wondering if LMN lesion signs such as fasiculation, hypotonia, etc are also included in ExtraPyramidal signs.

Yeah, there are tracts called ExtraPyramidal tracts - Rubospinal tract, Lateral vesitbulospinal tract, and so forth....
 
Yeah I would think it should be dorsiflexion (Babinski sign). Can anyone clarify this?

Here is what Kaplan says when it talks about subacute combined degeneration.

Subacute combined degeneration occurs with vitamin B12 deficiency. Patients will complain of distal paresthesias and weakness of the extremities followed by spastic paresis and ataxia. On exam there is a combined deficit of vibration and proprioception with pyramidal signs (plantar extension and hyperreflexia). Diagnosis is established by finding a low serum B12 and treatment is with vitamin B12 replacement.
 
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Can you explain a major difference between the twos to the level of USMLE? Thanks.

Here is how I understand. Please let me know if they are correct.

Pyramidal tracts = descending corticospinal tract (you have two - Lateral and Anterior - lateral for limbs and anterior for truncal)

Pyramidal signs = seen with UMN lesions.

I am confused about extrapyramidal signs/ tracts though. I saw somewhere that it means LMN signs, then in other place, it says it's of basal ganglia disorders.

Thanks again.
Extrapyramidal syndromes are movement disorders resulting from basal ganglia dysfunction. Depending on what part of the basal ganglia you're disrupting, you'll have different effects. When you're treating psychosis, some drugs will lower the levels of dopamine in the CNS, this has the effect of simulating Parkinson's disease. So the clinical picture will be of bradykinesia, hypotonia, tardive dyskinesia. On the other hand, one of the effects of treating true Parkinson's disease is that the patient doesn't respond well to levodopa therapy as well any more, and they experience "on-off" phenomenon where the patient fluctuates between dyskinesias and immobility due to abnormal regulation of dopamine levels and an abnormal physiological response to intermittent exogenous dosing.
 
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Thanks for the wiki.

For Pyramidal signs, I think it should be dorsiflexion instead of plantar extension because Pyramidal sing indicates an UMN lesion. Let me know if I am wrong..

Yeah, I am confused about ExtraPyramidal sings - I have seen dyskinesis/akinesis as being referred to as ExtraPyramidal signs.. But, I am wondering if LMN lesion signs such as fasiculation, hypotonia, etc are also included in ExtraPyramidal signs.

Yeah, there are tracts called ExtraPyramidal tracts - Rubospinal tract, Lateral vesitbulospinal tract, and so forth....

Lower motor neuron signs are pyramidal not extrapyramidal.
To put it super simply any lesion is the direct route from motor cortex-->corticospinal tract (upper motor neuron)-->lower motor neuron = WEAKNESS = PYRAMIDAL. Weakness is key as both upper and lower motor neurons lesions cause it. Of course, intrinsic muscle pathology and a whole load of other non neuro things can cause weakness.

As mentioned by the poster above MOVEMENT DISORDERS =EXTRAPYRAMIDAL. EPS are errors in MOTOR PLANNING pathways (not on the direct path from motor cortex to motor neuron) and do NOT characteristically cause weakness or spasticity (though cerebellar lesions can cause hypotonia). The primary motor cortex, the UMN, and the LMN (pyramidal tract) directly give the "marching orders" signals where as the extrapyramidal system refines them and removes the meaningless noise. So knock out the pyramidal "motherboard" and you cant move (weakness) but knock out the EPS "adjusters" and you can still move, but you'll move funny (ataxia) or get stuck (rigidity, bradykinesia, torticollis) or randomly flail (hemiballism) or have an overshoot tremor (cerebellar) or have writhing athetosis or dancing chorea (Huntingtons) etc etc
 
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Lower motor neuron signs are pyramidal not extrapyramidal.
To put it super simply any lesion is the direct route from motor cortex-->corticospinal tract (upper motor neuron)-->lower motor neuron = WEAKNESS = PYRAMIDAL. Weakness is key as both upper and lower motor neurons lesions cause it. Of course, intrinsic muscle pathology and a whole load of other non neuro things can cause weakness.

As mentioned by the poster above MOVEMENT DISORDERS =EXTRAPYRAMIDAL. EPS are errors in MOTOR PLANNING pathways (not on the direct path from motor cortex to motor neuron) and do NOT characteristically cause weakness or spasticity (though cerebellar lesions can cause hypotonia). The primary motor cortex, the UMN, and the LMN (pyramidal tract) directly give the "marching orders" signals where as the extrapyramidal system refines them and removes the meaningless noise. So knock out the pyramidal "motherboard" and you cant move (weakness) but knock out the EPS "adjusters" and you can still move, but you'll move funny (ataxia) or get stuck (rigidity, bradykinesia, torticollis) or randomly flail (hemiballism) or have an overshoot tremor (cerebellar) or have writhing athetosis or dancing chorea (Huntingtons) etc etc

Thank you! That's an awesome explaiantion !
 
Extrapyramidal system is a little different from extrapyramidal tract.
EXTRAPYRAMIDAL SYSTEM includes the basal ganglia and cerebellum. So EXTRAPYRAMIDAL DISORDERS are MOVEMENT DISORDERS like PD, HD, etc as explained above
PYRAMIDAL TRACT is the the corticobulbar tract and CST(that forms a pyramid in the medulla). Corticobulbar tract and CST are part of UMN
EXTRAPYRAMIDAL TRACT includes the rest of UMN like rubrospinal, reticulospinal, vestibulospinal
All extrapyramidal and pyramidal tracts project to UMNs, the final common pathway.
 
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Extrapyramidal system is a little different from extrapyramidal tract.
EXTRAPYRAMIDAL SYSTEM includes the basal ganglia and cerebellum. So EXTRAPYRAMIDAL DISORDERS are MOVEMENT DISORDERS like PD, HD, etc as explained above
PYRAMIDAL TRACT is the the corticobulbar tract and CST(that forms a pyramid in the medulla). Corticobulbar tract and CST are part of UMN
EXTRAPYRAMIDAL TRACT includes the rest of UMN like rubrospinal, reticulospinal, vestibulospinal
All extrapyramidal and pyramidal tracts project to UMNs, the final common pathway.

@Miracoli - can you comment on the symptoms associated with Extrapyramidal "TRACT" lesions? For Rubrospinal tract lesion, I know that there will be an extension of upper limbs but anything else should be expected with this lesion?
 
Lesion of extrapyramidal tracts gives decorticate or decerebrate rigidity.
Actually i found right now that BRS physio has a better note about this.
https://www.inkling.com/read/brs-physiology-linda-costanzo-5th/chapter-2/iii--motor-systems
  1. Motor centers and pathways
    • Pyramidal tracts (corticospinal and corticobulbar) pass through the medullary pyramids.
    • All others are extrapyramidal tracts and originate primarily in the following structures of the brain stem:
    1. Rubrospinal tract
      • originates in the red nucleus and projects to interneurons in the lateral spinal cord.
      • Stimulation of the red nucleus produces stimulation of flexors and inhibition of extensors.
    2. Pontine reticulospinal tract
      • originates in the nuclei in the pons and projects to the ventromedial spinal cord.
      • Stimulation has a general stimulatory effect on both extensors and flexors, with the predominant effect on extensors.
    3. Medullary reticulospinal tract
      • originates in the medullary reticular formation and projects to spinal cord interneurons in the intermediate gray area.
      • Stimulation has a general inhibitory effect on both extensors and flexors, with the predominant effect on extensors.
    4. Lateral vestibulospinal tract
      • originates in Deiters’ nucleus and projects to ipsilateral motoneurons and interneurons.
      • Stimulation causes a powerful stimulation of extensors and inhibition of flexors.
    5. Tectospinal tract
      • originates in the superior colliculus and projects to the cervical spinal cord.
      • is involved in the control of neck muscles.
 
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  1. Effects of transections above the spinal cord
    1. Lesions above the lateral vestibular nucleus
      • cause decerebrate rigidity because of the removal of inhibition from higher centers, resulting in excitation of α- and γ-motoneurons and rigid posture.
    2. Lesions above the pontine reticular formation but below the midbrain
      • cause decerebrate rigidity because of the removal of central inhibition from the pontine reticular formation, resulting in excitation of α- and γ-motoneurons and rigid posture.
    3. Lesions above the red nucleus
      • result in decorticate posturing and intact tonic neck reflexes.
 
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  1. Effects of transections above the spinal cord
    1. Lesions above the lateral vestibular nucleus
      • cause decerebrate rigidity because of the removal of inhibition from higher centers, resulting in excitation of α- and γ-motoneurons and rigid posture.
    2. Lesions above the pontine reticular formation but below the midbrain
      • cause decerebrate rigidity because of the removal of central inhibition from the pontine reticular formation, resulting in excitation of α- and γ-motoneurons and rigid posture.
    3. Lesions above the red nucleus
      • result in decorticate posturing and intact tonic neck reflexes.
Nice! Thanks.
 
Here is a Wiki explanation below that may help you.

Pyramidal signs basically mean plantar extension and hyperreflexia.

Extrapyramidal signs/symptoms are due to the side effects from dopamine blockade such as Dyskinesias (pseudoparkinsonism, dystonia, akathisia, tardive dyskinesia). Hope this helps.

In anatomy, the extrapyramidal system is a neural network that is part of the motor system that causes involuntary reflexes and movement, and modulation of movement (i.e. coordination). The system is called "extrapyramidal" to distinguish it from the tracts of the motor cortex that reach their targets by traveling through the "pyramids" of the medulla. The pyramidal pathways (corticospinal and some corticobulbar tracts) may directly innervate motor neurons of the spinal cord or brainstem (anterior (ventral) horn cells or certain cranial nerve nuclei), whereas the extrapyramidal system centers around the modulation and regulation (indirect control) of anterior (ventral) horn cells.

Extrapyramidal tracts are chiefly found in the reticular formation of the pons and medulla, and target neurons in the spinal cord involved in reflexes, locomotion, complex movements, and postural control. These tracts are in turn modulated by various parts of the central nervous system, including the nigrostriatal pathway, the basal ganglia, the cerebellum, the vestibular nuclei, and different sensory areas of the cerebral cortex. All of these regulatory components can be considered part of the extrapyramidal system, in that they modulate motor activity without directly innervating motor neurons.

The extrapyramidal system is very old and three of the four tracts of the human extrapyramidal system are clearly present in salamanders.[1][2]

The extrapyramidal tracts include parts of the following:[3]

Hello ppl. I'm from Brazil and I'm not a student of health courses. I saw the math about extra pyramidal and pyramidal subject. I'm a patient and the doctor said I have squizofreny but when I saw a study about risperidone versus haloperidol I saw that some adverse effects of risperidone are extrapyramidal effect and sedation but the extrapyramidal effect is something I saw here and got curiosity. So is that always motivated for lesions? About B12 deficit is it a problem that can get us trouble with extapyramidal effect? If I get more b12 from meat could I fight against that adverse effect? I'm having some involuntary movements at my hand but I wonder if could that be due risperidon extra pyramidal effect or deficit of b12? The last question is about the monotherapy of risperidone. spite of haldol could just risperidone be good? See ya bye and thanks
 
Hello ppl. I'm from Brazil and I'm not a student of health courses. I saw the math about extra pyramidal and pyramidal subject. I'm a patient and the doctor said I have squizofreny but when I saw a study about risperidone versus haloperidol I saw that some adverse effects of risperidone are extrapyramidal effect and sedation but the extrapyramidal effect is something I saw here and got curiosity. So is that always motivated for lesions? About B12 deficit is it a problem that can get us trouble with extapyramidal effect? If I get more b12 from meat could I fight against that adverse effect? I'm having some involuntary movements at my hand but I wonder if could that be due risperidon extra pyramidal effect or deficit of b12? The last question is about the monotherapy of risperidone. spite of haldol could just risperidone be good? See ya bye and thanks

Dear Henrique, first let me commend you on taking such an active role in your own care. Probably, one of the most important ways to maximize your treatment outcome is to educate yourself about your diagnosis and prescribed medications. As you have probably come to realize, this site is not for diagnosing or treating actual patients, nor commenting on the recommendations of your personal physician. With that in mind, I will say if you have concerns about certain supplements or vitamin deficiencies, I would encourage you to talk to your doctor. There are certain conditions and medications that can affect how your body incorporates vitamin B12 and there are ways of getting a B 12 level, if you believe that is an issue. As to medication side affects, both risperidone and haloperidol have the potential to affect what has been described above as the " extra pyramidal" system, causing involuntary and often unsettling movements. I hope that is not the case with you. I wish you the best of luck and encourage to remain your own strongest advocate.
 
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