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Episode Notes

Source / episode info

  • Episode: 374
  • Title: Divine Intervention Episode 374 – Spinal Cord Lesions (for Step 1-3)
  • Published: 2022-02-25
  • Source: Episode page

One-liner

This episode provides a comprehensive review of spinal cord syndromes, detailing the distinct patterns of sensory (dorsal column vs. spinothalamic tract) and motor deficits seen in conditions like Brown-Séquard syndrome, Central Cord Syndrome, Anterior Spinal Artery Syndrome, Subacute Combined Degeneration, and differentiating myelopathies from radiculopathies.

High-yield summary

  • Brown-Séquard Syndrome: Results from spinal cord hemisection (e.g., gunshot wound). Symptoms are ipsilateral loss of fine touch/vibration (Dorsal Columns) and contralateral loss of pain/temperature (Spinothalamic Tract), plus UMN signs on the same side as the lesion, and LMN signs at the level of the lesion.
  • Central Cord Syndrome: Damage to the center of the spinal cord (e.g., cervical trauma, syringomyelia). Classically presents with bilateral loss of pain and temperature sensation in a "cape-like" distribution, often affecting the upper extremities more severely.
  • Subacute Combined Degeneration: Caused by Vitamin B12 deficiency or impaired absorption (e.g., pernicious anemia, Crohn's disease). Affects both Dorsal Columns and Lateral Corticospinal Tract, leading to positive Romberg sign and UMN signs.
  • Anterior Spinal Artery Syndrome: Damage to the anterior two-thirds of the cord (e.g., following triple Aneurysm repair). Results in loss of all functions except fine touch, vibration, and proprioception (Dorsal Columns are spared).
  • Myelopathy vs. Radiculopathy: Myelopathy is a spinal cord problem; Radiculopathy is a nerve root problem. Myelopathies often present with bilateral symptoms or sensory levels; radiculopathies tend to be unilateral/lateral.
  • ALS: A pure motor neuron disease (UMN + LMN) that never involves sensory deficits. Treatment targets glutamate excitotoxicity using Riluzole.

Learning objectives

  • Differentiate the clinical presentations associated with various spinal cord syndromes (Brown-Séquard, Central Cord, Anterior Spinal Artery Syndrome).
  • Recognize the specific neurological findings related to Vitamin B12 deficiency and its impact on dorsal columns and corticospinal tracts.
  • Distinguish between myelopathy (spinal cord) and radiculopathy (nerve root) based on clinical patterns and physical exam findings.
  • Identify the characteristic motor neuron deficits seen in primary lower motor neuron diseases (SMA, ALS).
  • Interpret CSF findings associated with viral meningitis (e.g., West Nile Virus).

Board exam buzzwords

ConditionKey FindingAssociationBoard Exam Tip
Brown-Séquard SyndromeHemisection of spinal cordIpsilateral DC loss; Contralateral STT lossRemember the "split" pattern: one side for proprioception, opposite side for pain/temp.
Central Cord SyndromeBilateral Paresthesia (Cape distribution)Syringomyelia, Cervical traumaThe central location affects crossing fibers first, leading to bilateral sensory deficits.
Subacute Combined DegenerationPositive Romberg sign + UMN signsVitamin B12 deficiency; Pernicious anemiaMust have both dorsal column and corticospinal tract involvement for this diagnosis.
Anterior Spinal Artery SyndromePreservation of fine touch/vibrationDamage to anterior 2/3 of cord (e.g., AAA repair)The spared function is the most reliable diagnostic clue here.

Rapid review table

TopicKey PointContextExam Relevance
Myelopathy vs. RadiculopathyMyelopathy = Spinal Cord; Radiculopathy = Nerve RootA myelopathy often presents with bilateral symptoms or a sensory level; radiculopathy is typically unilateral/lateral.Use the pattern of deficits (e.g., dermatomes) to localize the problem.
Brown-Séquard SyndromeIpsilateral DC loss, Contralateral STT lossSpinal cord hemisection (e.g., gunshot wound).This classic triad is highly testable and requires remembering which deficit crosses where.
B12 DeficiencySubacute Combined DegenerationPernicious anemia, Crohn's disease, small bowel resection.Always check for both dorsal column signs (Romberg) AND UMN signs (hyperreflexia).
West Nile Virus MeningitisCSF: Mild pleocytosis (lymphocyte predominance), slightly elevated opening pressure, low glucose.Viral etiology; can cause severe meningoencephalitis.Differentiating viral vs. bacterial meningitis is key for appropriate empiric treatment.

Board-speak -> diagnosis

Board-speak / Vignette phraseDiagnosis / ConceptWhy it fits
A patient sustains a gunshot wound to the left side of the cervical cord, presenting with loss of fine touch/vibration on the left and loss of pain/temperature sensation on the right.Brown-Séquard SyndromeThis pattern perfectly matches hemisection damage: ipsilateral dorsal column deficit (left) and contralateral spinothalamic tract deficit (right).
A patient presents after a severe motor vehicle accident with bilateral sensory loss, predominantly affecting the upper extremities in a "cape" distribution.Central Cord SyndromeDamage to the central cord affects the crossing spinothalamic tracts bilaterally, leading to this classic pattern of pain/temperature loss.
A 65-year-old vegan presents with gait instability and positive Romberg sign, along with hyperreflexia.Subacute Combined Degeneration (B12 deficiency)B12 deficiency damages the dorsal columns (Romberg+) and lateral corticospinal tracts (UMN signs/hyperreflexia).
A patient undergoes surgery for an abdominal aortic aneurysm repair and subsequently develops profound weakness and loss of pain/temperature sensation, but retains fine touch and vibration sense.Anterior Spinal Artery SyndromeDamage to the anterior two-thirds of the cord spares the dorsal columns, resulting in preserved proprioception despite severe motor deficits.
A 7-month-old child presents with progressive muscle weakness, absent deep tendon reflexes, and loss of motor milestones.Spinal Muscular Atrophy (SMA)SMA is a lower motor neuron disease affecting anterior horn cells, leading to profound LMN signs in infancy.
A middle-aged man complains of difficulty playing the piano and swallowing, but all sensory exams are normal.Amyotrophic Lateral Sclerosis (ALS)ALS is a pure motor neuron disorder (UMN + LMN) that does not involve any sensory deficits.

Differential diagnosis / distinguishing features

Central Cord Syndrome

Key FeaturesDistinguishing FindingsNext Step
Bilateral sensory loss in a "cape" distribution, often affecting upper extremities first.Damage is central; commonly associated with syringomyelia or cervical trauma.Rule out compressive causes (e.g., tumor) and perform MRI to look for syrinx formation.

Subacute Combined Degeneration

Key FeaturesDistinguishing FindingsNext Step
Positive Romberg sign + UMN signs (hyperreflexia, spasticity).Requires deficiency of Vitamin B12; associated with malabsorption syndromes (Pernicious anemia).Measure serum Methylmalonic Acid (MMA) and Homocysteine levels. Supplementation (oral/IM) is the treatment.

Anterior Spinal Artery Syndrome

Key FeaturesDistinguishing FindingsNext Step
Loss of all functions except fine touch, vibration, and proprioception.Damage to the anterior two-thirds of the cord; often follows vascular surgery (e.g., AAA repair).Identify the underlying vascular cause or trauma site. Supportive care is primary management.

Cauda Equina Syndrome vs. Conus Medullaris Syndrome

Key FeaturesDistinguishing FindingsNext Step
Conus/Cauda: Myelopathy (Cord damage)Myelopathy: Often bilateral; UMN signs predominate; Sensory level may be present.MRI is required to visualize the cord vs. nerve roots.
Radiculopathy: Nerve Root DamageRadiculopathy: Typically unilateral or lateral; LMN signs predominate; Symptoms follow a dermatomal pattern.Electromyography (EMG) and Nerve Conduction Studies (NCS) are used for confirmation.

Management pearls

  • High Cervical Cord Injury: Any injury affecting C3-C5 roots/segments requires immediate consideration of respiratory failure, as these segments supply the diaphragm via the phrenic nerve; mechanical ventilation may be necessary.
  • B12 Deficiency Management: Treatment involves administering Vitamin B12 (e.g., 1000 mcg IM) to bypass potential gastrointestinal absorption issues seen in pernicious anemia or Crohn's disease.
  • ALS Management: While supportive care is paramount, Riluzole can be used to slow the progression by acting as an NMDA receptor antagonist and mitigating glutamate excitotoxicity.
  • Syringomyelia Workup: If central cord syndrome is suspected, MRI should be performed to look for a syrinx cavity (cystic dilation of the spinal canal).

Don't miss

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The key difference between myelopathy and radiculopathy lies in whether the pathology affects the spinal cord itself or the nerve roots exiting it.
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Dorsal Columns carry proprioception, fine touch, and vibration; damage leads to loss of these senses (positive Romberg).
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Spinothalamic Tracts carry pain and temperature information; damage is often contralateral to the lesion site.
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SMA: Is a lower motor neuron disease affecting anterior horn cells, leading to profound weakness in infancy.

Integration & clinical reasoning

  • Neurological Exam Integration: When evaluating spinal cord function, always systematically test: 1) Dorsal Columns (proprioception/vibration), 2) Spinothalamic Tracts (pain/temp), 3) Corticospinal Tract (UMN signs), and 4) LMN signs at the level of the lesion.
  • Vascular Integration: The anterior spinal artery is highly susceptible to compromise during major vascular surgeries (e.g., AAA repair), leading to predictable syndromes like Anterior Spinal Artery Syndrome.
  • Endocrine/Neuro Integration: While not directly related, understanding that peripheral neuropathy can mimic myelopathy requires ruling out metabolic causes (like B12 deficiency) before attributing symptoms solely to spinal cord damage.

OMM / COMLEX integration

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For COMLEX: know these viscerosomatics / Chapman points, but don't let OMM distract from emergent diagnosis and management.
  • Acute/Unstable Pathology: In any acute myelopathy or radiculopathy presentation, standard emergency management (ABC assessment, imaging, stabilization) takes absolute priority over OMT.
  • Spinal Cord Trauma: The principles of spinal cord injury classification and immediate immobilization are critical; manual traction and careful handling are paramount to prevent secondary damage.

Concept connections / cross-references

  • For detailed information on the general principles of neurological examination and sensory pathways, review [Episode 370].
  • Understanding motor neuron diseases like ALS is related to generalized neuromuscular function discussed in [Episode 365].

High-yield association table

ConditionAssociationMechanismClinical Significance
Brown-Séquard SyndromeSpinal cord hemisectionDamage affects tracts unilaterally (DC vs. STT).Requires careful mapping of deficits: ipsilateral DC, contralateral STT.
Central Cord SyndromeSyringomyeliaCystic dilation within the spinal canal damages central crossing fibers.Leads to a characteristic bilateral "cape" distribution of pain/temp loss.
Subacute Combined DegenerationVitamin B12 deficiencyDeficiency impairs myelin sheath maintenance in dorsal columns and lateral corticospinal tracts.Testing for MMA and Homocysteine is crucial for diagnosis confirmation.
Anterior Spinal Artery SyndromeAAA repair / Vascular traumaIschemia or direct damage to the anterior spinal artery.The preservation of fine touch/vibration (dorsal columns) is the hallmark finding.

Key terms glossary

TermDefinitionContextExample
MyelopathyDysfunction or disease affecting the spinal cord itself.Clinical presentation following trauma, tumor, or vascular compromise.Transverse myelitis (inflammation of the cord).
RadiculopathyDysfunction or disease affecting a specific nerve root.Compression or inflammation at the foramen exit point.Sciatica (compression of the sciatic nerve root).
Dorsal ColumnsFascicles carrying proprioception, fine touch, and vibration sense.Damage leads to loss of these senses; tested via Romberg sign/joint position sense.Subacute Combined Degeneration affects this pathway.
SyringomyeliaFormation of a fluid-filled cavity (syrinx) within the spinal cord parenchyma.Often seen in Central Cord Syndrome; can be idiopathic or secondary to trauma.Requires MRI confirmation and is associated with central sensory loss.

Study optimization

TopicStudy ApproachPriorityResources
Spinal SyndromesCreate a flow chart comparing the 4 major syndromes (Brown-Séquard, Central Cord, Anterior SA, B12).HighReview board vignettes focusing on pattern recognition.
Motor Neuron DiseasesDifferentiate pure motor vs. mixed UMN/LMN disorders; remember sensory sparing in ALS.MediumUse mnemonics for the signs (e.g., SMA = LMN only).
Differential DiagnosisPractice localizing deficits: Is it a root, the cord, or peripheral nerve?HighReview images of spinal sections to visualize tract damage.

Question pattern recognition

  • Pattern: Ipsilateral loss of fine touch/vibration + Contralateral loss of pain/temp -> Brown-Séquard Syndrome (Hemisection).
  • Pattern: Bilateral sensory loss, predominantly in the upper extremities, with preserved deep tendon reflexes -> Central Cord Syndrome (Syringomyelia).
  • Pattern: Positive Romberg sign and hyperreflexia -> Subacute Combined Degeneration (B12 deficiency) because both dorsal columns and corticospinal tracts are damaged.
  • Pattern: Symptoms that follow a dermatomal pattern, often unilateral/lateral -> Radiculopathy (Nerve root compression).

Test yourself

Common mistakes to avoid

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Mistake: Assuming that all spinal cord syndromes present with the same pattern of motor weakness. Correction: The specific location and type of damage (e.g., anterior vs. central) dictates which tracts are affected, leading to unique patterns.
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Mistake: Confusing myelopathy with radiculopathy based on symptoms alone. Correction: Always use physical exam findings (dermatomes vs. sensory levels; UMN vs. LMN predominance) and imaging (MRI) to localize the lesion correctly.
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Mistake: Forgetting that B12 deficiency affects both dorsal columns AND corticospinal tracts, leading to a combination of signs (Romberg + hyperreflexia).

Common traps

⚠️
Trap 1: The "Pure Motor" Trap: If a patient has weakness but no sensory deficits, think motor neuron disease (ALS) or an anterior cord syndrome.
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Trap 2: The Sensory Level Trap: A defined sensory level strongly suggests a myelopathy (spinal cord lesion), whereas dermatomal patterns suggest radiculopathy (nerve root).
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Trap 3: The "Spared Function" Trap: When presented with severe spinal deficits, remember which function is spared to pinpoint the exact location of damage (e.g., preserved fine touch in Anterior Spinal Artery Syndrome).

Original transcript with highlights

Original transcript with highlights

Okay, welcome. My name is Divine. This is episode 374 of the Divine intervention podcasts. And to this podcast, I'm going to be talking about the spinal cord lesions. So this is a continuation of the episode I started. I'm a few days ago actually, that was February 14th. I think I made that on Valentine's day from Namasteakin on the spinal cord, the spinal cord for step one to step three. So this is a full of these like the sequel to that podcast is on spinal cord lesions for step one to step three. Right? So the first thing I think I want to go ahead and start with is if you're taking the USMLSTEP2 CTO step three exams, within the next one month, I do have an NV Me testing and strategy scores coming up on the 21st of March. And then I have a 24-hour review course coming up between the 22nd to the 25th of March. So testing and strategy scores on a Monday and then the 24-hour review course from Tuesday to Friday. Again, I literally just completed the course today. And again, many people attended it and found it to be really helpful. So again, if you're interested, just go ahead and shoot me an email. And I'll be more than happy to point you in the right direction. So let's just go ahead and jump right into it. So what if they give you a question about a 25-year-old male and they tell you that he was shot. They tell you that oh, he was shot.

And now he has like, you know, they tell you that he has like, like, muscle weakness in his low extremities and they just tell you a bunch of different symptoms, right? They tell you that in his, like, right operative extremity, for example, they tell you that oh, he has lost pain and temperature sensation. And then in his left operative extremity, they tell you that he has lost fine-touch vibration and perception, right? And they tell you that oh, in his bilateral lower extremities, he has a positive Babinsky sign. Right? If you see that, what should you be thinking about? I'll really hope you're saying, oh, divine. It sounds like this person has bronzed quad syndrome, right? Bronzoquart syndrome. Right? Again, this thing is really rare, but it's something that is really testable. And why is it really testable? Because again, it's something that can integrate many different pieces of the spinal cord. So remember, the first thing with the bronzoquart syndrome is it's a spinal cord hemisection, right? You're literally messing up one half of the spinal cord, right? So let's just take things one by one, key to many of these spinal cord problems is just like many things in life, B-systematic. If you're systematic, you're going to be in good shape, right? So the thing is the dorsal columns are going to be messed up. Remember the dorsal columns? So let's say you have the problem on the right, right? Let's say, so let me just use a frame of reference.

Let's say, okay, let's say the problem is on the left, right? Let's say the problem is on the left, right? Your left spinal cord is messed up. Let's look at the pathways one by one. First, your dorsal columns are going to be messed up, right? So if your dorsal columns are messed up, remember your dorsal columns don't cross until they get to the midbrain. I mean until they get to the brainstem, the medallion. So since they've not crossed, you're going to have epsilateral symptoms. When you're left side, you're going to have loss of fine-touch vibration and perceptive information. But remember, your spinal thalamic tract crosses, right? So you're going to lose pain and temperature information on the contralateral side of the body, right? So you're going to lose pain and temperature information on the right, right? So if the problem is on the left, your dorsal column symptoms are going to be on the left and your, your, um, your spinal thalamic tract symptoms are going to be on the right. Now let me say something, I should probably correct myself. Let's assume that those people have the positive Babinsky in the left-low extremities, right? Because the thing is again, it's a spinal cord hemisection. Now, the thing is, those people, they're going to have upper motor neurons symptoms. But if you remember, the upper motor neurons, right, have already crossed in the cordon medulla, right? In the medallary pyramids.

So the thing is, those upper motor neurons symptoms they will have from the corticospinal tract, they're going to have it on the same side because the fibers have already crossed. So they're going to have like a positive, positive Babinsky on the left side. So we're assuming that this person's Gonshot wound was to the left spinal cord, right? And then you're also going to have lower motor neurons symptoms, right? Many times they're going to have it at the level of the lesion, right? They're going to have it at the level of the lesion. They're going to have it at the level of the lesion, right? So they're going to have lower motor neurons symptoms, like on the left sides of their bodies, right? And they're going to have upper motor neurons symptoms as well on the left side of their bodies, right? So again, those are the major tracks you see in the spinal cord. Again, it's just very high you to know these things. If you know these things, it's going to help you significantly on exams. Just always remember, whenever you get a spinal cord problem, ask yourself, is it affecting my drosol columns? Is it affecting the corticospinal tract? Is it affecting my upper motor neurons, right? Which is your corticospinal tract? Is it affecting my low motor neurons? That's the ventral horn or the anterior horn of the spinal cord, right? And is it affecting my spinal thalamic tract? Those are your pain and temperature fibers. Now, what if they give you a question about a patient?

They tell you that this patient, you know, was in a major motor vehicle accident, right? And they tell you that, oh, this patient has a history of spinal stenosis and that they suffered like very severe wear plashing jury. And then they tell you that, oh, the person has lost pain and temperature sensation and croutoch sensation, right? In their bilateral upper extremities. If you see that, I really want you to think about this person having what is called central cord syndrome, right? Central cord syndrome. Literally, the name tells you exactly what that means. Central cord syndrome is when you have a problem in the center of the spinal cord, right? In the center of the spinal cord. So if you damage the center of the spinal cord, the primary fibers, you're going to mess up. You're going to mess up those spinal thalamic tract fibers because if you remember from the last podcast that I made on the clutch spinal cord, I said that there's a part of the spinal cord called the central canal, where CSF flows through, right? The thing is in that central canal right in front of it is a region of the spinal cord called the anterior wide commissure. The spinal thalamic tract crosses in front of the anterior wide commissure. So if you have any problems in the center of the spinal cord, many times you're going to have pin and temperature loss in a bilateral distribution, right? Like you see the classically described, Cape Light Distribution, right? Central cord syndrome.

Actually, one of probably the more common causes of central cord syndrome, the emission and exam is syringo-maelia, right? Syringo-maelia. Remember, syringo-maelia happens when you have a cystic dilution of the central canal of the spinal cord. When you have that cystic dilution, the thing that's going to happen is that you're going to mess up again your cross-send spinal thalamic tract fibers. You're going to have a loss of pin and temperature information in a in a Cape Light Distribution. Now remember, syringo-maelia has an association with the Kiari-1 morpho-vation. I just remember that syringo-maelia, right? Like the fourth letter is an eye, kind of look like a one, right? Kiari-1 morpho-vation. That's a nice way to keep that in mind. So again, our friends at the MBM is one thing they've been doing in recent times on exams, is instead of giving you the words you know, then it just give you different terms. They can literally give you a syringo-maelia question and put a central cord syndrome as the answer, right? That's something just want to be prepared for on exams. And then what if they give you a question about a vegan? And they tell you that this vegan, you know, over the last like four months, have they having like a pins and needles sensation diffused around the body, right? And they tell you that this vegan, you know, has like parts of their bodies where they've lost pain and temperate, where they've lost a fine-touch vibration and perceptive information, right?

And they also tell you that they have like a positive Babinski sign, right? When you see all these peripheral neuropathes out and you're seeing like upper-moderated neurons symptoms, like you're seeing dossal colombus symptoms, I really want you to think about a sub-itute combined degeneration of the spinal cord, right? This is something that actually happens in people that have a B12 deficiency, right? They have a vitamin B12 deficiency. Remember vitamin B12 is very important for the appropriate function of your dossal columns and your lateral corticospinal tract. So if you have a B12 deficiency for any reason, because you're vegan, so you're not eating animal products, right? Or you have preneciacinemia, right? Where you pretty much, you have an autoimmune disease that has nuked your pridele cells, right? Or like intrinsic factor, right? Or you've nuked your terminal helium for any reason, right? Because you have like Crohn's disease, or you have a Celiac disease or things of that nature, or you've had like a small bowel reception. In those circumstances, you can get B12 deficiency, right? Don't forget B12 deficiency can cause a sub-acute combined degeneration of the cord, right? And in that subacute combined degeneration of the cord, you're missing of the corticospinal tract, right? And the dossal columns, right?

In fact, people that miss of their dossal columns is actually very high, or to know, on NBM exams, that those people are going to have a positive rhomburg test, right? So what is the mechanic of the, what are the mechanics of the rhomburg test? Well, remember, for you to know where your joints are in space, there are three things that help you do that. One is your vision. Two is your cranial nerve, eight is your vestibulococular nerve. And then three are your dossal columns. Of those three things, you need at least two working on every point in time for you to know exactly where your joint sign is in space. So if, for example, the dossal columns have been affected, it's not a big deal. They still have two out of three things helping them, vision and cranial nerve, eight. But when you tell them, oh, okay, you know what, go ahead and close your eyes, put your feet together, right? You close your eyes, you take away vision. Now they just, they just live with cranial nerve, eight. Those people are going to fall over, right? That's a positive rhomburg test. Remember, the rhomburg test is a test for dossal column function. It has nothing to do with the cerebellum. And then what if they give you a question about a person, they tell you that this person just had a triple-air repair, but that the person has been unable to move anything since the surgery ended. If you see that, what are you looking for?

I would really hope you're saying, oh, divine, this person likely has anterior spinal artery syndrome, right? And anterior spinal artery syndrome. Remember, anterior spinal artery syndrome arises because the anterior spinal artery in some cases can arise from an artery called the artery of a dhamcoids. I've said this in many podcasts, right? The thing is if you're fixing a triple-air and abdominal euricanurism, certain parts of the certain, yeah, abdominal euirror actually gives rise to a pretty large artery called the artery of a dhamcoids. The artery of a dhamcoids supplies certain levels of the spinal cord with the anterior spinal artery. So the thing that happens with people have anterior spinal artery syndrome is that you're going to lose everything in the spinal cord with the exception of the drossal columns. Those people will have no problems with fine touch, vibration, and perceptive sensation, but every other thing is pretty much gone, right? Because they're pretty much lost like the anterior two thirds of the spinal cord.

And one thing I want to go back and see is when people have central cord syndrome, I know I said that, you know, predominantly they're going to lose pain and temperature information, but every now and then those people can also have lower motor neuron symptoms because that central cord syndrome, depending on the extent of it, you can begin to pick up some, you can begin to mess up some fibers that constitute your lower motor neurons in the ventral horn or the anterior horn of the spinal cord, right? And then what if they give you a question about a seven-month-old child? They tell you that he has been losing his motor milestones and they tell you that he just has like profound diffuse muscle weakness and he has like the diffuse hyperreflexia, right? If you see that in an exam, what should you be thinking about? I would really hope you're seeing O' Divine, this child has spinal muscular atrophy. Remember, spinal muscular atrophy is also an MBM exam referred to as Wred Negh Hoffman disease, Wred Negh is spelled W-E-R-D-N-I-G and then Hoffman H-O-W-F-M-E-N, right? Wred Negh Hoffman disease, right? So remember, this is a problem with chromosome 5, right? It's actually an autosomal recessive disease, chromosome 5, autosomal recessive disease, right? And you have a mutation in a gene on chromosome 5 called the SMN1 gene, right? The survival motor neuron 1 gene, right?

So when you mess up the survival motor neuron 1 gene, the thing that's going to happen is that your lower motor neurons, this is a low motor neuron problem, right? Your low motor neurons in the spinal cord, they're not going to be surviving, they're going to die, right? So they're going to see a child that is losing motor milestones, right? Losing motor milestones, this is a low motor neuron problem. So that's something I want to keep at the back of your mind on exams. And then what if they give you a question about a middle-aged guy and he tells you that, you know, he's an accomplished musician, but he's having trouble like playing the piano, right? And they tell you that, you know, he's beginning to have like swallowing difficulties, but they tell you that he has no sense to have normalities on exams. If you see that, I'll really hope you're saying, oh, divine, this is ALS, in myotrophic lateral sclerosis, right? Remember, in myotrophic lateral sclerosis is a motor neuron disease. It's a combination of upper motor neuron problems and low motor neuron problems. The upper motor neurons, right? I'm going to be your quadricos spinal tracks that are messed up, right? But your low motor neuron problems, again, are going to be things like your ventral horn, your anterior horn in the spinal cord. These people are not going to have any sensory deficits, right? These people are not going to have any sensory deficits. Now, it's very high you to know that ALS, right?

It's called low garrics disease, right? You can treat it with right lusol, right? Because again, one of the thoughts as to why these neurons die is because of something called glutamate excitotoxicity, right? glutamate excitotoxicity. And the thing is glutamate has the ability to interact with NMG receptors. So if you give an NMG receptor antagonist like right lusol, right? That's going to help the person. I mean, it's not going to give you a life for much longer, right? But at least it helps. It helps somewhat, right? I remember people that have ALS, actually one of these strange people that somehow are eligible for Medicare. Because remember, friends at the NBM is the love to test insurance, right? Every now and then on these exams, right? And people that qualify for Medicare usually people people people over the age of 65, right? But again, if you have ALS, even if you are under 65, you can absolutely qualify for Medicare. People that also have nstitial disease also fit that build the fit that qualification, right? So again, ALS, amiotrophic lateral sclerosis is a motor neuron disease, is a combined upper and lower motor neuron problem. It's a pure motor neuron disease. There are no sensory deficits in people that have ALS, right? And then one thing I guess I want to discuss is remember, the anterior one of the spinal cord can be affected by many different viruses, right?

Like the West Nile virus loves to be affect, loves to affect the anterior one of the spinal cord, the polio virus, right? Loves to affect the anterior one of the spinal cord, right? So the thing is these things can cause lower motor neuron problems, right? That's why many people that have polio or like West Nile virus and it infects the anterior one of the spinal cord, they tend to have like motor weakness, right? Like all these lower motor neuron symptoms because again, it's the anterior horn that is messed up. Now one thing I want to say is that West Nile virus can also cause meningitis, right? It can cause a viral meningitis. So what are you going to find in viral meningitis in people that have a West Nile virus infection? Well remember, your CSF opening pressures, everything is like slightly increased, right? Like everything is slight environment in jihais, right? The CSF opening pressures will be slightly increased. They'll have like a slight leukocyteosis, but the bulk of that leukocyteosis is going to be lymphocyte because it's a viral infection, right? What you're going to notice that or the glucose is a little bit low, right? So just kind of keep those things in mind, right? Because West Nile virus can also cause meningitis and that meningitis can treat pretty deadly. I mean there is this shawai watch, a great great show, one of the main actors like in real life actually died from a West Nile virus meningitis.

Okay, and then remember I talked about how in B12 deficiency, I'm going to wrap up shortly, this is going to be a short podcast, right? So remember I talked about in B12 deficiency that you have a subacute combined degeneration of the spinal cord. I said that you know what, you're going to see a drossal column problem and in addition to that, you're going to see problems with your lateral corticospinal tract. Well let me tell you something, how can you differentiate B12 deficiency from TB's dorsalis. Remember TB's dorsalis is something in finding tertiary syphilis. TB's dorsalis does not involve the corticospinal tract. TB's dorsalis just involves the drossal columns, right? So it's going to be like a sex worker IV drug user stuff like that, right? That has a positive rumberg, right? But they have no upper motor neuron symptoms. If you see that, I want you to think about TB's dorsalis, right? Now one thing I want to talk about that many, many people mess up, in fact these are two things I want to talk about and then we wrap up. One is just differentiating conospidularis syndrome from quarter equina syndrome, right? The thing is when people have conospidularis syndrome, right? It's a problem with the actual spinal cord, right? It's a myelopathy, right? The actual spinal cord itself is messed up, right? The actual spinal cord itself is messed up, right? But when people have caught a equina syndrome, it's actually nerve roots that are messed up.

It's actually nerve roots that are messed up. And one of the best ways to distinguish conospidularis syndrome from quarter equina syndrome is that most people that have conospidularis syndrome, they'll have a predominance of upper motor neuron symptoms. But people that have caught a equina syndrome, they have a predominance of lower motor neuron symptoms, right? Corlox medularis syndrome is more of a myelopathy versus corlox medularis syndrome that is more of a radicalopathy. I'll talk about the difference between a myelopathy and a radicalopathy at the end of this podcast, right? And one other thing that is also really helpful is that people that have conospidularis syndrome, again because is the actual spinal cord that's affected, those people tend to have bilateral symptoms, right? Bilateral symptoms. But people that have caught a equina syndrome, they tend to have a lateral symptoms, right? Now the thing is, if you really think about it, people that have caught a equina syndrome, they actually tend to do better long term than people that have conospidularis syndrome. Why? Because in caught a equina syndrome is the peripheral nervous system that is affected, right? Again, remember, it's a nerve root problem, it's not a spinal cord problem. Corlox medularis syndrome is a spinal cord problem. Corlox medularis syndrome is a nerve root problem, right? Your nerve roots coming off from the spinal cord, they actually derived from your peripheral nervous system.

Your actual spinal cord is derived from your central nervous system, is derived from your neuro tube, right? So the thing is, your peripheral nervous system has a much better ability to regenerate than your central nervous system. That's why people that have caught a equina syndrome, they tend to heal much quicker than people that have conospidularis syndrome, right? So that's one thing I want to share. And then another thing I want to share, again, is my lopathy versus a radicalopathy. If you go into my neuro podcast that I made for the neurology shelf exams, I go into like way more detail on this. But the big thing I want to mention is that when a person has a my lopathy, they have a problem with the spinal cord. When a person has a radicalopathy, they have a problem with a nerve root. The thing is radicalopathy is the way be present on examples is the person is going to have a symptoms that study in the middle of the back and then they read it outwards, right? Read 18 outwards think of a radicalopathy, that's a nerve root problem, right? My lopathy is more of a spinal cord problem, the actual cord is messed up, right? And there are certain things that can tell you that, hmm, I'm likely dealing with my lopathy in this question, right? One classic tool is you'll notice that at the level of the lesion, those people have low motor neuron symptoms, but below the level of the lesion, those people are going to have upper motor neuron symptoms, right?

Because again, when you impinge the spinal cord in a certain part, the low motor neurons at that level are going to be messed up, right? But you're also messing up the upper motor neurons that are descending progressively through the spinal cord to supply low motor neurons a little lower down, right? So again, that's one classic sign of a my lopathy, like on a higher, like on a higher part of the body, you have low motor neuron symptoms, but on a lower part of the body, you're going to have upper motor neuron symptoms. That's a classic sign of a my lopathy. Another classic sign of a my lopathy is that the person is going to have a sensory level. You're going to notice that, wow, we know this defined level in the body, boom, the person is losing all of a particular kind of sensation. If you see that, that should get you thinking about some kind of my lopathy, right? That should get you thinking about some kind of my lopathy. Now, another thing that will also help you know that you're dealing with a my lopathy, I just look at the drossal column and spinal thalamic tract symptoms. If you see a drossal column problem in one extremity and a spinal thalamic tract problem in another extremity, then that localizes the problem to the spinal cord. That's actually a very easy way to know that you're dealing with a my lopathy on endemic exams.

And then finally, the thing I want to say is that if you damage any of your, any of your nerve roots from like C1 to C4, that person is going to need mechanical ventilation, right? Because remember, C345 keeps the diaphragm alive, right? So if you have like a high cervical cord injury, that can really, really make the person basically need mechanical ventilation. So I think I'm going to go ahead and stop here. Again, I really hope you find this podcast to be helpful. Again, as I do at the end of every podcast, I do offer one or one tutorial for many exams, step one, step two, CK, and step three. And then I also tell you for pre-clean comments, school exams, 30-year-clat shift shelf exams. And then I offer two flavors of three flavors, of course, is actually, I have an MBME test against strategies class. That's going to be taking place on the 21st of March from 2 to 4 30 PM, Mountain Standard Time. And then I have a 24-hour step two, CK step three, and you know, complex level two and three review course from the 22nd to the 25th of March. That's going to be from 70-M to 1 PM, Mountain Standard, I mean, Pacific Standard Time on each of those days. And the test taking course, again, is from 2 to 4 30 PM, Pacific Standard Time. So three hours behind these student time. And then I also have a step two CK school. Obviously, that also works for people taking step three or complex level two and three. But taking a U.S. Emily exam in the summer, it's a 40-person school.

It's going to run for 75 hours on Zoom. And we're going to review a ton of stuff. It's going to be like an expanded test taking strategy course. I made a dedicated podcast on that. I will encourage you to listen to that podcast if you can. And then I have all these podcasts on Apple podcasts, some Google podcasts, and on Spotify, right? At least the most recent 150. If you want everything from episode one, all the way to episode 374, I'll encourage you to go to the website, divineinterventionpodcasts.com. And if you actually subscribe with your Word Press account, you'll get an email notification whenever I make a new podcast. And then I also have a new website called divineinterventionlifelessens.com. Right? In fact, there is an Apple podcast associated with that. It's called the Divine Intervention Life Lessons Podcast. And in that podcast, you know, many people have emailed me, oh, divine, I love the life lessons you place at the end of your podcast. So I started our website right now. I believe I have like 62 or 63 episodes. I add like two every week of like 10 to 15 minutes, just short lessons, right? That I address things from a biblical perspective, right? Just how to solve common problems that humanity faces. So thank you for joining me today. Have a wonderful Friday. Have a wonderful weekend. And God bless you. Thank you.

Practice questions — USMLE style

Question 1 — Neurology

A 25-year-old male is involved in a gunshot wound to his left spinal cord. On examination, he exhibits the following findings: Right upper extremity: Loss of pain and temperature sensation. Left upper extremity: Loss of fine touch, vibration, and proprioception. Bilateral lower extremities: Positive Babinski sign. Which neurological syndrome best describes these findings?

  • A) Central cord syndrome
  • B) Subacute combined degeneration
  • C) Brown-Séquard syndrome
  • D) Anterior spinal artery syndrome

Answer: C. Explanation: Brown-Séquard syndrome results from a hemisection (damage to one half) of the spinal cord. Because the dorsal columns do not cross until the brainstem, damage on the left side causes ipsilateral loss of fine touch and vibration (left side). However, the spinothalamic tract crosses immediately after entering the spinal cord; therefore, damage on the left side results in contralateral loss of pain and temperature sensation (right side). The positive Babinski sign indicates an upper motor neuron lesion affecting the corticospinal tracts.

Question 2 — Neurology

A 68-year-old man presents following a severe motor vehicle accident. He has a history of spinal stenosis, and physical examination reveals bilateral weakness in his upper extremities with profound loss of pain and temperature sensation, described as having a "cape-like" distribution. His lower extremity function is relatively spared compared to the upper body deficits. What condition should be suspected based on this clinical presentation?

  • A) Brown-Séquard syndrome
  • B) Subacute combined degeneration
  • C) Central cord syndrome
  • D) Anterior spinal artery syndrome

Answer: C. Explanation: Central cord syndrome results from damage in the central portion of the spinal cord, often seen after trauma or due to syringomyelia. The spinothalamic tracts, which carry pain and temperature information, cross near the anterior white commissure (the center of the cord). Damage here leads to a characteristic bilateral loss of pain and temperature sensation in a cape-like pattern, while the more lateralized long tracts (dorsal columns and corticospinal tracts) are often spared or less severely affected.

Question 3 — Neurology

A vegan patient presents with chronic symptoms including paresthesias throughout his body, progressive weakness, and sensory deficits involving loss of fine touch, vibration, and proprioception in the lower extremities. Examination also reveals a positive Babinski sign. The physician suspects a nutritional deficiency causing combined degeneration of the spinal cord. What is the most likely underlying cause of this syndrome?

  • A) Tabes dorsalis
  • B) Vitamin B12 deficiency
  • C) Spinal epidural abscess
  • D) Guillain-Barré syndrome

Answer: B. Explanation: Subacute combined degeneration of the spinal cord, typically caused by Vitamin B12 deficiency (common in vegans or those with malabsorption), affects two major tracts: the dorsal columns (leading to loss of vibration/proprioception and positive Romberg sign) and the lateral corticospinal tracts (causing upper motor neuron signs like hyperreflexia and Babinski). Tabes dorsalis, conversely, only involves the dorsal columns and does not affect the corticospinal tract.

Question 4 — Neurology

A patient undergoes surgery for an abdominal aortic aneurysm repair, resulting in a temporary ischemic injury to the anterior spinal artery. Post-operatively, the patient develops profound weakness and sensory deficits. Examination reveals that he has preserved fine touch, vibration, and proprioception but has lost all pain and temperature sensation below the level of injury. Which anatomical region was most severely compromised?

  • A) Dorsal columns
  • B) Lateral corticospinal tracts
  • C) Anterior two-thirds of the spinal cord
  • D) Ventral horn (anterior horn)

Answer: C. Explanation: The anterior spinal artery supplies the anterior two-thirds of the spinal cord. Damage to this area, such as in anterior spinal artery syndrome, results in the loss of all structures housed there, including the spinothalamic tracts (responsible for pain and temperature). Crucially, the dorsal columns are located more posteriorly and are therefore spared, explaining the preservation of fine touch, vibration, and proprioception.

Quick fire review

What key finding suggests Brown-Séquard Syndrome?

Ipsilateral loss of fine touch/vibration (dorsal columns) and contralateral loss of pain/temperature (spinothalamic tract).

What is the classic association for Central Cord Syndrome?

Syringomyelia, which can be associated with a Chiari I malformation.

Which syndrome involves damage to the anterior two-thirds of the spinal cord, sparing only the dorsal columns?

Anterior Spinal Artery Syndrome.

What is the primary difference between Myelopathy and Radiculopathy?

Myelopathy is damage to the spinal cord (CNS); Radiculopathy is damage to a nerve root (PNS).

Which motor neuron disease is characterized by pure motor deficits, sparing all sensory function?

Amyotrophic Lateral Sclerosis (ALS).

What CSF findings are expected in West Nile Virus meningitis?

Slightly increased opening pressure, lymphocytic pleocytosis, and low glucose.

What specific deficit pattern characterizes a myelopathy versus a radiculopathy?

Myelopathy often presents with bilateral symptoms or sensory levels; Radiculopathy follows a dermatomal/myotomal pattern.

In B12 deficiency causing SCD, which two tracts are primarily affected?

Dorsal columns and Lateral corticospinal tract.

What is the key differentiator between Tabes Dorsalis and Subacute Combined Degeneration (SCD)?

SCD affects both dorsal columns AND lateral corticospinal tract; Tabes Dorsalis only affects the dorsal columns.

If a patient has symptoms affecting the anterior two-thirds of the spinal cord, what syndrome should be suspected?

Anterior Spinal Artery Syndrome.

What is the mechanism by which the Rhombburg test assesses function?

It tests proprioception and requires at least two working systems (Vision, CN VIII, Dorsal Columns) to know joint position in space.

Which condition causes lower motor neuron death due to a mutation in the SMN1 gene on chromosome 5?

Spinal Muscular Atrophy (SMA).

Quick recall / Anki-style questions

What specific deficit pattern characterizes a myelopathy versus a radiculopathy?

Myelopathy often presents with bilateral symptoms or sensory levels; Radiculopathy follows a dermatomal/myotomal pattern.

In B12 deficiency causing SCD, which two tracts are primarily affected?

Dorsal columns and Lateral corticospinal tract.

What is the key differentiator between Tabes Dorsalis and Subacute Combined Degeneration (SCD)?

SCD affects both dorsal columns AND lateral corticospinal tract; Tabes Dorsalis only affects the dorsal columns.

If a patient has symptoms affecting the anterior two-thirds of the spinal cord, what syndrome should be suspected?

Anterior Spinal Artery Syndrome.

What is the mechanism by which the Rhombburg test assesses function?

It tests proprioception and requires at least two working systems (Vision, CN VIII, Dorsal Columns) to know joint position in space.

Which condition causes lower motor neuron death due to a mutation in the SMN1 gene on chromosome 5?

Spinal Muscular Atrophy (SMA).