DIP Episode 506 - Weird But HY Spinal Cord Disorders (for Step 1-3)
Topic
Spinal cord anatomy and pathways; Demyelinating polyneuropathies (MS, NMO); Spinal cord compression; Nutritional deficiencies (B12, Copper).
Key Takeaway
Recognizing the specific clinical patterns—such as the combination of UMN/LMN signs in spinal cord infarction or the unique serological markers differentiating MS from NMOSD and transverse myelitis—is critical for diagnosing complex neurological disorders.
Episode Notes
Source / episode info
- Episode: 506
- Title: Divine Intervention Episode 506: Weird But HY Spinal Cord Disorders (for Step 1-3)
- Published: 2024-01-24
- Source: Episode page
One-liner
This episode emphasizes recognizing key spinal cord pathways (dorsal columns, corticospinal tract, spinothalamic tract), differentiating demyelinating syndromes (MS vs NMO vs TM), understanding the patterns of spinal cord infarction and nutritional deficiencies (B12/Copper), and mastering the workup and management of spinal cord compression.
High-yield summary
- Spinal Tracts: Dorsal columns carry vibration, fine touch, and proprioception; Corticospinal tract carries UMN signs; Spinothalamic tract carries pain/prick/temperature (loss is contralateral).
- Demyelinating Syndromes: MS presents with separated in space and time deficits, often associated with oligoclonal bands. NMOSD requires anti-NMO antibodies and typically involves optic neuritis. Transverse Myelitis follows a viral illness but lacks the specific serology or episodic nature of MS/NMOSD.
- Spinal Cord Infarction: Typically presents as an anterior spinal artery syndrome (anterior 2/3 involvement), sparing the dorsal columns, often following hypotension or aortic surgery.
- Nutritional Deficiencies: B12 deficiency causes subacute combined degeneration (posterior columns + corticospinal tract) and is associated with elevated MMA and homocysteine. Copper deficiency can be seen after bariatric surgery or zinc excess.
- Spinal Cord Compression Workup: Always start with an MRI. The management depends on the cause: steroids/surgery/radiation for masses; no steroids for infection/hematoma.
Learning objectives
- Identify the major ascending and descending tracts of the spinal cord and their corresponding clinical deficits.
- Differentiate between Multiple Sclerosis, Neuromyelitis Optica Spectrum Disorder, and Transverse Myelitis based on clinical course, serology, and imaging findings.
- Recognize the classic signs and risk factors associated with anterior spinal artery syndrome/spinal cord infarction.
- Correlate specific neurological deficits (e.g., macrocytic anemia, elevated MMA) with Vitamin B12 deficiency or Copper deficiency.
- Apply systematic approaches to diagnosing spinal cord compression based on clinical history (trauma, cancer, infection).
Board exam buzzwords
| Condition | Key Finding | Association | Board Exam Tip |
| Multiple Sclerosis (MS) | Separated in space and time deficits; Oligoclonal bands in CSF. | Optic neuritis (painful); Brain/Spine involvement. | Remember that MS is the most common cause, but always rule out NMOSD first if anti-NMO antibodies are positive. |
| Neuromyelitis Optica (NMOSD) | Anti-NMO IgG antibodies; Painful optic neuritis. | Attacks are often long-lasting and episodic. | The presence of anti-NMO antibodies is highly specific for this diagnosis, overriding other MS-like presentations. |
| Spinal Cord Infarction | Anterior spinal artery syndrome (anterior 2/3 involvement). | Hypotension (cardiac surgery); Aortic surgery; MI. | Always check the dorsal columns—they are typically spared in anterior cord infarcts. |
| Vitamin B12 Deficiency | Subacute combined degeneration of the spinal cord. | Elevated MMA and Homocysteine; Macrocyctic anemia. | The combination of elevated MMA/Homocystine and posterior column signs is pathognomonic for B12 deficiency. |
Rapid review table
| Topic | Key Point | Context | Exam Relevance |
| Spinal Tracts | Dorsal Columns (Vibration, Proprioception) vs Spinothalamic Tract (Pain/Temp). | Damage to dorsal columns causes ipsilateral loss of vibration; damage to spinothalamic tract causes contralateral loss. | Test knowledge of decussation points in the spinal cord and medulla. |
| MS vs NMOSD | MS: OC Bs, separated time/space. NMOSD: Anti-NMO IgG, long attacks. | Both cause myelitis; serology is key to differentiation. | If anti-NMO antibodies are positive, think NMOSD first. |
| B12 Deficiency | Subacute combined degeneration (Posterior columns + Corticospinal tract). | Macrocyctic anemia, elevated MMA/Homocysteine. | The combination of hematological and neurological findings is a classic board pattern. |
| Spinal Compression Workup | MRI is mandatory for all suspected compression. | Causes include trauma, abscess, tumor, or stenosis. | Knowing the "hook" (e.g., fever = abscess; history of AAA = pseudoaneurysm/hematoma) guides diagnosis. |
Board-speak -> diagnosis
| Board-speak / Vignette phrase | Diagnosis / Concept | Why it fits |
| A patient presents with sensory loss of pain and temperature that is contralateral to the lesion site. | Damage to Spinothalamic Tract | The tract crosses in the anterior white commissure, causing a decussation effect. |
| A 32-year-old female has painful optic neuritis and fluctuating motor weakness over years. CSF shows oligoclonal bands. | Multiple Sclerosis (MS) | Classic presentation of MS: separated in space and time; characteristic findings include OC Bs/elevated IgG index. |
| A patient develops flaccid paralysis after cardiac surgery due to hypotension, showing UMN signs but sparing dorsal column function. | Anterior Spinal Artery Syndrome / Spinal Cord Infarction | Hypotension or aortic surgery can cause ischemia affecting the anterior spinal cord segments (anterior 2/3). |
| A person has a history of bariatric gastric bypass and develops peripheral neuropathy. | Copper Deficiency | The duodenum is critical for copper reabsorption, making it susceptible to deficiency after bypassing this area. |
| Signs of UMN weakness at a lower level and LMN weakness at a higher level in the body. | Spinal Cord Compression (General Pattern) | This "reverse" pattern is highly characteristic of spinal cord pathology/compression. |
| A patient with myelitis has anti-NMO antibodies, episodic symptoms, and painful optic neuritis. | Neuromyelitis Optica Spectrum Disorder (NMOSD) | The specific serology (anti-NMO IgG) is the key differentiator from MS. |
Differential diagnosis / distinguishing features
Multiple Sclerosis vs Transverse Myelitis
| Key Features | Distinguishing Findings | Next Step |
| MS: Oligoclonal bands in CSF; symptoms are episodic. | TM: Associated with recent viral illness; symptoms are not typically episodic; no OC Bs/elevated IgG index. | Rule out infectious or inflammatory triggers (e.g., viral infection) and perform comprehensive serology. |
B12 Deficiency vs Copper Deficiency
| Key Features | Distinguishing Findings | Next Step |
| B12: Elevated MMA and Homocysteine; causes subacute combined degeneration. | Copper: History of bariatric surgery or zinc excess; copper deficiency is the primary issue. | Check for high-output GI history (e.g., gastric bypass) when considering metal deficiencies. |
Management pearls
- Spinal Cord Compression: Always obtain an MRI first. Management involves IV steroids, surgical decompression, and often radiotherapy (especially if due to malignancy).
- Infection/Hematoma vs Tumor: Do NOT give high-dose IV steroids for spinal cord compression caused by infection (abscess) or hemorrhage (hematoma), as this can worsen the condition.
- Liquid Tumors: For masses like leukemia or lymphoma causing compression, prioritize radiotherapy in addition to decompression and steroids.
- B12 Deficiency Treatment: Supplementation with Vitamin B12 is required; supplementation for copper deficiency should be considered if bariatric surgery history exists.
Don't miss
Integration & clinical reasoning
- Anatomy/Pathology: Understanding the specific tracts (dorsal vs spinothalamic) allows prediction of deficits based on lesion location in the spinal cord white matter.
- Endocrinology/Metabolic: The pattern recognition skills used for diagnosing myelitis are similar to those needed for metabolic disorders, requiring correlation of multiple lab findings (e.g., MMA + Homocysteine).
- Surgery/Trauma: Recognizing the risk factors for spinal cord infarction (hypotension, aortic surgery) is crucial in acute care settings following major procedures.
OMM / COMLEX integration
- Acute Spinal Cord Injury/Infarction: Standard emergency management (ABC, fluid resuscitation, neurosurgical consult) takes absolute priority over OMT. OMT should only be considered adjunctive after the patient is stabilized and primary causes of compression are addressed.
- Spinal Compression Pain: Localized pain or signs of nerve root irritation can sometimes be managed with targeted physical therapy/manual techniques (OMT), but this must never delay definitive imaging (MRI) or surgical consultation for compressive lesions.
Concept connections / cross-references
- For detailed information on peripheral neuropathies and demyelinating diseases, review [ Episode 37 ].
- Understanding general principles of myelopathy and UMN/LMN signs can be reinforced by reviewing spinal anatomy basics in [ Episode 12 ].
High-yield association table
| Condition | Association | Mechanism | Clinical Significance |
| Multiple Sclerosis (MS) | Oligoclonal bands in CSF; Separated time/space deficits. | Autoimmune demyelination of CNS white matter. | Requires careful differentiation from other myelopathies like NMOSD and TM. |
| Neuromyelitis Optica (NMOSD) | Anti-NMO IgG antibodies. | Autoimmunity targeting aquaporin-4 channels in the optic nerve/spinal cord. | The presence of these specific antibodies dictates treatment, often requiring immunosuppression beyond standard MS therapy. |
| Spinal Cord Infarction | Anterior spinal artery syndrome; Hypotension/Aortic surgery. | Ischemia affecting the anterior two-thirds of the cord (anterior 2/3). | Clinically important to test for dorsal column sparing when suspecting infarction. |
| Vitamin B12 Deficiency | Subacute combined degeneration. | Damage to posterior columns and corticospinal tracts due to impaired myelin synthesis. | The combination of macrocytic anemia, elevated MMA, and myelopathy is a classic triad. |
Key terms glossary
| Term | Definition | Context | Example |
| Anti-NMO IgG | Autoantibodies targeting Aquaporin-4 channels. | Used in the diagnosis of Neuromyelitis Optica Spectrum Disorder (NMOSD). | A patient with severe, long-lasting optic neuritis and myelitis testing positive for these antibodies. |
| Subacute Combined Degeneration | Demyelination affecting posterior columns and corticospinal tracts. | Seen in Vitamin B12 deficiency; affects proprioception/vibration and UMN function. | The classic triad of findings: sensory ataxia, spasticity, and macrocytic anemia. |
| Anterior Spinal Artery Syndrome | Ischemic damage limited to the anterior two-thirds of the spinal cord. | Caused by hypotension or aortic surgery; results in specific motor/sensory deficits. | Loss of pain/temperature sensation (spinothalamic) and UMN signs, but preserved vibration sense (dorsal columns). |
| Oligoclonal Bands | Immunoglobulin bands detected in the CSF that are not found in serum. | Suggests intrathecal immune activation; common finding in MS. | Used to support a diagnosis of MS when other causes of myelitis are ruled out. |
Study optimization
| Topic | Study Approach | Priority | Resources |
| Demyelinating Myelopathies | Create flowcharts comparing clinical presentation, serology, and CSF findings for MS vs NMOSD vs TM. | High (Board-level differential diagnosis) | Review board question banks focusing on neurological differentials. |
| Spinal Cord Syndromes | Memorize the specific deficits associated with each tract/syndrome (e.g., B12 = posterior columns; Infarct = anterior 2/3). | Medium-High (Pattern recognition) | Use mnemonics and association tables to link cause -> pattern of deficit. |
| Spinal Cord Compression | Create a decision tree: Symptoms -> MRI -> Identify Hook (Trauma, Cancer, Infection) -> Determine Treatment (Steroids vs No Steroids). | High (Management/Workup) | Focus on the contraindications for steroids (infection/hematoma). |
Question pattern recognition
- Pattern: Loss of vibration and proprioception combined with UMN signs. -> Points to posterior column damage, often seen in B12 deficiency or spinal cord infarction.
- Pattern: Flaccid paralysis following cardiac surgery or AAA repair. -> Highly suggestive of anterior spinal artery syndrome/spinal cord infarction due to hypotension or high pressure.
- Pattern: Myelitis with painful optic neuritis and positive anti-NMO antibodies, but negative MS lesions on MRI. -> Strongly suggests Neuromyelitis Optica Spectrum Disorder (NMOSD).
Test yourself
Common mistakes to avoid
Common traps
Original transcript with highlights
Original transcript with highlights
Welcome to episode 506 of the Divine Intervention Podcasts. In to this podcast we're going to be addressing a topic I love to call weird but high yield spinal cord disorders. Weird but high yield spinal cord disorders. These disorders that I'm going to talk about, you don't find them in many resources but they do show up on the USML Es. Step one, step two, step three. So I want to discuss them so you can basically have a collection, have it well organized in one podcast. So again, I will strongly encourage you, pay attention to this stuff. Don't sleep on it. So the first thing we're going to discuss before we jump into the spinal cord is the following. So what are the key pathways in the spinal cord? There's a ton but what are the ones that I really examine worth? Obviously in the posterior part of the spinal cord we have the drossal columns. The drossal columns and then we're going to give a bunch of vignettes here. In the drossal columns that's what controls vibration, perception, fine touch, fine touch, vibration, perception that's like the posterior third of the spinal cord. And then if you look around the posterior slash lateral sides of the spinal cord, that's where we have the cortical spinal tract. Remember at that point the cortical spinal tract has literally already crossed. The cortical spinal tract as we know crosses in the coda medala. And it's called cortical spinal because it starts in the cortex and ends in the spinal cord.
So the cortical spinal tract has already crossed. So whenever you have any drossal column problems, I mean any cortical spinal tract problems in the spinal cord, what you're going to notice is you're going to see the lateral symptoms. So if you damage the cortical spinal tract on the left side, you'll have left side at symptoms, cortical spinal tract on the right side, you'll have right side at symptoms. Since we already talked about drossal columns, if you also damaged the drossal columns in the spinal cord, you'll have the psalateral problems. You'll have it's lateral loss of vibration, fine touch and proprioception. Now the other major pathway in the spinal cord is clearly the spinal phalamic tract. Remember the spinal phalamic tract? You think of them as being very anterior and lateral in the spinal cord, very anterior and lateral in the spinal cord. Right? So they're like on the tips, the lateral tips, the lateral front tips. Sometimes it's just good to use a simple descriptor to get certain points across. The lateral front tips of the spinal cord, that's where we're going to find the spinal phalamic tract. Those things carry pain, pain prick and temperature. Pain, pain prick and temperature. Think of Power Point, PBT, pain, pain prick and temperature. Pain, pain prick and temperature. And if you damage the spinal phalamic tract in the spinal cord, you're going to notice, you're going to notice, you're going to notice what?
You're going to see a contralateral loss of pain, pain, pain, and temperature. It's going to be contralateral. Why? Because that's like one of those key pathways that crosses in the spinal cord. It crosses in the spinal cord. It crosses in the spinal cord. It crosses in the anterior white comission. That's why for person has a syringomylia, a problem with the central canal of the spinal cord, they can have that bilateral loss of pain, pain, and temperature. Pain prick and temperature loss in a keyplike distribution. So if you damage the spinal phalamic tract, notice everything is so far, I'm saying it's lateral, it's lateral. For drossal columns, I said it's lateral. For critical spinalized it's lateral. That's in the spinal cord. Remember, these problems, you see contralateral issues, if you hurt elsewhere, I'm just referring to the spinal cord. Spinal phalamic, you're going to see a contralateral loss of pain, pain, and temperature. And then another high-your-pathway, it's not really a pathway, but these are your lower motor neurons. These are going to be in the anterior part of your spinal cord. You're going to be more anterior in the middle, on both sides. Those lower motor neurons, they go straight to the neuromuscular junction, where they release a cellulcholine, so that they can act on the nicotinic acetylcholine receptors that we find on our skeletal muscles. So what's the deal with these? Well, these just go straight to the neuromuscular junction on the same side.
So guess what? When you damage the lower motor neurons, sometimes you call them the ventral horn, that is going to cause a person to have Ipsilateral weakness. Ipsilateral weakness. I remember there is a few things that can mess up these lower motor neurons. I've talked about them in other podcasts. I'm just going to give a quick drive by. But don't forget polio. Polio can cause lower motor neuron issues. Don't forget, West Nile virus. West Nile virus can cause lower motor neuron issues. Don't forget the spinal cord disorder, redening health man disease, that spinal musculotrophy, right? Or a more recessive problem, chromosome 5, in the SMN1 gene, cause a lower motor neuron issue as well. And they don't forget emailiotrophic lateral sclerosis. ALS. ALS is an upper and lower motor neuron disorder. So it damages both your cortical spinal tract, and it also damages your anterior horn, your ventral horn. Your anterior horn, your ventral horn, your lower motor neurons. So again, please, if you see any of these terms, it's the lower motor neurons that I've been referred to. They can be called lower motor neurons, they can be called anterior horn, they can be called ventral horn. Alright. So let's begin to maybe throw in a few. The thing is, these spinal cord disorders, many times the key way to recognize them is just by the clue. Recognize them by the clue.
So, because really if you think about it, when you have issues with the spinal cord, sometimes the problem can be within the cord itself. Sometimes you use the term intramedularity for that, but sometimes, or actually quite a number of times on the USML Es. When a person has a spinal cord problem, it's because of extrinsic compression. And again, remember if you damage the cortical spinal tract, since we said it already, you're going to see cellareroos symptoms. But whatever, if cellareroos symptoms you're going to see, what you're going to see is cellareroos symptoms like hyperreflexia, you're going to see spasticity, you're going to see spastic paralysis. And you're going to see a positive Babinski sign. A positive Babinski sign that is if cellarero. Remember that positive Babinski sign, sometimes on your exhalums. Instead of colline Babinski, because they know that's in every on key deck known to one kind, they'll call it an extensor planter response, an extensor planter response, an extensor planter response. Basically, you have a funny note of your tools. That is not normal. So if you damage the cortical spinal tract, you're going to see hyperreflexia, spasticity, right? A lot of spastic paralysis. You're going to see an extensor planter response. Now, and honestly, like you're going to find many of those symptoms specifically now.
In a person that has a coneous medallaris syndrome, coneous medallaris, coneous medallaris syndrome, you're going to see a lot of upper motor neuron symptoms. That's like a very nice clue that, man, this is probably coneous medallaris syndrome. Because many people tend to mess up coneous medallaris syndrome with Koda and Kwina syndrome. Koda and Kwina syndrome tends to present more with lower motor neuron symptoms. That's one way, honestly, I've pretty much always divided these things up, and it's been pretty helpful on the exams. So coneous medallaris, you're going to see a lot of upper motor neuron symptoms. Like, predominantly in the question, I'm going to see a lot of upper motor neuron symptoms. But in Koda and Kwina syndrome, you're going to see a lot of lower motor neuron symptoms, right? Like, you know, hyperreflexia or ear reflexia, you know, muscle weakness, things like that. Because Koda and Kwina syndrome, it's less of upper motor neuron issue. It's more of a lower motor neuron and nerve root issue. That's the way I kind of think about it. So Koda and Kwina is a lower motor neuron and nerve root issue. So you're going to see some radicalopathy symptoms as well. But coneous medallaris is more of like a straight-up upper motor neuron issue. Okay. So let's go ahead and talk through this, right? So what if they give you a question about a 32-year-old female? And they tell you that, you know, she has this, she has had bilateral or extrudy weakness for a few days.
And they tell you that three years ago, she had very painful, like she had to come to the emergency room because she had very painful eye. Well, clearly that's multiple sclerosis, right? That's clearly multiple sclerosis. That is clearly multiple sclerosis. Remember, those people are going to have neurological deficits that are separated in space and time. Right? There are many findings in MS, right? You can have like optic neuritis, painful vision loss, right? That's clearly an ophthalmological emergency. Obviously, in that case, you're going to shoot for those steroids. Are you going to give IV steroids? I have no other person's going to go permanently blind. Right? And this person again also has, you know, lower extrudy weakness on all these things. You see their symptoms just come and go, come and go, come and go, come and go. If you see that, think of MS. And MS is characteristic. You know, the MBM is tested in the female in her 30s. Don't get me wrong. And people that are not in their 30s get MS absolutely. But usually, over one minute majority of the time, an MS patient who exam is going to be in their 30s. But again, MS, how do you differentiate it from some other disorders? Because there are some other disorders that look like MS, whether or not MS. And our friends at the MBM is expected to know those disorders. And I guess one thing I'm going to say is that MS typically affects the brain and the spine. Typically, it affects the brain and the spine.
So that's why usually when people have MS, you're going to run MRI over the brain and the spine. But what if they give you a question about a person that, you know, they have these periodic paralysis. You notice that, man, they have these, you know, paralysis of the lower extremities that seems to come and go. Seems to come and go. Right? And the thing is, many times when they have these episodes, these episodes last pretty long. They last for a long period of time, but it's episodic. So it comes and goes. And you may even notice that they have this painful vision loss. So they have optic neuritis, just like you see in MS. Well, then they tell you in the question that, ooh, that they get brain imaging and they see nothing. They see nothing. And you're like, hmm, that's weird. I don't see those same white model lesions as I see for MS. And then they can tell you that, ooh, that they did some blood studies. And they find autoantibodies against NMO. Autoantibodies against N as a Nancy, M as in Mable, and O as in Oxford. Right? So they see anti-NMO antibodies. These are IgG antibodies. If you see this, I would really hope you're thinking about devex disease, devex disease, DEVIC. That's what NEME can be called. Or, you know, many of you know this as neuromylitis optica. Neuromylitis optica. Neuromylitis optica. So you're going to see a person having a lot of spinal cord problems, right? A lot of like, motor weakness and stuff like that.
You're going to see like spinal cord weakness that is periodic, right? So it's, it's basically episodic, right? But each episode lasts pretty long. And they even have optic neuritis. But again, you get brain imaging. You don't see the MS lesions. That's not MS. That's neuromylitis optica. And remember, one of the nice ways to know that, ooh, for sure, I'm dealing with neuromylitis optica is you're going to find IgG antibodies, some autoimmune disease. You find IgG antibodies against NMO, okay? And IgG antibodies against NMO. All right? And again, remember, another thing you may see for neuromylitis optica, or your exam is devex disease. You may see called devex disease. Okay. Now, what if they give you a question about a person, you know, this person has like some kind of viral infection, right? They have like a viral respiratory infection or a viral GI infection. And they you notice that over a few days, they begin to get like very weak. They start having all these sensory problems in the extremities and stuff like that. They have bowel, this bowel blood dysfunction, right? If you see this, honestly, and then they tell you that, ooh, that you check out the brain and you notice that, man, they don't have any characteristics, MS lesions on a brain MRI. If you see this, I want you to think of transverse myitis. I want you to think of transverse myitis.
Now, I know someone who may be like, come on, the vinyl like seriously, like, okay, this sounds a lot like MS, like, how are you going to differentiate it? And this sounds a lot like neuromylitis optica. How are you going to differentiate it? Okay, calm down, calm down, calm down. Let me explain. First things first, transverse myitis, the asymptoms are usually associated with an RNA, a recent viral infection, a recent viral infection. That's one, two, people that have transverse myitis, the asymptoms are not episodic. They have the asymptoms developed and it'll just last. It's usually like a one-time thing that you have, right? Although it could be recurring, but most times, right? You have a viral infection and then you notice afterwards, you see a lot of weakness, a lot of bowel blood dysfunction, right? And also, one fairly helpful feature with transverse myitis is they're going to have a lot of sensory problems. They're going to have a lot of sensory problems. Sensory problems, you may not see those, you may not, and you say you absolutely will not. You may not see those in neuromylitis optica, right? And one other thing that also helps with transverse myitis is that, again, if you check the brain, if you check the brain, if you check the brain for the characteristic MS lesions, you're not going to see those characteristic MS lesions, right?
Another thing that also helps with differentiating transverse myitis from MS is that typically in MS, if you check their CSF, you're going to see oligoclonal bands. You're going to see oligoclonal bands, or you know, sometimes they may tell you that you see an elevated IgG index, an elevated IgG index. But in people that have transverse myitis, you're not going to see oligoclonal bands in the on CSF studies, you're not going to see an elevated IgG index. So that's very, very helpful for differentiating MS from transverse myitis. And again, remember, neuromylitis optica, the asymptoms are episodic. Transverse myitis usually on the USMLS, their symptoms are not episodic. Also, in transverse myitis, again, you're not going to see these anti-NMO antibodies. You're going to see those anti-NMO antibodies in neuromylitis optica. And typically, people that have transverse myitis, they do not have optic neuritis, okay? They're going to have that painful, sodium-osate vision loss. Neuromylitis optica, right? Tens to have that optica neuritis, okay? In fact, look at the name neuromylitis optica, optica, eye, eye, eye, eye is affected, right? But again, transverse myitis, you don't see anything about the eyes in that. So hopefully with these, again, that's why I said this is a podcast on weird but high-yield spinal cord disorders. Again, sorry, we've got to know these things for your exams, right? Again, we're trying to score as high as possible on this podcast.
So you just got to go the extra, extra mile. So hopefully now you can clearly see the differences between MS, your mylitis optica, which was also called dewyx disease, and idiopathic transverse myitis. Okay, now what if they give you a question about a patient and they tell you that, oh, this patient, you know, they just had a cardiac surgery, right? Cardiac surgery just finished, right? Or you see a person that has like a lot of EVM affirmations, like a person that has an osler of veber or a unducendral. And then they tell you that, man, after cardiac surgery, this person is having a lot of, like these person just has this sudden, right? That you are not like this before surgery, but you have the sudden flaccid paralysis, they have a lot of weakness, they tell you that you've lost pain, pain, break, and you know, temperature sensation. If you see something like this, I really, really want you to think about a person that has literally infarcted their spinal cord. They've literally infarcted their spinal cords. Okay, they have literally infarcted their spinal cords. They've literally done what infarcted their spinal cords. So what are going to be the risk factors on your exams? You can see a person that has had a recent MI or a fib, right? Those people can from embolite in their hearts, those can flick off, go to one of the vessels that supplies the spinal cord, and you can get a spinal cord infarction.
You can also see this in a person that is very hypotensive from cardiovascular surgery, right? So like for example, a person that has just had a cardiac bypass, and you see that they have these symptoms, think of a spinal cord infarction, right? That hypotension can cause an ischemic infarction of the spinal cord, right? And also, if a person has had like surgery in their yoder, so like surgery for a triple A, like an abdominal aortic aneurysm, or a thoracic aortic aneurysm, those things can cause those people to also, if they have very high potency during the surgery, because those are very high resurgers, those things can certainly cause a person to have an infarction of the spinal cord, right? And also people that have EVMAL affirmation, remember an EVMAL affirmation, is when you have a direct connection from an artery to a vein, right? So you're pretty much skipping the capillaries, but remember the capillaries are kind of important, that's where you have gas exchange. So these people basically don't have good gas exchange that can cause issues. Now again, you may ask yourself, define, how do I know that these are spinal cord infarction? Well, look at the pattern, look at the pattern. Look at all the symptoms that I mentioned, the one symptom that I did not mention was what? I did not say anything about the dorsal columns.
Typically when people have spinal cord infarction on the USMLA exams, you're going to see corticospinal tract problems, you're going to see spinal phylamic tract problems, you're going to see ventral horn problems, but you will not see posterior column problems, you will not see dorsal column problems. So by the way, another thing for the dorsal columns, your posterior columns, just keep that in mind, why? Because they are posterior in the spinal cord, right? So you're going to see that pattern, many times when people have spinal cord infarctions, it's going to fit the anterior to thirds of the spinal cord, the anterior to thirds of the spinal cord. And again, this aortic surgery, especially triple A fixing and development of spinal cord infarction, that's a, you kind of want to know the relationship, right? Because the thing is this is this order called the order of adamcoids, adamcoids, adamcoids, adamcoids, adamcoids, the order of adamcoids. So that order of adamcoids is a branch of the order, especially if you have adamcoids. So if you're having like a triple A surgery and or you have a rupture triple A, the order of adamcoids can be infarcted and that's going to infarct many levels of the anterior to thirds of your spinal cord, right? So you're going to see like an anterior spinal artery syndrome. So again, please, in summary, infarction of the spinal cord problems, many times they're going to show up as anterior spinal artery syndrome.
So I'm going to keep that at the back of your mind. Again, that order of adamcoids I mentioned gives rise to against anterior spinal artery for quite a number of levels of the spinal cord. So you can get spinal cord infarction from that. All right. And then remember, what if they give you a question about a person and this person, you know, they tell you that they have a lot of, you know, loss of vibration, perception, fine touch loss, right? They tell you that they have like a sensory taxi, right? And they also tell you that, man, this person has a, you know, hyperreflexia, spastic paralysis and all these things, right? So if you notice, what am I focusing on here? I'm focusing a lot here on three groups of symptoms. Number one, number one, number one, I'm focusing on dorsal column problems, loss of vibration, fine touch perception, right? So dorsal columns gone. Number two, I'm focusing on a lot of upper motor neuron problems, right? Like spastic paralysis, hyperreflexia, extensive plantar response, which is also called the positive binski sign. And then also I'm talking about a sensory attack, yeah, a sensory attack, yeah, a sensory attack, yeah, right? Because the spinal cerebellar tracts also messed up. You put all those things together and they may tell you that, ooh, this person's, uh, um, hemoglobin is like seven, right? So it's pretty low and their mcv is like 112, right? So this person clearly has a macrositic anemia. These clearly clearly make sense as what?
As what? What are you telling me? I hope you're telling me, ooh, divine. This sounds a lot like b12 deficiency, okay? So this person has a vitamin b12 deficiency. This person has a vitamin b12 deficiency, okay? This person has a vitamin b12 deficiency. Please be careful. Our friends at the USML Es, sometimes they will not make the question a slam dunk. Instead of giving you the, because what made this question super easy? He's went all of a sudden talked about, um, the macrositic anemia. They will always give you the macrositic anemia. Please keep that in mind. Sometimes they can give you like a surrogate, right? So they can give you all these symptoms. And then you notice that, wow, this person's homocysteine levels are elevated and their methamalonic acid levels are also elevated. When you see that combination, that's a b12 deficiency. Remember, there are two causes of elevated methamalonic acid on your exams. Number one is going to be B12 deficiency. Remember, four needs does not elevate your methamalonic acid. But then if you also have a methamalonic acidemia, right? Because you have a problem in the enzyme that metabolizes methamalonic acid, that's more of a biochemical disorder, that's the one territory, that can also cause a person to have an elevated methamalonic acid. Right? So one thing that can also help here is the pattern. Because remember, B12 deficiency causes what? A subacute combined degeneration of the spinal cord. A subacute what?
Combined degeneration of the spinal cord. Subacute combined degeneration of the spinal cord. Right? You're going to mess up the, so it's a combined degeneration. So you're going to mess up two pathways in general. You're going to mess up the posterior columns, the brussel columns. You're going to mess up the corticospinal tract. But one thing that you can also kind of throw in there, one thing that you can kind of throw in there, you can fool into that, is damaged to the spinal cerebellar tract. That's why these people may have a sensory etaxia. Right? That's why they may have a sensory etaxia. And don't forget, don't forget, don't forget, when you have a B12 deficiency, right? Don't forget, when you have a B12 deficiency, you can also have the macrositic anemia. That's why I gave that clue in the first place. But again, the may even, I kill you now. So the USML is me even give you a B12 deficiency question. And the person will not have anemia. Just be careful, but literally be careful. Right? So the fact that you don't see that anemia does not mean the person doesn't have B12 deficiency. B12 deficiency does not always cause anemia. Okay? Well, I'm not going to go into the reasoning behind that. It's not very necessary for this, for this podcast. Now, what if they give you a question that looks a ton like B12 deficiency? It looks a lot like B12 deficiency. But then you notice that the person's methylmalonic acid levels are completely fine.
The homocystine levels are completely fine. And they tell you that, hmm, this person is being treated for Wilson's disease. Sorry, scratch what I said on being treated for Wilson's disease. But you see a person, the, okay, let me, let me take a step back. So you see a person, they seem to have like classic B12 deficiency symptoms. Right? So they have many of the upper motor neuron problems, cortical spinal tract, those so-called unproblems. And then they tell you that this person, you know, takes a supplement for, and they tell you that the homocystine levels are fine. The methylmalonic acid levels are fine. And they tell you that the person takes a supplement to make them not have the common code. If you see this, I honestly want you to think of corporate deficiency. You're like, what? What? Corporate deficiency? Yeah. I only think of corporate deficiency. So let me give you some clues that will tell you that, oh, this is corporate deficiency. You're going to see a question that looks an awful lot like B12 deficiency, okay? And we'll talk about B12 deficiency. But then you've got to notice some things that don't line up. Number one, the person will not have macrosidic anemia. Right? You may see that. They may not have macrosidic anemia. The homocystine levels will be fine. The methylmalonic acid levels will be fine. And then they'll give you a high-out history. Although again, sometimes some of these clues are giving. They don't give it.
But they love to give this high-out history with some of these questions. What's the high-out history? Basically, you may see a person that's taking an autonomous zinc, a person taking a ton of zinc. Right? Because many of these common-codes supplements have zinc in them. Zinc loves to bind up copper. That can cause a copper deficiency. Another classic one, the, the love this one on the exams, is a person that has had bariatric surgery. So a person that has like a, like, has had like a Ruin Y gastric bypass. Right? That's a big one. They love to test. Because many times when you have a Ruin Y gastric bypass, one of the big places you bypass in the GI tract is the Dwardnam. So many of the things that are absorbed in the Dwardnam, you start developing the efficiencies of those things if you've had a gastric bypass, if you've had bariatric surgery. So you see a person that has had bariatric surgery and they have like many of these B-12 symptoms. Once you think of copper deficiency, because copper is reabsorbed in the Dwardnam. That's pretty high yield actually, to know for example. Copper is in fact reabsorbed in the Dwardnam. Okay? So again, this is pretty high yield to make sure that you understand for, for your exams. And again, remember, I've kind of talked about this in previous podcasts. But whenever a person has a spinal cord problem, right? Like a general pattern. Right? So it is like a general pattern for spinal cord injury.
You're going to see upper boudonuron problems at the lower level in the body. And then you're going to see lower boudonuron problems at the same level, at a higher level in the body. So it's almost like there's a reverse. I've explained this in detail in other podcasts. But you're going to see upper boudonuron symptoms at a lower level in the body. And then you're going to see lower boudonuron symptoms at a higher level in the body. That's a very classic way to know that, oh, wait, this person likely has some kind of spinal cord problems. Okay? Some kind of spinal cord problems. Especially when you have spinal cord compression. These things I just mentioned, this pattern I just mentioned, something that's very characteristic of spinal cord compression. So again, you're going to see many of these symptoms. Many times you're also going to see things like bowel and blood dysfunction. You're going to see many of these problems. So again, if your spinal cord is being compressed, you may see neck pain, especially if you have a cervical neuropathy, you may see back pain. And again, you're going to see many of these symptoms we've talked about, right? Many of these symptoms, bowel blood dysfunction, right? All these upper boudonuron problems, depending on where it is, low boudonuron problems, the brain, and where it is. We've talked about all these things. Now, before we talk about causes of spinal cord compression or rep of this podcast again, I just want to put in a plug.
If you're studying for any of your USML exams, I have a course that can help you. So I have a step one class coming up in March, like Larry, the first or the seventh of March. All these classes over Zoom have a step two, step three course in February. And I also have a series of other courses in February for step one to step three, the NV Me Testicking Strategies course, that's two and a half hours long. That's on the 15th of February. The Biosdats classes of four hour class. It's on the 16th of February. And the social sciences and ethics classes are five hour class. That's on the 17th of February. Again, many people have taken this course and found them to be extremely helpful for the exams. I hate you not, extremely helpful for their exams. So I encourage you to check these courses out. I think you're going to find it to be extremely, extremely helpful. And then these courses are not lectures, right? They're pretty much almost all exclusively clinical scenarios, exam style problems. And then I use those to teach you the concepts and helping to integrate the concepts across multiple disciplines. And also don't forget that I have a 100 hours step two, step three course coming up in the month of. Lead April and most of me, leader, April and most of me. That's more for step two, step three. And I'm going to have another new class coming up soon. So just, just, should me an email through the website if you want some more information.
Or you can just email me at divineinterventionpodcasts.gmail.com. Podcasts with an S at the end. Divineinterventionpodcasts.gmail.com. Okay, so let's continue. So what if they give you, again, these classic science and symptoms of spinal cord compression? But then they give you like a hook. What do I mean by a hook? A hook is like some extra information that tells you that this is what's going on, right? So you see a person they have like science and symptoms of spinal cord compression. And you notice that the temperature is 102 degrees Fahrenheit. Clearly that's going to be an epidural abscess. That's going to be a spinal epidural abscess, right? Or they give you a question about a person that has these science and symptoms of spinal cord compression. And they were recently like in a motor vehicle accident. Well, unfortunately, this is a traumatic cause of spinal cord compression. Right? You probably had like some kind of vertebral fracture or something that's causing their issues. Or what if they give you a question about a patient? And they tell you that this patient, you know, the, you know, they've had a mastectomy in the past. And they're having signs and symptoms of spinal cord compression. That's cancer that has come back, right? That's pretty much like metastatic cancer. Remember, many cancers love to, love to metastasized to the spine, breast cancer, prostate cancer. I remember prostate cancer loves to use this a bachsin vertebral plexus.
That's a high old factor to know for your exams. The bachsin vertebral plexus to, you know, kind of seed to the spinal cord, right? So, or if they give you, you know, signs and symptoms of spinal cord compression and you see that it's more chronic. And you see it in a person that is really old and this person has like chronic back pain, chronic leg pain. Or you clearly want to think about spinal cord stenosis, right? Spinal stenosis, spinal stenosis. Or they give you a question about a person that again has signs and symptoms of spinal cord compression. And they tell you that, ooh, this person was recently diagnosed with E5 and was placed on anti-cualgulation. They want to think about some kind of spinal epidural hematoma, spinal epidural hematoma, okay? Spinal epidural hematoma. And here's the thing, whenever a person, whenever you suspect that a person has spinal cord compression, you always want to get an MRI, simple, simple, simple as that. Always get what? An MRI. Always get what? An MRI. Always get an MRI, right? Always get an MRI. And in general, you know, many times they don't go after treatment of these, but there are some things you probably want to know about treatment, right? Like, for example, if a person has like spinal cord compression and they have it because they have like cancer or whatever, you should clearly do two things for those people. Number one, so that's after you've got an MRI.
Number one, you're going to give steroids, you're going to give IV steroids, high-dose steroids, and they're going to send them for surgery, right? Let them get surgery with the compression. Actually, the third step you can add is radiotherapy, okay? So get the MRI, you're going to see the cause of spinal cord compression, and then how do you manage it? Number one, IV steroids, high-dose glucocorticoids number two, surgical decompression, right? And then number three, the person is going to get radiotherapy, right? And then, you know, if a person has a B12 problem or a copper problem, just supplement, right? That's why people that have had like gastric bypass, remember that biiatric surgery example I gave, with copper deficiency, don't be willing to get like copper, a bunch of supplementation, so they don't develop all these problems, right? And then obviously if it's an infection or whatever, right? Go ahead and treat them on the line infection, right? Transverse my lightest IV steroids as well, right? Transverse my lightest IV steroids as well. Now, please, never use IV steroids to treat a spinal cord compression that's caused by, like, infection or hematoma. Don't use steroids for that, that's not a good idea. You're going to be worse in those problems, right?
And one of the like hyper-specialized bits, again, this podcast, I'm sorry, it kind of sounds a little disorganized, but it's because these disorders are just kind of all over the place, but again, I promise you, this is a very, very high-yield podcast to know for your exams, right? But if a person has like these liquid tumors, I don't know how to say this, like liquid tumors that are causing spinal cord compression, right? So things like leukemia, right? All these blood cancers, leukemia, lymphoma, multiple malinoma and whatnot. These people, if they have spinal cord compression on your exams, I'll encourage you, pick the answer that says radiotherapy. Pick the answer that says radiotherapy. That's a much better answer for these people on your exams. I kid you not in terms of just treatment, in terms of just treatment. So we're going to go ahead and stop here. Again, I offer one on one, to learn for all the USMN exams, step one to step three, complex one to three, prickly and combative school exams, 30-ish off exams. I'm going to have review courses for step one, all the way to step three. The step one class is 25 hours long, step two classes, 20 hours long, and then I have a series of smaller classes that, again, people also find to be very helpful. And then I have these podcasts on Apple, Google and Spotify. I have a You Tube channel, that's where I post the videos that I make, so you can check those out.
And then also, I have another website called divininginterventionlifelessons.com. Every week I post two podcasts from a biblical perspective. I try to address a life lesson. We have almost 250 podcasts on there. There's actually an Apple podcast associated with that. I call the divininginterventionlifelessons.com podcast. And then I also help with ER As applications, you know, editing personal statements, brainstorming over personal statements, and all those things, more interviews. So if you're interested in many of these things, just shoot me an email and I'll be able to give you some more direction. So thank you for listening to me today. Please listen to those podcasts I promise you, and it's very high-yield. So have a wonderful rest of your day. God bless you and bye for now. Thank you.
Practice questions — USMLE style
Question 1 — Neurology/Metabolic
A 60-year-old man presents with progressive sensory ataxia and difficulty maintaining balance. On physical examination, he exhibits diminished vibratory sense and proprioception in a stocking-glove distribution, along with hyperreflexia and an extensor plantar response. Laboratory studies reveal macrocytic anemia and elevated methylmalonic acid (MMA) levels. Which vitamin deficiency is the most likely cause of this constellation of findings?
- A) Vitamin B6 deficiency
- B) Folate deficiency
- C) Copper deficiency
- D) Cobalamin (Vitamin B12) deficiency
Answer: D. The combination of macrocytic anemia, sensory ataxia due to posterior column involvement (loss of vibration/proprioception), and upper motor neuron signs (hyperreflexia, extensor plantar response) is classic for Vitamin B12 deficiency. This condition causes subacute combined degeneration of the spinal cord, affecting both the dorsal columns and the corticospinal tracts. Elevated MMA levels are highly specific to B12 deficiency because cobalamin is required for the metabolism of methylmalonyl-CoA.
Question 2 — Neurology/Inflammatory Myelitis
A 35-year-old woman presents with acute, fluctuating bilateral lower extremity weakness over several days. She also reports episodes of painful vision loss and has been diagnosed with anti-NMO (anti-neuronal myelin oligodendrocyte) antibodies. Initial brain MRI shows no characteristic demyelinating plaques typical of multiple sclerosis (MS). Which diagnosis best explains her clinical presentation?
- A) Multiple Sclerosis (MS), given the fluctuating nature of symptoms
- B) Transverse Myelitis, due to acute onset weakness
- C) Neuromyelitis Optica Spectrum Disorder (NMOSD), due to anti-NMO antibodies and optic neuritis
- D) Guillain-Barré Syndrome (GBS), due to peripheral nerve root involvement
Answer: C. The combination of episodic motor weakness, painful optic neuritis, and the presence of high titers of anti-NMO antibodies strongly points toward Neuromyelitis Optica Spectrum Disorder (NMOSD). While MS can cause fluctuating symptoms, NMOSD is characterized by these specific autoantibodies and often presents with severe optic neuritis and myelitis that may not show classic MS plaques on MRI. GBS typically involves peripheral nerve roots and is usually acute/ascending, while TM lacks the specific antibody marker seen here.
Question 3 — Neurology/Vascular Pathology
A 70-year-old man undergoes repair of a large abdominal aortic aneurysm (AAA). Two days post-surgery, he develops sudden onset weakness in his legs, loss of pain and temperature sensation below the level of injury, but retains intact vibratory and proprioceptive sense. Physical examination reveals preserved deep tendon reflexes at the knee joint. What is the most likely underlying spinal cord pathology?
- A) Brown-Séquard syndrome
- B) Anterior Spinal Artery Syndrome (ASA)
- C) Acute epidural abscess
- D) Cauda Equina Syndrome
Answer: B. The clinical pattern described—loss of pain and temperature sensation (spinothalamic tract involvement) combined with weakness (corticospinal tract/ventral horn involvement), but sparing the posterior columns (vibration/proprioception)—is characteristic of Anterior Spinal Artery Syndrome (ASA). This syndrome results from ischemia to the anterior two-thirds of the spinal cord, often seen following major vascular procedures like AAA repair. Brown-Séquard syndrome requires hemisection of the cord, and Cauda Equina Syndrome involves nerve root compression rather than a specific pattern of tract loss.
Question 4 — Neurology/Endocrine & Metabolism
A 25-year-old woman presents with progressive weakness and sensory deficits. She reports having recently undergone Roux-en-Y gastric bypass surgery. On examination, she has signs suggestive of peripheral neuropathy, but her serum homocysteine levels are normal, and her methylmalonic acid (MMA) levels are also normal. Which deficiency is most likely responsible for her neurological symptoms?
- A) Vitamin B12 deficiency
- B) Folate deficiency
- C) Copper deficiency
- D) Thiamine deficiency
Answer: C. The patient's history of gastric bypass surgery and the presence of peripheral neuropathy suggest malabsorption. While B12 deficiency (Option A) is a common complication, it would typically present with elevated MMA levels. Since both homocysteine and MMA are normal, copper deficiency is the most likely cause. Copper is reabsorbed in the distal ileum/ileocolic region, making it susceptible to malabsorption after bariatric surgery. Neurological symptoms from copper deficiency can mimic B12 deficiency.
Quick fire review
What pathway carries vibration, fine touch, and proprioception?
The Dorsal Columns (Posterior columns).
Where does the Corticospinal Tract cross, and what is the resulting pattern of symptoms if damaged unilaterally?
It crosses in the caudal medulla. Damage results in contralateral symptoms (e.g., left side damage $\rightarrow$ right side symptoms).
What are the key pathways that carry pain, prick, and temperature sensation, and where do they cross?
The Spinothalamic Tracts. They cross in the anterior white commissure, leading to a contralateral loss of pain/temp.
What is the classic presentation distinguishing Conus Medullaris Syndrome from Guillain-Barré Syndrome (GBS)?
CMS presents with predominantly Upper Motor Neuron (UMN) signs; GBS presents with Lower Motor Neuron (LMN) and nerve root symptoms.
If a patient has spinal cord infarction, which major sensory pathway is typically spared?
The Dorsal Columns (Posterior columns).
What are the three components of the classic biochemical triad seen in Vitamin B12 deficiency?
Macrocytic anemia, elevated methylmalonic acid (MMA), and elevated homocysteine.
Which spinal cord syndrome is characterized by a bilateral loss of pain/temperature sensation in a key-like distribution?
Syringomyelia.
What are the three primary risk factors for acute spinal cord infarction?
Recent Myocardial Infarction (MI), hypotension from cardiac surgery, or vertebral artery compromise (e.g., during AAA repair).
In B12 deficiency, which two specific pathways of the spinal cord are most commonly affected, leading to "combined degeneration"?
The Posterior Columns and the Corticospinal Tract.
What is the key difference in CSF findings between Multiple Sclerosis (MS) and Transverse Myelitis (TM)?
MS often shows oligoclonal bands or elevated IgG index; TM typically does not show these markers.
Which vitamin deficiency can cause copper malabsorption, especially after bariatric surgery or high zinc intake?
Copper deficiency.
When managing spinal cord compression due to cancer, what is the correct sequence of treatment modalities?
IV Steroids $\rightarrow$ Surgery $\rightarrow$ Radiotherapy. (Note: Do NOT use steroids for infection/hematoma).
Quick recall / Anki-style questions
Which spinal cord syndrome is characterized by a bilateral loss of pain/temperature sensation in a key-like distribution?
Syringomyelia.
What are the three primary risk factors for acute spinal cord infarction?
Recent Myocardial Infarction (MI), hypotension from cardiac surgery, or vertebral artery compromise (e.g., during AAA repair).
In B12 deficiency, which two specific pathways of the spinal cord are most commonly affected, leading to "combined degeneration"?
The Posterior Columns and the Corticospinal Tract.
What is the key difference in CSF findings between Multiple Sclerosis (MS) and Transverse Myelitis (TM)?
MS often shows oligoclonal bands or elevated IgG index; TM typically does not show these markers.
Which vitamin deficiency can cause copper malabsorption, especially after bariatric surgery or high zinc intake?
Copper deficiency.
When managing spinal cord compression due to cancer, what is the correct sequence of treatment modalities?
IV Steroids $\rightarrow$ Surgery $\rightarrow$ Radiotherapy. (Note: Do NOT use steroids for infection/hematoma).