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Interesting case discussion


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I've seen this a handful of times, but had a patient that was somewhat interesting today.

 

43 year old female with the complaint of the abrupt onset of right buttock and thigh pain after running. She complains of a burning pain that radiates through the buttock into the lateral thigh, anterior knee, and into the medial tibial area. There is some occasional tingling. She denies frank weakness. She complains of increased pain with sitting, walking, and prolonged standing. Valsalva maneuvers increase her pain. She denies the loss of bowel or bladder dysfunction or associated saddle paresthesias. The pain is not usually worse at night. Her symptoms have been present for 4 weeks.

 

Exam demonstrates quad and hip adductor weakness of -1 (we use a scale where 0 is normal), sensory to pinprick in the lower extremity is intact, reflexes show that ankle jerks are normal bilaterally, internal and external hamstring reflexes are normal, and left patella reflex is normal. Right patella reflex is -2.

 

MRI was obtained and demonstrates some scattered mild spondylosis, an old spondylolysis at L5-S1, and mild multilevel degenerative disc disease. At L2-3 there is a broad based disc bulge with compression of the right L3 nerve root in the lateral recess. There is no other evidence of nerve root compression.

 

The patient is started in therapy, and on a trial of Neurontin, which she started the day before she saw me. We agreed to give the therapy and gaba a try, and I would see her back in 2 weeks.

 

2 weeks later she's minimally better, and we decide to proceed with EMG (nerve root changes often don't show immediately on EMG, so ideally, 6 weeks is the best time to wait and do one). There is evidence of an L4 radiculopathy with active denervation, and fibs present in the rectus femoris, adductor longus, and vastus lateralis. Sensory nerve conductions were normal.

 

Based on this, I ordered an L3 TFESI with excellent resolution of her symptoms. The question is, why was an L3 nerve root compression causing an L4 radiculopathy? A bonus question would be, why were the sensory nerve conductions normal on EMG?

 

 

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Ok - I'm not a spine guy. Best educated guesses here, so no laughing and pointing.

 

1: I'm not certain why an L3-4 bulge would cause an L4 radiculopathy unless the bulge is providing some central canal pressure as well.

 

2: the EMG was abnormal without sensory change as the disc is impinging more on the anterior horn than the posterior.

 

I'm interested to hear the explanation on this.

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The spine is just weird sometimes and anything can happen, but having said that...

 

A far lateral 2-3 HNP could clip the L4 root, however your description of the MRI doesn't suggest a far lateral disc.

 

Perhaps she has an anomaly like a conjoint nerve root?

 

 

*Can you elaborate on your motor grading system and why you use it instead of the conventional?

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Im likely wrong since I havent worked in physiatry for a few years now and that was only for 6 months but i'll take a stab at it.

 

IIRC, L3 nerve root impingements usually affect the posterolateral thigh, anterior thigh and ant knee-which seems to be the L4 dermatone. This could be due to overlap. Sensory NCVs are usually nl in spinal radics because of this neural overlap (both L3 and L4 innervates quadriceps femoris muscle group). Motor NCV is likely delayed. Sensory NCV delays are found in peripheral radics like CTS etc. Rarely in central impingements unless there is demyelination (???)

 

BUUUT, What do I know im an HIV/FP guy now...lol Sent from my SAMSUNG-SGH-I537 using Tapatalk

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Okay....well, you are correct, it was NOT a far lateral disc. It was lateral recess stenosis.

 

As far as the second question, the reason that sensory conductions are preserved in radiculopathy is that the injury is occuring proximal to the dorsal root ganglion.

 

Now. On to the reason behind the L3 causing L4 symptoms and findings on EMG. For starters, there is significant overlap, with the patella reflex actually being a mix of L3, L4, and L5 (L4 is the predominant, but not the only innervation here). But her symptoms are occuring not just in areas of overlap, but in a predominant L4 territory which is why the EMG was interpreted as it was.

 

However, the nerves don't just leave the spine and go to the leg independently. In the lumbar spine, roots 1-4 form the lumbar plexus, with the L4 root typically forming the bifurcated "furcal" nerve which forms the division between the lumbar and sacral plexuses and is the only nerve that actually contributes to both of them. However, in about 20% of the population, these roots get mixed up and become either "prefixed" (L3 becoming the furcal nerve) or "postfixed" (L5 becoming the furcal nerve). This has implications because it can change innervation by one level than what is typically thought of.

 

In this patients case, she most likely has a prefixed lumbar plexus with the L3 nerve root acting as the furcal nerve, and by extension, the L4 root.

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