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Old 06-08-2011
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Question Embolus causing leg weakness and pain!

A 70-year-old woman with atrial fibrillation who is not taking anticoagulation medication “throws” an embolus and develops sudden weakness in her legs. She also has some associated pain in the legs and back. Which of the following would be expected on back and neurologic examination?

Answer
A. Absence of the Babinski reflex
B. Intact pain and temperature sensation over both lower legs
C. Intact vibration and proprioception in the feet
D. Spasticity would be present on inspection of the lower legs
E. Tenderness over the spinal process at the vertebral level of the embolus
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  #2  
Old 06-08-2011
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Default answer is d is think so

i think its d coz atrial fibrillation patients can also have embolus to brain and can cause upper motor neuron lesion and in that lesion there is muscle spasticity i hope its d..
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Old 06-08-2011
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More than one good answers here.

I would go with C. vibration and proprioception usually intact because of the lesion of spinal cord infarction is in anterior 2/3-watershed area sparing posterior columns. I think examiner is testing if you know the basic principle of watershed-ischemia prone area of spinal cord!

Other good answers are

1) yes-absent Babinski reflex in acute phase
2) spasticity of legs-can be the presenting feature too, although flaccid paralysis in acute phase (spinal shock)
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A. absence of the babinski reflex
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i think answer is d
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Clarification of onset of the symptoms should help us to differentiate between 3 good answers.

The question sounds very acute onset!!!!

If you see the patient within minutes of the onset-spinal shock stage, which classically present with acute flaccid paralysis, unable to void and absent babinski reflex!
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Option C (Intact vibration and proprioception in the feet) is correct. Vibration and proprioception are spared in spinal artery thrombosis, because they are in the posterior columns and not located in the anterior two thirds of the spinal cord that becomes infarcted.

Option A (Absence of the Babinski reflex) is incorrect. This absence is primarily an upper motor neuron finding.

Option B (Intact pain and temperature sensation over both lower legs) is incorrect. Pain and temperature sensation would be altered in spinal artery thrombosis distal to the level of infarction, because the anterior two thirds of the spinal cord is involved.

Option D (Spasticity would be present on inspection of the lower legs) is incorrect. Spasticity is primarily involved with upper motor neuron lesions.

Option E (Tenderness over the spinal process at the vertebral level of the embolus) is incorrect. The area at the level of the thrombosis would be painless to palpation, although there is a deeper pain radiating caudally. Palpable pain may be seen with infection.
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The Spinal Cord Segment

As soon as somatosensory fibers enter the spinal cord, protopathic and epicritic systems become, to a large degree, spatially segregated.



Figure 7-6 Segmental organization of somatosensory projections to the spinal cord. A, Protopathic system; B, Epicritic system.

Protopathic sensory fibers terminate primarily on neurons within the most dorsal, superficial regions of the dorsal horn, often referred to as Rexed's lamina I and II (Fig. 7-6A). Within this region, innumerable successive and parallel synapses occur in a complex neural network. Segmental networks within lamina I and II are linked to networks in adjacent spinal cord segments via propriospinal fibers (short ascending and descending pathways within the spinal cord) located in Lissauer's tract at the dorsal-most margin of the dorsal horn. Neural impulses entering the dorsal horn along the lightly myelinated (Aδ) and unmyelinated (C) peripheral fibers of the protopathic system encounter further transmission delays as they travel through the networks of the dorsal horn. Eventually, activation of neurons in lamina I and deeper lamina of the dorsal horn generates impulses in axons that cross the spinal cord in the anterior commissure near the central canal (not to be confused with the anterior commissure of the cerebrum) to the contralateral ventrolateral region of the white matter of the spinal cord. These axons ascend all the way to the brainstem and thalamus as the lateral spinothalamic tract. This anatomic organization, in which protopathic fiber pathways cross the spinal cord within one or two spinal levels of the point of entry of peripheral input, renders them particularly vulnerable to certain types of injury, as Case 7-7 illustrates.

Case 7-7 Lumbar Central Cord Syndrome
A 35-year-old woman presents with the chief complaint of numbness that has developed over the outer aspects of her thighs over the past month. On examination, she has sensory loss confined to an L2 distribution over the outer aspect of each thigh that maximally involves pain and temperature sensation (see Fig. 1-48A). She also has mild weakness of hip flexors, hyperactive knee and ankle jerks, and bilateral Babinski signs.

Comment: The fact that this patient has bilateral, symmetric sensory loss in the absence of polyneuropathy suggests a spinal cord lesion. This impression is confirmed by the presence of signs of damage to descending spinal cord motor pathways. She actually has a highly unusual central disk herniation at the T11-T12 level (most low back disk herniations occur at the L4-L5 and L5-S1 levels). This herniated disk compresses the spinal cord at the L2 level (recall the mismatch between spinal cord and vertebral body levels-[Fig. 1-49]). At some time, perhaps the occasion of the disk herniation, the trauma to the cord produced a small hemorrhage within the center of the cord (hematomyelia). As the hemorrhage resolved, a small cavity or syrinx was left in its place. This cavity, over time, has enlarged, something observed quite commonly in this situation. With enlargement, the cavity has particularly damaged the fibers of the protopathic system crossing in the anterior commissure of the cord. This damage produces abnormalities of pain and temperature sensation confined to the dermatomes corresponding to cord segments actually involved by the cavity. Cord segments below this level are spared because the ascending sensory tracts are spared. The cord compression or the syrinx has also produced subtle damage of descending lateral and ventral motor pathways, hence the hyper-reflexia and Babinski signs, and the mild proximal lower extremity weakness.

All epicritic sensory fibers enter the ipsilateral dorsal column of the spinal cord (Fig. 7-6B). From there, they follow one of two major trajectories. Some immediately enter the dorsal horn, send collaterals into ventral regions of the dorsal horn (subserving segmental proprioception), and ultimately terminate on or in the vicinity of α-motoneurons in the ventral horn (subserving motor functions). Others, with or without immediate collateral projections to the dorsal horn, travel rostrally in the ipsilateral dorsal column all the way to the dorsal column nuclei at the cervicomedullary junction. In addition, there are neurons within the dorsal horn itself that receive epicritic fiber synapses and project via the ipsilateral dorsolateral column to the dorsal column nuclei. Note that within the spinal cord, fibers of the protopathic system are crossed (travel contralateral to the side of the body they represent), whereas those of the epicritic system are uncrossed.

Taken from Medical Neuroscience by Nadeau et al

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Figure 7-10 Cross section of the spinal cord at the C5 level. The branches of the anterior spinal artery supplying the core of the spinal cord are illustrated on the right. Repeated anterior-posterior compression of the cord compresses these branches, resulting in the pattern of infarction shown on the left. The somatotopic organization of the lateral spinothalamic tract is also indicated on the left (S, sacral; C, cervical).
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Quote:
Originally Posted by miss patho View Post
Option C (Intact vibration and proprioception in the feet) is correct. Vibration and proprioception are spared in spinal artery thrombosis, because they are in the posterior columns and not located in the anterior two thirds of the spinal cord that becomes infarcted.

Option A (Absence of the Babinski reflex) is incorrect. This absence is primarily an upper motor neuron finding.

Option B (Intact pain and temperature sensation over both lower legs) is incorrect. Pain and temperature sensation would be altered in spinal artery thrombosis distal to the level of infarction, because the anterior two thirds of the spinal cord is involved.

Option D (Spasticity would be present on inspection of the lower legs) is incorrect. Spasticity is primarily involved with upper motor neuron lesions.
Ok admitted that this is a spinal artery thrombosis and it would affect pain and temp sensations. But I have a question about the babinski reflex.

Babinski reflex is present in UMNL. It is the fanning out and upward going plantars when you stroke the plantar surface of the foot.
When there is no UMNL, there should be no babinski reflex.
So in this case if it involves the spinal cord, shouldn't the babinski reflex be present? The explanation below says the opposite?

"Option A (Absence of the Babinski reflex) is incorrect. This absence is primarily an upper motor neuron finding."
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Quote:
Originally Posted by mle guy View Post
Ok admitted that this is a spinal artery thrombosis and it would affect pain and temp sensations. But I have a question about the babinski reflex.

Babinski reflex is present in UMNL. It is the fanning out and upward going plantars when you stroke the plantar surface of the foot.
When there is no UMNL, there should be no babinski reflex.
So in this case if it involves the spinal cord, shouldn't the babinski reflex be present? The explanation below says the opposite?

"Option A (Absence of the Babinski reflex) is incorrect. This absence is primarily an upper motor neuron finding."
Yes. I agree that it can be the case as I stated earlier!
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this q is confusing me toooooooo
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Old 06-20-2011
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Warning!

babinski positive = umln

in a normal patient they will fan the toe downwards!! babinski negaitve

try it on yourself

clinical it can also be called equiviocal, in that you cant differentiate
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Old 06-21-2011
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The Babinski’s sign can indicate UMN lesion constituting damage to the corticospinal tract. And emboli causing back pain and diffuse legs weakness wont be affecting the peripheral roots, its affecting the spinal cord (which is a CNS not PNS) that has a part of the descneding corticospinal tract at the level of emboli lesion. So its UMN and you expect to find babinski sign positive.
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Old 06-27-2011
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Guyz..there is nothing confusing about the question...It indeed is UMNL,but just look at the actueness of the problem...Initially,even in UMNL ,u can have flaccid paralysis and absent babinski's sign..These things appear with time..So the best option is really the one which is correct answer.
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Old 06-27-2011
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Quote:
Originally Posted by bigal View Post
babinski positive = umln

in a normal patient they will fan the toe downwards!! babinski negaitve

try it on yourself

clinical it can also be called equiviocal, in that you cant differentiate
You are right... All of us have no Babinski...

Besides that, you have to consider that all the tracts except the posterior columns are afected, therefore the flaccid features overwhelm the spastic features of the paralysis.

Just think this way: Why an UMN lesion causes spasticity? It is because the lower neurons do not have any regulation from UMN, therefore there is an excessive contraction (spastic)

A LMN lesion is flaccid because the signals that stimulate the muscle do not get to the muscle, therefore there is no muscle contraction.

In spinal cord lesion we have both UMN and LMN (because the anterior horn is gone as well) so, if you cannot send a signal to the muscle, it will be flaccid.
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