tag0620
Distinguished member
- Joined
- Nov 18, 2008
- Messages
- 175
- Diagnosis
- 11/2008
- Country
- US
- State
- ut
- City
- park city
Hi Everyone!
Sorry I've been absent...but I feel like we're in a "fight" for my husband's quality of life!
We've had so many Dr.'s not willing to look at other things...they are just deferring to that very hasty als diagnosis. We're in a weird "catch 22". We need surgery on this thoracic herniated disc to prove that he doesn't have als, but no one wants to do this very invasive surgery if he has als because it would be deemed un-necessary if he has it.
What I've found on this herniation...it's rare, it's usually caused by trauma (which means he's most likely been walking around with this spinal cord compression for 2 1/2 years!), it most likely could be compressing the anterior spinal artery that runs to the front of the spinal canal between t4/t9 (his herniation is at t6/t7 pressing directly back into the spinal cord, compressing it by at least 1/3), and it can present with upper AND lower motor neuron symptoms (ala als) as well as some other symptoms that he is now presenting with as well (cold legs and feet, purple feet, pins and needles in the left foot, no sensitivity to temperature changes in the left foot/lower leg).
There is a syndrome called "anterior spinal artery syndrome"
"Anterior Spinal Artery
On the anterior surface of the medulla, two branches from the vertebral arteries unite in the midline to form a single anterior spinal artery that descends the length of the spinal cord in the anterior median fissure (Figure 2.10). The sulcal arteries arising from the anterior spinal artery enter the spinal cord through the anterior median fissure. Successive sulcal arteries generally alternate in their distribution to the left and right side of the spinal cord (Figure 2.11), but occasionally a single sulcal artery will distribute to both sides (Figure 2.12). The sulcal arteries supply the anterior two-thirds of the spinal cord at any cross-sectional level. This is anclinically important feature of the anatomy of the spinal cord, because occlusion of the anterior spinal artery or its sulcal branches could result in anterior cord (spinal artery) syndrome (Figure 2.13). As in most vascular problems, the onset of signs and symptoms is rapid. Figure 2.13 shows the zone of distribution of the anterior spinal artery in the cross-hatched area. The posterior funiculus and horns are spared because these areas are supplied by the posterior spinal arteries. Initially, there is flaccid paralysis of the muscles in the body below the level of infarct because of spinal shock. In time, however, spastic paralysis and other upper motor neuron signs develop because of bilateral destruction of the corticospinal tracts. A variable degree of bowel and bladder dysfunction exists because of the interruption of the descending autonomic pathways. Initially, however, incontinence may be due to spinal shock. A cardinal sign of anterior cord syndrome is a dissociated sensory loss characterized by a loss of pain and temperature sensations (bilateral lateral spinothalamic tract lesion) with preservation of kinesthesia and discriminative touch sensations (sparing of posterior funiculi) in the body below the level of injury. Some patients develop painful dysesthesias about 6 to 8 months after the onset of neurologic symptoms. The source of this pain is unknown, but has been suggested to be attributed to the activation of previously latent pathways that mediate pain sensation. The anterior spinal artery is dependent on segmental contributions from anterior radicular arteries along the length of the spinal cord."
Here is a letter that our GP just wrote for us trying to get us the help we need on this thoracic injury...
"To Whom It May Concern,
My patient "J", has had bilateral lower extremity weakness, left greater than right, with associated muscle atrophy, that was intially progressive over months starting in Feb 2007. Since that time he has had waxing and waning weakness, and has had an impressive return of strength and muscle mass while taking a course of anabolic steroids. Mr. "J" has also developed slowly progressive bilateral, left greater than right lower leg parathesias including pain and coldness that is affected by body position. He has not at any time complained of upper extremity symptoms nor has he observed upper extremity muscle wasting.
Mr. "J"'s past medical history is only significant for a lumber spine fracture from a ski accident in Dec '06 with subsequent surgical fixation in Apr '08.
Mr. "J" has had a complete workup for his symptoms including a normal brain MRI, normal lp, normal labs except for positive antibodies for Rocky Mountain Spotted Fever for which he was given antibiotics, and a thoracic spine MRI which showed a large anterior disc protrusion which impinges on his spinal cord.
Mr. "J" was diagnosed with als after a brief meeting with a neurologist and since that diagnosis he has been unable to find anyone who will consider any other possible cause for his lower extremity weakness. Given the atypical symptoms and response to treatment, along with the presence of a significant thoracic disk protrusion, further workup as well as surgery to correct the spinal cord impingement is certainly warranted.
Thank you.
Sincerely,
Dr. R"
So...anyone have a take on this new info? Anyone think this letter from a "lowly" (haha) family practitioner will make any difference to a neurologist or specialized neuro surgeon?
AAARRRGGGHHH!
Hope everyone is doing ok!
Tracy
Sorry I've been absent...but I feel like we're in a "fight" for my husband's quality of life!
We've had so many Dr.'s not willing to look at other things...they are just deferring to that very hasty als diagnosis. We're in a weird "catch 22". We need surgery on this thoracic herniated disc to prove that he doesn't have als, but no one wants to do this very invasive surgery if he has als because it would be deemed un-necessary if he has it.
What I've found on this herniation...it's rare, it's usually caused by trauma (which means he's most likely been walking around with this spinal cord compression for 2 1/2 years!), it most likely could be compressing the anterior spinal artery that runs to the front of the spinal canal between t4/t9 (his herniation is at t6/t7 pressing directly back into the spinal cord, compressing it by at least 1/3), and it can present with upper AND lower motor neuron symptoms (ala als) as well as some other symptoms that he is now presenting with as well (cold legs and feet, purple feet, pins and needles in the left foot, no sensitivity to temperature changes in the left foot/lower leg).
There is a syndrome called "anterior spinal artery syndrome"
"Anterior Spinal Artery
On the anterior surface of the medulla, two branches from the vertebral arteries unite in the midline to form a single anterior spinal artery that descends the length of the spinal cord in the anterior median fissure (Figure 2.10). The sulcal arteries arising from the anterior spinal artery enter the spinal cord through the anterior median fissure. Successive sulcal arteries generally alternate in their distribution to the left and right side of the spinal cord (Figure 2.11), but occasionally a single sulcal artery will distribute to both sides (Figure 2.12). The sulcal arteries supply the anterior two-thirds of the spinal cord at any cross-sectional level. This is anclinically important feature of the anatomy of the spinal cord, because occlusion of the anterior spinal artery or its sulcal branches could result in anterior cord (spinal artery) syndrome (Figure 2.13). As in most vascular problems, the onset of signs and symptoms is rapid. Figure 2.13 shows the zone of distribution of the anterior spinal artery in the cross-hatched area. The posterior funiculus and horns are spared because these areas are supplied by the posterior spinal arteries. Initially, there is flaccid paralysis of the muscles in the body below the level of infarct because of spinal shock. In time, however, spastic paralysis and other upper motor neuron signs develop because of bilateral destruction of the corticospinal tracts. A variable degree of bowel and bladder dysfunction exists because of the interruption of the descending autonomic pathways. Initially, however, incontinence may be due to spinal shock. A cardinal sign of anterior cord syndrome is a dissociated sensory loss characterized by a loss of pain and temperature sensations (bilateral lateral spinothalamic tract lesion) with preservation of kinesthesia and discriminative touch sensations (sparing of posterior funiculi) in the body below the level of injury. Some patients develop painful dysesthesias about 6 to 8 months after the onset of neurologic symptoms. The source of this pain is unknown, but has been suggested to be attributed to the activation of previously latent pathways that mediate pain sensation. The anterior spinal artery is dependent on segmental contributions from anterior radicular arteries along the length of the spinal cord."
Here is a letter that our GP just wrote for us trying to get us the help we need on this thoracic injury...
"To Whom It May Concern,
My patient "J", has had bilateral lower extremity weakness, left greater than right, with associated muscle atrophy, that was intially progressive over months starting in Feb 2007. Since that time he has had waxing and waning weakness, and has had an impressive return of strength and muscle mass while taking a course of anabolic steroids. Mr. "J" has also developed slowly progressive bilateral, left greater than right lower leg parathesias including pain and coldness that is affected by body position. He has not at any time complained of upper extremity symptoms nor has he observed upper extremity muscle wasting.
Mr. "J"'s past medical history is only significant for a lumber spine fracture from a ski accident in Dec '06 with subsequent surgical fixation in Apr '08.
Mr. "J" has had a complete workup for his symptoms including a normal brain MRI, normal lp, normal labs except for positive antibodies for Rocky Mountain Spotted Fever for which he was given antibiotics, and a thoracic spine MRI which showed a large anterior disc protrusion which impinges on his spinal cord.
Mr. "J" was diagnosed with als after a brief meeting with a neurologist and since that diagnosis he has been unable to find anyone who will consider any other possible cause for his lower extremity weakness. Given the atypical symptoms and response to treatment, along with the presence of a significant thoracic disk protrusion, further workup as well as surgery to correct the spinal cord impingement is certainly warranted.
Thank you.
Sincerely,
Dr. R"
So...anyone have a take on this new info? Anyone think this letter from a "lowly" (haha) family practitioner will make any difference to a neurologist or specialized neuro surgeon?
AAARRRGGGHHH!
Hope everyone is doing ok!
Tracy