Guest guest Posted April 27, 2003 Report Share Posted April 27, 2003 At 03:01 PM 4/27/2003 -0700, you wrote: >The evidence just isn't in to say whether adult-onset >PLS is caused by cell body death, or axonal >degeneration. Autopsy data would provide the answers, >but no one is lining up for that research (G). I guess it's fortunate that the examinations that have been done have been published- if memory serves the articles I've read talked about cell body loss upon exam of deceased PLS patients. Sorry but I don't have the articles here at the house and can't get to the local university medical library. Lavon Quote Link to comment Share on other sites More sharing options...
Guest guest Posted April 27, 2003 Report Share Posted April 27, 2003 Would the MR Spectroscopy give us the same, or almost the same, information as the autopsy? Donna In PLS-FRIENDS , Lavon Lockwood <lockwood@t...> wrote: > At 03:01 PM 4/27/2003 -0700, you wrote: > >The evidence just isn't in to say whether adult-onset > >PLS is caused by cell body death, or axonal > >degeneration. Autopsy data would provide the answers, > >but no one is lining up for that research (G). > > I guess it's fortunate that the examinations that have been done have been > published- if memory serves the articles I've read talked about cell body > loss upon exam of deceased PLS patients. Sorry but I don't have the > articles here at the house and can't get to the local university medical > library. Lavon Quote Link to comment Share on other sites More sharing options...
Guest guest Posted April 27, 2003 Report Share Posted April 27, 2003 Hi Lavon, The article by Pringle et al (Primary Lateral Sclerosis: Clinical Features, Neuropathology and Diagnostic Criteria) states that at autopsy in one male PLS patient, there were reduced Betz cells in the precentral gyrus portion of the cortex. But there was also degeneration of the spinal cord. (pp. 501-505) The issue is which came first. The deceased in the Pringle paper had ascending PLS. (p. 499) He had very significant symptoms in the legs, hands, and arms. He was confined to a wheelchair within 4 years of developing symptoms. He could not speak. (p 499) If the cause of his PLS were axonal degeneration going back up the corticospinal tract to the neuronal cell bodies, then by the time he died one would expect to see a loss of cortical motor neurons as well as axons. This is what was seen on autopsy. Of course this doesn't rule out the possibility that the cell body died first--because the axons would die with the cell bodies. If the deceased had died while his symptoms were still in his legs, and if we could somehow read into the future to determine that he would develop PLS, then an autopsy would reveal whether his motor neurons were degenerating only at the axonal ends, or at the cell body in the cortex. Dr. Fink's 2002 HSP/PLS Research Update is helpful on this subject. He states: " It is not known in PLS which comes first: the degeneration of the nerve cell bodies in the brain or the degeneration of the long axons in the spinal cord that originate from these nerve cell bodies. " He also states: " The major pathologic changes for both PLS and HSP are found in the spinal cord. Both conditions show degenerationn of long nerve processes that begin in the brain (motor cortex) and extend down the spinal cord. These processes, known as corticopsinal tracts, degenerate in both HSP and PLS. Although the majority of pathologic changes in PLS and HSP occur in the spinal cord, there is evidence that brain neurons are also affected in PLS. There is also evidence that brain neurons are affected in at least some forms of HSP. " Based on the work of Drs. Pringle, Fink, and, most recently, Floeter, it currently cannot be scientifically challenged that it is unknown which comes first in PLS--axonal degeneration, or cell body death. There is no scientific battle on this issue. Scientists wait for the evidence. At this point, we just don't have the evidence. Mark > >The evidence just isn't in to say whether adult-onset > >PLS is caused by cell body death, or axonal > >degeneration. Autopsy data would provide the answers, > >but no one is lining up for that research (G). > > I guess it's fortunate that the examinations that have been done have been > published- if memory serves the articles I've read talked about cell body > loss upon exam of deceased PLS patients. Sorry but I don't have the > articles here at the house and can't get to the local university medical > library. Lavon Quote Link to comment Share on other sites More sharing options...
Guest guest Posted April 27, 2003 Report Share Posted April 27, 2003 Hi Donna, MRS produces images showing chemical concentrations in the human body. The issue here is the total loss or partial degeneration of neurons--something that can be seen at autopsy. I doubt very much that MRS would show this. To date, MRI and various x-ray technologies (including CT) show damage at the structural level. I am not aware of any current imaging technology that would show damage at the cellular level. If there were such a technology, diagnosing PLS would be much easier than it is now. Mark > > >The evidence just isn't in to say whether adult-onset > > >PLS is caused by cell body death, or axonal > > >degeneration. Autopsy data would provide the answers, > > >but no one is lining up for that research (G). > > > > I guess it's fortunate that the examinations that have been done > have been > > published- if memory serves the articles I've read talked about > cell body > > loss upon exam of deceased PLS patients. Sorry but I don't have > the > > articles here at the house and can't get to the local university > medical > > library. Lavon Quote Link to comment Share on other sites More sharing options...
Guest guest Posted April 27, 2003 Report Share Posted April 27, 2003 Hi Mark, Correct me if I'm wrong, but all Dr. Floeter's paper seems to say is that it is uncertain whether motor cortex neurons have been irreversibly lost, not what the primary process seems to be. She says " Experimental models have shown that NAA/Cr ratios can decline following deafferentation, and may reflect neuronal inactivity rather than loss of neurons. " based on the study below, and she goes on to say " Thus, it remains uncertain whether motor cortex neurons have been irreversibly lost in patients with ascending PLS. Future studies are needed to follow MRS serially among subgroups, and to provide pathologic correlation. " I would agree that we need further studies, and I would hope our neurons aren't irreversibly lost, but I'm not sure I read into this the same as you have. Dr. Fink's statements you refer to are not peer reviewed, so I don't take that as any more than his opinion. Don't get me wrong, I hold Dr. Fink in high esteem, I just don't think there is evidence to support his particular stance, and there isn't anything I can find to support it. Dr. Pringle had one patient in his PLS study that actually had diffuse Lewy body disease as the underlying pathology, even though he presented with PLS by clinical criteria. So I'm not sure I see any of these as a reason to doubt what has been thought of as the primary process in PLS. Also, classic ALS often times starts in an ascending fashion, one leg first, then the other, then onward up the body. So, go figure. But you are right, we just don't know for certain. I guess the only things certain are death and taxes! :0) Thomson Solana Beach, Ca Visit www.als-pls.org and www.geocities.com/mdmfoo/pls.html > Based on the work of Drs. Pringle, Fink, and, most recently, Floeter, > it currently cannot be scientifically challenged that it is unknown > which comes first in PLS--axonal degeneration, or cell body death. > > There is no scientific battle on this issue. Scientists wait for the > evidence. At this point, we just don't have the evidence. > > Mark Central nervous system trans-synaptic effects of acute axonal injury: a 1H magnetic resonance spectroscopy study. Rango M, Spagnoli D, Tomei G, Bamonti F, Scarlato G, Zetta L. Universita degli Studi di Milano, Istituto di Clinica Neurologica, Italy. N-acetylaspartate (NAA) has previously been proposed as a neuronal marker. 1H magnetic resonance spectroscopy (MRS) is able to detect NAA in brain, and decreases of NAA have been documented after brain injury. The reason for this decrease is not fully understood and neuron loss damage and " dysfunction " have all been proposed. It is hypothesized that acute central nervous system (CNS) deafferentation causes a trans-synaptic NAA decrease and that high resolution 1H MRS is able to detect such a decrease. To test this hypothesis, an experimental model was used in which axonal lesions were obtained by stretch injury in guinea pig right optic nerve (95-99% crossed fibers). The trans-synaptic concentration of NAA, total creatine (Cr), and the NAA/Cr ratio in lateral geniculate bodies (LGB) and superior colliculi (SC) sample extracts were measured 72 h later by high resolution 1H MRS. In the left LGB/SC, which is where right optic nerve fibers project, reductions of NAA and NAA/Cr were found whereas Cr levels were normal. NAA, NAA/Cr, and Cr values were all normal in the right LGB/SC. Histology and EM findings revealed no abnormalities. At 7 days, left LGB/SC NAA and NAA/Cr values were in the normal range. It was concluded that 1) acute deafferentation in the CNS causes a trans-synaptic decrease of NAA levels that can be detected by 1H MRS and 2) NAA decrease may be due to changes of NAA metabolism caused by functional neuronal inactivity rather than neuronal loss, injury or " dysfunction. " 1H MRS is a potential tool for the study of functional effect of CNS lesions in vivo. PMID: 7596262 [PubMed - indexed for MEDLINE] Quote Link to comment Share on other sites More sharing options...
Guest guest Posted April 28, 2003 Report Share Posted April 28, 2003 In a message dated 4/28/2003 4:10:41 PM Eastern Standard Time, markw732@... writes: > I have mild > sensory loss in my feet. > Mark I have pain/numbness in my feet. They named it Peripheral Neuropathy. Is that what you have also? Connie Quote Link to comment Share on other sites More sharing options...
Guest guest Posted April 28, 2003 Report Share Posted April 28, 2003 Hi , You're right--all I'm saying that it is currently unknown whether PLS begins (1) by degeneration in the far ends of the axons, or (2) by the death of the neuronal cell bodies in the motor cortex. Dr. Floeter wrote that " Thus, it remains uncertain whether motor cortex neurons have been irreversibly lost in patients with ascending PLS. " This was based on the possibility that PLS starts in the axons and then travels back toward the cell body. Dr. Floeter also found no MRI evidence of atrophy in the motor cortex. Her work compared PLSers with age matched controls. Previous work that showed cortical atrophy compared PLSers with college students. (Hardly a valid comparison.) Dr. Floeter also singled out ascending PLSers as a group whose symptoms seemed to be correlated to objective test measurement. She suggested that this may make them a good group for a genetic study. Like you, I was also removed from the study. In my case, I have mild sensory loss in my feet. Mark > Hi Mark, > Correct me if I'm wrong, but all Dr. Floeter's paper seems to say is that > it is uncertain whether motor cortex neurons have been irreversibly lost, > not what the primary process seems to be. She says " Experimental models > have shown that NAA/Cr ratios can decline following deafferentation, and may > reflect neuronal inactivity rather than loss of neurons. " based on the > study below, and she goes on to say " Thus, it remains uncertain whether > motor cortex neurons have been irreversibly lost in patients with ascending > PLS. Future studies are needed to follow MRS serially among subgroups, and > to provide pathologic correlation. " > > I would agree that we need further studies, and I would hope our neurons > aren't irreversibly lost, but I'm not sure I read into this the same as you > have. > > Dr. Fink's statements you refer to are not peer reviewed, so I don't take > that as any more than his opinion. Don't get me wrong, I hold Dr. Fink in > high esteem, I just don't think there is evidence to support his particular > stance, and there isn't anything I can find to support it. > > Dr. Pringle had one patient in his PLS study that actually had diffuse Lewy > body disease as the underlying pathology, even though he presented with PLS > by clinical criteria. > > So I'm not sure I see any of these as a reason to doubt what has been > thought of as the primary process in PLS. > > Also, classic ALS often times starts in an ascending fashion, one leg first, > then the other, then onward up the body. So, go figure. > > But you are right, we just don't know for certain. I guess the only things > certain are death and taxes! :0) > > Thomson > Solana Beach, Ca > Visit www.als-pls.org > and www.geocities.com/mdmfoo/pls.html > > > > Based on the work of Drs. Pringle, Fink, and, most recently, Floeter, > > it currently cannot be scientifically challenged that it is unknown > > which comes first in PLS--axonal degeneration, or cell body death. > > > > There is no scientific battle on this issue. Scientists wait for the > > evidence. At this point, we just don't have the evidence. > > > > Mark > > > > Central nervous system trans-synaptic effects of acute axonal injury: a 1H > magnetic resonance spectroscopy study. > > Rango M, Spagnoli D, Tomei G, Bamonti F, Scarlato G, Zetta L. > > Universita degli Studi di Milano, Istituto di Clinica Neurologica, Italy. > > N-acetylaspartate (NAA) has previously been proposed as a neuronal marker. > 1H magnetic resonance spectroscopy (MRS) is able to detect NAA in brain, and > decreases of NAA have been documented after brain injury. The reason for > this decrease is not fully understood and neuron loss damage and > " dysfunction " have all been proposed. It is hypothesized that acute central > nervous system (CNS) deafferentation causes a trans-synaptic NAA decrease > and that high resolution 1H MRS is able to detect such a decrease. To test > this hypothesis, an experimental model was used in which axonal lesions were > obtained by stretch injury in guinea pig right optic nerve (95-99% crossed > fibers). The trans-synaptic concentration of NAA, total creatine (Cr), and > the NAA/Cr ratio in lateral geniculate bodies (LGB) and superior colliculi > (SC) sample extracts were measured 72 h later by high resolution 1H MRS. In > the left LGB/SC, which is where right optic nerve fibers project, reductions > of NAA and NAA/Cr were found whereas Cr levels were normal. NAA, NAA/Cr, and > Cr values were all normal in the right LGB/SC. Histology and EM findings > revealed no abnormalities. At 7 days, left LGB/SC NAA and NAA/Cr values were > in the normal range. It was concluded that 1) acute deafferentation in the > CNS causes a trans-synaptic decrease of NAA levels that can be detected by > 1H MRS and 2) NAA decrease may be due to changes of NAA metabolism caused by > functional neuronal inactivity rather than neuronal loss, injury or > " dysfunction. " 1H MRS is a potential tool for the study of functional effect > of CNS lesions in vivo. > > PMID: 7596262 [PubMed - indexed for MEDLINE] Quote Link to comment Share on other sites More sharing options...
Guest guest Posted April 28, 2003 Report Share Posted April 28, 2003 With all this discussion of ascending PLS, what about descending PLS. Does anyone know anything about that. My speech has gone from bad to worse in a year. I am now beginning to feel some stiffness in my legs. I do not know what spacticity is. Is ascending and descending different, other than the direction? Re: Cell body vs Axon > Hi , > > You're right--all I'm saying that it is currently unknown whether PLS > begins (1) by degeneration in the far ends of the axons, or (2) by > the death of the neuronal cell bodies in the motor cortex. > > Dr. Floeter wrote that " Thus, it remains uncertain whether motor > cortex neurons have been irreversibly lost in patients with ascending > PLS. " This was based on the possibility that PLS starts in the axons > and then travels back toward the cell body. > > Dr. Floeter also found no MRI evidence of atrophy in the motor > cortex. Her work compared PLSers with age matched controls. > Previous work that showed cortical atrophy compared PLSers with > college students. (Hardly a valid comparison.) > > Dr. Floeter also singled out ascending PLSers as a group whose > symptoms seemed to be correlated to objective test measurement. She > suggested that this may make them a good group for a genetic study. > > Like you, I was also removed from the study. In my case, I have mild > sensory loss in my feet. > > Mark > > > > Hi Mark, > > Correct me if I'm wrong, but all Dr. Floeter's paper seems to say > is that > > it is uncertain whether motor cortex neurons have been irreversibly > lost, > > not what the primary process seems to be. She says " Experimental > models > > have shown that NAA/Cr ratios can decline following > deafferentation, and may > > reflect neuronal inactivity rather than loss of neurons. " based on > the > > study below, and she goes on to say " Thus, it remains uncertain > whether > > motor cortex neurons have been irreversibly lost in patients with > ascending > > PLS. Future studies are needed to follow MRS serially among > subgroups, and > > to provide pathologic correlation. " > > > > I would agree that we need further studies, and I would hope our > neurons > > aren't irreversibly lost, but I'm not sure I read into this the > same as you > > have. > > > > Dr. Fink's statements you refer to are not peer reviewed, so I > don't take > > that as any more than his opinion. Don't get me wrong, I hold Dr. > Fink in > > high esteem, I just don't think there is evidence to support his > particular > > stance, and there isn't anything I can find to support it. > > > > Dr. Pringle had one patient in his PLS study that actually had > diffuse Lewy > > body disease as the underlying pathology, even though he presented > with PLS > > by clinical criteria. > > > > So I'm not sure I see any of these as a reason to doubt what has > been > > thought of as the primary process in PLS. > > > > Also, classic ALS often times starts in an ascending fashion, one > leg first, > > then the other, then onward up the body. So, go figure. > > > > But you are right, we just don't know for certain. I guess the > only things > > certain are death and taxes! :0) > > > > Thomson > > Solana Beach, Ca > > Visit www.als-pls.org > > and www.geocities.com/mdmfoo/pls.html > > > > > > > Based on the work of Drs. Pringle, Fink, and, most recently, > Floeter, > > > it currently cannot be scientifically challenged that it is > unknown > > > which comes first in PLS--axonal degeneration, or cell body death. > > > > > > There is no scientific battle on this issue. Scientists wait for > the > > > evidence. At this point, we just don't have the evidence. > > > > > > Mark > > > > > > > > Central nervous system trans-synaptic effects of acute axonal > injury: a 1H > > magnetic resonance spectroscopy study. > > > > Rango M, Spagnoli D, Tomei G, Bamonti F, Scarlato G, Zetta L. > > > > Universita degli Studi di Milano, Istituto di Clinica Neurologica, > Italy. > > > > N-acetylaspartate (NAA) has previously been proposed as a neuronal > marker. > > 1H magnetic resonance spectroscopy (MRS) is able to detect NAA in > brain, and > > decreases of NAA have been documented after brain injury. The > reason for > > this decrease is not fully understood and neuron loss damage and > > " dysfunction " have all been proposed. It is hypothesized that acute > central > > nervous system (CNS) deafferentation causes a trans-synaptic NAA > decrease > > and that high resolution 1H MRS is able to detect such a decrease. > To test > > this hypothesis, an experimental model was used in which axonal > lesions were > > obtained by stretch injury in guinea pig right optic nerve (95-99% > crossed > > fibers). The trans-synaptic concentration of NAA, total creatine > (Cr), and > > the NAA/Cr ratio in lateral geniculate bodies (LGB) and superior > colliculi > > (SC) sample extracts were measured 72 h later by high resolution 1H > MRS. In > > the left LGB/SC, which is where right optic nerve fibers project, > reductions > > of NAA and NAA/Cr were found whereas Cr levels were normal. NAA, > NAA/Cr, and > > Cr values were all normal in the right LGB/SC. Histology and EM > findings > > revealed no abnormalities. At 7 days, left LGB/SC NAA and NAA/Cr > values were > > in the normal range. It was concluded that 1) acute deafferentation > in the > > CNS causes a trans-synaptic decrease of NAA levels that can be > detected by > > 1H MRS and 2) NAA decrease may be due to changes of NAA metabolism > caused by > > functional neuronal inactivity rather than neuronal loss, injury or > > " dysfunction. " 1H MRS is a potential tool for the study of > functional effect > > of CNS lesions in vivo. > > > > PMID: 7596262 [PubMed - indexed for MEDLINE] > > > > > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted April 28, 2003 Report Share Posted April 28, 2003 Connie, I have sensory loss--very mild sensory loss--in portions of my feet. I only notice it during a neurological exam. When the doc places a vibrating tuning fork on portions of the top of my feet, I feel nothing. Also, my sensation of hot and cold in those areas are diminished. Dr. Floeter worked this up in her exam of me at NIH. It knocked me out of the study. I do have pain in my feet, but I know the cause--the straps on my AFO's, and my shoelaces are on too tight. When I take my shoes and braces off, no more pain. (I just got new AFO's today--much pain, frequent removal of the AFO's.) Mark > In a message dated 4/28/2003 4:10:41 PM Eastern Standard Time, > markw732@y... writes: > > > I have mild > > sensory loss in my feet. > > > Mark > I have pain/numbness in my feet. They named it Peripheral Neuropathy. Is > that what you have also? Connie > > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted April 28, 2003 Report Share Posted April 28, 2003 Descending PLS (symptoms start in the mouth with speech difficulties and then descend down to the arms and legs) is more rare than ascending PLS. Dr. Floeter's paper mentioned 15 patients with " ascending PLS " . She also mentioned an additional 10 PLSers whose symptom progression was not ascending. Here's how she described them: " Multifocal group. Ten patients had a markedly asymmetric or patchy pattern of symptom spread. Region of symptom onset was variable: four began with arm symptoms or dysarthria (speech difficulties), one began with hemiparesis, and five began with leg symptoms, but as symptoms progressed. one or more limbs remained unaffected. A few patients in this group reported transient improvement or long periods of stability, rather than a steadily progressive course. One patient had moderate leg weakness to manual muscle testing in addition to spasticity. A few patients had pain or paresthesias, although no objective sensory loss was present on examination. Half of the patients had urinary urgency, which began on average 7.25 years (range 3 to 16 years) after onset of disease. Age at onset was 45.4 + or - 7.6 years, with a duration 8.4 + or - 8.1 years (range 3 to 30 years). " " Of the eight patients in this group followed more than a year, three returned for a follow-up examination and five were assessed by questionnaire. All reported worsening of symptoms. In six, worsening occurred within previously affected body regions. In two, an additional limb became symptomatic. One of the patients had begun using a walker, and one had undergone a baclofen pump placement. " Mark > > > Hi Mark, > > > Correct me if I'm wrong, but all Dr. Floeter's paper seems to say > > is that > > > it is uncertain whether motor cortex neurons have been irreversibly > > lost, > > > not what the primary process seems to be. She says " Experimental > > models > > > have shown that NAA/Cr ratios can decline following > > deafferentation, and may > > > reflect neuronal inactivity rather than loss of neurons. " based on > > the > > > study below, and she goes on to say " Thus, it remains uncertain > > whether > > > motor cortex neurons have been irreversibly lost in patients with > > ascending > > > PLS. Future studies are needed to follow MRS serially among > > subgroups, and > > > to provide pathologic correlation. " > > > > > > I would agree that we need further studies, and I would hope our > > neurons > > > aren't irreversibly lost, but I'm not sure I read into this the > > same as you > > > have. > > > > > > Dr. Fink's statements you refer to are not peer reviewed, so I > > don't take > > > that as any more than his opinion. Don't get me wrong, I hold Dr. > > Fink in > > > high esteem, I just don't think there is evidence to support his > > particular > > > stance, and there isn't anything I can find to support it. > > > > > > Dr. Pringle had one patient in his PLS study that actually had > > diffuse Lewy > > > body disease as the underlying pathology, even though he presented > > with PLS > > > by clinical criteria. > > > > > > So I'm not sure I see any of these as a reason to doubt what has > > been > > > thought of as the primary process in PLS. > > > > > > Also, classic ALS often times starts in an ascending fashion, one > > leg first, > > > then the other, then onward up the body. So, go figure. > > > > > > But you are right, we just don't know for certain. I guess the > > only things > > > certain are death and taxes! :0) > > > > > > Thomson > > > Solana Beach, Ca > > > Visit www.als-pls.org > > > and www.geocities.com/mdmfoo/pls.html > > > > > > > > > > Based on the work of Drs. Pringle, Fink, and, most recently, > > Floeter, > > > > it currently cannot be scientifically challenged that it is > > unknown > > > > which comes first in PLS--axonal degeneration, or cell body death. > > > > > > > > There is no scientific battle on this issue. Scientists wait for > > the > > > > evidence. At this point, we just don't have the evidence. > > > > > > > > Mark > > > > > > > > > > > > Central nervous system trans-synaptic effects of acute axonal > > injury: a 1H > > > magnetic resonance spectroscopy study. > > > > > > Rango M, Spagnoli D, Tomei G, Bamonti F, Scarlato G, Zetta L. > > > > > > Universita degli Studi di Milano, Istituto di Clinica Neurologica, > > Italy. > > > > > > N-acetylaspartate (NAA) has previously been proposed as a neuronal > > marker. > > > 1H magnetic resonance spectroscopy (MRS) is able to detect NAA in > > brain, and > > > decreases of NAA have been documented after brain injury. The > > reason for > > > this decrease is not fully understood and neuron loss damage and > > > " dysfunction " have all been proposed. It is hypothesized that acute > > central > > > nervous system (CNS) deafferentation causes a trans-synaptic NAA > > decrease > > > and that high resolution 1H MRS is able to detect such a decrease. > > To test > > > this hypothesis, an experimental model was used in which axonal > > lesions were > > > obtained by stretch injury in guinea pig right optic nerve (95- 99% > > crossed > > > fibers). The trans-synaptic concentration of NAA, total creatine > > (Cr), and > > > the NAA/Cr ratio in lateral geniculate bodies (LGB) and superior > > colliculi > > > (SC) sample extracts were measured 72 h later by high resolution 1H > > MRS. In > > > the left LGB/SC, which is where right optic nerve fibers project, > > reductions > > > of NAA and NAA/Cr were found whereas Cr levels were normal. NAA, > > NAA/Cr, and > > > Cr values were all normal in the right LGB/SC. Histology and EM > > findings > > > revealed no abnormalities. At 7 days, left LGB/SC NAA and NAA/Cr > > values were > > > in the normal range. It was concluded that 1) acute deafferentation > > in the > > > CNS causes a trans-synaptic decrease of NAA levels that can be > > detected by > > > 1H MRS and 2) NAA decrease may be due to changes of NAA metabolism > > caused by > > > functional neuronal inactivity rather than neuronal loss, injury or > > > " dysfunction. " 1H MRS is a potential tool for the study of > > functional effect > > > of CNS lesions in vivo. > > > > > > PMID: 7596262 [PubMed - indexed for MEDLINE] > > > > > > > > > > > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted April 28, 2003 Report Share Posted April 28, 2003 That's me! Lavon >and one had undergone a baclofen pump >placement. " Quote Link to comment Share on other sites More sharing options...
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