OK So this is weirder than your average..

[all buggered up]

OK So I partially broke my neck at c4567 area 6 years ago, but didnt know it at the time. I put the loss of function down to choreoathetosis/dystonic Cerebral palsy. Need Doctor Youngs advice on a few things...
I hate the anti parkinsons drugs have been addicted to them before the clarity of thought disappears as they deplete the brain of acetylcholine a neurotransmitter many of which are addictive and have very unpleasant side effects. I refuse to take these drugs as I cann't stand myself on them and neither can anyone else. The only alternative is to put me in a comma to keep me still enough while recovering, when I suggested this to the neurosurgeon its a no go. I need to be me at the end of the recovery.

Also because of the strength of my neck muscles isnt there a chance that the writhing of my body including the neck could re break the neck after weilding it leaving me worse off. So the drugs that I avoid now, I would have to be on for the rest of my life to keep the movements down to a minimum something that I won't do... The reason for the surgery is that I have pain and have a slow loss of sensation and movement in my good arm without which I am totally stuffed. If it were my right arm I would not consider the surgery but because its my least effected arm and with the ballism in the right shoulder and my thumb threatening to dislocate my right arm is vertually unusable. If I have to be on these drugs for the rest of my life I don't see the point of the surgery. I need my brain.

[cass]

hi dowdy. i sent you e a bit ago. want to chat? i'll go to a/v chat here.

[SCI-Nurse]

I have asked Dr Young to comment.

AAD

[cass]

bump. nobody has exp. with this type of issue? i know this poster personally. please.

[Wise Young]

Originally Posted by all buggered up

OK So I partially broke my neck at c4567 area 6 years ago, but didnt know it at the time. I put the loss of function down to choreoathetosis/dystonic Cerebral palsy. Need Doctor Youngs advice on a few things...
I hate the anti parkinsons drugs have been addicted to them before the clarity of thought disappears as they deplete the brain of acetylcholine a neurotransmitter many of which are addictive and have very unpleasant side effects. I refuse to take these drugs as I cann't stand myself on them and neither can anyone else. The only alternative is to put me in a comma to keep me still enough while recovering, when I suggested this to the neurosurgeon its a no go. I need to be me at the end of the recovery.

Also because of the strength of my neck muscles isnt there a chance that the writhing of my body including the neck could re break the neck after weilding it leaving me worse off. So the drugs that I avoid now, I would have to be on for the rest of my life to keep the movements down to a minimum something that I won't do... The reason for the surgery is that I have pain and have a slow loss of sensation and movement in my good arm without which I am totally stuffed. If it were my right arm I would not consider the surgery but because its my least effected arm and with the ballism in the right shoulder and my thumb threatening to dislocate my right arm is vertually unusable. If I have to be on these drugs for the rest of my life I don't see the point of the surgery. I need my brain.

Buggered, hi. I am sorry that I did not answer this earlier. I did not see this post until yesterday and have been thinking about it since. As you know, there is not a good answer to your question and I have been trying to figure out what is the best approach. I need to do some literature searches and will answer as soon as I can.

Wise.

[Wise Young]

All buggered,

Let me tell you what I am looking for.

1. I am thinking that there may be an approach to lesioning a part of the brain that would reduce the amount the movement. So, I am looking to see if there is any experience with this.

2. There is a possibility that botox can be used to weaken one or two of the neck muscles to reduce the amount of stress.

3. I am also looking for any new drugs that would slow or stop the movement.

Haven't found anything particularly convincing yet. I am continuing to look.

Wise.

[cass]

thx wise. he lives in australia but has been a guest in my house. i'll e him to make sure he knows of your input. again, ty very much. i know you're busy.

in chat, we wondered about a halo during the recovery period. i wouldn't wish that on anybody, but better than an induced coma, i'd think.

[all buggered up]

Thanks . I owe you both one ...

[all buggered up]

PS have thought about a halo,
but unless the muscles are controled any hard splinting will be automatically resisted this is part of the choreo-athetosis also weilding the neck will give my choreo athetosis a pont of resistance.. which will be destroyed ..I have no say... brain acts body follows...

[Wise Young]

ABU,

Here is what I have found so far. De Salles (1996) reported use of stereotaxic lesions of the ventrolateral nucleus or ventroposterior pallidium (globus pallidus) may reduce or eliminate motor dysfunction. It may be also possible to place stimulating electrodes into either of these two structures and ascertain whether these structures are active when you are undergoing choreoathetotic movements and inject local anesthesia (to stop the activity in those areas) to see if it reduces or stops the movement. This is to avoid the possibility of unnecessary trial-and-error in the lesioning process.

From what I know about choreoathetosis, it is not solely something that arises from the basal ganglia or thalamus. There have been some reports of choreoathetosis that results from cerebellar degeneration (Usui, et al. 1988). Also, neck muscles are very strong and I have not been able to find any reports of using botox to used for this purpose. I will keep adding to this, as I find more information:

1. De Salles AA (1996). Role of stereotaxis in the treatment of cerebral palsy. J Child Neurol 11 Suppl 1: S43-50. There is a renewed interest in basal ganglia surgery for improvement of motor symptoms in cerebral palsy. Rigidity, choreoathetosis, and tremor can be improved or abolished by a well-placed radiofrequency lesion, either in the ventrolateral nucleus of the thalamus or ventroposterior pallidum. The target is chosen based on the predominance of the symptoms in a given patient. A review of the main reports on surgery of the basal ganglia for cerebral palsy, as well as the author's data, shows that the surgery can have a remarkable impact on patients' quality of life when motor dysfunction is improved. An update of the physiopathology of cerebral palsy motor symptoms related to anatomic findings on experimental work, magnetic resonance imaging, and autopsy is used to rationalize surgery of the basal ganglia. Modern stereotactic technique based on exquisite demonstration of the basal ganglia anatomy by magnetic resonance imaging is described and supported by intraoperative electricophysiologic studies. The author stresses the importance of a multidisciplinary approach to provide the cerebral palsy patient with a comprehensive treatment plan before stereotactic surgery. Division of Neurosurgery, University of California Los Angeles School of Medicine 90024-6975, USA. http://www.ncbi.nlm.nih.gov/entrez/q...t_uids=8959461
   
2. Usui S, Beppu H, Hirose K, Tanabe H and Tsubaki T (1988). [A family of spino-cerebellar degeneration with disturbance of ocular movement, choreoathetosis, amyotrophy and dementia--a consideration in clinical features]. No To Shinkei 40: 953-61. Seven cases in a family of hereditary spino-cerebellar degeneration (SCD) similar to dentatorubro-pallido-Luysian atrophy (DRPLA) were reported. The clinical features of these cases were disturbance of ocular movement (limitation of ocular movement and slow eye movement (SEM], remarkable amyotrophy, choreoathetosis, dementia and sleep apnea. The brain CT's revealed marked atrophy in pons and cerebellum. Amyotrophy had been reported in the case of DRPLA, particular ataxo-choreoathetoid form (by Hirayama). Muscle biopsy was performed in these cases, which showed scattered small angulated fiber, severe atrophic fiber with pyknotic nuclear clump, fiber type grouping and small rounded fiber were mixed. These findings indicates neurogenic change of radiculoneuropathy type (by Tanabe). In many reported cases of DRPLA and SCD with amyotrophy, this type of muscle biopsy had not been recognized. In SCD with amyotrophy, a main lesion had existed on peripheral nerve. In this case, there was no definite clinical findings (sensory disturbance, delay of conduction nerve velocity, peripheral neuropathy in nerve biopsy). In recent years, several unclassified cases of SCD with amyotrophy had been reported, which had multi-system degeneration involving peripheral neuropathy. This case is similar to these cases, which is speculates multi-systemic lesions, not only DRPLA but also peripheral nerve involvement. On neuro-otological study, velocity of saccade was slow and persuit was reserved in proband case. In younger onset case, disturbance of saccade and pursuit was mild. In older progressive case, disturbance of saccade and pursuit was progressive and accompanied with severe limitation of ocular movement. Several autopsy cases of SEM had been reported.(ABSTRACT TRUNCATED AT 250 WORDS) Department of Neurology, Tokyo Metropolitan Neurological Hospital, Japan. http://www.ncbi.nlm.nih.gov/entrez/q...t_uids=3196499