Subclavian Steal Diagram

The eyes of the Border Collie

The "weakness" of the Border Collie is the frequency in this race two serious eye diseases: Eye Anomaly Collie (AOC) and the Progressive Atrophy of the Retina (APR). Here's a quick summary on the AOC from the site http://www.passionborder.com/

But first, a small photograph of the specimen most pampered ...



The anomaly of the eye Collie

This hereditary disease of the eye is caused by abnormal development in the eyeball with very different consequences depending on the dogs and the degree of damage.
The general characteristics of the AOC are: abnormal thinning of the choroid (vascular tissue present in the retina), lack of pigmentation of the latter and too low density of choroidal vessels may be more abnormal form. In more severe stages of vision can be altered to result in blindness, usually unilateral. There

2 forms of the disease: mild non-progressive who has a thinning of the choroid without vision loss (grades 1 and 2), and severe disease (grades 3 and 4).

1st Grade: Hypoplasia / dysplasia choroid
From the 45th day of gestation, can be detected by an ophthalmologist examination in puppies between 5-7 weeks to 2-3 months. If the anomaly is alone, there is no impact on visual skills.

second grade : Coloboma papillary or papillary-justa
The coloboma is a developmental anomaly of the choroid occur in stage embryo. It is with papillary or periphery, its size can vary and thus alter + or - the vision of a strong dog. At this stage it is associated with hypoplasia / dysplasia of the choroid.

3rd grade : Retinal detachment (partial or total)
The partial or total detachment associated with coloboma at this stage of the disease, bleeding may occur in this case.

fourth grade : intraocular hemorrhage
the Stade + severe. They occur in the presence of coloboma and retinal detachment but not systematically. The bleeding can lead to the formation of glaucoma in some cases.

The AOC is a congenital disease, in contrast to the RPA which is progressive development of choroidal hypoplasia and colobomas are present at birth and grow along with the eye itself, this explains that the diagnosis of the disease occurs when the dog is young (2 months-2 years) by the expression of early disease.
This disease is hereditary and caused by mutation, dogs suffering from a mild form can produce offspring that will affect a severe form.
The disease is inherited as an autosomal recessive monogenic fashion. The gene is located on chromosome No. 37 regardless of race.

Screening for disease:
-Examination of the fundus with an ophthalmoscope after dilating the pupil. The examination is more reliable on a dog 6 to 8 weeks because with age, the fundus may be distorted by pigmentation and mask the signs of the disease. This test should be conducted annually.
-DNA test, by request from a company, sampling kits are sent. The buccal swab should be made and authenticated by a veterinarian to be able to issue a certificate genetics. This test identifies the presence or absence of AOC but not its severity.


There is no cure for this disease, the only way to stop it is unfortunately the spacing of the reproduction of a dog suffering.

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nystagmus in image

Here are 2 small video nystagmus:

In the left eye: very asymmetric nystagmus, but not unilateral (right eye has a small vertical shaking)

In regard to right, squint pretty, but most of nystagmus ...

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Hence the usefulness of Botox ...

short history received by mail ...

I was sitting in the waiting room for my first appointment with a new dentist when I noticed his diploma hung on the wall. There was his name and I suddenly remembered a tall, dark with this name. It was in my high school class some 40 years ago and I was wondering if this could be the same boy who had cracked at the time?

When I entered the treatment room, I immediately dismissed the thought from my mind. This man, grizzled, balding and face marked deep wrinkles was too old to have been my secret love ... Although ...

After he examined my teeth, I asked him if he had gone to high school Henry IV.
"Yes, I he replied .
- When did you get your tank? I asked.
- 1972. Why do you ask?
- Well, you were in my class! did I exclaimed.

And then that horrible little old idiot son of a bitch asked me

teacher You were what?

...

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No implant The implant black black

bad, I would have really wanted one. But I am a "girl of 20 years," in the words of the optometrist, so it's not about me it will achieve this intervention. Argument: it would look smart in 15 years if they find a cure for my kind of trouble, that's my shot diplopia has more reason to be there, and I find myself still blind because of an implant blocking.
say I'm disappointed is an understatement. It's not when I'm 70 it will consider doing so. And even if we must remove the implant in 15 years, until it's always 15 years without double vision ... My double vision is not fresh (7 years), we could still start to think of ways a little more "sustainable", which combine efficiency and aesthetics. The filters are not one nor the other ...

Otherwise the rest, the optometrist took over the case, and casually, it makes 2 years that my condition is stable oculomotor . It can be summarized roughly as follows: state basic difference (left eye). But big spasms of the right medial left, impotence and abduction of the right eye, paralysis of the left superior rectus muscle, and nystagmus weird.

Regarding surgery oculomotor (2 years of stability, I could not not ask), response:
- I am the ideal indication for Faden-operation on my right medial left
- but 4 previous interventions with conventional surgery were very well justified, and each one has only complicate matters,
- I was also a clear indication of botulinum toxin, and it had no effect,
- so we shall refrain from any new gesture.

For some explanation of Faden-operation or operation wire Cüppers, see the 6th paragraph of this article

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Here is a summary of an article about a intervention that tempts me especially: the placement of an implant black. This summary
from the website of the French Association of Pediatric Ophthalmology and strabologie www.afsop.fr, and was written by Alain and Pierre Pêchereau Lebranchu.


antidiplopique treatment: black implant?

Subject: adjusting to the double vision is very variable depending on the patient, ranging from near indifference to a situation totally unbearable. In the latter case, insertion of an implant black seems to be a logical solution.

Materials and methods: Three patients suffering from intractable diplopia, it was proposed placement of an implant black. The implant was placed in the dominant eye after cataract surgery by phacoemulsification made.

Results: Despite its name, black implant passes a significant amount of light to a very low visual acuity and collect certain light sources. The decrease in luminance causes mydriasis allowing the entry of stray light at night. In all three cases, the only black implant placement resulted in a significant improvement in diplopia, but not its disappearance.
In all three cases, the creation of a miosis first by pilocarpine and by pupilloplastie surgery, resulted in the disappearance of diplopia.

Discussion: Some patients with diplopia and in a situation of extreme suffering develop a research strategy of double vision. There is a real addiction to double vision. To break this vicious circle, it is necessary to remove almost all visual information of eye dominated.

Conclusion: The treatment of diplopia by removing any visual information of an eye is possible. It is important to note that this solution is reversible if a serious accident occurred in the right eye.

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Review

intense photophobia and ERG CHU not really normal but not pathological nor frankly, that left little doubt about the good sensitivity of the cones can not be fixed. Then at least to be sure, the ophthalmologist had prescribed a comprehensive review to the clinic Sourdille: ERG, PEV, EOG sensory and visual field . I just received a copy of the minutes with the same curves plotted

:-) We start by visual field, which does not show a deficit above the left eye, normal view of ptosis and foveolar sensitivity not top, which nystagmus is the culprit. So we can say normal visual field.

It's the same with ERG dark adaptation and adjustment to the brightness, as well as sensory EOG , they show that my retina is fine, especially since this is my cones about them that had questions. The

VEP , on the right are slightly reduced in amplitude and latency limit, left normal latency but reduced amplitude frankly, with no detectable EPI for small checkerboard of 15 '. Blame the nystagmus.

So getting back to photophobia, the explanation is trivial: we know that awakens photophobia diplopia, nystagmus, and more. Two good reasons not to bear the light.

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Consult neuro retina, physiology

This morning I went to my consultation at the "center of reference for rare neuromuscular diseases" UHC, with the department head. Today's theme: failure of botulinum toxin . After explaining the neurologist city (ie botox at the base had not much to do in my eyes), I was anxious to have a slightly more elaborate explanation. The doctor who gave me injections is an ophthalmologist specializing strabologie in, and not a butcher's apprentice who is diversifying trying botox on anything that moves. I think we could from the basis that the botulinum toxin was a real indication of what a unit is easy to verify since it did not act and that my condition is always the same oculomotor, the other is a false question because even on a normal toxin is supposed to paralyze the muscles.

Well, consulting this morning still provided a good temper those comments. Indeed, regardless of whether the toxin has been shown or not: even though it would not have been, it would still have acted. If you realize this gesture in a normal subject, he causes oculomotor palsy, even though there is initially no spasm. So for him, he joined what the optometrist said, we can deduce that the origin of my troubles is downstream from the scope of action of botulinum toxin. As it acts at the neuromuscular junction, my oculomotor disorders would be strictly myogenic , including (pseudo) nystagmus (which happily survived injection).

If this explanation is correct, he seemed to understand that the treatment was severely compromised, there is no therapeutic means to stop these activities myogenic anarchic. Botulinum toxin effect is particularly effective on spasticity of neurogenic origin, but not directed to the muscle itself. Genetic analysis
launched two months ago would bring the better the diagnosis, if positive. You just wait ... 4 years? Go
time flies.

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Even less response

So yesterday, so it was my appointment with my neurologist at Nantes, I waited with great impatience. Well, a bit of disappointment for the answers I expected, he'll have to wait a bit ... He can not help me with the mystery of the failure of the toxin botulinum, it is "not sufficiently expert in this field" ...

Concerning a problem "second tier", but still important to me migraines. Beta-blockers were still pretty effective as maintenance treatment, since the number of crisis had diminished. But they are absolutely cons-indicated in combination with Mexitil, which treats myotonias. So we tried the last thing left to try: the tricyclic antidepressants. As this would be a shame to spoil the school, he prescribed the Cymbalta, which is one of the few to have no sedative effect. For

the channelopathy, nothing new, I just learned that genetic research that was launched was much largeque what I understood, with one hand ion channel analysis, and other analysis of genetic abnormalities responsible for progressive external ophthalmoplegia , in particular, mitochondrial citopathies .

To return to the botulinum toxin, the idea of a malformation of the neuromuscular junction is eliminated according to him, just as if this were the case, botulinum toxin would have been disastrous. We can not say she was ... He then told me to take appointment with Pr Pereon center rare neuromuscular disease, which is stalled on it. A little more waiting until June 30

Finally, do not stop there way visit to the optometrist on Monday in Toulouse.

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Mexitil green light cardiologist

A week after the resumption of Mexitil (just a reminder I had stopped after a few days because of gastrointestinal symptoms, to avoid any risk of arrhythmia hypokalemia), I find myself at home again the cardiologist to control everything. The

digestive problems returned from the 3rd day of treatment, but I waited firm foot to blow rice-banana-chocolate :-) Well we'll have to continue a diet adapted to this situation because Mexitil is intended for treatment on a long, sometimes very long term, it doesn encouraged him not to deal with other consequences Medoc side effects of initial treatment ...

Regarding heart rate, it is slow . After racing, my pulse was 50 beats per minute , which based on the Cardio is undoubtedly an effect of Mexitil. I-cons are listed all the humps heart, including beta-blockers, on pain of having to wear a pacemaker, which, again, would be a shame. The ECG also showed a arrhythmia (extra-systolic?) Which remains in tolerable. We will do a holter if I am still unwell or if I feel fibrillation. Finally

voltage side, it was 9 / 6. And there, mexiletine has nothing to do. J'épaississe just need a little. At the slightest blow as my "GI" in recent weeks, my muscle mass back, and it is not good for the tension, nor for my suspected channelopathy. So: eat salty liquorice and do sports! (The great sport that I am welcomes the idea ... ... ... to take the 30th degree).

So much for my little heart. I talked a little in passing the failure of botulinum toxin was the first time she had heard no immunological resistance to this toxin.
Next Tuesday, the neurologist appointment in Nantes. Deeply answers ...

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resistance to botulinum toxin Botox Injection

4 days after my second botox injection, I'm back at the optometrist this morning, to the same conclusion as last time: nothing happens. Or almost.
Yet he "put the dose (more than 10 IU), yet it I have not passed in the late morning, and yet her other patients have reacted well, some very next day. So we can not accuse a technical problem.

So according to the ophthalmologist, the hypothesis of immunological resistance is very unlikely for several reasons:
- the existence of resistance due to antibodies neutralizing botulinum toxin has not been proven,
- the doses used in ophthalmology are far too small to trigger such a reaction,
- the appearance of antibodies can be done only after several repeated injections, and certainly not soon the first time
- I asked if it was possible that one day I have eaten food contaminated with botulinum toxin and this has triggered an immune response, response: "we must not exaggerate, and botulism usually one realizes, "
- again, my left eyelid started to fall slightly (ptosis), which means that the toxin has spread and has an effect on my lifter eyelid ...

remains to understand why my reaction to botox eyelid, not my ocular muscles, while it's still where the injection was made! The ophthalmologist
I explained that botulinum toxin blocks the transmission at the neuromuscular junction, it is likely that the spasms and nystagmus have a myogenic origin strictly , making them insensitive to the effect of the toxin . I would not have a disruption of the order, but a pure muscle spasticity associated with something a bit "chaotic" muscles, which gives the appearance of nystagmus. Nystagmus which incidentally is not synchronous on the 2 eyes (sometimes unilaterally, sometimes on a vertical and horizontal eye on the other ...). For now, we embark on an explanation of this type. The ophthalmologist will still apply their views to the 2 strabologues CHU Nantes.

Regarding the retina : I gave him the report of the ERG increased to Nantes and leaves evoke a problem on the cone of the left eye. He said that the protocol used was insufficient to conclude, therefore he speak to the clinic Sourdille Nantes to make a complete study: ERG with dark adaptation, EPI, EOG and visual field. Then it turns out there actually reaching the retina, we could possibly make connections, which might help in the diagnosis ...

Wearing Tights And A Leotard

bis

The adventure begins after the incomprehensible failure of the first injection, at it again. So here I am back on Toulouse, family, and then yesterday morning at 8am entrance to the clinic St Nicolas, where I began to be known
:-) Everything was programmed by mail with the optometrist, so I am Arrival hands in pockets, no paper. Never mind, I filled up on the authorization for anesthesia, this fact sheet on the botox, the designation of a trustworthy person ... etc. All that I begin to know by heart. Then I'm in my room, the same as last time :-)
After the nurse who came do his little routine questioning, my ophthalmologist happening to me and ask how are you since last week, closely followed by another nurse who brings the required circumstances. Once the blue blouse and matching slippers slipped, she puts a catheter in the forearm and gives me a taste anxiolytic particularly disgusting, but very effective ... So effective that I do not remember much after that.

I do not remember having gone to the block with porter, for cons I have some "flashes" on what happened there: drops Biting eyes, the anesthesiologist with his cap in green card, the device voltage, and finally produces milky-white which fall directly into the arms of Morpheus, and the surgeon's hands.

All this had to take place around 10am, and spent the rest of the day sleeping off the anesthetic into my room. The ophthalmologist came to see me at the beginning of the afternoon to tell me that everything went well , perfect, enough to sleep on my 2 ears, by the way I did all afternoon . That evening, I resumed a little energy with a light meal but more than adequate. My blood pressure peaked at 8 / 4 and during the night, it does not improve because frankly I hold 9 / 3.
This morning, however, everything is better, I'm "in shape", I left the clinic at 11am, after getting my order Tobradex, the letter for my orthoptist and reporting. I received 0.2 mL or 10 IU of botulinum toxin into the right medial left, which is more than last time. I returned to see the optometrist's office Monday morning, and meanwhile I'm waiting to see if an effect occurs ...

Fence To Go Around Christmas Tree

Food Poisoning

Well, I ninth day of "gastro" , I finally decided to go see, for there to force feed myself almost exclusively Smecta, bananas and chocolate, the shape is gently trunk ... Not need an hour to find what I, the beginning is sadly obvious: it is the sandwich I bought at Nantes on Monday, 19 which definitely an insider. The good tuna sandwich with mayonnaise that takes looooongtemps ... The diagnosis is found: food poisoning.

9 of tension, 3 pounds lighter, it's time to move up a gear, I'm leaving home with my little the general requirement of anitbiotiques intestinal , and how to renew my stoc Smecta. And then of course still rice-banana-carrot, another 10 days like that and I'll eventually get used to it ...

Good if not, I still managed the feat of going to downtown Toulouse do my pre-orthoptic botox, without falling into the apples! (No no fruit it will wait a bit :-)). The divergence has increased slightly (40 diopters close, 22 below), also vertical strabismus (14 diopters), and nystagmus was his original injury that Nathalie had forgotten his camera, he was in the right eye vertical and horizontal the left eye when I looked up and left.

Then if a secretary St Nicolas Clinic called me to put some stuff in (I did not know my starting time, or my day off, not my type of anesthesia), and I'm very unpleasant impression of that I would have got it again last ... That is not in itself that bothers me is the fact that in early March I typed NOTHING to 1200km with the explanation that the toxin did not stand the wait too long. It would be a shame to repeat the same thing, botox adulterated, it's not worth seeing ...

Constant White Discharge

2 syncope in 2 days ...

It is what we might call a week very hectic.
Monday morning as I begin provided by my new treatment Mexitil (mexiletine). For lunch I buy a sandwich Nantes and 2 hours after I began to be malaaaade ... This time I spent my Monday night to Tuesday, vomiting, great, then Tuesday I was standing so I'm on probation despite my gastro beginner. Lunch (as in the morning) can not eat, and the afternoon I left early because really too bad. And then pretty uncomfortable on the tram, I fall into the apples, we had more than one passenger forces me to drink, but he did not press him when it was the return to FIG. I find myself all night for emergencies Hotel-Dieu of , where they say it is a malaise induced Mexitil, which can cause arrhythmia or bradycardia.

Good Wednesday unremarkable, I remain at home with my gastro which reaches its climax.

Thursday morning, I thought when I woke up it was better, and as I was less dependent on the toilet I decided to go to class, especially since the sagit DU strabologie. The morning went well, and the afternoon rebelotte I faints, that's what is called being noticed. I spend an ECG in the ophthalmology department, then the anesthesiologist decides me Emergency again, again because of Mexitil. J'ensuis stood at 21h, otherwise it's not funny, and yet I was lucky because they wanted to keep me heart! Yet it was a lease that I was better then as I had the next morning appointment with my cardiologist in town is a strong argument to get out.

This morning, as scheduled by appointment. I tell what happened, ECG yesterday where I was bradycardia to 44, and where I'm going bcp better. She did another ECG is completely normal , and finally explain why and how: I had gastroenteritis, which I probably caused a slight hypokalemia, Mexitil gold, which is an anti-arrhythmic paradoxically becomes very arrhythmogenic when hypokalemia is ... Therefore me to interrupt temporarily the processing time for a suitable diet for up potassium. Here I am condemned to banana split for the week, I'm going as penance :-)

Well, tomorrow, returning to Toulouse in order to celebrate my 20 years as a family, and for injection of botulinum toxin on 29!

Pregnant Lindsey Dawn

ERG, EMG and EMG pupillometry New

The series continues with 2:30 hours spent in the service of functional exploration of the Hotel-Dieu. In the order I had a pupillometry, an electro-rétinogramme, another EMG, and finally the blood for new DNA testing.

Then: The
pupillometry shows a speed of pupil constriction of 5.5 mm / s in the right eye and 4.3 mm / s to the left eye, which speeds are a little too low for my age.

The ERG shows discrete anomalies with a certain asymmetry of responses in photopic condition, "in favor of the predominantly left central lesions. As I always photophobia unexplained, it is preferable to have the advice of a specialist ophthalmologist in the retina.

Then I got a short video of my oculomotor unusual, so comment "looks like an inter-nuclear ophthalmoplegia upside down" and then a close-up that evokes a lot of oculomotor myotonias.

the EMG : Prof. Pereon chose to remake an EMG, to find these famous as myotonic missing last week. This time he pitched at the level of the orbicularis of the lower eyelid, although according to him it is never where we search the myotonias, but in any case well because he took after forced closure of the eyelids and reopening, he received several rounds myotonic. Then he did the same thing at the lip after he'd put the ice, and like several myotonic discharges. This explains the transition that I can not speak properly when it's cold ...
I also have a very rapid depletion of muscle reflexes / tendon because after 2 stimulations nothing answered.
This new test allows the shot to make sorting: the myotonias not found in the mitochondrial cytopathies, or in myasthenia gravis, so we dropped these tracks to return to channelopathies.

- The blood finally Genetic analysis of ion channels . The sample will be sent to Paris at the Pitie-Salpetriere, and I results in a delay of 3 to ... 12 months ...


PLAN ON THERAPEUTIC :


For my muscle condition (fatigue, myalgia and myotonias rebels ...): I Quit dantrolene and the lyrics, instead I'm leaving with a Order Mexitil (mexiletine) . It is a drug that is no longer marketed in France but who has an import when it's for the treatment of myotonia, which is the only effective molecule. It is available at the central pharmacy of the hospital. By cons it is necessary to have the green light on the cardiologically before starting, so I called my cardiologist this morning who told me it was impossible to reconcile the beta-blockers (lopressor) I takes for migraine headaches, with Mexitil, both of which are cardiac humps with a bonus for the arrhythmogenic effect Mexitil. So I have to stop Lopressor, then start mexiletine after 5 days, and examine cardiac (ECG + Holter) 1 week after controlling for tolerance.

Suite program : I provide a written description to the neurologist my type of nystagmus, I am examining the retina Mexitil I start mid-April, I heart my record on April 23 (day of my 20 years), I returned to Toulouse for a new injection of botulinum toxin 29 April, I resumed appointment with the neurologist to find another DMARD cons migraine, Case lopressor forces, and ... I await the test results!

What Else Can Look Like Cold Sores

and it continues to advance

Yesterday afternoon, I had an appointment at reference center for rare neuromuscular diseases Nantes to retake an EMG on the request of my neurologist Nantes. Arriving in the torture room, the doctor wants me smile all a "Happy Birthday!" it's very nice, it touches me deeply, but it was not my birthday :-) Small error on the date of birth, 23.4 became 24.3.

Professor Pereon was accompanied by an internal, 3 external and especially thanks to whom I could benefit from detailed explanations provided to them :-)
So I'm here to suspected disease Brody, you do not know, this is normal, including rare diseases there are also very rare, in this case only 6 cases in France are described. After a quick examination that identifies the various symptoms (myalgia, muscle fatigue, muscle stiffness sometimes, spasms, paralysis oculomotor, photophobia, nystagmus), we begin the EMG. The acquisitions were made on the muscles of the arm, hand and face, and show: an increment action potentials after a brief effort , which I understand is compatible with the disease Brody, followed by a decrement which was obtained only once and then without much meaning, it is still worth being re-explore the track myasthenia gravis, and finally a myogenic syndrome (" Multiphase course spread over a very small contraction). By cons got no myotonia, which bothers him a bit because the presence whether myotonic discharges is an important element in the direction of research, and here we are left with an EMG done in Toulouse which showed myotonic discharges and EMG did not show any day ... Knowing in addition that the disease does not cause Brody ... Not easy!

Well, no straight answer can not be absolved of this review, but the doctor told me:
- Brody's disease is "possible" , I'll do a blood test Tuesday that will be sent to the Pity -Salpetriere to test this hypothesis,
- myogenic syndrome may also be compatible with a mitochondrial the ocular symptoms also, especially oculomotor paralysis, and since this type of pathology can cause retinal problems and I am very photophobia, I'm going to check an ERG retinal
- need to do more tests, I do not know the nature, except that I realized that I would pedal a bicycle,
- if I MSSA are myogenic, that is not excluded, this may explain the failure of Botulinum toxin as it works by blocking transmission at the neuromuscular junction, it is therefore normal that there are insensitive myogenic disorders.

So after the program is: I returned Tuesday morning to serve functional investigations, we will do the blood test to analyze ion channel, an ERG and pupillometry.

A Tuesday ...