THE NYSTAGMUS IN DOWN CHILDREN: PRESENCE,
IMPLICATIONS AND RESULTS AFTER
DRUG THERAPY.
Summary.
A
polydrug therapy always using l-glutamine, pyridoxine, biotin and
diazepam among other drugs led to
disappearance of the nystagmus in 10 subjects, after, average, one year
and half treatment. It led to its reduction
in other eight, at checkups after 18-42 months.
Key words: Down’s
Syndrome; nystagmus; sex prevalence;
risk factors; drug therapy.
Drug
modulation of stress reactions
World
congresses on stress and other congresses
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The nystagmus is a term that refers on rhythmical and unintentional movements
of the eyes [1]. To understand the nystagmus we need know that the eye follows
a mobile object, or examines with the
look an object (even a written line ) with a slow movement, said even pursuit
movement or, better, fixative movement
[2].
In other words,
the slow movement comes from the effort to maintain the fixation on the object
that moves. When reading, it follows the need to move the fixation point on
every word, or on every letter of the line. In the first case the fixation follows the object. In the second the
fixation moves on objects that are in spins long a line, as it happens for our
writing, which goes from left to right, in a horizontal sense.
The return to the
departure position, to follow an other object (or the next line) happens
instead with a rapid movement, said saccadic movement [2]. In the pathological
nystagmus this type of movement is independent from their normal purpose, but
on the contrary they work against the
pupil fixation on the object to explore.
There is instead a
jerk nystagmus when the deviation of the
slow movement alternates with the rapid movement. The pathological nystagmus
can be horizontal, vertical and rotatory [1].
Since the will
does not control them, the eyeballs' movements of any nystagmus hinder the
object fixation. We recalled reading and
writing because two basic activities in school learning, and we can
understand how a visual trouble of these two fields can drive to negative
effects on learning.
Two were the
investigated aspects. The first refers on the presence of the nystagmus and its
possible correlation with risk factors or symptoms that usually accompany it.
We
sorted all with the nystagmus symptom. From them we collected the
following data:
- presence of prematurity or postmaturity [5];
Results.
Table 1:
Epidemiological and clinical data.
|
Nystagmus presence |
26/432 Ss |
6.02% |
|
Nystagmus type: horizontal jerking |
26 Ss |
100.00% |
|
Sex distribution |
16 F |
61.54% |
|
|
10 M |
38.46% |
|
Chromosomal diagnosis |
|
|
|
Trisomy 21 frees |
25 Ss |
96.15% |
|
Mosaicisms |
1 S |
3.85% |
|
Age at the first examination (in months) |
16-199 |
average: 67 |
Table 2:
Risk factors and squint presence .
|
Prematurity |
7 Ss |
31.82% |
|
Postmaturity |
1 S |
3.85% |
|
Low birthweigh |
0 Ss |
0.00 |
|
Prematurity + low birthweigh |
2 Ss |
7.69% |
|
|
||
|
Other risk factors pre-, peri- and neonatal |
|
|
|
Presence |
22 Ss |
84.62% |
|
No. for any S. |
1-8 |
Average: 2.27% |
|
Squint presence |
16 Ss |
61.54% |
|
l-glutamine |
90-250 Mg/die |
|
Pyridoxine |
125-250 Mg/die |
|
Biotin |
5 Mg/die |
|
Diazepam |
1-2 Mg/die |
|
Clinical result |
Nr. of Ss and % |
Therapy duration |
Therapy average |
|
Disappeared |
10 Ss = 38.46% |
6-48 months |
18 months |
|
Clearly diminished |
8 Ss = 30.77% |
18-42 months |
|
|
Unchanged |
5 Ss = 19.23% |
3-46 months |
|
|
No checkup |
3 Ss = 11.54% |
|
|
Females seem
affected in a decidedly higher rate than males, even if in Downs representative
samples, as it happens in our 432 subjects, the males/females ratio is always
favourable in the males, which are,
average one third more [6-7].
The horizontal
nystagmus type, is that usual of the
syndrome of Down.
The squint, as the
more frequent symptom accompanying the nystagmus, was in 61.54%, twice of what we had found again in the first
424 subjects of this same series.
As for the common
drugs everyone took, three of them,
glutamine, pyridoxine and diazepam are respectively a precursor of the
glutamate and of the GABA the first;
The second is the
catalyst of the enzyme (GAD) that transforms the glutamate into GABA; The third
works as a sensitizer of the type A
post-synaptic GABA receptor.
Pyridoxine and
biotin are found again increased, in normal people, exactly in the midbrain and
in the pons [8], the brain structures that seem involved in this type of
nystagmus.
This datum is completely new, and of difficult
interpretation.
References.
[2] Cambier
J., Masson M., Dehen H.: Neurologia. 4’ edizione italiana. Masson, Milano
1984: 74-75.
Author’s address: dr Renato COCCHI, via Rabbeno,3
renatococchi@libero.it
Drug
modulation of stress reactions
World congresses on stress and other congresses
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