CHILDHOOD
DEPRESSIONS
By
Renato Cocchi, a neurologist and a medical psychologist
(Italian translation / traduzione italiana)
Printed in 1985, and now republished without any
bibliographical updating and with the only variations between brackets.
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This text [Cocchi,
1985], whose importance in child neuropsychiatry goes always to become
greater, will reflect in a particular way, the views and the
therapeutic experience of the author. So, it is going far, in part, from ideas
and classification commonly approved.
Years of practice
and a wider angle of therapeutic results
in not predictable fields, as for the
current opinions about, do think that
this is a practicable road. This is not
only from a clinical point of view, but perfectly in accord with the new
neurophysiological basic research. It can drive to a more suitable
comprehension and therapy.
The idea of
depression - in childhood, because what concerns our interests, but the same
would pertain even to the adults'
depression - does not will regarded, as usually happens, as the mood
fall symptom. This last instead it is
only one of its symptoms, and not always present among others, but in the
inhibition sense.
Such inhibition (
or reduced functioning) will be considered at the origin of peculiar
symptoms that I will point out as defective symptoms,
due to a deficit of functionality. We
will however find other symptoms, as happens frequently, close to defective
symptoms. These other symptoms reflect the compensation action following to a
hyper-function of other neurochemical mechanisms.
I shall term those
as symptoms of compensation.
Following these premises, the depressive
illness is always a neuropsychological disorder (and in the child this is much
more evident that in the adult ). So, because the neural level involved is
that, more fine, of the synapse, than
that, more coarse, of the neuron.
To that it has to
add that the depressive illness is always a morbid condition that implicates
the whole body, in its neurovegetative, motor and intellectual components, besides
the affective one. This last, is responsible, to a large extent, of the
consequent impairment of psychological and social relationships, if they were
not already the cause of the illness
itself.
Since over,
it is evident the reference that we need to do to the notion of homeostasis. We mean
it as a strong trend of the body to the
best balance, where all vital functions, and neuropsychological ones work the
better they can do. A such balance is
the fruit of the selective adaptations made during millions of years in living organisms from the more simple, as
first appeared, till the human species.
It has to add that
a refined, adaptable organism, as it is the human one and its more complex
organ, the brain, although having reached high specialization levels, does not be led to totally outfit so
easily. To face it, there are many
adjusting mechanisms of reserve (compensatory mechanisms ) that can minimize
the followings of partial bad functioning.
Of course, as many
as compensations may be put into action,
then there are a limited number of them. So, it can happen that they not
succeed to face a damage that goes beyond the limits of tolerance of a
certain brain area that presides to a
peculiar function. So the brain can abandon that area and that function, even
if not entirely, because in this last case it would come out atrophy.
We can now
understand how, when it is not precise brain damage, the first to be disarmed
those areas which control the lastly acquired abilities (in order: Logical-formal
thought, fine motility, language) which are typical of the adult human being. The more primitive,
presiding to the neuro-vegetative life, will be more defended.
According to the
extent of the damage, and to the moment where the brain suffered from the
injury, the child will get those neuropsychological abilities compatible with
the precarious balance that came out. Of
course he will not have instead the more specialised abilities (see what
happens in the mental deficiency).
That is probably
creditable to the fact that exists a differential vulnerability of the
different brain areas, for which what preside more primitive functions result
even more protected. See, to this intention, what happens in some deep forms of
a coma, where nearly noticeable cerebral electric activity misses (At EEG check
) but where neurovegetative functions as respiration, digestion, blood
circulation, urine issue, thermoregulation etc., can instead be preserved.
It exists finally
an other aspect that starts to be often appraised. The brain damage corresponds
to the destruction of the struck brain area ( for which the impairment of the
function has its correspondent in the anatomical lesion)? Or are there any
damages where, even without any destruction, a functional blockade came out,
where its operative level is only sufficient to prevent the atrophy ( ex non
uso), but not enough to allow the
function operates?
That means that
the injured part can be replaced from a close area that assumes its tasks and
functions. Or it may even be of
reactivation type (the injured part, not working, but not destroyed, may find reactivation if adequate
neurochemical conditions can be reformed )?
However, it will
be as more efficient as smaller is the age of the subject, and when first the
therapeutic treatments become set out.
I did not
absolutely say that it does never work a secondary depression, the result
of a loss of self-esteem creditable to
the awareness of own infirmity, and its consequent social disability, (that however may always
be there!). A primary depression would
also have its room, in the sense here described.
On the
contrary this is the more frequent case in the practice of the
child neuropsychiatry. In these
depressions where the root was damage, it kept as limited to a functionality fall. The symptomatic
expression of which shows defective symptoms. When instead the entry in
operation of compensation mechanisms appears, we can then understand the effort
that the body does to maintain homeostasis, which has threatened to be, to
certain levels, upset.
Summary
As
childhood depression it is intending the inhibition to certain neurochemical
mechanisms, which cause defective symptoms, almost accompanied by the
compensating hyperfunction of other neurochemical mechanisms, from which
symptoms of compensation come out.
It appears more
evident that all the pathogenic agents that can act on the central nervous
system, - and I am speaking of physical, chemical, infectious mainly viral, and
psychological agents -, elicit mainly a
unique brain defensive answer.
This runs through
GABAergic mechanisms [in the range of reactions to stress].
The causes of the
childhood depression will be then mostly referred to physical, chemical,
infectious or psychological agents that
acted in this critical period. This type of formulation modifies entirely the
causality relationship, first because largely privileges, for a morbid
condition that would seem only psychic, factors that are mostly not psychological ones.
If in fact, for
any of the not psychological causes that I shall list, the child's emotional
threshold kept, and keeps altered and/or biological basic rhythms as the sleep
and the feeding keep modified, it is not difficult that happens, as we found,
that even better feelings of a mother
can drive to less emotional involvement.
The result of
it is that even the better mother, when
not vocated for the holiness, will counter-react, in the better case with the
affective indifference but, in the worse case -
luckily it happens rarely - with the murder of her son.
If, as roughly it has been done for many
years, and as often it keeps done, one just looks at the maternal feeling of hostility, and judges it
as the primary cause, not appraising its counter-reacting function. So one
risks of not only misunderstand the exact dynamics of the actual trouble, but
of applying therapeutic methods that, by force of it, will not
give the hoped results.
Moreover that
these methods on the one hand implicate a mother's responsibility, and so they
feed inadequacy and guilt feelings in her. On the other hand it is on this
supposed guilty mother that therapeutic treatment should find its ground.
It is possible
they are even in smaller number, since some injurious agents did not get their
best light.
When instead the depression is an accompanying
symptom of lesional illnesses of the central nervous system, the psychological
causes cannot be primary agents. The
psychological factors are the cause of that share of secondary depression that
may always add to a primary depression of any origin.
- prenatal causes:
Everything that reduces the supply of oxygen to the brain of the embryo and of
the fetus; Intrauterine infections; endogenous and exogenous intoxications,
among the last ones I have to remember the following of the psychostimulant
drugs abuse, from smoking to hard drugs;
burden anxiety states of the mother;
- perinatal
causes, the more frequent: Accelerated delivery, prolonged delivery, prematurity,
postmaturity, twin birth, complicated
delivery, neonatal respiratory distress,
not high hyperbilirubinemia, low birthweight, umbilical cord wound around to
the neck, or short, a caesarian section, even when previously decided, and not
after a suffering and prolonging delivery, blood change for RH incompatibility;
- postnatal
causes: Not heavy skull traumas, viral illnesses that produce light
encephalitis (flu, measles, but mainly the whooping cough), not burden
metabolic toxicoses, cardiac illnesses reducing brain oxygenation, followings
of viral hepatitis, results of kidney illnesses, long-lasting physical
illnesses prolong, psychic traumas (disturbed mother-child relationship, loss
of one or of both parents, entry in a foundling hospital, family atmosphere
seriously troubled).
The above
mentioned causes to different levels of the development of the child can
naturally add, as usually happens: One somatic cause + one psychological cause,
but even various somatic causes among them; Or still a hereditary
predisposition + a somatic cause + a psychological cause, and so on.
Summary.
The
causes of the childhood depression, beyond a possibly hereditary predisposition,
frequently, are the same that, when heavier, give the rise to the mental deficiency.
They can be listed as prenatal, perinatal and postnatal causes. To these
last we have to add psychological ones that, as primitive, are found only in
childhood depression, when this represents the only morbid picture.
Childhood depressions' frames of reference.
In the
intrauterine period the typical symptom of response to the stress is the
hypermotility (perhaps due to hyperfunction of exciting dopaminergic pathways
not more adequately controlled because
the fall of the inhibiting [A] GABAergic powers).
Further
confirmation of a fetal depression comes from the meconium tainted amnyotic
fluid, as seen when the amnyotic sack breaks up, at the delivery starting, and
considered the equivalent of the post-natal diarrhea.
- sleeping
reduction or loss, or alteration of rhythm sleeping-awakening (the baby has the
day for his night);
- continuous
crying;
- constipation;
- easiness to
upper respiratory tract infections;
- pallor.
Compensation
symptoms are:
- a sleeping time
increase (it drives to an increase availability of GABA neoproduction);
- increase of the
feeding or frank overeating (it to a larger introduction of some precursors
among which glucose and tryptophan);
- sucking the
thumb (it drives to an activation of large brain areas);
- increase of the
need of thermal-tactile contact with his mother, who becomes obliged to a
closer relationship, erroneously judged as an overprotection (while it has a
calming action);
- temper tantrums ( the make a suprarenal
incretion with a positive action on the low blood tension, and on the serotonin
neoproduction);
- rocking or
rocked (a calming action, for probable vestibular-limbic pathways);
- hypermotility
(an aggravation symptom of the
depression).
Other symptoms of
not easy classification:
- not infectious
gastroenterites, with diarrhea;
- persistence of
the milk crust;
- easiness to the
vomit;
- acetonemia, when
the child is feverish;
- febrile
convulsions;
- simple motor
delay, or simple delay of the language.
From the second
year to the entry in the primary school
defective symptoms of the childhood depression are:
- sleep disorders,
even only early-morning awakenings;
- poor appetite,
or reduced foods' choice [ie. Hyponeophagia];
- easy crying;
- constipation;
- easiness to
upper respiratory tract infections;
- pallor;
- asthenia;
- be sensitive to
cool;
- sadness;
- isolation;
- solitary game,
or with very few companions;
- behaviour difference
between morning and afternoon ( some are more serene in the morning,
others in the afternoon ).
Compensation symptoms, in this time, are:
- greediness for sweets
(it drives to increase the GABA neoproduction [throughout the Krebs' cycle];
- the active
search of coffee or wine (euphoriant drinks);
- diet preference
for the meat broth ( it contains glutamine and glutamate, precursors of the
GABA);
- accentuated
dependence from his mother;
- temper tantrums;
- need to put
himself to the centre of the attention (It increases the self-esteem?);
- the choice less
aged companions for games (with less-aged children the level of his own abilities
becomes suitable, and often, being then the more physically strong, he becomes
the bossy person);
- rocking;
-
"neurotic" masturbation (an adrenergic compensation the orgasm);
- hypermotility.
- stuttering;
- tics;
- sudden
diarrheas, for no known reason;
- bruxism during
the sleep;
- to talks in
one's sleep;
- pavor nocturnus;
- mood variations,
linked to weather changes;
- doing better
during the summer;
- brotherly
jealousy;
- bedwetting;
- loss of faeces;
- rituals before
eating, or when going to bed;
- panic refusal to
attend the nursery school (Is it similar to the school phobia?);
- simple delay of
the language and modest motor delay.
The entry in the
primary school, by itself, may reveal a
masked depression in children that did not make any evident discomfort till
that moment, or at least it seemed so.
- sleep disorders
(difficulty in falling asleep, or frequent awakenings during the night, or
early-morning waking up);
- poor appetite, or reduced foods' choice [ie.
hyponeophagia];
- easy crying;
- constipation;
- easiness to upper
respiratory tract infections;
- pallor;
- asthenia;
- be sensitive to
cool;
- frontal or
nape of the neck headache;
- sadness;
- emotional
inhibition;
- touchiness;
- solitary game,
or with less-aged friends;
- childish
language; motor awkwardness;
- learning
troubles, following attention, concentration, memory, ideation difficulties.
I noted those
compensation symptoms, in this period:
- overeating;
- greediness for
sweets (it drives to increase the GABA neoproduction [throughout the Krebs'
cycle];
- the active
search of coffee or wine or alcoholic drinks (euphoriant drinks);
- diet preference
for the meat broth ( it contains glutamine and glutamate, precursors of the
GABA);
- tendency to the order
and to the meticulousness (does have it anxiolytic action because it allows a
control on the surrounding reality?);
-
"neurotic" masturbation;
- need to put himself to the centre of the
attention ( a form of turned to impose dependence?);
- he does the
buffoon, mainly in the classroom ( it increases the self-esteem, by the growing
of the consideration of the peers' group);
- tendency to say lies or to the mythomany ( Another way
for being in the centre of the attention?);
- prevailing
choice of less-aged children for the game;
- hypermotility.
Other symptoms
often found, but of difficulty frames of reference:
- stuttering;
- tics;
- bedwetting;
- loss of faeces;
- sudden
diarrheas, without any evident cause;
- night bruxism;
- to talks in
one's sleep;
- pavor nocturnus;
- rituals, even
off before eating, or when going to bed;
- doing better during
the summer;
- mood variations,
related to weather changes;
- excess sweating;
- touchiness;
- self-pity;
- self-devaluation;
- avoiding of the
obstacle;
-
quarrelsomeness and/or brotherly
jealousy;
- certain forms of
the school phobia.
From the pubertal
period and in the adolescence the childhood depression, as for its symptoms,
get nearly all the features of the
adults' depression, inclusive the hope losing that can bring to the
attempted suicide or to the suicide.
It will miss however
a symptom not infrequent in the adult age, from the fourth life decade.
That is the idea (to half between the
depressive and the delusional one) of ruin.
The symptoms of the childhood depression are
inclined to dissociate from those of the
adult's depression, and so much more when the child has fewer years. Primarily, the childhood
depression has somatic symptoms of impaired basic biological rhythms (sleeping,
feeding, evacuation), symptoms of delay in the development of certain acquisitions
(language, motility and scholastic learning ) and psychic symptoms (from the
crying to the mood depression).
The
psychic symptoms become more frequent when the subject approaches to the adolescence,
an age in which doesn't exist many differences with the adult's depression of
the adult. Compensation symptoms, or by somatic pathways, are increasing the
functionality of GABAergic circuits, or are opposing the hypotension, or they
act through psychic pathways, by reducing the anxiety or increasing the
self-esteem.
Of course the
prognosis will be much worse as more serious is the depression, as less the
body could put into action compensation mechanisms, when larger is the involved
biological component, when first the depression came out and as more it lasted.
The fact that the
childhood depression was unknown for many years, and even today, in most cases,
does not have its diagnosis, does not
have still brought a sufficient amount of research on this topic, either the
depression was treated or not.
If it not was not
treated of, these are the clinical I think to should point up:
Some of them (I am referring to which acting on the
adrenaline and noradrenaline as aggressiveness, neurotic masturbation, a risk
situation's active search, etc.) can become an important component for the building of the adult personality;
- in other cases
however the body cannot overcome them by himself, neither can find an
acceptable compensation form, and in these cases case the defective symptoms
will be what build the subjects' personalities
( I am referring now, for example, the so-called introvert character);
- the fall of scholastic learning based on the depression
can heavily affect on all the academic
careers;
- forms of false
mental retardation on a depression base can settle in adult age in true mental
retardation, even if, usually, of a modest degree;
- always more
studies start to go out from which it results that psychiatric illnesses of the
adult age (depression, schizophrenia, drug addiction) have had psychopathological antecedent of an ignored childhood depression. That
happens with a greater rate than what would result from a random probability,
(till over 80% of the patients).
We do not know
however which rate of formerly depressed children has developed a psychiatric
illness in the adult age;
- we started to
suspect that in the preantibiotic era all a series of depressed children, with
the symptom "easiness to upper respiratory tract infections", died by
bronchopneumonia in their developmental age. With the current antibiotic
therapies this prognosis has practically disappeared, but this may have modified a "natural" selection for the
psychiatric illnesses. We observe that now we can to see Down's syndrome
persons aged 40 years, while 40 years ago a Down child of 10 years was a very
rare event.
The therapeutic
treatment, if well applied, can entirely modify the frame of the childhood
depression, and if early started and for
a suitable period, to overcome the possible accumulated delays. It is possible,
and there are the elements to think so, that a good antidepressant
treatment in childhood, can even prevent
a possible increasing of psychiatric troubles of the adult age, but there are
no studies on this topic.
Summary.
Therapeutic treatments.
When instead its
origin is indubitably a psychological or relational one, an individual
psychotherapy, or of the family, can be decisive by themselves, even if times
and costs are well heavy.
The same we can
say for an occupational therapy, or even for a psychomotor therapy, since the
effects of lowering of the so-called temper tantrums that this last
therapy has shown to possess.
Summary.
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