A NEW CASE OF PARESIS OF
THE FACIAL NERVE FOLLOWING A PROBABLY POST-FLU BELL'S PARALYSIS: RESULTS OF THE
ANTIDEPRESSANT AND ANTISTRESS DRUG THERAPY.
Renato Cocchi, a neurologist and a medical
psychologist.
(Three other texts on this topic)
Summary.
In a man of 33 years, after 98 days, an
antistress and antidepressant drug therapy are giving positive results on the
outcomes of the paresis of the left facial nerve of probable postflu origin.
The paresis of the facial nerve did not answer to the preceding therapies and
doesn't give signs of spontaneous improvement. The quick response to the
therapy has been perhaps favoured by the short lasting of the passed time,
(about three months) since the onset of the neuropathy.
Key words: Paralysis of Bell, facial
nerve, man, outcomes, stress, antistress therapy, antidepressant therapy,
results.
Drug modulation of stress reactions
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The paralysis of the facial nerve (or Bell's
paralysis) begins suddenly or within fewer hours, without any apparent cause.
As idiopathic paralysis, it rates about 75% of all the peripheral paralysis of
the facial nerve. As for predominant cases in winter (31.38%) and in autumn
(30.13%), which are statistically meaningful (Gonçalvel-Cohelo and coll.,
1997), there is someone debating such data.
In fact, for Danielides et al., 2001, there
is not instead any meaningful difference for the cool or half-cool periods of
the year, for the seasonal nature and for the monthly distribution.
Yet, Campbell and Brundage, 2002 affirmed
again that both the climate and the season are independent and predictive
factors of risk of the Bell's paralysis.
The natural evolution of the Bell's
paralysis is favourable, and 84% of the patients show a satisfactory recovery
without any treatment, but 16% suffer from outcomes that go from moderate to
serious degrees.
The prognosis of the Bell's paralysis is
generally much good. With or without any therapy mostly patients start to be
meaningfully better within two weeks, and about 80% recovers entirely within
three months.
In several ones, however, the symptoms can
last longer. In fewer cases, the symptoms may settle in stable way.
The prognosis is the function of the paresis
degree, the age of the patient, and the period where appeared the first signs
of recovery ( Jabor & Gianoli, 1996).
The state of the paralysis of the facial
nerve should be monitored through repeated electric examinations, preferably
with the EnoG (Moore, 1990).
I did not find exact information on what
happens to anyone who had an unfavourable outcome, and the conclusion that some
symptoms do not disappear anymore, seems, by now, the only one accepted.
Some elements, however (an idiopathic form,
age of the patient (Jabor & Gianoli, 1996), female prevalence
(Gon‡alvel-Cohelo and coll., 1997), possible action of the cool
(Gon‡alvel-Cohelo and coll., 1997; Campbell & Brundage, 2002), a link with
viral illnesses of the upper respiratory tract (Gon‡alvel-Cohelo and coll.,
1997; Campbell & Brundage, 2002), even mostly recoveries without any
treatment, but not totality of complete recoveries) induced me to think that
about some relationship with individual fragility, and then with possible
reactions of stress located to the facial nerve (Cocchi, 2003 ).
Here following I shall report an other case
in a subject with paretic outcomes after about three months of a facial nerve
paralysis, probably by cool, which I treated with antistress and antidepressant
drug therapy.
The case history.
A male person of 33 years at the first
consultation, for paresis of the left half-face for outcomes of the VII cranial
nerve paralysis (the facial nerve), which came out at the beginning of last
February. From the preceding Christmas he had a flu without fever. Two weeks
before, his brother had the same paralysis of the facial nerve, which recovered
after cortisone-based therapy.
A married man, he works as a clerk.
Following the prescription of a first consulted neurologist, who excluded a
paralysis from cool, he did an initial therapy of prednisone 50mg/die for five
days, then 25mg/die for other five days. He took even a B polyvitaminic
compound for one month, all without any result.
Fourteen days after the beginning of the
illness he consulted another neurologist, who required NMR without and with a
contrast medium. Following such an examination, made 50 days after the onset of
the illness, it permitted exclusively to see a greater impregnation of
gadolinium in the second tract of the left facial nerve "compatible with
inflammatory alteration still working." A third neurologist, who examined
him 57 days after the beginning of the paralysis, prescribed gabapentin
300-600mg/die + nimesulide 200mg/die for 10 days.
End April 2004, the first consultation.
There are evident paretic outcomes of the left facial nerve paralysis.
Paresis symptoms of the left half-face: He doesn't wrinkle his forehead; He denies any pain
to the exit hole of the ophthalmic branch of the facial nerve; His left eye is
more opened and cannot succeed to close well; The left nose-genal line is
missing; No pain occurs to the exit hole of the intermediary branch of the
facial nerve;
The lips are less moving; The right nostril
is more ample; The nos-labial fissure slightly moved to right; He doesn't
succeed to discover his teeth; No pain to the emergency hole of the mandibular
branch of the facial nerve. If he blows up the cheeks to blow, the swelling of
the cheek is more evident in the left side. He whistles badly, with an
indication of the whistle. The protruded tongue has normal direction. Now he
has light lingual paresthesias to the left. Now, he chews more to right side.
If tired, he has spasms of the orbicular muscle of the mouth, to the left side.
He has had feelings of cool, full unusual for him, but not before the evidence
of the paralysis.
Depression: He sleeps badly, with frequent awakenings. Often he
wakes up and goes to eat milk and sweet things. He doesn't use the intercourse
to ease his falling asleep.
Troubles of the half-brain dominance: He is not a "contrary Mary," and he does
not have inexplicable bad feelings. Currently he has intrusive thinking, with
focused thought on his illness. There is no need of counting for no reason.
Concentration difficulties occur.
Symptoms of stress: He does not wake up tired, suffers from the heat,
has normal greediness for sweet things [???] and for meat broth, but he has an
increased milk intake, mainly in the evening.
Since 7-8 months he suffers from headache, a
left migraine type, where he does labour to focus. In the evening he does not
bear the lights of the car that are coming from the opposite direction. After
the Bell's paralysis, he bears the confusion and the noise a few. There is no
drooling when he sleeps, nor buxism or muscular cramps. He doesn't have
breakfast at once. Not disbandment feelings, and rare faint feelings occur.
Rare colic and diarrhea happen. Usually he is an overactive man, and he doesn't
succeed to be without doing something.
The remote case history: It is unknown if he had born problems. In the first
year of life he ate a few, and had easiness to the upper respiratory tract
infections, but no paleness. There is information about his bowel function. He
did not have ADHD. At school he did not show any preference for Italian or
mathematics, but he was easy for the practical matters.
Test therapy (daily doses, by the oral via):
Glutamine 125mg; Pyridoxine 75mg; Carbamazepine 200mg; Amitriptyline 6-10mg;
Oxazepam 15mg.
Beginning June 2005, the first checkup after
35 drug therapy days. He is doing better. At night, he sleeps well. The left
half-face has become mobile. The ageusia of the left side of the tongue
diminished. Now, the inter-lips line is less falling to the left. He blows up
badly the left cheek. He doesn't wrinkle his forehead to the left side and
doesn't succeed to lift the lift eyebrow. As in past, he cannot wink with the
superior left eyelid. The left nose-genal plica is now more visible. He cannot
show the teeth to the left. Sometimes he chews even to the left. Spasms of the
orbicularis of the mouth to the left are missing.
Now, he is more vivacious, more clear on
improving his trouble, more serene. He says that he thinks always too much, but
not always to the illness. The need of drinking milk decreased. At the morning
he has breakfast. No more fainting feelings occurred, and so no more colic and
diarrhea. Lately he has a better concentration.
Therapeutic variation (daily doses, by the
oral via): Carbamazepine 300mg; Glutamine 250mg.
Beginning August 2005, the second checkup.
He improved either altogether either for the paretic outcomes of the Bell's
paralysis.
Now he is less tired and less anxious, too
because he spent 15 days of holiday by the sea. Whe awakening, he had anxiety
fits, but less than previously. The headache missed. His concentration improved
of more. He lost 9kg, without having done any diet, probably because he did not
wake up again during the night with attack of bulimia.
The facial paresis: The wrinkling of his
forehead too improved, it is still inadequate. Now he can close the sole left
eye, without any synkinesises with the right eye. She succeeds better in
lifting the left eyebrow. He does a little labour to lower the superior eyelid
and to lift the left inferior eyelid. In sunny days, the left eye has to be
protect with eye darkens. Not pain occurs to the emergency holes of the
branches of the facial nerve.
The left nose-genal plica is clearly
visible, even if a little less sunken than its right homologous. He moves well
the left wing of the nose. Now he blows well. His face asymmetry reduced and
the left mouth line nearly parallels that of the other side. Now he can show
the teeth nearly the same in both sides.
Usually, he chews even to the left. The
ageusia is not more improved, and the flavours are still attenuated. The words'
articulation runs better. He can spend the tongue on the teeth of the left
dental arches. There is, as new symptom, a feeling of the tremor in the
internal part of the left cheek.
Discussion.
The first checkup, planned for a possible
adjustment of the therapy, let see that several symptoms of the facial nerve
paresis were improving. A so quickly response could be creditable to individual
features of resistance, but more probably to the short time passed from the
onset of the Bell's paralysis.
Also the mood improved, previously of
depressive-reactive type, and other current symptoms of stress, but they were
probably preceding the facial nerve paralysis.
A strange datum with difficult
interpretation is that of the onset of the same morbid form in his brother 15
days before, which recovered following cortisone-based therapy. We may not
think to an infectious phenomenon, normally generally excluded as a direct
causal event. Even the different response to the cortisone-based therapy
suggests that we are dealing, somehow, with an independent event.
As compared to the other two cases I
described (Cocchi 2003; Cocchi 2004), this one differentiates for the
presumable origin, which is a post-flu one versus an idiopathic form (Cocchi,
2003) or a post-herpetic one (Cocchi, 2004). Even it, for the short time passed
since the onset to the beginning of the drug therapy I set up, being some
months versus one year in the first case (Cocchi, 2003), and two years and half
in the second case (Cocchi, 2004).
Much interesting it is the relationship between
body weight and the nighttime bulimic episodes. Missing the nighttime
awakenings and the bulimic impulses, in a few more than three months the
patient lowered nine kilograms, without having done any particular diet.
The increased milk and sweet things' intakes
probably were two compensation symptoms. They are producing a greater
introduction of precursors of brain neurotransmitters, the glucose for the
Krebs' cycle, for glutamate and GABA, and the tryptophan, of which the milk is
rich, for the synthesis of the serotonin. The glutamine prescription, another
precursor of the glutamate and of the GABA and that of the amitriptyline, a
serotonin uptake inhibitor, nearly surely regulated by other pathways the
deficient neurotransmitters, without more need of intake of foods as rich of
the respective precursors.
Conclusion.
After 98 days of an antistress and
antidepressant drug therapy positive results occurred on the outcomes a left
facial nerve paralysis of probable post-flu origin. The quick response to the
therapy suggests that it be elicited by the short time passed since the onset
of this neuropathy.
References
Campbell KE; Brundage JF. Effects of
climate, latitude, and season on the incidence of Bell's palsy in the US Armed
Forces, October 1997 to September 1999. Am J Epidemiol 2002 Jul 1;156(1):32-39.
Cocchi R. Need we recover the clinical idea
of an individual resistance to illnesses? August 2003
<www.stress-cocchi.net/index-it.htm/Speculation4.htm>.
Cocchi R. Stabilized outcomes of idiopathic
paralysis of the facial nerve (Bell's paralysis) and stress: An attempt of an
antistress drug therapy lasting 10 months. March 2003
<www.stress-cocchi.net/Other4.htm>.
Cocchi R. A woman with peripheral bilateral
paresis's followings of the facial nerve from herpetic neuritis, treated by
antistress therapy, June 2004 <www.stress-cocchi.net/Other12.htm>.
Danielides V; Nousia C-S; Patrikakos G;
Katsaraki A; Skevas A. Seasonal Distribution and Epidemiology of Bell's Palsy.
Oto-Rhino-Laryngologia-Nova 2001;11(3-4):151-156
Goncalves-Coelho TD; Pinheiro CN; Ferraz EV;
Alonso-Nieto JL. Clusters of Bell's palsy. Arq Neuropsiquiatr 1997
Dec;55(4):722-727
Jabor MA; Gianoli G. Management of Bell's
palsy. J La State Med Soc 1996 Jul;148(7):279-283
Moore GF. Facial nerve paralysis. Prim Care
1990 Jun;17(2):437-460
Posted on internet on September 2005. Copyright by Renato Cocchi, 2005.
Author's address: dr Renato COCCHI, via Rabbeno, 3
42100 Reggio Emilia
renatococchi@libero.it
Drug modulation of stress reactions
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