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Efectividad de Terapia Neural en pacientes con parálisis de Bell

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CASE STUDY
The Effectiveness of Neural Therapy in Patients With
Bell’s Palsy
Ferdi Yavuz, MD; Bayram Kelle, MD; Birol Balaban, MD
Abstract
This report describes the case of a 42-y-old man with a
type of facial nerve palsy of the lower motor neurons
(LMNs) on the right side, who was treated with neural
therapy. After exposure to cold weather, the patient had
Ferdi Yavuz, MD, is specialist of physical medicine and
rehabilitation at the Clinic of Physical Therapy and
Rehabilitation, Fizyocare Medical Center, in Ankara,
Turkey. Bayram Kelle, MD, is an assistant professor in
the Department of Physical Therapy and Rehabilitation,
Faculty of Medicine, Cukurova University, in Adana,
Turkey. Birol Balaban, MD, is a professor in the Clinic of
Physical Therapy and Rehabilitation, Fizyocare Medical
Center, and in the Department of Physical Therapy and
Rehabilitation, Faculty of Health Sciences, European
University of Lefke, in Lefke-Mersin, Turkey.
Corresponding author: Ferdi Yavuz, MD
E-mail address: [email protected]
T
his report describes the case of a 42-year-old man
with a type of facial nerve palsy of the lower motor
neurons (LMNs) on the right side, who was treated
with neural therapy. After exposure to cold weather, the
patient had suddenly developed difficulty in closing his
right eye and a deviation to the left in the angle of his
mouth. He had no previous medical illness and had no
history of trauma, smoking, alcohol intake, or blood
transfusion.
Examination of his other cranial nerves showed that
they were normal, and he had no cerebellar signs.
Magnetic resonance imaging (MRI) of the brain was
completed and did not reveal any obvious abnormality.
Serological tests for various infectious agents, including
40
Integrative Medicine • Vol. 15, No. 3 • June 2016
suddenly developed difficulty in closing his right eye
and a deviation to the left in the angle of his mouth. He
had no previous medical illness and had no history of
trauma, smoking, alcohol intake, or blood transfusion.
antibody tests for the syphilis antibody, Lyme (borreliosis)
immunoglobulin M (IgM), and Epstein-Barr virus capsid
antigen IgM, were all negative. After a differential diagnosis
had ruled out any secondary causes of facial nerve palsy
(Table 1),1 the patient was diagnosed with Bell’s palsy by a
neurologist.
Treatment with steroids and antiviral drugs had been
prescribed within 72 hours of the onset of the patient’s
Bell’s palsy. He had taken the drugs for 21 days without any
improvement. After the medical treatment, he was referred
to physiotherapy. Physiotherapy with exercise and
electrostimulation for a total of 21 sessions for a period of
4 consecutive weeks provided no clinical improvement.
Six weeks after the onset of the Bell’s palsy, the patient
was diagnosed with the LMN type of facial nerve palsy on
the right side (Figure 1). His facial nerve function was
measured as a having a House-Brackmann score of grade 4,
which reflects a moderate-to-severe dysfunction (Table 2).2
Six sessions with neural therapy were performed at
the authors’ outpatient clinic, with sessions 3 times per
week for 1 week and then 1 time per week for 3 weeks. All
of the 6 sessions took place, therefore, within a period of
4 weeks. No adverse events or side effects occurred.
During each neural-therapy session, subcutaneous
injections were performed using a 5-mL syringe with a
25-gauge, 1-inch (2.5-cm) needle. The deep autonomic
ganglia injection in each session used a 5-mL syringe
with a 27-gauge, 2-inch (5-cm) needle. The injections
were performed on the affected hemi face.
The subcutaneous injections were carried out along
the 5 branches of the facial nerve. The deep ganglia
injections were carried out for the autonomic ganglia of
Yavuz—Neural Therapy in Bell’s Palsy
Table 1. Causes of Secondary, Unilateral Facial Nerve
Palsy
Types of Causes Examples
Metabolic
Disease
• Diabetes
• Preeclampsia
Stroke
• Ipsilateral pontine infarction
• Pontine tegmental hemorrhage
Infection
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
Hansen’s disease (leprosy)
Otitis media
Mastoiditis
Herpes simplex infection
Varicella zoster infection
Ramsey–Hunt syndrome
Influenza viruses
Borreliosis
Cryptococcosis
Neurocysticercosis
Toxocariasis
Tuberculous meningitis
Parotitis and parotid abscess
Malignant external otitis
Syphilis
Surgery
• Removal of cerebellopontine
angle tumors
Trauma
• Head trauma (crush injury)
• Birth injury
Tumor
• Facial nerve neurinoma
• Cerebellopontine angle tumors
(neurinoma)
• Pons tumor
• Tumors of the petrosal bone
• Tumors of the middle ear
• Leucemia
• Tumors of the parotid gland
• Lymphoma
Immune System
Disorder
•
•
•
•
Drugs
• Interferon
• Linezolid
Other Causes
• Moebius syndrome
• Melkersson–Rosenthal
syndrome
• Sarcoidosis
• Histiocytosis X
• Autism
• Asperger’s syndrome
• Parkinson syndrome
Guillain–Barré syndrome
Miller–Fisher syndrome
Systemic lupus erythematodes
Myasthenia gravis
Yavuz—Neural Therapy in Bell’s Palsy
Figure 1. Examination of Facial Nerve Function Before
Neural Therapy
A
B
Note: Figure 1A shows inability to lift his right eyelid and
Figure 1B shows drooping corner of mouth and loss of
nasolabial fold on his right side.
Integrative Medicine • Vol. 15, No. 3 • June 2016
41
Table 2. House-Brackmann Scores
HBS Grade
1
• Normal, symmetrical function in all
areas
2
• Slight weakness on close inspection
• Complete eye closure with minimal effort
• Slight asymmetry of smile with maximal
effort
• Slight synkinesis, absent contracture or
spasm
3
•
•
•
•
4
•
•
•
•
•
•
Obvious disfiguring weakness
Inability to lift brow
Incomplete eye closure
Asymmetry of mouth with maximal effort
Severe synkinesis
Mass movement, spasms
5
•
•
•
•
•
•
Motion barely perceptible
Incomplete eye closure
Slight movement at corner of mouth
Synkinesis
Contracture
Usually absence of spasm
6
•
•
•
•
•
No movement
Loss of tone
No synkinesis
Contracture
Spasm
A
Obvious weakness but not disfigurement
Inability to lift eyebrow
Complete and strong eye closure
Asymmetrical mouth movement with
maximal effort
• Obvious but not disfiguring synkinesis
• Mass movement, spasms
Abbreviation: HBS, House-Brackmann score.
oticum and pterygopalatinum. A total of 10 mL of a
solution consisting of 0.4% lidocaine was used for each
subcutaneous injection, and 2 to 3 mL of a solution
consisting of 1% procaine was used for the infiltration of
the autonomic ganglia. After the 6 neural therapy sessions,
the patient’s House-Brackmann score was grade 1, which
describes a normal, symmetrical function in all areas
(Figure 2). Since the treatments occurred, the patient has
been asymptomatic, and no recurrence has been noted
during his follow-up visits.
A unilateral, peripheral, facial nerve palsy may have a
detectable cause (ie, may be a secondary facial nerve
palsy) or may be idiopathic (ie, primary, without an
42
Figure 2. Examination of Facial Nerve Function After
Neural Therapy
Integrative Medicine • Vol. 15, No. 3 • June 2016
B
Note: Figure 2A shows the patient can lift his right eyelid
and Figure 2B shows the patient can move his mouth
symmetrically. There is no sign with drooping corner of
mouth and loss of nasolabial fold.
obvious cause, such as Bell’s palsy).3-5 Secondary facial
nerve palsy can be due to various causes (Table 1) and is
generally less prevalent than Bell’s palsy at 25% versus
75%,6 respectively. Bell’s palsy was first described by
Friedreich7 in 1974 and is a diagnosis of exclusion.8
In the treatment of Bell’s palsy, many therapies consist
of corticosteroids, antiviral agents, exercise physiotherapy,
electrostimulation, and surgical decompression.
Corticosteroids and antivirals are strongly recommended
in the guideline for patients with Bell’s palsy. No
recommendations have been made regarding offering
exercise physiotherapy for acute facial nerve palsy of any
severity. However, exercise physiotherapy is weakly
Yavuz—Neural Therapy in Bell’s Palsy
recommended for patients with persistent facial muscle
weakness.9 The use of electrostimulation is also weakly
recommended for patients with Bell’s palsy of any severity.9
Facial nerve palsy can take up to 1 year to improve.10
Patients with incomplete palsy have a better prognosis
than patients with complete palsy.11 Without treatment,
the prognosis for complete Bell’s palsy is generally fair, but
approximately 20% to 30% of the patients are left with
varying degrees of permanent disability.5,8,12 Approximately
80% to 85% of patients recover spontaneously and
completely within 3 months, whereas 15% to 20%
experience some kind of permanent nerve damage.12
Neural therapy is an injection treatment that is
designed to repair the dysfunction of the autonomic
nervous system and shows its effects by correcting the
electrical condition of cells and nerves. Thus, the
bioelectric disturbance at a specific site or nerve ganglion
can be restored to normality. In neural therapy, local
anesthetics, usually procaine or lidocaine, are used. Neural
therapy involves the injection of local anesthetics into
peripheral nerves, autonomic ganglia, scar tissues,
endocrine glands, acupuncture points, trigger points, and
other tissues.13 Some clinical trials and case reports have
shown that neural therapy could be an effective treatment
for relieving pain and improving functional loss or
disability for patients with various disorders.14-16 However,
the effectiveness of neural therapy is still in question.17,18
Conclusion
The authors believe that this case review is the first
description of the effectiveness of neural therapy for patients
with Bell’s palsy. In the current case, the neural therapy was
used as an alternative treatment, which worked very well for
the patient’s recovery from Bell’s palsy.
Yavuz—Neural Therapy in Bell’s Palsy
Author Disclosure Statement
The authors declare that they have no conflicts of interest.
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