Neural Therapy in Peripheral Facial Paralysis Peripheral facial paralysis, which develops as a…
Peripheral facial paralysis, which develops as a result of peripheral involvement of the facial nerve (cranial nerve VII), is mostly benign in course, but because it disrupts one's appearance, it is a dramatic presentation that sends patients rushing to the doctor in great distress. When residual effects remain, it can also lead to severe psychological distress, especially in young patients. This is why treatment is important.
Hüseyin NAZLIKUL
CLINICAL FINDINGS
When the facial nerve is affected peripherally, a one-sided facial paralysis results. Symptoms appear as paresis of the facial muscles, hyperacusis (excessive sensitivity to sound), reduced tear and saliva secretion, and reduced taste sensation in the anterior two-thirds of the tongue. The last three functions listed above are carried out by the portion of the facial nerve up to the geniculate ganglion, which also includes the intermediate nerve branch. In a fully developed facial paralysis, all 3 branches are seen to be equally affected, and the eyelids do not close completely. In central-type facial paralysis, however, the eye can close because the forehead muscles are not affected, since fibers to the eye and forehead region also arrive from the opposite side. In the examination of motor functions, the patient is asked to raise the eyebrows, close the eyes, wrinkle the nose, show the teeth, smile, and puff out the cheeks.
CRYPTOGENIC PERIPHERAL FACIAL PARALYSIS
Cases of peripheral facial paralysis for which no cause is found are classified as cryptogenic. Cryptogenic peripheral facial paralysis is the most common form of peripheral facial paralysis.
EPIDEMIOLOGY AND FREQUENCY
It accounts for ¾ of all peripheral facial nerve lesions, with an annual incidence of approximately 25 per 100,000. It occurs at an equal rate in both sexes. It most commonly appears in adulthood.
PATHOGENESIS
Most claim that this is a cranial neuritis. Some researchers, on the other hand, claim that it is a viral infection, with the herpes simplex virus cited as the cause. It also occurs more frequently in cases of ischemia in the facial canal (Canalis Fallopii) and in diabetics. It is seen more frequently with age. It has been shown to develop more often in patients with arterial hypertension. Stimulation of the nerve during surgery has shown that edema developing in the inner ear causes a conduction block in the facial nerve extending from the entrance of the canal to the proximal portion of the geniculate ganglion. In other words, in facial paralysis, a conduction block develops within the canal as a result of edema.
CLINICAL COURSE
A few days before the disease begins, patients complain of pain behind the ear and in the neck on that side, followed by the development of one-sided facial paralysis. No clear triggering cause can be found. The degree of paralysis varies. Due to motor paresis, patients may drool while eating. Other findings are described above. In the majority of cases, approximately 90%, complete recovery occurs within 4-6 weeks. In cases that do not fully resolve, significant improvement is seen within 3-6 months. In 5-8% of cases, however, severe residual effects remain. These difficult-to-resolve cases are most often those of advanced age, those with complete paralysis at onset, and those showing severe axonal damage on electrophysiological testing.
Advanced age, hyperacusis, reduced taste sensation, severe paralysis, and severe denervation findings on electrophysiological testing are all indicators of a poor prognosis. In severe cases, residual findings such as contracture of the facial muscles at rest and synkinetic innervation due to faulty innervation may appear at a later stage. That is, the patient may tightly close the eyelid while showing the teeth, or the eyes may close tightly while puffing out the cheek on the paretic side. Rarely, a phenomenon called "crocodile tears," in which tearing occurs while eating, may also appear.
OTHER CAUSES OF FACIAL PARALYSIS
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Head trauma
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Skull base fractures
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Vasculitis
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Granulomatous diseases
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Melkersson-Rosenthal syndrome
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Encephalitis
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Mono- and polyneuropathies
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Middle ear infection
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Herpes infection
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Post-infectious facial paralysis
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Guillain-Barré Syndrome
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Borrelia infection
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Basal meningitis
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Tumor infiltration
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Iatrogenic causes following surgical interventions
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Others
CONVENTIONAL TREATMENT
In the treatment of cryptogenic facial paralysis, cortisone and antiviral treatment are applied. However, the effects of these treatments are also debated. No statistically significant difference has been found between those who use cortisone and those who do not. In a patient whose eye does not close, the eye must be covered, because keratitis can develop, and artificial tears and antibiotics should be given prophylactically.
In facial paralysis arising from other causes, treatment should target the underlying cause.
NEURAL THERAPY AS A SOLUTION-ORIENTED TREATMENT
In the neural therapy approach, a detailed patient history is especially important given the context in which facial paralysis appears. The timing of the problem's onset and whether it coincided with any illness, climate change, or psychological changes should be thoroughly investigated.
Following a comprehensive physical examination, the patient history should be revisited in depth. In this context, examining the Adler points is very important.
Prior illnesses, surgical interventions, the state of the intestines, and the person's psychological makeup must be evaluated.
The approach must first be local. The areas innervated by the paralyzed muscles on the affected side are locally stimulated.
The local application is followed by the segmental therapy approach.
Segmental treatment
C1-C7 cervical quadrant.
The close anatomical relationship between the jaw joint region and the parotid gland should be evaluated and examined.
Ganglion injection
INTERFERENCE FIELD THERAPY
In cases where a solution cannot be found, a thorough search for interference fields should begin. Taking the temporal relationship of the patient's history into account once again, illnesses experienced in childhood in particular, along with operations, living environment, work environment, medications used, and the state of the immune system should be investigated.
In cases where no response is obtained from the treatments above, interference field therapy is initiated.
Sources Used:
• Nazlikul, H: Nöralterapi Ders Kitabı
• Nazlikul, H: Nöralterapi Başka Bir Tedavi Mümkün
• H. Barop's Nöralterapi Atlası (Translated by H. Nazlikul)
• L. Fischer's Nöralterapi Kitabı (Translated by H. Nazlikul and Y. Tamam)
• James W. McNabb's Eklem ve Yumuşak Doku Enjeksiyonları (Translated by H. Nazlikul and Y. Tamam)
• Weinschenk, S: Neuraltherapie
• Fischer, L et: Lehrbuch Integrative Schmerztherapie