Central facial palsy
| Central facial palsy | |
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| Facial nerve and Bell's palsy. Image courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Central facial palsy, (also called colloquially central seven) is a symptom or finding characterized by paralysis or paresis of the lower half of one side of the face. It usually results from damage to upper motor neurons of the facial nerve.
Pathophysiology
The facial motor nucleus has dorsal and ventral divisions that contain lower motor neurons supplying the muscles of the upper and lower face, respectively.
- The dorsal division receives bilateral upper motor neuron input (i.e, from both sides of the brain).
- The ventral division receives only contralateral input (i.e, from the opposite side of the brain).
Thus, lesions of the corticobulbar tract between the cerebral cortex and the facial motor nucleus destroy or reduce input to the ventral division, but ipsilateral input (ie, from the same side) to the dorsal division is retained. As a result, central facial palsy is characterized by hemiparalysis or hemiparesis of the contralateral muscles of facial expression, but not the muscles of the forehead
History and Symptoms
Central facial palsy is the paralysis of the lower half of one side of the face. This condition is often caused by a stroke. This condition is often the result of damage of the upper motor neurons of the facial nerve. The facial motor nucleus contains ventral and dorsal areas that have lower motor neurons that supply the upper and lower face muscles. When central facial palsy occurs, there are lesions in the corticobulbar tract between the cerebral cortex. Because of these lesions, the facial motor nucleus will reduce or destroy input in the ventral division.[1] On the other hand, the ipsilateral input in the dorsal region is preserved. Therefore, central facial palsy is often characterized by either hemiparalysis or hemiparesis of the contralateral muscles in facial expression.[2]
On the other hand, the muscles on the forehead are left intact. Also, most patients will have lost voluntary control of the movement of the muscles in the face, however, the muscles in the face that are involved in spontaneous emotional expression will often remain intact.[2]
Central Facial palsy occurs in patients who are hemiplegic. Hemiplegic patients not only have dysfunctions in the facial expression but also a difficulty in communication. Other oropharyngeal functions such as sucking, swallowing, and talking are also impaired.[2]
Order of the Motor System and Facial Patterns
In older perspectives, the motor cortex is comprised of two distinct areas; however, this viewpoint is incorrect .[3] The motor cortex is located in the posterior parietal lobe, and has multiple areas that have anatomical and functional regions. Each area is involved in the circuitry of various inputs of sensory information. The motor and parietal areas are reciprocally intertwined and form a group of specialized circuits that work parallel to one another. These circuits transform sensory information into an action or movement. The parieto-frontal circuits are the basic compositions of the main elements of the cortical motor system. These circuits are dependent on the motor area in order to receive afferent information from the parietal areas. The input in one area is predominant, containing full amounts of information. The other input area is known as moderate or weak. When the input is moderate or weak, it contains additional secondary information. Each parietal area is connected to several motor areas. However, it only makes privileged contact with one motor area. There are exceptions to this, which include the prefrontal gyrus. In the prefrontal gyrus, the parietal area sends an equal amount of fibers to many motor areas.[3] This is interaction is vital because the activity in the facial muscles is due to voluntary control of the direct and indirect pathways that are corticobulbar pathways. Facial muscles will often respond to emotional influences by these pathways also. Most of our emotions are expressed more intensely on the left side than the right side of the face.[4] The reason for the asymmetry however, remains unclear. The most concluded theory for the asymmetry of emotions is that the right side of the hemisphere has an advantage in emotional processing than the left hemisphere.[4] In order to examine facial muscle movement often, transcranial magnetic stimulation (TMS) is used. Upper motoneuron lesions to the face often cause paralysis. The lesions will cause weakness in various areas of the face while other areas of the face are not impacted. This pattern of weakness often because the input of the motor neurons of the lower facial muscles is often maintained contralateral.[5] However, the strength of the muscles in the upper region of the face are preserved better than the muscles in the lower face. It was found that in many anataomical studies that cortical input from both hemispheres could reach motoneurons that supply muscles of all aspects of the face.[6] Through the combination of anterograde and retrograde tracing techniques in monkeys it was found that the facial nucleus, which supplies muscles of the lower face are innervated bilaterally. Using TMS, it has allowed many to see the activation of both hemispheres during facial expression and emotion. However, there have been some discrepancies with the use of this method. There have been differences in observations when using single and multiple needles as well as the areas of where the needles are placed. On the contrary, from electrical cortical mapping it was observed that bilateral movements were observed in the lower facial muscles compared to unilateral movements.[3] From anatomic studies on patients with unilateral infarction, motoneurons in the lower facial area were innervated bilaterally; however, there was predominance in contralateral areas of the lower face.[3]
Characteristics and Symptoms of Central Facial Paralysis
Central facial paralysis/palsy often has similar characteristics with stroke patients. Because of uncrossed areas from the ipsilateral and the supranuclear areas, movements in the frontal and upper orbcularis oculi are often spared.[4] Facial movement can be present on the affected side when the person expresses emotion. Damage to the central nervous system motor pathway from the cerebral cortex to the facial nuclei is found in the pons. This will lead to facial weakness that will spare various muscles in the face depending on the type of paralysis. The discrepancy of the weakness between the upper and lower facial muscles are due to the bilateral corticonuclear innervation from the upper facial muscles and contralateral corticonuclear innervation to the lower facial muscles.
Techniques In understanding the Facial Nerves
Through electrophysiological studies and neuronal tracing, these characteristics do not fully support the typical person with central facial palsy. Often, transcranial magnetic stimulation (TMS) is used to understand the bilateral corticonuclear projections of the lower facial motor neurons. This idea using bilateral innervation to the upper facial motor neurons is rarely tested by humans because of the afferent fibers in the trigeminal nerve are distributed over the head and face and could cause damage.[2] Therefore, supranuclear motor innervation of the facial musculature is difficult to examine because the circuitry is quite complex. There are only a few cases that are described in literature of central facial palsy and the absence of bilateral perioral muscle responses after TMS of the affected hemisphere. EMG responses are often used to observe the upper facial muscles, however, it is difficult to elicit by TMS. TMS often works by examining the motor cortex by recording the motor stroked potentials. At high stimulation strengths, this often will excite the trigeminal sensory afferents and will trigger a blink reflex. From the blink reflex, it contains the R1 ipsilateral and bilateral R2 component.[3] The reflex can then be recorded in the lower parts of the brain. The R1 component will limit the evaluation of the ipsilateral responses in the lower facial muscles.
Studies
In one study, the lab group primarily focused on the electrophysiological evaluation of corticonuclear descending fibers to the lower facial motor neurons in patients with central facial palsy, and the discussion of how central facial palsy can become mild from various recovery techniques.[1] It was found that in normal subjects, unilateral TMS stimulation of the motor cortex induced EMG responses from the perioral muscles. This finding supports other studies in favor that bilateral projection of the corticonuclear fibers of the lower facial muscles are present in humans and primates with normal function. Also, ipsilateral corticonuclear fibers were found in the lower facial muscles. This does not coincide with other papers; this variation could be from the selection of muscles used in the study as well as the different electrodes that were used in the study.
After the stroke, there were changes in the hemispheric organization of the lower facial muscles. First, the motor threshold was lowered and it was remarkable that it was possible to evoke the MEP even when the muscles were relaxed. This could indicate that the intracortical inhibitory mechanisms are weakened in the face associated cortex and there is no inhibition of these mechanisms. Also, the fibers that are contralateral to the normal side were the first to be activated stronger, and weeks after the stroke, these fibers had increased activation. This can be inferred that corticonuclear fibers in the unaffected hemisphere are needed and are important to recovery from a stroke. Changes in the amplitude enlargement of amplitude in these fibers could be detected by TMS stimulation from the unaffected hemisphere during the weeks after the stroke. This could mean that the hemisphere with no damage can be excited more frequently to corticonuclear fibers that are connected to the paretic lower facial muscles that are located both ipsilaterally and contralaterally. The study also explains that the increase in amplitude can not be due to electrode movement because the amplitude values of the responses from the intracranial facial nerve stimuli were not different on both sides of the face.
Central facial palsy due to stroke is often mild and incomplete because the ipsilateral and corticunuclear innervation recovers quite quickly. There often is hemispheric disinhibtion and cortical reorganization occurs rapidly. Other corticonuclear terminals and postsynaptic sensitivity could be major contributions to the rapid recovery of patients who have central facial palsy, but these inferences could not be confirmed.
Central facial paresis is rarely found to be chronic rather it is more of an acute stroke. However, in the chronic stage—after the stroke, and central facial paresis is still apparent, this could be due to a large middle cerebral artery infarction or direct destruction of facial cortical neurons and/or an decreased amount of innervation in the ipsilateral area that would not allow reinnervation of this area after the stroke. In the study, the patients that had central facial palsy had slower exciteable corticonuclear fibers in the lower facial muscles that were affected to the paretic mouth than the controls. However, this mechanism is still unknown.
The orbicularis oculi muscles are often examined in patients with facial paralysis. In the study, it was difficult to illicit any corticunuclear EMG responses from this area in both normal subjects and in patients with CFP.[1] This could be because the cortical links and synapses of the upper facial muscles are limited in function and TMS could not presynaptically stimulate the correct areas observed in paralysis. These areas are important because they will stimulate the presynaptic preterminals in cortical neurons. Also, this stimulation to the brain can not be studied on healthy human subjects. The upper facial muscle ME responses could not be innervated by TMS and the low threshold of blink reflexes often interferes with the nature of corticobulbar influences.[1]
Treatment
Electromyographical biofeedback or myofeedback could provide patients who suffer from central facial palsy the ability to create myo-elelctrical potentials that they will interpret. This method allows patients to receive information about muscle contraction that is normally subliminal.[2] Also, Electromyographical biofeedback will enable the patient to regain control of muscles that are involved in facial expression that have been atrophied. Brener’s model was one of the fist models to describe the circuitry of the role of feedback for voluntary control of physiological processes.[2] This method allows images of feedback that can produce effects on the voluntary control of motor responses. In his method, there are two central systems: an effector mechanism and feedback loops. There are central systems that are the central sensory integration system and the central motor system. The interaction of both of these systems enables the central motor pathways and a central feedback loop that will determine the activity of the effector system when it is innervated by the motor nerve[2]
From this pathway, self instruction will move in a pattern that is called a “response image”.[2] This response is often the actual movement of the directed response. Therefore, by knowing the loop, it allows full or dysfunctional proprioceptive feedback and exteroceptive control of the movement that is necessary in facial muscles.[2]
Neuro Developmental Treatment
From the knowledge of the sensimotor development it enabled others to distinguish the number of automatic reactions such as: balance, support, and automatic adaptations of muscle power changes to postures. Patients with hemiplegia will have movements that are lower level and less motor coordination. Patients often have to relearn these movements in order for them to continue or gain normal automatic transitions in the body. Therefore neuro developmental treatment (NDT) often will improve daily functioning and self help. This treatment is centered upon the restoration of the disabilities. Specifically, those who are hemiplegic have impaired sensimotor and neuropsychological functions.
Muscle regulation that is disturbed is often called hypo or hypertonic, that will cause abnormal patterns in movement. These automatic reactions are impaired, and patients must learn these movements and remember mentally and physically the positions. NDT uses techniques of muscle power through inhibiting and stimulating certain muscle groups which aim to lowering or increasing the the muscle tone. For facial expression, the therapist will often assist the patient in making several facial expressions by manipulating certain muscles with fingers. The patient will then try to imitate the expressions of the face. Also, speech therapy is used in order for word pronunciation to be corrected.
NDT is directed at the functioning of the whole body and not just only the face. Understanding the direct mechanisms of the face is needed in order to determine the dysfunction of specific muscles. Although NDT seems to be effective, spontaneous motor movement that is controlled was not examined. Other methods of recovery that are more effective and have a higher level of success should be analyzed.
References
- ↑ 1.0 1.1 1.2 1.3 Yildiz N, Ertekin C, Ozdemirkiran T; et al. (2005). "Corticonuclear innervation to facial muscles in normal controls and in patients with central facial paresis". J. Neurol. 252 (4): 429–35. doi:10.1007/s00415-005-0669-3. PMID 15726262.
- ↑ 2.0 2.1 2.2 2.3 2.4 2.5 2.6 2.7 2.8 van Gelder RS, Philippart SMM, Hopkins B (1990). "Treatment of Facial Paralysis of Cns-Origin: Initial Studies". International Journal of Psychology. 25 (2): 213–228. doi:10.1080/00207599008247858. ISSN 1464-066X.
- ↑ 3.0 3.1 3.2 3.3 3.4 Liscić RM, Zidar J (1998). "Functional organisation of the facial motor system in man". Coll Antropol. 22 (2): 545–50. PMID 9887611.
- ↑ 4.0 4.1 4.2 Meyer BU, Werhahn K, Rothwell JC, Roericht S, Fauth C (1994). "Functional organisation of corticonuclear pathways to motoneurones of lower facial muscles in man". Exp Brain Res. 101 (3): 465–72. PMID 7851513.
- ↑ Cruccu G, Berardelli A, Inghilleri M, Manfredi M (1990). "Corticobulbar projections to upper and lower facial motoneurons. A study by magnetic transcranial stimulation in man". Neurosci. Lett. 117 (1–2): 68–73. PMID 2290623.
- ↑ Triggs WJ, Ghacibeh G, Springer U, Bowers D (2005). "Lateralized asymmetry of facial motor evoked potentials". Neurology. 65 (4): 541–4. doi:10.1212/01.wnl.0000172916.91302.e7. PMID 16116113.
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