Central facial palsy

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Central facial palsy
Other namesCentral seven
Specialty Neurology   OOjs UI icon edit-ltr-progressive.svg

Central facial palsy (colloquially referred to as 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.

Contents

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) while 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 pons and the facial motor nucleus destroy or reduce input to the ventral division, but ipsilateral input (i.e. 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.

Signs 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 reduces or destroys input in the ventral division. [1] The ipsilateral input in the dorsal region is preserved.

Central facial palsy is often characterized by either hemiparalysis or hemiparesis of the contralateral muscles in facial expression. [2] Muscles on the forehead are left intact. Also, most patients have lost voluntary control of muscle movement in the face—however, muscles in the face involved in spontaneous emotional expression often remain intact. [2] Central Facial palsy occurs in patients who are hemiplegic. Such 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]

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 frontalis and upper orbicularis oculi are often spared. [3] 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 leads to facial weakness that spares 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.

The motor system and facial patterns

In contemporary perspectives, the motor cortex is composed of two distinct areas; however, this viewpoint is incorrect. [4] The motor cortex is located in the posterior frontal lobe, and has multiple areas with 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 depend on the motor area 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. Exceptions to this include the prefrontal gyrus, where the parietal area sends an equal amount of fibers to many motor areas. [4] This 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 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. [3] The reason for the asymmetry however, remains unclear, a commonly concluded theory is that the right side of the hemisphere has an advantage in emotional processing than the left hemisphere. [3] To examine facial muscle movement often, transcranial magnetic stimulation (TMS) is used. [3]

Upper motoneuron lesions to the face often cause paralysis. The lesions cause weakness in various areas of the face while not affecting other areas of the face. This pattern of weakness due to the input of the motor neurons of the lower facial muscles is often maintained contralateral. [5] 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 anatomical 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 has shown the activation of both hemispheres during facial expression and emotion. However, there have been some discrepancies with the use of this method including differences in observations when using single and multiple needles as well as the areas of where the needles are placed. Using electrical cortical mapping bilateral movements were observed in the lower facial muscles compared to unilateral movements. [4] 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. [4]

Diagnosis

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] Supranuclear motor innervation of the facial musculature is difficult to examine because the circuitry is quite complex, only a few cases 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, which often works by examining the motor cortex and recording the motor stroked potentials. At high stimulation strengths, this often excites the trigeminal sensory afferents and triggers a blink reflex. From the blink reflex, it contains the R1 ipsilateral and bilateral R2 component. [4] The reflex can then be recorded in the lower parts of the brain. The R1 component limits the evaluation of the ipsilateral responses in the lower facial muscles. [7]

Treatment

Electromyographical biofeedback or myofeedback could provide patients who have central facial palsy the ability to create myo-electrical potentials that they can interpret. This method provides patients with information about muscle contraction that is normally subliminal. [2] Electromyographical biofeedback enables the patient to regain control of muscles that are involved in facial expression that have been atrophied. Brener's model[ who? ] was one of the first models to describe the circuitry of the role of feedback for voluntary control of physiological processes. [2] His method allows images of feedback that can produce effects on the voluntary control of motor responses, it involves 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 determine the activity of the effector system when it is innervated by the motor nerve (figure 1). [2]

From this pathway, self instruction moves 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 sensorimotor development a number of other automatic reactions were distinguished, such as balance, support and automatic adaptations of muscle power changes to postures. [8] Patients with hemiplegia have movements that are lower level and less motor coordination, and often must relearn these movements to continue or gain normal automatic transitions in the body. [9] Neuro developmental treatment (NDT) often improves daily functioning and self-help. This treatment centers on reversing disabilities, specifically for patients who are hemiplegic with impaired sensorimotor and neuropsychological functions. [10] Muscle regulation that is disturbed, often called hypo or hypertonic, causes abnormal movement patterns. These automatic reactions are impaired, and patients must learn these movements and remember mentally and physically the positions. [11] [12]

NDT uses muscle power techniques through inhibiting and stimulating certain muscle groups, which aims to lower or increase muscle tone. [13] For facial expression, therapists often help the patient make facial expressions by manipulating specific muscles with their fingers. The patient then tries to imitate the facial expressions. [14] Speech therapy helps correct word pronunciation. [15] NDT is directed at the functioning of the whole body, and not just the face. [16] Understanding the direct mechanisms of the face is required to determine the dysfunction of specific muscles. [17] NDT seems to be effective, but spontaneous motor movement that is controlled was not examined. [18]

Research

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. The study also found that ipsilateral corticonuclear fibers were found in the lower facial muscles, which does not coincide with other papers. The variation could be from the selection of muscles used in the study as well as the different electrodes that were used.

The orbicularis oculi muscles are often examined in patients with facial paralysis. In the study, it was difficult to elicit any corticonuclear 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 stimulate the presynaptic terminals 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]

Related Research Articles

Hemiparesis, or unilateral paresis, is weakness of one entire side of the body. Hemiplegia is, in its most severe form, complete paralysis of half of the body. Hemiparesis and hemiplegia can be caused by different medical conditions, including congenital causes, trauma, tumors, or stroke.

<span class="mw-page-title-main">Trigeminal nerve</span> Cranial nerve responsible for the faces senses and motor functions

In neuroanatomy, the trigeminal nerve (lit. triplet nerve), also known as the fifth cranial nerve, cranial nerve V, or simply CN V, is a cranial nerve responsible for sensation in the face and motor functions such as biting and chewing; it is the most complex of the cranial nerves. Its name (trigeminal, from Latin tri- 'three', and -geminus 'twin') derives from each of the two nerves (one on each side of the pons) having three major branches: the ophthalmic nerve (V1), the maxillary nerve (V2), and the mandibular nerve (V3). The ophthalmic and maxillary nerves are purely sensory, whereas the mandibular nerve supplies motor as well as sensory (or "cutaneous") functions. Adding to the complexity of this nerve is that autonomic nerve fibers as well as special sensory fibers (taste) are contained within it.

<span class="mw-page-title-main">Pyramidal tracts</span> The corticobulbar tract and the corticospinal tract

The pyramidal tracts include both the corticobulbar tract and the corticospinal tract. These are aggregations of efferent nerve fibers from the upper motor neurons that travel from the cerebral cortex and terminate either in the brainstem (corticobulbar) or spinal cord (corticospinal) and are involved in the control of motor functions of the body.

The withdrawal reflex is a spinal reflex intended to protect the body from damaging stimuli. The reflex rapidly coordinates the contractions of all the flexor muscles and the relaxations of the extensors in that limb causing sudden withdrawal from the potentially damaging stimulus. Spinal reflexes are often monosynaptic and are mediated by a simple reflex arc. A withdrawal reflex is mediated by a polysynaptic reflex resulting in the stimulation of many motor neurons in order to give a quick response.

<span class="mw-page-title-main">Facial nerve paralysis</span> Medical condition

Facial nerve paralysis is a common problem that involves the paralysis of any structures innervated by the facial nerve. The pathway of the facial nerve is long and relatively convoluted, so there are a number of causes that may result in facial nerve paralysis. The most common is Bell's palsy, a disease of unknown cause that may only be diagnosed by exclusion of identifiable serious causes.

<span class="mw-page-title-main">Corticobulbar tract</span> Motor pathway in the brain connecting the motor cortex to the medullary pyramids

In neuroanatomy, the corticobulbartract is a two-neuron white matter motor pathway connecting the motor cortex in the cerebral cortex to the medullary pyramids, which are part of the brainstem's medulla oblongata region, and are primarily involved in carrying the motor function of the non-oculomotor cranial nerves. The corticobulbar tract is one of the pyramidal tracts, the other being the corticospinal tract.

<span class="mw-page-title-main">Abducens nucleus</span>

The abducens nucleus is the originating nucleus from which the abducens nerve (VI) emerges—a cranial nerve nucleus. This nucleus is located beneath the fourth ventricle in the caudal portion of the pons near the midline, medial to the sulcus limitans.

Monoplegia is paralysis of a single limb, usually an arm. Common symptoms associated with monoplegic patients are weakness, numbness, and pain in the affected limb. Monoplegia is a type of paralysis that falls under hemiplegia. While hemiplegia is paralysis of half of the body, monoplegia is localized to a single limb or to a specific region of the body. Monoplegia of the upper limb is sometimes referred to as brachial monoplegia, and that of the lower limb is called crural monoplegia. Monoplegia in the lower extremities is not as common of an occurrence as in the upper extremities. Monoparesis is a similar, but less severe, condition because one limb is very weak, not paralyzed. For more information, see paresis.

<span class="mw-page-title-main">Posterior cerebral artery</span> Artery which supplies blood to the occipital lobe of the brain

The posterior cerebral artery (PCA) is one of a pair of cerebral arteries that supply oxygenated blood to the occipital lobe, part of the back of the human brain. The two arteries originate from the distal end of the basilar artery, where it bifurcates into the left and right posterior cerebral arteries. These anastomose with the middle cerebral arteries and internal carotid arteries via the posterior communicating arteries.

<span class="mw-page-title-main">Sixth nerve palsy</span> Medical condition

Sixth nerve palsy, or abducens nerve palsy, is a disorder associated with dysfunction of cranial nerve VI, which is responsible for causing contraction of the lateral rectus muscle to abduct the eye. The inability of an eye to turn outward, results in a convergent strabismus or esotropia of which the primary symptom is diplopia in which the two images appear side-by-side. Thus, the diplopia is horizontal and worse in the distance. Diplopia is also increased on looking to the affected side and is partly caused by overaction of the medial rectus on the unaffected side as it tries to provide the extra innervation to the affected lateral rectus. These two muscles are synergists or "yoke muscles" as both attempt to move the eye over to the left or right. The condition is commonly unilateral but can also occur bilaterally.

<span class="mw-page-title-main">Facial motor nucleus</span>

The facial motor nucleus is a collection of neurons in the brainstem that belong to the facial nerve. These lower motor neurons innervate the muscles of facial expression and the stapedius.

Pseudobulbar palsy is a medical condition characterized by the inability to control facial movements and caused by a variety of neurological disorders. Patients experience difficulty chewing and swallowing, have increased reflexes and spasticity in tongue and the bulbar region, and demonstrate slurred speech, sometimes also demonstrating uncontrolled emotional outbursts.

<span class="mw-page-title-main">Foix–Chavany–Marie syndrome</span> Medical condition

Foix–Chavany–Marie syndrome (FCMS), also known as bilateral opercular syndrome, is a neuropathological disorder characterized by paralysis of the facial, tongue, pharynx, and masticatory muscles of the mouth that aid in chewing. The disorder is primarily caused by thrombotic and embolic strokes, which cause a deficiency of oxygen in the brain. As a result, bilateral lesions may form in the junctions between the frontal lobe and temporal lobe, the parietal lobe and cortical lobe, or the subcortical region of the brain. FCMS may also arise from defects existing at birth that may be inherited or nonhereditary. Symptoms of FCMS can be present in a person of any age and it is diagnosed using automatic-voluntary dissociation assessment, psycholinguistic testing, neuropsychological testing, and brain scanning. Treatment for FCMS depends on the onset, as well as on the severity of symptoms, and it involves a multidisciplinary approach.

Diplegia, when used singularly, refers to paralysis affecting symmetrical parts of the body. This is different from hemiplegia which refers to spasticity restricted to one side of the body, paraplegia which refers to paralysis restricted to the legs and hip, and quadriplegia which requires the involvement of all four limbs but not necessarily symmetrical. Diplegia is the most common cause of crippling in children, specifically in children with cerebral palsy. Other causes may be due to injury of the spinal cord. There is no set course of progression for people with diplegia. Symptoms may get worse but the neurological part does not change. The primary parts of the brain that are affected by diplegia are the ventricles, fluid filled compartments in the brain, and the wiring from the center of the brain to the cerebral cortex. There is also usually some degeneration of the cerebral neurons, as well as problems in the upper motor neuron system. The term diplegia can refer to any bodily area, such as the face, arms, or legs.

Premovement neuronal activity in neurophysiological literature refers to neuronal modulations that alter the rate at which neurons fire before a subject produces movement. Through experimentation with multiple animals, predominantly monkeys, it has been shown that several regions of the brain are particularly active and involved in initiation and preparation of movement. Two specific membrane potentials, the bereitschaftspotential, or the BP, and contingent negative variation, or the CNV, play a pivotal role in premovement neuronal activity. Both have been shown to be directly involved in planning and initiating movement. Multiple factors are involved with premovement neuronal activity including motor preparation, inhibition of motor response, programming of the target of movement, closed-looped and open-looped tasks, instructed delay periods, short-lead and long-lead changes, and mirror motor neurons.

A horizontal gaze palsy is a subtype of gaze palsy in which conjugate, horizontal eye movements are limited by neurologic deficits. Horizontal gaze palsies typically result from an ipsilateral pontine lesion or a contralateral frontal lobe lesion.

<span class="mw-page-title-main">Accessory nerve disorder</span> Disorder caused due to injury to the spinal accessory nerve (11th cranial nerve or Cranial Nerve XI)

Accessory nerve disorder is an injury to the spinal accessory nerve which results in diminished or absent function of the sternocleidomastoid muscle and upper portion of the trapezius muscle.

<span class="mw-page-title-main">Primary motor cortex</span> Brain region

The primary motor cortex is a brain region that in humans is located in the dorsal portion of the frontal lobe. It is the primary region of the motor system and works in association with other motor areas including premotor cortex, the supplementary motor area, posterior parietal cortex, and several subcortical brain regions, to plan and execute voluntary movements. Primary motor cortex is defined anatomically as the region of cortex that contains large neurons known as Betz cells, which, along with other cortical neurons, send long axons down the spinal cord to synapse onto the interneuron circuitry of the spinal cord and also directly onto the alpha motor neurons in the spinal cord which connect to the muscles.

<span class="mw-page-title-main">Smile surgery</span> Surgical procedure to restore smile

Smile surgery or smile reconstruction is a surgical procedure that restores the smile for people with facial nerve paralysis. Facial nerve paralysis is a relatively common condition with a yearly incidence of 0.25% leading to function loss of the mimic muscles. The facial nerve gives off several branches in the face. If one or more facial nerve branches are paralysed, the corresponding mimetic muscles lose their ability to contract. This may lead to several symptoms such as incomplete eye closure with or without exposure keratitis, oral incompetence, poor articulation, dental caries, drooling, and a low self-esteem. This is because the different branches innervate the frontalis muscle, orbicularis oculi and oris muscles, lip elevators and depressors, and the platysma. The elevators of the upper lip and corner of the mouth are innervated by the zygomatic and buccal branches. When these branches are paralysed, there is an inability to create a symmetric smile.

Alternating hemiplegia is a form of hemiplegia that has an ipsilateral cranial nerve palsies and contralateral hemiplegia or hemiparesis of extremities of the body. The disorder is characterized by recurrent episodes of paralysis on one side of the body. There are multiple forms of alternating hemiplegia, Weber's syndrome, middle alternating hemiplegia, and inferior alternating hemiplegia. This type of syndrome can result from a unilateral lesion in the brainstem affecting both upper motor neurons and lower motor neurons. The muscles that would receive signals from these damaged upper motor neurons result in spastic paralysis. With a lesion in the brainstem, this affects the majority of limb and trunk muscles on the contralateral side due to the upper motor neurons decussation after the brainstem. The cranial nerves and cranial nerve nuclei are also located in the brainstem making them susceptible to damage from a brainstem lesion. Cranial nerves III (Oculomotor), VI (Abducens), and XII (Hypoglossal) are most often associated with this syndrome given their close proximity with the pyramidal tract, the location which upper motor neurons are in on their way to the spinal cord. Damages to these structures produce the ipsilateral presentation of paralysis or palsy due to the lack of cranial nerve decussation before innervating their target muscles. The paralysis may be brief or it may last for several days, many times the episodes will resolve after sleep. Some common symptoms of alternating hemiplegia are mental impairment, gait and balance difficulties, excessive sweating and changes in body temperature.

References

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  7. ↑ "microblading courses" . Retrieved 13 July 2015.
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  9. ↑ Micera, Silvestro; Caleo, Matteo; Chisari, Carmelo; Hummel, Friedhelm C.; Pedrocchi, Alessandra (2020-02-19). "Advanced Neurotechnologies for the Restoration of Motor Function". Neuron. 105 (4): 604–620. doi:10.1016/j.neuron.2020.01.039. PMID   32078796.
  10. ↑ Pathak, Abhishek; Gyanpuri, Vyom; Dev, Priya; Dhiman, Neetu Rani (2021-11-29). "The Bobath Concept (NDT) as rehabilitation in stroke patients: A systematic review". Journal of Family Medicine and Primary Care . 10 (11): 3983–3990. doi: 10.4103/jfmpc.jfmpc_528_21 . ISSN   2249-4863. PMC   8797128 . PMID   35136756.
  11. ↑ Ganguly, Jacky; Kulshreshtha, Dinkar; Almotiri, Mohammed; Jog, Mandar (2021-04-16). "Muscle Tone Physiology and Abnormalities". Toxins. 13 (4): 282. doi: 10.3390/toxins13040282 . ISSN   2072-6651. PMC   8071570 . PMID   33923397.
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  13. ↑ Park, Eun-Young; Kim, Won-Ho (2017-06-07). "Effect of neurodevelopmental treatment-based physical therapy on the change of muscle strength, spasticity, and gross motor function in children with spastic cerebral palsy". Journal of Physical Therapy Science. 29 (6): 966–969. doi:10.1589/jpts.29.966. PMC   5468216 . PMID   28626301.
  14. ↑ Zwick, Julia C.; Wolkenstein, Larissa (March 2017). "Facial emotion recognition, theory of mind and the role of facial mimicry in depression". Journal of Affective Disorders. 210: 90–99. doi:10.1016/j.jad.2016.12.022. PMID   28024224.
  15. ↑ "What is speech therapy?", InformedHealth.org [Internet], Institute for Quality and Efficiency in Health Care (IQWiG), 2020-08-12, retrieved 2024-04-22
  16. ↑ Das, Sakti Prasad; Ganesh, G. Shankar (2019). "Evidence-based Approach to Physical Therapy in Cerebral Palsy". Indian Journal of Orthopaedics. 53 (1): 20–34. doi: 10.4103/ortho.IJOrtho_241_17 . ISSN   0019-5413. PMC   6394183 . PMID   30905979.
  17. ↑ Taylor, Alan; Mourad, Firas; Kerry, Roger; Hutting, Nathan (2021-11-02). "A guide to cranial nerve testing for musculoskeletal clinicians". Journal of Manual & Manipulative Therapy. 29 (6): 376–390. doi:10.1080/10669817.2021.1937813. ISSN   1066-9817. PMC   8725776 . PMID   34182898.
  18. ↑ Caroff, Stanley N. (2019-04-04). "Overcoming barriers to effective management of tardive dyskinesia". Neuropsychiatric Disease and Treatment. 15: 785–794. doi: 10.2147/NDT.S196541 . PMC   6459148 . PMID   31040678.
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