Bell Palsy
Facial Paralysis
Facial Nerve
Cerebral Palsy
Facial Nerve Diseases
Herpes Zoster Oticus
Lyme Neuroborreliosis
Rome
Moxibustion
Acupuncture Therapy
Ageusia
Acyclovir
Myoclonic Cerebellar Dyssynergia
Paralysis
Facial Nerve Injuries
Facial Muscles
High prevalence of varicella-zoster virus reactivation in herpes simplex virus-seronegative patients with acute peripheral facial palsy. (1/73)
Varicella-zoster virus (VZV) and herpes simplex virus (HSV) are considered to be the major causes of acute peripheral facial palsy (APFP). One hundred and forty-two patients with APFP were analyzed by serological assays and polymerase chain reaction analysis. Ramsay Hunt syndrome was diagnosed in 21 patients. Of the remaining 121 patients clinically diagnosed with Bell's palsy, VZV reactivation without zoster (zoster sine herpete) was detected in 35 patients (29%). The prevalence of antibodies to HSV among patients with Bell's palsy was significantly higher than the prevalence among those with VZV reactivation (Ramsay Hunt syndrome or zoster sine herpete). In contrast, a high incidence (88%) of VZV reactivation among HSV-seronegative patients with APFP was observed. Our data indicate that VZV is one of the major etiologic agents of clinically diagnosed Bell's palsy and that VZV reactivation causes APFP in most patients who lack antibodies to HSV. (+info)Detection of human herpesvirus 6 and varicella-zoster virus in tear fluid of patients with Bell's palsy by PCR. (2/73)
Human herpesvirus 6 DNA was detected by PCR in the tear fluid of 7 (35%) of 20 patients with Bell's palsy and of 1 (5%) of 20 healthy controls. Varicella-zoster virus was detected by PCR in the tear fluid of 2 of 20 Bell's palsy patients but in none of the tear fluids from 20 healthy controls. These findings suggest an association between human herpesviruses and Bell's palsy. (+info)Ramsay Hunt syndrome. (3/73)
The strict definition of the Ramsay Hunt syndrome is peripheral facial nerve palsy accompanied by an erythematous vesicular rash on the ear (zoster oticus) or in the mouth. J Ramsay Hunt, who described various clinical presentations of facial paralysis and rash, also recognised other frequent symptoms and signs such as tinnitus, hearing loss, nausea, vomiting, vertigo, and nystagmus. He explained these eighth nerve features by the close proximity of the geniculate ganglion to the vestibulocochlear nerve within the bony facial canal. Hunt's analysis of clinical variations of the syndrome now bearing his name led to his recognition of the general somatic sensory function of the facial nerve and his defining of the geniculate zone of the ear. It is now known that varicella zoster virus (VZV) causes Ramsay Hunt syndrome. Compared with Bell's palsy (facial paralysis without rash), patients with Ramsay Hunt syndrome often have more severe paralysis at onset and are less likely to recover completely. Studies suggest that treatment with prednisone and acyclovir may improve outcome, although a prospective randomised treatment trial remains to be undertaken. In the only prospective study of patients with Ramsay Hunt syndrome, 14% developed vesicles after the onset of facial weakness. Thus, Ramsay Hunt syndrome may initially be indistinguishable from Bell's palsy. Further, Bell's palsy is significantly associated with herpes simplex virus (HSV) infection. In the light of the known safety and effectiveness of antiviral drugs against VZV or HSV, consideration should be given to early treatment of all patients with Ramsay Hunt syndrome or Bell's palsy with a 7-10 day course of famciclovir (500 mg, three times daily) or acyclovir (800 mg, five times daily), as well as oral prednisone (60 mg daily for 3-5 days). Finally, some patients develop peripheral facial paralysis without ear or mouth rash, associated with either a fourfold rise in antibody to VZV or the presence of VZV DNA in auricular skin, blood mononuclear cells, middle ear fluid, or saliva. This indicates that a proportion of patients with "Bell's palsy" have Ramsay Hunt syndrome zoster sine herpete. Treatment of these patients with acyclovir and prednisone within 7 days of onset has been shown to improve the outcome of recovery from facial palsy. (+info)Symptomatic unruptured capillary telangiectasia of the brain stem: report of three cases and review of the literature. (4/73)
Three young patients with transient or intermittent focal neurological signs suggesting brain stem involvement are described, in whom high field MRI showed focal areas of hyperintensity in T2 weighted spin echo images, hypointensity in T2* weighted gradient echo images, and enhancement in postcontrast T1 weighted images consistent with unruptured capillary telangiectasia of the brain stem. The first patient was a 28 year old woman who complained of recurrent left ear tinnitus, exacerbated during the menstrual period; MRI demonstrated that the vascular anomaly involved the left acoustic pathway. The second patient was a 30 year old woman who had three episodes of paroxysmal left lip movement 4 weeks after child delivery; MRI showed capillary telangiectasia in the right corticonuclear pathway. The third patient, a 36 year old man, had a transient right Bell's palsy; MRI disclosed two circumscribed areas consistent with capillary telangiectasia in the left corticospinal tract and medial longitudinal fasciculus. Steroid receptors in the telangiectatic vessels walls might account for the recurrent and transient course seen in our two female patients. Awareness of the MRI features of capillary telangiectasia may help in defining the real incidence, clinical correlation, and the risk of haemorrhagic complications of these vascular malformations. (+info)Weather conditions and Bell's palsy: five-year study and review of the literature. (5/73)
BACKGROUND: Climatic or meteorological condition changes have been implicated in the pathogenesis of Bell's palsy (BP). We evaluate the influence of meteorological parameters, such as temperature, humidity, and atmospheric pressure, and their variation and covariation on the incidence of BP and present a review of the literature on the effect of meteorological conditions on facial nerve function. METHODS: A total of 171 cases of BP admitted to our Department over a five-year period were studied. The meteorological database included daily values of 13 distinct parameters recorded at the meteorological station of the University of Ioannina during this period. A relationship between each meteorological variable and the incidence of BP was investigated by applying (Chi2) test on data from 13 contingency tables. In addition, the influence of different weather types on the incidence of BP was also investigated. For this purpose Cluster Analysis was used to create eight clusters (weather types) for the Ioannina prefecture and (Chi2) test was applied on the contingency tables consisting of the days of BP cases for each cluster. RESULTS: No significant correlation was found either between BP and each distinct meteorological parameter or between BP and any specific weather. CONCLUSIONS: Meteorological conditions, such as those dominating in the Northwestern Greece, and/or their changes have little effect on the incidence of BP. Multicenter studies taking into account atmospheric pollution, and climatic differences between countries, are necessary to scrutinize the environmental effects on facial nerve function. (+info)Botulinum toxin treatment for hyperlacrimation secondary to aberrant regenerated seventh nerve palsy or salivary gland transplantation. (6/73)
AIM: To investigate the potential of botulinum toxin A for treating hyperlacrimation. METHODS: Three patients with unilateral symptoms of hyperlacrimation (diagnosed as "crocodile tearing") and one patient with a submandibular salivary gland transplant (SMGT) were studied. Tear production was quantified in the resting and stimulated (chewing or following exercise) state, using Schirmer's test and tear clearance. Lacrimal scintigraphy was used to assess outflow. Intraglandular injections (for patients with "crocodile tears") or periglandular injections (for the SMGT patient) of Dysport were administered in divided doses. RESULTS: Two of the three eyes with reported gustatory lacrimation had a higher Schirmer test result than their fellow eye following gustatory stimulation. Scintigraphy, with and without stimulation, confirmed a patent drainage system in these patients. The other patient demonstrated a functional obstruction to tear flow. After treatment patients with confirmed gustatory lacrimation and the SMGT patient had a marked reduction in tearing at 2 weeks. This effect lasted 3-4 months. There was no demonstrable improvement in the patient with epiphora secondary to functional obstruction. Two patients who had received intraglandular injections developed a ptosis, which resolved spontaneously. CONCLUSIONS: This study illustrates that gustatory lacrimation is a difficult diagnosis. In post-facial nerve palsy a functional element must always be considered. However, in confirmed hyperlacrimation botulinum toxin treatment is effective but side effects may occur. (+info)Association between Bell's palsy in pregnancy and pre-eclampsia. (7/73)
BACKGROUND: Previous published case series have suggested an association between the onset of Bell's palsy in pregnancy and the risk of pre-eclampsia and gestational hypertension. AIM: To evaluate the period of onset of Bell's palsy in pregnancy and the associated risk of adverse maternal and perinatal events, including the hypertensive disorders of pregnancy. STUDY DESIGN: Case series study of consecutive female patients. METHODS: Women presenting with Bell's palsy during pregnancy or the puerperium were identified by a hospital record review at five Canadian centres over 11 years. Information was abstracted about each woman's medical and obstetrical history, period of onset of Bell's palsy, and associated maternal complications, including pre-eclampsia and gestational hypertension as well as preterm delivery and low infant birth weight (<2500 g). These rates were compared to those previously described for the province of Ontario or for Canada. RESULTS: Forty-one patients were identified. Mean onset of Bell's palsy was 35.4 weeks gestation (SD 3.9). Nine (22.0%, 95%CI 10.8-35.7) were also diagnosed with pre-eclampsia and three (7.3%, 95%CI 1.4-17.1) with gestational hypertension, together (29.3%, 95%CI 16.5-43.9) representing nearly a five-fold increase over the expected provincial/national average. There were three twin births. The observed rates of Caesarean (43.6%) and preterm (25.6%) delivery, as well as low infant birth weight (22.7%), were also higher than expected, although the rate of congenital anomalies (4.5%) was not. CONCLUSIONS: The onset of Bell's palsy during pregnancy or the puerperium is probably associated with the development of the hypertensive disorders of pregnancy. Pregnant women who develop Bell's palsy should be closely monitored for hypertension or pre-eclampsia, and managed accordingly. (+info)Effects of climate, latitude, and season on the incidence of Bell's palsy in the US Armed Forces, October 1997 to September 1999. (8/73)
Bell's palsy is a relatively common disease characterized by the sudden onset of unilateral facial paralysis. Using a centralized surveillance system that contains demographic, military assignment, and medical encounter data of US military service members, the authors estimated rates, trends, and demographic correlates of risk of Bell's palsy during a 2-year period. Poisson regression was used to estimate the independent effects of climate, season, and latitude. From October 1997 to September 1999, there were 1,181 incident cases of Bell's palsy among US service members. The crude incidence rate was 42.77 per 100,000 person-years. Incidence rates increased with age and were higher among females, Blacks, Hispanics, married persons, and enlisted service members. Both climate (adjusted rate ratio for arid vs. nonarid climate = 1.34) and season (adjusted rate ratio for cold vs. warm months = 1.31) were independent predictors of risk of Bell's palsy. Latitude was not a statistically significant predictor when demographic, climate, and season effects were taken into account. The results are consistent with hypotheses regarding viral etiologies (e.g., reactivation of herpes simplex) of Bell's palsy. (+info)Bell palsy is a peripheral facial nerve palsy, which means that it is a weakness or paralysis of the facial nerves (cranial nerve VII) that causes sudden asymmetric weakness on one side of the face. The symptoms can vary from mild to severe and may include:
* Sudden weakness or paralysis on one side of the face
* Drooping of the mouth, causing difficulty with smiling, eating, drinking, or speaking
* Inability to close one eye
* Dryness of the eye and mouth
* Changes in taste sensation
* Discomfort around the jaw and behind the ear
* Headache
* Increased sensitivity to sound
The exact cause of Bell palsy is not known, but it is believed to be related to inflammation or swelling of the facial nerve. It may also be associated with viral infections such as herpes simplex virus or HIV. In most cases, Bell palsy resolves on its own within a few weeks to months, although some people may experience residual symptoms such as facial weakness or asymmetry. Treatment typically involves corticosteroids and antiviral medications, which can help reduce inflammation and speed up recovery.
Facial paralysis is a loss of facial movement due to damage or dysfunction of the facial nerve (cranial nerve VII). This nerve controls the muscles involved in facial expressions, such as smiling, frowning, and closing the eyes. Damage to one side of the facial nerve can cause weakness or paralysis on that side of the face.
Facial paralysis can result from various conditions, including:
1. Bell's palsy - an idiopathic (unknown cause) inflammation of the facial nerve
2. Trauma - skull fractures, facial injuries, or surgical trauma to the facial nerve
3. Infections - Lyme disease, herpes zoster (shingles), HIV/AIDS, or bacterial infections like meningitis
4. Tumors - benign or malignant growths that compress or invade the facial nerve
5. Stroke - damage to the brainstem where the facial nerve originates
6. Congenital conditions - some people are born with facial paralysis due to genetic factors or birth trauma
Symptoms of facial paralysis may include:
* Inability to move one or more parts of the face, such as the eyebrows, eyelids, mouth, or cheeks
* Drooping of the affected side of the face
* Difficulty closing the eye on the affected side
* Changes in saliva and tear production
* Altered sense of taste
* Pain around the ear or jaw
* Speech difficulties due to weakened facial muscles
Treatment for facial paralysis depends on the underlying cause. In some cases, such as Bell's palsy, spontaneous recovery may occur within a few weeks to months. However, physical therapy, medications, and surgical interventions might be necessary in other situations to improve function and minimize complications.
The facial nerve, also known as the seventh cranial nerve (CN VII), is a mixed nerve that carries both sensory and motor fibers. Its functions include controlling the muscles involved in facial expressions, taste sensation from the anterior two-thirds of the tongue, and secretomotor function to the lacrimal and salivary glands.
The facial nerve originates from the brainstem and exits the skull through the internal acoustic meatus. It then passes through the facial canal in the temporal bone before branching out to innervate various structures of the face. The main branches of the facial nerve include:
1. Temporal branch: Innervates the frontalis, corrugator supercilii, and orbicularis oculi muscles responsible for eyebrow movements and eyelid closure.
2. Zygomatic branch: Supplies the muscles that elevate the upper lip and wrinkle the nose.
3. Buccal branch: Innervates the muscles of the cheek and lips, allowing for facial expressions such as smiling and puckering.
4. Mandibular branch: Controls the muscles responsible for lower lip movement and depressing the angle of the mouth.
5. Cervical branch: Innervates the platysma muscle in the neck, which helps to depress the lower jaw and wrinkle the skin of the neck.
Damage to the facial nerve can result in various symptoms, such as facial weakness or paralysis, loss of taste sensation, and dry eyes or mouth due to impaired secretion.
Cerebral palsy (CP) is a group of disorders that affect a person's ability to move and maintain balance and posture. According to the Mayo Clinic, CP is caused by abnormal brain development or damage to the developing brain that affects a child's ability to control movement.
The symptoms of cerebral palsy can vary in severity and may include:
* Spasticity (stiff or tight muscles)
* Rigidity (resistance to passive movement)
* Poor coordination and balance
* Weakness or paralysis
* Tremors or involuntary movements
* Abnormal gait or difficulty walking
* Difficulty with fine motor skills, such as writing or using utensils
* Speech and language difficulties
* Vision, hearing, or swallowing problems
It's important to note that cerebral palsy is not a progressive condition, meaning that it does not worsen over time. However, the symptoms may change over time, and some individuals with CP may experience additional medical conditions as they age.
Cerebral palsy is usually caused by brain damage that occurs before or during birth, but it can also be caused by brain injuries that occur in the first few years of life. Some possible causes of cerebral palsy include:
* Infections during pregnancy
* Lack of oxygen to the brain during delivery
* Traumatic head injury during birth
* Brain bleeding or stroke in the newborn period
* Genetic disorders
* Maternal illness or infection during pregnancy
There is no cure for cerebral palsy, but early intervention and treatment can help improve outcomes and quality of life. Treatment may include physical therapy, occupational therapy, speech therapy, medications to manage symptoms, surgery, and assistive devices such as braces or wheelchairs.
Facial nerve diseases refer to a group of medical conditions that affect the function of the facial nerve, also known as the seventh cranial nerve. This nerve is responsible for controlling the muscles of facial expression, and it also carries sensory information from the taste buds in the front two-thirds of the tongue, and regulates saliva flow and tear production.
Facial nerve diseases can cause a variety of symptoms, depending on the specific location and extent of the nerve damage. Common symptoms include:
* Facial weakness or paralysis on one or both sides of the face
* Drooping of the eyelid and corner of the mouth
* Difficulty closing the eye or keeping it closed
* Changes in taste sensation or dryness of the mouth and eyes
* Abnormal sensitivity to sound (hyperacusis)
* Twitching or spasms of the facial muscles
Facial nerve diseases can be caused by a variety of factors, including:
* Infections such as Bell's palsy, Ramsay Hunt syndrome, and Lyme disease
* Trauma or injury to the face or skull
* Tumors that compress or invade the facial nerve
* Neurological conditions such as multiple sclerosis or Guillain-Barre syndrome
* Genetic disorders such as Moebius syndrome or hemifacial microsomia
Treatment for facial nerve diseases depends on the underlying cause and severity of the symptoms. In some cases, medication, physical therapy, or surgery may be necessary to restore function and relieve symptoms.
Herpes zoster oticus, also known as Ramsay Hunt syndrome type 2, is a viral infection that affects the facial nerve (cranial nerve VII). It is caused by the reactivation of the varicella-zoster virus, which is the same virus responsible for chickenpox. After an initial chickenpox infection, the virus can remain dormant in the body and later reactivate, causing herpes zoster oticus.
In this condition, the virus affects the geniculate ganglion of the facial nerve, leading to inflammation and damage to the nerve fibers. This results in various symptoms, including:
1. Painful rash around the ear, on the face, or in the mouth
2. Facial weakness or paralysis on one side of the face
3. Hearing loss, tinnitus (ringing in the ears), or vertigo (dizziness)
4. Loss of taste sensation on the anterior two-thirds of the tongue
5. Difficulty closing one eye, leading to dryness and irritation
Immediate medical attention is necessary for proper diagnosis and treatment, which typically involves antiviral medications and corticosteroids to reduce inflammation and speed up recovery. Early treatment can help minimize the risk of complications, such as permanent facial nerve damage or hearing loss.
Lyme neuroborreliosis (LNB) is a specific neurological manifestation of Lyme borreliosis, which is caused by the bacterium Borrelia burgdorferi. It is characterized by inflammation of the nervous system, particularly the peripheral and central nervous systems.
Involvement of the peripheral nervous system can present as radiculoneuropathy or cranial neuritis, leading to symptoms such as radiating pain, paresthesia, muscle weakness, and/or sensory loss in the affected areas. Involvement of the central nervous system may result in meningitis (inflammation of the membranes surrounding the brain and spinal cord), encephalitis (inflammation of the brain), or myelitis (inflammation of the spinal cord). These manifestations can cause symptoms such as headache, stiff neck, cognitive impairment, memory loss, mood changes, sleep disturbances, and, in rare cases, seizures.
LNB is typically diagnosed based on a combination of clinical presentation, laboratory tests (such as serological analysis or CSF examination), and sometimes supported by imaging studies. Treatment usually involves antibiotic therapy, which can be administered either orally or intravenously, depending on the severity and extent of the infection. Early diagnosis and treatment significantly improve the prognosis for LNB patients.
I'm sorry for any confusion, but "Rome" is not a medical term. It is the capital city of Italy and has great historical and cultural significance. If you have any medical questions or terms you would like defined, I would be happy to help!
Moxibustion is a traditional Chinese medicine (TCM) practice involving the burning of a mugwort-based herb called "moxa" close to or on specific points on the body, with the intention of stimulating chi (vital energy), encouraging healing, and preventing/treating diseases. The heat generated by moxa sticks or cones is believed to warm the meridians, dispel cold and dampness, and improve circulation. Practitioners may apply moxibustion directly on the skin, through an insulating material, or indirectly above the skin. It's often used in conjunction with acupuncture for various health issues, such as arthritis, digestive disorders, and gynecological conditions.
Acupuncture therapy is a form of traditional Chinese medicine that involves the insertion of thin needles into specific points on the body to stimulate the flow of energy (Qi), balance the vital force (Chi), and promote healing. It is based on the concept of meridians, or pathways, through which this energy flows. Acupuncture therapy is used to treat a variety of conditions, including pain, stress, anxiety, insomnia, digestive disorders, and reproductive health issues. According to Western medicine, acupuncture may work by stimulating the nervous system, increasing blood flow, and releasing natural pain-relieving chemicals called endorphins. It is generally considered safe when performed by a qualified practitioner using sterile needles.
Ageusia is a medical term that refers to the complete loss of taste. It can affect a person's ability to detect sweet, salty, sour, bitter, and savory flavors. Ageusia can be caused by various factors such as damage to the nerves responsible for transmitting taste signals to the brain, exposure to certain chemicals or radiation therapy, and some medical conditions like diabetes, hypertension, and upper respiratory infections. In some cases, ageusia may be temporary, while in others, it can be permanent. It is important to consult a healthcare professional if experiencing a loss of taste, as it could be a sign of an underlying health issue.
Acyclovir is an antiviral medication used for the treatment of infections caused by herpes simplex viruses (HSV) including genital herpes, cold sores, and shingles (varicella-zoster virus). It works by interfering with the replication of the virus's DNA, thereby preventing the virus from multiplying further. Acyclovir is available in various forms such as oral tablets, capsules, creams, and intravenous solutions.
The medical definition of 'Acyclovir' is:
Acyclovir (brand name Zovirax) is a synthetic nucleoside analogue that functions as an antiviral agent, specifically against herpes simplex viruses (HSV) types 1 and 2, varicella-zoster virus (VZV), and Epstein-Barr virus (EBV). Acyclovir is converted to its active form, acyclovir triphosphate, by viral thymidine kinase. This activated form then inhibits viral DNA polymerase, preventing further replication of the virus's DNA.
Acyclovir has a relatively low toxicity profile and is generally well-tolerated, although side effects such as nausea, vomiting, diarrhea, and headache can occur. In rare cases, more serious side effects such as kidney damage, seizures, or neurological problems may occur. It is important to take acyclovir exactly as directed by a healthcare provider and to report any unusual symptoms promptly.
Myoclonic cerebellar dyssynergia is not a widely recognized or formally defined medical term. However, based on its individual components, it can be inferred to refer to a neurological condition characterized by:
1. Myoclonus: These are sudden, involuntary jerking movements of a muscle or group of muscles. They typically occur as a result of hyperexcitability of the neurons in the brain that control movement (motor neurons).
2. Cerebellar: The cerebellum is a part of the brain responsible for coordinating muscle movements, maintaining posture and balance, and fine-tuning motor skills. When a condition is described as "cerebellar," it implies that there is some dysfunction or abnormality in this region of the brain.
3. Dyssynergia: This term refers to a lack of coordination between muscles and muscle groups during voluntary movements. It can result from damage to the cerebellum or other parts of the nervous system involved in motor control.
Therefore, myoclonic cerebellar dyssynergia could be interpreted as a condition characterized by involuntary muscle jerks (myoclonus) and impaired coordination of voluntary movements (dyssynergia), likely due to cerebellar dysfunction. However, it is essential to consult with a medical professional for an accurate diagnosis and treatment plan if you or someone else experiences symptoms that may align with this description.
Paralysis is a loss of muscle function in part or all of your body. It can be localized, affecting only one specific area, or generalized, impacting multiple areas or even the entire body. Paralysis often occurs when something goes wrong with the way messages pass between your brain and muscles. In most cases, paralysis is caused by damage to the nervous system, especially the spinal cord. Other causes include stroke, trauma, infections, and various neurological disorders.
It's important to note that paralysis doesn't always mean a total loss of movement or feeling. Sometimes, it may just cause weakness or numbness in the affected area. The severity and extent of paralysis depend on the underlying cause and the location of the damage in the nervous system.
Facial nerve injuries refer to damages or trauma inflicted on the facial nerve, also known as the seventh cranial nerve (CN VII). This nerve is responsible for controlling the muscles involved in facial expressions, eyelid movement, and taste sensation in the front two-thirds of the tongue.
There are two main types of facial nerve injuries:
1. Peripheral facial nerve injury: This type of injury occurs when damage affects the facial nerve outside the skull base, usually due to trauma from cuts, blunt force, or surgical procedures in the parotid gland or neck region. The injury may result in weakness or paralysis on one side of the face, known as Bell's palsy, and may also impact taste sensation and salivary function.
2. Central facial nerve injury: This type of injury occurs when damage affects the facial nerve within the skull base, often due to stroke, brain tumors, or traumatic brain injuries. Central facial nerve injuries typically result in weakness or paralysis only on the lower half of the face, as the upper motor neurons responsible for controlling the upper face receive innervation from both sides of the brain.
Treatment for facial nerve injuries depends on the severity and location of the damage. For mild to moderate injuries, physical therapy, protective eyewear, and medications like corticosteroids and antivirals may be prescribed. Severe cases might require surgical intervention, such as nerve grafts or muscle transfers, to restore function. In some instances, facial nerve injuries may heal on their own over time, particularly when the injury is mild and there is no ongoing compression or tension on the nerve.
Facial muscles, also known as facial nerves or cranial nerve VII, are a group of muscles responsible for various expressions and movements of the face. These muscles include:
1. Orbicularis oculi: muscle that closes the eyelid and raises the upper eyelid
2. Corrugator supercilii: muscle that pulls the eyebrows down and inward, forming wrinkles on the forehead
3. Frontalis: muscle that raises the eyebrows and forms horizontal wrinkles on the forehead
4. Procerus: muscle that pulls the medial ends of the eyebrows downward, forming vertical wrinkles between the eyebrows
5. Nasalis: muscle that compresses or dilates the nostrils
6. Depressor septi: muscle that pulls down the tip of the nose
7. Levator labii superioris alaeque nasi: muscle that raises the upper lip and flares the nostrils
8. Levator labii superioris: muscle that raises the upper lip
9. Zygomaticus major: muscle that raises the corner of the mouth, producing a smile
10. Zygomaticus minor: muscle that raises the nasolabial fold and corner of the mouth
11. Risorius: muscle that pulls the angle of the mouth laterally, producing a smile
12. Depressor anguli oris: muscle that pulls down the angle of the mouth
13. Mentalis: muscle that raises the lower lip and forms wrinkles on the chin
14. Buccinator: muscle that retracts the cheek and helps with chewing
15. Platysma: muscle that depresses the corner of the mouth and wrinkles the skin of the neck.
These muscles are innervated by the facial nerve, which arises from the brainstem and exits the skull through the stylomastoid foramen. Damage to the facial nerve can result in facial paralysis or weakness on one or both sides of the face.
Myositis is a medical term that refers to inflammation of the muscle tissue. This condition can cause various symptoms, including muscle weakness, pain, swelling, and stiffness. There are several types of myositis, such as polymyositis, dermatomyositis, and inclusion body myositis, which have different causes and characteristics.
Polymyositis is a type of myositis that affects multiple muscle groups, particularly those close to the trunk of the body. Dermatomyositis is characterized by muscle inflammation as well as a skin rash. Inclusion body myositis is a less common form of myositis that typically affects older adults and can cause both muscle weakness and wasting.
The causes of myositis vary depending on the type, but they can include autoimmune disorders, infections, medications, and other medical conditions. Treatment for myositis may involve medication to reduce inflammation, physical therapy to maintain muscle strength and flexibility, and lifestyle changes to manage symptoms and prevent complications.