This document provides detailed information on the anatomy and function of the facial nerve. It discusses the various parts of the facial nerve from its origin in the brainstem through its entire course. Key points include descriptions of the motor and sensory nuclei in the pons, the three parts of the facial nerve (intracranial, intratemporal, extracranial), its pathways through the fallopian canal and mastoid bone. Branches such as the chorda tympani are also outlined. Clinical disorders that can affect the facial nerve like Bell's palsy are summarized.
This document provides information on the surgical anatomy of the facial nerve. It begins with an introduction to the facial nerve and its functional components and nuclei. It then describes the different parts of the facial nerve from its intracranial portion to its extra-temporal portion in the neck. Several clinical considerations are discussed, including Bell's palsy, Ramsay Hunt syndrome, and Guillain-Barre syndrome. Surgical techniques for facial nerve repair are outlined, including nerve grafting and substitution techniques like hypoglossal-facial nerve crossover. In summary, this document details the anatomy and clinical implications of the facial nerve as well as surgical strategies for repairing injuries to this nerve.
Clinical anatomy of facial nerve and facial nerve palsy Ramesh Parajuli
The facial nerve is a mixed nerve that originates in the brainstem and has motor, sensory, and parasympathetic functions. It has several segments as it exits the brainstem and travels through the skull and internal auditory canal before exiting behind the ear. It gives off several branches and terminates in branches that innervate the muscles of facial expression. Facial nerve palsy can result from various causes like Bell's palsy, trauma, infection, tumors, or iatrogenic injuries. Clinical assessment and electrical tests can localize the site of injury which guides management including medications, physical therapy, or surgical interventions like decompression or repair.
The facial nerve has both sensory and motor components. It has nuclei in the pons that control muscles of facial expression, lacrimal and salivary glands, and taste sensation on the anterior tongue. The facial nerve exits the skull through the stylomastoid foramen and divides into branches that innervate muscles of the face, scalp and neck including the orbicularis oculi and orbicularis oris. It also communicates with adjacent cranial and spinal nerves to coordinate movements between branchial arches.
This document provides an overview of the muscles of the face. It begins with an introduction and outlines the various groupings of facial muscles, including topographic and functional groupings. It then describes each individual muscle in detail, covering origins, insertions, blood supply, nerve supply, and actions. Examples are given of how facial muscles contribute to different expressions. Clinical applications including facial paralysis and use of botulinum toxin injections are discussed. The document concludes with a brief section on skin tension lines and wrinkles.
The document discusses the muscles of facial expression (mimetic muscles) that are innervated by the facial nerve (cranial nerve VII). It describes the various muscle groups - orbicular, nasal, oral and others. It details each individual muscle, their origin, insertion and function. The document also discusses applied anatomy concepts like Bell's palsy, Parkinson's disease, Ramsay Hunt syndrome and others where these facial muscles are involved. It provides clinical features and diagnostic evaluation for certain conditions. Overall, the document is a detailed overview of the facial expression muscles, their function and involvement in various clinical scenarios.
This document provides an overview of facial nerve anatomy and management of Bell's palsy. It discusses the nuclei of origin, course, and branches of the facial nerve. Key points include that the facial nerve has motor and sensory roots that join to form the facial trunk. It passes through the internal acoustic meatus and facial canal before exiting through the stylomastoid foramen. The nerve then divides into five terminal branches that innervate facial muscles. Management of Bell's palsy focuses on these branches to restore facial expression. The document provides detailed information on the anatomy and function of the facial nerve and muscles.
The document discusses the facial nerve (cranial nerve VII) in three paragraphs or less:
The facial nerve controls muscles of the face and allows for facial expressions. It has both motor and sensory components that originate from different embryonic structures and nuclei. The nerve exits the skull through the stylomastoid foramen and gives off five terminal branches innervating various facial muscles. Facial nerve palsy can result from lesions along the nerve's course and have varying clinical presentations depending on the location of injury. Common causes include Bell's palsy, tumors, trauma, and infections. Differential diagnosis and management involve identifying the underlying etiology.
The facial nerve is a mixed nerve that arises from nuclei in the brainstem and controls muscles of facial expression. It has both motor and sensory functions. Clinically, facial nerve disorders can result in facial paralysis and loss of taste sensation on the anterior tongue. Evaluation involves physical examination and electrodiagnostic testing to localize the lesion. Bell's palsy is the most common cause of acute facial paralysis and typically resolves on its own, while Ramsay Hunt syndrome causes paralysis along with ear symptoms from varicella zoster virus reactivation.
This document provides information on the surgical anatomy of the facial nerve. It begins with an introduction to the facial nerve and its functional components and nuclei. It then describes the different parts of the facial nerve from its intracranial portion to its extra-temporal portion in the neck. Several clinical considerations are discussed, including Bell's palsy, Ramsay Hunt syndrome, and Guillain-Barre syndrome. Surgical techniques for facial nerve repair are outlined, including nerve grafting and substitution techniques like hypoglossal-facial nerve crossover. In summary, this document details the anatomy and clinical implications of the facial nerve as well as surgical strategies for repairing injuries to this nerve.
Clinical anatomy of facial nerve and facial nerve palsy Ramesh Parajuli
The facial nerve is a mixed nerve that originates in the brainstem and has motor, sensory, and parasympathetic functions. It has several segments as it exits the brainstem and travels through the skull and internal auditory canal before exiting behind the ear. It gives off several branches and terminates in branches that innervate the muscles of facial expression. Facial nerve palsy can result from various causes like Bell's palsy, trauma, infection, tumors, or iatrogenic injuries. Clinical assessment and electrical tests can localize the site of injury which guides management including medications, physical therapy, or surgical interventions like decompression or repair.
The facial nerve has both sensory and motor components. It has nuclei in the pons that control muscles of facial expression, lacrimal and salivary glands, and taste sensation on the anterior tongue. The facial nerve exits the skull through the stylomastoid foramen and divides into branches that innervate muscles of the face, scalp and neck including the orbicularis oculi and orbicularis oris. It also communicates with adjacent cranial and spinal nerves to coordinate movements between branchial arches.
This document provides an overview of the muscles of the face. It begins with an introduction and outlines the various groupings of facial muscles, including topographic and functional groupings. It then describes each individual muscle in detail, covering origins, insertions, blood supply, nerve supply, and actions. Examples are given of how facial muscles contribute to different expressions. Clinical applications including facial paralysis and use of botulinum toxin injections are discussed. The document concludes with a brief section on skin tension lines and wrinkles.
The document discusses the muscles of facial expression (mimetic muscles) that are innervated by the facial nerve (cranial nerve VII). It describes the various muscle groups - orbicular, nasal, oral and others. It details each individual muscle, their origin, insertion and function. The document also discusses applied anatomy concepts like Bell's palsy, Parkinson's disease, Ramsay Hunt syndrome and others where these facial muscles are involved. It provides clinical features and diagnostic evaluation for certain conditions. Overall, the document is a detailed overview of the facial expression muscles, their function and involvement in various clinical scenarios.
This document provides an overview of facial nerve anatomy and management of Bell's palsy. It discusses the nuclei of origin, course, and branches of the facial nerve. Key points include that the facial nerve has motor and sensory roots that join to form the facial trunk. It passes through the internal acoustic meatus and facial canal before exiting through the stylomastoid foramen. The nerve then divides into five terminal branches that innervate facial muscles. Management of Bell's palsy focuses on these branches to restore facial expression. The document provides detailed information on the anatomy and function of the facial nerve and muscles.
The document discusses the facial nerve (cranial nerve VII) in three paragraphs or less:
The facial nerve controls muscles of the face and allows for facial expressions. It has both motor and sensory components that originate from different embryonic structures and nuclei. The nerve exits the skull through the stylomastoid foramen and gives off five terminal branches innervating various facial muscles. Facial nerve palsy can result from lesions along the nerve's course and have varying clinical presentations depending on the location of injury. Common causes include Bell's palsy, tumors, trauma, and infections. Differential diagnosis and management involve identifying the underlying etiology.
The facial nerve is a mixed nerve that arises from nuclei in the brainstem and controls muscles of facial expression. It has both motor and sensory functions. Clinically, facial nerve disorders can result in facial paralysis and loss of taste sensation on the anterior tongue. Evaluation involves physical examination and electrodiagnostic testing to localize the lesion. Bell's palsy is the most common cause of acute facial paralysis and typically resolves on its own, while Ramsay Hunt syndrome causes paralysis along with ear symptoms from varicella zoster virus reactivation.
The facial nerve arises from nuclei in the brainstem and travels through the temporal bone, where it is vulnerable to injury. It innervates the muscles of facial expression and provides motor, sensory, and autonomic functions. Bell's palsy is an acute onset idiopathic peripheral facial nerve palsy that typically recovers within 3 weeks with treatment such as corticosteroids and antivirals.
This document provides an overview of the anatomy and embryology of the facial nerve (cranial nerve VII). It discusses the nuclei of origin, functional components, course through the skull and branches/distribution. Key points include that the facial nerve has motor, secretomotor and sensory fibers and exits the skull via the stylomastoid foramen. It describes associated ganglia like the geniculate ganglion and presents variations, disorders like Bell's palsy, and evaluation methods involving tests of motor/sensory function.
The facial nerve emerges from the brainstem and controls facial muscle expression. It has motor, sensory, and parasympathetic components. The nerve passes through the internal auditory canal into the middle ear. It can be injured through temporal bone fractures, surgery, Bell's palsy, or trauma. Facial nerve injuries are classified using the Sunderland or House-Brackmann system to describe the severity and prognosis. Physical exam involves testing facial muscle function to localize the site of injury.
This document discusses the anatomy of the face, including boundaries, skin layers, fascia, muscles, nerves, arteries, veins, and lymphatic drainage. It describes key facial muscles like the orbicularis oculi and orbicularis oris. The motor innervation of the face is outlined, with the facial nerve supplying muscles. The arterial blood supply is dominated by the facial artery. Applied anatomy concepts like Bell's palsy and trigeminal neuralgia are also briefly mentioned.
The document describes the anatomy of several areas of the face and head including the mandible, temporomandibular joint, outer, middle, and inner ear, nose, throat, oral cavity, eye, and basic jaw muscles. It provides detailed descriptions of the bones, cartilages, tissues, glands, and other structures that make up each anatomical area. Key structures are defined along with their functions in hearing, balance, facial movement, breathing, smell, taste, sight, and chewing.
facial nerve is the seventh cranial nerve supplies the submandibular, sublingual, lacrimal glands, the mucosal glands of the nose, palate, pharynx and taste fibres, and on being injured it leads to loss of lacrimation, loss of salivation, loss of taste sensation and paralysis of the muscles of facial expression.
The facial nerve is a mixed nerve that originates in the brainstem and has multiple branches that innervate muscles of facial expression and provide motor, sensory, parasympathetic, and taste functions. It exits the skull through the internal acoustic meatus and stylomastoid foramen, giving off branches along its course like the chorda tympani nerve. The facial nerve has motor, sensory, parasympathetic, and special sensory components that allow for facial muscle movement and provide various sensory functions like taste.
This document provides an overview of the facial nerve (cranial nerve VII) including its embryology, anatomy, course, branches and associated ganglia. It begins with a basic introduction and outlines the nuclei of origin in the brainstem. It then describes the facial nerve's course through six segments from the brainstem to the branches in the face. Several associated ganglia are also detailed, including the geniculate, submandibular and pterygopalatine ganglia. Congenital disorders involving the facial nerve are reviewed. Throughout, clinical relevance and applications to surgery are discussed.
The facial nerve has three nuclei and contains approximately 10,000 fibers. It exits the brainstem at the pontomedullary junction and travels through the internal acoustic meatus and fallopian canal. It has motor, parasympathetic, and sensory functions. Facial nerve palsy can result from various causes such as Bell's palsy, tumors, fractures, or inflammation. Diagnosis involves evaluating for signs of upper vs. lower motor neuron involvement. Treatment depends on the cause but may include corticosteroids, antivirals, or decompression surgery.
The facial nerve is the seventh cranial nerve that emerges from the brainstem and supplies motor innervation to the muscles of facial expression. It has three parts - a motor root, an intermedius nerve that carries taste and parasympathetic fibers, and branches that innervate the muscles of the face and neck. The facial nerve travels through the internal acoustic meatus, has three segments within the facial canal, and exits the skull through the stylomastoid foramen before branching within the parotid gland and terminating on individual facial muscles.
This document discusses the anatomy and surgical applications of the facial nerve. It begins with the basic anatomy and branches of the facial nerve. It then covers variations in branching patterns and surgical landmarks. It discusses differences between upper and lower motor neuron lesions. The remainder covers diagnostic tests, grading systems, medical and surgical management of facial nerve disorders including various repair and grafting techniques. Surgical procedures discussed include direct nerve repair, nerve grafting, cross facial nerve grafting and nerve crossovers using hypoglossal or spinal accessory nerves.
This document discusses the motor nerve supply of the face, with a focus on the facial nerve. It describes the anatomy and branches of the facial nerve in detail. Key points include that the facial nerve emerges from the brainstem between the pons and medulla, has motor, sensory and parasympathetic components, and gives off branches like the chorda tympani and greater petrosal nerve. The document outlines the course of the facial nerve through the skull and discusses its distribution and functional components. Surgical implications and complications of facial nerve injury during parotid surgery are also summarized.
This document provides an overview of the facial nerve (cranial nerve VII). It begins with definitions of nerves and nerve conduction. It then discusses the classification of the nervous system and provides an introduction to the facial nerve. The remainder of the document details the embryology, nuclei of origin, functional components, course, branches and distribution, ganglia, blood supply, surgical anatomy, applied aspects, and conclusion of the facial nerve. It provides diagrams and explanations of these various aspects of the facial nerve's anatomy and function.
The document discusses the anatomy of the muscles of facial expression and related structures. It can be summarized as follows:
1. The muscles of facial expression arise from the second branchial arch and are innervated by the facial nerve (CN VII). They allow for facial movements and expressions.
2. The main muscles involved include the frontalis, orbicularis oculi, corrugator supercilii, nasalis, orbicularis oris, and zygomaticus major and minor.
3. The facial artery and veins course through the face, supplying and draining the muscles and overlying skin. The arteries anastomose to provide redundant blood flow.
4. The facial
1. The face contains 17 muscles that are innervated by the facial nerve (CN VII) and control facial expressions. These include muscles around the eyes, nose, mouth, and other areas.
2. Damage to the facial nerve can cause total paralysis of the muscles on one side of the face, as seen in Bell's palsy. This prevents blinking, smiling, eye closing and other facial movements.
3. The orbicularis oculi muscle around the eye is important, as injury can cause ectropion where the lower eyelid droops and epip
Muscles of Fascial Expressions discusses the anatomy and development of facial muscles. It describes the origins, insertions, actions and nerve supply of each muscle. Examples of clinical conditions involving facial muscles are also provided, such as Bell's palsy (facial nerve paralysis), hemifacial spasm (involuntary muscle contractions on one side of face), and facioscapulohumeral muscular dystrophy (muscle weakness and wasting affecting face, shoulder blades and arms).
Facial nerve and its extracranial and intracranial rotssonambohra2
facial nerve its origin and insertion and its extracranial and intracranial roots and its branches and clinical significance and its related syndromes explained well along with treatment plan
The facial nerve develops from the second pharyngeal arch during gestation. It carries motor, sensory and parasympathetic fibers that innervate muscles of facial expression and glands. Bell's palsy is a temporary paralysis of the facial nerve causing drooping of the eyelid and mouth. It is diagnosed based on symptoms and ruled out other causes through tests. Treatment includes antiviral drugs, corticosteroids, facial exercises and physical therapy.
The facial nerve arises from nuclei in the brainstem and travels through the temporal bone, where it is vulnerable to injury. It innervates the muscles of facial expression and provides motor, sensory, and autonomic functions. Bell's palsy is an acute onset idiopathic peripheral facial nerve palsy that typically recovers within 3 weeks with treatment such as corticosteroids and antivirals.
This document provides an overview of the anatomy and embryology of the facial nerve (cranial nerve VII). It discusses the nuclei of origin, functional components, course through the skull and branches/distribution. Key points include that the facial nerve has motor, secretomotor and sensory fibers and exits the skull via the stylomastoid foramen. It describes associated ganglia like the geniculate ganglion and presents variations, disorders like Bell's palsy, and evaluation methods involving tests of motor/sensory function.
The facial nerve emerges from the brainstem and controls facial muscle expression. It has motor, sensory, and parasympathetic components. The nerve passes through the internal auditory canal into the middle ear. It can be injured through temporal bone fractures, surgery, Bell's palsy, or trauma. Facial nerve injuries are classified using the Sunderland or House-Brackmann system to describe the severity and prognosis. Physical exam involves testing facial muscle function to localize the site of injury.
This document discusses the anatomy of the face, including boundaries, skin layers, fascia, muscles, nerves, arteries, veins, and lymphatic drainage. It describes key facial muscles like the orbicularis oculi and orbicularis oris. The motor innervation of the face is outlined, with the facial nerve supplying muscles. The arterial blood supply is dominated by the facial artery. Applied anatomy concepts like Bell's palsy and trigeminal neuralgia are also briefly mentioned.
The document describes the anatomy of several areas of the face and head including the mandible, temporomandibular joint, outer, middle, and inner ear, nose, throat, oral cavity, eye, and basic jaw muscles. It provides detailed descriptions of the bones, cartilages, tissues, glands, and other structures that make up each anatomical area. Key structures are defined along with their functions in hearing, balance, facial movement, breathing, smell, taste, sight, and chewing.
facial nerve is the seventh cranial nerve supplies the submandibular, sublingual, lacrimal glands, the mucosal glands of the nose, palate, pharynx and taste fibres, and on being injured it leads to loss of lacrimation, loss of salivation, loss of taste sensation and paralysis of the muscles of facial expression.
The facial nerve is a mixed nerve that originates in the brainstem and has multiple branches that innervate muscles of facial expression and provide motor, sensory, parasympathetic, and taste functions. It exits the skull through the internal acoustic meatus and stylomastoid foramen, giving off branches along its course like the chorda tympani nerve. The facial nerve has motor, sensory, parasympathetic, and special sensory components that allow for facial muscle movement and provide various sensory functions like taste.
This document provides an overview of the facial nerve (cranial nerve VII) including its embryology, anatomy, course, branches and associated ganglia. It begins with a basic introduction and outlines the nuclei of origin in the brainstem. It then describes the facial nerve's course through six segments from the brainstem to the branches in the face. Several associated ganglia are also detailed, including the geniculate, submandibular and pterygopalatine ganglia. Congenital disorders involving the facial nerve are reviewed. Throughout, clinical relevance and applications to surgery are discussed.
The facial nerve has three nuclei and contains approximately 10,000 fibers. It exits the brainstem at the pontomedullary junction and travels through the internal acoustic meatus and fallopian canal. It has motor, parasympathetic, and sensory functions. Facial nerve palsy can result from various causes such as Bell's palsy, tumors, fractures, or inflammation. Diagnosis involves evaluating for signs of upper vs. lower motor neuron involvement. Treatment depends on the cause but may include corticosteroids, antivirals, or decompression surgery.
The facial nerve is the seventh cranial nerve that emerges from the brainstem and supplies motor innervation to the muscles of facial expression. It has three parts - a motor root, an intermedius nerve that carries taste and parasympathetic fibers, and branches that innervate the muscles of the face and neck. The facial nerve travels through the internal acoustic meatus, has three segments within the facial canal, and exits the skull through the stylomastoid foramen before branching within the parotid gland and terminating on individual facial muscles.
This document discusses the anatomy and surgical applications of the facial nerve. It begins with the basic anatomy and branches of the facial nerve. It then covers variations in branching patterns and surgical landmarks. It discusses differences between upper and lower motor neuron lesions. The remainder covers diagnostic tests, grading systems, medical and surgical management of facial nerve disorders including various repair and grafting techniques. Surgical procedures discussed include direct nerve repair, nerve grafting, cross facial nerve grafting and nerve crossovers using hypoglossal or spinal accessory nerves.
This document discusses the motor nerve supply of the face, with a focus on the facial nerve. It describes the anatomy and branches of the facial nerve in detail. Key points include that the facial nerve emerges from the brainstem between the pons and medulla, has motor, sensory and parasympathetic components, and gives off branches like the chorda tympani and greater petrosal nerve. The document outlines the course of the facial nerve through the skull and discusses its distribution and functional components. Surgical implications and complications of facial nerve injury during parotid surgery are also summarized.
This document provides an overview of the facial nerve (cranial nerve VII). It begins with definitions of nerves and nerve conduction. It then discusses the classification of the nervous system and provides an introduction to the facial nerve. The remainder of the document details the embryology, nuclei of origin, functional components, course, branches and distribution, ganglia, blood supply, surgical anatomy, applied aspects, and conclusion of the facial nerve. It provides diagrams and explanations of these various aspects of the facial nerve's anatomy and function.
The document discusses the anatomy of the muscles of facial expression and related structures. It can be summarized as follows:
1. The muscles of facial expression arise from the second branchial arch and are innervated by the facial nerve (CN VII). They allow for facial movements and expressions.
2. The main muscles involved include the frontalis, orbicularis oculi, corrugator supercilii, nasalis, orbicularis oris, and zygomaticus major and minor.
3. The facial artery and veins course through the face, supplying and draining the muscles and overlying skin. The arteries anastomose to provide redundant blood flow.
4. The facial
1. The face contains 17 muscles that are innervated by the facial nerve (CN VII) and control facial expressions. These include muscles around the eyes, nose, mouth, and other areas.
2. Damage to the facial nerve can cause total paralysis of the muscles on one side of the face, as seen in Bell's palsy. This prevents blinking, smiling, eye closing and other facial movements.
3. The orbicularis oculi muscle around the eye is important, as injury can cause ectropion where the lower eyelid droops and epip
Muscles of Fascial Expressions discusses the anatomy and development of facial muscles. It describes the origins, insertions, actions and nerve supply of each muscle. Examples of clinical conditions involving facial muscles are also provided, such as Bell's palsy (facial nerve paralysis), hemifacial spasm (involuntary muscle contractions on one side of face), and facioscapulohumeral muscular dystrophy (muscle weakness and wasting affecting face, shoulder blades and arms).
Facial nerve and its extracranial and intracranial rotssonambohra2
facial nerve its origin and insertion and its extracranial and intracranial roots and its branches and clinical significance and its related syndromes explained well along with treatment plan
The facial nerve develops from the second pharyngeal arch during gestation. It carries motor, sensory and parasympathetic fibers that innervate muscles of facial expression and glands. Bell's palsy is a temporary paralysis of the facial nerve causing drooping of the eyelid and mouth. It is diagnosed based on symptoms and ruled out other causes through tests. Treatment includes antiviral drugs, corticosteroids, facial exercises and physical therapy.
The facial nerve is the longest nerve in the bony canal. It contains both sensory and motor fibers and innervates the muscles of facial expression. The nerve develops from the second branchial arch and has nuclei in the lower pons connected to four nuclei. It exits the skull through the stylomastoid foramen and divides into branches in the parotid gland. The zygomatic and buccal branches are at risk during surgery on the zygomatic arch and cheek. Facial nerve paralysis can occur from lesions at different levels and have varying clinical presentations such as in Bell's palsy. Care must be taken during parotid and temporal bone surgeries due to the nerve's anatomy.
The document discusses the facial nerve (cranial nerve VII) in three sentences:
It originates in the brainstem and is a mixed nerve that controls facial muscle movement and taste sensation. It exits the skull through the stylomastoid foramen and gives off several branches as it passes through the parotid gland to innervate facial muscles. Disorders of the facial nerve can occur from various causes such as trauma, infections like Bell's palsy, or tumors and result in paralysis of the muscles on the same side of the face.
anatomy of facial nerve by tejpl singh.pptxAkanshaVerma97
The facial nerve is the 7th cranial nerve that has both motor and sensory components. It has a long intraosseous course through the skull bones. It originates in the brainstem and has nuclei in the pons. It travels through the cranial cavity, internal auditory canal, fallopian canal and exits through the stylomastoid foramen. It then divides in the parotid gland to innervate the muscles of facial expression. Key landmarks help identify the nerve during surgery including the processes cochleariform, incus, and pyramidal eminence. Supranuclear and infranuclear lesions cause different patterns of facial paralysis.
facial nerve is the 7th cranial nerve. it supplies the parts of the face and also the muscles of mastication. it helps in the expression of the face too.
The document describes the anatomy and function of the facial nerve (CN VII). It begins with the nuclei of origin in the brainstem and describes the intracrannial course through the facial canal. It then details the extracranial course through the parotid gland and branches to various muscles. The facial nerve is responsible for motor innervation to muscles of facial expression and neck, and also carries special sensory fibers for taste via the chorda tympani and parasympathetic fibers to glands. Damage to different parts of the facial nerve results in varied clinical deficits depending on the branches affected. Bell's palsy is described as the most common cause of facial paralysis with unknown etiology.
The facial nerve is the 7th cranial nerve with motor, parasympathetic, and sensory components. It has nuclei in the pons and medulla. The nerve exits the pons and travels through the internal acoustic meatus into the Fallopian canal. It gives off branches like the chorda tympani and exits at the stylomastoid foramen. Damage can cause Bell's palsy or Ramsay Hunt syndrome. Studies have mapped the nerve's relationship to anatomical landmarks to safely guide surgery on structures like the mandible and zygomatic arch.
This document provides information on the muscles of facial expression. It begins with an introduction to the facial musculature and its development. It then categorizes the muscles topographically and provides detailed anatomy of each muscle, including origin, insertion, vascular supply, innervation and action. Examples of facial expressions resulting from different muscle activations are summarized. Finally, some applied aspects are discussed, such as the modiolus and conditions affecting facial muscles like Myasthenia Gravis and Bell's Palsy.
The document discusses the embryological development of the facial nerve from the 3rd week of life through birth. It begins as the facioacoustic primordium in the 3rd week and develops further each week. By the 7th week the main branches are identifiable and multiple facial muscles have appeared. The facial nerve exits the skull at birth through the stylomastoid foramen but this moves medially with age. The anatomy and course of the facial nerve within the skull is also summarized, including its segments within the internal auditory canal and facial canal.
The facial nerve is the 7th cranial nerve. It is a mixed nerve that innervates the muscles of facial expression and provides sensory innervation to the face and taste sensation to the anterior two thirds of the tongue. During development, the facial nerve and muscles of facial expression differentiate between weeks 3-12 of gestation. Anatomically, the facial nerve has intracranial, intratemporal, and extracranial segments. In the parotid gland, it divides into temporal, zygomatic, buccal, marginal mandibular, and cervical branches which innervate the muscles of facial expression. The facial nerve is vulnerable in certain segments such as the mastoid and tympanic
FACIAL NERVE AND IT'S APPLIED ANATOMY AND IT'S SIGNIFICANCE FOR A DENTIST ALONG WITH THE CAUTIONS TO AVOID AN IATROGENIC INJURY TO FACIAL NERVE AND THE MANAGEMENT OF A PATIENT OF FACIAL NERVE DISORDER DURING ENDODONTIC PROCEDURES
The facial nerve (CN VII) is responsible for facial muscle movement and taste. It originates in the brainstem and travels through the facial canal in the temporal bone. The main branches innervate the muscles of facial expression. Facial paralysis can occur from lesions at different levels and have varying clinical presentations. Bell's palsy is an idiopathic acute facial paralysis that usually resolves over time with treatment. Evaluation and management depends on the severity and cause of injury.
Facial nerve and its applied aspect - seminar 3 [Autosaved].pptxdrpriyanka8
The document discusses the facial nerve (cranial nerve VII). It begins by classifying it as a mixed nerve that is predominantly motor and supplies the muscles of facial expression. It then covers the functional components and nuclei of the nerve, its intracranial and extracranial courses through various canals and foramina, its branches and distribution to various structures like the lacrimal gland and muscles of facial expression, clinical tests of its function, and applied aspects like Bell's palsy and Ramsay Hunt syndrome.
Anatomy(2) The skull and face The temporal region Infratemporal and pterygopa...Hamzeh AlBattikhi
This document provides an overview of the anatomy of the scalp, face, and temporal region. It describes the layers of the scalp including the skin, connective tissue, aponeurosis, and pericranium. It details the muscles of the scalp including the occipitofrontalis. It discusses the sensory and vascular supply as well as lymph drainage of the scalp. It then describes the bones, muscles, nerves, vessels, and lymph drainage of the face. Finally, it briefly mentions that the temporal region is located on the side of the head and contains the temporal lobe of the brain.
This document discusses the anatomy and functional components of the facial nerve (cranial nerve VII). It describes the course and branches of the facial nerve from its nuclei in the brainstem through the temporal bone. Key points include that the facial nerve has both motor and sensory fibers, and innervates the muscles of facial expression as well as the lacrimal and salivary glands. Tests to localize lesions of the facial nerve include the Schirmer test for lacrimation, stapedius reflex test, and taste/electrogustometry testing.
The trigeminal nerve is the 5th cranial nerve and is a mixed nerve responsible for sensation in the face and motor function of the muscles of mastication. It has 3 major divisions - the ophthalmic, maxillary, and mandibular nerves. The ophthalmic nerve provides sensory innervation to the upper face and eye region. The maxillary nerve provides sensory innervation to the mid face region including the maxillary teeth. The mandibular nerve provides sensory innervation to the lower face and motor innervation to the muscles of mastication.
The facial nerve originates from the brainstem and has both motor and sensory functions. It has 5 segments as it passes through the temporal bone: intracranial, meatal, labyrinthine, tympanic, and mastoid. Key landmarks help identify the nerve's location during middle ear and parotid surgery. The nerve gives off branches like the chorda tympani before terminating in 5 branches that innervate facial muscles. Precise knowledge of the facial nerve's anatomy is important for preventing injury during otologic and parotid procedures.
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Computer in pharmaceutical research and development-Mpharm(Pharmaceutics)MuskanShingari
Statistics- Statistics is the science of collecting, organizing, presenting, analyzing and interpreting numerical data to assist in making more effective decisions.
A statistics is a measure which is used to estimate the population parameter
Parameters-It is used to describe the properties of an entire population.
Examples-Measures of central tendency Dispersion, Variance, Standard Deviation (SD), Absolute Error, Mean Absolute Error (MAE), Eigen Value
Pictorial and detailed description of patellar instability with sign and symptoms and how to diagnose , what investigations you should go with and how to approach with treatment options . I have presented this slide in my 2nd year junior residency in orthopedics at LLRM medical college Meerut and got good reviews for it
After getting it read you will definitely understand the topic.
Discover the benefits of homeopathic medicine for irregular periods with our guide on 5 common remedies. Learn how these natural treatments can help regulate menstrual cycles and improve overall menstrual health.
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TEST BANK For Brunner and Suddarth's Textbook of Medical-Surgical Nursing, 14...Donc Test
TEST BANK For Brunner and Suddarth's Textbook of Medical-Surgical Nursing, 14th Edition (Hinkle, 2017) Verified Chapter's 1 - 73 Complete.pdf
TEST BANK For Brunner and Suddarth's Textbook of Medical-Surgical Nursing, 14th Edition (Hinkle, 2017) Verified Chapter's 1 - 73 Complete.pdf
TEST BANK For Brunner and Suddarth's Textbook of Medical-Surgical Nursing, 14th Edition (Hinkle, 2017) Verified Chapter's 1 - 73 Complete.pdf
Nano-gold for Cancer Therapy chemistry investigatory projectSIVAVINAYAKPK
chemistry investigatory project
The development of nanogold-based cancer therapy could revolutionize oncology by providing a more targeted, less invasive treatment option. This project contributes to the growing body of research aimed at harnessing nanotechnology for medical applications, paving the way for future clinical trials and potential commercial applications.
Cancer remains one of the leading causes of death worldwide, prompting the need for innovative treatment methods. Nanotechnology offers promising new approaches, including the use of gold nanoparticles (nanogold) for targeted cancer therapy. Nanogold particles possess unique physical and chemical properties that make them suitable for drug delivery, imaging, and photothermal therapy.
Breast cancer: Post menopausal endocrine therapyDr. Sumit KUMAR
Breast cancer in postmenopausal women with hormone receptor-positive (HR+) status is a common and complex condition that necessitates a multifaceted approach to management. HR+ breast cancer means that the cancer cells grow in response to hormones such as estrogen and progesterone. This subtype is prevalent among postmenopausal women and typically exhibits a more indolent course compared to other forms of breast cancer, which allows for a variety of treatment options.
Diagnosis and Staging
The diagnosis of HR+ breast cancer begins with clinical evaluation, imaging, and biopsy. Imaging modalities such as mammography, ultrasound, and MRI help in assessing the extent of the disease. Histopathological examination and immunohistochemical staining of the biopsy sample confirm the diagnosis and hormone receptor status by identifying the presence of estrogen receptors (ER) and progesterone receptors (PR) on the tumor cells.
Staging involves determining the size of the tumor (T), the involvement of regional lymph nodes (N), and the presence of distant metastasis (M). The American Joint Committee on Cancer (AJCC) staging system is commonly used. Accurate staging is critical as it guides treatment decisions.
Treatment Options
Endocrine Therapy
Endocrine therapy is the cornerstone of treatment for HR+ breast cancer in postmenopausal women. The primary goal is to reduce the levels of estrogen or block its effects on cancer cells. Commonly used agents include:
Selective Estrogen Receptor Modulators (SERMs): Tamoxifen is a SERM that binds to estrogen receptors, blocking estrogen from stimulating breast cancer cells. It is effective but may have side effects such as increased risk of endometrial cancer and thromboembolic events.
Aromatase Inhibitors (AIs): These drugs, including anastrozole, letrozole, and exemestane, lower estrogen levels by inhibiting the aromatase enzyme, which converts androgens to estrogen in peripheral tissues. AIs are generally preferred in postmenopausal women due to their efficacy and safety profile compared to tamoxifen.
Selective Estrogen Receptor Downregulators (SERDs): Fulvestrant is a SERD that degrades estrogen receptors and is used in cases where resistance to other endocrine therapies develops.
Combination Therapies
Combining endocrine therapy with other treatments enhances efficacy. Examples include:
Endocrine Therapy with CDK4/6 Inhibitors: Palbociclib, ribociclib, and abemaciclib are CDK4/6 inhibitors that, when combined with endocrine therapy, significantly improve progression-free survival in advanced HR+ breast cancer.
Endocrine Therapy with mTOR Inhibitors: Everolimus, an mTOR inhibitor, can be added to endocrine therapy for patients who have developed resistance to aromatase inhibitors.
Chemotherapy
Chemotherapy is generally reserved for patients with high-risk features, such as large tumor size, high-grade histology, or extensive lymph node involvement. Regimens often include anthracyclines and taxanes.
“Psychiatry and the Humanities”: An Innovative Course at the University of Mo...Université de Montréal
“Psychiatry and the Humanities”: An Innovative Course at the University of Montreal Expanding the medical model to embrace the humanities. Link: https://www.psychiatrictimes.com/view/-psychiatry-and-the-humanities-an-innovative-course-at-the-university-of-montreal
This presentation gives information on the pharmacology of Prostaglandins, Thromboxanes and Leukotrienes i.e. Eicosanoids. Eicosanoids are signaling molecules derived from polyunsaturated fatty acids like arachidonic acid. They are involved in complex control over inflammation, immunity, and the central nervous system. Eicosanoids are synthesized through the enzymatic oxidation of fatty acids by cyclooxygenase and lipoxygenase enzymes. They have short half-lives and act locally through autocrine and paracrine signaling.
2. Facial nerve is a mixed nerve (10,000 fibres)
motor root sensory root
(7000) (3000)
N. itermedius
Intracranial part (24mm)
Intratemporal part (28-30mm)
Extracranial part
3. Main Motor Nucleus
lies deep in the reticular formation of the lower part of the
pons.
The part of the nucleus that supplies the muscles of the
upper part of the face receives corticonuclear fibers from both
cerebral hemispheres.
The part of the nucleus that supplies the muscles of the
lower part of the face receives only corticonuclear fibers from
the opposite cerebral hemisphere.
4. • Motor Nuclei:
– Efferent fibers surround
nuclei of CN VI & form
small mounds on floor of 4th
ventricle
(facial colliculi)
• Exits at cerebellopontine angle
(CPA) Facial colliculus
5. Lie posterolateral to the main motor nucleus.
They are :
Superior salivatory nuclei: receives afferent
fibres from the hypothalamus through the
descending autonomic pathways. Information
concerning taste from the oral cavity received
from the nucleus of the solitary tract.
Lacrimal nuclei: receives afferent fibres from
the hypothalamus for emotional responses
and from the sensory nuclei of the trigeminal
nerve for reflex lacrimation secondary to
irritation of the cornea or conjunctiva.
6. It is the upper part of the nucleus of the tractus
solitarius and lies close to the motor nucleus
Sensations of taste travel through the peripheral
axons of nerve cells situated in the geniculate
ganglion on the seventh cranial nerve. The central
processes of these cells synapse on nerve cells in
the nucleus. Efferent fibres cross the median plane
and ascend to opposite thalamus and to a number
of hypothalamic nuclei. From the thalamus, the
axons of the thalamic cells pass through the
internal capsule and corona radiata to end in the
taste area of the cortex in the lower part of the
postcentral gyrus
7.
8.
9. Exits IAC via Fallopian canal
The facial nerve enters the
labyrinthine segment of its fallopian
canal through the meatal foramen,
which is the narrowest portion of
the entire canal and measures
approx. 0.68 mm in diameter.
The labyrinthine segment (4 mm in
length) makes up the first segment
of the bony fallopian canal and is
the narrowest and shortest portion
of the canal.
The labyrinthine segment is
posterocephalad to the cochlea,
anteromedial to the ampulla of the
superior semicircular canal, and
posterior to the vestibule.
Felt to be culprit in facial nerve
compression in Bell’s palsy & other
causes of nerve swelling
Fallopian Canal
10.
11. Progress to
geniculate ganglion
First genu
Start of tympanic
segment
◦ Gives rise to greater
superficial petrosal
nerve
Geniculate ganglion
12.
13. Fibers then course posteriorly under lateral semicircular canal in
middle ear (tympanic portion)
The prominence of the facial canal, lying above the posterior edge
of the promontory and the oval window, immediately below and
parallel to the prominence of the lateral semicircular canal. It runs
almost horizontally across the posterior half of the medial wall, then
turns to enter the posterior wall. The facial nerve courses through
the canal.
Tympanic Portion
14. MASTOID SEGMENT
Behind the base of the pyramidal
eminence the canal makes a broad
turn (second genu) to descend
vertically and somewhat laterally
through the mastoid process. In this
descending or vertical portion the
nerve may have a slight anterior
concavity. The canal normally lies
deep to the sutural groove between
the tympanic and mastoid portions
of the temporal bone.
Here last somatic & parasympathetic
fibers separate from facial nerve via
the chorda tympani nerve
The nerve exits through the
sytlomastoid foramen
Mastoid segment
15. Middle Ear and Mastoid Surgery:
◦ Processus cochleariformis
◦ Oval window and horizontal canal
◦ Short process of the incus
◦ Pyramid
16. Nerve exits stylomastoid foramen:
Facial nerve angles superiorly & anteriorly behind posterior
margin of vertical mandibular ramus
Postauricular nerve - external auricular and occipitofrontalis
muscles
Branches to the posterior belly of the digastric and stylohyoid
muscles
Enters parotid gland splitting it into a superficial and deep lobe
PES ANSERINUS
Temporal
Zygomatic
Buccal
Marginal mandibular
Cervical
17.
18. Parotid Surgery:
◦ Cartilaginous pointer
◦ Styloid process
◦ Posterior belly of digastric muscle
19. Small arteries derived from the
anteroinferior cerebellar branch of the
basilar artery,
The stylomastoid or occipital branches of
the external carotid, and
The petrosal arteries.
Insufficiency of the vascular supply to the
facial nerve, from whatever cause, is
regarded by some as one of the primary
causes of bell's palsy.
20. SVE (Special Visceral Efferent) — Motor to
striated muscles derived from the 2nd brachial
arch.
GVA (General Visceral Afferent) — Sensory
from visceral touch, temperature, and pain.
SVA (Special Visceral Afferent) — Taste
GVE (General Visceral Efferent) — Autonomic
innervation to mucosal, lacrimal, and salivary
glands.
GSA (General Somatic Afferent) — Sensory
from somatic touch, temperature, and pain.
21. Greater Superficial Petrosal Nerve (GSPN)
◦ GVA, GVE, SVA
Stapedial Nerve
◦ SVE
Chorda Tympani Nerve
◦ GVE, SVA
Posterior Auricular Nerve
◦ SVE, GSA
Facial Nerve (terminal branch)
◦ SVE
22. • Emerges from the geniculate
ganglion at the facial hiatus
and courses along the floor
of the middle cranial fossa
between layers of dura to
reach the foramen lacerum,
where it joins with the
carotid sympathetic nerves
to form the vidian nerve in
the vidian canal.
• After leaving the vidian
canal, they synapse with
postganglionic neurons in
the sphenopalatine ganglion
that innervate the lacrimal
gland and secretory glands
of the nose.
25. Innervation to muscles derived from the 2nd
branchial arch:
1. Stapedius muscle -- dampens movement of
the ossicles (inserts on stapes of middle ear)
2. Posterior auricular muscle -- posterior
movement of pinna
3. Stylohyoid muscle -- elevates hyoid bone
4. Posterior belly of digastric -- elevates hyoid
bone, depresses mandible
5. Muscles of facial expression -- blinking,
smiling, frowning, facial movements
26. Stapedius muscle dampens
movement of the ossicles
protecting the inner ear from
damage from loud noises
SVE
1. The Stapedius muscle dampens movement of the ossicles
27. The chorda tympani branch of the
facial nerve enters the middle ear
through the iter chordae posterius.
Passes forward and down between
the manubrium malleus and the long
process of the incus, then leaves the
cavity by passing through the
petrotympanic suture.
The chorda tympani has no function
in the middle ear. It contains both
parasympathetic fibres supplying the
submandibular and lingual glands
and taste fibres for the anterior two
third of the tongue.
After leaving the middle ear it joins
the lingual branch of V3 to be
distributed with that nerve.
28. Taste from the anterior
2/3 of the tongue
SVA
Chorda
tympani
32. Stylohyoid
muscle elevates
the hyoid bone.
Through the internal
Acoustic meatus
Through the
stylomastoid
foramen
The Stylohyoid muscle elevates the hyoid bone
Stylohyoid branch of
facial nerve
innervates stylohyoid
muscle
SVE
33. Through the
stylomastoid
foramen
The Posterior belly of digastric muscle elevates the hyoid bone
Posterior belly of
digastric branch of
facial nerve
innervates posterior
belly of digastric
muscle.
Posterior belly of
digastric muscle
elevates the
hyoid bone
SVE
Through the internal
acoustic meatus
34. A. Temporal branch (with zygomatic
branch) innervates orbicularis
oculi--closes eyelids
B. Zygomatic branch (with buccal
branch) innervates zygomaticus
major--smiling
C. Buccal branch innervates
buccinator--tenses cheek
D. Mandibular branch innervates
depressor angularis oris--
frowning
E. Cervical branch innervates
platysma -- lowers mandible,
tenses skin of anterior neck
*These are key innervations to the
muscles of facial expression.
However, each nerve branch
innervates multiple muscles and each
muscle receives multiple nerve
branches.
SVE
37. Buccal branch of
facial nerve innervates
Buccinator muscle.
SVE Contraction of the buccinator muscle
causes tensing of the cheek which
helps position food within the occusal plane
for chewing
39. Platysma muscle
Cervical branch of
facial nerve innervates
Platysma muscle.
Contraction of platysma
Muscle results in depression
of mandible.
SVE
40. Congenital bony dehiscences
may involve any part of the canal
most often found in the surroundings of the oval window,
located above and posterior to the oval window. During surgery
they should always be anticipated.
“As a rule they are less numerous and smaller in a well-
pneumatized temporal bone”.
The tiny shell of the facial canal can adhere to the jugular
dome, especially when the jugular bulb rises into the tympanic
cavity.
The facial canal may be dehiscent on its route to the
stylomastoid foramen.
41. Anomalies of the route of the facial
nerve
Classified under topographical aspects.
Frequently observed in cases of malformation and
are often associated with other abnormalities of the
external, middle, and inner ear.
An overhanging facial nerve might obstruct the
footplate.
The chorda tympani nerve origin may vary from1 to
11mm from the foramen, and in some cases the
origin is extratemporal.
Anomalous branching pattern of extratemporal
branches
42. • Endonerium
– Surrounds each nerve fiber
– Provides endoneural tube for regeneration
– Much poorer prognosis if disrupted
• Perinerium
– Surrounds a group of nerve fibers
– Provides tensile strength
– Protects nerve from infection
– Pressure regulation
• Epinerium
– Surrounds the entire nerve
– Provides nutrition to nerve
43.
44. – Class I (Neuropraxia)
• Conduction block caused by cessation of axoplasmic flow
• What one experiences when their leg “falls asleep”
• Full recovery
– Class II (Axonotmesis)
• Axons are disrupted
• Wallerian degeneration occurs distal to the site of injury
• Endoneural tube still intact
• Full recovery expected
– Class III (Neurotmesis)
• Neural tube is disrupted
• Poor prognosis
• If regeneration occurs, high incidence of synkinesis
(abnormal mass movement of muscles which do not
normally contract together)
45. ◦ Class IV
Epineurium remains intact
Perineurium, endoneurium, and axon disrupted
Poor functional outcome with higher risk for synkinesis
◦ Class V
Complete disruption
Little chance of regeneration
Risk of neuroma formation
46.
47. The facial nerve may be injured or become
dysfunctional anywhere along its course from
the brainstem to the face.
The paralysis may be supranuclear or
infranuclear.
48. Involves the upper motor neuron pathway
Usually a part of hemiplegia
Paralysis of lower part of face on contralateral side
Stroke, Lacunar infarcts
Brain abscess
Pontine glioma
Poliomyelitis
Multiple sclerosis
Progressive supranuclear palsy: Steele-Richardson-
Oleszewski syndrome
49. Lesion from facial nucleus to anywhere along the course of
facial nerve upto face
The disorder may even involve multiple segments of the
nerve.
The paralysis can be
Idiopathic
Trauma,
Systemic infection,
Acute or chronic otitis media,
Metabolic disorders,
Toxins,
Vasculitides,
Neurologic disorders,
Neoplasms (both benign and malignant),
Radiation therapy, and
Numerous other causes
50. Abrupt, unilateral, peripheral facial paresis or paralysis
without a detectable cause.
First described by Sir Charles Bell
60-70% cases
Pathophysiology – Impaired “axoplasmic” flow from
edema of facial nerve within fallopian canal
Other theories: viral infection, ischaemia, autoimmune
disorder
Rapid onset and evolution < 48 hours
May be associated with acute neuropathies of cranial
nerves V- X
Pain or numbness affecting ear, mid-face, tongue and
taste disturbances
Recurrences are more likely (2.5x) in patients with family
history, immunodeficiency or diabetes
51. The most alarming symptom of Bell's palsy is
paresis
Up to three quarters of affected patients think
they have had a stroke or have an intracranial
tumour.
52. Patients may also mention otalgia or aural
fullness and facial or retroauricular pain,
which is typically mild and may precede the
palsy.
A slow onset progressive palsy with other
cranial nerve deficits or headache raises the
possibility of a neoplasm
53. Bell's palsy causes a
peripheral lower motor
neurone palsy,
which manifests as the
unilateral impairment of
movement in the facial and
platysma muscles, drooping
of the brow and corner of
the mouth, and impaired
closure of the eye and
mouth.
54. Bell's phenomenon—upward diversion of the
eye on attempted closure of the lid—is seen
when eye closure is incomplete.
55. Bell palsy is a diagnosis of exclusion.
Other disease states or conditions that
present with facial palsies are often
misdiagnosed as idiopathic.
80-90% recover completely
◦ Over age 60, only 40% recover completely
56. Imaging in typical Bell’s palsy is not usually
necessary
◦ When necessary, MRI is best
Normal facial nerve distal to geniculate ganglion
may enhance
◦ Facial nerve proximal to geniculate ganglion does not
normally enhance
In patients with Bell’s palsy, enhancement of facial
nerve in fallopian & ICA is typical
57.
58. Clinical features
◦ Slower onset of symptoms
◦ Bilateral
◦ Recurrence
Numbness is not unusual
Progression beyond seven days
suggests another cause
59.
60. The main aims of treatment in the acute
phase of Bell's palsy are to speed recovery
and to prevent corneal complications.
Treatment should begin immediately to
inhibit viral replication and the effect on
subsequent pathophysiological processes
that affect the facial nerve.
Psychological support is also essential, and
for this reason patients may require regular
follow up.
61. Usual regimen is 1mg/kg/day for 1 week.
To be tapered in the 2nd week.
62. Cochrane review*:
“There is insufficient evidence about the effects of
corticosteroids for people with Bell's palsy, although their
anti-inflammatory effect might prevent nerve damage.”
*Salinas RA, Alvarez G, Ferreira J. Corticosteroids for Bell's palsy (idiopathic facial paralysis). Cochrane
Database of Systematic Reviews 2004, Issue 4. Art. No.: CD001942.
63. It seems logical in Bell's palsy because of the
probable involvement of herpes viruses.
Acyclovir, a nucleotide analogue, interferes
with herpes virus DNA polymerase and
inhibits DNA replication.
Usual regimen is 4000mg/24hrs divided into
5 doses for 7 to 10 days
64. Eye protection –artificial tears
Follow progression with serial examination
Facial nerve decompression
Progression to > 90% degeneration on ENoG
Performed before irreversible injury to the endoneural
tubules occurs (two weeks), will allow for axonal
regeneration to occur
65. Peripheral facial paralysis with erythematous vesicular rash in
the EAC, pinna or mouth
Caused by reactivation of varicella zoster virus (herpes virus
type 3)
◦ Herpes zoster oticus
Other cranial nerves, particularly trigeminal nerves (5th CN)
often involved
Rising titres of antibodies to VZV
Worse prognosis than Bell’s (complete recovery: 50%)
Important cause of facial paralysis in children 6-15 years old
67. Triad
◦ Recurrent orofacial
edema
◦ Recurrent facial palsy
(50-90%)
◦ Lingua plicata (fissure
tongue) – 25%
Lips become chapped,
fissured and red-brown
in appearance
Biopies identify
granulomatous changes
Facial nerve
decompression may be
indicated if facial
paralysis is severe and
recurrent
68. -Second most common cause of FN
paralysis behind Bell’s Palsy
-Represents 15% of all cases of FN
paralysis
-Most common cause of traumatic facial
nerve injury is temporal bone fracture
-Maxillofacial trauma
-Iatrogenic
69. 5% of trauma patients sustain a temporal bone fracture
– Three types
» LONGITUDINAL
Most common type – 70-80%
Fracture line parallel to long axis of petrous pyramid
Secondary to temporoparietal blunt force
Results in facial nerve paralysis in 25% of cases
» TRANSVERSE
10-20% of fractures
Fracture line perpendicular to long axis of petrous pyramid
Secondary to frontal or occipital blow
Results in facial nerve paralysis in 50% of cases
» MIXED
10% of temporal bone fractures
70. • Chang and Cass (1999) reviewed facial nerve
pathology of 67 longitudinal fractures and 11
transverse fractures where facial nerve paralysis
was known
– Longitudinal findings
• Perigeniculate region, tympanic segment
• 76% of cases showed bony impingement or intraneural
hematoma
• 15% showed a transected nerve
• 9% either had no pathologic findings or just neural edema
– Transverse findings
• Labyrinthine or mastoid segment
• 92% of cases showed transection
• 8% showed bony impingement or hematoma
71. -Typically results in FN injury in the extratemporal
segments
-Gun shot wounds cause both intratemporal and
extratemporal injuries
MC site- mastoid segment
GS wounds to temporal bone result in FN paralysis
in 50% of cases
Mixture of avulsion and blunt trauma to different
portions of the nerve
Much worse outcome when comparing GS related
paralysis to TB fracture related paralysis
72. – SURGICAL
• Most common overall surgery with FN injury is parotidectomy
• Most common otologic procedures with FN paralysis
– Mastoidectomy – 55% of surgical related FN paralysis
– Tympanoplasty – 14%
– Exostoses removal – 14%
– Stapedectomy
– Mechanism - direct mechanical injury or heat generated from
drilling
– Most common area of injury - tympanic portion due to its high
incidence of dehiscence in this area, and its relation to the
surgical field
• Unrecognized injury during surgery in nearly 80% of cases
74. Acute facial paralysis may result from
bacterial or tuberculous infection of
middle ear, mastoid & necrotizing otitis
externa
Incidence of facial paralysis with otitis
media: 0.16%
◦ Infection extends via bone
dehiscences to nerve in fallopian canal
leading to swelling, compression &
eventually vascular compromise &
ischemia
Immuno-compromised patients are at
risk for pseudomonas infection
Mastoiditis
Parotid & peri-parotid disease
HIV
Lyme disease
Meningitis
Chickenpox
Encephalitis
Poliomyelitis
Mumps
Mononucleosis
Leprosy
Influenza
Coxsackie virus
Malaria
Syphilis
Botulism
Mucormycosis
76. Neurogenic causes
Millard-Gubler syndrome
(abducens palsy with
contralateral hemiplegia
owing to lesion in base of
pons involving corticospinal
tract)
Opercular syndrome
(cortical lesion in facial
motor area)
Toxic
•Thalidomide (cranial nerves VI
and VII with atretic external
ears [Miehlke syndrome])
•Tetanus
•Diphtheria
•Carbon monoxide
•Lead intoxication
77. About 5% of cases of facial nerve paralysis
are caused by tumors
Characteristics of facial nerve palsy
Slow developing
Additional cranial nerve deficits
Recurrent ipsilateral involvement
Adenopathy
Palpable neck or parotid mass
78. 27% of patients with tumors involving the
facial nerve develop acute facial paralysis
Most common causes: schwannomas,
hemangiomas (usually near geniculate
ganglion) & perineural spread such as with
head and neck carcinoma, lymphoma &
leukemia
Other neoplasms can also involve the facial
nerve
◦ Adults: metatstatic disease, glomus tumors,
vestibular schwannomas & meningiomas
◦ Children: eosinophilic granuloma & sarcomas
79.
80.
81.
82. Glomus tumors arising
from jugular bulb
(jugulare) and/or middle
ear (tympanicum) may
involve the facial nerve
83. Common tumor
However, tends to produce facial paralysis
mostly when they attain a large size
84. Second most common
primary tumor of
cerebellopontine angle
Rarely results in facial
paralysis
86. History
Onset: Sudden vs. Gradual
Duration:
Rate of progression:– progressive loss of function or sudden
loss
○ Transected nerve -> sudden loss
○ Intraneural hematoma or impingement -> progressive loss
(better prognosis)
Recurrent or familial
recent surgery, facial/head trauma
Associated symptoms – hearing loss or vertigo (hint more toward a
temporal bone injury)
Medical history
87. Perform a full head and neck examination
Complete vs. incomplete
Segmental vs. uniform involvement
Unilateral vs. bilateral
Facial asymmetry
– Signs of facial injury (lacerations, hematomas, bruising)
– Exam head/scalp for signs of injury to help guide you to vector of force if head
trauma is involved
Otoscopic examination is a must
• Canal lacerations or step-offs
• Hemotympanum, TM perforation, drainage of blood or clear fluid from middle ear
• Polyposis or granulations in the ear canal may suggest cholesteatoma or
malignant otitis externa.
Tuning fork tests (Weber/Rinne) with a 512 Hz fork can help
determine if there is a conductive hearing loss
Cranial nerves assessment
Neurologic evaluation
Cerebellar signs
88. Localization of facial nerve lesion:
Central vs. Peripheral.
Peripheral
◦ Level of nucleus
◦ CPA level:
◦ Bony canal level: Topodiagnostics
◦ Outside the Temporal bone
89. Grade Characteristics
I. Normal facial function in all areas
II. Mild dysfunction •Slight weakness noticeable on close inspection
•Forehead - Moderate-to-good function
•Eye - Complete closure with minimal effort
•Mouth - Slight asymmetry
III. Moderate dysfunction
-First time you can notice a difference at rest
•Obvious but not disfiguring difference between the two sides
• Forehead - Slight-to-moderate movement
•Eye - Complete closure with maximum effort
•Mouth - Slightly weak with maximum effort
IV. Moderately severe dysfunction
-First time you have incomplete eye closure
-No forehead movement
•Obvious weakness and/or disfiguring asymmetry
• Forehead – No motion
•Eye - Incomplete closure
•Mouth - Asymmetric with maximum effort
V. Severe dysfunction •Only barely perceptible motion
•At rest, asymmetry
•Forehead – No movement
•Eye - Incomplete closure
•Mouth - Slight movement
VI. Total paralysis No movement
90. • Degree of electrical dysfunction
• Site of injury
• Helps determine treatment
• Can predict recovery of function – partial
paralysis is a much better prognosis than total
paralysis
• Divided into two categories
– Topographic tests
• Tests function of specific facial nerve branches
• Do not predict potential recovery of function
• Rarely utilized today
– Electro diagnostic tests
• Utilize electrical stimulation to assess function
• Most commonly used today
91. Intended to determine the level of facial nerve injury by
testing peripheral facial nerve function.
The underlying hypothesis is that injury to the facial nerve at
a particular location will affect all branches proximal to the
lesion, yet leave distal branches with normal function.
Schirmer test: if tearing is diminished the lesion is assumed
to be proximal to the point at which the greater superficial
petrosal nerve branches from the geniculate ganglion.
Immittance testing (abnormal stapedial muscle function
reflecting nerve impairment above the stapedial motor
branch),
Salivary secretion and taste testing (chorda tympani nerve
function).
92. To evaluate for concurrent SNHL or CHL
CHL – middle ear tumors, cholesteatomas,
other processes involving tympanic segment
SNHL – acoustic neuromas, meningiomas,
congenital cholesteatoma, others involving
CPA or IAC
93. • Compares amount of current required to illicit
minimal muscle contraction - normal side vs.
paralyzed side
• How it is performed
• A stimulating electrode is applied over the stylomastoid
foramen
• DC current is applied percutaneously
• Face monitored for movement
• The electrode is then repositioned to the opposite side, and
the test is performed again
• A difference of 3.5 mA or greater between the two
sides is considered significant
• Drawback - relies on a visual end point (subjective)
94. • Similar to the NET, except it utilizes
maximal stimulation rather than minimal
• The paralyzed side is compared to the
contralateral side
• Comparison rated as equal, slightly
decreased, markedly decreased, or absent
– Equal or slightly decreased response = favorable
for complete recovery
– Markedly decreased or absent response =
advanced degeneration with a poor prognosis
• Drawback - Subjective
95. Thought to be the most accurate of the electrodiagnostic
tests
How it works:
◦ Bipolar electrodes deliver an impulse to the FN at the
stylomastoid foramen
◦ Summation potential is recorded by another device
◦ The peak to peak amplitude is proportional to number of
intact axons
◦ The two sides are compared as a percentage of response
90% degeneration – surgical decompression should be
performed
Less than 90% degeneration within 3 weeks predicts 80 -
100% spontaneous recovery
Disadvantages: discomfort, cost, and test-retest variability
96. • Determines the activity of the muscle itself
• How it works
– Needle electrode is inserted into the muscle, and
recordings are made during rest and voluntary
contraction
• Normal = biphasic or triphasic potentials
• 10-21 days post injury - fibrillations
• 6-12 weeks prior to clinical return of facial
function – polyphasic potentials are recordable
– Considered the earliest evidence of nerve recovery
• Does not require comparison with normal side
97. CT scans
◦ Bony evaluation
◦ Locate middle ear, mastoid, and temporal bone pathology
Gadolinium enhanced MRI
◦ Utilized for soft tissue detail and CPA pathology
98. Incomplete recovery
Exposure keratitis
Synkinesis
Tics and spasms
Crocodile tears
Frey’s syndrome “gustatory sweating”
Psychological and social problems
Abnormal facial expressions
Mastication
Speech production
99.
100. • If transected during surgery
– Explore 5-10mm of the involved segment
– Stimulate both proximally and distally
• Response with 0.05mA = good prognosis;
further exploration not required
• If only responds distally = poor prognosis, and
further exposure is warranted
101. • If loss of function is noted following surgery, wait 2-3 hours and
then re-evaluate the patient.
• This should be ample time for an anesthetic to wear off
– Waited time and still paralysis
• Unsure of nerve integrity – re-explore as soon as possible
• Integrity of nerve known to be intact
– High dose steroids – prednisone at 1mg/kg/day x 10 days
and then taper
– 72 hours – ENoG to assess degree of degeneration
» >90% degeneration – re-explore
» <90% degeneration – monitor
if worsening paralysis occurs re-explore
if no regeneration, but no worsening, timing of exploration
or whether to is controversial
102. • Birth trauma and Extratemporal blunt trauma
– Recommend no surgical exploration
– >90% expected to regain normal/near normal recovery
• Complete paralysis following temporal bone fracture
– Likely nerve transection
– Surgical exploration
• Partial or delayed loss of function
– Approach similar to iatrogenic partial or delayed loss
– High dose steroids
– ENoG 72 hours
• >90% degeneration – explore
• < 90% degeneration – can monitor and explore at later date
depending on worsening or failure to regenerate
103. • Nerve may be injured along multiple segments
– localize injured site pre-operatively
– Full exposure of the nerve from IAC to the stylomastoid foramen
if can’t localize
• Approach to full exposure is based on patient’s auditory
and vestibular status
– Intact - Transmastoid/Middle cranial fossa approach
– Absent – Transmastoid/Translabyrinthine approach
• Diamond burs and copious irrigation is utilized to prevent
thermal injury
• Thin layer of bone overlying the nerve is bluntly removed
• Whether to perform neurolysis or not to open the nerve
sheath is debatable
– Recommended to drain hematoma if identified
104. Performed in severe cases when the facial nerve
is seriously deteriorating.
Patients are at risk for permanent paralysis and
have a poor prognosis without aggressive
intervention.
Research has shown that this procedure is
effective in improving outcomes in a selected
group of patients.
To be effective, the surgery must be performed
within 2 weeks of the onset of symptoms.
106. • Recovery of function takes around 4-6 months
• Nerve regrowth occurs at 1mm/day
• Goal is tension free, healthy anastomosis
• Rule is to repair earlier than later - controversial
– After 12-18 months, muscle reinnervation becomes less efficient
even with good neural anastomosis
– Some authors have reported improvement with repairs as far out
as 18-36 months
– Some recommend repair within 30 days, but others have found
superior results if done up to 12 months out
• 2 weeks following injury -> collagen and scar tissue
replace axons and myelin
– Nerve endings must be excised prior to anastomosis
107. • Best overall results of any surgical intervention
• Done if defect is less than < 2cm
– Mobilization of the nerve can give nearly 2cm of length
– With more mobilization comes devascularization
• Endoneurial segments must match - promotes
regeneration
• Ends should be sutured together using three to
four 9-0 or 10-0 monofilament sutures to bring
the epineurium or perineurium together
108. Approach is based on availability of proximal
nerve ending
Performed for defects > 2cm
Results in partial or complete loss of donor
nerve function
109. • Great auricular nerve
– Usually in surgical field
– Located within an incision made from the mastoid tip to the angle
of the mandible
– Can provide only upto 12cm of length
– Loss of sensation to lower auricle
• Sural nerve
– Located 1 cm posterior to the lateral malleolus
– Can provide 35cm of length
– Very useful in cross facial anastomosis
– Loss of sensation to lateral calf and foot
• Ansa Cervicalis
– Only utilized if neck dissection has been performed
• 92-95% of these patients have some return of facial
function
• 72-75% have good results (HB 3 or above)
110. • Requires that the patient have an intact distal nerve segment
and facial musculature suitable for reinnervation
– Determined by EMG and/or muscle biopsy
• Hypoglossal nerve
– Direct hypoglossal-to-facial graft
• Distal branch of facial nerve is attached to hypoglossal nerve
• 42-65% of patient’s expected to experience decent symmetry and
tone
• Complications – atrophy of ipsilateral tongue, difficulties with
chewing, speaking, and swallowing
– Partial hypoglossal-to-facial jump graft
• Uses a nerve cable graft, usually the sural nerve, to connect the
distal end of the facial nerve to a notch in the hypoglossal nerve
• Much fewer complications, but increased time
• May compared the results of direct VII-XII graft to the VII-XII jump
graft
Also known as Nerve transposition
112. • Facial-to-Facial Graft
Nerve Substitution
Is indicated when the nerve cannot be repaired in the
conventional manner.
In this procedure, another cranial nerve involved in
facial movement is connected to the damaged nerve
and takes over its function.
113. 113
– Options
• Single contralateral branch to distal nerve
anastomosis
• Multiple anastomoses from segmental branches to
segmental branches
– Best described is the use of a sural nerve graft to
connect the buccal branch on the contralateral
side to the distal nerve stump
– Most do not recommend this technique
• Weakness caused to the contralateral facial nerve
• Lack of power to control musculature resulting in
poor results
114.
115. Dynamic procedures
◦ Aim to reproduce movement in paralyzed face
◦ Improves symmetry at rest and in motion
Static procedures
◦ Alter the facial posture
◦ Alter the facial symmetry at rest
◦ Improve oral continence
◦ Improve nasal valve collapse
◦ No voluntary facial movement
116. Musculofascial transpositions:
◦ Move new muscles and nerves into the face to
take the place of the injured facial nerve.
Facial plastic procedures.
Prosthetics.
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117. 117
Involves taking a 1-2 cm band of the temporalis
muscle.
Rotating it from the temple region, over the
cheek bone and down, to attach to the corner of
the mouth.
When it is appropriately secured, the act of biting
down will result in elevation of the corner of the
mouth toward the cheekbone, just as in smiling.
121. In a combination muscle and nerve graft, two
procedures are performed several months apart.
Free muscle tissue is grafted from the leg to the
face following a cross-facial nerve graft.
The nerve graft becomes the nerve supply for the
healthy, transplanted muscle.
124. Is accomplished by one of
several techniques
Blepharoplasties: The eyebrow
can be repositioned by
performing a unilateral brow lift,
and matching the brow height
with the other side.
The eyelids can be addressed
using implantable eyelid springs
so that gravity assists with eye
closure.
Using lid gold weights
Canthoplasty
126. The collapse of the nasal sidewall
can be corrected either from the
outside or the inside of the nose.
Outside techniques involve
placing strips of suspension
material from the cheekbone,
under the skin, to the nasal
sidewall, and suspending the
nasal sidewall in its anatomic
position.
127. 12
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To widen the nasal cavity from the
inside, small cartilage grafts can be
inserted into the framework of the nose.