Describe the maxillary and mandibular nerves.

Maxillary nerve(V2) has 3 branches:
1)Zygomaticotemporal branch
2)Zygomaticofacial branch
3)Infra-orbital branch

-it exit the skull via foramen rotundum


Zygomaticotemporal
-exit zygomatic bone
-supply small area of anterior temple above the zygomatic arch

Zygomaticotfacial
-exit zygomaticofacial foramen
-supply skin on zygomatic bone

Infra-orbital
-exit maxilla via infra-orbital foramen and immediately divide into multi branch
-supply lower eye lid, side of nose, cheek and upper lip



Mandibular nerve (V3) has 3 branches as well:
1)Auriculotemporal branch
2)Buccal branch
3)Mental branch

-it exit the via foramen ovale


Auricotemporal
-enter the face posterior to the temporalmandibular joint
-passes through the parotid gland
-ascend just anterior to the ear
-supply external acoustic meatus & tympanic membrane & large area if temple

Buccal
-on the surface of buccinator muscle
-supply the cheek

Mental
-exit mandible via mental foramen
-immediately divide into multi branch
-supply skin and mucous membrane of lower lip and skin of chin


Contributed by Lawrence Oh

Anatomy Tasks : The Neck

a. Review the anatomy of the typical and atypical cervical vertebrae. (Shanthini)
b. Review atlanto-occipital and atlanto-axial articulations. (Lawrence)
c. Review trapezius & sternocleidomastoid & their relation to investing fascia (John); Explain how they define the anterior & posterior triangles. (Chris)
d. Explain how anterior triangle is subdivided; describe it's clinical significance. (Madhura)
e. Outline the features of the viscera of the neck - thyroid gland, cervical trachea & cervical oesophagus. (Ji Keon & Vivian)
f. Outline the fascial compartments of the neck & their contents. (Sri)

Please Note!
Special task for Christine: (Deep Fascia Regions) - Demonstrate the surface anatomy of the temporal, infratemporal & deep styloid regions and indicate clinical situations when this knowledge may be useful.

John

Temporal Fossa

The temporal fossa is a fan-shaped space that covers the lateral surface of the skull.

Boundaries:

Superior Margin: Pair of temporal lines (Superior and inferior temporal lines) that arch from the zygomatic process of the frontal bone to the supramastoid crest of the temporal bone
Lateral Margin: Temporal fascia, a fan-shaped aponeurosis overlying the temporalis muscle
Anterior Margin: Posterior surface of the zygomatic process of the frontal bone and the frontal process of the zygomatic bone
Inferior Margin: Zygomatic arch laterally; Infratemporal crest of the greater wing of the sphenoid medially

Contents:

Temporalis muscle:
Fanshaped muscle that orginates from the superior temporal line;
Fibres converge inferiorly to form a tendon which attaches to the anterior surface of the coronoid process of the mandible;
A powerful elevator of the mandible, retracts the mandible as well.
Innervated by the deep temporal nerves and blood supplied by the deep temporal arteries and middle temporal artery

Deep Temporal Nerves:
Usually 2 in number; originates from the anterior branch of the mandibular nerve(V3) in the infratemporal fossa;
Pass superiorly, around the infratemporal crest of the sphenoid bone, deep to the temporalis muscle to innervate it

Zygomaticotemporal Nerve:
Branch of the zygomatic nerve, a branch of the maxillary nerve (V2);
Originates in the pterygopalatine fossa; Penetrates temporal fascia to supply skin of the temple

Deep Temporal Arteries:
Usually 2 in number; Originate from the maxillary artery in the infratemporal fossa;
Travel superiorly with the deep temporal nerves; Anastomoses with Middle temporal arteries

Middle Temporal Artery:
A branch of the superficial temporal artery; Branches out just superior to the root of the zygomatic arch; Penetrates under the temporal fascia and goes deep to temporalis muscle; Supplies temporalis muscle and anastomoses with deep temporal arteries

Source: Gray's Anatomy for Students
Contributed by John Lee

Facial Nerve Palsy and Bell's Palsy

Hi everyone, sorry for putting this up so late. Remember Dr Lakshmi was asking us about the difference between a Facial nerve Palsy and a Bell's Palsy during the Facial and Parotid Regions Practical?

Well, hope what I found below will be able to shed some light on the confusion.

Facial nerve paralysis, or facial nerve palsy refers to the paralysis of the facial muscles. This disorder can have numerous causes. These includes
Trauma: such as birth trauma, skull base fractures, facial injuries, middle ear injuries, or surgical trauma.
Nervous system disease: including Opercular syndrome, Millard-Gubler syndrome.
Infection: of the ear or face, or Herpes Zoster of the facial nerve (Ramsey-Hunt syndrome).
Metabolic: diabetes mellitus or pregnancy.
Tumors: acoustic neuroma, schwannoma, cholesteatoma, parotid tumors, glomus tumors.
Toxins: alcoholism or carbon monoxide poisoning.

If no apparent cause can be found in a patient with facial nerve paralysis, then it is said to be idiopathic and the patient is diagnosed as having Bell's palsy (a diagnosis of exclusion). In other words, Bell's palsy is an idiopathic facial paralysis.

As the name suggests, there is no known etiology behind Bell's palsy as yet. Some schools of thought suggest that Bell's palsy is caused by a viral infection of the facial nerve with the most likely virus being the herpes simplex virus.

Bell's palsy is usually a self-limiting, non-life threatening condition that spontaneously remits within six weeks. The incidence is 15-40 new cases per 100,000 people per year in the US. It is one of the most common neurological disorders affecting the cranial nerves. There is no predominant age or racial predilection; however it is 3.3 times more common during pregnancy and slightly more common in menstruating females. In general, the incidence increases with advancing age.

The typical symptoms of Bell's palsy include:
Unilateral acute paralysis of facial muscles. The paralysis involves all muscles, including the forehead.
About half the time, there is numbness or pain in the ear, face, neck or tongue.
There is a preceding viral illness in 60% of patients.
There is a family history of Bell's palsy in 10% of patients.
Less than 1% of patients have bilateral problems.
There may be a change in hearing sensitivity (often increased sensitivity).

The proposed mechanism of injury of the facial nerve in Bell's palsy is:
Primary viral infection (herpes) sometime in the past.
The virus lives in the nerve (trigeminal ganglion) from months to years.
The virus becomes reactivated at a later date.
The virus reproduces and travels along the nerve.
The virus infects the cells surrounding the nerve (Schwann cells) resulting in inflammation.
There immune system responds to the damaged Schwann cells which and causes inflammation of the nerve and subsequent weakness or paralysis of the face.
The course of the paralysis and the recovery will depend upon the degree and amount of damage to the nerve.



Facial nerve palsy or Bell's palsy? You tell me! =)

Source: http://www.medicinenet.com/facial_nerve_problems/page3.htm

Contributed by: John Lee

Deep Facial Regions - Anatomy Tasks

This is just a reminder for the tasks that we are going to do on thursday, after the 2pm lecture.

1. Describe the temporomandibular joint. (Ji Keon)
2. Describe the muscles of mastication. (Shanthini)
3. Describe the maxillary artery and it's major branches. (Vivian)
4. Describe the maxillary and mandibular nerves. (Lawrence)
5. Describe the boundaries and contents of the temporal (John), infratemporal (Sree), and deep styloid regions (Madhura).
6. Group and list the foramina of these regions (temporal, infratemporal and deep styloid) ; describe contents. (Chris)
7. Demonstrate the surface anatomy of the regions and indicate clinical situations when this knowledge may be useful. (Christine)

Otalgia

Otalgia is defined as ear pain. Two separate and distinct types of otalgia exist. Pain that originates within the ear is primary otalgia; pain that originates outside the ear is referred otalgia.

Typical sources of primary otalgia are external otitis, otitis media, mastoiditis, and auricular infections. Most physicians are well trained in the diagnosis of these conditions. When an ear is draining and accompanied by tympanic membrane perforation, simply looking in the ear and noting the pathology can make the diagnosis. When the tympanic membrane appears normal, however, the diagnosis becomes more difficult.

Referred otalgia is a topic unto itself. Although many entities can cause referred otalgia, their relationship to ear pain must be identified. A categorical discussion of the workup, treatment, prognosis, demographics, and other issues is impossible because the various pathologies responsible for creating referred otalgia are so diverse.

By definition, referred otalgia is the sensation of ear pain originating from a source outside the ear.

To better understand referred otalgia, the physician first must understand the anatomic distribution of nerves associated with the ear. Irritation of these nerves, as well as irritation of distant branches of these nerves, can cause the perception of pain within the ear.

Pathophysiology: The sensory innervation of the ear is served by the auriculotemporal branch of the fifth cranial nerve, trigeminal nerve (CN V), the first and second cervical nerves, the tympanic (Jacobson) branch of the glossopharyngeal nerve, the auricular (Arnold) branch of the vagus nerve, and the sensory branches of the facial nerve. Neuroanatomically, the sensation of otalgia is thought to center in the spinal tract nucleus of CN V. Not surprisingly, fibers from CNs V, VII, IX, and X and cervical nerves 1, 2, and 3 have been found to enter this spinal tract nucleus caudally near the medulla. Hence, noxious stimulation of any branch of the aforementioned nerves may be interpreted as otalgia.

Causes: Dental disorders are the most common cause of referred pain to the ear. Of this group of disorders, temporomandibular dysfunctions account for the majority of patients. The auriculotemporal branch of the trigeminal nerve mediate pain, which is often perceived deep within the ear.

Within the oral cavity, the sensory innervation becomes quite complex. The tongue receives fibers from the glossopharyngeal nerve, the facial nerve, the trigeminal nerve and the vagus nerve posteriorly. All these nerves have distributions in the ear as well.

Sinusitis is another very common source of ear pain. The neural pathway is along V2, and the auriculotemporal nerve of V3, of CN V. Because the trigeminal nerve supplies the nasal cavity, patients with inflammatory mucosal contact points and nasal obstruction may develop symptoms in their ears.

Neck problems can also refer pain to the ears. These disorders include cervical osteoarthritis, cervical myofascial pain syndrome, and traumatic injuries. The cervical spine is sensitive and well supplied by the cervical nerve roots. Muscular pain from the trapezius or sternocleidomastoid may project postauricularly to the mastoid and occipital area.

Sensory branches of the vagus and glossopharyngeal nerves supply mucosal areas in the upper aerodigestive tract such as the nasopharynx, oropharynx, laryngopharynx, and larynx. The vagus continues caudally and supplies sensory enervation to the bronchus, esophagus, and heart as well. Irritative lesions at any of these sites may lead to secondary otalgia.

Tonsillitis and pharyngitis are very common causes of earaches in children. Less commonly, laryngitis, laryngeal tumors, esophagitis, and even angina pectoris may manifest as otalgia.

Sometimes, pain may be from irritation of the nerves themselves without an inciting source. These disorders are termed neuralgias. Neuralgias are typified by lancinating pain in the distribution of the involved nerve.

Source: http://www.emedicine.com/ent/topic199.htm

Contributed by John Lee

Palsies of the CN III, IV, VI

by Ji Keon LOOI

Oculomotor Palsy
Characteristic signs of a complete lesion of CN III:-

• Ptosis (drooping) of the superior eyelid, caused by paralysis of the levator palpebrae superioris.


• Eyeball (pupil) abducted and directed slightly inferiorly (down and out) because of unopposed actions of the lateral rectus and superior oblique.


• No pupillary (light) reflex (constriction of the pupil in response to bright light) in the affected eye


• Dilation of pupil, resulting from the interruption of parasympathetic fibers to the sphincter of the pupillae, leaving the dilator pupillae unopposed.


• No accommodation of the lens (adjustment to increase convexity for near vision) because of paralysis of the ciliary muscle.
  

Injury to the Trochlear Nerve
CN IV is rarely paralyzed alone. The nerve may be torn in severe head injuries because of its long intracranial course. Damage to CN IV nerve or its nucleus impair the ability to turn the affected eyeball inferomedially. The characteristic sign of trochlear nerve injury is diplopia (double vision) when looking down (e.g., when going down stairs). Diplopia occurs because the superior oblique normally assists the inferior rectus in depressing the pupil (directing the gaze downward) and is the only muscle to do so when the pupil is adducted. In addition, because the superior oblique is the primary muscle producing intorsion of the eyeball, the primary muscle producing extorsion (the inferior oblique) is unopposed when the superior oblique is paralyzed. Thus the direction of gaze and rotation of the eyeball about its anteroposterior axis is different for the two eyes, especially when looking downward and medially.

Injury to the Abducent Nerve
Because CN VI has a long intracranial course, it is often stretched when intracranial pressure rises, partly because of the sharp bend it makes over the crest of the petrous part of the temporal bone after entering the dura. A space-occupying lesion such as a brain tumor may compress CN VI, causing paralysis of the lateral rectus muscle. Complete paralysis of CN VI causes medial deviation of the affected eye—that is, it is fully adducted owing to the unopposed action of the medial rectus, leaving the person unable to abduct the eye. Diplopia is present in all ranges of movement of the eyeball, except on gazing to the side opposite the lesion.

Source: Moore and Agur; Essential Clinical Anatomy, Lippincott and Williams