eye and ear anatomy post lab

• Orbital rim:  Frontal, maxilla & zygomatic bones
• Superior wall: Frontal & Lesser wing of sphenoid
• lateral wall: Zygomatic & Greater wing of the sphenoid
• medial wall: Ethmoid, maxilla, Lacrimal & sphenoid
• Inferior wall: Maxilla, zygomatic & palatine
• Bones of the orbit

  A) frontal

  B) palatine

  C) ethmoid

  D) lacrimal

  E) sphenoid

  F) zygomatic

  G) maxilla

  
• What cranial nerves travel through the superior orbital fissure?

  CN III (Oculomotor n.), CN IV (Trochlear n.), CN V1 (Trigeminal nerve-ophthalmic division), CN VI (Abducens n.).
• What structures travel through the optic canal?

  CN II (Optic nerve), ophthalmic artery
• The ophthalmic artery is a branch of which artery?

  Internal carotid artery
• Remove the function of the lateral rectus muscle. Observe what happens to the eye. Why did the eye adduct?

  The lateral rectus and medial rectus acts antagonistically. The medial rectus primary function is to adduct the eye.
• Remove the function of the medial rectus muscle. Observe what happens to the eye when you move this eye to look towards the nose (i.e medially). Why did the eye fail to adduct?

  The lateral rectus and medial rectus acts antagonistically. The lateral rectus primary function is to abduct the eye.
• Remove the function of the 2 muscles that depress the eye. Observe what happens to the eye when you move the gaze downwards. Why is the eye ‘stuck’ to be looking upwards?

  The Inferior rectus and superior oblique normally acts synergistically to move the eye downwards, AND antagonistically with superior rectus and inferior oblique (which produces upwards action here). 
• Remove the function of the 2 muscles that elevates the eye. Observe what happens to the eye when you move the gaze upwards. Why is the eye ‘stuck’ to be looking downward?

  The Superior rectus and inferior oblique normally acts synergistically to move the eye upwards, AND antagonistically with inferior rectus and superior oblique (which produces downwards action here).
• Click on the cranial nerve setting for ‘CN III (Pupil)’. This turns the innervation of this cranial nerve ‘off’, simulating Oculomotor palsy. Observe what happens to the eye.

  Describe the position of the eye?

  Down and out OR Abducted and depressed.
• Explain why the eye is Down and out OR Abducted and depressed when CN III is paralysed?

  The superior oblique and lateral rectus are the two muscles still functioning each is innervated by other cranial nerves (Trochlear n. and Abducens n. respectively) thus these two muscles action will remain to move the eye down and out or abducted and depressed.
• Explain pupil dilates when CN III is damaged?

  When oculomotor nerve (CN III) is not ‘working’, the pupil loses ability to control the sphincter pupillae m. and thus cannot constrict in response to light.
• Match the eye movement with the extra-ocular muscle.

  A) inferior oblique

  B) superior rectus

  C) superior rectus and inferior oblique

  D) superior rectus

  E) inferior oblique

  F) lateral rectus

  G) medial rectus

  H) medial rectus

  I) lateral rectus

  J) superior oblique

  K) inferior rectus

  L) superior oblique and inferior rectus

  M) inferior rectus

  N) superior oblique

  
• Describe how in physical examination would you test the integrity of only the superior rectus?

  Direct patients gaze laterally (abduct the eye) and then ask to look upwards (H-test).

  
• Which structure would you find the most photoreceptors that are cones making it more specialised for sharp, detailed vision?

  Fovea

  
• In glaucoma, which structure is at risk of injury and why?

  The retina and the optic disc i.e optic nerve is at risk of injury due to compression caused by raised of intra-ocular pressure resulting from increase aqueous humour.

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• Why is the optic cup-to-disc ratio changed in the pathological glaucoma?

  Increased intra-ocular pressure risks causing death to optic nerve fibres this causes the optic disc to reduce in size.

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• What structure is likely blocked in glaucoma causing issues for the absorption of aqueous humour?

  Trabecular meshwork blocked and thus blocking drainage to scleral venous sinus (canal of Schlemm).

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• Clinical case: Glaucoma

  A) open angle

  B) closed angle

  C) acute

  D) chronic

  
• Treatment for chronic glaucoma: Reduce IOP by reducing production of aqueous humor (beta-blockers, protaglanding) or improve trabecular meshwork drainage via (Trabeculoplasty using lasers)
• Treatment for acute glaucoma: Reduce IOP by reducing aqueous humor, followed by Iridotomy- hole in iris. The hole allows fluid in the eye to circulate freely

  This helps to open up the drainage canal and reduce the risk of pressure rising in the eye
• In closed angle glaucoma, which structure is blocking the trabeculae meshwork?

  The iris.
• Sudden pupillary dilation typically induces closed angle glaucoma.

  What muscle structure is responsible for pupillary dilation and what provides it’s innervation?

  Dilator pupillae. Sympathetic innervation, nerve fibers from superior cervical ganglion.
• In glaucomoa, the shortening of this muscle radial fibers during pupillary light reflex (decreased light intensity e.g. entering a dark room) AND the subsequent contact between the iris and the lens when the iris is in a mid-dilated position causes pupillary block . This causes the peripheral iris to bow forward blocking the drainage angle, which can instigate a rapid rise in IOP because the aqueous humor in the posterior chamber has no route available to flow into the anterior chamber – it’s “door” is blocked off.
• OPEN ANGLE GLACOMA

  It's caused by the drainage channels in the eye becoming gradually clogged over time.

  
• Closed-angle glaucoma is caused by a blockage or narrowing of the drainage angle in the eye, where the cornea and iris meet. This blockage prevents the proper drainage of the aqueous humor (the fluid inside the eye), causing pressure to build up within the eye, leading to damage to the optic nerve.

  
• Explain how the external acoustic meatus can be manually manipulated to allow for clear visualisation of the tympanic membrane.  Why is this necessary?

  The external acoustic meatus does not follow a straight course. From the external opening it passes upward in an anterior direction, then turns slightly posteriorly still passing upward, and finally, turns again in an anterior direction with a slight descent. For examination purposes, observation of the external acoustic meatus and tympanic membrane can be improved by pulling the ear superiorly, posteriorly, and slightly laterally.
• What has caused this?

  A preceding viral/bacterial infection can cause mucosal inflammation in the nasopharynx and Eustachian tube(s).  The Eustachian tube(s) equalise pressure in the middle ear and assist with mucociliary clearance.  Obstruction secondary to inflammation of the Eustachian tube(s) prevents them from performing these functions effectively, resulting in fluid accumulating within the middle ear.  The presence of fluid is called an effusion.  It is responsible for the symptoms associated with Otitis media with effusion

  
• Why does this condition commonly affect children?

  The Eustachian tube is shorter and more horizontal in infants/young children than in older children and adults.  This renders it less effective at clearing the contents of the middle ear and equalising negative middle ear pressure.

  
• Which ear ossicle is attached to the tympanic membrane?

  Malleus
• Explain how this condition will lead to partial or complete hearing loss?

  Tympanic membrane retraction causes it to be stiffen, this reduces the ability for it to vibrate from sound waves.

  
• Reduced ossicular chain movement secondary to effusion. The ossicles transmit vibrations best when they’re in an air-filled environment.  A fluid-filled environment (effusion) impedes optimum sound wave conduction through the ossicles, which ultimately affects transmission of sound into the inner ear apparatus and, ultimately, to the auditory centres of the brain where sound waves are interpreted.

  
• Ossicular chain erosion – Longstanding, progressive TM retraction can lead to erosion of the ossicular chain.  This would present as worsening conductive hearing loss (again, the chain of sound transmission is compromised). 

  
• Diagnosis: Otitis media with effusion (OME) – colloquially known as “glue ear”

  Treatment: Placement of tympanostomy tubes (grommets) can both treat and prevent subsequent episodes of OME from developing by keeping the middle ear aerated for an extended period.

  Treatment/prevention methods for chronic OME include routine audiological testing, insertion of a tympanostomy tube (to facilitate middle ear ventilation) & ossicular chain reconstruction.

  
• Auditory ossicles (malleus, incus, stapes) are impeded from vibrating optimally in a fluid-filled environment.  Chronic TM retraction can also lead to them eroding.  This presents clinically as worsening conducting hearing loss. 
• Eustachian Tube is inflamed and narrowed secondary to a previous episode of acute otitis media or an upper respiratory tract infection.  This prevents effective mucociliary clearance which further occludes the Eustachian tube, reducing its ability to equalise middle ear pressure.