GEP (Life Control) Week 1 Flashcards
What are the devision of the brain
Forebrain
Cerebrum (outer):
Frontal lobe
Parietal lobe
Temporal lobe
Occipital lobe
Diencephalon (inner)
Thalamus
Hypothalamus
Midbrain
Tectum (roof/quadrigeminal plate)
Cerebral peduncles:
Crus cerebri
Tegmentum
Substantia nigra
Hindbrain
Brain stem:
Pons
Medulla Oblongata
Cerebellum
What is the cerebrum, what does it do and what does it consist of
Conscious thought processes and intellectual function
Memory storage, processing and retrieval
Conscious and subconscious regulation of skeletal muscle contraction
Frontal (motor activity, higher functioning)
Parietal (sensory areas [cortex])
Temporal (hearing)
Occipital (vision)
What are the motor and sensory regions of the cerebral cortex
What is the diencephalon
The diencephalon is beneath the cerebrum, and is the deep area of grey matter. Its main structures are the thalamus, which is the relay and processing centre, and the hypothalamus, which is involved in hormone production and emotional control.
What is the brainstem
Midbrain, Pons & Medulla Oblongata
Relay centre between brain and spinal cord
Reflex centres for autonomous control
What is the cerebellum and what does it consist of
Functions:
Coordination of complex somatic motor patterns
Balance
Refined movements
Describe the different regions of the skull
What are the different layers of the meninges and how CSF is made
What are the 12 cranial nerve
Oh Oh Oh To Touch And Feel Very Good Velvet Ah Heaven
What are axons, action potential and neurotransmitter
To discus neurotransmitters, we must quickly discuss how stimuli and responses travel through the nervous system. The brain, amongst other things is made up of neurons. These these have a main cell body which houses its nucleus, but then have losing finger like projections called axons. It is down these axons at action potentials are sent in response to a signal. Action potentials are when there is increase in voltage to the point of which a threshold potential is reached, this causes an influx of ions that causes depolarisation of the cell. This depolarisation spreads down the axon to the axon terminal. At this point, the axon terminal is connected to other neurons via synapses. These synapses allow to passage of impulse through neurons to desired areas. It is at these synapses that neurotransmitters play a pivotal role. As an action potential reaches the terminal, it depolarises the presynaptic membrane, which opens up calcium channels, causing an influx of calcium ions. This triggers the exocytosis of neurotransmitters from vesicles residing in the axon terminal into the synaptic cleft. These neurotransmitters then attach to receptors on the post synaptic membrane (another neuron), causing them to open and allow an influx of ions that fires off an action potential in the new neuron. Different neurotransmitters have different functions, some excitatory, some inhibitory.
What are the different types of neurotransmitter
What is the gross anatomy of the eye
Starting off with structure the eyes, it is highly sophisticated catcher of light. Through its structure is able to take in light, optimise its ability to excite receptors within the eye to provide a better image to process, before sending it down drive to be processed in the occipital lobe. The first main thing to state is that it is obviously spherical, allowing for it catch as much light as possible. It is made up of 3 layers.
The outer fibrous layer consists of the sclera and cornea, which are continuous with each other, the sclera is white, and the cornea (the anterior part of the eye) is transparent, allowing for light to enter the eye. The main function of this layer is to provide shape to the eye and support the deeper structures.
The next layer is the vascular layer, consisting of choroid vessels; that supplies the outer retina with nutrients; and the ciliary body. The body consists of muscle (meridonal fibres and circular fibres) and process, which allows a connection point to suspensory ligaments called zonules. The ciliary body has many important roles, mostly producing aqueous fluid humor. This is a fluid that (along with vitreous fluid) fills the eye, providing its structure. The fluid provides enough pressure to maintain the structure, and is accomplished through a delicate interplay between input and output of fluid that will be discussed later. A third component of this layer is the iris, which is found between the lens and the cornea, and what changes shape to control the entrance of light.
The final and most inner layer of the eye is the retina, which has the role of detecting light ad send the stimulus into the brain for processing. It is composed of two main layers, the pigmented outer layer (retinal pigment epithelium) which connects to the choroid layer, and a neural layer, which consists of photoreceptors called rods and cones, which are stimulated by light and send impulse down neurons. These neurons meet up at the optic disc, which creates the beginning of the optic nerve. On the centre of the posterior wall of the retina is a structure called the macula. It is a highly pigmented area, containing a depression called the fovea centralis, which contains a high concentration of cone photoreceptors, giving an area of high visual acuity. This is the area we use when reading for example.
What are the choroid and retina
The next layer is the vascular layer, consisting of choroid vessels; that supplies the outer retina with nutrients; and the ciliary body. The body consists of muscle (meridonal fibres and circular fibres) and process, which allows a connection point to suspensory ligaments called zonules. The ciliary body has many important roles, mostly producing aqueous fluid humor. This is a fluid that (along with vitreous fluid) fills the eye, providing its structure. The fluid provides enough pressure to maintain the structure, and is accomplished through a delicate interplay between input and output of fluid that will be discussed later. A third component of this layer is the iris, which is found between the lens and the cornea, and what changes shape to control the entrance of light.
The final and most inner layer of the eye is the retina, which has the role of detecting light ad send the stimulus into the brain for processing. It is composed of two main layers, the pigmented outer layer (retinal pigment epithelium) which connects to the choroid layer, and a neural layer, which consists of photoreceptors called rods and cones, which are stimulated by light and send impulse down neurons. These neurons meet up at the optic disc, which creates the beginning of the optic nerve. On the centre of the posterior wall of the retina is a structure called the macula. It is a highly pigmented area, containing a depression called the fovea centralis, which contains a high concentration of cone photoreceptors, giving an area of high visual acuity. This is the area we use when reading for example.
What are the muscles of the eyes and eyelid
Supporting structures of the eye include the eyelids and extraocular muscles. The eyelids obviously cover the eyes, providing protection to the eyes, as well as helping keep them lubricated (when we blink etc). It consists of 5 main layers (superficial to deep):
Skin and subcutaneous tissue
Orbicularis oculi (muscle that closes the eyelid, innervated by facial nerve)
Tarsal plates (glands to secrete oil into eye to prevent evaporation of tear film)
Levator apparatus (levator palpebrea superioris and superior tarsal muscle, opens eyelids, innervates buy occulomotor nerve)
Conjuctiva
*Sensory innervation: ophthalmic nerve (upper) and maxillary nerve (lower)
Innervation is important as something to look out for on examination is ptosis, which is caused then there is palsy of CNIII, causing the drooping eyelid.
What are the extraocular muscles of the eyes
The extraocular muscles allow for the movement of the eyes. They consist of six different muscles (for each eye), all allowing for a different movement of the eye: (see table)
SO4 LR6, rest are CNIII. Sometimes they are hard to comprehend, but the best way to remember them is to know that four rectus muscles, and these correspond to either up, down, left or right (in essence). The obliques are a little more complicated, but the best way to understand is to look at them using a YouTube video. See how if you pulled them, what movements they would make, and through that is becomes more manageable. But put simply, the obliques do the opposite of their name. Superior oblique helps the eye move down and out, the inferior helps the eye move up and out.
These are the main structures of the eye that should help us understand the processes that allow for converting light into visual images.
What are the directions and movements of the extraocular muscles
Describe the visual pathway
- Light hits cornea (tear film)
- Light is refracted (air->fluid medium)
- Fine focusing from lens
- Light hits retina
- Phototransdution
A light ray hits the eye at the cornea, which begins the process bending the light towards the retina through refraction. Refraction is phenomenon in which when light enters a different medium (i.e from gas to liquid) its trajectory is redirected. That is the level in which you need to understand refraction, as we just need to appreciate that as light hits the cornea, it is redirected towards the retina and more specifically towards the photoreceptors. To be even more specific, it is not the cornea itself that refracts light. A tear film (a lipid bilayer) in front of the cornea allows refraction to happen. The majority of the refraction required for light to hit the retina is done at this point. It then can pass through aqueous fluid within the anterior chamber and hits the lens. The lens then makes fine final adjustments to ensure the light hits the retina. It is here that Phototransduction occurs.
Phototransduction is the process in which light is converted to a sensory impulse, that is subsequently sent into the brain to be processed. This process involves several different cells.
What are the 2 type of photoreceptors and thier role
Two main types, rods and cones
Cones split into three other types, based on wavelength range they capture
Rods are scotopic, useful in dim light
Cones are phototopic, good for colour vision, visual acuity and edge detection
What is the process of phototransduction
When a light ray moves into a photoreceptor, it hits an opsin molecule, which converts the pigment from its cis form to a trans form, separating it from the opsin molecule. This opsin is the ‘activated’ and free to roam the cell. This free form of opsin is then able to activate a protein called transducin, which in turn is able to activate an enzyme called phosphodiesterase (PDE).
Usually in photoreceptors, when no light has been detected, gaunylate cyclase is able to convert GTP to cyclic GMP, which binds to channels on the photoreceptor membrane and allow ions into the cells, creating receptor potentials (similar to action potentials), which travels down the photoreceptor cell and releases the neurotransmitter glutamate. This causes an inhibitory post synaptic potential, preventing the release of neurotransmitters at the bipolar cell-ganglion cell synapse. With no neurotransmitter release, they do not send an impulse to ganglion cells, and no stimulus is sent down the optic nerve and to the brain.
When light is detected and PDE is produced, it breaks down cGMP (deactivating it), preventing it from binding to ion channels, which as a result close. No movement of ions into the photoreceptor repolarises the cell into a hyperpolarised state. This stops neurotransmitter release into the synaptic cleft between photoreceptor and bipolar cell. Little presence of glutamate stimulates the bipolar cell, keeping ions in the bipolar cell and depolarising the cell, allowing for potential to be sent through the cell. This causes the release of glutamate at the bipolar cell-ganglion cell synapse, causing an excitatory post synaptic potential. This action potential spreads down the ganglion axon, and conjoins with other axons towards the optic disc, forming the optic nerve.
This is the main process, but horizontal and Amacrine cells can be found at the different synaptic junctions (PR-BC, BC-GC respectively). Their role is to release various neurotransmitters that can inhibit and the surrounding cells. This prevents hypersensitivity to light, allowing for the stimulus to be very precise, increasing acuity.
Desribe the visual pathway
Signal sent down optic nerve. Nasal tracts decussate at the optic chiasm
Image is flipped (L->R) and inverted to create final image we perceive
At this point the optic nerve has been stimulated, and it sends the impulse down the optic nerve pathway in order for the image to be processed. The optic nerve leaves through the optic cavity and passes through the optic canal. It passes through the superior orbital fissure and converges with its contralateral counterpart at the optic chiasm (located superior to the sella turcica of the sphenoid bone). Here nerves fibres form the nasal aspect of the retina decussate and run along the contralateral side, this is so all images detected by the left side of the eyes (images from the right side) are processed in the left side of the brain. They travel down the optic tract to the Lateral Geniculate Nucleus (LGN), a second order sensory neuron in the thalamus. The LGN then sends to impulse along axons called optic radiations with loop through either the parietal or temporal lobs directly to the calcarine sulcus of the occipital lobe, where the image is processed. The route of the radiation corresponds with visual field, with parietal radiations corresponding with lower visual fields (and vice versa). The image from both eyes is merged to form a final image. Here, the body then inverts and flips it left to right to give us information that is correctly orientated within space. This is how our eyes and brain are light and convert it to an image.
We now have our image, which we the can create a response to. In terms of how the eyes can react, there are a number of things our eyes may do, mostly to create a better image for us to interpret.
Describe the pupillary light Reflex
- Pupils constriction/dilate in response to variable light levels
- Constriction is a parasympathetic response
- Stimulus sent to occipital lobe, which causes a bilateral efferent response via the Edinger-Westphal nucleus.
- Constriction of sphincter pupillae muscle->contriction of pupil
- Dilation is a sympathetic response
- Stimulus she to ciliospinal centre. Postsynaptic neurons pass down to cervical chain, then up carotid plexus to ophthalmic nerve
- Constriction of dilator pupillae muscle-> dilation of pupil
The first response from the body is to dilate or constrict the pupil. This is done depending on distance and light. If the object is too far away or too dark, the pupil can dilate to allow more light in. If too close or too bright, the pupil can constrict. This response is a balance between sympathetic and parasympathetic response. Parasympathetic innervation leads to pupillary constriction. A stimulus is sent to the occipital lobe, which then sends a bilateral response through the Edinger-Westphal nucleus near the occulomotor nerve nucleus. The efferent response then travels along the third cranial nerve and synapses at the cilliary ganglion, causing the sphincter pupillae muscle to contract, constricting the pupil.
Sympathetic innervation leads to pupillary dilation. Once the afferent impulse reaches to cortex it stimulates the ciliospinal centre. Post synaptic neurons take a convoluted path down the brain stem and exit at the cervical sympathetic chain and the superior cervical ganglion. They synapse at this ganglion, where third-order neurons travel through the carotid plexus and enter the orbit through the first division of the trigeminal nerve (Ophthalmic nerve). This stimulates constriction of the dilator pupillae muscle, dilating the eye.
It is important to note that whilst the stimulus may be unilateral, when forming an efferent response, the nuclei send bilateral signals, so that both eyes respond to the stimulus.
How does accommodation
- Fine focus done by lens
- Focuses light onto macular region (of concerted photoreceptors)
- High level of acuity
- Lens is thickened or narrowed to refract light so that it focuses onto this retina.
- In accommodation, ciliary body contracts, loosening zonules, thickening the lens, bending light to greater degree
- Stimulated by occulomotor nerve (CNIII)
Another response would be if the image was not focused. Whilst the majority of light is focused onto the retina via the cornea, fine focus is controlled by the lens. This is all to do with ensuring the light hits the macular area, where this a high concentration of photoreceptors which would increase acuity. If the image is blurred, this may be because the light ray is focused in front of or behind the retinal wall. In response to this, the lens can be made thicker or thinner in order to aim light onto retina. This done through use of the ciliary body and zonules. The zonules are suspensory ligaments, and when the ciliary muscle is at rest, the zonules are held taught, keeping the lens thinner and more concave. If an object is too close, then an impulse stimulates the cilliary ganglion (form CNIII) causing contraction of the ciliary muscle. This pulls on other ligaments that move the lens anteriorly, loosening the zonule and allowing the lens to thicken and become more convex.
What is convergence
A final response to an object being too close or not in focus would be to move the eyes. This is so that the eye can target photoreceptors closer to the macula of the eye, which has a higher concentration of photoreceptors and allows for greater acuity. The response from the extraocular muscles would be to make the eyes converge, that is make them come together. To do this, the medial rectus muscles would be stimulates via the occulomotor nerve, as well as the superior oblique which rotates the eyes inferiorly and medially. This would be done via stimulation of the abducens nerves (CNIV).
What is Visual Acuity Test
- Snellen chart most common test for visual acuity
- Read lowest line possible for each eye
- Score recorded as 6/X
- 6/6 normal vision
- 6/12 worsening vision (can see at 6m what should be seen at 12m)
The first usually performed is for visual acuity (the ability of the eye to distinguish shapes and details at a given distance). This is usually tested using a Snellen chart. The is asked to read the lowest line from a chart for each eye (chart is usually a 6m distance away). Score is recorded as 6/X, with 6/6 normal vision (can see at 6m what is normally read at 6m). An example of worsening vision would be 6/12 (see at 6m what is normally seen at 12m).
Also honourable mention to LogMAR exam, which is performed in hospitals.
How do we assess Visual fields and extraocular muslces
Confrontation exam to test visual fields (fields compared with your own)
Highlights issues with peripheral fields and ‘blind spot’
Asking patient to follow finger whilst you make H shape will highlight any extraocular muscle issues
Visual fields can be checked using confrontation, this is when you compare your visual field to the patient’s monocularly, by performing different movements (clinical skills will demonstrate these). During these movements you can also check for a blind spot (where the optic disc is). Movements will also show if there are any innervation issues, as certain movements that cannot be completed by the eye would correlate with a motor cranial nerve issue.
What are the common refractive errors
If we are testing the eyes for problems, what are common issues of the eyes?
One of the biggest issues that occurs in people all of the world is refractive errors that lead to an impaired ability to image focus. There are four very common refractive errors that occur in people, and these are myopia, hyper(metr)opia, presbyopia and astigmatism. Myopia and hyperopia of sophisticated terms for short and farsightedness. Here there is an issue with the actual shape of the eye. In people with myopia, they possess longer eyeballs than usual, which means that light focuses before the retina, causing a blurry image when it hits the retina. The lens relaxes so that the image focuses onto the retina. In hyperopic people, it is the opposite. The shortened eyeball means that light is focused behind the retina, so that the lens must use accommodation to bring the image back into focus. This is why they are farsighted, as they have already utilised their ability to accommodate and cannot accommodate further for objects that are too close to them.
Presbyopia is the loss of accommodation ability, usually through hardening of the proteins in the lens or weakening of the ciliary body. This often starts to happen at aged 50 before there is no accommodation left at around 65 years old. Presbyopia can seem similar to hyperopia as both require ‘reading’ glasses to help, but in hyperopia, there is still an ability to accommodate, it just cannot compensate for the shape of the eyeball.
Astigmatism occurs when there is an error in the shape of the cornea. With this there is an uneven image projected onto the retina, causing blurry vision.
What are visual field defects and how can they occur
Defects in visual fields can occur when there is a lesion in the nerve, or in the blood supply to that nerve
Depending on the location of the nerve, it will affect the visual field in a different way
Pre-chiasmal lesions: ipsilateral monocular visual field defect
Post-chiasmal lesions: homonymous visual field defects of the contra lateral side
Lesions compressing hemianopiathe chiasm (pituitary adenomas): bitemporal
These common problems with the eye are all to do with the eye itself, but often visual defects can occur due to lesions within the visual pathway. Where the lesion occurs determines the form and severity of the defect. Looking back at the visual pathway, lesions can occur in many areas. If there is a lesion of the (whole) optic nerve, this will prevent the whole image from that eye travelling to the occipital cortex, leading to total blindness (anopia) in that eye, also known as monocular anopia. If there is a lesion in the sagittal plane of the optic chiasm that cuts through the decussation of the nasal optic pathways, this prevents the temporal image form being processed. As a result, the problem is with the temporal view in both eyes, so bitemporal, and only half of the image in each eye is lost, giving us a hemianopia: bitemporal hemianopia. If the temporal pathway (the pathway that does not decussate, providing a nasal image) is damaged, then this results in patient blindness is the eye of the same side of the lesion. This is called a right or left nasal hemianopia. If there is an optic tract lesion, this will remove the contralateral side image in both eyes, as at this point all images have passed to the appropriate side for processing. If there is a right sided lesion, this would cause a left homonymous hemianopia (partial left blindness in both eyes). Lesions in the optic radiations lead to homonymous anopia in whatever quadrant that radiation corresponds to. For example, a lesion in the right parietal radiations would lead to a left homonymous superior quadrantanopia. The last area a lesion could occur would be in the occipital lobe itself. This would lead to homonymous hemianopia similar to that of the optic tract lesion, however there is a chance for macular sparing. This is due to the different blood supples. The occipital lobe receives blood from the posterior cerebral artery, whereas the macula is supplied by the middle cerebral artery. If a lesion in the PCA were to happen, the macula would still be supplied and therefore would still be seen by the patient.
What are the main causes of visual defect
What are cataracts
Damage to the lens over time, causing crystallin to denature. As a result, lens becomes opaque
Risk factors: UV exposure, diabetes, steroid use, smoking, ocular trauma
Management: reduce rate of progression though risk factor control
Management: surgery to replace lens: Phacoemulsification
The final two eye pathologies that you need to have a detailed understanding on are cataracts and glaucoma. This is because of how common they are around the world.
Cataracts is a condition of the lens. The lens of the eye contains crystallins, which keep the lens transparent. In cataracts, these cystallins can denature (mainly due to UV) and cause the lens to become opaque, altering visual acuity and colour perception. The two most common types of cataracts are cortical cataracts (new cortical fibres are produced concentrically, thickening and hardening the lens) and posterior subcapsular cataracts (migration and elongation of lens epithelial cells, Wedl cells). There are many risk factors for cataracts, mainly UV exposure, diabetes, steroid use, smoking and ocular trauma are most common. This process will often take many years to become severe and drastically impair quality of life. To slow the rate of disease progression, controlling of risk factors is the conservative management taken. But when symptoms are too severe, it is at that point that cataracts surgery can be performed. Also called Phacoemulsification, the opacified lens is broken down using US and the fragments are aspirated. A new lens is then implanted. This process can be completed in as quick as 5 minutes, with the patient returning several weeks later to perform surgery on the other eye. This new lens does not have the ability to accommodate, but usually when patients require surgery they are at an age where they have already lost the natural ability to accommodate anyway.
What is Glaucoma
Health intraocular pressure (IOP) of 14-24mmHg
In glaucoma >24mmHg
Increased IOP due to imbalance between aqueous humour production and outflow
Type depends on what is causing build up
Primary open angle glaucoma most common, resistance in outflow, with raised IOP causing ganglion damage over time->progressive blindness
Angle-closure glaucoma is acute and a medical emergency, causes redness and pain compared to open closure glaucoma.
In healthy eyes, pressure of the eye is controlled through flow of aqueous humour. This supplies oxygen and nutrients to the eye, as well as removing waste products. It is produced by non-pigmented epithelium on ciliary body. If flows into the position chamber around the lens before flowing through the iris into the anterior chamber. Outflow is then split into different route. 90% of outflow is through the trabecular network, in which humour drains through a trabecular network and out through the Canal of Schlemm and into episcleral vasculature. 10% outflows through the uveoscleral outflow, which drains into the urea and sclera of the eye. This constant flow maintains a intraocular pressure (IOP) of 14-21mmHg. In glaucoma, there is a problem with this balance of production and removal, leading to raised IOP. Glaucoma can be open or closed angle depending on the anatomical structure of the anterior chamber affecting flow. In primary open-angle glaucoma (the most common type), even though the iridocorneal angle appears open, there is increased resistance to the outflow through the trabecular mesh work. This causes IOP to raise, leading to ganglion cell death causing permanent visual loss (loss often in a pattern of interior->superior). It will often present with visual field defects, before examining a cupped optic disc and IOP >24mmHg. In angle-closure glaucoma, there is normally an acute rise in IOP due to narrowing of the anterior angle of the eye. Often a person will have a short eye length and shallower anterior chamber, causing reduced drainage. This is mediated by a pupillary block between the iris and the lens when the iris is in the mid-dilated position. This causes the peripheral iris to bow forward, blocking drainage and rapidly increasing IOP, typically >30mmHg. This is a medical emergency, so must be managed asap.
In POAG, there is more time to prevent the progression of optic nerve damage and present sight, mainly done by reducing IOP. This can be done medically or surgically:
Generic prostaglandin analogue (increased US outflow)
360 degree selective laser trabeculoplasty (SLT)
Trabeculectomy
Glaucoma filtration surgery
ACG is a medical emergency and IOP must be reduced asap. Along with analgesia, IOP is first stabilised using a triad of:
Beta-blockers (reduce aqueous production)
Pilocarpine (increase US outflow)
IV acetazolamide (reduces aqueous production)
*also topical steroids to reduce inflammation
Once controlled, a peripheral iridectomy is performed to allow a separate route for aqueous drained (though the iris).
Describe the gross anatomy of the ear
As we all know the main function of the ears is to enable to hear sound, but also helps with balance, particularly (postural equilibrium and coordination of head and eye movements). The ear is specially designed externally and internally to allow us to do this so well.
The ear can be split into three main sections, the external, middle and internal ear
Describe the anatomy of the external ear
The auricle or pinna, is musculocutaneous tissue attached to the skull, and is effectively cartilage covered in skin. It has numerous grooves and ridges (helix, crus and anti helix) that help direct sound into the canal. It is direct to the centre of the auricle, which is called the concha. This and the opening into the external acoustic canal (foramen) are covered by the Tragus (little flap of cartilage in front of opening)
Sound then enters the external acoustic meatus, which is a glorified chasm into the head made up of cartilage and fibrous membrane that directs sound onto the most medial part of the external ear; the tympanic membrane.
What is the tempanic membrane
Tympanic membrane is a thin membrane that stretches across the EAC
Vibrates in response to sound wave stimulus, causing vibration of ossicles found in the tympanic cavity of the middle ear
The tympanic membrane (aka the eardrum) is a thin membrane that stretches across the EAC. Upon sound waves striking it, it vibrates against some bones called the ossicles in the middle ear that help focus to sound onto the cochlea (in the inner ear). There are lots of landmarks on the tympanic membrane, with the two main sections being the Pars tensa and Pars flaccida. The centre of the tympanic membrane is called the Umbo, a connection point between the tympanic membrane and the most distal ossicle, the malleus.
What are the ossicles
Found in tympanic cavity
Three bones, malleus, incus & stapes
Amplify sound waves
Focus sound onto oval window of labyrinthine wall, into the cochlea
These ossicles can be found in the middle ear, also known as the tympanic cavity. This is roughly hexagonal cavity that its medial wall is called the labyrinthine wall, which has two windows (oval and round) that are important in transferring sound into the inner ear. Also found in the middle ear are the pharyngotympanic tube which is a cavity that helps to equalise pressure on both sides of the tympanic membrane. It extends into the pharynx, which is why when we swallow it helps the pressure in our ears during plane journeys for example. It is also why when we get throat infections, it pain can often radiate into the ear.
The ossicles are in fact 3 bones, called the malleus (hammer), incus (anvil) and stapes (stirrup). These take vibrations from the tympanic membrane and precisely focus them onto the oval window of the labyrinthine wall so that it can enter the inner ear. They are also able to amplify the sound, helping us hear smaller sounds. It is necessary to increase the force of these vibrations as sound waves lose intensity as they travel through the air of the EAC, meaning it would be more difficult to hear.
What is the inner ear and what does it consist off
Semicircular canals & vestibule- help for balance and coordination of head and eyes
Cochlea- important for converting sound waves into electrical impulse
The inner ear contains the semicircular canals, vestibule (helpful for balance etc) and cochlea, important for sound. (Latin for snail) It is a spiralled structure that is able to convert sound waves into electrical impulses, which it transports to the temporal lobe via the cochlear nerve. Which eventually becomes the eighth cranial nerve, vestibulocochlear nerve.
How does sound transduction occur
- Sound enters ear, causing tympanic membrane to vibrate
- Tympanic movement causes vibration of ossicles
- Information reaches stapes footplate, sending vibrations into bony labyrinth perilymph via oval window
- Vibration drawn into cochlea up the scala vestibuli
- This vibrates the cochlear duct, causing bending of hairs in basilar membrane (of CD, called stereocilia) against a tectorial plate
- This causes stereocilia to ‘fire’ and create an action potential that is sent down the cochlear nerve and into temporal lobe for processing
- Residual vibration enters scala tympani and out the round window, where it dissipates
The cochlea is very sophisticated, with the best way to describe anatomy being in the context of its physiology. Sound enters into the ear where it hits the tympanic membrane. The tympanic membrane then vibrates in response to the sound.
NB
Sounds of a lower pitch/frequency produce a slower rate of vibration.
Sounds of a lower volume/amplitude produce a less dramatic vibration.
The movements of the tympanic membrane vibrate the ossicles, passing on the information of frequency and amplitude. This information reaches the footplate of the stapes, which moves in a piston-like action, which sends vibrations into the bony labyrinth via the oval window. These vibrations pass through a fluid within the bony labyrinth called the perilymph.
NB Inferior to the oval window is the round window. This is important for the transfer of sound. As the cochlea is filled with fluid (perilymph), vibrations could not travel through the solid, bony structure. There needs to be a malleable area in order for the perilymph to be displaced as vibrations to pass through it. This is what the round window helps accomplishes, allowing vibrations into the bony labyrinth.
These vibrations are drawn into the (spiral system) cochlea, travelling from the base to apex via a cavity called scala vestibuli, and descending to the round window via the scala tympani.
NB Another structure around these scala is called the cochlear duct. Wedged in between both structures, it is filled with endolymph. The three structures are separated by membranes:
Reissner’s membrane (cochlear duct and scale vestibuli)
Basilar membrane (cochlear duct and scale tympani)
Vibrations from the scala vestibuli vibrate the flexible Reissner’s membrane, which vibrates the cochlear duct, which vibrates the Basilar membrane, which vibrates the scale tympani.
The organ of corti is a sophisticated structure situated in the basilar membrane and contains specialised hair cells closely covered by a structure called the tectorial membrane. When stimulated by vibrations, it bends these hairs against the tectorial membrane, causing hair cells to fire. This creates and action potential, which sends a nerve impulse to the brain via the cochlear nerve.
NB Different areas to the basilar membrane move variably in response to different frequencies of sound. Lower frequencies vibrate the basilar membrane close to the apex of the cochlea (vice versa). This is known as tonotopic organisation.
What is the auditory cortex
From the cochlear nerve, in joins up with the vestibular nerve to create CNVIII, vestibulocochlear nerve
What are the different ear examinations
One of the most basic ways is by using a tuning fork (512Hz). This apparatus causes vibrations that can be used to assess for hearing loss. There are three main types of hearing loss, which are conductive (canal blockage), sensorineural (cochlea and nerve issues) and mixed. A tuning fork can be used to distinguish between these different types. The two tests performed to determine the type of loss a person has are called the Rinne’s and Weber’s test. Rinne’s test is performed first. The fork is vibrated initially near the patient’s ear, and then placed on the mastoid process (behind ear). This is testing the quality of air and bone conduction. If normal (positive), air conduction should be louder. If pathological (negative), then bone conduction willl be louder. The issue with this is that there can be false positives and false negatives. These false results can imply sensorineural hearing loss. To test for this we use the Weber’s test. The tuning fork is vibrated and placed on the forehead of the patient. If there is no lateralisation, this is a healthy ear. If there is lateralisation to the ‘good ear’, this implies there is poor bone and air conduction in ht bead ear, implying SNHL. If there is lateralisation to the bad ear (side with BC>AC), this may be due to increased cochlear sensitivity on bad ear, making BC louder in bad ear than in good ear. This would imply CHL.
What is otoscopy and auditometry
Other exams can be performed, such at otoscopy to look at the tympanic membrane itself to look for damage or an EAC blockage (usually wax). Auditometry exams can also be performed to assess a person’s hearing ability and can give an indication into the form of hearing loss they have. Frequency is shown against the amplitude to which someone is able to hear said frequency. In age-related hearing loss, we lose higher frequencies first, so may show a drop off in ability to hear as the frequency increases.
What are the different types of hearing loss
There are 2 main types: Conductive and Sensorineural
There are many different causes to these types of hearing loss, with management dependent on the cause. For example, if there is a blockage, then this is removed (using drops or surgical intervention). Hearing aids can also be offered. There are many different types of hearing aids depending on the aetiology, they can be as basic hearing aids that help amplify the sound, or cochlear implant that works by creating an electrical impulse form sound waves in place of a defective cochlea.
