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Deep Learning Technology: Sebastian Arnold, Betty van Aken, Paul Grundmann, Felix A. Gers and Alexander Löser. Learning Contextualized Document Representations for Healthcare Answer Retrieval. The Web Conference 2020 (WWW'20)
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In mechanical anisocoria, this is the result of damage to the iris dilator muscle, which may be caused by trauma, angle-closure glaucoma, surgery such as cataract removal, or uveitis (inflammation of the eye). Slit lamp examination is often used as a diagnostic aid: damage to the dilator muscle is indicated by anisocoria when light intensity is lowered.Anisocoria refers to a common eye condition in which the two pupils differ in size.
A mydriatic is an agent that induces dilation of the pupil. Drugs such as tropicamide are used in medicine to permit examination of the retina and other deep structures of the eye, and also to reduce painful ciliary muscle spasm (see cycloplegia). Phenylephrine (e.g. Cyclomydril) is used if strong mydriasis is needed for a surgical intervention. One effect of administration of a mydriatic is intolerance to bright light (photophobia). Purposefully-induced mydriasis via mydriatics is also used as a diagnostic test for Horner's syndrome.
Relative afferent pupillary defect (RAPD) or Marcus Gunn pupil is a medical sign observed during the swinging-flashlight test whereupon the patient's pupils constrict less (therefore appearing to dilate) when a bright light is swung from the unaffected eye to the affected eye. The affected eye still senses the light and produces pupillary sphincter constriction to some degree, albeit reduced.
The most common cause of Marcus Gunn pupil is a lesion of the optic nerve (between the retina and the optic chiasm) or severe retinal disease. It is named after Scottish ophthalmologist Robert Marcus Gunn.
A second common cause of Marcus Gunn pupil is a contralateral optic tract lesion, due to the different contributions of the intact nasal and temporal hemifields.
Esophoria is an eye condition involving inward deviation of the eye, usually due to extra-ocular muscle imbalance. It is a type of heterophoria.
Causes include:
- Refractive errors
- Divergence insufficiency
- Convergence excess; this can be due to nerve, muscle, congenital or mechanical anomalies.
Unlike esotropia, fusion is possible and therefore diplopia is uncommon.
Anisocoria is a condition characterized by an unequal size of the eyes' pupils. Affecting 20% of the population, it can be an entirely harmless condition or a symptom of more serious medical problems.
Anisocoria is a common condition, defined by a difference of 0.4 mm or more between the sizes of the pupils of the eyes.
Anisocoria has various causes:
- Physiological anisocoria: About 20% of normal people have a slight difference in pupil size which is known as physiological anisocoria. In this condition, the difference between pupils is usually less than 1 mm.
- Horner's syndrome
- Mechanical anisocoria: Occasionally previous trauma, eye surgery, or inflammation (uveitis, angle closure glaucoma) can lead to adhesions between the iris and the lens.
- Adie tonic pupil: Tonic pupil is usually an isolated benign entity, presenting in young women. It may be associated with loss of deep tendon reflex (Adie's syndrome). Tonic pupil is characterized by delayed dilation of iris especially after near stimulus, segmental iris constriction, and sensitivity of pupil to a weak solution of pilocarpine.
- Oculomotor nerve palsy: Ischemia, intracranial aneurysm, demyelinating diseases (e.g., multiple sclerosis), head trauma, and brain tumors are the most common causes of oculomotor nerve palsy in adults. In ischemic lesions of the oculomotor nerve, pupillary function is usually spared whereas in compressive lesions the pupil is involved.
- Pharmacological agents with anticholinergic or sympathomimetic properties will cause anisocoria, particularly if instilled in one eye. Some examples of pharmacological agents which may affect the pupils include pilocarpine, cocaine, tropicamide, MDMA, dextromethorphan, and ergolines. Alkaloids present in plants of the genera "Brugmansia" and "Datura", such as scopolamine, may also induce anisocoria.
- Migraines
Exophoria can be caused by several factors, which include:
- Refractive errors - distance and near deviation approximately equal.
- Divergence excess - exodeviation is more than 15 dioptres greater for distance than near deviation.
- Convergence insufficiency - near exodeviation greater than distance deviation.
These can be due to nerve, muscle, or congenital problems, or due to mechanical anomalies. Unlike exotropia, fusion is possible in this condition, causing diplopia to be uncommon.
Exophoria is a form of heterophoria in which there is a tendency of the eyes to deviate outward. During examination, when the eyes are dissociated, the visual axes will appear to diverge away from one another.
The axis deviation in exophoria is usually mild compared with that of exotropia.
Miosis is excessive constriction of the pupil. The term is from Ancient Greek , "mūein", "to close the eyes.
The opposite condition, mydriasis, is the dilation of the pupil. Anisocoria is the condition of one pupil being more dilated than the other.
The Marcus Gunn pupil is a relative afferent pupillary defect indicating a decreased pupillary response to light in the affected eye.
In the swinging flashlight test, a light is alternately shone into the left and right eyes. A normal response would be equal constriction of both pupils, regardless of which eye the light is directed at. This indicates an intact direct and consensual pupillary light reflex. When the test is performed in an eye with an afferent pupillary defect, light directed in the affected eye will cause only mild constriction of both pupils (due to decreased response to light from the afferent defect), while light in the unaffected eye will cause a normal constriction of both pupils (due to an intact efferent path, and an intact consensual pupillary reflex). Thus, light shone in the affected eye will produce less pupillary constriction than light shone in the unaffected eye.
A Marcus Gunn pupil is distinguished from a total CN II lesion, in which the affected eye perceives "no" light. In that case, shining the light in the affected eye produces no effect.
Anisocoria is absent. A Marcus Gunn pupil is seen, among other conditions, in optic neuritis. It is also common in retrobulbar optic neuritis due to multiple sclerosis but only for 3–4 weeks, until the visual acuity begins to improve in 1–2 weeks and may return to normal.
Physiological anisocoria is when human pupils differ in size. It is generally considered to be benign, though it must be distinguished from Congenital Horner's syndrome, pharmacological dilatation or other conditions connected to the sympathetic nervous system.
The prevalence of physiological anisocoria has not been found to be influenced by the sex, age, or iris color of the subject.
When detected during childhood, without any other symptoms and when other disorders are discarded through clinical tests, it should be considered a developmental or genetic phenomenon.
Asymmetric pupil or dyscoria, potential causes of anisocoria, refer to an abnormal shape of the pupil which can happens due to developmental and intrauterine anomalies.
Tropicamide is used as a mydriastic agent during cataract surgery. Anticholinergics such as atropine, hyoscyamine, and scopolamine antagonize the muscarinic acetylcholine receptors in the eye. By blocking these receptors, the pupils are no longer capable of constriction and dilation results. Such alkaloids present in many plants of the family "Solanaceae" may also induce mydriasis when used
The neurotransmitter norepinephrine regulates many physiological processes in the body and brain. One of them is the autonomic constriction and contraction of certain muscles. The psychoactive drug cocaine potently inhibits the normal reuptake of norepinephrine into presynaptic nerve terminals, resulting in an increased level of extracellular norepinephrine. Amphetamines also potently release and prevent the reuptake of norepinephrine. The released norepinephrine then proceeds to bind to adrenergic receptors, and the biological effects of norepinephrine finally occur. When a solution of cocaine is dropped into the eye, this process takes place and the end result is dilation of the pupil. Cocaine itself is not typically used for this task, however. Any potent norepinephrine reuptake inhibitor or release agent should be capable of such an effect.
Opiates such as morphine and heroin do not cause pupil dilation. Instead they cause miosis (pupil contraction). Mydriasis occasionally occurs during opiate rebound and withdrawal.
Superior limbic keratoconjunctivitis is an ocular disease characterized by episodes of recurrent inflammation of the superior cornea and limbus, as well as of the superior tarsal and bulbar conjunctiva.
Even though the pathophysiology remains unclear, it is thought that mechanical trauma from tight upper lids or loose redundant conjunctiva could lead to the disruption of normal epithelium. This mechanical hypothesis is supported by the increased lid apposition of exophthalmic thyroid patients, who are known to have an increased incidence of superior limbic keratoconjunctivitis.
Patients present with red eye, burning, tearing, foreign body sensation, mild photophobia. Inflammation and thickening of the conjunctiva is observed, especially at the limbus.Lubrication is an effective treatment for this pathology.
There is no current cure for superficial siderosis, only treatments to help alleviate the current symptoms and to help prevent the development of further symptoms. If a source of bleeding can be identified (sources are frequently not found), then surgical correction of the bleeding source can be performed; this has proved to be effective in halting the development of further symptoms in some cases and has no effect on symptoms that have already presented.
Patients with superficial siderosis are often treated with deferiprone, a lipid-soluble iron chelator, as this medication has been demonstrated to chelate iron in the central nervous system.
While on this drug you will need a frequent blood test (weekly) to keep an eye on the blood levels as this drug is known to lower certain blood levels such as the neutrophils and WBC (white blood count) and etc. While it is ok if these levels go low in the average person, if they go low while taking Deferiprone Ferriprox it can cause life threatening infections that can result in death.
Alleviation of the most common symptom, hearing loss, has been varyingly successful through the use of cochlear implants. Most people do not notice a large improvement after successful implantation, which is most likely due to damage to the vestibulocochlear nerve (cranial nerve VIII) and not the cochlea itself. Some people fare far better, with a return to near normal hearing, but there is little ability to detect how well a person will respond to this treatment at this time.
Light entering the eye strikes three different photoreceptors in the retina: the familiar rods and cones used in image forming and the more newly discovered photosensitive ganglion cells. The ganglion cells give information about ambient light levels, and react sluggishly compared to the rods and cones. Signals from photosensitive ganglion cells have multiple functions including acute suppression of the hormone melatonin, entrainment of the body's circadian rhythms and regulation of the size of the pupil.
The retinal photoceptors convert light stimuli into electric impulses. Nerves involved in the resizing of the pupil connect to the pretectal nucleus of the high midbrain, bypassing the lateral geniculate nucleus and the primary visual cortex. From the pretectal nucleus neurons send axons to neurons of the Edinger-Westphal nucleus whose visceromotor axons run along both the left and right oculomotor nerves. Visceromotor nerve axons (which constitute a portion of cranial nerve III, along with the somatomotor portion derived from the Edinger-Westphal nucleus) synapse on ciliary ganglion neurons, whose parasympathetic axons innervate the iris sphincter muscle, producing miosis. This occurs because sympathetic activity from the ciliary ganglion is "lost" thus parasympathetics are not inhibited.
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Non-surgical therapies include:
- Shoe modifications: wearing shoes that have a wide toe box, and avoiding those with pointed toes or high heels.
- Oral nonsteroidal anti-inflammatory drugs may help in relieving the pain and inflammation.
- Injections of corticosteroid are commonly used to treat the inflammation.
- Bunionette pads placed over the affected area may help reduce pain.
- An ice pack may be applied to reduce pain and inflammation.
Surgery is often considered when pain continues for a long period with no improvement in these non-surgical therapies.
Both eccentric loading and extracorporeal shockwave therapy are currently being researched as possible treatments for tendinosis. One study found both modalities to be equally effective in treating tendinosis of the Achilles tendon and more effective than a 'wait and see' approach. Other treatments for which research is on-going includes vitamin E, vitamin B6, nitric oxide, Platelet Rich Plasma (PRP), and stem cell injections.
One study found increased achilles tendon healing in rats supplemented with high doses of vitamin C, which is needed for collagen synthesis.
Treatment typically is supportive and includes monitoring and observation.
The first-line treatment for a muscular strain in the acute phase include five steps commonly known as P.R.I.C.E.
- Protection: Apply soft padding to minimize impact with objects.
- Rest: Rest is necessary to accelerate healing and reduce the potential for re-injury.
- Ice: Apply ice to induce vasoconstriction, which will reduce blood flow to the site of injury. Never ice for more than 20 minutes at a time.
- Compression: Wrap the strained area with a soft-wrapped bandage to reduce further diapedesis and promote lymphatic drainage.
- Elevation: Keep the strained area as close to the level of the heart as is possible in order to promote venous blood return to the systemic circulation.
Immediate treatment is usually an adjunctive therapy of NSAID's and Cold compression therapy. Controlling the inflammation is critical to the healing process. Cold compression therapy acts to reduce swelling and pain by reducing leukocyte extravasation into the injured area. NSAID's such as Ibuprofen/paracetamol work to reduce the immediate inflammation by inhibiting Cox-1 & Cox-2 enzymes, which are the enzymes responsible for converting arachidonic acid into prostaglandin. However, NSAIDs, including aspirin and ibuprofen, affect platelet function (this is why they are known as "blood thinners") and should not be taken during the period when tissue is bleeding because they will tend to increase blood flow, inhibit clotting, and thereby increase bleeding and swelling. After the bleeding has stopped, NSAIDs can be used with some effectiveness to reduce inflammation and pain.
A new treatment for acute strains is the use of platelet rich plasma (PRP) injections which have been shown to accelerate recovery from non surgical muscular injuries.
It is recommended that the person injured should consult a medical provider if the injury is accompanied by severe pain, if the limb cannot be used, or if there is noticeable tenderness over an isolated spot. These can be signs of a broken or fractured bone, a sprain, or a complete muscle tear.
Keratoconjunctivitis is inflammation ("-itis") of the cornea and conjunctiva.
When only the cornea is inflamed, it is called "keratitis"; when only the conjunctiva is inflamed, it is called "conjunctivitis".
There are several potential causes of the inflammation:
- Keratoconjunctivitis sicca is used when the inflammation is due to dryness. ("Sicca" means "dryness" in medical contexts.) It occurs with 20% of rheumatoid arthritis patients.
- The term "Vernal keratoconjunctivitis" (VKC) is used to refer to keratoconjunctivitis occurring in spring, and is usually considered to be due to allergens.
- "Atopic keratoconjunctivitis" is one manifestation of atopy.
- "Epidemic keratoconjunctivitis" is caused by an adenovirus infection.
- "Infectious bovine keratoconjunctivitis" (IBK) is a disease affecting cattle caused by the bacteria "Moraxella bovis".
- "Pink eye in sheep and goat" is another infectious keratoconjunctivitis of veterinary concern, mostly caused by "Chlamydophila pecorum"
- "Superior limbic keratoconjunctivitis" is thought to be caused by mechanical trauma.
- "Keratoconjunctivitis photoelectrica" (arc eye) means inflammation caused by photoelectric UV light. It is a type of ultraviolet keratitis. Such UV exposure can be caused by arc welding without wearing protective eye glass, or by high altitude exposure from sunlight reflected from snow ("snow blindness"). The inflammation will only appear after about 6 to 12 hours. It can be treated by rest, as the inflammation usually heals after 24–48 hours. Proper eye protection should be worn to prevent keratoconjunctivitis photoelectrica.
Floppy eyelid syndrome is a disease whose most prominent features often include floppy upper eyelids that can be easily everted, as well as papillary conjunctivitis. It is often associated with patients with high body mass index and obstructive sleep apnea.
Floppy eyelid syndrome is thought to revolve around the upregulation of elastin-degrading enzymes, as well as mechanical factors. These can cause instability of the eyelid scaffold, resulting in the malposition of the eyelid.
There are varying types of intervention for ankyloglossia. Horton "et al.," have a classical belief that people with ankyloglossia can compensate in their speech for limited tongue range of motion. For example, if the tip of the tongue is restricted for making sounds such as /n, t, d, l/, the tongue can compensate through dentalization; this is when the tongue tip moves forward and up. When producing /r/, elevation of the mandible can compensate for restriction of tongue movement. Also, compensations can be made for /s/ and /z/ by using the dorsum of the tongue for contact against the palatal rugae. Thus, Horton "et al." proposed compensatory strategies as a way to counteract the adverse effects of ankyloglossia and did not promote surgery. Non-surgical treatments for ankyglossia are typically performed by Orofacial Myology specialists, and involve using exercises to strengthen and improve the function of the facial muscles and thus promote proper function of the face, mouth and tongue
Intervention for ankyloglossia does sometimes include surgery in the form of frenotomy (also called a frenectomy or frenulectomy) or frenuloplasty. This relatively common dental procedure may be done with soft-tissue lasers, such as the CO laser. However, authors such as Horton "et al." are in opposition to it. According to Lalakea and Messner, surgery can be considered for patients of any age with a tight frenulum, as well as a history of speech, feeding, or mechanical/social difficulties. Adults with ankyloglossia may elect the procedure. Some of those who have done so report post-operative pain.
A viable alternative to surgery for children with ankyloglossia is to take a wait-and-see approach. Ruffoli "et al." report that the frenulum naturally recedes during the process of a child's growth between six months and six years of age;
Treatment for this condition entails the maintenance of intravascular volume. Additionally, the following can be done as a means of managing FES in an individual:
- Albumin can be used for volume resuscitation
- Long bone fractures should be attended to immediately (surgery)
- Mechanical ventilation