STUDY - Technical - New Dacian's Medicine
Eye and
Vision Disorders (8)
Translation Draft
I'll be as "expeditive" as in the previous post...
Orbital tumors produce progressive, painless exophthalmia. The most common primary tumors are hemangioma, lymphangioma, neurofibroma, dermoid cyst, optic nerve glioma and mixed benign tumors of the tear gland. Metastatic orbital tumors commonly occur in breast carcinoma, lung carcinoma and lymphoma. Establishing the diagnosis by suction with a fine needle, followed by emergency radiotherapy, can sometimes save sight.
Cavernous carotid fistulas with anterior orbital drainage produce exophthalmia, diplopia, glaucoma and the appearance of sinuous red conjunctival vessels. Direct fistulas usually occur as a result of trauma. They are easily diagnosed due to dramatic signs caused by high-flow sanding and high pressure. Indirect fistulas or dural arteriovenous malformations occur more likely spontaneously, especially in older women. The signs are more subtle, and the diagnosis is frequently missed.
The combination of mild exophthalmia, diplopia, muscle enlargement and eye congestion is commonly confused with thyroid ophthalmopathy. The presence of a noise at the auscultation of the head, or reported by the patient, is a valuable indication for diagnosis. Imaging examinations reveal an enlarged upper ophthalmic vein in the orbits. Cavernous carotid sunts can be removed by intravascular embolization.
Let's get to the ptozes now! Blepharoptosis is an abnormal fall of the eyelid. Unilateral or bilateral ptosis may be congenital, following dysgenesis of the upper eyelid muscle or abnormal insertion of the aponevrosis of this muscle on the eyelid. Acquired ptosis can evolve so slowly that the patient does not realize the existence of the problem.
Observing older photos is useful for dating your debut. The existence of a history of trauma, eye surgery, contact lens use, diplopia, systemic symptoms (e.g. dysphagia or weakness of peripheral muscles) or a family history of ptosis should be investigated. Variable ptosis that worsens towards the end of the day is typical for myasthenia gravis.
Examination should focus on arguments for exophthalmia, masses or palpebral deformities, inflammation, pupil inequality or limitation of motility. The width of the palpebral fissures shall be measured with the head looking straight to quantify the degree of ptosis. Ptosis will be underestimated if the patient lifts the eyebrows compensatingly with the help of the frontal muscle.
Mechanical ptosis occurs in many elderly patients due to the extent and surplus of skin and palpebral subcutaneous adipose tissue (dermatochalasis). The additional weight of these deformed tissues causes the eyelid to fall. Enlargement or deformation of the eyelid following infection, tumours, trauma or inflammation also produces ptosis on a purely mechanical basis.
Aponevrotic ptosis is a dehiscence or acquired stretch of the aponevrotic tendon that binds the lifting muscle of the eyelid to the posterior face of the eyelid. It usually occurs in elderly patients, probably due to loss of connective tissue elasticity. Aponevrotic ptosis is also a frequent sechele of palpebral edema following infections or closed trauma of the eye socket, cataract surgery or the use of hard contact lenses.
Myogenous ptosis includes myasthenia gravis and a number of rare myopathys that occur with ptosis. The term chronic progressive external ophthalmoplegy refers to a group of systemic diseases produced by mutations in mitochondrial DNA. As the name shows, the most important signs are slow lysting progressive ptosis and limitation of eye movements. In general, diplopia is a late syndrome because all eye movements are reduced equally. In the Kearns-Sayre variant, retinal pigmentation changes and cardiac conduction disorders occur.
Biopsy of peripheral muscles reveals characteristic "irregular red fibers". Oculopharyngeal dystrophy is a distinct dominant autosomal condition, onset in middle age, characterized by ptosis, limitation of eye movements and dysphagia. Myotonic dystrophy, another dominant autosomal condition, produces ptosis, ophthalmopares, cataracts and pigment retinopathy. Patients experience muscle fatigue, myotonia, frontal baldness and cardiac abnormalities.
Neurogenic ptosis occurs due to a lesion that affects the innervation of either of the two muscles that open the eyelid: Muller's muscle or the upper eyelid lift muscle. Examination of the pupil helps to differentiate the two possibilities. In Horner syndrome, the eye with ptosis has a larger or normal pupil. If the pupil is normal and the movements of the eyeball are complete.
In oculomotor nerve paralysis, the eye with ptosis has a larger or normal pupil. if the pupil is normal, but the movements of adduction, lifting and descent are limited, there is the possibility of oculomotor nerve paralysis with the pupil's sparing. Rarely, a lesion affecting the small central subnucleus of the oculomotor complex as produces bilateral ptosis with normal pupils and eye movements.
I'll continue with the diplopia. First, it should be checked whether diplopia persists in the eye and after covering the other eye. If it persists, the diagnosis is monocular diplopia. The cause is usually intrinsic to the eye and therefore has no severe implications for the patient.
Corneal aberrations (e.g. keraconus, pteringioma), uncorrected refractive defects, cataracts or fovea traction may cause monocular diplopia. Sometimes it is a simulated symptom or a symptom of a psychiatric condition.
Diplopia improved by covering an eye is binocular diplopia and is due to disturbance of the alignment of the eyeballs. The nature of diplopia (simple image doubling or partial vertical displacement of images), how to start, duration, intermitence, diurnal variations and associated neurological or systemic symptoms should be studied.
If the patient experiences diplopia during the examination, the motility test will reveal a deficiency corresponding to the patient's symptoms. However, the subtle limitation of eyeball trips is often difficult to detect. For example, a patient with a moderate paralysis of the left abducens nerve may apparently have complete eye movements, despite the accusation of horizontal diplopia on the left-hand gaze.
In this situation, the cover test provides a more sensitive method for demonstrating poor alignment of the eyeballs. The test should be performed with the head looking straight, then with the head turned and tilted in each direction. In the example above, the cover test with the head turned to the right will maximize the movement of the eye in order to fix the target evoked by the cover test. Sometimes the cover test performed in an asymptomatic patient, as part of a routine examination, will reveal an eye deviation.
If the eye movements are complete and the alignment deficit of the eyeballs is the same in all directions of the eye (concomitant deviation), the diagnosis is strabismus. In this condition, found in about 1% of the population, the conjugation of the movements of the eyeballs is affected in the neonatal period or in early childhood.
To avoid diplopia, visual projection from the eye that does not achieve conjugation is suppressed. In some children, this situation leads to vision disturbance (amblyopia or "lazy" eye) of the deviated eye. Binocular diplopia occurs to a wide range of conditions: infectious, neoplastic, metabolic, degenerative, inflammatory and vascular.
The nature of diplopia, neurogenic or following the limitation of the movements of the eyeballs, must be identified by a condition located in orbit. Pseudotumora of the orbit, myositis, infections, tumors, thyroid disorders and muscle catching (for example, due to a cominutive fracture) produce restrictive diplopia.
The diagnosis is confirmed by the practice of a forced ab/adduction test in the office. After performing local anesthesia, the doctor catches the eye with the help of a forceps and pulls in the direction of deficient movement. if the rotational movement of the eyeball encounters resistance, it means that a restrictive process is present. The usefulness of this test is limited by the lack of popularity among patients, in practice, the diagnosis of the restriction being established by identifying other associated signs and symptoms, local disease of the orbit.
Myasthenia gravis is a major cause of diplopia. Diplopia is often intermittent, variable and is not limited to any of the individual eye movements controlled by the oculomotor nerve. Pupils are always normal. Variable ptosis may be present. Many patients have a purely ocular form of the disease, with no signs of systemic muscle fatigue.
The diagnosis can be confirmed by intravenous injection of edrofonium or by a test for acetylcholine antireceptor antibodies. The negative results of these tests do not exclude diagnosis. Botulism following food poisoning or infection of a wound can mimic ocular myasthenia. After the exclusion of restrictive diseases of the orbit and myasthenia gravis, damage to a cranial nerve that irritates the extrinsic musculature of the eye remains the most likely cause of binocular diplopia.
The oculomotor nerve (third cranial nerve) irritates the medial, lower and upper right muscles, the lower oblique muscle, the upper eyelid lift muscle and the sphincter of the iris. Oculomotor nerve paralysis produces ptosis and pupil dilation, the eye being deflected "down and out", due to the activity of the right lateral and upper oblique muscles to which no resistance is resisted. This combination of signs is very clear.
Diagnosis of an early or partial paralysis of the oculomotor nerve is somewhat more difficult to achieve. In this situation, any combination of ptosis, midriasis and weakness of the eye muscles innervated by the oculomotor nerve can be encountered. Frequent serial examinations during the evolutionary phase of paralysis along with a high degree of suspicion prevent the diagnosis from being missed.
The appearance of oculomotor nerve paralysis with pupillary damage, regardless of its degree, in an otherwise healthy patient, especially when accompanied by pain, raises suspicion of aneurysm of the Willis polygon. If the MRI examination does not reveal any compressive lesions, an arteriogram will be performed for the purpose of excluding a posterior communicative artery aneurysm or basilar artery.
If the pupil is perfectly normal, and all other components of oculomotor nerve paralysis are present, aneurysm is such a small possibility that angiogram is rarely indicated. Damage to the oculomotor nucleus in the rosral mesencephalus produces signs that differ from those caused by a lesion of the nerve itself. Bilateral ptosis is present, as the lifting muscle is innervated from a single central subnucleus.
Hypotonia of the controlled upper right muscle is also present, as it is inervated from the oculomotor nucleus on the opposite side. Sometimes both upper right muscles are hypotons. Isolated damage to the neurological nucleus reveals additional signs that suggest damage to the brain stem through infarction, hemorrhage, tumors or infections.
I'm going to continue tomorrow with the oculomotor muscle problems...
I'll be as "expeditive" as in the previous post...
Orbital tumors produce progressive, painless exophthalmia. The most common primary tumors are hemangioma, lymphangioma, neurofibroma, dermoid cyst, optic nerve glioma and mixed benign tumors of the tear gland. Metastatic orbital tumors commonly occur in breast carcinoma, lung carcinoma and lymphoma. Establishing the diagnosis by suction with a fine needle, followed by emergency radiotherapy, can sometimes save sight.
Cavernous carotid fistulas with anterior orbital drainage produce exophthalmia, diplopia, glaucoma and the appearance of sinuous red conjunctival vessels. Direct fistulas usually occur as a result of trauma. They are easily diagnosed due to dramatic signs caused by high-flow sanding and high pressure. Indirect fistulas or dural arteriovenous malformations occur more likely spontaneously, especially in older women. The signs are more subtle, and the diagnosis is frequently missed.
The combination of mild exophthalmia, diplopia, muscle enlargement and eye congestion is commonly confused with thyroid ophthalmopathy. The presence of a noise at the auscultation of the head, or reported by the patient, is a valuable indication for diagnosis. Imaging examinations reveal an enlarged upper ophthalmic vein in the orbits. Cavernous carotid sunts can be removed by intravascular embolization.
Let's get to the ptozes now! Blepharoptosis is an abnormal fall of the eyelid. Unilateral or bilateral ptosis may be congenital, following dysgenesis of the upper eyelid muscle or abnormal insertion of the aponevrosis of this muscle on the eyelid. Acquired ptosis can evolve so slowly that the patient does not realize the existence of the problem.
Observing older photos is useful for dating your debut. The existence of a history of trauma, eye surgery, contact lens use, diplopia, systemic symptoms (e.g. dysphagia or weakness of peripheral muscles) or a family history of ptosis should be investigated. Variable ptosis that worsens towards the end of the day is typical for myasthenia gravis.
Examination should focus on arguments for exophthalmia, masses or palpebral deformities, inflammation, pupil inequality or limitation of motility. The width of the palpebral fissures shall be measured with the head looking straight to quantify the degree of ptosis. Ptosis will be underestimated if the patient lifts the eyebrows compensatingly with the help of the frontal muscle.
Mechanical ptosis occurs in many elderly patients due to the extent and surplus of skin and palpebral subcutaneous adipose tissue (dermatochalasis). The additional weight of these deformed tissues causes the eyelid to fall. Enlargement or deformation of the eyelid following infection, tumours, trauma or inflammation also produces ptosis on a purely mechanical basis.
Aponevrotic ptosis is a dehiscence or acquired stretch of the aponevrotic tendon that binds the lifting muscle of the eyelid to the posterior face of the eyelid. It usually occurs in elderly patients, probably due to loss of connective tissue elasticity. Aponevrotic ptosis is also a frequent sechele of palpebral edema following infections or closed trauma of the eye socket, cataract surgery or the use of hard contact lenses.
Myogenous ptosis includes myasthenia gravis and a number of rare myopathys that occur with ptosis. The term chronic progressive external ophthalmoplegy refers to a group of systemic diseases produced by mutations in mitochondrial DNA. As the name shows, the most important signs are slow lysting progressive ptosis and limitation of eye movements. In general, diplopia is a late syndrome because all eye movements are reduced equally. In the Kearns-Sayre variant, retinal pigmentation changes and cardiac conduction disorders occur.
Biopsy of peripheral muscles reveals characteristic "irregular red fibers". Oculopharyngeal dystrophy is a distinct dominant autosomal condition, onset in middle age, characterized by ptosis, limitation of eye movements and dysphagia. Myotonic dystrophy, another dominant autosomal condition, produces ptosis, ophthalmopares, cataracts and pigment retinopathy. Patients experience muscle fatigue, myotonia, frontal baldness and cardiac abnormalities.
Neurogenic ptosis occurs due to a lesion that affects the innervation of either of the two muscles that open the eyelid: Muller's muscle or the upper eyelid lift muscle. Examination of the pupil helps to differentiate the two possibilities. In Horner syndrome, the eye with ptosis has a larger or normal pupil. If the pupil is normal and the movements of the eyeball are complete.
In oculomotor nerve paralysis, the eye with ptosis has a larger or normal pupil. if the pupil is normal, but the movements of adduction, lifting and descent are limited, there is the possibility of oculomotor nerve paralysis with the pupil's sparing. Rarely, a lesion affecting the small central subnucleus of the oculomotor complex as produces bilateral ptosis with normal pupils and eye movements.
I'll continue with the diplopia. First, it should be checked whether diplopia persists in the eye and after covering the other eye. If it persists, the diagnosis is monocular diplopia. The cause is usually intrinsic to the eye and therefore has no severe implications for the patient.
Corneal aberrations (e.g. keraconus, pteringioma), uncorrected refractive defects, cataracts or fovea traction may cause monocular diplopia. Sometimes it is a simulated symptom or a symptom of a psychiatric condition.
Diplopia improved by covering an eye is binocular diplopia and is due to disturbance of the alignment of the eyeballs. The nature of diplopia (simple image doubling or partial vertical displacement of images), how to start, duration, intermitence, diurnal variations and associated neurological or systemic symptoms should be studied.
If the patient experiences diplopia during the examination, the motility test will reveal a deficiency corresponding to the patient's symptoms. However, the subtle limitation of eyeball trips is often difficult to detect. For example, a patient with a moderate paralysis of the left abducens nerve may apparently have complete eye movements, despite the accusation of horizontal diplopia on the left-hand gaze.
In this situation, the cover test provides a more sensitive method for demonstrating poor alignment of the eyeballs. The test should be performed with the head looking straight, then with the head turned and tilted in each direction. In the example above, the cover test with the head turned to the right will maximize the movement of the eye in order to fix the target evoked by the cover test. Sometimes the cover test performed in an asymptomatic patient, as part of a routine examination, will reveal an eye deviation.
If the eye movements are complete and the alignment deficit of the eyeballs is the same in all directions of the eye (concomitant deviation), the diagnosis is strabismus. In this condition, found in about 1% of the population, the conjugation of the movements of the eyeballs is affected in the neonatal period or in early childhood.
To avoid diplopia, visual projection from the eye that does not achieve conjugation is suppressed. In some children, this situation leads to vision disturbance (amblyopia or "lazy" eye) of the deviated eye. Binocular diplopia occurs to a wide range of conditions: infectious, neoplastic, metabolic, degenerative, inflammatory and vascular.
The nature of diplopia, neurogenic or following the limitation of the movements of the eyeballs, must be identified by a condition located in orbit. Pseudotumora of the orbit, myositis, infections, tumors, thyroid disorders and muscle catching (for example, due to a cominutive fracture) produce restrictive diplopia.
The diagnosis is confirmed by the practice of a forced ab/adduction test in the office. After performing local anesthesia, the doctor catches the eye with the help of a forceps and pulls in the direction of deficient movement. if the rotational movement of the eyeball encounters resistance, it means that a restrictive process is present. The usefulness of this test is limited by the lack of popularity among patients, in practice, the diagnosis of the restriction being established by identifying other associated signs and symptoms, local disease of the orbit.
Myasthenia gravis is a major cause of diplopia. Diplopia is often intermittent, variable and is not limited to any of the individual eye movements controlled by the oculomotor nerve. Pupils are always normal. Variable ptosis may be present. Many patients have a purely ocular form of the disease, with no signs of systemic muscle fatigue.
The diagnosis can be confirmed by intravenous injection of edrofonium or by a test for acetylcholine antireceptor antibodies. The negative results of these tests do not exclude diagnosis. Botulism following food poisoning or infection of a wound can mimic ocular myasthenia. After the exclusion of restrictive diseases of the orbit and myasthenia gravis, damage to a cranial nerve that irritates the extrinsic musculature of the eye remains the most likely cause of binocular diplopia.
The oculomotor nerve (third cranial nerve) irritates the medial, lower and upper right muscles, the lower oblique muscle, the upper eyelid lift muscle and the sphincter of the iris. Oculomotor nerve paralysis produces ptosis and pupil dilation, the eye being deflected "down and out", due to the activity of the right lateral and upper oblique muscles to which no resistance is resisted. This combination of signs is very clear.
Diagnosis of an early or partial paralysis of the oculomotor nerve is somewhat more difficult to achieve. In this situation, any combination of ptosis, midriasis and weakness of the eye muscles innervated by the oculomotor nerve can be encountered. Frequent serial examinations during the evolutionary phase of paralysis along with a high degree of suspicion prevent the diagnosis from being missed.
The appearance of oculomotor nerve paralysis with pupillary damage, regardless of its degree, in an otherwise healthy patient, especially when accompanied by pain, raises suspicion of aneurysm of the Willis polygon. If the MRI examination does not reveal any compressive lesions, an arteriogram will be performed for the purpose of excluding a posterior communicative artery aneurysm or basilar artery.
If the pupil is perfectly normal, and all other components of oculomotor nerve paralysis are present, aneurysm is such a small possibility that angiogram is rarely indicated. Damage to the oculomotor nucleus in the rosral mesencephalus produces signs that differ from those caused by a lesion of the nerve itself. Bilateral ptosis is present, as the lifting muscle is innervated from a single central subnucleus.
Hypotonia of the controlled upper right muscle is also present, as it is inervated from the oculomotor nucleus on the opposite side. Sometimes both upper right muscles are hypotons. Isolated damage to the neurological nucleus reveals additional signs that suggest damage to the brain stem through infarction, hemorrhage, tumors or infections.
I'm going to continue tomorrow with the oculomotor muscle problems...
A rewarding weekend,
fun... But also understanding, love and gratitude!!!
Dorin, Merticaru