STUDY - Technical - New Dacian's Medicine
Eye and
Vision Disorders (9)
Translation Draft
I take advantage of the fact that it's Sunday and I don't have "to waste" time at work, so I'm going to do a slightly more consistent job now because I want to finish with this "sector" of disease signs... Let's move on with the oculomotor nerve problems!
The damage to the structures adjacent to the oculomotor nerve beams in its downward path through the mesencephalus gave rise to a number of classical entities. In Nothnagel syndrome, damage to the upper cerebellar peduncle causes ipsilateral oculomotor paralysis and contralateral cerebellar ataxia.
In Benedikt syndrome, damage to the red nucleus causes ipsilateral oculomotor paralysis and contralateral tremor, chorea and athetosis. Claude syndrome includes features of both of the aforementioned syndromes, by damaging both the red nucleus and the upper cerebellar peduncles. In Weber syndrome, damage to the cerebral peduncles causes ipsilateral oculomotor paralysis with contralateral hemiparesis. In the subarachnoid space, the oculomotor nerve is vulnerable to aneurysms, meningitis, tumors, infarction and compression.
In cerebral hernia, the nerve is trapped between the edge of the tentorium and the one of the temporal lobe. Oculomotor paralysis can also occur as a result of torsiation and mesencephalic haemorrhages during brain engagement. In the cavernous sinus, oculomotor paralysis occurs due to carotid aneurysms, cavernous carotid fistules, cavernous sinus thrombosis, tumors (pituitary adenoma, pituitary meningioma, metastases), herpes-zoster infection and Tolosa-Hunt syndrome.
The etiology of an isolated paralysis of the oculomotor nerve, without damage to the pupil, often remains obscure even after neuroimaging examinations and numerous laboratory tests. Most cases are assumed to be the result of microinfarctization of the nerve, somewhere along its path from the brain stem to orbit. Usually, the patient complains of pain.
Diabetes, hypertension and vascular diseases are major risk factors. As a rule, recovery is spontaneous over several months. If this does not occur or if symptoms develop, the diagnosis of paralysis by microinfarctization of the oculomotor nerve will be reconsidered. Aberrant regeneration is common if the oculomotor nerve is damaged by trauma or compression (tumors, aneurysms).
The wrong connection of the neoformed nerve fibers to the lifting muscle of the eyelid and the right muscles causes the eyelid to rise to the downward gaze or abstraction. The pupil also contracts with the attempt to add, lift or lower the eyeball. Aberrant regeneration is not found after oculomotor paralysis caused by microvascular infarction and therefore invalidates this diagnosis.
Let's now move to the nucleus of the trochlear nerve (fourth cranial nerve) which is located in the mesencephalus, caudal of the oculomotor nerve complex. Its fibers leave the brain stem at the dorsal level and cross to irritate the contralateral upper oblique muscle. The main actions of this muscle consist in the downward and lateral orientation of the eyeball. Therefore, paralysis leads to hypertropy and excyclotorsion.
Cyclotorsion is rarely observed in patients. Instead, patients accuse vertical diplopia, especially when reading or when looking down. Vertical diplopia is also exacerbated by the tilt of the head to the side of the eye with paralysis and is improved by the tilt of the head in the opposite direction. This "head tilt test" is an important feature for diagnosis.
Isolated paralysis of the trochlear nerve occurs through all the aforementioned causes, to the oculomotor nerve, except the aneurysm. The trochlear nerve is particularly vulnerable to closed head trauma. The mechanism is unknown, but the free edge of the tentorium can come into contact with the nerve during a strong blow. most isolated trochlear nerve paralysis is idiopathic and as a result diagnosed by exclusion as "microvascular".
Spontaneous improvement occurs within a few months in most patients. A bottom-based prism (conveniently applied to the patient's glasses as a Grip Fresnel lens) can serve as a temporary method of improving diplopia. If the paralysis does not resolve, the eyes can be realigned by surgically adjusting other eye muscles.
The abducens nerve (sixth cranial nerve) irritates the right lateral muscle. Paralysis of the abducens produces horizontal diplopia, more serious to the gaze to the side of the lesion. The lesion of the nucleus has different consequences, because the nucleus of the abducens contains interneurons that send projections on the path of the medial longitudinal beam to the medial subnucleus of the contralateral oculomotor complex. Therefore, a lesion of the abducens nucleus causes total paralysis of lateral movements, following weakening of both the ipsilateral lateral right muscle and the contralateral medial right muscle.
Foville syndrome following dorsal pontine lesion includes lateral vision paralysis, ipsilateral facial paralysis and contralateral hemiparesis due to damage to corticospinal downward fibers. Millard-Gubler syndrome following ventral pontine lesion is similar, except for eye signs. There is only weakening of the right lateral muscle, instead of paralysis of vision, because the abducens beam is damaged to a much greater extent than the nucleus. Infarctions, tumors, hemorrhages, vascular malformations and multiple sclerosis are the most common etiologies of abducens paralysis with origin in the brain stem.
After leaving the ventral bridge, the abducens nerve walks along the clivus, penetrates the dura to the rocky bone and penetrates the cavernous sinus. On its arachnoid route, the abducens nerve is susceptible to meningitis, tumors (meningiomas, cordomas, carcinomatous meningitis), subarachnoid hemorrhages, trauma and compression through aneurysms or dolicoectatic vessels.
At the level of the rocky apex, mastoiditis can cause deafness, pain and ipsilateral paralysis of abducens (Gradenico syndrome). In the cavernous sinus, the abducens nerve may be affected by carotid aneurysms, cavernous carotid fistula, tumors (pituitary adenoma, meningioma, nasopharyngeal carcinoma), herpes infections and Tolosa-Hunt syndrome. Unilateral or bilateral paralysis of abducens is a classic sign of intracranial hypertension.
Diagnosis is confirmed if papillary edema is observed on the examination of the bottom of the eye. The mechanism is still controversial, but is probably correlated with the rostro-caudal displacement of the brain stem. The same phenomenon is responsible for paralysis of abducens following intracranial hypotension (e.g. after lumbar puncture, spinal anesthesia or dural spontaneous extravasation of cerebrospinal fluid).
Treatment of abducens paralysis is oriented towards prompt correction of the underlying cause. However, in many cases, the case remains obscure despite the thorough assessment. As mentioned above, for isolated trochlear and oculomotor paralysis, it is assumed that most cases are microvascular infarctions, as they occur frequently in diabetics or in the case of other vascular risk factors. Some cases may evolve as post-infectious mononeuritis (e.g. following a flu).
The bandage of the eye or the temporary application of a prism will relieve diplopia until remission of paralysis. If recovery is incomplete, eye muscle surgery can almost always align the eyeballs, at least in the primary position. A patient with abducens paralysis, which does not improve, should be re-evaluated for occult etiology (e.g. cordom, carcinomatous meningitis, cavernous carotid fistula, myasthenia gravis).
Multiple paralysis of the motor eye nerve should not be attributed to spontaneous microvascular phenomena affecting more than one cranial nerve at a time. This remarkable coincidence occurs, however, especially in diabetic patients, but the diagnosis is established only retrospectively, after the exclusion of all other diagnostic variants.
Neuroimaging examinations should be focused on the cavernous sinus, upper orbital fissure and orbital apex, where all three motor eye nerves are in close proximity. In diabetic or immunodepressed host, fungal infection (Aspergillus, Mucorales, Cryptococcus) is a common cause of multiple paralysis of motor eye nerves.
In patients with systemic neoplasia, carcinomatous meningitis is a possible diagnosis. Cytological examination may be negative despite repeated sampling of cerebrospinal fluid. Eaton-Lambert paraneoplastic myasthenic syndrome can also cause ophthalmoplegia. Giant (temporal) cell arthritis sometimes manifests itself with diplopia, following ischemic paralysis of extrinsic eye muscles. Fisher syndrome, an ocular variant of Guillain-Barre syndrome, can produce ophthalmoplegia with areflexia and ataxia. Often ataxia is moderate, and areflexia is overlooked, because the doctor's attention is focused on the eyes.
Supernuclear disorders of eye-fixing are frequently confused with multiple paralysis of the motor eye nerve. For example, Wernicke's encephalopathy can produce nystagmus and a partial horizontal and vertical fixation deficiency, which mimics a combined paralysis of the abducens and oculomotor nerve. This disorder occurs in malnourished or alcoholic patients and can be remitted by taking thiamine. Infarctions, haemorrhages, tumors, multiple sclerosis, encephalitis, vasculitis and Whipple's disease are other important causes of supranuclear disorders of eye-catching.
The frontal eye field of the cerebral cortex is involved in the production of the exceptifs to the contralateral part. After the emispheric stroke, the eyes usually deviate to the part of the lesion due to the unhindered action of the frontal eye field in the normal hemisphere. Over time, this remittance deficit. Seizures generally have the opposite effect, with the eyes becoming conjugated to the opposite side of the irritant outbreak.
Parietal injuries affect smooth tracking of targets moving to the side of the lesion. Bilateral parietal lesions produce Balint syndrome, characterized by deterioration of eye-hand coordination (optical ataxia), difficulty in initiating voluntary eye movements (eye apraxia) and visual disorientation in space (simultagnosia). The descending cortical impulses that mediate the horizontal fixation of the gaze finally converge at the bridge level.
Neurons in the paramedian pontine reticulated formation are responsible for controlling the conjugation of the gaze to the same side. They project directly into the nucleus of ipsilateral abducens. Damage to either the paramedian pontine reticulated formation or the abducens nucleus produces ipsilateral paralysis of the conjugated gaze. In both cases, the lesion produces almost identical clinical syndromes, with the following exception: vestibular stimulation (by oculocephalic or caloric maneuver) will be able to conjugate the eyes to the side, in the patient with a lesion of the paramedian pontine reticulated formation, but not in the patient with abducens nucleus lesion.
Internuclear ophthalmoplegia is due to damage to the medial longitudinal beam that ascends from the abducens nucleus from the points to the oculomotor nucleus of the mesencephalus (by the term "internuclear"). Damage to the fibers that transmit the conjugated signal from the connecting interneurons of the abducens nucleus to the right contralateral medial motor neurons, makes it impossible to add when trying to turn the gaze to the side.
For example, a patient with a left internuclear ophthalmoplegia will experience slow or absent adduction movements in the left eye. A patient with bilateral damage to the medial longitudinal beam will have bilateral internucleation ophthalmoplegia. Multiple sclerosis is the most common cause, although tumors, strokes, trauma or any process in the brain stem may be responsible for internuclear ophthalmoplegia. The syndrome "one and a half" is due to a combined lesion of the medial longitudinal beam and nucleus abducens on the same side. The patient's only horizontal eye movement is the abstraction of the eye on the other side.
Vertical fixation of the gaze is controlled from the mesencephalus. The neural circuits affected in the vertical fixation disorders of the gaze are not yet well established, but the lesions of the interstitial rostrial nucleus of the medial longitudinal beam and the cajal interstitial nucleus produce the supranuclear paresis of the gaze upwards, downwards or all vertical eye movements. Distal ischemia of the basilar artery is the most common etiology. Oblique deviation refers to a vertical defect in the conjugation of the eyes, which is usually constant in all positions of the eye. It has a low value for the location of the lesion, as the oblique deviation has been reported as a result of lesions in large regions of the brain stem and cerebellum.
Parinaud syndrome (dorsal mesencephalic syndrome) is a distinct supranuclear disorder of vertical fixation of the eye, due to damage to the upper commision. It's a classic sign of hydrocephalus through aqueductal stenosis. Tumors of the pineal region (germinomas, pineoblastomas), cysticercosis and strokes also produce Perinaud syndrome.
Characteristics of the syndrome include: loss of eye-up (and sometimes downward), convergence-retraction nystagmus when trying to look up, eye deviation down (sunset sign), eyelid retraction (Collier sign), oblique deviation, pseudoparalysis of abducens and dissociation of light-distance pupil adjustment reflexes. Vertical eye-fixing disorders, especially downward-looking fasteners, are an early feature of progressive supranuclear paralysis. Fine movements are affected late in the course of the disease. Parkinson's disease, Huntington's Korea and olivopontocerebel degeneration can also affect vertical eye fixation.
Nistagmus is a rhythmic oscillating motion of the eyeballs, which normally occurs following vestibular and optokinetic stimulation or abnormal in a wide variety of diseases. Blindness following the disorders of the anterior visual paths in the early years of life produces complex, search-like nystagmus with irregular and jerky pendulum (sinusoidal) oscillations. This nystagmus is commonly referred to as congenital nystagmus, an inappropriate term, since nystagmus is commonly acquired in early childhood. Sometimes it develops in a normal child.
The jerky nistagmus is characterized by a removal of the target, followed by a rapid corrective jerk. By convention, the nystagmus is named after the rapid phase. The jerky nistagmus can be oriented higher, lower, horizontal (left or right) and torsional. The characteristics of the nystagmus may vary with the position of the gaze. many patients will not realize the existence of nystagmus. Others will accuse a subjective movement of the go-go environment (oscillopsie), corresponding to the nystagmus. Fine nistagmus can be difficult to identify when examining the eyes. Observation of nystagmoid movements of the optic disc at ophthalmoscopy is a sensitive method of detecting the subtle degrees of nystagmus. slot lamp is also useful.
The nystagmus evoked by fixing the gaze is the most common form of jerky nystagmus. When the eyes are kept in an eccentric position in the orbits, they have a normal tendency to return to the primary position. The subject compensates by making the correcting point to maintain the deflected position of the eyes. Many normal patients present moderate lystagmus evoked by fixation of the gaze. The exaggerated nistagmus evoked by fixation of the gaze can be induced by drugs (sedatives, anticonvulsants, alcohol), muscular paresis, myasthenia, demyelinating disorders and pontocerebel angle lesions, brain stem and cerebellum.
Vestibular nistagmus occurs due to labyrinthine dysfunction (Meniere's disease), the vestibular nerve or the vestibular nucleus of the brain stem. Peripheral vestibular nystagmus frequently occurs in discrete attacks with symptoms of nausea and vertigo. It can be associated with tinnitus and hearing-so-called. Sudden change in the position of the head can cause or exacerbate symptoms.
The downward-oriented nistagmus occurs consecutively to injuries adjacent to the craniocervical junction (Chiari malformation, basilar invasion). It has also been reported in stroke of the brain stem or cerebellum, lithium or anticonvulsant poisoning and multiple sclerosis. Upward oriented nistagmus is associated with lesions of pontine tegumentum through infarction, demyelination or tumors.
Opsoclonus is a rare, dramatic disorder of eye movements, consisting of bouts of consecutive seizures (sequencemania). When the dry scans are limited to the horizontal plane, the term eye flutter is preferred. It is a sign of neuroblastoma, encephalitis, trauma or paraneoplastic syndrome. It has been reported as a benign, transient phenomenon in otherwise healthy patients, probably as a consequence of mild occult viral encephalitis.
Pfui!!! Right now, I really don't have anything to talk about. I'm done with eye and vision disorders, and tomorrow I'm starting with presentations about smell, taste and hearing disorders...
I take advantage of the fact that it's Sunday and I don't have "to waste" time at work, so I'm going to do a slightly more consistent job now because I want to finish with this "sector" of disease signs... Let's move on with the oculomotor nerve problems!
The damage to the structures adjacent to the oculomotor nerve beams in its downward path through the mesencephalus gave rise to a number of classical entities. In Nothnagel syndrome, damage to the upper cerebellar peduncle causes ipsilateral oculomotor paralysis and contralateral cerebellar ataxia.
In Benedikt syndrome, damage to the red nucleus causes ipsilateral oculomotor paralysis and contralateral tremor, chorea and athetosis. Claude syndrome includes features of both of the aforementioned syndromes, by damaging both the red nucleus and the upper cerebellar peduncles. In Weber syndrome, damage to the cerebral peduncles causes ipsilateral oculomotor paralysis with contralateral hemiparesis. In the subarachnoid space, the oculomotor nerve is vulnerable to aneurysms, meningitis, tumors, infarction and compression.
In cerebral hernia, the nerve is trapped between the edge of the tentorium and the one of the temporal lobe. Oculomotor paralysis can also occur as a result of torsiation and mesencephalic haemorrhages during brain engagement. In the cavernous sinus, oculomotor paralysis occurs due to carotid aneurysms, cavernous carotid fistules, cavernous sinus thrombosis, tumors (pituitary adenoma, pituitary meningioma, metastases), herpes-zoster infection and Tolosa-Hunt syndrome.
The etiology of an isolated paralysis of the oculomotor nerve, without damage to the pupil, often remains obscure even after neuroimaging examinations and numerous laboratory tests. Most cases are assumed to be the result of microinfarctization of the nerve, somewhere along its path from the brain stem to orbit. Usually, the patient complains of pain.
Diabetes, hypertension and vascular diseases are major risk factors. As a rule, recovery is spontaneous over several months. If this does not occur or if symptoms develop, the diagnosis of paralysis by microinfarctization of the oculomotor nerve will be reconsidered. Aberrant regeneration is common if the oculomotor nerve is damaged by trauma or compression (tumors, aneurysms).
The wrong connection of the neoformed nerve fibers to the lifting muscle of the eyelid and the right muscles causes the eyelid to rise to the downward gaze or abstraction. The pupil also contracts with the attempt to add, lift or lower the eyeball. Aberrant regeneration is not found after oculomotor paralysis caused by microvascular infarction and therefore invalidates this diagnosis.
Let's now move to the nucleus of the trochlear nerve (fourth cranial nerve) which is located in the mesencephalus, caudal of the oculomotor nerve complex. Its fibers leave the brain stem at the dorsal level and cross to irritate the contralateral upper oblique muscle. The main actions of this muscle consist in the downward and lateral orientation of the eyeball. Therefore, paralysis leads to hypertropy and excyclotorsion.
Cyclotorsion is rarely observed in patients. Instead, patients accuse vertical diplopia, especially when reading or when looking down. Vertical diplopia is also exacerbated by the tilt of the head to the side of the eye with paralysis and is improved by the tilt of the head in the opposite direction. This "head tilt test" is an important feature for diagnosis.
Isolated paralysis of the trochlear nerve occurs through all the aforementioned causes, to the oculomotor nerve, except the aneurysm. The trochlear nerve is particularly vulnerable to closed head trauma. The mechanism is unknown, but the free edge of the tentorium can come into contact with the nerve during a strong blow. most isolated trochlear nerve paralysis is idiopathic and as a result diagnosed by exclusion as "microvascular".
Spontaneous improvement occurs within a few months in most patients. A bottom-based prism (conveniently applied to the patient's glasses as a Grip Fresnel lens) can serve as a temporary method of improving diplopia. If the paralysis does not resolve, the eyes can be realigned by surgically adjusting other eye muscles.
The abducens nerve (sixth cranial nerve) irritates the right lateral muscle. Paralysis of the abducens produces horizontal diplopia, more serious to the gaze to the side of the lesion. The lesion of the nucleus has different consequences, because the nucleus of the abducens contains interneurons that send projections on the path of the medial longitudinal beam to the medial subnucleus of the contralateral oculomotor complex. Therefore, a lesion of the abducens nucleus causes total paralysis of lateral movements, following weakening of both the ipsilateral lateral right muscle and the contralateral medial right muscle.
Foville syndrome following dorsal pontine lesion includes lateral vision paralysis, ipsilateral facial paralysis and contralateral hemiparesis due to damage to corticospinal downward fibers. Millard-Gubler syndrome following ventral pontine lesion is similar, except for eye signs. There is only weakening of the right lateral muscle, instead of paralysis of vision, because the abducens beam is damaged to a much greater extent than the nucleus. Infarctions, tumors, hemorrhages, vascular malformations and multiple sclerosis are the most common etiologies of abducens paralysis with origin in the brain stem.
After leaving the ventral bridge, the abducens nerve walks along the clivus, penetrates the dura to the rocky bone and penetrates the cavernous sinus. On its arachnoid route, the abducens nerve is susceptible to meningitis, tumors (meningiomas, cordomas, carcinomatous meningitis), subarachnoid hemorrhages, trauma and compression through aneurysms or dolicoectatic vessels.
At the level of the rocky apex, mastoiditis can cause deafness, pain and ipsilateral paralysis of abducens (Gradenico syndrome). In the cavernous sinus, the abducens nerve may be affected by carotid aneurysms, cavernous carotid fistula, tumors (pituitary adenoma, meningioma, nasopharyngeal carcinoma), herpes infections and Tolosa-Hunt syndrome. Unilateral or bilateral paralysis of abducens is a classic sign of intracranial hypertension.
Diagnosis is confirmed if papillary edema is observed on the examination of the bottom of the eye. The mechanism is still controversial, but is probably correlated with the rostro-caudal displacement of the brain stem. The same phenomenon is responsible for paralysis of abducens following intracranial hypotension (e.g. after lumbar puncture, spinal anesthesia or dural spontaneous extravasation of cerebrospinal fluid).
Treatment of abducens paralysis is oriented towards prompt correction of the underlying cause. However, in many cases, the case remains obscure despite the thorough assessment. As mentioned above, for isolated trochlear and oculomotor paralysis, it is assumed that most cases are microvascular infarctions, as they occur frequently in diabetics or in the case of other vascular risk factors. Some cases may evolve as post-infectious mononeuritis (e.g. following a flu).
The bandage of the eye or the temporary application of a prism will relieve diplopia until remission of paralysis. If recovery is incomplete, eye muscle surgery can almost always align the eyeballs, at least in the primary position. A patient with abducens paralysis, which does not improve, should be re-evaluated for occult etiology (e.g. cordom, carcinomatous meningitis, cavernous carotid fistula, myasthenia gravis).
Multiple paralysis of the motor eye nerve should not be attributed to spontaneous microvascular phenomena affecting more than one cranial nerve at a time. This remarkable coincidence occurs, however, especially in diabetic patients, but the diagnosis is established only retrospectively, after the exclusion of all other diagnostic variants.
Neuroimaging examinations should be focused on the cavernous sinus, upper orbital fissure and orbital apex, where all three motor eye nerves are in close proximity. In diabetic or immunodepressed host, fungal infection (Aspergillus, Mucorales, Cryptococcus) is a common cause of multiple paralysis of motor eye nerves.
In patients with systemic neoplasia, carcinomatous meningitis is a possible diagnosis. Cytological examination may be negative despite repeated sampling of cerebrospinal fluid. Eaton-Lambert paraneoplastic myasthenic syndrome can also cause ophthalmoplegia. Giant (temporal) cell arthritis sometimes manifests itself with diplopia, following ischemic paralysis of extrinsic eye muscles. Fisher syndrome, an ocular variant of Guillain-Barre syndrome, can produce ophthalmoplegia with areflexia and ataxia. Often ataxia is moderate, and areflexia is overlooked, because the doctor's attention is focused on the eyes.
Supernuclear disorders of eye-fixing are frequently confused with multiple paralysis of the motor eye nerve. For example, Wernicke's encephalopathy can produce nystagmus and a partial horizontal and vertical fixation deficiency, which mimics a combined paralysis of the abducens and oculomotor nerve. This disorder occurs in malnourished or alcoholic patients and can be remitted by taking thiamine. Infarctions, haemorrhages, tumors, multiple sclerosis, encephalitis, vasculitis and Whipple's disease are other important causes of supranuclear disorders of eye-catching.
The frontal eye field of the cerebral cortex is involved in the production of the exceptifs to the contralateral part. After the emispheric stroke, the eyes usually deviate to the part of the lesion due to the unhindered action of the frontal eye field in the normal hemisphere. Over time, this remittance deficit. Seizures generally have the opposite effect, with the eyes becoming conjugated to the opposite side of the irritant outbreak.
Parietal injuries affect smooth tracking of targets moving to the side of the lesion. Bilateral parietal lesions produce Balint syndrome, characterized by deterioration of eye-hand coordination (optical ataxia), difficulty in initiating voluntary eye movements (eye apraxia) and visual disorientation in space (simultagnosia). The descending cortical impulses that mediate the horizontal fixation of the gaze finally converge at the bridge level.
Neurons in the paramedian pontine reticulated formation are responsible for controlling the conjugation of the gaze to the same side. They project directly into the nucleus of ipsilateral abducens. Damage to either the paramedian pontine reticulated formation or the abducens nucleus produces ipsilateral paralysis of the conjugated gaze. In both cases, the lesion produces almost identical clinical syndromes, with the following exception: vestibular stimulation (by oculocephalic or caloric maneuver) will be able to conjugate the eyes to the side, in the patient with a lesion of the paramedian pontine reticulated formation, but not in the patient with abducens nucleus lesion.
Internuclear ophthalmoplegia is due to damage to the medial longitudinal beam that ascends from the abducens nucleus from the points to the oculomotor nucleus of the mesencephalus (by the term "internuclear"). Damage to the fibers that transmit the conjugated signal from the connecting interneurons of the abducens nucleus to the right contralateral medial motor neurons, makes it impossible to add when trying to turn the gaze to the side.
For example, a patient with a left internuclear ophthalmoplegia will experience slow or absent adduction movements in the left eye. A patient with bilateral damage to the medial longitudinal beam will have bilateral internucleation ophthalmoplegia. Multiple sclerosis is the most common cause, although tumors, strokes, trauma or any process in the brain stem may be responsible for internuclear ophthalmoplegia. The syndrome "one and a half" is due to a combined lesion of the medial longitudinal beam and nucleus abducens on the same side. The patient's only horizontal eye movement is the abstraction of the eye on the other side.
Vertical fixation of the gaze is controlled from the mesencephalus. The neural circuits affected in the vertical fixation disorders of the gaze are not yet well established, but the lesions of the interstitial rostrial nucleus of the medial longitudinal beam and the cajal interstitial nucleus produce the supranuclear paresis of the gaze upwards, downwards or all vertical eye movements. Distal ischemia of the basilar artery is the most common etiology. Oblique deviation refers to a vertical defect in the conjugation of the eyes, which is usually constant in all positions of the eye. It has a low value for the location of the lesion, as the oblique deviation has been reported as a result of lesions in large regions of the brain stem and cerebellum.
Parinaud syndrome (dorsal mesencephalic syndrome) is a distinct supranuclear disorder of vertical fixation of the eye, due to damage to the upper commision. It's a classic sign of hydrocephalus through aqueductal stenosis. Tumors of the pineal region (germinomas, pineoblastomas), cysticercosis and strokes also produce Perinaud syndrome.
Characteristics of the syndrome include: loss of eye-up (and sometimes downward), convergence-retraction nystagmus when trying to look up, eye deviation down (sunset sign), eyelid retraction (Collier sign), oblique deviation, pseudoparalysis of abducens and dissociation of light-distance pupil adjustment reflexes. Vertical eye-fixing disorders, especially downward-looking fasteners, are an early feature of progressive supranuclear paralysis. Fine movements are affected late in the course of the disease. Parkinson's disease, Huntington's Korea and olivopontocerebel degeneration can also affect vertical eye fixation.
Nistagmus is a rhythmic oscillating motion of the eyeballs, which normally occurs following vestibular and optokinetic stimulation or abnormal in a wide variety of diseases. Blindness following the disorders of the anterior visual paths in the early years of life produces complex, search-like nystagmus with irregular and jerky pendulum (sinusoidal) oscillations. This nystagmus is commonly referred to as congenital nystagmus, an inappropriate term, since nystagmus is commonly acquired in early childhood. Sometimes it develops in a normal child.
The jerky nistagmus is characterized by a removal of the target, followed by a rapid corrective jerk. By convention, the nystagmus is named after the rapid phase. The jerky nistagmus can be oriented higher, lower, horizontal (left or right) and torsional. The characteristics of the nystagmus may vary with the position of the gaze. many patients will not realize the existence of nystagmus. Others will accuse a subjective movement of the go-go environment (oscillopsie), corresponding to the nystagmus. Fine nistagmus can be difficult to identify when examining the eyes. Observation of nystagmoid movements of the optic disc at ophthalmoscopy is a sensitive method of detecting the subtle degrees of nystagmus. slot lamp is also useful.
The nystagmus evoked by fixing the gaze is the most common form of jerky nystagmus. When the eyes are kept in an eccentric position in the orbits, they have a normal tendency to return to the primary position. The subject compensates by making the correcting point to maintain the deflected position of the eyes. Many normal patients present moderate lystagmus evoked by fixation of the gaze. The exaggerated nistagmus evoked by fixation of the gaze can be induced by drugs (sedatives, anticonvulsants, alcohol), muscular paresis, myasthenia, demyelinating disorders and pontocerebel angle lesions, brain stem and cerebellum.
Vestibular nistagmus occurs due to labyrinthine dysfunction (Meniere's disease), the vestibular nerve or the vestibular nucleus of the brain stem. Peripheral vestibular nystagmus frequently occurs in discrete attacks with symptoms of nausea and vertigo. It can be associated with tinnitus and hearing-so-called. Sudden change in the position of the head can cause or exacerbate symptoms.
The downward-oriented nistagmus occurs consecutively to injuries adjacent to the craniocervical junction (Chiari malformation, basilar invasion). It has also been reported in stroke of the brain stem or cerebellum, lithium or anticonvulsant poisoning and multiple sclerosis. Upward oriented nistagmus is associated with lesions of pontine tegumentum through infarction, demyelination or tumors.
Opsoclonus is a rare, dramatic disorder of eye movements, consisting of bouts of consecutive seizures (sequencemania). When the dry scans are limited to the horizontal plane, the term eye flutter is preferred. It is a sign of neuroblastoma, encephalitis, trauma or paraneoplastic syndrome. It has been reported as a benign, transient phenomenon in otherwise healthy patients, probably as a consequence of mild occult viral encephalitis.
Pfui!!! Right now, I really don't have anything to talk about. I'm done with eye and vision disorders, and tomorrow I'm starting with presentations about smell, taste and hearing disorders...
A pleasant, restful
Sunday, full of understanding, love and gratitude!.
Dorin, Merticaru