פרק 13 Chapter 13 Disorders of Ocular Movement and Pupillary Function Flashcards
בת 20 עם מחלה פסיכיאטרית ברקע מגיע למיון בתלונה שלא מצליחה להוריד את העיניים כלפי מטה.
מה הטיפול במצב זה?
מדובר ב
occulogyral crises
והטיפול הוא תרופה אנטיכולינרגית
Another unusual disturbance of gaze is the oculogyric Crisis, or spasm, which consists of a tonic spasm of conjugate deviation of the eyes, usually upward and less frequently, laterally or downward. Recurrent attacks,
sometimes associated with spasms of the neck, mouth, and tongue muscles and lasting from a few seconds to an hour or two, were pathognomonic of postencephalitic Parkinsonism in the past. Now this phenomenon is observed as an acute reaction in patients being given phenothiazine and related neuroleptic drugs and in Niemann-Pick disease. The pathogenesis of these ocular spasms is not known. In the drug-induced form, upward deviation of the eyes is often associated with a report by the patient of peculiar obsessional thoughts;
the entire syndrome can be terminated by the administration of an anticholinergic medication such as benztropine.
מטופל הטוען שהוא עיוור
איזו בדיקה תוכיח לנו שהוא אכן רואה?
optokinetic nystagmus
Complete feigned blindness is disproved by observing the normal ocular jerk movements
in response to a rotating optokinetic drum or strip,
or by noting that the patient’s eyes follow their own image in a mirror that is moved in front of them.
An important additional fact about OKN is that the
ability to evoke it in all directions proves that the patient is not blind. Each eye can be tested separately to exclude monocular blindness. Thus the test is of particular value in the examination of hysterical patients and malingerers who claim that they cannot see, and of neonates and infants.
additional facts about specific lesions:
* Parietal Lobe Lesions – loss of pursuit in direction of the lesion
- Frontal Lobe Lesions – no fast phase correction in the direction opposite the lesion
בן 46 , מזה 5 ימים כאבים סביב עין שמאל מלווים כפל ראיה ואודם בעין שמאל.
CTV פגם מילוי ב
- cavernous sinus משמאל
איזה ממצא בבדיקה אופייני למצב זה?
א. הפרעה בחדות הראיה בעין שמאל
ב. הפרעה בתחושת פנים באזור המצח משמאל
ג. הפרעה בחוש הריח
ד. חולשת שרירי פנים משמאל
הפרעה בתחושת פנים באיזור המצח משמאל.
חייל שנחבל קלות בראשו ממדף נמוך ללא אובדם הכרה נבדק בחדר המיון, בבדיקתו בניסיון אבדוקציה יש רטרקציה של גלגל העין.
במה מדובר?
1. DUANE
2. Mobius
Patients with the Duane retraction syndrome type 1 (absent sixth nerve) have limited abduction and on adduction show characteristic retraction of the globe because of co-contraction of the medial rectus and lateral rectus muscles
A congenital form of bilateral abducens palsy is associated with bilateral facial paralysis (Mobius syndrome) (6+7)
מטופלת עם downbeat nystagmus וחוסר יכולת לדכא את הVOR בפיקסציה. איפה הפגיעה?
1. מידבריין טגמנטום
2. דנטייט נוקלאוס
3. פלוקולוס
4. מידל צרבלר פדנקל
Floculor nodular lobe
איזו תנועת עיניים תיפגע בדימום אוקסיפיטו-פריאטלי
הפרעה ב
smooth pursuit
בכיוון האיפסי לטרלי
The pathways for smooth pursuit movements are less well defined. One probably originates in the posterior parietal cortex and the adjacent temporal, and anterior occipital cortex (area MT of the monkey) and descends to
the ipsilateral dorsolateral pontine nuclei. Also contributing to smooth pursuit movements are projections from the frontal eye fields to the ipsilateral dorsolateral pontine nuclei. The latter, in turn, project to the flocculus and dorsal vermis of the cerebellum, which provide stability
for the pursuit movements. However, for the purposes of clinical work, lesions of the posterior parietal cortex are the ones known to impair pursuit toward the damaged side.
OKN- parietal lesions lead to loss of pursuit
- Frontal Eye Fields – סקאדות לצד הקונטראלטראלי
- PARIETAL – SMOOTH PURSUIT IPSILATERAL
מי המבנים המעורבים בהוראה לתנועות הוריזונטליות?
FEF
PPRF
CN6
MLF
CN3
מי המבנים המעורבים בהוראה לתנועות עיניים ורטיקליות
RiMLF
INC
Posterior commisure
3rd nerve nucleus
- The riMLF lies at the junction of the midbrain and thalamus, at the rostral end of the medial longitudinal fasciculus, just dorsomedial to the rostral pole of the red nucleus. It functions as the “premotor” nucleus with “burst cells” for the production of fast (saccadic) vertical
versional and torsional movements. Input to the riMLF arises both from the PPRF and the vestibular nuclei. Each riMLF projects mainly ipsilaterally to the oculomotor and trochlear nuclei, but each riMLF is also connected to its counterpart by fibers that traverse the posterior commissure. Bilateral lesions of the riMLF or of their interconnections in the posterior commissure are more common than unilateral ones, and cause a loss either of downward saccades or of all vertical saccades. - The INC is a small collection of cells that lies just caudal to the riMLF on each side. Each nucleus projects to the motor neurons of the opposite elevator muscles (superior rectus and inferior oblique) by fibers that cross
through the posterior commissure, and it projects ipsilaterally and directly to the depressor muscles (inferior rectus and superior oblique). The functional role of the
INC appears to be in holding eccentric vertical gaze, especially after a saccade; it is also integral to the vestibuloocular Reflex. Lesions of the INC produce a *vertical gaze-evoked and torsional nystagmus, and an ocular tilt reaction and probably slow all conjugate eye movements,
mainly vertical ones. * - Lesions of the posterior commissure are common; they interrupt signals crossing to and from the INC and the riMLF.
A lesion here **characteristically produces a paralysis of upward gaze and of convergence, often associated with mild mydriasis, accommodative loss, convergence
nystagmus, lid retraction (Collier “tucked lid” sign), and, less commonly, ptosis. This constellation is the Parinaud Syndrome**, also referred to as the pretectal, dorsal midbrain,
or sylvian aqueduct syndrome (see ‘‘Vertical Gaze
Palsy” further on). In some instances, only a restricted combination of these signs is seen. The same syndrome may be produced by unilateral lesions of the posterior commissure, presumably by interrupting bidirectional connections from the riMLF and INC.
With acute lesions of the commissure, there is a tonic downward deviation of the eyes and lid retraction (“setting-sun sign”).
מסלול של תנועות סקאדות ורטיקליות
The riMLF lies at the junction of the midbrain and thalamus, at the rostral end of the medial longitudinal fasciculus, just dorsomedial to the rostral pole of the red nucleus. It functions as the “premotor” nucleus with “burst cells” for the production of fast (saccadic) vertical
versional and torsional movements. Input to the riMLF arises both from the PPRF and the vestibular nuclei. Each riMLF projects mainly ipsilaterally to the oculomotor and trochlear nuclei, but each riMLF is also connected to its counterpart by fibers that traverse the posterior commissure. Bilateral lesions of the riMLF or of their interconnections in the posterior commissure are more common than unilateral ones, and cause a loss either of downward saccades or of all vertical saccades.
מסלול של תנועות
puirsuit ורטיקליות
- The INC is a small collection of cells that lies just caudal to the riMLF on each side. Each nucleus projects to the motor neurons of the opposite elevator muscles (superior rectus and inferior oblique) by fibers that cross
through the posterior commissure, and it projects ipsilaterally and directly to the depressor muscles (inferior rectus and superior oblique). The functional role of the
INC appears to be in holding eccentric vertical gaze, especially after a saccade; it is also integral to the vestibuloocular Reflex. Lesions of the INC produce a *vertical gaze-evoked and torsional nystagmus, and an ocular tilt reaction and probably slow all conjugate eye movements,
mainly vertical ones. *
ניד ורטיקלי עם מרכיב רוטטורי במבט מעלה
The functional role of the
INC appears to be in holding eccentric vertical gaze, especially after a saccade; it is also integral to the vestibuloocular reflex.
**Lesions of the INC produce a vertical
gaze-evoked and torsional nystagmus, and an ocular tilt reaction and probably slow all conjugate eye movements, mainly vertical ones.
Cerebellar nodules
Periodic alternating nystagmus is a remarkable horizontal jerking that periodically (every 90 seconds or so) changes direction, interposed with a brief neutral period during which the eyes show no nystagmus, or jerk downward. Alternating nystagmus is seen with lesions in the lower brainstem but has also been reported with Creutzfeldt-Jakob disease, hepatic encephalopathy, lesions of the cerebellar nodulus, carcinomatous meningitis,anti-GAD antibodies, and varied other processes.
More types of nystagmus:
-
Upbeat nystagmus: demyelination, stroke, tumours, wernicke (?anterior cerebellar vermis,
Pontomedullary?) - Downbeat Nystagmus: medullary-cervical areas – e.g. syringobulbia, chiari, basilar invagination, Demyelinating plaques. Wernicke’s, brainstem encephalitis, cerebellar degeneration with opsoclonus’, flocoulus lesions, lithium intoxiction, magnesium depletion, anti GAD association.
- Gaze evoked, round nystagmus, downbeat nystagmus – cerebellar disease
- Pendular Nystagmus – congenital, acquired: leukodystrophies, MS, toulene intoxication, occulomasticatory myoarrhythmia of whipple,
- Convergence Nystagmus - PARINAUD, DORSAL MIDBRAIN SYNDROME
- See Saw Nystagmus - torsional – vertical oscillation – sellar and parasellar masses (conjoined with hemianopia), after pituitary surgery
-
Nystagmus of Labyrinthine Origin
horizontal or vertical unidirectional jerk nystagmus, often with a slight torsional Component ,suppressed by fixation,beats in most cases away from the side of the lesion and increases as the eyes are turned in the direction of the quick phase (the Alexander law), characteristically has an additional torsional component. Tinnitus and hearing loss are often associated with disease of the peripheral labyrinthine mechanism; also, vertigo, nausea, vomiting, and staggering may accompany
מטופל מתייצג עם המיאנופסיה ביטמפורלית וניסטגמוס.
איזה ניסטגמוס נראה?
א. pendular
ב. See saw
ג. convergence
See Saw
- See saw nystagmus is a torsional-vertical oscillation in which the intorting eye moves up and the opposite (extorting) eye moves down, then both move in the reverse direction. It is occasionally observed in conjunction with chiasmatic bitemporal hemianopia caused by sellar or parasellar masses and after pituitary surgery
More types of nystagmus:
* Convergence nystagmus refers to a rhythmic oscillation in which a slow abduction of both eyes is followed by a quick movement of adduction, usually accompanied by quick rhythmic retraction movements of the eyes (nystagmus retractorius, retraction nystagmus) and by one or more features of the Parinaud-dorsal midbrain syndrome. There may also be rhythmic movements of the eyelids or a maintained spasm of convergence, best brought out on attempted elevation of the eyes on command or downward rotation of an
OKN drum. These unusual phenomena all point to a lesion of the upper midbrain tegmentum and are usually manifestations of vascular disease, traumatic damage, or tumor, notably pinealoma that compresses this region.
- Periodic alternating nystagmus is a remarkable horizontal jerking that periodically (every 90 seconds or so) changes direction, interposed with a brief neutral period during which the eyes show no nystagmus, or jerk downward. Alternating nystagmus is seen with lesions in the lower brainstem but has also been reported with Creutzfeldt-Jakob disease, hepatic encephalopathy, lesions of the cerebellar nodulus, carcinomatous meningitis,anti-GAD antibodies, and varied other processes.
-
Upbeat nystagmus: demyelination, stroke, tumours, wernicke (?anterior cerebellar vermis,
Pontomedullary?) - Downbeat Nystagmus: medullary-cervical areas – e.g. syringobulbia, chiari, basilar invagination, Demyelinating plaques. Wernicke’s, brainstem encephalitis, cerebellar degeneration with opsoclonus’, flocoulus lesions, lithium intoxiction, magnesium depletion, anti GAD association.
- Gaze evoked, round nystagmus, downbeat nystagmus – cerebellar disease
- Pendular Nystagmus – congenital, acquired: leukodystrophies, MS, toulene intoxication, occulomasticatory myoarrhythmia of whipple,
-
Nystagmus of Labyrinthine Origin
horizontal or vertical unidirectional jerk nystagmus, often with a slight torsional Component ,suppressed by fixation,beats in most cases away from the side of the lesion and increases as the eyes are turned in the direction of the quick phase (the Alexander law), characteristically has an additional torsional component. Tinnitus and hearing loss are often associated with disease of the peripheral labyrinthine mechanism; also, vertigo, nausea, vomiting, and staggering may accompany
במי מהבאים לא נראה תמונה של
downbeat nystagmus?
1. Cerebellum
2. chiari malformation
3. labyrinthitis
4. lithium
5. syrnix
labyrinthitis
Nystagmus of Labyrinthine Origin
This is predominantly a horizontal or vertical unidirectional jerk nystagmus, often with a slight torsional Component, that is evident when the eyes are close to the central position and changes minimally with the direction of gaze. It is more prominent when visual fixation is eliminated (conversely, it is suppressed by fixation).
Vestibular nystagmus of peripheral (labyrinthine) origin beats in most cases away from the side of the lesion and increases as the eyes are turned in the direction of the quick phase (the Alexander law).
In contrast, nystagmus of brainstem and cerebellar origin is most apparent when the patient fixates upon and follows a moving target and the direction of nystagmus changes with the direction of gaze.
Labyrinthine-vestibular nystagmus is horizontal, vertical, or oblique, and that of purely labyrinthine origin characteristically has an additional torsional component. Tinnitus and hearing loss are often associated with disease of the peripheral labyrinthine mechanism; also, vertigo, nausea, vomiting, and staggering may accompany disease of any part of the labyrinthine-vestibular apparatus or its central connections.
other types of nystagmus
- ** Downbeat nystagmus** , which is always of central origin, is characteristic of lesions in the medullary-cervical region such as syringobulbia, Chiari malformation (most commonly), basilar invagination, and demyelinating plaques. It has also
been seen with Wernicke disease and may be an initial sign of either paraneoplastic brainstem encephalitis or cerebellar degeneration with opsoclonus. Downbeat nystagmus, usually in association with oscillopsia, has also been observed in patients with lithium intoxication or with profound magnesium depletion Cases associated with antibodies against glutamic acid decarboxylase (GAD), a substance that has a documented relationship to the stiff man syndrome have been reported by Antonini and colleagues and by other groups. Whether this antibody explains the idiopathic cases of downbeat nystagmus is not known. - Periodic alternating nystagmus is a remarkable horizontal jerking that periodically (every 90 seconds or so) changes direction, interposed with a brief neutral period during which the eyes show no nystagmus, or jerk downward. Alternating nystagmus is seen with lesions in the lower brainstem but has also been reported with Creutzfeldt-Jakob disease, hepatic encephalopathy, lesions of the cerebellar nodulus, carcinomatous meningitis,anti-GAD antibodies,
-
Upbeat nystagmus: demyelination, stroke, tumours, wernicke (?anterior cerebellar vermis,
Pontomedullary?) - Gaze evoked, round nystagmus, downbeat nystagmus – cerebellar disease
- Pendular Nystagmus – congenital, acquired: leukodystrophies, MS, toulene intoxication, occulomasticatory myoarrhythmia of whipple,
- Convergence Nystagmus - PARINAUD, DORSAL MIDBRAIN SYNDROME
- See Saw Nystagmus - torsional – vertical oscillation – sellar and parasellar masses (conjoined with hemianopia), after pituitary surgery
מה יעזור באבחנה של
congenital nystagmus?
1. הוריזונטלי במבט שמאלה וורטיקלי במבט מעלה
2. הפאזה המהירה היא עם כיוון תנועת התוף בבדיקת OKN
3. סיבוב של הראש עם כיוון הניד
4. מתגבר בקונברגציה
הפאזה המהירה עם כיוון התוף בבדיקת
OKN
The nystagmus is always binocular and in one plane; i.e., it will remain horizontal even during vertical movement. It is mainly pendular (sinusoidal) except in extremes of gaze, when it comes to resemble jerk nystagmus. Head oscillation may accompany the nystagmus and is probably compensatory. With eye movement recordings it displays a feature unique among nystagmus, an exponentially increasing velocity of the slow phase.
Indications as to the congenital nature of nystagmus are that it remains horizontal in all directions of gaze; it is suppressed during convergence and may be associated with odd head positions or with head oscillations and with strabismus. Also characteristic is a paradoxical response to optokinetic testing, in which the quick phase is in the same direction as the drum rotation.
איזה עצב קרניאלי נפגע בשכיחות הגבוהה ביותר לאחר טראומה ?
CN- 4
שיתוק עצב 4
- טראומה במקום הראשון! (כמעט ב 50% מהמקרים), כנראה עקב המסלול הארוך והמוצלב.
- כמעט ולעולם לא יהיה מעורב עקב אנוריזמה (גם לא 6) וזה מעיד עד כמה אנוריזמות לא נפוצות באזור האינפראקלינואיד (בניגוד לסופראקלינואיד המערב את עצב 3)
- הרבה מקרים אידיופאטיים
- VZV, עקב הקירבה של עצב 4 למעטפת של הטריג’מינל.
- ייתכן משני לסוכרת אם כי גם הרבה פחוץ נפוץ מ 6
- Brown syndrome – כליאה של הסופריור אובליק, במצב כזה בנוסף לחולשה יהיה כאב בארובת העין ומבחינה קלינית יהיה דומה לטולוסה האנט.
- Increased ICP אבל שוב בסבירות נמוכה בהרבה מעצב 6.
לעיתים מתרחש בשיורגן, לופוס מסיבה לא ידועה*
- Superior oblique myokimia - אירועים חוזרים של תנועות גלגל העין, דיפלופיה המופיעה לסירוגין, לרוב מתואר בהופעה שפירה (ייתכן משנית ללחץ של סעיף מהעורק הבזילרי) אך יכולה להופיע גם ב
pontine glioma או ב MS.
ניתן לטיפול בעזרת קרבאמזאפין
מה נראה קלינית בפגיעה בעצב קרניאלי
3
4
6
הפרעה במבט הצידה (3+6)
When infraclinoid retrocavernous compressive Lesions, such as aneurysms and tumors, affect the oculomotor Nerve, they tend to also involve all three divisions of the trigeminal nerve.
In the posterior portion of the cavernous sinus, the first and second trigeminal divisions are involved along with the oculomotor nerves;
In the anterior portion, only the ophthalmic division of the trigeminal nerve is affected.
The fourth and sixth nerves are practically never involved by aneurysm. This reflects the relative infrequency of carotid artery aneurysms in the infraclinoid portion of the cavernous sinus, where they could impinge on the sixth nerve. (In contrast, supraclinoid aneurysms commonly involve the third nerve.)
מי יפגע בסבירות הגבוהה ביותר מאנוריזמה?
CN3, 4,6
קודם 3 אחר כך 6 ובסוף 4
The oculomotor nerve, soon after it emerges from the brainstem, passes between the superior cerebellar and posterior cerebral arteries. The nerve (and sometimes the posterior cerebral artery) may be compressed at this point by herniation of the uncal gyrus of the temporal lobe through the tentorial opening .
The sixth nerve, after leaving the brainstem, sweeps upward along the clivus and then runs alongside the third and fourth
cranial nerves; together they course anteriorly, pierce the dura just lateral to the posterior clinoid process, and run in the lateral wall of the cavernous sinus, where they are closely applied to the internal carotid artery and first and second divisions of the fifth nerve.
When infraclinoid retrocavernous compressive
lesions, such as aneurysms and tumors, affect the oculomotor nerve, they tend to also involve all three divisions of the trigeminal nerve.
In the posterior portion of the cavernous sinus, the first and second trigeminal divisions are involved along with the oculomotor nerves;
in the anterior portion, only the ophthalmic division of the trigeminal nerve is affected.
Just posterior and superior to the cavernous sinus, the oculomotor nerve crosses the terminal portion of the internal carotid artery at its junction with the posterior communicating artery. An aneurysm at this site frequently damages the third nerve; this serves to localize the site of compression or bleeding.
Table 13-1_DISEASES EXHIBITING UPGAZE OR VERTICAL GAZE PALSY
posterior commissure
Lesions of the posterior commissure are common; they interrupt signals crossing to and from the INC and the riMLF. A lesion here characteristically produces a paralysis of upward gaze and of convergence, often associated with mild mydriasis, accommodative loss, convergence nystagmus, lid retraction (Collier “tucked lid” sign), and, less commonly, ptosis. This constellation is the** Parinaud syndrome, also referred to as the pretectal, dorsal midbrain,
or sylvian aqueduct syndrome**
In some instances, only a restricted combination of these signs is seen. The same syndrome may be produced by unilateral lesions of the posterior
commissure, presumably by interrupting bidirectional connections from the riMLF and INC. With acute lesions of the commissure, there is a tonic downward deviation of the eyes and lid retraction (“setting-sun sign”). The MLF is the main conduit of signals that control vertical gaze from the vestibular nuclei in the medulla to the midbrain centers. For this reason, with internuclear ophthalmoplegia, along with the characteristic adductor paresis on the affected side, vertical pursuit and the VOR are impaired. This is most evident when there are bilateral
internuclear ophthalmoplegias. Vertical deviation of the ipsilateral eye (skew) may be seen in cases of unilateral internuclear ophthalmoplegia.
ד. קוקאין מרחיב את האישון על ידי מניעת ספיגת נוראדרנלין בסינפסה
- Atropinics dilate the pupils by paralyzing the parasympathetic nerve endings;
- physostigmine constrict the pupils, by inhibiting cholinesterase activity at the neuromuscular junction.
-
pilocarpine constrict by direct stimulation of
the sphincter muscle of the iris. - Epinephrine and phenylephrine Dilate the pupils by direct stimulation of the dilator Muscle.
- Cocaine dilates the pupils by preventing the reabsorption of norepinephrine into the nerve endings.
- apraclonidine, a weak direct alpha-agonist drug has been shown to reliably reverse the anisocoria of Horner syndrome and has become the preferred drug for testing. Normally apraclonidine does not exert significant dilatory effect, but with denervation hypersensitivity that accompanies Horner syndrome, the miotic pupil dilates in response to the drug.
מה נכון לגבי תסמונת הורנר?
1. בצורתו המולדת קשור להטרוכרומיה של האיריס
2. מופיע בדיסקציה של עורק ורטברלי
3. פטוזיס מלא
4. אנאיזוקוריה מחמירה באור
- בצורתו המולדת קשור להטרוכרומיה של האיריס
Horner Syndrome
Interruption of the sympathetic fibers result in miosis and ptosis (because of paralysis of the pupillary dilator muscle and of Milller muscle, respectively). The lesion may be central, between the hypothalamus and the points of exit of sympathetic fibers from the spinal cord (CS to T3, mainly T2), or peripheral, in the cervical sympathetic chain, superior cervical ganglion, or along the carotid artery.
A congenital form caused by perinatal injury, usually of the sympathetic chain in the neck is seen regularly in our clinics. A hereditary form of the Horner syndrome (autosomal dominant) is also known, usually but not always associated with a congenital absence of pigment in the affected iris (heterochromia iridis).
To the ophthalmic findings may be added loss of sweating on the same side of the face and redness of the conjunctiva. The entire complex is called the Horner syndrome, Bernard-Horner syndrome, or oculosympathetic palsy. The pupillary change may be subtle and may require covering the eyes or dimming the room lights to observe the lack of expected mydriasis on one side.
Most cases are caused by peripheral interruption of the sympathetic chain but the same effect may be produced by ipsilateral lesions of the sympathetic tract in the medulla or cervical cord. The pattern of sweating may be helpful in localizing the lesion in the following manner:
* With lesions at the level of the common carotid artery, loss of sweating involves the entire side of the face.
* With lesions distal to the carotid bifurcation, loss of sweating is not found or is confined to the medial aspect of the forehead and side of the nose.
Retraction of the eyeball (enophthalmos), considered a component of the syndrome, is probably an illusion created by narrowing
of the palpebral fissure.
ד. בעורק ה
common carotid
The pattern of sweating may be helpful in localizing the lesion in the following manner:
* With lesions at the level of the common carotid artery, loss of sweating involves the entire side of the face.
* With lesions distal to the carotid bifurcation, loss of sweating is not found or is confined to the medial aspect of the forehead and side of the nose.
צעיר עם אנאיזוקוריה (שמאל גדול מימין), מחמירה באור. לאחר פילוקרפין 1% אין שינוי באישונים. מה האבחנה?
א. Right horner
ב. Adie’s pupil
ג. Atropinic mydriasis
ד. שיתוק עצב 3
ה. Simple anisocoria
ג. atropinic mydriasis
מטופל עם מיוזיס- האישון מתכווץ בתגובה לאפקרלונידין.
בתגובה להידרוקסיאמפתמין אין תגובה של האישון. מה טיב הפגיעה?
post ganglionic horner syndrome
בחולה שסובל מתסמונת הורנר משמאל מעל שבוע: מה התגובה שתופיע לאחר טפטוף של שתי טיפות
apraclonidine 0.5% בכל עין ?
א. התכווצות בולטת יותר של אישון שמאל
ב. התכווצות בולטת יותר של אישון ימין
ג. הרחבה בולטת יותר של אישון שמאל
ד. הרחבה בולטת יותר של אישון ימין
הרחבה בולטת יותר של אישון שמאל
Table 13-6_CHARACTERISTICS OF ARGYLL ROBERTSON AND ADIE PUPIL
בן 31 ללא מחלות רקע ידועות, מתלונן על כפל ראייה במבט לצדדים, בבדיקתו הגבלה בביצוע אדוקציה של העיניים דו”צ. איזה מהבאים צפוי שיופיע בבדיקתו?
1. האישונים יהיו לא שווים, כאשר האישון הימני רחב יותר
2. במבט ימינה מופיע ניד הוריזונטלי של העין הימנית
3. האישונים לא יגיבו לאור ויגיבו להתקרבות
4. במבט מעלה העין הימנית אינה עולה
5. צניחת עפעף בעין ימין
- במבט ימינה מופיע ניד הוריזונטלי של העין הימנית
(bilateral INO)
ביהמיספרלית!
Caloric-induced nystagmus Labyrinthine stimulation-e.g.,
Cold water induces a slow tonic Deviation of the eyes toward the irrigated ear and a compensatory nystagmus in the opposite direction; warm water does the reverse. Thus the acronym taught to generations of medical students: COWS, or “cold opposite, warm same,“ to refer to the direction of the fast phase of the induced nystagmus. The slow tonic component reflects impulses originating in the semicircular canals, and the fast component is a corrective movement.
* In comatose patients, the fast “corrective” phase of nystagmus is lost and the eyes are tonically deflected to the side irrigated with cold water or away from the side irrigated
with warm water; this position may be held for 2 to 3min. Brainstem lesions disrupt these vestibuloocular Reflexes;
* In normal subjects, the nystagmus usually persists for 90 to 120 s, although the range is considerably larger. Nausea and symptoms of excessive reflex vagal activity may occur in sensitive individuals.
Simultaneous irrigation of both canals with cold water causes a tonic downward deviation of the eyes with nystagmus (quick component) upward. Bilateral irrigation with warm water yields a tonic upward movement and nystagmus in the opposite direction (“cold upward, warm down, referring again to the fast phase of nystagmus; “CUWD”). Caloric testing will reliably answer whether the vestibular end organs react, and comparison of the responses from the two ears will indicate which one is paretic. Recording of eye movements during the test allows quantification of these responses
אם אין אף תגובה- פגיעה בגזע. אם יש תגובה אך אין ניד- פגיעה ביהמיספרלית
Table 13-2
ACTIONS OF THE EXTRAOCULAR MUSCLES
Table 13- 3
MAIN CAUSES OF INDIVIDUAL AND COMBINED OCULOMOTOR PALSIES
Table 13- 4
CAUSES OF PAINFUL OPHTHALMOPLEGIA
Table 13-5
CAUSES OF COMPLETE OPHTHALMOPLEGIA
Figure 13-1. The supranuclear pathways subserving horizontal gaze to the left. The pathway originates in the right frontal cortex, descends in the internal capsule, decussates at the level of the rostral pons, and descends to synapse in the left pontine paramedian reticular formation (PPRF). Further connections with the ipsilateral sixth nerve nucleus and contralateral medial longitudinal fasciculus are also indicated. The right MLF (green line) is labeled between the abducens and oculomotor nuclei and the vestibular nuclei (VN) are shown on the right. LR, lateral rectus; MLF, medial longitudinal fasciculus; MR, medial rectus.
Figure 13-2. Pathways for the control of vertical eye movements. The main structures are the interstitial nucleus of Cajal (INC), the rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF), and the subnuclei of the third nerve, all located in the dorsal midbrain. Voluntary vertical movements are initiated by the simultaneous activity of both frontal cortical eye fields. The riMLF serves as the generator of vertical saccades and the INC acts tonically to hold eccentric vertical gaze. The INC and riMLF connect with their contralateral nuclei via the posterior commissure, where fibers are subject to damage. Projections for upgaze cross through the commissure before descending to innervate the third nerve nucleus, while those for downgaze may travel directly to the third nerve, thus accounting for the frequency of selective upgaze palsies (see text). The MLF carries signals from the vestibular nuclei, mainly ipsilaterally, to stabilize the eyes in the vertical plane (VOR) and maintain tonic vertical position.
Figure 13-3. Topographic arrangement of oculomotor fascicular fibers in the mesencephalon. CCN, central caudal nucleus; IO, inferior oblique; IR, inferior rectus; LP, levator palpebrae; MR, medial rectus; P, pupil; SR, superior rectus. (From Ksiazek SM, Slamovits TL, Rosen CE, et al: Fascicular arrangement in partial oculomotor paresis. Am J Ophthalmol 118: 97, 1994. With permission.)
Figure 13-4. A. Midbrain in horizontal section, indicating the effects of lesions at different points along the intramedullary course of the third-nerve fibers. A lesion at the level of oculomotor nucleus results in homolateral third-nerve paralysis and homolateral anesthesia of the cornea. A lesion at the level of red nucleus results in homolateral third-nerve paralysis and contralateral ataxic tremor (Benedikt and Claude syndromes). A lesion near the point of exit of third-nerve fibers results in homolateral third-nerve paralysis and crossed corticospinal tract signs (Weber syndrome; see Table 44-2). B. Brainstem at the level of the sixth-nerve nuclei, indicating effects of lesions at different loci. A lesion at the level of the nucleus results in homolateral sixth- and seventh-nerve paralyses with varying degrees of nystagmus and weakness of conjugate gaze to the homolateral side. A lesion at the level of corticospinal tract results in homolateral sixth-nerve paralysis and crossed hemiplegia (Millard-Gubler syndrome).
Figure 13- 5.
The cavernous sinus and its relation to the cranial nerves.
A. Base of the skull; the cavernous sinus has been removed on the right.
B. The cavernous sinus and its contents viewed in the coronal plane.
Figure 13-6.
Muscles chiefly responsible for vertical movements of the eyes in different positions of gaze. (Adapted by permission from Cogan DG: Neurology of theOcular Muscles, 2nd ed. Springfield, IL, Charles C Thomas, 1956.)
Figure 13-7.
Diplopia fields with individual muscle paralysis. The red Maddox rod is in front of the right eye and gives rise to the straight line image, and the fieldsare projected as the patient sees the images.
A. Paralysis of right lateral rectus. Characteristic: right eye does not move to the right. Field: the vertical red line is displaced to the right and the separation of images increases on looking to the right.
B. Paralysis of right medial rectus. Characteristic: right eye does not move to the left. Field: horizontal crossed diplopia increasing on looking to the left.
C. Paralysis of right inferior rectus. Characteristic: right eye does not move downward when eyes are turned to the right. Field: vertical diplopia (with the red line, seen by the right eye, displaced inferiorly) increasing on looking to the right and down.
D. Paralysis of right superior rectus. Characteristic: right eye does not move upward when eyes are turned to the right. Field: vertical diplopia (with red line displaced superiorly) increasing on looking to the right and up.
E. Paralysis of right superior oblique. Characteristic: right eye does not move downward when eyes are turned to the left. Field: vertical diplopia (with red line displaced inferiorly) increasing on looking to the left and down.
F. Paralysis of right inferior oblique. Characteristic: right eye does not move upward when eyes are turned to the left. Field: vertical diplopia (with red line displaced superiorly) increasing on looking to the left and up.
Figure 13-8.
MRI of orbital pseudotumor showing bilateral swelling of the extraocular muscles and adjacent orbital contents. A “streaming” appearance of the fat as shown in the right retroorbital compartment is characteristic. The process in this patient responded to corticosteroids.
Figure 13-9. Diagram of the pathways subserving the pupillary light reflex. (Redrawn with permission from Bradford CA [ed]: Basic Ophthalmology, 7th ed. San Francisco, American Academy of Ophthalmology,
1975.)
Figure 13-10. Congenital Horner syndrome on the patient’s left. In addition to the miosis and ptosis, the patient’s left iris is gray in color and the right, brown.
Figure 13-11. A schematic approach for sorting out the nature of anisocoria. (Adapted by permission from Thompson and Pilley.)
