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"Vision into pairs", also known as diplopia, the principle of double vision is that the imaging of one eye falls on the concave of the macula, while the imaging of the other eye does not fall on the
concave.
The image that falls on the concave is never clearer than the image that does not fall on the fovea, so two images
are formed.
There are many causes of diplopia, most of which are caused by weakness or paralysis of the extraocular muscles
.
The extraocular muscles are controlled by cranial nerves, and diseases of cranial nerves or the brain itself may cause diplopia, as well as lesions of extraocular muscles, muscle-nerve junctions, oculomotor nerves and their nuclei
.
Next, let's dissect the cause
of diplopia in this case.
First look at the basic information
of the patient, male, 45 years old, mainly due to "intermittent headache for 1 week, vision in double 3 days" admission
.
The patient had intermittent headache without obvious triggers 1 week ago, for the right hemisphere pulsating dull pain, with the right temporal region as the center, each pain lasted about 10-20s, several pain attacks a day, no obvious regularity, did not pay attention, 3 days ago there was no obvious trigger for the appearance of double eye vision, the most obvious when looking up, accompanied by right eyelid lifting difficulty and eyebrow arch pain discomfort, can not be relieved after rest, no significant aggravation after fatigue, not accompanied by dizziness, Limb numbness and weakness, etc.
, visited our hospital, ophthalmology outpatient clinic after fundus examination to eliminate eye diseases, then visited our outpatient clinic, with "extraocular muscle paralysis (cause to be investigated)" admitted to hospital
.
Since the onset of the disease, the patient's spirit and diet have been acceptable, sleep is poor, urine and urine are normal, and there is no significant change
in body weight.
Previous physical health, family history, personal history is not special
.
▌Physical examination:
Cardiopulmonary and abdominal examination showed no obvious abnormalities
。 Sharp speech, double pupil is large and equicircle, right upper eyelid is weak to lift, right eye direct and indirect light reflex dull, left eye sensitive to light reflex, right eye upward vision restriction, double vision, bilateral frontal lines and nasolabial folds symmetrical, tooth mouth angle is not biased, tongue extension is centered, limb muscle strength, muscle tone is normal, bilateral limb tendon reflex symmetrical existence, bilateral Pap sign negative, meningeal stimulation sign negative
.
▌Preliminary diagnosis:
diplopia (to be investigated); Cerebral infarction (?) ）； Cerebral aneurysms (?) ）； Myasthenia gravis (?) ）； Intracranial mass lesions (?) ）
。
How about localization and qualitative diagnosis?
▌Localization diagnosis: Figure 1.
Localization diagnosis ▌Qualitative diagnosis:
Middle-aged male patients, acute onset, acute cerebrovascular disease can not be excluded; The patient had intermittent throbbing headache 1 week ago, and the intraocular muscles were affected at the same time, which could not be ruled out due to metabolic diseases; The patient begins with drooping eyes and face, double vision, and myasthenia
gravis cannot be excluded.
So we improved the relevant inspections in a targeted manner:
Figure 2.
Skull MRA
In summary, further qualitative diagnosis: head MRI did not indicate acute infarction foci and aneurysm→ etc.
, did not support acute cerebrovascular disease and intracranial mass lesions; The patient began with drooping eyes and face, double vision, no abnormalities in the current electroneurography and negative neostigmine test→ which does not support myasthenia gravis; Glucose tolerance test does not support diabetes → so diabetic-related peripheral nerve damage is not considered →; At present, the possibility of painful ophthalmoplegia is considered to be high, and it is necessary to improve orbital imaging to further clarify
.
Orbital MRI: thickening of the mucosa of the right ethmoid sinus and left maxillary sinus, and no abnormalities on MRI scan of the remaining orbit (Fig.
3).
Figure 3.
Orbital MRI skull enhancement MRI: MRI
enhancement did not show obvious abnormal enhancement
.
Thoracic magnetic scan non-contrast scan: MRI shows no significant abnormal reinforcement
.
Perfect lumbar puncture: cerebrospinal fluid biochemistry, cerebrospinal fluid routine analysis normal range, acid fast, ink staining: negative
.
Cerebrospinal fluid testing does not support demyelinating disease
.
At present, it is considered that painful ophthalmoplegia syndrome (Tolosa-Hunt Syndrome) is very likely, and oral hormone therapy is given at the same time as gastric protection, potassium supplementation, calcium supplementation and other prevention of hormonal side effects
.
After 3 days of hormone therapy, the patient's right upper eyelid was raised stronger than the front, the right eyelid was enlarged compared with the front, and the distance between the reality and the virtual image was shortened, and the treatment was effective
.
What is THS?
THS is an idiopathic granulomatous inflammation from the cavernous sinus to the supraorbital fissure and apex that compresses blood vessels and neural structures
within the cavernous sinus.
In 1954, Tolosa first reported a patient with periorbital pain, ipsilateral oculomotor nerve (III.
, IV.
, VI.
) palsy and decreased corneal reflexes.
Cerebral angiography shows stenosis from the end of the internal carotid artery to the siphon, and autopsy reveals epiarteritis
.
In 1961, Hunt reported 6 similar patients, all of which showed periorbital pain and III.
, IV.
, VI.
cranial nerve palsy, symptoms were relieved or recurred for months or years, including cerebral angiography, various examinations and surgeries did not find cavernous sinus abnormalities, and were completely relieved by glucocorticoid therapy, named "painful ophthalmoplegia"
.
In 1996, Smith reported 5 more cases and called them THS
.
Common causes of THS are summarized in the following table:
Table 1.
Common causes
of THS: Diagnosis and differential diagnosis
of THS▌Diagnostic criteria[1].
1.
One or more unilateral orbital pain, which can last for several weeks if not treated;
2.
Extraocular muscle paralysis + granulomatous lesions (confirmed by magnetic resonance or biopsy);
3.
Ophthalmoplegia and pain occur at the same time, or ophthalmoplegia appears within 2 weeks of pain;
4.
Pain and ophthalmoplegia relieved within 3 days after adequate use of hormones;
5.
Exclude other diseases
.
▌Differential diagnosis [2] 1.
Aneurysm: Aneurysm of the skull base artery ring or internal carotid artery
can cause oculomotor and/or
Extensor nerve palsy, an internal carotid aneurysm in the cavernous sinus, can cause oculomotor, trochlear spread, and trigeminal nerve ophthalmic branch paralysis, called cavernous sinus syndrome
.
Aneurysms of the posterior cerebral artery, superior cerebellar artery, and posterior communicating artery can cause oculomotor palsy, but generally do not cause trochlear nerve palsy
alone.
2.
Infection
of intraorbital or postorbital inflammation can cause paralysis of the oculomotor nerve and produce the following syndromes
.
(1) Temporal bone apex syndrome: In patients with otitis media and chronic mastoiditis, inflammation develops into the skull and destroys the temporal apex, which can cause the syndrome
.
Clinically, bilateral endotropia invades the semilunar ganglia, which can cause facial numbness or pain
.
(2) Neuritis: For patients with paranasal sinusitis, paralysis of oculomotor, trochlear and extensor nerves may occur
.
(3) Superior orbital fissure syndrome and orbital apical syndrome: patients with pituitary tumor, myringitis, and paranasal sinusitis, when the disease invades the supraorbital fissure and optic nerve foramen, there can be paralysis of the oculomotor, trochle, extensor nerve and trigeminal nerve ophthalmic branches, that is, supraorbital fissure syndrome, if there is visual impairment, it is called orbital apex syndrome
.
(4) Other infections: various meningitis such as tuberculous purulent, viral, fungal meningitis, can affect the oculomotor and trochlear nerve, paralyzing; Orbital cellulitis can cause ophthalmoplegia; Encephalitis can cause nuclear ophthalmoplegia; Shingles, chickenpox, and mumps can also cause ophthalmoplegia
.
3.
Head trauma, orbital fracture and intraorbital hemorrhage, which can lead to paralysis of extraocular muscles,
and the upper and lower oblique muscles are the most vulnerable; Orbital apical fractures can lead to oculomotor, trochlea, extensor palsy, and damage to the ophthalmic branch of the trigeminal nerve, because the oculomotor nerve and parasympathetic nerve are severely damaged, and due to sympathetic and parasympathetic dysfunction, the pupil size can be normal and the light response disappears
.
hiatus hernia caused by intracranial hematoma on one side, ipsilateral oculomotor nerve palsy and contralateral hemiplegia; Damage to the ciliary ganglion
leads to paralysis of the intraocular muscles.
4.
Patients with cerebral arteriosclerotic angiopathy
cerebral arteriosclerosis and hypertension, often suddenly appear ophthalmoplegia, which may be due to brainstem hemorrhage, subarachnoid hemorrhage or blockage of blood vessels supplying the nerve trunk or nerve nucleus, and can also be because of hardened blood vessels such as posterior cerebral artery, superior cerebellar artery compression to make eye movement, Schlear nerve palsy, endoauditory artery and anterior inferior cerebellar artery sclerosis caused by extensor nerve palsy
.
5.
Myasthenia
gravis is a common cause of ophthalmoplegia, and the striated muscles of each muscle or limb innervated by the medulla oblongata can be affected, but extraocular muscle involvement is more common
.
6.
Other
such as diabetic ophthalmoplegia with oculomotor nerve, extensor nerve palsy is more common, because the mydriatic fiber is located in the peripheral part above the oculomotor nerve, not susceptible to ischemic damage generally does not appear pupil changes, which is very different from the mydriasis caused by oculomotor nerve palsy caused by aneurysm; ophthalmoplegic migraine, which occurs during or after an attack (oculomotors, extensor nerve palsy, and diplopia); Extraocular muscular dystrophy can also occur with ptosis of both eyelids and progressively progresses to paralysis of all extraocular muscles
.
Treatment of THS
Clinical analysis of 10 cases of painful ophthalmoplegic syndrome[J].
Modern Chinese Drug Application,2015,9(02):72-73.
) Li Bin.
Analysis of the etiology of extraocular muscle paralysis in 80 cases with compound as the first symptom[J].
Journal of Clinical Ophthalmology,2014,22(02):165-168.
)
Where to see more neurological clinical knowledge?
Come to the "doctor's station" and take a look 👇
A case learns a disease
"Vision into pairs", also known as diplopia, the principle of double vision is that the imaging of one eye falls on the concave of the macula, while the imaging of the other eye does not fall on the
concave.
The image that falls on the concave is never clearer than the image that does not fall on the fovea, so two images
are formed.
There are many causes of diplopia, most of which are caused by weakness or paralysis of the extraocular muscles
.
The extraocular muscles are controlled by cranial nerves, and diseases of cranial nerves or the brain itself may cause diplopia, as well as lesions of extraocular muscles, muscle-nerve junctions, oculomotor nerves and their nuclei
.
Next, let's dissect the cause
of diplopia in this case.
First look at the basic information
of the patient, male, 45 years old, mainly due to "intermittent headache for 1 week, vision in double 3 days" admission
.
The patient had intermittent headache without obvious triggers 1 week ago, for the right hemisphere pulsating dull pain, with the right temporal region as the center, each pain lasted about 10-20s, several pain attacks a day, no obvious regularity, did not pay attention, 3 days ago there was no obvious trigger for the appearance of double eye vision, the most obvious when looking up, accompanied by right eyelid lifting difficulty and eyebrow arch pain discomfort, can not be relieved after rest, no significant aggravation after fatigue, not accompanied by dizziness, Limb numbness and weakness, etc.
, visited our hospital, ophthalmology outpatient clinic after fundus examination to eliminate eye diseases, then visited our outpatient clinic, with "extraocular muscle paralysis (cause to be investigated)" admitted to hospital
.
Since the onset of the disease, the patient's spirit and diet have been acceptable, sleep is poor, urine and urine are normal, and there is no significant change
in body weight.
Previous physical health, family history, personal history is not special
.
▌Physical examination:
Cardiopulmonary and abdominal examination showed no obvious abnormalities
。 Sharp speech, double pupil is large and equicircle, right upper eyelid is weak to lift, right eye direct and indirect light reflex dull, left eye sensitive to light reflex, right eye upward vision restriction, double vision, bilateral frontal lines and nasolabial folds symmetrical, tooth mouth angle is not biased, tongue extension is centered, limb muscle strength, muscle tone is normal, bilateral limb tendon reflex symmetrical existence, bilateral Pap sign negative, meningeal stimulation sign negative
.
▌Preliminary diagnosis:
diplopia (to be investigated); Cerebral infarction (?) ）； Cerebral aneurysms (?) ）； Myasthenia gravis (?) ）； Intracranial mass lesions (?) ）
。
How about localization and qualitative diagnosis?
▌Localization diagnosis: Figure 1.
Localization diagnosis ▌Qualitative diagnosis:
Middle-aged male patients, acute onset, acute cerebrovascular disease can not be excluded; The patient had intermittent throbbing headache 1 week ago, and the intraocular muscles were affected at the same time, which could not be ruled out due to metabolic diseases; The patient begins with drooping eyes and face, double vision, and myasthenia
gravis cannot be excluded.
So we improved the relevant inspections in a targeted manner:
- Oral glucose tolerance test (OGTT test): blood glucose 8.
74mmol/L in 2 hours, the remainder is within the normal range
.
- Biochemical total, urinalysis, glycated hemoglobin, five alpha + male tumor, five suspected blood, five hepatitis B + C antibody, fecal analysis showed no obvious abnormalities
. - Plain scan of head + chest showed no abnormalities
. - Skull DWI+MRA: No abnormally high signal
was seen in head DWI imaging.
Localized stenosis of the P1 segment of the right posterior cerebral artery and the siphon portion of the left internal carotid artery (Figure 2).
Figure 2.
Skull MRA
- Skull MRI + SWI: non-contrast MRI scan of the head showed no obvious abnormalities
.
Skull SWI imaging showed no abnormally low signal
. - Electroneurography repeated frequency electrical stimulation: there were no characteristic changes in the low-frequency stimulation of the right orbicularis oculi muscle and trapezius muscle, and the low-frequency and high-frequency stimulation of the left little finger extensor muscle showed no characteristic changes
. - Neostigmine test: negative, no significant improvement
in right eye face drooping and right eyeball restriction after administration of neostigmine.
In summary, further qualitative diagnosis: head MRI did not indicate acute infarction foci and aneurysm→ etc.
, did not support acute cerebrovascular disease and intracranial mass lesions; The patient began with drooping eyes and face, double vision, no abnormalities in the current electroneurography and negative neostigmine test→ which does not support myasthenia gravis; Glucose tolerance test does not support diabetes → so diabetic-related peripheral nerve damage is not considered →; At present, the possibility of painful ophthalmoplegia is considered to be high, and it is necessary to improve orbital imaging to further clarify
.
Orbital MRI: thickening of the mucosa of the right ethmoid sinus and left maxillary sinus, and no abnormalities on MRI scan of the remaining orbit (Fig.
3).
Figure 3.
Orbital MRI skull enhancement MRI: MRI
enhancement did not show obvious abnormal enhancement
.
Thoracic magnetic scan non-contrast scan: MRI shows no significant abnormal reinforcement
.
Perfect lumbar puncture: cerebrospinal fluid biochemistry, cerebrospinal fluid routine analysis normal range, acid fast, ink staining: negative
.
Cerebrospinal fluid testing does not support demyelinating disease
.
At present, it is considered that painful ophthalmoplegia syndrome (Tolosa-Hunt Syndrome) is very likely, and oral hormone therapy is given at the same time as gastric protection, potassium supplementation, calcium supplementation and other prevention of hormonal side effects
.
After 3 days of hormone therapy, the patient's right upper eyelid was raised stronger than the front, the right eyelid was enlarged compared with the front, and the distance between the reality and the virtual image was shortened, and the treatment was effective
.
What is THS?
THS is an idiopathic granulomatous inflammation from the cavernous sinus to the supraorbital fissure and apex that compresses blood vessels and neural structures
within the cavernous sinus.
In 1954, Tolosa first reported a patient with periorbital pain, ipsilateral oculomotor nerve (III.
, IV.
, VI.
) palsy and decreased corneal reflexes.
Cerebral angiography shows stenosis from the end of the internal carotid artery to the siphon, and autopsy reveals epiarteritis
.
In 1961, Hunt reported 6 similar patients, all of which showed periorbital pain and III.
, IV.
, VI.
cranial nerve palsy, symptoms were relieved or recurred for months or years, including cerebral angiography, various examinations and surgeries did not find cavernous sinus abnormalities, and were completely relieved by glucocorticoid therapy, named "painful ophthalmoplegia"
.
In 1996, Smith reported 5 more cases and called them THS
.
Common causes of THS are summarized in the following table:
Table 1.
Common causes
of THS: Diagnosis and differential diagnosis
of THS▌Diagnostic criteria[1].
1.
One or more unilateral orbital pain, which can last for several weeks if not treated;
2.
Extraocular muscle paralysis + granulomatous lesions (confirmed by magnetic resonance or biopsy);
3.
Ophthalmoplegia and pain occur at the same time, or ophthalmoplegia appears within 2 weeks of pain;
4.
Pain and ophthalmoplegia relieved within 3 days after adequate use of hormones;
5.
Exclude other diseases
.
▌Differential diagnosis [2] 1.
Aneurysm: Aneurysm of the skull base artery ring or internal carotid artery
can cause oculomotor and/or
Extensor nerve palsy, an internal carotid aneurysm in the cavernous sinus, can cause oculomotor, trochlear spread, and trigeminal nerve ophthalmic branch paralysis, called cavernous sinus syndrome
.
Aneurysms of the posterior cerebral artery, superior cerebellar artery, and posterior communicating artery can cause oculomotor palsy, but generally do not cause trochlear nerve palsy
alone.
2.
Infection
of intraorbital or postorbital inflammation can cause paralysis of the oculomotor nerve and produce the following syndromes
.
(1) Temporal bone apex syndrome: In patients with otitis media and chronic mastoiditis, inflammation develops into the skull and destroys the temporal apex, which can cause the syndrome
.
Clinically, bilateral endotropia invades the semilunar ganglia, which can cause facial numbness or pain
.
(2) Neuritis: For patients with paranasal sinusitis, paralysis of oculomotor, trochlear and extensor nerves may occur
.
(3) Superior orbital fissure syndrome and orbital apical syndrome: patients with pituitary tumor, myringitis, and paranasal sinusitis, when the disease invades the supraorbital fissure and optic nerve foramen, there can be paralysis of the oculomotor, trochle, extensor nerve and trigeminal nerve ophthalmic branches, that is, supraorbital fissure syndrome, if there is visual impairment, it is called orbital apex syndrome
.
(4) Other infections: various meningitis such as tuberculous purulent, viral, fungal meningitis, can affect the oculomotor and trochlear nerve, paralyzing; Orbital cellulitis can cause ophthalmoplegia; Encephalitis can cause nuclear ophthalmoplegia; Shingles, chickenpox, and mumps can also cause ophthalmoplegia
.
3.
Head trauma, orbital fracture and intraorbital hemorrhage, which can lead to paralysis of extraocular muscles,
and the upper and lower oblique muscles are the most vulnerable; Orbital apical fractures can lead to oculomotor, trochlea, extensor palsy, and damage to the ophthalmic branch of the trigeminal nerve, because the oculomotor nerve and parasympathetic nerve are severely damaged, and due to sympathetic and parasympathetic dysfunction, the pupil size can be normal and the light response disappears
.
hiatus hernia caused by intracranial hematoma on one side, ipsilateral oculomotor nerve palsy and contralateral hemiplegia; Damage to the ciliary ganglion
leads to paralysis of the intraocular muscles.
4.
Patients with cerebral arteriosclerotic angiopathy
cerebral arteriosclerosis and hypertension, often suddenly appear ophthalmoplegia, which may be due to brainstem hemorrhage, subarachnoid hemorrhage or blockage of blood vessels supplying the nerve trunk or nerve nucleus, and can also be because of hardened blood vessels such as posterior cerebral artery, superior cerebellar artery compression to make eye movement, Schlear nerve palsy, endoauditory artery and anterior inferior cerebellar artery sclerosis caused by extensor nerve palsy
.
5.
Myasthenia
gravis is a common cause of ophthalmoplegia, and the striated muscles of each muscle or limb innervated by the medulla oblongata can be affected, but extraocular muscle involvement is more common
.
6.
Other
such as diabetic ophthalmoplegia with oculomotor nerve, extensor nerve palsy is more common, because the mydriatic fiber is located in the peripheral part above the oculomotor nerve, not susceptible to ischemic damage generally does not appear pupil changes, which is very different from the mydriasis caused by oculomotor nerve palsy caused by aneurysm; ophthalmoplegic migraine, which occurs during or after an attack (oculomotors, extensor nerve palsy, and diplopia); Extraocular muscular dystrophy can also occur with ptosis of both eyelids and progressively progresses to paralysis of all extraocular muscles
.
Treatment of THS
small
knot
In conclusion, when diagnosing the nature of ophthalmoplegia, not only cavernous sinus lesions should be considered, but further examination must be carried out to exclude diseases
such as intracranial mass lesions and aneurysms.
Clinical analysis of 10 cases of painful ophthalmoplegic syndrome[J].
Modern Chinese Drug Application,2015,9(02):72-73.
) Li Bin.
Analysis of the etiology of extraocular muscle paralysis in 80 cases with compound as the first symptom[J].
Journal of Clinical Ophthalmology,2014,22(02):165-168.
)
Where to see more neurological clinical knowledge?
Come to the "doctor's station" and take a look 👇
