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A 64-years-old male patient presented to our
Department with 10-days history of horizontal
diplopia. He first noted symptoms when
gazing to the left which is relieved by
occlusion of one of his eyes
His past history revealed hypertension &
Diabetes mellitus
No history of headache,N.&V., numbness or
any associated neurological symptom
he denied any head trauma or surgery
No history of fatigability
No history of hearing loss,Vertigo ,no weight
loss
VA 6/6 (both eyes)
Face turn to the left ,Normal lid
,fatigability is -ve,no RAPD,LT incomitant
esotropia 20 degree far>near ,limitation
of abduction in the left eye ,has
binocular hoizontal diplopia,
normal fundi.
systemic examination ;nothing significant
A.Neurogenic(6 th n. palsy)
B.Restricted medial rectus m. (trauma,inflammatory
pseudotumor or myositis,thyroid eye disease)
C.Spasm of near reflex
D.Mysthenia gravis
Cranial nerve VI, also known as the abducens nerve, innervates the ipsilateral lateral
rectus (LR), which functions to abduct the ipsilateral eye.
It has the longest subarachnoid course of all the cranial nerves; therefore, its
syndromes are similar to those of the fourth nerve because of their long intracranial
courses.
The sixth nerve nucleus is located in the pons, just ventral to the floor of the fourth
ventricle and just lateral to the medial longitudinal fasciculus (MLF). About 40% of its
neurons project into the ipsilateral MLF only to cross over to the contralateral side and
ascend to innervate that contralateral medial rectus subnucleus to participate in
contralateral eye adduction
Isolated cases are mostly due to vascular causes such as
hypertension, arteriosclerosis, and diabetes. Tumors are a much more
common diagnosis in children, unless they occur after upper respiratory
tract infections.
Nuclear
Fascicular
BasilarIntracavernus
Orbital
Elevated intracranial pressure can result in downward displacement
of the brainstem, causing stretching of the sixth nerve secondary to
its anatomic location within the Dorello canal. This is believed to be
the reason that about 30% of patients with pseudotumor cerebri
have an isolated abducens nerve palsy.
Subarachnoid space lesions can be causes of abducens nerve
palsy (eg, hemorrhage, infection, inflammation, space-occupying
tumor, cavernous sinus mass). Inflammatory (eg, postviral,
demyelinating, sarcoid, giant cell arteritis)
Vascular
Metabolic (eg, vitamin B, Wernicke-Korsakoff syndrome)
Neoplasm (children) - Pontine glioma
Infectious (eg, Lyme disease, syphilis)
Congenital absence of the sixth nerve (eg, Duane syndrome)
Trauma, particularly if it results in a torsional head motion
Post–lumbar tap
A typical workup of a sixth nerve palsy
involve
excluding paresis of other cranial nerves (including VII and
VIII), checking ocular muscle motility, and evaluating pupillary
responsiveness.
Checking deep tendon reflexes (DTRs) and motor function to
exclude corticospinal tract involvement also is important
Complete blood cell (CBC) count
Glucose levels
Glycosylated hemoglobin (HbA1C)
Erythrocyte sedimentation rate and/or C-reactive protein
Rapid plasma reagin test
Fluorescent treponemal antibody-absorption test
Lyme titer
Antinuclear antibody test
Imaging Studies
Patients younger than 50 years specially no vasculopathic history
Associated pain or other neurologic abnormality
Bilateral sixth nerve palsy
Papilledema
In the event no marked improvement is seen or other nerves become
involved
ifMRI results are negative
An LP should be considered
Tensilon test
Chest imaging
Cerebral angiography
Truly isolated cases often are benign. They can be followed with a serial
examination, at least every 6 weeks, over a 6-month period to note
decreasing symptoms (diplopia) and resolution of the paretic lateral rectus
(increasing motility).[
Children with sixth nerve palsy who are in the amblyopic age group can be
treated with an alternating patching to decrease their chances of developing
any amblyopia in the paretic eye. Additionally, prescribing the full amount of
hyperopic correction helps to decrease the esodeviation by relaxing the
child's accommodative effort
Adult patients and those children beyond the amblyopic age can be patched
or have their lenses "fogged" with clear tape or nail polish to reduce their
diplopia.
Fresnel prisms also can be prescribed as an alternative
Older patients in whom giant cell arteritis is a consideration should start
the standard treatment with prednisone or intravenous
methylprednisolone as soon as possible
Botulinum toxin A (Botox) has been used in the treatment of adult
patients with acute sixth CN palsies to prevent contracture of the
ipsilateral medial rectus muscle and to restore binocular vision.
If after 6 months of follow-up care the remaining deviation is
still unacceptable and is too large to be corrected with prisms,
surgical corrective options should be discussed with the
patient.
The procedure that is chosen depends on the remaining
function of the lateral rectus and the experience of
the surgeon.
If some residual function exists in the lateral rectus, a graded
recession/resection is the procedure of choice.
When little or no residual function is present, a transposition
procedure, such as the Hummelsheim or the Jensen, can be
used, along with, in appropriate patients, weakening the
antagonist ipsilateral medial rectus.
Thank you

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6 th nerve palsy

  • 1.
  • 2. A 64-years-old male patient presented to our Department with 10-days history of horizontal diplopia. He first noted symptoms when gazing to the left which is relieved by occlusion of one of his eyes His past history revealed hypertension & Diabetes mellitus No history of headache,N.&V., numbness or any associated neurological symptom he denied any head trauma or surgery No history of fatigability No history of hearing loss,Vertigo ,no weight loss
  • 3. VA 6/6 (both eyes) Face turn to the left ,Normal lid ,fatigability is -ve,no RAPD,LT incomitant esotropia 20 degree far>near ,limitation of abduction in the left eye ,has binocular hoizontal diplopia, normal fundi. systemic examination ;nothing significant
  • 4.
  • 5. A.Neurogenic(6 th n. palsy) B.Restricted medial rectus m. (trauma,inflammatory pseudotumor or myositis,thyroid eye disease) C.Spasm of near reflex D.Mysthenia gravis
  • 6.
  • 7. Cranial nerve VI, also known as the abducens nerve, innervates the ipsilateral lateral rectus (LR), which functions to abduct the ipsilateral eye. It has the longest subarachnoid course of all the cranial nerves; therefore, its syndromes are similar to those of the fourth nerve because of their long intracranial courses. The sixth nerve nucleus is located in the pons, just ventral to the floor of the fourth ventricle and just lateral to the medial longitudinal fasciculus (MLF). About 40% of its neurons project into the ipsilateral MLF only to cross over to the contralateral side and ascend to innervate that contralateral medial rectus subnucleus to participate in contralateral eye adduction Isolated cases are mostly due to vascular causes such as hypertension, arteriosclerosis, and diabetes. Tumors are a much more common diagnosis in children, unless they occur after upper respiratory tract infections.
  • 8.
  • 9.
  • 11. Elevated intracranial pressure can result in downward displacement of the brainstem, causing stretching of the sixth nerve secondary to its anatomic location within the Dorello canal. This is believed to be the reason that about 30% of patients with pseudotumor cerebri have an isolated abducens nerve palsy. Subarachnoid space lesions can be causes of abducens nerve palsy (eg, hemorrhage, infection, inflammation, space-occupying tumor, cavernous sinus mass). Inflammatory (eg, postviral, demyelinating, sarcoid, giant cell arteritis) Vascular Metabolic (eg, vitamin B, Wernicke-Korsakoff syndrome) Neoplasm (children) - Pontine glioma Infectious (eg, Lyme disease, syphilis) Congenital absence of the sixth nerve (eg, Duane syndrome) Trauma, particularly if it results in a torsional head motion Post–lumbar tap
  • 12. A typical workup of a sixth nerve palsy involve excluding paresis of other cranial nerves (including VII and VIII), checking ocular muscle motility, and evaluating pupillary responsiveness. Checking deep tendon reflexes (DTRs) and motor function to exclude corticospinal tract involvement also is important
  • 13.
  • 14. Complete blood cell (CBC) count Glucose levels Glycosylated hemoglobin (HbA1C) Erythrocyte sedimentation rate and/or C-reactive protein Rapid plasma reagin test Fluorescent treponemal antibody-absorption test Lyme titer Antinuclear antibody test Imaging Studies
  • 15. Patients younger than 50 years specially no vasculopathic history Associated pain or other neurologic abnormality Bilateral sixth nerve palsy Papilledema In the event no marked improvement is seen or other nerves become involved
  • 16. ifMRI results are negative An LP should be considered Tensilon test Chest imaging Cerebral angiography
  • 17. Truly isolated cases often are benign. They can be followed with a serial examination, at least every 6 weeks, over a 6-month period to note decreasing symptoms (diplopia) and resolution of the paretic lateral rectus (increasing motility).[ Children with sixth nerve palsy who are in the amblyopic age group can be treated with an alternating patching to decrease their chances of developing any amblyopia in the paretic eye. Additionally, prescribing the full amount of hyperopic correction helps to decrease the esodeviation by relaxing the child's accommodative effort Adult patients and those children beyond the amblyopic age can be patched or have their lenses "fogged" with clear tape or nail polish to reduce their diplopia. Fresnel prisms also can be prescribed as an alternative
  • 18. Older patients in whom giant cell arteritis is a consideration should start the standard treatment with prednisone or intravenous methylprednisolone as soon as possible Botulinum toxin A (Botox) has been used in the treatment of adult patients with acute sixth CN palsies to prevent contracture of the ipsilateral medial rectus muscle and to restore binocular vision.
  • 19. If after 6 months of follow-up care the remaining deviation is still unacceptable and is too large to be corrected with prisms, surgical corrective options should be discussed with the patient. The procedure that is chosen depends on the remaining function of the lateral rectus and the experience of the surgeon. If some residual function exists in the lateral rectus, a graded recession/resection is the procedure of choice. When little or no residual function is present, a transposition procedure, such as the Hummelsheim or the Jensen, can be used, along with, in appropriate patients, weakening the antagonist ipsilateral medial rectus.