- •Preface
- •Transient Binocular Visual Loss
- •Migraine with Typical Visual Aura
- •Congenitally Elevated Optic Disc
- •Optic Disc Coloboma
- •Optic Pit
- •Morning Glory Optic Disc Anomaly
- •Optic Disc Hypoplasia
- •Typical Optic Neuritis
- •Atypical Optic Neuritis
- •Arteritic Anterior Ischemic Optic Neuropathy
- •Posterior Ischemic Optic Neuropathy
- •Hypotensive Ischemic Optic Neuropathy
- •Toxic Optic Neuropathy
- •Dominantly Inherited Optic Neuropathy
- •Leber Hereditary Optic Neuropathy
- •Sphenoid Meningioma
- •Optic Nerve Sheath Meningioma
- •Craniopharyngioma
- •Pituitary Adenoma
- •Optic Glioma (Pilocytic Astrocytoma of Optic Nerves or Chiasm)
- •Anterior Visual Pathway Intracranial Aneurysm
- •Traumatic Optic Neuropathy
- •Radiation Optic Neuropathy
- •Graves Optic Neuropathy
- •Papilledema
- •Hypertensive Optic Neuropathy
- •Paraneoplastic Optic Neuropathy
- •Diabetic Papillopathy
- •Homonymous Hemianopia
- •Cerebral (Retrogeniculate, Cortical) Blindness
- •Visual Agnosia
- •Visual Spatial And Attentional Disturbances
- •Orbital Myositis
- •Graves Disease
- •Genetic Extraocular Myopathy
- •Myasthenia Gravis
- •Third Cranial Nerve Palsy
- •Fourth Cranial Nerve Palsy
- •Sixth Cranial Nerve Palsy
- •Unilateral Ophthalmoplegia
- •Bilateral Ophthalmoplegia
- •Direct Carotid–cavernous Fistula
- •Indirect (Dural) Carotid–cavernous Fistula
- •Internuclear Ophthalmoplegia
- •Skew Deviation
- •Dorsal Midbrain (Pretectal) Syndrome
- •Paramedian Thalamic or Midbrain Syndrome
- •Paramedian Pontine Syndrome
- •Dorsolateral Medullary (Wallenberg) Syndrome
- •Acute Upgaze Deviation
- •Acute Downgaze Deviation
- •Omnidirectional Slow Saccades
- •Omnidirectional Saccadic Pursuit
- •Congenital Ocular Motor Apraxia
- •Acute Horizontal Gaze Deviation
- •Ping Pong Gaze
- •Physiologic Nystagmus
- •Congenital Motor Nystagmus
- •Congenital Sensory Nystagmus
- •Monocular Pendular Nystagmus of Childhood
- •Spasmus Nutans
- •Peripheral Vestibular Nystagmus
- •Acquired Binocular Pendular Nystagmus
- •Sidebeat, Upbeat, and Downbeat Nystagmus
- •Epileptic Nystagmus
- •Convergence–retraction “Nystagmus”
- •Voluntary “Nystagmus”
- •Superior Oblique Myokymia
- •Square Wave Jerks
- •Ocular Flutter and Opsoclonus
- •Ocular Dysmetria
- •Ocular Bobbing
- •Tonic Pupil
- •Argyll Robertson Pupils
- •Tectal (Dorsal Midbrain) Pupils
- •Pharmacologically Dilated Pupil
- •Mydriatic Pupil of Third Cranial Nerve Palsy
- •Mydriatic Pupil of Traumatic Iridoplegia
- •Episodic Pupil Dilation
- •Horner Syndrome
- •Ptosis
- •Lid Retraction
- •Apraxia of Eyelid Opening
- •Benign Essential Blepharospasm
- •Hemifacial Spasm
- •Index
• 13 SECTIONDisorders Eyelid
Hemifacial Spasm
Key Facts
•Involuntary contraction of facial muscles on one side • Generally no underlying disease, but some patients have old ipsilateral facial palsy • Believed to result from pathologic excitability of facial nerve
•In some patients, surgical exploration shows compression of facial nerve at its exit from brainstem by aberrant artery
• this abnormality is generally not visible with brain imaging
•Botulinum toxin injections into affected side of face are usually temporarily effective • For refractory cases, suboccipital craniectomy with placement of Gelfoam between facial nerve and aberrant artery is an option
Clinical Findings
•Involuntary contraction of facial muscles on one side • Upper face, including orbicular oculi, usually most prominently involved • No other pertinent findings unless pre-existing facial palsy causes ipsilateral facial weakness and ipsilateral deviation of mouth (postparetic facial contracture) and abnormal coactivation of facial muscles (facial synkinesis)
Ancillary Testing
•MRI with attention to brainstem—extrinsic and intrinsic brainstem lesions may rarely cause hemifacial spasm
Treatment
•Botulinum toxin injected into affected side of face is usually temporarily effective
• For refractory cases, suboccipital craniectomy with placement of Gelfoam between facial nerve and aberrant artery is an option
Prognosis
•Botulinum toxin injections generally relieve symptoms for 3–4 months
• Craniectomy usually effective, but there is a small risk of stroke or deafness
A B
Fig. 13.5 Patient with left hemifacial spasm. (A) Upper and lower facial muscles are contracted. (B) Botulinum toxin injections are given subcutaneously in the brow, eyelids, and cheek.
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C
Fig. 13.5, con’t (C) One day later, the facial muscle contraction has disappeared.
Fig. 13.6 Hemifacial spasm. Axial T2 MRI shows compression of the seventh cranial nerve (black arrows) by a vessel indenting its root entry zone (white arrow) in the caudal pons. (From Rahman EA et al. Am J Ophthalmol 2002; 133:854–856, with permission.)
Spasm Hemifacial
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