Abnormal Eye Movements

• Optokinetic Nystagmus
• Toward involved (lesioned) hemisphere is lost
• Right parietal lesion causes impared smooth tracking to right
• Vertical eye movements
• Under bilateral control of cortex and upper brainstem
• Pretectal fibers of midbrain tegmentum, involve fibers of posterior commissure near superior colliculus
• Rostral MLF at junction of midbrain and thalamus
• Medial cells serve upgaze; lateral cells serve downgaze (initially are medial and commingle with upgaze fibers)
• Lesion of both medial RiMLF causes complete vertical gaze palsy
• Lateral lesion causes isolated downgaze palsy (rare)
• Saccades – fast conjugate eye movements, voluntary
• Generalized in contralateral frontal lobe (area 8)
• Smooth Pursuit – slow involuntary movement generated in ipsilateral occipital lobe (area 18 and 19)
• Hypermetria (overshooting) – midline cerebellar lesion
• Inability to initiate voluntary movements (vertically or horizontally)
• May be congenial (Cogan syndrome, ataxia-telangiectasia)
• Impaired Smooth Pursuit with slow, hypotonic saccades – caused by Parkinson’s, Huntington’s, Progressive Supranuclear Palsy
• Midbrain lesion or in region of posterior commissure – interfere with conjugate movements in vertical plane (seen in Nieman-Pick)
• Parinaud’s syndrome – vertical gaze palsy (usually upgaze)
• Mydriasis; loss of convergence and papillary light reflexes
• Refractory nystagmus or lid retraction (Collier’s sign)
• Congenital Ocular Motor Apraxia (Cogan’s Syndrome)
• Abnormal eye and head movements during attempts to change position of eyes
• Effects of Lesions
• Right cerebral lesion produces right eye deviation, left hemiparesis
• Right PPRF lesion produces left eye deviation, left hemiparesis, left CN VI/VII palsies
• CN III lesion produces ipsilateral CN III palsy (down and out)
• CN III + Red nucleus lesion also produces contralateral tremor (Benedikt’s syndrome)
• CN III + pyramid lesion produces contralateral hemiparesis (Weber’s syndrome)
• CN VI+VII + pyramid lesion produces cranial nerve deficits and contralateral hemiparesis (Millard-Gubler syndrome)
• Cavernous lesions
• Retrocaverous compressive lesions(infraclinoid extradural aneurysms/tumor) – involve V1, V2, V3, III, IV, VI
• Posterior cavernous sinus – V1, V2, III, IV, VI
• Anterior cavernous sinus – VI, III, VI, VI
• CN IV lesion – difficulty with downward gaze, especially with adduction
• Paralyzed eye tends to look up and in (opposite of CN III lesion)
• Bielchowski’s sign – head tilt to opposite shoulder because of paralyzed intortion
• Inferior oblique intorts abducted eye, depresses adducted eye
• Spasmus Mutans – pendular nysyagmus of infancy
• Any direction, one eye predominates, worse when head immobilized
• Vertical Nystagmus
• Upbeat – can be demyelinating; caused by vascular, tumors
• Downbeat – always central; caused by Wenickes, syringobulbia, Chiari, basilar invagination
• Course Horizontal Nystagmus – can be caused by CP angle tumors
• Convergence Nystagmus – after accompanied by nystagmus retractorius in Parinaud syndrome
• Usually lesion of upper midbrain tegmentum or pinealoma
• Seesaw Nystagmus – torsional-vertical oscillation; caused by sella or parasellar masses
• Palatal Nystagmus – lesion of central tegmental tract
• Oscillopsia – illusionary movement of environment
• Associated with lesion of labyrinth (such as aminoglycoside toxicity)
• Opsoclonus – rapid, conjugate oscillations of eyes in all positions
• Childhood form associated with ataxia, myoclonus; responds to ACTH
• Ophthalmoplegia
• Internuclear Ophthalmoplegia (INO)
• Ipsilateral adduction palsy, preserved convergence, contralateral monocular nystagmus
• Caused by lesion of pontine or midbrain MLF
• One-and-a-Half Syndrome
• Ipsilateral gaze palsy with an ipsilateral INO
• Only horizontal eye movement is abduction of contralateral eye
• Caused by pontine lesion of MLF and PPRF