I.
II.
III.
IV.
Intro to Homonymous Hemianopsia
A. Manifestation of retrochiasmal afferent visual pathway disease
1.Path includes: optic tracts, LGN, optic radiations, and striate cortex
B. Statistics
1.Most common neuro-ophth. presentation of retrochiasmal path disturbance is HH
2.Prevelance estimated at 0.8% in gen pop over 49 yrs old
3.Estimated 1 million new cases of hemi and quad VF loss per year in Us extrapolated from data
on strokes, trauma, and tumors
Etiology
A. Most common causes of HH in 904 cases (in adults): CVA (69.6%), Trauma (13.6%), Tumor
(11.3%), Brain surgery (2.4%) , demylination (1.4%)1
B. In children, neoplasm or their assoc. biopsy or removal were the most common cause (Ped. Series
from Children’s Hospital of Philadelphia)2
C. CVA
1.Ischemic/ Infarct (58.9%)
-85% of strokes
2.Hemorrhagic(10.9%)3
-15% of all strokes are hemorrhagic
a. 2/3 of intracranial bleeds are SAH (subarachnoid heme)
1. SAH commonly caused byrupture ofvessels on or near surface of the brain or
ventricles (e.g. aneurysm or vasc. Malformation)
2. SAH bleeding mainly into CSF
b. Intracerebral heme
1. Caused by rupture of arteries within brain substance (e.g. HTN hemorrhage
or vasc. malformation)
Anatomy/Location – Most common lesion locations were occipital lobes (45%) and optic radiations
(32.2%), Multiple (11.4%), Optic Tract (10.2%), LGN (1.3%). 4
A. Optic Tract VF defects
1.most often caused by mass lesion.
2.VA’s remain normal
3.Cerebral peduncle may be affected by compressive lesion and lead to hemiparesis on the side
of the hemianopia.
B. LGN VF defects
1.rare due to highly anastomotic blood supply.
2.Associated with homonymous Sectoropia based on anterior or posterior choroidal artery
infarction 5
C. Optic Radiation VF defects can vary in density
1.Temporal superior defect
2.Parietal inferior defect
3.PITS mnemonic (Parietal Inferior/Temporal Superior)
D. Occipital lesion (normal OKN). May produce macular sparing due to dual blood supply. HH central
scotoma possible if only the tip of the occipital lobe affected. Sparing of the Temporal crescent
possible if lesions does not involve the anterior striate cortex. Most commonly PCA stroke
E. LM case with sparing of temporal crescent
F. MG case of macroaneurysm of MCA with superior L quadrantanopsia
G. ML case with inferior R quadrantanopsia
H. MB case with strict full HH from occipital lobe infarct
Blood supply review with consequences
A. MCA (2/3 of all infarcts) can cause:
1.HH, Hemiparesis and sensory loss.
2.Aphasia and neglect may also be evident depending on side involved and extent of ischemia.
3.HH due to MCA strokes may be assoc with deficits in the fronto-parietal, parietal, and parietotemporal regions.
4.Anterior MCA strokes produce motor findings and Broca’s (non-fluent) aphasia.
5.Posterior MCA strokes produce more sensory deficits and Wernicke’s (fluent) aphasia.
B. PCA
1.Complete HH and hemianesthesia (loss of all sensation) with stroke of the perforating
branches
1
Zhang X.. Et. al. Homonymous hemianopias: Clinical-anatomic correlations in 904 cases. Neurology 2006; 66:906-910.
Liu GT, Galetta SL. Homonymous hemifield loss in children. Neurology. 1997;49:1748-1749.
3
Same as 1
4
Zhang X.. Et. al. Homonymous hemianopias: Clinical-anatomic correlations in 904 cases. Neurology 2006; 66:906-910.
2
5
Liu GT, et. Al. Neurophthalmology: Diagnosis and Management. Philadelphia: Saunders, 2001.
V.
VI.
VII.
VIII.
2.Macular sparing may occur due to MCA collateral supply
3.Dyslexia and dyscalculia may occur
4.Memory impairment
C. MCA and PCA provide dual blood supply at the LGN and tip of occipital lobe
Natural Course of HH
A. Natural History of HH (Zhang)
1.263 cases reviewed
2.Spontaneous improvement of HH in at least 50% of pts. seen within 1 month of injury
3.In most cases, improvement occurs within first 3 mo after injury
4.Spontaneous improvement after 6 mo should be interpreted with caution
B. Macular sparing
1.HH with macular sparing is considered to classically result from occipital lesions, specifically
occipital infarctions in the distribution of the PCA. (Trobe JD)
2.Macular sparing occurs in locations other than the occipital lobes in almost 50% of cases.
However, another classic cause of macular sparing is poor fixation as the subject tries to
compensate for the HH. (Zhang)
Accompanying symptoms/diagnoses
A. Unilateral Spatial Neglect
1.Subtypes
B. Language and visual processing disorders
1.Temporal lobe lesion may produce personality changes, complex partial seizures, memory
deficits, fluent aphasia (if dominant side), or Kluver-Bucy syndrome (hypersexuality, placidity,
hyperorality, visual and auditory agnosia, and apathy) with involvement of ant temp lobes
bilaterally.
2.Parietal lobe lesions
a. Dominant side (Left Brain typically): conduction aphasia, Gerstmann syndrome (finger
agnosia, agraphia, acalculia, and R-L disorientation) and tactile agnosia
b. Non-dominant (Right Brain): Left Neglect, topographic memory loss, apraxia of
construction and dressing
c. HH due to deep parietal lesion may by assoc. with defective OKN response when
targets are moved toward side of lesion. Slow pursuits will be defective toward side of
lesion. Problems due to co-involvement of optic radiations and adjacent descending
corticobulbar fibers from the parieto-occipitotemporal pursuit area
C. Optic Tract lesion – Cerebral peduncle may be affected by compressive lesion and lead to hemiparesis
on the side of the hemianopia
D. Occipital lesions have normal OKN
Neuro Evaluation in Optometric Setting
A. Ocular health evaluation and refraction first
B. Visual Field Testing
1.HVF 30-2 (gives testing for macular sparing, misses temporal crescent)
2.HVF 120 pt 3 zone (adjunct to 30-2, not detailed for mac sparing)
3.Goldmann VF (addresses full field, less time consumed with “blind” side, skilled perimetrist
needed)
C. Unilateral spatial neglect testing
a. Line bisection
b. Cancellation test
c. Drawing (Clock dial)
d. Extinction of fields – reveals mild form of neglect
D. Reading acuity
1.MNRead
E. Additional testing
1.Motility/ BV testing
2.OKN Drum
3.Visual Information Processing
a. Figure Ground testing
b. Spatial Orientation
c. Visual word recall efficiency
Vision Rehabilitation
A. Timeline of rehab in relation to onset of symptoms
1.Natural Course of HH
a. Best chance of recovery in first three months. Neurology often starts that time line
after patient comes out of coma if that is part of story
2.Early rehab of HH (<3 mo) may be productive and help with other therapies
3.Goal is to improve function and independence
B. VF Expansion for hemianopsia and quadrantanopsia
IX.
X.
XI.
1.Why? Because scanning to blind side requires significant effort
2.“Early alert” or “early detection” systems
3.Treatments attempt to:
a. Decrease amount of gaze shift needed to see periphery on defective side (Sector or
Gottlieb )
b. Bring missing visual field info into “seeing” VF (EP Horizontal)
C. Saccadic vision training
1.E.G. Wayne’s saccadic fixator, Accuvion 1000
2.Improve scanning techniques
D. VRT (Vision Restoration Therapy)
1.Based on concept of neuroplasticity
2.Average of 5 degrees field recovery
E. Simple non-optical techniques
1.“Anchoring”
2.Line guide/Typoscope
3.Shift page orientation
F. Prism Adaptation therapy
1.Management of Unilateral Spatial Neglect
2.High amount of yoked prism OU with Base toward defect
3.Residual shift in attention toward area neglected
G. Driving
1.Best accomplished with team approach
2.CDRS, Neuropsychologist, Neurologist
Anomalies
A. Unilateral spatial neglect without hemianopia
B. Alzheimer’s visual variant
Cases
A. JN, Right HH from internal carotid artery/posterior communicating artery aneurysm with subarachnoid
hemorrhage
B. DS, Left HH with left neglect, from GBM Grade IV in occipital lobe and resected
C. EJ, Left HH from CVA with left neglect and L hemiparesis
Conclusions
A. Retrochiasmal pathway assoc with HH, but specific location of injury gives additional info on overall
picture
B. Awareness of symptoms beyond HH can clue practitioner in on probable location of infarct and other
possible problems