Alexander CFlint, University of California, San Francisco, 505 Parnassus Avenue, Room M-830, Box 0114, San Francisco CA 94143-0114alexander.flint@gmail.com
John P. Loh, John C.M. Brust
Submitted January 04, 2006
We appreciate the comments of Dr. Clatworthy et al regarding
our Neuroimage. [1] We also found our patient's description of
worsened visual hallucinations during light stimulation interesting and unusual.
The patient was clear in describing her experiences -- her
ability to
draw her hallucinations and her construction of a 'hemifield mask' using
her
eyeglasses made it seem likely that the exacerbation of her hallucinations
by
light was a real phenomenon. While our patient's relatively brief
experience of these hallucinations was a relief to her, the short duration
of
the phenomena prevented further testing as suggested by Dr. Clatworthy.
The two categories of proposed mechanisms are plausible.
Based
on the timing of events in our patient's experience, we would favor the
first
mechanism (direct visual projections to higher cortical regions in the
absence
of V1 function). Our patient informed us that she noted the element of
light
exacerbation as soon as her visual hallucinations began. The visual
hallucinations themselves occurred quite early in the course of her
homonymous hemianopia (within the first day). Also, from the onset of her
hemianopia, she could not recall seeing any 'real world' visual stimuli
within
the region of her field defect.
While these observations do not exclude
the
possibility of a rapidly developed functional plasticity of projections
from an
incompletely damaged primary visual cortex, they seem to us to make it
less
likely than a mechanism involving disinhibited projections from the LGN to higher visual cortical centers.
As Dr. Clatworthy's group points out, these hypothetical mechanisms
could
be tested with functional imaging. Since the phenomenon appears to be both
rare and short-lived, it unfortunately may be difficult to study from a
practical
perspective.
We appreciate the comments of Dr. Clatworthy et al regarding our Neuroimage. [1] We also found our patient's description of worsened visual hallucinations during light stimulation interesting and unusual.
The patient was clear in describing her experiences -- her ability to draw her hallucinations and her construction of a 'hemifield mask' using her eyeglasses made it seem likely that the exacerbation of her hallucinations by light was a real phenomenon. While our patient's relatively brief experience of these hallucinations was a relief to her, the short duration of the phenomena prevented further testing as suggested by Dr. Clatworthy.
The two categories of proposed mechanisms are plausible. Based on the timing of events in our patient's experience, we would favor the first mechanism (direct visual projections to higher cortical regions in the absence of V1 function). Our patient informed us that she noted the element of light exacerbation as soon as her visual hallucinations began. The visual hallucinations themselves occurred quite early in the course of her homonymous hemianopia (within the first day). Also, from the onset of her hemianopia, she could not recall seeing any 'real world' visual stimuli within the region of her field defect.
While these observations do not exclude the possibility of a rapidly developed functional plasticity of projections from an incompletely damaged primary visual cortex, they seem to us to make it less likely than a mechanism involving disinhibited projections from the LGN to higher visual cortical centers.
As Dr. Clatworthy's group points out, these hypothetical mechanisms could be tested with functional imaging. Since the phenomenon appears to be both rare and short-lived, it unfortunately may be difficult to study from a practical perspective.