Concept: Cortical blindness
Calcium channel blockers are commonly prescribed medications; calcium channel blocker overdose is becoming increasingly prevalent. The typical presentation of a calcium channel blocker overdose is hypotension and decreased level of consciousness. We describe a case of a calcium channel blocker overdose that led to bilateral cortical blindness, a presentation that has not previously been reported.
Allocentric sense is one of the major components that underlie spatial navigation [1, 2]. In blind patients, the difficulty in spatial exploration is attributed, at least partly, to the deficit of absolute direction perception [3, 4]. In support of this notion, we announce that blind adult rats can perform spatial tasks normally when externally provided with real-time feedback of their head directions. Head-mountable microstimulators coupled with a digital geomagnetic compass were bilaterally implanted in the primary visual cortex of adult rats whose eyelids had been sutured. These “blind” rats were trained to seek food pellets in a T-shaped maze or a more complicated maze. Within tens of trials, they learned to manage the geomagnetic information source to solve the mazes. Their performance levels and navigation strategies were similar to those of normal sighted, intact rats. Thus, blind rats can recognize self-location through extrinsically provided stereotactic cues.
We describe a 69-year-old patient with superior altitudinal hemianopia who contentiously denied having any visual impairment after stroke in the lower banks of both calcarine fissures. Although the patient did not produce intentional responses to visual stimuli in the blind fields, he showed reduced reaction times to stimuli presented in the inferior visual fields when they were primed by identical stimuli in the superior blind fields. Furthermore he showed left extinction to the double stimulation and delayed reaction times for left unprimed stimuli in the inferior fields. Based on these findings we discuss the possibility that blindsight and right hemisphere damage might be both necessary conditions for denying bilateral blindness.
- The Journal of neuroscience : the official journal of the Society for Neuroscience
- Published over 6 years ago
Cortical blindness refers to the loss of vision that occurs after destruction of the primary visual cortex. Although there is no sensory cortex and hence no conscious vision, some cortically blind patients show amygdala activation in response to facial or bodily expressions of emotion. Here we investigated whether direction of gaze could also be processed in the absence of any functional visual cortex. A well-known patient with bilateral destruction of his visual cortex and subsequent cortical blindness was investigated in an fMRI paradigm during which blocks of faces were presented either with their gaze directed toward or away from the viewer. Increased right amygdala activation was found in response to directed compared with averted gaze. Activity in this region was further found to be functionally connected to a larger network associated with face and gaze processing. The present study demonstrates that, in human subjects, the amygdala response to eye contact does not require an intact primary visual cortex.
Resolution of Anton-Babinski syndrome after systemic thrombolysis and mechanical thrombectomy with a stentriever
- Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia
- Published about 2 years ago
Anton-Babinski syndrome is a rare neuropsychiatric syndrome characterized by bilateral cortical blindness and anosognosia with visual confabulation. We present the case of a patient presenting with occlusion of both posterior cerebral arteries (PCA), with Anton-Babinski syndrome, completely solved after combined systemic thrombolysis and mechanical thrombectomy with a stent-retriever.
Total bilateral blindness in the setting of facial transplantation is a controversial matter. Some transplant teams exclude these candidates, while others accept them onto their facial transplant waiting list. Using 3 cases, the clinical and ethical complexity of total bilateral blindness is explored. Guidance (medical, psychological, and social) for total bilateral blindness as both an inclusion and exclusion criterion is provided, with the stipulation that total bilateral blindness should not be an automatic exclusion criterion for facial transplantation. Additionally, guidance for corneal transplant in facial transplant candidates is discussed. Suggestions for posttransplant disability assistance for patients with total bilateral blindness are also provided.
The superior colliculus is sensitive to gestalt-like stimulus configuration in hemispherectomy patients
- Cortex; a journal devoted to the study of the nervous system and behavior
- Published over 3 years ago
Patients with cortical blindness following a lesion to the primary visual cortex (V1) may retain nonconscious visual abilities (blindsight). One intriguing, though largely unexplored question, is whether nonconscious vision in the blind hemifield of hemianopic patients can be sensitive to higher-order perceptual organization, and which V1-independent structure underlies such effect. To answer this question, we tested two rare hemianopic patients who had undergone hemispherectomy, and in whom the only post-chiasmatic visual structure left intact in the same side of the otherwise damaged hemisphere was the superior colliculus (SC). By using a variant of the redundant target effect (RTE), we presented single dots, patterns composed by the same dots organized in quadruple gestalt-like configurations, or patterns of four dots arranged in random configurations, either singly to the intact visual hemifield or bilaterally to both hemifields. As reported in a number of prior studies on blindsight patients, we found that bilateral stimulation yielded faster reaction times (RTs) than single stimulation of the intact field for all conditions (i.e., there was an implicit RTE). In addition to this effect, both patients showed a further speeding up of RTs when the gestalt-like, but not the random shape, quadruple patterns were projected to their blind hemifield during bilateral stimulation. Because other retino-recipient subcortical and cortical structures in the damaged hemisphere are absent, the SC on the lesioned side seems solely responsible for such an effect. The present results provide initial support to the notion that nonconscious vision might be sensitive to perceptual organization and stimulus configuration through the pivotal contribution of the SC, which can enhance the processing of gestalt-like or structured stimuli over meaningless or randomly assembled ones and translate them into facilitatory motor outputs.
In many functional magnetic resonance imaging (fMRI) studies blind humans were found to show cross-modal reorganization engaging the visual system in non-visual tasks. For example, blind people can manage to understand (synthetic) spoken language at very high speaking rates up to ca. 20 syllables/s (syl/s). FMRI data showed that hemodynamic activation within right-hemispheric primary visual cortex (V1), bilateral pulvinar (Pv), and left-hemispheric supplementary motor area (pre-SMA) covaried with their capability of ultra-fast speech (16 syllables/s) comprehension. It has been suggested that right V1 plays an important role with respect to the perception of ultra-fast speech features, particularly the detection of syllable onsets. Furthermore, left pre-SMA seems to be an interface between these syllabic representations and the frontal speech processing and working memory network. So far, little is known about the networks linking V1 to Pv, auditory cortex (A1), and (mesio-) frontal areas. Dynamic causal modeling (DCM) was applied to investigate (i) the input structure from A1 and Pv toward right V1 and (ii) output from right V1 and A1 to left pre-SMA. As concerns the input Pv was significantly connected to V1, in addition to A1, in blind participants, but not in sighted controls. Regarding the output V1 was significantly connected to pre-SMA in blind individuals, and the strength of V1-SMA connectivity correlated with the performance of ultra-fast speech comprehension. By contrast, in sighted controls, not understanding ultra-fast speech, pre-SMA did neither receive input from A1 nor V1. Taken together, right V1 might facilitate the “parsing” of the ultra-fast speech stream in blind subjects by receiving subcortical auditory input via the Pv (= secondary visual pathway) and transmitting this information toward contralateral pre-SMA.
- The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry
- Published about 4 years ago
The incidence of cortically induced blindness is increasing as our population ages. The major cause of cortically induced blindness is stroke affecting the primary visual cortex. While the impact of this form of vision loss is devastating to quality of life, the development of principled, effective rehabilitation strategies for this condition lags far behind those used to treat motor stroke victims. Here we summarize recent developments in the still emerging field of visual restitution therapy, and compare the relative effectiveness of different approaches. We also draw insights into the properties of recovered vision, its limitations and likely neural substrates. We hope that these insights will guide future research and bring us closer to the goal of providing much-needed rehabilitation solutions for this patient population.
Partial cortical blindness is a visual deficit caused by unilateral damage to the primary visual cortex, a condition previously considered beyond hopes of rehabilitation. However, recent data demonstrate that patients may recover both simple and global motion discrimination following intensive training in their blind field. The present experiments characterized motion-induced neural activity of cortically blind (CB) subjects prior to the onset of visual rehabilitation. This was done to provide information about visual processing capabilities available to mediate training-induced visual improvements. Visual Evoked Potentials (VEPs) were recorded from two experimental groups consisting of 9 CB subjects and 9 age-matched, visually-intact controls. VEPs were collected following lateralized stimulus presentation to each of the 4 visual field quadrants. VEP waveforms were examined for both stimulus-onset (SO) and motion-onset (MO) related components in postero-lateral electrodes. While stimulus presentation to intact regions of the visual field elicited normal SO-P1, SO-N1, SO-P2 and MO-N2 amplitudes and latencies in contralateral brain regions of CB subjects, these components were not observed contralateral to stimulus presentation in blind quadrants of the visual field. In damaged brain hemispheres, SO-VEPs were only recorded following stimulus presentation to intact visual field quadrants, via inter-hemispheric transfer. MO-VEPs were only recorded from damaged left brain hemispheres, possibly reflecting a native left/right asymmetry in inter-hemispheric connections. The present findings suggest that damaged brain hemispheres contain areas capable of responding to visual stimulation. However, in the absence of training or rehabilitation, these areas only generate detectable VEPs in response to stimulation of the intact hemifield of vision.