Despite the concern that has been expressed about potential method biases, and the pervasiveness of research settings with the potential to produce them, there is disagreement about whether they really are a problem for researchers in the behavioral sciences. Therefore, the purpose of this review is to explore the current state of knowledge about method biases. First, we explore the meaning of the terms “method” and “method bias” and then we examine whether method biases influence all measures equally. Next, we review the evidence of the effects that method biases have on individual measures and on the covariation between different constructs. Following this, we evaluate the procedural and statistical remedies that have been used to control method biases and provide recommendations for minimizing method bias.

Sources of Method Bias in Social Science Research and Recommendations on How to Control It

Over the last 2 decades, a large number of neurophysiological and neuroimaging studies of patients with schizophrenia have furnished in vivo evidence for dysconnectivity, ie, abnormal functional integration of brain processes. While the evidence for dysconnectivity in schizophrenia is strong, its etiology, pathophysiological mechanisms, and significance for clinical symptoms are unclear. First, dysconnectivity could result from aberrant wiring of connections during development, from aberrant synaptic plasticity, or from both. Second, it is not clear how schizophrenic symptoms can be understood mechanistically as a consequence of dysconnectivity. Third, if dysconnectivity is the primary pathophysiology, and not just an epiphenomenon, then it should provide a mechanistic explanation for known empirical facts about schizophrenia. This article addresses these 3 issues in the framework of the dysconnection hypothesis. This theory postulates that the core pathology in schizophrenia resides in aberrant N-methyl-D-aspartate receptor (NMDAR)-mediated synaptic plasticity due to abnormal regulation of NMDARs by neuromodulatory transmitters like dopamine, serotonin, or acetylcholine. We argue that this neurobiological mechanism can explain failures of self-monitoring, leading to a mechanistic explanation for first-rank symptoms as pathognomonic features of schizophrenia, and may provide a basis for future diagnostic classifications with physiologically defined patient subgroups. Finally, we test the explanatory power of our theory against a list of empirical facts about schizophrenia.

/pdf/dysconnection-in-schizophrenia-from-abnormal-synaptic-305n6j3pxf.pdf

Dysconnection in Schizophrenia: From Abnormal Synaptic Plasticity to Failures of Self-monitoring

Dynamics of Active Sensing and perceptual selection

THE human brain is the instrument of the high powers of intelligence that distinguish man from all other living creatures. The secret of man's most distinctive attribute is hidden in the texture of his brain, and perhaps will never be fully revealed. Yet from time to time, with the growth of knowledge and the discovery of new methods of approach, we can profitably return to this greatest of all biological problems and get new glimpses of the factors that have made man what he is. Two considerations make the present time appropriate for taking stock of the state of our knowledge of these matters. The emergence of a clearer understanding of the sequence of structural changes in the brain and body of man's ancestors enables us to interpret the physiological factors involved in the widening and deepening of the intellectual powers and to appreciate the conditions essential for the attainment of-such mental growth. In the second place, the new points of view regarding the functions of the cerebral cortex that have emerged from Dr. Henry Head's suggestive clinical investigations prompt one to examine the brain anew and endeavour to integrate the results of his brilliant analysis with those revealed in the study of the evolution of the brain. Whether or not it is yet possible fully to correlate the facts and conclusions of these two disciplines into one coherent body of doctrine, it is well worth while to make the attempt to do so, if for no other reason than to direct attention to new problems that call for solution.

The Human Brain

A broad range of evidence regarding the functional organization of the vertebrate brain - spanning from comparative neurology to experimental psychology and neurophysiology to clinical data - is reviewed for its bearing on conceptions of the neural organization of consciousness. A novel principle relating target selection, action selection, and motivation to one another, as a means to optimize integration for action in real time, is introduced. With its help, the principal macrosystems of the vertebrate brain can be seen to form a centralized functional design in which an upper brain stem system organized for conscious function performs a penultimate step in action control. This upper brain stem system retained a key role throughout the evolutionary process by which an expanding forebrain - culminating in the cerebral cortex of mammals - came to serve as a medium for the elaboration of conscious contents. This highly conserved upper brainstem system, which extends from the roof of the midbrain to the basal diencephalon, integrates the massively parallel and distributed information capacity of the cerebral hemispheres into the limited-capacity, sequential mode of operation required for coherent behavior. It maintains special connective relations with cortical territories implicated in attentional and conscious functions, but is not rendered nonfunctional in the absence of cortical input. This helps explain the purposive, goal-directed behavior exhibited by mammals after experimental decortication, as well as the evidence that children born without a cortex are conscious. Taken together these circumstances suggest that brainstem mechanisms are integral to the constitution of the conscious state, and that an adequate account of neural mechanisms of conscious function cannot be confined to the thalamocortical complex alone.

http://www.summer12.isc.uqam.ca/page/docs/readings/Merker-Bjorn/Merker-Consciousness%20without%20a%20cerebral%20cortex.pdf

Consciousness without a cerebral cortex: a challenge for neuroscience and medicine.

https://www.cell.com/current-biology/pdf/S0960-9822(04)01044-9.pdf

Saccades differentially modulate human LGN and V1 responses in the presence and absence of visual stimulation.

Blinking suppresses the neural response to unchanging retinal stimulation.

Visual fMRI responses in human superior colliculus show a temporal--nasal asymmetry that is absent

Eye patching has revealed enhanced saccadic latencies or attention effects when orienting toward visual stimuli presented in the temporal versus nasal hemifields of humans. Such behavioral advantages have been tentatively proposed to reflect possible temporal-nasal differences in the retinotectal pathway to the superior colliculus, rather than in the retinogeniculate pathway or visual cortex. However, this has not been directly tested with physiological measures in humans. Here, we examined responses of the human superior colliculus (SC) to contralateral visual field stimulation, using high spatial resolution fMRI, while manipulating which hemifield was stimulated and orthogonally which eye was patched. The SC responded more strongly to visual stimulation when eye-patching made this stimulation temporal rather than nasal. In contrast, the lateral geniculate nucleus (LGN) plus retinotopic cortical areas V1-V3 did not show any temporal-nasal differences and differed from the SC in this respect. These results provide the first direct physiological demonstration in humans that SC shows temporal-nasal differences that LGN and early visual cortex apparently do not. This may represent a temporal hemifield bias in the strength of the retinotectal pathway, leading to a preference for the contralateral hemifield in the contralateral eye.

https://www.physiology.org/doi/pdf/10.1152/jn.00835.2006

Richard Sylvester

Papers

Saccades differentially modulate human LGN and V1 responses in the presence and absence of visual stimulation.

Blinking suppresses the neural response to unchanging retinal stimulation.

Visual fMRI responses in human superior colliculus show a temporal--nasal asymmetry that is absent

Visual fMRI Responses in Human Superior Colliculus Show a Temporal–Nasal Asymmetry That Is Absent in Lateral Geniculate and Visual Cortex

Combined orientation and colour information in human V1 for both L-M and S-cone chromatic axes.