What distinguishes the right and left cerebral hemispheres from each other?

3.2.8 Cerebral Lateralization

As mentioned in the previous sections, each of the two cerebral hemispheres is functionally distinct. This is known as cerebral lateralization or cerebral dominance. In most cases, the left hemisphere contains the general interpretive and speech centers and is responsible for language-based skills. Tasks, such as reading, writing, and speaking, are dependent on processing done in the left cerebral hemisphere. Additionally, the premotor cortex involved with control of hand movements is larger on the left side for right-handed individuals than for left-handed individuals. The left hemisphere is also important in performing analytical tasks, such as mathematical calculations and logical decision-making.

The right hemisphere analyzes sensory information and relates the body to the sensory environment. Interpretive centers in the left hemisphere let you identify familiar objects via sensory inputs such as smell, touch, sight, taste, and feel. For example, the right hemisphere plays a significant role in facial recognition and understanding three-dimensional relationships. It is also important for analyzing emotional context in a conversation (e.g., distinguishing between a threaten remark “Get lost!” and a question “Get lost?”). People with damage to the right hemisphere may be unable to add emotional inflections to their own words.

Metencephalon.

The ventral portion of the pons provides for connections between each cerebral hemisphere and the contralateral cerebellar hemisphere. Pontine nuclei receive input from each of the cerebral lobes and give rise to a large number of pontocerebellar fibers that enter into the cerebellum through the massive middle cerebellar peduncle (Fig. 2-50). Most of these fibers, but not all, cross the midline before entering into the cerebellum, where they project mostly to the cerebellar hemisphere.

The cerebellum is an exceptionally large structure in the human brain. It is a phylogenetically old structure that receives ascending input from most of the sensory systems and descending input from the cerebral cortex. The surface of the cerebellum is marked by numerous narrow folds that increase the cortical surface area. The cerebellum is attached to the brainstem by three pairs of peduncles that contain afferent and efferent fibers. Afferent fibers come from several sources, including the inferior olivary cortex, pontine nuclei, vestibular fibers, and spinocerebellar tract. Deep cerebellar nuclei provide the main output of the system. Output projections include those to the red nucleus, pontine nuclei, vestibular nuclei, and ventral lateral and ventral anterior thalamus.

The cerebellum is particularly important in sensory-motor integration and coordination, although the precise function of the cerebellum varies from one part to the next, according to its interconnectivity with the rest of the nervous system. For example, those portions of the cerebellum receiving sensory input from the vestibular system help to maintain balance and equilibrium. The cerebellum plays an important role in the control of muscle tonus, especially in relationship to locomotion, postural reflexes, and nonstereotyped behaviors. Lesions of the cerebellum cause a number of significant deficits. Impairments of equilibrium, posture, and skilled motor activity are common. Normally smooth movements often become jerky, rapid movements are slowed, and target-directed movements often miss their mark.

Specification of cortical parcellation.

The evolution of the mammalian brain is characterized by an enormous expansion of the cerebral hemispheres accompanied by a multiplication of the cortical areas each with its distinctive cytoarchitecture, extrinsic connectivity and physiology. The multiplicity of cortical areas, their diverse specializations as well as their implication in higher mental function remain important issues in developmental neurobiology.

One unexpected finding is that early enucleation leads to a much reduced extent of area 17. Our results (Dehay et al., 1989) along with those of Pasko Rakic (1988) show that the overall cytoarchitecture of area 17 appears relatively normal in enucleates despite a gross disturbance of the gyral pattern of the occipital lobe. These results have deep implications concerning the mechanisms involved in areal specification. Basically, there are three mechanisms which could contribute to a reduced area 17. (1) Reduced production of area 17 (either a reduction of the pool of area precursors and/or in their mode of proliferation). (2) Shrinking of area 17 (once area 17 has been produced, there could be a decrease in cell size and volume of neuropile coupled with increased levels of cell death). (3) Reduction of peripheral specification of a non-committed cortical plate (according to this hypothesis, the developing cortical plate is a uniform sheet of cells, none of which are committed to a particular areal fate. Hence the reduced number of thalamic fibers subsequent to enucleation claim or specify a smaller area 17). All three mechanisms contribute to the areal size reduction. However, quantitative measurements of cell densities and the topographical relationship of area 17 to adjacent cortical areas show that (2) and (3) above make only a negligible contribution (Dehay et al., 1991). The major influence of the sensory periphery seems therefore to be by modulation of the proliferation of area 17 precursors, for which there is substantial evidence both in invertebrates and vertebrates (see Dehay et al., 1991 for a review of this literature).

Early enucleation despite leading to a reduced production of area 17 was not found to change either the thickness of area 17 (in terms of microns or numbers of cells) nor the lamination. Further cytochrome oxidase blobs in layers 2/3 were also present (Dehay et al., 1989; Kuljis and Rakic, 1990). The cytochrome oxidase blobs form a regular repeating lattice in area 17 which is directly related to the functional architecture of this area (see Martin, 1988 for a review). This raises the question of whether the areal reduction of striate cortex in excess of 70% has influenced the periodicity of the cytochrome oxidase blobs. We found that blob separation in the enucleate showed an 8% linear reduction which exactly fitted the calculated areal reduction resulting from the shrinking of striate cortex due to the reduction of neuropile and cell size (Kennedy et al., 1990).

The fact that the reduction of area 17 was not accompanied by an equivalent reduction in the mean blob separation indicates that two levels of specification need to be distinguished. The first occurs early in development, is critically dependent on the presence of the two eyes and determines the areal dimensions of area 17, at least partly by modulating the levels of cell death and proliferation. The second is independent of the sensory periphery, operates after the determination of the areal borders and specifies the periodicity of the cytochrome oxidase blobs.

4.1 STFT analysis result relative to the lesion location

A comparison of Patient 1 and the reference is shown in Figure 2. Columns with odd numbers correspond to left cerebral hemisphere, otherwise to the right side.

As it can be seen from Figure 2, the DFBEP, the AFBEP and the AD of the healthy person are generally symmetrical between left and right cerebral hemisphere. However, the DFBEP of left cerebral hemisphere is higher than that of the right side, while the AFBEP and the AD are opposite to it with respect to the patient 1. AD is a better indicator than AFBEP when compared the frequency band energy percentage of left and right cerebral hemisphere.

Then the average values of the DFBEP, the AFBEP and the AD of left and right cerebral hemisphere of patient 1-10 are calculated respectively. The results are shown in Table 3. Figure 3 depicting symmetry between left and right cerebral hemisphere are drawn according to the data of Table 3

Table 3. The average values of the DFBEP, the AFBEP and the AD of left and right cerebral hemisphere

NoDFBEPAFBEPADReDFBEPAFBEPADLRLRLRLRLRLR10.700.350.050.220.081.0110.270.280.430.354.934.1320.850.710.030.090.050.1620.500.480.110.110.360.3330.620.370.070.180.140.7530.540.540.100.100.230.2540.620.360.070.240.151.0340.430.440.190.170.850.6450.580.240.090.330.202.3650.370.390.320.264.212.8760.750.560.040.110.060.2660.500.500.120.130.310.3270.610.790.090.040.230.0570.490.510.100.100.270.2780.250.580.360.132.800.3280.500.500.110.120.300.3290.590.800.150.040.400.0690.380.390.290.252.662.03100.570.670.130.070.310.12100.490.530.130.110.330.27

No: Patient number; L(R): Left (Right) cerebral hemisphere; Re: Refence episode.

As it can be seen from Figure 3, the average of the DFBEP, the AFBEP and the AD of the healthy person are generally symmetrical between left and right cerebral hemisphere. However, with respect to the left cerebral infarction patients, the average of the DFBEP of left cerebral hemisphere is higher than that of the right side, while average of the AFBEP and the AD are the other way around. The same results are observed with respect to the right cerebral infarction patients.

To summarize the results obtained from first ten patients, it can be seen that DFBEP is relatively higher, AFBEP and AD are relatively lower when the lesion exists in corresponding cerebral area, thus, DFBEP, AFBEP and AD can be used as indicators to monitor patient condition.

8.2 Pathology

Acute severe HA causes cerebral edema, with cerebral swelling and symmetrical parenchymal lesions, but sparing of the brainstem and cerebral hemispheres [7]. Edema sufficient to raise intracranial pressure (ICP) may result in uncal herniation and fatal brain stem compression [122]. 1H magnetic resonance spectroscopy (MRS) imaging shows increased brain glutamine [13]. At autopsy, primates with severe hyperammonemic encephalopathy have cerebral edema, herniation of the cerebellar tonsils, and astrocyte swelling on microscopy, but no demonstrable abnormalities of neurons or nerve axons [118]. Brain magnetic resonance imaging (MRI) of human infants some months after prolonged severe neonatal HA shows hypomyelination and cystic changes of the white matter, myelination delay, ventricular dilatation, and hypodensity of the basal ganglia and thalamus [13,14,123]. At autopsy, additional findings have been spongiform changes at the gray–white matter junction and in the deep gray matter, with Alzheimer type II cells on microscopy [13,124]. These cells are enlarged abnormal astrocytes with decreased cytoplasmic density, large pale nuclei, and a prominent nucleolus and increases in the numbers of mitochondria and in the endoplasmic reticulum. They indicate chronic ongoing HA [10,14,122,125]. With MRI, adults with partial enzyme deficiencies, even those who are asymptomatic and have a normal IQ, may have reversible white matter lesions in the cingulum and frontal and motor cortex. These involve tracts involved with executive function and working memory. Patients with chronic HA may have persisting white matter damage. With 1H MRS imaging brain glutamine is increased and the osmolyte, myoinositol, is decreased. Choline is decreased in the frontal cortex, perhaps indicating cell membrane dysfunction [7,13]. Preliminary evidence from 13C MRS studies suggested a glutamate neurotransmission defect in adults with partial OTC deficiency [13]. Autopsy data for humans presenting with chronic HA after infancy are largely restricted to patients with chronic liver disease, in whom other factors contribute to brain damage. They have Alzheimer type II cells on brain histology [10,122,125]. However there are data for a chronically hyperammonemic animal, the spfmouse, which has partial OTC deficiency. The brain size is decreased but the ventricles are enlarged. In the striatum, there is a selective loss of medium spiny neurons and other changes with a pattern characteristic of an excitotoxic mechanism of cell death [112].

Neurofibrillary Tangles and Tau

Neurofibrillary tangles are found within the cell bodies of affected neurons in the hippocampus, neocortex, and certain other regions of the cerebral hemispheres and brain stem. As seen under the electron microscope, they consist largely of clusters unbranched fibrillary structures, twisted into a spiral, or helix (Wischik et al., 1985) (Fig. 3). The twisted structures are described as paired helical filaments. They have a minimum diameter of about 10 nm, and the twists are 80 nm apart. Aggregated filaments within nerve processes are referred to as neuropil threads. Neurofibrillary tangles are found in adults with Down's syndrome and in a handful of other neurological disorders, where they occur without neuritic plaques.

The paired helical filaments are composed of tau, a protein associated with microtubules. Microtubules are part of the internal skeleton of a nerve cell. Tau protein, which is found primarily in nerve axons, has number of sites that can accept a phosphate group. The tau protein in paired helical filaments has an excessive number of phosphate groups. It is this chemical modification that prevents typical binding to microtubules and leads the tau protein to aggregate into paired helical filaments.

Aggregates of hyperphosphorylated tau brought into a nerve cell may form a template for the misfolding of hyperphosphorylated tau proteins inside the cell. New tau aggregates are thereby formed, and this process is thought to propagate from one neuron to others with which it maintains connections (de Calignon et al., 2012; Liu et al., 2012).

This process of cell to cell spread may partially explain the distribution of pathological change in the brain. In the absence of obvious dementia, neurofibrillary tangles, when present in old age, are largely confined to larger neurons of the hippocampus, the adjacent entorhinal and transentorhinal cortex, and the amygdala. Other affected brain areas include basal forebrain neurons that use the neurotransmitter acetylcholine, locus coeruleus neurons that use noradrenalin, and midline brainstem neurons that use serotonin. The transentorhinal region of the temporal lobes may be the earliest affected region of the cerebrum, but tau pathology occurs even earlier in the locus coeruleus and other brainstem nuclei (Braak et al., 2011). In more severe stages of the illness, virtually the entire cerebral cortex is affected, sparing until late in the disease course primary motor cortex concerned with volitional movement and primary sensory areas concerned with touch, hearing, and vision. Amyloid may also undergo spread from one neuron to another through axon and dendrite connections (Nath et al., 2012).

There are other disorders characterized by tau accumulation and neurofibrillary tangles. These are referred to as tauopathies and include progressive supranuclear palsy, corticobasal degeneration, and a variant of frontotemporal dementia. Chronic traumatic encephalopathy is a tauopathy that results from repeated brain trauma.

Introduction

The old fathers of anatomy paid little attention at the cerebral cortex and is has rightly been remarked, that their drawings of the cerebral hemispheres resembled more a plate of macaroni than the organ of the human mind. Interest of scientists in the cortical anatomy began in the last century and was at its peak at the beginning of our century. One of those were Economo and Koskinas, who presented in over 700 pages of their publication from 1925 not only gross descriptions of the cortical surface, but also detailed measurements of cortical thickness and cytoarchitectonic characteristics. Especially interested in the occipital lobe was Filimonoff (1932, 1933), who published some detailed papers on the variability of the occipital cortex in human and non-human primates. He also not only presented surface and section anatomy, but a lot of tables with various measurements of sulcal length and relations. Other comprehensive publications on the human cortex came from Bailey and Bonin (1951) and on the primate cortex from Conolly (1950).

In our days there is again growing interest in the surface anatomy of the brain, which is documented by the very recently published extensive atlas of surface anatomy of the human brain by Ono et al. (1990). The main reasons for this is, that the technique of nuclear magnetic resonance makes it possible to study all anatomical features very detailed in a patient's brain. The detailed knowledge of surface and section anatomy of the brain is the prerequisite for an exact localization of pathological processes and planning of neurosurgical operations.

2 Ephapsis

In 1975, Freeman did not yet have a clear understanding of the mechanism which could bring the billions of neurons that make up each human cerebral hemisphere into global order within a few thousandths of a second. In 2006 however, he published with Vitiello a seminal paper [6] which offers an answer. Freeman and Vitiello start with an observation:

The dominant mechanism for neural interactions by axodendritic synaptic transmission should impose distance-dependent delays on the EEG oscillations owing to finite propagation velocities and sequential synaptic delays. It does not. Neural populations have a low velocity information and energy transfers and high velocity of spread of phase transitions.

The answer to this puzzle may be provided by Carver Mead's Collective Electrodynamics [7] or Giuseppe Vitiello's Quantum Field Theory (QFT) [8], both of which differ drastically from Quantum Mechanics. Freeman speculates that wave packets he observed act as a bridge from quantum dynamics at the atomic level through the microscopic pulse trains of neurons to macroscopic properties of large populations of neurons. Field theory of many-body systems allows for phase transition by spontaneous break of symmetry (SBS) or event-related potential (ERP). SBS is always accompanied by the dynamical formation of collective waves (Nambu—Goldstone modes or bosons) that span the whole system. These ordering waves (bosons) condense in the system ground state and ordering is a result of this boson condensation. Examples of macroscopically observed patterns are phonons (elastic waves) in crystals and the magnons (spin waves) in magnets.

Freeman and Vitiello propose that the physical nature of SBS carrier wave is a dipole wave in which the 3D-rotational (electric) axis is spontaneously broken. They believe that cortical boson condensate, or its wave packet, may explain the rapid course of perception: how neocortex can respond to the impact of photons from a face in a crowd on a handful of retinal neurons mixed among many impulses elicited by light from the crowd. Phase transition of order from disorder emerges suddenly: the neural vapor as it were condenses into neural droplets, the first step in recognition within a few tens of milliseconds, which is insufficient for classical models.

Boson condensate enables an orderly description of the phase transition that includes all levels of macroscopic, mesoscopic, and microscopic organization of the cerebral patterns that mediate the integration of animal with its environment. Dendritic trees may interact by ephapsis of the ionic currents from their neighbors densely packed in neuropil. No one knows how ephaptic transmission works, but the candidate mechanism may include coupling through water dipoles, because both the intracellular and extracellular compartments are weak ionic solutions, comprised of more than 80% water, with high electrical conductivity on either side of the lipid layers. This is in good agreement with Carver Mead's observation in Collective Electrodynamics that electric dipoles coupling is million time stronger than coupling of magnetic dipoles. Nambu-Goldstone (NG) theorem predicts that the quanta have zero mass and thus they can span the whole system volume without inertia.

According to Freeman, cognitivists assign the starting point for analysis to the sensory receptors in the skin. Bundles of axons serve as channels to carry the information to the brainstem and eventually information converges in thalamus where it is already subdivided and classified by the receptors in respect to its features such as color, motion, or tonal modulation. These researchers view thalamus as acting like a postmaster to deliver the bits of information to destinations that have already been assigned by the sensory receptors. They think that stimulus salience selects the information for transmission to cortex. Pulses represent primitive elements of sensation, or features. The primary cortex combines these representations of features into representations of objects and transmits them into adjacent association areas; a combination of lines and colors might make up a face, a set of phonemes might form a sentence, and a sequence of joint angles might represent a gesture after a “binding” process is executed. The problem is that so far cognitivists have not been able to show where that happens or in what way perception differs from sensation or where the information in perception changes into information for action.

Freeman assigns the starting point to the limbic system, not the sensory receptors. Hippocampus is a part of surface of each cerebral hemisphere, only buried deep inside the medial temporal lobe. It is more like the hub of spider web than the memory bank or CPU of a computer. Entorhinal cortex, which interacts with so many other parts of the brain, is the main source of input and output from hippocampus and it, rather than thalamus, performs multisensory convergence, followed by spatial localization of events and temporal sequencing of them into hippocampus, which cooperates with other areas to form multisensory perceptions and coordinates learning, remembering, and recall. Perception starts with attention and expectations in the limbic system (indicated in the picture below by the asterix) and is transmitted from there by corollary discharges to all sensory cortices in the process of preafference. A new hypothesis forms and it is confirmed or denied by modified sensory input resulting from anticipatory organism action.

Which of the following distinguishes the right and left cerebral hemisphere from each other quizlet?

What are the functional differences between the two cerebral hemispheres?

How are the right and left cerebral hemispheres specialized for different functions?