Functional disconnection

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Functional disconnection is the disintegrated function in the brain in the absence of anatomical damage, in distinction to physical disconnection of the cerebral hemispheres by surgical resection, trauma or lesion. Applications have included alexia without agraphia [1] dyslexia, [2] persistent vegetative state and minimally conscious state [3] as well as autistic spectrum disorders. [4] Functional disconnection itself is not a medically recognized condition. It is a theoretical concept used to facilitate research into the causes and symptoms within recognized conditions. [5]

History

In 1977, Witleson reported [6] that developmental dyslexia may be associated with (i) bi-hemisphere representation of spatial functions, in contrast to the unitary right hemisphere control of these functions observed in normal individuals. The bilateral neural involvement in spatial processing may interfere with the left hemisphere's processing of its own specialized functions and result in deficient linguistic, sequential cognitive processing and in overuse of the spatial, holistic cognitive mode, reflecting a functional disconnection syndrome in these individuals confirmed by Leisman in the 1980s [2] and in the 2000s. [7]

The concept of functional disconnection developed further with Stachowiak and Poeck in 1976. [8] who reported on a case in 1976 of a 67-yr-old male with hemianopia resulting from a cerebrovascular accident resulting in pure alexia and a color naming deficit that he suggested was due to a functional disconnection mechanism. He noted that the underlying disconnection mechanism is improved by the facilitating effect of unblocking methods (in the tactile, somesthetic, auditory, and visual systems), so that pathways other than the one impaired by the brain lesion are used.

In 1998, Fritson [9] presented a mechanistic account of how dysfunctional integration among neuronal systems arises, based on the central role played by synaptic plasticity in shaping the connections. He hypothesized that the pathophysiology of schizophrenia is expressed at the level of modulation of associative changes in synaptic efficacy; specifically the modulation of plasticity in those brain systems responsible for emotional learning and emotional memory in the postnatal period. This modulation is mediated by ascending neurotransmitter systems that: (i) have been implicated in schizophrenia; and (ii) are known to be involved in consolidating synaptic connections during learning. The pathophysiology results in a disruption of the reinforcement of adaptive behavior consistent with the disintegrative aspects of the disorder. Kim and colleagues in 2003 [10] further described the disconnection hypothesis in schizophrenia as the result of a prefrontal-parietal lobe functional disconnection, particularly prefrontal dissociation and abnormal prefrontal-parietal interaction during working memory processing.

The concept of functional disconnection developed still further when it was applied to the understanding of the nature of autistic spectrum disorder. Geschwind and Levitt in 2007 [11] suggested a model of the symptoms of autism in which higher-order association areas of the brain (that normally connect to the frontal lobe) are partially disconnected during development, thereby explaining the heterogeneity of autism etiology. The autism group at Cambridge University [12] provided evidence that the functional connectivity of medial temporal lobe structures specifically is abnormal in people with Asperger’s syndrome, at least during fearful face processing. Melillo and Leisman have similarly concluded that a functional disconnection syndrome is a basis for explaining the symptoms of autistic spectrum disorder. [13]

Related Research Articles

<span class="mw-page-title-main">Asperger syndrome</span> Former neurodevelopmental diagnosis

Asperger syndrome (AS), also known as Asperger's, is a neurodevelopmental condition characterized by significant difficulties in social interaction and nonverbal communication, along with restricted and repetitive patterns of behavior and interests. The syndrome is no longer recognized as a diagnosis in itself, having been merged with other conditions into autism spectrum disorder (ASD). It was considered to differ from other diagnoses that were merged into ASD by relatively unimpaired spoken language and intelligence.

Agraphia is an acquired neurological disorder causing a loss in the ability to communicate through writing, either due to some form of motor dysfunction or an inability to spell. The loss of writing ability may present with other language or neurological disorders; disorders appearing commonly with agraphia are alexia, aphasia, dysarthria, agnosia, acalculia and apraxia. The study of individuals with agraphia may provide more information about the pathways involved in writing, both language related and motoric. Agraphia cannot be directly treated, but individuals can learn techniques to help regain and rehabilitate some of their previous writing abilities. These techniques differ depending on the type of agraphia.

<span class="mw-page-title-main">Parietal lobe</span> Part of the brain responsible for sensory input and some language processing

The parietal lobe is one of the four major lobes of the cerebral cortex in the brain of mammals. The parietal lobe is positioned above the temporal lobe and behind the frontal lobe and central sulcus.

<span class="mw-page-title-main">Frontal lobe</span> Part of the brain

The frontal lobe is the largest of the four major lobes of the brain in mammals, and is located at the front of each cerebral hemisphere. It is parted from the parietal lobe by a groove between tissues called the central sulcus and from the temporal lobe by a deeper groove called the lateral sulcus. The most anterior rounded part of the frontal lobe is known as the frontal pole, one of the three poles of the cerebrum.

In psychology, theory of mind refers to the capacity to understand other people by ascribing mental states to them. A theory of mind includes the knowledge that others' beliefs, desires, intentions, emotions, and thoughts may be different from one's own. Possessing a functional theory of mind is considered crucial for success in everyday human social interactions. People utilise a theory of mind when analyzing, judging, and inferring others' behaviors. The discovery and development of theory of mind primarily came from studies done with animals and infants. Factors including drug and alcohol consumption, language development, cognitive delays, age, and culture can affect a person's capacity to display theory of mind. Having a theory of mind is similar to but not identical with having the capacity for empathy or sympathy.

Mind-blindness, mindblindness or mind blindness is a theory initially proposed in 1990 that claims that all autistic people have a lack or developmental delay of theory of mind (ToM), meaning they are unable to attribute mental states to others. According to the theory, a lack of ToM is considered equivalent to a lack of both cognitive and affective empathy. In the context of the theory, mind-blindness implies being unable to predict behavior and attribute mental states including beliefs, desires, emotions, or intentions of other people. The mind-blindness theory asserts that children who delay in this development will often develop autism.

<span class="mw-page-title-main">Behavioral neurology</span>

Behavioral neurology is a subspecialty of neurology that studies the impact of neurological damage and disease upon behavior, memory, and cognition, and the treatment thereof. Two fields associated with behavioral neurology are neuropsychiatry and neuropsychology. In the United States, 'Behavioral Neurology & Neuropsychiatry' has been recognized as a single subspecialty by the United Council for Neurologic Subspecialties (UCNS) since 2004.

Pure alexia, also known as agnosic alexia or alexia without agraphia or pure word blindness, is one form of alexia which makes up "the peripheral dyslexia" group. Individuals who have pure alexia have severe reading problems while other language-related skills such as naming, oral repetition, auditory comprehension or writing are typically intact.

<span class="mw-page-title-main">Brain asymmetry</span> Term in human neuroanatomy referring to several things

In human neuroanatomy, brain asymmetry can refer to at least two quite distinct findings:

<span class="mw-page-title-main">Classic autism</span> Neurodevelopmental condition

Classic autism, also known as childhood autism, autistic disorder, (early) infantile autism, infantile psychosis, Kanner's autism,Kanner's syndrome, or just autism, is a neurodevelopmental condition first described by Leo Kanner in 1943. It is characterized by atypical and impaired development in social interaction and communication as well as restricted, repetitive behaviors, activities, and interests. These symptoms first appear in early childhood and persist throughout life.

<span class="mw-page-title-main">Gerstmann syndrome</span> Neuropsychological disorder caused by damage to the inferior parietal lobule

Gerstmann syndrome is a neuropsychological disorder that is characterized by a constellation of symptoms that suggests the presence of a lesion usually near the junction of the temporal and parietal lobes at or near the angular gyrus. Gerstmann syndrome is typically associated with damage to the inferior parietal lobule of the dominant hemisphere. It is classically considered a left-hemisphere disorder, although right-hemisphere damage has also been associated with components of the syndrome.

Educational neuroscience is an emerging scientific field that brings together researchers in cognitive neuroscience, developmental cognitive neuroscience, educational psychology, educational technology, education theory and other related disciplines to explore the interactions between biological processes and education. Researchers in educational neuroscience investigate the neural mechanisms of reading, numerical cognition, attention and their attendant difficulties including dyslexia, dyscalculia and ADHD as they relate to education. Researchers in this area may link basic findings in cognitive neuroscience with educational technology to help in curriculum implementation for mathematics education and reading education. The aim of educational neuroscience is to generate basic and applied research that will provide a new transdisciplinary account of learning and teaching, which is capable of informing education. A major goal of educational neuroscience is to bridge the gap between the two fields through a direct dialogue between researchers and educators, avoiding the "middlemen of the brain-based learning industry". These middlemen have a vested commercial interest in the selling of "neuromyths" and their supposed remedies.

<span class="mw-page-title-main">Autism spectrum</span> Neurodevelopmental disorder

Autism, formally called autism spectrum disorder (ASD) or autism spectrum condition (ASC), is a neurodevelopmental disorder characterized by deficits in social communication and social interaction, and repetitive or restricted patterns of behaviors, interests, or activities, which can include hyper- and hyporeactivity to sensory input. Autism is a spectrum disorder, meaning that it can manifest very differently in each person. For example, some are nonspeaking, while others have proficient spoken language. Because of this, there is wide variation in the support needs of people across the autism spectrum.

<span class="mw-page-title-main">Imprinted brain hypothesis</span> Conjecture on the causes of autism and psychosis

The imprinted brain hypothesis is an unsubstantiated hypothesis in evolutionary psychology regarding the causes of autism spectrum and schizophrenia spectrum disorders, first presented by Bernard Crespi and Christopher Badcock in 2008. It claims that certain autistic and schizotypal traits are opposites, and that this implies the etiology of the two conditions must be at odds.

<span class="mw-page-title-main">Disconnection syndrome</span> Collection of neurological symptoms

Disconnection syndrome is a general term for a collection of neurological symptoms caused – via lesions to associational or commissural nerve fibres – by damage to the white matter axons of communication pathways in the cerebrum, independent of any lesions to the cortex. The behavioral effects of such disconnections are relatively predictable in adults. Disconnection syndromes usually reflect circumstances where regions A and B still have their functional specializations except in domains that depend on the interconnections between the two regions.

The development of an animal model of autism is one approach researchers use to study potential causes of autism. Given the complexity of autism and its etiology, researchers often focus only on single features of autism when using animal models.

Sex and gender differences in autism exist regarding prevalence, presentation, and diagnosis.

Hypercalculia is "a specific developmental condition in which the ability to perform mathematical calculations is significantly superior to general learning ability and to school attainment in maths." A 2002 neuroimaging study of a child with hypercalculia suggested greater brain volume in the right temporal lobe. Serial SPECT scans revealed hyperperfusion over right parietal areas during performance of arithmetic tasks.

Autism's symptoms result from maturation-related changes in various systems of the brain. Although it is not well understood how autism occurs, there have been attempts to describe the mechanisms involved. Conceptually, one can divide its development into two areas: the pathophysiology of brain structures and processes associated with autism, and the neuropsychological linkages between brain structures and behaviors. The behaviors appear to have multiple pathophysiologies.

The pathophysiology of autism is the study of the physiological processes that cause or are otherwise associated with autism spectrum disorders.

References

  1. ↑ Sroka H, Solsi P, Bornstein B (1973). "Alexia without agraphia with complete recovery". Confinia Neurologica. 35 (3): 167–176. doi:10.1159/000102840. PMID   4541303.
  2. 1 2 Leisman G, Ashkenazi A (1980). "Aetiological factors in dyslexia: IV. Cerebral hemispheres are functionally equivalent". International Journal of Neuroscience. 11 (3): 157–164. doi:10.3109/00207458009147581. PMID   7440087.
  3. ↑ Leisman G, Koch P (2009). "Networks of conscious experience: computational neuroscience in understanding life, death, and consciousness". Reviews in the Neurosciences. 20 (3–4): 151–176. doi:10.1515/revneuro.2009.20.3-4.151. PMID   20157986. S2CID   40003252.
  4. ↑ Melillo R, Leisman G (2009). "Autistic spectrum disorders as functional disconnection syndrome". Reviews in the Neurosciences. 20 (2): 111–131. doi:10.1515/revneuro.2009.20.2.111. PMID   19774789. S2CID   13724127.
  5. ↑ Guy Boulton (November 14, 2010). "Doctors skeptical of center's claims". Milwaukee Journal Sentinel . Archived from the original on November 24, 2014. Retrieved November 24, 2014.
  6. ↑ Witelson SF (1977). "Developmental dyslexia: two right hemispheres and none left". Science. 195 (4275): 309–311. Bibcode:1977Sci...195..309W. doi:10.1126/science.831280. PMID   831280.
  7. ↑ Leisman G (2002). "Coherence of hemispheric function in developmental dyslexia". Brain and Cognition. 48 (2–3): 157–164. doi:10.1006/brcg.2001.1394. PMID   12030482. S2CID   14064120.
  8. ↑ StachowiakF-J, Poeck K. (1976). "Functional disconnection in pure alexia and color naming deficit demonstrated by facilitation methods". Brain and Language. 3 (1): 135–143. doi:10.1016/0093-934X(76)90010-9. PMID   1268693. S2CID   39696728.
  9. ↑ Friston KJ (1998). "The disconnection hypothesis". Schizophrenia Research. 30 (2): 115–125. CiteSeerX   10.1.1.159.9437 . doi:10.1016/s0920-9964(97)00140-0. PMID   9549774. S2CID   10981981.
  10. ↑ Kim JJ, Kwon JS, Park HJ, Youn T, Kang DH, Kim MS, Lee DS, Lee MC (2003). "Functional disconnection between the prefrontal and parietal cortices during working memory processing in schizophrenia: A[15(O)]H2O PET study". American Journal of Psychiatry. 160 (5): 919–923. doi:10.1176/appi.ajp.160.5.919. PMID   12727696.
  11. ↑ Geschwind DH, Levitt P (2007). "Autism spectrum disorders: developmental disconnection syndromes". Current Opinion in Neurobiology. 17 (1): 103–111. doi:10.1016/j.conb.2007.01.009. PMID   17275283. S2CID   7970237.
  12. ↑ Welchew DE, Ashwin C, Berkouk K, Salvador R, Suckling J, Baron-Cohen S, Bullmore E (2005). "Functional disconnectivity of the medial temporal lobe in Asperger's syndrome". Biological Psychiatry. 57 (9): 991–998. doi:10.1016/j.biopsych.2005.01.028. PMID   15860339. S2CID   3145422.
  13. ↑ Melillo R, Leisman G (2009). Neurobehavioral disorders of childhood: An evoloutionary perspective. New York, NY: Springer. ISBN   978-1-4419-1232-9.
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