Cognition: 4th Translation
Tanskane, P., Valkama, M., Haapea, M., Barnes, A., Ridler, K., Miettunen, J., Murray
Background:
Past studies on low birth weight and preterm birth have reported a higher incidence of abnormal structural neural anatomy and cognitive deficits in childhood and adolescence. Few studies have investigated follow-up into adulthood outcomes associated with brain structure and adult cognition. Premature births and low birth weight infants are vulnerable to brain injury during the neonatal period and are prone to structural brain abnormalities. Individuals born with abnormalities have been linked to reduced neurocognitive function. Recent interest in moderated low birth to mild preterm birth after 32 to 37 of gestational weeks which account for most of preterm labors has been the focus of this research.
Theory:
Research from an earlier study reported educational difficulties in children who were born with low birth weights and premature birth at age 14 and at age 24. These individuals were reported to have a higher incidence of mental retardation as well.
Findings:
Researchers have studied individuals in a cohort of preterm birth and low birth weight to adulthood at the ages of 33-35 years to examine the effects on education, occupational, and cognitive function. They collected data from questionnaires on school performances, testing of visual spatial working memory, visual object learning, executive functions, visual object learning, and verbal learning. Magnetic resonance imaging (MRI) was conducted on these individuals at age 33-35 years. Structural images were evaluated for neuro anatomical abnormalities. Findings from this study showed that children born preterm or low birth weight were born below developmental age by as much as 13% for low birth weight and 8% for preterm birth. Their school grades were found to be slightly lower than the control group. In adulthood subjects were found to have a lower educational level than the control group. In addition, low birth weight individuals were found to be unemployed more often than the control group. Individuals born with low birth weight or born preterm were found to show lower scores in verbal learning. Interestingly, there were no significant differences between the groups in categorization, visual spatial working memory, or visual object learning. MRI scans did not reveal any abnormalities in most subjects except of one individual in this study.
Clinical Applications:
We would consider decreased cognitive functions and abnormal brain structure as a brain injury condition as a result of low birth weight or preterm birth. But do we want to label individuals early in their development at risk for diminished adulthood functioning? Or do would we want to do early intervention? I guess it is all on how we look at things. I believe as occupational therapists we can provide intervention to these individuals and prevent poor outcomes with early interventions and guidance.
Take Home Point:
It is interesting that our birth weight or premature birth may influence our future adult function. One of my professors and principle investigator at the Center for Perinatal Biology at Loma Linda University School of Medicine had many interesting theories when a woman is ready to give birth. He mentioned the amount of lipid (fat) of a fetus may play an important role in the timing of birth. But what is the cause of preterm birth? This is what we were researching at LLU. I worked in the lab as a master’s anatomy student doing research on the innervation of the cervix before birth in mice and the connections to the spinal cord. Ask me anything about the spinal cord of the mouse or its cervix two days before birth, it is my specialty! It was interesting work and I saw the plasticity of the nervous system in action before the time of birth, it is amazing! One day before birth the cervix which is normally a hard inflexible structure becomes a loose and flexible passage way for the fetus. Without this change vaginal birth is not possible and the safety of the mother and child may be endangered. This is what excites me about the nervous system it is full of surprises and I never ceases to a look at it in wonder.
Mary Groves, M.S. Anatomy, OTR/L
Cognition:Third Translation
Scotto-Lomassese, S., Nissant, A., Mota, T., Neant-Fery, M., Oosstra, B. A., Greer, C. A., Lledo, P., Trembleau, A., & Caille, I. (2011). Fragile X Mental Retardation Protein Regulates New Neuron Differentiation in Adult Olfactory Bulb. The Journal of Neuroscience, 31, 6, 2205-2215.
Background:
Fragile X syndrome (FXS) is congenital disorder attributed to regions of the X chromosomes that separate or break off under certain cell processes which causes chromosomal abnormalities. Fragile X syndrome is characterized by mental retardation, large ears, prominent jaw, and pale blue irides. Male children are more affected than female children. Fragile X syndrome is second to Down syndrome as a cause of mental retardation.
Theory:
Fragile X mental retardation protein (FMRP) is a RNA-binding protein which is important for the expression in neurons, dendrites, and dendritic spines. Without FMRP due to the inhibition of the gene FMR1 leads to Fragile X syndrome (FXS). Studies on the neuro-pathological findings from FX patients have suggested a hyper production of dendritic spines in the cortical neurons. It has also been suggested that the postsynaptic spines which typically are excitatory enhance synaptic excitation and may contribute to an increase in epilepsy in FX patients.
Findings:
The purpose of this study was to find if dendritic malformation had a direct affect on FXS. Here is yet another example of the importance of cellular architecture and the functioning of synaptic processes of the nervous system. The shape and design of the smallest structures of our bodies have a profound effect on its function. The importance of the dendrite spines can not be over emphasized. Our understanding of cognition and learning processes is dependant on these structures for providing increased synaptic impulses and networking in complex connections. These processes require experience-dependant plasticity which means we need lots of dendrite spines to increase the synapses which receive these neural impulses. Learning and cognitive development requires increased dendritic spine density for synaptic functions. Any deviation from the architecture of the dendrites may affect this function and has been attributed to the cause of some forms of mental retardation and mental disorders. Findings of this study showed that FMRP was necessary for the expression of dendritic plasticity which may be attributed to a cause of FXS.
Clinical Applications:
Has a parent ever asked you why their baby was born with Down’s syndrome or some other disorder? Doctors give their medical opinion as to why, they talk about genes and chromosomes that miss read the DNA transcription as it unfolds at the start of conception. What does this mean to someone who may face a future caring for a child who may need total care for the rest of their lives? For many of these disorders we do not have answers to their cause and more importantly can we give a good and reassuring response to the parent’s questions as to why? How do we comfort and provide hope? How do we manage a parent’s pain and fear? For these answers, we as practitioners need to reach into our knowledge base and provide support and understanding for our patients and their parents. We need to hear their story because others in the medical field may not. They need to tell us their story and feel it because it is important to their understanding and ours.
Take Home Point:
It is always a challenge working with children with mental or physical disabilities but I have noticed that every parent assumes the care of their child with different approaches to their acceptance as a human being and their hope for their child’s future. I have friends whose daughter was born with arthrogryposis. This is a congenital disorder of the musculoskeletal system, the degree of severity ranges from mild muscle impairment to sever loss of muscle tissue and joint mobility. They were in shock when their daughter was born, they were not expecting this. They soon became experts learning about arthrogryposis, caring, and advocating for their daughter. My family and I became friends with them and Jane (not her real name) when she was in the second grade and the first thing you notice about her was her smile and humor. She uses a motorized wheel chair with a chin control to move around. Jane requires total care for her ADLs because she was born with the most sever type of arthrogryposis, she has no muscles in her extremities. Today, Jane is a corporate lawyer and on her off time litigates for disabled persons pro bono. She enjoys sailing in the San Francisco
Mary Groves, M. S., OTR/L
Glossary:
Dendrites: process which are part of the neuron and receives neural impulses.
Dendritic Spines: found in pyramidal neurons in the neocortex and are part of the dendrites. Spines increase the synaptic surface of dendrites.
Irides: plural for iris
Cognition : Second Translation
Naismith, S.L. and Lewis, S. J. G. (2011). “DASH” symptoms in patients with Parkinson’s disease: Red flags for early cognitive decline. Journal of Clinical Neuroscience, Vol. 8, 352-355.
Background:
Dementia associated with Parkinson’s disease (PDD) may affect 25% of patients with Parkinson’s disease (PD). This condition represents an additional level of care for persons with PDD. Identifying the “red flags” will help care givers and health professional’s information when to recommend additional intervention and pharmaceutical recommendations.
Theory:
Studies have identified motor dysfunction, later age of onset, and severity of symptoms with a greater risk of dementia in patients with Parkinson’s disease. Additional research has investigated the behavioral changes connected to PD. These changes include visual hallucinations, delusions, psychosis, depression, apathy, anxiety, and sleep disturbances and have been noted to be very common with PDD.
Findings:
The purpose of this study was to examine the relationship between cognitive functioning and four self-rated questions addressing depression, anxiety, sleep disturbances, and hallucinations (DASH). Their findings concluded a high correlation with neuropsychological tests that utilized executive or frontal cortical functioning. This suggests that the DASH score may prove to be an easy screening instrument to identify early cognitive involvement associated with PDD.
Clinical Applications:
Cognitive changes in a client with PD may involve frontal cortex and synaptic changes of the neurons which has been suggested in recent research. Knowing the extent of these cognitive changes in our clients is important and the DASH provides us with an additional tool to work with. Our client’s physician may not be aware of these cognitive changes and reporting these would be of value for the medical care of the client. Changes in medication could be suggested such as a cholinesterase inhibitor.
Take Home Point:
So why did I chose this research? First there is a high relationship between PD and cognitive dysfunction and second I have an interest in knowing when things turn for the worse. My mother had dementia and I will never forget the day I knew things had turned for my mother. She started to hallucinate and she was seeing people in her car and she thought they were trying to steal it. I would look in the driveway and no one was in the car. But my mother insisted and I could only go with it and I tried to chase the people in the car away. This is when I looked like a fool and the neighbors confirm what they had thought of me for years, she is crazy! This was a freighting moment for my mother and my self. I knew changes were occurring with my mother but I would have liked to known the extent of these changes. I can only think what is going on with my clients who have PD and their care givers when they notice cognitive changes, they must be frightened and worry what is going to happen now? It may not be that comforting knowing the extent of these cognitive changes but it gives you time to prepare for these changes. There are many assessments for PD, the Parkinson’s Disease Questionnaire (PDQ-39) assesses quality of life, Beck Depression Inventory-II (BDI-II) just to name a couple. But I am always on the look out for other assessments which will provide further information for my clients and there loved ones.
Glossary:
Dementia – a syndrome of failing memory and progressive loss of intellectual process due to continuing degenerative disease in the brain.
Cognition
H. Kasai, M. Fukuda, S. Watanabe, A. Hayashi-Takagi, and J. Noguchi (2010). Structural dynamics of dendritic spines in memory and cognition. Trends in Neurosciences, Vol. 33. ( 3), 121-129.
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| Pyramidal Neuron |
Background:
Recent research on the morphology of dendrite structures in pyramidal neurons suggest these structures may play a role in functional memory and cognition. Dendrites are the branch like structures found protruding from the body of a neuron. These structures receive impulses from other neurons’ axons which synapse on these structures and transmit information to the neuron. Neuron transmissions may be excitatory or inhibitory. Pyramidal cells are found in the Neocortex (gray matter), Purkinje cells in the cerebellum, and spiny neurons in the basal ganglia. Pyramidal cells in the cortex are excitatory neurons and use glutamate transmitters.
Dendritic spines are dynamic which means they are constantly changing in size and volume. Spines increase the synaptic area of the dendrite surface and are protein rich in their molecular structure (actin). This protein composition allows for rapid reformation of spines within 30 to 60 minutes as the dendrites are stimulated by synaptic activity. Researchers have also correlated larger older spines with long term memory for motor and sensory memory. Smaller spines were found to be constantly changing in volume and size, which suggests that the function of theses structures are very fluid, and adapt to impulse activity of these neurons. The dynamic nature of these pyramidal dendritic spines suggests a relationship, linking adaptive spine dynamics and cognitive processing. There has also been a correlation between abnormal spine morphology and spine density with some mental disorders including, schizophrenia, mental retardation, and autism.
Theory: Donald Hebb’s basis for learning and memory is dependant on synaptic activity, with high synaptic densities
Recent studies using photon imagery have demonstrated that spine growth was associated with long term potentials (synaptic activity) which indicate the application of Hebb’s learning theory to the level of the single synapse- plasticity, and its dependence on synaptic activity. Learning and memory depend on a high activity of synaptic processing and a high level of synaptic densities.
Findings:
Neuronal plasticity in dendritic spines may be responsible for long term memory and cognitive functioning. Because dendritic formation and enlargement is dependant on synaptic remodeling, as seen in the adult Neocortex as well; this relationship indicates a foundation for stable memory formation. It has also been suggested that there is a possible relationship between spine dynamics and cognitive processing. Increased intrinsic synaptic contacts within these structures are important to the visual cortex, Broca’s area, and the pre-frontal lobes as well as other neocortical areas of the brain. When memory is mentioned in this article they are refereeing to memory for motor and sensory functions. Cognition is related to the complex connections required to relate information received within the Neocortex and transmitted to other areas of the central nervous system (CNS) as opposed to specific areas of memory and cognition. Neural networks provide the connections for these functions and have a close relationship to high synaptic activity. In a broad interpretation of these findings, we can conclude that the intense activity of dendritic spines provides millions of synaptic connections which function for memory of a task, or processing for a cognitive task as we live our daily lives.
Deformation of dendritic spines has been associated with mental illnesses such as schizophrenia, mental retardation, and autism. Abnormalities in dendritic spines and mental disorders tended to be abnormally small and immature. They also suggested that abnormal spines may not maintain synaptic functions normally produced by typical dendritic spines. The relationship between dendritic spines and schizophrenia has been observed by reduced densities of dendritic spines in the pre-frontal lobe.
Clinical Applications:
The remodeling of these dendritic spines plays a role in memory and cognition. As therapist, we challenge and engage our clients in occupational activities to improve function. As we guide our clients in theses activities, we are stimulating neuronal growth and plasticity. Using sensory and motor functions will stimulate these dendritic spines within the Neocortex and their pyramidal neurons. Basal ganglia structures will be stimulated by gross motor activities and Cerebellar neurons will be activated by trunk and limb activities and balance activities as well. Cognitive activities stimulate the growth of these structures as well. Consider a therapist working with a person with impaired motor control. If I wanted to increase synaptic activity, I would want to use a more dynamic activity, say doing an activity which is functional versus picking up cones. The cone activity would not give enough stimuli to the dendritic spines in the pyramidal neurons once the cortex became use to this activity. But if you chose to do an activity which involved changes in motor speed, visual attention, and environmental changes this would not bore the pyramidal neurons and the dendritic spines would be increasing their synaptic connections.
Take Home Point:
I consider this a water shed article, when I was in OT school we learned neuroanatomical structures and function. But we need to ask ourselves questions on how these structures interconnect because our nervous system works in so many other ways other than just going from point A to point B. It is much more dynamic and complex to just memorize structures. We need to understand how our nervous system is integrated to other regions of our body and other areas of the nervous system as well.
When I think of these structures in the brain and their functions, I now think of the pyramidal neurons and how they are dependent on the synaptic stimulation for the functioning of these neurons. Occupational therapists have been stimulating these neural structures for years but we did not give a specific name or location to these vital synaptic connections. Now, when I am working with a client, I will say, “Let’s grow some dendritic spines!”
Mary Groves, M.S. Anatomy, OTR/L
Glossary:
Neocortex- the out most surface of the cortex which contains six layers of neurons,
including the pyramidal neurons
Basal ganglia- collection of nuclei deep in the cortex. These include the caudate nucleus,
putamen, and the globus pallidus. These structures are associated with stereotypic and automated movements.
Hebb, Donald O. - creator of the Hebbian Theory. This describes a basic mechanism for
Synaptic plasticity the increase in synaptic efficacy arises from the Presynaptic cell’s repeated and persistent stimulation of the postsynaptic cell.
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| The Neuron Forest |
