How is Obstructive Sleep Apnea (OSA) is caused by Neural Dysfunction in children?

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Many parents have observed inadequate sleep in children is associated with daytime behavioral problems and poor academic functioning. A fact-less well-recognized by clinicians and the general the public is that sleep-related breathing disorders, which occur in two to 10% of children depending on how they are defined can have a significant impact even among children who have normal sleeping hours.

One of the most severe nocturnal breathing diseases, obstructive sleep apnea (OSA), includes partial or complete breathing blockage recurrently during sleep, resulting in intermittent low level of oxygen in the blood and probably sleep disruption. The frontal and hippocampal regions of the brain, which are implicated in the regulation of behavior and memory, respectively, appear to be most vulnerable to OSA, but the evidence is indirect.

Proton magnetic resonance spectroscopy (MRS), a non-invasive neuroimaging technique is used to detect chemical metabolites linked to neural dysfunction, to shed more direct light on the neural functioning of children with OSA.

The Study Findings

In comparison, children with OSA have significantly lower on tests of overall intelligence and some aspects of higher-level thinking called “executive functions,” but the groups did not vary on tests of sustained attention, or motor skills. Tests of memory did not give significant differences between the groups, but the effect sizes were large enough to suggest that significant effects might have been found in a larger sample. MRS specified that those with OSA had abnormal metabolites in the left hippocampus and right frontal cortex.

Implications for Brain Development and Clinical Practice

These parallel findings of shortage on measures of behavioral and brain functioning in children with OSA are sobering and gives support to concerns that OSA, if it is not treated, it may cause substantial long-term adverse effects. The developing brain does not just unfold in a predestined genetic process. But, it builds upon itself at every level, with development by the interaction of genes with the immediate cellular surroundings. That surrounding is estimated by the child's life experiences (e.g., reactions to OSA-related behavioral disturbances) and physiological functioning (e.g., OSA-related oxygen deprivation or sleep disruption). Due to this, untreated childhood OSA may have a specifically marked long-term impact.

Pediatricians and other health-care professionals must increase their consistency in screening for symptoms of OSA. Sleep is seldom addressed in most pediatric clinics, even though clinical screening tools are easy to use for testing. This lack of clinical attention runs difficult to current evidence from sleep medicine and developmental neuroscience, which suggests that early disorder diagnosis and treatment should be a high priority.

Limitations of the Study

The studies in current research withstand replication because they are consistent with adult studies that have shown similar abnormalities using MRS, and with current theories of the mechanisms behind the daytime deficits observed in individuals with OSA. Yet, more research is needed to verify and build on these theories. MRS gives indirect indices of neural dysfunction (not necessarily neuron death), and it is not clear whether those indices will become normal with effective OSA treatment or what long-term effects might continue. Similarly, although the current theories gave tantalizing suggestions of developmental effects, few children below the age 10 were able to tolerate the sedative-free MRS procedure, as they should be lying still during the scan. As a result, the high-risk period for OSA in preschool and early grade school remains are still not mainly considered by this study. By targeting on relatively severe cases, the study also is not considered for milder forms of sleep-disordered breathing, which are more prevalent than severe forms and which have been found to rise in the risk for behavioral problems. At last, these theories will need to be replicated in completely community-based samples. Children who are referred for clinical estimation in a sleep clinic are likely to have other problems that brought them to their concern of referring professionals in the first place.

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Alzheimer Disease – Different Drug discoveries

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Alzheimer Disease:

Alzheimer illness (AD) is among the most widely recognized reasons for dementia around the world. Affirmed drugs for the manifestations of AD dementia has a peripheral advantage, and no new treatments have been endorsed in recent years. There are no endorsed medications for the anticipation of AD dementia. The absence of strong therapeutics comes notwithstanding serious endeavors by people in general and private research network to find them. There have been around 450 disapproved clinical drug discoveries since the last endorsement by the Food and Drug Administration. There is an increase in people who are affected by AD and different dementias around the world, and nations around the world are contributing generously funding to invigorate essential and translational research with expectations of growing new therapeutics for the treatment and aversion of AD and other dementia.

Complexity for drug design:

Clinical-pathologic discoveries, numerous from network-based that incorporate brain autopsy, are revealing insight into the complex nature of the AD dementia phenotype. This complexed nature, to a great extent the consequence of blended dementia and neural save has significant implications for clinical drug design and its discovery.

The data paint a picture of cognitive decline, MCI, and AD dementia resulting from a complex interaction between the accumulations of one or more brain pathologies in the context of a brain that is more or less resilient to these pathologies. This complexity has major implications for both clinical drug design and its discovery.

Implications of complexity for drug discovery:

Imagine a drug that targets the amyloid-β. Theories suggest that AD pathology is responsible for about a third of the variance of cognitive decline if one includes the effects of both amyloid-β and NFT [7]. One can enhance a study for amyloid-β with PET scans or CSF amyloid-β, but the theory still needs to be powered to affect only that portion of the cognitive trajectory associated along with this pathology. It is not clear that most theories have explicitly powered their trials in this way.

Currently, trials targeting a single molecular marker (i.e., amyloid-β) are costly, also requiring many other expensive PET scans. By difference, imagine neural reserve as a therapeutic endpoint. There is no developmental pressure to form systems that protect the brain from other brain pathology of old age, let alone different systems that give protection from different pathologies. Hence, finding that myriad factors alter the trajectory of cognitive decline agnostic to fundamental brain pathologies is expected. A hypothetical therapeutic endpoint that targets neural reserve could be used to counterbalance any and likely all common brain pathologies that alter cognition. The basic approach to design a clinical trial, assuming a relatively safe agent, would be a large research of cognitive decline among people at a slightly increased risk of cognitive decline. Depending on the expected effect size, such a theory would likely want a minimum of less than a thousand subjects followed for a maximum four years. Although several issues are to be addressed, neural reserve gives a new pattern for approaching the treatment and prevention of AD and indeed all dementia syndromes.

What are the various Neuromuscular diseases and it’s treatment?

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Neuromuscular diseases consists a wide range of disorders damaging the peripheral nervous system, which consists of all the motor and sensory nerves from all over the body that connects the brain and spinal cord. Progressive muscle weakness is the primary condition of these disorders. Many of these disorders are curable if the treatment is given early and appropriately. In fact, further disability can be inhibited and potentially reversed. Determining the exact nature of the disease will also allow understanding all the implications of a particular disease and, if it’s hereditary, what it might mean for family and offspring.

Diseases:

•          Diabetic neuropathy – nerves affected by the diabetes
•          Amyotrophic lateral sclerosis (Lou Gehrig’s Disease) and different motor neuron diseases –       cells that control voluntary muscle activity is damaged
•          Toxic neuropathy – pain, and weakness caused by toxic substances
•          Small fiber neuropathy – affects the nerve endings of the skin
•          Autonomic neuropathies – damage to nerves that affects the heart, blood pressure, body             temperature, digestion and more
•          Muscular disorders, hereditary:

Ø  Congenital myopathies – muscle weakness existing at birth

Ø  Muscular dystrophy – a group of disorders involving muscle weakness       

Ø  Metabolic myopathies – the breakdown of muscles, cramping syndromes, exercise intolerance, including mitochondrial disorders

•         Muscular disorders, acquired:

Ø  Inclusion body myositis – inflammatory muscle disease includes weakness and difficulty swallowing

Ø  Dermatomyositis – inflammatory muscle disease includes muscle weakness and skin rash

Ø  Polymyositis – includes muscle weakness and inflammation

Ø  Necrotizing myopathy – extensive muscle destruction

•          Neuromuscular junction disorders (a problem at the location where nerves connect with             muscles):

Ø  Myasthenia gravis – communication problem between nerves and muscles results in muscle weakness and muscle fatigue.

Ø  Lambert-Eaton Syndrome – often coincides with cancer, causing muscle weakness.

Diagnosis:

                  During the process of electro diagnostics, small electrical impulses are applied to the nerves and electrical responses are recorded. This helps to determine whether there is a loss of nerve fibers or a problem with the wrapping (insulation) of the nerves. A small acupuncture-size needle can also be inserted into the muscles to listen to the activity of neuron and determine if there is a primary muscle disorder. Several tests can also be performed which includes repetitive stimulation method for the neuromuscular junction, autonomic nerve testing and single-fiber EMG (Electromyography) for assessing transmission at the neuromuscular junction. Treatment varies widely, depending on the diagnosis and other factors. Few treatments include medical therapy, including immunosuppressive drugs, pain management, and assistive devices. Apheresis is a technique which takes out antibodies in the blood associated with a neuromuscular disease that causes weakness and other disorders.