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Microglial Priming in Alzheimer’s Disease

Microglial Priming in Alzheimer’s Disease

Alzheimer�s disease (AD) is one of the most common types of dementia among older adults. Research studies have demonstrated that pathological changes in the human brain, whether directly or indirectly, can ultimately cause loss of synaptic function, mitochondrial damage, microglial cell activation, and neuronal cell death. However, the pathogenesis of AD is not yet fully understood and there is currently no definitive treatment for the neurological disease. Research studies have demonstrated that the activation and priming of microglial cells may contribute to the pathogenesis of AD. �

 

A proinflammatory status of the central nervous system (CNS) can also cause changes in the function of the microglial cells or microglia. Neuroinflammation is closely associated with the activation of microglia and astrocytes which are connected to a variety of neurological diseases by the synthesis and secretion of inflammatory mediators such as iNOS, ROS, and proinflammatory cytokines. According to research studies, microglial priming is also caused by the inflammation of the CNS. �

 

Therefore, whether microglial priming is the result or the cause of neuroinflammation is still controversial. Microglial cell activation commonly causes an increase of A? and tau proteins as well as a decrease of neurotrophic factors, ultimately leading to the loss of healthy brain cells or neurons and the development of neuritic plaques and neurofibrillary tangles which are closely associated with AD. With the progression of Alzheimer’s disease, changes from neuronal dysfunctions which may have no obvious symptoms to memory loss and cognitive impairment may become more noticeable. �

 

Microglial Priming, Neuroinflammation, and AD

 

Although the accurate and detailed, fundamental role of the microglial cells continues to be discovered and explained, there is a consensus among many researchers that primed microglia are associated with the inflammatory response of the CNS in AD. It has also been determined that neuroinflammation caused by microglial priming is mainly associated with aging, systemic inflammation, gene regulation, and blood-brain barrier impairment. The purpose of the article below is to discuss how microglial priming and neuroinflammation in Alzheimer’s disease can be caused due to a variety of risk factors. �

 

Aging

 

Aging is considered to be one of the main risk factors for AD and it is generally followed by chronic, systemic up-regulation of pro-inflammatory factors and a considerable decrease in an anti-inflammatory response. This change from homeostasis to an inflammatory state occurs through age-related elements which cause an imbalance between anti-inflammatory and pro-inflammatory systems. Microglia is primed into an activated state which can increase the consistent neuroinflammation and inflammatory reactivity in the aged human brain. Research studies have demonstrated that microglia in the brain of rodents developed an activated phenotype during aging characterized by the increased expression of CD11b, CD11c, and CD68. �

 

Systemic Inflammation

 

Recent research studies have determined that the neuroinflammation from primed microglial cells can also cause the pathogenesis of AD. Continuous activation of microglia can promote the synthesis and secretion of pro-inflammatory cytokines and trigger a pro-inflammatory response, ultimately causing neuronal damage. Neuroinflammation is an early symptom in the progression of AD. The microglia can have a tremendous effect on the inflammation of the human brain. �

 

The inflammation and health issues of the CNS can be associated with systemic inflammation through molecular pathways. One research study demonstrated that ROS development of primed microglia decreases the levels of intracellular glutathione and increases nitric oxide in NADPH oxidase subunit NOX2. Moreover, researchers demonstrated that these simultaneously occurring processes ultimately cause the development of more neurotoxic peroxynitrite. This is demonstrated in rodents with peripheral LPS or proinflammatory cytokines, such as TNF-?, IL-1?, and IL-6, IL-33. �

 

The outcome measures of numerous research studies have demonstrated that systemic inflammation can cause microglial activation. The results of the research studies emphasize the variability of the inflammatory response in the human brain associated with AD and the underlying health issues associated with systemic inflammation and neuroinflammation, as shown in Table 1. MAPK (mitogen-activated protein kinase) signaling pathways regulate mechanisms of the eukaryotic cell and microglial MAPK can also cause an inflammatory response to the aged brain with AD. Furthermore, chronic or continuous systemic inflammation causes neuroinflammation, resulting in the onset and accelerating the progression of AD. �

 

Table 1 Effects of Inflammatory Cytokines in AD | El Paso, TX Chiropractor

Genetic Regulation

 

In the aging human brain, gene regulation has ultimately been associated with an innate immune response. Recent preclinical, bioinformatics, and genetic data have demonstrated that the activation of the brain immune system is associated with the pathology of AD and causes the pathogenesis of this neurological disease. Genome-wide association studies (GWAS), functional genomics, and even proteomic evaluations of cerebrospinal fluid (CSF) and blood have demonstrated that dysfunctional immune pathways from genic mutation are risk factors in LOAD, which is the vast majority of AD. �

 

GWAS have become a fundamental tool in the screening of genes as well as demonstrating several new risk genes associated with AD. Apolipoprotein E (APOE) ?4allele is one of the most considerable and well-known risk genes for sporadic AD and this mutation ultimately increases the risk of neurological disease onset by 15 times in homozygous carriers and by three times in heterozygous carriers. Further research studies have demonstrated how microglial cell function can be affected through a variety of rare mutations which have demonstrated to have an increased risk factor of Alzheimer’s disease. �

 

An extracellular domain mutation of the TREM2 gene has also demonstrated an almost identical extent with APOE?4 in increasing the risk factor of AD. TREM2 is increasingly demonstrated on the surface of microglia and mediates phagocytosis as well as the removal of neuronal debris. Additionally, several other genes, such as PICALM, Bin1, CLU, CR1, MS4A, and CD33 have been demonstrated as risk genes for AD. Most of the risk mutation genes are expressed by microglial cells. �

 

Blood-Brain Barrier (BBB) Impairment

 

The blood-brain barrier (BBB) is a specialized barrier commonly developed between the blood and the brain by tight liner sheets consisting of specific endothelial cells and tight junctions or structures which connects a variety of cells together. The CNS is fundamental for the human body, and the BBB is fundamental for the CNS. The BBB and the blood-nerve barrier develop a defense system to control the communications of cells and soluble factors between blood and neural tissue where it plays a considerable role in maintaining and regulating the homeostasis of the CNS and peripheral nervous system. �

 

With development, continuous inflammation can also cause damage to the BBB. This damage can ultimately cause loss of hypersensitive neurons, neuroinflammatory regions, and focal white matter impairment following the damage. The compromised BBB also allows more leukocytes to enter into the CNS where an immune response can be aggravated by brain microglia under the condition of peripheral inflammation. These processes may ultimately be under the control of chemokine and cytokine signaling which can also have an effect on brain microglial cells as well as other health issues in AD. �

 

By way of instance, it has been determined that TNF-?, IL-17A, and IL-1? can reduce the tight junctions and eliminate the BBB. Loss of BBB integrity and abnormal expression of tight junctions are associated with neuroinflammation. Several research studies also demonstrated in an animal model of AD that the vulnerability of BBB to inflammation increases. Current evidence has also demonstrated that the BBB integrity is fundamental while further evidence of the BBB may demonstrate a new treatment approach for AD associated with microglial priming as shown in Figure 2 below. �

 

Microglial Priming and AD | El Paso, TX Chiropractor

Conclusion

 

Microglia play a fundamental role in maintaining and regulating the homeostasis of the CNS’s micro-environment. If the balance of the homeostasis of the human brain is interrupted, the microglial cells can be activated to restore the balance in the CNS by defending against the stimulation and protecting the structure and function of the brain. However, chronic and continuous stimulation can trigger microglia into a state known as microglial priming, which is more sensitive to potentially minor stimulation, causing a variety of health issues, such as central sensitization, chronic pain, and fibromyalgia. �

 

Microglial priming mainly causes the boost of A?, tau protein as well as neuroinflammation and reduces neurotrophic factors which can cause the loss of healthy brain cells or neurons as well as the development of neuritic plaques and neurofibrillary tangles which are associated with Alzheimer’s disease. Although this �double-edged sword� plays a fundamental role, it can increase the progression of abnormal protein development and aggravate neuronal loss and dysfunction. However, research studies have ultimately demonstrated that aging can cause the progression of AD and there’s not much we can do about it. �

 

El Paso Chiropractor Dr. Alex Jimenez

Microglial cells play a fundamental role as the protectors of the brain and they ultimately help maintain as well as regulate the homeostasis of the CNS microenvironment. However, continuous stimulation can cause the microglia to trigger and activate at a much stronger state which is known as microglial priming. Once the microglial cells go into protective mode, however, primed microglia can become much more sensitive to even minor stimulation and they have a much stronger possibility of reacting towards normal cells. Microglial priming has been associated with neuroinflammation and Alzheimer’s disease (AD) as well as central sensitization and fibromyalgia. – Dr. Alex Jimenez D.C., C.C.S.T. Insight

 

AD is one of the most common types of dementia among older adults. However, the pathogenesis of AD is misunderstood and there is no definitive treatment for the neurological disease. Research studies have ultimately demonstrated that the activation and priming of microglial cells may contribute to the pathogenesis of AD. The scope of our information is limited to chiropractic, musculoskeletal and nervous health issues as well as functional medicine articles, topics, and discussions. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900 . �

 

Curated by Dr. Alex Jimenez �

 


 

Additional Topic Discussion: Chronic Pain

 

Sudden pain is a natural response of the nervous system which helps to demonstrate possible injury. By way of instance, pain signals travel from an injured region through the nerves and spinal cord to the brain. Pain is generally less severe as the injury heals, however, chronic pain is different than the average type of pain. With chronic pain, the human body will continue sending pain signals to the brain, regardless if the injury has healed. Chronic pain can last for several weeks to even several years. Chronic pain can tremendously affect a patient’s mobility and it can reduce flexibility, strength, and endurance.

 

 


 

Neural Zoomer Plus for Neurological Disease

Neural Zoomer Plus | El Paso, TX Chiropractor

 

Dr. Alex Jimenez utilizes a series of tests to help evaluate neurological diseases. The Neural ZoomerTM Plus is an array of neurological autoantibodies which offers specific antibody-to-antigen recognition. The Vibrant Neural ZoomerTM Plus is designed to assess an individual�s reactivity to 48 neurological antigens with connections to a variety of neurologically related diseases. The Vibrant Neural ZoomerTM Plus aims to reduce neurological conditions by empowering patients and physicians with a vital resource for early risk detection and an enhanced focus on personalized primary prevention. �

 

Formulas for Methylation Support

 

Xymogen Formulas - El Paso, TX

 

XYMOGEN�s Exclusive Professional Formulas are available through select licensed health care professionals. The internet sale and discounting of XYMOGEN formulas are strictly prohibited.

 

Proudly,�Dr. Alexander Jimenez makes XYMOGEN formulas available only to patients under our care.

 

Please call our office in order for us to assign a doctor consultation for immediate access.

 

If you are a patient of Injury Medical & Chiropractic�Clinic, you may inquire about XYMOGEN by calling 915-850-0900.

xymogen el paso, tx

 

For your convenience and review of the XYMOGEN products please review the following link.*XYMOGEN-Catalog-Download

 

* All of the above XYMOGEN policies remain strictly in force.

 


 

Microglial Priming in the Central Nervous System

Microglial Priming in the Central Nervous System

Microglial cells make up about 10 to 15 percent of all the glial cells in the human body, which can be found in the central nervous system (CNS) and play a fundamental role in the human brain. Microglial cells are responsible for maintaining and regulating changes in the physiological and pathological condition of the CNS by changing their morphology, phenotype and function. In an average physiological state, the microglial cells are continuously in charge of controlling their environment. �

 

However, when the homeostasis of the brain is interrupted, the microglia change into an amoeba-like shape and become a phagocyte where they can actively reveal a variety of antigens. If the homeostasis interruption in the CNS continues, the microglial cells will then trigger at a much stronger state, which is known as microglial priming. Microglia are the “Bruce Banner” of the CNS. However, once they go into protective “Hulk” mode, primed microglia become much more sensitive to stimulation and they have a much stronger possibility of reacting to stimulation, even reacting towards normal cells. �

 

Microglial Cells are Bruce Banner and Hulk in CNS | El Paso, TX Chiropractor

 

Microglial priming can become a double-edged sword. As a matter of fact, primed microglia are created from different phenotypes of microglia and the phenotypes are context-dependent, which means they are associated to the sequence and duration of their exposure to different varieties of stimulation in a variety of pathologies. In the article below, we will demonstrate the effect of microglial priming on the central nervous system (CNS), especially in neurological diseases. �

 

Role of Microglial Cells in the CNS

 

Microglial cells are commonly found in the central nervous system (CNS), where they are considered to be one of the most flexible types of brain cells. Microglial cells are created from precursor cells found within mesoderm bone marrow, or more specifically found in the mesodermal yolk sac, and they are divided in different densities throughout several regions of the brain. As mentioned above, microglia will remain in a dormant state when the homeostasis of the brain remains stable. �

 

Microglia have a small cell body and morphological branches which extend towards all directions to help maintain and regulate the overall function of the CNS. Changes in their microenvironment can trigger microglia into an “activated� state. Research studies have demonstrated that microglia play a fundamental role in brain development and a variety of functions, including synaptic pruning and clearing out cell debris. Moreover, microglia create an immune surveillance system in the human brain and control fundamental processes associated with a variety of pathologies, including the clearance and uptake of A? and abnormal tau protein as well as the production of neurotrophic factors and neuroinflammatory factors. �

 

Microglial Priming Overview

 

Microglial priming activates when continuous interruptions in the brain’s microenvironment trigger a much stronger microglial response compared to an initial interruption which simply triggers microglial activation. Primed microglia in the CNS are also much more sensitive to possibly minor stimulation. This increased response involves microglial proliferation, morphology, physiology, and biochemical markers or phenotype. However, these changes will ultimately promote an increase in cytokines and inflammation mediator production which can have a tremendous impact on synaptic plasticity, neuronic survival, individual cognitive and behavioral function. Below is an overview of the effects of microglial priming in the CNS. �

 

Mechanisms of Microglial Priming in the CNS

 

The microenvironment of the central nervous system (CNS), by way of instance, is one of the main factors which can affect the microglial cells. Increased oxidative stress, lipid peroxidation and DNA damage associated with brain aging can all commonly trigger microglial priming. Another common factor for microglial priming includes traumatic brain injury. Research studies have shown that traumatic CNS injury activates microglia as well as the development of primed microglia. �

 

Many research studies have also shown that both focal and diffuse traumatic brain injury increase inflammation in the brain associated with microglia and astrocytes. CNS infections can also trigger microglial priming where viruses are the main cause of CNS infection. Both DNA and RNA viruses can trigger microglial priming including microglia and astrocytes. Recent research studies have shown that complement dysfunction can change the expression of complement receptors and trigger microglial priming after continuous activation following a variety of functions, including synapse maturation, immune product clearance, hematopoietic stem/progenitor cells (HSPC) mobilization, lipid metabolism, and tissue regeneration. �

 

Moreover, research studies have shown that there is increased priming of the microglia in a variety of neurological diseases. By way of instance, microglial cells with a morphological phenotype are found in large numbers in the human brain. In the last several years, research studies have suggested that neuroinflammation can continuously activate the microglia and trigger microglial priming. Furthermore, all of the previously mentioned situations are closely associated with neuroinflammation. Research studies have also demonstrated that neuroinflammation, as well as microbial debris and metabolic effects, are associated with central sensitization in neurological diseases, such as fibromyalgia, also referred to as the “brain on fire”. �

 

In the context of the previous situations mentioned above, microglia are primed though a series of pro-inflammatory stimulation, such as lipopolysaccharide (LPS), pathogenetic proteins (e.g., A?), ?synuclein, human immunodeficiency virus (HIV)-Tat, mutant huntingtin, mutant superoxide dismutase 1 and chromogranin A. There is also a variety of signaling pathways and it is common for different types of cells to express special pattern recognition receptors (PRRs) which can affect inflammatory signaling pathways. By way of instance, several signaling pathways, known as pathogen-associated molecular patterns (PAMPs), which can commonly increase in infected tissue, could also control microbial molecules. �

 

Additionally, peptides or mislocalized nucleic acids identified as misfolded proteins through a series of pathways, known as danger-associated molecular patterns (DAMPs), can also cause microglial priming. Toll-like receptors (TLRs) and carbohydrate-binding receptors commonly function in these pathways. There are also many different receptors found in microglia, including triggering receptors expressed on myeloid cells (TREM), Fc? receptors (Fc?Rs), CD200 receptor (CD200R), receptor for advanced glycation end products (RAGE), chemokine receptors (CX3CR1, CCR2, CXCR4, CCR5, and CXCR3), which can be recognized and mixed in with other signaling pathways, although some pathways are still not clear. �

 

Consequences of Microglial Priming in the CNS

 

Microglia show a low rate of mitosis in their normal state and a high rate of proliferation after microglial priming, showing that the microglia have the ability to affect cell turnover and pro-inflammation stimulation. With continued stimulation, microglia activate from their resting state, changing into amoeboid microglial cells in morphology. However, the changes in the shape of the microglia cannot differentiate the characteristics of microglial activation and the function of primed microglia depends on their phenotypes which are associated with receptors and molecules which they create and recognize. �

 

The different types of tissue macrophages, under microenvironmental impetus, are able to differentiate M1 and M2 phenotypes. First, M1 polarization, also known as classical activation, ultimately needs interferon-? (IFN-?) to be mixed with TLR4 signaling which then causes the production of inducible nitric oxide synthases (iNOS), reactive oxygen species (ROS), proinflammatory cytokines, and finally, ultimately reduces the release of neurotrophic factors, ultimately causing inflammation with increased markers of main histocompatibility complex II (MHC II), interleukin-1? (IL-1?) and CD68. �

 

Moreover, M2 polarization, also known as alternative activation, is ultimately believed to be associated with tissue-supportive in the situation of wound healing, reducing inflammation and improving tissue repair of collagen form. They trigger in response to IL-4 and IL-13 in vivo. M2 polarization is characterized by the increased expression of neurotrophic factors, proteases, enzymes arginase 1 (ARG1), IL-10 transforming growth factor-? (TGF-?), scavenger receptor CD206 and coagulation factors as well as improving phagocytic activity. As a matter of fact, there are currently no clear boundaries between the two polarizations and the M1 phenotype shares many similar characteristics with the M2 phenotype. �

 

Another phenotype of primed microglia, known as acquired deactivation, has been recently discovered. This new phenotype overlaps with M2 and has the ability to improve anti-inflammatory and functional recovery. Additionally, a research study conducted ultra-structural analyses and identified a brand-new phenotype, known as �dark microglia�, which is rarely seen in the microglial cell’s resting state. Systemic inflammation triggers microglia into an activated state to promote cell and tissue recovery and achieve homeostasis. Microglial priming is ultimately the second interruption in the CNS microenvironment. �

 

The primed microglia is a double-edged sword for brain health. Many research studies in vivo and in vitro have shown that neurological diseases are associated with microglial activation. The inflammatory phenotypes of the microglia create neurotoxic factors, mediators and ROS which can affect the CNS. Primed microglia play a fundamental and beneficial role in neuronal regeneration, repair, and neurogenesis. Primed microglia are also much more sensitive and respond much stronger to brain injury, inflammation, and aging as well as increase the activation of microglial cells by switching from an anti-inflammation, potentially protective phenotype to a pro-inflammation destructive phenotype, as shown in (Figure 1). �

 

Figure 1 Microglial Priming and Altering | El Paso, TX Chiropractor

 

In the early stages of microglial priming, the ability and function to phagocytize cell debris, misfolded proteins, and inflammatory medium are increased where more protective molecules, such as IL-4, IL-13, IL-1RA, and scavenging receptors, are created. The changes can affect wound healing and damage tissue repairment, neuron protection, and homeostasis recovery. Classically activated microglia (M1) make up a large proportion of all microglia and promote an increased creation of neurotoxic factors, such as IL-1?, TNF-?, NO and H2O2 (6), where more microglia are primed immediately afterward. �

 

This increased and extended neuroinflammation caused by primed microglia can ultimately be associated with the development and clustering of the protein tau and A?. Furthermore, it can lead to loss of neurons as well as the decrease of cognitive function and memory, such as in Alzheimer’s disease. Although the mechanisms are not clear enough, people have reached an agreement that primed microglia cause a chronic proinflammatory response and a self-perpetuating cycle of neurotoxicity. And this is believed to be the key factor in brain health issues resulting in neurological diseases. �

 

Microglia are known as the protectors of the brain and they play a fundamental role in maintaining as well as regulating the homeostasis of the CNS microenvironment. Constant stimulation causes the microglia to trigger at a much stronger state, which is known as microglial priming. Microglial cells are the “Bruce Banner” of the CNS. However, once they go into protective “Hulk” mode, primed microglia become much more sensitive to stimulation and they have a much stronger possibility of reacting to stimulation, even reacting towards normal cells. �- Dr. Alex Jimenez D.C., C.C.S.T. Insight

 

Microglial cells make up about 10 to 15 percent of all the glial cells in the human body, which can be found in the central nervous system (CNS) and play a fundamental role in the human brain. Microglial cells are responsible for maintaining and regulating changes in the physiological and pathological condition of the CNS. The scope of our information is limited to chiropractic, musculoskeletal and nervous health issues as well as functional medicine articles, topics, and discussions. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900 . �

 

Curated by Dr. Alex Jimenez �

 


 

Additional Topic Discussion: Chronic Pain

 

Sudden pain is a natural response of the nervous system which helps to demonstrate possible injury. By way of instance, pain signals travel from an injured region through the nerves and spinal cord to the brain. Pain is generally less severe as the injury heals, however, chronic pain is different than the average type of pain. With chronic pain, the human body will continue sending pain signals to the brain, regardless if the injury has healed. Chronic pain can last for several weeks to even several years. Chronic pain can tremendously affect a patient’s mobility and it can reduce flexibility, strength, and endurance.

 

 


 

Neural Zoomer Plus for Neurological Disease

Neural Zoomer Plus | El Paso, TX Chiropractor

 

Dr. Alex Jimenez utilizes a series of tests to help evaluate neurological diseases. The Neural ZoomerTM Plus is an array of neurological autoantibodies which offers specific antibody-to-antigen recognition. The Vibrant Neural ZoomerTM Plus is designed to assess an individual�s reactivity to 48 neurological antigens with connections to a variety of neurologically related diseases. The Vibrant Neural ZoomerTM Plus aims to reduce neurological conditions by empowering patients and physicians with a vital resource for early risk detection and an enhanced focus on personalized primary prevention. �

 

Formulas for Methylation Support

 

Xymogen Formulas - El Paso, TX

 

XYMOGEN�s Exclusive Professional Formulas are available through select licensed health care professionals. The internet sale and discounting of XYMOGEN formulas are strictly prohibited.

 

Proudly,�Dr. Alexander Jimenez makes XYMOGEN formulas available only to patients under our care.

 

Please call our office in order for us to assign a doctor consultation for immediate access.

 

If you are a patient of Injury Medical & Chiropractic�Clinic, you may inquire about XYMOGEN by calling 915-850-0900.

xymogen el paso, tx

 

For your convenience and review of the XYMOGEN products please review the following link.*XYMOGEN-Catalog-Download

 

* All of the above XYMOGEN policies remain strictly in force.

 


 

Diagnosis of Central Nervous System Infections Part 2

Diagnosis of Central Nervous System Infections Part 2

Central nervous system, or CNS, infections can be life-threatening if they are not diagnosed and treated early. Because CNS infections are non-specific, determining an accurate diagnosis can be challenging. The nucleic acid in vitro amplification-based molecular methods are starting to be utilized for routine microbial diagnosis. These molecular methods have improved beyond conventional diagnostic techniques with increased sensitivity and specificity. Moreover, molecular methods utilized on cerebrospinal fluid samples are considered the new standard for diagnosis of CNS infections caused by pathogens. �

 

Molecular methods for the diagnosis of CNS infections offers a variety of monoplex and multiplex PCR assays to diagnose several types of health issues. Pan-omic molecular platforms can also help diagnose CNS infections. Although molecular methods are utilized for the diagnosis of CNS infections, the outcome measures for these diagnostic techniques must be carefully identified by healthcare professionals. The following article discusses conventional diagnostic techniques and molecular methods utilized for the diagnosis of central nervous system infections, their application, and future approaches. �

 

Molecular Methods in the Diagnosis of CNS Infections

 

Because of increased sensitivity and specificity, nucleic acid in vitro amplification-based molecular methods has tremendously improved the ability to diagnose CNS infections in a reasonable and effective time frame. Several PCR-derived techniques have also ultimately increased the flexibility and rigor of currently available diagnostic techniques. �

 

Reverse transcriptase, or RT,-PCR was developed to increase RNA targets. Its utilization plays a fundamental role in the diagnosis of RNA-virus infections as well as managing their reaction to treatment. Timely access to enterovirus RT-PCR outcome measures has demonstrated shorter hospital stays, reduced unnecessary antibiotic utilization, and decreased ancillary laboratory evaluations and tests. Broad-range rRNA PCR techniques, which utilize a single pair of primers targeting conserved regions of genes, have been utilized to diagnose bacterial pathogens and herpes viruses in the CSF. Isothermal amplification-based techniques. including loop-mediated isothermal amplification or LAMP, have been developed to offer a diagnosis within several minutes to hours. Table 2 demonstrates commercial molecular in vitro diagnostic devices, or IVD, which have been cleared by the US Food and Drug Administration, or FDA, for diagnosis of microbial pathogens in CSF. �

 

Monoplex Assays

 

A conventional molecular method involves three phases: sample extraction, target nucleic acid amplification, and amplicon detection. One of the first molecular assays successfully utilized for the diagnosis of CNS infections was utilized for the diagnosis of HSV in cerebrospinal fluid or CSF. PCR became the test of choice when research studies demonstrated that CSF PCR was similar to culture of brain tissue for diagnosis of HSV encephalitis and meningitis. Many PCR based methods for the diagnosis of herpes and enteroviruses have become available with increased sensitivity compared to viral culture. �

 

Real-time PCR with nucleic acid amplification and amplicon detection further improved the transition to molecular methods in clinical laboratories. Unlike conventional PCR, the real-time system is a �closed� system and it overcomes the fundamental problem of carryover contamination. At the time of manuscript preparation, three molecular assays utilized to help diagnose HSV and enteroviruses in CSF have ultimately been approved by the FDA as demonstrated in Table 2 of the previous article. � Real-time PCR-based methods are the main diagnostic technique utilized to help diagnose the Zika virus, which was first reported in Uganda in 1947, and is now a worldwide concern after the virus spread widely in Brazil and Central America. Research studies developed a one-step RT-PCR assay utilized to diagnose the Zika virus in human serum with a limited detection of 7.7pfu/reaction. Along with plasma, the Zika virus RNA can be diagnosed through urine and plasma within the first 2 weeks after symptoms have manifested. In March 2016, the FDA approved a trioplex-PCR assay under emergency use authorization for the simultaneous diagnosis of Zika, Chikungunya, and Dengue viruses in serum, urine, CSF and amniotic fluid. The RT-PCR assay utilizes dual labeled hydrolysis probes with a LOD of 1.54�10 4 GCE/ ml of Zika virus in serum. �

 

Introduction of real-time PCR based diagnostic assays have affected early and effective diagnosis of several bacterial infections. Isothermal amplification-based molecular assays have excellent performance characteristics and they don’t require any specialized equipment. These assays are fundamental for the utilization of on or near point-of-care testing. LAMP-based methods have been utilized to diagnose Neisseria meningitis, Streptococcus pneumoniae, Haemophilus influenzae type b, M. tuberculosis, and JEV in the CSF. The Xpert MTB/RIF assay has tremendously improved regulation of tuberculosis by offering an integrated and automated system which allows quick clinical decision making in a POC or near-care context. Several research studies have utilized the Xpert MTB/RIF to evaluate the diagnosis of M. tuberculosis in CSF from TB meningitis. In a meta-analysis of thirteen research studies, the pooled sensitivity of the Xpert assay was 80.5 percent, or 95 percent CI 59.0 percent to 92.2 percent, against culture and 62.8 percent, or 95 percent CI 47.7 percent to 75.8 percent, against composite standard. Utilizing a large volume of sample, of at least 8�10 ml, is necessary for testing CSF and centrifugation can cause considerable improvements in yield. Despite the lack of standardization for sample processing, WHO has allowed testing CSF with the automated Xpert MTB/RIF assay as the first-line test over conventional microscopy. �

 

Multiplex Assays

 

Simplicity makes multiplex molecular assays fundamental for the diagnosis of a panel of microbial targets. Several multiplex PCR assays have been developed to diagnose bacterial pathogens in CSF targeting the most common causes of meningitis: S. pneumoniae, N. meningitis, H. influenzae, L. monocytogenes, S. agalactiae, S. aureus, E. coli, and M. pneumoniae. A multiplex PCR followed by Luminex suspension array can simultaneously diagnose eight bacterial and viral pathogens in CSF, including N. meningitis, S. pueumoniae, E. coli, S. aureus, L. monocytogenes, S. agalactiae, HSV-1/2, and VZV, among others. �

 

Considering the variety of pathogens involved in CNS infection, application of comprehensive molecular panels with multiple bacterial and viral targets have improved the efficiency of diagnosis. The BioFire FilmArray Meningitis/Encephalitis panel is currently the only FDA cleared multiplex assay utilized for the diagnosis of six bacterial, such as Escherichia coli K1, Haemophilus influenzae, Listeria monocytogenes, Neisseria meningitides, Streptococcus agalactiae and Streptococcus pneumoniae, seven viral, such as cytomegalovirus, enterovirus, HSV-1, HSV-2, human herpesvirus 6 or HHV-6, human parechovirus and VZV, as well as a single fungal, such as Cryptococcus neoformans/gattii, target in CSF as demonstrated in Table 2. The integrated FilmArray system takes about an hour, with only 2 minutes of hands-on time. During the preparation of the manuscript, two research studies demonstrated the performance of this assay. Utilizing 48 samples from gram stain negative CSF samples from suspected cases of meningitis, research studies demonstrated that this system diagnosed more viral pathogens, such as EBV. Four cases of WNV and a single case of Histoplasma were not diagnosed by this assay. Among HIV infected patients in Uganda, the test performance demonstrated increased sensitivity and specificity for the diagnosis of Cryptococcus. Although the FilmArray Meningitis/Encephalitis panel offers a quick diagnosis of CNS infections, further research studies are needed to determine its performance for a variety of targets and other high-risk populations. �

 

Co-infections are frequently found among immunocompromised patients and can ultimately be challenging to diagnose for clinicians. The multiplex design allows simultaneous diagnosis of multiple targets on the same sample. One research study utilized a panel of monoplex and multiplex molecular assays to conduct a prospective cohort research study in Uganda to comprehensively evaluate the etiology of meningitis among HIV-infected adults. Among the 314 HIV-infected patients with meningitis, EBV co-infection was diagnosed with Cryptococcus, M. tuberculosis, or other viral pathogens. EBV in CSF in these settings is not completely understood although a single research study associated increased EBV viral load as a marker of poor outcome measures in patients with bacterial meningitis and EBV co-infection/ reactivation, among others. �

 

Pan-Omic Molecular Assays

 

Technological improvements in metagenomic deep sequencing have increased its utilization for clinical diagnosis of CNS infections. Several research studies have demonstrated its ability to solve diagnostic technique problems which challenge the limits of traditional laboratory testing. Due to sterile status and protection by BBB, CSF and brain biopsies are fundamental to further explore the utilization of this technology for pathogen diagnosis. Metagenomics was successfully utilized to establish a diagnosis of neuroleptospirosis in a 14-year-old boy with severe combined immunodeficiency who also suffered from recurrent bouts of fever, headache, and coma. Similarly, high-throughput RNA sequencing performed on brain biopsy from an 18-month-old boy with encephalopathy diagnosed a new Astrovirus as the cause. Despite the utilization of metagenomics for the diagnosis of infectious disease, there are many technological and practical concerns which need to be addressed before this form of diagnostic testing can become mainstream and part of the clinical standard of care. �

 

Other promising advances have occurred in transcriptomics, proteomics and metabolomics. Host and microbial microRNA or miRNA, profiles have been utilized for a variety of inflammatory and infectious diseases. Two miRNAs, miR-155 and miRNA-29b, were reported as potential biomarkers for JEV infection and treatment targets for anti-JEV therapy. Host neural epidermal growth factor, including 2 and apolipoprotein B in CSF, was able to diagnose tuberculous meningitis with 83.3 percent to 89.3 percent sensitivity and 75 percent to 92 percent specificity. CSF metabolite profiling has been reported to be useful in the classification, diagnosis, epidemiology, and treatment assessment of CNS infections in HIV patients. CSF metabolic profile analysis demonstrated bioenergetic adaptation in regulating shifts of HIV-infected patients. �

 

Outcome Measures Associated with Diseases

 

Diagnosis of an etiologic agent in patients with CNS infections needs consideration of the most common causative organisms, the available diagnostic techniques and molecular methods for these agents, and the highest-yield clinical specimens for evaluation and testing. Knowledge of the epidemiology and clinical presentation of specific agents is fundamental in selecting which diagnostic methods are appropriate for patients. Animal or vector exposures, geographic location, recent travel history, season of the year, exposure of ill contacts, and occupational exposures should be considered. �

 

When selecting appropriate pathogen-specific molecular diagnostic methods, the following factors should be considered. CSF is the optimal specimen for PCR testing for patients with meningitis or meningoencephalitis. While indirect evidence can be determined by testing other specimen types, attempts should be made to obtain CSF samples early before treatment can compromise yield. Time of testing from the manifestation of symptoms is fundamental to understand and rule out false-negative results and recommend retesting within a certain time frame. By way of instance, HSV PCR can commonly render false-negative results if CSF sample is obtained very early or late in the process of HSE infection. Host health is also known to affect test performance characteristics. Immunocompromised patients are at risk for infection by a variety of opportunistic pathogens, by way of instance HHV-6, JC virus, Toxoplasma encephalitis in bone marrow transplant recipients and patients with HIV. Often, infection can be more severe, such as WNV, and challenging to diagnose in this population. Table 3 below demonstrates practical recommendations on application and pitfalls of molecular test for the diagnosis of CNS infections. �

 

Table 3 Molecular Methods in Detecting CNS Infections 1 | El Paso, TX Chiropractor Table 3 Molecular Methods in Detecting CNS Infections 2 | El Paso, TX Chiropractor

 

Furthermore, a positive nucleic acid amplification testing results are considered to be complicated by the fact that some viruses survive latently in macrophages or neurologic tissues even if they’re incidentally diagnosed by sensitive molecular techniques without an actual pathogenic role which can potentially lead to overtreatment. Utilization of adjunctive biomarkers which help determine active replication is being explored to overcome this drawback in research studies. �

 

Historically, the diagnosis of microbiologic agents in patients with CNS infections has been hindered by the low yield of CSF culture for viral and fastidious bacterial organisms, delays in CNS production of organism-specific antibodies, and challenges in determining optimum samples for testing. The nucleic acid in vitro amplification-based molecular diagnostic methods and techniques have a wider and better application in clinical microbiology practice. The monoplex assay will likely be the main platform utilized for urgent, random-access, low throughput assays. Multiplex assays have the additional benefit of diagnosing multiple targets and mixed infections. As the volume of CSF sample retrieved is often small, multiplex assays enable comprehensive diagnostic analysis with a low amount of sample, obviating the need for repeated lumbar punctures. The clinical relevance and cost-effectiveness of simultaneous multi-pathogen diagnosis strategies need further research studies. Application of pan-omic techniques in challenging to diagnose CNS infections is the new exciting frontier, the technology is promising but routine implementation is expected to be slow due to various challenges, such as lack of applicable regulatory guidelines and adaptation in the clinical setting, although the outcome measures are promising. �

 

As previously mentioned, central nervous system, or CNS, infections can be life-threatening health issues if they are not accurately diagnosed and properly treated. However, determining a diagnosis of CNS infections can be challenging for many clinicians. Fortunately, a variety of diagnostic techniques and molecular methods can ultimately help determine the source of CNS infections and other health issues. These diagnostic techniques and molecular methods have tremendously improved over the years, as previously mentioned, and more of these evaluations are being utilized in clinical settings to accurately diagnose CNS infections for proper treatment. – Dr. Alex Jimenez D.C., C.C.S.T. Insight

 

In part 2 of our “Diagnosis of Central Nervous System Infections” article, we discussed the molecular methods and the pan-omic molecular assays which are utilized in the diagnosis of CNS infections as well as how specific testing outcome measures have ultimately been associated with clinical diseases and health issues. The scope of our information is limited to chiropractic, musculoskeletal and nervous health issues as well as functional medicine articles, topics, and discussions. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900 . �

 

Curated by Dr. Alex Jimenez �

 


 

Additional Topic Discussion: Chronic Pain

 

Sudden pain is a natural response of the nervous system which helps to demonstrate possible injury. By way of instance, pain signals travel from an injured region through the nerves and spinal cord to the brain. Pain is generally less severe as the injury heals, however, chronic pain is different than the average type of pain. With chronic pain, the human body will continue sending pain signals to the brain, regardless if the injury has healed. Chronic pain can last for several weeks to even several years. Chronic pain can tremendously affect a patient’s mobility and it can reduce flexibility, strength, and endurance.

 

 


 

Neural Zoomer Plus for Neurological Disease

Neural Zoomer Plus | El Paso, TX Chiropractor

Dr. Alex Jimenez utilizes a series of tests to help evaluate neurological diseases. The Neural ZoomerTM Plus is an array of neurological autoantibodies which offers specific antibody-to-antigen recognition. The Vibrant Neural ZoomerTM Plus is designed to assess an individual�s reactivity to 48 neurological antigens with connections to a variety of neurologically related diseases. The Vibrant Neural ZoomerTM Plus aims to reduce neurological conditions by empowering patients and physicians with a vital resource for early risk detection and an enhanced focus on personalized primary prevention. �

 

Formulas for Methylation Support

 

Xymogen Formulas - El Paso, TX

 

XYMOGEN�s Exclusive Professional Formulas are available through select licensed health care professionals. The internet sale and discounting of XYMOGEN formulas are strictly prohibited.

 

Proudly,�Dr. Alexander Jimenez makes XYMOGEN formulas available only to patients under our care.

 

Please call our office in order for us to assign a doctor consultation for immediate access.

 

If you are a patient of Injury Medical & Chiropractic�Clinic, you may inquire about XYMOGEN by calling 915-850-0900.

xymogen el paso, tx

 

For your convenience and review of the XYMOGEN products please review the following link.*XYMOGEN-Catalog-Download

 

* All of the above XYMOGEN policies remain strictly in force.

 


 

Diagnosis of Central Nervous System Infections Part 1

Diagnosis of Central Nervous System Infections Part 1

The central nervous system, or CNS, plays a fundamental role in the pathogenesis of infection. The CNS is regulated by the blood-brain barrier or BBB, however, it can still be exposed to a microbial invasion from a contiguous focus, hematogenous dissemination, or intraneural passage of organisms. A variety of environmental or commensal bacteria, viruses, fungi, protozoa, or parasites can enter the CNS and cause a variety of infections and health issues. Central nervous system infections can ultimately cause headache, stiff neck, vomiting, fever, photophobia, and focal neurological symptoms. �

 

What are Central Nervous System Infections?

 

CNS infections are characterized according to their affected region. Infection of the brain, spinal cord, and meninges results in meningitis, encephalitis, brain abscess, and myelitis. Infections can affect single or multiple regions of the brain, such as meningoencephalitis and encephalomyelitis. Moreover, CNS infections are characterized as acute, sub-acute, chronic, or recurrent based on their duration. Meningitis can cause headache, neck stiffness, fever, and photophobia over a period of hours to days. Encephalitis can cause brain parenchymal inflammation which can ultimately cause lethargy to coma. Last but not least, Myelitis can cause inflammation of the spinal cord including headache, fever, and paraparesis or paralysis. �

 

Diagram of Central Nervous System and Pathogens.

 

One of the most fatal CNS infections, acute bacterial meningitis, with three to five cases for every 100,000 people in the United States, has a mortality rate of 6 percent to 26 percent. Approximately 4,000 cases of acute bacterial meningitis occur in the U.S. every year with about 500 deaths. The frequent cause of acute bacterial meningitis includes Streptococcus pneumoniae, group B Streptococcus, Neisseria meningitides, Haemophilus influenzae, and Listeria monocytogenes. �

 

CNS infections caused by viruses are more common and are mostly mild and self-limited. However, these can manifest as meningitis and/or encephalitis. CNS infections caused by viruses can vary due to region and season. Non-polio enteroviruses are responsible for the majority of meningitis and/or encephalitis cases from late spring to fall. CNS infections due to herpes simplex viruses, or HSV, are associated with sporadic encephalitis and meningitis with severe sequelae if left untreated. �

 

Diagnosis of CNS Infections

 

Diagnosis of microbial pathogens is fundamental for treatment. Methods and techniques utilized in clinical microbiology laboratories include direct microscopic examination, and culture techniques as well as antigen and antibody detection assays. However, each method and technique has several essential limitations. By way of instance, direct microscopic examination of CSF restricted sensitivity and specificity. The sensitivity of culture for enteroviruses is between 65 percent to 75 percent with average retrieval time of 3.7 to 8.2 days. Moreover, several serotypes of enteroviruses, especially Coxsackievirus A strains, are well-known to be non-cultivable and frequently grow poorly. Because enteroviruses are missing a common antigen found throughout a variety of serotypes, universal antigen and/or antibody diagnosis is impossible. Diagnosis of CNS HSV infections through methods and techniques utilized to determine culture sensitivity from CSF is tremendously poor. The presence of HSV IgG antibodies in CSF can ultimately be utilized to determine a diagnosis, however, the production is delayed until day 10 or day 12 after infection and it is not considered ideal for early diagnosis.

 

Methods and Techniques for Diagnosis of Central Nervous System Infections.

 

Diagnostic techniques, especially PCR based amplification, have developed a variety of mainstay tools to help determine the diagnosis of microbial pathogens in CSF. Molecular methods have demonstrated greater diagnosis rates than other diagnostic techniques. One research study demonstrated that 16S rRNA PCR-based assays were able to diagnose the causative organism in 65 percent of banked CSF samples compared to 35 percent when utilizing culture and microscopy. In another research study, diagnosis based on diagnostic techniques like molecular methods were utilized to optimize antibiotic treatment of patients with infectious meningitis when conventional methods and techniques demonstrated a negative outcome measure. Molecular methods and diagnostic techniques utilized on CSF samples are a fundamental standard when compared to the culture standard in the diagnosis of CNS infections caused by viruses which are challenging to diagnose. �

 

The diagnosis of CNS infections has tremendously changed over the last several years. PCR-based molecular methods have become a fundamental element in the clinical microbiology laboratory, providing tools for an accurate diagnosis. As demonstrated in Table 2, a variety of commercial molecular assays have been cleared by the Food and Drug Administration, or FDA, for the diagnosis of microbial pathogens. The approved assays for pathogen detection in the CNS are shown below. �

 

FDA Assays for Pathogen Detection in the CNS.

 

However, there are still several challenges in molecular diagnostic techniques and methods. Utilizing a combination of conventional diagnostic techniques and molecular methods, research studies demonstrated that in approximately 62 percent of patients with encephalitis, an etiologic organism could not be identified. Researchers have started to focus on developing advanced techniques and methods. In the following series of articles, we will demonstrate an update on the current conventional and molecular platforms utilized for the diagnosis of CNS infections. We will also demonstrate a preview on the potential clinical application of future technologies, including pan-omic assays. The emphasis of the following series of articles is to demonstrate optimal test selection in the clinical scenario for the diagnosis of CNS infection. �

 

Conventional Microbiology Methods and Techniques

 

Microscopic Examination

 

A positive CSF Gram stain confirms the diagnosis of bacterial meningitis. The sensitivity of the Gram stain for the diagnosis of bacterial meningitis is approximately 60 percent to 80 percent in patients not on antimicrobial treatment and approximately 40 percent to 60 percent in patients on antibacterial treatment. In one research study, Gram stain diagnosed as much as 90 percent Streptococcus pneumoniae and 50 percent Listeria monocytogenes in CSF collected from patients with bacterial meningitis confirmed by PCR 26 techniques and methods. Two organisms which are frequently diagnosed by microscopy include Mycobacterium tuberculosis by acid-fast bacillus, or AFB, staining and Cryptococcus neoformans by India ink or Gram stain. However,� the sensitivities of these techniques and methods are poor and culture is generally utilized instead. �

 

Culture

 

Culture of brain tissue can demonstrate a positive diagnosis of CNS infections, however, getting biopsies are tremendously invasive and frequently avoided unless a clinician determines that they are absolutely necessary. CSF sampling is most commonly performed to diagnose CNS infection. CSF viral, bacterial, including mycobacterial, and fungal cultures are fundamental in the diagnosis of infectious meningitis. However, CSF cultures in these cases are extremely low. Another disadvantage of CSF bacterial culture is that it generally requires up to 72 hours to determine a final diagnosis. A recent research study demonstrated that CSF mycobacterial culture had a sensitivity of 22 percent and a specificity of 100 percent in the diagnosis of tuberculosis meningitis. For viruses, utilizing monoclonal antibodies through culture increased the speed and specificity. However, due to time and sensitivity, CSF viral culture is frequently unable to determine a diagnosis. �

 

Rapid Antigen Detection

 

Cryptococcal antigen is the most commonly utilized antigen assay for CNS infections. The test utilizes Cryptococcus capsular polysaccharide antigens in CSF through enzyme immunoassay to determine a diagnosis. In a single research study which evaluated patients less than 35 years of age with CNS cryptococcosis, overall sensitivity and specificity of 93 percent to 100 percent and 93 percent to 98 percent were shown. Cryptococcus is a neurotropic fungus. Polysaccharide serum antigen titers with host immune status are frequently utilized to determine the need for a lumbar puncture to evaluate the patient for CNS health issues. The baseline peak titer of polysaccharide antigen in serum or CSF has demonstrated fundamental prognostic significance with an increased titer, or peak titer less than 1:1024, associated with antifungal therapy failure. �

 

The diagnosis of galactomannan, or GM, antigen and 1,3 ?-D-glucan, or BDG, in CSF, can help in the diagnosis of CNS aspergillosis or other invasive fungal infection such as fusariosis. Increased BDG in serum and CSF is associated with fungal infections. Measuring the levels of BDG is a beneficial biomarker in the evaluation of fungal CNS infection. It was recently demonstrated that patients receiving effective antifungal therapy demonstrated a decrease in CSF BDG concentrations with less than 31pg/ml and for this reason, BDG titers in CSF are a beneficial biomarker when monitoring response to treatment. �

 

For acute bacterial meningitis, a rapid antigen assay can help diagnose for a pneumococcal capsular antigen. Several research studies have demonstrated the utilization of M. tuberculosis-specific antigens in CSF for the diagnosis of tuberculosis meningitis. M. tuberculosis Early Secreted Antigenic Target 6, or ESAT-6, has been utilized for tuberculosis meningitis. �

 

Serology

 

Serological diagnosis of CNS infections is determined by identifying IgM antibodies or by demonstrating an increase in neutralizing antibody titers between acute- and convalescent-phase CSF. Due to a delay in antibody response when symptoms have manifested, a negative antibody test cannot be utilized to rule out infections and retesting may be required. Moreover, in specific populations, such as immunocompromised patients, the tests may not offer optimum sensitivity. In most instances, nucleic acid amplification tests have surpassed antibody-based detection as the test of choice. For several CNS infections, these assays play a fundamental role. CSF IgM is the most commonly utilized test for West Nile virus, or WNV, infections. Antibodies may manifest in as soon as 3 days and may continue for up to 3 months. However, its accuracy is challenged by high cross-reactivity with other flaviviruses and associated vaccines. Antibodies in recombinant WNV E proteins can determine where cross-reacting viruses co-circulate or determine which patients have been immunized. �

 

Fundamental serological assays for CNS infections are utilized for the diagnosis of neurosyphilis. Neurosyphilis is determined by a positive CSF venereal disease research laboratory, or VDRL, test. Diagnosis of varicella-zoster virus, or VZV, IgG in CSF is the most common technique and/or method for the diagnosis of VZV associated with CNS infection. �

 

Central nervous system, or CNS, infections can ultimately be life-threatening health issues if they are not diagnosed and treated early. Determining an accurate diagnosis of CNS infections can be challenging. Fortunately, a variety of diagnostic techniques and molecular methods can help determine the source of CNS infections. These diagnostic techniques and molecular methods have tremendously improved over the years and more and more of these evaluations are being utilized in clinical settings to accurately diagnose CNS infections for early treatment. – Dr. Alex Jimenez D.C., C.C.S.T. Insight

 

In part 2 of our “Diagnosis of Central Nervous System Infections” article, we will ultimately discuss the molecular methods and the pan-omic molecular assays which are utilized in the diagnosis of CNS infections as well as discuss how specific testing outcome measures are associated with clinical diseases and health issues. The scope of our information is limited to chiropractic, musculoskeletal and nervous health issues as well as functional medicine articles, topics, and discussions. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900 . �

 

Curated by Dr. Alex Jimenez �

 


 

Additional Topic Discussion: Chronic Pain

 

Sudden pain is a natural response of the nervous system which helps to demonstrate possible injury. By way of instance, pain signals travel from an injured region through the nerves and spinal cord to the brain. Pain is generally less severe as the injury heals, however, chronic pain is different than the average type of pain. With chronic pain, the human body will continue sending pain signals to the brain, regardless if the injury has healed. Chronic pain can last for several weeks to even several years. Chronic pain can tremendously affect a patient’s mobility and it can reduce flexibility, strength, and endurance.

 

 


 

Neural Zoomer Plus for Neurological Disease

Neural Zoomer Plus | El Paso, TX Chiropractor

Dr. Alex Jimenez utilizes a series of tests to help evaluate neurological diseases. The Neural ZoomerTM Plus is an array of neurological autoantibodies which offers specific antibody-to-antigen recognition. The Vibrant Neural ZoomerTM Plus is designed to assess an individual�s reactivity to 48 neurological antigens with connections to a variety of neurologically related diseases. The Vibrant Neural ZoomerTM Plus aims to reduce neurological conditions by empowering patients and physicians with a vital resource for early risk detection and an enhanced focus on personalized primary prevention. �

 

Formulas for Methylation Support

 

Xymogen Formulas - El Paso, TX

 

XYMOGEN�s Exclusive Professional Formulas are available through select licensed health care professionals. The internet sale and discounting of XYMOGEN formulas are strictly prohibited.

 

Proudly,�Dr. Alexander Jimenez makes XYMOGEN formulas available only to patients under our care.

 

Please call our office in order for us to assign a doctor consultation for immediate access.

 

If you are a patient of Injury Medical & Chiropractic�Clinic, you may inquire about XYMOGEN by calling 915-850-0900.

xymogen el paso, tx

 

For your convenience and review of the XYMOGEN products please review the following link.*XYMOGEN-Catalog-Download

 

* All of the above XYMOGEN policies remain strictly in force.

 


 

Protein Folding and Neurological Disease

Protein Folding and Neurological Disease

We often think of proteins are nutrients found in the food we eat and the main component of muscles, however, proteins are microscopic molecules located inside of cells which actually perform a variety of fundamental roles. The function of a protein depends on its shape, and when protein formation goes awry, the resulting misshapen proteins can cause numerous health issues, such as when proteins neglect their essential roles or when they form a sticky, clumpy clutter inside of cells. Protein formation is an error-prone procedure and mistakes along the way have been associated with neurological diseases. �

 

There are approximately 20,000 to over 100,000 unique types of proteins found inside a common human cell. Why so many? Proteins are the workhorses of the human cell. By way of instance, several of these proteins are structural, lending stiffness and rigidity to thin neurons or muscle tissues. Other proteins shuttle them to new places and bind to specific molecules and others catalyze responses. A property of proteins is possible through diversity and specificity in their role when they fold. �

 

Why Proteins Fold into a Functional Shape

 

A protein generally begins in the cell as a lengthy chain of about 300 building blocks known as amino acids. There are 22 different types of amino acids and their order decides what protein chain will fold onto itself. After folding, two types of structures will generally form. Several regions of the protein chain coil into slinky-like formations known as “alpha-helices,” while other regions fold into zigzag patterns known as “beta-sheets,” which resemble the folds of a paper fan. �

 

Both of these structures may interact to form complex structures. In one protein structure, many beta-sheets wrap themselves around to form a hollow tube. The tube is also generally short where the overall structure resembles snakes (alpha-helices) emerging out of a can (beta-sheet tubing ). Moreover, several other protein structures with descriptive names include the “beta-barrel,” that the”beta-propeller,” the”alpha/beta-horseshoe,” as well as the “jelly-roll fold”. �

 

These intricate structures allow proteins to perform their variety of roles in the cell. The “snakes in a can” protein, when embedded into a cell membrane, creates a tube which enables traffic in and out of cells. Other proteins form contours with pockets known as “active sites” which are perfectly shaped to bind to a certain molecule like a lock and key. By bending into different shapes, proteins can do different functions. To draw an analogy, all vehicles are made from steel, while a bus, dump truck, crane, or Zamboni are shaped to execute their very own tasks however races are won by the slick shape of a racecar. �

 

Why Protein Folding Sometimes Fails

 

Protein folding ultimately allows a protein to take a functional shape, however, it’s an intricate procedure which can sometimes fail. According to research studies, protein folding can go wrong due to three major reasons: �

 

  1. A person may have a mutation which affects an amino acid in the protein chain, making it difficult for a specific protein to locate its favored fold or “native” state. This is how it is for mutations, such as those contributing to cystic fibrosis or sickle cell anemia. These mutations are found in the DNA sequence or “gene” which encodes one special protein. Therefore, these types of inherited mutations affect only that protein and its related function.
  2. On the other hand, protein folding failure can be seen as an ongoing and much more general procedure which affects several proteins. When proteins are made, the structure which reads the instructions from DNA to produce the long chains of amino acids can make errors. Researchers estimate that the ribosome makes mistakes in as many as 1 in every 7 proteins. These mistakes can make the proteins which are resultantly inclined to continue to fold improperly.
  3. Even though an amino acid chain does not have any mutations or mistakes, it may still not reach its own preferred folded shape because proteins don’t fold properly 100 percent of their time. Protein folding becomes much more difficult if the conditions in the cell change due to external factors such as temperature and acidity.

 

A collapse in protein folding can cause a variety of neurological diseases and researchers hypothesize that many health issues are associated with folding problems. There are two problems which exist in cells which don’t protein fold correctly. �

 

One type of problem, known as “loss of function,” results when not enough of a particular protein folds correctly, causing a lack of “specialized functions” necessary to perform a particularly important role. By way of instance, imagine a correctly folded protein is shaped to bind a toxin and split it into noxious compounds. Without enough of that protein accessible, the toxin will build-up to damaging levels. In another instance, a protein may be responsible for metabolizing sugar which can then be utilized by the cell for energy. The cell will grow due to lack of energy if not enough of this protein is accessible. The reason the cell becomes ill, in these cases, is because of a lack of one particular folded, functional protein. Cystic fibrosis, Tay-Sachs disease, Marfan syndrome, and some types of cancer are examples of health issues which result when one type of protein is unable to perform its role. Who knew that one type of protein out of thousands may be so significant? �

 

Proteins folding may also impact the overall health and wellness of the cell regardless of the utilization of the protein. When proteins fail to fold into their functional state, the consequent misfolded proteins could be contorted into shapes which are harmful to the crowded cell environment. Most proteins have sticky, “water-hating” amino acids which they bury deep inside their own core. Misfolded proteins utilize these parts on their exterior, such as a chocolate-covered candy which has been crushed to reveal a gooey center. These misfolded proteins commonly stick together to form clumps known as “aggregates.” Researchers discovered that the accumulation of misfolded proteins plays a fundamental role in several neurological diseases, including Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, and Lou Gehrig’s (ALS) disease, however, researchers are still working to discover exactly how these misfolded molecules affect the well-being of the cells. �

 

One misfolded protein ultimately stands out from among the rest and it deserves particular attention. The “prion” protein in Creutzfeldt-Jakob disease, also known as mad cow disease, is an illustration of a misfolded protein gone rogue. This protein isn’t simply irreversibly misfolded, however, it also transforms other functional proteins into a similar twisted condition. �

 

How Cells Protect from Misfolded Proteins

 

Recent research studies have demonstrated that protein misfolding often occurs inside of cells. Fortunately, cells also have many systems in place and are accustomed to coping with this issue by refolding or destroying aberrant protein formations. � Appropriately known as chaperones, these structures accompany proteins throughout the folding procedure, enhancing a protein’s odds of folding properly and even allowing several misfolded proteins the opportunity to refold. Chaperones are proteins themselves. There are many distinct types of chaperones. A few chaperones supply safety to proteins, isolated from other molecules. Production of many chaperones is fostered when a cell encounters high temperatures or other states which can ultimately make protein folding more difficult, therefore, providing these chaperones the alias, “heat shock proteins.” �

 

The following line of cell defense against misfolded proteins is known as the proteasome. If misfolded proteins linger in the cell, they will be targeted for destruction by this structure, which chews proteins up and spits them out. The proteasome is similar to a center, permitting the cell to reuse amino acids to create proteins. The proteasome itself is not a single protein but many acting collectively. Proteins frequently interact to form larger structures. By way of instance, a human sperm’s tail is a structure made of various types of proteins which work together to produce a rotary engine which propels the sperm. �

 

Protein Folding and Misfolding Overview

 

Why is it that some misfolded proteins can evade systems such as chaperones and the proteasome? How can the neurological diseases previously mentioned above be caused by sticky misfolded proteins? Do some proteins misfold more often than others? These questions are at the forefront of research studies seeking to understand the health issues which ultimately result if protein fold goes awry as well as protein biology. The broad world of proteins, using its great assortment of shapes, bestows cells with capacities that allow for life to exist and allow for its diversity (e.g., the differences between eye, skin, lung or heart cells, and also the differences between species). But perhaps this is one of the many reasons why the word “protein” comes from the Greek word “protas,” meaning “of primary significance” and indeed they seem to be. �

 

Protein folding is a complex, physiochemical process by which a protein “folds” or assumes a functional shape to be able to perform their biological function. Proteins are nutrients we obtain from the food we eat and they are considered to be one of the main components of muscles, however, proteins play a wide variety of fundamental roles in the human body. According to research studies, protein misfolding can cause a variety of health issues, including neurological diseases. – Dr. Alex Jimenez D.C., C.C.S.T. Insight

 

The purpose of the article above is to describe protein folding and how it’s associated with neurological diseases. Neurological diseases are associated with the brain, the spine, and the nerves. The scope of our information is limited to chiropractic, musculoskeletal and nervous health issues as well as functional medicine articles, topics, and discussions. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900 . �

 

Curated by Dr. Alex Jimenez �

 


 

Additional Topic Discussion: Chronic Pain

 

Sudden pain is a natural response of the nervous system which helps to demonstrate possible injury. By way of instance, pain signals travel from an injured region through the nerves and spinal cord to the brain. Pain is generally less severe as the injury heals, however, chronic pain is different than the average type of pain. With chronic pain, the human body will continue sending pain signals to the brain, regardless if the injury has healed. Chronic pain can last for several weeks to even several years. Chronic pain can tremendously affect a patient’s mobility and it can reduce flexibility, strength, and endurance.

 

 


 

Formulas for Methylation Support

 

Xymogen Formulas - El Paso, TX

 

XYMOGEN�s Exclusive Professional Formulas are available through select licensed health care professionals. The internet sale and discounting of XYMOGEN formulas are strictly prohibited.

 

Proudly,�Dr. Alexander Jimenez makes XYMOGEN formulas available only to patients under our care.

 

Please call our office in order for us to assign a doctor consultation for immediate access.

 

If you are a patient of Injury Medical & Chiropractic�Clinic, you may inquire about XYMOGEN by calling 915-850-0900.

xymogen el paso, tx

 

For your convenience and review of the XYMOGEN products please review the following link.*XYMOGEN-Catalog-Download

 

* All of the above XYMOGEN policies remain strictly in force.

 


 

What is Cerebrovascular Disease?

What is Cerebrovascular Disease?

Cerebrovascular disease is characterized as a group of diseases, conditions, and disorders which ultimately affects the blood vessels and the blood supply to the human brain. Brain damage can occur when a blockage, malformation, or hemorrhage prevents the brain cells from receiving enough oxygen. Cerebrovascular disorders can include stroke, transient ischemic attack or TIA, aneurysm, and vascular malformation. �

 

Cerebrovascular disease can develop due to a variety of health issues, such as atherosclerosis, where the arteries become narrow; thrombosis or embolic arterial blood clot, which is a blood clot in an artery of the brain; or cerebral venous thrombosis, which is a blood clot in a vein of the brain. �

 

In the United States, cerebrovascular disease is one of the most common causes of death. In 2017, it caused about 44.9 deaths per 100,000 individuals or 146,383 deaths in total. Fortunately, people can decrease their risk of developing cerebrovascular disease. In the following article, we will describe the types, the symptoms, the diagnosis, and the treatment for cerebrovascular disease and how to prevent them. �

 

Cerebrovascular Disease Symptoms

 

The symptoms of cerebrovascular disease are commonly based on the region of the health issue and its effect on the brain. � Different types of cerebrovascular disease may have different symptoms, however, common symptoms can include: �

 

  • a severe and sudden headache
  • hemiplegia or paralysis on one side of the human body
  • weakness on one side, also known as hemiparesis
  • confusion
  • difficulty communicating, including slurred speech
  • losing vision on one side
  • loss of balance
  • becoming unconscious

 

Emergency Response

 

The American Stroke Association promotes the public knowledge of the F.A.S.T. acronym as a way to help people recognize the warning signs of a stroke or any other type of cerebrovascular disease to take action immediately, including: �

 

  • face drooping
  • arm weakness
  • speech difficulty
  • time to call 911

 

Immediate medical attention is fundamental if anyone demonstrates symptoms of a cerebrovascular disease attack because these may ultimately have long-term effects if not treated immediately, such as cognitive impairment and paralysis. �

 

Types of Cerebrovascular Disease

 

Stroke, TIA, and subarachnoid hemorrhage are several types of cerebrovascular disease. Aneurysms and hemorrhages may cause acute health issues. Blood clots can affect the brain directly or indirectly from other regions of the human body.

 

Ischemic Stroke

 

Ischemic strokes occur when a blood clot or atherosclerotic plaque blocks a blood vessel which supplies blood to the brain. A clot or thrombus may develop in a narrow artery. A stroke occurs when a blood supply deficiency causes brain cell death.

 

Embolism

 

An embolic stroke is the most common type of ischemic stroke. An embolism occurs when a clot breaks off from another region in the human body and travels to the brain and blocks a smaller artery. People who have arrhythmias, which are health issues associated with irregular heart rhythm, are more vulnerable to developing an embolism as well as other health issues. �

 

A tear in the lining of the carotid artery, which is found in the neck, can ultimately cause an ischemic stroke. The tear allows blood circulation to flow between the layers of the artery, reducing blood flow to the brain, and causing it to become narrow. �

 

Hemorrhagic Stroke

 

Hemorrhagic strokes occur when a blood vessel in part of the brain weakens and pops open, causing blood to flow into the brain. The leaking blood puts pressure on the brain tissue, causing edema, which can ultimately damage brain tissue. The hemorrhage may cause parts of the brain to lose their supply of oxygen-rich blood, causing a variety of other health issues. �

 

Cerebral Aneurysm or Subarachnoid Hemorrhage

 

A cerebral aneurysm or subarachnoid hemorrhage can occur due to structural health issues associated with the blood vessels of the brain. An aneurysm is a bulge which in the arterial wall which may rupture and bleed. A subarachnoid hemorrhage occurs when a blood vessel ruptures and bleeds between two membranes in the brain, damaging brain cells. �

 

Cerebrovascular Disease Causes

 

Cerebrovascular disease develops due to a variety of factors. If damage occurs to a blood vessel in the brain, it won’t be able to deliver enough or any blood to the necessary region of the brain. The deficiency of blood can affect the delivery of oxygen and brain cells can begin to die. Brain damage is irreversible. �

 

Immediate medical attention is fundamental to decrease a person’s risk of long-term brain damage and increase their chances of survival. Atherosclerosis is a key cause of cerebrovascular disease. This occurs when cholesterol levels, as well as inflammation in the brain’s arteries, cause cholesterol to build-up. This plaque may restrict or completely obstruct blood circulation into the brain, causing a cerebrovascular disease attack, including a stroke or TIA. �

 

Risk Factors

 

Stroke is the most common type of cerebrovascular disease. The risk of stroke increases with age, especially if a person or their close relatives have previously had a cerebrovascular disease attack. The risk doubles every 10 years, between 55 and 85 years of age. However, a stroke can occur at any age, even during infancy. � Factors which increase the risk of stroke and other types of cerebrovascular disease include: �

 

  • hypertension, which the American College of Cardiology defines as blood pressure of 130/80 mm Hg or higher
  • smoking
  • obesity
  • poor diet and lack of exercise
  • diabetes
  • blood cholesterol levels of 240 milligrams per deciliter (mg/dl) or higher

 

The same factors can increase a person’s risk of developing a cerebral aneurysm. However, people with a congenital anomaly or previous head trauma may also be at risk of developing a cerebral aneurysm. Pregnancy can also increase the risk of developing cerebral venous thrombosis which is a blood clot affecting a vein in the human brain. � Other risk factors of cerebrovascular disease include: �

 

  • Moyamoya disease, a progressive condition which causes a blockage of the cerebral arteries and their major branches
  • venous angiomas, which affect around 2 percent of the U.S. population and rarely bleed or cause symptoms
  • a vein of Galen malformation, an arterial disorder which develops in a fetus during pregnancy

 

Certain drugs and/or medication, as well as other health issues, can make the blood more likely to clot and also increase the risk of ischemic stroke. Hormone replacement therapy or HRT may also increase the risk of a cerebrovascular disease attack in people who currently have atherosclerosis or carotid artery disease, among other health issues. �

 

Cerebrovascular Disease Diagnosis

 

Any cerebrovascular disease can be considered a medical emergency and anybody who recognizes the symptoms must contact 911 for support and evaluation. Early diagnosis is fundamental to reduce brain damage. In the clinic, a doctor will ask about the person’s medical history and search for specific neurological, motor, and sensory health issues, including: �

 

  • changes in vision or visual fields
  • reduced or altered reflexes
  • abnormal eye movements
  • muscle weakness
  • decreased sensation

 

A doctor may also utilize a cerebral angiography, vertebral angiogram, or carotid angiogram to identify a vascular abnormality, such as a blood clot or a blood vessel health issue. These include injecting dye to demonstrate any clots as well as their size and form on MRI or CT imaging. �

 

A CAT scan will also help a doctor diagnose hemorrhagic strokes as it can distinguish between blood, bone, and brain tissue. However, it does not reveal damage from an ischemic stroke in the first phases. An MRI scan may detect early-stage strokes. An electrocardiogram (EKG or ECG) may diagnose cardiac arrhythmia which is a risk factor for embolic strokes. �

 

Cerebrovascular Disease Treatment

 

A cerebrovascular disease requires emergency treatment. Rapid diagnosis and treatment are crucial because a person must receive stroke drugs and/or medications from the beginning of their symptoms. In the case of an acute stroke, the emergency group may administer a medicine known as tissue plasminogen activator (tPA) which breaks up the blood clot. �

 

A neurosurgeon must evaluate a person who has had a brain hemorrhage. They may perform surgery to decrease the pressure which bleeding causes in the brain. A carotid endarterectomy involves making an incision in the carotid artery and removing the plaque. This allows blood to flow again. The surgeon then repairs the artery with sutures or a graft. �

 

Several patients may need carotid angioplasty and stenting which involves a doctor inserting a balloon-tipped catheter into the artery so that the artery reopens when they inflate the balloon. Then, the doctor matches a slim, metal mesh tube, or stent, within the carotid artery to improve blood flow in the formerly blocked artery. The stent helps to prevent the artery from closing-up or collapsing following the procedure.

 

Cerebrovascular Disease Rehabilitation

 

Because a cerebrovascular disease attack can cause irreversible brain damage, people can experience temporary or permanent disability. For this reason, they may require a variety of supportive and rehabilitative treatments so that they can keep as much function as possible. These may ultimately include: �

 

  • Physical therapy: The goal is to restore mobility, flexibility, and upper and/or lower extremity function.
  • Speech therapy: This helps improve communication and regain speech after a stroke or cerebrovascular disease attack.
  • Occupational therapy: This can help access facilities which support a return to work and daily life.
  • Psychological therapy: Physical disability can create unexpected emotional demands and often requires intensive readjustment. A person may benefit from visiting a psychiatrist, psychologist, or counselor after experiencing a cerebrovascular disease attack if they feel overwhelmed.

 

Cerebrovascular Disease Prevention

 

Techniques and methods which can ultimately help reduce the risk of cerebrovascular disease include: �

 

  • no smoking
  • getting at least 150 minutes of moderate to intense exercise and/or physical activity every week
  • eating a balanced diet which supports vascular health, such as the DASH diet
  • maintaining a healthy body weight
  • managing blood cholesterol and blood pressure with diet as well as drugs and/or medications, if necessary

 

People with heart arrhythmia should seek immediate medical attention from a healthcare professional and discuss whether they should be taking a blood thinner to prevent strokes. �

 

Stroke and other cerebrovascular diseases may lead to death but with immediate medical attention, a partial or full recovery is possible. Patients with cerebrovascular disease should follow their healthcare professional’s instructions and lifestyle modifications to ultimately help decrease the prospect of a cardiovascular disease attack. �

 

Decreasing the Risk of Stroke

 

Taking blood platelet inhibitors, including, Dipyridamole, Ticlopidine, and clopidogrel, can decrease the chance of stroke before it occurs. These can help prevent stroke in people who have a medical history or higher prospect of experiencing a cerebrovascular disease attack. �

 

Doctors recommended people to take a daily dose of aspirin to decrease the chance of a heart attack or stroke. However, current guidelines recommend people to take aspirin only if they’re at risk of experiencing cardiovascular disease because aspirin increases the risk of bleeding. � Doctors prescribe statins to manage high cholesterol levels and reduce the risk of ischemic stroke and heart attack. �

 

As previously mentioned above, cerebrovascular disease is identified as a group of diseases, conditions, and disorders which affects the blood vessels and the blood flow supply to the human brain. There are several types of cerebrovascular diseases and their diagnosis and treatment depends on the type and severity. Prompt treatment and lifestyle modifications can improve the outlook of a patient with cerebrovascular disease. Chiropractors are qualified and experienced to help patients with cerebrovascular disease recover from their symptoms. – Dr. Alex Jimenez D.C., C.C.S.T. Insight

 

The purpose of the article above is to describe cerebrovascular disease and its effect on overall health and wellness. Neurological diseases are associated with the brain, the spine, and the nerves. The scope of our information is limited to chiropractic, musculoskeletal and nervous health issues as well as functional medicine articles, topics, and discussions. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900 . �

 

Curated by Dr. Alex Jimenez �

 


 

Additional Topic Discussion: Chronic Pain

 

Sudden pain is a natural response of the nervous system which helps to demonstrate possible injury. By way of instance, pain signals travel from an injured region through the nerves and spinal cord to the brain. Pain is generally less severe as the injury heals, however, chronic pain is different than the average type of pain. With chronic pain, the human body will continue sending pain signals to the brain, regardless if the injury has healed. Chronic pain can last for several weeks to even several years. Chronic pain can tremendously affect a patient’s mobility and it can reduce flexibility, strength, and endurance.

 

 


 

Formulas for Methylation Support

 

Xymogen Formulas - El Paso, TX

 

XYMOGEN�s Exclusive Professional Formulas are available through select licensed health care professionals. The internet sale and discounting of XYMOGEN formulas are strictly prohibited.

 

Proudly,�Dr. Alexander Jimenez makes XYMOGEN formulas available only to patients under our care.

 

Please call our office in order for us to assign a doctor consultation for immediate access.

 

If you are a patient of Injury Medical & Chiropractic�Clinic, you may inquire about XYMOGEN by calling 915-850-0900.

xymogen el paso, tx

 

For your convenience and review of the XYMOGEN products please review the following link.*XYMOGEN-Catalog-Download

 

* All of the above XYMOGEN policies remain strictly in force.

 


 

What is Cerebral Perfusion Pressure?

What is Cerebral Perfusion Pressure?

Cerebral perfusion pressure, or CPP, is the net pressure gradient which carries oxygen to brain tissue. It is measured by the difference between the mean arterial pressure, or MAP, and the Intracranial Pressure, or ICP,� which is measured in millimeters of mercury (mm Hg). Regulating CPP is fundamental in the treatment of patients with intracranial pathology, including shock, hemodynamic distress, and traumatic brain injury. �

 

Although the average CPP is generally between 60 and 80 mm Hg, these values may change to the left or to the right depending on individual physiology. MAP and ICP has to be measured together because CPP is a calculated measure. Regulating CPP at hemodynamically unstable conditions with abnormal ICP or in cases of intracranial pathology will reduce the chance of ischemic brain injury. �

 

  • CPP = MAP – ICP

 

Cerebral Perfusion Pressure Physiology

 

CPP and ICP

 

At its own average range of 60 to 80 mm Hg, the CPP is determined by the ICP and the mean arterial pressure. Under regular standards, the ICP is between 5 and 10 mm Hg which has a reduced effect on the CPP than the MAP in clinical circumstances not associated with intracranial pathology. ICP is generally measured through intracranial pressure transduction.

 

Physiologically, the ICP is a function of intracranial compliance. Intracranial compliance is the relationship between the ICP and the volume of the intracranial cavity including cerebrospinal fluid, or CSF, brain tissue as well as arterial and venous blood volume. Because the skull is a fixed and rigid anatomic space, the ICP can increase if the intracranial volume increases while intracranial compliance decreases. As the ICP increases or intracranial compliance decreases, CPP also decreases. �

 

Several processes determine that ICP continues to stay within the average range for the longest extended period of time possible, especially throughout periods of affected intracranial volume and compliance. As volume adds to the intracranial space, CSF can shift into the spinal subarachnoid space, causing the ICP to continue significantly unchanged. As volume increases due to a growing space-occupying lesion, brain tissue edema or blood, this process ultimately becomes overwhelming, and ICP begins to increase substantially. �

 

Cerebral blood flow, or CBF, is also a fundamental factor in ICP homeostasis. Cerebral auto-regulation makes sure that steady blood flow is maintained in the brain over a wide range of physiologic alterations. When blood pressure decreases, auto-regulation causes cerebral vasodilation and an increase in CBF and cerebral blood volume, maintaining ICP and CPP. However, when blood pressure increases, auto-regulation causes cerebral vasoconstriction and a decrease in CBF with a decrease in cerebral blood volume, also regulating ICP and CPP. Too many changes outside of average CBF ranges can cause brain ischemia and injury. �

 

CPP and MAP

 

Because ICP in its average ranges is a considerably small number, the CPP generally depends on the mean arterial pressure. MAP is the normal blood pressure during one cardiac cycle which can be measured through invasive hemodynamic monitoring or calculated by the systolic blood pressure, plus two times the diastolic blood pressure, divided by three. The average range of MAP is 70 to 100 mm Hg. �

 

The average arterial pressure can be affected due to everyday activities, such as rest, stress, and exercise or physical activities. However, if the ICP continues to stay the same, the average arterial pressure can change across its significantly wide range without tremendously decreasing or increasing the CPP. As a matter of fact, CPP and CBF will continue to stay considerably unchanged across a wider range of MAP (50 � 150 mm Hg) than normal due to cerebral auto-regulation and vasoconstriction or vasodilation of cerebral vasculature. �

 

For patients with hypertension, the auto-regulation setpoint changes, decreasing the average arterial pressure associated with the patient�s normal arterial pressure, which causes vasodilation to increase CBF. Patients with lower than normal average arterial pressure at baseline will have auto-regulatory vasoconstriction as a reaction to an increase in their significant average MAP, to return CBF to baseline. When looking at CBF and CPP in the context of the patient�s average MAP, it is clinically significant based on the regulation of intracranial pathology and hemodynamic derangements. �

 

Cerebral Perfusion Pressure Complications

 

Diagnosing and treating cerebral perfusion pressure complications necessitates measuring both the ICP and the MAP. The MAP may be quantified through the utilization of invasive hemodynamic processes, most frequently cannulation of a peripheral artery such as the radial or femoral artery. The MAP may also be measured with a non-invasive blood pressure cuff by applying the formula mentioned above utilizing the systolic and diastolic blood pressures. � Intracranial pressure is generally measured through an intracranial pressure transduction device. The most common and most accurate method or technique is utilizing an intraventricular monitor. The intraventricular dimension of ICP is the normal standard. An intraventricular catheter is inserted into a hole drilled in the skull and into the lateral ventricle to gauge the pressure of the CSF. The benefit of an intraventricular catheter is that CSF could be eliminated, if needed, to decrease ICP. Considerable complications for the ICP include a possibility of bleeding, infection, and difficulty with proper placement. Options include sub-dural and intra-parenchymal monitors. �

 

The ICP can be measured non-invasively through several methods and techniques, including transcranial Doppler ultrasonography or TCD. TCD utilizes a temporal window to evaluate the speed of blood flow through the middle cerebral artery. Systolic and diastolic average flow velocity is utilized to determine a pulsatility index. The pulsatility index was determined to be closely associated with ICP in several research studies as well as be associated with ICP in other research studies. Therefore, it is not suggested to use TCD as a substitute for direct ICP dimension. Invasive diagnosis and treatment of the MAP through an arterial cannula and the ICP through an intraventricular catheter will give a continuous and accurate calculation of CPP. �

 

Cerebral Perfusion Pressure Clinical Significance

 

Two general types of pathologic health issues can ultimately occur where the regulation of the CPP is fundamental, such as intracranial pathology, where ICP regulation is essential and hemodynamic instability/shock where MAP regulation is the most essential. Intracranial pathology involves space-occupying lesions, such as tumors, epidural and subdural hematoma or severe intraparenchymal hemorrhage and cerebral edema as seen after ischemic injury, traumatic brain injury or acute hepatic encephalopathy. In these circumstances, average CPP depends on decreasing the ICP into a normal range as soon as possible while regulating the MAP. When CPP is normal, it’s fundamental to keep in mind that every individual’s brain tissue has a CPP that is “normal” in the context of that individual patient’s physiology, which may be affected by other health issues, such as hypertension or cardiovascular disease. Moving towards a more dynamic direction of the average CPP utilizing the patient’s personal auto-regulatory capacity. These diagnosis and treatment approaches involve more frequent and sophisticated monitoring and might not be readily available for widespread utilization. �

 

In the instance of considerable traumatic brain injury, significant cerebral edema can decrease intracranial compliance and CSF, developing an increased ICP or intracranial hypertension. Auto-regulatory mechanisms and techniques may or may not function normally and when ICP continues to be elevated, CPP will decrease causing further injury through an ischemic process. In circumstances such as these, together with starting the measures for decreasing the ICP, it is essential to prevent hypotension (MAP – ICP = CPP) and in some instances, allowing hypertension to reasonably occur. �

 

In circumstances of instability, the ICP is considerably stable as cerebral auto-regulation is undamaged. In the instance of hypotension, the MAP decreases due to blood loss, or hemorrhagic shock, intravascular leak, or distributive shock, and decreased cardiac output, or cardiogenic shock, and the CPP also decreases. It’s the association between MAP and CPP which carries resuscitation guidelines to recommend regulating a MAP greater than or equal to 65 mm Hg. With a normal ICP, this threshold must make sure that a CPP of 55 to 60, the minimum necessary to stop cerebral ischemic injury, is ultimately maintained. As in the circumstance of ICP and cerebral auto-regulation, the goal of MAP is to be within the context of an individual patient’s evaluation hemodynamic function. Patients with untreated hypertension must have increased MAP goals to maintain proper CBF and CPP. �

 

As previously mentioned in the following article, cerebral perfusion pressure, or CPP, is the net pressure gradient which affects cerebral blood flow to the brain, also known as brain perfusion. According to healthcare professionals, the CPP, or cerebral perfusion pressure, must be constantly regulated within a specific limit because too little pressure or too much pressure could potentially cause a variety of brain health issues. Cerebral perfusion pressure may be associated with a variety of neurological diseases. – Dr. Alex Jimenez D.C., C.C.S.T. Insight

 

The purpose of the article is to discuss cerebral perfusion pressure and its association with neurodegenerative diseases. Neurological diseases are associated with the brain, the spine, and the nerves. The scope of our information is limited to chiropractic, musculoskeletal and nervous health issues as well as functional medicine articles, topics, and discussions. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900 . �

 

Curated by Dr. Alex Jimenez �

 


 

Additional Topic Discussion: Chronic Pain

 

Sudden pain is a natural response of the nervous system which helps to demonstrate possible injury. By way of instance, pain signals travel from an injured region through the nerves and spinal cord to the brain. Pain is generally less severe as the injury heals, however, chronic pain is different than the average type of pain. With chronic pain, the human body will continue sending pain signals to the brain, regardless if the injury has healed. Chronic pain can last for several weeks to even several years. Chronic pain can tremendously affect a patient’s mobility and it can reduce flexibility, strength, and endurance.

 

 


 

Formulas for Methylation Support

 

Xymogen Formulas - El Paso, TX

 

XYMOGEN�s Exclusive Professional Formulas are available through select licensed health care professionals. The internet sale and discounting of XYMOGEN formulas are strictly prohibited.

 

Proudly,�Dr. Alexander Jimenez makes XYMOGEN formulas available only to patients under our care.

 

Please call our office in order for us to assign a doctor consultation for immediate access.

 

If you are a patient of Injury Medical & Chiropractic�Clinic, you may inquire about XYMOGEN by calling 915-850-0900.

xymogen el paso, tx

 

For your convenience and review of the XYMOGEN products please review the following link.*XYMOGEN-Catalog-Download

 

* All of the above XYMOGEN policies remain strictly in force.

 


 

Apoptosis in Neurological Diseases

Apoptosis in Neurological Diseases

Neural cell death can occur both during the development and throughout the pathophysiology of the nervous system. Two different types of cell death, known as necrosis and apoptosis, are involved in pathological neuronal loss, however, apoptosis is the process of programmed cell death during development. All types of cells will go through apoptosis. This mechanism controls neuronal growth where an excess of neurons is produced and only those which form connections with the target structures will receive enough survival factors. The remaining neurons will then ultimately go through death and removal. �

 

Apoptosis continues throughout life and it is the main process involved in the elimination of surplus, unwanted, damaged or aged cells. Dysregulation of apoptosis is demonstrated after damage or injury as well as in neurodegeneration and in tumorigenesis. Treatment approaches which influence the apoptotic pathway offer valuable therapeutic options in a wide variety of pathological states. The purpose of the article is to describe the significance of apoptosis in neurological diseases. �

 

What is Apoptosis?

 

Apoptosis is the well-conserved and highly controlled process of cell death involved in the removal of unnecessary, surplus, aged or damaged cells. Dysregulation of apoptosis can ultimately develop mutated cells which can result in malformations, autoimmune diseases, and even cancer. Abnormal apoptosis can also result in the elimination of healthy cells which can occur in health issues such as infection, hypoxic-ischaemic injury, neurodegenerative or neuromuscular diseases, and AIDS. �

 

Apoptosis is different from necrotic cell death. In necrosis, cell death is caused by an external factor and involves the early loss of tissue, damage to organs, and the leakage of cytoplasmic contents, leading to the recruitment of phagocytes which can cause an acute inflammatory reaction. In contrast, apoptosis is often considered cell suicide. According to research studies, cells which die due to apoptosis retain membrane and organelle structure and function until late in the process while still developing plasma membrane blebbing, reduced cytoplasmic volume, chromatin condensation, and nuclear fragmentation. �

 

In the final phases, cell fragments wrapped in plasma membrane pull away as apoptotic bodies which are then phagocytosed by healthy cells. The removal of cell debris also occurs in the absence of an inflammatory response, and this silent, quick, and efficient elimination of apoptotic cells mean that apoptosis can be difficult to find in cells. However, as many as 50 percent of the cells in developing adulthood may go through apoptosis where less than 1 percent of cells are apoptotic at any one time. �

 

Apoptosis in the Nervous System

 

Programmed cell death by apoptosis occurs in several developmental processes, such as body sculpting and removal of self-reacting resistant cells as well as sexual organ growth and gamete formation. The general principle of growth in multicellular organisms involves the development of excess numbers of cells, where the excess or unwanted cells are then removed by apoptosis through the development of functional organs. In the developing nervous system, apoptosis has been demonstrated to occur in neural tube formation and continues throughout terminal differentiation of the neural system. �

 

A growing number of neurotrophic factors, such as nerve growth factor family, including both the neurokines and development factors like insulin-like growth variables (IGF-I and IGF-II), encourage the survival of several types of neurons. Targeted disruption of genes encoding these factors or their receptors demonstrate that neurotrophic factors are significant for the development of specific neuronal populations. Neurotrophic factors function by binding to specific receptors in the cell membrane. Moreover, the effects of NGF offer a good illustration of the subtle command the system permits. �

 

The nerve growth factor receptor has high and low affinity components. It will function as a survival factor if it binds to the high-affinity trkA receptor but it will also cause apoptosis of retinal neurons or oligodendrocytes once it binds to the low-affinity receptor p75 in the absence of trkA. Nerve growth factor in the extracellular environment is consequently able to control neural development by both boosting the growth of several types of cells as well as the removal of other cells. �

 

In some cases, however, concentrated genetic disruption of neurotrophic factors or their receptors may leave the central nervous system seemingly unaffected, demonstrating that these variables can ultimately become biased. According to research studies, it has now become evident that the control of neuronal survival does not only depend on the supply of trophic molecules by the targets but also on activity, humoral factors, and trophic support from glia or glial cells. �

 

Furthermore, neurons don’t simply undergo programmed cell death during differentiation. Apoptosis appears to regulate cell numbers in systems as diverse as the disappearance of the germinal layer during the third trimester of pregnancy, the sexual differentiation of the medial preoptic nucleus where apoptosis is controlled by testosterone, lineages throughout the olfactory epithelium, oligodendrocyte development in the optic nerve, and the development of Schwann cells in the peripheral nervous system. Programmed cell death occurs in a variety of other processes in the developing nervous system. �

 

Apoptosis in Nervous System Injuries & Diseases

 

Although apoptosis is a fundamental process involved in the developing nervous system, apoptosis can ultimately be involved in a variety of nervous system injuries and diseases. In most cases, the connection between a specific mutation or trauma as well as the activation of apoptotic cascades remains evasive. An overview of a developing list of neurological diseases in which apoptosis has been implicated as a significant pathological mechanism is provided below. �

 

Neuronal Injury

 

Cerebral hypoxic-ischaemic injury is a cause of neurological injury and death. Magnetic resonance spectroscopy studies have demonstrated that transient hypoxia-ischemia contributes to a biphasic disturbance of cerebral energy metabolism. Related to the biphasic energy collapse, two waves of cell death appear to follow hypoxic-ischaemic injury in the developing brain. Immediate neuronal death is most likely due to necrosis resulting from the accumulation of calcium ions. �

 

Delayed cell death caused by hypoxic-ischemic injury appears to involve further mechanisms with increasing data which demonstrates that in the delayed phase, cell death occurs by apoptosis. The amount of apoptosis is directly associated with the magnitude of ATP depletion during hypoxia-ischemia. Apoptosis can occur in the brains of newborn babies following birth asphyxia and sudden intrauterine death. Apoptosis can also be notable in white matter injury in newborn babies. �

 

Apoptosis may continue for months after an hypoxic-ischaemic injury due to constant changes in cerebral energy metabolism in infants during the months after birth asphyxia. Following focal neural injury, apoptosis has been discovered in remote regions from the initial damage. After severe spinal cord injury in reptiles, apoptosis of oligodendrocytes occurs in distant degenerating fiber tracts and after forebrain injury in rats, apoptosis was demonstrated in the cerebellum. �

 

The apoptotic loss of oligodendrocytes could consequently be a potential source of secondary demyelination in paraplegia and in the chronic degeneration related to multiple sclerosis. Further research studies must be performed in order to provide further evidence on the role of apoptosis in this type of injury which begins from the report of which Bcl-2 expression boosts the growth and regeneration of retinal axons. Apoptosis in neuronal injury can be demonstrated in a variety of ways. �

 

Neural Cancers

 

A connection between apoptosis and the cell cycle is demonstrated in carcinogenesis where proto-oncogenes, such as c-fos, c-jun, and c-myc, can activate apoptosis and promote cell division while inactivation of the pro-apoptotic p53 tumor suppressor gene is a frequent mark of human neoplasia. By way of instance, in a number of gliomas, the reduction of wild p53 activity was connected to tumor progression, possibly leading to resistance to chemotherapy and radiotherapy. �

 

Although there have been reports of Bcl-2 overexpression in glioma cell lines, the correlation between the anti-apoptotic effect of this gene and malignancy is not yet clear. However, a homolog of Bcl-2, the brain associated apoptosis gene (BRAG-1), is found predominantly in the brain, and it is upregulated in human gliomas as a rearranged transcript. As demonstrated above, the process of apoptosis can also be significant in the development of neural cancers, according to research studies. �

 

Infectious Disease

 

Apoptosis may play a role in HIV encephalopathy. In the brain, the virus reproduces primarily in microglia which it enters through the CD4 receptor. Although the activation of microglia is believed to be the main reason for adrenal loss and demyelination, neurons die by apoptosis in HIV encephalopathies because of HIV mediated alterations in astrocyte function and aberrant stimulation of NMDA receptors or due to nitric oxide from the activation of inducible nitric oxide synthase. �

 

In subacute sclerosing panencephalitis, widespread apoptotic death was demonstrated to develop in the brain, although no correlation was observed between viral load, lymphocyte infiltration, and the number of apoptotic cells. DNA fragmentation indicative of apoptosis was detected in scrapie-infected sheep and mice brains, suggesting a function associated with cell death in spongiform encephalopathies. Apoptosis may also ultimately be involved in another infectious disease. �

 

Neurodegeneration

 

Spinal muscular atrophy is associated with mutations in the survival of motor neuron and neuronal apoptosis inhibitory protein (NAIP) enzymes. NAIP is closely related to the baculovirus inhibitor of apoptosis protein and inhibits apoptosis in many cell types. This implies that mutations in NAIP could deregulate apoptosis in spinal motor nerves, causing their death. Recent studies emphasize the importance of anti-apoptotic genes in cerebral protection which can rescue neurons. �

 

Apoptosis has also been implicated in retinal dystrophies such as retinitis pigmentosa. In this case, apoptosis results from mutations in the three photoreceptor genes, rhodopsin, peripherin, and the ?-subunit of cyclic guanosine monophosphate di esterase, resulting in photoreceptor degeneration. The absence of c-fos prevents apoptosis in those cells is unknown. Moreover, defined neurotrophins and growth factors injected intraocularly in animal models of retinal degeneration improve photoreceptor survival, suggesting that the apoptotic cascade can be obstructed by supplying exogenous survival signs. �

 

The mutation underlying Huntington’s disease is an expanded trinucleotide which is fundamental for normal development and can be regarded as a cell survival gene. Transgenic models demonstrated increased apoptosis in the neurons of an embryonic neuroectoderm. During apoptosis, caspase-3 (apopain) is improved by a gain of function associated with the triplet expansion. This is supported by the overexpression of specific trinucleotide repeats in transgenic mice. �

 

Most cerebellar ataxias are associated with neuronal loss. Ataxia-telangiectasia, caused by mutations in the ATM gene, is considered to have an apoptotic component. ATM shares extensive and significant homology with the DNA dependent protein kinases involved in DNA damage responses at different cell cycle checkpoints and is downregulated in most patients with ataxia-telangiectasia. The simple fact that inappropriate p53 mediated apoptosis is the major cause of death in ataxia-telangiectasia cells suggests that the mutation causes improper triggering of apoptosis by otherwise non-lethal DNA injury. �

 

From the familial form of amyotrophic lateral sclerosis gain of function, mutations in the gene encoding copper-zinc superoxide dismutase (sod-1) develop a dominant pro-apoptotic sign. Although cell harm by the accumulation of free radicals can trigger apoptosis, these mutants can induce apoptosis both in nerve cells in culture and in transgenic mice. Mental retardation in Down’s syndrome has also been associated with abnormal apoptosis. Although cortical neurons from fetal Down’s syndrome brains are different, they then degenerate and undergo apoptosis, according to research studies. �

 

Degeneration is blocked by treatment with free radical scavengers, suggesting that a defect in the metabolism of reactive oxygen species is the trigger for apoptosis. In Parkinson’s disease, the death of dopaminergic neurons in the substantia nigra was demonstrated to occur through apoptosis and may be obstructed by delivery of glial-derived neurotrophic factor. Alzheimer’s disease is associated with the progressive accumulation of ?-amyloid protein which is the fundamental component of neural plaques. The ?-amyloid peptide can cause neurons to undergo apoptosis in vitro research studies. �

 

Inherited Metabolic Disease

 

Furthermore, few data suggest that the acute encephalopathy associated with maple syrup urine disease is because of the induction of apoptosis by an accumulating metabolite of leucine, ?-keto isocaproic acid. This compound is a potent inducer of apoptosis in central nervous system glial cells and the result is significantly enhanced in the presence of leucine. Phenylalanine and leucine do not induce apoptosis in this system, suggesting that this result is ultimately unique. �

 

There are two ways in which a cell can die, necrosis and apoptosis. While necrosis occurs due to an external factor which harms the cell, apoptosis follows a controlled, predictable routine. Apoptosis is generally known as programmed cell death. Apoptosis, or programmed cell death, has many fundamental functions in the developing structures of the human body, however, research studies have demonstrated that abnormal apoptosis can be associated with the development of a variety of neurological diseases. – Dr. Alex Jimenez D.C., C.C.S.T. Insight

 

The purpose of the article above is to discuss the process of apoptosis, or cell death, in neurodegenerative diseases. Neurological diseases are associated with the brain, the spine, and the nerves. The scope of our information is limited to chiropractic, musculoskeletal and nervous health issues as well as functional medicine articles, topics, and discussions. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900 . �

 

Curated by Dr. Alex Jimenez �

 


 

Additional Topic Discussion: Chronic Pain

 

Sudden pain is a natural response of the nervous system which helps to demonstrate possible injury. By way of instance, pain signals travel from an injured region through the nerves and spinal cord to the brain. Pain is generally less severe as the injury heals, however, chronic pain is different than the average type of pain. With chronic pain, the human body will continue sending pain signals to the brain, regardless if the injury has healed. Chronic pain can last for several weeks to even several years. Chronic pain can tremendously affect a patient’s mobility and it can reduce flexibility, strength, and endurance.

 

 


 

Formulas for Methylation Support

 

Xymogen Formulas - El Paso, TX

 

XYMOGEN�s Exclusive Professional Formulas are available through select licensed health care professionals. The internet sale and discounting of XYMOGEN formulas are strictly prohibited.

 

Proudly,�Dr. Alexander Jimenez makes XYMOGEN formulas available only to patients under our care.

 

Please call our office in order for us to assign a doctor consultation for immediate access.

 

If you are a patient of Injury Medical & Chiropractic�Clinic, you may inquire about XYMOGEN by calling 915-850-0900.

xymogen el paso, tx

 

For your convenience and review of the XYMOGEN products please review the following link.*XYMOGEN-Catalog-Download

 

* All of the above XYMOGEN policies remain strictly in force.

 


 

Understanding the Life and Death of a Neuron

Understanding the Life and Death of a Neuron

For many years, most neuroscientists believed we were born with all the neurons we were ever going to carry in our brains. As children, we may develop new neurons to help create the pathways, known as neural circuits, which function as information highways between different regions of the brain. However, scientists believed that after a neural circuit was created, developing any new neurons could interrupt the flow of information and disable the brain’s communication system. �

 

Introduction to Brain Basics

 

In 1962, scientist Joseph Altman questioned this belief when he saw evidence of neurogenesis, or the birth of neurons, in a region of an adult rat’s brain known as the hippocampus. He then reported that newborn neurons migrated from their birthplace in the hippocampus to other regions of the brain. In 1979, another scientist, Michael Kaplan, proved Altman’s findings in the rat brain and in 1983, Kaplan found neural precursor cells in the forebrain of an adult monkey. �

 

In the early 1980s, a scientist attempting to explain how birds learn how to sing suggested that neuroscientists should once again analyze neurogenesis in the adult brain and start to determine how it can make sense. In several experiments, Fernando Nottebohm and his team revealed that the numbers of neurons in the forebrains of male canaries tremendously increased during the mating season. This was the same time in which the birds had to learn new songs to attract females. �

 

However, why did these bird’s brains create new neurons during such a vital time in learning? Nottebohm believed it was because new neurons helped keep new song patterns inside the neural tissues of the forebrain, or the region of the brain which regulates complex behaviors. These new neurons made learning possible. If birds developed new neurons to help them remember and learn new song patterns, Nottebohm believed that the brains of mammals may also be able to do the same. �

 

Elizabeth Gould discovered evidence of newborn neurons in a different region of the brain in monkeys. Fred Gage and Peter Eriksson also demonstrated that the adult human brain developed new neurons in a similar region. For several neuroscientists, neurogenesis in the adult brain is still an unproven theory. However, other neuroscientists believe that the evidence provides interesting possibilities associated with the role of adult-generated neurons in memory and learning. �

 

Architecture of the Neuron

 

The central nervous system, which includes the brain and the spinal cord, consists of two primary types of cells: the neurons and the glia. Glia outnumber neurons in several regions of the brain, however, neurons are the key structures in the brain. Neurons are information messengers. They utilize electrical impulses and chemical signals to transfer information between different regions of the brain and between the brain and the rest of the nervous system. Everything we think, feel, and do would be impossible without the utilization of neurons and the glial cells, known as astrocytes and oligodendrocytes. �

 

Neurons have three primary parts including a cell body and two extensions known as an axon and a dendrite. Within the cell body is a nucleus, which regulates the cell’s activities and holds the cell’s genetic material. The axon is characterized by a very long tail and it transfers messages from the cell. Dendrites are characterized similar to that of the branches of a tree and they receive messages from the cell. Neurons communicate with one another by sending chemicals, known as neurotransmitters, across a very small region, known as a synapse, found between the axons and the dendrites of adjacent neurons. � There are three types of neurons:

 

  • Sensory neurons: Transfer information from the sense organs, such as the eyes and ears, to the brain.
  • Motor neurons: Manage voluntary muscle activity and transfer messages from nerve cells in the brain to muscles.
  • All other neurons are known as interneurons.

 

Scientists believe that neurons are the most varied type of cell in the human body. Within these three types of neurons are hundreds of different types of neurons, each with specific message-carrying abilities. The way these neurons communicate with one another by establishing connections is ultimately what makes people unique in how we think, feel, and act. �

 

Birth of the Neuron

 

The range to which new neurons are created in the brain has been a controversial topic among neuroscientists for many years. Meanwhile, although nearly all neurons are currently present in our brains by the time we’re born, there’s recent evidence to support that neurogenesis, or the scientific word utilized to describe the birth of neurons, is a lifelong procedure. Neurons are born in regions of the brain which are full of neural precursor cells, known as neural stem cells. These cells have the potential to develop all, if not all, of the different types of neurons and glia found in the brain. Neuroscientists have discovered how neural precursor cells function in the laboratory. Although this may not be exactly how these cells behave when they are in the brain, it gives us data about how they may function when they are in the brain’s environment. �

 

The science of stem cells is still very recent and could ultimately change with further discoveries, however, researchers have discovered enough evidence to support as well as to be able to demonstrate how neural stem cells create the other cells of the brain. Neuroscientists refer to this as a stem cell’s lineage and it is similar in principle to the concept of a family tree. �

 

Neural stem cells increase by dividing into two and creating two new stem cells, two early progenitor cells, or one of each. When a stem cell divides to create another stem cell, it is believed to self-renew. This new cell has the potential to make more stem cells. When a stem cell divides to create an early progenitor cell, it is said to differentiate. Differentiation is when a new cell is more technical in structure and function. An early progenitor cell doesn’t have the potential of a stem cell to create several different types of cells. It can only make cells within their distinct lineage. Early progenitor cells may self-renew or go in either of two ways. One type will develop astrocytes. The other type will develop neurons or oligodendrocytes. �

 

Migration of the Neuron

 

Once a neuron is born, it must go to the region of the brain where it will function. But, how does a neuron understand where to go? And, what helps it get there? Neuroscientists have determined that neurons utilize two different methods to travel:

 

  • Several neurons migrate by following the long fibers of cells known as radial glia. These fibers extend from the inner layers to the outer layers of the brain. Neurons glide along the fibers until they reach their destination.
  • Neurons also travel by using chemical signals. Scientists have found special molecules on the surface of neurons, known as adhesion molecules, which bind with similar molecules on nearby glial cells or nerve axons. These chemical signals will also ultimately help guide the neuron to its final destination in the brain.

 

Not all neurons are successful in their journey. Scientists believe that only one-third of these neurons will reach their destination. Some cells die during the process of neuronal growth. Some neurons may also survive, but end up where they don’t belong. Mutations in the genes which regulate migration create regions of misplaced or abnormal neurons which can cause disorders, such as epilepsy. Scientists believe that schizophrenia is partially caused by misguided neurons. �

 

Differentiation of the Neuron

 

When a neuron reaches its destination, then it must begin to perform its initial function. This final measure of differentiation is one of the most misunderstood sections of neurogenesis. Neurons are in charge of the transfer and uptake of neurotransmitters, or chemicals which deliver information between cells. Depending on its location, a neuron may perform the role of a sensory neuron, a motor neuron, or an interneuron, sending and receiving specific neurotransmitters. �

 

In the developing brain, a neuron depends on molecular signals from other cells, including astrocytes, to determine its form and location, the type of transmitter it creates, and to which other neurons it can connect. These newborn cells establish neural circuits, or data pathways that connect from neuron to neuron, which is determined during adulthood. However, in the mature brain, neural circuits are already developed and neurons must find a way to fit in. As a new neuron settles in, it starts to look like enclosing cells. It then develops an axon and dendrites and begins to communicate with its neighbors. �

 

Death of the Neuron

 

Although neurons are the longest living cells within the human body, large numbers of them often die during migration and differentiation. The lives of some neurons can sometimes take unexpected turns. Several health issues associated with the brain, the spinal cord, and the nerves are the consequence of the unnatural deaths of neurons and supporting cells. �

 

  • In Parkinson’s disease, neurons which create the neurotransmitter dopamine die off at the basal ganglia, a region of the brain which controls body movements. This causes difficulty initiating movement.
  • In Huntington’s disease, a genetic mutation causes the over-production of a neurotransmitter known as glutamate, which kills neurons in the basal ganglia. As a result, individuals twist and writhe uncontrollably.
  • In Alzheimer’s disease, unusual proteins build up in and around neurons in the neocortex and hippocampus, sections of the brain which manage memory. When these neurons die, people lose their ability to remember and perform regular tasks. Physical damage to the brain and other regions of the central nervous system can also kill nerves.

 

Injury to the brain, or damage caused by a stroke, can kill nerves completely or gradually starve them of the oxygen and nutrients they need to survive. Spinal cord injury may disrupt communications between the brain and nerves when these lose their link to axons located under the site of injury. These neurons survive but they may lose their ability to communicate. �

 

Conclusion to Brain Basics

 

Scientists hope that by understanding more about the life and death of neurons, they could develop treatment options and perhaps even cures for brain diseases and disorders which ultimately affect the lives of many people in the United States. �

 

The most current research studies suggest that neural stem cells can generate many, if not all, of the several types of neurons located in the brain and the nervous system. Determining how to control these stem cells from the laboratory into specific types of neurons can develop a new supply of brain cells to replace the ones which have been damaged or died. �

 

Treatment approaches may also be created to take advantage of growth factors and other signaling mechanisms within the brain which tells precursor cells to make new neurons. This will make it easy to fix, reshape, and renew the brain from within. �

 

A neuron is characterized as a nerve cell which is considered to be the basic building block of the central nervous system. Neurons are similar to other cells in the human body, however, neurons are responsible for transferring and transmitting information throughout the human body. As previously mentioned above, there are also several different types of neurons which are in charge of a variety of functions. Understanding the life and death of neurons is essential to help understand the mechanisms of neurological diseases and hopefully their treatment and cure.� – Dr. Alex Jimenez D.C., C.C.S.T. Insight

 

The purpose of the article is to understand the life and death of neurons and how these relate with neurological diseases. Neurological diseases are associated with the brain, the spine, and the nerves. The scope of our information is limited to chiropractic, musculoskeletal and nervous health issues as well as functional medicine articles, topics, and discussions. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900 . �

 

Curated by Dr. Alex Jimenez �

 


 

Additional Topic Discussion: Chronic Pain

 

Sudden pain is a natural response of the nervous system which helps to demonstrate possible injury. By way of instance, pain signals travel from an injured region through the nerves and spinal cord to the brain. Pain is generally less severe as the injury heals, however, chronic pain is different than the average type of pain. With chronic pain, the human body will continue sending pain signals to the brain, regardless if the injury has healed. Chronic pain can last for several weeks to even several years. Chronic pain can tremendously affect a patient’s mobility and it can reduce flexibility, strength, and endurance.

 

 


 

Formulas for Methylation Support

 

Xymogen Formulas - El Paso, TX

 

XYMOGEN�s Exclusive Professional Formulas are available through select licensed health care professionals. The internet sale and discounting of XYMOGEN formulas are strictly prohibited.

 

Proudly,�Dr. Alexander Jimenez makes XYMOGEN formulas available only to patients under our care.

 

Please call our office in order for us to assign a doctor consultation for immediate access.

 

If you are a patient of Injury Medical & Chiropractic�Clinic, you may inquire about XYMOGEN by calling 915-850-0900.

xymogen el paso, tx

 

For your convenience and review of the XYMOGEN products please review the following link.*XYMOGEN-Catalog-Download

 

* All of the above XYMOGEN policies remain strictly in force.

 


 

The Annual Cost of Neurological Disease in the US

The Annual Cost of Neurological Disease in the US

Neurological diseases are characterized as health issues associated with the brain, the spine, and the nerves which connect them. Neurological disease is considered to be one of the most prevalent health issues with a high burden to the patients, their families, and society. However, there are now estimates of the burden of neurological diseases in the United States. �

 

Neurological Disease Prevalence and Costs

 

The most prevalent and costly neurological diseases, according to several recent research studies, include Alzheimer disease and other dementias, chronic low back pain, stroke, traumatic brain injury, migraine headaches, epilepsy, multiple sclerosis, spinal cord injury, and Parkinson’s disease. Many other neurological diseases were excluded due to their mixed etiologies. �

 

The most common neurological disorders described above cost the United States approximately $789 billion in 2014, which may increase as the elderly population increases between 2011 and 2050, according to a research study published in the Annals of Neurology. The research study demonstrates the price of the serious annual financial burden in the US and has been demonstrated as healthcare professionals have suggested budget reductions for federally-funded research studies. �

 

According to these demographic statistics, the American Neurological Association, or the ANA, commissioned a research study by former ANA marketing committee and public advocacy committee chair Clifton L. Gooch, MD, currently professor and chair of the Department of Neurology in the University of South Florida’s Morsani College of Medicine in Tampa. �

 

The research study, the Burden of Neurological Disease in the United States: A Summary Report and Call to Action, demonstrated the annual cost of the most prevalent neurological diseases, including Alzheimer’s disease and other dementias, chronic low back pain, stroke, traumatic brain injury, migraine headaches, epilepsy, multiple sclerosis, spinal cord injury, and Parkinson’s disease. Neurological disease ultimately affects an estimated 100 million people in the United States every year and, together with the costs of stroke and dementia alone, these are estimated to total over $600 billion by 2030. �

 

Figure demonstrating the annual costs of the most common neurological diseases.

 

Funding for Neurology in the United States

 

The tremendous and sustained capital investments made in cardiovascular and cancer research studies beginning in the 1970s have considerably increased lifespan. Ironically, however, the number of older adults who have a higher chance of developing neurological diseases have increased, which has developed a growing outbreak among healthcare professionals. �

 

“Preliminary research studies, including those of cancer, focus considerable research study investment to the neurological diseases which are impacting the quality of life and mortality of more and more people in the United States every year,” stated Gooch, referring to the $1.8 billion in funding for cancer and neurology research approved by Congress in 2016. �

 

“We hope the findings of the report will serve as a wake-up call to Congress to improve much needed clinical and basic research funding necessary to discover treatments which can mitigate, and finally cure, the considerable amount of neurological diseases which have developed profound consequences in our patients as well as for the national economy.” �

 

“The future of funding for neurological research studies was an issue in 2012 when the ANA voted to support this particular research study,” stated ANA President Barbara G. Vickrey, MD, MPH. “With the reductions now being suggested to the NIH funding from the President of the United States, this has become of even greater concern today. As representatives of the scholars working to eradicate these health issues, we feel we must raise our collective perceptions, armed with the facts.” �

 

Annual Cost of Neurological Disease Overview

 

Researchers gathered the information from the research study through a complete review of the world literature among the most prevalent and costly neurological diseases in the United States. To be conservative, researchers focused on the prevalence and cost estimates they considered to be the most comprehensive and accurate, excluding neurological diseases, such as depression and chronic pain, which frequently have mixed etiologies beyond primary nervous system injury. �

 

“A complete accounting of all neurological diseases would considerably increase price tag estimates,” wrote the authors of the research study. Indirect and direct costs for the most common neurological diseases previously mentioned above, have been demonstrated in the research study and were estimated according to maintenance standards for each health issue. �

 

Alzheimer’s disease and other dementias accounted for $243 billion of their $789 billion total, while chronic lower back pain represented $177 billion, and stroke represented $110 billion.�As well as documenting the fiscal costs of neurological disease, Gooch and his USF colleagues ultimately recommend an action plan for reducing the burden of these health issues through infrastructure investment in neurological research and enhanced clinical management of neurological disorders. �

 

Many research studies have demonstrated how several of the most common neurological diseases pose a serious annual financial burden in the United States. The most prevalent and costly neurological health issues, such as Alzheimer’s disease and other dementias, chronic low back pain or sciatica, as well as stroke, among other common neurological diseases mentioned above, have been estimated to have an annual cost totalling $789 billion in 2014, according to research studies. These annual costs have also been demonstrated to considerable increase further over time.� – Dr. Alex Jimenez D.C., C.C.S.T. Insight

 


 

The purpose of the article is to demonstrate the annual cost of several of the most prevalent neurological diseases. Neurological diseases are associated with the brain, the spine, and the nerves. The scope of our information is limited to chiropractic, musculoskeletal and nervous health issues as well as functional medicine articles, topics, and discussions. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900 . �

 

Curated by Dr. Alex Jimenez �

 


 

Additional Topic Discussion: Chronic Pain

 

Sudden pain is a natural response of the nervous system which helps to demonstrate possible injury. By way of instance, pain signals travel from an injured region through the nerves and spinal cord to the brain. Pain is generally less severe as the injury heals, however, chronic pain is different than the average type of pain. With chronic pain, the human body will continue sending pain signals to the brain, regardless if the injury has healed. Chronic pain can last for several weeks to even several years. Chronic pain can tremendously affect a patient’s mobility and it can reduce flexibility, strength, and endurance.

 

 


 

Formulas for Methylation Support

 

Xymogen Formulas - El Paso, TX

 

XYMOGEN�s Exclusive Professional Formulas are available through select licensed health care professionals. The internet sale and discounting of XYMOGEN formulas are strictly prohibited.

 

Proudly,�Dr. Alexander Jimenez makes XYMOGEN formulas available only to patients under our care.

 

Please call our office in order for us to assign a doctor consultation for immediate access.

 

If you are a patient of Injury Medical & Chiropractic�Clinic, you may inquire about XYMOGEN by calling 915-850-0900.

xymogen el paso, tx

 

For your convenience and review of the XYMOGEN products please review the following link.*XYMOGEN-Catalog-Download

 

* All of the above XYMOGEN policies remain strictly in force.