Tag Archives: Central Nervous System

Exploring Spinal Cord Injuries

June 1, 2015

The Evolving Science Of Spinal Cord Injuries

Spinal cord InjuryThe most important structure that plays the role of a link between the body and the brain is the spinal cord. It extends from the medulla oblongata of the brain through to the level of the first lumbar vertebrae. It is a cylindrical structure of nervous tissue that is composed of white and grey matter. On each of its sides, two consecutive rows of nerve roots emerge. These roots distally join forming the 31 pairs of spinal nerves. It is housed within the vertebral column. The spinal cord makes up approximately only 2% of the central nervous system but has very vital functions.

A spinal cord injury refers to any damage to any part of the spinal cord or damage of nerves at the spinal canal’s end. Below the site of the injury, there often occur permanent changes in sensation, strength and other body functions.

The subject of spinal cord injuries is not a new one. Many people are familiar with it and understand its financial implications. Many families have had to put up with hefty hospital bills after a spinal cord injury of a member. Special equipment like wheelchairs have had to be purchased to assist victims of spinal cord injury. Some victims even lose their jobs after a spinal cord injury due to inability to perform their tasks at the work place. This is a very serious financial blow to them considering the fact that they require large amounts of money to lead a normal life.

There is a complete relationship between the physical, financial, emotional and social implications of spinal cord injuries. For example when one suffers a spinal cord injury, they get paralyzed which calls for the purchase of special equipment. In some cases paralysis may lead to loss of a job. When one loses a job, they become emotionally affected and thus their social life is also greatly affected.

Spinal cord injuries are of different levels and seriousness depending on the site of injury. The vertebrae that make up the spinal column are grouped into sections. Since spinal injuries affect body functions below the site of injury, the higher the sight of injury, the more severe the dysfunction that results.

Spinal cord injury cure has been the focus of science for so long. New strategies are being developed and old strategies are being revised to make them better and improve their efficacy.

Regenerative strategies

The last two decades have witnessed tremendous efforts in attempt to enhance regeneration of spinal cord axon though many techniques. These techniques include neutralization of neurite inhibition, synthetic channel implantation, various cell transplantation and administration of neurotrophic factors. Some of these strategies have been applied to animal models and they have been so promising to the extent that their potential human application is being explored by clinicians. The main factor limiting recovery from a spinal cord injury has been attributed to the failure of the central nervous system to regenerate. All these strategies aim at making it possible for the axons in the central nervous system to regenerate. Expectations become high with the identification of growth inhibitory molecules in the central nervous system. It was thought that neutralizing these factors would allow for functional axonal regeneration in the central nervous system. But as happens to most seemingly bright researches, the dark side finally showed in this. There exist mixed results of therapeutic approaches that were based on this assumption. Neurons are suggested to differ in their regenerative abilities through similar extracellular environments by recent data. These neurons have also been shown by recent data to undergo a developmental loss of intrinsic regenerative ability. Intrinsic regenerative abilities are mediated by factors that include expression of:

  • Cytoskeletal proteins mediating the axon growth mechanics
  • Receptors for inhibitory molecules
  • Molecules in the intracellular signaling cascades mediating response to chemoattractive and chemorepulsive cues.
  • Surface molecules permitting adhesion of axon to cells in the growth path

Sharply contrasting to axon development, its regeneration involves internal protrusive forces. Micro tubules generate these forces either by transporting other skeletal elements like neurofilaments to the tip of the axon or through their own elongation. It is the complexity of the regeneration program that casts a dark shadow on the progress.

Multi- cell therapy

Spinal cord injuryTransplantation of cells replaces the damaged neural tissues and restores function after spinal cord injury. Successful results have been obtained with different cell types including adult neural stem cells, mesenchymal stem cells, fetal tissue, embryonic stem cells and myelin producing cells.

In transplants of fetal tissue combined with neurotrophic factors, axonal growth has been seen. Transplanting polymer guiding channels with Schwann’s cells also helps in achieving novel axonal growth towards a cell transplant.

It is important to note that enough immune suppression is needed lest the cell transplant will be rejected. Attention is currently focused on mesenchymal stem cells to try and circumvent this immunological rejection of transplanted cells. After transplantation, they differentiate into desired cells.

Even though multiple studies have shown success of these multi-cell strategies, it is still not clearly understood what mechanisms lead to functional improvement following transplant.

For more information about bone marrow transplant and stem cell transplantation, visit www.awaremednetwork.com. Dr. Dalal Akoury has years of experience in integrative medicine and will be of assistance.

While at it, visit http://www.integrativeaddiction2015.com to learn about the upcoming integrative addiction conference 2015. The conference will deliver unique approaches to telling symptoms of addiction and how to assist patients of addiction.

The Evolving Science Of Spinal Cord Injuries

 

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Methamphetamine Use May Risk Development of Parkinson’s Disease

March 25, 2015

Methamphetamine Use May Predispose Consumers to Future Development of Parkinson’s Disease

There are several neurodegenerative disorders but it will still not be right for anybody to talk about neurodegenerative disorders without mentioning the Parkinson’s disease. This disorder is the second most common after Alzheimer’s disease and it is affecting approximately ten million people worldwide. The probability of a person suffering from this disease increases with age with most people being diagnosed after the age of 50. Early in the course of the disease, the most obvious symptoms are movement-related. These include shaking, rigidity, slowness of movement, and difficulty with walking and gait. However, the symptoms worsens as time passes by, these may include cognitive and behavioral problems with dementia commonly occurring in the advanced stages of the disease. Other symptoms include sensory, sleep, and emotional problems. PD is caused by degeneration of midbrain dopaminergic neurons that project to the striatum. The loss of striatal dopamine is responsible for the major symptoms of the disease. Although a small proportion of cases can be attributed to known genetic factors, most cases of PD are idiopathic. While the etiology of dopaminergic neuronal demise is mysterious, a combination of genetic susceptibilities, age, and environmental factors seems to play a critical role. Dopamine degeneration process in PD involves abnormal protein handling, oxidative stress, mitochondrial dysfunction, excitotoxicity, apoptotic processes, and microglial activation or neuroinflammation.

methamphetamine

Studies on animals on methamphetamine toxicity

Studies done on animals have shown that methamphetamine can cause long-term dopamine terminal damage as well as dopamine neuronal body loss. In rodents, repeated administration of methamphetamine causes a decrease in dopaminergic markers such as tyrosine hydroxylase (TH) and dopamine transporter. Accompanied by a reduction in TH activity, reduced levels of dopamine and its metabolites and decreased levels of vesicular monoamine transporter 2 (VMAT2). These effects occur primarily in the striatum but also in the cortex, thalamus, hypothalamus and hippocampus. Methamphetamine induces neurotoxicity in a dose-dependent manner as do other amphetamine-derivatives like MDMA. Although partial recovery of TH and dopamine transport fibers occurs after methamphetamine administration, methamphetamine-induced neurotoxicity is persistent. In mice, the greatest dopaminergic fiber loss is seen 24 hours after methamphetamine administration. Neurotoxic effects persist for more than seven days after methamphetamine exposure and one month after MDMA exposure. Drugs that induce PD symptoms and TH loss such as MPTP in mice also show a partial recovery with time in nonhuman monkeys and mice. The time courses and degrees of TH and dopamine transport fiber recovery after methamphetamine or after MDMA exposure are similar, suggesting terminal regrowth, as these two proteins are independently regulated. Researchers have also noted that there is partial recovery of dopamine levels in the striatum strongly suggesting that the regrown terminals are functional. However the mechanisms responsible for partial recovery are not known, but it is speculated that it might involve compensatory sprouting and branching as has been reported for regrowth following MPTP-induced damage. Dopamine terminal recovery has also been described in rhesus monkeys and velvet monkeys, although it appears to occur on a slower timescale than in mice. Methamphetamine-induced dopaminergic damage persists for more than 12 weeks in velvet monkeys and more than 3 years in rhesus monkeys, demonstrating the persistence of methamphetamine-induced brain damage.

Methamphetamine Toxicity in the Substantia Nigra

This drug doesn’t only cause fiber loss in TH but also produces dopamine cell body loss in the substantia nigra as shown in tests in mice that were treated with 3 methamphetamine injections (5 mg/kg) at 3-hour intervals. From the counts it is evident that 20 to 25% dopaminergic cell loss, measured at different time are linked to exposure to methamphetamine. The observed pattern of TH-stained neuron loss is very similar to the pattern of Nissl-stained neuron loss, indicating that neuronal loss is specific to dopaminergic neurons. Dopamine cell body loss was confirmed via staining with Fluoro-Jade, a general marker of neuronal degeneration that fluoresces after administration of known dopaminergic toxins such as 6-OHDA and MPTP. Fluoro-Jade stains scattered neurons degenerated in the substantia nigra after methamphetamine treatment. there is a possibility that the lack of complete recovery of TH fibers in the striatum is related to the loss of dopaminergic neurons in the Substantia nigra similar to what occurs in Parkinson’s disease.

methamphetamine

Increased Risk of Parkinson’s Disease in Methamphetamine Abusers

There are literatures that have linked the abuse of amphetamine to the later development of PD. In a report of a study done by Callaghan and his colleagues, there is an increase in of PD in methamphetamine users in an epidemiological investigation based on data from California statewide hospital discharge records. The researchers identified 1,863 methamphetamine users, 9,315 patients hospitalized for appendicitis as a nondrug control group, and 1,720 cocaine users as a drug control group. All subjects were aged at least 50 years, had been hospitalized in California between 1990 and 2000, and had been followed for up to 10 years after discharge. The methamphetamine user group showed an elevated incidence of PD, with a 165% higher risk for development of PD than the patients from the control group. the results have been confirmed by the same group after doing the same research but in a much broader scope; 40,000 people hospitalized for methamphetamine versus 200,000 for appendicitis and 35,000 for cocaine and a 16-year follow-up period. From these two studies it is evident that methamphetamine use increases the chances of PD development in adulthood.

Drug abuse, addiction and independence are problems that people grapple with every day. These problems need to be treated effectively through integrative medicine. Dr. Dalal Akoury (MD) is an expert at this.  Call her on (843) 213-1480 for help.

Methamphetamine Use May Predispose Consumers to Future Development of Parkinson’s Disease

 

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Striatum Methamphetamine Toxicity

March 22, 2015

Methamphetamine Toxicity in the Striatum

The striatum is a crucial part of the brain. This part of the brain plays very important roles but it can be adversely affected by the use of stimulants and other drugs of leisure. Substances such as cocaine and methamphetamine produce their primary effects inside the brain by boosting the presence of dopamine which is a neurotransmitting chemical that activates the pleasure-producing neurons contained within the limbic system. As stated above the limbic system includes the hippocampus, along with several other brain structures. According to the results of two separate studies published in 2008 in the Journal of Neuroscience and Biological Psychiatry, the presence of either cocaine or methamphetamine alters normal adult neurogenesis inside the hippocampus and damages this region’s ability replenish its neuron supply.  It is no longer news that methamphetamine intoxication causes long-lasting damage to dopamine nerve endings in the striatum. However the mechanisms underlying this neurotoxicity are not yet known but oxidative stress has been linked to it.

methamphetamine

 

Microglia are the major antigen-presenting cells in brain and when activated, they secrete an array of factors that cause neuronal damage. Astoundingly, very little work has been directed at the study of microglial activation as part of the methamphetamine neurotoxic cascade. It has been report that methamphetamine activates microglia in a dose-related manner and along a time course that is coincident with dopamine nerve ending damage. Through tests done on mice scientists have discovered that prevention of methamphetamine toxicity by maintaining treated mice at low ambient temperature prevents drug-induced microglial activation. MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) not only damages dopamine nerve endings and cell bodies but also  causes extensive microglial activation in striatum as well as in the substantia nigra. Contrastingly, methamphetamine causes neither microglial activation in the substantia nigra nor dopamine cell body damage.

Dopamine transporter antagonists do not mimic the effect of methamphetamine on microglia. Hyperthermia, a prominent and dangerous clinical response to methamphetamine intoxication, has been also ruled out as the cause of microglial activation. Together, these data suggest that microglial activation represents an early step in methamphetamine-induced neurotoxicity. Other neurochemical effects resulting from methamphetamine-induced overflow of dopamine into the synapse, but which are not neurotoxic, do not play a role in this response.

Methamphetamine use on the rise despite effects

The use of methamphetamine has been on the rise despite the fact that it is a powerful stimulant drug that has adverse effects when abused as most people do. According to the UN Office on Drugs and Crime reported recently that abuse of amphetamines, including designer drugs such as methamphetamine and 3, 4-methylenedioxymethamphetamine, now exceeds that of cocaine and heroin on a global scale. This presents no sign that its use will decline any soon. Past researchers were able to establish a fact that methamphetamine causes persistent reductions of function in dopamine nerve endings of animals and humans. Methamphetamine neurotoxicity has been under intense study for over 20 years, but still there is much that still remains to be learned about how this dangerous drug causes damage to dopamine nerve endings. The theory that revolves around oxidative stress has been at the top of the speculations. Drug-induced oxidative stress is an attractive construct that can account for many of the effects of methamphetamine on the dopamine nerve ending such as inhibition of tyrosine hydroxylase activity as well as reductions in the dopamine transporter and the vesicle monoamine transporter. This may even be an early event that leads eventually to methamphetamine-induced apoptosis. However, the source of the reactant species that mediate methamphetamine-induced damage is not known.

methamphetamine

Due to their crucial roles they play in mediating the mediating damage to the nervous system, Microglia has attracted considerable attention. Immune like in many ways  these interesting cells become activated by damage and then transmigrate to sites of injury where they can secrete an array of factors  like cytokines, prostaglandins, nitric oxide, and superoxide that are known to have detrimental effects on neurons. However, the role of microglia in methamphetamine-induced damage to the dopamine system has received little attention. In 1994 a researcher, Bowyer and his colleagues noted for the first time that methamphetamine resulted in activation of microglia in striatum of treated rats. These investigators concluded that microglia were increased in response to nerve ending damage and were not apparently a cause of it.  Recently, another research was conducted to give an in-depth analysis of the effect of methamphetamine on striatal gene expression. Numerous genes linked to microglia were activated significantly within hours of methamphetamine intoxication, suggesting the possibility that microglial activation occurs earlier in the methamphetamine toxic cascade than previously thought.

Today there are researchers who are building on the initial analysis of methamphetamine and report the pharmacological characterization of microglial activation by methamphetamine in striatum. As mentioned before, striatum is an area dense in dopamine nerve endings and is known to be targeted for damage by methamphetamine. Microglial activation coincides with the onset of methamphetamine-induced damage in striatum and the extent of this effect is related to the degree of damage to dopamine nerve endings. Numerous nontoxic effects exerted by methamphetamine, such as inhibition of the DAT, increases in synaptic levels of dopamine, activation of D1 and/or D2 DA receptors, and hyperthermia, cannot explain methamphetamine-induced microglial activation.

Finally, this is still a dark area and there is need for more literature so as to establish the mechanism of methamphetamine toxicity on the striatum. Needless to say, Drug abuse, addiction and independence are problems that people grapple with every day. These problems need to be treated effectively through integrative medicine. Dr. Dalal Akoury (MD) is an expert at this.  Call her on (843) 213-1480 for help.

Methamphetamine Toxicity in the Striatum

 

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Natural Remedies for Insomnia Caused By Addiction

March 18, 2015

Use of Chamomile, HOPS, Passion Flower, Valerian Roots, Californian Poppy for Insomnia Caused By Addiction

According to National Sleep Foundation, insomnia is difficulty falling asleep or staying asleep, even when a person has the chance to do so. People with insomnia can feel dissatisfied with their sleep and usually experience the symptoms of poor sleep that may deter them from enjoying healthy lifestyles. This disease can affect people of all ages but adults are the major victims.

This foundation further stresses that, sleep is essential for a person’s health and wellbeing. But still there are millions of people who do not get enough sleep and many suffer from lack of sleep. NSF conducted survey between 1999-2004 that revealed that at least 40 million Americans suffer from over 70 different sleep disorders and 60 percent of adults report having sleep problems a few nights a week or more. Most of those with these problems go undiagnosed and untreated. In addition, more than 40 percent of adults experience daytime sleepiness severe enough to interfere with their daily activities at least a few days each month – with 20 percent reporting problem sleepiness a few days a week or more. Furthermore, 69 percent of children experience one or more sleep problems a few nights or more during a week.

insomnia

However insomnia can also be caused by addiction. And so far it is one of the serious symptoms of addiction. Drugs of abuse for example alcohol has been shown to interfere with normal sleep patterns since they disrupt particular neurotransmitters in the brain which control or regulate sleep. When these neurotransmitters are disrupted, disturbances can result. Small amounts of alcohol can cause early sedation or sleepiness, and is often used as a sedative. However, the use of alcohol as an effective sedative can be extremely misleading because the side effects that can result are usually even more harmful and detrimental to the natural sleep cycle. For instance, due to the natural elimination of alcohol from the body, arousal and sleep fragmentation can occur and the second half of the sleep period can be drastically interrupted. This is due to the fact that, although alcohol will cause sedation, it will also decrease rapid eye movement sleep in the first half of the night resulting in the rebound of rapid eye movement sleep later in the night.  Here are some of the natural ways through which addiction induced insomnia can be treated.

Passion flower

Passion flower is a good remedy for sleep disorders that had been previously got approved in the U.S as an over the counter sedative and sleep aid. However by this time its safety and effectiveness had not been approved and it was consequentially taken off market. This product can be used alone or in combination with other herbs to help cure insomnia that is induced by drug addiction. Some researchers opined that when passion flower tea is taken an hour before going to bed it may help to improve the quality of sleep. However there is still need for evidence to show it does all these effectively.

California poppy- also known as Eschscholzia californica, California poppy is a good remedy for sleep disorders. It works as a sedative and is known to promote sleep. Currently it can be found in different herbal remedies sold in the U.S for cure of insomnia, as relaxants and therapies for anxiety. Owing to its mild sedative and analgesic properties, it can be given safely to children. Clinical and laboratory work on California poppy has clearly demonstrated the plant’s sedative and anti-anxiety properties.  It has also been shown to improve both sleep latency and quality. You can use it solely or in combination with other herbs to help cure insomnia.

Hops – scientifically its known as Humulus lupulus

insomniaThe use of Hops dates back to early 1900s when Eclectic physicians used it as a sedative specifically for insomnia due to worry or nerve. This herb that is used as a major flavoring component of beer has been used for a long time to cure insomnia, nervousness, and restlessness. Hops pillows are sometimes used for mild insomnia. Having been used successfully in the past, trying it won’t hurt you.

Chamomile:  is scientifically known as Anthemis nobilis. This herb has been used as sedative for a long time and can be safely used with children as well as adults. In South America, Europe and Mexico chamomile tea is a common beverage that is honored for its effectiveness in curing such conditions as irritability, restlessness and insomnia both in children and adults. What’s more? Its oil can also be used in bathing waters to help soothe nerves. Its oil can also be used for massage. Chamomile is still one of the sought after sedatives with proven effectiveness.

 

Valerian: is scientifically known as Valeriana officinalis.  This is a common herb in the U.S where it is used widely for cure of insomnia restlessness and nervousness. This herb can reduce the time people take before falling asleep and is known to shorten sleep latency. When used it reduces chances of a person waking up in the night. As a herbal sedative, valerian has many benefits yet no known side effects that synthetic sedatives are loathed for. It can be used in combination with Hops, California poppy and chamomile among others.

These herbs are an excellent way to help you fight insomnia naturally. We at AWAREmed health and wellness center are dedicated to finding the best natural solutions to health problems. You can visit us at Myrtle Beach South Carolina where you will be attended to by Dr. Dalal Akoury (MD) who has vast experience in integrative medicine for lifestyle diseases.

Use of Chamomile, HOPS, Passion Flower, Valerian Roots, Californian Poppy for Insomnia Caused By Addiction

 

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GABA Restoration In Addiction Therapy

March 8, 2015

Role of GABA restoration in addiction therapy

There are several drugs of pleasure that people use today. The problem is not exactly in the use of the drugs but rather in the effects they create in the brain. Addiction contrary to what many people think is not a problem with how frequent you take a drug but what even a single puff of or drop of a drug will cause to your brain and the entire nervous system. Composed of the individual nerve cells also known as neurons the nervous system serves as the network in the body. Without this network all communications between the nerve cells will be broken and a person will be incapacitated to even do a simple task as blinking. Typically, nerve signals are transmitted through the length of a neuron as an electrical impulse. When a nerve impulse reaches the end of the neuron it can jump over to the next cell using chemical messengers called neurotransmitters. Therefore without the neurotransmitters the nerves will not be able to send impulses over to other nerve cells in order to initiate specific actions. The neurotransmitters have vital functions in the central nervous system. In the central nervous system these neurotransmitters send impulses between neurons. The functions of the neurotransmitters is not limited to the central nervous system alone but are also crucial in the peripheral nervous system where they send impulses between neurons and gland cells. The peripheral nervous system is composed of nerves that link the central nervous system to the rest of the body.

There are two types of neurotransmitters, the inhibitory transmitters which are known to restore calm in the brain especially after the use of leisure drugs that are known to induce euphoric effects by raising the levels of dopamine and the excitatory neurotransmitters that fires the brain. GABA is one of the inhibitory neurotransmitters that counter the effects of leisure drugs and restores calm in the brain.

GABA restoration

GABA is one of the most abundant neurotransmitters in the central nervous system, and especially in the cerebral cortex. The brain cortex is where thinking occurs and sensations are interpreted. As mentioned above GABA is the primary inhibitory neurotransmitter brain and it helps in tranquillizing stressful, anxious and worrying thoughts. What happens with most drugs of leisure is that they cause instability in the brain leading to anxiety, stress and even depression. These are symptoms of low GABA. Addiction is a cause of low GABA as most drugs deplete GABA. There are several ways through which this can be medically corrected but those with addiction issues usually turn to their drugs as a means of self-medication but this only worsens the situation leading to anxiety and depression. Tranquilizers and downers are no better solutions to low GABA symptoms but finding a safe GABA regulation therapy may help in addiction treatment. The other cause for use of downers and tranquilizers is the rise in the level of norepinephrine. A rise in this neurotransmitter often induces the use of cannabis sativa.

The roles of GABA in the Brain

Made from glutamate in the brain cells, GABA works as an inhibitory neurotransmitter blocking nerve impulses. It is this neurotransmitter that inhibits the actions of dopamine when elevated in level by drug use. Glutamate acts as an excitatory neurotransmitter and when bound to adjacent cells encourages them to fire and send a nerve impulse. However, GABA does the opposite and tells the adjoining cells not to calm, not to send an impulse.

To those with inadequate level of GABA the activities of the excitatory neurotransmitters will not be inhibited and therefore the impulses they send will not be regulated and this often leads to anxiety disorders such as panic attacks, seizures, addiction, Parkinson’s disease and cognitive impairment.

GABA is the most effective neurotransmitter in inhibiting the transmission of nerve impulses from one neuron to another. When this happens it restores calmness in the brain however when drugs are used they inhibit the release of GABA, when GABA release is inhibited there will be more nerve transmissions occurring. These drugs inhibit the release of GABA by causing molecules to bind on neurons near GABA reducing its effect on the neurons. Benzodiazepines and other drugs are known to work in this style, they may also mimic the activities of GABA thereby inhibiting its transmission.

GABA rESTORATION

Need For GABA restoration in addiction Treatment

After a long term use of certain drugs, the level of GABA will be depleted to a point where it will be at an all-time low. This will lead to myriad of complications as the nerve impulses will be unregulated. This will lead to such problems as anxiety, depression, cognitive impairment and seizures among other diseases. Without restoring the level of GABA to healthy limits, any attempt to treat an addict will be ineffective.

Finally, Drug addiction treatment is a complex procedure that needs the input of an experienced integrative doctor. the health of neurotransmitters matters a lot and now that it is known that some drugs depletes these neurotransmitters there is need for treatment of addiction in a manner that restores the functions of the entire nervous system. This is why here at AWAREmed we are dedicated to finding the best solutions to addiction and dependence on substances. Dr. Dalal Akoury (MD) is always in the mood of helping any patient to be addiction free. Do not hesitate to call on her for help in managing any sort of chronic pain as well as other diseases.

Role of GABA restoration in addiction therapy

 

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