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Post-Traumatic Seizures and Anxiety



  • Post-Traumatic Seizures and Anxiety
  • Case Reports in Medicine
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  • Since the risk of recurrence after a single late post-traumatic seizure is over .. abdominal rising feeling), psychic (fear or sense of impending doom, anxiety. PTE and post-traumatic seizures (PTS) have both been used to describe . article by Bushnik et al., these issues include anxiety, depression, poor self- esteem. Post-traumatic epilepsy (PTE) is by definition from a focal (localized) injury, and the frontal and temporal lobes are the most frequently affected.

    Post-Traumatic Seizures and Anxiety

    According to AIP, traumatic memories left insufficiently processed lead to distorted thoughts and problematic behaviors and reactions Shapiro, The primary goal of EMDR is to encourage processing of the trauma memory with the underlying hypothesis that processing will help correct distorted thoughts and maladaptive behaviors.

    Both sertraline brand name: Zoloft and paroxetine brand names: Pexeva, Paxil are SSRIs that increase the neurotransmitter serotonin in the synaptic cleft therefore increasing brain activity stimulated by serotonergic stimulation by inhibiting its reuptake.

    While SSRIs can be effective, the results of the medication have not been shown to last after discontinuation. Although Prolonged Exposure is highly supported and evidence based, patients may be interested in other new treatment options and alternatives. There are other treatment methods with some preliminary research support that may also help individuals with PTSD. Although not yet empirically supported, researchers are working to strengthen these up and coming treatment options to be viable treatment alternatives or enhancements to PE.

    Virtual reality methodologies have been used as a way to enhance engagement in existing Prolonged Exposure therapy. Especially when people have experienced combat-related traumas, the use of virtual reality enables patients to be immersed in safe and controllable situations that will allow them to confront their traumas. Virtual reality headsets can provide the patient with auditory and visual experiences which simulate situations related to their past traumas and lessen the need for patients to recall all of the details on their own.

    The use of virtual reality seems like a promising addition to Prolonged Exposure and its use has been supported in many preliminary studies. However, further controlled and standardized studies are needed to standardize treatment protocol and examine treatment outcomes.

    One of the main limitations of VR is that the scenarios are developed for very specific situations and each traumatic event would require a new VR environment. This would be very expensive, and potentially limit the accessibility of the already underutilized treatment of PE.

    TMS is a type of treatment most commonly used for hard to treat depression. Although the specifics of how TMS works are unclear, it is thought to activate areas of the brain responsible for mood control by delivering a painless magnetic pulse. The initial results have been promising but limited, and further control trials should be conducted to examine the clinical application of TMS as a treatment for PTSD. This treatment would focus on increasing the ability to be present in the moment, increasing the connection between the self and the body, and personal growth.

    PTSD is a disorder that many people experience with varying frequency. In general, roughly 3. Additionally, women were more than twice as likely as men to have PTSD both in the last year and during their lifetime. PTSD rates are even worse still in inner city populations, with a lifetime prevalence of about Anyone experiencing a traumatic event has some risk for developing PTSD.

    Any type of traumatic experience can increase the risk for PTSD. For example, sexual assault, physical assault, combat, natural disaster, and car accidents are all examples of traumatic experiences, and each of these are associated with increased risk for PTSD.

    Some people have a higher chance of developing PTSD in response to trauma based on factors present before the trauma. Biological factors, such as inherited genes, can make us more or less likely to respond to a traumatic event with symptoms of PTSD. Additionally, growing up in a stressful environment or experiencing other traumas in the past can increase the chance that a person will respond to trauma with PTSD. The experience of mental health or psychological symptoms prior to trauma can also increase the chance that an individual will experience PTSD symptoms in response to trauma.

    Although each of these factors increase the risk for developing PTSD, it does not mean that PTSD is inevitable for an individual with these risk factors. In fact, many people with these risk factors do not go on to develop PTSD in response to trauma. It is also possible to develop PTSD even if you do not have any risk factors prior to the experience of trauma.

    Most people experience PTSD-like symptoms in the weeks after a traumatic event. For many, these symptoms begin to go away on their own and they experience a natural recovery. For others, these symptoms linger for longer at least one month and that is when a diagnosis of PTSD is made. Similarly, being discouraged from talking about or disclosing trauma can also increase the chance that an individual develops PTSD. The experience of other major life stressors soon after trauma can also increase the chance of developing PTSD symptoms.

    Following trauma, positive social support and connection are thought to be important in promoting psychological healing and recovery. For adults, within the last 12 months, approximately 3. PTSD is rarely the only concern a person has once the disorder becomes chronic. In fact, PTSD is second only to depression in the likelihood of a person presenting with multiple psychiatric diagnoses.

    For instance, people with PTSD are twice as likely as someone without PTSD to have gastrointestinal concerns, are over three times as likely to have a metabolic or autoimmune issue, and two and a half times more likely to have a neurological problem. There are varying ideas about why this comorbidity is so prevalent, but the self-medication hypothesis has the most support. People often find this solution quite helpful in the short-term, but over time, usually leaves a person with two chronic, interconnected, and very debilitating problems that are difficult to tease apart from one another.

    This is particularly problematic for this group of individuals because PTSD has a unique impact on SUD treatment that few other psychiatric disorders have.

    The presence of PTSD often leads to early SUD treatment dropout, a more rapid relapse rate to substance use after SUD treatment ends, and a more complicated presenting list of problems at the beginning of treatment. The good news is that more and more research is now confirming that these two disorders can be treated simultaneously without increasing the risk for SUD treatment failure.

    The key at this point is to train clinicians to treat both disorders at the same time versus continuing to adhere to the idea of obtaining a period of sobriety first and then working on trauma related symptoms later.

    Similarly, the co-morbid rates of borderline personality disorder BPD and PTSD vary by study, however, it is agreed upon that these two disorders often co-occur. Once again, either of these disorders alone can be incredibly debilitating, but when paired together the course of treatment can be much more complicated. It is suggested that some of the most dangerous behaviors associated with BPD suicidality and non-suicidal self-injury like cutting can be very effective at reducing the distress caused by PTSD symptoms.

    As with initial substance use, these behaviors often bring short term relief from PTSD symptoms but unfortunately, what seems to occur in the long term, is a painful and chronic back and forth between ongoing PTSD symptoms and the need for coping with those symptoms by relying on self-injurious behaviors.

    Once again, by delivering a concurrent treatment model for both presenting problems, addressing the symptoms of PTSD enhances the outcomes of DBT. The exact opposite actually occurs. The take home message is that concurrently treating both disorders sooner versus later gives a person the best chance at recovery from both.

    The prevalence rates for eating disorders anorexia nervosa, bulimia nervosa, binge eating disorder in the United States vary by gender and disorder anywhere from 0. As one researcher reported, eating disorders have the highest mortality rates of any mental illness. Of particular concern is the comorbidity of binging and purging behaviors and PTSD.

    For example, when a person with anorexia also engages in binging and purging behaviors their risk for PTSD is significantly greater than those who are mainly engaged in restrictive behaviors. Once again, the relationship between binging and purging is associated with an effective short term relief from PTSD related distress. Research indicates that those who engage in binging and purging experience a self-soothing short-term experience that is very relieving and likely to increase the use of those behaviors the next time a person feels distress associated with their PTSD symptoms.

    Therefore, another chronic and vicious cycle of relying on certain coping behaviors in the short term that ultimately creates two difficult disorders to address over the long term.

    Therefore, again, the treatment goal is to provide concurrent treatment for both disorders simultaneously. This remains an idea that is growing more popular within the ED field but actual implementation of treatment research demonstrating how concurrent treatment in this population could be done effectively remains scarce.

    For those not familiar with PNES, this can be an extraordinarily debilitating disorder without a lot of evidence based treatments for it. Therefore, PNES is a diagnosis given due to the symptoms of seizures but the seizures are conceived of as symptoms of an underlying psychological condition which means PNES must be treated by mental health professionals. Especially interesting is that when the PTSD is effectively treated, out of 13 pilot cases, all experienced a significant decrease in seizure frequency and many experienced their seizures stopping completely.

    By addressing PTSD, clinicians are also more effectively able to treat a variety of other comorbid conditions that are functionally related to the development of PTSD. Immediate and early seizures belong to the group of provoked seizures and they do not define epilepsy since they are not underlying a pathogenic mechanism that chronically predisposes the patient to manifest epileptic seizures [ 2 ].

    Post-traumatic epilepsy is determined by the presence of late seizures and therefore unprovoked. Post-traumatic epilepsy PTE is the most frequent cause of epilepsy in young adults as they are more at risk of the exposure to head injury [ 3 , 4 ]. Traumatic head injury TBI represent one of the most important epilepsy risk factors in children, with increased epilepsy risk 7.

    The study of PTE epidemiology stems from the analysis of military records at the beginning of the twentieth century, with reference to the American Civil War, to the First World War, to the Second World War and other more recent studies have been carried out on traumatized soldiers from the Korean War and the War in Vietnam [ 7 - 11 ].

    Severe traumatic brain injuries tend to correlate with an increased risk of developing early and late post-traumatic seizures compared to mild and moderate TBIs [ 12 ]. Obtaining reliable epidemiological data on the frequency of epilepsy in patients with TBI requires prospective studies with long periods of follow-up at least 10 years.

    Although, at a distance of years, it is difficult to establish, with certainty, a direct cause-effect correlation between head trauma and incident epilepsy In industrialized countries the proportion of epilepsy attributed to brain injuries is higher in past studies than in recent ones [ 4 , 13 ]. TBIs and other risk factors have actually modified their frequency over time; the reasons are attributable to modification in socio-economic status and amelioration in emergency health care.

    However, improved survivorship of severe traumatized patients could increase proportion of PTE in future epidemiological investigations. Early PTSs occur in various series of cases with a variable frequency comprised between 2. In the infant population early epileptic seizures are much more frequent compared to late seizures and they very often tend to occur as immediate seizures within 24h [ 16 ].

    In general, severe TBIs are associated with a high frequency of early crises, with rates that in adults are times higher in comparison with mild and moderate TBIs [ 17 ].

    Frequency rates of late PTSs are variable in different studies with values comprised between 1. PTE frequency and incidence studies in military populations inevitably show higher rates compared to studies carried out in the general population, with regard to a higher risk of severe TBIs. A patient with mild TBI shows a normalization of the risk incidence ratio 1.

    Epidemiological studies have generally revealed a higher risk of early and late seizures in relation to the severity of the head injury [ 18 ]. The characteristics of the trauma and the presence of any associated lesions represent risk factors for a successive development of early and immediate PTSs or late PTSs.

    A recent study [ 19 ] that retrospectively compared a population of subjects without head injury non TBI group and subjects with moderate and severe TBI with skull fracture revealed, on behalf of the latter, a relative risk of In the past, Jennet [ 20 ] showed that the presence of compound depressed skull fractures was associated to a higher general risk of early and late PTSs.

    The studies found the following risk factors for early epileptic seizures: Risk factors for late PTSs are acute subdural hematomas, acute subdural hemorrhage, multiple brain contusions, age over 35, transient amnesia which lasts more than 24 hours and male gender [ 19 ]. Some studies have considered the presence of early PTSs as a risk factor for late PTSs in adults [ 20 , 21 ], but this is certainly not true for the infant population [ 20 ] and according to Annegers [ 14 ], it is not even a risk factor for the adult population.

    Acute subdural hematoma is the intracranial lesion which has highest risks of developing both early and late PTIs. The role of genetic susceptibility that regulate response to cerebral injury is not clear; most of epidemiological studies did not found that family history of epilepsy could represent a significant risk factor for early and late PTSs [ 22 ]. Patients with PTE in most cases have focal epilepsy or focal epilepsy with a secondary generalization.

    The clinical characteristics of the seizures depend on the location of the lesion and the precocity of the secondary generalization. In patients with a history of trauma in childhood less than five years can manifest mesial temporal lobe epilepsies, as a trauma in the temporal region at an early age can induce the appearance of mesial temporal sclerosis [ 23 , 24 ].

    The infant population undoubtedly has a higher probability of SE compared to the adult one. Patients with high frequencies of PTSs during the first year after injury have a low probability of remission. There are several structural, physiological and biochemical modifications occuring in a brain after a head injury. A cranial trauma creates a potentially epileptogenic brain damage through a number of different mechanisms, which are not yet fully elucidated.

    In fact, different pathogeneses recognize early seizures and late seizures. The studies in this regard made use of animal and in vitro models with PTE.

    In , Willmore [ 26 ] used an animal model where iron ferric chloride was injected into the cortex of rats, with an evidence of epileptiform anomalies in EcoG recordings after convulsive epileptic seizures. Direct inoculations of hemoglobin into brain cortex were used in other animal models [ 27 ] recently; some authors studied a PTE model induced by lateral fluid percussion of the rat cortex, with the detection of an increased susceptibility to seizures at a distance of 30 days [ 28 ].

    In vitro models, thin layers of hippocampus are used in order to evaluate the response of the micro cortexes correlated to mechanic injuries or any changes in the concentrations of neurotransmitters. Immediate and early seizures are considered direct reactions of a brain damage and they are correlated to an altered vessel regulation of the local cerebral blood flow, to an alteration of the hematic-encephalic barrier and to an increase of the intracranial pressure with focal or diffused presence of ischemic, hemorrhagic, inflammatory or necrotic damage [ 29 ].

    The results of studies conducted on animal models of chronic epilepsy have suggested that late seizures are caused by two main pathogenic pathways: The result of this sequence of events is a reduction of the chronic convulsive threshold of a group of neuronal cells. The excitotoxic mechanism is explained by the extra cellular increase of excitatory amino acids immediately after injury, with increased levels of glutamate and aspartatic acid [ 30 ].

    These traumatized cells tend to assume excitatory aminoacids more readily than controls and present increased expression of the sodium-coupled neutral amino acid transporters subtypes 1 SNAT1 and subtypes 2 SNAT 2 [ 31 ]. Traumatized in vitro cells tend to form axonal sprouting with a higher immunoreactivity to GAP 43 Grown Associated Protein ; these cells show an altered excitability, evidenced by the presence of synaptic potentials with prolonged post-synaptic components [ 32 ].

    According to some authors [ 33 ], the impaired neuronal plasticity in injured brain areas can promote the appearance of focal dysplasia if TBI occurs soon after birth when the process of neuronal migration is not yet fully completed. In patients with seizures at a short distance from cranial trauma it is necessary to exclude other potential causes of provoked seizures. A trauma patient often presents conditions of metabolic and circulatory instability, with high probability of alteration in the biochemical parameters, such as hyponatremia, which may lower the epileptogenic threshold.

    Case Reports in Medicine

    One of the problems that can occur after a traumatic brain injury (TBI) is seizures. Although most people who have a brain injury will never have a seizure, it is. The diagnosis may be suspected in patients with seizures related to mild TBI and in patients with a history of post-traumatic stress disorder (PTSD), said Martin. We present a year old man who developed nocturnal attacks after experiencing psychological trauma: seeing a colleague fall and die in.

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    One of the problems that can occur after a traumatic brain injury (TBI) is seizures. Although most people who have a brain injury will never have a seizure, it is.

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