Cognitive Processing Therapy (CPT) for Trauma and PTSD

Phobia Release Program

The curative methods that are described in the 5-Day Phobia Release Course are psychologically proven and are vouched for by many phobic patients, who no longer feel the fear. Each technique is something that you can perform them on your own. Each technique is easy, described in plain, ordinary English and requires no more than a couple of minutes to do. In all, the course contains 9 exercises, organized into 5 days for your convenience. You also receive some background information about Neuro-Linguistic Programming and references for further reading on Nlp if you are interested in learning more.

Phobia Release Program Summary


4.6 stars out of 11 votes

Contents: E-book And Audio Course
Author: Jan Heering
Price: $67.00

My Phobia Release Program Review

Highly Recommended

The very first point I want to make certain that Phobia Release Program definitely offers the greatest results.

This ebook does what it says, and you can read all the claims at his official website. I highly recommend getting this book.

Download Now

Posttraumatic Stress Disorder

There is extensive clinical evidence that NE plays a role in human anxiety. Well-designed psychophysiological studies have been conducted that have documented heightened autonomic or sympathetic nervous system arousal in combat veterans with chronic PTSD. Because central noradrenergic and peripheral sympathetic systems function in concert (Aston-Jones et al. 1991), the data from these psychophysiology investigations are consistent with the hypothesis that noradrenergic hyperreactivity in patients with PTSD may be associated with the conditioned or sensitized responses to specific traumatic stimuli. There is some evidence that baseline levels of NE are consistently altered in combat-related PTDS. Women with PTSD secondary to childhood sexual abuse had significantly elevated levels of catecholamines (NE, epinephrine, DA) and cortisol in 24-h urine samples (Lemieux and Coe 1995). Sexually abused girls excreted significantly greater amounts of catecholamine metabolites, metanephrine,...

Basal HPA Hormone Levels in PTSD

The first report on cortisol levels in PTSD was that of Mason et al. who found that the mean 24-h urinary excretion of cortisol was significantly lower in combat Vietnam veterans with PTSD compared to psychiatric patients in four other diagnostic groups (Mason et al. 1986). The authors noted surprise at the fact that cortisol levels were low, since certain clinical features such as depression and anxiety in PTSD might have been expected to be associated with increased activity of the pituitary-adrenal cortical system. Since this initial observation, the majority of the evidence supports the conclusion that cortisol alterations in PTSD are different from those observed in acute and chronic stress, and major depression, but more importantly, that the HPA axis appears to be regulated differently.

Glucocorticoid Receptors in PTSD

Lymphocyte and brain GRs have been found to share similar regulatory and binding characteristics (Lowy 1989). A greater number of 8 00 a.m., but not 4 00 p.m., mononuclear leukocytes (presumably lymphocyte) type II GRs was reported in Vietnam veterans with PTSD compared to a normal comparison group (Yehuda et al. 1991b). Subsequently, Yehuda et al. reported an inverse relationship between 24-h urinary cortisol excretion and lymphocyte GR number in PTSD and depression (i.e., low cortisol and increased receptor levels were observed in PTSD, whereas in major depressive disorder, elevated cortisol and reduced receptor number were observed) (Yehuda et al. 1993a). Although it is not clear whether alterations in GR number reflect an adaptation to low cortisol levels or some other alteration, the observation of an increased number of lymphocyte GRs provided the basis for the hypothesis of an increased negative feedback inhibition of cortisol secondary to increased receptor sensitivity (Yehuda...

The Cholecystokinin Tetrapeptide Challenge Test in PTSD

Cholecystokinin tetrapeptide (CCK)-4 is a potent stimulator of ACTH. Kellner et al. administered a 50-pg bolus of CCK-4 to subjects with PTSD and found substantially attenuated elevations of ACTH in PTSD, which occurred despite comparable ACTH levels at baseline (Kellner et al. 2000). Cortisol levels were lower in PTSD at baseline, but rose to a comparable level in PTSD and control subjects. However, the rate of decline from the peak was faster, leading to an overall lower total cortisol surge. The attenuated ACTH response to CCK-4 is compatible with the idea of CRF overdrive in PTSD, and is a similar to the administration of CRF. That less ACTH can produce a similar activation of the adrenalgland, butamorerapid sensitive negative feedback inhibition secondary to increased glucocorticoid receptor activity at the pituitary. Although the comparatively greater effects on cortisol relative to ACTH is also compatible with an increased sensitivity of the adrenal gland to ACTH, rather than...

Putative Models of HPA Axis Alterations in PTSD

Cortisol levels are most often found to be lower than normal in PTSD, but can also be similar to or greater than those in comparison subjects. Findings of changes in circadian rhythm suggest that there may be regulatory influences that result in a greater dynamic range of cortisol release over the diurnal cycle in PTSD. Together, these findings imply that although cortisol levels may be generally lower, the adrenal gland is certainly capable of producing adequate amounts of cortisol in response to challenge. The model of enhanced negative feedback inhibition is compatible with the idea that there may be transient elevations in cortisol, but would suggest that when present, these increases would be shorter-lived due to a more efficient containment of ACTH release as a result of enhanced GR activation. This model posits that chronic or transient elevations in CRF release stimulate the pituitary release of ACTH, which in turn stimulates the adrenal release of cortisol. However, an...

The Dexamethasone Suppression Test in PTSD

The initial DST studies in PTSD using the 1.0-mg dose of DEX did not considerthepossibility ofahypersuppressiontoDEX andtestedthe hypothesis that patients with PTSD might show a nonsuppression of cortisol similar to patients with major depressive disorder. A large proportion of the PTSD subjects studied also met criteria for major depression. Four (Dinan et al. 1990 Halbreich et al. 1989 Kosten et al. 1990 Reist et al. 1995) out of five (Kudler et al. 1987) of the earlier studies noted that PTSD did not appear to be associated with Cortisol nonsuppression, using the established criterion of 5 pg 100 ml at 4 00 p.m. A more recent study did not use the established criterion to determine nonsuppression, but nonetheless reported a greater mean cortisol in PTSD compared to normal subjects at 8 00 a.m. (Thaller et al. 1999). In this study, Thaller et al. reported that DEX resulted in 67 suppression in PTSD ( 34) compared to 85 suppression in comparison (n 17) subjects. Similarly, Atmaca et...

The Naloxone Stimulation Test in PTSD

Another strategy for examining CRF activity involves the assessment of ACTH and cortisol after administration of agents that normally block the inhibition of CRF. Naloxone increases CRF release by blocking the inhibition normally exerted by opioids in the hypothalamus. Naloxone was administered to 13 PTSD patients and 7 normal comparison subjects (Hockings et al. 1993). Of the PTSD subjects, 6 7 showed an increased ACTH and cortisol response to naloxone. These findings appear to contradict those of Smith et al. (1989) who showed a blunted ACTH response to CRF however, here too the absence of information about ambient CRF complicates the interpretation of these findings. This finding is noteworthy for illustrating that only a proportion of subjects in a particular group may exhibit evidence of pituitary adrenocortical alterations.

The CRF Challenge Test and ACTH Stimulation Test in PTSD

A study of eight PTSD subjects demonstrated that the ACTH response to CRF is also blunted (Smith et al. 1989). However, although the authors noted a uniform blunting of the ACTH response, this did not always occur in the context of hypercortisolism. Furthermore, although the ACTH response was significantly blunted, the cortisol response was not (however, though not statistically significant, it should be noted that the area under the curve for cortisol was 38 less than controls). Bremner et al. also observed a blunted ACTH response to CRF in women with PTSD as a result of early childhood sexual abuse (Bremner et al. 2003b). Yehuda et al. previously suggested that the blunted ACTH response in PTSD might reflect an increased negative feedback inhibition of the pituitary secondary to increased GR number or sensitivity (Yehuda et al. 1995a). This explanation supports the idea of CRF hypersecretion in PTSD, and explains the pituitary desensitization and resultant lack of hypercortisolism...

Post Traumatic Stress Disorder

The Diagnostic and Statistical Manual of Mental Disorders, 4th ed. (American Psychiatric Association 1994), defines PTSD as an anxiety disorder generated when a person has experienced or witnessed a stressful event that involves death, the threat of death, or serious bodily injury to the self or to another person and which causes reactions characterized by intense fear and feelings of helplessness or of terror (American Psychiatric Association 1994). PTSD is a disorder classically associated with war. The syndrome had been referred to variously as traumatic neurosis, war neurosis, or stress response syndrome (de Pa l 1995) before the current name was adopted by the American Psychiatric Association and the World Health Organization. PTSD no longer is diagnosed only in ex-combatants. It is seen in a wide range of groups, such as casualties of traffic accidents patients suffering from terminal illness, physical abuse, or any type of violence and, especially, victims of sexual assault...

Cortisol Levels Over the Diurnal Cycle in PTSD

Among the many potential methodologic problems associated with 24-h urine collections is the possibility that persons who are asked to collect 24-h samples at home may not provide complete collections. To the extent that there may be a systematic bias in protocol nonadherence between subjects with and without PTSD, in that the former might be more likely to miss collections than the latter, this could contribute to observed low cortisol levels. One of the initial rationales for performing a comprehensive circadian rhythm analysis was to corroborate and extend findings from the 24-h urine excretion studies and those using single-point estimates (Yehuda et al. 1990). An initial study of cir-cadian parameters in PTSD was conducted by obtaining 49 consecutive blood samples from three groups of subjects Vietnam combat veterans with PTSD, subjects (largely veterans) with major depression, and non-psychiatric comparison subjects every 30 min over a 24-h period under carefully controlled...

Urinary Cortisol Levels in PTSD

The initial report of sustained, lower urinary cortisol levels in PTSD highlighted the disassociation between cortisol and catecholamine levels in PTSD. Norepinephrine and epinephrine levels assayed from the same urine specimens revealed elevations in both of these catecholamines, while cortisol levels in PTSD fell within the normal range of 20-90 pg day, indicating that the alteration was not in the hypoadrenal or endocrinopathologic range (Mason et al. 1986). This finding established the expectation that alterations in basal levels of cortisol might be subtle, and not easily differentiated from normal values (Mason et al. 1986). Table 1 shows that this is in fact the case. Whereas the majority of studies has found evidence of low Cortisol in PTSD, it is clear that group differences are not always present between subjects with and without PTSD. The inconsistency in published reports examining urinary 24-h cortisol levels has been widely noted. There are numerous sources of potential...

Neuroendocrine Aspects of PTSD

2 Basal HPA Hormone Levels in 2.1 Urinary Cortisol Levels in 2.2 Cortisol Levels Over the Diurnal Cycle in 2.5 Correlates of Cortisol in 2.6 CRF Levels in 2.7 ACTH Levels in 3 Glucocorticoid Receptors in 4.1 The Dexamethasone Suppression Test in 4.2 The Cholecystokinin Tetrapeptide Challenge Test in PTSD 386 4.4 The CRF Challenge Test and ACTH Stimulation Test in PTSD 389 4.5 The Naloxone Stimulation Test in 6 Putative Models of HPA Axis Alterations in PTSD 392 Abstract This chapter discussed how neuroendocrine findings in posttraumatic stress disorder (PTSD) potentially inform hypothalamic-pituitary-adrenal (HPA) alterations in PTSD and highlight alterations relevant to the identification of targets for drug development. Most studies demonstrate alterations consistent with an enhanced negative feedback inhibition of cortisol on the pituitary, an overall hyperreactivity of other target tissues (adrenal gland, hypothalamus), or both in PTSD. However, findings of low cortisol and...

MDMA and Posttraumatic Stress Disorder

Held at Esalen Institute in 1985, where the state of knowledge concerning MDMA was reviewed, one of the conclusions was that victims of child abuse and sexual attack experienced the most dramatic benefits (Greer 1985). Grinspoon and Bakalar (1986) stated, MDMA might also help in working through loss and trauma. Peter Stafford, in his Psychedelics Encyclopedia, also speaks of the effectiveness of MDMA in treating, rape, childhood abuse, and post-war stress syndromes and discusses specific cases of people finding beneficial results from MDMA-assisted psychotherapy (Stafford 1992). Eisner (1989) discusses the potential benefits for female victims of sexual assault who undergo MDMA-assisted psychotherapy as well as his personal understanding of how these benefits accrue. In addition, some first-person accounts of PTSD sufferers have described how they benefited from treatment that included MDMA (Adamson 1985). MDMA has a unique ability to facilitate and accelerate the therapeutic process...

Correlates of Cortisol in PTSD

Even in cases where there is failure to find group differences, there are often correlations within the PTSD group with indices of PTSD symptom severity. Baker et al. (1999) failed to find group differences between Vietnam veterans with PTSD compared to non-exposed controls, but did report a negative correlation between 24-h urinary cortisol and PTSD symptoms in combat veterans. A negative correlation between baseline plasma cortisol levels and PTSD symptoms, particularly avoidance and hyperarousal symptoms, were observed in adolescents with PTSD (Goenjian et al. 2003). Rasmusson et al. (2003) failed to observe a significant difference in urinary cortisol between premenopausal women with PTSD and healthy women, but noted an inverse correlation between duration since the trauma and cortisol levels, implying that low cortisol is associated with early traumatization. This finding is consisted with Yehuda and colleagues' observation of an inverse relationship between childhood emotional...

CRF Levels in PTSD

There have been three published reports examining the concentration of corticotrophin-releasing factor (CRF) in cerebrospinal fluid (CSF) in PTSD. The assessment of CSF CRF does not necessarily provide a good estimate of hypothalamic CRF release, but rather, an estimate of both hypothalamic and extrahypothalamic release of this neuropeptide (Yehuda and Nemeroff 1994). An initial report using a single lumbar puncture indicated that CRF levels were elevated in combat veterans with PTSD (Bremner et al. 1997). A second study, examining serial CSF sampling over a 6-h period by means of an indwelling catheter, also reported significantly higher CSF CRF concentrations, but did not observe a relationship between CRF and 24-h urinary cortisol release (Baker et al. 1999). A third report demonstrated that PTSD subjects with psychotic symptoms had significantly higher mean levels of CRF than either subjects with PTSD without psychotic symptoms or controls subjects (Sautter et al. 2003).

ACTH Levels in PTSD

Among the challenges in assessing pituitary activity under basal conditions is the fact that the normal positive and negative feedback influences on the pituitary can mask the true activity of this gland. Because the pituitary mediates between CRF stimulation from the hypothalamus and the inhibition of ACTH release resulting from the negative feedback of adrenal corticosteroids, baseline ACTH levels may appear to be normal even though the pituitary gland may be receiving excessive stimulation from CRF. In most studies ACTH levels in PTSD patients were reported to be comparable to non-exposed subjects. The majority of studies has reported no detectible differences in ACTH levels between PTSD and comparison subjects even when cortisol levels obtained from the same sample were found to be significantly lower. This pattern was observed in Kellner et al. who reported that cortisol levels were 41 lower, but that ACTH levels were only 7.4 lower in PTSD compared to normals (Kellner et al....

Specific Phobia

The key feature of specific phobia is an intense and persistent fear of circumscribed situations or specific stimuli (e.g. exposure to animals, blood). Confrontation with the situation or stimulus provokes almost invariably an immediate anxiety response. Often, the situation or stimulus is therefore avoided or endured with considerable dread. Adolescents and adults with this disorder recognize that this anxiety reaction is excessive or unreasonable, but this may not be the case in children. For a diagnosis according to DSM-IV, the avoidance, fear or anxious anticipation of the phobic stimulus must interfere with the persons daily life or the person must be markedly distressed about having the phobia. Further, the phobic reactions are not better explained by another mental disorder, such as, for example, social phobia.

Syndromes of Anxiety and Their Treatment

Posttraumatic Stress Disorder (PTSD) PTSD occurs after a traumatic experience that is potentially life-threatening. Symptoms include reexperiencing the event through intrusive recollections, nightmares, flashbacks, avoidance of people and situations similar to the events of the trauma, and persistent symptoms of increased arousal such as insomnia, hypervigilance, and an exaggerated startle response. control over the symptoms of PTSD. You may find psychotherapy helps to free you from the influence of the trauma in your life, though this work can be painful, difficult, and time-consuming. There are no medications to cure PTSD, but they can minimize the intensity of some of the symptoms. SSRIs can lessen the intensity of anxiety, flashbacks, and improve sleep. TCAs and MAOIs can do the same thing but tend to cause more side effects. Benzos can minimize the anxiety and improve sleep, but are habit-forming and tend to lose their effectiveness after some months. You will go through a period...

Pregnancy Category C

Like other stimulants, cocaine may improve mood, self-confidence, and sociability. Taking the drug for such purposes may be recreational or for self-medication of psychological distress for example, a strong association exists between posttraumatic stress disorder and cocaine use. Cocaine can temporarily enhance work performance whether the task be manual labor or intellectual concentration. A century ago railroad engineers, dock workers, and cotton pickers were reported to be using the drug for that purpose, and it also received experimental military use in that pre-amphetamine era. On an occasional basis cocaine can help accomplish intense intellectual effort, such as staying awake all night to finish a piece of writing, and on a regular basis, cocaine can help accomplish dull repetitive tasks requiring close mental attention. As with other stimulants, steady use can eventually worsen work ability as a person's physical reserves are exhausted and as a person becomes emotionally...

Review of Linkage and Association Studies of Anxiety Disorders

Or have shown to have no association in previous studies (Lappalainen et al. 1998). The two linkage studies (Kennedy et al. 2001 Stein et al. 1998b) of social phobia have been examined by the same group and found to be negative. One genome scan for simple phobia has been performed with a LOD score of 3.17 on chromosome 14 (Gelernter et al. 2003). One positive-association study (Comings et al. 1996) of posttraumatic stress disorder with the A1 allele of the dopamine (D2) receptor polymorphism was not replicated in a subsequent study (Gelernter et al. 1999).

Health Testimonials W

Though I have tried, I know that I can't really imagine what he must feel. This has been the hardest thing either of us has ever dealt with, and for the most part, have had no help in doing so. Garrett now suffers from PTSD as well, due to the fact he was sleeping when the event occurred, which is coupled with the minor traumatic brain injury, both aggravating each other. He is in constant pain. Phantom pains in his arm, where he feels he has electricity running through it or says he feels as if his hand is still there and constantly opening and closing. Constant headaches. Pain in his back, his side, and legs. Terrible trouble sleeping and reoccurring night terrors when he does sleep. Depression. Anxiety. Yet Somehow he goes on each day, and tries to hold onto the hope of one day things getting better. I am humbled by his perseverance in the darkest of hours, and the absolute love of life that he so terribly wants to be able to act on once again. After the first year, having no...

Other Antidepressant Agents

Bupropion Buproprion-SR has been found to be effective in the treatment of social anxiety disorder, and to be ineffective in PD, and also in an open-label study with PTSD. Mirtazapine Mirtazapine may be effective in the treatment of panic disorder and generalized anxiety disorder. Mirtazapine has also been studied in patients with chronic PTSD results from small studies indicate it may also be efficacious as an adjuvant in the treatment of PTSD. In OCD, small studies with mirtazapine (as primary treatment or augmentation of SSRI medication) suggest possible benefit, even an acceleration of treatment response. Nefazodone The efficacy of nefazodone has been assessed in open-label studies in PTSD results suggest that this agent may decrease the core symptoms of PTSD, improve sleep, and decrease symptoms of anger. It may be helpful for patients who are refractory to SSRI treatment.

Cellular Mechanisms of Stress Induced Structural Plasticity

Chronic or severe stress is a well-known precipitant of some forms of anxiety and depressive disorders, and it is likely that stress-induced alterations in neuronal plasticity may underlie functional changes. Stress exposure in experimental animals can result in dendritic remodeling and atrophy in hippocampal CA3 pyramidal neurons (Margarinos et al. 1996 Sousa et al. 2000 Watanabe et al. 1992) as well as decreased hippocampal volume and neurogenesis (Czeh et al. 2001 Gould et al. 1997). These findings, along with observations of decreased hippocampal volume seen clinically in association with PTSD and depression (Bremner et al. 1995 Sheline et al. 1996), and the observation that clinically effective antidepressant treatments can reverse stress-induced changes in neuronal structure (Magarinos et al. 1999), have suggested the potential relevance of stress-induced structural alterations to affective disorders (Duman et al. 2000 Manji et al. 2001 Nestler et al. 2002).

Intracellular Signaling Pathways Involved in Fear Memory

Anxiety represents a state of heightened vigilance and fear, but pathological anxiety can be distinguished from fear in that it is inappropriately evoked and may persist in the absence of real threat or danger. The study of conditioned fear has provided detailed information on the neural circuitry and intracellular mechanisms that are important to fear responses and their long-term retention. The description of neural circuitry and the mechanisms underlying disorders of fear memory such as posttraumatic stress disorder (PTSD) may also be relevant to other anxiety states that share common neural substrates.

Betablocker Medications

These medicines are most useful for treatment of anxiety syndromes and disorders with somatic symptoms associated with increased adrenergic tone. Propranolol in doses of 10 to 40 mg day has been used for performance anxiety, on an as-needed basis. Recent research on PTSD suggests a different role for the beta-blocker medications. It appears that traumatic memories may be reduced by medications that prevent presynaptic norepinephrine release (such as alpha-2-adrenergic agonists or opioids), or block postsynaptic norepinephrine receptors, blocking a cycle that is mediated by noradrenergic hyperactivity in the basolateral amygdala. There are two controlled studies of trauma victims presenting to emergency rooms suggesting that post-trauma treatment with propranolol can decrease subsequent PTSD symptoms.

Modulation of Fear Learning

The ways in which learning and memory mechanisms are recruited by fear-inducing stimuli as well as knowledge about how a conditioned cue can come to lose its ability to elicit a fear response are of great significance to strategies for the clinical management of anxiety states, and may be particularly relevant to PTSD. Continued investigation of the intracellular molecular mechanisms that allow fear responses to come under the control of cues in the environment and the elements that are critical to the persistence of such responses will help define new, more selective targets for pharmacological intervention.

Observations About Baseline Cortisol Based on Single Estimates of Plasma or Saliva

Table 2 provides a summary of cortisol levels in studies that specifically obtained 8 00 a.m. cortisol concentrations, and highlights the lack of uniform findings in relation to cortisol levels, possibly reflecting the above-mentioned methodologic considerations. Of particular note, however, is Boscarino's report of low cortisol in a large epidemiologic sample of over 2,000 Vietnam veterans with PTSD compared to those without PTSD, which implies that to consistently observe low morning cortisol would require an extremely large sample size (Boscarino 1996). The magnitude of difference between PTSD and non-PTSD subjects at 8 00 a.m. was very modest there was only a 4 difference between veterans with and without current or lifetime PTSD. Cortisol levels were significantly lower in combat veterans with very high exposure (17.9 pg day) compared to those with no or low exposure (19.1 pg day). The finding of an inverse relationship between combat exposure severity and 8 00 a.m. cortisol...

Clinical Presentation

Overall, the core element of all anxiety disorders is the occurrence of an anxiety reaction that may vary widely in terms of intensity, frequency, persistence, trigger situations, severity and consequences and other qualifying features. Anxiety disorders as defined in the current DSM-IV can be described in terms of the situations, objects or thoughts which provoke anxiety, the specific expression of anxiety in terms of autonomic, and cognitive or motoric features, as well as the specific behaviours used to cope with the provoked anxiety. In some disorders anxiety is expressed mainly in physiological reactions such as heart palpitations (panic disorder), in others primarily by avoidance (specific phobias), and still others by cognitive symptoms such as obsessions or worries (obsessive-compulsive disorder, generalized anxiety disorder). Table 1 gives an overview of the key features of major anxiety disorders included in DSM-IV.

Comorbidity Within the Anxiety Disorders

Although less studied, epidemiological investigation has also shown that there is a considerable degree of overlap within the anxiety disorders. In the NCS, associations (in terms of ORs) within different forms of anxiety disorders were found to range between 3.8 and 12.3 for generalized anxiety disorder, 5.8 and 11.9 for agoraphobia, 4.9 and 8.5 for specific phobia, and 3.8 and 7.8 for social phobia (Wittchen et al. 1994 Magee et al. 1996). The strongest comorbidity was found between panic disorder and agoraphobia, due to the fact that agoraphobia with panic disorder and agoraphobia without panic were not distinguished in the diagnostic criteria of agoraphobia. Interestingly, only about one third of the respondents who meet criteria for DSM-III-R agoraphobia additionally reported panic attacks. This result confirms earlier results found in the ECA and Zurich study (Angst and Dobler-Mikola 1985 Weissman et al. 1986) that panic seems to be involved only in a minority of people with...

Selective Serotonin Reuptake Inhibitors

And posttraumatic stress disorder (PTSD) sertraline for obsessive-compulsive disorder (OCD) and PTSD . In clinical practice, the SSRIs have become the first-line treatment for panic disorder because of their overall safety and tolerability, their safety in overdose, and their low potential for addiction and withdrawal.

Intensification Of Conventional Therapeutic Mechanisms

The therapeutic potential of the reliving of emotionally important episodes from childhood seems to involve two important elements. One of them is a deep release of pent-up energies and their peripheral discharge in the form of emotional and physical abreaction. The second is conscious integration of the content that is now devoid of affective charge. This is made possible by the double orientation or dual role that individuals can assume in the LSD state, either simultaneously or in an alternating fashion. On the one hand, they experience full and complex age-regression to early life periods when the traumatic events took place on the other hand, they also have access to the position corresponding to their chronological age at the time of the LSD session. In this way, it becomes possible to reevaluate from an adult point of view the relevance of events that were once overwhelming for the immature organism. The replay of early biographical events is thus experienced by a subject svho...

Findings of Cortisol in the Acute Aftermath of Trauma

Recent data have provided some support for the idea that low cortisol levels may be an early predictor of PTSD rather than a consequence of this condition. Low cortisol levels in the immediate aftermath of a motor vehicle accident predicted the development of PTSD in a group of 35 accident victims consecutively presenting to an emergency room (Yehuda et al. 1998). Delahanty et al. (2000) also reported that low cortisol levels in the immediate aftermath of a trauma contributed to the prediction of PTSD symptoms at 1 month. In a sample of 115 people who survived a natural disaster, cortisol levels were similarly found to be lowest in those with highest PTSD scores at 1 month post-trauma, however cortisol levels were not predictive of symptoms at 1 year (Anisman et al. 2001). Similarly, lower morning, but higher evening cortisol levels were observed in 15 subjects with high levels of PTSD symptoms 5 days following a mine accident in Lebanon compared to 16 subjects with lower levels of...

The Debilitating Medical Conditions Advisory Panel

The Oregon Health Division (OHD) convened an advisory panel in February of 2000 to review nine petitions requesting the inclusion of eight new conditions on the list of debilitating medical conditions. (Two petitions were submitted for PTSD.) All nine petitions were submitted by either the patient or a family member of a person suffering from the disorder in question. These petitions, all for the inclusion of psychiatric conditions, were post traumatic stress disorder (2 petitions), During the afternoon all of the petitioners were heard from, five in person and three by telephone. Their testimony was unpolished yet sincere as they each described significant improvement in their psychiatric symptoms from Cannabis use. The petitioner with bipolar disorder described that he had remained out of the hospital for 11 years because Cannabis controlled his mood swings. The two petitioners suffering from PTSD both described Cannabis' antianxiety effects that diminished the intensity of...

Memorandum from the Multidisciplinary Association for Psychedelic Studies MAPS

MAPS has sponsored and assisted researchers in gaining approval to proceed with several studies involving MDMA (Ecstasy), and psilocybin. Currently, a study is underway in South Carolina investigating the use of MDMA to facilitate psychotherapy in patients with posttraumatic stress disorder (PTSD), with promising results. Similar MAPS-sponsored studies using MDMA-assisted psychotherapy to treat PTSD are fully-approved in Israel and under review in Switzerland. A study at Harvard Medical School testing MDMA to ease anxiety associated with advanced-stage cancer has received final approved from the DEA on 19 January 2006 and will begin soon. A completed pilot study at the University of Arizona-Tucson found positive benefits from the effects of psilocybin in reducing symptoms of obsessive-compulsive disorder (OCD).

Psychiatric Drugs Poison or Panacea

There is a great deal of information about psychiatric problems and drugs in the media. Pharmaceutical companies have developed many new psychiatric drugs in the last decade, which they promote at public events and in popular magazines. Celebrities like Mike Wallace, Patty Duke, William Styron, and Lawton Chiles have gone public with their problems and their experiences with medication. Many people not in the public eye have told their stories on television, in print, and on radio talk shows. Television shows like Frontline and Sixty Minutes have focused on psychiatric problems such as attention deficit disorder, posttraumatic stress disorder, and the debate over the reality of sexual abuse.

Pharmacotherapy for Specific Psychiatric Disorders

Substance-induced disorders (particularly stimulant intoxication and alcohol or sedative-hypnotic withdrawal) can resemble generalized anxiety disorder or panic attacks, and thus, as with depression, at least a two week period of abstinence is preferable prior to initiating pharmacotherapy, although again there is room for judgment. Other anxiety disorders, such as social phobia, agoraphobia, PTSD, or OCD, have distinctive symptoms that do not overlap with symptoms of toxicity or withdrawal. Behavioral approaches are effective for many anxiety disorders and should be considered, first alone and then as a supplement to pharmacotherapy. Antide-pressants are effective for panic disorder or generalized anxiety disorder and have less abuse potential than the benzodi-azepines. Buspirone may be beneficial for generalized anxiety disorder at a dose of at least 45 mg day. If a benzodiazepine is still preferred, expert opinion (supported by some experimental evidence) suggests that the safest...

Cortisol Levels in Response to Stress

The potential significance of the findings of an increased range of cortisol is that the HPA axis may be maximally responsive to stress-related cues in PTSD, whereas major depressive disorder may reflect a condition of minimal responsiveness to the environment. That is, an enhanced amplitude-to-mesor ratio describes a system with particularly low background activity and, accordingly, a potentially increased capacity to respond to environmental cues. In support of this, Liberzon et al. observed an increased cortisol but not increased corticotropin (ACTH) response in combat veterans with PTSD compared to controls who were exposed to white noise and combat sounds (Liberzon et al. 1999). Elizinga et al. also observed that women with PTSD related to childhood abuse had substantially higher salivary cortisol levels in response to hearing scripts related to their childhood experiences compared to controls, who had relatively lower cortisol levels in response to hearing scripts of other...

Mental Health Problems Associated With Mdma

Like other mind-altering drugs, MDMA was perceived as one with few adverse effects when it was first introduced. However, as its use spread from psychotherapy into the general community, it became linked with a variety of mental health problems. When MDMA was used as an aid to psychotherapy in the late 1970s, therapists characterized the effects as feelings of empathic understanding for others and a release of emotions. Since then, however, there have been reports of confusion, anxiety, amnesia, panic attacks, depression, mania (excessive excitation), suicide, insomnia, nightmares, depersonalization (feeling unreal), derealization (feeling that the surroundings are unreal), hallucinations, flashbacks, post-traumatic stress disorder (PTSD), paranoia and other persistent false beliefs, other types of psychosis, automatic or repetitive behavior, dissociative disorders, irritability and aggression with mood swings, tolerance, dependence, and increased risk of problems with other drugs...

Panic Disorder and Agoraphobia

Panic disorder is comorbid with episodes of depression at some stage in the majority of cases (Stein et al. 1990), with social anxiety disorder and to a lesser extent GAD and PTSD, and with alcohol dependence and personality disorder. Comorbidity results in increased severity and poor response to treatment. Panic disorder is associated with a significantly increased risk of suicide, and this is increased further by the presence of comorbid depression (Lepine et al. 1993).

The Metyrapone Stimulation Test

Whereas both the results of the DST and CCK challenge tests are consistent with the idea of an enhanced negative feedback inhibition in PTSD, these alter ations do not directly imply that an enhanced negative feedback inhibition is a primary disturbance in PTSD. Yehuda et al. used the metyrapone stimulation test as a way of providing further support for the enhanced negative feedback hypothesis (Yehuda et al. 1996a). Metyrapone prevents adrenal steroidogenesis by blocking the conversion of 11-deoxycortisol to cortisol, thereby unmasking the pituitary gland from the influences of negative feedback inhibition. If a sufficiently high dose of metyrapone is used such that an almost complete suppression of cortisol is achieved, this allows a direct examination of pituitary release of ACTH without the potentially confounding effects of differing ambient cortisol levels. When metyrapone is administered in the morning when HPA axis activity is relatively high maximal pituitary activity can be...

Clinical Implications

Most basic researchers and clinicians believe that detailed knowledge about cellular mechanisms underlying the formation and extinction of aversive memories will lead to the development of novel therapeutic strategies for the treatment of human anxiety disorders. Our current knowledge about these mechanisms largely arises from results obtained in animal experiments. However, the transferability of such experimental data to the human situation depends on the validity of the experimental models chosen. Numerous sets of criteria have been developed for evaluating experimental models (McKinney and Bunney 1969 Willner 1984 Newport et al. 2002). Human psychiatric disorders may develop as a consequence of genetic and developmental predisposition that affect sensitivity to life stress and the initiation of pathological processes. Consequently, it appears rather unlikely that comprehensive animal models can be developed that accurately reflect the human situation (Shekhar et al. 2001). These...

Medications for Opiate Dependence

A pragmatic drawback of methadone maintenance is that regulations stipulate that it can only be administered at specially licensed clinics that require frequent attendance (daily at the outset) and that are not even available in many geographic regions. This can be a practical constraint or a disincentive for many patients. On the other hand, it has been shown that the effectiveness of methadone maintenance depends upon regular counseling in conjunction with the medication, which is a requirement of methadone clinics, and more severely dysfunctional patients probably benefit from the structure imposed by clinic rules. Furthermore, many of the better methadone clinics offer primary medical and psychiatric care, which is important since chronic opiate-dependent patients often have multiple medical problems (e.g., hepatitis B and C, HIV) and psychiatric problems (e.g., depression, PTSD).

Tricyclic Antidepressants

This group includes compounds with actions on a range of neurotransmitter systems. Their antidepressant efficacy is mediated by reuptake inhibition of serotonin and noradrenaline, although side-effects such as sedation may also be useful. Their use in anxiety disorders is supported by a long history of clinical experience and a reasonable evidence base from controlled trials. Studies support the use of clomipramine (a potent serotonin reuptake inhibitor) in panic disorder and OCD (Lecrubier et al. 1997 Clomipramine Collaborative Study Group 1991), of imipramine in panic disorder and GAD (Cross-National Collaborative Panic Study 1992 Rickels et al. 1993), and of amitriptyline in PTSD (Davidson et al. 1993a). No controlled studies support the use of TCAs in social anxiety disorder.

Adverse Aftereffects Of Lsd Psychotherapy

The changes caused by activation of different levels of COEX systems are usually not very dramatic and stay within the range of various neurotic and psychosomatic manifestations, unless the activated layer is from very early childhood and or its emotional charge is excessive. When an important COEX system is activated and remains unresolved, the subject experiences in the post-session period an intensification of the clinical symptoms related to this system and perceives the environment with specific distortions reflecting its content. In addition, he or she may manifest a tendency to exteriorize the general theme of the system, or certain specific characteristics of one of its layers, in the treatment situation and in various aspects of everyday life. He or she may show peculiar idiosyncrasies and overreact to certain circumstances. The behavior of subjects under these conditions can involve complicated psychological maneuvers that tend to provoke specific reciprocal attitudes in the...

Clinical Experience With Mdmaassisted Psychotherapy

GG I'm a psychiatrist in private practice. I have a small outpatient psychotherapy practice, and I also work half-time in a residential treatment center for post-traumatic stress disorder (PTSD), mosdy with patients who have experienced sexual or physical abuse in childhood. They also generally have depression and other mood disorders, eating disorders, attention-deficit hyperactivity disorder (ADHD), and addictions. It's a very intense patient population. They come to our program from all around the country after being in hospitals for about a month. It's a residential program designed for afterhospital care. I'm the psychiatrist there, and I evaluate patients and prescribe medications. JH You've mentioned two areas I want to spend more time on. The first is PTSD. You have worked specifically with people with this diagnosis, who have a history of physical or psychic trauma. Can you describe how an MDMA-assisted psychotherapy session might help people to process some of this trauma GG...

Memory Decay and Extinction

Everyone experiences how memories may dissipate with time. Responsible for this phenomenon might be spontaneous forgetting, the suppression of memory retrieval and memory extinction. Spontaneous forgetting describes the loss of learned performances that is often observed when time elapses between memory acquisition and memory retrieval. It results from different processes (Bouton et al. 1999). First, memory traces might dissipate over time. Second, information might increasingly interfere with retrieval of the original memory in a proactive or retroactive manner. Third, memory retrieval might be disturbed transiently or permanently (e.g. following head injury or stroke). Fourth, a recent study suggests that neurogenesis in the dentate gyrus might play a role in the clearance or destabilisation of outdated hippocampal memory traces after systems reconsolidation, thereby saving the hippocampus from overload (Feng et al. 2001). Furthermore, on confrontation with reminders of unpleasant...

Summary and Conclusions

Significant progress has been made in understanding the neurobiology of fear memory, including the signal transduction cascades that are activated and required for the formation of long-term fear memory. This has resulted in hypothesis-based novel targets and strategies for fear-related disorders, including PTSD. This progress has resulted in part from the well-defined models and neural circuitry for fear conditioning, which provides a system for testing the role of specific signaling molecules. Progress on anxiety has been limited to information resulting from the use of effective anxiolytic drugs, primarily the benzodiazepines and behavioral models that were designed to test for drugs of this class. However, this has not led to fundamental information regarding the neurobiology of anxiety. Development of better models of anxiety will provide information on the neural circuitry underlying this disorder. This information is critical for further characterization of the...

A Mil ii yiiiiiiiiiiiiiiiiiiii

Cells of all their normal afferents and in many cases you cut their axons. You cut the axon of the very cell you are recording, but you are unaware that has occurred. But there are many different traumatic events that take place when you extract the slice. The behavior of the cells is quite abnormal if you look at it carefully.

Syndromes of Psychosis and Their Treatment

Psychotic symptoms can be a secondary phenomenon originating in another disorder. Thyroid conditions, epilepsy, brain tumors, multiple sclerosis, and syphilis can cause psychotic symptoms. It is important to exclude these causes before treatment. Steroids, stimulants, amphetamines, cocaine, hallucinogens, marijuana, and PCP can also cause psychotic symptoms. It is essential to stop taking any drug that may be causing psychotic symptoms. Psychotic symptoms can also occur in bipolar disorder, depression, dementia, and posttraumatic stress disorder.

Cholecystokinin Tetrapeptide Challenge

CCK-B receptor agonists such as pentagastrin or CCK-4 (25-50 pg i.v.) have panic-like anxiogenic effects in humans (Table 1). Panic patients and patients suffering from posttraumatic stress disorder, however, are more sensitive than healthy controls to the anxiogenic effects of CCK-4 (e.g., DeMontigny et al. 1989 Radu et al. 2002). Pretreatment with a CCK-B receptor antagonist is able to reverse both the autonomic and anxiogenic effects of pentagastrin (Lines et al. 1995). The safety, reliability, and dose-dependence of the anxiogenic effects of CCK-4 as well as the similarity of effect to naturalistic panic are strong, rendering CCK-4 an attractive probe of anxiety. CCK-4-induced panic has a characteristic physiological activation curve that only lasts about 2-3 min (Bradwejn et al. 1995). Like sodium lactate-induced panic, CCK-4-induced attacks are accompanied by hyperventilation. Increases in regional cerebral blood flow as measured by PET scans have been described in the...

Neural Mechanisms of Anxiety and Fear

May account for common clinical observation in panic disorder, PTSD that sensory and cognitive stimuli associated with or resembling the frightening experience elicit panic attacks, flashbacks, and autonomic symptoms This hypothesis leads to several predictions that may have relevance to the discovery of novel therapeutics for anxiety disorders. It suggests that blocking NMDA receptors in the amygdala during learning should impair short-and long-term fear memory. This has been demonstrated in rodents (Walker et al. 2000 Rodrigues et al. 2001). Valid human models of fear conditioning and the availability of the NMDA receptor antagonist memantine should permit this hypothesis to be tested clinically (Grillon 2002). If memantine impairs the acquisition of fear in humans, it may have utility in the prevention and treatment of anxiety disorders such as posttraumatic stress disorder (PTSD), and panic disorder. Blockade of VGCCs appears to block long-term but not short-term memory (Bauer et...


This calming and sleep-inducing substance is probably the most frequently prescribed drug in the benzodiazepine class. Alprazolam is used mainly to help persons suffering from panic attacks and other anxiety disorders, but it is not recommended for posttraumatic stress disorder. The compound can dramatically lessen premenstrual syndrome (PMS) and is routinely given to women of child-bearing age. Improvement of PMS is not invariable, however, and two careful experiments yielded results showing little benefit. Theoretical reasons and results from a rat experiment suggest that alprazolam may help maintain bone mass. That action may be especially important to athletes and elderly women, who commonly suffer loss of bone mass an affliction making breakage easier. The drug has been tested as an asthma treatment with encouraging results, though reasons for success are unclear. Some researchers believe the drug has potential in diabetes control. In an experiment measuring alprazolam's...


These behaviors are also seen in other psychiatric syndromes. Learning disabilities can impair comprehension and performance in school and masquerade as ADHD, especially if a child reacts to the failure by excessive motor activity. Children who are oppositional by nature may have difficulty functioning in school in a manner that looks like ADHD. Hyperactivity, excessive speech, dis-tractible thinking, and irritability are often seen in bipolar disorder, and the two can be difficult to tease apart. Some people have both syndromes. People with anxiety or posttraumatic stress disorder can be chronically restless, always on the go, easily distractible, impulsive, and irritable. Excessive use of caffeine or the use of marijuana, cocaine, or alcohol can also cause some of these symptoms.

Pregnancy Category D

Clonazepam is not recommended for persons suffering from narrow-angle glaucoma. The compound may worsen respiratory disease. The substance increases saliva production. It often makes people tired, interferes with muscular coordination, and can impede decision making such effects hinder ability to operate dangerous machinery. Dozens of less common adverse effects are described, ranging from skin rash to painful gums. One case report concludes that clonazepam may promote porphyria, a body chemistry disorder that can make a person violent and supersensitive to light, but such a result is virtually unheard of. A review of medical records of men being treated for posttraumatic stress disorder suggested that the drug may commonly inhibit sexual performance in such a population. Some persons suffer from a disquieting affliction called apnea in which they temporarily stop breathing case reports say clonazepam can cause apnea attacks. An experiment noted a rebound effect when people...

Phobic Disorders

Though there are far fewer controlled family and twin studies of the other anxiety subtypes, all of the phobic states (i.e., specific phobia, agoraphobia) have also been shown to be familial (Fyer et al. 1995 Noyes et al. 1987 for review, see Merikangas and Angst 1995). The average relative risk of phobic disorders in the relatives of phobics is 3.1. Stein et al. (1998a) found that the familial aggregation of social phobia could be attributed to the generalized subtype of social phobia. Data from the Virginia Twin Study report the estimated total heritability for phobias to be 0.35 (Kendler et al. 1992).


There is emerging evidence that links the role of genetic factors to the vulnerability to stress-related psychopathology, such as PTSD. An investigation of twin pairs from the Vietnam Twin Registry reported that inherited factors accounted for up to 32 of the variance of PTSD symptoms beyond the contribution of trauma severity (True et al. 1993). The molecular neurobiological abnormalities that underlie these findings have not been elucidated. Two relatively small association studies which evaluated D2 dopamine receptor polymorphisms in PTSD yielded contradictory results (Comings et al. 1996 Gelernter et al. 1999). A preliminary study found an association between the dopamine transporter (DAT) polymorphism and PTSD (Gelernter et al. 1999). Volumetric magnetic resonance imaging investigations demonstrated a smaller hippocampal volume in PTSD patients (Bremner et al. 1995 Bremner et al. 1997 Gurvits et al.

Chapter Three

It was a fascinating and absorbing time during that first study of LSD. Sid and I were very involved with the psyches and complications of our subjects patients, our colleagues, and almost anyone who had had LSD or was working with it. Certainly our study proved to both of us beyond the shadow of a doubt that LSD was one of the most potent therapeutic tools in existence. Also that it was a powerful drug for teaching observers could watch as patients went through levels of their defensive system, layer by layer, down to core problems. It was amazing how observers could follow, see, and understand the structure and the process. We also learned about the power and the process of abreaction of past traumatic events as we watched and recorded successful solutions of difficulties emerge from the recapitulation of pasttime events, accompanied by emotional turmoil and often explosive actions and vocalizations.


PRECAUTIONS Warnings It is habit-forming. Clonazepam, like all benzo-diazepines, is physically and psychologically habit-forming. People who have experienced traumatic events in their lives and have chronic anxiety are especially prone to developing dependence. Prolonged use is associated with a range of problems. Use for more than four weeks is not recommended. If you stop clonazepam


PRECAUTIONS Warnings It is habit-forming. Diazepam, like all benzodiazepines, is physically and psychologically habit-forming. People who have experienced traumatic events in their lives and have chronic anxiety are especially prone to developing dependence. Prolonged use is associated with a range of problems. Use for more than four weeks is not recommended. If you stop diazepam after more than four weeks of daily use you will probably experience withdrawal symptoms (see below). Seizures can occur if it is stopped abruptly, so consultation with your physician is essential if you wish to stop. Tests needed before starting None. Alcohol Alcohol must be avoided entirely. The simultaneous use of di-azepam and alcohol is extremely dangerous because it can cause you to stop breathing. The combination can cause death. Use in pregnancy There is a higher rate of babies born with a cleft palate to mothers who took benzodiazepines during pregnancy. The elderly are especially sensitive to the...


As a class, benzodiazepines are efficacious for the treatment of many anxiety disorders, including panic disorder, social anxiety disorder, generalized anxiety disorder, alcohol withdrawal, and situational anxiety. Although obsessive-compulsive disorder falls within the taxonomy of anxiety disorders, benzodiazepines do not seem to be particularly effective in treating these patients. The BZDs may be contraindicated in the ongoing treatment of PTSD though open-label studies have suggested efficacy, a recent double-blind study found no benefit, and it is believed that BZDs may cause depression in such patients and potentially worsen the course of the disorder. There are concerns about dependency and stigma associated with the use of benzodiazepine medications.


PRECAUTIONS Warnings It is habit-forming. Estazolam, like all benzodi-azepines, is physically and psychologically habit-forming. People who have experienced traumatic events in their lives and have chronic anxiety are especially prone to developing dependence. Prolonged use is associated with a range of problems. Use for more than four weeks is not recommended. If you stop estazolam after more than four weeks of daily use you will probably experience withdrawal symptoms (see below). Tests needed before starting None. Alcohol Alcohol must be avoided entirely. The simultaneous use of estazolam and alcohol is extremely dangerous because it can cause you to stop breathing. The combination can cause death. Use in pregnancy There is a higher rate of babies born with a cleft palate to mothers who took benzodiazepines during pregnancy. The elderly are especially sensitive to the effects of benzodiazepines and may experience pronounced side effects at low doses (see chapter 4).


The HPA axis alterations in PTSD support the idea that HPA axis alterations are complex and might be associated with different aspects of PTSD, including risk for the development of this disorder. For the findings to coalesce into an integrative neuroendocrine hypothesis ofPTSD, it would be necessary to assert that (1) some features of the HPA axis may be altered prior to the exposure to a focal trauma (2) that components of the HPA axis are not uniformly regulated (e.g., circadian rhythm patterns, tonic cortisol secretion, negative feedback inhibition, and the cortisol response to stress are differentially mediated (3) that the system is dynamic, and may therefore show transient increases or hyperre-sponsivity under certain environmental conditions that (4) other regulatory influences might affect HPA axis regulation in PTSD and probably (though not necessarily), that (5) there might be different biologic variants of PTSD with relatively similar phenotypic expressions, as is the case...


Data from epidemiological studies consistently have shown that anxiety disorders are more common in women than in men. On average, anxiety disorders are about twice as frequent in women (Kessler et al. 1994 Alonso et al. 2004 Jacobi et al. 2004). Although there are variations across the specific forms of anxiety disorders (female male ratio ranging between 1.5 and 2.5), the overall higher risk for women remains stable. The lifetime and 12-month prevalences of agoraphobia, specific phobia, generalized anxiety disorder, panic disorder and posttraumatic stress disorders are approximately twice as prevalent among women as men (Eaton et al. 1991 Kessler et al. 1994 Magee et al. 1996 Bijl et al. 1998 Alonso et al. 2004 Jacobi et al. 2004). Across the surveys, smaller sex differences were found for social phobia and OCD (Magee et al. 1996 Bijl et al. 1998 Alonso et al. 2004 Jacobi et al. 2004).

Life Events

And the subsequent development of anxiety disorders (Ernst et al. 1993 Fer-gusson et al. 1996 Kessler et al. 1997 Bijl et al. 1998 Chartier et al. 2001 DeGraaf et al. 2002). Molnar et al. (2001) evaluated on the basis of the NCS data the relationship between child sexual abuse and subsequent mental disorders. They found that, among women, child sexual abuse increases the risk for agoraphobia, panic disorder, posttraumatic stress disorder and social phobia. Among men, only posttraumatic stress disorder was associated with child sexual abuse. Similar specific findings were recently reported by MacMillan et al. (2001) who found significant associations between child sexual abuse and subsequent anxiety disorders only among women. Other life events that have been investigated include parental divorce, death of parents and early separation from parents, but to date these factors have not consistently been proved as risk factors for the development of anxiety disorders.


PRECAUTIONS Warnings It is habit-forming. Quazepam, like all benzodiazepines, is physically and psychologically habit-forming. People who have experienced traumatic events in their lives and have chronic anxiety are especially prone to developing dependence. Prolonged use is associated with a range of problems. Use for more than four weeks is not recommended. If you stop quazepam after more than four weeks of daily use, you will probably experience withdrawal symptoms (see below). Tests needed before starting None. Alcohol Alcohol must be avoided entirely. The simultaneous use of quazepam and alcohol is extremely dangerous because it can cause you to stop breathing. The combination can cause death. Use in pregnancy There is a higher rate of babies born with a cleft palate to mothers who took benzodiazepines during pregnancy. The elderly are especially sensitive to the effects of benzodiazepines and may experience pronounced side effects at low doses (see chapter 4).


This category contains various drugs that are licensed for the treatment of psychotic disorders. Their effects are mediated via antagonism of D2 dopamine receptors in the limbic system and cortex. They are loosely divided into two groups older classical drugs such as haloperidol and chlorpromazine that are potent D2 blockers and atypical antipsychotics that have a lower affinity for D2 receptors but also block 5-HT2 receptors. The history of clinical use of classical antipsychotics as major tranquillisers has little support from controlled trials (El-Khayat and Baldwin 1998). Evidence is greatest in OCD for the augmentation of SSRI treatment with haloperidol (McDougle et al. 1994) and the atypical drugs risperidone (McDougle et al. 2000) and quetiapine (Atmaca et al. 2002). Recent controlled trials have reported benefits for the atypical drug olanzapine in social anxiety disorder (Barnett et al. 2002) and in addition to SSRIs in PTSD (Stein et al. 2002). Open studies are reporting...

Mental Disorders

Posttraumatic Stress Disorder (PTSD) and Substance Use Disorders. Lifetime prevalence of SUDs in general population samples of individuals with PTSD ranges from 21 to 43 percent (Jacobsen et al., 2001). In a review of clinical samples of SUDs, lifetime PTSD has ranged from 26 to 52 percent, and current PTSD from 15 to 41 percent (Schafer & Najavits, 2007). Rates of PTSD SUD comorbidity may vary with specific substances as well. In a sample drawn from the Australian general population (Mills et al., 2006), alcohol use disorders were the most common SUDs among individuals with PTSD, with a prevalence of 24.1 percent. Among individuals with SUDs, PTSD was most prevalent among those with opioid use disorders (33.2 ) and sedative use disorders (28.5 ), compared to 5.4 percent of individuals with alcohol use disorders and 5.2 percent with cannabis use disorders. Several mechanisms may explain the association between PTSD and SUDs. One is the self-medication hypothesis, which posits that...


PRECAUTIONS Warnings It is habit-forming. Temazepam, like all benzo-diazepines, is physically and psychologically habit-forming. People who have experienced traumatic events in their life and have chronic anxiety are especially prone to developing dependence. Prolonged use is associated with a range of problems. Use for more than four weeks is not recommended. If you stop temazepam after more than four weeks of daily use you will probably experience withdrawal symptoms (see below). Tests needed before starting None. Alcohol Alcohol must be avoided entirely. The simultaneous use of temazepam and alcohol is extremely dangerous because it can cause you to stop breathing. The combination can cause death. Use in pregnancy There is a higher rate of babies born with a cleft palate to mothers who took benzodiazepines during pregnancy. The elderly are especially sensitive to the effects of benzodiazepines and may experience pronounced side effects at low doses (see chapter 4).


SSRIs have been approved for the treatment of the majority of anxiety disorders, except agoraphobia and specific phobia. The mechanisms of action responsible for SSRIs' anxiolytic activity remain to be fully delineated. Understanding of pre- and postsynaptic receptor regulation with chronic treatment and cross-system effects are critical in furthering our understanding of these drugs. Increasing specificity may improve clinical efficacy.


The effects of -adrenergic blockade on the consolidation of traumatic memories has been an area of special interest for the treatment of posttraumatic stress disorder (PTSD), and recently the first randomized controlled study on the effects of propranolol in the prevention of PTSD was published. Pittmann and coworkers (2002) could demonstrate that propranolol may reduce PTSD


PRECAUTIONS Warnings It is habit-forming. Flurazepam, like all ben-zodiazepines, is physically and psychologically habit-forming. People who have experienced traumatic events in their lives and have chronic anxiety are especially prone to developing dependence. Prolonged use is associated with a range of problems. Use for more than four weeks is not recommended. If you


According to the various schools of traditional psychoanalytic thought, the dissolution of neuroses is a lengthy process, whose progress depends on penetrating layers of character armoring and identifying the root causes of unhealthy fixations. Hoping to shorten the duration of treatment by accelerating the pace of resistance dissolution practitioners, have turned to pharmaceuticals as an adjunct to the therapeutic process. Thus, upon discovery of the unique properties of hallucinogenic agents during the 1950's, LSD gained widespread popularity as a therapeutic agent, while mescaline remained obscure, as it was used by comparatively few practitioners. Patients under the influence of these substances confronted long repressed traumatic events as they began to surface and enter conscious awareness. In some cases, such emerging traumatic experiences had been repressed since early childhood. Medical records and case histories indicate that many patients not only remembered, but actually...


PRECAUTIONS Warnings It is habit-forming. Clorazepate, like all benzodiazepines, is physically and psychologically habit-forming. People who have experienced traumatic events in their lives and have chronic anxiety are especially prone to developing dependence. Prolonged use is associated with a range of problems. Use for more than four weeks is not recommended. If you stop clo-razepate after more than four weeks of daily use you will probably experience withdrawal symptoms (see below). Seizures can occur if it is stopped abruptly, so consultation with your physician is essential if you wish to stop. Tests needed before starting None. Alcohol Alcohol must be avoided entirely. The simultaneous use of clorazepate and alcohol is extremely dangerous because it can cause you to stop breathing. The combination can cause death. Use in pregnancy There is a higher rate of babies born with a cleft palate to mothers who took ben-zodiazepines during pregnancy. The elderly are especially sensitive...

Neuroactive Steroids

While no data on the role of 3a-reduced neuroactive steroids in PTSD or its treatment in panic disorder patients have been published to date, opposite changes to those seen in major depression have emerged. At baseline, patients with panic disorder had significantly increased concentrations of the positive allosteric modulators 3a,5a-THP and 3a,50-THP, together with sig


PRECAUTIONS Warnings It is habit-forming. Chlordiazepoxide, like all benzodiazepines, is physically and psychologically habit-forming. People who have experienced traumatic events in their lives and have chronic anxiety are especially prone to developing dependence. Prolonged use is associated with a range of problems. Use for more than four weeks is not recommended. If you stop chlordiazepox-


Another significant, psychotherapeutically valuable characteristic of LSD inebriation is the tendency of long forgotte n or suppressed contents of experience to appear again in consciousness. Traumatic events, which are sought in psychoanalysis, may then become accessible to psychotherapeutic treatment. Numerous case histories tell of experiences from even the earliest childhood that were vividly recalled during psychoanalysis under the influence of LSD. This does not involve an ordinary recollection, but rather a true reliving not a r miniscence, but rather a r viviscence, as the French psychiatrist Jean Delay has formulated it.


PRECAUTIONS Warnings It is habit-forming. Lorazepam, like all benzodiazepines, is physically and psychologically habit-forming. People who have experienced traumatic events in their lives and have chronic anxiety are especially prone to developing dependence. Prolonged use is associated with a range of problems. Use for more than four weeks is not recommended. If you stop lorazepam after more than four weeks of daily use you will probably experience withdrawal symptoms (see below). Seizures can occur if it is stopped abruptly, so consultation with your physician is essential if you wish to stop. Tests needed before starting None. Alcohol Alcohol must be avoided entirely. The simultaneous use of lo-razepam and alcohol is extremely dangerous because it can cause you to stop breathing. The combination can cause death. Use in pregnancy There is a higher rate of babies born with a cleft palate to mothers who took benzodiazepines during pregnancy. The elderly are especially sensitive to the...


The use of antidepressants in the treatment of depression remains the best-understood use of these medications however, there is a growing list of other indications for antidepressants, including panic disorder (PD), obsessive-compulsive disorder (OCD), bulimia and posttraumatic stress disorder (PTSD). Many of these illnesses respond best to combination treatment modalities that include medication and various forms of psychotherapy.