Anxiety is an emotion characterized by an unpleasant state of inner turmoil, often accompanied by nervous behavior such as pacing back and forth, somatic complaints, and rumination. It includes subjectively unpleasant feelings of dread over anticipated events. [need quotation to verify]Anxiety is a feeling of uneasiness and worry, usually generalized and unfocused as an before (or thesis) (CBT) for anxiety disorders including post-traumatic stress disorder, obsessive-compulsive disorder, panic disorder, generalized anxiety May 04, · Anxiety disorder due to a medical condition includes symptoms of intense anxiety or panic that are directly caused by a physical health problem. Generalized anxiety disorder includes persistent and excessive anxiety and worry about activities or events — even ordinary, routine issues. The worry is out of proportion to the actual circumstance
Anxiety disorders - Symptoms and causes - Mayo Clinic
Try out PMC Labs and tell us what you think. Learn More. Functional imaging studies have reported with remarkable consistency hyperactivity in the orbitofrontal cortex OFCanterior cingulate cortex ACCand caudate nucleus of patients with Obsessive-Compulsive Disorder OCD.
These findings have often been interpreted as evidence that abnormalities in cortico-basal ganglia-thalamo-cortical loops involving the OFC and ACC are causally related to OCD. This interpretation remains controversial, however, because such hyperactivity may represent either a cause or a consequence of the symptoms.
This article analyzes the evidence for a causal role of these loops in producing OCD in children and adults. The article first reviews the strong evidence for anatomical abnormalities in thesis on generalized anxiety disorder loops in patients with OCD.
These findings are not sufficient to establish causality, however, because anatomical alterations may themselves be a consequence rather than a cause of the symptoms, thesis on generalized anxiety disorder. The article then reviews three lines of evidence that, despite their own limitations, permit stronger causal inferences: the development of OCD following brain injury, pediatric autoimmune neuropsychiatric disorders associated with streptococcal infection, and neurosurgical lesions that attenuate OCD.
Converging evidence from these various lines of research supports a causal role for the cortico-basal ganglia-thalamo-cortical loops that involve the OFC and ACC in the pathogenesis of OCD in children and adults. It affects an estimated 50 million people worldwide Sasson et al.
OCD is typically characterized by the presence of both obsessions and compulsions, although the presence of either obsessions or compulsions alone is sufficient to make the diagnosis of OCD DSM-IV.
Obsessions are recurrent, persistent, thesis on generalized anxiety disorder, and intrusive ego-dystonic thesis on generalized anxiety disorder, impulses, or images; compulsions are repetitive behaviors or mental acts that are executed with the goal of preventing or reducing distress, or preventing some dreaded event or situation DSM-IV. The age of onset of OCD seems to have a bimodal distribution, with a peak in childhood at approximately 10 years of age and another in early adulthood Geller, ; Geller, Biederman, Jones, Shapiro et al.
Estimates of the prevalence of OCD among adolescents are of approximately 2 — 3. Childhood- and adult-onset OCD differ in several ways. Taylor, Most brain imaging studies that include adults with OCD use mixed samples that include adults with childhood- and adult-onset OCD. Given the evidence that brain activity differs in adults with childhood- versus adult-onset OCD Busatto et al.
In addition, many studies report only the mean and standard deviation of age of illness onset, which are inadequate to characterize what are likely to be bimodal distributions. Consequently, knowing whether findings apply to all adults with OCD or only to those with childhood- or adult-onset OCD is impossible for most existing studies that include adults with OCD. In addition, few studies have compared the neural correlates of OCD across children and adults, severely limiting our knowledge of their similarities and differences.
One of the aims of this review is to begin to redress this gap by systematically evaluating the similarities and differences in findings from studies of the neural bases of pediatric and adult OCD. We should note, however, that differences in findings across these age groups may be due to several factors. We list four, thesis on generalized anxiety disorder, non-exhaustive possibilities.
First, any such differences may be a consequence of comparing children with OCD with mixed samples that include adults with childhood-onset OCD and adults with adult-onset OCD. If childhood-onset OCD is a distinct biological subtype, this comparison confounds age or developmental effects with the effects of illness subtype. Second, such differences may be a consequence of compensatory behavioral, cognitive, or affective responses, which may be more developed — or simply different — in adults.
Third, such differences may reflect the differences in phenomenology between pediatric and adult OCD Geller, Biederman, Jones, Park et al. Fourth, such thesis on generalized anxiety disorder may be a consequence of brain development, thesis on generalized anxiety disorder, affecting either the neural systems directly involved in the symptoms of OCD or closely related systems.
Much of our understanding of the pathophysiology of OCD has been derived from functional neuroimaging studies. Combinations of these categories are also possible: one can, for example, image cognitive activation or symptom provocation before and after treatment Lazaro et al.
These findings have generally been interpreted as evidence that abnormalities in these or closely related areas cause OCD e. Two studies have compared resting blood flow before and after pharmacological treatment in children with OCD Castillo et al. One of these studies Diler et al. The findings of this study were largely consistent with the findings in adults, including hyperactivity at rest in the caudate and ACC of treatment-naïve children, which declined following treatment.
The other study Castillo et al. We are not aware of any symptom provocation studies in children with OCD, thesis on generalized anxiety disorder. The situation has shifted in recent years, with the publication of a large number of cognitive activation studies in adults with OCD, using a wide variety of cognitive tasks with an emphasis on executive function tasks.
Rather than attempting to survey this large and varied literature, though, we wish to highlight a general difficulty with interpreting cognitive activation studies that applies across tasks. Typically, a given cognitive task only activates those areas involved in the cognitive processes required to perform the task. Whether and how the cognitive processes involved in the tasks that have been used to study OCD may relate to the symptoms of OCD is not always obvious, thesis on generalized anxiety disorder.
For example, most cognitive activation studies of Thesis on generalized anxiety disorder have used inhibitory control tasks. However, the relevance of those studies to understanding the symptoms of OCD depends on the unproven assumption that those symptoms relate directly to a deficit in inhibitory control. The symptoms of OCD have indeed been suggested to be a consequence of deficient inhibitory control, with obsessions arising from a failure to inhibit intrusive thoughts, thesis on generalized anxiety disorder, and compulsions arising from a failure to inhibit certain behaviors Chamberlain et al.
Robinson et al. The presence of deficits in inhibitory control in so many disorders with such widely varying phenotypes suggests caution in interpreting such deficits as the root cause of OCD. Despite these limitations, cognitive activation studies can certainly be informative. Early cognitive activation studies, for example, found that healthy controls recruited the striatum during performance of an implicit habit learning task, whereas patients with OCD recruited the hippocampus, despite similar behavioral performances across the groups Rauch et al.
If so, the performance of patients with OCD should suffer more than that of healthy controls when a secondary task that taxes working memory is introduced, and this was confirmed experimentally Deckersbach et al, thesis on generalized anxiety disorder. These studies show that even in the absence of obvious differences in behavioral performance, cognitive activation studies may highlight differences in neural activity that reflect compensatory strategies.
On the other hand, the pathogenic relation, if any, of deficits in implicit habit learning and the symptoms of OCD remains unclear. However, from the idea that OCD prominently involves exaggerated habits the compulsionsone could equally plausibly have predicted the opposite pattern of findings — that the habit learning system in OCD should be especially powerful and effective.
This highlights again the difficulties with interpreting the relevance thesis on generalized anxiety disorder cognitive tasks and cognitive activation studies for the pathogenesis of OCD. Several CBGTC loops exist, and they seem to run largely parallel courses through the basal ganglia Alexander et al. Each of these thesis on generalized anxiety disorder receives inputs from multiple cortical areas and then projects back to one of its cortical areas of origin, thereby partly closing the loop Alexander et al.
No consensus exists in the literature about exactly how many such loops there are, but a particularly influential formulation proposes the existence of five loops, whose target areas are a the supplementary motor area, b the frontal eye fields, c the dorsolateral prefrontal cortex DLPFCd the lateral OFC; and e the ACC Alexander et al. The main site in the striatum through which the CBGTC loops involving the OFC and ACC run is the head of the caudate nucleus Alexander et al.
The net effect of the direct pathway is excitatory and the net effect of the indirect pathway is inhibitory Figure 1so these pathways are sometimes said to form positive and negative feedback loops, respectively.
The direct pathway runs from cortex to the striatum, then directly to the globus pallidus internal segment GPi and substantia nigra pars reticulata SNrthen to the thalamus, thesis on generalized anxiety disorder, and finally back to cortex. Arrows represent excitatory glutamatergic connections and circles represent inhibitory GABAergic connections. The direct pathway contains an even number of inhibitory connections 2so its net effect from cortex back to cortex is excitatory.
The indirect pathway contains an odd number of inhibitory connections 3so its net effect from cortex back to cortex is inhibitory. These symptoms are in the motor domain, but different symptoms may occur if the balance of the direct and indirect pathways is compromised in non-motor CBGTC loops, thesis on generalized anxiety disorder. This theory of OCD is not without difficulties, though.
In particular, thesis on generalized anxiety disorder, it does not explain why patients with OCD should have specific obsessions, as opposed to obsessing about everything. This can be unpacked into two, related questions.
The first is why one finds great similarity in the contents of obsessions cross-culturally Sasson et al. This suggestion also fails to explain why some patients with OCD will, for example, obsess about germs and wash compulsively, whereas others may obsess about whether they have locked the doors to their house and check the locks compulsively.
As noted above, the findings that in patients with OCD the OFC, ACC, and caudate nucleus are hyperactive at rest, become more active under symptom provocation, thesis on generalized anxiety disorder show less activity following treatment, have generally been interpreted as evidence that hyperactivity in these areas generates the symptoms of OCD e.
Several alternative interpretations of these findings are, however, equally plausible, thesis on generalized anxiety disorder. We know, for example, that when healthy controls are exposed to pictures depicting OCD-relevant scenes specifically, pictures that are washing-relevant, checking-relevant, and hoarding-relevant and are asked to imagine related scenarios e.
A related, though slightly different idea is that hyperactivation of the OFC, thesis on generalized anxiety disorder, ACC, and caudate nucleus simply reflects the need to inhibit compulsive behavior during the scan Peterson, Further support for this idea comes from the findings that the OFC, ACC, and caudate are activated in a variety of tasks that require the suppression of a prepotent response Peterson, Consistent with the idea that OFC activity plays an inhibitory role, keeping the obsessions, compulsions, or anxiety in check, greater activation of the OFC during symptom provocation is associated with a smaller increase in reported symptoms with the provocation Adler et al.
If OFC hyperactivity played a role in causing, rather than in inhibiting symptoms, then greater activation of the OFC during symptom provocation should be associated with a greater, not a lesser, increase in symptoms. Our goal is not to suggest that one of these various interpretations is the correct one. Instead, thesis on generalized anxiety disorder, we wish to emphasize that all are consistent with the findings that the OFC, ACC, and caudate nucleus are hyperactive at rest, become more active under symptom provocation, and show less activity following treatment.
For example, if the activation of these areas reflects an attempt thesis on generalized anxiety disorder inhibit symptoms, such activation could be expected to be higher at rest in patients with OCD than in healthy controls, to increase with symptom provocation, when such inhibition becomes more necessary, and to decrease after treatment, when such inhibition becomes less necessary.
The problem with interpreting these activations as the cause of the symptoms is that these functional imaging findings are inherently correlational: they demonstrate only that activity in these areas correlates with a symptomatic state in OCD.
One might hope that anatomical imaging studies would resolve the difficulties in establishing a causal role for these areas in OCD. However, much evidence suggests that repeatedly engaging in a class of behaviors or cognitive processes can change brain structure Lazar et al.
Thus, even anatomical differences in the brains of patients with OCD may be a consequence rather than a cause of the disorder. This highlights the usefulness of studying patients with OCD as close to symptom onset as possible, thesis on generalized anxiety disorder, when such epiphenomenal changes may be less prominent. OCD is, however, often diagnosed thesis on generalized anxiety disorder after the onset of symptoms, making this strategy relatively impractical.
The problem is that, like functional imaging studies, anatomical studies only provide thesis on generalized anxiety disorder about the correlates of the disorder. Other lines of evidence may, however, help establish causality in humans, thesis on generalized anxiety disorder.
We will explore three such lines of evidence. First, certain brain lesions due to accidents, stroke, and other naturalistic causes seem to cause OCD. Third, several neurosurgical procedures make localized lesions in attempts to provide symptom-relief in severe, treatment-refractory cases of OCD.
Each of these lines of evidence has important limitations in establishing a causal role for abnormalities in specific brain regions in producing OCD. First, studies of OCD as a consequence of brain injury typically involve a small number of subjects who have diffuse lesions that vary greatly across subjects.
Furthermore, demonstrating that lesions that affect certain brain circuits result in OCD does not, per se, prove a pathogenic role for those circuits in most cases of OCD. Third, neurosurgical studies lack appropriate controls, and the mechanisms by which they attenuate OCD symptoms are not fully understood. Moreover, an improvement in symptoms following certain neurosurgical lesions does not, per se, prove that the circuits that were lesioned caused the symptoms just as having a gastric bypass surgery and losing weight as a result does not prove that the cause of excess weight was an enlarged stomach.
We will therefore review thesis on generalized anxiety disorder of these lines of evidence in turn. Volumetric studies thesis on generalized anxiety disorder the volumes of specific regions of interest ROIs in the brain. Proton magnetic resonance spectroscopy 1 H-MRS studies measure the concentrations of certain metabolites in ROIs. NAA levels may be more sensitive than volumetric measures to detect neuronal abnormalities Bartha et al.
DSM Generalized Anxiety Disorder
, time: 13:31Anxiety - Wikipedia
Childhood- Versus Adult-Onset OCD. The age of onset of OCD seems to have a bimodal distribution, with a peak in childhood (at approximately 10 years of age) and another in early adulthood (Geller, ; Geller, Biederman, Jones, Shapiro et al., ).Estimates of the prevalence of OCD among adolescents are of approximately 2 – % (Flament et al., ; May 04, · Anxiety disorder due to a medical condition includes symptoms of intense anxiety or panic that are directly caused by a physical health problem. Generalized anxiety disorder includes persistent and excessive anxiety and worry about activities or events — even ordinary, routine issues. The worry is out of proportion to the actual circumstance In this case, it can be classified as an anxiety disorder. Anxiety disorders include panic disorder, posttraumatic stress disorder (PTSD), and obsessive-compulsive disorder (OCD). These forms of anxiety are common and require treatment. You can start your essays on anxiety by looking for inspiration from sample papers
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