Social Phobia
Excessive fear of social or performance settings is accompanied by extreme anxiety when the Pt is exposed to these situations. Generalized social phobia involve fear in most social interactions, public speaking. Patients often have very severe impairments in their daily lives. Social phobia usually begins in the midteens, sometimes after an embarrassing incident. It lasts throughout the patient's life, with exacerbations during times of stress.
Differentiate from panic d/o, which has no clear precipitant.
Si & Sx: Severe anxiety or panic attract. Avoidance of phobic situations and dread being embarrassed. Pts have low self-esteem and may be underachievers. Anxiety may be evident with even minimal contact, and other anxiety or mood d/o are often present. Adults have insight that their fear is unwarranted but children usually do not.
Tx: Behavior therapy, MAOIs and antidepressants, SSRIs, and buspirone may also be useful. BB can be used for stage fright, to block tachycardia and prespiration.
Acute Stress Disorder
During a traumatic event, the patient experiences a sense of detachment or numbed emotion, a lack of awareness, depersonalization, or dissociative amnesia. Dissociative symptoms follow the trauma, with numbed emotions, guilt, or an inability to experience pleasure. As in PTSD, the patient relives the event and tries to avoid related stimuli.
On physical exam, injury resulting from the recent trauma may be evident.
Symptoms must last at least 2 days and less than 4 weeks, after which the diagnosis of PTSD applies. Also symptoms occur within 1 month of exposure to stressor. Supportive therapy may be helpful.
Post-Traumatic Stress Disorder
PTSD develop after experiencing or witnessing a traumatic event. It develops within 3 months of the event (acute). Half of patients recover completely within 3 more months, whereas others have symptoms for more than a year.
Chronic symptoms >3 months, with delayed onset (onset of symptoms at least 6 months after stressor) PTSD may coexist with other anxiety d/o or with depression. Social supports and personal history can affect the development of PTSD, although it can occur in patients without any apparent predisposition.
Increased susceptibility: In most trauma-exposed persons (e.g., 78% of those exposed to combat), PTSD does not develop after the exposure. The intensity of the trauma and individual susceptibility interact to influence the likelihood of PTSD. Factors associated with increased susceptibility include female sex, childhood trauma, fewer years of schooling, prior mental disorders, exposure to four or more traumatic events, and a history of exposure to interpersonal violence.
Signs and symptoms: Dreams, memories, and flashbacks of the trauma are prominent and intrusive symptoms causing distressing memories, nightmares, and dissociative symptoms.The resulting psychological distress is severe. Pt. try to avoid settings that trigger memories, but may, at the same time, be amnestic of the trauma. They typically feel detached, numb, unemotional, and unable to experience pleasure. Survivor guilt, self-destructive behavior, somatization, and social withdrawal are common. Anxiety and hypervigilance are often seen, and increased autonomic arousal (rapid heart rate and increased sweating) may be noted on exam.
Dx: For a dx to apply, a Pt. must experience a traumatic event and have felt intense fear, helplessness, or horror. Hypervigilance, mentally reliving the event, and avoiding associated stimuli occur for at least 1 month for diagnosis of acute PTSD and for more than 3 months for diagnosis of chronic PTSD.
MRI studies show reduced hippocampal volume in some individuals with PTSD when compared with controls.
Two recently validated, short questionnaires have improved clinical screening for PTSD: the 4-item Primary Care PTSD Screen (PC-PTSD) and the 17-item PTSD Checklist (PCL). The PCL also quantifies the severity of symptoms and can be used to monitor the response to treatment. To better target the intervention, the clinician should assess the interference of symptoms with the patient’s daily life, memory, concentration, sleep, and self-care. The patient should also be assessed for concurrent depression, suicidal ideation, alcohol and drug use, and ongoing environmental pressures.
Tx: Counseling. Give benzodiazepines acutely for anxiety symptoms. SSRIs, TCAs, MAOIs, and SSRIs may all be useful. Psychotherapy is also effective.
Therapies for PTSD include psychological, pharmacologic, and innovative interventions. Trauma-focused cognitive behavioral therapy (CBT) is the best-supported psychological intervention for PTSD. CBT revisits distressing elements of the traumatic events and consequent avoidance and cognitive distortions. Most patients with PTSD (e.g., 74% of affected war veterans) receive some form of pharmacologic treatment, including antidepressant agents, anxiolytic or sedative–hypnotic agents, and antipsychotic agents (prescribed, respectively, for 89%, 61%, and 34% of those receiving pharmacotherapy). Effect sizes for antidepressants in patients with PTSD are relatively small. These agents alleviate symptoms but rarely induce remission, and there is a substantial risk of relapse on discontinuation. Paroxetine and sertraline are approved by the Food and Drug Administration for the treatment of PTSD. In addition, venlafaxine and nefazodone have been recommended for PTSD; mirtazapine, trazodone, and prazosin have been used for insomnia and nightmares; and topiramate has been used in patients with PTSD and alcohol use disorder.
Neurofeedback trains patients to regulate PTSD-associated brain dysfunction by exposing them to malleable real-time displays of brain activity (mostly electroencephalographic displays). Preliminary studies show that changing brain-wave activity or connectivity on functional magnetic resonance imaging with the use of neurofeedback alleviates PTSD symptoms. Transcranial magnetic stimulation is a noninvasive brain-stimulation procedure that can alter neuronal activity through the administration of magnetic pulses to dedicated brain areas. Preliminary studies suggest that transcranial magnetic stimulation of the right dorsolateral prefrontal cortex has a positive effect. Cycloserine, a partial agonist of the glutamatergic N-methyl-d-aspartate (NMDA) receptor, has been evaluated for its capacity to enhance extinction learning (i.e., a reduction in a learned response) during cognitive behavioral therapy, with conflicting results. There is also considerable interest in endocannabinoid modulators. Finally, preliminary data suggest that intravenous ketamine, a glutamate NMDA receptor antagonist, rapidly reduces the severity of PTSD symptoms, but further evidence is required to substantiate its clinical use.
Specific Phobia
Most common phobia. Previously called simple phobias, specific phobia is the fear of a particular object or situation. Pts have a persistent, unreasonable, intense fear of situations, circumstances, or objects. These include fear of being injured, of losing control, or of fainting. Most have childhood onset, and may or may not have traumatic events or panic attacks may predispose the patient to developing a phobia. Women are diagnosed with these d/o more frequently than men.
The object in question immediately provokes a panic attack or excessive anxiety. The level of severity is related to the proximity to the object and to the patient's capacity to escape. Instead of panic attacks, some Pts may have vasovagal responses, particularly with phobias to blood, needles, or injury. In avoiding the phobic object, patient may have significant impairment in social or occupational functioning. Adult Pts generally have some insight into the unwarranted nature of their fears.
It is differentiated from PTSD and acute stress d/o, which has a history of a traumatic event. There is no known eliciting events in phobic d/o associated with the onset of symptoms.
Tx: Behavior therapy. Exposure therapy (involves increasing exposure to stimulus in order to induce habituation and decreased anxiety). Benzodiazepines and BB are helpful when given prior to exposure.
Generalized Anxiety Disorder. "Worry Wart"
Dxtic Criteria:
A. Excessive anxiety and worry (apprehensive expectation), occurring more days than not for at least 6 mo, about a number of events or activities (such as work or school performance). In GAD, multiple life circumstances, not just one, are causing the anxiety. Interferes with daytime functioning.
B. The person finds it difficult to control the worry.
C. The anxiety and worry are associated with 3 or more of the following six symptoms (with at least some sx present for more days than not for the past 6 mo): (1) restlessness or feeling keyed up or on edge; (2) being easily fatigued; (3) difficulty concentrating or mind going blank; (4) irritability; (5) muscle tension; (6) sleep disturbance (difficulty falling or staying asleep, or restless unsatisfying sleep).
Mnemonic: REDIMS:
Restlessness or feeling keyed up or on edge
Easy fatigability
Difficulty concentratinG
Irritability
Muscle tension
Sleep disturbance
D. The focus of the anxiety and worry is not confined to features of an Axis I disorder, e.g., the anxiety or worry is not about having a panic attack (as in panic disorder), being embarrassed in public places (as in social phobia), being contaminated (OCD), being away from home or close relatives (as in separation anxiety disorder), gaining wt (as in anorexia nervosa), having multiple physical complaints (as in somatization disorder), or having a serious illness (as in hypochondriasis), and the anxiety and worry do not occur exclusively during PTSD.
E. The anxiety, worry, or physical sx cause clinically significant distress or impairment in social, occupational, or other important areas of functioning.
F. The disturbance is not due to the direct physiologic effects of a substance (e.g., a drug of abuse, a med) or general med condition (hypothyroidism) and does not occur exclusively during a mood disorder, a psychotic disorder, or a pervasive developmental disorder.
Tx: Supportive psychotherapy, including relaxation techniques and biofeedback. SSRIs, venlafaxine, buspirone, and benzodiazepines.
Buspirone is the best option for people with occupations where driving or machinery is involved, as there is no sedation or cognitive impairment. No withdrawal syndrome.
Obsessive-Compulsive Disorder
An obsession is a recurrent thought, feeling, idea, or image that is unpleasant and intrusive but cannot be controlled by the patient. Common obsessions concern contamination, order, frightening images or doubts, or disturbing sexual images. Pts try to suppress or counteract their obsessions, they realize it is unreasonable and excessive (i.e., there is insight). A compulsion is a repeated mental or motor behavior performed to lessen anxiety, usually following the desired goal . Common compulsions are repetitive checking, washing, counting, and stereotyped ordering (e.g., alphabetizing soup cans).
The severe, recurrent obsessions or compulsions that characterize OCD cause the patient significant distress and may require excessive time to complete. It should take up at least >1 h/day time.
Epidemiology: OCD begins in the late teens and early 20s but one third of the Pts show symptoms of OCD before age 15. Men and women have equal rates of this diagnosis. Most patients have exacerbations at stressful times. There is high rate of concordance with Tourette's syndrome and other tic disorders.
Etiology: Behavioral models of OCD propose that obsessions and compulsions are produced and sustained through classic and operant conditioning. It is also seen after head injury or seizure d/o. They may be a biological basis for this disorder as studies have shown that monozygotic twins have a higher concordance rate than dizygotic twins. The neurotransmitter serotonin has been implicated as a mediator in obssessive thinking and compulsive behavior. The anatomy of OCD is thought to include orbital frontal cortex, caudate nucleus, and globus pallidus. The caudate appears to be involved in the acquisition of maintenance of habit and skill learning, and interventions that are successful in reducing obsessive-compulsive behaviors also decrease metabolic activity measured in caudate.
In patients with obsessive-compulsive disorder (OCD), structural and volumetric abnormalities have been identified by up-to-date neuroimaging techniques both in the prefrontal region and in the basal ganglia (striatum, thalamus, amygdala). The dysfunction of these regions also has been proved by neuroimaging techniques. These alterations can be described as dopaminergic hyperfunction in the prefrontal cortex and serotonergic hypofunction in the basal ganglia. The dysfunction of the so-called 'cortico-striato-thalamic' loops is strongly linked to the symptoms of OCD, where the dopamine is the most dominant neurotransmitter. The ascending serotonergic projections from the raphe nuclei restrain and control the function of these loops. Thus, when serotonergic hypofunction is present, the predominantly dopaminergic loops became overactive, which has been confirmed by neuroimaging techniques and by neurocognitive tests as well.
The linkage of the two predominant neurotransmitter systems affected in OCD can be the reason for the fact that SSRIs have limited success in the treatment of OCD symptoms. In recent international, multicentric studies, the treatment of SSRI non-responder subgroup of OCD patients were supplemented by antipsychotics with dopaminergic activity. Many studies have confirmed the beneficial effect of these antidopaminergic substances on the hyperactive cortico-striato-thalamic loops in OCD.
The investigation of these dysfunctional loops is also connected to the genetic background of OCD, because some of the candidate gene regions of OCD are coding proteins of the dopamine synthesis (for example: COMT).
Signs and symptoms: Onset is gradual, beginning in early adulthood, but childhood onset is not rare. It has a waxing and waning course, but some cases may show a steady deterioration in psychosocial functioning. Pts may avoid settings that evoke obsessions or compulsions. Sleep disturbances, alcohol use, and feelings of guilt are common. Skin problems from cleaning, chafed and reddened hands; alopecia (from repetitive hair pulling, or trichotillomania) compulsions may be found on physical examination.
Diagnosis: Obessions and compulsions may require excessive time or cause severe distress. Adult patients must have some degree of insight, realizing that the behaviors are unusual. Obsessive sx in psychotic d/o may be misdiagnosed as OCD. You can differentiate psychosis form OCD by looking for a lack of insight and loss of contact with reality.
Comorbidities: depression, other anxiety d/o, eating d/o, and tics.
Tx: TCA (clomipramine) 25-250 mg/d, but is poorly tolerated due to its anticholinergic and sedative effects at these doses. Its efficacy is unrelated to antidepressant activity.
Fluoxetine, 5-60 mg/d, fluvoxamine 25-300 mg/d, and sertraline 50-150 mg/d are better thean clomipramine with less side effect profile. Only 50-60% show improvement with phamacotherapy alone. In treatment resistant cases, augmentation with other serotonergic agents, such as buspirone, or with a neuroleptic or benzodiazepine may be beneficial. After achieving a therapeutic response, long term maintenance is usually indicated.
Behavioral therapy are often effective. Most patients improve, although one-third later develop major depression.
Anxiety Due to Medical Conditions and Medications: Anxiety and panic attacks can be caused by medical disorders. Thyroid disorders, hyoglycemia, pheochromocytoma, COPD, cardiac arrhythmias, and CHF may all bring about symptoms of anxiety or panic. The diagnosis is supported by an appropriate temporal relation between the medical condition and the anxiety disorder. Sympathomimetic substances such as amphetamine, cocaine, and caffeine may also cause symptoms of anxiety. Corticosteroids, alcohol and sedative withdrawal states.
Do not give Cymbalta (duolexetine) in Hep C or liver disease.
Adjustment disorder: This is a normal psychological reaction (anxiety, depression, irritability) that occurs soon after profound changes in a person's life, such as divorce, migration, or birth of a handicapped child. Symptoms are not severe enough to be classified in another category. Adjustment d/o in not a true anxiety d/o.
Tx: Do not treat these patients with medications instead provide counseling to help with the patient adjust to the life stressor.