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Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study surveys Vietnamese refugees attending two psychiatric clinics to determine both the prevalence of panic disorder (PD) as well as panic attack subtypes in those suffering PD. A culturally valid adaptation of the SCID-panic module (the Vietnamese Panic Disorder Survey or VPDS) was administered to 100 Vietnamese refugees attending two psychiatric clinics. Utilizing culturally sensitive panic probes, the VPDS provides information regarding both the presence of PD and panic attack subtypes during the month prior to interview. Of 100 patients surveyed, 50 (50%) currently suffered PD. Among the 50 patients suffering PD, the most common panic attack subtypes during the previous month were the following: "orthostatic dizziness" (74% of the 50 panic disorder patients [PDPs]), headache (50% of PDPs), wind-induced/temperature-shift-induced (24% of PDPs), effort-induced (18% of PDPs), gastro-intestinal (16% of PDPs), micturition-induced (8% of PDPs), out-of-the-blue palpitations (24% of PDPs), and out-of-the-blue shortness of breath (16% of PDPs). Five mechanisms are adduced to account for this high PD prevalence as well as the specific profile of subtypes: 1) a trauma-caused panic attack diathesis; 2) trauma-event cues; 3) ethnic differences in physiology; 4) catastrophic cognitions generated by cultural syndromes; and 5) a modification of Clark's spiral of panic.
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PMID:Panic disorder among Vietnamese refugees attending a psychiatric clinic: prevalence and subtypes. 1173 65

People exposed to high altitudes often experience somatic symptoms triggered by hypoxia, such as breathlessness, palpitations, dizziness, headache, and insomnia. Most of the symptoms are identical to those reported in panic attacks or severe anxiety. Potential causal links between adaptation to altitude and anxiety are apparent in all three leading models of panic, namely, hyperventilation (hypoxia leads to hypocapnia), suffocation false alarms (hypoxia counteracted to some extent by hypocapnia), and cognitive misinterpretations (symptoms from hypoxia and hypocapnia interpreted as dangerous). Furthermore, exposure to high altitudes produces respiratory disturbances during sleep in normals similar to those in panic disorder at low altitudes. In spite of these connections and their clinical importance, evidence for precipitation of panic attacks or more gradual increases in anxiety during altitude exposure is meager. We suggest some improvements that could be made in the design of future studies, possible tests of some of the theoretical causal links, and possible treatment applications, such as systematic exposure of panic patients to high altitude.
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PMID:High altitudes, anxiety, and panic attacks: is there a relationship? 1221 35

We examined the feasibility, acceptability, and therapeutic efficacy of a culturally adapted cognitive-behavior therapy (CBT) for twelve Vietnamese refugees with treatment-resistant posttraumatic stress disorder (PTSD) and panic attacks. These patients were treated in two separate cohorts of six with staggered onset of treatment. Repeated measures Group x Time ANOVAs and between-group comparisons indicated significant improvements, with large effect sizes (Cohen's d) for all outcome measures: Harvard Trauma Questionnaire (HTQ; d = 2.5); Anxiety Sensitivity Index (ASI: d = 4.3); Hopkins Symptom Checklist-25 (HSCL-25), anxiety subscale (d = 2.2); and Hopkins Symptom Checklist-25, depression subscale (d = 2.0) scores. Likewise, the severity of (culturally related) headache-and orthostasis-cued panic attacks improved significantly across treatment
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PMID:CBT for Vietnamese refugees with treatment-resistant PTSD and panic attacks: a pilot study. 1563 22

We enrolled six patients suffering from refractory chronic cluster headache in a pilot trial of neurostimulation of the ipsilateral ventroposterior hypothalamus using the stereotactic coordinates published previously. After the varying durations needed to determine optimal stimulation parameters and a mean follow-up of 14.5 months, the clinical outcome is excellent in three patients (two are pain-free; one has fewer than three attacks per month), but unsatisfactory in one patient, who only has had transient remissions. Mean voltage is 3.28 V, diplopia being the major factor limiting its increase. When the stimulator was switched off in one pain-free patient, attacks resumed after 3 months until it was turned on again. In one patient the implantation procedure had to be interrupted because of a panic attack with autonomic disturbances. Another patient died from an intracerebral haemorrhage that developed along the lead tract several hours after surgery; there were no other vascular changes on post-mortem examination. After 1 month, the hypothalamic stimulation induced resistance against the attack-triggering agent nitroglycerin and tended to increase pain thresholds at extracephalic, but not at cephalic, sites. It had no detectable effect on neurohypophyseal hormones or melatonin excretion. We conclude that hypothalamic stimulation has remarkable efficacy in most, but not all, patients with treatment-resistant chronic cluster headache. Its efficacy is not due to a simple analgesic effect or to hormonal changes. Intracerebral haemorrhage cannot be neglected in the risk evaluation of the procedure. Whether it might be more prevalent than in deep-brain stimulation for movement disorders remains to be determined.
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PMID:Hypothalamic stimulation in chronic cluster headache: a pilot study of efficacy and mode of action. 1568 58

Panic disorder is one of the most common anxiety disorders and has a lifetime prevalence of 3-5%. Panic attacks can begin at any age, but commonly have their onset in early adulthood between the ages of 20 and 40 years. Naturalistic data has shown that panic disorder has a chronic and relapsing course. Panic disorder is reported to be associated with an increased risk of suicidal behavior and comorbid psychiatric diagnoses such as depression and substance abuse. Currently, recommended treatment modalities for panic disorder include the use of antidepressant pharmacotherapy and/or cognitive behavioral therapy. Paroxetine is unique among the selective serotonin reuptake inhibitors since, in addition to its effect on the CNS serotonergic neurotransmission, it also has mild noradrenergic properties demonstrated to be effective in the treatment of anxiety disorders and depression. Paroxetine treatment has the potential to cause weight gain and sexual dysfunction, primarily anorgasmia and ejaculatory dysfunction for the long term. In the short-term, treatment causes nausea, gastrointestinal disturbances, irritability, headaches and eating and sleeping difficulties. Paroxetine is an example of an selective serotonin reuptake inhibitor agent, which has been well studied in the treatment of panic disorder and is efficacious and well-tolerated. Paroxetine pharmacotherapy has been recommended to be continued for 1 year as specified in the treatment guidelines set by the American Psychiatric Association in the treatment of panic disorder.
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PMID:Paroxetine in panic disorder: clinical management and long-term follow-up. 1585 60

Primary chronic cluster headache (CCH) is a rare but severe pain syndrome and pathophysiological explanations are still missing. PET studies revealed activation in the hypothalamus and therefore it became a target for therapeutic deep brain stimulation (DBS). A case of a 39-year-old woman and a literature review are presented. The patient suffered from left-sided primary CCH for 14 months. The headache was resistant to any pharmacological therapy or treatment was limited by major drug side effects. Using a stereotactic approach a quadripolar lead was inserted in the left posterior hypothalamus. A test trial was performed and attack frequency, intensity, and adverse events were noted. Intraoperative test stimulation evoked typical side effects like tachycardia, diplopia and panic attacks. During the trial test a marked reduction in frequency and intensity of CCH was recorded. After 7 days the stimulation device was implanted subcutaneously. DBS with implantation of a lead in the ipsilateral inferior posterior hypothalamus is an experimental treatment option and should be offered to selected patients in a prospective controlled clinical trial. Data concerning the long-term follow-up need to be collected.
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PMID:[Deep brain stimulation in the posterior hypothalamus for chronic cluster headache. Case report and review of the literature]. 1640 29

General population studies suggest a non-casual association (comorbidity) between migraine, major depression and anxiety disorders (panic attack disorder, obsessive-compulsive disorder, generalised anxiety disorder). The risk of developing affective and anxiety disorders is not increased uniformly in the different migraine subtypes, but it is more elevated in migraine with aura patients. The relationship between migraine and depression is "bi-directional" (i. e., migraineurs have a more than three-fold risk of developing depression compared with non-migraine patients, while depression patients that have never suffered from migraine before have a more than three-fold risk of developing migraine compared with nondepressed patients) and specific (i. e., the presence of migraine or severe non-migraine headache increases a patient's risk of developing depression or panic attack disorder, whereas the presence of depression or panic attack disorder is associated with a greater risk of developing migraine, but not severe non-migraine headache). Comorbidity with psychiatric disorders has also been described for chronic tension-type headache and for chronic daily headache, although these findings are based only on clinical population data.
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PMID:Psychiatric comorbidity and headache: clinical and therapeutical aspects. 1668 33

The identification of comorbid disorders in migraineurs is important since it may impose therapeutic challenges and limit treatment options. Moreover, the study of comorbidity might lead to improve our knowledge about causes and consequences of migraine. Comorbid neuropathologies in migraine may involve mood disorders (depression, mania, anxiety, panic attacks), epilepsy, essential tremor, stroke, and white matter abnormalities. Particularly, a complex bidirectional relation exists between migraine and stroke, including migraine as a risk factor for cerebral ischemia, migraine caused by cerebral ischemia, migraine as a cause of stroke, migraine mimicking cerebral ischemia, migraine and cerebral ischemia sharing a common cause, and migraine associated with subclinical vascular brain lesions.
J Headache Pain 2006 Sep
PMID:Comorbid neuropathologies in migraine. 1676 30

Catecholamine-producing tumors may arise in the adrenal medulla (pheochromocytomas) or in extraadrenal chromaffin cells (secreting paragangliomas). Their prevalence is about 0.1% in patients with hypertension and 4% in patients with a fortuitously discovered adrenal mass. An increase in the production of catecholamines causes symptoms (mainly headaches, palpitations and excess sweating) and signs (mainly hypertension, weight loss and diabetes) reflecting the effects of epinephrine and norepinephrine on alpha- and beta-adrenergic receptors. Catecholamine-producing tumors mimic paroxysmal conditions with hypertension and/or cardiac rhythm disorders, including panic attacks, in which sympathetic activation linked to anxiety reproduces the same signs and symptoms. These tumors may be sporadic or part of any of several genetic diseases: familial pheochromocytoma-paraganglioma syndromes, multiple endocrine neoplasia type 2, neurofibromatosis 1 and von Hippel-Lindau disease. Familial cases are diagnosed earlier and are more frequently bilateral and recurring than sporadic cases. The most specific and sensitive diagnostic test for the tumor is the determination of plasma or urinary metanephrines. The tumor can be located by computed tomography, magnetic resonance imaging and metaiodobenzylguanidine scintigraphy. Treatment requires resection of the tumor, generally by laparoscopic surgery. About 10% of tumors are malignant either at first operation or during follow-up, malignancy being diagnosed by the presence of lymph node, visceral or bone metastases. Recurrences and malignancy are more frequent in cases with large or extraadrenal tumors. Patients, especially those with familial or extraadrenal tumors, should be followed-up indefinitely.
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PMID:Pheochromocytomas and secreting paragangliomas. 1715 52

Our aim was to observe the induction of anxiety symptoms and panic attacks by a caffeine challenge test in panic disorder (PD) patients (DSM-IV) and their healthy first-degree relatives. We randomly selected 25 PD patients, 27 healthy first-degree relatives of probands with PD, and 22 healthy volunteers with no family history of PD. In a randomized double-blind experiment performed over two occasions 7 days apart, 480 mg caffeine and a caffeine-free solution were administered in a coffee form. Using specific panic attack criteria, 52.0% (n=13) PD patients, 40.7% (n=11) first-degree relatives (chi2=1.81, df=1, P=0.179), and none of the control subjects had a panic attack after the test (chi2=51.7, df=2, P<0.001). In this caffeine challenge test, PD patients and their first-degree relatives were more sensitive than healthy volunteers to the panic attack symptoms but less sensitive to headache, increase in blood pressure, and insomnia. Our data suggest that there is an association between panic attacks after the intake of 480 mg of caffeine in PD patients and their first-degree relatives. There is a clear differentiation of PD patients and their first-degree relatives by a caffeine test from the healthy group.
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PMID:A caffeine challenge test in panic disorder patients, their healthy first-degree relatives, and healthy controls. 1782 63


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