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

The authors report two cases of pseudotumor cerebri in patients taking lithium for treatment of bipolar disorder. Pseudotumor cerebri is a poorly understood syndrome characterized by chronic headaches, bilateral papilledema, and increased intracranial pressure without localized neurologic signs or symptoms, intracranial mass, or hydrocephalus. Ventriculography, computed tomography, and nuclear magnetic resonance imaging reveal normal or small ventricles. Multiple etiologies may include Vitamin A toxicity, obesity, head trauma, hypothyroidism or hyperthyroidism, prolonged steroid therapy or its withdrawal, Addison's disease, Cushing's disease, pituitary insufficiency, and lithium therapy. Patients treated with lithium whose antidiuretic hormone-cyclic adenosine monophosphate mechanism is disturbed are most likely to develop pseudotumor cerebri via disregulation of sodium balance, thyroid-stimulating hormone production, and glucose metabolism. The authors recommend careful medical monitoring to avoid iatrogenic effects of lithium, including pseudotumor cerebri.
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PMID:Pseudotumor cerebri associated with lithium therapy in two patients. 203 32

Cluster headache and manic depressive illness share in common similarities like: periodic symptomatology, accessibility to lithium therapy, abnormalities in circadian rhythm of cortisol. Though, in contrast to periodic depression, D.S.T. was found normal in 9 patients with cluster headache.
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PMID:[Dexamethasone test in cluster headache]. 383 Jun 94

Three patients were initially seen with headache, blurred vision, and papilledema while taking lithium carbonate for their respective bipolar affective disorder. A diagnosis of pseudotumor cerebri was made in each case when a thorough evaluation revealed only elevated intracranial pressure. Two of the patients had complete resolution of their symptoms and papilledema after discontinuing use of the drug. Increased intracranial pressure with papilledema persisted in the third patient when she failed to adjust psychiatrically, necessitating continuance of the lithium carbonate therapy. A history of lithium carbonate ingestion should be sought in patients with the syndrome of pseudotumor cerebri. All patients receiving this drug should have a regular funduscopic examination.
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PMID:Pseudotumor cerebri secondary to lithium carbonate. 392 28

We are reporting a case of manic depressive illness in a patient with a falxial chondroma in the right parietal region. Neurological symptoms were absent except for right hemicranial headache and examination was normal, prior to the presentation with mania. The mania responded to psychotropics. Subsequent evaluation with a head CT scan using contrast enhancement showed a 2.5 x 2 cm high density mass which on craniotomy and biopsy was noted to be a chondroma. For two years following removal, the patient remained euthymic without medication. To our knowledge, this is the fourth reported case of a chondroma in the parietal region and the first case of secondary mania associated with such a tumor.
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PMID:Silent solitary right parietal chondroma resulting in secondary mania. 828 25

The levels of N-acetyl-beta-glucosaminidase (NAG) in urine from 35 patients with bipolar affective disorder were compared with scores for the 90 items (symptoms) of the Symptom Checklist (SCL-90). There were significant negative correlations between NAG levels and 23 of the SCL-90 variables (symptoms). These symptoms could be grouped into the following categories: anxiety, unusual or psychotic thinking, suicidal thinking, dysphoria, irritability, nausea, headaches, memory problems, and loss of interest. Serotonin abnormalities may play a role in the production of many of these symptoms. The hypothesis that NAG could be a marker for a serotonin activity is discussed.
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PMID:Association of levels of N-acetyl-beta-glucosaminidase with specific psychiatric symptoms in bipolar patients. 834 66

A 10-week open-label trial of fluvoxamine was conducted for male Vietnam combat veterans with chronic PTSD. Subjects were excluded if they met full current criteria for panic disorder or agoraphobia, and lifetime criteria for psychosis, bipolar disorder, or organic mental syndrome. Repeated MANOVA was performed to determine change over time. Fluvoxamine was well tolerated; side effects were observed primarily early in treatment with headache, insomnia, sedation, and gastrointestinal distress being most frequent. Fluvoxamine was effective for treating the core intrusion, avoidance, and arousal symptoms of PTSD. Large treatment effects were seen by 4-6 weeks, and maintained at 10 weeks. The magnitude of change was greater than has been previously reported for antidepressant treatment of male Vietnam combat veterans with PTSD.
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PMID:Open trial of fluvoxamine treatment for combat-related posttraumatic stress disorder. 869 84

The efficacy and safety of tianeptine were compared, in the course of a multicentre randomised, double-blind, parallel group study, to those of placebo in the treatment of Major Depressions and Bipolar Disorder, Depressed with or without melancholia, without psychotic features. After a 1-week run-in placebo period, 126 depressed out-patients presenting DSM-III-R Major Depression or Bipolar Disorder, Depressed, with a total MADRS score of at least 25, were treated for 42 days with either tianeptine (25-50 mg/day) or placebo. Efficacy assessments were MADRS, CGI, HARS, Zung Depression Self Rating Scale and a VAS. Better efficacy of tianeptine was shown, and confirmed by covariance analyses, in final MADRS scores of the intention-to-treat population, of patients treated for at least 14 days and of completers; also in CGI items 1 and 2, MADRS item 10, and VAS. The results confirmed the efficacy of tianeptine (mean dosage: 37.5 mg/day) in the treatment of Major Depression and Bipolar Disorder, Depressed, with or without melancholia, compared to placebo. Tianeptine's acceptability did not differ from that of placebo. For adverse events, a higher incidence of headaches was found with tianeptine.
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PMID:Placebo-controlled study of tianeptine in major depressive episodes. 901 20

Migraine is a highly prevalent episodic headache disorder. When migraine and depression occur together, therapeutic opportunities, as well as limitations, exist. The effective treatment of both migraine and depression begins with making an accurate diagnosis and explaining it to the patient. Behavioral interventions, such as maintaining a regular schedule, getting adequate sleep and exercise, and giving up tobacco, are often useful. In addition, patients with comorbid depression often need supportive psychotherapy. Patients with depression often need antidepressant therapy independent of their migraine attack frequency. Although the mechanism of antidepressants in headache prophylaxis is unknown, it is not the result of treating masked depression. Preventive migraine medication is usually given daily to decrease the frequency of migraine attacks. For the patient with migraine and depression, use an antidepressant. While tricyclic antidepressants may be more effective for migraine, selective serotonin reuptake inhibitors are just as effective for depression and have fewer side effects. For the patient with migraine and epilepsy, or migraine and manic depressive illness, divalproex sodium is the drug of choice. Drug combinations are commonly used for patients with refractory headache disorders. Some combinations, such as antidepressants and beta-blockers, are suggested even in depressed patients.
Cephalalgia 1998 Feb
PMID:Comprehensive management of headache and depression. 953 72

Calcium (Ca) and magnesium (Mg) are involved in many processes related to depression. Evaluations of serum and plasma Ca and Mg levels in depressive disorders do not show consistent results. The few studies that examined their cerebrospinal fluid (CSF) levels tended to find no differences between depressed patients and controls. Because both hypercalcemia and hypomagnesemia are associated with depression, and as Mg may function as a Ca antagonist, it is suggested that the relationship between these cations could be different in depressed patients and controls. We examined CSF and serum Ca and Mg in acutely depressed patients diagnosed as having major depressive disorder or being in a depressive episode of bipolar disorder. Controls were subjects undergoing lumbar puncture as part of an evaluation for headache or suspected meningitis and found to demonstrate no physical or mental disorder. Serum and CSF Ca/Mg ratios were found to be elevated in the depressed patients compared with the controls. A retrospective analysis of previous trials assessing serum/plasma or CSF Ca and Mg does not seem to refute the findings of this study. We further discuss our findings in their relation to the acuteness of the depressive disorders.
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PMID:High serum and cerebrospinal fluid Ca/Mg ratio in recently hospitalized acutely depressed patients. 1007 61

Research efforts to identify and understand the pathophysiology of schizophrenia and bipolar illness are limited by the inability to study neuronal tissue of living patients. An alternative to sampling brain tissue from living patients is to measure neuronal proteins found in cerebral spinal fluid. One such candidate protein is synaptosomal-associated protein 25kDa. Our hypothesis is that the level of this protein in cerebral spinal fluid may be a marker of neuronal pathology. Cerebral spinal fluid from headache, schizophrenic, bipolar, and control subjects was used to measure the SNAP-25 level by quantitative dot blotting. Schizophrenic subjects had significantly elevated levels of SNAP-25 as compared to headache and control subjects. However, there was no significant difference between the bipolar group and schizophrenic or control groups. This study reports on a potentially useful clinical marker in schizophrenia, and the presence of elevated cerebral spinal fluid SNAP-25 may indicate alterations in neuronal functioning.
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PMID:CSF SNAP-25 in schizophrenia and bipolar illness. A pilot study. 1063 77


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