Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

While mania usually occurs as a phase of manic-depressive disease, it can occur in association with organic dysfunction--medical and pharmacological--in patients with no history of affective disorder. In reviewing the literature, we have found that mania occurs secondary to drugs, infection, neoplasm, epilepsy, and metabolic disturbances. These cases are best considered secondary manias. They suggest that mania--like, for example, hypertension--is a syndrome with multiple causes and that with further research many manic syndromes currently considered primary will be shifted into the secondary category. Furthermore, the concept of secondary mania casts doubt on any unitary or single-agent hypothesis of the etiology of mania and supports the notion of a continuum of psychopathologic syndromes. Clinicians are alerted to the existence of this syndrome and are urged to screen for it when conditions warrant.
 ...
PMID:Secondary mania: manic syndromes associated with antecedent physical illness or drugs. 75 97

Six patients with the diagnosis of acute mania were treated with high doses of the beta-adrenergic blocking agent propranolol. One of these patients was treated during two manic phases. Psychopathologic change during treatment was rated daily by a psychiatrist not informed on the patients medication. The IMPS (Inpatient Multidimensional Psychiatric Scale) was used. Three cases were placebo-controlled under double blind conditions. Four times we had a second medication period, twice with propranolol and once with oxprenolol and dexpropranolol respectively. Propranolol was administered every 4 h (six times per day), starting with single doses of 20-40 mg. Doses were increased individually under control of pulse rate, blood pressure, and ECG. Augmentation of doses was continued until an effect on manic symptomatology was undoubtedly seen or until therapy had to be discontinued because of side-effects. In four patients definite improvement of manic symptomatology could be achieved during altogether five manic phases within usually two treatment periods of 5-15 days. Manic behavior disappeared completely in two of these patients. The effective dosage of propranolol varied between 280 and 2320 mg per day. All of the improved patients relapsed after discontinuation of the drug. In the only case on dexpropranolol (5 days up to 900 mg daily) the effect was questionable. No extrapyramidal side-effects were observed. In one patient treatment was discontinued because of lack of cooperation, in another because of extrasystoles. Gastrointestinal bleeding occurred in the patient who received dexpropranolol. This complication was possibly due to other medication. Other side-effects were insomnia, hypertension, precordial pain, abdominal pain as well as the expected hypotension and bradycardia. The significance of these results regarding the catecholamine hypothesis of manic-depressive illness is discussed.
 ...
PMID:[The effect of the beta-adrenergic blocking agent propranolol in mania (author's transl)]. 99 94

Secondary mania is increasingly recognized clinically, and consists of acute exhibition of manic symptoms without past or family history of affective disorder. It has been reported with toxic and metabolic disturbances, primary and metastatic brain tumors, epilepsy, and cerebrovascular events. A multifactorial etiology has been suggested. We report two men, 52 and 56 years old, who developed grandiosity, sleeplessness, irritable mood, hyperactivity, and paranoid and religious delusions, with attempted violence in one case. Both had no premorbid psychiatric history and were healthy except for hypertension. One patient had a normal neurologic examination, and the other had mild left hemiparesis and hyperreflexia. EEGs, brainstem auditory-evoked responses, and median nerve somatosensory-evoked potentials were normal. Magnetic resonance studies demonstrated infarction of the ventral pons (on the right in the patient with left-sided signs and on the left in the patient with normal neurologic examination). The two patients responded to lithium carbonate and neuroleptics and have not had further psychiatric symptoms in 18 months of follow-up. These cases emphasize the relationship of late-onset mania with predisposing brain disease, and they suggest that brainstem disturbances can influence mood, sleep, libido, and thought.
 ...
PMID:Secondary mania after ventral pontine infarction. 213 93

Diet clearly influences neurotransmission. This can be important in grossly undernourished children. It can also be important in children in whom normal homeostatic mechanisms governing food intake are bypassed. Subtle differences in behavior can occur with physiologic variation in food intake. Components of foods can also be used as drugs. Starvation can impair neuronal maturation and can have lasting effects upon behavior and intellectual performance. The extent of starvation's impact upon the brain depends upon whether undernutrition occurred during a critical phase in brain development. Short-term fasting has small, but significant, effects upon intellectual performance. Even when gross malnutrition is not present, subtle changes in diet may modulate brain function. Tryptophan, tyrosine, and choline in the diet are used as precursors for neuronal synthesis of serotonin, dopamine and norepinephrine, and acetylcholine, respectively. It is likely that the brain's sensitivity to certain components of the diet exists to permit monitoring of food intake by the central nervous system. Tryptophan, tyrosine, and choline may be useful in treatment of humans with sleep disorders, pain depression, mania, hypertension, shock, or dyskinesias. Other components of the diet that may affect behavior include food additives, sugar, and caffeine. Food additives may exacerbate hyperactive symptoms in a small proportion of children with attention deficit disorder. Given that there is little potential for harm and that there is a subpopulation that may respond, a trial of a diet that contains no food additives may be a valid diagnostic approach for children with attention deficit disorder who do not respond to stimulant therapy or for children for whom stimulant therapy is not desired. Refined sugar has been blamed for many behavioral abnormalities. Subtle effects of carbohydrate upon behavior have been reported, but the existing data do not support the hypothesis that sucrose or fructose exert special effects upon neurotransmission. Caffeine is easily detected as a stimulant by humans, but it has little effect upon cognitive function. Administration of large doses of vitamins has no beneficial effect in most humans with schizophrenia, attention deficit disorder, autism, Down's syndrome, or drug addiction. Large doses of niacinamide may even be harmful, as they may cause hepatic damage.
 ...
PMID:Dietary influences on neurotransmission. 302 51

A case is reported in which abrupt cessation of long term reserpine therapy for hypertension was followed by hallucinations and mania. Reserpine is thought to induce a denervation sensitivity to dopamine in the basal ganglia and chemotactic trigger zone in man and to catecholaminergic agents in the basal ganglia and mesolimbic system in animals. Conceivably, a parallel supersensitivity in the mesolimbic area could have occurred in this patient and accounted for the psychiatric symptoms. This supersensitivity and the possibility that it may, like tardive dyskinesia, be persistent should be considered when reserpine or similar drugs are used for prolonged periods.
 ...
PMID:Reserpine withdrawal psychosis: the possible role of denervation supersensitivity of receptors. 709 68

Phencyclidine (PCP), a widely abused drug currently, has multiple pharmacological actions, including psychotomimetic [1], anesthetic [2], sympathomimetic [2], anticholinergic [3-7], and dopaminergic [8-10]. Similarly, PCP intoxication in man can present with diverse symptoms: schizophrenia-like delusions and hallucinations; mania; violence, dyskinetic, catatonic, or stereotyped movements; hypertension; and coma [11, 12]. There is general agreement that the treatment of PCP intoxication includes support of vital functions and acidification of the urine [13]. However, there is no known specific antidote for PCP toxicity. Although diazepam [13], haloperidol [14, 15], and chlorpromazine [16] have been reported to improve the agitation and psychotic symptoms caused by PCP, the therapeutic efficacy of these agents has rarely been documented with objective clinical measures. Recently we found that intramuscular physostigmine and haloperidol [17, 18] improved several symptoms of acute PCP intoxication as measured by the Brief Psychiatric Rating Scale (BPRS) [19].
 ...
PMID:Phencyclidine intoxication: assessment of possible antidotes. 713 17

The authors report a case of acute mania induced by perindopril (Coversyl) in a 57 year old man with no prior history of mental illness. This Angiotensin-Converting Enzyme Inhibitor (ACEI) had been introduced eight days prior to the first signs of excitation, in order to treat recently diagnosed arterial hypertension. Without proof of reintroduction, and on the basis of clinical observations, the attribution appears plausible. Similar observations have been made for other molecules in this class of medication, such as captopril (Lopril). A review of literature regroups recent data concerning psychotropic effects of ACEIs. Several reports claim that captopril clearly acts as an antidepressant. Studies on the mood or the quality of life of treated hypertensive patients show ACEIs to have an euphoric-type positive effect compared to other anti-hypertensive treatments. Captopril and perindopril also act like potential antidepressants in experimental models of antidepression. Furthermore, pharmacologic data confirm that the most lipophilic ACEIs penetrate the central nervous system and argue in favor of the role of these molecules in activating central opioides. As these data provide evidence of mood swing in some patients, but also of an overall benefit in hypertensive populations, the clinical importance of the antidepressant effect of ACEIs needs further investigations.
 ...
PMID:[Psychotropic effects of angiotensin-converting enzyme inhibitors: what are the arguments?]. 852 71

Concurrent use of herbs may mimic, magnify, or oppose the effect of drugs. Plausible cases of herb-drug interactions include: bleeding when warfarin is combined with ginkgo (Ginkgo biloba), garlic (Allium sativum), dong quai (Angelica sinensis), or danshen (Salvia miltiorrhiza); mild serotonin syndrome in patients who mix St John's wort (Hypericum perforatum) with serotonin-reuptake inhibitors; decreased bioavailability of digoxin, theophylline, cyclosporin, and phenprocoumon when these drugs are combined with St John's wort; induction of mania in depressed patients who mix antidepressants and Panax ginseng; exacerbation of extrapyramidal effects with neuroleptic drugs and betel nut (Areca catechu); increased risk of hypertension when tricyclic antidepressants are combined with yohimbine (Pausinystalia yohimbe); potentiation of oral and topical corticosteroids by liquorice (Glycyrrhiza glabra); decreased blood concentrations of prednisolone when taken with the Chinese herbal product xaio chai hu tang (sho-salko-to); and decreased concentrations of phenytoin when combined with the Ayurvedic syrup shankhapushpi. Anthranoid-containing plants (including senna [Cassia senna] and cascara [Rhamnus purshiana]) and soluble fibres (including guar gum and psyllium) can decrease the absorption of drugs. Many reports of herb-drug interactions are sketchy and lack laboratory analysis of suspect preparations. Health-care practitioners should caution patients against mixing herbs and pharmaceutical drugs.
 ...
PMID:Herb-drug interactions. 1076 66

We examined the prevalence of HIV, general medical, and psychiatric comorbidities by age based on a recent multisite cohort of HIV infected veterans receiving care: the Veterans with HIV/AIDS 3 Site Study (VACS 3). VACS 3 includes 881 adult patients with HIV infection enrolled between June 1999 and July 2000. Providers reported their patients' CDC-defined HIV comorbidities, general medical comorbidities (based on Duke and Charlson comorbidity scales), and psychiatric comorbidity. Mean age of participants was 49 years and 54% were African-American. The most common HIV comorbidities were oral candidiasis (21%), peripheral neuropathy (16%), and herpes zoster (16%). The most common general medical comorbidities included chemical hepatitis (53%), hypertension (24%), and hyperlipidemia (17%). The mean number of HIV and general medical comorbidities experienced by patients were respectively 1.1 and 1.4 (P < .001). Older (> or = 50 years) HIV-infected patients experienced a greater number of general medical comorbidities than those < 50 years (respectively 1.7 versus 1.2, P < .001). There was no significant difference in mean HIV comorbidity number by age. Based on patient report, 46% had significant depressive symptoms (> or = 10 on 10-item CES-D) and 21% reported at-risk drinking (> or = 8 on AUDIT). Providers reported 32% of patients had anxiety, 4% mania, 4% schizophrenia, and 11% cognitive impairment/dementia. General medical and psychiatric comorbidities constituted a higher disease burden for HIV-infected veterans than HIV comorbidities. Whether these comorbidities are due to antiretroviral drug toxicity or are age or lifestyle-associated conditions, the substantial prevalence of these "non-HIV" comorbidities suggest an important role for general medical and psychiatric management of HIV-infected patients.
 ...
PMID:General medical and psychiatric comorbidity among HIV-infected veterans in the post-HAART era. 1175 Feb 6

Psychiatric manifestations are frequently associated with pernicious anemia including depression, mania, psychosis, dementia. We report a case of a patient with vitamin B12 deficiency, who has presented severe depression with delusion and Capgras' syndrome, delusion with lability of mood and hypomania successively, during a period of two Months. Case report - Mme V., a 64-Year-old woman, was admitted to the hospital because of confusion. She had no history of psychiatric problems. She had history of diabetes, hypertension and femoral prosthesis. The red blood count revealed a normocytosis with anemia (hemoglobin=11,4 g/dl). At admission she was uncooperative, disoriented in time and presented memory and attention impairment and sleep disorders. She seemed sad and older than her real age. Facial expression and spontaneous movements were reduced, her speech and movements were very slow. She had depressed mood, guilt complex, incurability and devaluation impressions. She had a Capgras' syndrome and delusion of persecution. Her neurologic examination, cerebral scanner and EEG were postponed because of uncooperation. Further investigations confirmed anemia (hemoglobin=11,4 g/dl) and revealed vitamin B12 deficiency (52 pmol/l) and normal folate level. Antibodies to parietal cells were positive in the serum and antibodies to intrinsic factor were negative. An iron deficiency was associated (serum iron=7 micromol/l; serum ferritin concentration=24 mg/l; serum transferrin concentration=3,16 g/l). This association explained normocytocis anemia. Thyroid function, hepatic and renal tests, glycemia, TP, TCA, VS, VDRL-TPHA were normal. Vitamin B12 replacement therapy was started with hydroxycobalamin 1 000 ng/day im for 10 days and iron replacement therapy. Her mental state improved dramatically within a few days. After one week of treatment the only remaining symptoms were lability of mood, delusion of persecution, Capgras' syndrome but disappeared totally 9 days after the beginning of the treatment. A neurologic examination was possible because of cooperation. All the tendon reflexes of inferior members were absent. The plantars were in flexion and there was a left inferior member hypoesthesia. The cerebral scan and EEG were normal. Fundic biopsy, realized by fibroscopy, revealed fundic atrophia and intestinal metaplasia compatible with Biermers' disease. The iron deficiency exploration concluded diet deficiency. Mme V. appeared euphoric, her speech was very rapid with play on words and overactivity. This hypomania state totally disappeared 3 days after. Six Months after her hospitalisation, she presented an hypothyroidism (TSH=3,780; T3=1,35; T4=1,08). A thyroid hormones replacement was started and she continued to receive Monthly B12 replacement. Discussion - This case report illustrates psychiatric manifestations of Biermers' disease. The clinical arguments in favour are: white woman, more than 60 Years old, no history of psychiatric problems, atypical symptoms (confusional state with psychiatric symptoms), fluctuation of symptoms (severe depression with confusional state, delusion of persecution and Capgras' syndrome; delusion with lability of mood and hypomania), dramatic improvement after 9 days of vitamin B12 replacement therapy. The biological arguments are: anemia, vitamin B12 deficiency, normal folate level, atrophia and fundic metaplasia, positive antibodies to parietal cells in the serum, association between Biermers' disease and autoimmune disease (Haschimoto thyroidite). Psychiatric manifestations can occur in the presence of low serum B12 levels but in the absence of the other well recognized neurological and haematological abnormalities of pernicious anemia. Mental or psychological changes may precede haematological signs by Months or Years. They can be the initial symptoms or the only ones. Verbank et al. described the case of a patient with vitamin B12 deficiency in whom hypomania, paranoia and depression had been successively presented during a period of 5 Years before anemia have been developed. The case of Mme V. is similar in the succession of severe depression with delusion of persecution and Capgras' syndrome, delusion with lability of mood and hypomania, during a period of two Months. This report seems to be the first one of a sequence of several psychiatric states with pernicious anemia during a period of two Months with normocytosis anemia. To illustrate this illness we reviewed the literature regarding psychopathology associated with B12 deficiency. The most common psychiatric symptoms were depression, mania, psychotic symptoms, cognitive impairment and obsessive compulsive disorder. The neuropsychiatric severity by vitamin B12 deficiency and the therapeutic efficacy depends on the duration of signs and symptoms. Conclusion - We recommend consideration of B12 deficiency and serum B12 determinations in all the patients with organic mental disorders, atypical psychiatric symptoms and fluctuation of symptomatology. B12 levels should be evaluated with treatment resistant depressive disorders, dementia, psychosis or risk factors for malnutrition such as alcoholism or advancing age associated with neurological symptoms, anemia, malabsorption, gastrointestinal surgery, parasite infestation or strict vegetarian diet. In first intention, B12 deficiency should be researched by serum B12 determination (normal 200-950 pg/ml). Studies of methylmalonic acid and homocysteine showed that they are very sensitive functional indicators of cobalamin status especially when other evidence of cobalamin (B12) deficiency was equivocal. Measurement of methylmalonic acid (normal 73-271 nmol/l) and homocysteine (normal 5,4-13,9 micromol/l) should not replace the measurement of serum cobalamin.
 ...
PMID:[Psychiatric manifestations of vitamin B12 deficiency: a case report]. 1502 91


1 2 3 Next >>