Input: Long term hormone therapy for perimenopausal and postmenopausal women. BACKGROUND: Hormone therapy (HT) is widely used for controlling menopausal symptoms and has also been used for the management and prevention of cardiovascular disease, osteoporosis and dementia in older women. This is an updated version of the original Cochrane review first published in 2005. OBJECTIVES: To assess the effect of long - term HT on mortality, cardiovascular outcomes, cancer, gallbladder disease, cognition, fractures and quality of life. SEARCH STRATEGY: We searched the following databases to November 2007: Trials Register of the Cochrane Menstrual Disorders and Subfertility Group, Cochrane Central Register of Controlled Trials, MEDLINE, EMBASE, Biological Abstracts. Also relevant non - indexed journals and conference abstracts. SELECTION CRITERIA: Randomised double - blind trials of HT versus placebo, taken for at least one year by perimenopausal or postmenopausal women. HT included oestrogens, with or without progestogens, via oral, transdermal, subcutaneous or transnasal routes. DATA COLLECTION AND ANALYSIS: Two authors independently assessed trial quality and extracted data. MAIN RESULTS: Nineteen trials involving 41, 904 women were included. In relatively healthy women, combined continuous HT significantly increased the risk of venous thrombo - embolism or coronary event (after one year' s use), stroke (after three years), breast cancer and gallbladder disease. Long - term oestrogen - only HT significantly increased the risk of venous thrombo - embolism, stroke and gallbladder disease (after one to two years, three years and seven years' use respectively), but did not significantly increase the risk of breast cancer. The only statistically significant benefits of HT were a decreased incidence of fractures and (for combined HT) colon cancer, with long - term use. Among women aged over 65 who were relatively healthy (i. e. generally fit, without overt disease) and taking continuous combined HT, there was a statistically significant increase in the incidence of dementia. Among women with cardiovascular disease, long - term use of combined continuous HT significantly increased the risk of venous thrombo - embolism. One trial analysed subgroups of 2839 relatively healthy 50 to 59 year old women taking combined continuous HT and 1637 taking oestrogen - only HT, versus similar - sized placebo groups. The only significantly increased risk reported was for venous thrombo - embolism in women taking combined continuous HT: their absolute risk remained low, at less than 1 / 500. However, this study was not powered to detect differences between groups of younger women. AUTHORS' CONCLUSIONS: HT is not indicated for the routine management of chronic disease. We need more evidence on the safety of HT for menopausal symptom control, though short - term use appears to be relatively safe for healthy younger women.

cardiovascular disease

osteoporosis

dementia

cancer

gallbladder disease

fractures

Menstrual Disorders

venous thrombo - embolism

stroke

breast cancer

gallbladder disease

venous thrombo - embolism

stroke

gallbladder disease

breast cancer

fractures

colon cancer

dementia

cardiovascular disease

venous thrombo - embolism

venous thrombo - embolism

oestrogens

progestogens

oestrogen

oestrogen

progestogens

venous thrombo - embolism

progestogens

venous thrombo - embolism

progestogens

venous thrombo - embolism

progestogens

venous thrombo - embolism

oestrogens

gallbladder disease

oestrogens

gallbladder disease

oestrogens

gallbladder disease

oestrogen

gallbladder disease

oestrogen

gallbladder disease

oestrogen

gallbladder disease

oestrogen

gallbladder disease

oestrogen

gallbladder disease

oestrogen

gallbladder disease

oestrogens

stroke

oestrogens

stroke

oestrogen

stroke

oestrogen

stroke

oestrogen

stroke

oestrogen

stroke

oestrogens

venous thrombo - embolism

oestrogens

venous thrombo - embolism

oestrogens

venous thrombo - embolism

oestrogens

venous thrombo - embolism

oestrogen

venous thrombo - embolism

oestrogen

venous thrombo - embolism

oestrogen

venous thrombo - embolism

oestrogen

venous thrombo - embolism

oestrogen

venous thrombo - embolism

oestrogen

venous thrombo - embolism

oestrogen

venous thrombo - embolism

oestrogen

venous thrombo - embolism

oestrogens

dementia

oestrogens

dementia

oestrogen

dementia

oestrogen

dementia

oestrogen

dementia

oestrogen

dementia

progestogens

dementia

progestogens

dementia


Input: Passage of mannitol into the brain around gliomas: a potential cause of rebound phenomenon. A study on 21 patients. AIM: Widespread use of mannitol to reduce brain edema and lower elevated ICP in brain tumor patients continues to be afflicted by the so - called rebound phenomenon. Leakage of mannitol into the brain parenchyma through an altered BBB and secondary reversal of osmotic gradient is considered the major cause of rebound. This has only been demonstrated experimentally in animals. As a contribution to this issue we decided to research the possible passage of mannitol into the brain after administration to 21 brain tumor patients. METHODS: Mannitol (18% solution; 1 g / kg) was administered as a bolus to patients (ten had malignant glioma, seven brain metastases and four meningioma) about 30 minutes before craniotomy. During resection, a sample of the surrounding edematous white matter was taken at the same time as a 10 ml venous blood sample. Mannitol concentrations were measured in plasma and white matter by a modified version of the enzyme assay of Blonquist et al. RESULTS: In most glioma patients, mannitol concentrations in white matter were 2 to 6 times higher than in plasma (mean 3. 5 times). In meningioma and metastases patients plasma concentrations of mannitol were higher than white matter concentrations except in three cases with infiltration by neoplastic cells. CONCLUSIONS: The results of our study show that even after a single bolus, mannitol may leak through the altered BBB near gliomas, reversing the initial plasma - to - blood osmotic gradient, aggravating peritumoral edema and promoting rebound of ICP.

mannitol

mannitol

mannitol

mannitol

Mannitol

Mannitol

mannitol

mannitol

mannitol

gliomas

brain edema

elevated ICP

brain tumor

brain tumor

malignant glioma

metastases

meningioma

edematous

glioma

meningioma

metastases

gliomas

edema

mannitol

elevated ICP

mannitol

elevated ICP

mannitol

elevated ICP

mannitol

elevated ICP

Mannitol

elevated ICP

Mannitol

elevated ICP

mannitol

elevated ICP

mannitol

elevated ICP

mannitol

elevated ICP


Input: Can lidocaine reduce succinylcholine induced postoperative myalgia? This study was undertaken to determine the effect of lidocaine pretreatment on reduction of succinylcholine - induced myalgia in patients undergoing general anesthesia for gynecological surgery. One hundred and thirty - five patients were assigned to one of three groups in a prospective, double blind, randomized manner. Group PS, the control group, received normal saline and succinylcholine 1. 5 mg x kg (- 1); Group LS, lidocaine 1. 5 mg x kg (- 1) and succinylcholine 1. 5 mg x kg (- 1); Group PR, normal saline and rocuronium 0. 6 mg x kg (- 1). Morphine 0. 1 mg x kg (- 1) iv was given for premedication and all patients were monitored with a noninvasive blood pressure monitor, ECG and pulse oximetry. Anesthesia was induced with 5 mg. kg (- 1) thiopental iv. followed by succinylcholine (Group PS, LS) or rocuronium (Group PR) for tracheal intubation. Following administration of these agents, the presence, and degree of fasciculation were assessed visually on a four point scale by one investigator who was blinded to the drug administered. The blood pressure and heart rate of each patient were monitored on nine occasions. Twenty - four hours later, any myalgia experienced was assessed according to a structured questionaire and graded by a four point scale by one investigator blinded to the intraoperative management. The results indicate that muscle fasciculation was not found in Group PR while the patients in Group LS had a lower incidence of muscle fasciculation than those in Group PS (p < 0. 001). At 24 h, the incidence of myalgia was higher in Group PS than in Group LS and PR (p < 0. 05). A correlation was not found between the incidence of myalgia and the occurrence of muscle fasciculation. The changes in systolic and diastolic blood pressure and heart rate were not significant among the three groups. In conclusion, where succinylcholine is used, lidocaine is proven to be the useful pretreatment agent for the reduction of postoperative myalgia.

lidocaine

succinylcholine

lidocaine

succinylcholine

succinylcholine

lidocaine

succinylcholine

rocuronium

Morphine

thiopental

succinylcholine

rocuronium

succinylcholine

lidocaine

postoperative myalgia

myalgia

fasciculation

myalgia

muscle fasciculation

muscle fasciculation

myalgia

myalgia

muscle fasciculation

postoperative myalgia

succinylcholine

fasciculation

succinylcholine

muscle fasciculation

succinylcholine

muscle fasciculation

succinylcholine

muscle fasciculation

succinylcholine

fasciculation

succinylcholine

muscle fasciculation

succinylcholine

muscle fasciculation

succinylcholine

muscle fasciculation

succinylcholine

fasciculation

succinylcholine

muscle fasciculation

succinylcholine

muscle fasciculation

succinylcholine

muscle fasciculation

succinylcholine

fasciculation

succinylcholine

muscle fasciculation

succinylcholine

muscle fasciculation

succinylcholine

muscle fasciculation

succinylcholine

fasciculation

succinylcholine

muscle fasciculation

succinylcholine

muscle fasciculation

succinylcholine

muscle fasciculation

succinylcholine

fasciculation

succinylcholine

muscle fasciculation

succinylcholine

muscle fasciculation

succinylcholine

muscle fasciculation

succinylcholine

postoperative myalgia

succinylcholine

postoperative myalgia

succinylcholine

postoperative myalgia

succinylcholine

postoperative myalgia

succinylcholine

postoperative myalgia

succinylcholine

postoperative myalgia

succinylcholine

postoperative myalgia

succinylcholine

postoperative myalgia

succinylcholine

postoperative myalgia

succinylcholine

postoperative myalgia

succinylcholine

postoperative myalgia

succinylcholine

postoperative myalgia


Input: Open - label assessment of levofloxacin for the treatment of acute bacterial sinusitis in adults. PURPOSE: To evaluate the efficacy and safety of levofloxacin (500 mg orally once daily for 10 to 14 days) in treating adult outpatients with acute bacterial sinusitis. PATIENTS AND METHODS: A total of 329 patients enrolled in the study at 24 centers. All patients had a pre - therapy Gram' s stain and culture of sinus exudate obtained by antral puncture or nasal endoscopy. Clinical response was assessed on the basis of signs and symptoms and sinus radiograph or computed tomography results. Microbiologic cure rates were determined on the basis of presumed plus documented eradication of the pre - therapy pathogen (s). RESULTS: The most common pathogens were Haemophilus influenzae, Streptococcus pneumoniae, Staphylococcus aureus, and Moraxella catarrhalis. Of 300 clinically evaluable patients, 175 (58%) were cured and 90 (30%) were improved at the post - therapy evaluation, resulting in a clinical success rate of 88%. Thirty - five patients (12%) clinically failed treatment. The microbiologic eradication rate (presumed plus documented) among 138 microbiologically evaluable patients was 92%. Microbiologic eradication rates (presumed plus documented) of the most common pathogens ranged from 93% (M. catarrhalis) to 100% (S. pneumoniae) at the post - therapy visit. All but one of the 265 patients who were cured or improved at post - therapy returned for a long - term follow - up visit; 243 (92%) remained well 4 to 6 weeks after therapy; and 21 (8%) had a relapse of symptoms. Adverse events considered to be related to levofloxacin administration were reported by 29 patients (9%). The most common drug - related adverse events were diarrhea, flatulence, and nausea; most adverse events were mild to moderate in severity. CONCLUSION: The results of this study indicate that levofloxacin 500 mg once daily is an effective and safe treatment for acute bacterial sinusitis.

levofloxacin

levofloxacin

levofloxacin

levofloxacin

sinusitis

sinusitis

diarrhea

flatulence

nausea

sinusitis

levofloxacin

flatulence

levofloxacin

flatulence

levofloxacin

flatulence

levofloxacin

flatulence

levofloxacin

diarrhea

levofloxacin

diarrhea

levofloxacin

diarrhea

levofloxacin

diarrhea

levofloxacin

nausea

levofloxacin

nausea

levofloxacin

nausea

levofloxacin

nausea


Input: Clinical evaluation on combined administration of oral prostacyclin analogue beraprost and phosphodiesterase inhibitor cilostazol. Among various oral antiplatelets, a combination of a novel prostacyclin analogue beraprost (BPT) and a potent phosphodiesterase inhibitor cilostazol (CLZ) may result in untoward clinical effects due to possible synergistic elevation of intracellular cAMP (cyclic adenosine 3', 5' - monophosphate). Thereby, a clinical study of the combined administration of the two agents was attempted. Twelve healthy volunteers were assigned to take BPT / CLZ in the following schedule; BPT: 40 micrograms at day 1 and 120 micrograms t. i. d. from day 7 to 14, CLZ: 200 mg t. i. d. from day 3 to 14. At various time intervals, physical examination and blood collection for ex vivo platelet aggregation and determination of intraplatelet cAMP were performed. Throughout the observation period, no significant alteration in vital signs was observed. Seven out of 12 subjects experienced headache of a short duration accompanying facial flush in one and nausea in one, especially after ingestion of CLZ. All of these symptoms, probably caused by the vasodilating effect of the two agents, were of mild degree and no special treatment was required. Intraplatelet cAMP content was gradually but significantly increased to 9. 84 + / - 4. 59 pmol per 10 (9) platelets at day 14 in comparison with the initial value (6. 87 + / - 2. 25 pmol). The platelet aggregability was significantly suppressed at various time intervals but no additive or synergistic inhibitory effect by the combined administration was noted. In conclusion, the combined administration of BPT / CLZ is safe at doses used in the study, though the beneficial clinical effect of the combined administration has yet to be elucidated.

prostacyclin

beraprost

cilostazol

prostacyclin

beraprost

BPT

cilostazol

CLZ

cAMP

cyclic adenosine 3', 5' - monophosphate

BPT

CLZ

BPT

CLZ

cAMP

CLZ

cAMP

BPT

CLZ

platelet aggregation

headache

facial flush

nausea

cilostazol

facial flush

cilostazol

facial flush

CLZ

facial flush

CLZ

facial flush

CLZ

facial flush

CLZ

facial flush

CLZ

facial flush

cilostazol

nausea

cilostazol

nausea

CLZ

nausea

CLZ

nausea

CLZ

nausea

CLZ

nausea

CLZ

nausea

beraprost

headache

beraprost

headache

BPT

headache

BPT

headache

BPT

headache

BPT

headache

beraprost

facial flush

beraprost

facial flush

BPT

facial flush

BPT

facial flush

BPT

facial flush

BPT

facial flush

cilostazol

headache

cilostazol

headache

CLZ

headache

CLZ

headache

CLZ

headache

CLZ

headache

CLZ

headache

beraprost

nausea

beraprost

nausea

BPT

nausea

BPT

nausea

BPT

nausea

BPT

nausea


Input: Gastrointestinal tolerability of etoricoxib in rheumatoid arthritis patients: results of the etoricoxib vs diclofenac sodium gastrointestinal tolerability and effectiveness trial (EDGE - II). OBJECTIVE: A randomised, double - blind study to compare the gastrointestinal (GI) tolerability, safety and efficacy of etoricoxib and diclofenac in patients with rheumatoid arthritis (RA). PATIENTS AND METHODS: A total of 4086 patients (mean age 60. 8 years) diagnosed with RA were enrolled and received etoricoxib 90 mg daily (n = 2032) or diclofenac 75 mg twice daily (n = 2054). Use of gastroprotective agents and low - dose aspirin was allowed. The prespecified primary end point consisted of the cumulative rate of patient discontinuations due to clinical and laboratory GI adverse experiences (AEs). General safety was also assessed, including adjudicated thrombotic cardiovascular event data. Efficacy was evaluated using the Patient Global Assessment of Disease Status (PGADS; 0 - 4 point scale). RESULTS: Mean (SD; maximum) duration of treatment was 19. 3 (10. 3; 32. 9) and 19. 1 (10. 4; 33. 1) months in the etoricoxib and diclofenac groups, respectively. The cumulative discontinuation rate due to GI AEs was significantly lower with etoricoxib than diclofenac (5. 2 vs 8. 5 events per 100 patient - years, respectively; hazard ratio 0. 62 (95% CI: 0. 47, 0. 81; p < or = 0. 001)). The incidence of discontinuations for hypertension - related and oedema - related AEs were significantly higher with etoricoxib (2. 5% and 1. 1% respectively) compared with diclofenac (1. 5% and 0. 4% respectively; p < 0. 001 for hypertension and p < 0. 01 for oedema). Etoricoxib and diclofenac treatment resulted in similar efficacy (PGADS mean changes from baseline - 0. 62 vs - 0. 58, respectively). CONCLUSIONS: Etoricoxib 90 mg demonstrated a significantly lower risk for discontinuing treatment due to GI AEs compared with diclofenac 150 mg. Discontinuations from renovascular AEs, although less common than discontinuations from GI AEs, were significantly higher with etoricoxib.

etoricoxib

etoricoxib

diclofenac sodium

etoricoxib

diclofenac

etoricoxib

diclofenac

aspirin

etoricoxib

diclofenac

etoricoxib

diclofenac

etoricoxib

diclofenac

Etoricoxib

diclofenac

Etoricoxib

diclofenac

etoricoxib

rheumatoid arthritis

rheumatoid arthritis

RA

RA

thrombotic cardiovascular

GI AEs

hypertension

oedema

hypertension

oedema

GI AEs

GI AEs

etoricoxib

oedema

etoricoxib

oedema

etoricoxib

oedema

etoricoxib

oedema

etoricoxib

oedema

etoricoxib

oedema

etoricoxib

oedema

etoricoxib

oedema

etoricoxib

oedema

etoricoxib

oedema

etoricoxib

oedema

etoricoxib

oedema

etoricoxib

oedema

etoricoxib

oedema

Etoricoxib

oedema

Etoricoxib

oedema

Etoricoxib

oedema

Etoricoxib

oedema

etoricoxib

oedema

etoricoxib

oedema

diclofenac sodium

GI AEs

diclofenac sodium

GI AEs

diclofenac sodium

GI AEs

diclofenac

GI AEs

diclofenac

GI AEs

diclofenac

GI AEs

diclofenac

GI AEs

diclofenac

GI AEs

diclofenac

GI AEs

diclofenac

GI AEs

diclofenac

GI AEs

diclofenac

GI AEs

diclofenac

GI AEs

diclofenac

GI AEs

diclofenac

GI AEs

diclofenac

GI AEs

diclofenac

GI AEs

diclofenac

GI AEs

diclofenac

GI AEs

diclofenac

GI AEs

diclofenac

GI AEs

diclofenac

GI AEs

diclofenac

GI AEs

diclofenac

GI AEs

etoricoxib

hypertension

etoricoxib

hypertension

etoricoxib

hypertension

etoricoxib

hypertension

etoricoxib

hypertension

etoricoxib

hypertension

etoricoxib

hypertension

etoricoxib

hypertension

etoricoxib

hypertension

etoricoxib

hypertension

etoricoxib

hypertension

etoricoxib

hypertension

etoricoxib

hypertension

etoricoxib

hypertension

Etoricoxib

hypertension

Etoricoxib

hypertension

Etoricoxib

hypertension

Etoricoxib

hypertension

etoricoxib

hypertension

etoricoxib

hypertension


Input: Placebo - level incidence of extrapyramidal symptoms (EPS) with quetiapine in controlled studies of patients with bipolar mania. OBJECTIVES: To evaluate extrapyramidal symptoms (EPS), including akathisia, with quetiapine in patients with bipolar mania. METHODS: Data were analyzed from four similarly designed, randomized, double - blind, 3 - to 12 - week studies. Two studies evaluated quetiapine monotherapy (up to 800 mg / day) (n = 209) versus placebo (n = 198), with lithium or haloperidol monotherapy as respective active controls. Two studies evaluated quetiapine (up to 800 mg / day) in combination with a mood stabilizer (lithium or divalproex, QTP + Li / DVP) (n = 196) compared to placebo and mood stabilizer (PBO + Li / DVP) (n = 203). Extrapyramidal symptoms were evaluated using the Simpson - Angus Scale (SAS), the Barnes Akathisia Rating Scale (BARS), adverse event reports and anticholinergic drug usage. RESULTS: The incidence of EPS - related adverse events, including akathisia, was no different with quetiapine monotherapy (12. 9%) than with placebo (13. 1%). Similarly, EPS - related adverse events with QTP + Li / DVP (21. 4%) were no different than with PBO + Li / DVP (19. 2%). Adverse events related to EPS occurred in 59. 6% of patients treated with haloperidol (n = 99) monotherapy, whereas 26. 5% of patients treated with lithium (n = 98) monotherapy experienced adverse events related to EPS. The incidence of akathisia was low and similar with quetiapine monotherapy (3. 3%) and placebo (6. 1%), and with QTP + Li / DVP (3. 6%) and PBO + Li / DVP (4. 9%). Lithium was associated with a significantly higher incidence (p < 0. 05) of tremor (18. 4%) than quetiapine (5. 6%); cerebellar tremor, which is a known adverse effect of lithium, may have contributed to the elevated rate of tremor in patients receiving lithium therapy. Haloperidol induced a significantly higher incidence (p < 0. 001) of akathisia (33. 3% versus 5. 9%), tremor (30. 3% versus 7. 8%), and extrapyramidal syndrome (35. 4% versus 5. 9%) than quetiapine. No significant differences were observed between quetiapine and placebo on SAS and BARS scores. Anticholinergic use was low and similar with quetiapine or placebo. CONCLUSIONS: In bipolar mania, the incidence of EPS, including akathisia, with quetiapine therapy is similar to that with placebo.

extrapyramidal symptoms

EPS

bipolar mania

extrapyramidal symptoms

EPS

akathisia

bipolar mania

Extrapyramidal symptoms

EPS

akathisia

EPS

EPS

EPS

akathisia

tremor

tremor

tremor

akathisia

tremor

extrapyramidal syndrome

bipolar mania

EPS

akathisia

quetiapine

quetiapine

quetiapine

lithium

haloperidol

quetiapine

lithium

divalproex

QTP

Li

DVP

Li

DVP

quetiapine

QTP

Li

DVP

Li

DVP

haloperidol

lithium

quetiapine

QTP

Li

DVP

Li

DVP

Lithium

quetiapine

lithium

lithium

Haloperidol

quetiapine

quetiapine

quetiapine

quetiapine

haloperidol

extrapyramidal symptoms

haloperidol

EPS

haloperidol

extrapyramidal symptoms

haloperidol

EPS

haloperidol

Extrapyramidal symptoms

haloperidol

EPS

haloperidol

EPS

haloperidol

EPS

haloperidol

EPS

haloperidol

extrapyramidal syndrome

haloperidol

EPS

haloperidol

extrapyramidal symptoms

haloperidol

EPS

haloperidol

extrapyramidal symptoms

haloperidol

EPS

haloperidol

Extrapyramidal symptoms

haloperidol

EPS

haloperidol

EPS

haloperidol

EPS

haloperidol

EPS

haloperidol

extrapyramidal syndrome

haloperidol

EPS

Haloperidol

extrapyramidal symptoms

Haloperidol

EPS

Haloperidol

extrapyramidal symptoms

Haloperidol

EPS

Haloperidol

Extrapyramidal symptoms

Haloperidol

EPS

Haloperidol

EPS

Haloperidol

EPS

Haloperidol

EPS

Haloperidol

extrapyramidal syndrome

Haloperidol

EPS

haloperidol

tremor

haloperidol

tremor

haloperidol

tremor

haloperidol

tremor

haloperidol

tremor

haloperidol

tremor

haloperidol

tremor

haloperidol

tremor

Haloperidol

tremor

Haloperidol

tremor

Haloperidol

tremor

Haloperidol

tremor

lithium

extrapyramidal symptoms

lithium

EPS

lithium

extrapyramidal symptoms

lithium

EPS

lithium

Extrapyramidal symptoms

lithium

EPS

lithium

EPS

lithium

EPS

lithium

EPS

lithium

extrapyramidal syndrome

lithium

EPS

lithium

extrapyramidal symptoms

lithium

EPS

lithium

extrapyramidal symptoms

lithium

EPS

lithium

Extrapyramidal symptoms

lithium

EPS

lithium

EPS

lithium

EPS

lithium

EPS

lithium

extrapyramidal syndrome

lithium

EPS

Li

extrapyramidal symptoms

Li

EPS

Li

extrapyramidal symptoms

Li

EPS

Li

Extrapyramidal symptoms

Li

EPS

Li

EPS

Li

EPS

Li

EPS

Li

extrapyramidal syndrome

Li

EPS

Li

extrapyramidal symptoms

Li

EPS

Li

extrapyramidal symptoms

Li

EPS

Li

Extrapyramidal symptoms

Li

EPS

Li

EPS

Li

EPS

Li

EPS

Li

extrapyramidal syndrome

Li

EPS

Li

extrapyramidal symptoms

Li

EPS

Li

extrapyramidal symptoms

Li

EPS

Li

Extrapyramidal symptoms

Li

EPS

Li

EPS

Li

EPS

Li

EPS

Li

extrapyramidal syndrome

Li

EPS

Li

extrapyramidal symptoms

Li

EPS

Li

extrapyramidal symptoms

Li

EPS

Li

Extrapyramidal symptoms

Li

EPS

Li

EPS

Li

EPS

Li

EPS

Li

extrapyramidal syndrome

Li

EPS

lithium

extrapyramidal symptoms

lithium

EPS

lithium

extrapyramidal symptoms

lithium

EPS

lithium

Extrapyramidal symptoms

lithium

EPS

lithium

EPS

lithium

EPS

lithium

EPS

lithium

extrapyramidal syndrome

lithium

EPS

Li

extrapyramidal symptoms

Li

EPS

Li

extrapyramidal symptoms

Li

EPS

Li

Extrapyramidal symptoms

Li

EPS

Li

EPS

Li

EPS

Li

EPS

Li

extrapyramidal syndrome

Li

EPS

Li

extrapyramidal symptoms

Li

EPS

Li

extrapyramidal symptoms

Li

EPS

Li

Extrapyramidal symptoms

Li

EPS

Li

EPS

Li

EPS

Li

EPS

Li

extrapyramidal syndrome

Li

EPS

Lithium

extrapyramidal symptoms

Lithium

EPS

Lithium

extrapyramidal symptoms

Lithium

EPS

Lithium

Extrapyramidal symptoms

Lithium

EPS

Lithium

EPS

Lithium

EPS

Lithium

EPS

Lithium

extrapyramidal syndrome

Lithium

EPS

lithium

extrapyramidal symptoms

lithium

EPS

lithium

extrapyramidal symptoms

lithium

EPS

lithium

Extrapyramidal symptoms

lithium

EPS

lithium

EPS

lithium

EPS

lithium

EPS

lithium

extrapyramidal syndrome

lithium

EPS

lithium

extrapyramidal symptoms

lithium

EPS

lithium

extrapyramidal symptoms

lithium

EPS

lithium

Extrapyramidal symptoms

lithium

EPS

lithium

EPS

lithium

EPS

lithium

EPS

lithium

extrapyramidal syndrome

lithium

EPS

lithium

tremor

lithium

tremor

lithium

tremor

lithium

tremor

lithium

tremor

lithium

tremor

lithium

tremor

lithium

tremor

Li

tremor

Li

tremor

Li

tremor

Li

tremor

Li

tremor

Li

tremor

Li

tremor

Li

tremor

Li

tremor

Li

tremor

Li

tremor

Li

tremor

Li

tremor

Li

tremor

Li

tremor

Li

tremor

lithium

tremor

lithium

tremor

lithium

tremor

lithium

tremor

Li

tremor

Li

tremor

Li

tremor

Li

tremor

Li

tremor

Li

tremor

Li

tremor

Li

tremor

Lithium

tremor

Lithium

tremor

Lithium

tremor

Lithium

tremor

lithium

tremor

lithium

tremor

lithium

tremor

lithium

tremor

lithium

tremor

lithium

tremor

lithium

tremor

lithium

tremor

haloperidol

akathisia

haloperidol

akathisia

haloperidol

akathisia

haloperidol

akathisia

haloperidol

akathisia

haloperidol

akathisia

haloperidol

akathisia

haloperidol

akathisia

haloperidol

akathisia

haloperidol

akathisia

Haloperidol

akathisia

Haloperidol

akathisia

Haloperidol

akathisia

Haloperidol

akathisia

Haloperidol

akathisia


Input: Contribution of the sympathetic nervous system to salt - sensitivity in lifetime captopril - treated spontaneously hypertensive rats. OBJECTIVE: To test the hypothesis that, in lifetime captopril - treated spontaneously hypertensive rats (SHR), the sympathetic nervous system contributes importantly to the hypertensive effect of dietary sodium chloride supplementation. METHODS: Male SHR (aged 6 weeks) that had been treated from conception onward with either captopril or vehicle remained on a basal sodium chloride diet or were fed a high sodium chloride diet. After 2 weeks, the rats were subjected to ganglionic blockade and 2 days later, an infusion of clonidine. RESULTS: Lifetime captopril treatment significantly lowered mean arterial pressure in both groups. Intravenous infusion of the ganglionic blocker hexamethonium resulted in a rapid decline in MAP that eliminated the dietary sodium chloride - induced increase in MAP in both groups. Infusion of the central nervous system alpha2 - adrenergic receptor agonist clonidine also resulted in a greater reduction in MAP in both groups of SHR that were fed the high (compared with the basal) sodium chloride diet. CONCLUSIONS: In both lifetime captopril - treated and control SHR, the sympathetic nervous system contributes to the pressor effects of a high sodium chloride diet.

captopril

captopril

dietary sodium chloride

captopril

sodium chloride

sodium chloride

clonidine

captopril

hexamethonium

dietary sodium chloride

alpha2 - adrenergic receptor agonist

clonidine

sodium chloride

captopril

sodium chloride

hypertensive

hypertensive

hypertensive

increase in MAP

dietary sodium chloride

hypertensive

dietary sodium chloride

hypertensive

dietary sodium chloride

hypertensive

dietary sodium chloride

increase in MAP

dietary sodium chloride

hypertensive

dietary sodium chloride

hypertensive

dietary sodium chloride

hypertensive

dietary sodium chloride

increase in MAP


Input: Dose - related beneficial and adverse effects of dietary corticosterone on organophosphorus - induced delayed neuropathy in chickens. Tri - ortho - tolyl phosphate (TOTP), 360 mg / kg, po, and 0, 0' - diisopropyl phosphorofluoridate (DFP), 1 mg / kg sc, were administered to adult White Leghorn chickens 24 hr after they were placed on diets containing 0 to 300 ppm corticosterone. Supplemented diets were continued until clinical signs and lesions of delayed neuropathy appeared. Although low concentrations (less than or equal to 50 ppm) of corticosterone had beneficial effects on TOTP - induced neuropathy, greater than or equal to 200 ppm exacerbated clinical signs in chickens given either TOTP or DFP. Neurotoxic esterase activities 24 hr after TOTP or DFP were less than 20% of values measured in chickens not given organophosphorous compounds. Chickens given 200 ppm corticosterone without TOTP or DFP had significantly elevated activity of plasma cholinesterase and significantly inhibited activity of liver carboxylesterase. Degenerating myelinated fibers were also evident in distal levels of the peripheral nerves of chickens given TOTP or DFP.

corticosterone

organophosphorus

Tri - ortho - tolyl phosphate

TOTP

0, 0' - diisopropyl phosphorofluoridate

DFP

corticosterone

corticosterone

TOTP

TOTP

DFP

TOTP

DFP

organophosphorous

corticosterone

TOTP

DFP

TOTP

DFP

neuropathy

neuropathy

neuropathy

Neurotoxic

Degenerating myelinated fibers

0, 0' - diisopropyl phosphorofluoridate

Degenerating myelinated fibers

DFP

Degenerating myelinated fibers

DFP

Degenerating myelinated fibers

DFP

Degenerating myelinated fibers

DFP

Degenerating myelinated fibers

DFP

Degenerating myelinated fibers

0, 0' - diisopropyl phosphorofluoridate

neuropathy

0, 0' - diisopropyl phosphorofluoridate

neuropathy

0, 0' - diisopropyl phosphorofluoridate

neuropathy

DFP

neuropathy

DFP

neuropathy

DFP

neuropathy

DFP

neuropathy

DFP

neuropathy

DFP

neuropathy

DFP

neuropathy

DFP

neuropathy

DFP

neuropathy

DFP

neuropathy

DFP

neuropathy

DFP

neuropathy

DFP

neuropathy

DFP

neuropathy

DFP

neuropathy

Tri - ortho - tolyl phosphate

Degenerating myelinated fibers

TOTP

Degenerating myelinated fibers

TOTP

Degenerating myelinated fibers

TOTP

Degenerating myelinated fibers

TOTP

Degenerating myelinated fibers

TOTP

Degenerating myelinated fibers

TOTP

Degenerating myelinated fibers

Tri - ortho - tolyl phosphate

neuropathy

Tri - ortho - tolyl phosphate

neuropathy

Tri - ortho - tolyl phosphate

neuropathy

TOTP

neuropathy

TOTP

neuropathy

TOTP

neuropathy

TOTP

neuropathy

TOTP

neuropathy

TOTP

neuropathy

TOTP

neuropathy

TOTP

neuropathy

TOTP

neuropathy

TOTP

neuropathy

TOTP

neuropathy

TOTP

neuropathy

TOTP

neuropathy

TOTP

neuropathy

TOTP

neuropathy

TOTP

neuropathy

TOTP

neuropathy

TOTP

neuropathy


Input: In vivo characterization of a dual adenosine A2A / A1 receptor antagonist in animal models of Parkinson' s disease. The in vivo characterization of a dual adenosine A (2A) / A (1) receptor antagonist in several animal models of Parkinson' s disease is described. Discovery and scale - up syntheses of compound 1 are described in detail, highlighting optimization steps that increased the overall yield of 1 from 10. 0% to 30. 5%. Compound 1 is a potent A (2A) / A (1) receptor antagonist in vitro (A (2A) K (i) = 4. 1 nM; A (1) K (i) = 17. 0 nM) that has excellent activity, after oral administration, across a number of animal models of Parkinson' s disease including mouse and rat models of haloperidol - induced catalepsy, mouse model of reserpine - induced akinesia, rat 6 - hydroxydopamine (6 - OHDA) lesion model of drug - induced rotation, and MPTP - treated non - human primate model.

adenosine A2A / A1 receptor antagonist

adenosine A (2A) / A (1) receptor antagonist

haloperidol

reserpine

6 - hydroxydopamine

6 - OHDA

MPTP

Parkinson' s disease

Parkinson' s disease

Parkinson' s disease

catalepsy

akinesia

reserpine

akinesia

haloperidol

catalepsy


Input: An extremely rare case of delusional parasitosis in a chronic hepatitis C patient during pegylated interferon alpha - 2b and ribavirin treatment. During treatment of chronic hepatitis C patients with interferon and ribavirin, a lot of side effects are described. Twenty - three percent to 44% of patients develop depression. A minority of patients evolve to psychosis. To the best of our knowledge, no cases of psychogenic parasitosis occurring during interferon therapy have been described in the literature. We present a 49 - year - old woman who developed a delusional parasitosis during treatment with pegylated interferon alpha - 2b weekly and ribavirin. She complained of seeing parasites and the larvae of fleas in her stools. This could not be confirmed by any technical examination. All the complaints disappeared after stopping pegylated interferon alpha - 2b and reappeared after restarting it. She had a complete sustained viral response.

delusional parasitosis

chronic hepatitis C

chronic hepatitis C

depression

psychosis

psychogenic parasitosis

delusional parasitosis

pegylated interferon alpha - 2b

ribavirin

ribavirin

pegylated interferon alpha - 2b

ribavirin

pegylated interferon alpha - 2b

pegylated interferon alpha - 2b

delusional parasitosis

pegylated interferon alpha - 2b

psychogenic parasitosis

pegylated interferon alpha - 2b

delusional parasitosis

pegylated interferon alpha - 2b

delusional parasitosis

pegylated interferon alpha - 2b

psychogenic parasitosis

pegylated interferon alpha - 2b

delusional parasitosis

pegylated interferon alpha - 2b

delusional parasitosis

pegylated interferon alpha - 2b

psychogenic parasitosis

pegylated interferon alpha - 2b

delusional parasitosis

ribavirin

delusional parasitosis

ribavirin

psychogenic parasitosis

ribavirin

delusional parasitosis

ribavirin

delusional parasitosis

ribavirin

psychogenic parasitosis

ribavirin

delusional parasitosis

ribavirin

delusional parasitosis

ribavirin

psychogenic parasitosis

ribavirin

delusional parasitosis


Input: Possible neuroleptic malignant syndrome related to concomitant treatment with paroxetine and alprazolam. A 74 - year - old man with depressive symptoms was admitted to a psychiatric hospital due to insomnia, loss of appetite, exhaustion, and agitation. Medical treatment was initiated at a daily dose of 20 mg paroxetine and 1. 2 mg alprazolam. On the 10th day of paroxetine and alprazolam treatment, the patient exhibited marked psychomotor retardation, disorientation, and severe muscle rigidity with tremors. The patient had a fever (38. 2 degrees C), fluctuating blood pressure (between 165 / 90 and 130 / 70 mg mm Hg), and severe extrapyramidal symptoms. Laboratory tests showed an elevation of creatine phosphokinase (2218 IU / L), aspartate aminotransferase (134 IU / L), alanine aminotransferase (78 IU / L), and BUN (27. 9 mg / ml) levels. The patient received bromocriptine and diazepam to treat his symptoms. 7 days later, the fever disappeared and the patient' s serum CPK levels were normalized (175 IU / L). This patient presented with symptoms of neuroleptic malignant syndrome (NMS), thus demonstrating that NMS - like symptoms can occur after combined paroxetine and alprazolam treatment. The adverse drug reaction score obtained by the Naranjo algorithm was 6 in our case, indicating a probable relationship between the patient' s NMS - like adverse symptoms and the combined treatment used in this case. The involvement of physiologic and environmental aspects specific to this patient was suspected. Several risk factors for NMS should be noted in elderly depressive patients whose symptoms often include dehydration, agitation, malnutrition, and exhaustion. Careful therapeutic intervention is necessary in cases involving elderly patients who suffer from depression.

neuroleptic malignant syndrome

depressive symptoms

psychiatric

insomnia

loss of appetite

agitation

psychomotor retardation

muscle rigidity

tremors

fever

extrapyramidal symptoms

fever

neuroleptic malignant syndrome

NMS

NMS

NMS

NMS

depressive

dehydration

agitation

malnutrition

depression

paroxetine

alprazolam

paroxetine

alprazolam

paroxetine

alprazolam

creatine

aspartate

alanine

bromocriptine

diazepam

paroxetine

alprazolam

alprazolam

neuroleptic malignant syndrome

alprazolam

neuroleptic malignant syndrome

alprazolam

NMS

alprazolam

NMS

alprazolam

NMS

alprazolam

NMS

alprazolam

neuroleptic malignant syndrome

alprazolam

neuroleptic malignant syndrome

alprazolam

NMS

alprazolam

NMS

alprazolam

NMS

alprazolam

NMS

alprazolam

neuroleptic malignant syndrome

alprazolam

neuroleptic malignant syndrome

alprazolam

NMS

alprazolam

NMS

alprazolam

NMS

alprazolam

NMS

alprazolam

neuroleptic malignant syndrome

alprazolam

neuroleptic malignant syndrome

alprazolam

NMS

alprazolam

NMS

alprazolam

NMS

alprazolam

NMS

paroxetine

neuroleptic malignant syndrome

paroxetine

neuroleptic malignant syndrome

paroxetine

NMS

paroxetine

NMS

paroxetine

NMS

paroxetine

NMS

paroxetine

neuroleptic malignant syndrome

paroxetine

neuroleptic malignant syndrome

paroxetine

NMS

paroxetine

NMS

paroxetine

NMS

paroxetine

NMS

paroxetine

neuroleptic malignant syndrome

paroxetine

neuroleptic malignant syndrome

paroxetine

NMS

paroxetine

NMS

paroxetine

NMS

paroxetine

NMS

paroxetine

neuroleptic malignant syndrome

paroxetine

neuroleptic malignant syndrome

paroxetine

NMS

paroxetine

NMS

paroxetine

NMS

paroxetine

NMS


Input: Pilocarpine seizures cause age - dependent impairment in auditory location discrimination. Children who have status epilepticus have continuous or rapidly repeating seizures that may be life - threatening and may cause life - long changes in brain and behavior. The extent to which status epilepticus causes deficits in auditory discrimination is unknown. A naturalistic auditory location discrimination method was used to evaluate this question using an animal model of status epilepticus. Male Sprague - Dawley rats were injected with saline on postnatal day (P) 20, or a convulsant dose of pilocarpine on P20 or P45. Pilocarpine on either day induced status epilepticus; status epilepticus at P45 resulted in CA3 cell loss and spontaneous seizures, whereas P20 rats had no cell loss or spontaneous seizures. Mature rats were trained with sound - source location and sound - silence discriminations. Control (saline P20) rats acquired both discriminations immediately. In status epilepticus (P20) rats, acquisition of the sound - source location discrimination was moderately impaired. Status epilepticus (P45) rats failed to acquire either sound - source location or sound - silence discriminations. Status epilepticus in rat causes an age - dependent, long - term impairment in auditory discrimination. This impairment may explain one cause of impaired auditory location discrimination in humans.

Pilocarpine

pilocarpine

Pilocarpine

seizures

impairment in auditory location discrimination

status epilepticus

seizures

status epilepticus

deficits in auditory discrimination

status epilepticus

status epilepticus

status epilepticus

seizures

seizures

status epilepticus

Status epilepticus

Status epilepticus

impairment in auditory discrimination

impaired auditory location discrimination

Pilocarpine

status epilepticus

Pilocarpine

status epilepticus

Pilocarpine

status epilepticus

Pilocarpine

status epilepticus

Pilocarpine

status epilepticus

Pilocarpine

status epilepticus

Pilocarpine

Status epilepticus

Pilocarpine

Status epilepticus

pilocarpine

status epilepticus

pilocarpine

status epilepticus

pilocarpine

status epilepticus

pilocarpine

status epilepticus

pilocarpine

status epilepticus

pilocarpine

status epilepticus

pilocarpine

Status epilepticus

pilocarpine

Status epilepticus

Pilocarpine

status epilepticus

Pilocarpine

status epilepticus

Pilocarpine

status epilepticus

Pilocarpine

status epilepticus

Pilocarpine

status epilepticus

Pilocarpine

status epilepticus

Pilocarpine

Status epilepticus

Pilocarpine

Status epilepticus

Pilocarpine

impairment in auditory location discrimination

Pilocarpine

deficits in auditory discrimination

Pilocarpine

impairment in auditory discrimination

Pilocarpine

impaired auditory location discrimination

pilocarpine

impairment in auditory location discrimination

pilocarpine

deficits in auditory discrimination

pilocarpine

impairment in auditory discrimination

pilocarpine

impaired auditory location discrimination

Pilocarpine

impairment in auditory location discrimination

Pilocarpine

deficits in auditory discrimination

Pilocarpine

impairment in auditory discrimination

Pilocarpine

impaired auditory location discrimination


Input: Cardiovascular risk with cyclooxygenase inhibitors: general problem with substance specific differences? Randomised clinical trials and observational studies have shown an increased risk of myocardial infarction, stroke, hypertension and heart failure during treatment with cyclooxygenase inhibitors. Adverse cardiovascular effects occurred mainly, but not exclusively, in patients with concomitant risk factors. Cyclooxygenase inhibitors cause complex changes in renal, vascular and cardiac prostanoid profiles thereby increasing vascular resistance and fluid retention. The incidence of cardiovascular adverse events tends to increase with the daily dose and total exposure time. A comparison of individual selective and unselective cyclooxygenase inhibitors suggests substance - specific differences, which may depend on differences in pharmacokinetic parameters or inhibitory potency and may be contributed by prostaglandin - independent effects. Diagnostic markers such as N - terminal pro brain natriuretic peptide (NT - proBNP) or high - sensitive C - reactive protein might help in the early identification of patients at risk, thus avoiding the occurrence of serious cardiovascular toxicity.

cyclooxygenase inhibitors

cyclooxygenase inhibitors

Cyclooxygenase inhibitors

cyclooxygenase inhibitors

prostaglandin

N - terminal pro brain natriuretic peptide

NT - proBNP

myocardial infarction

stroke

hypertension

heart failure

cardiovascular toxicity

cyclooxygenase inhibitors

hypertension

cyclooxygenase inhibitors

hypertension

Cyclooxygenase inhibitors

hypertension

cyclooxygenase inhibitors

hypertension

cyclooxygenase inhibitors

stroke

cyclooxygenase inhibitors

stroke

Cyclooxygenase inhibitors

stroke

cyclooxygenase inhibitors

stroke

cyclooxygenase inhibitors

myocardial infarction

cyclooxygenase inhibitors

myocardial infarction

Cyclooxygenase inhibitors

myocardial infarction

cyclooxygenase inhibitors

myocardial infarction

cyclooxygenase inhibitors

heart failure

cyclooxygenase inhibitors

heart failure

Cyclooxygenase inhibitors

heart failure

cyclooxygenase inhibitors

heart failure


Input: Predictors of decreased renal function in patients with heart failure during angiotensin - converting enzyme inhibitor therapy: results from the studies of left ventricular dysfunction (SOLVD) BACKGROUND: Although angiotensin - converting enzyme inhibitor therapy reduces mortality rates in patients with congestive heart failure (CHF), it may also cause decreased renal function. Little information is available to predict which patients are at highest risk for this complication. OBJECTIVE: To quantify specific clinical predictors of reduction in renal function in patients with CHF who are prescribed angiotensin - converting enzyme inhibitor therapy. METHOD: We analyzed data from the Studies of Left Ventricular Dysfunction (SOLVD), a randomized, double - blind, placebo - controlled trial of enalapril for the treatment of CHF. There were 3379 patients randomly assigned to enalapril with a median follow - up of 974 days and 3379 patients randomly assigned to placebo with a mean follow - up of 967 days. Decreased renal function was defined as a rise in serum creatinine > / = 0. 5 mg / dL (44 micromol / L) from baseline. We used time - to - event analysis to identify potential predictors of decrease in renal function including age, baseline ejection fraction, baseline creatinine, low systolic blood pressure (< 100 mm Hg), history of hypertension, diabetes, and use of antiplatelet, diuretic, and beta - blocker therapy. RESULTS: Patients randomly assigned to enalapril had a 33% greater likelihood of decreased renal function than controls (P =. 003). By multivariate analysis, in both the placebo and enalapril groups older age, diuretic therapy, and diabetes were associated with decreased renal function, whereas beta - blocker therapy and higher ejection fraction were renoprotective. Older age was associated with a greater risk of developing decreased renal function in both groups, but significantly more so in the enalapril group (enalapril: risk ratio [RR] 1. 42 per 10 years, 95% confidence interval [CI] 1. 32 - 1. 52 with enalapril; placebo: RR 1. 18, 95% CI 1. 12 - 1. 25). Diuretic therapy was likewise associated with a greater risk of decreased renal function in the enalapril group (RR 1. 89, 95% CI 1. 70 - 2. 08) than in the placebo group (RR 1. 35, 95% CI 1. 09 - 1. 66). Conversely, enalapril had a relative renoprotective effect (RR 1. 33, 95% CI 1. 13 - 1. 53) compared with placebo (RR 1. 96, 95% CI 1. 57 - 2. 44) in patients with diabetes. A lower risk of renal impairment was seen in both groups with beta - blocker therapy (RR 0. 70, 95% CI 0. 57 - 0. 85) and higher baseline ejection fraction (RR 0. 93 per 5% increment, 95% CI 0. 91 - 0. 96). CONCLUSIONS: Enalapril use caused a 33% increase in the risk of decreased renal function in patients with CHF. Diuretic use and advanced age increased this risk. Diabetes was associated with an increased risk of renal impairment in all patients with CHF, but this risk was reduced in the enalapril group compared with the placebo group. beta - Blocker therapy and higher ejection fraction were renoprotective in all patients regardless of therapy.

decreased renal function

heart failure

left ventricular dysfunction

congestive heart failure

CHF

decreased renal function

reduction in renal function

CHF

Left Ventricular Dysfunction

CHF

Decreased renal function

hypertension

diabetes

decreased renal function

diabetes

decreased renal function

decreased renal function

decreased renal function

diabetes

renal impairment

decreased renal function

CHF

Diabetes

renal impairment

CHF

angiotensin

angiotensin

angiotensin

enalapril

enalapril

creatinine

creatinine

diuretic

enalapril

enalapril

diuretic

enalapril

enalapril

enalapril

Diuretic

enalapril

enalapril

Enalapril

Diuretic

enalapril

enalapril

decreased renal function

enalapril

decreased renal function

enalapril

reduction in renal function

enalapril

Decreased renal function

enalapril

decreased renal function

enalapril

decreased renal function

enalapril

decreased renal function

enalapril

decreased renal function

enalapril

renal impairment

enalapril

decreased renal function

enalapril

renal impairment

enalapril

decreased renal function

enalapril

decreased renal function

enalapril

reduction in renal function

enalapril

Decreased renal function

enalapril

decreased renal function

enalapril

decreased renal function

enalapril

decreased renal function

enalapril

decreased renal function

enalapril

renal impairment

enalapril

decreased renal function

enalapril

renal impairment

enalapril

decreased renal function

enalapril

decreased renal function

enalapril

reduction in renal function

enalapril

Decreased renal function

enalapril

decreased renal function

enalapril

decreased renal function

enalapril

decreased renal function

enalapril

decreased renal function

enalapril

renal impairment

enalapril

decreased renal function

enalapril

renal impairment

enalapril

decreased renal function

enalapril

decreased renal function

enalapril

reduction in renal function

enalapril

Decreased renal function

enalapril

decreased renal function

enalapril

decreased renal function

enalapril

decreased renal function

enalapril

decreased renal function

enalapril

renal impairment

enalapril

decreased renal function

enalapril

renal impairment

enalapril

decreased renal function

enalapril

decreased renal function

enalapril

reduction in renal function

enalapril

Decreased renal function

enalapril

decreased renal function

enalapril

decreased renal function

enalapril

decreased renal function

enalapril

decreased renal function

enalapril

renal impairment

enalapril

decreased renal function

enalapril

renal impairment

enalapril

decreased renal function

enalapril

decreased renal function

enalapril

reduction in renal function

enalapril

Decreased renal function

enalapril

decreased renal function

enalapril

decreased renal function

enalapril

decreased renal function

enalapril

decreased renal function

enalapril

renal impairment

enalapril

decreased renal function

enalapril

renal impairment

enalapril

decreased renal function

enalapril

decreased renal function

enalapril

reduction in renal function

enalapril

Decreased renal function

enalapril

decreased renal function

enalapril

decreased renal function

enalapril

decreased renal function

enalapril

decreased renal function

enalapril

renal impairment

enalapril

decreased renal function

enalapril

renal impairment

enalapril

decreased renal function

enalapril

decreased renal function

enalapril

reduction in renal function

enalapril

Decreased renal function

enalapril

decreased renal function

enalapril

decreased renal function

enalapril

decreased renal function

enalapril

decreased renal function

enalapril

renal impairment

enalapril

decreased renal function

enalapril

renal impairment

enalapril

decreased renal function

enalapril

decreased renal function

enalapril

reduction in renal function

enalapril

Decreased renal function

enalapril

decreased renal function

enalapril

decreased renal function

enalapril

decreased renal function

enalapril

decreased renal function

enalapril

renal impairment

enalapril

decreased renal function

enalapril

renal impairment

Enalapril

decreased renal function

Enalapril

decreased renal function

Enalapril

reduction in renal function

Enalapril

Decreased renal function

Enalapril

decreased renal function

Enalapril

decreased renal function

Enalapril

decreased renal function

Enalapril

decreased renal function

Enalapril

renal impairment

Enalapril

decreased renal function

Enalapril

renal impairment

enalapril

decreased renal function

enalapril

decreased renal function

enalapril

reduction in renal function

enalapril

Decreased renal function

enalapril

decreased renal function

enalapril

decreased renal function

enalapril

decreased renal function

enalapril

decreased renal function

enalapril

renal impairment

enalapril

decreased renal function

enalapril

renal impairment

diuretic

decreased renal function

diuretic

decreased renal function

diuretic

reduction in renal function

diuretic

Decreased renal function

diuretic

decreased renal function

diuretic

decreased renal function

diuretic

decreased renal function

diuretic

decreased renal function

diuretic

renal impairment

diuretic

decreased renal function

diuretic

renal impairment

diuretic

decreased renal function

diuretic

decreased renal function

diuretic

reduction in renal function

diuretic

Decreased renal function

diuretic

decreased renal function

diuretic

decreased renal function

diuretic

decreased renal function

diuretic

decreased renal function

diuretic

renal impairment

diuretic

decreased renal function

diuretic

renal impairment

Diuretic

decreased renal function

Diuretic

decreased renal function

Diuretic

reduction in renal function

Diuretic

Decreased renal function

Diuretic

decreased renal function

Diuretic

decreased renal function

Diuretic

decreased renal function

Diuretic

decreased renal function

Diuretic

renal impairment

Diuretic

decreased renal function

Diuretic

renal impairment

Diuretic

decreased renal function

Diuretic

decreased renal function

Diuretic

reduction in renal function

Diuretic

Decreased renal function

Diuretic

decreased renal function

Diuretic

decreased renal function

Diuretic

decreased renal function

Diuretic

decreased renal function

Diuretic

renal impairment

Diuretic

decreased renal function

Diuretic

renal impairment


Input: Pemoline induced acute choreoathetosis: case report and review of the literature. BACKGROUND: Pemoline is an oxazolidine derivative that is structurally different from amphetamines and used in the treatment of attention deficit disorder. Pemoline has not been commonly associated in the literature as a cause of acute movement disorders. The following case describes two children acutely poisoned with pemoline who experienced profound choreoathetosis. CASE REPORT: Two, 3 - year - old male, identical twin siblings presented to the emergency department after found playing with a an empty bottle of pemoline originally containing 59 tablets. The children had a medical history significant for attention deficit disorder previously treated with methylphenidate without success. This was their first day of pemoline therapy. The choreoathetoid movements began 45 min to 1 h after ingestion. The children gave no history of prior movement disorders and there was no family history of movement disorders. The children received gastrointestinal decontamination and high doses of intravenous benzodiazepines in an attempt to control the choreoathetoid movements. Despite treatment, the children continued to have choreoathetosis for approximately 24 hours. Forty - eight hours after admission, the children appeared to be at their baseline and were discharged home. CONCLUSION: Pemoline associated movement disorder has been rarely reported in the acute toxicology literature. The possibility of choreoathetoid movements should be considered in patients presenting after pemoline overdose.

Pemoline

Pemoline

oxazolidine

amphetamines

Pemoline

pemoline

pemoline

methylphenidate

pemoline

benzodiazepines

Pemoline

pemoline

choreoathetosis

attention deficit disorder

movement disorders

choreoathetosis

attention deficit disorder

choreoathetoid

movement disorders

movement disorders

choreoathetoid

choreoathetosis

movement disorder

choreoathetoid

overdose

Pemoline

overdose

Pemoline

overdose

Pemoline

overdose

pemoline

overdose

pemoline

overdose

pemoline

overdose

Pemoline

overdose

pemoline

overdose

Pemoline

choreoathetosis

Pemoline

choreoathetosis

Pemoline

choreoathetoid

Pemoline

choreoathetoid

Pemoline

choreoathetosis

Pemoline

choreoathetoid

Pemoline

choreoathetosis

Pemoline

choreoathetosis

Pemoline

choreoathetoid

Pemoline

choreoathetoid

Pemoline

choreoathetosis

Pemoline

choreoathetoid

Pemoline

choreoathetosis

Pemoline

choreoathetosis

Pemoline

choreoathetoid

Pemoline

choreoathetoid

Pemoline

choreoathetosis

Pemoline

choreoathetoid

pemoline

choreoathetosis

pemoline

choreoathetosis

pemoline

choreoathetoid

pemoline

choreoathetoid

pemoline

choreoathetosis

pemoline

choreoathetoid

pemoline

choreoathetosis

pemoline

choreoathetosis

pemoline

choreoathetoid

pemoline

choreoathetoid

pemoline

choreoathetosis

pemoline

choreoathetoid

pemoline

choreoathetosis

pemoline

choreoathetosis

pemoline

choreoathetoid

pemoline

choreoathetoid

pemoline

choreoathetosis

pemoline

choreoathetoid

Pemoline

choreoathetosis

Pemoline

choreoathetosis

Pemoline

choreoathetoid

Pemoline

choreoathetoid

Pemoline

choreoathetosis

Pemoline

choreoathetoid

pemoline

choreoathetosis

pemoline

choreoathetosis

pemoline

choreoathetoid

pemoline

choreoathetoid

pemoline

choreoathetosis

pemoline

choreoathetoid


Input: Continuous subcutaneous administration of mesna to prevent ifosfamide - induced hemorrhagic cystitis. Hemorrhagic cystitis is a major potential toxicity of ifosfamide that can be prevented by administering mesna along with the cytotoxic agent. Mesna is generally administered by the intravenous route, although experience with oral delivery of the drug has increased. The continuous subcutaneous administration of mesna has the advantage of not requiring intravenous access. In addition, subcutaneous delivery of the neutralizing agent will not be associated with the risk of inadequate urinary mesna concentrations, such as in a patient taking oral mesna who experiences severe ifosfamide - induced emesis and is unable to absorb the drug. Limited clinical experience with continuous subcutaneous mesna administration suggests it is a safe, practical, and economic method of drug delivery that permits ifosfamide to be administered successfully in the outpatient setting.

mesna

ifosfamide

ifosfamide

mesna

Mesna

mesna

mesna

mesna

ifosfamide

mesna

ifosfamide

hemorrhagic cystitis

hemorrhagic

cystitis

Hemorrhagic cystitis

Hemorrhagic

cystitis

toxicity

emesis

ifosfamide

hemorrhagic cystitis

ifosfamide

cystitis

ifosfamide

Hemorrhagic cystitis

ifosfamide

cystitis

ifosfamide

hemorrhagic cystitis

ifosfamide

cystitis

ifosfamide

Hemorrhagic cystitis

ifosfamide

cystitis

ifosfamide

hemorrhagic cystitis

ifosfamide

cystitis

ifosfamide

Hemorrhagic cystitis

ifosfamide

cystitis

ifosfamide

hemorrhagic cystitis

ifosfamide

cystitis

ifosfamide

Hemorrhagic cystitis

ifosfamide

cystitis

mesna

hemorrhagic cystitis

mesna

hemorrhagic

mesna

Hemorrhagic cystitis

mesna

Hemorrhagic

mesna

hemorrhagic cystitis

mesna

hemorrhagic

mesna

Hemorrhagic cystitis

mesna

Hemorrhagic

Mesna

hemorrhagic cystitis

Mesna

hemorrhagic

Mesna

Hemorrhagic cystitis

Mesna

Hemorrhagic

mesna

hemorrhagic cystitis

mesna

hemorrhagic

mesna

Hemorrhagic cystitis

mesna

Hemorrhagic

mesna

hemorrhagic cystitis

mesna

hemorrhagic

mesna

Hemorrhagic cystitis

mesna

Hemorrhagic

mesna

hemorrhagic cystitis

mesna

hemorrhagic

mesna

Hemorrhagic cystitis

mesna

Hemorrhagic

mesna

hemorrhagic cystitis

mesna

hemorrhagic

mesna

Hemorrhagic cystitis

mesna

Hemorrhagic

mesna

cystitis

mesna

cystitis

mesna

cystitis

mesna

cystitis

Mesna

cystitis

Mesna

cystitis

mesna

cystitis

mesna

cystitis

mesna

cystitis

mesna

cystitis

mesna

cystitis

mesna

cystitis

mesna

cystitis

mesna

cystitis

ifosfamide

hemorrhagic

ifosfamide

Hemorrhagic

ifosfamide

hemorrhagic

ifosfamide

Hemorrhagic

ifosfamide

hemorrhagic

ifosfamide

Hemorrhagic

ifosfamide

hemorrhagic

ifosfamide

Hemorrhagic


Input: Modification of drug action by hyperammonemia. Pretreatment with ammonium acetate (NH4Ac) (6 mmol / kg s. c.) approximately doubled the time morphine - treated mice remained on a hot surface and similarly increased muscular incoordination by diazepam, but NH4Ac treatment alone had no effect. Thus, hyperammonemia is capable of altering drug action and must be considered along with impaired drug metabolism in enhanced drug responses associated with liver disease. Experiments in vitro showed that acetylcholine - induced catecholamine release from bovine adrenal medulla is depressed as much as 50% by 0. 3 mM NH4Ac and KCl - induced contractions of guinea - pig ileum were inhibited 20% by 5 mM NH4Ac. Addition of excess calcium reversed the depression in both tissues, but calcium - independent catecholamine release by acetaldehyde was not blocked by NH4Ac. These results suggested that ammonia blocks calcium channels. Parallels in the actions of NH4Ac and the calcium channel blocker verapamil support this concept. Both verapamil (10 mg / kg i. p.) and NH4Ac pretreatment enhanced morphine analgesia - and diazepam - induced muscular incoordination and antagonized amphetamine - induced motor activity, and neither verapamil nor NH4Ac affected the convulsant action of metrazol. The data suggest that hyperammonemia exerts a calcium channel blocking action which enhances the effects of central nervous system depressants and certain opioid analgesics.

hyperammonemia

incoordination

hyperammonemia

liver disease

depression

analgesia

incoordination

hyperammonemia

ammonium acetate

morphine

diazepam

acetylcholine

catecholamine

KCl

calcium

calcium

catecholamine

acetaldehyde

ammonia

calcium

calcium

verapamil

verapamil

morphine

diazepam

amphetamine

verapamil

metrazol

calcium

diazepam

incoordination

diazepam

incoordination

diazepam

incoordination

diazepam

incoordination

ammonium acetate

incoordination

ammonium acetate

incoordination

incoordination

incoordination

incoordination

incoordination

incoordination

incoordination

incoordination

incoordination

incoordination

incoordination

incoordination

incoordination

incoordination

incoordination

incoordination

incoordination


Input: Risk of nephropathy after consumption of nonionic contrast media by children undergoing cardiac angiography: a prospective study. Despite increasing reports on nonionic contrast media - induced nephropathy (CIN) in hospitalized adult patients during cardiac procedures, the studies in pediatrics are limited, with even less focus on possible predisposing factors and preventive measures for patients undergoing cardiac angiography. This prospective study determined the incidence of CIN for two nonionic contrast media (CM), iopromide and iohexol, among 80 patients younger than 18 years and compared the rates for this complication in relation to the type and dosage of CM and the presence of cyanosis. The 80 patients in the study consecutively received either iopromide (group A, n = 40) or iohexol (group B, n = 40). Serum sodium (Na), potassium (K), and creatinine (Cr) were measured 24 h before angiography as baseline values, then measured again at 12 -, 24 -, and 48 - h intervals after CM use. Urine samples for Na and Cr also were checked at the same intervals. Risk of renal failure, Injury to the kidney, Failure of kidney function, Loss of kidney function, and End - stage renal damage (RIFLE criteria) were used to define CIN and its incidence in the study population. Accordingly, among the 15 CIN patients (18. 75%), 7. 5% of the patients in group A had increased risk and 3. 75% had renal injury, whereas 5% of group B had increased risk and 2. 5% had renal injury. Whereas 33. 3% of the patients with CIN were among those who received the proper dosage of CM, the percentage increased to 66. 6% among those who received larger doses, with a significant difference in the incidence of CIN related to the different dosages of CM (p = 0. 014). Among the 15 patients with CIN, 6 had cyanotic congenital heart diseases, but the incidence did not differ significantly from that for the noncyanotic patients (p = 0. 243). Although clinically silent, CIN is not rare in pediatrics. The incidence depends on dosage but not on the type of consumed nonionic CM, nor on the presence of cyanosis, and although CIN usually is reversible, more concern is needed for the prevention of such a complication in children.

nephropathy

nephropathy

CIN

CIN

cyanosis

renal failure

Injury to the kidney

Failure of kidney function

Loss of kidney function

renal damage

CIN

CIN

renal injury

renal injury

CIN

CIN

CIN

congenital heart diseases

CIN

cyanosis

CIN

contrast media

contrast media

contrast media

CM

iopromide

iohexol

CM

iopromide

iohexol

sodium

potassium

K

creatinine

Cr

CM

Cr

CM

CM

CM

contrast media

nephropathy

contrast media

nephropathy

contrast media

CIN

contrast media

CIN

contrast media

renal damage

contrast media

CIN

contrast media

CIN

contrast media

CIN

contrast media

CIN

contrast media

CIN

contrast media

CIN

contrast media

CIN

contrast media

nephropathy

contrast media

nephropathy

contrast media

CIN

contrast media

CIN

contrast media

renal damage

contrast media

CIN

contrast media

CIN

contrast media

CIN

contrast media

CIN

contrast media

CIN

contrast media

CIN

contrast media

CIN

contrast media

nephropathy

contrast media

nephropathy

contrast media

CIN

contrast media

CIN

contrast media

renal damage

contrast media

CIN

contrast media

CIN

contrast media

CIN

contrast media

CIN

contrast media

CIN

contrast media

CIN

contrast media

CIN

CM

nephropathy

CM

nephropathy

CM

CIN

CM

CIN

CM

renal damage

CM

CIN

CM

CIN

CM

CIN

CM

CIN

CM

CIN

CM

CIN

CM

CIN

CM

nephropathy

CM

nephropathy

CM

CIN

CM

CIN

CM

renal damage

CM

CIN

CM

CIN

CM

CIN

CM

CIN

CM

CIN

CM

CIN

CM

CIN

CM

nephropathy

CM

nephropathy

CM

CIN

CM

CIN

CM

renal damage

CM

CIN

CM

CIN

CM

CIN

CM

CIN

CM

CIN

CM

CIN

CM

CIN

CM

nephropathy

CM

nephropathy

CM

CIN

CM

CIN

CM

renal damage

CM

CIN

CM

CIN

CM

CIN

CM

CIN

CM

CIN

CM

CIN

CM

CIN

CM

nephropathy

CM

nephropathy

CM

CIN

CM

CIN

CM

renal damage

CM

CIN

CM

CIN

CM

CIN

CM

CIN

CM

CIN

CM

CIN

CM

CIN

CM

nephropathy

CM

nephropathy

CM

CIN

CM

CIN

CM

renal damage

CM

CIN

CM

CIN

CM

CIN

CM

CIN

CM

CIN

CM

CIN

CM

CIN

iopromide

nephropathy

iopromide

nephropathy

iopromide

CIN

iopromide

CIN

iopromide

renal damage

iopromide

CIN

iopromide

CIN

iopromide

CIN

iopromide

CIN

iopromide

CIN

iopromide

CIN

iopromide

CIN

iopromide

nephropathy

iopromide

nephropathy

iopromide

CIN

iopromide

CIN

iopromide

renal damage

iopromide

CIN

iopromide

CIN

iopromide

CIN

iopromide

CIN

iopromide

CIN

iopromide

CIN

iopromide

CIN

iohexol

nephropathy

iohexol

nephropathy

iohexol

CIN

iohexol

CIN

iohexol

renal damage

iohexol

CIN

iohexol

CIN

iohexol

CIN

iohexol

CIN

iohexol

CIN

iohexol

CIN

iohexol

CIN

iohexol

nephropathy

iohexol

nephropathy

iohexol

CIN

iohexol

CIN

iohexol

renal damage

iohexol

CIN

iohexol

CIN

iohexol

CIN

iohexol

CIN

iohexol

CIN

iohexol

CIN

iohexol

CIN


Input: A case of ventricular tachycardia related to caffeine pretreatment. Suboptimal seizure duration is commonly encountered in electroconvulsive therapy practice, especially in older patients with higher seizure thresholds. Intravenous caffeine is commonly used to improve seizure duration and quality in such patients and is generally well tolerated aside from occasional reports of relatively benign ventricular ectopy. We describe a patient with no previous history of cardiac disease or arrhythmia who developed sustained bigeminy and 2 brief runs of ventricular tachycardia after caffeine administration. Although intravenous caffeine is generally well tolerated, the clinician should be aware of the potential for unpredictable and serious ventricular arrhythmias.

ventricular tachycardia

seizure

seizure

seizure

ventricular ectopy

cardiac disease

arrhythmia

ventricular tachycardia

ventricular arrhythmias

caffeine

caffeine

caffeine

caffeine

caffeine

seizure

caffeine

seizure

caffeine

seizure

caffeine

seizure

caffeine

seizure

caffeine

seizure

caffeine

seizure

caffeine

seizure

caffeine

seizure

caffeine

seizure

caffeine

seizure

caffeine

seizure

caffeine

ventricular tachycardia

caffeine

ventricular tachycardia

caffeine

ventricular tachycardia

caffeine

ventricular tachycardia

caffeine

ventricular tachycardia

caffeine

ventricular tachycardia

caffeine

ventricular tachycardia

caffeine

ventricular tachycardia

caffeine

ventricular ectopy

caffeine

ventricular ectopy

caffeine

ventricular ectopy

caffeine

ventricular ectopy


Input: Optical coherence tomography can measure axonal loss in patients with ethambutol - induced optic neuropathy. PURPOSE: To map and identify the pattern, in vivo, of axonal degeneration in ethambutol - induced optic neuropathy using optical coherence tomography (OCT). Ethambutol is an antimycobacterial agent often used to treat tuberculosis. A serious complication of ethambutol is an optic neuropathy that impairs visual acuity, contrast sensitivity, and color vision. However, early on, when the toxic optic neuropathy is mild and partly reversible, the funduscopic findings are often subtle and easy to miss. METHODS: Three subjects with a history of ethambutol (EMB) - induced optic neuropathy of short -, intermediate -, and long - term visual deficits were administered a full neuro - ophthalmologic examination including visual acuity, color vision, contrast sensitivity, and fundus examination. In addition, OCT (OCT 3000, Humphrey - Zeiss, Dublin, CA) was performed on both eyes of each subject using the retinal nerve fiber layer (RNFL) analysis protocol. OCT interpolates data from 100 points around the optic nerve to effectively map out the RNFL. RESULTS: The results were compared to the calculated average RNFL of normal eyes accumulated from four prior studies using OCT, n = 661. In all subjects with history of EMB - induced optic neuropathy, there was a mean loss of 72% nerve fiber layer thickness in the temporal quadrant (patient A, with eventual recovery of visual acuity and fields, 58% loss; patient B, with intermediate visual deficits, 68% loss; patient C, with chronic visual deficits, 90% loss), with an average mean optic nerve thickness of 26 + / - 16 microm. There was a combined mean loss of 46% of fibers from the superior, inferior, and nasal quadrants in the (six) eyes of all three subjects (mean average thickness of 55 + / - 29 microm). In both sets (four) of eyes of the subjects with persistent visual deficits (patients B and C), there was an average loss of 79% of nerve fiber thickness in the temporal quadrant. CONCLUSIONS: The OCT results in these patients with EMB - induced optic neuropathy show considerable loss especially of the temporal fibers. This is consistent with prior histopathological studies that show predominant loss of parvo - cellular axons (or small - caliber axons) within the papillo - macular bundle in toxic or hereditary optic neuropathies. OCT can be a valuable tool in the quantitative analysis of optic neuropathies. Additionally, in terms of management of EMB - induced optic neuropathy, it is important to properly manage ethambutol dosing in patients with renal impairment and to achieve proper transition to a maintenance dose once an appropriate loading dose has been reached.

ethambutol

ethambutol

Ethambutol

ethambutol

ethambutol

EMB

EMB

EMB

EMB

ethambutol

optic neuropathy

axonal degeneration

optic neuropathy

tuberculosis

optic neuropathy

optic neuropathy

optic neuropathy

visual deficits

optic neuropathy

visual deficits

visual deficits

visual deficits

optic neuropathy

optic neuropathies

optic neuropathies

optic neuropathy

renal impairment

ethambutol

visual deficits

ethambutol

visual deficits

ethambutol

visual deficits

ethambutol

visual deficits

ethambutol

visual deficits

ethambutol

visual deficits

ethambutol

visual deficits

ethambutol

visual deficits

Ethambutol

visual deficits

Ethambutol

visual deficits

Ethambutol

visual deficits

Ethambutol

visual deficits

ethambutol

visual deficits

ethambutol

visual deficits

ethambutol

visual deficits

ethambutol

visual deficits

ethambutol

visual deficits

ethambutol

visual deficits

ethambutol

visual deficits

ethambutol

visual deficits

EMB

visual deficits

EMB

visual deficits

EMB

visual deficits

EMB

visual deficits

EMB

visual deficits

EMB

visual deficits

EMB

visual deficits

EMB

visual deficits

EMB

visual deficits

EMB

visual deficits

EMB

visual deficits

EMB

visual deficits

EMB

visual deficits

EMB

visual deficits

EMB

visual deficits

EMB

visual deficits

ethambutol

visual deficits

ethambutol

visual deficits

ethambutol

visual deficits

ethambutol

visual deficits

ethambutol

optic neuropathy

ethambutol

optic neuropathy

ethambutol

optic neuropathy

ethambutol

optic neuropathy

ethambutol

optic neuropathy

ethambutol

optic neuropathy

ethambutol

optic neuropathy

ethambutol

optic neuropathies

ethambutol

optic neuropathies

ethambutol

optic neuropathy

ethambutol

optic neuropathy

ethambutol

optic neuropathy

ethambutol

optic neuropathy

ethambutol

optic neuropathy

ethambutol

optic neuropathy

ethambutol

optic neuropathy

ethambutol

optic neuropathy

ethambutol

optic neuropathies

ethambutol

optic neuropathies

ethambutol

optic neuropathy

Ethambutol

optic neuropathy

Ethambutol

optic neuropathy

Ethambutol

optic neuropathy

Ethambutol

optic neuropathy

Ethambutol

optic neuropathy

Ethambutol

optic neuropathy

Ethambutol

optic neuropathy

Ethambutol

optic neuropathies

Ethambutol

optic neuropathies

Ethambutol

optic neuropathy

ethambutol

optic neuropathy

ethambutol

optic neuropathy

ethambutol

optic neuropathy

ethambutol

optic neuropathy

ethambutol

optic neuropathy

ethambutol

optic neuropathy

ethambutol

optic neuropathy

ethambutol

optic neuropathies

ethambutol

optic neuropathies

ethambutol

optic neuropathy

ethambutol

optic neuropathy

ethambutol

optic neuropathy

ethambutol

optic neuropathy

ethambutol

optic neuropathy

ethambutol

optic neuropathy

ethambutol

optic neuropathy

ethambutol

optic neuropathy

ethambutol

optic neuropathies

ethambutol

optic neuropathies

ethambutol

optic neuropathy

EMB

optic neuropathy

EMB

optic neuropathy

EMB

optic neuropathy

EMB

optic neuropathy

EMB

optic neuropathy

EMB

optic neuropathy

EMB

optic neuropathy

EMB

optic neuropathies

EMB

optic neuropathies

EMB

optic neuropathy

EMB

optic neuropathy

EMB

optic neuropathy

EMB

optic neuropathy

EMB

optic neuropathy

EMB

optic neuropathy

EMB

optic neuropathy

EMB

optic neuropathy

EMB

optic neuropathies

EMB

optic neuropathies

EMB

optic neuropathy

EMB

optic neuropathy

EMB

optic neuropathy

EMB

optic neuropathy

EMB

optic neuropathy

EMB

optic neuropathy

EMB

optic neuropathy

EMB

optic neuropathy

EMB

optic neuropathies

EMB

optic neuropathies

EMB

optic neuropathy

EMB

optic neuropathy

EMB

optic neuropathy

EMB

optic neuropathy

EMB

optic neuropathy

EMB

optic neuropathy

EMB

optic neuropathy

EMB

optic neuropathy

EMB

optic neuropathies

EMB

optic neuropathies

EMB

optic neuropathy

ethambutol

optic neuropathy

ethambutol

optic neuropathy

ethambutol

optic neuropathy

ethambutol

optic neuropathy

ethambutol

optic neuropathy

ethambutol

optic neuropathy

ethambutol

optic neuropathy

ethambutol

optic neuropathies

ethambutol

optic neuropathies

ethambutol

optic neuropathy


Input: Effects of the cyclooxygenase - 2 specific inhibitor valdecoxib versus nonsteroidal antiinflammatory agents and placebo on cardiovascular thrombotic events in patients with arthritis. There have been concerns that the risk of cardiovascular thrombotic events may be higher with cyclooxygenase (COX) - 2 - specific inhibitors than nonselective nonsteroidal antiinflammatory drugs (NSAIDs). We evaluated cardiovascular event data for valdecoxib, a new COX - 2 - specific inhibitor in approximately 8000 patients with osteoarthritis and rheumatoid arthritis treated with this agent in randomized clinical trials. The incidence of cardiovascular thrombotic events (cardiac, cerebrovascular and peripheral vascular, or arterial thrombotic) was determined by analyzing pooled valdecoxib (10 - 80 mg daily), nonselective NSAID (diclofenac 75 mg bid, ibuprofen 800 mg tid, or naproxen 500 mg bid) and placebo data from 10 randomized osteoarthritis and rheumatoid arthritis trials that were 6 - 52 weeks in duration. The incidence rates of events were determined in all patients (n = 7934) and in users of low - dose (< or = 325 mg daily) aspirin (n = 1051) and nonusers of aspirin (n = 6883). Crude and exposure - adjusted incidences of thrombotic events were similar for valdecoxib, NSAIDs, and placebo. The risk of serious thrombotic events was also similar for each valdecoxib dose. Thrombotic risk was consistently higher for users of aspirin users than nonusers of aspirin (placebo, 1. 4% vs. 0%; valdecoxib, 1. 7% vs. 0. 2%; NSAIDs, 1. 9% vs. 0. 5%). The rates of events in users of aspirin were similar for all 3 treatment groups and across valdecoxib doses. Short - and intermediate - term treatment with therapeutic (10 or 20 mg daily) and supratherapeutic (40 or 80 mg daily) valdecoxib doses was not associated with an increased incidence of thrombotic events relative to nonselective NSAIDs or placebo in osteoarthritis and rheumatoid arthritis patients in controlled clinical trials.

valdecoxib

valdecoxib

valdecoxib

diclofenac

ibuprofen

naproxen

aspirin

aspirin

valdecoxib

valdecoxib

aspirin

aspirin

valdecoxib

aspirin

valdecoxib

valdecoxib

thrombotic

arthritis

thrombotic

osteoarthritis

rheumatoid arthritis

thrombotic

thrombotic

osteoarthritis

rheumatoid arthritis

thrombotic

thrombotic

Thrombotic

thrombotic

osteoarthritis

rheumatoid arthritis

aspirin

thrombotic

aspirin

thrombotic

aspirin

thrombotic

aspirin

thrombotic

aspirin

thrombotic

aspirin

thrombotic

aspirin

Thrombotic

aspirin

thrombotic

aspirin

thrombotic

aspirin

thrombotic

aspirin

thrombotic

aspirin

thrombotic

aspirin

thrombotic

aspirin

thrombotic

aspirin

Thrombotic

aspirin

thrombotic

aspirin

thrombotic

aspirin

thrombotic

aspirin

thrombotic

aspirin

thrombotic

aspirin

thrombotic

aspirin

thrombotic

aspirin

Thrombotic

aspirin

thrombotic

aspirin

thrombotic

aspirin

thrombotic

aspirin

thrombotic

aspirin

thrombotic

aspirin

thrombotic

aspirin

thrombotic

aspirin

Thrombotic

aspirin

thrombotic

aspirin

thrombotic

aspirin

thrombotic

aspirin

thrombotic

aspirin

thrombotic

aspirin

thrombotic

aspirin

thrombotic

aspirin

Thrombotic

aspirin

thrombotic


Input: A randomized, placebo - controlled, crossover study of ephedrine for SSRI - induced female sexual dysfunction. The objective of this study was to determine whether ephedrine, an alpha - and beta - adrenergic agonist previously shown to enhance genital blood flow in women, has beneficial effects in reversing antidepressant - induced sexual dysfunction. Nineteen sexually dysfunctional women receiving either fluoxetine, sertraline, or paroxetine participated in an eight - week, double - blind, placebo - controlled, cross - over study of the effects of ephedrine (50 mg) on self - report measures of sexual desire, arousal, orgasm, and sexual satisfaction. Although there were significant improvements relative to baseline in sexual desire and orgasm intensity / pleasure on 50 mg ephedrine 1 - hr prior to sexual activity, significant improvements in these measures, as well as in sexual arousal and orgasmic ability also were noted with placebo. These findings highlight the importance of conducting placebo - controlled trials for this condition.

ephedrine

ephedrine

fluoxetine

sertraline

paroxetine

ephedrine

ephedrine

sexual dysfunction

sexual dysfunction

sexually dysfunctional

fluoxetine

sexual dysfunction

fluoxetine

sexual dysfunction

fluoxetine

sexually dysfunctional

paroxetine

sexual dysfunction

paroxetine

sexual dysfunction

paroxetine

sexually dysfunctional

sertraline

sexual dysfunction

sertraline

sexual dysfunction

sertraline

sexually dysfunctional


Input: Erectile dysfunction occurs following substantia nigra lesions in the rat. Erectile function was assessed 6 weeks following uni - and bilateral injections of 6 - hydroxydopamine in the substantia nigra nucleus of the brain. Behavioral apomorphine - induced penile erections were reduced (5 / 8) and increased (3 / 8) in uni - and bilateral lesioned animals. Intracavernous pressures, following electrical stimulation of the cavernous nerve, decreased in lesioned animals. Lesions of the substantia nigra were confirmed by histology. Concentration of dopamine and its metabolites were decreased in the striatum of substantia nigra lesioned rats. Lesions of the substantia nigra are therefore associated with erectile dysfunction in rats and may serve as a model to study erectile dysfunction in Parkinson' s disease.

Erectile dysfunction

erectile dysfunction

erectile dysfunction

Parkinson' s disease

6 - hydroxydopamine

apomorphine

dopamine

6 - hydroxydopamine

Erectile dysfunction

6 - hydroxydopamine

erectile dysfunction

6 - hydroxydopamine

erectile dysfunction


Input: Potential therapeutic use of the selective dopamine D1 receptor agonist, A - 86929: an acute study in parkinsonian levodopa - primed monkeys. The clinical utility of dopamine (DA) D1 receptor agonists in the treatment of Parkinson' s disease (PD) is still unclear. The therapeutic use of selective DA D1 receptor agonists such as SKF - 82958 (6 - chloro - 7, 8 - dihydroxy - 3 - allyl - 1 - phenyl - 2, 3, 4, 5 - tetrahydro - 1H - 3 - benzaze pine hydrobromide) and A - 77636 ([1R, 3S] 3 - [1' - admantyl] - 1 - aminomethyl - 3, 4 - dihydro - 5, 6 - dihydroxy - 1H - 2 - benzo pyran hydrochloride) seems limited because of their duration of action, which is too short for SKF - 82958 (< 1 hr) and too long for A - 77636 (> 20 hr, leading to behavioral tolerance). We therefore conducted the present acute dose - response study in four 1 - methyl - 4 - phenyl - 1, 2, 3, 6 - tetrahydropyridine (MPTP) - exposed cynomolgus monkeys primed to exhibit levodopa - induced dyskinesias to evaluate the locomotor and dyskinetic effects on challenge with four doses (from 0. 03 to 1. 0 mg / kg) of A - 86929 ([-] - [5aR, 11bS] - 4, 5, 5a, 6, 7, 11b - hexahydro - 2 - propyl - 3 - thia - 5 - + + + azacyclopent - 1 - ena [c] phenathrene - 9 - 10 - diol), a selective and full DA D1 - like receptor agonist with an intermediate duration of action. Levodopa and the DA D2 - like receptor agonist, LY - 171555 ([4aR - trans] - 4, 4a, 5, 6, 7, 8, 8a, 9 - o - dihydro - 5n - propyl - 2H - pyrazo lo - 3 - 4 - quinoline hydrochloride) were also used for comparison. Acute administration of A - 86929 was as efficacious in alleviating MPTP - induced parkinsonism as levodopa and LY - 171555, but was less likely to reproduce the levodopa - induced dyskinesias in these animals than with either LY - 171555 or subsequent challenge of levodopa. Selective stimulation of the DA D1 receptor may provide better integration of neural inputs transmitted to the internal segment of the globus pallidus (referred to as the basal ganglia output) compared with levodopa and selective DA D2 receptor agonist. Potent DA D1 receptor agents with an intermediate duration of efficacy such as A - 86929 (approximately 4 hr at higher doses tested) are potential therapeutic tools in PD and merit further attention.

dopamine

A - 86929

levodopa

dopamine

DA

DA

SKF - 82958

6 - chloro - 7, 8 - dihydroxy - 3 - allyl - 1 - phenyl - 2, 3, 4, 5 - tetrahydro - 1H - 3 - benzaze pine hydrobromide

A - 77636

[1R, 3S] 3 - [1' - admantyl] - 1 - aminomethyl - 3, 4 - dihydro - 5, 6 - dihydroxy - 1H - 2 - benzo pyran hydrochloride

SKF - 82958

A - 77636

1 - methyl - 4 - phenyl - 1, 2, 3, 6 - tetrahydropyridine

MPTP

levodopa

A - 86929

[-] - [5aR, 11bS] - 4, 5, 5a, 6, 7, 11b - hexahydro - 2 - propyl - 3 - thia - 5 - + + + azacyclopent - 1 - ena [c] phenathrene - 9 - 10 - diol

DA

Levodopa

DA

LY - 171555

[4aR - trans] - 4, 4a, 5, 6, 7, 8, 8a, 9 - o - dihydro - 5n - propyl - 2H - pyrazo lo - 3 - 4 - quinoline hydrochloride

A - 86929

MPTP

levodopa

LY - 171555

levodopa

LY - 171555

levodopa

DA

levodopa

DA

DA

A - 86929

parkinsonian

Parkinson' s disease

PD

dyskinesias

dyskinetic

parkinsonism

dyskinesias

PD

levodopa

dyskinesias

levodopa

dyskinetic

levodopa

dyskinesias

levodopa

dyskinesias

levodopa

dyskinetic

levodopa

dyskinesias

Levodopa

dyskinesias

Levodopa

dyskinetic

Levodopa

dyskinesias

levodopa

dyskinesias

levodopa

dyskinetic

levodopa

dyskinesias

levodopa

dyskinesias

levodopa

dyskinetic

levodopa

dyskinesias

levodopa

dyskinesias

levodopa

dyskinetic

levodopa

dyskinesias

levodopa

dyskinesias

levodopa

dyskinetic

levodopa

dyskinesias

1 - methyl - 4 - phenyl - 1, 2, 3, 6 - tetrahydropyridine

parkinsonian

1 - methyl - 4 - phenyl - 1, 2, 3, 6 - tetrahydropyridine

parkinsonism

MPTP

parkinsonian

MPTP

parkinsonism

MPTP

parkinsonian

MPTP

parkinsonism


Input: Deaths from local anesthetic - induced convulsions in mice. Median convulsant (CD50) and median lethal (LD50) doses of three representative local anesthetics were determined in adult mice to evaluate the threat to life of local anesthetic - induced convulsions. The CD50 and LD50, respectively, were 57. 7 and 58. 7 mg / kg for bupivacaine, 111. 0 and 133. 1 mg / kg for lidocaine, and 243. 4 and 266. 5 mg / kg for chloroprocaine. When given intraperitoneally, bupivacaine thus was only about twice as toxic as lidocaine and four times as toxic as chloroprocaine. Convulsions always preceded death, except after precipitous cardiopulmonary arrest from extreme doses. A CD50 dose of local anesthetic (causing convulsions in 50% of mice) was fatal in 90% of bupivacaine - induced seizures, in 57% of the chloroprocaine group, and in 6% of the lidocaine group. The narrow gap between convulsant and lethal doses of local anesthetics indicates that untreated convulsions present much more of a threat to life than heretofore appreciated.

convulsions

convulsions

Convulsions

cardiopulmonary arrest

convulsions

seizures

convulsions

bupivacaine

lidocaine

chloroprocaine

bupivacaine

lidocaine

chloroprocaine

bupivacaine

chloroprocaine

lidocaine

lidocaine

convulsions

lidocaine

convulsions

lidocaine

Convulsions

lidocaine

convulsions

lidocaine

seizures

lidocaine

convulsions

lidocaine

convulsions

lidocaine

convulsions

lidocaine

Convulsions

lidocaine

convulsions

lidocaine

seizures

lidocaine

convulsions

lidocaine

convulsions

lidocaine

convulsions

lidocaine

Convulsions

lidocaine

convulsions

lidocaine

seizures

lidocaine

convulsions

chloroprocaine

convulsions

chloroprocaine

convulsions

chloroprocaine

Convulsions

chloroprocaine

convulsions

chloroprocaine

seizures

chloroprocaine

convulsions

chloroprocaine

convulsions

chloroprocaine

convulsions

chloroprocaine

Convulsions

chloroprocaine

convulsions

chloroprocaine

seizures

chloroprocaine

convulsions

chloroprocaine

convulsions

chloroprocaine

convulsions

chloroprocaine

Convulsions

chloroprocaine

convulsions

chloroprocaine

seizures

chloroprocaine

convulsions

bupivacaine

convulsions

bupivacaine

convulsions

bupivacaine

Convulsions

bupivacaine

convulsions

bupivacaine

seizures

bupivacaine

convulsions

bupivacaine

convulsions

bupivacaine

convulsions

bupivacaine

Convulsions

bupivacaine

convulsions

bupivacaine

seizures

bupivacaine

convulsions

bupivacaine

convulsions

bupivacaine

convulsions

bupivacaine

Convulsions

bupivacaine

convulsions

bupivacaine

seizures

bupivacaine

convulsions


Input: Myoclonic, atonic, and absence seizures following institution of carbamazepine therapy in children. Five children, aged 3 to 11 years, treated with carbamazepine for epilepsy, had an acute aberrant reaction characterized by the onset of myoclonic, atypical absence and / or atonic (minor motor) seizures within a few days. When the carbamazepine was discontinued, two of the children returned to their former state very quickly, two had the minor motor seizures resolve in 3 and 6 months, and one had the seizures persist. The child in whom the seizures persisted was later found to have ceroid lipofuscinosis. The other children are doing well on other anticonvulsants.

Myoclonic, atonic, and absence seizures

Myoclonic, atonic, and absence seizures

absence seizures

epilepsy

myoclonic, atypical absence and / or atonic (minor motor) seizures

myoclonic, atypical absence and / or atonic (minor motor) seizures

atypical absence and / or atonic (minor motor) seizures

seizures

seizures

seizures

ceroid lipofuscinosis

carbamazepine

carbamazepine

carbamazepine

carbamazepine

Myoclonic, atonic, and absence seizures

carbamazepine

absence seizures

carbamazepine

myoclonic, atypical absence and / or atonic (minor motor) seizures

carbamazepine

atypical absence and / or atonic (minor motor) seizures

carbamazepine

Myoclonic, atonic, and absence seizures

carbamazepine

absence seizures

carbamazepine

myoclonic, atypical absence and / or atonic (minor motor) seizures

carbamazepine

atypical absence and / or atonic (minor motor) seizures

carbamazepine

Myoclonic, atonic, and absence seizures

carbamazepine

absence seizures

carbamazepine

myoclonic, atypical absence and / or atonic (minor motor) seizures

carbamazepine

atypical absence and / or atonic (minor motor) seizures

carbamazepine

Myoclonic, atonic, and absence seizures

carbamazepine

myoclonic, atypical absence and / or atonic (minor motor) seizures

carbamazepine

Myoclonic, atonic, and absence seizures

carbamazepine

myoclonic, atypical absence and / or atonic (minor motor) seizures

carbamazepine

Myoclonic, atonic, and absence seizures

carbamazepine

myoclonic, atypical absence and / or atonic (minor motor) seizures


Input: Naloxone reversal of hypotension due to captopril overdose. The hemodynamic effects of captopril and other angiotensin - converting enzyme inhibitors may be mediated by the endogenous opioid system. The opioid antagonist naloxone has been shown to block or reverse the hypotensive actions of captopril. We report a case of an intentional captopril overdose, manifested by marked hypotension, that resolved promptly with the administration of naloxone. To our knowledge, this is the first reported case of captopril - induced hypotension treated with naloxone. Our experience demonstrates a possible role of naloxone in the reversal of hypotension resulting from captopril.

Naloxone

captopril

captopril

angiotensin - converting enzyme inhibitors

naloxone

captopril

captopril

naloxone

captopril

naloxone

naloxone

captopril

hypotension

overdose

hypotensive

overdose

hypotension

hypotension

hypotension

angiotensin - converting enzyme inhibitors

hypotension

angiotensin - converting enzyme inhibitors

hypotensive

angiotensin - converting enzyme inhibitors

hypotension

angiotensin - converting enzyme inhibitors

hypotension

angiotensin - converting enzyme inhibitors

hypotension

angiotensin - converting enzyme inhibitors

overdose

angiotensin - converting enzyme inhibitors

overdose


Input: Carbamazepine - induced cardiac dysfunction. Characterization of two distinct clinical syndromes. A patient with sinus bradycardia and atrioventricular block, induced by carbamazepine, prompted an extensive literature review of all previously reported cases. From the analysis of these cases, two distinct forms of carbamazepine - associated cardiac dysfunction emerged. One patient group developed sinus tachycardias in the setting of a massive carbamazepine overdose. The second group consisted almost exclusively of elderly women who developed potentially life - threatening bradyarrhythmias or atrioventricular conduction delay, associated with either therapeutic or modestly elevated carbamazepine serum levels. Because carbamazepine is widely used in the treatment of many neurologic and psychiatric conditions, the recognition of the latter syndrome has important implications for the use of this drug in elderly patients.

Carbamazepine

carbamazepine

carbamazepine

carbamazepine

carbamazepine

carbamazepine

cardiac dysfunction

bradycardia

atrioventricular block

cardiac dysfunction

sinus tachycardias

overdose

bradyarrhythmias

atrioventricular conduction delay

psychiatric

Carbamazepine

atrioventricular block

Carbamazepine

atrioventricular conduction delay

carbamazepine

atrioventricular block

carbamazepine

atrioventricular conduction delay

carbamazepine

atrioventricular block

carbamazepine

atrioventricular conduction delay

carbamazepine

atrioventricular block

carbamazepine

atrioventricular conduction delay

carbamazepine

atrioventricular block

carbamazepine

atrioventricular conduction delay

carbamazepine

atrioventricular block

carbamazepine

atrioventricular conduction delay

Carbamazepine

bradycardia

Carbamazepine

bradyarrhythmias

carbamazepine

bradycardia

carbamazepine

bradyarrhythmias

carbamazepine

bradycardia

carbamazepine

bradyarrhythmias

carbamazepine

bradycardia

carbamazepine

bradyarrhythmias

carbamazepine

bradycardia

carbamazepine

bradyarrhythmias

carbamazepine

bradycardia

carbamazepine

bradyarrhythmias

Carbamazepine

sinus tachycardias

carbamazepine

sinus tachycardias

carbamazepine

sinus tachycardias

carbamazepine

sinus tachycardias

carbamazepine

sinus tachycardias

carbamazepine

sinus tachycardias


Input: Glutamatergic neurotransmission mediated by NMDA receptors in the inferior colliculus can modulate haloperidol - induced catalepsy. The inferior colliculus (IC) is primarily involved in the processing of auditory information, but it is distinguished from other auditory nuclei in the brainstem by its connections with structures of the motor system. Functional evidence relating the IC to motor behavior derives from experiments showing that activation of the IC by electrical stimulation or excitatory amino acid microinjection causes freezing, escape - like behavior, and immobility. However, the nature of this immobility is still unclear. The present study examined the influence of excitatory amino acid - mediated mechanisms in the IC on the catalepsy induced by the dopamine receptor blocker haloperidol administered systemically (1 or 0. 5 mg / kg) in rats. Haloperidol - induced catalepsy was challenged with prior intracollicular microinjections of glutamate NMDA receptor antagonists, MK - 801 (15 or 30 mmol / 0. 5 microl) and AP7 (10 or 20 nmol / 0. 5 microl), or of the NMDA receptor agonist N - methyl - d - aspartate (NMDA, 20 or 30 nmol / 0. 5 microl). The results showed that intracollicular microinjection of MK - 801 and AP7 previous to systemic injections of haloperidol significantly attenuated the catalepsy, as indicated by a reduced latency to step down from a horizontal bar. Accordingly, intracollicular microinjection of NMDA increased the latency to step down the bar. These findings suggest that glutamate - mediated mechanisms in the neural circuits at the IC level influence haloperidol - induced catalepsy and participate in the regulation of motor activity.

NMDA

haloperidol

amino acid

amino acid

dopamine

haloperidol

Haloperidol

glutamate

NMDA

MK - 801

NMDA

N - methyl - d - aspartate

NMDA

MK - 801

haloperidol

NMDA

glutamate

haloperidol

catalepsy

catalepsy

catalepsy

catalepsy

catalepsy

haloperidol

catalepsy

haloperidol

catalepsy

haloperidol

catalepsy

haloperidol

catalepsy

haloperidol

catalepsy

haloperidol

catalepsy

haloperidol

catalepsy

haloperidol

catalepsy

haloperidol

catalepsy

haloperidol

catalepsy

Haloperidol

catalepsy

Haloperidol

catalepsy

Haloperidol

catalepsy

Haloperidol

catalepsy

Haloperidol

catalepsy

haloperidol

catalepsy

haloperidol

catalepsy

haloperidol

catalepsy

haloperidol

catalepsy

haloperidol

catalepsy

haloperidol

catalepsy

haloperidol

catalepsy

haloperidol

catalepsy

haloperidol

catalepsy

haloperidol

catalepsy


Input: Metabotropic glutamate 7 receptor subtype modulates motor symptoms in rodent models of Parkinson' s disease. Metabotropic glutamate (mGlu) receptors modulate synaptic transmission in the central nervous system and represent promising therapeutic targets for symptomatic treatment of Parkinson' s disease (PD). Among the eight mGlu receptor subtypes, mGlu7 receptor is prominently expressed in the basal ganglia, but its role in restoring motor function in animal models of PD is not known. The effects of N, N' - dibenzhydrylethane - 1, 2 - diamine dihydrochloride (AMN082), the first selective allosteric activator of mGlu7 receptors, were thus tested in different rodent models of PD. Here, we show that oral (5 mg / kg) or intrastriatal administration (0. 1 and 0. 5 nmol) of AMN082 reverses haloperidol - induced catalepsy in rats. AMN082 (2. 5 and 5 mg / kg) reduces apomorphine - induced rotations in unilateral 6 - hydroxydopamine (6 - OHDA) - lesioned rats. In a more complex task commonly used to evaluate major akinetic symptoms of PD patients, 5 mg / kg AMN082 reverses the increased reaction time to respond to a cue of bilateral 6 - OHDA - lesioned rats. In addition, AMN082 reduces the duration of haloperidol - induced catalepsy in a mGlu7 receptor - dependent manner in wild - type but not mGlu7 receptor knockout mice. Higher doses of AMN082 (10 and 20 mg / kg p. o.) have no effect on the same models of PD. Overall these findings suggest that mGlu7 receptor activation can reverse motor dysfunction associated with reduced dopamine activity. Selective ligands of mGlu7 receptor subtypes may thus be considered as promising compounds for the development of antiparkinsonian therapeutic strategies.

glutamate

glutamate

N, N' - dibenzhydrylethane - 1, 2 - diamine dihydrochloride

haloperidol

apomorphine

6 - hydroxydopamine

6 - OHDA

6 - OHDA

haloperidol

dopamine

Parkinson' s disease

Parkinson' s disease

PD

PD

PD

catalepsy

akinetic

PD

catalepsy

PD

haloperidol

catalepsy

haloperidol

catalepsy

haloperidol

catalepsy

haloperidol

catalepsy