Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A wide variety of conditions seen in medical practice can produce memory impairment (amnesia). Normal aging, depression, and anxiety are commonly associated with memory difficulties, as are many neurologic conditions. Systemic illnesses can impair memory by injuring vulnerable limbic regions sensitive to hypoxia or hypoglycemia. Commonly used over-the-counter and prescription medications can likewise cause amnesia. These conditions disrupt memory in characteristic ways. Recent studies suggest that immediate, recent, and remote memory functions have different neuroanatomic substrates, as do the processes of registration, retention, and retrieval. New classifications have emerged to explain the evidence for multiple memory subsystems. The neuropharmacology of memory now includes several peptides in addition to cholinergic and noradrenergic pathways. Critical limbic regions have been discovered that mediate memory consolidation, and neuronal mechanisms such as long-term potentiation are being implicated in the unique capacity of these areas to permit new learning to take place.
 ...
PMID:Amnestic disorders. Pathophysiology and patterns of memory dysfunction. 215 98

Anaesthesia for elective direct current cardioversion (DCC) was induced with propofol (Diprivan) 1.2 mg/kg in 28 patients and with 0.2 mg/kg etomidate (Hypnomidate) in 20 patients. These mostly high risk patients (NYHA class II to III) were successfully treated with defibrillation. Blood pressure and heart rate were recorded before and after induction and at 2 minutes intervals up to 20 minutes after DCC. Both anaesthetic agents caused mild hypotension. Heart rate did not change significantly after induction but fell significantly after DCC from the mean value of 124 +/- 26 bpm and 122 +/- 37 bpm to 94 +/- 19 bpm and to 91 +/- 19 bpm in propofol and etomidate treated patients respectively. Four patients became apnoeic necessitating assisted ventilation for approximately four minutes. All propofol treated patients had rapid recovery times and opened eyes on command within 5.6 +/- 1.9 minutes after induction, and were fully orientated about 4 minutes later also. Complete amnesia was observed in all patients in this group. In contrast etomidate induced anaesthesia did not cause respiratory depression, but the recovery time was longer. Four patients of this group complained of recall of DCC. In 7 patients due to involuntary movements or myoclonus, after induction with etomidate reliable EKG monitoring appeared to be difficult.
 ...
PMID:[Anesthesia for cardioversion. A comparison of propofol and etomidate]. 220 24

We have studied the effect of i.v. flumazenil 0.01 mg kg-1 on the amnesia and sedation caused by midazolam 2 mg and 5 mg i.v. in volunteers in order to determine the relationship between the actions of the antagonist on these two effects. Midazolam caused dose-dependent central neural depression as assessed by critical flicker fusion frequency, and dose-dependent amnesia for word cards. In subjects given flumazenil 5 min after administration of midazolam, fusion frequency readings and memory were restored to levels comparable to those before midazolam administration. These two effects of flumazenil were similar in time course and extent, suggesting that they share the same mechanism of action. Flumazenil given alone had no effect on memory. The study has demonstrated anterograde amnesia following benzodiazepine administration and antagonism by flumazenil. There was neither retrograde amnesia nor retrograde antagonism of amnesia.
 ...
PMID:Effect of flumazenil on midazolam-induced amnesia. 222 35

Flunarizine hydrochloride (FZ), a calcium entry blockade, has been used nationwide in Japan as a cerebral active vasodilator since October, 1984. The present paper reports 31 cases of FZ-induced Parkinsonism, depression and akathisia, referred to our hospital between October 1986 and September 1988. Out of the 31 patients, four including two with Parkinson's disease and one each with progressive supranuclear palsy and olivopontocerebellar atrophy showed worsening of their parkinsonian symptoms within a few months after FZ administration. The remaining 27 patients (7 males and 20 females) newly developed Parkinsonism after treatment with FZ. Symptoms appeared one week to two years (mean: 6.1 months) after starting FZ of a daily dose of 10 mg. FZ had been used in 6 patients for cerebrovascular episodes confirmed by clinical history or brain CT, and in the remainder, for dizziness, light-headedness, hypertension, amnesia or hypochondric neurotic complaints. Akinesia and bradykinesia progressed rather rapidly after onset, and patients became unambulatory within several months. Symptoms had worsened, and L-dopa, anticholinergic drugs, and bromocriptine had been ineffective until FZ was discontinued. Their Parkinsonism was characterized by marked akinesia, bradykinesia, and moderate rigidity. Masked face was seen in most of them. Tremor was absent at rest, and induced in 12 patients by posture and/or action. Sixteen patients were accompanied by depression, and five, by akathisia. Improvement began several weeks after withdrawal of FZ, and most patients recovered almost completely within a few months although mild rigidity and bradykinesia remained in some.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Parkinsonism, depression and akathisia induced by flunarizine, a calcium entry blockade--report of 31 cases]. 258 81

1. Firing thresholds and conduction latencies of single myelinated axons in frog sciatic nerves were monitored during impulse activity in vitro. Resting threshold and the activity dependence of threshold were studied as a function of the concentration of two inhalational anaesthetic agents, halothane and enflurane. 2. At concentrations comparable to those obtained during general anaesthesia both agents produced biphasic effects on the resting threshold. A step increase in the partial pressure of anaesthetic was followed first by a transient lowering of threshold, then by a slow rise to a steady-state level above the original baseline. Step decreases in anaesthetic were followed by transient rises before threshold dropped. Transients lasted 20-30 min. During these threshold transients, the average latency of impulse conduction changed monotonically. The prolongation of latency following an increase in anaesthetic was progressive, reaching steady state concurrently with threshold (20 min to greater than 1 h). 3. The anaesthetics reduced the long-lasting increased threshold ('depression') which normally follows repetitive impulse activity in axon membrane. 4. These actions of halothane at concentrations of 0.25-2.7% (0.14-1.54 mM) and enflurane at concentrations of 0.62-3.08% (0.35-1.73 mM) on resting threshold and on the activity-dependent increase in threshold increased monotonically with anaesthetic concentration. 5. The effects on excitability at steady state are consistent with block of voltage-dependent Na+ and K+ channels by these inhalational agents. Reduced depression may occur because the anaesthetics reduce the net ion transfer per impulse, slowing the substrate-driven Na+-K+-ATPase and thereby reducing electrogenic hyper-polarization. 6. The finding that general anaesthetics inhibit depression at clinically relevant concentrations supports the possibility that general anaesthesia is produced by inhibition of processes that modulate excitability of nerve membrane. We suggest that general anaesthetics produce unconsciousness and amnesia because they disrupt activity-dependent processes, which may thus remove temporal 'context' essential for interpreting nerve impulse patterns.
 ...
PMID:Effects of halothane and enflurane on firing threshold of frog myelinated axons. 261 30

The neurotransmitter acetylcholine is important in memory function, and low brain concentrations may be associated with cognitive impairment. Our hypothesis was that atropine, a centrally acting anticholinergic drug known to cause amnesia, confusion, and delirium, may further exacerbate the amnesia and/or confusion resulting from electroconvulsive therapy (ECT) when used as a preanesthetic, and that the peripherally acting glycopyrrolate would by comparison decrease these side effects. We randomly administered glycopyrrolate versus atropine in equivalent doses as the preanesthetic agent to 20 consecutively admitted geriatric patients with major depression, for whom ECT was the clinical treatment of choice. Patients were matched for age, Hamilton Scale for Depression, and baseline performance on the Buschke Selective Reminding Task (BSRT). We found no significant difference in outcome between patients treated prior to ECT with atropine versus glycopyrrolate, as assessed by the above measures. We conclude from this study that atropine is no more deleterious to memory than is glycopyrrolate when given before ECT.
 ...
PMID:Glycopyrrolate versus atropine in post-ECT amnesia in the elderly. 266 13

The differential diagnosis of Alzheimer's disease is a problem that arises in different circumstances. At an advanced stage of the disease the symptoms are so typical that the clinical diagnosis can be made immediately. Complementary examinations (i.e. essentially computerized tomography) are performed to exclude other causes of amnesia and dementia, notably curable dementias. The diagnosis may be more difficult at the early stage of the disease in patients with only slight disorders of memory or certain types of depression. The same applies to cases with unusual presentation, focal symptoms, episodes of confusion, or delirium and hallucinations.
 ...
PMID:[Differential diagnosis of Alzheimer's disease]. 270 60

A variety of manipulations which interfere with the activity of the striatum, including cholinergic blockade and spreading depression, produce amnesia. However, it has been demonstrated that with overtraining, striatal spreading depression and injections of anticholinergic drugs do not produce memory deficits in positively-rewarded tasks. In the present experiment 2% lidocaine was injected into the striatum shortly after training of passive avoidance, using three levels of footshock (0.2, 0.3, and 0.4 mA). Highly significant retention deficits were produced when the lower intensities were studied; in contrast, the animals trained with 0.4 mA showed near-perfect performance. The data show that the enhanced learning experience, which may be equivalent to overtraining, also protects against memory deficits in negatively-rewarded behaviors, and suggest that it induces a transfer of mnemonic functions from the striatum to other neural structures.
 ...
PMID:Retrograde amnesia induced by lidocaine injection into the striatum: protective effect of the negative reinforcer. 273 89

We studied the parameters of suggested posthypnotic amnesia (initial deficit in recall, reversibility, and temporal disorganization of the initial material partially recalled during amnesia) in 132 psychiatric inpatients with DSM-III diagnoses of schizophrenia (N = 25), eating disorders (N = 77), alcoholism (N = 12), and major affective disorder (depression) (N = 18). We compared the findings on these patients with normal student control groups on the Stanford Hypnotic Susceptibility Scale (SHSS:C) posthypnotic suggestion item. In general, the small patient subgroups showed posthypnotic amnesia on each of these criteria in similar fashion to normal student populations. Highly hypnotizable patients were more likely to recall their hypnotic experiences in a more random order than the temporally more accurate sequence shown by low-hypnotizable subjects. Schizophrenic patients initially recalled fewer of their hypnotic experiences (indicating some cognitive deficit), and eating disorder patients initially recalled more of their experiences than other patient groups or normal subjects. Nevertheless, all patient subgroups showed significant additional recall after the reversibility cue. The results support the robustness of posthypnotic amnesia in psychiatric patients.
 ...
PMID:Suggested posthypnotic amnesia in four diagnostic groups of hospitalized psychiatric patients. 277 18

An infusion of propofol was compared with intravenous boluses of diazepam as sedation for minor oral surgery under local anaesthesia in 12 healthy patients who had elective bilateral surgical extraction of lower third molars; the patients served as their own controls. Plasma catecholamine, vasopressin and cortisol concentrations were determined from repeated blood samples. The total administered dose of propofol was 3.93 (SD 1.34) mg/kg and of diazepam 0.28 (SD 0.07) mg/kg. No cardiovascular depression or airway problems occurred. Other side effects were also rare but some discomfort on injection was frequent with propofol. Recovery times were faster after propofol than after diazepam as assessed by the Maddox wing and visual analogue scales. Propofol also provided better amnesia compared to diazepam at the time of the extraction of the teeth. Eight of the 12 patients subjectively preferred propofol sedation. There was no hormonal stress response in either group.
 ...
PMID:Propofol infusion for sedation in outpatient oral surgery. A comparison with diazepam. 280 18


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>