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)

We report two patients who developed an acute, profound, and permanent sensory deficit after treatment with massive doses of parenteral pyridoxine. Aside from rapid onset, their clinical picture resembles that described in chronic pyridoxine neurotoxicity. It also is consonant with experimental models of acute pyridoxine intoxication and is probably secondary to a sensory ganglion neuronopathy. These patients also had transient autonomic dysfunction, mild weakness, nystagmus, lethargy, and respiratory depression. These previously undocumented features may be attributable to either the preservative used in the parenteral pyridoxine preparation or to the exceptionally high doses of pyridoxine these patients received.
 ...
PMID:Acute sensory neuropathy-neuronopathy from pyridoxine overdose. 282 81

Elevation and intorsion of one eye and synchronous depression and extorsion of the other eye characterize a half cycle of seesaw nystagmus. Reversal of these movements constitutes the second half cycle, forming the "seesaw"-like movements. Based on analysis of the ocular oscillation characteristics of the cases of seesaw nystagmus reported in the literature, including the two new cases we present, we postulate that seesaw nystagmus is another type of ocular oscillation brought about by an unstable visuovestibular interaction control system. Nonavailability of retinal error signals to the inferior olivary nucleus essential for vestibuloocular reflex adaptation due to complete chiasmal dissection makes the system less stable. This system instability is further accentuated by the pursuit feedback element. The intact inferior olivary nucleus-nodulus connections in seesaw nystagmus would explain the 180 degrees phase difference that distinguishes it from the midline form of oculopalatal myoclonus, where these connections are likely disrupted.
 ...
PMID:Seesaw nystagmus. Role of visuovestibular interaction in its pathogenesis. 297 81

Ingestion of ethylene glycol was responsible for severe azotemia, acidosis, and abnormal anionic gap value in a pygmy goat. Clinical signs consisted of ataxia, polydipsia, decreased rumen motility, and constipation. Nervous signs included depression, absence of menace response, vertical nystagmus, and terminal convulsions. Four days after onset of clinical signs, antidotal treatment was ineffective. Lesions and oxalate crystals in the kidney were typical of ethylene glycol or plant oxalate toxicosis in other species. Toxicologic analysis revealed ethylene glycol in the rumen content and glycolic acid in urine and ocular fluid.
 ...
PMID:Ethylene glycol toxicosis in a pygmy goat. 319 47

1. The multiunit EMG activity of the forelimb extensor muscle triceps brachii was recorded in precollicular decerebrate cats, either at rest or during roll tilt of the animal at 0.15Hz, +/- 10 degrees leading to sinusoidal stimulation of labyrinth receptors. Both the spontaneous EMG activity as well as the labyrinthine-induced EMG responses were tested before and after pontine microinjection of a cholinergic agonist. 2. Local injection of the cholinergic agonist carbachol into the dorsal aspect of the pontine tegmentum (usually 0.25 microliter, 0.01-0.2 microgram/microliter) produced a state of postural atonia, and abolished both the spontaneous EMG activity as well as the EMG responses of the triceps brachii to sinusoidal stimulation of labyrinth receptors. This suppression was generally ipsilateral to the side of the injection and persisted throughout the episode of postural atonia, but sometimes it involved also the contralateral limbs. In these instances it could be accompanied by a spontaneous nystagmus, interspersed at regular intervals with bursts of rapid eye movements. 3. Similar effects were also obtained following injection of carbachol in the gigantocellular tegmental field (FTG) (0.25 microliter, 0.5-1.0 microgram/microliter). However, this structure was not critically responsible for the phenomena reported above, which persisted unaltered after kainic acid lesion of the FTG performed ipsilaterally to the side of the pontine injection. 4. Local infusion of the muscarinic blocker atropine sulphate reversed the effects of carbachol injection into the dorsal aspect of the pontine tegmentum, thus indicating that muscarinic receptors were involved. 5. It is postulated that the postural atonia as well as the tonic depression of vestibulospinal reflexes, which occur in the decerebrate cat after local injection of a cholinergic agonist depends, at least in part, on the activation of cholinoceptive neurons located in dorsal pontine reticular structures. These may in turn excite medullary reticulospinal neurons, which are finally responsible for the inhibition of extensor motoneurons.
 ...
PMID:Inhibition of vestibulospinal reflexes following cholinergic activation of the dorsal pontine reticular formation. 319 35

Transfer of activity generated by prior optokinetic (OK) stimuli of one minute's duration to nystagmus induced in darkness by a subsequent vestibular stimulus consisting of step velocities to and from 40 degrees/s-1 was studied in 10 normal subjects. Four types of OK stimuli were used: (a) full field 'passive'; (b) full field 'active'; (c) full field in the presence of optic fixation, and (d) small OK drum stimulation. Transfer (T) was evident under all conditions and resulted in an enhancement of the vestibulo-ocular (VO) response when activity from the two stimuli were in the same direction (S) and a suppression when in the opposite (O). Expressed by the equation: Formula See Text. the respective transfer values obtained for the above conditions were (a) 66%, (b) 58%, (c) 22%, and (d) 54%. In all tests, rightward OK drum movement was more effective than leftward. In respect of passive OKN the resultant response can be well represented as the algebraic summation of the expected optokinetic after-nystagmus (OKAN) and the VO response, though opposing OKAN is more effective than enhancing. Passive OKN is more effective than active and this can be accounted for by the small contribution made by retinal slip in the former (the indirect path). Surprisingly, the small drum proved almost as effective as active OKN in terms of transfer. Fixation in the presence of full-field OK stimuli induces a non-directionally specific depression of the subsequent VO response, implying that retinal slip could contribute to the mechanism of VO response suppression.
 ...
PMID:Transfer of optokinetic activity to vestibular nystagmus. 326 Apr 39

Despite the widespread use of non-steroidal anti-inflammatory drugs (NSAIDs), the current number of reported cases of poisoning is small. However, with the introduction of 'over-the-counter' preparations of NSAIDs in some countries (e.g. ibuprofen in the UK and USA) an increased incidence of acute poisoning from this group of drugs can be expected. Conventionally, NSAIDs are divided into the following groups based on their chemical structure: arylpropionic acids, indole and indene acetic acids, heteroarylacetic acids, fenamates, phenylacetic acids, pyrazolones and oxicams. Unless NSAIDs are ingested in substantial overdose, acute poisoning with these agents does not usually result in significant morbidity or mortality. In most cases the clinical features are mild and confined to the gastrointestinal and central nervous systems, though acute renal failure, hepatic dysfunction, respiratory depression, coma, convulsions, cardiovascular collapse and cardiac arrest may complicate severe poisoning. Arylpropionic acid derivatives were thought initially to have a low order of toxicity in overdose but, in addition to anticipated gastrointestinal symptoms, headache, tinnitus, hyperventilation, sinus tachycardia, hypoprothrombinaemia, haematuria, proteinuria and acute renal failure have been described. In addition, drowsiness, coma, nystagmus, diplopia, hypothermia, hypotension, respiratory depression and cardiac arrest have been reported in severe cases of poisoning. Oxyphenbutazone and phenylbutazone are considerably more toxic in overdose. Complications of severe poisoning include coma, convulsions, hepatic dysfunction, acute renal failure, sodium and water retention, haematuria, cardiovascular collapse, respiratory alkalosis, metabolic acidosis, hypoprothrombinaemia and thrombocytopenia. In contrast, indomethacin appears to be much less toxic. In addition to gastrointestinal symptoms, indomethacin taken in overdose induces headache, tinnitus, dizziness, lethargy, drowsiness, confusion, disorientation and restlessness. Only 1 case of acute sulindac poisoning has been reported in the literature. A 16-year-old boy was admitted with hypokalaemia (2.2 mmol/L), transient granulocytosis and 'scanty' haematemesis after ingesting 12 g sulindac. No case of acute tolmetin poisoning have been reported. The fenamates (flufenamic acid, meclofenamic acid, mefenamic acid, tolfenamic acid) are, with the exception of mefenamic acid, not as widely prescribed as other groups of NSAIDs. In overdose, mefenamic acid may result in nausea, vomiting, diarrhoea, muscle twitching, convulsions and coma.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Acute poisoning due to non-steroidal anti-inflammatory drugs. Clinical features and management. 353 13

Actions and interactions of buprenorphine (BUP) and amitriptyline (AMI) on performance and respiration were studied double-blind and cross-over in 12 healthy volunteers. After one-week pretreatments with AMI or placebo, the subjects received on Day 8 placebo, BUP or AMI so that the final treatments were 1) placebo, 2) acute AMI 50 mg, 3) acute BUP, 4) subchronic AMI + acute BUP and 5) subchronic AMI. The subacute treatments were started at two-week intervals. A Mapleson D rebreathing circuit including a pneumotachograph and an infrared capnograph was employed to study drug effects on respiration. Minute volume and end-tidal carbon dioxide as well as psychomotor performance were measured and the blood samples taken on Day 8 before the drug intake and 2 and 4 h thereafter. The performance tests included tracking, choice reaction, flicker fusion, exophoria, nystagmus, digit symbol substitution and the subjective assessment of mood. BUP depressed respiration, and subchronic AMI increased this depression. Both BUP and acute AMI 50 mg each alone impaired various measures of performance and rendered the subjects drowsy, feeble, mentally slow and muzzy but subchronic AMI did not enhance BUP effects. BUP increased plasma prolactin levels similarly after both pretreatments. The results suggest that both BUP and AMI moderately affect psychomotor performance but the interaction between these agents is mild and restricted mainly to respiration.
 ...
PMID:Psychomotor, respiratory and neuroendocrinological effects of buprenorphine and amitriptyline in healthy volunteers. 369 7

In this study of ibuprofen overdose, symptoms developed in 19% of patients (24 of 126)--in 7% of children (6 of 88) and in 47% of adults (18 of 38). Central nervous system depression, seizures, gastrointestinal disturbances, bradycardia, hypotension, apnea, abnormal renal functions, hematuria, nystagmus, and blurred vision were observed. No patients became symptomatic more than four hours after ingestion. There was no significant difference (P greater than .05) between symptomatic and asymptomatic adult groups in either total milligrams or milligram-per-kilogram amounts ingested by history. Pediatric patients who became symptomatic had a mean ingestion by history of 440 mg/kg; those who remained asymptomatic had a mean ingestion by history of 114 mg/kg (P less than .001). No patients ingesting less than 99 mg/kg by history developed any symptoms. Two children had seizures or apnea and one died. Ibuprofen occasionally may cause serious toxicity in overdose.
 ...
PMID:Ibuprofen overdose: 126 cases. 377 88

Effects of intravenous administration of the serotonin precursor tryptophan (TRP) on serum prolactin, neuromotor function, subjective mood, and blood pressure and pulse were determined in nine depressed patients before and during placebo-controlled treatment with the monoamine oxidase inhibitor (MAOI) tranylcypromine. Tranylcypromine significantly increased the prolactin response to TRP. Four patients developed a distinctive neuromotor syndrome following TRP during tranylcypromine, but not placebo, treatment. Symptoms included hyperreflexia, ankle clonus, nystagmus, incoordination, tremor, myoclonic jerks, and nausea. There were no differences in peak prolactin, mood, or autonomic responses between patients with and without the syndrome, but those with the syndrome had received active tranylcypromine for a significantly shorter duration. Tranylcypromine had little effect on TRP-induced changes in mood or autonomic function, except for a modest enhancement of the TRP-induced rise in diastolic blood pressure. These results suggest that tranylcypromine treatment may enhance serotonin function in depression.
 ...
PMID:Effects of tranylcypromine treatment on neuroendocrine, behavioral, and autonomic responses to tryptophan in depressed patients. 403 56

1. Perfusion of 1% procaine into the cerebral ventricles of conscious dogs produced mild paresis, defaecation, vomiting, jerky movements of eyelids, brisk nystagmus, increase in amplitude of respiration and sometimes loss of consciousness. Procaine 2% produced paralysis, loss of consciousness and sometimes respiratory depression.2. Procaine 2% perfused into the cerebral ventricles of dogs under chloralose anaesthesia produced an initial increase in amplitude of respiration, which preceded its final depression, which is due primarily to procaine and only partly to a change in pH.3. The site of action for the initial increase in amplitude of respiration was in the fourth ventricle, for it did not occur on perfusion of procaine into the cranial subarachnoid space.4. Perfusion of spinal subarachnoid space with procaine is enough to cause respiratory failure even when the procaine does not reach the medulla.
 ...
PMID:Procaine perfused into cerebral ventricles and subarachnoid space in conscious and anaesthetized dogs. 568 94


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