Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0033377 (prolapse)
 11,717 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This is the first report of unilateral palatal myoclonus with which two different ocular movements were synchronized. A 55-year-old woman was admitted to our hospital due to intubation and dysarthria of sudden onset after three similar attacks for these four years. On admission right ptosis, hypalgesia in the right face, right facial nerve palsy, dysarthria, bilaterally increased deep tendon reflexes and trunkal ataxia were noted. Continuous repetitive contractions at 110/min frequencies were observed in the left soft palate, pharynx and larynx. On electronystagmography and electro-magnetic search coil system (Skala system), two different ocular movements, i.e., rotary oscillation with torsion and nystagmus to the right, successively alternated each other at random during eyelids closure. They were synchronized with palatal myoclonus. True nystagmus synchronized with palatal myoclonus has not been reported. When she calculated, rotary oscillation disappeared. In sleep polygraphy, rotary oscillation reduced in amplitude in stage 1 and disappeared in stages 2, 3, 4 and REM. On the other hand, the nystagmus reduced in amplitude in stage 1 and 2 and disappeared in stages 3, 4 and REM. The direction of nystagmus was converted to the left in stages 1 and 2. Similarly, in a drowsy state induced by intravenous injection of 7 mg diazepam, the direction of the nystagmus was converted to the left. On brain magnetic resonance imaging (MRI) right inferior olive was identified as a well circumscribed, enlarged increased signal area on T2-weighted and proton density-weighted images in addition to the lesions of infarcts in left corona radiata, posterior limb of right internal capsule and tegmentum pontis.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Unilateral palatal myoclonus with peculiar ocular movements--neurotological studies and MRI]. 275 41

4-Amino-6-methoxy-1-phenyl-pyridazinium methyl sulfate (ameziniummetilsulfate, LU 1631, Regulton), in this study briefly called amezinium, was tested for possible central effects taking particular account of the mechanisms of action found for this substance in other studies. 1. The most conspicuous action of amezinium was in modifying reserpine-induced ptosis and reserpine-induced hypothermia. When amezinium is given before reserpine, the ED50 values are 0.15 and 3.9 mg/kg p.o. for both mouse and rat. These effects can be explained by a peripheral site of action since peripheral sympathomimetic effects can also be demonstrated in this dose range. Higher doses (10 mg/kg and upwards p.o.) were required to abolish reserpine-induced hypothermia 17 h after reserpine administration, an effect which probably requires a central site of action. But for imipramine, desipramine and pargyline the effective doses are the same in both experimental models (administration before and after reserpine, respectively). 2. Amezinium potentiated the effect of a threshold dose of L-dopa. Based on the central symptoms, higher doses (10 mg/kg p.o.) were also required for this effect. 3. With blood pressure increasing doses, the sleeping-waking pattern was modified in that duration and number of REM-episodes were reduced; in cats there was no parallel increase of wakefulness whilst in rats there was a slight relative increase of wakefulness. 4. Amezinium, particularly at high doses (46.4 mg/kg and upwards), exhibited a central depressant effect on the spontaneous behaviour of mice and rats and on orientational hyperactivity of mice. Based on the modification of aggregation toxicity, the effect of methamphetamine was reduced. In no dose range was there any evidence of methamphetamine-like effects (increase of motor activity, inhibition of food intake and increase of aggregation toxicity). 5. Amezinium did not affect the duration of hexobarbital anaesthesia or the coordination of mice on a rotating rod. 6. The acute toxicity of amezinium in mice and rats was low. The oral LD50 for mice was 1630 mg/kg and for rats 1410 mg/kg.
 ...
PMID:Pharmacology of amezinium, a novel antihypotensive drug. VI. Effect on central nervous functions. 719 73

We examined the effect of 7-nitro indazole (7-NI, 2.5-50 mg/kg, i.p.), an inhibitor of central nitric oxide (NO) synthesis, on general behaviour and sleep. The results show that 7-NI induces ptosis, a loss of the righting reflex and decrease of the EEG amplitudes. Furthermore, a duration of slow wave sleep (SWS) and REM sleep decreased, while the latencies of SWS and REM sleep increased. The effects of 7-NI on general behaviour and sleep were partially antagonized by intraventricular administration of the NO precursor, L-arginine (600 micrograms). These findings indicate that 7-NI induces a state of prominent central depression associated with motor deficit and decrease in sleep stages and wakefulness. It further suggests that NO exerts a significant excitatory effect on the neuronal structure involved in the regulation of locomotion and vigilance.
 ...
PMID:Sleep and nitric oxide: effects of 7-nitro indazole, inhibitor of brain nitric oxide synthase. 877 77