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)

Dextrorphan HCl (Ro 01-6794/706) is an NMDA receptor antagonist with clinical potential for administration in an elderly population of acute ischemic stroke patients. In vivo experience with such patients demonstrated a consistent pharmacologic effect/adverse experience profile that is typical of an NMDA receptor antagonist (e.g., nystagmus, nausea, vomiting, agitation, somnolence, hallucinations and hypertension). For the most part, these pharmacologic effects were mild to moderate in severity; short-lived; reversible; not life-threatening and subjectively tolerated. The most serious pharmacologic effect produced by dextrorphan administration was hypotension, which occurred within a well-defined window of 90 minutes from the start of the loading dose infusion in patients who received 200 mg/hr or greater loading dose infusions. In all cases it was reversible without neurologic sequelae. Careful review of demographic and pharmacokinetic parameters did not demonstrate any overriding factor(s) to the production of hypotension other than the rate of the loading dose infusion. Severe hypotension, severe decreased levels of consciousness and respiratory depression should not be generally expected at loading doses less than 200 mg/hr. In summary, dextrorphan can be safely given to an elderly population of ischemic stroke patients as a loading dose rate below 200 mg/hr and as a maintenance dose rate between 50-90 mg/hr for 24 hours when patients are monitored carefully for pharmacologic effects.
 ...
PMID:Safety, tolerability and pharmacokinetics of the N-methyl-D-aspartate antagonist Ro-01-6794/706 in patients with acute ischemic stroke. The Dextrorphan Study Group and Hoffmann-La Roche. 748 11

See-saw nystagmus is an uncommon but highly characteristic eye movement disorder comprising intorsion and elevation of one eye, with synchronous extorsion and depression of the other. It generally has a pendular waveform and is due to a midline, extrinsic, suprasellar mass lesion compressing or invading the brainstem bilaterally at the meso-diencephalic junction. This report deals with the clinical and MRI findings in three patients (and binocular three-dimensional quantitative oculographic findings in one patient) with a jerk waveform see-saw nystagmus due in each case to a unilateral meso-diencephalic lesion. In each patient the torsional component of the nystagmus fast phases rotated the upper poles of the eyes toward the side of the lesion. Jerk see-saw nystagmus can be clinically indistinguishable from pendular see-saw nystagmus and from the torsional-vertical nystagmus which occurs with medullary lesions. We propose that jerk see-saw nystagmus is due to unilateral inactivation of the torsional eye-velocity integrator, thought to be in the interstitial nucleus of Cajal, with sparing of the torsional fast-phase generator, thought to be in the adjacent rostral interstitial nucleus of the medial longitudinal fasciculus.
 ...
PMID:Jerk-waveform see-saw nystagmus due to unilateral meso-diencephalic lesion. 792 66

Subjective contrast sensitivity for the stationary and horizontally drifting vertical stripe patterns was measured in normal subjects and in patients with glaucoma, optic neuritis and optic atrophy. Contrast sensitivity was also determined objectively using an eye movement reflex (optokinetic nystagmus) recorded by means of electro-oculography. The contrast sensitivity for the drifting stripe patterns in normal subjects was characterized by a depression of sensitivity at the high spatial frequency and an increased contrast sensitivity at the low spatial frequency in comparison with the results of stationary stripe patterns. The measurement of contrast sensitivity for the horizontally drifting vertical stripe patterns was found to be more sensitive for detection of minor damage to the optic nerve than that for the stationary patterns. The results of the subjective contrast sensitivity and the objective one determined using an eye movement reflex showed a good correlation.
 ...
PMID:Contrast sensitivity for the stationary and drifting vertical stripe patterns in patients with optic nerve disorders. 827 41

Psychogenic dizziness is defined as recurring or persistent symptoms of balance dysfunction, inconsistent with organic vestibular disease as determined by history, clinical examination and pertinent investigations, and consistent with emotional origin. Of 1,335 patients seen in our dizziness clinic between January 1988 and August 1991, psychogenic dizziness was diagnosed in 180 (13.5%) patients. There were 67 men and 113 women aged from 12 to 77 years (mean age 40.2 years). The characteristics of psychogenic dizziness are: (1) continuous dizziness for long periods of time; (2) younger patients; (3) predominant female; (4) associated symptoms of panic attack, such as headache, breathlessness, nausea, sleep disturbance, paresthesias, anxiety and palpitation; (5) symptoms of aggravation due to stressful life events; (6) normal neurotological bedside examination; (7) hyperventilation reproduced accurately. The electronystagmographic results of 74 patients show normal bithermal caloric responses in 47 patients (63.5%), caloric hyperactivity in 21 patients (28.4%), canal paresis in four patients (5.4%), canal paresis with directional preponderance in two patients (2.7%), large random voluntary eye swings or severe blinking in 35 patients (47.3%), and spontaneous nystagmus (slow phase velocity < 6.5 degrees/s) in four patients (5.4%). There were 31 patients who consulted psychiatrists with diagnoses of anxiety (51.6%), depression (16.1%), insomnia (12.9%), psychosomatic disorder and adjustment disorder. Treatment of patients with psychogenic dizziness must be directed at the underlying anxiety. Psychiatric consultation is necessary.
 ...
PMID:[Psychogenic dizziness]. 848 48

Smooth pursuit and other eye movements were quantitatively studied in patients with chronic schizophrenia to characterize the pattern and severity of eye movement abnormalities in this disorder. Twenty-one patients with schizophrenia, 13 patients with other psychiatric disorders (manic-depressive psychosis, schizoaffective disorder, depression and obsessive-compulsive disorder), and 19 normal subjects were studied. Horizontal eye movements were recorded with DC electro-oculography and analyzed by an online computer system. Eye velocity and closed-loop gain of pursuit, optokinetic nystagmus (OKN), vestibulo-ocular response (VOR) and visual-vestibular interactions were calculated. The latency, accuracy and peak velocity-amplitude relationships of voluntary saccades were measured. The group mean gains of pursuit and OKN of the schizophrenic patients were significantly lower than those of the normal subjects. Suppression of the VOR by fixation was impaired, and the latency of saccades was prolonged. However, the differences in group mean values were small in magnitude, and the frequencies of outliers among the schizophrenic patients were low. The patients with other psychiatric disorders had a similar pattern and severity of eye movement abnormalities. The frequency and severity of eye movement abnormalities in schizophrenic patients are lower than those indicated by previous studies that used different techniques of analysis.
 ...
PMID:Eye movements in schizophrenia. 859 20

An outbreak of polioencephalomalacia affected 16 of 46 Swaledale lambs and five of 25 Scottish blackface lambs 15 to 32 days after they were introduced to an ad libitum concentrate ration containing 0.43 per cent sulphur. The clinical signs were acute and included depression central blindness and head-pressing, but no hyperaesthesia, nystagmus, dorsiflexion of the neck or opisthotonos were observed. Treatment of the affected lambs with vitamin B1, dexamethasone and antibiotics was associated with a prolonged recovery period, though no further cases were identified after vitamin B1 had been given parenterally to all the lambs at risk.
 ...
PMID:Sulphur-induced polioencephalomalacia in lambs. 873 Jun 74

See-saw nystagmus is an uncommon but characteristic kind of nystagmus. Typically there is intorsion and elevation of one eye and simultaneous extorsion and depression of the other eye. The nystagmus can be of pendular-waveform or jerk-waveform. The pendular-waveform see-saw nystagmus is commonly due to a midline meso-diencephalic, bilaterally compressing mass. The jerk-waveform see-saw nystagmus is mostly due to a unilateral lesion in the meso-diencephalic junction. For explanation, a current theory assumes a unilateral lesion of the interstitial nucleus of Cajal sparing the rostral interstitial nucleus of the medial longitudinal fascicle. Another concept suggests a lesion of the vertical vestibulo-ocular-reflex. We report two patients with jerk-waveform see-saw nystagmus. In both patients an internuclear ophthalmoplegia was found additionally. The origin was a unilateral brainstem infarction in both cases. We explain the symptomatology of see-saw nystagmus and discuss the actual theories of its origin.
 ...
PMID:[See-saw nystagmus. Clinical aspects, diagnosis, pathophysiology: observations in 2 patients]. 876 3

Carboplatin preferentially destroys inner hair cells (IHCs) and type-I spiral ganglion neurons while sparing outer hair cells (OHCs). Loss of IHCs and type-I ganglion cells is associated with a significant reduction of the compound action potential (CAP). However, the cochlear microphonic (CM) potential and distortion product otoacoustic emissions (DPOAEs) remain normal, indicating that the OHCs are functionally intact. In the vestibular system, carboplatin selectively destroys type-I hair cells and their afferent neurons. Damage of type-I vestibular hair cells and their afferent terminals is associated with significant depression of nystagmus induced by cold, caloric stimulation. Histochemical studies revealed a rapid decrease in succinate dehydrogenase (SDH) staining in IHCs soon after carboplatin treatment, and staining intensity remained depressed in surviving IHCs for at least 1 month after carboplatin treatment. These results suggest that carboplatin depresses the metabolic function in surviving IHCs. Several lines of evidence suggest that free radicals may contribute to carboplatin-induced sensory cell damage. Intracochlear infusion of L-buthionine-[S,R]-sulfoximine (BSO), which depletes intracellular glutathione (GSH), increases IHC and OHC loss. Previous in vitro studies have shown that neurotrophin 4/5 (NT-4/5) promotes the survival of spiral ganglion neurons from cisplatin ototoxicity. In vivo perfusion of NT-4/5 promoted the survival of spiral ganglion neurons, but did not protect the hair cells.
 ...
PMID:Selective loss of inner hair cells and type-I ganglion neurons in carboplatin-treated chinchillas. Mechanisms of damage and protection. 1084 92

An eight-month-old girl presented with congenital exotropia and latent nystagmus. Further evaluation revealed congenital ptosis of the left eye and restriction of the elevation, depression and adduction of the left eye. A diagnosis of congenital oculomotor palsy was made. At the age of three months she had been examined by the neurologist because of retarded psychomotor development. All laboratory investigations were normal. At the age of eight months, a CT scan of the brain and orbit was found to be normal. The patient was treated for amblyopia. At the age of five, strabismus surgery was performed, and a large fibrous tumor encapsulating the superior and lateral rectus muscle was found. A biopsy was taken and pathology showed fibrous tissue containing a hair. Based on the clinical history, the diagnosis of a perinatally ruptured orbital dermoid cyst was made. Review of the previous CT and an additional CT showed enlargement of the left lateral orbital wall with a notch in the lateral wall, indicative of a dermoid cyst.
 ...
PMID:Perinatally ruptured dermoid cyst presenting as congenital oculomotor palsy. 1085 51

Zolpidem, a non-benzodiazepine hypnotic, was identified in the blood of 29 subjects arrested for impaired driving. Zolpidem concentrations ranged from 0.05 to 1.4 mg/L (mean 0.29 mg/L, median 0.19 mg/L). In the subjects whose cases we reviewed where zolpidem was present with other drugs and/or alcohol, symptoms reported were generally those of CNS depression. Symptoms included slow movements and reactions, slow and slurred speech, poor coordination, lack of balance, flaccid muscle tone, and horizontal and vertical gaze nystagmus. In five separate cases, where zolpidem was the only drug detected (0.08-1.40 mg/L, mean 0.65 mg/L, median 0.47 mg/L), signs of impairment included slow and slurred speech, slow reflexes, disorientation, lack of balance and coordination, and "blacking out." Although no quantitative relationship between blood concentrations and degree of driving impairment is currently possible, it is reasonable to conclude that because of its specific activity as a sleep inducer, blood concentrations consistent with therapeutic doses of zolpidem have the potential to affect driving in a negative way, and that concentrations above the normal therapeutic range would further impair a person's level of consciousness and driving ability.
 ...
PMID:Zolpidem and driving impairment. 1121 Aug 92


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