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

A 24-year-old woman had bilateral pendular nystagmus, foveal hypoplasia, 360-degree peripheral retinal rosettes, and hypoplastic ora serrata of nongenetic origin. Kinetic perimetry revealed a generalized constriction of the field. Flicker perimetry revealed general depression of the critical flicker frequencies in the entire field. A slight increase of the threshold for light sensitivity after dark adaptation was noted from 10 to 30 degrees. Haidinger brush phenomenon was abnormal. Color vision was normal. The electroretinogram revealed mild abnormalities in the photopic flicker response. The visual-evoked response, recorded by local macular stimulation, was abnormal. The relationship of foveal hypoplasia to peripheral retinal rosettes in this case may have been caused by an intercurrent infection during the late stages of embryogenesis.
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PMID:Foveal hypoplasia and bilateral 360-degree peripheral retinal rosettes. 43 72

Patients from a polydrug abuse treatment program were titrated with either secobarbital or methaqualone, their primary drug of abuse, to a state of mild intoxication, consisting of lateral and vertical nystagmus, ataxia, slurred speech, and drownsiness. The mean dose required to produce each sign was compared to that determined in a similarly treated control group. Tolerance to secobarbital was more easily demonstrated than tolerance to methaqualone, and nystagmus was the least sensitive indicator of patient tolerance. The individual signs were also cumulated into a graded rating scale of central nervous system depression which would be related to the dose administered. Tolerence was easily demonstrated at the higher stages of toxicity for secobarbital in the overall patient population, but tolerance to methaqualone was only unequivocal in the subjects indicating a relatively high frequency of abuse. Tolerance to methaqualone occurred at the lower stages of toxicity, suggesting that there is a difference between tolerance to secobarbital and tolerance to methaqualone. There was no indication that patients who also abuse alcohol are more tolerant than their patient counterparts. The patients who also had a history of amphetamine abuse, however, were less tolerant than the nonusers of these drugs.
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PMID:Dose-response studies on tolerance to multiple doses of secobarbital and methaqualone in a polydrug abuse population. 49 34

Cattle consuming only Kochia scoparia in a pasture southeastern Colorado became ill. Clinical signs were lacrimation, depression, anorexia, nystagmus, head pressing, and recumbency. Some cattle died acutely, with the only clinical signs being recumbency, nystagmus, and occasionally opisthotonos. Pathologic findings were pulmonary edema and congestion, hepatic necrosis and fibrosis, necrosis of proximal convoluted tubular epithelium in the kidneys, epidermal necrosis of lightly pigmented areas, and laminar cerebrocortical necrosis. When the cattle were removed from the pasture, the problem ceased.
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PMID:Polioencephalomalacia and photosensitization associated with Kochia scoparia consumption in range cattle. 50 Apr 79

A simple manifestation of the memorial processes is the so called reversed postoptokinetic nystagmus (RPN), a trace phenomenon elicited in the rabbit by prolonged (60 min) optokinetic (OK) stimulation. Electrophysiological analysis of RPN indicated that the underlying neural trace is weakened, but not suppressed by spreading depression in the cerebral cortex or superior colliculus. An asymmetry of RPN is brought about by unilateral 6-OHDA lesion on substantia nigra. Electroconvulsive shock applied immediately after a period of OK stimulation blocks the subsequent RPN without interfering with OKN. About 70 percent of neurons in the vestibular complex changed their activity during OKN and RPK. The changes consisted in most cases of an excitation accompanying OKN and inhibition during RPN. The OKN-RPN related reacti6ns were also abundant in flocculus but significant activity changes during RPN were less frequent in this structure. Units in midbrain reticular formation reacted both during OKN and RPN in a similar fashion as the vestibular ones. On the other hand units in the cerebellar deep nuclei and brachium conjunctivum were only weakly influenced by OKN and/or RPN. It is suggested that the neural trace of RPN develops in the vestibular complex and vestibulocerebellum as a part of the process compensating the effect of continued optokinetic stimulation. Flocculus participates in input processing of the optokinetic stimulation whereas reticular formation mediates signal transmission to oculomotor and higher integrating centers. The trace, revealed by sudden cessation of the eliciting stimulus in absence of visual reference signals is probably the neural substrate of the so called motion habituation and visual hallucinations. As other compensatory phenomena in the motor system, RPN has features of instrumental (it improves the organisms control of environment) and classical (it is automatically established and involuntarily emitted) conditioning.
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PMID:Reversed postoptokinetic nystagmus: a model of plasticity in the vestibuloocular system. 54 5

Changes in behavior and electrical activity of primary vestibular neurons were observed following injection of lidocaine hydrochloride into the middle ear of cats. After injection the cats exhibited head and ocular nystagmus, head and neck deviation and pupillary changes. Mean preinjection resting discharge rate for first order vestibular neurons was 46.0 spikes/sec. Two hours after lidocaine application the resting rate decreased to a mean of 22.2 spikes/sec and then recovered to 43.0 spikes/sec four hours, and 47.4 spikes/sec six hours after the experimental treatment. The increment sensitivity (increased rate of firing) of horizontal canal neurons to constant angular acceleration for the control period was 2.0 extra spikes/sec/deg/sec2; two hours after the application, 70% of the recorded neurons were unresponsive to angular acceleration or tilt. The sensitivity after four hours was 1.0 spikes/sec/deg/sec2 and 2.1 spikes/sec/deg/sec2 at six hours. The distinct depression of sensitivity by lidocaine at four hours compared to normal mean resting rate at this time suggests these functions may be governed by two modes of action in the receptor or first order afferents.
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PMID:Response of first order vestibular neurons to lidocaine hydrochloride. 62 8

The bias of slow phase velocity (SPV) of optokinetic nystagmus (OKN) caused by an acute labyrinthine lesion was examined in 8 patients using differnet optokinetic stimulus velocities. In all patients a directional preponderance of OKN-SPV was found corresponding to spontaneous nystagmus. This was due to enhancement of nystagmus SPV to the side of the lesion and depression of SPV in the opposite horizontal direction. The preponderance of OKN on the average increased with the intensity of spontaneous nystagmus and decreased along with recovery. These vestibularly induced differences in OKN-SPV range up to 70%. A differentiation is discussed between OKN preponderances caused by labyrinthine lesions and brain stem lesions.
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PMID:Computer analysis of optokinetic nystagmus in patients with spontaneous nystagmus of peripheral vestibular origin. 69 89

A systematic search for cases of adult-onset hereditary ataxia was conducted on location in Scotland. The investigation resulted in the discovery of eight pedigrees with 42 patients of whom 16 were alive in 1975. Nine patients were examined by the authors and recent hospital records were available on the remaining seven. The clinical features were quite variable. In declining order of frequency, findings were gait and limb ataxia, dysarthria, hyperreflexia, extrapyramidal motor disturbances, impaired vibratory sense, spasticity, defects of extraocular movements and nystagmus, reflex depression, Babinski signs, impaired joint position sense, muscle weakness, optic atrophy, and mental abnormalities. Foot deformity occurred only once. Inheritance was compatible with autosomal dominant transmission, but complicated by consanguinity in two families. The minimum prevalence was calculated as 0.31/100,000. Autopsy in two members in one family revealed olivopontocerebellar degeneration.
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PMID:Adult-onset hereditary ataxia in Scotland. 90 33

A calcifying aponeurotic fibroma involving the soft tissue and bone of the occipital area compressed and attenuated the cerebellum and brainstem of a 9-year-old female dog of mixed breeding. Clinical signs included a head tilt to the left; gait ataxia; anisocoria, with a midly dilated left pupil; horizontal nystagmus, with the fast phase to the right; and a mild depression of the level of consciousness. The signs were sequential and progressive.
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PMID:Calcifying aponeurotic fibroma in a dog. 111 57

Phencyclidine is now one of the most frequently used main ingredients of "street drug" preparations. Its effects are highly dose dependent and three varieties of acute intoxication have been seen clinically associated with different dosages and routes of administration. Most persons using phencyclidine smoke it sprinkled on parsley in low doses. The presence of horizontal and vertical nystagmus associated with hypertension in a patient who is agitated or comatose are diagnostic of a phencyclidine intoxicated state. Sensory isolation and intravenous administration of diazepam in the event of seizure activity have proved effective in the treatment of acute intoxicated states. Phencyclidine has pronounced behavioral toxicity and several deaths due to this agent have now been documented. It is unknown whether seizure activity or respiratory depression is the primary cause of death in pharmacological overdoses.
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PMID:Phencyclidine--states of acute intoxication and fatalities. 121 Mar 29

In nine cases of phencyclidine hydrochloride poisoning, early signs of overdose included drowsiness, nystagmus, miotic pupils, blood pressure elevation, increased deep tendon reflexes, ataxia, anxiety, and agitation. In more severe cases, seizures, spasticity, and opisthotonos were seen in addition to deep coma and respiratory depression. Treatment included removal by emetics or lavage, hydration, and a quiet, reassuring environment. Spasticity, agitation, and ocular manifestions responded to diazepam. Psychiatric intervention was instituted after the patients were stable and no longer agitated.
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PMID:Phencyclidine. Nine cases of poisoning. 124 71


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