Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028738 (nystagmus)
 7,431 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We describe two patients with unusual neuro-ophthalmologic complications during long-term therapy with lithium carbonate given for bipolar affective disorder, "benign" intracranial hypertension in one, and downbeat nystagmus, with oscillopsia in the other. A review of the literature is proposed. Though rare, such neuro-ophthalmologic manifestations are worth being recognised since they usually disappear with cessation--when possible--of lithium therapy.
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PMID:[2 rare neuro-ophthalmologic complications of long-term treatment with lithium salts]. 250 94

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.
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PMID:Eye movements in schizophrenia. 859 20

A 47-year-old man with a 15-year history of bipolar disorder treated with anti-depressants, lithium carbonate or neuroleptics was admitted because of marked difficulty in gait and speech. At the age 45, he was unable to walk without bilateral assists and became a wheel-chair state. There was no family history and his mother, father and younger sister were neurologically free. General physical examinations revealed no abnormalities. Neurologically, he was moderately demented (mini mental state examination: 18/30) and showed bilateral horizontal gaze nystagmus, parkinsonism, cerebellar ataxia, dysarthria and moderate spastic paraparesis. No involuntary movements were noted. Wet blood smear showed acanthocytes, while blood chemistries revealed no abnormalities including levels of serum creatine kinase, hepatic enzymes and blood beta-lipoprotein. Kell antigen expressions of the red blood cells were within normal limit. Western blot analysis with anti-chorein antibody detected normal chorein expression levels of the red blood cells. Cranial MRI showed severe symmetric atrophy of the frontotemporal lobes, caudate nuclei, putamen, and brainstem. Also, MRI-gradient echo showed symmetric iron accumulation in the medial portion of the globus pallidus without surrounding high intensity areas, so called "eye-of-the-tiger sign". Genetic analyses revealed no mutations in the PANK2 and PLA2G6 genes. Therefore, he was diagnosed as idiopathic neurodegeneration with brain iron accumulation (NBIA). These findings suggest that NBIA is heterogeneous and other additional genes remain to be found.
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PMID:[Adult-onset case of idiopathic neurodegeneration with brain iron accumulation without mutations in the PANK2 and PLA2G6 genes]. 1982 96

Dextromethorphan (DXM) has unique toxicity that may be difficult to diagnose. We present a case of a young woman who presented to our emergency department (ED) initially diagnosed with recurrent seizures. Paramedics brought a 19-year-old woman to the ED. Witnesses noted "shaking," which the patient did not recall. The patient denied fever, antecedent trauma, or neurological complaint. She was recently administered lamotrigine for bipolar disorder. She was a former alcoholic with no history of developing withdrawal. She admitted to marijuana use but denied use of any other illicit substances. Her vital signs and physical examination were unremarkable. She had a normal brain computed tomography, electrocardiogram, and laboratory evaluation. There was no alcohol detected. Her urine drug screen was negative for opiates, benzodiazepines, cocaine, amphetamines, barbiturates, phencyclidine, and tricyclic antidepressants. She was diagnosed with new-onset seizure and discharged home. No abnormalities were seen in the brain magnetic resonance imaging scan and electroencephalogram. She was scheduled for a cardiac syncope workup, but never followed through. Two months later, she presented to the hospital again for a similar complaint. Coworkers reported witnessing sudden tonic-clonic movements and confusion. On ED presentation, the patient was tachycardic with a heart rate of 110 beats/min and had horizontal nystagmus. She was alert with a flat affect. She did not recall events but answered questions appropriately. Repeat radiographic and laboratory evaluations were normal including urine drug screen and computed tomography. Upon questioning, she admitted to abusing DXM for the past several months. A serum DXM level at this time was 988.3 ng/mL. She was admitted to the hospital for 24 hours without sequelae. All further diagnostic testing was cancelled, and she was referred to a drug rehabilitation program. Abuse of DXM is increasing in incidence. The serum level of our patient was almost 10-fold greater than the reported therapeutic level. The toxicity of DXM is unique, and abuse should be considered in all patients presenting to the ED with new-onset seizure. Dextromethorphan abuse should be considered in young adults who present with previously undiagnosed seizure activity.
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PMID:Dextromethorphan abuse masquerading as a recurrent seizure disorder. 2137 23

Lithium salts have been used in treatment of depression and bipolar disorder for more than 50 years. Neurotoxic side-effects such as nystagmus, ataxia, tremor, fasciculation, clonus, seizure and even coma have been well described in the literature. We present a case of generalised peripheral neuropathy following lithium intoxication. It is a rare presentation with delayed onset and characterised by a rapid downhill course. Diagnosis was confirmed by nerve conduction tests, which showed axonal neuropathy. Despite the profound neurological effects of this toxicity, it is readily reversible with supportive care and the prognosis is good.
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PMID:A rare neurological complication due to lithium poisoning. 2286 82

We report a case of lithium-induced downbeat nystagmus and horizontal gaze palsy in a 62-year-old woman who was treated for a bipolar affective disorder with lithium carbonate for one month. At presentation serum lithium was within therapeutic range. No alternative causes of the ocular motility disturbances were found, and the patient improved significantly as lithium carbonate was discontinued.
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PMID:Lithium-Induced Downbeat Nystagmus and Horizontal Gaze Palsy. 2734 48

We report the case of a 76-year old lady under lithium carbonate for a bipolar disorder who presented with a suspected optic neuritis. A typical lithium-induced downbeat nystagmus was observed. Discontinuation of lithium therapy resulted in frank improvement in visual acuity and disappearance of the nystagmus.
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PMID:Lithium-induced downbeat nystagmus. 2926 83