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 examined six patients who developed blurring or oscillopsia as a result of downbeat nystagmus while being treated with lithium carbonate. Of these six plus six previously described similar patients, all but two developed downbeat nystagmus insidiously as an isolated disorder in the setting of otherwise satisfactory therapeutic control, without clinical or biochemical evidence of acute lithium intoxication. Only six of these 12 patients were able either to reduce or to stop taking lithium, and in only two of these six did the downbeat nystagmus improve or remit.
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PMID:Lithium-induced downbeat nystagmus. 249 96

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

Lithium carbonate has recently been used in the treatment of manic diseases. However, since the marginal range between therapeutic and toxic doses is very narrow, close attention should be paid to the development of adverse reactions in its application. Lithium intoxication is manifested by neurological symptoms. Neurotological tests were performed on a patient with lithium intoxication that occurred in the course of psychiatric treatment of mania. The observed sequelae included marked downbeat vertical nystagmus and truncal ataxia. The main lesions in the present case were considered to be located in the cerebellum. Close observation, including neurotological tests, is of greatest importance because in cases of lithium intoxication the development of cerebellar as well as brainstem disorders must not be overlooked.
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PMID:A case of lithium intoxication with downbeat vertical nystagmus. 313 40

Two patients who were treated with lithium for psychiatric illness developed primary position downbeat nystagmus. Previous reports have suggested that lithium causes this type of nystagmus, but other known causes were present in most cases. Several months after stopping the lithium, one patient had marked resolution, while the second patient had only minimal improvement. Valproate sodium proved to be useful in suppressing the nystagmus in the second patient. Lithium carbonate is a cause of primary position downbeat nystagmus. The nystagmus may be permanent or require several months of abstinence for improvement.
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PMID:Lithium-induced downbeat nystagmus. 275 17

In this case study, lithium carbonate, used to control bipolar disorders, is postulated to be the cause of downbeat nystagmus; the degree of nystagmus could be correlated with the dosage and serum level of the drug. All tests for anatomic lesion were negative, including metrizamide cisternography.
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PMID:Downbeat nystagmus as a side effect of lithium carbonate: case report. 392

Downbeat nystagmus developed in a 67-year-old hypomagnesemic woman while she was receiving lithium carbonate for depression. This nystagmus abated each time lithium carbonate therapy was withdrawn, and no alternative causes of nystagmus were demonstrated. However, this nystagmus occurred despite serum lithium carbonate levels in the nontoxic range. Total-body magnesium deficiency may have enhanced the toxic effect of lithium carbonate on cerebellomedullary connections.
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PMID:Downbeat nystagmus. Long-term therapy with moderate-dose lithium carbonate. 662 91

Benign paroxysmal positional vertigo (BPPV) is a common vestibular disorder that results in brief periods of vertigo and nystagmus, when the head is tipped relative to gravity. Symptoms are commonly attributed to the pathological presence of heavy calcium carbonate particles within the lumen of the semicircular canal(s)-a condition termed canalithiasis. In the present work, we induced canalithiasis in an animal model (oyster toadfish, Opsanus tau) by introducing heavy glass microbeads into the lumen of the lateral semicircular canal. Bead movement under the action of gravity and canal afferent nerve discharge were recorded in vivo. When the head was oriented nose-down, beads moved toward the nose and the lateral canal afferent discharge rate increased. Afferents that normally encoded angular velocity during oscillatory head rotations responded with tonic increases in the discharge rate during gravity-dependent bead movement. Other afferents, such as the units that rapidly adapt to a step increase in angular head velocity, responded with an initial increase in discharge rate followed by a period of adaptation. Afferent responses occurred in the complete absence of head movement and quantify the pathological inputs to the brain that arise from canalithiasis. The magnitude and time course of the responses reported here are sufficient to explain the symptoms of BPPV.
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PMID:Afferent responses during experimentally induced semicircular canalithiasis. 1722 24

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

Benign paroxysmal positional vertigo (BPPV) is the most common cause of recurrent vertigo and has a lifetime prevalence of 2.4% in the general population. Benign paroxysmal positional vertigo is caused when calcium carbonate material originating from the macula of the utricle falls into one of the semicircular canals. Due to their density relative to the endolymph, they move in response to gravity and trigger excitation of the ampullary nerve of the affected canal. This, in turn, produces a burst of vertigo associated with nystagmus unique to that canal. Recognition of this condition is important not only because it may avert expensive and often unnecessary testing, but also because treatment is rapid, easy, and effective in >90% of cases. Two well-established methods of treating BPPV are discussed and explained in this article along with a brief discussion of the most commonly used method for treatment of horizontal canal BPPV. Recurrence rates approach 50% in those followed for at least 5 years.
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PMID:Benign paroxysmal positional vertigo. 1983 61

Benign positional vertigo (BPV) is the most common cause of episodic vertigo. It results from activation of semicircular canal receptors by the movement of calcium carbonate particles (otoconia) which dislodge from the otolith membranes. During changes in head position, the otoconia either float freely within the semicircular canal duct (canalithiasis) or adhere to and move with the cupula of the canal (cupulolithiasis). BPV from canalithiasis evokes brief spells of vertigo lasting seconds and can be diagnosed at the bedside by provoking paroxysmal vertigo and nystagmus on tilting the head in the plane of the affected canal. The nystagmus has a unique rotational axis perpendicular to the affected canal. The Dix-Hallpike test is a simple means of confirming the diagnosis in patients presenting with episodic vertigo or imbalance. Audiovestibular tests are only indicated if a symptomatic primary underlying inner ear disease is suspected. In over 80% of patients, BPV can be treated successfully with a single bedside Epley (particle-repositioning) manoeuvre, which can be performed by any medical practitioner.
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PMID:Practical neurology--4: Dizziness on head movement. 2206 84


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