Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004134 (ataxia)
 15,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Lithium was found to be a selective (i.e., it antagonized aggression at doses that did not produce concurrent neuromuscular impairment) antagonist of isolation-induced aggressive behavior in mice following repeated (subacute) administration for five days. Acute (single dose) administration of lithium failed to inhibit aggression. At atiaggressive doses, lithium did not produce ataxia as measured by the inclined-screen or rotarod procedures. The mechanism of this action is discussed in terms of a possible influence on serotonergic mechanisms.
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PMID:Inhibition of fighting in isolated mice following repeated administration of lithium chloride. 56 35

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

Lithium toxicity can produce persistent and possibly permanent neurologic damage involving multiple areas of the nervous system, often including the cerebellum. Such cases, though rare, may continue to occur since lithium salts are widely used. In this report we describe the neurologic presentation, rehabilitation management, and outcome of treatment in such a patient. Her persistent neurologic syndrome was dominated by features of cerebellar dysfunction. Deficits in speech, swallowing, activities of daily living, transfers, and ambulation were identified and a rehabilitation program was implemented. Therapeutic rehabilitative techniques focused on compensatory mechanisms for ataxia and incoordination. Though her basic neurologic status did not change substantially, she did respond well to rehabilitative measures with significant functional gains and the patient was returned to her prior living arrangement.
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PMID:Rehabilitation in lithium toxicity: case report. 406 31

Two patients exhibited permanent neurological deficits following relatively uncomplicated episodes of lithium intoxication. Lithium toxicity alone appears to result in a fairly consistent combination of neurological findings, including deficits in recent memory, limb and truncal ataxia, and choreoathetosis or parkinsonism. The potential role of early hemodialysis in preventing these permanent deficits is discussed.
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PMID:Permanent neurological deficits due to lithium toxicity. 683 76

Lithium is widely used, and most of its side effects are well established and recognized. Persistent neurologic sequelae or dysfunctions are not common, but they are serious side effects. They usually persist after acute toxicity following accidental or suicidal overdose or during maintenance therapy, when toxicity is more insidious. The irreversible neurologic sequelae are generally cerebellar signs, especially ataxia and dysarthria. Risk factors are sometimes present and recognizable, but more often they are not well identified. Persistent neurologic handicaps greatly reduce the quality of life and are difficult to manage. Lithium toxicity can be avoided by conservative prescribing, care in combining drug therapies, and, above all, educating the patient and caregivers to recognize early signs of the condition. A review of the literature is presented, together with vignettes of a further seven cases.
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PMID:Irreversible lithium neurotoxicity: an overview. 926 Jul 27

Lithium has many medical and psychiatric uses. These include cluster and migraine headaches, alcoholism, impulsive behavior, and bipolar disorder. Toxicity from lithium can occur by overdose (intentional or accidental) or, more commonly, from alteration in its clearance by the kidney. We present two cases of lithium toxicity. The first is a 57-year-old male who presented with confusion, ataxia, and lethargy. The second case involves a 52-year-old female with bizarre behavior who was unable to care for herself. Both patients received dialysis and recovered without sequelae.
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PMID:Lithium toxicity: two case reports. 1213 13

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

Lithium is one of the oldest psychotropic drugs with a well-known narrow therapeutic range and the drugs that interact with lithium elimination are well established. However, patients are still admitted to the emergency department with lithium toxicity due to often overlooked interactions with concomitant drugs. We report on two patients, admitted to the emergency department, with lithium toxicity. One patient presented with aphasia and ataxia, showing moderate toxicity. The other was referred due to coma, illustrating severe lithium toxicity. In both cases, a non-steroidal anti-inflammatory drug was the underlying cause. We highlight the mechanism of this drug-drug interaction and underline the need for thoughtful use of other medications in patients taking lithium. Special attention has to be paid for the non-steroidal antiinflammatory drugs due to the low threshold of prescribing them for the control of acute pain and its availability as free over-the-counter drugs.
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PMID:Drug-related admissions due to interaction with an old drug, lithium. 2457 42

Lithium is a commonly prescribed treatment for bipolar affective disorder. However, treatment is complicated by lithium's narrow therapeutic index and the influence of kidney function, both of which increase the risk of toxicity. Therefore, careful attention to dosing, monitoring, and titration is required. The cause of lithium poisoning influences treatment and 3 patterns are described: acute, acute-on-chronic, and chronic. Chronic poisoning is the most common etiology, is usually unintentional, and results from lithium intake exceeding elimination. This is most commonly due to impaired kidney function caused by volume depletion from lithium-induced nephrogenic diabetes insipidus or intercurrent illnesses and is also drug-induced. Lithium poisoning can affect multiple organs; however, the primary site of toxicity is the central nervous system and clinical manifestations vary from asymptomatic supratherapeutic drug concentrations to clinical toxicity such as confusion, ataxia, or seizures. Lithium poisoning has a low mortality rate; however, chronic lithium poisoning can require a prolonged hospital length of stay from impaired mobility and cognition and associated nosocomial complications. Persistent neurological deficits, in particular cerebellar, are described and the incidence and risk factors for its development are poorly understood, but it appears to be uncommon in uncomplicated acute poisoning. Lithium is readily dialyzable, and rationale support extracorporeal treatments to reduce the risk or the duration of toxicity in high-risk exposures. There is disagreement in the literature regarding factors that define patients most likely to benefit from treatments that enhance lithium elimination, including specific plasma lithium concentration thresholds. In the case of extracorporeal treatments, there are observational data in its favor, without evidence from randomized controlled trials (none have been performed), which may lead to conservative practices and potentially unnecessary interventions in some circumstances. More data are required to define the risk-benefit of extracorporeal treatments and their use (modality, duration) in the management of lithium poisoning.
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PMID:Lithium Poisoning. 2751 79

Lithium is used as a first line treatment in bipolar disorder. The neuroprotective effects of lithium in this indication tend to be well known and are mediated by its action on two enzymes: glycogen synthase kinase-3 and inositol monophosphatase-1. Preclinical and clinical studies seek to evaluate the neuroprotective effect of lithium in neurodegenerative disorders. The aims of this literature review is to gather clinical studies that investigated the efficacy of lithium in neurodegenerative diseases, using a systematic method based on PubMed data. Results were found concerning Alzheimer's disease and related dementias, Huntington's disease, amyotrophic lateral sclerosis and spino-cerebellar ataxia. Lithium exposure showed a potential neuroprotective effect in studies on psychiatric populations with a lower prevalence of Alzheimer's disease in exposed patients. In patients with mild cognitive impairment, lithium would be associated with clinical improvement and a lower level of cerebrospinal phosphorylated tau protein. Lithium would allow at least a partial improvement in symptoms, including suicidal thoughts, in Huntington's disease. Despite several positive case reports and short studies, further controlled researches have failed to substantiate any positive effects of lithium exposure in amyotrophic lateral sclerosis. In spinocerebellar ataxia, introduction of lithium may be of benefits in terms of improvement of cerebellar symptoms. Large randomized controlled trials are required to asses the effect of early exposure lithium in these indications, based on reliable biological markers of disease.
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PMID:Neuroprotective effects of lithium: what are the implications in humans with neurodegenerative disorders? 2940 Feb 98


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