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PubMed1991

Lithium neurotoxicity.

Lithium is potentially toxic to many parts of the central and peripheral nervous systems. Clinical lithium neurotoxicity may appear at any time during therapy and probably often goes unrecognised, at least for a time. Acute lithium toxicity has a mortality of 15%, and 10% of survivors suffer permanent neurological sequelae that are largely unpredictable though persons with the longest and most clinically severe intoxication are probably at highest risk. Even rapidly effective treatment with haemodialysis will not always protect against permanent residual neurological deficits. Lithium may also produce neurotoxic syndromes which develop chronically. There is a large variation among patients in relation to what constitutes a toxic serum lithium level. Both acute and chronic toxicity can occur with therapeutic range serum lithium levels. Failure to appreciate this fact may lead to delays in diagnosis and treatment, placing the patient at risk of permanent neurological damage or death. The diagnosis of lithium intoxication is largely clinical though the EEG may help if typical though non-specific EEG changes are present. If available, the red cell:plasma lithium ratio may be a sensitive indicator of intoxication. Prompt and effective treatment is indicated once the diagnosis of lithium intoxication is made. Prevention of intoxication, which requires the active involvement of both the doctor and patient, is crucial.

Acute Disease↗
PubMed1976

The effect of lithium on the permeability response induced in the collecting duct by antidiuretic hormone.

The diffusional and osmotic water permeability of collecting ducts in isolated papillae of rats' kidneys were measured in papillae taken from normal and lithium pretreated rats. The diffusional water permeability of collecting ducts in papillae from normal rats in the absence of ADH was 4.1 +/- 0.2 (S.E.M.) (n = 18) muM s-1 increasing to 7.2 +/- 0.6 mum s-1 with ADH. Values obtained with lithium (10 mM) in the medium, perfusate or both and in papillae taken from lithium pretreated rats did not differ significantly from the above. The cyclic AMP content of the papillae taken from normal rats was 83 +/- 6 pm mg protein in the absence of ADH and increased to 196 +/- 12 (n = 13) with 500 mu units ml-1 ADH. Lithium 10 mM in the medium did not alter this response. Papillae from lithium pretreated rats had a similar basal level of cyclic AMP but the increment in a lithium (10 mM) medium after ADH was significantly less. These results indicate that the impaired water handling of lithium treated rats is probably not due to a failure of the membrane to increase its permeability to water after ADH. Though lithium does alter the production of cyclic AMP this is not believed to be important regarding any alteration in water permeability. We believe it is probable that lithium interferes with sodium chloride transport at some more proximal nephron segment thereby producing the syndrome of polyuria.

Animals↗
PubMed1990

Effect of diuretic and antidiuretic agents on lithium clearance as a marker for proximal delivery.

Diuretic drugs have marked effects on lithium clearance. The magnitude and mechanism of the effect depend not only on the site of action of the diuretic but also on the sodium intake of the subject as well. In sodium restricted rats all diuretics except the thiazides increase FeLi and abolish distal lithium uptake. The increase in FeLi produced by proximal and loop diuretics are associated with changes in proximal delivery. Amiloride, on the other hand, increases FeLi solely through inhibition of distal lithium uptake. Therefore, this agent is useful to detect lithium reabsorption beyond the proximal tubule. Additionally the values for FeLi obtained after amiloride administration may provide the best quantitative estimate for proximal delivery in conditions where distal lithium uptake is a consideration. Antidiuretic agents, especially those which potentiate ADH activity, may also have marked effects on lithium clearance. NSAID's and dDAVP are able to significantly reduce FeLi even in sodium loaded animals. As this occurs without a change in proximal delivery, these agents increase lithium reabsorption in distal nephron segments preferentially. Thus, estimates of proximal delivery determined by lithium clearance are not valid in the presence of these agents. Experimental conditions which produce high levels of endogenous ADH or potentiate the action of endogenous ADH may also adversely effect FeLi as a quantitative marker for proximal delivery. Whether there are other drugs which disrupt the ability of lithium clearance to function as a marker for proximal delivery requires further study.

Animals↗
PubMed1978

Prediction of lithium response in affective disorders.

Lithium carbonate has established itself as an effective therapeutic agent in primary affective disorders. As not all the patients with primary affective disorders respond to lithium therapy, it is necessary to identify responders prior to treatment. The important indicators of favourable lithium response include a definitive diagnosis of primary affective disorder, occurrence of less than four episodes of mania and depression within one year, psychotic features during both manic as well as depressive episodes, "grandiose-elated" picture during manic episodes; a family history of bipolar illness and response of affected family members to lithium treatment. While those with more than four episodes are not likely to respond to lithium therapy, those with episodes less frequent than once a year or two may not need prophylactic lithium. Among the depressed, hypersomnic depressed patients respond to lithium combined with a monoamine oxidase inhibitor. In addition to clinical predictors of response to lithium treatment, there are a number of pharmacokinetic, neurophysiological and biochemical indices which have been employed as supplementary predictors of response to lithium therapy.

Age Factors↗
PubMed1979

Enhancing the efficacy of lithium treatment by combined use with diuretics and low sodium diets: a preliminary report.

Because reports have indicated that sodium metabolism may bear some influence on manic-depressive illness, the present study was designed to test the efficacy of sodium depletion in enhancing lithium's therapeutic effect. Twenty-seven manic patients refractory to lithium doses producing therapeutic serum lithium levels were subjected to lithium alone, lithium in combination with a thiazide diuretic, and lithium in combination with a low sodium diet. Results indicated that such combinations could be helpful in reducing manic symptoms in the majority of patients without engendering undue toxicity. While mechanisms of action remain to be elucidated, it appears that such combinations may be safely administered to those manic patients not responding to lithium alone or to those requiring lithium but suffering either a lithium-induced nephrogenic diabetes insipidus or other severe side effects. However, caution is still advised in employing these combinations until further, better controlled research substantiates these preliminary data.

Adolescent↗
PubMed1980

Lithium enhancement of central 5-HT transmission induced by 5-HT precursors.

The effects of acute and chronic lithium chloride administration on synaptic transmission between bulbospinal norepinephrine (NE) or 5-hydroxy-tryptamine (5-HT) pathways and sympathetic preganglionic neurons were tested in unanesthetized, spinal cats. Discharges recorded from sympathetic preganglionic white rami were evoked by stimulation of spinal reflex pathways or descending excitatory pathways in the cervical spinal cord. Acute lithium administration (2 meq/kg) produced insignificant depression of the reflex pathway but markedly depressed transmission through the intraspinal pathway, an effect that was prevented by depletion or blockage of 5-HT. These observations and the failure of lithium to alter the typical effects of L-dopa on both pathways indicate that lithium does not affect transmission through the excitatory NE pathway. L-Tryptophan (1,0 mg/kg) alone produced little or no depression of either pathway, but 3--4 hr after lithium, this dose of L-tryptophan gradually depressed transmission through both pathways by about 20%. After chronic lithium pretreatment (1 meq/kg twice a day for 3 days), L-tryptophan rapidly depressed transmission through spinal reflex and intraspinal pathways by 40% and 50% respectively. Chronic lithium pretreatment also more than doubled the depression of transmission through both pathways produced by 30 mg/kg of 5-HTP. The average of plasma lithium levels 8--10 hr after the last chronic dose was 1.5 meq/liter. These results support the proposal that lithium increases the uptake of L-tryptophan and 5-HTP by central 5-HT terminals and thereby enhances 5-HT synthesis which is reflected in increased transmission at central 5-HT synapses.

5-Hydroxytryptophan↗
PubMedDate not supplied

Reversible resistance to the phosphaturic effect of db-cAMP in lithium-treated rats.

Acute lithium administration (5 mmol/kg b.w.) to parathyroidectomized (PTX) rats induces extracellular acidosis, lower plasma phosphate concentration and increased phosphate reabsorption. The present studies evaluate the effect of lithium administration on tissue phosphate distribution, metabolites content in the kidneys and renal phosphate, 2-oxoglutarate and citrate transport in the presence and absence of db-cyclic AMP. Lithium decreased plasma and renal phosphate concentrations and increased phosphate concentration in the skeletal muscle, db-cyclic AMP was not phosphaturic in lithium-treated PTX rats. In PTX rats infused with 20 mM phosphate lithium depressed fractional phosphate excretion induced by db-cyclic AMP from 20 +/- 0.3% to 3.2 +/- 1.0%. However, metabolic or respiratory acidosis restored the responsiveness to db-cyclic AMP. Citraturia and ketoaciduria induced by lithium were depressed in db-cyclic AMP-treated rats. Kidney citrate and 2-oxoglutarate concentrations increased drastically, ATP level fell significantly whereas cAMP content did not change after lithium. We conclude that lithium administration increases phosphate uptake by the muscle which largely accounts for hypophosphatemia. The kidney responds with increased phosphate reabsorption independent of plasma and kidney phosphate concentrations, and with refractoriness to the phosphaturic effects of db-cyclic AMP. Acute lithium administration to rats induces extracellular acidosis and, probably, renal intracellular alkalosis as reflected by citraturia and ketoaciduria as well as the renal metabolite profile. The phosphaturic responsiveness to db-cyclic AMP is dependent, at least in part, on intracellular pH.

Animals↗
PubMedDate not supplied

The effects of lithium treatment on cation transport processes in erythrocytes of patients with affective illnesses.

The effect of lithium administration on cation transport processes in erythrocytes was investigated in 26 patients with affective illnesses. The measures of ouabain-dependent sodium and potassium transport, Na+K+ATP-ase activity and lithium-sodium countertransport in erythrocytes were taken before and after 14 days of lithium therapy. In eleven patients an additional assay was made, following 3-12 months of continuous lithium administration. A significant increase in sodium and potassium transport as well as Na+K+ATP-ase activity was found after 14 days of lithium therapy, while the intensity of lithium-sodium countertransport markedly decreased. Maintenance treatment with lithium tended to stabilize these changes on the altered level. A role of cation transport in the mechanism of lithium action is discussed. It is suggested that an increment of erythrocyte active cation transport may accompany the normothymic effect of lithium.

Adolescent↗
PubMed1981

Granulopoietic effects of lithium on human bone marrow in vitro.

Although studies in mice suggest that lithium enhances granulopoiesis by increasing the production of colony stimulating factor (CSF), results using human assay systems have varied. We have studied the action of lithium on the in vitro proliferation of normal human bone marrow (BM) granulocytic progenitor cells (CFUc) and on CSF production by human peripheral blood (PB) mononuclear cells (MNC). In the absence of exogenous CSF, lithium increased the number of "spontaneous" BM CFUc (P less than 0.05). This effect was abolished by removal of phagocytic cells, suggesting that lithium does not affect CFUc directly, but rather acts via a phagocytic cell. Lithium variably increased BM CFUc when PB MNC feeder layers were employed as the CSF source. This stimulation was most pronounced when the number of cells in the feeder layer was low, i.e., suboptimal CSF. Incubation with 1 meq/L lithium, increased (P less than 0.05) CSF production by PB MNC. Addition of lithium to BM cultures containing optimum CSF did not increase, but in fact decreased, the number of CFUc. These studies indicate that lithium increases CSF production by both PB and BM MNC. Furthermore, the stimulatory effects of lithium occur when CSF levels in the culture system are low.

Animals↗
PubMed1995

Lithium tremor.

BACKGROUND: Tremor is a common problem for patients taking lithium, but little is known about its true prevalence, its effect on compliance, and effective treatments. METHOD: The data base of the Lithium Information Center in Madison, Wis., was searched for articles relating to lithium tremor. RESULTS: Studies show a wide range of incidence of lithium tremor--4% to 65%--due to differences in defining and reporting this side effect. While lithium tremor often decreases with time on lithium, other treatment options include changing the dose or preparation of lithium, decreasing or eliminating other drugs, and treating with beta-blocking drugs, primidone, fatty acids, or potassium. Severe tremor may be a sign of lithium toxicity. CONCLUSION: Patients should be evaluated for lithium tremor on a regular basis. Diagnostic criteria should be standardized by a double-blind, random assignment, multicenter study that could also investigate proposed treatments.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

Efficacy of divalproex vs lithium and placebo in the treatment of mania. The Depakote Mania Study Group.

OBJECTIVE: To compare the effectiveness of divalproex sodium with that of lithium and placebo in patients with acute mania. DESIGN: Randomized, double-blind, parallel-group study of treatment outcomes in patients with manic-depressive illness. PATIENTS: A total of 179 hospitalized, acutely manic patients meeting the Research Diagnostic Criteria for manic disorder, approximately half of whom had been nonresponsive to lithium previously, were studied at nine university-affiliated hospitals. INTERVENTIONS: After a minimum 3-day washout period, random assignment for 21 days to divalproex, lithium, or placebo in a 2:1:2 ratio. Dosage of divalproex and lithium was increased if tolerated to a target concentration of 1041 mumol/L (150 micrograms/mL) or 1.5 mmol/L (conventionally expressed as milliequivalents per liter), respectively. MAIN OUTCOME MEASURES: Primary outcome measures were changes in the Mania Rating scale derived from the Schedule for Affective Disorders and Schizophrenia. RESULTS: Intent-to-treat analysis for efficacy was based on data from 68, 35, and 73 patients in the divalproex, lithium, and placebo groups, respectively. Groups were initially comparable except that all eight patients with four or more manic episodes in the previous year were in the divalproex group. In 30%, 33%, and 51% of the above groups, treatment was prematurely terminated due to lack of efficacy, with fewer premature terminations from divalproex than placebo (P = .017). The proportions of patients improving at least 50% were higher for divalproex and lithium groups than for the placebo group: 48% for divalproex (P = .004) and 49% for lithium (P = .025) vs 25% for placebo. Divalproex was as effective in rapid-cycling manic patients as in other patients. CONCLUSIONS: Both divalproex and lithium were significantly more effective than placebo in reducing the symptoms of acute mania. The efficacy of divalproex appears to be independent of prior responsiveness to lithium.

Acute Disease↗
PubMed1993

Lithium nephrotoxicity.

After nearly two decades of concern and controversy surrounding the long-term effects of lithium on the kidney, the fact that lithium is capable of causing a major disturbance in water balance, manifest as polyuria and secondary polydipsia, remains undisputed. A decreased urinary concentrating ability (nephrogenic diabetes insipidus) with a disturbed responsiveness of the distal nephron to the action of ADH (vasopressin) is demonstrable, and the symptoms are largely reversible on cessation of lithium or reduction of the dose. An acute histological lesion of the distal nephron, corresponding to the site of lithium inhibition of the action of ADH, and consisting of epithelial cellular swelling and glycogen deposition, also appears to be readily reversible. Of greater concern is the development of a progressive impairment of urinary concentrating ability in patients on long-term maintenance therapy--especially those with a history of acute lithium toxicity and those additionally treated with neuroleptics. This functional lesion is not always reversible, and the underlying renal histology is a chronic focal interstitial nephropathy. Interestingly, some psychiatric patients never exposed to lithium have demonstrated similar renal histology. There is very little evidence that stable maintenance lithium therapy, without episodes of acute intoxication, is associated with a reduction of glomerular filtration rate. Episodes of acute lithium intoxication are largely predictable, and therefore avoidable, provided appropriate precautions are taken. Patients with polyuria and impaired urinary concentrating ability are at increased risk of acute lithium toxicity because of excessive renal losses of fluid, and these symptoms should be treated in the first instance with dosage reduction.(ABSTRACT TRUNCATED AT 250 WORDS)

Glomerular Filtration Rate↗
PubMed1977

Lithium: modification of behavioral activity and brain biogenic amines in developing hyperthyroid rats.

Daily treatment of neonatal rats with 1-triiodothyronine for 30 days increased locomotor activity as well as the synthesis and presumably, release of brain norepinephrine, dopamine and 5-hydroxytryptamine. Whereas administration of lithium carbonate (60 mg/kg) to normal rats for 10 days, beginning from the 20th day of age, produced no significant effect, this antimanic drug significantly decreased the observed increase in spontaneous locomotor activity in l-triiodothyronine-treated rats. Lithium treatment in normal rats increased the activity of striatal tyrosine hydroxylase, but produced no significant effect on the endogenous levels of norepinephrine and dopamine in several discrete brain regions examined. Lithium, enhanced deamination of catecholamines as evidenced by increased level of 3,4-dihydroxyphenylacetic acid and monoamine oxidase activity in normal rats. The activity of catechol o-methyltransferase was decreased to 82 and 59% in midbrain and crebral cortex of normal rats, respectively. Furthermore, chronic treatment with lithium increased endogenous levels of tryptophan, tryptophan hydroxylase, 5-hydroxytryptamine and its metabolite, 5-hydroxyindoleacetic acid, in normal animals. In contrast to the effects seen in normal rats, admininstration of lithium in l-triiodothyronine-treated animals significantly decreased tyrosine hydroxylase as well as dopamine and its metabolite, 3,4-dihydroxyphenylacetic acid, suggesting that this antimanic drug reduced the synthesis and turnover of dopamine. However, the steady-state levels of norepinephrine were raised in hypothalamus, pons-medulla, midbrain and striatum of lithium-treated hyperthyroid rats. As seen in normal animals, lithium in l-triidothyronine-treated rats increased trytophan, tryptophan hydroxylase and 5-hydroxytryptamine levels, but decreased the concentration of 5-hydroxyindoleacetic acid. The results show that the suppressed behavioral activity seen in lithium-treated hyperthyroid rats may be associated with decreased synthesis of norepinephrine and dopamine in the brain. Finally, the effects exerted by lithium on the brain catecholamine metabolizing system of young hyperthyroid rats were not similar to those seen in normal rats of the corresponding age group.

Animals↗
PubMed1996

A cross-sectional study of parkinsonism and tardive dyskinesia in lithium-treated affective disordered patients.

BACKGROUND: The purpose of this study was to investigate the prevalence of extrapyramidal symptoms (EPS) and tardive dyskinesia (TD) in affective disordered patients treated with lithium and to study the association of these symptoms with medication and other factors. METHODS: This cross-sectional study was carried out in all consenting outpatients attending an affective disorders clinic in a psychiatric hospital. The study sample consisted of 130 stable outpatients: 110 with bipolar disorder, 18 with unipolar (major) depression, and 2 with atypical affective disorder. At the time of evaluation, 110 patients were receiving lithium, 37 in combination with antidepressants and 19 with neuroleptics, and 40 had a history of neuroleptic treatment during the previous 6 months. The patients were assessed with the Extrapyramidal Symptom Rating Scale (ESRS) for parkinsonism, akathisia, dystonia, and TD. The prevalence of these symptoms was calculated for all patients and by current lithium and neuroleptic intake. Multiple linear regression analysis was used to investigate the relationship between the ESRS subscale scores and gender, age, diagnosis, and medication type. RESULTS: The prevalence of tremor was 20.8%; hypokinetic parkinsonism, 7.7%; akathisia, 4.6%; dystonia, 3.8%; and TD, 9.2%. Tremor was associated with lithium and neuroleptic intake; hypokinesia was associated with neuroleptic treatment and age; and TD was associated with neuroleptic, lithium, and tricyclic intake and age. Seven of 51 patients taking lithium but without a history of neuroleptic treatment during the previous 6 months presented symptoms of TD. CONCLUSION: The combination of lithium and neuroleptics was associated with a high prevalence of EPS. The presence of TD in lithium-treated patients not treated with neuroleptics for at least 6 months is consistent with the hypothesis that lithium may exacerbate the vulnerability of affective disordered patients to dyskinesias.

Adult↗
PubMed1977

[Lithium-powered cardiac pacemakers. A survey of 3 years' clinical experience (author's transl)].

In addition to the lithium-iodine cell which has been in clinical use since 1972, the following lithium-based power sources for cardiac pacemakers are available: The lithium-silver chromate cell (SAFT), the lithium-thionylchloride-battery (G.T.E.), the lithium-cupric sulfide cell (DuPont) and the lithium-lead iodide cell (Mallory). These batteries differ not only in their energy providing chemical reaction and their components (liquid electrolyte or not), but also in their capacity and discharge characteristics. Out of 244 lithium-powered pacemakers implanted during the past 3 years, 5 pulse generators had to be removed due to electronic circuit failure, whereas battery failure has not been observed up till now. Sensing problems were registered in 8 cases probably due to the specific properties of the entrance filter and entrance resistance of the pacer. In some cases, however, they were caused by poor electrode position. One pacemaker model, powered with the WGL702 cell, frequently gave rise to skin necrosis, Newer models have more favourable dimensions and lower specific weight. The capacity of their batteries is sufficient for middle to long-term stimulation when using current saving electrodes. Because of the well-known advantages of the lithium-cells in comparison to conventional Mallory batteries, together with the favorable clinical results, only lithium-powered pacemakers have been implanted in our hospital since 1977.

Electrodes↗
PubMed1998

Neurobiology of lithium: an update.

Lithium remains a first-line approach for the treatment of acute mania and the prophylactic management of manic-depressive illness, yet the underlying neurobiological mechanisms remain as yet undefined. In this paper we critically examine the accumulated preclinical and clinical evidence for the action of lithium in the brain and suggest areas that may be most productive for future investigation, i.e., membrane transport systems, neurotransmitter receptor regulation, second messenger generating systems, protein kinase C (PKC) regulation, and gene expression. In their experimental design, preclinical investigations have often jeopardized the physiologic relevance of their studies by a relative lack of attention to issues such as therapeutic concentrations, acute versus chronic exposure, and a lack of adequate cation and/or psychotropic controls. Future studies should account for the established prophylactic efficacy of lithium, the higher risk for relapse into mania after abrupt discontinuation, the ability of lithium to stabilize recurrent depression associated with unipolar disorder, and the efficacy of lithium in the treatment of refractory major depressive disorder in the presence of an antidepressant. Studies of the action of lithium in receptor mediated phosphoinositide signaling in the brain over the past several years have opened up heuristic lines of investigation that stem from lithium's uncompetitive inhibition of the enzyme inositol monophosphatase. Subsequent studies involving regulation of inositol transport, PKC isozymes and activity, and the expression of the major PKC substrate MARCKS (myristoylated alanine-rich C-kinase substrate) have offered potential avenues for understanding the complexity of the action of long-term lithium in the brain. These studies will offer us a better understanding of the neuroanatomical sites of action of lithium and together with ongoing clinical investigations using brain imaging in patients with manic-depressive illness a more complete understanding of the pathophysiology of this disease.

Bipolar Disorder↗
PubMed2001

Two phase morphology limits lithium diffusion in TiO(2)(anatase): a (7)Li MAS NMR study.

7Li magic angle spinning solid-state nuclear magnetic resonance is applied to investigate the lithium local environment and lithium ion mobility in tetragonal anatase TiO(2) and orthorhombic lithium titanate Li(0.6)TiO(2). Upon lithium insertion, an increasing fraction of the material changes its crystallographic structure from anatase TiO(2) to lithium titanate Li(0.6)TiO(2). Phase separation occurs, and as a result, the Li-rich lithium titanate phase is coexisting with the Li-poor TiO(2) phase containing only small Li amounts approximately equal to 0.01. In both the anatase and the lithium titanate lattice, Li is found to be hopping over the available sites with activation energies of 0.2 and 0.09 eV, respectively. This leads to rapid microscopic diffusion rates at room temperature (D(micr) = 4.7 x 10(-12) cm(2)s(-1) in anatase and D(micr) = 1.3 x 10(-11) cm(2)s(-1) in lithium titanate). However, macroscopic intercalation data show activation energies of approximately 0.5 eV and smaller diffusion coefficients. We suggest that the diffusion through the phase boundary is determining the activation energy of the overall diffusion and the overall diffusion rate itself. The chemical shift of lithium in anatase is independent of temperature up to approximately 250 K but decreases at higher temperatures, reflecting a change in the 3d conduction electron densities. The Li mobility becomes prominent from this same temperature showing that such electronic effects possibly facilitate the mobility.

Journal Article↗
PubMed2002

Equilibrium lithium transport between nanocrystalline phases in intercalated TiO(2) anatase.

Microcrystalline TiO(2) with an anatase crystal structure is used as an anode material for lithium rechargeable batteries, and also as a material for electrochromic and solar-cell devices. When intercalated with lithium, as required for battery applications, TiO(2) anatase undergoes spontaneous phase separation into lithium-poor (Li(0.01)TiO(2)) and lithium-rich (Li(0.6)TiO(2)) domains on a scale of several tens of nanometres. During discharge, batteries need to maintain a constant electrical potential between their electrodes over a range of lithium concentrations. The two-phase equilibrium system in the electrodes provides such a plateau in potential, as only the relative phase fractions vary on charging (or discharging) of the lithium. Just as the equilibrium between a liquid and a vapour is maintained by a continuous exchange of particles between the two phases, a similar exchange is required to maintain equilibrium in the solid state. But the time and length scales over which this exchange takes place are unclear. Here we report the direct observation by solid-state nuclear magnetic resonance of the continuous lithium-ion exchange between the intermixed crystallographic phases of lithium-intercalated TiO(2). We find that, at room temperature, the continuous flux of lithium ions across the phase boundaries is as high as 1.2 x 10(20) s(-1) m(-2).

Journal Article↗