Samples, John R.

Starr, Arnold

PubMed

Samples, JR

Starr, A

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UC IrvineUC Irvine Previously Published WorksTitleNeurology-epitomes of progress: lithium toxicity in the central nervous system.Permalinkhttps://escholarship.org/uc/item/9w8271fvJournalArizona Medicine, 127(2)ISSN0093-0415AuthorsSamples, JRStarr, APublication Date1977-08-01Copyright InformationThis work is made available under the terms of a Creative Commons Attribution License, availalbe at https://creativecommons.org/licenses/by/4.0/ Peer reviewedeScholarship.org Powered by the California Digital LibraryUniversity of CaliforniaEPITOMES-NEUROLOGYsystemic hypertension develops as well as pul-monary hypertension, and there are significantcardiac arrhythmias, including ventricular tachy-cardia, during the apnea. Apnea occurs duringinspiration and a salient clinical sign in these pa-tients is the occurrence of loud snoring. A simplescreening procedure consists of recording thesound of the patient's respirations during earlysleep by means of a cassette tape recorder at thepatient's bedside at home or in the hospital. Iffindings are suspicious, a polygraphic study ofnocturnal sleep is indicated. At present no effec-tive drug therapy has been found and treatmentconsists of tracheostomy, so prompt otolaryn-gologic consultation is indicated. Symptomatologyis totally reversed by this procedure. In the otherform of sleep apnea (so-called central apnea), noobstruction is encountered and respiratory effortceases. In this form of the disorder, tracheostomyis less helpful.JON F. SASSIN, MDREFERENCESKales A: Sleep disorders: Recent findings in the diagnosis andtreatment of disturbed sleep. N Engl J Med 290:487-499, Feb 28,1974Guilleminault C: Insomnia with sleep apnea, a new syndrome.Science 181:856-858, Aug 31, 1973Lithium Toxicity in theCentral Nervous SystemLITHIUM CARBONATE is the accepted treatment ofacute hypomania and mania. The mild side effectscommonly experienced include nausea, vomiting,diarrhea, fatigue and weakness. Polydipsia andpolyuria commonly occur and may be due to inhi-bition of the action of antidiuretic hormone.There may be a fine, mild resting tremor of thehands which is responsive to treatment with pro-panolol. The serious signs and symptoms of cen-tral nervous toxicity of lithium usually appearwith serum concentrations greater than 1.5 mEqper liter and include lethargy, lightheadedness andconfusion, accompanied by ataxia, drowsiness,slurred speech, tinnitus, blurred vision and pro-found weakness. The features of severe intoxica-tion are striking and usually appear either overseveral days of lithium therapy or following anacute overdose. A patient with severe, acutelithium intoxication presents with tremor, in-creased neuromuscular irritability, increased deeptendon reflexes, nystagmus, confusion and evenconvulsions. Nonneurologic signs of intoxicationinclude vomiting and acute diarrhea. All of thesesigns may progress to stupor, coma and eventualdeath. It is generally thought that life-threateninglithium intoxication does not occur below serumlevels of 3.0 mEq per liter. However, the thresh-old for intoxication may be lowered in elderlypatients and in patients taking other medicationsincluding the anticholinesterases and haloperidol.There have been some patients with toxic neuro-logic manifestations in whom serum lithium levelswere within the accepted therapeutic range. Alter-ations in lithium tolerance may be produced bytrauma, infection and sodium restricted diets.Severe lithium toxicity has been reported in awoman with a viral infection causing high feverand a serum lithium level of 1.0 mEq per liter.An electroencephalogram in a patient who islithium intoxicated may show a variety ofchanges. Status epilepticus has been reported inpreviously nonepileptic patients with lithium con-centrations in the therapeutic range. The rela-tionship of lithium to seizures was studied in 16epileptics in whom only one instance of increasedclinical seizure activity was reported. In ten ofthe 16 patients there was a clear reduction inseizure frequency during lithium therapy. Thecontinuous use of lithium for more than eightmonths has been reported to be associated withincreased muscle tone. The development of thealtered muscle tone appears to be directly re-lated to the duration of lithium maintenancetherapy and is not relieved by benztropine, anantiparkinson drug. Rarely, patients taking lithiumcan develop choreoathetosis. Patients exposed toelevated lithium levels for prolonged periods havesurvived with permanent damage to the cere-bellum and basal ganglia.In assessing lithium toxicity, the clinical signsare the most important means of detecting in-toxication. Serum levels may be used for con-firmation, but it should always be kept in mindthat toxicity may occur with serum levels in thetherapeutic range. When signs of serious intoxi-cation are noted, lithium administration shouldbe stopped immedately. As a pharmacologicallyactive cation, lithium is not metabolized in thebody, but is excreted by the kidneys. The serumhalf life of lithium is usually about 16 hours.Hemodialysis, or, if hemodialysis is not available,peritoneal dialysis may be used effectively tolower serum lithium levels. Long-duration hemo-132 AUGUST 1977 * 127 * 2EPITOMES-NEUROLOGYdialysis for 12 to 16 hours will avoid a reboundeffect due to the slow movement of lithiumbetween intracellular and extracellular compart-ments. The usual cause of death in cases of acuteoverdose is pneumonia or shock. With appro-priate attention to cardiac, renal and pulmonaryfunction, and to the maintenance of fluid andelectrolyte balance, the recovery of patients withsigns and symptoms of acute lithium toxicity willbe optimal.JOHN R. SAMPLES, MDARNOLD STARR, MDREFERENCESBaldessarini RJ, Lipinski JR: Lithium salts: 1970-1975. AnnIntern Med 83:527-533, Oct 1975Erwin CW, Gerber CJ, Morrison SD: Lithium carbonate andconvulsive disorders. Arch Gen Psych 28:646-648, May 1973Hartitzsch B, Hoenich NA, Leigh RJ, et al: Permanent neuro-logical sequelae despite haemodialysis for lithium intoxication.Brit Med J 4:757-759, Dec 1972Syndrome of Infant BotulismSINCE THE RECOGNITION of infant botulism abouta year ago, at least 20 cases have been reportedfrom various parts of the United States. The in-cidence of the disease process is, therefore, morecommon than originally anticipated. Both boysand girls who have been previously healthy areaffected in early infancy, and over a period ofone to two days the ability to suck and swallowis lost, head control is greatly diminished toabsent, and the cry is weak. They may be con-stipated. Cranial nerve abnormalities includeptosis, sluggish pupillary light reflexes, decreasedextraocular motility, a paucity of facial mobilityand a decreased gag reflex. The muscle tone andstretch reflexes are reduced. Careful electrophys-iologic investigation shows small, short motorunit potentials or small compound muscle actionpotentials (CMAP) amplitude with an increasein CMAP amplitude with repetitive stimulation ashas been described earlier in patients withbotulism.The botulinal toxin may not be identified inthe serum but the toxin, as well as Clostridiumbotulism organisms, have been identified in stoolspecimens. No botulinal toxin has been identifiedfrom the stool of clinically normal humans.The question, of course, is how do infants getbotulism? Some of the infant patients were breast-fed and others received commercial formula, inaddition to a variety of infant foods. The C.botulinum spore is ubiquitous, but after intensiveepidemiological investigations, no source of thebotulinal toxin has been identified. It has beensuggested, therefore, that there may be an in vivoproduction of the botulinal toxin, as shown tooccur in other forms of animal life.Although three known patients have had re.-spiratory arrests, all patients with infant botulismhave recovered, receiving general supportive care.None of the patients from California have re-ceived antitoxin. There has been no evidencethat infant botulism is related to the sudden in-fant death syndrome.Botulism should be considered in infant pa-tients in whom there has been rapid onset ofweakness, with or without abnormalities of cranialnerve function. Careful electrophysiological in-vestigation should be carried out, and specimensof blood and stool should be sent to laboratoriesequipped for identification of the botulinal toxin.BRUCE 0. BERG, MDREFERENCESPickett J, Berg B, Chaplin E, et al: Syndrome of botulism ininfancy: Clinical and electrophysiological study. N Engl J Med295:770-772, Sep 30, 1976Berg B: Syndrome of infant botulism. Pediatrics 59:321-323,Mar 1977Cherington M: Botulism: Ten-year experience. Arch Neurol 30:432-437, Jun 1974Gutmann L, Pratt L: Pathophysiologic aspects of human botu-lism. Arch Neurol 33:175-179, Mar 1976Arnon S, Midura T, Clay S, et al: Infant botulism: Epidemio-logical, clinical and laboratory aspects. JAMA 237:1946-1951, May2, 1977Shvedov L: Observations on the formation of a toxin in thedigestive tract of animals infected orally with a type A strain ofClostridium botulinum. Zh Mikrobiol Epidemiol smmunobiol 31:106, Jan 1960Treatment of Multiple Sclerosiswith Adrenal Cortical SteroidsTHE CAUSE AND CURE of multiple sclerosis (Ms)still elude us and many therapies are used tocontrol the symptoms or slow the recurrent in-flammatory-degenerative process. The possibleimmunological basis of- the demyelination hasbeen treated without success by transfer factor,antithymocyte globulin or azathioprine (ImuranQ).For several years, adrenal corticosteroids or ACTHhave been tried, and it seems appropriate to re-view the current status of this controversialtherapy.When a patient is in an acute relapse and failsto respond to bed rest and simple supportiveTHE WESTERN JOURNAL OF MEDICINE 133

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Neurology-epitomes of progress: lithium toxicity in the central nervous system.

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Neurology—Epitomes of Progress: Lithium Toxicity in the Central Nervous System

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