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J Am Board Fam Pract: first published as 10.3122/jabfm.8.5.400 on 1 September 1995. Downloaded from Syndrome In Parkinson ni{/l[(' M. Wc>iss, Mn

Parkinson disease is a progressively debilitating cent, white cell count 14,500 I11llll with 7H per­ disease of the extrapyramidal motor system. cent segmented ncutrophils, 17 pcrcent lympho­ Components of , as well as depression, cytes, no band cells, and a platelet count of have been recently rccognized as part of the syn­ 276X 103/111111'. Urinalysis was unremarkable as drome. As psychopharmacology bccomcs more were results of a urine toxicology screening test. advanced in the treatment of clusters of symptoms, His ammonia level was 330 mg/dL. new pitfalls arise. The "serotonin syndrome" is a An electrocardiogram showed sinus tachycar­ complic1tion of the use of dia, and findings on a chest radiograph were inhibitors (MAOls) and selective serotonin re­ within normal limits. Computed tOlllography uptake inhibitors (SSRls). The former are used as (CT) of his head showed cvidcnce of a right sub­ anti parkinson drugs, ,lS well as , occipital craniotomy but no mass, midline shift, and includc (Nardil), tranylc}11romine infarct, or hemorrhage. Findings from a lumbar (Parnate), and (Eldepryl). The latter puncture were unremarkable. make up the newer genen1tion of antidepressants, Meanwhile, further history was obtained from such as (Prozac), (Paxil), and the patient's f~lIni!y, who said that the patient had (Zoloft). A casc is presented that serves had Parkinson disease for 16 years. Carbidopa­ to illustrate the drug interactions and review the levodopa (Sinemet) therapy began 3 years after syndrome. the disease onset, and the improved A 50-year-old man was found outside a nearby his symptoms substantially. He denied any history f{)od outlet in a state of agitation with generalized of or drug use. His surgical history spasms. Paramedics wcre called, and the patient was noteworthy for removal of a right cerebellar was brought to the emergcncy department. arteriovenous malformation that was incidentally On arrival, his temperature was )(17°F rectally, discovered on CT of his head, which was per­ 1971119 I11ml Ig, heart ratc 12 H/min, formed for evaluation of the Parkinson disease 10 and rcspiratory rate 40/min. The patient was in­ years prior to admission. coherent and had -like muscle trcmors of He was taking large doses of carhidopa-Ievo­

both upper and lower extremities. Neurologic dopa, 251250 four times a day, and a sustained­ http://www.jabfm.org/ examination was notable for rapid, dyskinetic release form (Sinemet CR), 501200 two tahlets movements mainly in the hands and feet bilater­ each day. In addition, he was taking selegiline, ally. I Ie had moderate rigidity in both upper and 10 mg/cl. The patient had been prescribed sertra­ lower cxtremities, his deep tendon reflexcs were line, 50 mg/d, for depression 2 weeks prior to ad­ 2 + bilaterally, and his toes were downgoing. mission. He had been forced to retire from his job Laboratory data wcre as follows: sodium 155 as a chemical engineer at the California Institute mEq/L, potassiulll 5.0 mEq/L, chloride 113 mEq/L, of 'Ilxhnology because of his Parkinson disease on 4 October 2021 by guest. Protected copyright. bicarbonate 24 mEq/L, blood urea 21 and had become despondent ahout his physical mg/dL, creatinine I.H mg/dL, glucose 94 mg/dL. detcrioration. He had no recent history of expo­ The creatininc kinase was 1029 U/L, with an MB sure to ,1Il inhalationa] anesthetic or a neuroleptic fraction of 6.5 U/mL, and index 0.6 pcrcent. The medication. hcmoglobin was I.~.H g/dL, hematocrit 40 per- The patient was thought to have the neuro­ leptic malignant syndrome despite no history of medication ingestion. He was ad­ Sui>lllitted, revised, 12 :\by I (!'!5. mitted to thc intensive care unit for further obser­ Frolll the Dcpartillent of Faillily ,\ledicine, Kaiser I'enna­ vation. Levodopa, , and supportive nente ,\lediC:11 Center, Fontana, California. Address reprint therapies were administered, and he improvcd rC'lIll'sts to l)i:lIle ,\1. \\'eiss, :\11), Departillent of Faillily ;\ledi­ cine, Kaiser l'erlllanente :\1edical Center, ()<)() I Sierra Avenne, overnight. The selegiline and sertraline were dis­ FonLl1la, CA ()]l.l5. continued. Thirty-six hours after admission he

4-00 JABFP Sept.~(kt. 1t)95 Vol. H No.5 J Am Board Fam Pract: first published as 10.3122/jabfm.8.5.400 on 1 September 1995. Downloaded from was transferred from the intensive care unit to a Some drawbacks observed with selegiline are ward bed, never requiring intubation. He did suf­ that it irreversibly inhibits MAO-B, it tends to be fer from a component of with nonselective for MAO-B at higher doses (thereby subsequent renal insufficiency. Total creatinine creating risk for the " cheese" effect), kinase reached a peak of 30,000 UIL. Renal func­ and it has somewhat weak metabo­ tion returned to normal with hydration and alka­ lites. Newer drugs are being actively investigated linization of the urine. Two and one-half days to overcome these problems,f' after admission, the patient was released in stable condition. All blood, urine, and cerebrospinal The Serotonin Syndrome fluid cultures remained negative. Clinical depression is now recognized as occur­ ring in nearly 50 percent of patients with Parkin­ Discussion son disease. To treat these patients fully, anti­ Parkinson DtsellSe depressants are being prescribed in ever-growing Paralysis agitans, or Parkinson disease, was first numbers. Clinicians are becoming increasingly described in 1817.1 Occurring sporadically in the familiar with the third-generation antidepressants general population, it is a progressive, debilitating as a result of their circumscribed side-effect pro­ disorder with its first onset in mid to late life. De­ file/ and it is common to find patients on fluoxe­ spite extended research the cause is not well un­ tine and sertraline as opposed to the older tricy­ derstood. Two related conditions resulting in simi­ clic antidepressants. lar symptoms are postencephalitis As a result a new syndrome known as the sero­ and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyri­ tonin syndrome has come to be recognized.8- 16 1t dine (MPTP) intoxication (a drug of abuse) pro­ results from a combination of MAOIs with selec­ viding evidence for an environmental insult. tive serotonin reuptake inhibitors (SSRIs), such as L-, , fluoxetine, and Clinical Syndrome sertraline. Clinically, the serotonin syndrome is Symptoms of the full-blown syndrome are unmis­ similar to the neuroleptic malignant syndrome takable - stooped posture; stiff, slow move­ that occurs when antipsychotic are ments; impassive facies; and rhythmic at combined with receptor blockers.17 rest. Symptoms generally begin asymmetrically include the acute onset of and progress to symmetric involvement. There is , , , , dia­ no paralysis, but the progressive tremor and stiff­ phoresis, tremor, , and incoordination. ness make activities of daily living nearly impossi­ Resolution is usually equally rapid, in contrast to http://www.jabfm.org/ ble in the end stages of disease. Deep tendon re­ the neuroleptic malignant syndrome, which can flexes, as well as sensory perception, remain take up to 1 to 2 weeks to resolve fully. intact. Nearly one-half of patients suffer from de­ The syndrome occurs in both sexes and in pressive symptoms. adults of all ages. There have been 38 cases reported during the past 12 years. The typical 'J'reatment scenario is one in which medications are being The mainstay of treatment has been to provide an altered for a variety of reasons - efficacy, side on 4 October 2021 by guest. Protected copyright. exogenous source of dopamine. The timing of effects - and an overlap between the serotonin this intervention is critical, because dopamine re­ reuptake inhibitors and the MAOIs causes hyper­ placement is not without side effects, including stimulation of brain-stem and spinal-cord seroto­ precipitation of , the on-off phenome­ nin receptors. It is now recommended that a full non (sudden variation in response), mental confu­ 5 weeks lapse after discontinuing fluoxetine and sion, and loss of efficacy. before starting MAOI treatment. More recently, the selective monoamine oxi­ In the case described, a selective MAO-B in­ dase B (MAO-B) inhibitor selegiline2 has been hibitor was taken with sertraline. Although found to delay by 1 year the need for levodopa ther­ MAO-A rather than MAO-B is specific for sero­ apy.3,4 The most intriguing hypothesized mode of tonin , there have been reports impli­ action is the inhibited production of free radicals cating MAO-B inhibition in a nonspecific reac­ ·, 5 that cause lipid membrane degra danon m neurons. tion with serotonin reuptake inhibitors. It is

Serotonin Syndrome 401 J Am Board Fam Pract: first published as 10.3122/jabfm.8.5.400 on 1 September 1995. Downloaded from currently not advised to prescribe selegiline with 5. DAIATOP: a llIulticente,' controlled in any of the selective serotonin reuptake inhibitors. early Parkinson's disease. Arch Neurol I I)se); Treatment consists of removing the offending 4(>:1 052 -60. 6. Fowler .IS, Volkow NU, Logan j, Schlyer Uj, agents and providing supportive therapy. Active MacGregor RR, Wang (;.1, et al. MOlloallline oxi­ serotonin ant.l27. Neurol JI)I)3; Conclusion 43: I 1)8..j.-92. 7. Rickels K, Schweizer E. Clinical overview of seroto­ This case shows the hazard of polypharmacy nin reuptake inhibitors . .I Clin 1990; in the patient with the diagnoses of Parkinson 51 (Suppl B):9-12. disease and depression. Ib treat patients in this 8. Sternbach H. The serotonin syndrome. Am J Psy­ specialized group, it might be necessary to rely chi'ltry 1991; 148:705-13. on the older generation of antidepressants. If 9. SlIchowersky 0, DeVries jD. Interaction of HlIoxe­ those medications are not tolerated, then care­ tine and selegiline. CanJ Psychiatry 1(1)0; 35:571-2. 10. Bhatara VS, Bandettini Fe. Possihle interaction he­ ful consideration of the most efficacious drug tween sertraline and . Clin Pharm regimen must be made to avoid life-threatening 1993; 12:222-5. complications. II. Feighner JP, Boyer WF, lyler Dt, Nehorsky RJ. Ad­ verse consequences of tluoxetine-MAOI comhina­ tion therapy.J Clin Psychiatry 1990; 51:222-5. 12. Sternbach H. Danger of MA01 therapy after tlu{)xe­ References tine withdrawal. Lancet 19f\8; 2:R50-1. I. Richardson EP Jr, Beal Mf~ MartinJB. Degenerative 13. Graham PM, Ilett KF. Danger of MACH therapy of the . Tn: Braunwald E, after Huoxetine withdrawal. Lancet 198R; 2:255 -(lo Isselbacher KJ, Petersdorff RG, 'Nilson JD, Martin 14. Brennan D, MacManus M, Howe j, McLoughlin J. JB, Fauci AS. Harrison's principles of i!lternalmedi­ "Neuroleptic malignant syndrome" without neuro­ cine. 11th cd. New Y<)rk: McGraw-Hill, 1987:2017-9. leptics. BrJ Psych 19R8; 152:578-9. 2. Drugs used in extrapyramidal movement disorders. 15. Kline SS,Mauro LS, Scala-Bamett DM, Zick D. Sero­ In: Drug evaluations. Annual. Chicago: American tonin syndrome versus neuroleptic malignant syn­ Medical Association, 1994:383-408. drome as a cause of death. Clin Pharm 19R9; 8:510-4. 3. Effect of deprenyl on the progression of disahility in 16. MontastrucjL, Chamontin B, SenanlJM, 'fran MA, early Parkinson's disease. The Parkinson Study Rascol 0, Llau ME, et al. Pseudophaeochro1l1o­ Group. N Engl] Met! 1989; 321:1364-71. cytoma in a parkinsonian patient treated with Huoxe­ 4. Effects of tocopherol and deprenyl on the progres­ tine plus selegiline. Lancet 1993; 321 :555. sion of disability in early Parkinson's disease. The 17. Pearlman CA. Neuroleptic malignant syndrome: a Parkinson Study Group. N EnglJ Med 1993; review of the literatul'e. J Clin Psychopharmacol http://www.jabfm.org/ 328:176-83. 1986; 6:257-73. on 4 October 2021 by guest. Protected copyright.

402 JABFP Sept.-Oct. 1(1)5 Vol. 8 No.5