Neuroleptic Malignant-Like Syndrome and Lithium

Köehler, Philipp; Mirandolle, J. F.

doi:10.1016/s0140-6736(88)90985-3

Cited by 15 publications

(3 citation statements)

References 6 publications

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“…22 Lithium has been implicated in some cases of NMS in patients with Parkinson's disease during levodopa withdrawal. 23 These cases suggest that the addition of lithium critically disturbs an already unstable dopaminergic system. Lithium also has been implicated in the recurrence of NMS in two patients.…”

Section: Neuroleptic Malignant Syndromementioning

confidence: 99%

Acute Lithium Intoxication and Neuroleptic Malignant Syndrome

2003

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A 45-year-old man was admitted to our hospital after taking an intentional overdose of 90 sustained-released lithium tablets (450 mg each). The patient was stabilized with three sessions of hemodialysis. On day 7 of his hospital stay, his serum lithium level was 0.5 mEq/L. On day 10, he developed high fever, tachypnea, muscle rigidity, rhabdomyolysis, acute renal insufficiency, mental confusion, and obtundation. His creatine kinase level was 698 IU/L, serum creatinine 3.5 mg/dl. Late-onset neuroleptic malignant syndrome (NMS) was diagnosed. The patient died after developing acute renal failure and acute respiratory distress syndrome. Clinicians should be aware that lithium may cause NMS independent of other neuroleptic agents.

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Section: Neuroleptic Malignant Syndromementioning

confidence: 99%

Acute Lithium Intoxication and Neuroleptic Malignant Syndrome

2003

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“…Other non-neuroleptic drugs causing NMS include amoxipine [7], phenytoin intoxication [8], sulpiride [9], trimipramine [10], tiapride [11], lithium [12], biperidin [13], clozapine plus lithium [14], phenelzine plus lithium [15], and clozapine and carbamazepine [16]. Heroin is known to cause rhabdomyolysis but not NMS [24].…”

Section: Discussionmentioning

confidence: 99%

“…Most cases of NMS occur following the administration of neuroleptic drugs. Recently, the syndrome has been described in patients on nonneuroleptic drugs [7][8][9][10][11][12][13][14][15][16][17] and after the withdrawal of certain drugs, especially antiParkinson medication [18,19]. This paper describes four cases of NMS recently encountered; one following levodopa/bromocriptine withdrawal, one probably due to heroin "snorting" and two related to neuroleptic administration.…”

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confidence: 99%

Four Cases of Neuroleptic Malignant Syndrome

et al. 1992

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The neuroleptic malignant syndrome (NMS) is a relatively uncommon, sometimes fatal, idiosyncratic drug reaction usually associated with the administration of neuroleptic drugs. The syndrome is characterized by generalized rigidity, fever, altered consciousness or mutism, tremor, autonomic dysfunction, tachypnea, elevated serum creatinine phosphokinase, leukocytosis and myoglobinuria. We report four cases of NMS; one following levodopa/bromocriptine withdrawal, two related to neuroleptic administration and one following heroin use. There are no previous reports linking heroin to NMS. The syndrome is thought to result from acute dopaminergic blockage or dopamine depletion. Levodopa, bromocriptine or both are recommended as specific treatment for this condition. Most cases of NMS occur following the administration of neuroleptic drugs. Recently, the syndrome has been described in patients on nonneuroleptic drugs [7][8][9][10][11][12][13][14][15][16][17] and after the withdrawal of certain drugs, especially antiParkinson medication [18,19]. This paper describes four cases of NMS recently encountered; one following levodopa/bromocriptine withdrawal, one probably due to heroin "snorting" and two related to neuroleptic administration. While heroin is known to produce rhabdomyolysis, there are no previous reports of its producing NMS. Case 1A 14-year-old Saudi female was brought to the hospital unresponsive. Forty days prior to admission trifluoperazine and imipramine were prescribed for agitation, anxiety, confusion and paranoia. She did not respond and eight days prior to admission these drugs were replaced by haloperidol 3 mg b.i.d. She developed progressive sluggishness, falling down spells, opisthotonic events, urinary incontinence and finally became unresponsive.On examination, her blood pressure was 104/60 mm Hg, pulse rate 150/min, respirations 40-60/ min and temperature was 38.9°C. There were bruises and abrasions on her shins. She respondedminimally to pain. Pupils were mid-position and reacted sluggishly. The limbs moved symmetrically· There was generalized rigidity including neck muscles and a fine tremor of the hands. Tendon reflexes were symmetrical and the plantar responses normal. Pertinent laboratory data: white blood count (WBC) was 16,000/mm 3 . Urinalysis was strongly positive for blood using the dip stick, but microscopic examination showed 0-1 red blood cells (RBC) per high powered field (HPF) strongly suggesting myoglobinuria. Serum lactic dehydrogenase (LDH) was 4,599 U/L, serum glutamic oxaloacetic transaminase (SGOT) 1381 U/L, serum glutamic pyruvic transaminase (SGPT) 236 U/L, total bilirubin 25 μmοl/L and direct bilirubin 6 μιηοΙ/L. Lumbar puncture opening pressure was 230 mm of water. Cerebrospinal

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Neuroleptic Malignant Syndrome

Factor¹

2005

Drug Induced Movement Disorders

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Neuroleptic Malignant-Like Syndrome and Lithium

Cited by 15 publications

References 6 publications

Acute Lithium Intoxication and Neuroleptic Malignant Syndrome

Acute Lithium Intoxication and Neuroleptic Malignant Syndrome

Four Cases of Neuroleptic Malignant Syndrome

Neuroleptic Malignant Syndrome

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