Neuroleptic malignant syndrome

Causes and risk factors

NMS is classified among the acute complications of psychopharmacotherapy. The primary triggers are potent antipsychotic drugs (e.g., haloperidol and thiopropazate). The syndrome may manifest either during active treatment or upon sudden discontinuation of the medication.

The probability of developing this complication increases in the presence of the following predictors:

• Prior organic CNS lesion (history of).
• Initially poor tolerability of prescribed medications.
• Appearance of pronounced parkinsonism symptoms within the very first days of drug therapy.

Clinical presentation and laboratory markers

NMS can be suspected based on a combination of neurological, autonomic, and somatic disorders.

Main clinical manifestations:

• Extrapyramidal disorders: pronounced muscular rigidity (sharp increase in muscle tone).
• Autonomic dysfunction: hyperthermia, unstable blood pressure (both hypertension and hypotension may occur), tachycardia, and profuse diaphoresis.
• Alteration of mental status: altered consciousness of varying depth.
• Skeletal muscle involvement: rhabdomyolysis, which clinically manifests as myalgia.

Laboratory findings show:

• Significant elevation of creatine phosphokinase (CPK), creatinine, transaminases, and erythrocyte sedimentation rate (ESR).
• Changes in the complete blood count: leukocytosis against the background of lymphopenia.
• Markers of muscle breakdown — myoglobinemia and myoglobinuria — appear in the blood and urine. These pose a direct threat of developing acute kidney injury (AKI).

Principles of treatment

NMS management requires emergency measures, often in an intensive care setting. The treatment algorithm includes:

1. Immediate discontinuation of all neuroleptics.
2. Infusion therapy to correct water-electrolyte balance (saline solutions, 5% glucose, plasma, and dextrans are used).
3. Restoration of dopaminergic activity (bromocriptine, amantadine, and levodopa preparations are prescribed).
4. Administration of muscle relaxants (diazepam) to protect muscle tissue from further damage.
5. Prescription of glucocorticoids (for cerebral edema prevention) and heparin sodium (for thrombosis prevention).

Plasmapheresis demonstrates high efficacy. In cases where the patient does not have deep impairment of consciousness (sopor, coma, amnesia), electroconvulsive therapy (ECT) may be used.

Malignant hyperthermia as a variant of NMS

Malignant hyperthermia is distinguished as a specific variant of neuroleptic malignant syndrome. Its key difference is the absence of pronounced neurological symptoms (no muscle rigidity or tremor).

It is frequently associated with clozapine use and in some cases may resolve without specific therapy. However, a sharp rise in body temperature poses a serious danger: metabolic acidosis, hyperkalemia, hypermagnesemia, and DIC syndrome may develop.

Class and exam questions

What else to study on this topic

• Serotonin syndrome: clinical features and treatment
• Anticholinergic delirium in psychotropic drug use
• Agranulocytosis as a complication of psychopharmacotherapy
• Principles of treatment for acute neuroleptic poisoning
• Acute allergic reactions to psychotropic drugs

Other topics in the section "Chapter 28. Psychiatric Emergencies"

Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.