MYOGLOBINURIA, MALIGNANT HYPERTHERMIA, NEUROLEPTIC MALIGNANT SYNDROME AND SEROTONIN SYNDROME

This chapter is a brief overview of the evaluation and diagnosis of patients with neuromuscular disorders. This includes the history and examination in order to help differentiate them, as well as to determine useful ancillary tests that will help reach a final diagnosis, that could lead to treatment, which is discussed in other chapters. We also describe electromyography and histological tests, providing examples of their most important features. Basic concepts of imaging and genetic tests are also discussed. This will be covered and expanded in detail in other chapters.

Spasm is a descriptive term for an involuntary muscle contraction. When painful, spasms are often referred to as cramps. The anatomical origin of spasms always involves muscles, but the causative mechanism can be localized within the muscle or in other areas of the nervous system.

Describir un caso de rabdomiolisis asociada a uso de quetiapina y lamotrigina en adolescente tratado por trastorno afectivo bipolar.

Descripción del caso clínico, análisis de los factores asociados y revisión no sistemática de la literatura relevante.

Varón de 18 años de edad con trastorno afectivo bipolar, tratado farmacológicamente con quetiapina y lamotrigina, que tras 2 semanas de entrenamiento físico presentó rabdomiolisis. La quetiapina y el ejercicio se han asociado a rabdomiolisis. No se ha encontrado el mecanismo que media tal asociación, si bien se plantea disfunción neuromuscular e incremento en la permeabilidad sarcomérica.

Este caso clínico permite observar la interacción compleja de los psicofármacos y la actividad física en un paciente psiquiátrico adolescente, y la aparición de una complicación médica potencialmente letal.

To describe a case of rhabdomyolysis associated with the use of quetiapine and lamotrigine in an adolescent treated for bipolar disorder.

Description of the clinical case, analysis of the associated factors and a non-systematic review of the relevant literature.

An 18 year old male, with bipolar disorder and treated pharmacologically with quetiapine and lamotrigine, after two weeks of physical activity presents with rhabdomyolysis. Quetiapine and exercise have been associated with rhabdomyolysis. The mediator mechanism of this association has not been found, although it has been established that there is neuromuscular dysfunction and an increase in sarcomere permeability.

This clinical case allowed the complex interaction between antipsychotic agents and increased physical activity to be observed in a psychiatric adolescent patient, as well as the appearance of a potentially lethal medical complication.

Fluoxetine is one of the most prescribed psychotropic medications, and is an agent of increasing interest for environmental toxicology. Fish and other aquatic organisms are excellent models to study neuroactive small molecules like fluoxetine. However, prone to variance due to experimental factors, data obtained in these models need to be interpreted with caution, using proper experimental protocols, study designs, validated endpoints as well as well-established models and tests. Choosing the treatment protocol and dose range for fluoxetine and other serotonergic drugs is critical for obtaining valid test results and correct data interpretation. Here we discuss the value of aquatic models to study fluoxetine effects, based on prior high-quality research, and outline the directions of future translational studies in the field. We review fluoxetine-evoked phenotypes in acute vs. chronic protocols, discussing them in the contact of complex role of serotonin in behavioral regulation. We conclude that zebrafish and other aquatic models represent a useful in-vivo tool for fluoxetine pharmacology and (eco)toxicology research.

Rhabdomyolysis is due to severe muscle damage from acquired or genetic causes. Myoglobin, a major component of cardiac and skeletal muscle, is released into the blood and is excreted in the kidneys. Excessive levels can lead to myoglobinuria and potentially acute renal failure. The causes of myoglobinuria may be acquired as in crush injury, excess exercise, toxins, infectious diseases, or inherited as metabolic (glycogen or glycolytic disorders) or nonmetabolic (muscular dystrophies) disorders. Diagnosis is required to establish the nature of myoglobin release and therapy is dependent on the cause. Regardless of cause, treatment of acute renal failure is essential as well as management of associated concomitants, such as hyperkalemia or hypo- or hypercalcemia. Mortality may be up to 10%.