From the Guidelines
Clonus on physical examination is most likely caused by serotonergic drug use, particularly when accompanied by hyperreflexia, as these symptoms are highly diagnostic for serotonin syndrome. This condition can be precipitated by medications or drug toxicity reactions, and differentiating it from other medication-induced syndromes is crucial, as treatment may differ depending on the underlying etiology 1. The clinical presentation of serotonin syndrome often includes myoclonus, which occurs in slightly more than half of cases, as well as clonus and hyperreflexia, which are considered highly diagnostic features when seen in the context of serotonergic drug use.
Some key points to consider when evaluating clonus on physical examination include:
- The presence of clonus and hyperreflexia in a patient taking serotonergic drugs, such as SSRIs, can establish the diagnosis of serotonin syndrome 1
- Other potential causes of clonus, such as stroke, multiple sclerosis, spinal cord injury, brain trauma, cerebral palsy, and metabolic disorders, should be considered in the differential diagnosis
- The pathophysiology of clonus involves interruption of the normal inhibitory signals from the brain to the spinal cord, resulting in exaggerated stretch reflexes
- Clonus can be elicited by rapidly dorsiflexing the foot and maintaining pressure, or by quickly extending the wrist or patella, and the presence of sustained clonus generally indicates significant upper motor neuron pathology.
In terms of morbidity, mortality, and quality of life, it is essential to promptly recognize and treat serotonin syndrome, as it can be a life-threatening condition if left untreated 1. Therefore, when clonus is observed on physical examination, particularly in the context of serotonergic drug use, it is crucial to consider serotonin syndrome as a potential diagnosis and to initiate appropriate treatment promptly.
From the Research
Causes of Clonus
- Clonus is a series of involuntary, rhythmic, muscular contractions, and relaxations that may be caused by interruption of the upper motor neuron fibers, such as stroke, multiple sclerosis, or by metabolic alterations, such as severe hepatic failure or serotonin syndrome 2
- Upper motor neuron diseases, such as stroke and spinal cord injury, can produce alterations in muscle tissue in association with neural damage, leading to clonus 3
- Clonus can also be caused by a combination of increased reflex gain and enlarged tissue viscoelasticity, as seen in patients with stroke and spinal cord injury 3
- Spasticity, a disorder of the sensorimotor system, can also contribute to clonus, particularly in patients with upper motor neuron lesions 4
Mechanisms of Clonus
- The mechanism underlying clonus is not solely related to muscle stretch, but rather involves the interaction of central mechanisms and peripheral events 5
- Clonus may be attributed to the action of a central oscillator, rather than just recurrent muscle-tendon stretch 5
- The hyperexcitability of the alpha motoneuron pool at the segmental level can also contribute to clonus, particularly in patients with upper motor neuron syndrome 4
Clinical Implications
- Clonus can have a significant impact on activities of daily living and can pose challenges to comfort, self-care, hygiene, and appearance, particularly in patients with upper extremity clonus 6
- Intramuscular botulinum toxin-A injections have been shown to reduce spasticity and improve quality of life in patients with clonus 6