Clonus, characterized by rhythmic, involuntary muscle contractions and relaxations, is a neurological sign often associated with upper motor neuron lesions. Its presence, typically alongside hyperreflexia, serves as a crucial indicator in neurological examinations. This article delves into the intricacies of clonus, focusing on its differential diagnosis, elicitation techniques, clinical significance, and the vital role of an interprofessional healthcare team in patient management. Understanding clonus and its diverse presentations is essential for accurate diagnosis and effective patient care.
Understanding Clonus: Mechanisms and Physiology
The precise physiological mechanisms underlying clonus are still under investigation, but current theories point towards disruptions within the nervous system’s control of muscle stretch reflexes. Two primary hypotheses attempt to explain this phenomenon.
Theories of Clonus
One theory suggests that clonus arises from a self-perpetuating cycle of peripheral muscle stretch reflex reactivation. In this model, each muscle contraction triggers the subsequent stretch reflex, creating a continuous oscillatory loop. Alternatively, another theory proposes a central nervous system origin, where an initial stimulus activates the stretch reflex, but a persistent central signal then commands the muscles to continue contracting rhythmically, even without ongoing peripheral stimulation. It is plausible that a combination of both peripheral and central mechanisms contributes to the manifestation of clonus.
Neurophysiological Basis
The hyperexcitability of muscle stretch circuits, a hallmark of clonus, stems from reduced tonic inhibition of motor neurons involved in the monosynaptic stretch reflex. This disinhibition typically occurs due to lesions affecting descending motor pathways, particularly the dorsal reticulospinal tract. These lesions can be located anywhere along the pathway from the cerebral cortex down to the spinal cord. The descending motor nerves normally exert an inhibitory influence on alpha and gamma motor neurons. When this inhibitory effect is diminished, the muscle stretch reflex circuit becomes hyperexcitable, leading to clonus and the commonly associated hyperreflexia. Therefore, clonus is a significant indicator of upper motor neuron dysfunction.
The rhythmic frequency of clonus varies depending on the joint and the associated nerve pathways. Joints with shorter nerve pathways, such as the wrist and fingers, exhibit higher frequency oscillations compared to joints with longer pathways, like the ankle. This difference is attributed to the time required for nerve signal conduction to and from the spinal cord.
The ankle joint, innervated by the S1/S2 nerve roots, is the most frequent site for clonus testing. However, clonus can be assessed in other locations, including:
- Jaw jerk (Masseter reflex): Trigeminal nerve, elicited by tapping the chin.
- Patellar reflex (Knee jerk): L2-L4 nerve roots (primarily L4), tested by tapping the patellar tendon.
- Biceps reflex: C5-C6 nerve roots, tested at the biceps tendon in the antecubital fossa.
- Triceps reflex: C7-C8 nerve roots (primarily C7), tested at the triceps tendon above the olecranon.
Eliciting Clonus: A Step-by-Step Guide
A significant advantage of clonus assessment is its simplicity, requiring no specialized equipment. The technique mirrors that of eliciting muscle stretch reflexes, involving a quick stretch to the muscle tendon in a relaxed joint, typically positioned at approximately 90 degrees of flexion. For clonus specifically, sustained pressure is maintained on the joint after the initial stretch to facilitate and appreciate the rhythmic oscillations.
Ankle Clonus Technique
To assess for ankle clonus:
- Position the patient with a relaxed leg, the ankle passively flexed to around 90 degrees, and the knee also slightly flexed if possible. Support the leg with your non-testing hand.
- Place your hand on the dorsum of the patient’s forefoot.
- Briskly dorsiflex the foot and maintain continuous dorsiflexion pressure.
- Palpate for rhythmic plantarflexion and relaxation cycles. Each cycle constitutes a “beat” of clonus. Observe the rhythm and count the number of beats. The initial beat is often the most pronounced, with subsequent beats diminishing in duration but maintaining a consistent frequency after the first few oscillations. Slight foot eversion during dorsiflexion can sometimes enhance the response.
Clinical examination of ankle clonus is typically demonstrated in upper motor neuron lesions or serotonin syndrome. Contributed by RS Menon, MD
Knee Clonus Technique
To assess for knee clonus:
- Position the patient supine with the knee fully extended and leg muscles completely relaxed.
- Using your fingers, briskly displace the patella distally (towards the foot).
- Maintain gentle, sustained pressure in the distal direction.
- Palpate for rhythmic proximal (cephalad) movements of the patella followed by relaxation. Each cycle represents a beat of knee clonus.
Other Sites for Clonus Testing
While ankle and knee clonus are most frequently assessed, clonus can be elicited and evaluated at other joints using similar principles of brisk stretch and sustained pressure appropriate to the joint being tested.
Clinical Significance of Clonus and Differential Diagnosis
Clonus, while sometimes physiological in specific populations, is generally indicative of underlying pathology, particularly in adults. In term infants, a few beats of clonus may be considered within the normal range due to physiological hyperreflexia, but sustained clonus is not typical. In adults, clonus is usually pathological. Sustained clonus, defined as more than 10 beats, is a significant finding, often documented as “sustained clonus” or a reflex grade of “5” (exceeding the standard reflex scale of 0-4).
Clonus as a Sign of Upper Motor Neuron Lesions
As a clinical sign, clonus is a hallmark of hyperreflexia and part of the upper motor neuron syndrome. It frequently co-occurs with other upper motor neuron signs, including spasticity (increased muscle tone) and weakness. The presence of these signs, especially in combination and within the clinical context, strongly suggests an insult to the central nervous system.
Differential Diagnosis of Clonus: Neurological Conditions
The differential diagnosis for clonus is broad, encompassing a range of neurological conditions that affect the upper motor neuron pathways. These include:
- Vascular events: Stroke (cerebrovascular accident) is a common cause of new-onset clonus, particularly when accompanied by other focal neurological deficits.
- Infections: Encephalitis and meningitis, infections affecting the brain and meninges respectively, can lead to widespread neurological dysfunction including clonus.
- Congenital conditions: Cerebral palsy, a group of disorders affecting movement and posture, often manifests with upper motor neuron signs including clonus, particularly in children.
- Autoimmune disorders: Multiple sclerosis (MS), an autoimmune disease affecting the myelin sheath of nerve fibers in the brain and spinal cord, is a well-known cause of upper motor neuron signs, including clonus and spasticity.
- Traumatic injuries: Spinal cord injury can disrupt descending motor pathways, resulting in clonus and other upper motor neuron deficits below the level of the lesion.
Clonus in Serotonin Syndrome and Toxicological Causes
Beyond structural neurological lesions, clonus is a critical diagnostic criterion in serotonin syndrome, a potentially life-threatening condition caused by excessive serotonergic activity in the central nervous system. Serotonin syndrome is often drug-induced, associated with medications that increase serotonin levels, such as:
- Psychiatric medications: Monoamine oxidase inhibitors (MAOIs), selective serotonin reuptake inhibitors (SSRIs), serotonin-norepinephrine reuptake inhibitors (SNRIs), and tricyclic antidepressants (TCAs).
- Substance abuse: Cocaine, ecstasy (MDMA), and amphetamines.
- Other medications: Tramadol (an SNRI-like analgesic) and certain antiemetics.
In the context of suspected drug overdose, particularly with serotonergic agents like tramadol, clonus assessment is invaluable. Studies have shown clonus to be a predictive factor for seizure risk in tramadol overdose.
Common Signs of Serotonin Syndrome. Serotonin syndrome signs include increased bowel sounds (may have diarrhea), hyperreflexia (greater in lower extremities), clonus (greater in lower extremities), autonomic instability (often hypertensive), diaphoresis.
Physiological Clonus vs. Pathological Clonus
Distinguishing between physiological and pathological clonus is critical for accurate diagnosis. Physiological clonus, as seen in some infants, is transient and typically involves only a few beats. Pathological clonus, in contrast, is more sustained, often involving numerous beats and associated with other neurological signs and symptoms. The clinical context, patient age, and presence of other neurological findings are essential in differentiating between these two.
The Role of Clonus in Healthcare and Interprofessional Care
The ease and speed of clonus assessment, along with its lack of equipment requirements, make it a highly valuable tool in various healthcare settings. Nurses, medical students, primary care providers, and specialists are all trained to perform this examination. It is routinely used in the evaluation of patients suspected of having upper motor neuron syndromes, such as those at risk of stroke or with altered mental status.
Clear documentation of clonus findings is essential for effective communication within the interprofessional healthcare team. While detailed descriptions of the elicitation technique and observed clonus characteristics are ideal, noting reflex grades (e.g., “4” or “5”) can also be a concise method of recording the finding.
When clonus is detected during a physical examination, it necessitates further investigation. Referral to a neurologist is often warranted to determine the underlying etiology. Pharmacist consultation is crucial, particularly to evaluate medication lists for potential drug-induced causes, such as serotonin syndrome. Once the diagnosis is established and a treatment plan is initiated, ongoing communication and collaboration within the interprofessional team are vital to monitor patient progress and optimize outcomes. This collaborative approach ensures comprehensive patient care, from initial detection to ongoing management of conditions associated with clonus.
Conclusion
Clonus is a clinically significant neurological sign that provides valuable insights into the integrity of upper motor neuron pathways and overall neurological function. Its presence necessitates a thorough differential diagnosis to identify the underlying cause, ranging from structural neurological lesions to toxicological and metabolic conditions. The simplicity of clonus assessment makes it an accessible and crucial component of the neurological examination, facilitating early detection and guiding appropriate management strategies within an interprofessional healthcare framework. A comprehensive understanding of clonus, its elicitation, and differential diagnosis is paramount for healthcare professionals in delivering optimal patient care.
