In the Netherlands a young man named Jan was admitted to the emergency room. He and his friends had been to a rave. His friends say he started twitching and having muscle spasms which progressed until he was 'stiff as a board.' On examination, staff found a marked increase in muscle tone and hyperreflexia involving facial and limb muscles. In his pocket, he had unmarked dark yellow tablets with dark flecks. Analysis of the tablets showed them to contain a mixture of ecstasy and strychnine. Ecstasy would not cause this clinical picture, but strychnine, which blocks glycine receptors, could. Explain how.

Verified step by step guidance

1. Understand the role of glycine in the central nervous system: Glycine is an inhibitory neurotransmitter that primarily acts in the spinal cord and brainstem. It binds to glycine receptors on neurons, causing an influx of chloride ions, which hyperpolarizes the neuron and makes it less likely to fire.
2. Recognize the effect of strychnine on glycine receptors: Strychnine is a potent antagonist of glycine receptors. By blocking these receptors, strychnine prevents glycine from exerting its inhibitory effects, leading to increased neuronal excitability.
3. Connect the inhibition of glycine receptors to muscle spasms: Without the inhibitory action of glycine, there is an unchecked excitatory input to motor neurons. This results in continuous firing of motor neurons, leading to muscle spasms and increased muscle tone, as seen in Jan's symptoms.
4. Relate hyperreflexia to the lack of inhibition: Hyperreflexia, or exaggerated reflexes, occurs because the normal inhibitory pathways that modulate reflex arcs are disrupted. The absence of glycine-mediated inhibition allows reflexes to be more pronounced.
5. Summarize the clinical picture: The combination of muscle spasms, increased muscle tone, and hyperreflexia is consistent with the effects of strychnine poisoning, which blocks glycine receptors and removes inhibitory control over motor neurons.

Key Concepts

Strychnine Mechanism of Action

Strychnine is a potent neurotoxin that primarily acts as a competitive antagonist at glycine receptors in the central nervous system. By blocking these receptors, strychnine disrupts the inhibitory neurotransmission that glycine normally mediates, leading to increased neuronal excitability. This results in symptoms such as muscle spasms and rigidity, as seen in Jan's case, where the lack of inhibition causes excessive muscle contraction.

Glycine Receptors

Glycine receptors are ligand-gated ion channels that mediate inhibitory neurotransmission in the spinal cord and brainstem. When glycine binds to these receptors, it typically allows chloride ions to enter the neuron, leading to hyperpolarization and reduced neuronal firing. Inhibition of these receptors by substances like strychnine can lead to a loss of this inhibitory effect, resulting in hyperreflexia and increased muscle tone, contributing to the clinical symptoms observed.

Hyperreflexia and Muscle Tone

Hyperreflexia refers to an exaggerated response to stimuli, often resulting from an imbalance between excitatory and inhibitory signals in the nervous system. In Jan's case, the blockade of glycine receptors by strychnine leads to a predominance of excitatory signals, causing increased muscle tone and spasms. This clinical presentation is characterized by stiffness and involuntary muscle contractions, which are hallmark signs of strychnine poisoning.