The withdrawal reflex is a spinal reflex intended to protect the body from damaging stimuli. It is a polysynaptic reflex, causing stimulation of sensory, association, and motor neurons. In this article we will discuss the basic anatomy, the neural pathways and also the clinical relevance of this reflex.
|Mechanism||1. Noxious stimulus -> excites the sensory nociceptor
2. Tignal travels through a primary sensory neuron -> enters the dorsal horn of the spinal cord
3. The neuron synapses with an interneuron
4. The interneuron synapses with an alpha motor neuron
5. The motor command leaves via the ventral horn -> excites the ipsilateral (same side) flexor muscle group
6. In parallel, motor neurons that supply the ipsilateral extensor compartment receive signals from inhibitory neurons and supply the antagonist muscles -> reciprocal inhibition
|Clinical relations||Overriding of the reflex, transverse myelitis|
This article will discuss the mechanism and importance of the withdrawal reflex.
The withdrawal reflex is defined as an automatic withdrawal of an extremity (e.g. a hand) from a painful stimulus. Unlike deep tendon reflex, the withdrawal reflex is polysynaptic.
The basic mechanism by which it works is the following:
- a noxious stimulus, such as heat or pain, will excite the sensory nociceptor e.g. a heat receptor on the person’s skin
- the signal travels through a primary sensory neuron, which will enter the dorsal horn of the spinal cord
- the neuron will then will synapse with an interneuron within the spinal cord itself
- next, the interneuron will synapse with an alpha motor neuron
- subsequently, this will leave via the ventral horn, and will supply excitatory input to the ipsilateral (same side) flexor muscle group
- in parallel, motor neurons that supply the ipsilateral extensor compartment will receive signals from inhibitory neurons and supply the antagonist muscles. This is known as ‘reciprocal inhibition'. The overall result will consist of pulling the limb away from the noxious stimulus within half a second.
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It is worth noting, that at the same time the sensory neuron synapses with the ipsilateral motor neuron, it also synapses with the contralateral motor neuron. This will send signals up the spinal cord and cause the person to contract muscles that will move the centre of gravity of the person to prevent them falling once they withdraw from the stimulus. This will act to stabilize the contralateral part of the person’s body. For example, it will prepare the contralateral leg in order to stabilize the body and prevent the person falling. The stimulation of the contralateral half of the body for stabilization is known as the crossed extension reflex.
Under normal conditions, a noxious stimulus will occur before the flexor reflex will occur. However, squeezing a limb can cause the same response. This suggests that the spinal cord can modify and modulate the sensitivity of the local circuitry to a variety of sensory inputs.
Overriding of the reflex
Drunk, drugged or unconscious patients will not exhibit this reflex. The body can also be made to override the reflex.
This is a demyelinating condition of the spinal cord caused by multiple sclerosis, viruses (herpes simplex, enteroviruses, cytomegalovirus) and certain fungal infections (mycoplasma pneumonia). It often leads to:
- motor weakness
- diminished reflexes
- autonomic dysfunction
- sensory dysfunction
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