8.3 The Spark

Time To Read

4–7 minutes

Date Last Modified

Age 35


Anti-MAG peripheral neuropathy

1

Radiating Leg Pain & Numbness After a ‘Clear’ Crash 

2

Symmetric Loss of Light-Touch & Vibration

3

Slowed Nerve Conduction 

4

Synapse Intact — the Fault Is Upstream

5

Anti-MAG Antibodies 

6

A Map Pointing at Two Nerve Roots

7

Anti-MAG, Sensory-Predominant Peripheral Neuropathy

The conduction study clipped electrodes to Stina’s legs and timed how fast her nerves answered. The signals were there — but late, dragging behind where they should have been, worst in the longest nerves running to her feet. “Mild, nonspecific slowing,” the report concluded, and it was filed. To Stina it confirmed only that the numbness was real and measurable. What no one said out loud was that slowed conduction is not random noise; it is the specific signature of insulation that has come loose.

A neuron at rest holds a voltage across its membrane — the resting membrane potential, about −70 millivolts inside relative to outside, maintained by ion pumps and channels that sort sodium (Na⁺), potassium (K⁺), and other ions. When a stimulus pushes the membrane past a threshold, voltage-gated Na⁺ channels snap open, Na⁺ floods in, and the voltage spikes — an action potential, the all-or-nothing electrical signal. It then races down the axon. On a myelinated axon it doesn’t crawl; it leaps from one bare gap to the next — the nodes of Ranvier — in saltatory conduction, which is what makes signaling fast. Strip or loosen the myelin and the leap fails: the signal must crawl, and conduction slows — exactly Stina’s result.

Notice the ions. Na⁺ and K⁺ run the action potential, and Ca²⁺ — the calcium that built her bone and contracted her muscle earlier in the course — is about to take the lead role at the synapse. The same calcium thread now wires the nervous system.

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