Head Injuries and Neuroinflammation: Part I
In practice, I regularly see patients who suffer from persistent muscle spasms, balance issues, headaches, exhaustion, and heightened sensitivity to smells and sounds. Often these symptoms have persisted for years. They may have seen many practitioners without relief, and feel hopeless about their ability to heal.
The cause may be glial (pronounced GLEE-uhl) priming, which is a shift from a healthy brain to an inflamed brain.
Part I: Glial Priming
To understand glial priming, it's important to look at the different types of brain cells, and the functions they perform.
Types of Brain Cells and Their Functions
Let's take a look at the cells that make up the brain. Neurons are the brain cells that send messages to all parts of the body. The average brain has about 100 billion of them, making up just 10% of all brain cells. The other 90% are called glial cells, from the Greek word for glue. When glial cells were first discovered, it was thought that they mostly just held the neurons in place. More recent research has shown that glial cells are the support system for neurons.
Astroglia, or astrocytes, are glial cells that have long projections that attach to blood vessels and neurons, and act as the go-between to provide nutrients from the bloodstream to the neurons. They are what makes up the blood-brain barrier. They protect the neurons from any blood-borne infection. Astrocytes also clean up synapses (the gaps between one neuron and another) of leftover neurotransmitters after a nerve has fired, helping the neuron get ready to fire again.
Oligodendrocytes (AH-li-go-DEN-dro-sites) are glial cells that make myelin, the substance that insulates nerve axons (the long threadlike part of a neuron that carries the nerve impulse). Without myelin, nerve impulses would 'short-circuit', or not arrive at their targets, much like an electrical wire that has lost its insulating coating. This is what happens in Multiple Sclerosis, one of the demyelinating diseases.
The most important type of glial cell when considering neuroinflammation is microglia, which has been the subject of a great deal of recent study. Microglia, in a healthy brain, are nearly-stationary cells which act like 'hall monitors' for the neurons in their midst. These healthy microglia have long arms that reach into the surrounding tissue, secreting neural growth factors, and trimming synapses for nerve connections that are no longer needed.
Microglia have the ability to change their shape and their function when a traumatic event (like a head injury) happens. In this case, the microglial cells go through a series of changes which allow them to react to the damage caused to their region of the brain.
These steps are known as Microglial Activation and Microglial Priming. Let's look at these steps:
Microglial Activation: during this process, Microglial cells begin the change from "hall monitor cells" to "search-and-destroy cells". The long arms they had when life was calm and happy begin to shorten, and the cells begins to move, drawn to damaged neurons, where instead of secreting growth factors (healing substances), they begin to secrete toxins that dissolve damaged neurons. Microglial Activation is a response to a 'first hit'-- a traumatic brain injury (TBI), an overwhelming infection like meningitis (brain inflammation/ infection), or an emotionally traumatizing event, such as a sexual assault.
Microglial Priming happens after the 'second hit' usually another TBI. Priming completes the process of loss of the microglial 'arms', and the cell becomes highly mobile, joining other primed glial cells which collectively attack damaged and healthy neurons. This creates more debris in that brain region, triggering further attack on both healthy and damaged brain tissues. In short, a positive feedback loop, or vicious cycle is created.
In Part II, we'll discuss what happens next.
Richard Nuzzi, DC
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