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Understanding potential brain damage in woodpeckers

Pileated Woodpecker. Photo by Raven Ouellette

A typical woodpecker can hammer a tree trunk 20 times per second (12,000 times per day) with its head moving forward about 7m/sec. Upon striking wood, it can decelerate at a rate 1,200 times the force of gravity (1,200 g). All of this with little, if any, brain damage.

Humans? Not so much. We can handle 2-3 g on roller coasters, but 4-6 g for even a few seconds can be fatal for most. Jet fighter pilots are trained to handle 9 g for a second or two. Even then, most pilots wear special bodysuits that prevent blood from pooling in their legs. Rarely does a human tolerate higher g forces, but it happens.

In 1976, Peter May and colleagues (Lancet 307:1347-48) reviewed factors that allow woodpeckers to prevent the forces of slamming their bills into trees from damaging their brains and causing their eyes to pop out. The research suggested that an understanding of the protective mechanisms of woodpeckers might be applied to humans in a form of biomimicry.

Woodpecker adaptations that reduce the effects of g forces begin with a sturdy tripod of two strong legs and a stiff tail. With two toes forward and two backward, a woodpecker can clamp and hold onto bark or wood. This base allows the bird to draw its bill away from the tree and fire it forward with rapid acceleration.

brain damage in woodpeckers
A curving complex of cartilage and bone within a woodpecker’s head permits the bird to extend and store its exceptionally long tongue. The illustration depicts a Northern Flicker. Illustration by Denise Takahashi

A strong skull

Woodpeckers have a thicker, stronger skull than other birds. The strong, boney bill is encapsulated in a tough membrane that continues to regenerate cells at the tip to keep the bill sharp. Just before striking wood, the lower mandible slides forward to make first contact with the tree. This initial and large force is channeled back through the lower skull, tongue, and neck muscles to avoid direct contact with the brain.

The woodpecker brain is small and more tightly enclosed in the brain case (cranium) than other birds (or humans). Consequently, there is less space and less cerebrospinal fluid in which the brain can “slosh” around. A brain that moves within the cranium will hit cranial bones with greater velocity, which could cause greater brain damage. Additionally, the lining of the woodpecker cranium has more rough, uneven surfaces that reduce brain movement following tree hammering than the smooth bones of other birds.

The lower jaw of woodpeckers articulates with the skull through the quadrate bone, which cushions the pecking force, thereby reducing the force transmitted to the skull and brain.

The hyoid apparatus is a very long cartilage, bone, and muscle structure that attaches to the base of the tongue and allows the bird to extend its tongue a greater distance into insect galleries and tunnel under tree bark to extract insect larvae. A problem is how to store the long hyoid apparatus. Cleverly, the hyoid projects back from the base of the tongue into the throat. There, it splits into a “Y” shape, with the side branches passing through sheaths between muscle and skin, from the throat up the sides of the neck and behind and over the top of the skull, usually ending in the right nostril.

The hyoid segments have boney centers and compliant cartilage around the outside. When forces from striking a tree reach the boney tongue, it is transferred to the hyoid, which acts much like a seat belt, dampening the transmitted forces.

Birds have a third eyelid (nictitating membrane) that moves sideways over the eye just prior to pecking, protecting the eye from wood splinters and acting as a “seat belt,” holding the eyeball in place.

Some researchers suggest that as much as 99 percent of the force generated by the rapid deceleration of the woodpecker bill is dissipated through the above structural adaptations.

Questions about brain damage

This has drawn the attention of persons concerned with repetitive traumatic brain injury (TBI) in athletes involved with contact sports, such as football, soccer (heading), hockey, and boxing. Repetitive TBI is suspected to lead to chronic traumatic encephalopathy (CTE), although the mechanism is not yet known. CTE is a nonreversible, degenerate brain pathology. At present, there are no biological markers that allow diagnosis in living humans. Instead, a diagnosis is made by postmortem examination of brain tissue.

The nervous system consists of the brain, spinal cord, and a host of nerve cells (neurons), both within the brain and spinal cord and as a network throughout the body. A typical nerve cell consists of a cell body and narrow, elongate projections (think electrical wires) called dendrites, which transmit messages to cells and axons that carry messages from cells.

An electrical impulse passes along axons, causing a chemical messenger to be released at their ends, going through a short junction (synapse) and inducing an impulse in a dendrite of another cell. Axons and dendrites are kept long and straight by microtubules that surround them. The structure of the microtubules, in turn, is maintained by a long-chained protein called tau. With repetitive TBI, inflammation occurs, which attracts specialized nerve cells (microglia) to the damaged area. Microglia function like white blood cells in that they are phagocytic (i.e., they engulf dead cells and cellular debris).

Tau is regulated by proteins that attach or remove phosphates from it. Inflammation, however, dysregulates the attachment of phosphates, creating hyperphosphorylated tau proteins, which separate from the microtubules, causing cell axons and dendrites to lose their proper shape and form tangles, with cell death soon to follow.

During brain tissue examination, a special stain applied to the brain tissue on a slide will turn black in the presence of hyperphosphorylated tau and axon and dendritic tangles. The presence of black spots confirms CTE.

It has been assumed for years that woodpeckers do not suffer brain damage from hammering on trees because changes in behavior have not been observed. Because woodpecker brain tissues had not been examined for damage from pecking, George Farah and colleagues at Boston University Medical School did an initial examination reported in 2018 (PloS 13 (2) e0191526). They examined brain tissue from 10 different woodpeckers and found that 8 of them tested positive for CTE, although the damage was not excessive.

The significance of finding limited tau damage in the woodpecker brain is not yet known. More work must be done to replicate the known studies and to understand the results better. Might woodpeckers suffer from some form of CTE? Have woodpeckers developed a biochemical mechanism to counteract the effects of hyperphosphorylated tau? Degenerative brain diseases in humans, such as dementia, Alzheimer’s, and Parkinson’s, all involve the hyperphosphorylation of tau.

Woodpeckers entertain us with bold colors, unusual undulating flight, and dynamic drumming. If you observe one excavating, take time to watch and think of all the problems that were overcome for that to happen. Woodpeckers are truly among the most amazing of birds.

This article was first published in Eldon Greij’s “Those Amazing Birds” column in the September/October 2021 issue of BirdWatching magazine. It updates Eldon’s 2013 column on why woodpeckers can hammer without getting headaches.

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Eldon Greij

Eldon Greij

Eldon Greij (1937-2021) was professor emeritus of biology at Hope College, located in Holland, Michigan, where he taught ornithology and ecology for many years. He was the founding publisher and editor of Birder’s World magazine and the author of our popular column “Those Amazing Birds.”

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