Damage to brain's association fibers? Does it heal?

Question

Let's say damage was sustained to the Superior longitudinal fasciculus bundle II in the caudal-inferior parietal cortex. If said region was cut what could be the resulting behavior and more importantly, would the region ie. said fibers heal themselves. Is the damage permanent?

Answer 1

That's a loaded question and depends on the type of damage and the severity. For the most part the brain does in fact repair itself and does so daily. More information such as etiology and patient history would be needed but as a rule here's what I have for you:

White matter tracts such as the superior longitu-

dinal fasciculus, fronto-occipital fascicu-

lus, uncinate fasciculus, extreme capsule,

and inferior longitudinal fasciculus. These

white matter tracts underlie brain regions

associated with cognitive and emotional

function. In depressed patients but not

comparison subjects, volumes of three of

these regions correlated with executive

function; whole brain white matter hy-

perintensities correlated with executive

function; whole brain white matter corre-

lated with episodic memory, processing

speed, and executive function; and whole

brain gray matter correlated with process-

ing speed.

SLF II is the major component of SLF and originates in the caudal-inferior parietal cortex and terminates in the dorsolateral prefrontal cortex.

SLF II connects to the caudal inferior parietal cortex which controls spatial attention and visual and oculomotor functions. This suggest the SLF II provides the prefrontal cortex with parietal cortex information regarding perception of visual space. Since these bundles are bi-directional, working memory in the prefrontal cortex may provide the parietal cortex with information to focus spatial attention and regulate selection and retrieval of spatial information.

One of the most pervasive types of injury following even a minor trauma is damage to the nerve cell's axon through shearing; this is referred to as diffuse axonal injury. This damage causes a series of reactions that eventually lead to swelling of the axon and disconnection from the cell body of the neuron. In addition, the part of the neuron that communicates with other neurons degenerates and releases toxic levels of chemical messengers called neurotransmitters into the synapse, damaging neighboring neurons through a secondary neuroexcitatory cascade. Therefore, neurons that were unharmed from the primary trauma suffer damage from this secondary insult. Many of these cells cannot survive the toxicity of the chemical onslaught and initiate programmed cell death, or apoptosis. This process usually takes place within the first 24 to 48 hours after the initial injury, but can be prolonged.

In the healthy brain, the chemical glutamate functions as a neurotransmitter, but an excess amount of glutamate in the brain causes neurons to quickly overload from too much excitation, releasing toxic chemicals. These substances poison the chemical environment of surrounding cells, initiating degeneration and programmed cell death. Studies have shown that a group of enzymes called matrix metalloproteinases contribute to the toxicity by breaking down proteins that maintain the structure and order of the extracellular environment. Other research shows that glutamate reacts with calcium and sodium ion channels on the cell membrane, leading to an influx of calcium and sodium ions into the cell. Investigators are looking for ways to decrease the toxic effects of glutamate and other excitatory neurotransmitters.

The brain attempts to repair itself after a trauma, and is more successful after mild to moderate injury than after severe injury. Scientists have shown that after diffuse axonal injury neurons can spontaneously adapt and recover by sprouting some of the remaining healthy fibers of the neuron into the spaces once occupied by the degenerated axon. These fibers can develop in such a way that the neuron can resume communication with neighboring neurons. This is a very delicate process and can be disrupted by any of a number of factors, such as neuroexcitation, hypoxia (low oxygen levels), and hypotension (low blood flow). Following trauma, excessive neuroexcitation, that is the electrical activation of nerve cells or fibers, especially disrupts this natural recovery process and can cause sprouting fibers to lose direction and connect with the wrong terminals.

The use of stem cells to repair or replace damaged brain tissue is a new and exciting avenue of research. A neural stem cell is a special kind of cell that can multiply and give rise to other more specialized cell types. These cells are found in adult neural tissue and normally develop into several different cell types found within the central nervous system. Medical researchers are investigating the ability of stem cells to develop into neurotransmitter-producing neurons, specifically dopamine-producing cells. Researchers are also looking at the power of stem cells to develop into oligodendrocytes, a type of brain cell that produces myelin, the fatty sheath that surrounds and insulates axons. One study in mice has shown that bone marrow stem cells can develop into neurons, demonstrating that neural stem cells are not the only type of stem ce