FEAR ON THE BRAIN

We often think of fear as a temporary state. It is an emotional and physiological reaction to an external stimulus that usually subsides once the stimulus ends. However, certain types of fear, namely prolonged or life-threatening, can cause permanent changes in our brains. This is why Post Traumatic Stress Disorder can be such a difficult disorder to treat.

The fear response starts in a region of the brain called the amygdala. When triggered, other areas of the brain are activated in order to prepare us for fight or flight, i.e. Motor functions. It also triggers the release of stress hormones and our sympathetic nervous system. Ultimately, making us more efficient at times of danger: muscles grow due to increased heart rate and breathing and gastrointestinal system slows down.

However, a different part of the brain called the hippocampus, which is closely connected to the amygdala along with the prefrontal cortex mitigate the fear by interpreting the threat in its context. For example, if you encountered a shark in open waters vs. a shark in an aquarium, your experience of fear would vary significantly given the context. This is because the hippocampus and the prefrontal cortex judge the context and then dampen the amygdala’s fear response. Generally speaking, this neurophysiological process is rather straightforward when we are talking about isolated and mild to moderate fear events. When we are discussing prolonged or life-threatening events, that is altogether a different story.

Researchers from the Tulane University School of Science and Engineering and Tufts University School of Medicine found that the stress neurotransmitter norepinephrine, also known as noradrenaline, facilitates fear processing in the brain by stimulating inhibitory neurons in the amygdala to generate a repetitive bursting pattern of electrical discharges. This is particularly the case when there is persisting fear, or an extreme amount of fear being triggered. This bursting pattern of electrical activity changes the frequency of brain wave oscillation in the amygdala from a resting state to an aroused state that promotes the formation of fear memories.

This changes the electrical discharge pattern in the amygdala, which transitions the brain to a state of heightened arousal that facilitates memory formation and fear memory. Because of the neurophysiological alterations, patients with PTSD often struggle with re-experiencing of traumatic events and hyper-vigilance.

Disorders of anxiety and fear include phobias, social phobia, generalized anxiety disorder, separation anxiety, PTSD and obsessive-compulsive disorder without appropriate treatment can become chronic and debilitating. Without understanding the neurophysiological basis of fear, it’s difficult to appreciate how to really help individuals that are often paralyzed by their fears. Treating anxiety disorders such as PTSD is not as simple as enlisting them in talk therapy. Rather, it is considering how best to rewire their brains from the heightened state due to the electrical discharges and the neurophysiological changes. The best form of treatment is conjunctive therapy with behavioral, cognitive and neurochemical (medications) approaches. Combined, these could help the individual normalize the brain function.

In my practice, I encounter patients regularly that have been involved in catastrophic injuries, varying from construction site accidents to transit accidents. What I often see is along with their head injuries, patients are often dealing with the residual effects from the fear/anxiety related to the accident itself. Thus, it is important that we take note of the effects of fear on the brain as these can often cause insidious problems that compound patient recovery.

BASELINE BRAIN FUNCTION: TESTING FOR PREMORBID FUNCTIONING

With the increasing accessibility of information these days, individuals are becoming more aware of the fragility of the brain. From an athlete’s risk of concussions during a football game to the possibility of a brain contusion from a car accident, there is more concern around brain injuries than ever before.

As a result of this increased awareness, the demands on the field of neurology and its subspecialties have grown. This growth has also raised more questions. One common recurring question is, how do doctors determine the chronicity and severity of a neurological injury.

Doctors often rely on brain imaging to determine diagnosis, treatment and prognosis. MRIs are the most accurate type of brain scan science has to offer (at the moment) and they are effective in identifying hematomas, hemorrhages, and cerebral edemas, but not so effective at identifying other types of brain injuries. For example, MRIs usually cannot detect any abnormalities in a patient with traumatic brain injury. It isn’t until much later that an MRI or a CT scan is able to detect brain atrophy from a TBI (results when dead or injured brain tissue is reabsorbed following the injury). At that time, it is much too late to implement any reversable treatments. Since brain scans are often unremarkable in these cases, we must rely on other clinical tools to properly diagnose and treat these injuries.

Since microscopic injuries to the brain cause long term problems, it is key to detect them early in order to adequately treat them. One of the methods employed to do so is through baseline cognitive testing. Baseline cognitive tests are measures that neuropsychologists administer to assess brain function during a healthy state. Following a concussion, neuropsychologists can use a post-injury test (and compare against your baseline cognitive test) to help determine the severity of the injury and the treatment you’ll need.

In my practice, I work a lot with professional athletes and especially football players. Since concussion protocols have been put into place, the National Football League has implemented a baseline cognitive test for all incoming athletes called the ImPact. This allows team doctors to re-examine the athlete when a head injury occurs and compare test results at the time of injury to their baseline. From the results, the doctors are able to identify a) if an injury occurred, b) the severity of the injury, and c) the treatment required.

But what happens when there’s been a neurological insult, and we have no baseline tests? What then can we compare the post-injury test to in order to determine if there has been an injury?  And its level of chronicity and severity? This is where the importance of premorbid testing comes in!

A test of premorbid functioning estimates an individual's pre-morbid (pre-injury) cognitive functioning. Similar to that of baseline testing, a pre-morbid test allows us to determine a) if an injury occurred, b) the severity of the injury, and c) the treatment that is needed. The difference is that in this case, the test takes place after the injury, and we are estimating the pre-morbid level of functioning using empirically based measures and collateral information.

Empirically based measures are standardized assessment procedures that assess for crystallized intelligence. Crystallized intelligence is information that relies on accumulated knowledge, such as vocabulary and reading. Generally speaking, these are not vulnerable to brain damage, with the exception of patients with aphasias (communication disorders) due to damage to the Wernicke’s or Broca’s areas in the brain. In patients with aphasia, the LOFT (Lexical-Orthographic Familiarity Test) can be used. This is a forced-choice recognition task based on lexical familiarity judgments. In studies on aphasic patients, it was found that when compared to non-brain damaged individuals, their scores on the LOFT were statistically insignificant, meaning aphasic patients were not affected in their ability to perform on this test.

Combining the results from empirically based measures with clinical impressions derived from socioeconomic variables such as the patient's level of academic, occupational, social and interpersonal relation areas, neuropsychologists can confidently generate a premorbid estimate of cognitive functioning. This is particularly important in the medical-legal field when doctors are asked to consider pre-existing conditions and apportion when there are pre-existing factors.

More often than not, we do not have a brain MRI or CT scan from before a neurological insult. Individuals typically are not getting a brain scan when they are healthy. Similarly, individuals are not getting a neurocognitive evaluation or baseline cognitive test when they are healthy. This means doctors are typically not provided baseline studies. It is therefore important that we always include premorbid testing to help us determine the individual’s premorbid level of cognitive functioning. This is the only way in which we can effectively determine whether there was truly an injury and the chronicity and the severity of the injury.

Without understanding what the starting point is, doctors cannot truly appreciate what, if any, change has occurred.

THE PAINED BRAIN

According to the Centers for Disease Control and Prevention, in 2021, the prevalence of chronic pain among U.S. adults ranged from 20.5% to 21.8%. With such a large subgroup of the population persistently in pain, let’s discuss what happens to our brain when we experience pain.

When our bodies experience pain, there are four steps that occur: i) transduction, ii) transmission, iii) modulation and iv) perception. The first step - transduction - is where the peripheral tissue (i.e. Skin) feels a mechanical sensation (i.e. Heat via the nociceptors). The second step - transmission - is where the sensation is passed through to the central nervous system via the axon of the nociceptors in the spinal cord and through to the brain. The third step - modulation - is where the brain alters the intensity of the signal depending on the circumstance one is in. Truly an evolutionary gift, this allows us to survive circumstances where we cannot afford to react to pain as it is. For example, if you were running from a mountain lion and broke your toe, you would be able to ignore the pain and keep on running until the threat was cleared. Pain perception is modulated at several areas in the brain including the dorsal root ganglion, the spinal cord dorsal horn, the reticular system of the brainstem, and the cortical areas of the brain. Finally, the fourth step - perception - is where we actually interpret and experience the pain in the cortex of the brain.

In light of the above, pain is clearly not just an objective processing of a stimulus.  It is dependent upon neural processing in the spinal cord and several brain regions; it’s more than a pattern of nociceptive action potentials (when a neuron sends information down an axon). Action potentials ascending the spinothalamic tract are decoded by the thalamus, sensorimotor cortex, insular cortex, and the anterior cingulate to be perceived as an unpleasant sensation that can be localized to a specific region of the body. Action potentials ascending the spinobulbar tract are decoded by the amygdala and hypothalamus to generate a sense of urgency and intensity. Combined, they integrate sensations, emotions, and cognitions, resulting in our perception of the pain. This is good news because it means we can train ourselves to experience less pain as it is not purely a mechanical process, but rather an emotional and cognitive one too.

When we are referring to chronic pain (pain persisting beyond 3 months), however, this is another subject altogether. Individuals with chronic pain develop changes in their brain and nervous system over time.  The signal pathway to the brain can become hyper-sensitized and hyper-reactive, whereby the persisting pain and emotional reaction to it creates a compounding effect leading to a vicious cycle that categorically causes a neurological disorder. These changes cause the brain to continuously send out pain signals even when there are none. Besides the persistence of pain, individuals with chronic pain can develop hyperalgesia (extreme sensitivity to pain). This occurs when the body's pain receptors become damaged or sensitized. This is why an antidepressant is often prescribed to chronic pain patients as the neurochemistry within chronic pain patients is usually altered in comparison to those without.

In addition to neurochemical changes in the central nervous system, studies prove that chronic pain causes regional brain atrophy, namely to the aforementioned regions. Correspondingly, it cause changes to one’s neurocognitive functioning. A study by the VA San Diego Healthcare System found that individuals with chronic pain show deficits in attention, working memory, learning and memory, processing speed, and executive function. These findings have been repeated by numerous other studies around the world. Chronic pain can also interfere with our daily activities (i.e. Working, physical activities and social activities) and lead to depression, anxiety, and trouble sleeping; all of which could further exacerbate the problem. This tells us that not only does chronic pain affect neural pathways, but it also affects our neuropsychiatric functioning.

Since pain is an unobvious symptom, one that many find difficulty empathizing with, by understanding what happens to one’s brain when they experience pain (and chronic pain specifically) the hope is that more compassion is extended to those struggling with these types of pain. It’s a condition that undoubtedly changes one’s neurophysiology, with specific impacts on the central nervous system, brain functioning, and emotional wellbeing over time. So the next time you encounter a family member, friend, or coworker that struggles with back pain, arthritis, or neuropathy, take a moment to reflect on the toll this has taken on their mind, body, and brain and perhaps offer some consideration.