How Brain Inflammation Might Impact Stroke Recovery

After a stroke, one barrier to recovery is chronic brain inflammation that continues past the first month of a stroke.

This process – referred to as neuroinflammation – is moderated by several inflammatory messengers that continue to be released from small cells supporting damaged neurons in the brain. Specifically, these inflammatory messengers may continue to be released by glial cells, endothelial cells and white blood cells for months after the stroke event.

The severity of neuroinflammation can be impacted by the number of white blood cells at the site of injury, the quality of blood flow in the area, ongoing swelling in the brain, and even the extent of stress and inflammation affecting the body.

In this blog post, we will explore how neuroinflammation affects a person’s ability to regain key cognitive functions after a stroke.

Understanding Neuroinflammation

Neuroinflammation is a complex biological response which can either augment or hinder recovery from stroke. In the first weeks after a stroke, the initial inflammatory response is critical for the repair of damaged neurons and the protection of surviving cells in the brain. For example, inflammation helps the immune system to ‘clean up’ damaged parts of the brain in these first few weeks. However, many people recovering from stroke enter into a chronic ‘inflammatory cascade’ that delays or prevents a return of function.

So, how does neuroinflammation shape the brain after a stroke?

The Acute Phase (1st Month after a Stroke)

Broadly speaking, strokes are either caused by a major bleed or a blood clot affecting at least one of the brain’s blood vessels. We categorize these into haemorrhagic and ischemic strokes, respectively.

When a stroke disrupts blood flow to a part of the brain, entire groups of neurons quickly become deprived of oxygen and other nutrients. This leads to the death of key neurons, and an urgent need to restructure (a.k.a. remodel) the brain’s structural connections. In the first month after a stroke, inflammation is what helps the immune system to rapidly repair this damage. We call this the acute phase of a stroke.

The Chronic Phase (1st Year after a Stroke)

About four weeks after a stroke, there is a gradual transition away from acute inflammation in the brain. The inflammatory response gradually diminishes around this time, which allows neuroplasticity to take place.

Neuroplasticity refers to the brain’s ability to repair itself by forming new connections between neurons. This process is fundamental to learning and achieving an optimal recovery after a stroke; however, neuroinflammation disrupts the physiological balance required for neuroplasticity to occur.

To relearn things after a stroke, the brain needs to build new connections between neurons (synapses) so they can fire in a meaningful way. You can think of this as building new ferry routes to connect various islands to each other. Neurons that develop new connections with each other would achieve neuroplasticity; however, chronic inflammation blocks this process, making learning much more difficult.

First, inflammation often interferes with the release of neurotransmitters by neurons in the brain. Inflammatory messengers not only block the travel of some neurotransmitters (ferry boats) but they can also block the uptake of these signals by neurons (close the ports on the islands).

Synaptic pruning, or the loss of connections between neurons in the brain, is more likely to occur when neuroinflammation exists over a long period of time.

This is because inflammation in the brain also changes the biochemical environment between the neurons, essentially creating choppy waters that are difficult for the ferry boats to cross. As a result, stroke survivors may find it hard to encode and retrieve new information, hindering their relearning efforts in these choppy seas.

So, while inflammation plays a critical role in repairing damaged tissue after a stroke, it can also provoke serious thinking and memory problems when inflammation continues for too long after a stroke.

When Neuroinflammation is a Barrier to Learning

Healthcare professionals working with people recovering from stroke are likely to focus on other clinical issues, and might overlook the importance of inflammation in the stroke recovery process.

However, chronic neuroinflammatory processes are known to:

• Prolong or slow the stroke recovery process;
• Increase the work of relearning after a stroke; and,
• Increase the level of frustration experienced by patients attempting to restore normal brain function.

To explain these effects, it is important to explain how people ‘cross the learning barrier’ during their stroke recovery process.

‘Crossing the learning barrier’ marks a significant milestone in stroke rehabilitation. It signifies the point where individuals easily reclaim lost skills and integrate them into their daily lives.

Take, for instance, the challenge of learning how to walk again after a stroke.

Walking might initially feel overwhelming, noticing significant changes in your brain’s control of movement. As neuroplasticity occurs and new neural pathways are formed, however, walking becomes easier. You begin to walk more, which in turn improves your ability to walk further.

Chronic inflammation in the brain might delay your recovery, preventing you from crossing this learning barrier. This makes walking feel impossible for much longer than it should after a stroke event.

To cross the learning barrier, your brain must first have the ability to form new connections between neurons (neuroplasticity). This allows you to build new motor action patterns, for example. Walking no longer feels like a challenge, and instead becomes a regular activity you can undertake in your daily life. This shift increases the amount of time you spend “practicing” walking, relying upon the skill more frequently in your daily life.

While the journey of relearning to walk after a stroke may seem arduous, several strategies show promise in mitigating neuroinflammation to facilitate a more rapid course of recovery. This may include pharmacological interventions, lifestyle modifications, and specific rehabilitation techniques.

Key to your recovery is a focus on managing brain inflammation to promote maximal neuroplasticity. By reducing the extent of chronic inflammation within the brain, we can more easily cross the learning barrier and design more impactful stroke rehabilitation exercises.