What is Thalamic Pain Syndrome?

Thalamic pain syndrome is an unfortunate outcome following a cerebrovascular accident (CVA) to the thalamus, usually from a stroke. It is centralized, neuropathic pain that is associated with temperature changes. Patients experience extreme levels of pain to typically non-painful stimuli (3). It used to be known as Dejerine-Roussy syndrome, but is more commonly known as central post-stroke pain. This term encompasses all types of pain syndromes following a stroke and are not specific to a thalamic event.

How Common is Thalamic Pain Syndrome?

There are an estimated 56,000 cases of central post-stroke pain that occur annually, 20-33% of which are due to thalamic stroke. Despite being common, diagnosis is can be challenging because thalamic pain syndrome onset may occur anywhere from months to years after the event. Majority of patients develop pain within a month of their stroke, an estimated 18% within the first 6 months and another 18% develop pain at 6 months post-CVA (19). 

What are the Symptoms of Thalamic Pain Syndrome?

Tissue damage is an appropriate reason for the brain to recognize a stimulus as painful. Sensations of touch and mild temperature changes are not, however they become painful to a person with thalamic pain syndrome. Inappropriate painful responses to normally non-painful stimuli is called allodynia. Potentially painful stimuli being worse than expected is called hyperalgesia. Both are present in thalamic pain syndrome (3). Thalamic pain syndrome is also correlated with mood changes, fatigue, sleep disturbances, pain catastrophizing, and cognitive changes. Depending on the area affected by the stroke, muscle strength, cranial nerves, balance and speech may also be affected (20). 


What Happens in the Brain During Thalamic Pain Syndrome?

The thalamus is a deep brain structure that acts as the relay station for all sensory information within the brain. When we are exposed to sensory information from the environment, this affects our peripheral nervous system, which conducts information into the central nervous system (CNS). As sensory input enters the CNS, it is projected to the thalamus through the spinothalamic tract. The thalamus receives this input, integrates it with other sensory input, and relays the signal to the appropriate areas of the cerebral cortex where it can be interpreted. 


Thalamic function is compromised in thalamic pain syndrome. The thalamus is usually injured by a stroke occurring in the area. It may be caused by an ischemic stroke or a hemorrhagic stroke. A stroke occurs when a blood vessel in the brain is either blocked or ruptured. Both of these will cause the parts of the brain that rely on blood from that blood vessel to become damaged or die.

Central post-stroke pain can develop from a lesion anywhere along the course of the spinothalamic tract (21).

There is a thalamus on the right and left sides of the brain. An injury to one side of the thalamus causes sensory dysfunction on the opposite side of the body and face (3). 

The ventral posterolateral nucleus of the thalamus has an intrinsic network of GABAergic neurons, which causes the intrinsic inhibition of ventral posterolateral nucleus. The VPL is a primary relay for sensation from the body, including for pain information. Stroke affecting the lateral thalamus causes loss of this VPL inhibition by decreasing activation of the thalamic nucleus, which in turn causes the activation of cortical areas resulting in pain. The slow return of neuronal function after stroke or trauma explains the timing of the pain. The disinhibition of temperature-sensing fibers (primarily those that sense cold) is likely be the cause of painful perception of cold sensations, known as allodynia (19). 

Thalamic pain syndrome is a type of centralized pain, meaning the dysfunction is occurring in the CNS. Loss of pain modulation mechanisms from damage to the thalamus, spinothalamic tract, or parietal lobe can cause severe windup in the mechanisms associated with the perception of pain, as mechanisms that would normally inhibit pain are lost (22).

How is Thalamic Pain Syndrome Diagnosed?

A physical and neurological examination can reveal signs associated with thalamic pain syndrome and other regions affected by a stroke. Diagnostic criteria for thalamic pain syndrome include facial and head pain within 6 months of an ischemic or hemorrhagic stroke, and an MRI demonstrating a vascular lesion in the appropriate region of the brain. The pain cannot be explained by another mechanism (23).

How is Thalamic Pain Syndrome Generally Treated?

Thalamic pain syndrome is generally treated as a chronic pain and centralized pain case, with analgesic medication (3). Other therapies usually considered include physical therapy, deep brain stimulation, radiation therapy and cognitive-behavioral therapy. 

The residual motor, cognitive, and neurologic problems from stroke are usually addressed by physical, occupational, and speech therapy. While these are undoubtedly helpful, as recovery slows most therapy programs shift focus toward teaching the individual to compensate for their impaired function, rather than attempting to restore the functions and capacities that have been lost. 

 

How is the NeuroRescue Program Different?

One of the fundamental problems seen in stroke is what is called a diaschisis. Neurons need 3 main things to survive: glucose, oxygen, and activation. Neurons need to be continuously stimulated in order for them to continue replicating all of the protein and cellular components they need to survive and keep firing efficiently. When someone suffers a stroke, neurons that are supplied by the involved blood vessel are deprived of glucose and oxygen. Unfortunately, most of these will die off unless blood flow is rapidly restored. 

There is nothing that we or anyone else can do to bring back the neurons that have been lost. However, the dead neurons are usually not entirely responsible for the symptoms seen after a stroke.  

This is because of the diaschisis phenomenon. Each neuron receives activation signals from an average of 10,000 other neurons.  This input will either excite or inhibit the neuron, but either way, the presence of this activation causes it to keep replicating protein and stay healthy. If the neuron is outside of the vascular distribution of a stroke, it may still be affected if enough of the neurons that activate it are lost. When neurons die in a stroke, the neurons that they stimulate, even though they have a different blood supply and are not directly affected by the stroke, will undergo diaschisis and start to break down. They will lose endurance, will not be able to sustain high rates of firing, and will tend to fatigue and fail. This will be the case even though they still have a normal supply of glucose and oxygen. 

If these remaining fragile neurons affected by diaschisis are not properly activated, they will ultimately die off. If they are overstimulated and caused to fire at a rate that they cannot withstand, they will also be lost (24). 

However, if another neuron or pathway that supplies input to the fragile cells can be found, and these can be stimulated to activate the damaged neurons at a rate that they can withstand, they can be used to rebuild the function in the injured cells.

This is exactly the basis of all of our NeuroRescue stroke rehabilitation therapies. We use cutting edge neurodiagnostic technologies and examination procedures to not only identify what areas of your system are damaged, but also what systems are still present but impacted by diaschisis. We identify pathways that we can harness to rebuild the function of the fragile systems. We determine the exact frequency and intensity of stimulation of these pathways that leads to positive plastic changes without overstimulation. We then employ several of a vast array of therapies, chosen specifically for the unique needs of your system, to maximize your functional recovery.

Our therapies are constantly evolving, and are on the cutting edge of neurorehabilitation. Everything we do for rehabilitation is supported by the latest neuroscience research. 

We use a wide array of neurostimulation strategies in restoring function after a stroke. Electrical therapies can be harnessed to stimulate neurons in the brain through the peripheral nervous system. There are many different kinds of currents and applications that we employ, but these are collectively known as repetitive peripheral sensory stimulation. RPSS has been demonstrated to be effective in restoring function in patients suffering from stroke hemiparesis (5).

Photobiomodulation is another form of neurostimulation, using low level laser and LED light frequencies to help rebuild endurance and metabolic function in neurons after stroke. We use several different types of laser and LED systems for stroke rehabilitation. Research shows that these can be very helpful to improve function in strokes and vascular injuries (6,7).

Hyperbaric oxygen therapy can prove useful in cases of stroke. Cells that have been deprived of oxygen for a time but not lost have been shown to improve in function when patients receive hyperbaric (above normal atmospheric pressure) oxygen treatment. Hyperbaric therapy can be an important adjunct to our therapies, and allows us to rehabilitate patients faster and more effectively without fatigue (8).

We regularly use Transcranial Magnetic Stimulation, which is an extremely effective form of neurostimulation in the treatment of stroke. Transcranial Magnetic Stimulation uses an MRI-strength magnet to apply a focused beam of electromagnetic energy through the skull and directly to the injured areas of the brain. This treatment is safe, comfortable, with minimal rare side effects. More importantly, it is extremely effective for helping people manage chronic pain and restore motor function after stroke (9,10). It has been demonstrated as helpful specifically for thalamic pain syndrome in the literature as well (15). We have such great success with our TMS treatment that we installed our second TMS unit this year. We use TMS in conjunction with our other therapies discussed here to significantly improve our patient outcomes. 

It is extremely common that people can develop balance difficulties after suffering a stroke. This greatly increases the risk of injury from falls, including further traumatic brain injuries. We go to great lengths to ensure that all of our patients have their fall risk reduced through precise vestibular therapy, which is part of every NeuroRescue program. Vestibular therapy has been shown to be very effective to improve balance after a stroke (11).

Vision can very commonly be impaired after suffering a stroke. It is common for people to develop difficulty visually mapping their world, holding their eyes still on targets, following moving objects, and processing complicated visual environments. In many cases, an entire visual field can be lost through damage to visual pathways. We use several types of visual exercises and rehabilitation to help resolve these difficulties, tailored to the unique needs of the patient. The effectiveness of visual therapies has solid support in neuroscience literature (12). 

Specific types of eye movement exercises have been shown to be helpful in not only restoring visual function, but also in restoration of cognitive and executive function. Specific eye movement therapies have been shown help with cognitive retraining [13], and have demonstrated significant improvement in brainwaves and reduction in symptom scales after strokes (14).

We also use a number of unique therapies to help your brain remap your body and restore movement patterns after strokes. Sometimes the best way to restore appropriate sensation is by using a technique called mirror therapy (MT). MT provides different visual representations of the impaired limb by mirroring the good limb while engaging in sensory and movement exercises (16). Mirror therapy is particularly helpful when employed in a virtual reality environment (17), and we regularly see rapid changes in sensory and motor function when using our Virtualis VR system. And physical exercises and soft tissue rehabilitation techniques can be helpful once central neurological function has been addressed. In particular, joint manipulation and mobilization can lead to significant improvement in pain perception in chronic post-stroke pain (18).

How Does the NeuroRescue Program Work?

We design your unique NeuroRescue Program to be among the most comprehensive diagnostic and therapeutic protocols available today. We create individual NeuroRescue Programs based on a comprehensive analysis of every relevant neurological system and pathway, using gold-standard, cutting edge neurodiagnostic technologies and examination procedures and state-of-the-art therapies. 

 

We begin with your Discovery Day, wherein we perform a comprehensive history of not only your condition, but also of your life on a timeline. This allows us to dive deeply into your case and see all of the factors that led to where you are now. It helps us uncover hidden problems and associated conditions that may be making it difficult for you to move your recovery forward.

 

Our examination allows us to identify the areas and pathways of your brain that have been directly and indirectly affected by your stroke. We do this by precisely quantifying the function of your visual, vestibular, and proprioceptive systems through computerized analysis of your eye movements, your inner ear reflexes, and your balance in a host of different sensory conditions. 

 

We employ technologies including Videooculography and Saccadometry to measure several classes of eye movements. We use Video Head Impulse Testing to measure the function of your inner ear, and Computerized Dynamic Posturography to assess your balance in different sensory conditions.

 

We use NeuroSensoryMotor Integration testing to evaluate hand-eye coordination and cognition, and Virtualis testing to assess dynamic eye tracking and perception of vertical in a virtual reality environment. 

 

We combine all of this with a comprehensive physical and neurological examination of your sensory, motor, autonomic, and cognitive systems. We review any relevant laboratory testing, radiological imaging, and prior neurodiagnostic testing, and integrate that information with our findings.

 

We use this information to identify which parts of your nervous system are working properly, which systems are struggling, and the precise point at which your systems fatigue. 

 

We can then design a NeuroRescue Program that is unique and specific to your brain, and yours alone. Your NeuroRescue Program works to rejuvenate and reintegrate the damaged neurons and pathways in your central nervous system. It works to improve energy, endurance, and functional capacity within your involved fragile systems. 

 

We use our technologies and procedures to not only see what we need to address, but also when it is time to stop and let you rest. We address your impaired neurological function from multiple angles of therapy, and provide metabolic support to improve neurological recovery. 

 

While we cannot bring back neurons that have been lost, your NeuroRescue Program allows us to take the pathways that remain and maximize their efficiency and endurance. And by focusing on the integration of systems, we can do more than just get pathways working better, we can get them working together again. This gives us our best opportunity to get your pain under control and return you to living a healthy, vibrant, and fulfilling life. 

 

Your Next Best Step:

Living with thalamic pain syndrome is challenging, but there is hope for recovery and remission.  To see if the NeuroRescue Program is right for you, contact one of our patient care coordinators to schedule your Discovery Day.

And remember, it’s never too late to start getting better.


References:

1. https://www.stroke.org/en/about-stroke/stroke-symptoms

2. https://www.cdc.gov/stroke/types_of_stroke.htm

3. https://www.ncbi.nlm.nih.gov/books/NBK554490/#:~:text=The%20prevalence%20of%20thalamic%20pain,stroke%2C%20diagnosis%20is%20often%20difficult

4. https://en.wikipedia.org/wiki/Stroke#Ischemic_2 

5. https://pubmed.ncbi.nlm.nih.gov/32269549/

6. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5723531/

7. https://pubmed.ncbi.nlm.nih.gov/29131369/

8. https://pubmed.ncbi.nlm.nih.gov/27132523/

9. https://pubmed.ncbi.nlm.nih.gov/27132523/

10. https://pubmed.ncbi.nlm.nih.gov/29111342/

11. https://pubmed.ncbi.nlm.nih.gov/30040765/

12. https://pubmed.ncbi.nlm.nih.gov/29792389/

13. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4700208/

14. https://pubmed.ncbi.nlm.nih.gov/26834698/

15. https://pubmed.ncbi.nlm.nih.gov/31853195/

16. https://pubmed.ncbi.nlm.nih.gov/29492272/

17. https://pubmed.ncbi.nlm.nih.gov/29156493/

18. https://pubmed.ncbi.nlm.nih.gov/29557687/ 

19. https://www.ncbi.nlm.nih.gov/books/NBK519047/

20. https://www.ncbi.nlm.nih.gov/books/NBK554490/

21. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6112889/

22. https://pubmed.ncbi.nlm.nih.gov/2919091/

23. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7812148/

24. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6728715/

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