Central Post-Stroke Pain: The Burning Pain That Comes From the Brain, Not the Body

Central post-stroke pain is a nerve pain caused by the stroke damaging the brain’s own pathways for sensation, so that the weak side burns, freezes or aches even though the limb itself is not injured. It usually begins within 1 to 3 months of the stroke, and estimates of how many survivors develop it range from about 1% to 35%, depending on how studies define and measure it¹.

I did not get this one, and I want to be clear about that from the start. I had the shoulder, the fatigue, the arm that would not do as it was told. But a man in my stroke group, a retired electrician who had had his stroke a few months before mine, described his left leg as “standing in a bucket of ice that is also on fire”, and for the best part of a year nobody could tell him why. His scans had not changed. His leg looked fine. He was told, more than once, that it would settle. This article is the explanation he wanted and did not get, and it sits inside the wider picture of neuro-rehabilitation.

What central post-stroke pain actually is

Central post-stroke pain (CPSP) is a type of neuropathic pain: pain produced by damage to the nervous system itself, here the parts of the brain that carry and interpret pain and temperature, rather than by injury to skin, muscle or joint. The thalamus, a relay station deep in the brain that passes sensory information on to the cortex, is the classic site, but strokes outside the thalamus can cause it too¹.

The simplest way I have found to think about it is a fire alarm with a damaged wire. Nothing is burning, but the system that is supposed to report burning has been disrupted and now sends the signal anyway, or turns ordinary signals into alarms. That is why the pain is real, sometimes severe, and yet nothing shows up when a doctor examines the arm or leg. Clinicians group central pain with the other kinds of pain that can follow a stroke, such as shoulder pain, pain linked to spasticity and headache, and the commonest combinations are central pain with spasticity pain or with shoulder pain¹.

What it feels like

The pain is usually described as burning, freezing, pricking, aching or squeezing, felt on the side of the body affected by the stroke, and it often sits alongside numbness or an odd, altered feeling in the same area. In one review of the evidence, abnormal sensations were reported by about 85% of people with CPSP, and burning by around 82% in one of the studies it summarised¹.

Two features help tell it apart from other pains. The first is that it often comes with a sensory change: the skin can feel numb, wooden or “not mine”, and yet hurt. The second is allodynia, where things that should not hurt do. A bedsheet across the foot, a shirt sleeve, a draught, a cold glass in the hand. Cold is a particularly common trigger; in one study summarised in the same review, almost two thirds of people with CPSP had pain brought on by cold¹. My friend could not sleep with the duvet touching his leg and ended up building a frame at the foot of the bed out of a clothes airer.

Many people also notice that the pain is worse when they are tired, stressed or low, which fits what we know about how the brain amplifies or dampens pain signals. That is not the same as saying it is “in your head”. It is in your head, in the literal sense that the damaged wiring is there, and it is still a physical problem.

When it starts and who gets it

CPSP most often appears within about 1 to 3 months after the stroke, but it can start within the first month or develop a year or more later, which is one reason it is easily missed. It is more common in the months after hospital than in the first days, so the people who notice it first are usually the survivor and the family at home, not the ward team¹.

The wide range in the figures, from about 1% to 35%, tells you more about how hard it is to measure than about any one person’s risk. Studies use different definitions, follow people for different lengths of time and include different kinds of stroke¹. What the evidence does agree on is that strokes affecting the sensory pathways, especially in or near the thalamus, carry a higher risk. If you already have altered sensation on the weak side, it is worth knowing CPSP exists so that a new burning or freezing pain does not get waved away.

Why it gets missed

Central pain is often overlooked because the person looks well, the scan has not changed, the limb examines normally, and the pain can start weeks after anyone was checking. It also overlaps with other common problems after a stroke, such as shoulder pain after stroke and the aching that comes with spasticity, and a person can have more than one at once.

There is a communication problem layered on top. Some survivors have aphasia and cannot easily describe the quality of a pain; some have changes in attention or memory; and some, like a lot of men I met, simply say “it’s fine” because complaining feels like failing at recovery. NICE’s stroke rehabilitation guideline lists pain among the things a holistic assessment after stroke should cover, and points to its separate neuropathic pain guidance for managing nerve pain². In practice, that assessment is far better if you bring words to it. “Burning on the outside of my left calf, worse at night, and the sheet touching it makes it jump” gives a doctor far more to work with than “my leg’s bad”.

How it is treated

CPSP is treated mainly with medicines that act on nerve pain rather than ordinary painkillers, chosen and adjusted by a doctor, and usually alongside non-drug approaches; the aim is to bring the pain down to a level you can live and rehabilitate with, since a complete cure is often not possible. Paracetamol and anti-inflammatory drugs target tissue damage and inflammation, which is not what is driving central pain, so they tend to help little¹.

The medicines most often used are from the families that treat other nerve pain. The review of the evidence describes amitriptyline, an older antidepressant used at low doses for pain, as the main first-line option, with lamotrigine and the gabapentinoids (gabapentin and pregabalin) as other choices, and notes that the research base is small and the results variable¹. I am deliberately not giving doses here. These drugs interact with others that many stroke survivors take, can cause drowsiness and dizziness that matter a great deal if your balance is already shaky, and need to be started and changed by a doctor who knows your whole picture.

For people whose pain does not respond to medicines, specialist pain services sometimes use other approaches. The evidence review lists exercise therapies, TENS and acupuncture, which tend to give temporary relief, mirror therapy, and, in specialist centres, forms of brain stimulation such as repetitive transcranial magnetic stimulation¹. None of these is a guaranteed fix, and some are not widely available, but they are worth asking about if the standard route has failed.

Living with it during rehabilitation

Central pain and rehabilitation affect each other: pain disrupts sleep, mood and the ability to practise, and staying active, pacing and treating low mood can in turn change how much the pain dominates. NICE asks for rehabilitation sessions to be tailored to ongoing medical needs such as post-stroke fatigue and to take account of the person’s mood on the day², and pain that wrecks sleep and concentration belongs in the same conversation, managed alongside therapy rather than after it.

What helped my friend most, once he finally had a name for it, was the combination rather than any single thing. A medicine that took the edge off at night, so he slept. A physiotherapist who changed his sessions to the mornings, before the pain built up. A rule about keeping the leg warm, because cold was his worst trigger. And treatment for the low mood that had crept in during the months when nobody believed him; post-stroke depression is common enough on its own, and chronic pain makes it more likely. He still has the pain. He describes it now as “background”, which from him is a considerable improvement.

If you recognise this, the next step is not more reading. It is an appointment where you describe the pain precisely and ask, directly, whether it could be central post-stroke pain. What treatment suits you is a question for your own doctor and rehabilitation team, who can examine you and know the rest of your medical history. A website can only help you ask the right question.