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HEADACHE & PAIN SYNDROMES

Central Pain Syndrome in Hyderabad: Burning Pain After Stroke or Spinal Injury — Recognised, Assessed, and Treated at KIMS

Expert assessment of post-stroke central pain (Dejerine-Roussy syndrome), spinal cord injury pain, MS pain, and syringomyelia- related central pain — with first-line amitriptyline and pregabalin, lamotrigine for refractory PSCP, neuromodulation (SCS, MCS, DBS, TMS), and psychological and rehabilitation support at KIMS Neuroscience, Secunderabad, Hyderabad.

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Central pain syndrome is a chronic pain condition arising from damage to the central nervous system — brain or spinal cord — rather than from a peripheral nerve or body tissue. The most common cause is stroke (post-stroke central pain in 8–10% of stroke survivors, also called Dejerine-Roussy syndrome when from the thalamus). The pain typically develops weeks to months after the CNS injury — not immediately. The clinical hallmark is the allodynia paradox: pain in an area of reduced sensation. The damaged spinothalamic pathways become hyperexcitable, generating pain signals spontaneously. Amitriptyline has the strongest evidence for post-stroke central pain. Lamotrigine has RCT evidence. MCS, DBS, and SCS are available at KIMS for refractory cases.

What it is: Pain from CNS damage (brain or spinal cord) — not from a peripheral nerve. Arises in areas corresponding to the damaged CNS region, often with co-existing sensory loss (anaesthesia dolorosa).
Most common cause: stroke: Post-stroke central pain (Dejerine-Roussy when thalamic) in 8–10% of stroke survivors. Onset weeks–months after stroke, not at the time. Thalamic strokes: contralateral burning face and arm; cold allodynia characteristic.
Spinal cord injury: Central pain in 60–80% of SCI patients. Below-level SCI pain: diffuse burning in entire area below injury, including areas with no sensation. Often more disabling than the paralysis itself.
MS pain: Demyelinating lesions in spinothalamic tract or thalamus. 25–50% of MS patients. Uhthoff phenomenon: pain worsened by heat (hot showers, exertion). Cooling measures and same neuropathic agents.
First-line at KIMS: Amitriptyline (strongest evidence for post-stroke pain) · Pregabalin/gabapentin · Lamotrigine (specific RCT evidence for PSCP, titrate slowly) · Duloxetine when TCAs not tolerated.
Refractory options at KIMS: Ketamine infusions (NMDA) · Repetitive TMS over motor cortex · Motor cortex stimulation (MCS, surgical epidural electrode) · DBS · SCS for SCI central pain. Realistic goal: 30–50% reduction allowing function.
Contact KIMS: 040-44885000 · Stroke pain assessment · SCI pain pathway · MS pain · Syringomyelia neurosurgical coordination · Emergency: 040-46324365

Fact	Details
Definition	Pain arising from CNS damage (brain or spinal cord) · Not peripheral nerve or tissue injury · Allodynia paradox: pain in an area of reduced sensation
Post-stroke (Dejerine-Roussy)	8–10% of stroke survivors · Onset 1–6 months post-stroke · Burning, aching, shooting · Thalamic stroke = contralateral face and arm with cold allodynia
SCI central pain	60–80% of SCI patients · At-level (severe burning, stabbing) and below-level (diffuse burning in entire area below injury) · Among most refractory neuropathic pain
MS central pain	25–50% of MS · Demyelinating plaques in spinothalamic tract · Uhthoff phenomenon: pain worsens with heat · Cooling + neuropathic agents at KIMS
First-line medications	Amitriptyline (strongest PSCP evidence) · Pregabalin/gabapentin · Lamotrigine (RCT evidence in PSCP) · Duloxetine (when TCAs not tolerated)
Neuromodulation at KIMS	TMS (non-invasive, short-term) · Motor cortex stimulation (MCS) · DBS · SCS (for SCI central pain) · Ketamine infusions for central sensitisation
Prognosis	Complete relief often not achievable · Realistic goal: 30–50% reduction in intensity that allows return to function · Multidisciplinary approach essential

About This Condition

Central Pain Syndrome at a Glance

The essential facts that shape how central pain syndrome is recognised, attributed, and managed at KIMS — from its origin in CNS rather than peripheral injury, through stroke as the most common cause, to the allodynia paradox that distinguishes it from peripheral neuropathic pain.

What it is

A chronic pain condition arising from damage to, or dysfunction of, the central nervous system (brain or spinal cord) — rather than from injury to a peripheral nerve or body tissue. Central pain can follow stroke, spinal cord injury, multiple sclerosis, traumatic brain injury, syringomyelia, or other CNS lesions. The pain arises in areas of the body that correspond to the damaged CNS region, often with co-existing sensory loss (anaesthesia dolorosa — pain in a numb area).

The most common cause: stroke

Post-stroke central pain (PSCP) — also called Dejerine-Roussy syndrome when from thalamic involvement — occurs in approximately 8–10% of stroke survivors. It typically develops weeks to months after the stroke, not immediately. The pain is usually described as constant burning, aching, or stabbing in the hemiparetic limbs, face, or trunk. It is frequently undertreated in India because it develops after the acute stroke phase has passed and rehabilitation attention has moved on.

Other causes

Spinal cord injury (SCI): pain develops in approximately 60–80% of SCI patients, both at and below the injury level. MS: central pain in approximately 25–50% of MS patients. Traumatic brain injury. Syringomyelia. Cervical myelopathy (post-decompressive central pain). Any CNS lesion affecting the spinothalamic tract (pain and temperature pathways) is particularly associated with central pain.

The allodynia paradox

Central pain is characterised by the paradox of pain with sensory loss — the patient has reduced sensation in the painful area but burning or aching pain that can be provoked by the lightest touch (allodynia), cold stimuli, or emotional stress. This paradox is the clinical hallmark and distinguishes central pain from peripheral neuropathic pain.

Appointment

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About This Condition

The Pain That Arrived Three Months After the Stroke

A 67-year-old man in Hyderabad had a right thalamic ischaemic stroke 4 months ago. He recovered reasonably well — mild left arm weakness and some sensory change, but walking independently. His family brings him to KIMS because of a new complaint that has developed over the past 6 weeks: a constant burning sensation in his left arm and left side of his face, rated 6–7/10 continuously, worse at night and when the arm is touched or exposed to cold water. He describes it as “fire under the skin.” His left arm is numb to light touch, but paradoxically, the lightest touch causes the burning to flare severely.

At KIMS, this is recognised immediately as post-stroke central pain — specifically thalamic pain (Dejerine-Roussy syndrome), arising from the thalamic lesion that disrupted the spinothalamic pain-processing circuitry. The onset weeks after the stroke (not at the time of the stroke) is characteristic — central pain develops as the CNS reorganises following the injury, typically within 1–6 months of stroke.

Treatment is started at KIMS: amitriptyline 25mg at night (most evidence-based agent for post-stroke central pain); pregabalin 75mg twice daily (added if amitriptyline provides partial relief); and referral to the KIMS pain psychologist for the significant depression that accompanies chronic post-stroke pain.

Central pain is one of the most underrecognised consequences of stroke in India. The acute stroke is managed, rehabilitation begins, and then, weeks later, severe burning pain emerges — frequently attributed to musculoskeletal causes or inadequately treated. At KIMS, any stroke patient who develops new pain weeks to months after their stroke is assessed specifically for central pain syndrome.

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Speak directly with our central pain specialist team — neurology, pain medicine, neurosurgery (DBS / MCS / craniocervical decompression), and rehabilitation coordinated under one roof. No referral required. Monday to Saturday.

040-44885000Emergency line: 040-46324365

Recognising Central Pain

Causes and Clinical Presentations of Central Pain

Central pain is driven by damage to specific CNS structures — the thalamus and spinothalamic tract after stroke, the spinal cord after injury, demyelinating lesions in MS, and the expanding syrinx of syringomyelia. Each cause has a characteristic distribution and clinical presentation that is specifically assessed at KIMS.

Post-stroke central pain — the most common

Occurs in approximately 8–10% of stroke survivors. Most commonly from strokes involving the thalamus, thalamocortical pathways, or the spinothalamic tract in the brainstem or cortex. Onset typically 1 to 6 months after stroke. Described as burning, aching, shooting, or pressing. Always in the territory corresponding to the stroke — contralateral hemiparesis and hemibody pain in thalamic strokes; face and arm in lateral medullary (Wallenberg) strokes. Allodynia from cold stimuli is particularly characteristic of thalamic pain.

Spinal cord injury pain — at-level and below-level

Central pain develops in approximately 60–80% of spinal cord injury patients. At-level pain: at or within a few segments of the injury level — often severe burning and stabbing. Below-level pain: diffuse burning or aching in the entire area below the injury, including areas that are completely denervated. Below-level SCI pain is among the most severe and refractory forms of central pain, significantly impairing quality of life and rehabilitation participation. The pain persists even in complete injuries where no sensation is transmitted through the damaged cord.

Multiple sclerosis pain

Central pain in MS arises from demyelinating lesions in the spinothalamic tract or thalamus. Affects approximately 25–50% of MS patients and is one of the most common sources of severe disability in MS. Lhermitte’s sign (electric-shock sensation down the spine on neck flexion) is a characteristic MS symptom from posterior column demyelination. Trigeminal neuralgia in MS patients arises from a demyelinating plaque at the trigeminal root entry zone. Chronic burning pain in MS limbs is treated with the same agents as other central pain syndromes.

Syringomyelia

A fluid-filled cavity (syrinx) within the spinal cord, most commonly from Chiari malformation or a previous spinal cord injury. Syrinx expansion progressively damages the central cord — the crossing spinothalamic fibres are affected first, producing a "cape-like" distribution of pain and temperature loss across the shoulders and upper arms, with burning pain in that distribution. Surgical management of the underlying Chiari malformation or syrinx drainage at KIMS is coordinated with the neurosurgical team.

Treatment

Treatment at KIMS — Pharmacological First-Line, Selective Opioid Use, Neuromodulation for Refractory Cases, and Psychological Support

Pharmacological Treatment

Pharmacological Treatment — Antidepressants First

Amitriptyline has the strongest evidence for post-stroke central pain of any agent. Starting at 10–25mg at night, titrated to 50–75mg if tolerated. Acts by enhancing descending noradrenergic and serotonergic pain inhibition. Also improves sleep and mood, which are significantly affected in central pain patients. In older adults or those with cardiac disease: nortriptyline or duloxetine preferred.

Pregabalin 150–600mg/day or gabapentin 900–3,600mg/day: second-line or add-on to amitriptyline. Particularly effective for the allodynia and shooting pain components of central pain. Combination of amitriptyline and pregabalin is commonly required at KIMS for adequate central pain control.

Lamotrigine 200–400mg/day: has specific evidence for post-stroke central pain (one of few agents shown in RCT to be effective). Requires very slow titration to avoid Stevens-Johnson syndrome risk.

Opioids — Limited Role

Opioids — Carefully Considered, Not First-Line

Opioids have a limited and carefully considered role in central pain. Tramadol (weak mu-opioid and SNRI mechanism) has some evidence for central neuropathic pain.

Strong opioids are rarely the right answer for chronic central pain — they carry tolerance, dependence, and cognitive side-effect risks that significantly impair the stroke or SCI rehabilitation process. At KIMS, opioids are not used as first-line therapy for central pain.

Psychological & Rehabilitation

Psychological and Rehabilitation Interventions

Depression, anxiety, and sleep disruption are near-universal co-morbidities in central pain syndrome and must be treated alongside the pain itself.

CBT for chronic pain is the most evidence-based psychological intervention. Graded activity and occupational therapy adapted for the specific CNS injury (stroke, SCI). Hydrotherapy for pain-limited movement. Sleep management with melatonin or low-dose amitriptyline.

Neuromodulation — SCS

Spinal Cord Stimulation (SCS)

Evidence for SCI-related central pain and for post- stroke central pain in some studies. Particularly effective for the below-level burning pain of SCI. KIMS provides SCS for eligible patients.

Neuromodulation — MCS

Motor Cortex Stimulation (MCS)

Surgically placed epidural electrode over the motor cortex, which modulates thalamic pain circuits via descending inhibitory pathways. Evidence for post- stroke thalamic pain that has failed pharmacological management. Requires neurosurgical expertise. Discussed at KIMS for severe refractory post-stroke pain.

Neuromodulation — DBS

Deep Brain Stimulation (DBS)

Stimulation of the periaqueductal grey or sensory thalamus for refractory central pain. Performed in specialist neurosurgical centres. the KIMS Neuroscience team's extensive DBS experience at KIMS is relevant for this indication.

Neuromodulation — TMS

Transcranial Magnetic Stimulation (TMS)

Repetitive TMS over the motor cortex has evidence for short-term reduction in central neuropathic pain. Non- invasive, available at KIMS for eligible patients as an adjunctive treatment.

Related Conditions

Central Pain Syndrome belongs to the family of headache and pain syndromes evaluated and managed at KIMS Neuroscience:

Complex Regional Pain Syndrome Trigeminal Neuralgia Paroxysmal Hemicrania Headache & Pain Syndromes (Master)

FAQs

Frequently Asked Questions

Yes — and the delayed onset is characteristic of central pain syndrome. Post-stroke central pain typically develops weeks to months after the stroke, not at the time of the stroke. The pain arises as the central nervous system reorganises following the injury — the damaged spinothalamic pathways become hyperexcitable and generate spontaneous pain signals. The thalamus is the most common stroke location to produce this — thalamic pain (Dejerine-Roussy syndrome) produces burning pain in the contralateral face and arm, often with extreme sensitivity to cold (cold allodynia). At KIMS, any stroke patient with new pain developing in the weeks after their stroke is assessed for central pain syndrome. The most evidence-based treatment is amitriptyline. Please call 040-44885000.

This is the paradox of central pain: the areas below the injury level can produce burning, aching pain even though no normal sensation can pass through the damaged spinal cord. The pain arises not from the body part itself, but from the damaged and reorganised neural circuits in the spinal cord and brain above the injury. The cord above the injury becomes hyperexcitable — it generates pain signals spontaneously without any peripheral input. This below-level SCI pain is one of the most severe forms of neuropathic pain and is rated as the most distressing consequence of SCI by many patients, often more disabling than the paralysis itself. Pregabalin, gabapentin, and amitriptyline are the first-line medications. Spinal cord stimulation has evidence for SCI central pain. Call 040-44885000.

Partial relief on amitriptyline and pregabalin combined is the common scenario for post-stroke central pain — it is a difficult pain syndrome and complete relief is often not achievable. Options at KIMS for the next step: adding lamotrigine (which has specific RCT evidence for post-stroke central pain, titrated slowly); duloxetine if amitriptyline causes excessive side effects; low-dose ketamine infusions for central sensitisation; repetitive TMS over the motor cortex (non-invasive, short-term benefit, can be repeated); and for the most refractory cases, motor cortex stimulation (surgically implanted epidural electrode) or deep brain stimulation. The realistic goal is meaningful reduction in pain intensity (30–50% reduction allows functional improvement) rather than complete elimination. Please call 040-44885000 for a specialist review.

What you are describing is Uhthoff’s phenomenon — worsening of MS symptoms, including pain, with heat. In MS, demyelinated nerve fibres conduct electrical signals less reliably than normal, and heat further reduces conduction reliability. This applies to pain-transmitting fibres as much as to motor fibres. Central pain in MS is therefore frequently heat-sensitive, worsening in hot weather, with exercise, or in a hot bath. Management: cool showers rather than hot; cooling vests or neck wraps during exertion; avoiding unnecessary heat exposure during flares. The pharmacological management remains the same: amitriptyline, pregabalin, or lamotrigine for the central pain itself, with consideration of disease-modifying therapy for the underlying MS. Please call 040-44885000.

Syringomyelia causes central pain by the expanding fluid cavity in the spinal cord damaging the crossing spinothalamic fibres. The pain distribution is characteristically cape-like: across the shoulders, upper arms, and chest, in a shawl pattern. Surgery addresses the underlying cause: if the syrinx is associated with a Chiari malformation, posterior fossa decompression (craniocervical decompression, which The KIMS Neuroscience team performs at KIMS) can allow the syrinx to drain and stabilise, halting or reversing progression. If the syrinx is from a different cause (post-traumatic, secondary to a tumour), syringosubarachnoid or syringopleural shunting may be performed. Surgery does not always resolve the existing pain — it prevents further progression. Pharmacological central pain treatment (pregabalin, amitriptyline) addresses the pain during and after surgical management. Please call 040-44885000 for a KIMS assessment.

Burning, aching, or stabbing pain that arrived weeks or months after a stroke, spinal cord injury, MS, or syringomyelia. Pain in a numb area. Light touch that triggers severe burning. Central pain syndrome is a real, diagnosable, and treatable neurological pain condition — not a psychological consequence of the underlying CNS injury.

At KIMS Neuroscience, Secunderabad, Hyderabad, central pain syndrome is assessed as a specific neurological pain diagnosis — not dismissed as a psychological consequence of stroke or injury. Amitriptyline and pregabalin are the first-line treatments. Lamotrigine, TMS, SCS, and DBS are available for refractory central pain. Call 040-44885000.

040-44885000

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