22. Chronic pain / muscle tension in ADHD

Author: Ulrich Brennecke
Review (March 2024): Dipl.-Psych. Waldemar Zdero
Completely revised: December 2024

• 1. Chronic pain and ADHD
• 2. Axial pain and ADHD
• 3. Increased muscle tension in ADHD
• 4. Medication for chronic pain
  • 4.1. ADHD medication reduces chronic pain associated with ADHD
  • 4.2. Other medications for chronic pain
• 5. Causal pathways for chronic pain, increased muscle tone and fibromyalgia

1. Chronic pain and ADHD¶

People with ADHD often show increased sensitivity to pain. High ADHD scores correlated with increased pain¹
ADHD also correlates with chronic pain.²³ Children with ADHD had a 45% increased risk of weekly pain. Hyperactivity/impulsivity had a 133% increased risk of frequent pain, inattention a 17% increased risk. Multiple pains were more common in girls with hyperactivity than in boys with hyperactivity (51.4% vs. 27.9%). 25% of girls with ADHD-C and 20% of boys with ADHD-C had weekly headaches and/or abdominal pain, compared with 11% to 13% of children without these symptoms (+127% to +53%).⁴
Children and adolescents suffer from chronic pain

• to 20 %⁵
• to 20.8 % (meta-analysis, k = 19, n = 1,043,878)⁶
  • Headache and skeletal muscle pain: 25.7 % (meta-analysis, k = 19, n = 1,043,878)⁶
  • Chronic pain and pain intensity in patients with ADHD are associated with muscular dysregulation.⁷
• The prevalence rates of chronic pain in children and adolescents in a meta-analysis varied considerably:⁸
  • Headaches: 8 % to 83 %
  • Abdominal pain: 4 % to 53 %
  • Back pain: 14 % to 24 %
  • Skeletal muscle pain: 4% to 40%
  • multiple pain: 4 % to 49 %
  • other pain: 5 % to 88 %.

Similar symptoms are increased sensitivity to stress and increased sensitivity to punishment. See also Emotional dysregulation.

Girls are more likely to have chronic pain than boys, except for back pain and skeletal muscle pain (meta-analysis, k = 19, n = 1,043,878).⁶
Of 100 women with ADHD or ASD, 76% reported chronic pain.⁹ Chronic widespread pain (CWP), the main symptom of fibromyalgia, was almost twice as common in ADHD (39%) as in ASD.
The most frequently mentioned painful areas of the body were

• Lower back (47 %)
• Neck (37 %)
• Shoulder (35 %)
• Head (32 %, related to ADHD)
• Stomach (30 %)
• Arms / hands (30 %)
• Upper back (27 %)
• Knee (27 %)
• Hip / thigh (18 %)
• Calves / feet (16 %)
• Breast (4 %)

ADHD correlates with an increased incidence of¹⁰

• Fibromyalgia¹¹
• chronic pain in the lower back¹²
• idiopathic orofacial pain ¹³
• chronic abdominal pain⁹
• Burning mouth syndrome
  • 92.2% of persons with ADHD showed ADHD¹⁴

Pain is associated with reduced tonic dopamine firing, which causes increased phasic dopamine firing in the nucleus accumbens.¹⁵ This is consistent with Grace’s model of decreased tonic and increased phasic dopamine firing in ADHD. See also Tonic and phasic dopamine in explanatory models for ADHD In the section Dopamine in the chapter Neurological aspects.
People with chronic pain show reduced responsiveness within the mesolimbic dopamine system to meaningful stimuli, reduced D2 receptor binding, reduced presynaptic dopamine activity in the striatum at rest and after an acute pain stimulus.¹⁶ In animals, chronic pain leads to decreased c-Fos activation in the VTA, decreased total dopamine levels and decreased D2 receptors in the striatum.¹⁶
Conversely, a reduction of dopamine in the brain by acute depletion of the dopamine precursors phenylalanine and tyrosine caused increased subjective pain sensitivity (the degree to which pain was perceived as unpleasant) without altering the sensory perception of pain.¹⁷
In 6-OHDA mice, in which dopamine synthesis is chemically damaged and which thus represent an ADHD animal model, an increased sensitivity to pain was found. The pain sensitivity was presumably mediated by α- and β-adrenergic and D2/D3 receptors. Atomoxetine¹⁸ such as MPH¹⁹ was able to reduce the increased pain sensitivity in ADHD.
Stimulation of the substantia nigra, one of the two most important sources of dopamine in the brain, causes pain relief by activating spinal cord neurons via dopaminergic signaling pathways.²⁰²¹²² Painful stimuli cause a release of dopamine in the dorsolateral striatum, which correlates with the subjective perception of pain intensity. The ventral striatum is also clearly associated with the emotional dimension of the human pain process and the expectation of pain.²³
Increased sensitivity to pain correlated with certain dopaminergic gene variants (DAT1 and MAO-A, but not DRD4).²⁴

In children with chronic pain (without headaches) an ADHD prevalence of 15 to 25 %, i.e. 2 to 5 times higher (meta-analysis).²⁵
72.5% of adults referred to a pain clinic for chronic pain and a probable somatic syndrome disorder met the diagnostic criteria for ADHD.²⁶ Of 60 adults with chronic non-specific lower back pain, 31.5% had ADHD.¹²
Psychiatric patients with chronic pain show a higher prevalence of ADHD than psychiatric patients without chronic pain.⁷
Children with ADHD showed a prevalence of chronic pain of up to 66% (at least weekly pain for more than 3 months). Stimulant treatment reduced the rate of chronic pain. Another study found a reduced perception of pain in adolescents with ADHD, which disappeared with stimulant treatment.²⁵
Of young women with ADHD and/or ASD, 76.6%⁹ and 75.9% reported chronic pain, respectively, compared to 45.7% of unaffected young women²⁷.
80% of the people with ADHD studied reported chronic pain.²⁸

A population study over 15 years found significantly higher rates of various pain conditions in children with ADHD prior to their ADHD diagnosis:²⁹

• Headaches (+ 16 %)
• Earache (+ 30 %)
• Sore throat (+ 8 %)
• Sprains and strains (+ 23 %)
• more frequent use of painkillers
  • Paracetamol (+ 19 %)
  • Ibuprofen (+ 37 %)

One study found ADHD in 25 of 30 patients with refractory orofacial pain (83.3%; women: 20).³⁰
ADHD was associated with a 32% increased risk of migraine, while the risk of tension headaches was unchanged.³¹³² Children with migraine had a 2.6-fold risk of ADHD, while the prevalence of migraine in children in general was 3.76%. Migraines correlated particularly with hyperactivity and impulsivity, not inattention.³³ Children with ADHD have a 2.6-fold risk of migraine in ADHD, whereas the prevalence of migraine in children in general was 9.9% in this study³²

In Parkinson’s disease, which is also characterized by dopamine deficiency, 30 to 50 % of people with ADHD suffer from increased sensitivity to pain.³⁴ This can be improved by dopaminergic medication³⁵, e.g. levodopa or deep brain stimulation.³⁶
Conversely, the perception of pain is reduced in schizophrenia, which is associated with increased dopamine levels.³⁷

2. Axial pain and ADHD¶

Chronic pain in patients with ADHD is characterized by widespread and axial pain that starts early. This “ADHD pain” is qualitatively different from chronic pain in patients without ADHD.⁷
Axial pain occurred in 86.6% of persons with ADHD, in 50% of those not diagnosed with ADHD, and in 21.4% of those who also did not have subclinical ADHD.
People with subclinical ADHD showed the same muscular dysregulation as people with ADHD.⁷
While ADHD is a predictor of “axial pain”, affective disorders, anxiety disorders or personality disorders were not.⁷

The axial muscles are:

• Head and neck muscles
• Spinal muscles
• Other trunk muscles
• Pelvic floor muscles

Axial muscles regulate and control posture and are constantly used to maintain the naturally unstable upright position. Muscular dysregulation has a significant impact here and could lead to high muscle tone with consequent widespread pain and lower back pain³⁸

• Erector spinae
• Latissimus dorsi
• Iliopsoas
  • connects the lumbar spine with the lower limbs
  • Iliopsoas spasms can increase lumbar lordosis and lumbar pain³⁹

Gene variants that correlate with neck or shoulder pain causally increase the risk of ADHD.⁴⁰

3. Increased muscle tension in ADHD¶

ADHD is often associated with increased muscle tension. This is not an expression of hyperactivity or a fundamental motor dysfunction. There are high-performance athletes with ADHD; they are unlikely to have severe motor dysfunction. Nevertheless, increased muscle tension can also be observed in them.

Muscle tension, especially in the shoulder/neck area, occurs much more frequently with ADHD.
An orthopaedist explained to us that during sleep, the muscles further away from the trunk (spine) relax first, while those at the spine relax last. These need undisturbed deep sleep in order to relax. Accordingly, muscle tension could also be a consequence of impaired sleep in ADHD.
One study found that computer work and sleep problems correlated with chronic shoulder and neck pain.⁴¹

MPH can help with increased muscle tension.⁴²
Our impression in the ADxS forum is that increased muscle tension is reported more frequently with lisdexamfetamine.

With regard to fibromyalgia, which is often associated with greatly increased muscle tension, helpful treatment with very low doses of naltrexone (0.5 to 4.5 mg instead of the usual 150 mg) has been reported. The treatment is said to be virtually free of side effects.^4344454647 Naltrexone is a long-acting competitive opioid antagonist that is also used to treat alcohol and opioid dependence. One person with ADHD told us that the low-dose naltrexone also helped with the ADHD symptoms.
Paracetamol was repeatedly mentioned as a treatment option.
Magnesium is also helpful.
Myotonolytics (e.g. methocarbamol, tolperisone, tetrazepam, flupirtine, tizanidine, baclofen, pridinol, eperisone or methocarbamol) have a muscle-relaxing effect by inhibiting polysynaptic reflex conduction in the spinal cord and in subcortical centers. However, they are less suitable for long-term use and have significant side effects. Tizanidine and cyclobenzaprine have a sedative effect and can help with existing sleep problems.⁴⁸ Methocarbamol and metaxalone are slightly less sedating, but probably also less effective. Dizziness and drowsiness are reported with all myotonolytics.

4. Medication for chronic pain¶

4.1. ADHD medication reduces chronic pain associated with ADHD¶

MPH can remedy the increased sensitivity to pain in people with ADHD.^4930135051
Atomoxetine^{5253 54} and guanfacine⁵⁵ have also been shown to reduce chronic pain in people with ADHD. Clonidine, like guanfacine an alpha-adrenoceptor agonist, is helpful for ADHD and chronic pain.
US President John F. Kennedy is said to have had ADHD.⁵⁶ Kennedy also suffered from chronic lower back pain, for which he successfully took amphetamine medication.⁵⁷

31.8% of patients with various types of chronic pain who were referred to a psychiatrist in a pain clinic were diagnosed with ADHD. 21 of them received ADHD medication (methylphenidate and/or atomoxetine). ADHD symptoms improved in 20 of the 21 (95.5%). In 14 out of 21 (66.7 %), their pain symptoms improved at the same time, on average by 4.6 points (64.7 %) on the Pain Numerical Rating Scale (NRS). Among the 7 medicated patients with persistent chronic non-specific lower back pain, the pain symptoms of all 7 (100 %) improved, on average by 4.3 points (65.3 %) on the NRS.⁵⁸

4.2. Other medications for chronic pain¶

Risperidone⁵³ and aripiprazole⁵⁹ are also said to be helpful for chronic pain.

Tricyclic antidepressants have long been the most important drugs for the treatment of chronic neuropathic pain, but have high side effects.⁶⁰ TCAs were also previously used to treat ADHD (especially imipramine).
Antiepileptic drugs such as gabapentin, carbamazepine and lamotrigine are also helpful.⁶⁰ Due to the massive withdrawal side effects, which are similar to withdrawal from opioids or alcohol and often enough require hospitalization, gabapentin is recommended at best as a last resort and with special information about the associated problems.
Baclofen, mexiletine and clonidine can also be helpful for selected people with ADHD.⁶⁰

5. Causal pathways for chronic pain, increased muscle tone and fibromyalgia¶

According to Stray, motor disinhibition and increased muscle tone in ADHD are directly associated with dysregulation of the dopamine and noradrenaline systems.⁶¹
It is fitting that the increased muscle tone in ADHD is reduced by methylphenidate⁶² and that a noradrenaline reuptake inhibitor (orphenadrine, Norflex®) serves as a skeletal muscle relaxant. Noradrenaline reuptake inhibitors are also used as ADHD medication (atomoxetine, viloxazine).

One study reports an increased sphingomyelin/ceramide ratio in patients with lower back pain⁶³ (which is also a typical form of ADHD). The acid sphingomyelinase (ASM, sphingomyelin phosphodiesterase 1, encoded by the ADHD candidate gene SMPD1) Degrades sphingomyelin to ceramide. If sphingomyelin is high and ceramide is low, this indicates weak S-ASM. With this in mind, FIASMA (ASM inhibitors) such as amitriptyline could be detrimental and increase the risk of muscle tension. Whether this idea is supportive for ADHD remains to be seen

So far, pain sensitivity has only been researched in two model animals with ADHD:¹⁰

SHR, an animal model for ADHD, showed

• weakened pain suppression (analgesia) in the event of harmful stimuli⁶⁴
• a decrease in noradrenaline in the posterior horn of the spinal cord in response to nociceptive stimuli. An increase would be normal.⁶⁵ The decrease indicates reduced endogenous pain suppression (analgesia) in ADHD.¹⁰
• showed more active noradrenaline synthesis under pain conditions⁶⁵ SHR:
  • more noradrenaline synthesizing enzymes in the posterior horn of the spinal cord
  • higher extracellular noradrenaline levels in the posterior horn of the spinal cord
• excessive noradrenaline synthesis in a pain-free state could cause overexpression of NET and downregulation of the α2A receptor. This could lead to decreased norepinephrine activity during NSIA and attenuated descending pain inhibition.¹⁰ SHR showed:
  • more noradrenaline transporters in the posterior horn of the spinal cord
  • fewer α2A receptors in the posterior horn of the spinal cord
• Atomoxetine reduced sensitivity to pain⁶⁵

6-hydroxydopamine (6-OHDA) mice, another ADHD animal model, showed⁶⁶

• as a sign of increased basic nociceptive sensitivity
  • increased licking of the hind legs in response to thermal or mechanical stimuli
  • increased sensitization to pathological inflammatory stimuli
• in the lamina II of the posterior horn of the spinal cord were
  • the inhibitory synaptic connections remain unchanged
  • the excitatory compounds were significantly increased
    • this could promote pain sensitization

• Pain sensitivity in 6-OHDA) mice is probably mediated by¹⁸
  • Α-adrenergic receptors
  • Β-adrenergic receptors
  • D2 receptors
  • D3 receptors
• Increased spontaneous activity of the ACC-PI signaling pathway.⁶⁶ The ACC-PI pathway (from the ACC to the posterior insula, PI) controls central sensitization mechanisms. ADHD-induced ACC-PI activity can increase or decrease pain sensitivity and possibly trigger hyperactivity (ergomania).¹⁰
  • Caused by sex-specific neuroinflammatory response to dopamine (DA) neuron loss by 6-OHDA⁶⁷
    • Males: Dopamine loss triggered inflammation only in the ACC
      • Consequences:
        • Hyperactivity
        • No increased sensitivity to pain (no hyperalgesia)
    • Females: Dopamine loss triggered inflammation in the ACC-PI signaling pathway
      • Consequences:
        • No hyperactivity
        • Increased sensitivity to pain (hyperalgesia)
      • May explain why
        • Prevalence of fibromyalgia^{6869 70 71} and other pain disorders⁷²⁷³ is higher in women
        • Hyperactivity is less common in women
  • Increased ACC activity in response to mechanical stimulation of the contralateral hind limb⁶⁶
    • Resulting in increased firing rate in second-order nociceptive neurons in the dorsal horn of the spinal cord
      • Thereby further lowering the pain threshold
  • Inhibition of the ACC-PI pathway suppressed the action potentials of the posterior horn and increased the pain threshold⁶⁶
• Atomoxetine could reduce sensitivity to pain¹⁸

See also Chronic pain and muscle tension in ADHD - neurophysiological correlates