Investigators concluded that the therapeutic effectiveness of antiparkinsonian medications is short and limited for intolerable abdominal pain.
A recently published study of 6 patients with Parkinson disease (PD) with intolerable abdominal pain highlighted the rarity of this symptom, and suggested that it alleviates quality of life. On CT scans, maximal rectus abdominis thickness and relative muscle thickness ratio of patients with abdominal pain were significantly higher than those without pain.1
All patients had difficulty with daily living while in pain, and had food intake decreased which led to body weight reductions in some patients. In 3 patients, palpable muscle contraction was evident and lower limb pain occurred in 2 patients. Pain occurred daily for patients often during the night, not related to the timing of food intake, pain in two patients was related to wearing-off.
Lead author Hiroshi Kataoka, MD, associate professor of neurology at Nara Medical University, Nara, Japan, and colleague wrote, “the therapeutic usefulness of antiparkinsonian medications, including levodopa and long-acting dopamine agonists, is short and limited for intolerable abdominal pain, and rasagiline or memantine might be associated with pain for some periods. Requiring a high dose of levodopa, such as levodopa-carbidopa intestinal gel or deep brain stimulation, is effective for persistent intolerable abdominal pain.”1
Investigators collected medical records between 2006 and 2022 from 6 patients with PD(age range 71–85 years; 3 men), including the disease course before and after the onset of abdominal pain. The Hoehn–Yahr stage, disease duration, and daily levodopa equivalent dose were 3.1 (±0.7), 107 (±44) months, and 636.7 (±451.4) mg/day, respectively. Maximal thickness of rectus muscles at the L4 and L5 corpus vertebral level of the abdomen on axial computed tomography was calculated. Relative muscle thickness ratio was calculated by dividing maximal thickness and distance from fascia between bilateral rectus muscles of the abdomen and the dorsal part of the corpus vertebrae.
Abdominal pain occurred 2 months after addiction of zonisamide (25 mg/day), 1 month after the withdrawal of ropinirol (1 mg/day), 2 months after addition of catechol O-methyltransferase inhibitor (500 mg/day), or 2 months after withdrawal of zonisamide (50 mg/day). All patients had constipation, and 3 patients reported axial motor symptoms. Before the onset of abdominal pain, the mean duration of levodopa intake was 72 (±32) months. Treatment durations of pramipexole, ropinirol, and cabergoline were 6, 12, and 81 months whereas rotigotine and ropinirole were 3 and 7 years, respectively.
Patient 1 displayed constant hypertonic activity in the rectus abdominis on surface electromyography. After the levodopa equivalent daily dose was increased in five out of six patients, severity of abdominal pain mildly reduced. Or abdominal pain reduced mildly by infusing mepivacaine or lidocaine to the rectus muscles of the abdomen in 2 patients, apomorphine in 1 patient, etizolam in 1 patient, and tramadol in 1 patient. Rasagiline showed to be moderately effective with effectiveness maintained for 10 months.
Treatment with levodopa-carbidopa intestinal gel for several weeks was pain-free for patient 6. Pain in both the abdomen and lower limbs was relieved after bilateral subthalamic nucleus-deep brain stimulation in patient 5. Several years after onset of abdominal pain, CT scans on patient 6 showed marked retention of colon gas. Both maximal thickness (8.7 mm) and relative muscle thickness ratio (0.05) were minimal among patients with abdominal pain.
Kataoka and colleague noted, “The pathophysiology seems to vary, and our observations found wearing-off of related pain and muscle contraction, suggesting dystonia. Among persistent abdominal pain, organic abnormalities, such as the precursor state of megacolon, may be lurking.”1
Previous research conducted by Kataoka and colleagues observed two patients with painful abdominal contractions associated with abdominal muscle hypertrophy and the current study demonstrated similar results.2 “The hypertrophy of the rectus abdominis muscle might be derived from persistent muscle contractions because surface electromyography showed constant hypertonic activity in the rectus muscles of the abdomen in Patient 1,” Kataoka and colleague wrote.1