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Episode two of the Gastric and Small Bowel Motility chapter covers the episodic and functional presentations where the structural workup comes back clean and the pattern carries the diagnosis: cyclic vomiting syndrome, cannabinoid hyperemesis, chronic intestinal pseudo-obstruction, and functional dyspepsia. Reading dilated bowel or delayed emptying as mechanical disease misleads you every time. Each condition is answered by naming the pattern, not by another motility drug.
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Welcome to Board Pearls. This is episode two of two of the Gastric and Small Bowel Motility chapter, in the Stomach and Small Bowel Disorders module. This episode is the episodic and functional presentations: cyclic vomiting syndrome, cannabinoid hyperemesis, intestinal pseudo-obstruction, and functional dyspepsia. They share one puzzle: the structural workup comes back clean, so the pattern carries the diagnosis, and reading the imaging as mechanical misleads you every time.
Start with cyclic vomiting syndrome. The definition is stereotyped attacks of severe nausea and vomiting lasting hours to days, separated by symptom-free intervals of weeks to months, with the attacks resembling each other in onset, duration, and severity. The word doing the diagnostic work is stereotyped: the patient describes their attack the same way every time, and between attacks there's no chronic nausea and no daily medication need. In fact, emptying between attacks is normal or even fast, which is exactly what separates this from gastroparesis on a scintigraphy study. The biology maps onto migraine, and this isn't incidental: many patients have a personal or family history of migraine, the same triggers set off both, and that link is why the drugs that prevent attacks are the migraine preventives and the ones that abort them include triptans. The biology drives the pharmacology. The attack itself runs in four phases, and naming them is what separates this from ordinary chronic nausea: a symptom-free interval, a prodrome of nausea and pallor and impending vomiting, an intense but self-limited emetic phase, and a recovery back to baseline. A patient who describes that four-phase rhythm, attack after attack, is handing you the diagnosis.
Treatment splits into preventing attacks and aborting them, and prevention borrows straight from migraine, with a low-dose tricyclic at bedtime as the favored agent and topiramate next, plus options like propranolol and mirtazapine. Aborting an active attack means fluids, ondansetron, and a benzodiazepine for the nausea and the panic-like component, with a triptan added when the attack looks like a migraine variant, which it often does, and lifestyle work on sleep and stress underneath it all.
Now cannabinoid hyperemesis, which is the cannabis-driven look-alike and the most heavily tested differential here, because the cycle looks identical. The patient has years of regular cannabis use and develops the same episodic stereotyped vomiting, and the history that gives it away is the hot shower: hot showers or baths produce dramatic temporary relief, so the bathing becomes compulsive, sometimes for hours, sometimes with scalding water, and the patient gets agitated when made to leave it, often unable to say why it helps. That compulsive hot-water bathing is the hallmark. The mechanism explains it: chronic THC dysregulates a receptor that both hot water and capsaicin activate directly, which is why the shower works and why capsaicin cream on the abdomen gives partial relief in the emergency department, exploiting the same pathway. The teaching point is that the bathing isn't psychiatric, it's the patient self-administering a receptor agonist. And the cure is stopping cannabis, with resolution over a week or two, though addiction support is usually needed. Tricyclics don't work here and ondansetron alone isn't enough; when standard antiemetics fail in an active episode, the add-ons are topical capsaicin, haloperidol, and a benzodiazepine.
So the two favored stems are mirror images. A young adult with stereotyped vomiting, daily cannabis, and dramatic hot-shower relief: the answer is stop cannabis, not start a tricyclic. A young adult with migraines, a family history of migraine, no cannabis, and stereotyped episodic vomiting: the answer is a bedtime tricyclic. Same cycle, different right answers, and the decision rests on two history features, hot-water bathing and daily cannabis on one side, migraine biology on the other. Two related conditions round this out: chronic nausea and vomiting syndrome, which is continuous rather than stereotyped attacks, and rumination, which is effortless regurgitation of just-eaten food within minutes, no retching and no nausea, with a pressure study showing the abdominal-strain event, treated by diaphragmatic breathing.
Now pseudo-obstruction, where the imaging shows dilated bowel with no transition point. It splits in two. The acute colonic form, Ogilvie syndrome, is a hospital-onset problem in postoperative, trauma, and critically ill patients, driven by electrolyte disturbances, opioids, and autonomic imbalance, and it's covered fully in chapter thirty-one. The short version: a cecal diameter over twelve centimeters and distension lasting beyond several days sharply raise the perforation risk, conservative management for a couple of days succeeds in most, and failure or marked dilation triggers intravenous neostigmine with cardiac monitoring, then colonoscopic decompression for refractory cases.
The condition this episode centers on is chronic intestinal pseudo-obstruction, defined as severe chronic impairment of intestinal propulsion producing recurrent obstruction symptoms with no occluding lesion, so distension, vomiting, inability to pass stool, and weight loss with dilated small bowel on imaging but no transition point on any study. It's rare, and about half of adult cases are secondary to an identifiable disease. The pathophysiology splits three ways, and the distinction matters because the workup follows the lesion. A neuropathic problem is a disorder of the enteric nerves with structurally normal muscle, so on manometry the contractions are of normal strength but uncoordinated. A myopathic problem is a disorder of the muscle itself, so the pattern of contractions is preserved but the force is low. And a pacemaker problem is loss of the interstitial cells of Cajal, so the slow-wave rhythm itself is abnormal. Many secondary causes show mixed patterns over time.
The secondary differential is wide, and it's worth holding as a structured list. Connective tissue diseases lead, with systemic sclerosis the prototype: most scleroderma patients have gut involvement, and the course shifts from an early neuropathic phase to a later myopathic one as the muscle fibroses, so late manometry shows low-amplitude contractions, the imaging hallmark is a markedly dilated duodenum, and stasis breeds bacterial overgrowth that adds bloating, diarrhea, and malabsorption. Amyloid infiltrates the muscle as a myopathic pattern. Endocrine causes like thyroid disease, hyperparathyroidism, and diabetes give mixed patterns. Neurologic diseases like Parkinson and autonomic neuropathy give neuropathic patterns. And in a young cachectic patient, a mitochondrial disorder enters the differential, with the named entity presenting with eye-movement problems, white-matter changes, neuropathy, and severe dysmotility.
Paraneoplastic pseudo-obstruction is the favored vignette and deserves its own attention: an older patient with a smoking history, rapidly progressive new dysmotility, weight loss out of proportion to symptoms, and dilated small bowel with no cutoff, sometimes with orthostatic hypotension or sensory neuropathy signaling autonomic involvement. The paraneoplastic antibody panel comes back positive, most often anti-Hu, and the tumor is usually small cell lung cancer, so chest CT finds it and PET is the next step if the chest CT is unrevealing, with treatment of the cancer sometimes stabilizing the motility. The vignette to lock in is the older smoker with new dysmotility and weight loss, in whom the answer is chest CT and an oncologic workup, not another motility drug. Iatrogenic causes, opioids and anticholinergics, round out the secondary list, and the rest are idiopathic.
The workup runs in a fixed order. First exclude mechanical obstruction with imaging and endoscopy. Then confirm the dysmotility and find its level, with emptying and transit studies across the stomach, small bowel, and esophagus. Then characterize the lesion with antroduodenal manometry, the most specific test for confirming the diagnosis and calling it neuropathic or myopathic, though it's available only at specialized centers. And full-thickness intestinal biopsy at laparoscopy is reserved for genuine uncertainty, because it's invasive. The manometry read is mechanical once you remember what it sees: normally, fasting shows the migrating motor complex cycling through its phases, and eating replaces it with a sustained fed pattern. Neuropathic disease shows normal-strength but disorganized contractions with the propagated phase absent or misdirected; myopathic disease shows low-amplitude contractions with the pattern preserved. Paraneoplastic disease and early scleroderma look neuropathic; late scleroderma and amyloid look myopathic. Alongside, you screen for the secondary causes with thyroid tests, scleroderma antibodies, the paraneoplastic panel with a chest CT, and metabolic testing when mitochondrial disease is suspected.
Management is mostly supportive. Nutrition is the cornerstone, oral when tolerated, jejunal feeding when it isn't, and parenteral nutrition for the patients with true intestinal failure. Bacterial overgrowth is essentially universal and adds to the symptoms, controlled with rotating antibiotic courses to limit resistance. Prokinetics are tried despite limited evidence, with prucalopride preferred and pyridostigmine used to enhance cholinergic signaling, while octreotide has fallen out of favor because it can actually slow small-bowel transit and worsen overgrowth. Surgery is limited, venting distended loops or, in the most severe cases with chronic pain from massively dilated bowel, resection that commits the patient to lifelong parenteral nutrition, with transplantation reserved for the few with intestinal failure and serious parenteral-nutrition complications.
Finally, functional dyspepsia, the most common upper-GI complaint in clinic, where most patients have no structural explanation and the pathophysiology overlaps heavily with gastroparesis. The criteria require one or more of four bothersome symptoms with no structural disease to explain them: postprandial fullness, early satiation, epigastric pain, and epigastric burning, present for months. Two subtypes come from which symptoms dominate, and the subtype drives therapy. Postprandial distress syndrome is dominated by fullness and early satiation, and its mechanism is a motor-and-sensory problem of the upper stomach, impaired accommodation plus hypersensitivity to distension. Epigastric pain syndrome is dominated by pain or burning, and its mechanism is visceral hypersensitivity. Many patients overlap, but the dominant symptom guides treatment. The broader pathophysiology is multifactorial, impaired accommodation producing early satiety, delayed emptying in a subset producing the gastroparesis overlap, visceral hypersensitivity, low-grade duodenal inflammation, and a post-infectious subset after acute gastroenteritis, with anxiety and depression as common comorbidities through the gut-brain connection. Symptoms don't reliably separate organic from functional disease, which is why the workup matters.
That workup runs on the alarm-feature framework. The alarm features, which mandate prompt endoscopy and shift you toward an organic cause, are significant unintentional weight loss, progressive dysphagia or odynophagia, unexplained iron-deficiency anemia or bleeding, persistent vomiting, a family history of upper-GI cancer, a palpable mass or nodes, and new-onset symptoms over age sixty. So the rule is: under sixty with no alarm features, start with noninvasive H. pylori test-and-treat, and if negative or still symptomatic after eradication, an empiric acid-blocker trial for a few weeks; but at sixty or older, or with any alarm feature, scope first, because the cancer risk rises in that group.
Treatment after excluding organic disease is subtype-targeted. Acid suppression is first-line for both subtypes but works more reliably in the pain subtype, given for a few weeks and stopped if there's no response, since doubling the dose doesn't help. H. pylori eradication is done in every infected patient regardless of subtype, because it's the one intervention with a durable effect on the underlying disease, even if the benefit is modest. Prokinetics are reserved for the fullness subtype after acid suppression and eradication fail, with metoclopramide the approved option under the same twelve-week cap for tardive dyskinesia. Buspirone is worth understanding by mechanism: it relaxes the upper stomach, so it helps the patient whose problem is impaired accommodation, and the favored stem is exactly that, normal emptying, impaired accommodation, fullness-type symptoms, in whom buspirone is the answer. Neuromodulators are second-line for refractory disease, and here tricyclics are favored over the serotonin-based antidepressants, at low bedtime doses, reducing hypersensitivity and pain, most reliably in the pain subtype, given a two-to-three-month trial before calling failure. Mirtazapine is the favored neuromodulator when dyspepsia comes with weight loss, because it fights nausea and stimulates appetite, so the thin patient with early satiety and weight loss is the mirtazapine vignette. And behavioral therapies, gut-directed CBT and hypnotherapy, have real independent evidence by modulating the gut-brain connection, so the patient who's failed the drugs, has concurrent stress, and wants a non-drug option is the one you route to gut-directed CBT or hypnotherapy. Periodic attempts to taper off chronic acid suppression are appropriate, since many patients can come off once stable.
So pull the three together. The shared puzzle was a clean structural workup with the pattern carrying the diagnosis. In cyclic vomiting it's the stereotyped four-phase attack with well intervals and migraine biology, answered with a bedtime tricyclic; in cannabinoid hyperemesis it's the same cycle with daily cannabis and compulsive hot-water bathing, answered by stopping cannabis. In chronic pseudo-obstruction it's dilated bowel with no transition point, where manometry sorts neuropathic from myopathic and the older-smoker vignette flips you toward paraneoplastic disease and a chest CT. And in functional dyspepsia it's the subtype applied after the alarm-feature framework, with the fullness subtype routing to buspirone and prokinetics, the pain subtype to acid suppression and a tricyclic, and mirtazapine reserved for the thin patient with weight loss. In every one, the structural test rules out structural disease, and the right therapy comes from naming the pattern.
The next chapter pivots to the acute upper GI bleed, where the whole question is what you do in the first hours: restrictive transfusion, pre-endoscopic erythromycin and risk scoring, agent-specific anticoagulant reversal, dual therapy at the ulcer, and acid-suppression dosing matched to the recurrence risk.