Peripheral autonomic disorders, including autonomic neuropathies, lead to autonomic failure, a condition characterized by reduced autonomic function. The clinical manifestations involve multiple organ systems: in the cardiovascular system, orthostatic hypotension, postprandial hypotension, and supine/hypertension; in the gastrointestinal tract, gastroparesis, constipation, and diarrhea; and in the lower urinary tract, an underactive bladder. Peripheral autonomic disorders predominantly affect the postganglionic autonomic nerves, resulting in characteristic clinical features. The management of autonomic symptoms relies primarily on non-pharmacological interventions, with pharmacological therapy introduced when these measures are insufficient. This article reviews the clinical features, underlying pathophysiology, and treatment of symptoms associated with peripheral autonomic disorders.

Diabetic autonomic neuropathy is a clinically important component of diabetic neuropathy involving the cardiovascular, gastrointestinal, genitourinary, sudomotor, pupillary, and glucose counterregulatory systems. Cardiovascular autonomic neuropathy (CAN) has been extensively studied and is clinically relevant because of its association with adverse cardiovascular and renal outcomes. Early CAN is frequently silent and may only be recognized by reduced heart rate variability or abnormal cardiovascular autonomic reflex testing. As CAN progresses, patients develop resting tachycardia, reduced exercise tolerance, orthostatic or postprandial hypotension, abnormal nocturnal blood pressure regulation, and perioperative hemodynamic instability. Non-cardiovascular manifestations include gastroparesis, bowel and bladder dysfunction, erectile dysfunction, sudomotor and pupillary abnormalities, and impaired hypoglycemic awareness. The underlying mechanisms involve chronic hyperglycemia, glycemic variability, dyslipidemia, insulin resistance, oxidative and mitochondrial stress, inflammation, microvascular injury, and impaired axon-glial support. Clinically, evaluation should begin with a systematic symptom review, neurological examination, supine and standing blood pressure measurements, and heart rate assessment, followed by organ-specific testing if indicated. Treatment was based on comprehensive risk factor control and symptom-directed management.

Parkinson disease and pure autonomic failure are α-synucleinopathies that lead to peripheral autonomic neuropathy. These autonomic disturbances include well-known symptoms, such as orthostatic hypotension and constipation, and often overlooked symptoms, including supine hypertension and gastroparesis. This article describes the characteristics of diverse peripheral autonomic symptoms of α-synucleinopathies and discusses therapeutic interventions available in daily clinical practice and their impact on prognosis, in the absence of established disease-modifying drugs.

Gastroparesis, a chronic motility disorder, is a diagnosis of exclusion that necessitates careful evaluation for structural and surgically correctable causes. Although the medical differential diagnosis emphasizes functional etiologies, anatomic abnormalities are often under-recognized despite guideline recommendations for thorough endoscopic and structural assessment. Symptoms such as nausea, vomiting, early satiety, and delayed gastric emptying may be indistinguishable from true motility disorders. We present two patients initially diagnosed with gastroparesis whose symptoms were ultimately driven by surgical pathology. Case 1 describes a 70-year-old woman with persistent nausea and vomiting, weight loss, epigastric abdominal pain, and delayed gastric emptying on scintigraphy, initially scheduled for gastric peroral endoscopic myotomy (G-POEM) for presumed gastroparesis. Intraoperative endoscopy revealed gastric volvulus as the underlying etiology, prompting conversion to definitive surgical repair. Gastric volvulus, while rare, may be complicated by ischemia or perforation, highlighting the importance of timely differentiation from gastroparesis. Case 2 describes a 53-year-old woman with intractable nausea, vomiting, and inability to tolerate oral intake following a Roux-en-Y gastric bypass (RYGB). Surgical exploration revealed a Roux-en-O configuration with twisted limbs causing impaired drainage, ultimately requiring bypass reversal and pyloroplasty. The Roux-en-O configuration is a rare but serious complication of RYGB involving misplaced anastomoses that create a blind loop, resulting in obstruction and gastroparesis-like symptoms. Clinicians should maintain heightened suspicion for structural pathology in patients with atypical presentations, previous surgery, or refractory symptoms, as delayed diagnosis can lead to life-threatening complications.

Thirty-five-year-old female presents with a history of chronic constipation, gastroparesis, chronic lower abdominal pain, and anxiety. She is diagnosed with colonic inertia and undergoes a total abdominal colectomy with ileorectal anastomosis. She initially does well with resolution of her constipation; however, she continues to complain of persistent lower abdominal pain, debilitating enough to keep her from working at full capacity.

Background Gastric motility problems are a commonly overlooked complication of type 2 diabetes mellitus (T2DM). Diabetic autonomic neuropathy and dysfunction of the interstitial cells of Cajal are believed to be the main underlying mechanisms. Electrogastrography (EGG) is a simple, noninvasive method for studying gastric electrical activity. There are limited data on gastric electrical abnormalities in Indian patients with T2DM. This study was designed to estimate the prevalence of such abnormalities and to examine whether they are related to long-term glycemic control and duration of diabetes. Methods This cross-sectional observational study was conducted at the Department of Physiology, Gandhi Medical College, Bhopal. A total of 130 adult patients with T2DM were enrolled. Surface EGG was recorded using a BIOPAC MP36 data acquisition system (BIOPAC Systems Inc., Goleta, CA, USA) before and after a standardized test meal. Gastric slow waves were classified as bradygastria (0.5 to <2 cpm), normogastria (2 to 4 cpm), or tachygastria (>4 to 9 cpm) using a delta T-based wave-count method applied over a standardized 22-minute analyzable window. Dominant frequency (DF), dominant power, instability coefficients, and power ratio were also calculated. Abnormal gastric electrical rhythm (AGER) was defined as normogastria of 70% or less, DF outside the 2 to 4 cpm range, or a postprandial PR of 1 or less. Spearman correlation was used to assess associations between EGG parameters and HbA1c and duration of diabetes. Results The mean age of participants was 49.91 ± 9.28 years, and the mean HbA1c was 9.92 ± 2.62%. AGER was found in 92.3% of participants before the meal and in 91.5% after the meal. The proportion of normogastria was markedly low (preprandial, 39.5%; postprandial, 46.6%), whereas bradygastria was high (preprandial, 44.4%; postprandial, 38.3%). Despite these rhythm abnormalities, DF remained within the normal range in both states (2.80 and 3.00 cpm). Instability coefficients were elevated (0.57 preprandial and 0.54 postprandial) and were comparable to values reported in diabetic gastroparesis. No significant correlation was found between any EGG parameter and HbA1c or duration of diabetes (all p > 0.05). Conclusions Most patients with T2DM in this study showed substantial subclinical gastric myoelectrical dysfunction, even in the absence of GI symptoms. This included markedly reduced normogastria, elevated bradygastria, and unstable pacemaker activity. No significant association was observed between EGG parameters and HbA1c or reported duration of diabetes. These findings raise the possibility that factors other than long-term glycemic control and disease duration may contribute to gastric myoelectrical dysfunction in T2DM. Further controlled longitudinal studies are needed to explore this.

Hyperprolactinemia accompanied by headache and visual symptoms commonly prompts pituitary imaging to rule out prolactinoma. Several medications can elevate serum prolactin into ranges that overlap with prolactin-secreting adenomas, and metoclopramide, a dopamine D2 receptor antagonist used for gastroparesis and nausea, is among the most frequent offenders. Headache and blurred vision are also listed as adverse effects, reproducing the symptomatic triad clinicians associate with a pituitary tumor. We describe a 22-year-old woman with polycystic ovary syndrome who presented with a prolactin level of 160.3 ng/mL, intermittent blurry vision, and chronic headaches managed with onabotulinumtoxinA through neurology. Pituitary MRI was unremarkable. Despite repeated direct questioning, her initial medication history included only losartan. Metoclopramide was identified through deliberate review of outside gastroenterology records, where it had been prescribed for chronic constipation. One month after discontinuation, prolactin levels had returned to normal at 11.2 ng/mL. Menstrual function showed initial improvement, as she experienced her first menstrual cycle after approximately one year of amenorrhea. However, regular menses did not fully resume; cycles remained irregular, likely in the setting of her underlying polycystic ovary syndrome (PCOS). This case illustrates how drug-induced hyperprolactinemia can be missed when the medication list is incomplete, particularly in fragmented care settings, and how deliberate review of outside documentation can spare patients unnecessary imaging.