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Ganglion cells in achalasia of the cardia

C W Adams, R H Brain, J R Trounce

    Virchows Archiv. A, Pathological Anatomy and Histology
    |November 22, 1976
    PubMed

    Insights

    Achalasia (a condition affecting the esophagus) shows significant loss of myenteric ganglion cells, suggesting an active disease process. Oesophageal spasm may represent an early stage of achalasia.

    Area of Science:

    • Gastroenterology
    • Neuropathology
    • Oesophageal Pathophysiology

    Background:

    • Achalasia, oesophageal spasm, and scleroderma are conditions affecting oesophageal motility.
    • The role of the myenteric plexus in these conditions is not fully understood.
    • Histopathological examination is crucial for diagnosing and understanding oesophageal disorders.

    Purpose of the Study:

    • To investigate the histopathological changes in the myenteric plexus in achalasia, oesophageal spasm, and scleroderma.
    • To compare these changes with control groups (carcinoma and reflux oesophagitis).
    • To determine if neuronal loss or inflammation is the primary cause of these conditions.

    Main Methods:

    • Histopathological examination of oesophageal biopsies.
    • Analysis of myenteric ganglion cells and neuronal integrity.
    • Comparison of patient groups with control groups.

    Main Results:

    • Achalasia cases showed near-complete loss of myenteric ganglion cells in the upper oesophagus and partial loss in the lower oesophagus.
    • Neuronal chromatolysis in achalasia indicated an active disease process.
    • Oesophageal spasm cases exhibited similar neuronal loss to the lower oesophagus in achalasia, suggesting a potential link.
    • Scleroderma showed ganglion cell loss, but the myenteric plexus was involved by the disease process.
    • Control groups did not display ganglion cell loss or chromatolysis.

    Conclusions:

    • Achalasia involves significant loss of myenteric ganglion cells, supporting an active pathological process.
    • Oesophageal spasm may represent an early or incomplete form of achalasia.
    • The findings suggest a primary neuronal disorder in achalasia, rather than preganglionic fibre issues or inflammation.

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