Medical Terminology Daily - Est. 2012

Medical Terminology Daily (MTD) is a blog sponsored by Clinical Anatomy Associates, Inc. as a service to the medical community. We post anatomical, medical or surgical terms, their meaning and usage, as well as biographical notes on anatomists, surgeons, and researchers through the ages. Be warned that some of the images used depict human anatomical specimens.

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A Moment in History

Jean George Bachman

Jean George Bachmann
(1877 – 1959)

French physician–physiologist whose experimental work in the early twentieth century provided the first clear functional description of a preferential interatrial conduction pathway. This structure, eponymically named “Bachmann’s bundle”, plays a central role in normal atrial activation and in the pathophysiology of interatrial block and atrial arrhythmias.

As a young man, Bachmann served as a merchant sailor, crossing the Atlantic multiple times. He emigrated to the United States in 1902 and earned his medical degree at the top of his class from Jefferson Medical College in Philadelphia in 1907. He stayed at this Medical College as a demonstrator and physiologist. In 1910, he joined Emory University in Atlanta. Between 1917 -1918 he served as a medical officer in the US Army. He retired from Emory in 1947 and continued his private medical practice until his death in 1959.

On the personal side, Bachmann was a man of many talents: a polyglot, he was fluent in German, French, Spanish and English. He was a chef in his own right and occasionally worked as a chef in international hotels. In fact, he paid his tuition at Jefferson Medical College, working both as a chef and as a language tutor.

The intrinsic cardiac conduction system was a major focus of cardiovascular research in the late nineteenth and early twentieth centuries. The atrioventricular (AV) node was discovered and described by Sunao Tawara and Karl Albert Aschoff in 1906, and the sinoatrial node by Arthur Keith and Martin Flack in 1907.

While the connections that distribute the electrical impulse from the AV node to the ventricles were known through the works of Wilhelm His Jr, in 1893 and Jan Evangelista Purkinje in 1839, the mechanism by which electrical impulses spread between the atria remained uncertain.

In 1916 Bachmann published a paper titled “The Inter-Auricular Time Interval” in the American Journal of Physiology. Bachmann measured activation times between the right and left atria and demonstrated that interruption of a distinct anterior interatrial muscular band resulted in delayed left atrial activation. He concluded that this band constituted the principal route for rapid interatrial conduction.

Subsequent anatomical and electrophysiological studies confirmed the importance of the structure described by Bachmann, which came to bear his name. Bachmann’s bundle is now recognized as a key determinant of atrial activation patterns, and its dysfunction is associated with interatrial block, atrial fibrillation, and abnormal P-wave morphology. His work remains foundational in both basic cardiac anatomy and clinical electrophysiology.

Sources and references
1. Bachmann G. “The inter-auricular time interval”. Am J Physiol. 1916;41:309–320.
2. Hurst JW. “Profiles in Cardiology: Jean George Bachmann (1877–1959)”. Clin Cardiol. 1987;10:185–187.
3. Lemery R, Guiraudon G, Veinot JP. “Anatomic description of Bachmann’s bundle and its relation to the atrial septum”. Am J Cardiol. 2003;91:148–152.
4. "Remembering the canonical discoverers of the core components of the mammalian cardiac conduction system: Keith and Flack, Aschoff and Tawara, His, and Purkinje" Icilio Cavero and Henry Holzgrefe Advances in Physiology Education 2022 46:4, 549-579.
5. Knol WG, de Vos CB, Crijns HJGM, et al. “The Bachmann bundle and interatrial conduction” Heart Rhythm. 2019;16:127–133.
6. “Iatrogenic biatrial flutter. The role of the Bachmann’s bundle” Constán E.; García F., Linde, A.. Complejo Hospitalario de Jaén, Jaén. Spain
7. Keith A, Flack M. The form and nature of the muscular connections between the primary divisions of the vertebrate heart. J Anat Physiol 41: 172–189, 1907.


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This is a series of articles on depression and published as a community service. The information in these articles follow our Privacy and Security Guidelines and cannot be construed as medical guidance. For additional information and counseling, consult with your physician or the appropriate health care professional of your choice. You can also find information on Transcranial Magnetic Stimulation (TMS) here. For the initial article on this series click here.

The medical term meaning "cause" is [etiology]. As you talk to a physician or research on the causes of depression knowing this term will come in handy. Most likely, the etiology of depression is a combination of genetic, biological, environmental, and psychological factors.

Depressive pathologies are disorders of the brain. Brain-imaging technologies, such as Magnetic Resonance Imaging (MRI), have shown that the brains of patients who have depression are physically different than those of non-depressed individuals. This is important to understand. A depression patient is not a "mental" or "crazy" person in the fact that there is an underlying physical brain disorder causing the depression. They are not "faking it" and the treatment must look into getting the brain back into a normal physical pattern. 

The following images show a Positron Emission Tomography (PET) scan of both a non-depressed and a depressed individuals. In these images the areas of the brain involved in mood, thinking, sleep, appetite, and behavior appear different. These images do not reveal why the depression has occurred, only that a depressed brain is physically different from a non-depressed brain.

PET scan showing the physical differences between a depressed and a non-depressed brain
Click on the image for a larger view

Some types of depression tend to run in families, indicating a genetic base for the pathology. However, depression can occur in people without family history of depression. Scientists are studying certain genes that may make some people more prone to depression. Some genetics research indicates that risk for depression results from the influence of several genes acting together with environmental or other factors. In addition, trauma, the loss of a loved one, a difficult relationship, long winter seasons, or any stressful situation may trigger a depressive episode. Other depressive episodes may occur with or without an obvious trigger.

Who is at risk?

Major depressive disorder is one of the most common mental disorders in the United States. Each year about 6.7% of U.S adults experience major depressive disorder. Women are 70 % more likely than men to experience depression during their lifetime.  Non-Hispanic blacks are 40% less likely than non-Hispanic whites to experience depression during their lifetime.  The average age of onset is 32 years old. Additionally, 3.3% of 13 to 18 year olds have experienced a seriously debilitating depressive disorder.

Depression also may occur with other serious medical illnesses such as heart disease, stroke, cancer, HIV/AIDS, diabetes, and Parkinson's disease. People who have depression along with another medical illness tend to have more severe symptoms of both depression and the medical illness, more difficulty adapting to their medical condition, and more medical costs than those who do not have co-existing depression. Treating the depression can also help improve the outcome of treating the co-occurring illness

Source: National Institute of Mental Health

Next article: Types of Depression