What is the difference between tetanus and tetany?

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Type of article: Point of View

E.S.Prakash, School of Medicine, Faculty of Medical and Health Sciences,
Asian Institute of Medicine, Science & Technology, 08100 Bedong, Kedah Darul Aman, Malaysia. E-mail: medicalphysiologyonline [at] gmail [dot] com

Submitted 1 Jan 2008; accepted 16 Jan 2008; published 16 Jan 2008.

Here is a common dialog between a physiology teacher and an undergraduate student during a physiology examination:
Teacher: What is the difference between tetanus and tetany?
Student: Tetanus is a disease caused by Clostridium tetani whereas tetany is a consequence of hypocalcemia.
Teacher: You are correct.

My comments: While there is nothing really wrong with the above dialog, it reads as though tetanus and tetany are two different things. My point is, in a mechanistic sense, there is little difference between tetanus and tetany but this is not commonly noted. Let me explain.

The clinical condition "tetanus", caused by Clostridium tetani, is characterized by painful muscle spasms and rigidity; this is because the toxin tetanospasmin which C. tetani produces is a powerful inhibitor of the release of glycine, an inhibitory neurotransmitter, from Renshaw cells in the spinal cord. When this happens, unrestrained high frequency discharge of alpha motor neurons results in sustained skeletal muscle contractions that we call tetanus.

Experimentally, for example with a frog sciatic nerve-gastrocnemius muscle preparation, we "tetanize" the muscle by stimulating the sciatic nerve supplying the muscle (or the muscle itself) at high frequencies (called tetanizing frequencies); in other words, we are exciting α-motor neurons supplying the muscle at high frequencies. Strictly speaking, a muscle is said to be tetanized completely if there is no relaxation between successive contractions. To be tetanized, skeletal muscle needs to be stimulated at a frequency greater than or at least equal to the reciprocal of the contraction period in seconds.

Hypocalcemia is said to increase neuromuscular excitability by reducing the magnitude of depolarization necessary to initiate changes in the Na and K conductance that produce an action potential [1]. The carpopedal spasm that occurs in hypocalcemia is evidence of increased neuromuscular excitability and must be due to increased discharge of motor neurons supplying the corresponding muscles. Indeed, Mullin and colleagues [2] have demonstrated the occurrence of opisthotonus, pleurothotonus, and rigidity of abdominal musculature in experimental dogs in which hypocalcemia was induced by injecting calcium poor solutions into the cisterna magna. Thus, the neuromuscular consequences of tetanotoxin and hypocalcemia are similar.

Conflict of interest: the author is the editor of Medical Physiology Online.

References:

1. Ganong WF. Chapter 2. Excitable Tissue: Nerve; In: Review of Medical Physiology, 22nd edition, Mc Graw Hill Co, New York, 2005.

2. Mullin FJ, Hastings AB, and Lees WM. Neuromuscular responses to variations in calcium and potassium concentrations in the cerebrospinal fluid. Am J Physiol 1938; 121: 477-481. [Link]

Please cite this article as: Prakash ES. What is the difference between tetanus and tetany? Medical Physiology Online [serial online] article 3; volume 1: 2008; available from http://www.medicalphysiologyonline.org

Some rights reserved © 2008 E.S.Prakash. This is an open access article distributed under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by-nc-sa/3.0/

Guest editor for this manuscript: Dr. Madanmohan, Jawaharlal Institute of Postgraduate Medical Education and Research, Pondicherry, India. E-mail: drmadanmohan123 [at] gmail [dot] com

Conflict of interest: E.S.Prakash invited me to review this manuscript. He was my student from 2001 through 2006. We have worked and published several articles together.

Correction: The correct citation of the paper by Mullin FJ et al should be Am J Physiol 1938; 121: 719-727, and not Am J Physiol 1938; 121: 477-481 as mentioned in the original article. I thank P Pavithran, Student advisor for Medical Physiology Online for alerting me of this error.