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We present, below, the second part of this article by Dr. Prof. Villalaín Blanco, of obligatory reading to study in depth the subject of the rigor mortis of the corpse of the man of the Shroud. The conclusion of the article, next week. Although it is a bit long, it is worth spending a few minutes on it.

Notes on cadaveric rigidity

From the medical point of view, there are two distinct types of muscle contraction, structurally similar, but with different enzymatic sequences. Indeed, postmortem contraction has no practical function and only reveals the attainment and depletion of muscle energy reserves after cellular death.


As death occurs, it creates a state of relaxation or generalized muscle flaccidity, and then, slowly and gradually, a process of muscle contraction is established. The rigor mortis, therefore, would be the state of temporary and progressive muscular tension that occurs after death (Louis, one of the pioneers of Forensic Medicine, writes in his fourth letter: “For research done with all the accuracy possible for me, and that I have continued for many years without interruption, I have seen more than five hundred individuals at the time of death, i.e. at the moment of the absolute cessation of body movement, the joints begin to become rigid even before natural heat decreases").

It is accompanied by changes in the biochemical pattern: lactate production, muscle acidity, and loss of adenosine triphosphate (ATP). It is characterized by a marked decrease in muscle extensibility and loss of recovery of the deformity of muscle fibers.


All muscles become rigid whether they are of smooth fiber or striated fiber, as a general rule. The organs that have smooth muscle fiber, the heart and diaphragm, are rigid from 30 minutes to two hours after death. Striated skeletal muscle fiber starts to become rigid three to six hours after death.

The rigidity appears gradually and has a lot to do, in our experience, with the body position: In a supine body position, with the head raised up to the body plane, it occurs in the following order, according to most authors: lower jaw and orbicular muscles of the eyelids, face, neck, arms, legs, trunk. In other positions, the production order varies with the position. The body ends up forming a solid block, fixed by the rigor mortis. But the sequence with which with rigor mortis is established is not uniform for the different authors: According to Nysten’s schemes, rigidity begins at the jaw and neck, followed by the trunk, upper limbs and lower limbs. Brouardel wrote that rigor mortis begins with the seminal vesicles, probably thinking of asphyctic cases, and follows with the jaw, neck and other muscles. Barahona said that it starts with the lower jaw, quickly followed by the neck and eyelids, then the legs, and finally, the muscles of the upper limbs and trunk. According to Sommer-Larcher, it is initiated at the jaw, almost simultaneously in the lower limbs and neck, then the arms. Brouardel says the stiffness of the lower limbs is prior to the above, that the finger muscles keep the rigidity longer and that the organ that was the last to enter into rigidity is also the last to lose it. This is due to the variability that it offers, in the experience of the authors, and to the ignorance that existed for the oldest concerning the physicochemistry of the phenomenon.

In any case, an athletic isometric contraction is instituted, highlighting the muscular relief, with slight flexor predominance. On the contrary, given the importance of the degree of muscular hydration or dehydration, if the body remains inverted upright with the feet higher, the rhythm becomes reversed. In the case of crucifixion, the upper body dehydration and the lower congestion and edema cause the rigidity to begin very quickly above and slowly in the lower part.

In normal conditions, for a well-fed individual with the nervous and muscular system intact and in natural death, rigidity begins in the temporomadibular articulation between two and four hours after death. Subsequently it extends throughout the musculature, being complete within 8-12 hours and maximal at 24 hours. It begins to disappear after 36-48 hours and ends two to four days after death. It is now widely called the Niderkorn rule, according to which the rigidity is early before three hours; normal between three and six hours; late between six and nine hours, and very late after this timeline.

Mallach published an impressive study in 1964. According to this author, rigidity begins between two and eight hours, with a standard deviation higher than five. The period leading up to it ranges from half an hour to seven, with a standard deviation of 3 ± 2. These figures were determined measures assessing 26 publications between 1811 and 1960. Complete rigidity ranged between six and ten hours with variations between 2 and 20, evaluating 28 publications in the same period with a standard deviation of 8 ± 1 on the subject. The average figures are approximate. Schleyer already noted the “considerable dogmatism” with which the books deal with the subject. Shapiro, Lyel, Stemmer, Cleveland and others have noted that the variability in the figures considered is due to the fact that rigor mortis is the expression of a physical-chemical process and the available data have very different origins: some come from bodies laid out on a bed; others on an autopsy table and those examined have died in extreme situations, internal or external, the corpses of the injured and those obtained experimentally originate from small muscle masses and small laboratory animals that are not comparable to a entire human body.

Where, as in the case of the Shroud image, there is rigidity that is apparently early, let us see what the bibliography collects in that respect. Indeed, Brown-Sequard published the case of a soldier who died of typhoid fever complicated by deep exhaustion. In this case the rigidity preceded the cardiac arrest by three minutes. The same author described how in cholera cases with the presence of cramps, rigidity commences early in the affected muscles. Bonnet says the stiffness starts (immediately?) after death occurs, reaches its fullness at fifteen hours and then slowly disappears. Nysten has drawn attention to how, in cases of marasmus and general cachexia from pulmonary tuberculosis or stomach cancer, the rigidity is also very early, scarse and short. Sommer fixed the start from ten minutes to seven hours after death. Peiró refers to this time period as between ten minutes and 16 or 18 hours. According to the observations of Oscar Freire Institute in Sao Paulo, which has vast experience, rigor mortis occurs within the first hour after death; Maschka never saw it before an hour and a half; Niderkorn and Hofmann mark it at two hours, complete within three hours; Sydney Smith in three hours or shortly before; Borri, Strassmann or Balthazard, three hours. Therefore, the literature describes early cases, similar to that presented by the Man of the Shroud. The speed of appearance and the shortness of the rigidity are also known in the case of forced or fatigued animals being hunted, five minutes after death. Vock et al. have published a case of instantaneous stiffness in a case of tetany. There have been reports of instantaneous stiffness, especially cases with seizures, e.g. strychnine poisoning or organophosphate insecticides; Morgagni has cited cases of sudden death where the rigidity was present almost immediately; Sommer, Muller and many others have seen that rigidity occurs earlier after acute and cachectic illnesses, sometimes almost instantly. Balthazard references rigidity that may appear immediately after death in those who have succumbed to tetanus or strychnine poisoning; Brown-Sequard, in subjects who died from infectious diseases.

Mechanism of production

The mechanism is currently absolutely and precisely unknown; however, there are many proven data and applicable results of research in recent years. Several biochemical theories have been proposed, all very complex and only partially proven but, synthesizing as much as possible, it can be argued that the ATP (adenosintriphosphoric) becomes ADP (adenosindiphosphoric), releasing a molecule of phosphoric acid. The latter provides the phosphate needed for ATP resynthesis, using energy-giving glycogen. When the glycogen reserve is exhausted, it lacks the energy to resynthesize ATP, which definitely becomes ADP, causing contraction of myosin. Therefore the glycogen reserve is critical and in the case of a subject who has died like the Man of the Shroud, it necessarily had to be minimal.


Casper outlines the evolution of rigor mortis, similar to how Camps does it under the following scheme, which applies to forensic practice:

– If the body is warm and relaxed, death came less than three hours before.

– If the body is warm and partially rigid, death occurred between 3 and 8 hours before (2-9 hours under the Camps scheme).

– If the body is cold and rigid, postmortem interval is 8 to 36 hours (over 9 hours according to Camps).

– If the body is cold and limp, the postmortem interval is greater than 36 hours.

Niederkorn, after studying the evolution of rigor mortis in 113 cadavers, obtained the following results: In two cases it was complete at two hours; in 76 cases, the rigidity was complete between 4 and 7 hours; in 31 cases, after 4 hours; in 14 cases, it occurred after 5 hours; in 20 cases, after 6; and in 11 cases, after 7 hours; and in another two, after 13 hours of evolution.

Bendall distinguished three phases in the progress of rigor mortis: phase of delay or prerigor, rapid phase, and post-rigor phase; the latter phase has no interest for our purposes because we are studying established rigidity.

The delay phase maintains the muscle properties. It is characterized in that the ATP figures remain unchanged, while the values ​​of phosphocreatinine and pH decrease rapidly. The ATP is converted into ADP and this, together with the hydrogen ions and phosphorus, reacts with the glucose released from glycogen stores. In this phase one third of the ADP is reconverted by means of creatine using phosphocreatinine. Therefore the glycogen reserve is critical in the process.

The rapid phase is characterized by the loss of extensibility and the beginning of pronounced shortening in the muscular fiber. The loss of ATP is initiated along with the accompanying formation of ammonia due to dephosphorylation and deamination of the adenine nucleotides. Inosine triphosphate (ITP) and inosine diphosphate (IDP) appear, which peak at the end of the phase.

Therefore, from our particular point of view, in relation to the establishment of rigor mortis, the amount of glycogen is inversely proportional to the time required to initiate it. This is a factor that we have noted, very important in the death of Jesus.

Furthermore, glycogen stores are related to pH; low pH (5.6) reflects high levels of glycogen; high numbers (7.2) indicate low or no reserves. Acetate content runs parallel to the figures of glycogen, so glycogen figures are referred to in lactate units, so that one unit of lactate equals a half unit of glucose derived from glycogen.

In the whole mechanism calcium also plays an important role, as trigger of the rigor and the pathogenic mechanism of initiation. In our case the numbers of calcium should be correct and rather high in a subject used to the great outdoors, with no signs of rickets or calcium deficiencies.


Nysten defined the “Law of rigor mortis,” determining that the intensity and duration are related, so that when the rigidity is early, the intensity is limited and brief, whereas if delayed, it is noted and prolonged. Keep in mind that there are processes that do not follow these rules (electrocution, deaths from cold, fatigue). Its presentation is accelerated when metabolic activity is great at the time of death, in febrile states, in exertion, or during the summer.

In practice the duration of the rigor varies greatly and depends, according to Bendall, on the initial amount of phosphocreatinine and glycogen deposits, all conditioned by the temperature. At a constant temperature of 98.6° F. the rigor can vary from half an hour in an exhausted subject to four or more hours in a subject that is rested and fed. It is a general phenomenon in all animals (rabbit, steer, lamb, man) but there are always exceptions such as frogs and whales that have long delays, or chickens that start very quickly. Therefore, in the experimental data on animals, it is very important to know and appreciate the species before making rapid traspolaciones.


Gisbert points out, like all modern writers, that in the implementation phase “rigidity can be overcome by applying some force, with the limbs recovering their flaccidity, but after some time the process recommences, with the muscles becoming rigid once again.” According to Thoinot, and as a general rule, it can be argued that, under normal conditions, if within the first 7-8 hours we overcome the rigidity by applying an external force, it is restored spontaneously, although less evident, in a period of four to six hours. After eight or nine hours the rigidity is not recoverable. In the case of the Shroud, the shoulder rigidity is overcome in order to place the arms on the abdomen.

Also one must keep in mind that in the active phase, the stiffness is of such intensity that the force may cause tears and Gisbert himself adds, “in the second phase or state period, the rigidity is almost invincible without producing tears or fractures.” We now know, and experience confirms, that once the rigidity is established, the force that must be applied is considerable, and may cause fibrillary breakage, joint dislocation or malposition, a repetitive phenomenon in autopsy rooms when the stiffness is overcome to initiate autopsy. This is a point that should also be considered in the case being studied, because the shoulder subluxation, presented by the Man of the Shroud, whose explanation has been attempted in so many ways, clearly has this origin. Rigidity in this case was fully established.

In the resolution phase, if the rigidity is overcome, it is not recovered. Louis said, many years ago, that if a stiff joint is forced, it becomes indifferent to all movements, a simplistic approach from a pioneer of forensic medicine, because many authors, especially Thoinot, have pointed out this extreme when they affirm that this is valid for the active period, since the joints if forced start the process of becoming rigid again after a few hours. Niederkorn has concluded in his study that if the rigidity is overcome in the active period, it is restablished with an intensity that is inversely proportional to the postmortal period. At 20 hours the phenomenon is no longer produced.

Development and modifying circumstances

Rodriguez Pazos has drawn attention to the paucity of research done on human skeletal muscle. Most of the research on muscle cell death has been done on myocardium and little on skeletal muscle, mostly on animal bodies, hence the existing opinions that often depend more on subjectivity and the authors’ experience than on rigorous experimental measurements.

There are also numerous factors that have been collected in forensic literature throughout the years, which determine the onset of rigidity, according to the above overview. Therefore, in order to calculate how and when the body produces the rigidity, it is necessary to consider the extrinsic or external circumstances, as well as those of the subject.

From this point of view it is necessary to analyze the death of Jesus Christ through the known data, which are corroborated on the Shroud of Turin and the Sudarium of Oviedo, in order to, in view of this data, analyze it as modifying factors.

Death on the cross is primarily asphyxial death. In the image on the Shroud, there are reflected two repeated positions caused by the "air hunger" experienced by the victim. This situation involved an enormous muscular exercise, increased fatigue, accumulation of metabolites, muscle pain and repeated cramps, lymphocytosis and then neutrophilia (35,000 cells), hypersecretion of the adrenal glands that causes increased compensatory arterial tension, decreased eosinophils and increased fibrinolytic activity.

Subjects who have died by hanging have an intense fever of about 104-105.8° F. and higher, hypoglycemia with pronounced weakness, profuse sweating, blurred vision, headache, palpitations, nausea, even vomiting, and severe dehydration due to lack of fluid replacement, exercise, loss of breath and bleeding. Consequently, there is intense thirst.

As a result of the diversion of fluid to the intratissue space and peripheral blood deviation to the lower planes, the general dehydration is accentuated, especially in the upper half of the body.

On this general asphyxia picture was being imposed the shock that, in the case of Jesus was manifold: First a psychogenic shock that he experienced in the Garden of Olives, which caused loss of water and blood and softened the skin to future injury. Secondly neurogenic shock originated due to continuous pain experienced throughout the Passion (crown of thorns, beatings, abuse, flogging and median nerve injury), powered by the undoubted emotional component caused by knowledge and logic sensibility.

Third, hypovolemic shock caused by blood loss due to hematidrosis, bleeding from the scourging and crucifixion with intense thirst that increased anxiety and pain. Hypovolemic shock would be the root cause because it causes hypoxic damage at the level of microcirculation, abduction and hypostasis of the blood, increased vascular wall permeability, tissue acidosis, closure of vascular circuits, reduced blood volume, from venous return and cardiac output, decreased plasma volume, increased platelet aggregation, release of plasma triggers, increased vasopressin and angiotensin, pulmonary shock with profound alteration of the ratio of ventilation/perfusion, and pulmonary edema that is enhanced by the component distribution.

Fourth, distributive shock caused by asphyxiation and by the anomalous hanging position that presupposes vertical immobility, which causes a progressive fall in blood pressure, as seen in the abnormal pendulous abdominal image.

Finally, cardiogenic shock causes metabolic cardiac alterations and the final arrest of the heart.

This view is confirmed by the Sudarium of Oviedo, according to which the subject died hanging, as a result of heart failure that caused great pooling and pulmonary edema.

Intrinsic circunstancias

Empirically, Brown-Sequard had found that the stiffness depends on the condition and integrity of the musculature. A natural death without nutritional affectaton, muscular integrity, and violence causes intense, lasting, and late rigidity. In the Man of the Shroud muscle masses are tremendously bruised and contusions are numerous, which cover 50% of the body, as calculated by Diggio. Therefore, the degree of muscular integrity was very poor. Following Nysten’s laws, in muscular subjects and individuals with good nutrition, stiffness is delayed, intense and lasting; conversely, the destruction and muscular injuries cause stiffness that is early, short and weak. For the same reason in individuals who are tired and exhausted, as in the case of Jesus, the rigidity appears close and weak (Brown-Sequard). One must also consider the possible prior violent muscular activity, caused by transfers, abuse and asphyxia crisis on the cross. Husband has studied some of the factors influencing the stiffness, including violent exercise prior to death. In these cases the stiffness rapidly disappears and is early, weak and short. In all cases, the availability of glycogen and adenosinetriphosphatase is lower and both substances are essential in the development of the stiffness. In this type of death hypoglycemia is the rule as the glycogen stores depleted. Thus, muscle activity, acidity and fever shorten the process.

Sex is a conditioning factor to be taken into account, not only in the rigidity process but also morphometrically and histochemically. Brooke and Engel have described these differences that, together with age, modify the contractive functionality. In the man it is more intense, late and lasting than in the woman, but the physical deterioration of Christ makes it so that this factor cannot be measured.

Age influences equally. In children and the elderly it is is precocious, weak and short. Thus prepubertal, pubertal, juvenile and average rigidity have been described, where rigidity becomes intense, late and lasting. In the case we are studying, it is an adult subject, but badly damaged by abuse; therefore this factor is not applicable.

Type of death is another element that brings great variability. Fever causes a precocious rigidity, short and weak. In the case of Christ, the fever at death had to be extremely high. The same happens when preceded by a long agony. In these cases the stiffness is also early, weak and short. An agony with seizures (tetanus, stricnine intoxication, alkaloid poisoning (Taylor), or insecticides) causes a rigidity that is early, intense and long. This effect is known in many other types of intoxication, such as CO, As, or chloroform, which also make it early, intense and long, due to convulsions preceding death. Electrocution, which causes a death with strong muscle spasm or convulsions, causes rigidity that is early, intense and long, as Lombroso himself described.

Factors of external origin

The outside temperature, as was the case with the interior, is very important in the establishment and, above all, in tanatocronological evolution. As stiffness is the result of a biochemical process, the temperature greatly influences it; generally outside heat makes the rigidity early and intense and its conclusion is also rapid.

Nysten had already shown that rigor mortis increases with temperature; Kussmaul, Husband, Morgenstern, Foster et al., Bendall and Davey, among so many others, have also recorded it. Both exterior and interior heat (especially fever) makes the rigidity early and intense, and its conclusion also rapid. In the experimental series carried out ​​by Brier and Freund, high environmental temperatures have produced very early rigidities; from 122° F. the time varies between instantaneous and 15 minutes, reaching full rigidity between 10 and 45 minutes. In contrast, it is admitted by all authors that cold causes delayed and prolonged stiffness. Below 50° F. it is usually not observed.

Today we know that rigor mortis is developed in three distinct phases (already discussed in detail above):

– Delay phase that maintains the muscle properties.

– Rapid phase characterized by loss of extensibility and the beginning of pronounced shortening in the muscle fiber.

– Post-rigor stage in which the muscle makes itself extensible again, but to a lesser extent than in the first phase.

These phases, according to research conducted at the Langfootf Institute for Research on flesh, can vary considerably as do the premortem circumstances and the temperature and provides the following variants that are summarized below:

– In well-fed animals immobilized pharmacologically before death, with ambient temperature of 62.6° F., and with ambient temperature of 98° F. Not applicable to our case.

– Animals that are agitated or suffer seizures before or during death: The duration of the rigor is more limited.

– Animals that are hungry or starving, sedated before death: The total duration of the rigor is diminished.

These variations are due to the different amount of deposits of ATP, phosphocreatinine and glycogen, as well as the type of initial pH of rigor. The muscles of agitated animals exhibit very low levels of ATP, phosphocreatinine and glycogen and a pH value that is low because of the amount of lactate produced during the premortem agitation.

Bendall has also observed that the muscular work in rigor mortis increases with temperature and high pH values​​. Muscular acidity has been invoked as a trigger, but if we take away the acidity by means of acid monoiodoacetic poisoning, rigidity also appears. Today the rigor mortis is classified as rigor acid, characterized by being of great length and synchronism with temperature, and rigor alkaline, with pH above 7.2 of rapid onset, even at room temperature, and which causes a great hardening and shortening of the muscle fiber. It favors the predominance of red type musculature and stress or struggle during the agony. This is perfectly applicable to the case of the Man of the Shroud.

The importance of muscular hydration has indeed been shown, which delays it, while dehydration accelerates it. The degree of hydration is also essential. For this reason, when there is anasarca, or edema, the excess hydration makes its appearance difficult. It can even appear at a different rate in the limbs according to their water content. This phenomenon explains the upper limb rigidity being higher than the lower limbs, which is described by the authors.

Muscle dehydration causes immediate rigidity, as Lacassagne and Martin have reported, by injecting dehydrating chemicals (chloroform, calcium chloride), which was checked by Küsmaul (lime water, potash, vinegar, nitrated water and potassium carbonate) and by Coze using chloroform. In such cases the rigidity appears quickly. This happens in dehydrating diseases (cholera, heavy bleeding, cachexia, death by thirst) and varying degrees of stiffness may be obtained experimentally by regionally injecting the muscle mass. Large hemorrhages act equally to greatly reduce tissue hydration and then the stiffness becomes early, weak and short. Throughout the Passion of Jesus, a progressive dehydration is maintained; the very fact of nudity on the cross facilitates copious sweat evaporation and accentuated dehydration.

Therefore, in view of the foregoing in relation to the intrinsic and extrinsic modifier causes acting on the rigidity, it is consistent and rational than the stiffness would have occurred at an early stage.


Differential diagnosis

There are a series of scenarios of postmortem muscular contraction that can simulate rigor mortis and require, therefore, differentiation based on the data we have in relation to the death of Jesus:

In the medical literature identification problems could be provided in the following cases:

– Firstly cataleptic hysterical, hypnotic or schizophrenic rigidity that has caused death misdiagnosis due to faulty, superficial examination. A brief clinical study demonstrates the vitality of the subject and the lack of other cadaveric phenomena; forced rigidity immediately recovers its position; electrical stimulation causes muscle response. On the Shroud the lesion data and cadaveric signs are many and of such a nature that they make it impossible to maintain, from the point of view of forensic expertise, that the Man of the Shroud was alive.

– Rigidity by postmortem heat is another possibility that in this case is excluded in the absence of corporal signs of burning. It is due to denaturalization and precipitation of muscle proteins by heat. It is a permanent stiffness that when forced produces muscle tears. Furthermore, the general morphology of the scenario completes the diagnosis.

– Possible rigidity from cold can also be excluded given the characteristics of the image, its background and historical data. It is due to freezing of the corpse. The pressure of the muscles produces a characteristic crack from breakage of the ice crystals that have originated at the intracellular level. Once thawed, specifically cadaveric rigidity reappears.

– Another hypothesis that has come to be considered in studies of rigor mortis is possible decerebrate rigidity. This is a generalized hypertonic contracture of skeletal muscle, with rigid extension of all four limbs in the upper internal rotation with adduction of the lower limbs, and opisthotonos inclination of the neck and trunk. It comes in peduncular lesions, massive cerebral hemorrhage. Typical example among Spaniards is that of the fatally stabbed bull, a case of rigidity instantaneous with the injury. It also should be excluded because, while constituting a spastic reflex scenaro, the bull is unable to retain the posture it had at the moment of death.

– Decorticate rigidity. It originates in injuries above the brainstem, immediately close to the hemispheres or bilateral intrahemispheres. In that case we find the subject with a rigid extension of the legs and hypertonic flexion of the upper extremities. For the same reasons it may also be excluded.

– Tetanus. There may be a generalized spasticity due to the diffuse action of the toxin on the nervous system with the release of peripheral motoneurons, but the contracture that originates is different from what is offered on the Shroud.

– Cadaveric Spasm: This is a special rigidity of vital character that appears at the time of death, fixing the position of the body. It can be general or partial, segmental, from the physiognomy or posture.

In these cases, the rigidity is established without any transition, immediately after the rearward muscular contraction. This contraction is held fixed and with unchanged posture. The rigidity that would follow merely fixes and accentuates the spasm. Etienne Martin defines the cadaveric spasm as the persistence after death of a spasm given voluntarily in life and that continues in the corpse. There is, therefore, no prior period of relaxation.

It originates in preference to violent deaths by firearms, injuries to the nervous system, especially accompanied by cerebral hemorrhages, and violent deaths accompanied by convulsions, deaths from lightning and asphyxia, especially by drowning, tetanus, strichnic poisonings, proven by Sommer, Haen, Gentz​​, Küsmaul, Tourdes and many forensic pathologists. This is an antigravity muscle contracture, which by its nature is easily detectable. Arnaud, Perier, Chenu, in the wars of Italy and Crimea; Neudurfer, Brinton, in the wars of succession; Rossbach in the Franco-Prussian War, also described in our Civil War and, in general, on all battlefields.

It is a very rare phenomenon. Polson and Gee, in 20 years of practice, saw only two cases. Schneider adds that most of the cases reported in the literature are of war or secondary to electrocution. Bauman has shown how most of these cases occur when there are head injuries, brain or brainstem, and thoracic injuries with possible gas embolism.

Its mechanism is not well known. Most of the authors, following Brown-Sequard, explain the spasm by neural mechanisms, although in these cases the bulboprotuberancial region is not directly concerned. In them, the injuries causing death would determine an inhibition that the marrow would release. Thanks to that, the muscular system would retain its vitality and would even exaggerate it sometimes, setting the body in the posture it had at the time of death. For Magnus and Sherrington, for Laves and Prokop, it would be a form of decerebrate rigidity; however, we have pointed out above the differences that exclude this etiology. For Perez Argilés it would be due to a release of acetylcholine. In any case the mechanism is not yet known in detail, however, its existence is an undeniable reality. Peiró proposes, as a differentiator of the rigidity of a vital contracture, mechanically forcing muscular action. If it is stiff, the limb remains in the new position and it does not occur in vital contractures that attempt to return to the initial position.

Delgado Roig gives as an example of a generalized spasm the image of Christ's Atonement of the Seville Museum Guild, attributed to Marcos Cabrera. Adalberto Pazzini has described the same phenomenon in numerous representations of the crucifixion of Christ of the thirteenth century. In the medical field, Le Bec, in 1925, Barbet, Hynek, and De Vicentiis relate the phenomenon to the effort and muscular tetanization Christ suffered on the cross, to which we must add the full range of additional pathologies that sharpened the scenario.

However, in the present case there is a datum that allows exclusion. Thoinot noted that “a major difference exists between early stiffness and cadaveric spasm, as the first assumes prior muscle relaxation, the shorter it is, the sooner the muscles become stiff. In cadaveric spasm it does not exist, however there is intermediate relaxation, immediately succeeding muscle contraction and rigidity. The result is that the early stiffness, as rapid as we might guess, cannot set the body in a posture adopted during the last moments of life when this position is contrary to the laws of gravity. Muscle relaxation intervenes in fact to destroy this position, which remains fixed, rather in the cadaveric spasm.” There is eyewitness testimony that allows us to exclude a possible cadaveric spasm and it is provided by John in his Gospel (John, 19. 30), “and he bowed his head and gave up his spirit.” The cervical inclination is secondary to muscle relaxation. There was, therefore, a prior period of relaxation before proper stiffness was instituted.

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