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CHANGES IN THE MUSCLES AFTER DEATH

After death, all muscles of the body (voluntary, involuntary and cardiac) pass through 3states:-
(i) Primary relaxation [primary flaccidity]
(ii) Rigor mortis [RM] and
(iii) Secondary relaxation [Secondary flaccidity].

Q). Short note on Primary relaxation?


A). Definition - Primary relaxation [or flaccidity] is complete relaxation of muscles in the period immediately after somatic death and no cellular
death. All muscles of the body begin to relax soon after death.
Salient features: (1) Relaxation of skeletal muscle causes following changes:
(i) Contact flattening [flattening of muscles in contact with the surface, eg gluteal and scapular muscles, when body is supine]
(ii) Eyelids – lose tension
(iii) Lower jaw - falls
(iv) joints become flexible
(2) Muscular irritability and response to mechanical or electrical stimuli persist.
(3) Peristalsis may occur in the bowel, and ciliary movements and movements of white cells may continue.
(4) Discharges of the dying motor neurons may stimulate small groups of muscle cells and lead to focal twitching, although these decrease with
time.
(5) Anaerobic chemical processes may continue in the tissue cells, e.g., the liver cells may dehydrogenate ethyl alcohol to acetic acid, and complex
chemical changes may occur in the muscles.
(6) Pupils react to atropine or physostigmine but not to light.
(7) Relaxation of involuntary muscle [Loss of muscle tone in the sphincters ] causes following changes:
(i) pyloric sphincter - duodenal contents move up->bile staining of stomach walls
(ii) anal sphincter - emptying of rectum,
(iii) bladder sphincter – emptying of bladder
(8) Persists – muscles are relaxed as long as the ATP content remains sufficiently high to permit the splitting of the actin-myosin cross bridges,
throughout supravital period [i.e. about 3 h]. All cellular functions continue as in supravital period
(9) Muscle protoplasm – slightly alkaline.

Q) Write a short note on Rigor Mortis?


A) (I) Definition - Rigor mortis [L. rigor, stiffness; mortis, death] (syn cadaveric rigidity; death stiffening, RM) is a state of stiffening of muscles,
with very little shortening of fibers, that occurs soon after death.

(II) Mechanism of RM: Rigor mortis is a physico-chemical change that occurs within muscles. A voluntary muscle consists of bundles of long fibres.
Each fibre is formed of densely packed myofibrils extending through its whole length. A sarcomere is the basic unit of a muscle. Sarcomeres are
multi-protein complexes composed of Actin (thin filaments) and Myosin (thick filaments). Proteins constitute 80% of dry muscle weight. Contractile
proteins constitute 60% of all muscle proteins [(Of these, the main proteins are actin (20%) and myosin (60%).

(1) During life in a relaxed state – Myosin remains in a "hydrated" state due to the presence of ATP molecules on its surface, which remain
"adsorbed" to its surface. The ATP molecules keep the muscle in a hydrated state (and thus soft and supple). ATP is responsible for elasticity
and plasticity of the muscle. Actin filaments interdigitate with the myosin filaments only to a small extent.

(2) During life in a contracted state - Under the influence of a nerve impulse, actin filaments are drawn into the arrays of myosin filaments (much
like pistons into cylinders). This causes the muscle to contract. There is appreciable shortening of sarcomere. During life, the separation of the actin
and myosin filaments, and the energy needed for contraction are dependent on adenosinetriphosphate (ATP) The ATP molecules present on the
surface of the myosin molecule prevent a permanent cross-linkage between actin and myosin filaments. Note that the cross-linkages are not quite
reaching the myosin filaments.

(3) Supply of ATP during life: Three metabolic systems are responsible for maintaining a continuous supply of ATP in the muscle:
(i) Phosphagen system.
(ii) Glycogen-lactic acid system.
(iii) Aerobic system.

(4) Metabolism of ATP: - The dephosphorylation of ATP by the action of ATPase produces ADP and phosphate, and a large amount of energy,
which is used for muscle contraction. The free phosphate then engages in a phosphorylation reaction that converts glycogen to lactic acid. The lost
ATP is replaced during life by resynthesis, which is dependent upon the supply of glycogen. The lactic acid enters blood stream and reconverted to
glycogen in the liver. At the time of somatic death, enough ATP is present in the muscle to maintain relaxation.

(5) Mechanism of muscles contraction after death - After death the ATP is progressively and irreversibly destroyed leading to increased
accumulation of lactates and phosphates in the muscles. There is no resynthesis of ATP. The postmortem alteration of ATP is due to
dephosphorylation and deamination. Postmortem loss of integrity of the muscle cell sarcoplasmic reticulum allows calcium ions to flood the
contractile units of the muscle fibres (sarcomeres) initiating the binding of actin and myosin molecules and mimicking the normal contraction
process. Normal relaxation in life is achieved by energy-dependent (ATP-driven) pumping of calcium back across the membrane of the
sarcoplasmic reticulum, but this fails after death because of membrane disruption and lack of ATP, due to which increased calcium level in the
sarcomeres causes muscle contraction.

(6) After death -Two conditions may prevail (i) either the muscle was robust with abundant supply of glycogen and ATP or (ii) the muscle was
depleted (starvation, violent exertion just before death) of glycogen and ATP. In both cases, slightly different course ensues,

(i) When muscle was robust with abundant supply of glycogen and ATP - Anaerobic glycolysis continues to occur, producing more ATPs. This
results in formation of lactic and pyruvic acids [lactic acid content of resting muscle during life is 0.03%; during RM->0.3%]. Muscle pH decrease.
When the pH reaches 5.8, glycolysis stops. Anyway by this time, very little glycogen remains in the muscle. From this point on, ATP molecules
continue to deplete from the surface of myosin. When they are completely consumed, "permanent”, irreversible cross-linkages form between actin
and myosin filaments (actinomyosin complex). There is no appreciable shortening of sarcomere. During life muscle is alkaline [pH 7.3]. Since the
pH of muscle reaches 5.8 (acidic), the rigor (produced under initial conditions of abundant glycogen and ATP) is known as acid rigor,

(ii) Muscle was depleted with minimal glycogen stores - Lactic and pyruvic acids are not formed. Rigor occurs, but muscle remains alkaline
[alkaline rigor].

(7) Chemical conditions required for onset of RM: (i) ATP – RM starts when ATP has fallen to 85% of normal. When the ATP is reduced to a
critical level (85% of the normal), the overlapping portions of myosin and actin filaments combine as rigid link of actomyosin, which is viscous and
inextensible, and causes hardness and rigidity of muscle rigor. The rigidity of the muscle is at its maximum, when the level of ATP is reduced to
15% and lactic acid level is 0.3%. If at the time of death itself, ATP have reduced to this level [due to consumption of ATP due to violent activity
during life], muscles may immediately go in contraction after death [Biochemical explanation of cadaveric spasm],
(ii) Free Ca++ ions- Rigor is inhibited by calcium binding agents eg EDTA.

(8) Strength of muscle decreases. Load required for tearing fresh muscle->8kg/cm2. Load required to tear muscle in RM -> 4-6kg/cm2.

(9) Integrity of nervous system - RM does not depend upon it. It is concerned with muscles only. Thus it would appear (i) in an amputated limb
[even though the person may be alive] and
(ii) Even in a person who was paralyzed [eg poliomyelitic] during life. It however appears more slowly and is less intense due to lesser muscle mass
(iii) it appears even in meat kept for longer periods, making it harder.

(10) Development of RM – Before rigor mortis develops, the body can be moved to any posture and the rigor will fix in that posture. When rigor is
developing, the extremities can be moved and the rigor, temporarily overcome, develops later and fixes the extremities in their new position,
although the rigidity will be less than other symmetrical groups which have not been disturbed. Skeletal muscle contains two types of fibres. (i) Type
I (red) which are rich in mitochondria with dominant oxidative metabolism. (ii) Type II (white) which are relatively poor in mitochondria with dominant
glycolytic metabolism. Rigor occurs at different times in the above types of muscles.

(11) Artificial breaking of RM - If the rigor is broken before it is fully developed; a variable extent of rigidity will reappear. The fibres which are still
slack and some others which are not fully contracted, retain capacity for reversible binding of myosin heads to actin filaments. Re-establishment of
rigor occurs due to contraction of such fibres. However once fully established, breaking of RM in joints is irreversible. If force is applied when rigor is
fully developed, stiffness is broken up permanently and the rigid muscles may show postmortem ruptures. Frequent handling of the body breaks
the rigor in certain places, leaving a patchy distribution.

(12) Persistence – Rigor persists until the onset of putrefaction. The actin-myosin complex is trapped in a state of contraction until it is physically
disrupted by the onset of putrefaction. This process is characterized by proteolytic detachment of actin molecules from the ends of the sarcomeres,
and consequent loss of the structural integrity of the contractile units which breaks down proteins including the actinomyosin complex. The muscles
then soften and relax. Muscles become limp again [secondary relaxation].

(III). Order of appearance of Rigor - RM is of great importance in food industry; handling, packing, processing, and freezing of fish should be
avoided when it is in rigor.
(1) Methods to assess RM - Several methods have been developed to assess the extent of RM in fishes. These include:
(a) visual assessment by extent of sag
(b) measurement of flexibility of fish by rigor index method [by determination of the extent of sag of the tail]
(c) monitoring isometric muscle tensions and shear strength
(d) Mechanical rigorometer

(2) Order of appearance in all muscles - Cardiac muscle [ Myocardium becomes rigid in 1 hour] -> Involuntary muscles -> Voluntary muscles
(3) RM in Heart – may simulate hypertrophy
(4) Features of RM - When rigor is fully developed, the entire body is stiff, the muscles shortened, hard and opaque; knees, hips, shoulders and
elbows are slightly flexed and fingers and toes often show a marked degree of flexion.
(5) RM in involuntary muscles may result in misleading artifacts:-
(i) Arrectores Pilorum – rigor of erector pilae muscles attached to the hair follicles, causes:
(a) Cutis anserina or goose skin – roughness, pimpling or goose-flesh appearance of the skin with elevation of the cutaneous hairs.
(b) Hair may erect and may appear longer. This has given rise to the myth that hair continue to grow after death,
(c) Five o'clock shadow — The term refers to beard stubble that is visible late in the day, usually around 5 o’clock, on men who have shaved their
faces that morning. Beard may give this appearance due to erection of hair, and may lead an inexperienced investigator to conclude that death
occurred around 5 pm.
(ii) Iris - may affect each iris different producing anisocoria [unequal size of pupils]
(iii) Rigor in cremaster muscle causes the testes to be drawn up into the groin; and rigor in dartos muscle can compress testes and epididymis –
these lead to postmortem extrusion of semen out of seminal vesicles through urethral meatus and present at the tip of penis
(iv) Rarely, if the uterus is in labour at the time of death, the rigor mortis may cause the uterus to contract and expel the foetus
(v) Heart - In the heart, rigor causes ventricles to contract which may be mistaken for left ventricular hypertrophy. This can be excluded by
measuring weight, estimating the relative size of left side and measuring ventricular thickness.
(vi) Facial grimacing - Muscle relaxation immediately after death with opening of the eyes and mouth and subsequent fixation in rigor mortis often
occur after death, giving the face the appearance of grimacing, but this does not reflect whether the individual's last moments were of fear or fright.

(6) Nysten's law [Proximo-distal progression of RM] - is applicable to voluntary muscles. It states that muscles which are nearest to the brain go
into rigor first, and those which are farthest go into rigor last. It begins in the eyelids, neck and lower jaw and passes upwards to the muscles of the
face, and downwards to the muscles of the chest, upper limbs, abdomen and lower limbs and lastly in the fingers and toes. The lactic acid enters
blood stream and reconverted to glycogen in the liver. In individual limbs, it usually progresses from above downwards. Such a sequence is not
constant, symmetrical or regular. In individual limbs, it disappears in the same order in which it has appeared. Rigor mortis always sets in, increases
and decreases gradually Thus RM appears in this order: eyelids [1-2 h] -> jaw TMJ] [3 h] -> upper limbs [6 h] -> lower limbs [9 h] -> fingers
and toes [12 h]. [After French pathologist Pierre-Hubert Nysten (1774- 1817), who enunciated the law in 1811].

(7) Theories - Since RM is a physicochemical process, it must start simultaneously in all muscles. Thus it is not clear why RM should appear in a
proximo-distal fashion. Following theories attempt to explain this paradox:-

(i) Shapiro's theory [1950] - According to this theory, rigor mortis does not follow the anatomical sequence usually described. He suggests that as
rigor mortis is a physicochemical process, it is most likely to develop simultaneously in all the muscles, although the changes are more easily
first detected in the smaller masses than in the larger. The proximodistal progression is more apparent than real, for the sequence is determined
by the bulk and kind of muscle involved.
(a) Proximal joints [eg temporomandibular joint, elbow joint] have shorter and less bulky muscles around them as compared to distal joints [eg hip]
which have larger muscles,
(b) At any given point in time, longer length of larger muscles allows more movement of joints than shorter muscles even when both are in the same
degree of RM.
(c) This gives an impression that shorter muscle have gone into RM earlier. If so, why small muscles of fingers and toes are last to stiffen,
(d) Shapiro explains that stiffening of these muscles is not due to muscles around finger joints, but due to stiffening of larger muscles more
proximally located, whose tendons end in fingers and toes.

(ii) Red muscle theory- Rigor mortis progresses [rapidly in red than in white muscle fibres. Masticatory muscles have red fibres. This rigor mortis
appears earlier in jaws.
(iii) Insertion of tendon theory - Insertion of tendon and its length determines movement of joint. If it is short [as in TMJ], it is immobilized earlier; if
longer as in fingers and toes, they are immobilized later.

(iv) Cooling theory - Distal muscles cool faster due to larger surface area. RM appears late, as it depends on temp.

(v) Supply of glycogen and ATP molecules at the time of death is more in larger muscles than in smaller muscles. Thus larger muscles take longer
to deplete their ATP supply.

(IV). Time of onset and Duration of RM


(1) Onset - In India, it begins 1 to 2 hours after death and takes further 1 to 2 hours to develop and gets well established in the entire body in 6 h
in summer. In temperate countries, it begins in 3 to 6 hours and takes further 2 to 3 hours to develop. The so called rule of 12 [march of rigor] is
not applicable in tropical countries.[ as per Reddy]
(2) Duration - In India, (i) usually in winters - it lasts 24 to 48 hours and, (ii) in summers – it lasts 18 to 36 hours. It may begin to disappear in about
12 hours. In temperate regions - It lasts for 2 to 3 days. Times are variable, because of many extrinsic and intrinsic factors. When rigor sets in early,
it passes off quickly and vice versa.[ as per Reddy]
(3) Rigor mortis appears - in the entire body in 12 hours
(4 ) Persists - for another 12 hours
(5) Then disappears - in next 12 hours in the same proximo-distal fashion in which it appeared. The body is again relaxed in 36 h [secondary
relaxation]

(V). Demonstration of RM
A. In skeletal muscles:
(1) Eyelids - try to open eyelids gently
(2) Jaws - Try opening jaw and see whether they can be opened easily or not
(3) Upper limbs – Trying bending and extending the hands at shoulders, elbows and wrists and note rigidity at all joints. Alternatively upper limb
may be held in such a position that forearm should be free to fall with gravity. If it remains in place, the elbow is in rigor mortis
(4) Lower limbs - Trying bending and extending the lower limbs at hips, knees and ankles and note rigidity at all joints. Alternatively lower limb may
be held in such a position that leg should be free to fall with gravity. If it remains in place, the leg is in rigor mortis.
(5) Fingers and toes - try opening the fist, if it is closed. Then try bending and extending fingers, thumbs, toes etc.
(6) Note the degree (absent, minimal, moderate, advanced or complete) and distribution.

B. In cardiac and smooth muscles:


(1) Heart - appears tougher and more “solid” in RM. In animals, it has been demonstrated (i) by a Hg manometer connected with the ventricular
cavity by a tube either passed through the ventricular wall or introduced through the auricle, and (ii) by observing the height to which the blood rises
in a vertical tube of small caliber pushed through the cardiac wall into the cavities; the tube has a sharp bevelled point and is washed out with 25%
MgS04, soln just before using. A minute snip is made through the epicardium to permit the entrance of the point of the tube.

(2) Smooth muscles - There is no convincing way to demonstrate RM in smooth muscles [eg trachea, intestines, bladder etc]. Hg manometer
connected to bladder etc may be used to determine pressure. The most convincing way to demonstrate RM in all muscles is by E/m.
(VI). Conditions altering onset and duration of RM
All the following conditions can be easily explained on the basis of formation of actinomyosin complex. If muscular ATP reserve was more at the
time of death, and its consumption slower after death, it would take longer to deplete and RM would develop late, and vice-versa.
i. Age
(1) Rigor mortis appears in all ages, even in fetuses. It is wrongly taught sometimes that RM does not appear in fetuses <7 m. As long as there is
muscle, the actinomyosin complex would form, and RM would set in. Muscles in a fetus begin to form at 8 weeks. A fetus <8 weeks may not show
RM simply because he does not have muscle.
(2) Stillborn fetuses at full term- would develop RM. RM has no value as a sign of live-birth.
(3) In children and old people - feeble; develops rapidly; passes away early
(4) Healthy adults -strong and well marked; develops slowly; lasts longer; passes away late.

ii. Nature of death


(1) RM sometimes absent in - septicemia
(2) RM appears early and passes away early [duration short] in:-
(i) Conditions causing great exhaustion and wasting –
(a) bacterial infections [esp gas gangrene, where putrefaction begins early]
(b) cancer
(c) cholera
(d) starvation
(e) tuberculosis
(f) typhoid
(ii) Death preceded by convulsions - (a) DDT, (b) OP, (c) Strychnine, (d) Tetanus
(iii) Violent deaths - (a) Cut throat (b) Electrocution (c) Firearms (d) Lightning

(3) RM appears late and passes away late in: (i) Apoplexy (ii) Asphyxia (iii) CO (iv) Hemorrhage [severe] (v) Neuromuscular disorders
(vi) Perfusion with normal saline (vii) Pneumonia

iii. Muscular state


(1) Muscles healthy and were at rest before death -> Onset slow, duration long, strength substantial
(2) Emaciated, weak persons -> Onset slow, duration short, strength weak
(3) (i) convulsions (ii) Exercise [heavy and violent] (iii) Exhaustion (iv) Fatigue (v) Running [excessive as to save from assailant. Rigor appears
quicker in legs than other body parts] (vi) Strenuous work (vii) Struggle - >Onset rapid, duration short

iv. Atmospheric conditions


(1) Cold dry weather -> Onset slow, duration long
(2) Hot weather -> Onset rapid, duration short [because of the increased breakdown of ATP]
(3) Extremely hot environment – RM may disappear in 12 hours after death as decomposition begins.
(4) Refrigerated condition – RM may persist for 3-4 days.
(VII). MLI of Rigor Mortis
(1) It is a sign of death
(2) Helps in estimation of TSD to some extent - from the practical angle, corpses may be divided into three categories depending upon the
progression of rigor mortis:
S. No Rigor Mortis Time since death
1 Body is still warm, without any Rigor mortis About a couple of hours previously
2 Rigor progressing but not established in the entire body Death within about 4-12 hours previously
3 Rigor mortis well developed in the entire body Death beyond 9-12 hours
To bring better approximation, degree and extent of rigor in the various parts of the body should be determined

(3) It indicates position of body at the time of death. If for examples arms are in rigidity extending up in air, it may indicate that they were initially
resting on a chair, which was subsequently moved away.

(vii) Antenatal Rigor mortis


(1) Few cases of rigor mortis before death [antenatal rigor mortis] have been described.
(2) In one case, it developed in a live patient after cardiac surgery. Factors responsible were intense low cardiac output status, use of unusually high
dose of inotropic and vasopressor agents and sepsis.
(3) Antenatal RM in heart - has been described after open heart surgery. It is an ischemia related, irreversible contraction of heart [stone heart]
(4) It is of importance when determining TSD.

Q) What are the other forms of stiffening which simulate Rigor Mortis?
A) Conditions simulating RM are:
1) Heat stiffening:
(i) Temperature causing heat stiffening - When a body is exposed to temperatures above 65°C, a rigidity is produced
(ii) Intensity of rigidity - which is much more marked than that found in rigor mortis.
(iii) Depends on factors - The degree and depth of the change depends on the intensity of the heat and the time for which it was applied.
(iv) Usually seen in - It is seen in deaths from burning, high voltage electric shock and from falling into hot liquid.
(v) Mechanism - Heat causes stiffening of the muscles, because the tissue proteins are denatured and coagulated as in cooking.
(vi) Appearance of muscles - The muscles are contracted, dessicated or even carbonised on the surface. A zone of brownish pink 'cooked meat’ is
seen under this, overlying normal red muscle.
(vii) Changes in posture, especially flexion of the limbs occur due to muscle contraction (Pugilistic or Boxer’s attitude).
(viii) Persists – The heat stiffening cannot be broken down by extending the limbs as in RM and will persists until the muscles and ligaments soften
from decomposition and the normal rigor mortis does not occur.
(ix) Shortening of muscle fibres – Unlike RM, heat stiffening is associated with considerable shortening of muscle fibres.
(x) Changes of heat stiffening have nothing to do with the life or the cause or manner of death in any way.

2) Cold stiffening:
(i) Temperature causing cold stiffening - When a body is exposed to freezing temperatures (-5°C or lower) before acid metabolites appear in the
muscles
(ii) Mechanism - the tissues become frozen and stiff, due to freezing of the body fluids and solidification of subcutaneous fat simulating rigor.
(iii) Rigor mortis – process of rigor mortis is suspended in such cases until thawing takes place. When the body is subjected to thawing, true RM
appears with great rapidity and passes off very quickly.
(iv) Condition of body - The body is extremely cold and markedly rigid.
(v) Forcible flexion - When the joints are forcibly flexed, crepitus may be felt due to breaking of frozen fluid in the joint space. Ice breaks in the
synovial fluid with a sudden sharp sound..
(vi) Misleading ligature mark - Hardening of the subcutaneous fat especially in infants sometimes makes the skin-folds rigid, which may be mistaken
for ligature mark. However, they coincide with the skin creases, are deepest at the front and do not exhibit any petechiae, abrasions or patterning as
might be expected in the seat of the groove of the ligature.

3) Chemical stiffening [embalming]

4) Gas stiffening (Gas Rigor):


(1) In about 2-3 days after death, putrefactive gases collect in s/ c tissues, muscles and around joints to stiffen the joints [putrefactive rigor mortis].
(2) Both upper and lower limbs are abducted, flexed and rigid; hands are open and fingers wide apart.
(3) The rigidity persists till gases escape during advanced putrefaction.
(4) This condition is especially seen in bodies recovered from water.

5). Cadaveric spasm or instantaneous rigor [Write a short note on cadaveric spasm?]
Definition - Cadaveric spasm [syn cataleptic rigidity, instantaneous rigidity, instantaneous rigor, and postmortem spasm] is a rare condition, where
the group of muscles which have been actively working and contracted at the moment of death becomes stiff and rigid immediately after death
without passing through the stage of primary relaxation. As such, the change preserves the exact attitude of the person at the time of death for
several hours afterwards.
Salient features:
(1) Predisposing conditions: It occurs especially in cases of intense physical and/or emotional activity.
(i) Cerebral hemorrhage
(ii) CNS injuries [eg Firearm wounds to the head]
(iii) Convulsant poisons [eg strychnine]
(iv) Excitement
(v) Exhaustion
(vi) Fatigue
(vii) Fear
(viii) Pain [severe]
(ix) Sudden death
(x) Drowning

(2) Last action - of the person is preserved or "frozen" for several hours after death

(3) Mechanism – Obscure and unclear. Some theories are


(i) ATP depletion at time of death- appears most attractive. Muscular contraction starts during last moments of life, i.e. neuromuscular stimulation,
but contraction is retained because of low levels of ATP [please see above-> mechanism of RM].
(ii) Failure of chemical processes- required for active muscle relaxation to occur during molecular death.
(iii) Adrenocortical exhaustion – Most improbable and controversial. It is said to impair re-synthesis of ATP after death. The theory automatically
implies that re-synthesis occurs after death in other cases. This has never been experimentally proved.

(4) Muscles involved- usually a single group of voluntary muscles and frequently involve the hands. Rarely entire body as seen in soldiers shot in
battle [battle-field rigidity],
Case studies –
(a) On one occasion, a soldier was seen in a kneeling posture apparently taking aim with his rifle. It was dark and he was told to get up. When he
failed to obey, someone pushed his shoulder, and his dead body fell over,
(b) In another instance, all wounded soldiers were dead and their entire bodies frozen as wax statues. A wounded soldier was seen holding his
water bottle as if drinking from it. The incident became known as “The Teaparty”.
(c) Rossbach (1870) describes the case of 6 soldiers who were killed by a shell. The head of one preserved his laughing expression, present at the
moment of death. The head of another had been blown off. He remained in a sitting position with cup still in his hand,
(d) Battle of Worth (1870) - at the third charge of the Cuirassiers, a horse was seen going at full speed with a headless rider. The mutilated corpse
was that of M. de la Futzun de Lacarre, Colonel of the 3rd Regiment of Cuirassiers, who had been decapitated by a cannon-ball,
(e) A man, wounded in the left breast at Belmont, Missouri, found a stray mule, which he succeeded in mounting. Whilst in the act of riding the
animal he died; but his corpse retained in an upright mounted position. When it became necessary to appropriate the mule to the use of a living
wounded soldier, the body was found to be so firmly and rigidly set, as to demand a certain amount of positive force to free the mule from the clasp
of the legs.

(5) Cannot be simulated - No other condition simulates cadaveric spasm and it cannot be produced by any method after death.
Eg by keeping the weapon in victim's hands. Case studies –
(a) R. v. Saville, 1844 — The prisoner was tried for murdering his wife by cutting her throat. In the deceased woman’s hand was found a razor, but it
appeared to be very loosely grasped. There was no blood on the hand holding the razor. The razor in this case had been placed in the hands of the
woman after death,
(b) R. v. Gardner [CCC, Oct, 1862] — The victim (a woman) died from several wounds in the throat [cut throat]. After death a table-knife was found
lying loosely in her right hand, but the back of the blade was toward the palm, and the weapon in the direction of the length of the body. It was
shown that the chief cut could not have been self-inflicted with the right hand. The knife had been placed in her hand after death. This was a case of
murder

(6) Disappearance – Very great force is required to overcome stiffness. lt passes without interruption into normal rigor mortis and disappears when
rigor disappears.

(7 ) MLI: (i) Differentiation between AM and PM drowning- by grass, weeds, leaves etc found firmly grasped in hands
(ii) Occasionally, in case of suicide the weapon, e.g., pistol or knife is seen firmly grasped in the victim's hand which is a strong presumptive
evidence of suicide. Attempts may be made to simulate this condition in order to conceal murder. Attempts to put weapon in victim's hands after
murdering him does not produce the same tight grip. Ordinary rigor does not produce the same firm grip of a weapon, and the weapon may be
placed in the hand in a way which could not have been used by a suicide.
(iii) Objects grasped in fist - of victim may give information about the assailant, eg hair, pieces of cloth [eg piece of shirt pocket], buttons etc. In fact
in all suspected homicide cases, the pathologist should first pay attention to the fists.

(8) Case studies:


(i) R. v. Ellison [Bodmin Assizes, 1845] — Hairs (gray and brown), corresponding in all respects to the hair of the prisoner, were found tightly
grasped in the hands of the murdered woman. This led to his conviction,
(ii) Tidy (1882) - described case of two lovers, who took cyanide for committing suicide. They were found folded in each other’s arms because of
cadaveric spasm,
(iii) Spilsbury (1944) - Describes the case of a woman who died of cerebral hemorrhage in her bath. She was found dead seated upright in the
bathtub. She held a sponge in her hand which was raised half way to her face

Q) What are the differences between Rigor Mortis and cadaveric spasm?
A)
S.No Feature Rigor Mortis Cadaveric Spasm
1 Onset 1- 2 h after death in skeletal muscles. Stage of primary Instantaneous. Stage of primary flaccidity is absent
flaccidity is present.
2 Mechanism Breakdown of ATP below critical level sometime after Complete exhaustion of ATP at the moment of death
death itself [ not clearly known]
3 Predisposing factors None. Occurs in all cases. But may be hastened or Excitement, exhaustion, fear, nervous tension, sudden
delayed by some factors death, Violent struggle, etc.
4 Molecular death Occurs Does not occur
5 On touching Body is cold Body is warm
6 Muscle reaction Acidic Alkaline
7 Muscles involved All muscles. Both voluntary and involuntary Voluntary muscles only; that too in a single group of
muscles usually
8 Simulated by Heat rigor, cold rigor, gas stiffening, and chemical None. Cannot be produced by any method after death.
stiffening. Freezing and exposure to temperature above
65°C will produce rigor
9 Primary relaxation Seen Not seen
10 Degree of muscle Not marked. Moderate force can overcome it Marked. Very great force is required to overcome it
stiffening
11 Electrical stimuli Muscles will not respond Muscles in cadaveric spasm would not respond, but
other muscles would
12 Duration of stay About 12-24 hours A few hours, until replaced by rigor mortis.
13 MLI Indicate TSD Indicates manner of death, and last action undertaken
by victim.

Q) Short note on Secondary Relaxation?


A) Secondary relaxation [or flaccidity] is complete relaxation of muscles after rigor mortis has passed away.
Salient features: (1) Mechanism - 3 theories
(i) Action on muscles of alkaline liquids produced by putrefaction
(ii) Excessive acid rproduced during RM causes dissolution of myosin
(iii) Autodigestion – enzymes developed in dead muscles which dissolve myosin.
(2) Secondary relaxation in heart may result in dilatation of the atria or ventricles which may mimic pathologic dilatation (antemortem dilatation) of
the chambers, or myocardial degeneration. Because of RM and secondary relaxation appearing in heart, it is not possible to opine if heart stopped
in systole or diastole.

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