85

Neuropsychiatric Casualties of Nuclear, Biological, and Chemical Warfare

Chapter 4

NEUROPSYCHIATRIC CASUALTIES OF

NUCLEAR, BIOLOGICAL, AND

CHEMICAL WARFARE

FRANKLIN D. JONES, M.D., F.A.P.A.*

INTRODUCTION

CHEMICAL WARFARE

Physiological Effects of Nerve Agents

Physiological Effects of Other Agents

Neuropsychiatric Syndromes Associated With Chemical Warfare

BIOLOGICAL WARFARE

Physiological Effects of Biological Agents

Neuropsychiatric Casualties of Biological Agents

NUCLEAR WARFARE AND DISASTERS

Physical Effects of Nuclear Warfare

Electromagnetic Pulse Effects of Nuclear Warfare

Physiological Casualties of Nuclear Warfare

Neuropsychiatric Casualties of Nuclear Warfare

Laser and Microwave Radiation

Treatment of Neuropsychiatric Casualties of Nuclear Warfare

SUMMARY AND CONCLUSION

*Colonel (ret), Medical Corps, U.S. Army; Clinical Professor, Uniformed Services University of the Health Sciences, Bethesda, Maryland; Past

President and Secretary and current Honorary President of the Military Section, World Psychiatric Association; formerly Psychiatry and

Neurology Consultant, Office of The Surgeon General, U.S. Army
War Psychiatry

86

Kerr Eby Match Sellers, Class of ’17 1918

Kerr Eby was initially a member of the Ambulance Corps in the U.S. Army in World War I, then transferred

to the Engineers, and went to the front lines in France. His painting depicts a group of soldiers blinded

during a gas attack. Whereas the neuropsychiatric casualties of other forms of warfare may present as

individuals, the casualties of nuclear, biological, and chemical warfare are most often seen as groups

because the agent, whatever it may be, is delivered in a dispersed form to affect as many troops as possible.

The title, Match Sellers, refers to a possible occupation, from a previous era, for these soldiers when they

return home.

Art: Courtesy of US Center of Military History, Washington, DC.
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Neuropsychiatric Casualties of Nuclear, Biological, and Chemical Warfare

INTRODUCTION

Although outlawed by both the Hague Convention1 and the Geneva Convention,2 chemical warfare continues to exist along with potential use of

nuclear and biological warfare. In recent wars it

has been alleged that the former Soviets used mycotoxins against Afghan guerrillas and that Vietnam

used “yellow rain” (mycotoxins) in Cambodia and

Laos. Iraq used chemical agents against Iranian

soldiers and Kurdish rebels, and had the ability to

use them against coalition forces in the Persian Gulf

War. The long history of the use of such agents is

likely to continue. This usage has usually occurred

when one side has, or believes that it has, superiority in such weaponry. During World War II, the

Germans had a superior capability in the form of

nerve agents; but, believing the Allies to have a

similar capability, they did not use them. There is,

therefore, a compelling argument in favor of the

deterrent effect of parity in chemical warfare capability. Tear gas and nausea-producing agents, which

were not designated as prohibited agents by the

Hague1

 and Geneva2 conventions, were used by

U.S. forces in Vietnam.3–5 Exhibit 4-1 reveals the

frequency of alleged usage of chemical and biological weapons since World War I. This review indicates that the U.S. armed forces or modern armies

must be prepared for the possible use of such agents

in future wars.

The use of tactical (battlefield) nuclear weapons

is possible not only between the major powers but

also between smaller industrialized and nonindustrialized nations. In addition to the nations known

to have nuclear arsenals in 1992 (United States,

Russia, Ukraine, Khazakstan, Great Britain, France,

China, and India), a number of countries had nuclear

weapons or were developing them (South Africa,

Israel, Pakistan, Iraq, and possibly North Korea,

Iran, and Brazil). Most industrialized European

nations are capable of developing such weapons if

they choose to do so. Furthermore, the potential for

terrorists to steal nuclear weapons or to make primitive devices also exists. Mental health workers

must plan for tactical and strategic nuclear exchanges.6 Strategic nuclear exchanges will be addressed in terms of disaster planning. This chapter

will address the psychiatric aspects of tactical

nuclear weapons and nonnuclear radiation threats

after first discussing chemical and biological warfare which appear more likely to exist on the battlefield than nuclear warfare.

CHEMICAL WARFARE

and in July 1917, mustard gas. Other gases were

tried, including arsenic compounds and cyanide,

but with limited success. Mustard gas was the most

successful. During World War I, chlorine and mustard gas killed or injured more than a million soldiers and civilians.

Although the U.S. Army entered late in the war,

31% of all American battle casualties were due to

gas.7 Russian gas casualties amounted to half a

million, of which 10% were fatalities. The Russian

Army suffered twice the number of casualties and

5-fold the number of deaths secondary to gas than

any other combatant.8

The forerunners of modern chemical nerve agents

were developed by German chemists during

the 1930s as a by-product of insecticide research.

By the end of World War II, about 12,000 tons

of Tabun (Ga) and small amounts of Sarin (Gb)

and Soman (Gd) were synthesized, most of

which fell into Soviet hands. As mentioned, the

Germans did not use these weapons because they

Ancient artwork and documents reveal the use of

chemical agents. Three-thousand-year-old Assyrian

bas reliefs depict the use of liquid fire. Irritant or

toxic smoke or fumes were used at the sieges of

Syracuse (413 BC) and Rhodes (304 BC). Such agents

were used for both their asphyxiating and incendiary effects but were not very effective.7

At the Hague Congress in 1899, all countries

represented, except the United States, pledged to

refrain from using suffocating or poisonous gases.

The U.S. delegate felt that it was illogical to say that

gas was inhumane while bombs, bullets, and other

methods of warfare were more humane.7

Just 15 years later, the modern use of poison gas

began in earnest during World War I. In August

1914, the French used tear gas against German

troops. On the pretext that this was chemical warfare, in April 1915, the Germans attacked French

troops by releasing 180 tons of chlorine in a cloud

north of Ypres. This attack was devastating. In

December 1915, the Germans introduced phosgene
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88

Data sources: [1899–1970] Stockholm International Peace Research Institute. The Problem of Chemical and Biological Warfare. Vol 1:

The Rise of CB Weapons. New York: Humanities Press; 1971: 1–5, 141–212, 212–230. [1980–1991] Author research.

EXHIBIT 4-1

CHRONOLOGY OF CHEMICAL AND BIOLOGICAL WARFARE ALLEGATIONS

1899: Hague Council outlawed use of chemical warfare (CW)

1915–1918: World War I—Both sides used chemical agents extensively

1919–1921: Russian Civil War—Both sides perhaps, Whites definitely, used CW

Early 1920s: British forces in Middle East—Both sides allegedly used CW

Mid 1920s: Morocco—Spanish used mustard gas in 1925; French allegedly used it

Early 1930s: China—Governor of Manchuria used CW against insurgents

1935–1936: Ethiopia—15,000 of total 50,000 Ethiopian casualties were from CW agents used by Italy

1936: Spain—Probably only tear gas used by Fascists

1937–1945: China—CW used by Japanese but probably irritants initially, mustard later; Japanese experimented

with bacteria on human prisoners

1939–1945: World War II—Poles in 1939 used mustard gas defensively; Germans used chemical and bacterial

agents in crimes against civilians in concentration camps; Japanese used cyanide hand grenades on U.S.

forces in Pacific; U.S. forces had mustard gas available but the only casualties from its use were Americans

accidentally exposed.

1945–1949: China—Civil War—Alleged use of CW by Nationalists

1947: Indochina—Alleged use of CW by French

1949: Greece—Civil War—Sulfur dioxide allegedly used by government (first military use of sulfur dioxide was

in the same area 2300 years earlier when the Peloponnesians besieged Platea)

1951–1952: Korea—United States allegedly used CW and biological warfare, admits only to tear gas

1957: Cuba—Castro forces allegedly used mustard gas

1958: Rio de Oro—French and Spanish allegedly used CW in Sharan, Morocco, area

1958: China—Nationalists allegedly used CW from Quemoy against the mainland

1963-1967: Yemen—Egyptian forces allegedly used CW (multiple gases) in Yemeni Civil War

1965–1971: United States used tear gas in Vietnam; others were alleged

1968: Guinea and Bissau—Portugal allegedly used gas

1969: Palestine—Palestine Liberation Organization accused Israel of using gas warfare

1970: Angola—Portugal was accused of gas warfare

1970: Rhodesia (now Zimbabwe)—Government was accused of poisoning a rebel water supply

1980s: Afghanistan—Soviets allegedly used CW, particularly mycotoxins, especially early in the war

Early 1980s: Cambodia and Laos—Vietnam allegedly used mycotoxins in “yellow rain”

1980s: Iraq used several chemicals, including mustard gas and nerve agents, against Iranian ground troops. In

1988, hundreds of Kurdish civilians and Iranian soldiers were killed by Iraqi mustard and cyanide gas in

territory captured by Iran; Iran allegedly retaliated with CW

1991: Iraq had chemical agents but did not use them during the U.N. attack on Iraq. Iraq was close to developing

a nuclear capability.
89

Neuropsychiatric Casualties of Nuclear, Biological, and Chemical Warfare

mistakenly believed that the Allies also possessed

them.

Many armies expect that chemical weapons will

be used in any major conflict. Modern military

doctrine assumes that combat operations will continue in the presence of toxic chemicals. As of 1990,

training in the use of protective masks and clothing

started at the grade school level in schools in the

former Soviet Union and continued through adolescence and into the military service. Soviet troops

were routinely trained to fight while wearing protective masks and clothing, and chemical defense

personnel were integral to Soviet fighting units

down to the company level.9 Training of Soviet

troops included exposure in protective gear to active diluted nerve agents. Psychological conditioning to fighting in a chemical environment was also

heavily stressed.8 Soviet chemical weapons were

believed to consist predominantly of the nerve

agents (particularly Soman), cyanide and mustard,10,11 and possibly mycotoxins. With the demise

of the Soviet Union and Warsaw Pact, the threat of

major warfare and use of NBC warfare is lessened;

however, terrorist use of such weapons remains a

real threat. This is exemplified by the March 1995

use of Sarin in the Tokyo subway system terrorist

attack, reportedly by the religious cult Aum Supreme Truth. The attack resulted in 10 deaths and

over 1,000 injuries.12

Iraq used mustard and nerve agent13 in its war

against Iran after the tide of the war had turned in

Iran’s favor. Iraqi Republican Guard units, which

had been trained to fight on the contaminated battlefield, enabled Iraq to win the limited counteroffensive which finally brought Iran to accept a grudging

cease-fire. The threat of Iraqi chemical weapons

was taken seriously during the 1991 Persian Gulf

War. Many troops were given prophylactic pyridostigmine as pretreatment for nerve agent exposure.

The U.S. units were frequently in mission-oriented

protective posture (MOPP) gear. No cases of Iraqi

chemical weapons’ use were documented, although

there were numerous chemical alarms sounded.

Since the Persian Gulf War, the media have reported that several thousand veterans have complained of miscellaneous symptoms including fatigue, trouble concentrating and remembering,

pares-thesias, hair loss, joint pains, skin rashes,

respiratory and gastrointestinal problems, and caustic (irritating) semen.14 Many show severe emotional distress as they testify before Congress or the

news media that similar symptoms are affecting

their spouses and children (who they also fear are

subject to birth defects). Many of the sufferers (and

one congressman) attribute this “Persian Gulf Syndrome” (which is perhaps more appropriately labeled “Possible Persian Gulf Illnesses”) on either

trace quantities of Iraqi chemical or biological agents,

or on the U.S. pretreatment drug pyridostigmine or

the vaccinations against anthrax. Another suspect

is radiation from the depleted uranium used as

antitank ammunition or additional armor for tanks.

The difficulty of confirming or excluding any of

these hypotheses illustrates the high ambiguity of

the NBC threat and the severe stress that ambiguity

causes.

Physiological Effects of Nerve Agents

The “nerve agents” are derived from organophosphorus compounds related to commercially

available insecticides such as parathion and

diazinon. They are extremely toxic. For example,

0.8 mg of Soman or 0.4 mg of agent VX can be lethal.

Other nerve agents include Sarin and Tabun, which

can penetrate ordinary clothes with ease, making

special suits necessary for protection. Nerve agents

in the liquid state can penetrate unbroken skin, and

one or two droplets on the skin can be fatal if not

removed immediately.15 The addition of thickening

compounds to these agents can increase persistence, resulting in a contact hazard that may last for

weeks.11

Nerve agents are irreversible inhibitors of acetylcholinesterase, an enzyme that is present throughout the central nervous system, the skeletal muscles,

numerous glands, and other cholinergically innervated organs. Poisoning with these agents leads to

an inability to break down acetylcholine. An excess of

acetylcholine in the synapses results, leading to a

functional denervation state or subsensitivity of the

post-synaptic receptor in response to overwhelming

stimulation.16 The resulting symptoms of cholinergic

overstimulation include lacrimation, salivation, nausea, hyperpnea, rhinorrhea, bronchoconstriction, vomiting, muscle twitching, progressive respiratory paralysis, and death. The usual cause of death is

respiratory paralysis, which may be central in origin.17 Autopsy studies of animals who survived

exposure to nerve agents revealed extensive damage to limbic neurons.18 This suggests that human

survivors of nerve agent poisoning may suffer serious, permanent personality changes.

The detailed treatment of acute poisoning with

nerve agents is beyond the scope of this book; however, the mainstay of treatment is atropine. Cur-
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90

rently U.S. soldiers are provided with three

autoinjectors, each with 2 mg of atropine, for selfadministration in the field. As further therapy,

atropine is administered until significant side effects appear. Atropinization is usually maintained

for at least 24 to 48 hours. As much as 10 to 40 mg

of atropine may be necessary in the first 24 hours.19,20

Some studies21 indicate that scopolamine, which

apparently enters the brain more readily than atropine, may be more effective than atropine in treating the central nervous system effects of nerve agent

poisoning.

Treatment protocols20,22–24 andmilitary manuals25–28

all call for treatment with pralidoxime (Protopam

or 2-PAM chloride), which, by removing the bound

agent from the enzyme, reactivates the enzyme.23,24

While oximes are effective antagonists to many

cholinesterase inhibitors, they also produce side

effects. Furthermore, some nerve agents are refractory to currently available oximes; this is particularly true of Soman, the predominant nerve agent in

the former Soviet Union arsenal.29 The current

standard oxime of the U.S. Army, pralidoxime chloride, is administered by the slow intravenous route

along with atropine in the Mark I autoinjector.

Plans now include pretreatment with pyridostigmine 30 mg every 8 hours prior to anticipated

exposure. This does not prevent symptoms but

greatly increases the efficacy of atropine and

pralidoxime. Pyridostigmine is itself a “nerve agent”

which temporarily protects some acetylcholinesterase enzyme from deactivation by the enemy’s

nerve agents. Diazepam 10 mg is also issued as

an anticonvulsant to be administered with the

third autoinjector or if the casualty is convulsing,

with the goal of decreasing the chances of lasting

brain damage. Genetic engineering may allow

the development of a more effective antidote in

the future. This is suggested by the discovery of

an enzyme in squid nerves that hydrolyzes and

detoxifies Soman.30

If a nerve agent is used, many soldiers will receive only low doses by virtue of location or protective measures; this low-level poisoning may be accepted as a calculated risk or may even go

undetected. If a nerve agent is used, many more

soldiers will receive only very low doses than will

receive high doses, by virtue of their location or

protective measures. Some low-dose exposure may

be accepted as a calculated risk. The first symptom

of minimal exposure of the eyes to nerve agent

vapor (at 1⁄30th to 1⁄50th of the lethal dose) is pinpoint

pupils.25 This does not grossly impair vision in

bright light, but causes dimming of vision and may

impair performance in the low levels of artificial

illumination inside vehicles or tents (tactical operations centers) and/or at the critical times of predawn and dusk. Soldiers with pinpoint pupils

would be seriously impaired and at a dangerous

disadvantage in night operations under blackout

conditions. At slightly higher doses, the soldiers

also have eye discomfort on focusing, blurred vision, headaches, jitteriness, and runny noses to further distract them.25 These symptoms could involve

all members of a squad, platoon, or company, to

greater or lesser degree. The pinpoint pupils remain marked for 24 hours, before gradually improving over several days. The soldiers may well be

fearful of further NBC or conventional attack, unwilling to venture out after dark, and prone to

overreact to threats until adequate vision returns.

Experience with human exposure to the chemically related organophosphate insecticides suggests

that, in cases of chronic exposure to low concentrations, psychiatric symptoms may predominate over

physical ones. Impaired thinking, judgment, attention, and short-term memory are likely, but toxic

delirium may also be present. The cognitive deficits

may persist many months, even after treatment,

along with irritability, mood changes, depression,

and insomnia with nightmares. Acetylcholinesterase inhibitors have been found to precipitate

psychotic symptoms in predisposed individuals.31

Behavioral manifestations of nerve agent poisoning that antedate, follow, or occur independently

of somatic symptoms19 may be most prominent in

individuals who have been exposed to sublethal

doses or in those who have recovered from the

somatic effects of poisoning. Acute organophosphorus intoxication produces cognitive impairment with difficulty in concentration, confusion,

and drowsiness.31,32 Airplane crashes of cropduster pilots may be due to acute intoxication with

organophosphorus compounds.33 Chronically-exposed agricultural workers have complained of forgetfulness, difficulty in thinking, visual impairment, and drowsiness. These deficits were

quantified by sophisticated testing.34 Another

study32 showed that chronically-exposed workers

had higher levels of anxiety than matched controls.

Chronic exposure has also been associated with

increased anxiety, possibly causing misdiagnosis of

combat stress reactions.35 Memory also appears to

be impaired by organophosphate poisoning.20 Significant impairment of cognition, vigilance, and

memory may make it difficult for a minimallyexposed soldier to perform the often complex tasks

that will be required.
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Neuropsychiatric Casualties of Nuclear, Biological, and Chemical Warfare

Poisoning with nerve agents may cause other

psychiatric disturbances that mimic psychological

as opposed to organic disorders. Depression has

been observed as a prominent symptom in accidental poisoning.22,31,36 The severity of depression seems

to be related to the severity of poisoning and the

degree of acetylcholinesterase inhibition. This

depressogenic effect of nerve agents is suggested by

the observation that the reversible cholinesterase

inhibitor, physostigmine, can normalize mood in

manic patients and can cause depression in normal

persons.37,38 Could the same be true for the pretreatment drug, pyridostigmine, in some soldiers? Nerve

agent toxicity has also been associated with complaints of “excessive” dreaming, nightmares, insomnia, and delirium.22,32 Treatment with anticholinergic agents seems to reduce these symptoms.22

Nerve agents may also lower the threshold for convulsive seizures. These could be mimicked by

pseudoseizures in tense, anxious persons, creating

a problem for differential diagnosis.

It is possible that nerve agents can cause psychosis,

by altering the dopaminergic-cholinergic balance in

mesolimbic structures. Anticholinesterases reportedly activate symptoms in schizophrenic patients.36

One study39 reported that a higher percentage of agricultural workers exposed to toxic agents developed

psychotic illnesses than would have been expected.

These results have not been confirmed, however.

In summary, the data on the subacute and chronic

physiological effects of exposure to organophosphorus poisons reveal substantial risk of depression and sleep disturbances, decreased cognitive

abilities, and a slight risk of psychosis and anxiety

disorders.40

Added to the dangers of nerve agent poisoning

are effects of antidotes, which may outweigh the

danger of potential exposure to nerve agents. Selfinjection of atropine by the soldier after exposure to

nerve agents may be lifesaving, but inappropriate

self-injection may lead to a central anticholinergic

syndrome with delirium. If a false alarm (or a

deliberate attempt to make oneself a casualty) leads

to the administration of chemical warfare antidotes

in the absence of the appropriate agent, serious

psychological symptoms are likely. Atropine in

low doses produces blurred vision, tachycardia,

dry mouth, sweat suppression with increased risk

of heat stroke, urinary retention, and perhaps impaired thinking, judgment, insight, and short-term

memory. Even in the 2 to 6 mg range available for

early self-administration, atropine may give some

individuals a toxic anticholinergic delirium with

disorientation, agitation or stupor, paranoid delusions, and visual and tactile hallucinations lasting 8

to 16 hours. TAB (TMB-4 [an oxime], atropine, and

benactyzine), an antidote combination formerly used

by the U.S. Air Force and U.S. Navy/Marine Corps,

was virtually guaranteed to produce psychosis with

visual hallucinations in its standard dose.30 While

the presence of anticholinesterase nerve agents in

the body may partially counteract such psychiatric

side effects, it is unlikely that agent and antidote

will exactly cancel each other.

Studies conducted at the U.S. Army Aeromedical

Research Laboratory demonstrated that experienced

helicopter pilots can fly helicopters, although seriously impaired, after receiving 4 mg of atropine.

“Effects were seen most often ... in terms of aircraft

control problems, vision disturbances, impaired

tracking, reduced cortical activation, and decreased

cognitive skills. These problems indicate helicopter

tactical flight is dangerous after an unchallenged 4

mg dose. Other types of flight should also be

avoided for at least 12 hours after atropine.”41(p.857)

Following the administration of large doses of

atropine, symptoms progress from tachycardia and

dryness of the mouth to ataxia, hallucinosis, and

confusion. In a study performed at Edgewood

Arsenal,42 subjects administered large doses of atropine became unable to pay attention, carry out

instructions, speak coherently, or perform calculations. Significantly, soldiers who had impaired

judgment failed to recognize their degree of general

impairment and resented assistance. In this study,

chlorpromazine, strongly anticholinergic itself, potentiated the adverse mental effects of anticholinergic agents. This takes on added significance in

view of the widespread use of phenothiazines to

treat anxiety symptoms in Vietnam.43,44

Treatment of atropine-type psychoses should not

include phenothiazines, which produce anticholinergic side effects of their own, although haloperidol

may be used. Current definitive treatment is with

the carbamate, physostigmine, but this requires

careful and prolonged intravenous titration.

The effects of atropine resemble those of another

class of chemical agents, the incapacitants. Agent

BZ (3-quinuclidinyl Bensylate) is a strong antimuscarinic compound that for some time was kept in

the arsenal of U.S. chemical weapons. It produces

hallucinations and psychological incapacitation

similar to that produced by atropine, but is more

specific and longer lasting (24–48 h) than atropine.

The burden of self-diagnosis is formidable, particularly considering the fact that other agents or

even anxiety may mimic early symptoms of nerve

agent poisoning. Under battle conditions, with
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92

oncoming shells producing smoke or spreading tear

gas, with troops dispersed and communications

strained, the apprehension and ambiguities may

unavoidably lead to individual or group decisions

to administer antidotes when exposure to nerve

agents has not, in fact, occurred.45

Whether due to mistaken self-administration of

antidotes or exposure to antimuscarinic agents, the

possibility of significant numbers of casualties

with anticholinergic poisoning must be considered.

One example of troops thus exposed was in 1676,

when British troops in Jamestown, Virginia, ingested Jimson (“Jamestown”) Weed (Datura stramonium) and suffered mass anticholinergic poisoning.46 Bizarre behavior and amnesia allegedly lasted

for 11 days. The soldiers, who had to be confined

to prevent them from injuring themselves, were

very negligent of personal hygiene. More recently,

combativeness or hyperactivity was noted in 10%

of a series of 212 cases of stramonium intoxication.47 Hallucinations occurred in 99 of the 212

cases, and 5 deaths were directly attributable to

psychosis.

The failure to maintain adequate self-care behavior such as keeping dry, maintaining adequate hydration, and attending to personal hygiene has been

noted as a cause of soldier ineffectiveness.48,49 Reported effects of high doses of anticholinergic agents

on soldiers include impaired performance in timing

and vigilance tasks, in firing rifles or running an

obstacle course; ataxia; blurred vision; inability to

perform calculations; and disruption of communication between individuals.42 Possible effects in the

field might include failure to observe discipline,

failure to conserve drinking water, failure to wear

protective clothing, misinterpretation of visual or

auditory signals, misidentification of individuals,

failure to maintain silence, and increased risk of

heat stroke. Anticholinergic syndromes can be reversed with physostigmine,50 but this drug is not

easy to use in the field. There are storage problems

and it requires careful titration in use. Furthermore, as mentioned earlier, physostigmine can produce serious depression in normal persons, and the

same problem of inappropriate use described with

atropine exists.

In summary, nerve agents present numerous

problems in practical therapeutics for the psychiatrist. Both the agents themselves and their antidotes may have significant behavioral effects, and

the military psychiatrist may be called upon to

treat, and to advise other physicians on how to

treat, these problems.

Physiological Effects of Other Agents

Cyanide

Other chemical agents also may be encountered.

Cyanide gas, a nonpersistent agent, is especially

dangerous because it may saturate the active material in gas mask filters and render them useless. A

combination of cyanide and a nerve agent would

be particularly deadly. The early symptoms of

cyanide exposure are anxiety, confusion, giddiness,

and hyperventilation. These symptoms can also

be caused by stress, and could lead to unnecessary medication with cyanide antidotes. In civilian

situations, antidotes to cyanide have often been

administered inappropriately.51,52 Chronic exposure

to low levels of cyanide could lead to mental changes

as was seen when cyanide compounds were

used therapeutically.53 The effects of administration of large doses of anticholinergic agents to

soldiers who have been poisoned with cyanide

is unknown. Atropinization may conceal the

symptoms of cyanide poisoning or may increase

its lethality.

Incapacitating Agents

Tear-gas agents have been extensively used in

war as most countries have interpreted the Hague

and Geneva accords against gas warfare as not

applying to these agents. Intended to be used as

harassing agents, their lethality is very low.

Nonlethal incapacitating agents may exert their

own direct effects on psychological functioning (like

the anticholinergic BZ). Those reportedly used in

Afghanistan appear to cause temporary unconsciousness or immobilization. Incapacitants may

also provoke inappropriate responses by mimicking the early symptoms of more lethal agents. The

tear gases may be confused with the lacrimationproducing nerve gases. Vomiting agents may stimulate fears of having been irradiated or exposed to

biological agents. Adamsite, in this class, reportedly also may cause depression.11

Mustard

Mustard gas was responsible for the majority

of gas casualties during World War I. It is considered an obsolete agent by the U.S. but the former

Soviets were believed to have stockpiles of it,8 and it

was used by Iraq against Iran. Mustard gas is

unique for its insidious method of action and its
93

Neuropsychiatric Casualties of Nuclear, Biological, and Chemical Warfare

latency of several hours before burns and blisters

appear. It can present a contact hazard for weeks.

Sulfur mustard (bis[2-chloroethyl] sulfide) is a

powerful alkylating agent that can produce severe

skin burns and pulmonary injury if inhaled. Very

low doses of mustard produce painful conjunctivitis of the eyes which lasts for days to weeks,

severely impairing vision.54 As with nerve agent,

blindness on the battlefield, even if known to be

temporary, can produce anxiety, dependency, and

other psychological as well as management problems. Higher-dose contact burns the eyes and causes

permanent blindness as well as disfiguring facial

burns. The potential psychological impact of these

is discussed in Chapter 14, Disabling and Disfiguring Injuries. Blistering of exposed hands could also

leave long-term physical and emotional scars. In

soldiers without protective overgarments, mustard

tends to produce blisters at the moist creases of the

body, notably the genital region. Psychological

reactions to genital injuries are also discussed in

Chapter 14.

Blister agents (mustard gas, Lewisite) have been

noted to produce chronic psychological symptoms

of apathy and depression55 in addition to their severe and delayed dermatologic, pulmonary, and

systemic lesions. Phosgene, a suffocant gas, keeps

active the traditional World War I terror of gas

attack as producing a horrible sensation of the lungs

filling with fluid, with the added threat that it

permanently inactivates the charcoal in one’s mask

or overgarment. Phosgene’s delay of several hours

before the first symptoms, and the dangerous worsening of symptoms by physical exercise, was especially unnerving, even to those not actually exposed.56

Mycotoxins

The mycotoxins (thought to have been used by

the Soviets and their allies in Southeast Asia and

Afghanistan) produce terrifyingly rapid symptoms

of vomiting, tissue necrosis, and failure of blood

coagulation. Psychotic symptoms and bizarre behavior have not been mentioned prominently in

current accounts; however, such psychiatric symptoms have been prominent in historical natural outbreaks of “St. Vitus’ Dance” and “tarantism,” which

are now attributed to contamination of food grains

by ergot derivatives from other fungal toxins. Mental symptoms may also become significant if mycotoxin patients are kept alive by treatment of the

otherwise rapidly fatal symptoms.

Neuropsychiatric Syndromes Associated With

Chemical Warfare

Large-scale gas warfare during World War I presented special problems. In addition to the “physical” casualties of chemical warfare, there were “psychological” casualties and syndromes. One of these

was “gas hysteria,” which usually occurred in small

epidemics, threatening the integrity of entire units

until remedial measures were taken.57,58 This “epidemic” effect is seen in the following World War I

episode:

One morning a large number of soldiers were returned to the field hospital diagnosed as gas casualties. The influx continued for about eight days

and the number of patients reached about 500. The

divisional gas officer failed to find any clinical

evidence of gas inhalation or burning.... Most of

the patients had the fixed conviction that they had

been gassed and would usually describe all the

details with convincing earnestness and generally

with some dramatic quality of expression.... It was

obvious on examination that they were not really

gassed. Further, it was inconceivable that they

should be malingerers.57(pp318–319)

Acute symptoms of gas hysteria often mimicked

some of the symptoms of gas poisoning and included dyspnea, coughing, and burning of the skin.

Aphonia was also seen prominently.59 For those in

whom the symptoms persisted, the term “gas neurosis” was applied.60 The degree of exact exposure

to gas was unrelated to the symptoms presented.

Dramatic symptoms were seen, such as tics and

blepharospasm,59 as well as “unconscious movements of the hands like clawing at the throat or

removing a mask.”60(p214) The patients presented

with signs of air hunger and anxiety with alterations of consciousness, but no organic basis for the

symptoms was found. One author suggested that

gas neurosis patients “are particularly amenable to

suggestion and rest. Optimism based on exact

diagnosis and sincere faith in ultimate recovery is

excellent therapy.”60(p214) However, some of the gas

neuroses continued until long after the war and

were rewarded with compensation.57 It should be

remembered that during World War I there were

approximately twice as many gas neurosis cases as

there were gas exposure cases.57

Chemical warfare is still perceived as choking off

one’s breath. In spite of the complicated chemical

properties of modern agents, respiratory symptoms

are likely to predominate in conversion reactions.
War Psychiatry

94

This is reinforced by current military training requiring wearing protective clothing while tear gas

agents are used to simulate poison gases.

More recently, similar conversion symptoms have

been reported in the aftermath of chemical attacks

in Afghanistan and Cambodia,8 with aphonia and

catatonic symptoms predominating. More generally, the mere act of donning protective gear will

increase the soldier’s sense of isolation from peers

and decrease intragroup communication and support, factors that have been shown to be important

in maintaining morale and probably in decreasing

the incidence of psychiatric casualties.61

Gas warfare is perceived much as it was in 1918,

as “awe inspiring” with “unbelievable horrors.”60

During World War I, units that were otherwise

stressed, having spent long periods in combat under arduous conditions, were at much higher risk

for “gas hysteria.” This risk increased still further if

relief was anticipated but did not arrive on schedule.57 This aspect will loom large in any future midor high-intensity conflict, with the extremely highpressure, continuous combat operations that are

expected.48,61

As long as the nuclear, biological, and chemical

(NBC) threat is an active, serious threat, protective

masks and overgarments must be worn, certainly

for brief periods and perhaps for prolonged ones.

The protective gear distorts visual, auditory, and

tactile perception; impairs fine motor coordination;

increases physical effort, frustration, and fatigue;

and increases psychiatric casualties in simulation

exercises.62,63 These effects may be especially disruptive to the performance of medical functions;

however, modifications of protective gear for medical treatment64,65 as well as approaches to triage

have been proposed.66 The protective ensembles

retain body heat and increase the risk of heat exhaustion and heat stroke, which may present with

mental symptoms and be difficult to diagnose in

full MOPP (mission-oriented protective posture)

gear. During a Scud missile attack by Iraq on Israel

in January 1991, several elderly persons died of

heart attacks while in gas masks.

The restrictions on eating, drinking, elimination,

and hygiene functions, along with other discomforts and interference with sleep, can affect morale

as well as physiological well-being. Decreased ability to recognize comrades and gauge their mood or

resolve may lessen unit cohesion and increase the

sense of helpless isolation (a prime factor in battle

fatigue). Claustrophobic panic, premature unmasking (which may be imitated by others), spatial disorientation, and paranoid reactions to impaired sensory functioning may also occur. Such adverse

reactions are exacerbated when visibility is further

restricted by darkness, smoke, or vegetation. Gas

mask phobia proved to be a significant problem in

the Allied invasion of Iraq in 1991.67

Field studies and training exercises which test

troops in force-on-force battles using the MILES

(multiple integrated laser engagement system) to

score who “shoots” whom have shown an alarming

increase in friendly fire casualties (“fratricide”) by

insufficiently trained troops in the protective ensemble. Whereas only about 1 in 20 soldiers or

vehicles is “shot” by their own side in conventional

battles, the rate rises as high as 1 in 5 in full missionoriented protective postures.68,69 This is attributable to the combination of impaired vision and

hearing plus the jumpiness this provokes. Fratricide, of course, is very disruptive of morale. Rigorous training is needed to reduce the risk.

Factors that predispose to psychiatric casualties

include the rates of wounding in the unit, lack of

sleep, and lack of prior combat experience.70–72

Chemical attacks might increase psychiatric casualties by exacerbating all three of these factors.45,73

Chemical weapons create fear of the unknown, a

potent effect in inexperienced troops. Usually,

troops entering combat will be, for the most part,

untested in battle. Lack of sleep has produced

hallucinations in troops during extended training

exercises74–76 and is a factor predisposing to combat

psychiatric reactions.

With the possibility of high-intensity, continuous combat, psychiatric services will be strained to

the limit. Because this country is committed against

the initial use of chemical weapons, U.S. forces

would be the first to suffer from chemical attacks,

with the concomitant psychiatric casualties. Lack

of experience in chemical warfare and the psychiatric syndromes arising from the physiological effects

of chemical agents and their antidotes may lead to

misdiagnosis and mistreatment. This may lead to

decreased unit effectiveness at critical times. The

difficulties in decontaminating large numbers of

exposed soldiers may lead to removing them to

centralized decontamination stations well to the

rear. Many soldiers who might be medically fit to

return to their units might develop an evacuation

syndrome that would increase their resistance to

returning to combat. In the 1982 Israeli incursion

into Lebanon, some Israeli combat stress casualties
95

Neuropsychiatric Casualties of Nuclear, Biological, and Chemical Warfare

were evacuated by air to Israel, while others were

appropriately treated in forward areas. Almost all

of the forward-treated cases, but few of the rearevacuated cases, returned to combat.77

In summary, the psychological casualties

of chemical warfare may well outnumber and

prove more costly in personnel losses than the

physical casualties, as occurred in World War I.78

However, it should be noted that most veteran

soldiers in World War I adapted to the threats

and discomforts of chemical warfare. They often

“preferred” this risk of chemical attack to those of

high explosive shells and machine gun bullets because the protective equipment and good training

allowed them to improve their odds of survival

better.79

Reports of biological warfare go back many centuries. One example is the introduction of smallpox

to the American Indians by early settlers who gave

or sold them infected blankets or trinkets.80 However, in modern times the use of biological warfare

agents appears to have been rare.

The United States did not have an offensive or

defensive biological warfare capability until toward

the end of World War II.80 The nascent program

focused on anthrax and botulinus toxins primarily.

An anthrax plant received authorization to produce

a million bombs and progress was being made in

short-range dispersal techniques for botulin in paste

form. Figure 4-1 shows a probable descendent of

the World War II anthrax dispersal bomb. Moreover, there is evidence that research was conducted

with brucellosis, psittacosis, tularemia, and the respiratory disease, glanders. In addition, botanical

toxins and viruses were being explored with the

aim of destroying Japanese vegetable gardens and

rice crops. Tactical, rather than moral, considerations prevented the use of defoliants in World War

II. They were later used in Vietnam, in the form of

Agent Orange.

Rumors that a 1979 mishap with anthrax in the

former Soviet Union produced scores of casualties

at Sverdlovsk have been replaced by verified accounts that such a mishap actually occurred.81 Iraq

was suspected of working towards developing anthrax as a weapon. That led to the decision of the

United States to vaccinate many personnel in the

Persian Gulf campaign with an experimental anthrax vaccine. Many of the same considerations of

chemical warfare apply to biological warfare; however, a major difference is the self-perpetuating

effect of live biological agents. This can produce

fear of contagion, which may severely impair relationships among troops and interfere with proper

care of casualties. The near-panic responses of

some persons in casual contact with victims of the

practically noncontagious (except through sexual

contact and shared needles) acquired immunodeficiency syndrome (AIDS) illustrate the validity of

this factor.

Physiological Effects of Biological Agents

A number of viral, bacterial, and rickettsial agents

have been identified as potential weapons, both for

their psychological effects and the terror those effects produce in exposed troops. Anticipated psychiatric casualties of biological warfare will be included in a general discussion. It is, however,

possible that an enemy could develop neurotropic

viral agents that could produce primarily psychiatric symptoms.82 Tables 4-1, 4-2, and 4-3 show agents

considered by Malek80 to have a biological warfare

potential.

Neuropsychiatric Casualties of Biological

Agents

Contagious biological organisms, like persistent

transmissible chemical agents, would require quarantine and special handling. This would surely

have widespread psychological effects on buddycare and attitudes toward strangers, stragglers, and

refugees. Within the medical system, the impact of

invisible, patient-borne threats to other patients

and to the treating personnel would reintroduce an

old but now rarely encountered psychological as

well as occupational stress, which may be difficult

to cope with under field conditions. In World War

I, entire medical/surgical teams were temporarily

incapacitated by eye damage from mustard vapor

brought into the operating room on wounded patients who had not yet shown any effects of their

own exposure.

BIOLOGICAL WARFARE
War Psychiatry

96

Fig. 4-1. Patent application of R. L. Le Tourneau for a light high-explosive bomb for dispersing toxic and insecticidal

aerosols, 1955. Le Tourneau’s patent application reveals the technological ingenuity he employed in continuing the

production of gas warfare mechanisms. This technological interest continued for the next several decades with the

development of safer binary weapons (ie, chemicals were inactive until combined at the time of actual use).

Photograph: U.S. Patent and Trademark Office, Arlington, Va.
97

Neuropsychiatric Casualties of Nuclear, Biological, and Chemical Warfare

TABLE 4-1

POSSIBLE BIOLOGICAL WARFARE AGENTS—BACTERIAL

Adapted with permission from Malek I. Biological weapons. In: Rose S, ed. CBW: Chemical and Biological Warfare. Boston, Mass:

Beacon Press; 1969: 60–61.

TABLE 4-2

POSSIBLE BIOLOGICAL WARFARE AGENTS—VIRAL

Adapted with permission from Malek I. Biological weapons. In: Rose S, ed. CBW: Chemical and Biological Warfare. Boston, Mass:

Beacon Press; 1969: 60–61.

Table 4-1 is not shown because the copyright permission granted to the Borden Institute, TMM, does

not allow the Borden Institute to grant permission to other users and/or does not include usage in

electronic media. The current user must apply to the publisher named in the figure legend for

permission to use this illustration in any type of publication media.

Table 4-2 is not shown because the copyright permission granted to the Borden Institute, TMM, does

not allow the Borden Institute to grant permission to other users and/or does not include usage in

electronic media. The current user must apply to the publisher named in the figure legend for

permission to use this illustration in any type of publication media.
War Psychiatry

98

TABLE 4-3

POSSIBLE BIOLOGICAL WARFARE AGENTS—RICKETTSIAL, FUNGAL, TOXIC

Adapted with permission from Malek I. Biological weapons. In: Rose S, ed. CBW: Chemical and Biological Warfare. Boston, Mass:

Beacon Press; 1969: 60–61.

NUCLEAR WARFARE AND DISASTERS

quently falls to earth to contaminate it (fallout).

While an air detonation produces the greatest blast

damage, few particles are drawn into the atmosphere to mix with radioactive bomb debris so there

is little residual contamination from fallout. Nuclear

explosions over water produce massive vaporization and an intensely radioactive rainfall as well as

a 50- to 100-foot tidal wave capable of drowning a

coastal city.

Electromagnetic Pulse Effects of Nuclear Warfare

A high altitude electromagnetic pulse (EMP) is a

radiated electromagnetic wave caused by the detonation of a nuclear weapon above the earth’s atmosphere. A 3.3 megaton nuclear weapon, detonated

400 km above the center of the United States, can

produce sufficient electromagnetic radiation to

cover the entire country; and, if detonated over

Europe, most of the continent would be affected.84

Vandre, et al,84 in simulated EMP tests, showed that

by creating power surges in standard field medical

equipment, an EMP would render about 65% of

In some countries the use of nuclear weapons is

a practical rather than a moral issue. An attack

could be launched by tactical missile forces and

fighter bombers.73 There is concern that portable

tactical nuclear weapons from the stockpiles of the

former Soviet Union or from unstable states might

fall into the hands of terrorists who could use them

against cities. Industrial disasters like that at

Chernobyl could release nuclear radiation to contaminate large areas and require military intervention to minimize the damage, evacuate the population, and maintain order.

Physical Effects of Nuclear Warfare

The energy generated by a typical tactical nuclear

explosion consists of blast and shock waves (45% of

the energy produced), light and heat (35%), initial

radiation (5%), and residual fallout radiation (about

15%).83 A ground detonation, vaporizing soil and

melting granite and clay, results in large amounts of

debris drawn by vacuum into the fireball, where it

is mixed with radioactive bomb debris and subseTable 4-3 is not shown because the copyright permission granted to the Borden Institute, TMM, does

not allow the Borden Institute to grant permission to other users and/or does not include usage in

electronic media. The current user must apply to the publisher named in the figure legend for

permission to use this illustration in any type of publication media.
99

Neuropsychiatric Casualties of Nuclear, Biological, and Chemical Warfare

such equipment useless. The more modern and

integrated the equipment, the greater the vulnerability to an EMP power surge.

An American Medical Association (AMA) report

of the Board of Trustees indicated that civilian medical facilities would be equally devastated.85 The

AMA noted that in addition to medical equipment,

telephone and other telecommunication equipment,

computers and electronic equipment involved in

life support systems, and diagnostic testing and

other equipment utilizing solid state components

are particularly vulnerable.

In a related paper, Vandre, et al,86 described

methods to minimize the vulnerability of equipment to EMP effects by keeping wiring near the

ground, keeping it short, unplugging unused power

equipment, running power cabling and tents in a

north-south direction (thereby avoiding running

power cabling in an east-west direction), and placing sensitive equipment in standardized shelters.

By following such procedures Vandre, et al86 estimated that 88% or more of unplugged field medical

equipment could be kept functional in the event of

EMP. The AMA noted that the increasing use of

fiber optic components would decrease the effects

of EMP because they are not vulnerable to the EMP

surge. They recommended use of standby diesel

generators to provide emergency power.85

Physiological Casualties of Nuclear Warfare

Studies of the effects of nuclear weapons on humans, with the exception of a few accidental radiation victims (particularly in Chernobyl), focus on

the effects of the Hiroshima and Nagasaki bombings. A useful bibliography has been prepared by

the Atomic Bomb Casualty Commission.87

Initial physical casualties are due to the blast and

shock, heat, and nuclear radiation. Later, casualties

are primarily from nuclear radiation. The initial

effects are most closely related to the proximity and

size of the fireball. At Hiroshima and Nagasaki

more than 80% of the population within 0.6 of a mile

of ground zero were casualties, and over 90% of

these casualties were killed. In contrast, of individuals who were beyond approximately 1.6 miles

from ground zero, less than 5% were killed.88 These

findings suggest that troop dispersal will be the

primary defensive strategy in nuclear war. Burns

accounted for two thirds of the initial deaths at

Hiroshima and for one half of the total deaths.

About 30% of those who died in Hiroshima had

received lethal doses of radiation; however, this

was not always the immediate cause of death.

There are two major biological effects of radiation in excess of 100 rad (a measure of the dose

absorbed from ionizing radiation equal to 100 ergs

per gram): (1) cell membrane damage leading to

cellular and vascular leakage affecting especially

brain and lungs, and (2) loss of reproductive capacity in stem cells.87 Different tissues of the body show

different sensitivities to ionizing radiation. In general, the radiosensitive cells are found in lymphoid

tissue, bone marrow, spleen, organs of reproduction, and gastrointestinal tract. Of intermediate

sensitivity are skin, lungs, and liver. Muscle, nerve,

and adult bones are least sensitive.88

The medical manifestations of radiation damage

can be conveniently divided into three time phases:

initial, latent, and final.88 During the initial phase,

exposed persons may experience nausea, vomiting,

headache, dizziness, and malaise. The onset time

decreases and the severity of these symptoms increases with increasing dose. During the latent

phase, exposed persons will experience few, if any,

symptoms and will be able to carry on normal

functions. The final phase is characterized by illness

that requires hospitalization of people who have

received the higher doses. The symptoms experienced in the initial phase will recur and be accompanied by skin hemorrhages, diarrhea, and sometimes loss of hair. At higher doses, seizures and

prostration may occur. The final phase is ended by

either recovery or death. These effects are summarized in Table 4-4 and Figure 4-2.

Persistent radioactive contamination is quite similar to persistent mustard gas in many of its effects.

Presumed “psychological fallout” is an unseen hazard that produces delayed illness in all bodily systems that involve rapid cellular reproduction (ie,

distressing gastrointestinal symptoms, impaired

wound healing, and increased susceptibility to infection and hemorrhage). Early death may occur

unless sophisticated medical support is given. Survivors are at increased risk of death from cancer.

Acute irradiation from a nuclear explosion (without concurrent disabling burn or blast injury) puts

the military medical-ethical dilemma of these conditions into even starker relief. In the absence of

quantitative dosimetry for each exposed patient (a

difficult task in itself), how are the massed casualties

to be triaged into those who are expected to die

(“expectant”) and those who can reasonably be saved

with the over-used resources that remain? What is to

be done with those fatally exposed who can still

function? Should they be told the prognosis? Should

they be discharged “RTDTD” (“Return To Duty To

Die”), perhaps to carry out high-risk delaying ac-
War Psychiatry

100

TABLE 4-4

SUMMARY OF POTENTIAL MILITARY EFFECTIVENESS OF RADIATION CASUALTIES

Onset of Duration of Incidence

Radiation initial incapacity effectiveness Later incapacity of Death

in rems from vomiting, etc. (latency) (onset to duration) (time)

0–100 None 100% None None

100–200 3–6 h to 1 d 1 d to 2 wk 10–14 d to 4 wk None

200–600 1⁄2–6 h to 2 d 1–2 d to 4 wk 1–4 wk to 1–8 wk 0%–90%

2–12 wk

600–1,000 15–30 min to 2 d 2 d to 5–10 d 5–10 d to 1–4 wk 90%–100%

1–6 wk

1,000–5,000 5–30 min to 1 d 0 to 7 d 2 to 10 d 100%

2–14 d

Over 5,000 Almost immediately None Almost immediately 100%

1–2 d

Adapted from Glasstone S, Dolan PJ. The Effects of Nuclear Weapons. 3rd ed. Washington, DC: US GPO; 1977: 580–581.

Organs Affected by Ionizing Radiation

Range 0–100 rems Subclinical range 100–1,000 rems Therapeutic range Over 1,000 rems Lethal range

100–200 rems 200–600 rems 600–1,000 rems 1,000–5,000 rems Over 5,000 rems

Clinical Therapy Therapy

Role of therapy surveillance effective promising Therapy palliative

Leading organ Hematopoietic tissue Gastrointestinal tract Central nervous system

Characteristic None below 50 rems Moderate Severe leukopenia; Diarrhea, fever, Convulsions, tremor,

signs leukopenia hemorrhage; infections; disturbance of ataxia, lethargy

epilation above 300 rems electrolyte balance

Critical period

postexposure —— 1–6 wk 2–14 d 1–48 h

Fig. 4-2. Summary of clinical effects of acute ionizing radiation. Adapted from Glasstone S, Dolan PJ. The Effects of

Nuclear Weapons. 3rd ed. Washington, DC: US GPO; 1977: 580-581.

convey some of the moral and psychological implications that the Army Medical Department

(AMEDD), the line military, and the exposed individuals themselves would have to deal with.

Triage by scarce medical resources is obviously

the best way to preserve lives. This is critical in an

operational sense in that the medical resources

should be expended in helping those who are most

likely to be able to return to duty.

tions, “kamikaze” attacks, and operations in contaminated areas? What medications should they be

given for symptom relief to improve their efficiency?

Could those who cannot be discharged provide the

answer to the shortage of whole blood in the combat

zone? Will there be a place for euthanasia on the

battlefield to end suffering and preserve other lives

through allocation of medical resources, as suggested by Swann?89 Such mind-chilling questions
101

Neuropsychiatric Casualties of Nuclear, Biological, and Chemical Warfare

Neuropsychiatric Casualties of Nuclear Warfare

Although nuclear devices have been used twice

in warfare, no one has actually fought a nuclear

war. Neuropsychiatric casualties of nuclear warfare, therefore, must be inferred from studies of the

primarily civilian victims of the nuclear explosions

at Hiroshima and Nagasaki; from the disasters in

Goiânia, Brazil, and Chernobyl, Ukraine; from a

small number of imperfect simulations, such as the

Desert Rock I, IV, and V studies; and from extrapolations from situations of extreme stress such as that

during disasters or combat. The following sections

will briefly review some of these studies.

Hiroshima and Nagasaki

There have only been about 20 useful studies of

the psychological reactions to nuclear explosions;

many of these are autobiographical accounts. Although retrospective, one of the best reviews of the

physical, social, and psychological toll of nuclear

devices is that of a Japanese committee commissioned by the cities of Hiroshima and Nagasaki.

This report was first published in Japan in 1979; an

English translation was published in 1981.90 This

review concluded that organic forms of mental illness among survivors were not prominent.

In one study91 of 50 survivors at Omura Hospital

in Japan, psychoneurological observations were

made 2 to 3 weeks after exposure, the following

month, and about 3 to 4 months after exposure.

Only 4 of the 50 patients were diagnosed as having

mental disorder in the initial stage. In the intermediate stage, some patients, especially those suffering thermal burns, showed neurasthenia-like symptoms. In the later stage, those suffering a specific

diathesis tended to develop neuroses. These were

considered indirect effects of physical deterioration.

Acute radiation illness was considered to be the only

direct effect of the atomic bomb on the human

psychoneurological system. Konuma91 has argued

that complaints of “agony,” lassitude, fatigability,

and other symptoms constitute a “diencephalic syndrome,” which can be diagnosed even in the absence

of physical examination signs or abnormal laboratory findings. The presumption is that hematologic

or other direct radiation effects on nerve cell membranes have damaged the vegetative nervous system. However, the severe losses (of relatives, physical capacities, and material resources) experienced

by many of the victims could readily produce a

depressive syndrome with many of these characteristics, particularly in a vulnerable personality.

Psychological studies were not conducted until

years or decades after the event. Furthermore,

disability compensation, social ostracism, and other

factors colored the survivors’ remembrances. Nevertheless, a fairly common response pattern was

described in the 1952 study by Kubo,90 who studied

54 victims from 1949 to 1952. Most of them had been

1 to 3 km from the bomb hypocenter. Kubo found

that most were “startled” by the initial flash and fell

down and covered their eyes in an “instinctive”

withdrawal from the stimulus, while some turned

to face the flash.

The blast, causing widespread damage, produced

a feeling of “mental blankness” lasting for a few

minutes. This was followed by attempts to escape

the area of destruction and an inability to make

clear judgments. Many of the victims aimlessly

followed fleeing crowds until eventually they

reached places where they felt safe; there they were

given food and shelter. Most experienced a degree

of recovery by the second day, but from 1 to 3 weeks

later radiation sickness began to appear. This was,

to most, a totally mysterious illness with high fever;

bleeding from gums, throat, nose, and uterus; loss

of hair; and fatigue. This produced high levels of

anxiety, particularly as apparently uninjured persons began to die from intercurrent illness or other

causes. The need for early treatment to prevent

irreversible damage and death has been expressed.92

Goiânia and Chernobyl

Although the focus here is on short-term radiation effects, recognition of the longer-term effects of

increased risk for cancer, sterility, and diminished

life span may play an acute role in demoralizing the

combatants. The Goiânia, Brazil, tragedy in which

a small town was exposed to cesium isotopes from

a medical device, reveals the potential for social

disruption from radiation exposure. Many of the

exposed individuals were shunned by friends and

neighbors. Exports of produce from Goiânia

dropped precipitously.

Similar effects were reported in the Chernobyl

disaster in the Ukraine. Of 148 persons subjected to

radiation effects of the Chernobyl atomic energy

electrical plant accident and treated at Kiev Mental

Hospital from 1986 through 1990, reactive psychoses were observed in only 11 cases and this was

mainly during the 2 to 4 months after the disaster

when the production of stress was maximal. It

appears that stress, resulting in various psychopathological conditions including, rarely, psychosis, is paramount in producing psychiatric symp-
War Psychiatry

102

toms, rather than biological effects of ionizing radiation on central nervous system tissue.93

Extrapolation Studies

William James94 appears to have been the first

psychologist to systematically document the reactions of persons to disasters in his report of responses to the 1906 San Francisco earthquake

and fire. It was not, however, until the late 1940s

that Tyhurst95 did field studies of two apartment

house fires, a marine fire, and a flash flood from

which detailed clinical and actuarial reports could

be made. He formulated reactions during three

overlapping phases: (1) impact, (2) recoil, and (3)

post-trauma. During impact, reactions are automatic and can be separated into three main groups.

The first of these is an “effective” group of about

12% to 25% who remain “cool and collected,” and

who appreciate and respond appropriately to the

situation. The second group is characterized as a

“normal” group, because this is the largest number

(three fourths of the survivors), who are stunned

and bewildered. Individuals in this group show a

restricted field of attention and lack of awareness of

subjective feelings or emotion; however, they

display the physiological concomitants of fear,

and automatic or reflex behavior. The last group of

10% to 15%, the “ineffectives,” display manifestly

inappropriate responses: confusion, paralyzing

fear, inability to move or “freezing,” and “hysterical” crying or screaming. During recoil there is a

gradual return to normalcy; however, excessive

dependency is common during the first day or two.

The post-trauma reactions usually involve withdrawal, nightmares, anxiety, and pressured, repetitious recounting of the traumatic event. These

responses are well known to psychiatrists and will

not be addressed here.

Caldwell, Ranson, and Sacks96 discussed potential reactions of a civilian population under atomic

attack and applied Tyhurst’s95 formulations of the

impact of disasters on communities. High among

their considerations were expectations of group

panic. Panic, however, occurs only rarely and in

circumstances such that an overwhelming trauma

is experienced or expected and all avenues of possible escape but one are closed.

Simulation Studies: Desert Rock I, IV, V

In Desert Rock I97 an augmented airborne battalion combat team experienced an atomic bomb burst

from a position in the open about 7 miles from the

aerial explosion in October 1951. Attitude assessment, factual information questionnaires, and polygraph examinations at various times before and

after the explosion were given to the participants

and to control populations at the same base (Fort

Campbell, Kentucky) and at another distant base

(Fort Lewis, Washington).

The most significant finding was that anxiety

concerning some of the bomb’s effects persisted at a

high absolute level throughout the entire experiment. It was also found that the better-educated

were better informed, expressed more self-confidence, and experienced less anxiety. A disproportionate number of soldiers who experienced physiological disturbances on the day of the maneuver

were in the lower-educated group. The few highereducated men with physiological reactions differed

from other higher-educated men only in having had

greater difficulty adjusting to their roles in the U.S.

Army.97

Desert Rock IV,98 staged in May 1952, differed

from Desert Rock I in that the participants were

armored infantry troops who were stationed 4 miles

from ground zero in trenches, and they witnessed

the explosion of an atomic bomb emplaced on a

tower rather than an aerial bomb. In all, the reactions of about 1,200 men from the 1st Armored

Division, including those not involved in the maneuver, were tested from mid-May to mid-June

1952. Findings included the following:

1. Troops showed marked improvement in

knowledge about atomic effects as the result of a 4-hour indoctrination at Desert

Rock on the day before the atomic bomb

explosion.

2. The soldiers were most successful in learning the kind of information that had to do

with personal injury (eg, blindness, sterility, impotence). They tended, just after the

indoctrination, to overestimate the potential dangers of the atomic bomb more than

they did earlier or later.

3. The indoctrination appeared to lessen the

fear the troops felt about being on an atomic

bomb maneuver.

4. In contrast to the changes noted above, soldiers’ attitudes other than fear toward

atomic maneuvers and the U.S. Army were

not appreciably altered as a result of the

indoctrination.

5. There was no evidence that fear made any

troops incapable of carrying out their duties just after the detonation; in fact, no
103

Neuropsychiatric Casualties of Nuclear, Biological, and Chemical Warfare

grossly disorganizing fear was observed at

any time during the research. The spectacle

of the blast apparently had complex effects

upon soldiers’ fears: In comparison to the

previous night, less fear was expressed by

the soldiers in answer to direct questions 15

minutes after the explosion, whereas more

fear was revealed at this time by indirect

(projective) tests.

6. The troops apparently were neither more

nor less afraid of the effects of the bomb

after they had seen the damage it had done

in the forward area.

7. A material increase in the proportion of

troops who would volunteer to go on another atomic bomb maneuver, and to occupy a position as close or even closer to

ground zero, was recorded just after the

bomb explosion.

8. The high point of troops’ confidence in themselves and their outfits and in the experts’

ability to use the atomic bomb safely apparently was reached just after they had completed the maneuver.

Desert Rock V found similar responses among

officers.99

Vineberg Report

The Vineberg Report”100 has remained the standard reference concerning potential psychiatric casualties in a nuclear war. Vineberg reviewed the

relevant literature from a number of stressful situations including aerial bombing of cities (including

Hiroshima and Nagasaki), the disasters’ literature,

the behavior of personnel in combat, and psychological mechanisms involved in coping with extreme stress such as major surgery or terminal illness. Based on these studies he formulated a model

for nuclear combat.

Vineberg was reasonably optimistic about the

ability of a well-trained, highly-motivated soldier

to hold up, even when facing inevitable death. His

general conclusion was that a soldier would act in

tactical nuclear combat much as he had always

acted in combat. He did feel that because of the

greater stress there would be greater numbers of

psychological casualties, but he did not foresee a

sharp quantitative change in responses to such stress.

As in conventional warfare, psychiatric casualties

would arise as a function of cumulative stress related to the duration of exposure to combat and the

intensity of combat. Vineberg did not believe that

nuclear warfare would result in a breakdown of

authority relationships resulting in amoral, lawless, and asocial behavior in civilian or military

populations. Altogether, the Vineberg Report was

reassuring to military commanders. This optimism

had been reflected in the earlier “Clark Report,”101

in which Clark had estimated total casualties of

enlisted men in a unit to range from 4% to 23% in an

infantry battalion under atomic attack and concluded that losses ranging from 40% to 70% would

have to occur before the unit would be completely

demoralized. Perhaps in keeping with this optimism, the NATO handbook, Emergency War Surgery,

102 while addressing mass casualties in thermonuclear warfare, was silent about psychiatric

casualties.

The author does not share the optimism of

Vineberg and others that while psychiatric casualties must be considered, they will not prove decisive in nuclear warfare. Such factors may well have

been decisive in the defeat of France early in World

War II.103 Since 1965, neutron weapons capable of

surgically killing living beings in precisely designated targets have been developed by the United

States. Conventional weapons of near-nuclear capability in terms of blast and overpressure effects

now exist, and these may be mistaken for nuclear

devices.

Furthermore, it would be naive to believe that

nuclear weapons would not be accompanied by

chemical and biological warfare. A particularly

horrible dilemma might face the irradiated soldier

in a chemical environment who must remove his

protective mask or die from aspiration of his own

radiation-induced vomitus.

Laser and Microwave Radiation

One other form of radiation injury deserves mention because it will be encountered today on any

conventional battlefield. The nonionizing electromagnetic radiation of current laser range finders

and designators (U.S. forces’ as well as the enemy’s)

will produce injuries ranging from covert retinal

burns to sudden catastrophic blindness at distances

of several kilometers in unprotected eyes (and further in those using optical instruments). Lasers of

great power may be developed as direct weapons as

well. This invisible threat with its especially frightening consequences could affect the willingness of

troops to look toward the enemy and use weapons’

sights, and might stimulate conversion reactions of

hysterical blindness as an expression of battle fatigue.
War Psychiatry

104

Treatment of Neuropsychiatric Casualties of

Nuclear Warfare

The nature of modern combat with its high noise

levels, burning flesh, random death, and sleep and

sensory deprivation suggests the kinds of psychiatric casualties to expect even in the absence of nuclear

weapons.104 The largest group, unless evacuation is

possible, is likely to be the “psychological shock” or

“disaster-fatigue” cases encountered in mass casualty incidents. The disaster-fatigue casualties will

probably occur primarily in the first few hours and

days of the initiation of hostilities. Glass and colleagues105,106 applied Tyhurst’s formulations to the

atomic battlefield and established the concept of

treating such casualties similarly to combat fatigue;

hence, their use of the term “disaster fatigue.” This

treatment consists of replenishing physiological

needs (rest, nutrition, sleep) as necessary, and giving the individuals simple tasks to perform. In this

setting, the expectancy that they are “normal” and

effective is just as important as on the nonnuclear

battlefield.

The treatment of disaster-fatigue casualties must

emphasize education and preparation as the critical

elements in minimizing these casualties. Obviously, the main target of psychiatric intervention

should be the 50% to 80% of “normal” dazed persons who can be given simple tasks to aid their

recovery from the psychological shock. The small

hysterical group may require sedation; however,

this may fixate symptoms. Glass105 has pointed out

the need in these cases for a positive expectancy just

as in traditional combat fatigue. The most important element in minimizing these casualties, however, is prevention. It is well known that psychological trauma can be minimized by decreasing the

suddenness of the traumatic event; for example, a

sudden bereavement, as in the death of a spouse in

an accident, is more likely to produce psychiatric

morbidity than death of the spouse following a long

illness. It is as if time were available for a cognitive

desensitization. To prevent these casualties, repeated exposure to as realistic a battle experience as

possible must be part of the soldier’s training.

Aside from their destructive potential both from

blast and radiation effects, nuclear weapons produce in most people a not unwarranted fear verging

on hysteria, a fear conditioned by hundreds of media exposures to nuclear holocaust. The mere threat,

therefore, of nuclear weapons may result in psychiatric casualties with a primarily psychological etiology. Cataclysmic, unconventional warfare introduces new forms of psychopathology. Long periods of anxious waiting in shelters or in hermetic

tanks, and long wearing of masks and NBC protection cause psychic vulnerability106–109 as reported in

the Persian Gulf War.67,110

In the event of actual nuclear attack, the direct

effect of nuclear flash and blast would have a terrorizing psychological consequence. The extended

material destruction and numerous victims create a

sense of helplessness and vulnerability that undermines the fighter’s morale. Observations of

Hiroshima and Nagasaki survivors reveal a collective behavior of “shock-inhibition-stupor” followed

by attempts to escape.111 This is similar to behaviors

in earthquakes and similar catastrophes.

Even in the case of threatened use of unconventional weapons, psychopathological behaviors

should be expected. The terror of an unknown

death with the mythic fantasy of disappearing in

the nuclear flash (like the man from Hiroshima

reduced to his shadow) and the conviction that one

can neither be protected nor cured from radiation

sickness are powerful psychological factors. The

normal ambiguity of the battleground will be magnified by dispersal and loss of communications due

to the destruction of all but hard-wire communications by the nuclear EMP. In such circumstances

rumors may magnify in a contagious manner leading to collective panic. Even well-controlled fighters will experience increased levels of anxiety, leading at the minimum to increased numbers of combat

fatigue casualties, already expected to be as high as

one-to-one, that is, one combat fatigue to one

wounded in action, due to the stress of modern

continuous warfare. Added to this stress would be

concern about family (especially when accompanying U.S. forces in Europe and Korea), a factor found

to be important in Israeli casualties during the 1973

Yom Kippur War, increasing the likelihood of breakdown.

While realistic training and strong unit cohesion

fostered by good leadership leading to high levels

of fitness and morale will minimize psychiatric

casualties in even this hellish combat environment,

concrete steps should be undertaken now to minimize such casualties and make best use of all

resources in the event of nuclear war. Information

on the diagnosis and management of neuropsychiatric casualties of NBC warfare should be widely

disseminated. Realistic training in a partially

contaminated NBC environment should continue.

This training should involve not only combat arms

troops but also combat-support troops, who may
105

Neuropsychiatric Casualties of Nuclear, Biological, and Chemical Warfare

be even more likely than combat troops to suffer

chemical and nuclear attacks as the enemy attempts

to disrupt logistical support. Education to combat

rumors and fear of the unknown must be emphasized.

Fatally irradiated soldiers should receive every

possible palliative treatment, including narcotics,

to prolong their utility and alleviate their physical

and psychological distress. Depending on the

amount of fatal radiation, such soldiers may have

several weeks to live and to devote to the cause.

Commanders and medical personnel should be familiar with estimating survival time based on onset

of vomiting (see Table 4-4). Physicians should be

prepared to give medications to alleviate diarrhea,

and to prevent infection and other sequelae of radiation sickness in order to allow the soldier to serve as

long as possible. The soldier must be allowed to make

the full contribution to the war effort. He will already

have made the ultimate sacrifice. He deserves a

chance to strike back, and to do so while experiencing as little discomfort as possible.

In summary, a wide range of chemical, biological, and nuclear threats exist. Many are invisible,

persistent, have delayed effects, or are contagious.

Delivery means may be nonspecific, ubiquitous, or

covert. Detection methods are often inadequate.

Early signs and symptoms of exposure may be

nonspecific and common. The consequences of

delaying treatment may be irreversible and fatal.

Since Pavlov’s studies with dogs, scientists have

known that a requirement to discriminate between

ambiguous stimuli typically produces severe anxiety, stereotyped, sometimes bizarre behavior, or

both. This behavior must be expected to some

extent in any combat against a foe known to be

capable of using NBC weapons, even if those weapons are not actually employed.

A variety of maladaptive psychological reactions

may be evoked by the threat of NBC warfare. Anxiety may lead to heightened susceptibility to rumors

of the use of NBC warfare. This, in turn, could

provoke undue concern, not only for self and

unit, but also for the safety of dependent families if

they are in the area at risk. Preoccupation with

early warning symptoms may encourage individual hypochondriasis and increase the baseline

demand for medical attention. Group amplification of stress and hyperventilation symptoms may

cause epidemics of “gas hysteria,” as seen in World

War I. Even panic flight may occur if units feel

completely unprepared or if protective measures

seem inadequate (as they may in a hysterical

epidemic). There may also be excessive concern

with decontamination (perhaps leading to dermatologic problems), and overavoidance of possible

sources of exposure (possibly causing dehydration,

malnutrition, or even refusal to obey orders).

On the other hand, there may be inappropriate

fatalism or overconfidence leading to abandonment

of NBC protective equipment and of sensible precautions.

Even without “gas hysteria,” the added fear

and uncertainty about NBC use will probably increase the incidence of acute stress reactions (“battle

fatigue”). Rates as high as one case of transitory

battle fatigue per one wounded in action have been

projected based on historical data. Medical personnel are not immune to battle fatigue and must become familiar not only with its various presentations and basic treatment but also with its

prevention.

Psychological stresses that seem unendurable

have been described, but history proves that welltrained, cohesive units can come to accept such

horrors as commonplace. Effective deterrence requires not only thinking about the unthinkable but

obviously being prepared to deal with it. The psychological threats of NBC warfare have implications for psychological preparation that are especially relevant to the medical departments of the

armed services, and to National Guard and reserve

units. For example, training should avoid the traditional one-shot CS (tear gas) exposure exercise,

which classically conditions somatic and anxiety

symptoms to the protective mask. Such training

resulted in significant gas-mask phobia cases in the

Persian Gulf War. Instead, frequent practical exercises are needed to foster familiarity, confidence,

and the special skills required to function in an NBC

battlefield. Future warfare has aspects similar to

mass-casualty disasters, which produce large numbers of psychological casualties among uninjured

witnesses. Perhaps military units should train in

naturally occurring disaster incidents. NBC warfare is an exceedingly unpleasant prospect to consider; however, failure to prepare for it only increases the risk of its use.

SUMMARY AND CONCLUSION
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106

ACKNOWLEDGEMENT

The author wishes to acknowledge the assistance of Paul Newhouse, M.D., Department of Psychiatry,

College of Medicine, University of Vermont; James Stokes, M.D., Colonel, Medical Corps, U.S. Army,

Chief, Combat Stress Actions Office, Academy of Health Sciences, Army Medical Department Center

and School, Fort Sam Houston; and Gregory Belenky, M.D., Colonel, Medical Corps, U.S. Army,

Director, Division of Neuropsychiatry, Walter Reed Army Institute of Research, in portions of this

chapter.

REFERENCES

1. Hague Convention IV Respecting the Laws and Customs of War on Land. 18 October 1907. The Hague, The

Netherlands. Section 2, Chapter 1, Article 23A.

2. Geneva Convention for the Amelioration of the Condition of the Wounded and Sick in Armed Forces in the

Field. 12 August 1949. Geneva, Switzerland. April 21–August 12, 1949.

3. Nielands JB. Harvest of Death. New York: The Free Press; 1972.

4. Bestwick FW. Chemical agents used in riot control and warfare. Hum Toxicol. 1983;2:247–256.

5. Vien NK. Chemical Warfare, Vietnamese Studies. Hanoi, Vietnam: Xunhasaka; 1971: 175–178.

6. Jones FD, Stokes JW, Newhouse PA, Belenky GL, Crocq L. Neuropsychiatric casualties of chemical, biological

and nuclear warfare. In: Pichot P, Berner P, Wolf R, Thau K, eds. Psychiatry. The State of the Art. Vol 6. New

York: Plenum Publishing; 1985: 539–543.

7. Vedder EB. Medical Aspects of Chemical Warfare. Baltimore, Md: Williams & Wilkins; 1925.

8. Westerhoff SH. CBR Protection of Soviet Ground Forces. [Defense Intelligence Report DDB-1600-5-80] Washington, DC: Defense Intelligence Agency; 1980.

9. US Department of State. Reports of the Use of Chemical Weapons in Afghanistan, Laos and Kampuchea. Washington, DC; August 1980.

10. Meselson M, Robinson JD. Chemical warfare and chemical disarmament. Sci Am. 1980;242(4):38–47.

11. Medical Manual of Defense Against Chemical Agents. 5th ed. London: Her Majesty’s Stationery Office; 1972.

12. Reid TR. New cults flourish in a changed Japan. Washington Post. 27 March 1995. Vol 112: A1, A16.

13. United Nations, Security Council. Report of the mission dispatched by the Secretary-General to investigate

allegations of the use of chemical weapons in the conflict between the Islamic Republic of Iran and Iraq.

S/17911, March 12, 1986.

14. Why are we sick: Persian Gulf War leaves legacy of illness and broken faith. Army Times. 25 April 1994: 16–17.

15. Cookson J, Nottingham J. A Survey of Chemical and Biological Warfare. London: Sheep and Ward; 1969.

16. Heath DF. Organophosphorus Poisons. New York: Pergamon Press; 1961.

17. Gonsalves SF, Borison H. Atropine resistant central respiratory stimulants by bethanechol in cats. J Pharmacol

Exp Ther. 1980;214:297–305.
107

Neuropsychiatric Casualties of Nuclear, Biological, and Chemical Warfare

18. Petras JM. Soman neurotoxicity. Fundam Appl Toxicol. 1981;1:242.

19. Grob D, Harvey AM. The effects and treatment of nerve gas poisoning. Am J Med. 1953;14:52–63.

20. Nambu T, Nolte CT, Jackrel J, Grob D. Poisoning due to organophosphorus insecticides. Am J Med. 1971;50:475–

92.

21. Janowsky D, Ziegler M, Risch SC, Gillin JC. Antagonistic effects of scopolamine and atropine on the physostigmine response in man. Milit Med. 1987;152(11):579–581.

22. Sidell FR. Soman and sarin: Clinical manifestations and treatment of poisoning by organophosphates. Clin

Toxicol [now J Toxicol Clin Toxicol]. 1974;7(1):1–17.

23. Wills JH. Pharmacology of anticholinesterases: CSW special publication 2-14. Army Chemical Center, Md: US

Army Chemical Warfare Laboratories, Physiology Division, Directorate of Medical Research; 1958.

24. Sidell FR, Groff WA. Intramuscular and intravenous administration of small doses of 2-pyridinium aldoxime

methochloride to man. J Pharm Sci. 1971;60:1224–1228.

25. US Department of the Army. Treatment of Chemical Agent Casualties and Conventional Military Chemical Injuries.

Washington, DC:DA; February 1990. Field Manual 8-285: 2-2, 2-3.

26. US Department of the Navy. Treatment of Chemical Agent Casualties and Conventional Military Chemical Injuries.

Washington, DC: Naval Medical Command; February 1990. NAVMED P-5041.

27. US Department of the Air Force. Treatment of Chemical Agent Casualties and Conventional Military Chemical

Injuries. Randolph Air Force Base, Tex: Air Force Management Engineering Agency; February 1990. Air Force

Manual 160-11.

28. US Department of the Army. Clinical Notes on Chemical Casualty Care. Aberdeen, Md: US Army Medical Research

Institute of Chemical Defense; 14 August 1990. Technical Memorandum 90-1.

29. Chipman M, Sidell FR. A Review of the Efficacy and Clinical Pharmacology of the Chloride and Methanesulfonate Salts

of Pyridium 2-Aldoxime. Edgewood Arsenal, Md: US Army Biomedical Laboratory; 1980.

30. Hoskin FCG, Roush AH. Hydrolysis of nerve gas by squid-type diisopropyl phosphoroflouridate hydrolyzing

enzyme on agarose resin. Science. 1982;215:1255–1257.

31. Bowers MB, Goodman E, Sim VM. Some behavioral changes in man following anticholinesterase administration. J Nerv Ment Dis. 1964;138:383–389.

32. Levin HS, Rodnitzky RL. Behavioral effects of organophosphate pesticides in man. Clin Toxicol [now J Toxicol

Clin Toxicol]. 1976;9(3):391–405.

33. Wood W, Gabrica J, Brown HW, Watson M, Benson WW. Implication of organophosphate pesticide poisoning

in the plane crash of a duster pilot. Aerosp Med [now Aviat Space Environ Med]. 1971;42:1111–1113.

34. Metcalf DR, Holmes HH. EEG, psychological and neurological alterations in humans with organophosphorus

exposure. Ann N Y Acad Sci. 1969;160:357–365.

35. Levin HS, Rodnitzky RL, Mick DL. Anxiety associated with exposure to organophosphate compounds. Arch Gen

Psychiatry. 1976;33:225–228.

36. Rountree DW, Nevin S, Wilson A. The effects of diisopropyl flourophosphonate in schizophrenia and manic

depressive psychosis. J Neurol Neurosurg Psychiatry. 1950;13:47–59.

37. Davis KL, Berger PA, Hollister LE, Defraites E. Physostigmine in mania. Arch Gen Psychiatry. 1978;35:119–122.
War Psychiatry

108

38. Janowsky DS, El-Yousef MK, Davis JM, Sekerke HJ. Parasympathetic suppression of manic symptoms by

physostigmine. Arch Gen Psychiatry. 1973;28:542–547.

39. Gershon S, Shaw FH. Psychiatric sequelae of chronic exposure to organophosphorus insecticides. Lancet

1961;1:1371–1374.

40. Meyerhoff JL. Neurochemical and Behavioral Effects of Anticholinergic Drugs. Washington, DC: Medical Neurosciences Department, Walter Reed Army Institute of Research. Manuscript. 1980.

41. Caldwell JA Jr, Stephens RL, Carter DJ, Jones HD. Effects of 2mg and 4mg atropine sulfate on the performance

of US Army helicopter pilots. Aviat Space Environ Med. 1992;63(10):857–864.

42. Ketchum JS, Sidell FR, Crowell EB Jr, Aghajanian GK, Hayes AH Jr. Atropine, scopolamine, and ditran:

Comparative pharmacology and antagonists in man. Psychopharmacology (Berlin). 1973;28:121–145.

43. Datel WE, Johnson AW Jr. Psychotropic Prescription Medication in Vietnam. Available from Defense Technical

Information Center, Alexandria, Va. No. ADA097610. 1978.

44. Jones FD, Johnson AW. Medical and psychiatric treatment policy and practice in Vietnam. J Soc Issues.

1975;31(4):49–65.

45. Jones FD. Combat psychiatry in modern warfare. In: Adelaja O, Jones FD, eds. War and its Aftermath. Lagos,

Nigeria: John West; 1983: 63–77.

46. Beverley R. History and Present State of Virginia, Book 2. Chapel Hill, NC: North Carolina University Press; 1947: 24.

47. Gowdy JM. Stramonium intoxication—review of symptomatology in 212 cases. JAMA. 1972;221(6):585–587.

48. Belenky GL, Jones FD. The evacuation syndrome in military exercises: A model of the psychiatric casualties of

combat. In: Mangelsdorff AD, Furukawa PT. Proceedings: Users’ Workshop on Combat Stress. Washington, DC:

Defense Technical Information Center, Alexandria, VA. No. ADA 152464. September 1981: 140–142.

49. Jones FD. Lessons of war for psychiatry. In: Pichot P, Berner P, Wolf R, Thau K, eds. Psychiatry: The State of the

Art. Vol 6. New York: Plenum; 1985: 515–519.

50. Duvoisin RC, Katz R. Reversal of central anticholinergic syndrome in man by physostigmine. JAMA.

1968;206(9):1963–1965.

51. Bryson DD. Cyanide poisoning (Letter to the editor). Lancet. 1978;1(8055):92.

52. Gosselin RE, Hodge HC, Smith HP, Gleason MN, eds. Clinical Toxicology of Commercial Products. 4th ed.

Baltimore, Md: Williams & Wilkins; 1976: 105–112.

53. Barnett HOM, Jackson MV, Spaulding WB. Thiocyanate psychosis. JAMA. 1951;147(16):1554–1558.

54. Willems JL. Clinical Management of Mustard Gas Casualties. Ghent, Belgium: University of Ghent Medical School;

1989: 11. Vol 3: Supplement to Annales Medicinae Militaris Belgicae.

55. Grinstad B, ed. BC Warfare Agents. Stockholm: Forsvarets Forskningsanstalt; 1964.

56. Fisher GJB. Chemicals in War: A Treatise on Chemical Warfare. New York: McGraw-Hill; 1937: 156.

57. Salmon TW, Fenton N, eds. In the American Expeditionary Forces [Section 2]. Neuropsychiatry. Vol. 10. In: The

Medical Department of the United States Army in the World War. Washington, DC; Office of The Surgeon General,

US Army; 1929.

58. Miller E. Neurosis in War. New York: Macmillan. 1944.
109

Neuropsychiatric Casualties of Nuclear, Biological, and Chemical Warfare

59. Mott FW. War Neuroses and Shell Shock. London, England: Oxford University Press; 1919: 105.

60. Hulbert HS. Gas neurosis syndrome. Am J Insanity [now Am J Psychiatry]. 1920;77:213–216.

61. Ingraham LH, Manning FJ. Psychiatric battle casualties. Milit Rev. 1980;60(8):19–29.

62. Brooks FR, Xenakis SN, Ebner DG, Balson PM. Psychological reactions during chemical warfare training. Milit

Med. 1983;148(3):232–235.

63. Fullerton CS, Ursano RJ. Health care delivery in the high-stress environment of chemical and biological warfare.

Milit Med. 1994;159:524–528.

64. Bennion SD. Designing of NBC protective gear to allow for adequate first aid. Milit Med. 1982;147(11):960–962.

65. Burgin WW, Gehring LM, Bell TL. A chemical field resuscitation device. Milit Med. 1982;147(10):873–876.

66. Xenakis SN, Brooks FR, Burgin WW, Balson PM. A model for training combat medics for chemical warfare. Fort

Sam Houston, Tex: US Academy of Health Sciences. Unpublished manuscript. 1983.

67. Took KJ, Ritchie EC, Sandman LM. Letters to the editor on gas mask phobia. Milit Med. 1992;157(8):A10–A11.

68. Draper ES, Lombardi JJ. Combined arms in a nuclear/chemical environment. In: Force Development Testing

and Experimentation, CANE FDTE: Summary evaluation report, phase 1. Fort McClellan, Ala: US Army

Chemical School; 1986.

69. Taylor HL, Orlansky J. The effects of wearing chemical warfare combat clothing on human performance.

Alexandria, Va: Institute for Defense Analysis, IDAP 2433; August 1991: iii-3.

70. Glass AJ. Observations upon the epidemiology of mental illness in troops during warfare. Presented at the

Symposium on Social Psychiatry, Walter Reed Army Institute of Research; April 1957; Washington, DC.

71. Jones FD. Combat stress: Tripartite model. Int Rev Army Navy Air Force Med Serv. 1982;55:247–254.

72. Noy S. Division-based psychiatry in intensive war situations. J R Army Med Corps. 1982;128:105–116.

73. Belenky GL, Newhouse P, Jones FD. Prevention and treatment of psychiatric casualties in the event of a war in

Europe. Int Rev Army Navy Air Force Med Serv. 1982;55:303–307.

74. Belenky G. Unusual visual experiences reported by subjects in the British Army study of sustained operations,

Exercise Early Call. Milit Med. 1979;144(10):695–696.

75. Haslam DR. The effects of sleep loss and recovery sleep upon the military performance of the soldier. Int Rev

Army Navy Air Force Med Serv. 1981;54:103–116.

76. Sodetz FJ. Some constraints on the management of sleep and fatigue. Revue Internationale des Services de Sante.

1981;54:97–100.

77. Belenky GL, Tyner CF, Sodetz FJ. Israeli Battle Shock Casualties: 1973 and 1982 [Report WRAIR NP-83-4].

Washington, DC: Walter Reed Army Institute of Research; 1983.

78. Cadigan FD. Battleshock, the chemical dimension. J R Army Med Corps. 1982;128:89–92.

79. Marshall SLA. Bringing Up the Rear: A Memoir. San Rafael, Calif: Presidio Press; 1979: 15.

80. Malek I. Biological weapons. In: Rose S, ed. CBW: Chemical and Biological Warfare. Boston, Mass: Beacon Press;

1969: 48–61.
War Psychiatry

110

81. Abramova FA, Grinberg LM, Yampolskaya OV, et al. Pathology of inhalational anthrax in 42 cases from the

Sverdlovsk outbreak of 1979. Proc Natl Acad Sci USA. 1993;90:2291–2294.

82. Meyerhoff JC. Personal Communication, 1984.

83. Eastwood M. The medicine of nuclear warfare: A clinical dead end. Lancet. 1981:1(8232):1252–1253.

84. Vandre RH, Tesche FM, Kleber J, Blanchard JP. Electromagnetic pulse (EMP), Part 1: Effects on field medical

equipment. Milit Med. 1993;158(4):233–236.

85. AMA Board of Trustees, Electromagnetic pulse and its effects. JAMA. 1992;268(5):639–641.

86. Vandre RH, Tesche RM, Klebers J, Blanchard JP. Electromagnetic pulse (EMP), Part 2: Field-expedient ways to

minimize its effects on field medical treatment facilities. Milit Med. 1993;158(5):285–289.

87. Atomic Bomb Casualty Commission. Bibliography of Publications Concerning Effect of Nuclear Explosions 1945—

1960. Washington, DC: US GPO; 1961.

88. Glasstone S, Dolan PJ. Biological effects. The Effects of Nuclear Weapons. 3rd ed. Washington, DC: US GPO; 1977:

541–559.

89. Swann SW. Euthanasia on the battlefield. Milit Med. 1987;152(11):545–549.

90. Committee for the Compilation of Materials on Damage caused by the Atomic Bombs in Hiroshima and

Nagasaki, eds. Hiroshima and Nagaski: The Physical, Medical and Social Effects of the Atomic Bombings. Ishikawa E,

Swain DL, Trans. New York: Basic Books; 1981.

91. Konuma M. Neuropsychiatric case studies on the atomic bomb casualties at Hiroshima. In: Research in the Effects and

the Influences of the Nuclear Bomb Test Explosions. Vol 2. Tokyo: Japan Society for the Promotion of Science; 1956.

92. Stokes JW. Neuropsychiatric casualties of NBC and conventional warfare. Presented at Division and Combat

Psychiatry Course, Army Medical Department; April 1982; Colorado Springs, Colo.

93. Revenok AA. Structural-dynamic characterization of reactive psychoses in persons subjected to the effect of

ionizing radiation as a result of the Chernobyl AES disaster. JAMA. 1991;268(11):1406.

94. James W. On some mental effects of the earthquake. In: Memories and Studies. New York: Longmans, Green; 1911:

207–226.

95. Tyhurst JS. Individual reactions to disaster: The natural history of psychiatric phenomena. Am J Psychiatry.

1951;107:764–769.

96. Caldwell JM, Ranson WW, Sacks JG. Group panic and other mass disruptive reactions. US Armed Forces Med J.

1951;2(4):541–567.

97. Bordes PA, Finan JL, Hochstim JR, McFann HH, Schwartz SG. Desert Rock I: A Psychological Study of Troop

Reactions to an Atomic Explosion. Washington, DC: Human Resources Research Office, George Washington

University. TR-1. February 1953.

98. Desert Rock IV: Reactions of an Armored Infantry Battalion to an Atomic Bomb Maneuver. Washington, DC: Human

Resources Research Office, George Washington University. TR-2. August 1953.

99. White BW. Desert Rock V: Reactions of Troop Participants and Forward Volunteer Officer Groups to Atomic Exercises.

Washington, DC: Human Resources Research Office, George Washington University; August 1953.

100. Vineberg R. Human Factors in Tactical Nuclear Combat. Human Resources Research Office, George Washington

University, Washington, DC. TR 65-2. April 1965.
111

Neuropsychiatric Casualties of Nuclear, Biological, and Chemical Warfare

101. Clark DK. Casualties as a Measure of the Loss of Combat Effectiveness of an Infantry Battalion. Chevy Chase, Md:

Operations Research Office, Johns Hopkins University. ORO-T-289. August 1954.

102. Emergency War Surgery: First United States Revision of the Emergency War Surgery, NATO Handbook. Washington,

DC: US GPO, Department of Defense; 1975.

103. Cline WR, Rath FH. The concept of the army as a psychiatric casualty. J R Army Med Corps. 1982;128:79–88.

104. Romo J, Schneider RJ. Disaster, psychiatric casualties and implications for future war. J R Army Med Corps.

1982;128:93–99.

105. Glass AJ. Management of mass psychiatric casualties. Milit Med. 1956;118(4):335–342.

106. Glass AJ, Drayer CS, Cameron DC, Woodward WD. Psychological first aid in community disasters. JAMA.

1954;156:36–41.

107. Crocq L, Lefebvre P, Girard V. Considerations sur l’evolution des conceptions en psychopathologie de guerre.

Revue de Medecine Psychosomatique. 1965;7(3):253–262.

108. Crocq L. Guerre NBC et panique collective. Revue des Corps de Sante des Armees. 1970;11(4):483–497.

109. Doutheau C, Crocq L, Sailhan M. Panic and catastrophe behaviour. In Pichot P, Berner P, Wolf R, Thau K, eds.

Psychiatry: The State of the Art. Vol 6. New York: Plenum Press; 1985: 471–478.

110. Ritchie EC. Treatment of gas mask phobia. Milit Med. 1992;157:104–106.

111. Gregory GA, Lawson TR, Brooks FR. Behavioral Science Support in the Theater of Operations: Casualty Generation Study.

San Antonio, Tex: Behavioral Sciences Division, Directorate of Training, Academy of Health Sciences; 1979.