During World War I, British troops found themselves exposed to a range of blast injuries, particularly before the introduction of the steel helmet at the beginning of 1916. Engaged in static trench warfare, frontline soldiers experienced artillery barrage and mortar attacks, together with the threat of devastating mines. It is estimated that 60% of deaths in World War I were caused by shrapnel
(8) . Lt. Col. John Rhein, consultant in neuropsychiatry to the American Expeditionary Force, reported that 50% to 60% of soldiers with shell shock admitted to his base hospital claimed to have been concussed; for example, “a man states that he had lost consciousness or memory after having been blown over by a shell”
(9) .
Shell Shock
Head wounds and brain injury following exposure to exploding ordnance were recognized as a significant cause of invalidity in the opening phase of World War I. These casualties offered Gordon Holmes, consultant neurologist to the British Expeditionary Force, an unprecedented opportunity to test the localization of brain function. Cerebral trauma found itself at the cutting edge of military medicine. But what appeared to be a straightforward association between cause (shell explosion) and effect (head wound) soon became clouded and a cause of controversy.
Increasing numbers of soldiers who had been close to a detonation without receiving a head wound presented at casualty clearing stations with puzzling symptoms. They suffered from amnesia, poor concentration, headache, tinnitus, hypersensitivity to noise, dizziness, and tremor but did not recover with hospital treatment
(10) . Diagnosis became problematic because their clinical presentation was similar in many respects to that of soldiers who had experienced cerebral injury. The term “shell shock” evolved in an attempt to describe cases that arose in the context of exploding ordnance but where enduring symptoms could not be linked to the presence of an obvious organic lesion. Shell shock entered the medical debate in February 1915 with the publication of a paper on the subject in
Lancet by Capt. C.S. Myers, a specialist in psychological medicine
(6) .
In the spring of 1915, after bitter fighting at the second battle of Ypres, the number of shell shock cases increased, but the military made no significant progress in understanding the disorder, and still less in designing an effective management strategy. This was partly a question of priorities. The British Army struggled to open sufficient hospital accommodation for the wounded in France
(11) . The rapid growth of the British Expeditionary Force and unexpected levels of bacterial infection created pressing medical priorities, forcing shell shock to a lowly position on the military agenda for 1915. As a result, shell shock patients were transferred to base hospitals in France and the U.K. for observation in general wards
(12) . Without an informed treatment strategy, this puzzling disorder spread throughout the British Army. By the autumn of 1916, with manpower losses following the Somme offensive, the issue of shell shock finally came to the fore. The flow of casualties from the front had to be stemmed and an effective intervention devised to return combat troops to active duty.
Because shell shock was characterized by a wide range of common symptoms, it was open to multiple etiological explanations. At first, forces of compression and decompression were thought to cause a cerebral lesion, a form of commotio cerebri
(5) . Frederick Mott, then Britain’s leading neuropathologist, who was recruited by the War Office to discover the etiology of the disorder, argued that in extreme cases shell shock could be fatal if intense commotion affected “the delicate colloidal structures of the living tissues of the brain and spinal cord,” arresting “the functions of the vital centers in the medulla”
(13) . It was also speculated that the disorder resulted from damage to the CNS from carbon monoxide released by the partial detonation of a shell or mortar
(14) . In other words, shell shock was formulated as an organic problem even though the pathology remained unclear.
However, research conducted in 1915 and 1916 by Myers, consultant psychologist to the British Expeditionary Force, led to a new hypothesis
(15) . Based on his own observations, an increasing appreciation of the stress of trench warfare, and the finding that many shell-shocked soldiers had been nowhere near an explosion but had identical symptoms to those who had, Myers suggested a psychological explanation
(16) . For these cases, the term “emotional,” rather than “commotional,” shock was proposed. The psychological explanation gained ground over the neurological in part because it offered the British Army an opportunity to return shell-shocked soldiers to active duty. Increasingly short of frontline troops, any initiative that promised to restore soldiers to fitness was attractive. As a result, in November 1916, Arthur Sloggett, Director General of Army Medical Services, authorized two new classifications: “effects of explosion (wound)” for those who were unable to perform their duties as a soldier as a result of direct contact with “a specific explosion … without producing a visible wound” and “nervousness” for those whose symptoms were characterized by anxiety
(17) . In addition, four dedicated units were set up in France close to the front line (“forward psychiatry”) for acute cases. Furthermore, specialist base hospitals were established for those already suffering from chronic effects (notably at Maghull, Craiglockhart, and the Maudsley). Considerable resources were diverted toward the investigation and clinical management of this apparently novel disorder.
A further problem encountered by the physicians at these specialist units, whether in France or the U.K., was to establish a definitive link between any explosion and subsequent symptoms. Without an organic lesion, any soldier in a war zone with symptoms of fatigue, memory loss, or dizziness had to be considered a potential shell shock case. Regimental medical officers were required to state on casualty forms whether a serviceman had been close to a detonation or not, but in the heat of battle with other pressing duties, this information was rarely provided
(18) .
When the United States entered the war in April 1917, U.S. military authorities faced the same steep learning curve. A month later, Maj. Thomas Salmon was ordered to the U.K. and France to study the question of shell shock and make recommendations for U.S. Army policy
(19) . In essence, he proposed a system of forward psychiatry supported by a large specialist “clearing hospital for mental cases,” which led to the creation of Base Hospital No. 117, set up at La Fauche
(20) . Despite this careful planning, shell shock spread through the American Expeditionary Force and rose to significant levels during the Argonne offensive
(21) .
Scale of the Disorder
During World War I, 10% of British battle casualties were categorized as some form of shell shock or neurasthenia
(22) . In October 1917, Salmon reported that shell shock was responsible for one-seventh of all discharges from the British Army, and one-third if wounds were excluded
(7) . By the end of 1918, the British government had awarded 32,000 war pensions for shell shock, a figure that would rise dramatically once soldiers were discharged from the forces
(23) .Shell shock had initially caught the popular imagination in part because it was thought to be related to a genuine medical emergency, a head wound or neurological lesion. As Southard observed, the term “compared with the more acutely terrible and life-in-the-balance thing we know as traumatic or surgical shock”
(24) . In 1917, however, when it had become clear that many cases of shell shock were not directly related to a head injury, military medical authorities attempted to restrict use of the diagnosis. Servicemen invalided from the front were given a preliminary label of “not yet diagnosed, nervous,” and those who failed to recover but had no visible cerebral injury were then classified as “neurasthenic.” Disputes over the etiology and management of shell shock served to inhibit further the design of an effective protocol. The involvement of the media and politicians, ostensibly to support the claims of individual veterans, added an emotive element that distorted policy and research
(25) . In November 1917, for example, Myers was denied permission to submit a paper on shell shock to the
British Medical Journal because orders had been issued to the press bureau that nothing regarding the disorder should be released to newspapers
(26) .