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Suggested Citation:"The Chronic Neurological Deficit." National Research Council. 1961. Follow-Up Study of Head Wounds in World War II, by a. Earl Walker and Seymour Jablon. Washington, DC: The National Academies Press. doi: 10.17226/18529.
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Suggested Citation:"The Chronic Neurological Deficit." National Research Council. 1961. Follow-Up Study of Head Wounds in World War II, by a. Earl Walker and Seymour Jablon. Washington, DC: The National Academies Press. doi: 10.17226/18529.
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Suggested Citation:"The Chronic Neurological Deficit." National Research Council. 1961. Follow-Up Study of Head Wounds in World War II, by a. Earl Walker and Seymour Jablon. Washington, DC: The National Academies Press. doi: 10.17226/18529.
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Suggested Citation:"The Chronic Neurological Deficit." National Research Council. 1961. Follow-Up Study of Head Wounds in World War II, by a. Earl Walker and Seymour Jablon. Washington, DC: The National Academies Press. doi: 10.17226/18529.
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Suggested Citation:"The Chronic Neurological Deficit." National Research Council. 1961. Follow-Up Study of Head Wounds in World War II, by a. Earl Walker and Seymour Jablon. Washington, DC: The National Academies Press. doi: 10.17226/18529.
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Page 39
Suggested Citation:"The Chronic Neurological Deficit." National Research Council. 1961. Follow-Up Study of Head Wounds in World War II, by a. Earl Walker and Seymour Jablon. Washington, DC: The National Academies Press. doi: 10.17226/18529.
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Page 40
Suggested Citation:"The Chronic Neurological Deficit." National Research Council. 1961. Follow-Up Study of Head Wounds in World War II, by a. Earl Walker and Seymour Jablon. Washington, DC: The National Academies Press. doi: 10.17226/18529.
×
Page 41
Suggested Citation:"The Chronic Neurological Deficit." National Research Council. 1961. Follow-Up Study of Head Wounds in World War II, by a. Earl Walker and Seymour Jablon. Washington, DC: The National Academies Press. doi: 10.17226/18529.
×
Page 42
Suggested Citation:"The Chronic Neurological Deficit." National Research Council. 1961. Follow-Up Study of Head Wounds in World War II, by a. Earl Walker and Seymour Jablon. Washington, DC: The National Academies Press. doi: 10.17226/18529.
×
Page 43
Suggested Citation:"The Chronic Neurological Deficit." National Research Council. 1961. Follow-Up Study of Head Wounds in World War II, by a. Earl Walker and Seymour Jablon. Washington, DC: The National Academies Press. doi: 10.17226/18529.
×
Page 44
Suggested Citation:"The Chronic Neurological Deficit." National Research Council. 1961. Follow-Up Study of Head Wounds in World War II, by a. Earl Walker and Seymour Jablon. Washington, DC: The National Academies Press. doi: 10.17226/18529.
×
Page 45
Suggested Citation:"The Chronic Neurological Deficit." National Research Council. 1961. Follow-Up Study of Head Wounds in World War II, by a. Earl Walker and Seymour Jablon. Washington, DC: The National Academies Press. doi: 10.17226/18529.
×
Page 46
Suggested Citation:"The Chronic Neurological Deficit." National Research Council. 1961. Follow-Up Study of Head Wounds in World War II, by a. Earl Walker and Seymour Jablon. Washington, DC: The National Academies Press. doi: 10.17226/18529.
×
Page 47
Suggested Citation:"The Chronic Neurological Deficit." National Research Council. 1961. Follow-Up Study of Head Wounds in World War II, by a. Earl Walker and Seymour Jablon. Washington, DC: The National Academies Press. doi: 10.17226/18529.
×
Page 48
Suggested Citation:"The Chronic Neurological Deficit." National Research Council. 1961. Follow-Up Study of Head Wounds in World War II, by a. Earl Walker and Seymour Jablon. Washington, DC: The National Academies Press. doi: 10.17226/18529.
×
Page 49
Suggested Citation:"The Chronic Neurological Deficit." National Research Council. 1961. Follow-Up Study of Head Wounds in World War II, by a. Earl Walker and Seymour Jablon. Washington, DC: The National Academies Press. doi: 10.17226/18529.
×
Page 50
Suggested Citation:"The Chronic Neurological Deficit." National Research Council. 1961. Follow-Up Study of Head Wounds in World War II, by a. Earl Walker and Seymour Jablon. Washington, DC: The National Academies Press. doi: 10.17226/18529.
×
Page 51
Suggested Citation:"The Chronic Neurological Deficit." National Research Council. 1961. Follow-Up Study of Head Wounds in World War II, by a. Earl Walker and Seymour Jablon. Washington, DC: The National Academies Press. doi: 10.17226/18529.
×
Page 52
Suggested Citation:"The Chronic Neurological Deficit." National Research Council. 1961. Follow-Up Study of Head Wounds in World War II, by a. Earl Walker and Seymour Jablon. Washington, DC: The National Academies Press. doi: 10.17226/18529.
×
Page 53
Suggested Citation:"The Chronic Neurological Deficit." National Research Council. 1961. Follow-Up Study of Head Wounds in World War II, by a. Earl Walker and Seymour Jablon. Washington, DC: The National Academies Press. doi: 10.17226/18529.
×
Page 54
Suggested Citation:"The Chronic Neurological Deficit." National Research Council. 1961. Follow-Up Study of Head Wounds in World War II, by a. Earl Walker and Seymour Jablon. Washington, DC: The National Academies Press. doi: 10.17226/18529.
×
Page 55
Suggested Citation:"The Chronic Neurological Deficit." National Research Council. 1961. Follow-Up Study of Head Wounds in World War II, by a. Earl Walker and Seymour Jablon. Washington, DC: The National Academies Press. doi: 10.17226/18529.
×
Page 56
Suggested Citation:"The Chronic Neurological Deficit." National Research Council. 1961. Follow-Up Study of Head Wounds in World War II, by a. Earl Walker and Seymour Jablon. Washington, DC: The National Academies Press. doi: 10.17226/18529.
×
Page 57
Suggested Citation:"The Chronic Neurological Deficit." National Research Council. 1961. Follow-Up Study of Head Wounds in World War II, by a. Earl Walker and Seymour Jablon. Washington, DC: The National Academies Press. doi: 10.17226/18529.
×
Page 58
Suggested Citation:"The Chronic Neurological Deficit." National Research Council. 1961. Follow-Up Study of Head Wounds in World War II, by a. Earl Walker and Seymour Jablon. Washington, DC: The National Academies Press. doi: 10.17226/18529.
×
Page 59
Suggested Citation:"The Chronic Neurological Deficit." National Research Council. 1961. Follow-Up Study of Head Wounds in World War II, by a. Earl Walker and Seymour Jablon. Washington, DC: The National Academies Press. doi: 10.17226/18529.
×
Page 60
Suggested Citation:"The Chronic Neurological Deficit." National Research Council. 1961. Follow-Up Study of Head Wounds in World War II, by a. Earl Walker and Seymour Jablon. Washington, DC: The National Academies Press. doi: 10.17226/18529.
×
Page 61
Suggested Citation:"The Chronic Neurological Deficit." National Research Council. 1961. Follow-Up Study of Head Wounds in World War II, by a. Earl Walker and Seymour Jablon. Washington, DC: The National Academies Press. doi: 10.17226/18529.
×
Page 62
Suggested Citation:"The Chronic Neurological Deficit." National Research Council. 1961. Follow-Up Study of Head Wounds in World War II, by a. Earl Walker and Seymour Jablon. Washington, DC: The National Academies Press. doi: 10.17226/18529.
×
Page 63
Suggested Citation:"The Chronic Neurological Deficit." National Research Council. 1961. Follow-Up Study of Head Wounds in World War II, by a. Earl Walker and Seymour Jablon. Washington, DC: The National Academies Press. doi: 10.17226/18529.
×
Page 64
Suggested Citation:"The Chronic Neurological Deficit." National Research Council. 1961. Follow-Up Study of Head Wounds in World War II, by a. Earl Walker and Seymour Jablon. Washington, DC: The National Academies Press. doi: 10.17226/18529.
×
Page 65
Suggested Citation:"The Chronic Neurological Deficit." National Research Council. 1961. Follow-Up Study of Head Wounds in World War II, by a. Earl Walker and Seymour Jablon. Washington, DC: The National Academies Press. doi: 10.17226/18529.
×
Page 66
Suggested Citation:"The Chronic Neurological Deficit." National Research Council. 1961. Follow-Up Study of Head Wounds in World War II, by a. Earl Walker and Seymour Jablon. Washington, DC: The National Academies Press. doi: 10.17226/18529.
×
Page 67
Suggested Citation:"The Chronic Neurological Deficit." National Research Council. 1961. Follow-Up Study of Head Wounds in World War II, by a. Earl Walker and Seymour Jablon. Washington, DC: The National Academies Press. doi: 10.17226/18529.
×
Page 68
Suggested Citation:"The Chronic Neurological Deficit." National Research Council. 1961. Follow-Up Study of Head Wounds in World War II, by a. Earl Walker and Seymour Jablon. Washington, DC: The National Academies Press. doi: 10.17226/18529.
×
Page 69
Suggested Citation:"The Chronic Neurological Deficit." National Research Council. 1961. Follow-Up Study of Head Wounds in World War II, by a. Earl Walker and Seymour Jablon. Washington, DC: The National Academies Press. doi: 10.17226/18529.
×
Page 70
Suggested Citation:"The Chronic Neurological Deficit." National Research Council. 1961. Follow-Up Study of Head Wounds in World War II, by a. Earl Walker and Seymour Jablon. Washington, DC: The National Academies Press. doi: 10.17226/18529.
×
Page 71
Suggested Citation:"The Chronic Neurological Deficit." National Research Council. 1961. Follow-Up Study of Head Wounds in World War II, by a. Earl Walker and Seymour Jablon. Washington, DC: The National Academies Press. doi: 10.17226/18529.
×
Page 72
Suggested Citation:"The Chronic Neurological Deficit." National Research Council. 1961. Follow-Up Study of Head Wounds in World War II, by a. Earl Walker and Seymour Jablon. Washington, DC: The National Academies Press. doi: 10.17226/18529.
×
Page 73
Suggested Citation:"The Chronic Neurological Deficit." National Research Council. 1961. Follow-Up Study of Head Wounds in World War II, by a. Earl Walker and Seymour Jablon. Washington, DC: The National Academies Press. doi: 10.17226/18529.
×
Page 74
Suggested Citation:"The Chronic Neurological Deficit." National Research Council. 1961. Follow-Up Study of Head Wounds in World War II, by a. Earl Walker and Seymour Jablon. Washington, DC: The National Academies Press. doi: 10.17226/18529.
×
Page 75
Suggested Citation:"The Chronic Neurological Deficit." National Research Council. 1961. Follow-Up Study of Head Wounds in World War II, by a. Earl Walker and Seymour Jablon. Washington, DC: The National Academies Press. doi: 10.17226/18529.
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Page 76

Below is the uncorrected machine-read text of this chapter, intended to provide our own search engines and external engines with highly rich, chapter-representative searchable text of each book. Because it is UNCORRECTED material, please consider the following text as a useful but insufficient proxy for the authoritative book pages.

Chapter HI THE CHRONIC NEUROLOGICAL DEFICIT A. INTRODUCTION In general, reparative and recuperative processes tend to reduce a neuro- logical defect for about 2 years. Rehabilitation and special training may be effective over a somewhat longer period of time, but usually in an adult the neurological dysfunction reaches a plateau after 3 to 5 years and in the ensuing next few years regresses very little. It seems probable that an examination made 7 to 10 years after injury will represent the relatively stable state of the nervous system—in other words, the end result of the natural healing processes and the various special therapies. To evaluate this state, all aspects of nervous function must be investigated in order to assess the overall condition of the individual. In this study special emphasis has been placed on certain aspects, such as the presence of headaches or convulsions, but it is planned to present in this chapter the neurological status at the time of the follow-up examination, and, by correlating the abnormalities with the varying conditions operating at the time of injury and shortly thereafter, to determine the factors which may be important in their production. B. GENERAL SURVEY A glance at the summary table 40 of the chronic neurological deficits indicates that even years after injury few men who suffered a head wound considered themselves perfectly normal, although almost half had no ab- normal findings on neurological examination. Granted that the wound- ing in this series is much more serious than in the ordinary civilian series of head injuries, it is still remarkable that 81 percent of patients 7 to 8 years after injury were suffering headaches. This is not, however, a higher fre- quency than that reported by Rawling (100), who found 88 percent of his English patients suffering headaches 2 years after injury, by Alajouanine et al. (4), who reported 87 percent of the French head injuries in 1914-18 having cephalalgia, nor by Gliddon (54), who stated that 87 percent of his Canadian veterans of World War I had headaches as long as 19 years after wounding. Similarly, German military casualties suffering head injuries had a high incidence of headache, Brun (24) reporting 77 percent and Usbeck (128) 85 percent. The more favorable outcome of civilian injuries, probably less severe and to a younger population, is apparent from Pennington and Mearin's (97) review of 4,822 male naval inductees. Thirteen percent of these men had suffered craniocerebral injuries, 473 being so mild that consciousness was impaired less than 10 minutes, 69 having a period of unconsciousness between 10 and 60 minutes, and 110, classified as severe, being out a longer period. Some years after the injury only 4 percent of the mildly injured, 19

Table 40.—General Summary of Neurological Status at Time of Follow-up Symptomatology Normal 63 Posttraumatic syndrome 419 Headache 183 Other and unknown 74 Total 739 Objective finding No neurological deficit 346 Hemiplegia or hemiparesis 159 Hemianopsia 68 Cortical sensory impairment 148 Aphasia 59 Mental impairment 102 Cranial nerve palsy 175 Cerebellar syndrome 7 Other 13 Unknown 2 Total 739 percent of the moderately injured, and 29 percent of the severely injured group had neurological symptoms referable to the effects of the accident. That 57 percent of the wounded in this series should have a full-blown posttraumatic syndrome is also quite remarkable. In men with some neurological disability, hemiparesis, usually associated with hemihypesthesia, was common. As might be expected, a large pro- portion of these men (15 percent) had an aphasia, which may be a greater disability than paralysis of an extremity. That almost 15 percent of the patients had some mental impairment emphasizes a fact often overlooked, namely, that organic brain disease does give rise to mental aberration vary- ing from simple memory loss and confusion to profound dementia. It is further enlightening to note that almost one-fourth of the wounded in this series had some evidence of cranial nerve impairment. This is probably an indication of the destructiveness of present-day high velocity missiles. On the other hand, the paucity of cerebellar syndromes is likely due to the same factor since violence in the posterior fossa is apt to be incompatible with life. C. NEUROLOGICAL SYMPTOMATOLOGY For a short time almost all persons sustaining a head injury sufficient to cause an impairment of consciousness experience such symptoms as head- ache, dizziness, amnesia, mental confusion, nervousness, etc. These have been recognized as temporary sequelae, but their persistence is considered, in general, as abnormal. The duration of these immediate posttraumatic symptoms varies in different individuals and according to severity of the wounding. Cedr- mark (27) stated that 25 percent of patients suffering various civilian head wounds considered themselves well in 10 days, and 50 percent were free of symptoms in 3.5 weeks and 75 percent in 10 weeks. Those patients having no skull fractures had a median at 3 weeks and those having fractures had 36

a median at 9 weeks, but, strangely, almost 50 percent of the latter had some complaints as long as 3 to 10 years. Russell (107), in a series of 200 cases, noted that symptoms lasted less than 2 months in 80 cases (40 percent) and more than 18 months in 79 cases (40 percent), but 61 percent of working men and women returned to their usual tasks within 2 months after injury. Denny-Brown (36) states that 55 percent of a series of 200 cases of head injury had symptoms in convalescence, of which only 8 percent were due to demonstrable organic disease. The remainder seemed to be related to psychologic features, especially anxiety concerning occupation, compensa- tion, family, or, more generally, the future. Akerlund (3), in a series of civilian head injuries, found that 37 percent were back at work in 2 weeks, 69 percent in 4 weeks, and 89 percent in 8 weeks. Certain sequelae of a head injury have been recognized to fall into a fairly consistent clinical picture, which has been termed the posttraumatic syndrome or concussion state. Typically this includes headaches, dizziness, tinnitus, lack of ability to concentrate, nervousness, anxiety, and, less com- monly, other mental symptoms. For the purpose of this discussion, any patient complaining of any three symptoms (usually including headache and dizziness) has been considered as having the posttraumatic syndrome; a person with less than three such complaints has had his symptoms coded individually. Accordingly, patients considered to have the posttraumatic syndrome often have many more than three of the above complaints. This arbitrary definition of the syndrome vitiates analysis of the individual complaints.2 Examination of the present series of head-injured patients for these general symptoms at the times of discharge and of follow-up (table 41) reveals an interesting contrast. At the time of discharge, averaging approximately 9 months after in- jury, 42 percent of the patients did not complain of any neurological symp- toms. But at the time of examination 6 to 7 years after injury, only 9 percent were free of such complaints. Did 33 percent of the men conceal such symptoms or did they develop the symptoms later? Since the major- Table 41.—Comparison of General Symptomatology at Discharge From Service and at Follow-up At discharge from service At discharge from service Complaint At follow-up Complaint At follow-up None 309 63 18 22 Posttraumatic syn- drome Impaired memory 26 20 11 127 419 4 Headache 241 183 Other 48 5 Irritability or nerv- 6 70 Unknown 5 Dizziness 94 49 Total 739 739 Easy fatiguability .... 4 28 1 Drs. Friedman and Mikropolous have made a separate study of posttraumatic headache at the New York center, and the data are presented in appendix 1.

s =« e o « a 1 .a. I I G I S I e 5 • J3 B O .*.*.* 00 a 8 CN O O Cv sO >-"i-" K Number .-o o oooc* Percent 8 t-' sd soOs CO | CM ^ in in m a a «O CMOONCO i 7 c Os 00 ^" 00 &. ft V g Os MSS* OH CM Number CM 00 VH Percent O 8 or^^^ c*•) en en ^— . i * °"s= a O mr~ ooo B o CO VD -rf O E o i n C N *-i S £ H o> en ON en <^- J8 P 'O ^-i oo r^- a 1 | o a ci * 1 ^ i? i ^i§ It 1 0 IJjl 38

ity were released by CDD (Certificate of Discharge for Disability) and expected disability compensation, it would seem improbable that such symp- toms, which might increase their awards, would not be mentioned. The hospital clinical records were scrutinized with care, so that it can be assumed that few men with symptoms were missed. In other series of head-injured in World War II (82, 136), the percentage of such patients having head- ache or the posttraumatic syndrome at or near the time of discharge is 22 to 54 percent, which would suggest that the figure given here is correct. If this is accepted, then, the stresses of civilian life would seem to have been sufficient to produce further symptoms. This delay in the onset of post- traumatic symptoms has been noted by many writers. Roussy and Lhermitte (104) called this interval the phase of incubation or contempla- tion. Adler (1) believes this interval varies in length according to the severity of the physical injury, being delayed until the patients recover physically and are faced again with their obligations. This type of reac- tion, originating in a conflict between a sense of duty and self-respect and the patient's idea of self-preservation, is designated a conflict neurosis by Symonds (123). Denny-Brown (35) believes that this accounts for the surgical opinion that severely injured patients often fail to develop this syn- drome since the surgeon discharges the patient before the symptoms arise. Ruesch and Bowman (106) believe that patients with brain damage tend to improve, whereas those with an unstable pretraumatic personality, even if not so injured, worsen. Bay (12) also emphasized the necessity of assessing the premorbid mental structure in patients with posttraumatic complaints. On analysis of the 309 men who were asymptomatic at discharge, it is found that only 40 are so at follow-up, 136 have the posttraumatic syn- drome, 80 suffer headaches, and lesser numbers suffer other posttraumatic symptoms. On the other hand, only 24 (6 percent) of those men having any symptoms at discharge were without complaints 7 to 8 years later. In the group of 127 men having posttraumatic syndrome at discharge, only 9 were entirely free of symptoms at follow-up, and in the group of 241 men suffering headache at discharge, only 6 were free of neurological com- plaints at the time of follow-up examination. This, then, suggests that only about 6 percent of men having neurological complaints 9 months after a head injury will become completely free of them in time. On the contrary, there is an excellent chance that posttraumatic symptoms may be reprecipi- tated after a free interval of some months. It is interesting to speculate as to the cause of this recrudescence of symptoms. Were these more neurotic individuals who could not stand the stresses or were they more severely wounded persons? If the table showing symptomatology at time of follow-up is analyzed in terms of the factors at the time of wounding, it becomes evident that a higher percentage of patients with mild head injuries than with severe brain damage are without symptoms (table 42). There is little difference in the frequency of posttraumatic syndrone as between men in R-I groups 3 and 4, but the mildly wounded patients in group 1 have less posttraumatic syndrome than the more severely wounded men in groups 3 and 4. The men in R-I group 2 were, it will be remembered, selected from a roster of 680803—62 1

Table 43.—Correlation of Neurological Symptomatology at Follow-up With Various Characteristics of the Wound and Early Complications Neurological symptomatology at follow-up Characteristics of wound and early complications Total Posttrau- Head- ache Other symp- toms Number of men Percent None matic syndrome Percentage distribution All men 739 100.0 8.5 56.7 24.8 10.0 Brain laceration: None 238 497 4 100.0 100.0 100.0 10.9 55.5 57.0 100.0 25.6 24.5 8.0 11.1 Present 7.4 Location of wound: Frontal 251 100. 1 100.0 100.0 100.0 7.6 9.4 9.6 4.0 57.4 56.5 53.5 61.4 24.7 22.0 26.7 24.4 10.4 12.1 10.2 10.2 Parietal 372 187 176 Temporal Occipital Immediate neurological deficit: None 417 100.0 8.6 54.7 29.7 7.0 Hemiplegia, hemi- anopsia, aphasia 233 89 100.0 100.0 6.4 13.5 60.5 56.2 17.6 15.5 10.1 Other and unknown .... Complications: None 20.2 Infection or fungus ccrebri 552 100.0 9.1 55.4 27.2 8.3 76 65 46 100.0 99.9 99.9 7.9 1.5 13.0 61.8 14.5 24.6 13.0 15.8 13.8 15.2 Hematoma 60.0 58.7 Other Foreign bodies: None 297 195 100.0 100.0 9. 1 9.2 56.9 51.8 26.3 26.7 7.7 12.3 Bone only Metal, with or with- out bone 210 100.0 100.0 7.1 18.1 59.5 64.9 22.4 16.2 11.0 10.8 Unknown 37 Healing: Primary. ... 485 103 151 99.9 100.0 100.0 8.0 9.7 9.2 54.2 56.3 64.9 27.4 19.4 19.9 10.3 14.6 6.0 Secondary Period of uncon- sciousness: None 146 100.0 100.1 100.0 100.0 100.0 11.0 8.5 11.5 5.4 7.6 41.1 41.1 6.8 7.9 5.8 8.1 13.9 0-2 hours 165 52 57.6 75.0 68.9 57.6 26.1 7.7 17.6 20.9 2-24 hours 1-7 days 74 302 Other and unknown . . . men receiving compensation from the Veterans Administration for resi- duals of a head wound, so it is not surprising that few of them are without symptoms. The apparent decrease in proportions of headaches in category 4 is due to the increase in the frequency of concomitant symptoms. Few, however, of the specific factors of wounding—the type, location, depths, or 40

size of the wound—seem to influence significantly the frequency of the posttraumatic syndrome, headache, etc., seen at follow-up (table 43). Even the immediate neurological deficit does not seem to be related to symptomatology or the posttraumatic syndrome at follow-up. One factor with some relation to symptomatic status at follow-up is the presence of initial complications; only 1 of 65 men with an initial hematoma was asymptomatic at follow-up. Finally, the initial period of unconsciousness appears to be associated with symptomatic status at follow-up; in general, longer periods of unconsciousness seem prognostic of multiple complaints at follow-up. However, men not rendered unconscious by the head wound were no more frequently asymptomatic than men having a period of trau- matic unconsciousness. On the other hand, posttraumatic symptoms correlate well with person- ality and intelligence. In table 44, it is apparent that the patients with the posttraumatic syndrome have high hysteria, depression and hypochondriasis scores, and relatively high psychasthenia and schizophrenia scores in the Minnesota Multiphasic Personality Test. Although the group with one or two posttraumatic symptoms have somewhat higher scores than the asymp- tomatic group, statistical significance is attained only in the hysteria score. This is of clinical importance as it suggests that the population having post- traumatic symptoms have, on the whole, a different personality type from the general population. That this is a psychoneurotic type cannot be said since the number of cases bearing that diagnosis, except in the Boston group, is very small. That the basic types are different is further borne out upon an analysis of the IQ's of the various groups (table 45). It is apparent that the group with posttraumatic symptoms has a high percentage of men with low intelligence and a low percentage of men with high intelligence. This is further demonstrated by the observation that the percentage of mentally deteriorated men is significantly higher in the group with posttraumatic syndrome than in the asymptomatic group (table 46). An analysis of the work and social adjustment (tables 47 and 48, respec- tively) brings out the fact that patients with the posttraumatic syndrome are likely to have difficulties in both of these spheres. Which is cause and which is effect cannot be stated; even that there is any causal relationship is not certain since both phenomena may be under the influence of another factor. It is of interest that in the group having the posttraumatic syn- drome only 8.8 percent attended school after discharge, whereas 16.5 percent of the mono- or disymptomatic group and 25.4 percent of the asymptomatic group did so. The home adjustment of the group with posttraumatic syndrome was much better than their social or work rehabilitation; in fact, in this regard there is little difference in the three groups, which may simply be a reflection of the fact that the patients were receiving disability compensation sufficient to enable them to live at a satisfactory level with their woes. In this series the family adjustment seemed to be about the same in the men having a posttraumatic syndrome and those not so afflicted; the only possible exception might be the divorce or separation rate of 11.4 percent (8 of 70) in the "nervous" men, as opposed to a 5.3 percent incidence in men not so classified. 41

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Table 45.—Correlation of Wechsler-Bellevue Intelligence Scale With Neurological Symptomatology at Follow-up Symptom Number tested Percentage of cases with IQ, <89 90-119 >120 Total No symptoms 57 237 389 1.8 8.9 i17. 0 63.2 35.1 25.3 »11.6 100.0 100.0 100.0 One or 2 symptoms 65.8 71.5 PosttrauniHtic syndrome Total 683 12.9 68.8 18.3 100.0 i Statistically significant. The percentage for the subgroup with symptoms differs from that in the symptom-free group with P <\05. Table 46.—Correlation of Mental Deterioration, Determined by Wechs- ler-Bellevue Intelligence Scale, With Neurological Symptomatology at Follow-up Abnormally deteriorated for age Number tested Symptom Number Percent 57 237 389 4 40 102 7.0 16.9 '26.2 One or 2 symp Posttraumatic s ,oms yndrome Total... 683 146 21.4 1 Statistically significant. The percentage for the subgroup with symptoms differs from that in the symptom-free group with P <.05. Table 47.—Correlation of General Work Progress With Neurological Symptomatology at Follow-up Number tested Work progress Symptom Regressed Un- changed Pro- gressed Unclassi- fied Total Percentage distribution No symptoms One or 2 symp- toms 63 257 419 7.9 15.2 25.3 22.2 20.2 29.4 68.3 63.0 44.1 1.6 1.6 1.2 100.0 100.0 100.0 Posttraumatic Total 739 20.3 25.6 52.8 1.4 100.0 43

Table 48.—Correlation of Social Adjustment Wiih Neurological Symptomatology at Follow-up Symptom Number Social adjustment Good Percentage distribution Poor Other and unknown Total 63 257 419 90.5 86.4 70.2 7.9 1.6 2.7 2.1 100.0 100.0 100.0 10.9 27.7 Total 739 77.5 20.2 2.3 100.0 The posttraumatic state was recognized as a frequent sequel to head injuries almost a century ago. Many years ago Friedmann (49) and others described as a syndrome a constellation of symptoms consisting of headache, dizziness, mental disturbances as noted above, and an intolerance to alcohol This train of disorders was attributed to actual physical damage to the brain or disordered intracranial vasomotor control Since that time much has been written on the subject without solving the basic problem. Two schools of thought have developed—the one con- sidering the syndrome essentially organic and the other believing it to be a neurosis. Arguing for the first view in the early part of this century was Aschaffenburg (7), more recently Penfield (94), who emphasized the role of dural adhesions, McConnell (84, 85, 86), who found excess subdural fluid in the intracranial cavity, and Watts et al. (137), who considered the contusion of the scalp to be related to the syndrome. On the other side, Charcot (28) assumed the symptoms to be purely functional. This view- point is still prevalent but placed in a somewhat different setting. It is agreed generally that a patient who develops a neurosis after a head injury (and it may be of any type—hysterical, anxiety, terror, neurasthenia, or hypochondriacal) had the basic neurotic personality before the head injury. As Minkowski (90) stated, the "pretraumatic factors" are tripped by the head injury into the neurotic state. Courville (30) maintains that this is typically quite distinct from the posttraumatic syndrome, being characterized by mental alertness, emotional depression, exaggeration of preexisting personality defects, elaboration of symptoms both in statement and be- havior, the presence of hysterical components, and the multiplicity, change- ability, and indefiniteness of the symptoms. The two conditions— posttraumatic syndrome and posttraumatic neurosis, Strauss and Savitsky (120) emphasize, may not be independent clinical entities. Schilder (114) 44

believes that the organic concussion syndrome may facilitate attitudes of a neurotic character and precipitate a type of neurosis different from the usual traumatic neurosis following injuries of other parts of the body. That this neurosis builds upon the warp and woof of the acute concussion syndrome is understandable. The findings in this series of head-injured patients would seem to indicate that the two conditions are very closely associated and that stresses and strains which might produce a pure neurosis in a noninjured person induce a recrudescence of posttraumatic symptoms in the head-injured. Often the recurrent headache resembles the vascular type of cephalalgia which is associated with tension states. In fact, Friedman et al. (47) found that the responses to drugs in posttraumatic and psychogenic headaches were very similar and believed that the pathogenesis was closely related. The mental symptoms—nervousness, anxiety, mental confusion, lack of concentration, impaired mentation, etc.—are almost as common and some- times more disabling than the nervous symptoms of headache, dizziness, etc. Adler (1) emphasizes that the posttraumatic mental symptoms are present in approximately 31.5 percent of cases after civilian injuries. The most common type is the posttraumatic anxiety state which was present in her series in 48 of 200 patients and frequently accompanied headache and dizziness, nightmares, or other physical sequelae of the injury. It has been suggested that cranioplasty might prevent the syndrome of the trephine, which is practically identical to the posttraumatic syndrome. Gardner (51), in particular, emphasized the movements of the brain with each arterial or venous pulsation. Grantham and Landis (58) noted that 54 of 100 patients with calvarial defects complained of headache, but that cranioplasty relieved only 16 of these and precipitated headaches in 4 other patients. Eleven of 24 men having vertigo were relieved after cranioplasty. Grant and Norcross (57) also suggest that cranioplasty relieves the headache and dizziness in the syndrome of the trephined. They report complete relief of headache in 5 of 20 cases. The incidence of the posttraumatic syndrome in this series was not influenced by the presence or absence of a skull plate. Because most of these posttraumatic complaints are subjective, little can be noted on clinical examination. However, a few of the alterations were Table 49.—Examiner's Evaluation of Mental Status at Follow-up Mental status Number of men Mental status Number of men Normal 609 3 10 22 12 5 Impaired judgment or men- tation Uncooperative Irritability 77 22 19 Others Total 739 45

subject to verification. Irritability was noted by the examiner in some of the 70 patients who complained. Other aspects of the mental status are subject to clinical and psychological testing, and these results will be con- sidered at this point. D. MENTAL STATUS A rather large number of mental aberrations were noted, although the majority of the patients had no complaints referable to their mental status. In table 49 the detailed breakdown of the findings referable to the mental state is given. Only the category of impaired judgment or mentation is sufficiently large to warrant correlations; this abnormality seems to be related to the severity of injury (table 50) and the various factors influencing it, but not to the location of the wound (table 51). That deficiency in mentation is related both to a low intelligence (table 52) and mental deterioration (table 53) is understandable. However, al- terations in personality fail to correlate with impaired mentation, as indi- cated in table 54. Moreover, patients in whom examiners noted other alterations, particularly depression, euphoria, and irritability, had elevated scores for all elements of the personality scale, most of them, indeed, sig- nificantly elevated. Mentation was examined by two series of tests: One, the ability to re- peat forward and backward certain numbers and to give the names of four presidents of the United States of America, and the other, the ability to carry out the serial subtraction test. The first test, mainly dependent upon memory, is roughly correlated with the severity of injury (table 55) in that patients with very minor injuries had few errors, whereas more than 25 percent of the more severely injured men made three or more errors. Whether or not brain laceration had occurred does not seem to be a promi- nent factor in this test (table 56), nor is the location of the lesion significant (table 57). Similarly, the various individual factors influencing the sever- ity of wounding, namely, the diameter, depth of debridement, and compli- cations, do not correlate with the ability to carry out these memory tests. Patients without a neurological deficit made fewer errors than individuals having a gross disability (table 58). Most patients were able to carry out the serial 7 test with no more than two errors (table 59). The severity of wounding does not seem to be a strong determinant of impairment in this test, but the proportion of men in group 4 who made three or more errors was significantly higher at the 5-percent level than the corresponding proportion in group 3. It would seem that the memory and serial 7 tests are dependent upon more general factors than localized damage of the brain, and hence reflect only weakly the varying grades of brain wounding. The findings in these tests do cor- relate strongly with the intelligence and deterioration scores (table 60). In fact, the serial 7 and memory tests might be considered the clinician's in- telligence test. 46

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Table 51.—Relationship of Mental Status to Location of Wounding Location of wounding Mental status Frontal Parietal Temporal Occipital Num- ber Per- cent Num- ber Per- cent Num- ber Per- cent Num- ber Per- cent Total 251 100.1 372 100.0 ' 187 100.1 176 100.0 Normal 204 81.3 10.8 296 48 28 79.6 12.9 7.5 157 17 13 84.0 9.1 7.0 146 22 8 83.0 12.5 4.5 Impaired judgment or mentation 27 20 Other abnormalities of mental status 8.0 Table 52.—Relationship of Mental Status to Wechsler-Bellevue Intelligence Scale Mental itatus Number Total Perc< MUage wit tilQ tested <89 90-119 >120 Total 683 100.0 12.9 68.8 18.3 Normal 562 100.0 10.1 68.7 21.2 Impaired judgment or mentation . . Other abnormalities in mental status . 71 100.0 100.0 25.4 73.2 64.0 1.4 10.0 50 26.0 Table 53.—Relationship of Mental Status to Mental Deterioration as Determined by Wechsler-Bellevue Abnormally deterio- rated for age Mental status Number tested Number Percent Total 683 145 21.2 Normal 562 71 50 90 38 17 16.0 i53.5 '34.0 Impaired judgment or mentation Other and unknown . . i Statistically significant. Percentage differs from that for men of normal mental status, P <. 01.

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Table 56.—Correlation of Memory With Cerebral Wounding 0—2 errors 575 150 77.8 20.3 187 50 78.6 21.0 385 99 77.5 19.9 3 1 75.0 25.0 I> 3 errors .... Test not done or unsatis- 14 1.9 1 .4 13 2.6 Table 57. — Correlation of Memory With Location of Wounding Location of wounding Memory Frontal Parietal Temporal Occipital Num- ber Per- cent Num- ber Per- cent Num- ber Per- cent Num- ber Per- cent Total 251 100.0 372 100.1 187 100.0 176 100.0 0—2 errors . 192 51 76.5 20.3 287 75 77.2 20.2 148 31 79.1 16.6 133 38 75.6 21.6 Test not done or unsatis- 8 3.2 10 2.7 8 4.3 5 2.8 Toble 58. — Correlation of Memory With Neurological Deficit Immediate neurological deficit Memory Total None Hemiparesis Other and unknown Num- ber Per- cent Num- ber Per- cent Num- ber Per- cent Num- ber Per- cent Total 739 100.0 417 100.0 148 100.0 174 99.9 >3 errors. . 575 150 77.8 20.3 344 72 82.5 17.3 102 39 68.9 26.4 129 39 74.1 22.4 51

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t APHASIA That disturbances of speech result from cerebral injuries has long been known and is usually attributed to damage to the dominant hemisphere. Yet in young individuals the ability of the cerebrum to compensate for im- pairment in speech functions seems remarkable, for a relatively small num- ber of patients sustaining head injuries, even of the dominant hemispheres, complained of aphasic troubles, and even fewer had overt manifestations. Of 636 patients who did not complain of aphasic disturbances, only 6 were found to have clinical evidence of speech impairment, and of the 103 who complained of trouble, approximately one-third had no clinical evidence of aphasia. Thirty-seven patients complained of difficulties in all aspects of speech (global aphasia) and 26 of a specific anomia. The changes in aphasia with the passage of time are also of interest. There were 99 patients noted to be aphasic at the time of debridement; of these, 57 had apparent speech disturbances at the time of discharge approx- imately 9 months after injury. Seven to 8 years later only 34 of them were noted to have clinical manifestations of aphasia. On the other hand, of the 42 men with initial aphasia, which was not observed at the time of discharge, 11 were said by the examiner to have aphasia at follow-up. It seems reasonable to believe that these men who were aphasic at the time of injury and also at follow-up were probably so affected at the time of dis- charge, even though the records do not note it. On this assumption, the following is found: Aphasic at injury, 99 (100 percent) Still aphasic at 9 months, 68 (68.7 percent) Still aphasic at follow-up, 45 (45.5 percent) On the other hand, there are some patients whose aphasic symptoms develop or become aggravated after debridement, perhaps as the result of the operative procedures, or vascular or infective complications. This ap- parently happened to 25 patients in this series; that is, there were 25 who were not noted to be aphasic at the time of injury, but who were found to be so at follow-up. In 11 of the 25, speech difficulties were already noted at discharge, while for 14 men, evidence of speech difficulty was at no time noted in the Army clinical records. The evidence, then, is of marked improvement and even recovery in more than half of patients who were aphasic immediately after a head wound. Nearly a third recovered during the first 6 to 8 months, and nearly a quarter more improved during the subsequent 7 to 8 years. The side of the lesion was predominantly left in aphasic right-handed patients, although some of these men had their major wound on the right side (table 61). However, the 7 left-handed persons suffering head wounds who had aphasia also had left-sided lesions. This would seem to emphasize the fact that left-handedness is not necessarily associated with dominance of the right hemisphere, a fact which has been noted previously (43). It further lends support to the concept that unilateral (usually left) representa- 54

tion of speech is the most prevalent form of cerebral organization in sinis- trals. In general, wounds of the left hemisphere were more disabling than comparable wounds of the right side of the brain; of 286 patients with right hemispheral wounds, 61 percent had no immediate neurological deficit, whereas of 312 patients with left hemispheral wounds, only 48 percent were without deficit. Table 61.—Correlation of Handedness, Side of Wounding, and Aphasia Handedness Side of injury Num- ber Percent aphasic Right . Right . . . 286 5. 9 Right Left 312 21.2 Left. Right . , 20 0 Left Left 27 25.9 Right 11 27.3 Ambidextrous and unknown Left 7 14.3 Bilateral 76 5.3 Total 739 13.3 It is obvious that the severity of injury (and all factors relating to it) was strongly correlated with the presence or absence of an aphasia (table 62). However, the location of the wound did not seem to be a very important determinant of aphasic difficulties (table 63). Global aphasia was much more common in patients with foreign bodies within the brain than was a nominal type of aphasia (table 64). That the speech mechanisms are of great importance in mental functions, even in formal intelligence testing, is apparent from the scores on the Wechsler-Bellevue tests. Those patients having aphasia tended to be in the lower range of intelligence, and fewer of them had superior IQ's as com- pared to nonaphasic patients. Moreover, almost half (46 percent) of the 87 aphasic patients had abnormal deterioration as compared to 17.6 percent of the 592 patients with normal speech. As a further corollary of the above generalization is the fact that speech is essential to most occupations, and its impairment is a serious handicap to business success. In fact, as mentioned before, a speech defect may be a greater handicap than a hemiplegia or monoplegia. This hindrance became apparent in the analysis of the occu- pational status. The aphasic men had difficulty in their work so that almost half (42 percent) regressed and only 29 percent advanced, while the corresponding percentages for the nonaphasic were 17 percent and 57 percent. Similarly, aphasia seemed to have considerable influence on the social adjustment, some 46 percent of aphasics not having a satisfactory adjustment compared to 19 percent of the normally speaking men. How- ever, economic and home adjustments were not significantly influenced by speech impairment 680802—62 8 55

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F. APRAXIA There were 27 patients with apraxic difficulties, whereas 708 patients seemed to have no such disturbances. Those patients having apraxic diffi- culties were all in the more severe group of cerebrally wounded, that is, in groups 3 and 4 (table 65), and the majority had a marked hemiparesis. The disturbances occurred in 24 right-handed men, with involvement in 10 instances of the right and 12 instances of the left hemisphere. G. OLFACTORY DISTURBANCES Olfactory disturbances were uncommon in this series, less than 6 percent of patients having any complaints referable to smell (table 66). Although wounds of the frontal region were more frequently associated with olfactory disturbances than injuries of other regions, the later also were accompanied by impairment of smell (table 67), perhaps as the result of contrecoup laceration of the orbitofrontal region. As might be expected, other factors of wounding did not seem to be related to olfactory alterations except that unilateral or bilateral anosmia was associated with severe injuries. These findings are similar to Leigh's (77) observations in a series of 1,000 head- injured patients. He found impairment of smell in 72 cases and stated that recovery occurred in only 6 cases. No observations were available on re- covery in this series. Parosmia was noted in 12 of Leigh's cases and in 11 percent of patients in this series. This symptom may develop some time after injury. H. VISUAL DISTURBANCES Visual disturbances are rather common in head-injured patients. As seen in table 68, a field defect occurred in almost 10 percent of cases. The presence or absence of a visual disturbance correlated well with the severity of the injury, the mildly injured patients being unlikely to have symptoms referable to the visual system (table 69). Although diplopia and blurred vision did not seem to be related to wounding of any particular part of the brain, blindness, as would be expected, was much more commonly found with wounds of the frontal region since these implicated the optic nerve and tract; hemianoptic defects were found in patients having injuries of the posterior parietal, temporal, and particularly the occipital region (table 70). Nearly 24 percent of the cases of occipital wounds had lasting field defects. The course of patients having visual disturbances is of interest. Of the 55 patients observed to be hemianoptic at the time of debridement, only 36 were noted in the records to have visual field disturbances at discharge, while at the time of examination 38 had contralateral, 1 an ipsilateral, and 1 a bilateral hemianopsia. It would, therefore, seem that regression of a hemianoptic defect may occur in approximately 30 percent of cases. Eighteen men were recorded at discharge as having field disturbances which were not noted at debridement, so that a total of 54 men had field defects when separated from service, and 5, or 9.3 percent, of these had no visual signs at follow-up, evidnce that late recovery may sometimes occur. 59

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Table 66.—Olfactory Symptoms at Follow-up Symptom Number of men Symptom Number of men None 684 Unknown 6 11 Anosmia 25 Total 739 Other 13 Table 67.—Correlation of Olfactory Disturbances With Location of Wounding Location" of wounding Symptom Frontal Parietal Temporal Occipital Num- ber Per- cent Num- ber Per- cent Num- ber Per- cent Num- ber Per- cent Total 251 100.0 372 100.0 187 100.0 176 100.0 None 223 6 88.8 2.4 6.8 2.0 344 7 7 14 92.5 1.9 1.9 3.8 176 1 5 5 94.1 0.5 2.7 2.7 164 2 93.2 1.1 1.7 17 5 3 7 4.0 Table 68.—Visual Disturbances Subjective complaint Number of men Objective findings Number of men 578 Normal 645 18 Blind1 7 Blurred vision — bilateral 38 Vision impaired 23 27 Homonymous hemianopsia, 6 contralateral 63 Field defect 55 Homonymous hemianopsia, Other 17 3 5 Other 5 Unknown 3 Total number of cases. . . 739 Total number of cases. . . 739 i Includes patients who had one eye enucleated. ' Excludes patients who had an eye enucleated. •1

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Table 7O.—Correlation of Visual Disturbances With Location of Wounding Location of wounding Disturbance Frontal Parietal Temporal Occipital Num- ber Per- cent Num- ber Per- cent Num- ber Per- cent Num- ber Per- cent Total 251 100.0 372 100.0 187 100.0 176 100.0 No symptoms 197 6 13 22 7 6 78.5 2.4 5.2 8.8 2.8 2.4 289 12 18 9 33 11 77.7 3.2 4.8 2.4 8.9 3.0 146 5 8 10 12 6 78.1 2.7 4.3 5.3 6.4 3.2 116 2 9 2 42 5 65.9 1.1 5.1 1.1 23.9 2.8 T)ip\opia Blindness Field defect Injury to the peripheral visual structures, the optic nerve or bulb, is not uncommon in head injuries. Turner (127) found 25 cases of optic nerve injury in 1,550 head injuries, and Russell (108) found 8 such cases in 600 patients. Brandle (21) gives an incidence of 0.7 percent in head injuries. In this series some 25 patients had an eye enucleated because of injury to the orbit, 7 patients were blind in 1 eye, and 23 patients had some visual impairment. On ophthalmoloscopic examination 19 of these patients with impaired eyesight had optic atrophy in one or both eyes. Over a period of time considerable improvement may occur in the vision of patients with traumatic damage to the optic nerve. Turner (127) states that if recovery is going to occur, light perception begins to return about the fourth day and the recoverable vision has returned by the end of a month. Bryson (25) noted that the prognosis is poor if light perception has not returned in 2 months, if the pupil is inactive, and if there is early disc pallor. Askenasy et al. (9) conclude that an immediate amaurosis will not be bene- fited by surgery. Hooper (68) points out that some cases of traumatic blindness are caused by a contusion with small petechial hemorrhages in the optic nerve and that recovery may occur, although, in general, the prog- nosis is poor. Landolt (75) found fractures in the sphenoidal ridge in 75 percent of his series of traumatic optic nerve lesions. Blurred vision does not seem to correlate with specific factors of wounding nor with objective evidence of impaired vision since 29 of 39 patients so complaining had normal vision. However, it may be a manifestation of the posttraumatic syndrome, for every one of the 39 men complaining of blurred vision had posttraumatic symptoms, and 29 had the full-blown syndrome. I. ACOUSTIC DISTURBANCES Complaints referable to hearing were quite common (table 71), although objective auditory defects were less frequent. Tinnitus was the most com- mon complaint, and impaired hearing was almost as frequent. These com- 63

plaints, however, were not correlated with the severity of injury or any of its component factors (table 72). The fact that wounds in the mastoid area were more frequently associated with auditory disturbances (table 73) than were wounds of other regions would fit in with the recognized oc- currence of eighth nerve lesions as the result of basal temporal fractures. The chances of recovery from tinnitus are not very good. Of the 24 men who were reported to have had noises in one or both ears at the time of separation from service, only 5 had no auditory symptoms at follow-up. Of the 715 men without tinnitus at discharge, 62.5 percent were without auditory symptoms at follow-up; 126 (19.0 percent) complained of tinnitus. If one accepts Mygind's (91) figures as applying generally, approximately 50 percent of head-injured men, if examined within the first week of injury, would have otoscopic changes such as tears in the drum, and hemorrhages behind the tympanic membrane. Hence, many of these changes must resolve, leaving the patient asymptomatic. Table 71.—Auditory Disturbances Disturbances of hearing Subjective complaints Objective findings None 456 587 Tinnitus: Contralateral to side wounded 36 Ipsilateral to side wounded 80 Bilateral 81 Impaired hearing: Contralateral to side wounded 32 27 Ipsilateral to side wounded 71 89 Bilateral 26 19 Deafness: Contralateral to side wounded 5 5 Ipsilateral to side wounded 20 9 Bilateral 1 1 Other and unknown 5 4 Total number of cases 739 739 Table 72.—Correlation of Auditory Findings With Severity of Wounding R-I group Finding 1 2 3 4 Num- ber Per- cent Num- ber Per- cent Num- ber Per- cent Num- ber Per- cent Total . . 99 100.0 182 100.0 362 100.0 96 100.0 None 83 15 1 0 83.8 15.2 1.0 .0 147 30 5 0 80.8 16.5 2.7 .0 282 69 77.9 19.1 1.9 1.1 74 19 2 1 77.1 19.8 2.1 1.0 Deafness 7 4 Other and unknown 64

Table 73.—Correlation of Auditory Findings With Location of Wounding Finding Frontal Parietal Location Temporal Occipital Num- ber Per- cent Num- ber Per- cent Num- ber Per- cent Num- ber Per- cent Total 246 100.0 372 100.0 163 100.0 176 100.0 None 209 32 2 3 85.0 13.0 .8 1.2 294 70 79.0 18.8 1.1 1.1 116 38 6 3 71.2 23.3 3.7 1.8 131 38 4 3 74.4 21.6 2.3 1.7 Inipairpd hearing ........ Deafness 4 4 Other and unknown The tinnitus may be associated with normal hearing. Only 41.7 percent of the patients with aural noises complained of some degree of impairment of hearing, as compared to 20.3 percent of the group without tinnitus, and 58.3 percent were found to have some auditory disability, as compared to 19.4 percent of the group with no aural symptoms. Late symptoms referable to the vestibular portion of the acoustic nerve were rare, for, as Linthicum and Rand (80) state, they tend to disappear early. Although dizziness is a common complaint, rarely is it due to vesti- bular involvement. If true vertigo is present, as Baumoel and Marks (11) note, abnormalities in the caloric responses may persist for some weeks after the whirling sensation has disappeared. Grove (59) emphasizes asymmetri- cal vestibular sensitivity as a source of symptoms. Positional vertigo, Gor- don (56) states, following a head injury usually clears in a few months. However, dizziness, as a more general complaint, is prone to persist in- definitely after a head injury. In this series approximately two-thirds of the cases had some such symptoms over 7 to 8 years. Rawling (100) re- ported 77 percent of his cases complained of this disturbance, Gliddon (54) that 58 percent of head-injured men had dizziness, some as long as 19 years after their injury, and, in Germany, Brun (24) noted that 47.9 percent of men with open head injuries suffered dizziness for 9 years or more. J. OTHER CRANIAL NERVES Nerves to the extraocular muscles were rarely involved; in 18 cases only was there such impairment—14 times in the ipsilateral and 4 times in the globe contralateral to the injury (table 74). There were eight examples of sixth cranial nerve weakness, six being on the side of wounding. Ani- socoria was also relatively uncommon, being found in 39 cases, of which the contralateral pupil was the larger in 21 instances. In spite of an anisocoria, the light response was normal in both eyes in 12 of the cases. When the reflex was impaired it usually occurred in the ipsilateral eye. Although facial sensation and movement were examined and coded with the cranial nerves, their impairment in this series was usually supranuclear and hence, strictly speaking, not the result of involvement of a cranial nerve. 65

Impairment of facial sensation to pinprick and touch was noted in 80 cases, usually associated with a hemihypesthesia; in 13 of these cases there was an impairment of sensation ipsilateral to the side of injury not associated with an apparent peripheral nerve injury. In some additional 27 cases ipsi- lateral sensory impairment seemed to be due to an injury of the peripheral branches of the trigeminal nerve. Facial movement was impaired on the side opposite cerebral wounding in 75 cases and on the same side in 27 cases, but 16 of the latter seemed to be due to extracranial peripheral injuries of the facial nerve. In two cases there was bilateral facial paresis. The 9th and 10th cranial nerves were involved in only two cases in this series, causing impairment of deglutition. Table 74.—Impairment of Other Cranial Nerves Nerve and type of impairment Number of men Nerve and type of impairment Number of men Ocular motor nerves: Impairment extraocular movement: 14 Contralateral to wound .... Fifth cranial nerve: Trigeminal hypesthesia (central) : 7 Contralateral to wound .... 4 Ipsilateral to wound 13 Anisocoria: Ipsilateral larger 18 Contralateral to wound .... Seventh cranial nerve: 67 Gontralateral larger 21 Facial paresis (central) : Impairment light reflex: 11 Ipsilateral to wound 20 Contralateral to wound . . . 75 K. DISTURBANCES OF THE MOTOR SYSTEM It is of interest that most patients who complained of weakness had ob- jective paresis upon examination. At follow-up, 513 patients had no symp- toms of motor impairment. Of these, 485 had normal power and another 9 patients had weakness due to a peripheral wound so that only 19 (3.7 per- cent) had paresis attributable to the head wound. Complaints of mono- paresis were less likely to be associated with a demonstrable weakness than symptoms of hemiparesis. Of the 76 patients complaining of isolated paresis of face, arm, or leg, 33 (43.4 percent) had no impairment of strength on examination; of the 70 who complained of unilateral arm and leg weakness, 13 (18.6 percent) had no paresis; and of the 32 complaining of hemiparesis, only 1 had no demonstrable impairment. Motor disturbances usually were referred to as weakness of the ex- tremities opposite the wound, as may be seen in table 75. However, some patients complained of weakness on the ipsilateral side and a few had weakness of both legs. The degree of weakness, both subjectively and ob- jectively, was correlated with the severity of injury and with all factors which modify that aspect of wounding (table 76). Reflecting this is the fact that paresis occurred in approximately 25 percent of patients having primary healing and in over 50 percent of patients with secondary healing. Weakness was more common in parietal lobe wounds, although present in wounds of all parts of the brain (table 77). Perhaps as a corollary of this, 66 .-*»

Table 75.—Impairment of Motor Power Weakness Subjective complaints Objective findings None 513 546 Arm: Contralateral to side wounded 37 34 Ipsilateral to side wounded 6 7 Leg: Contralateral to side wounded 18 22 Ipsilateral to side wounded 3 2 Arm and leg: Oontralateral to sid^ wounded 66 55 Ipsilateral to side wounded 4 9 Entire side: Contralateral to side wounded 32 20 Ipsilateral to side wounded 3 1 Weakness not cine to head injury 34 32 23 11 Total 739 739 Table 76.—Correlation of Motor Disturbances With Severity of Wounding R-I group Motor disturbance 1 2 3 4 Num- ber Per- cent Num- ber Per- cent Num- ber Per- cent Num- ber Per- cent Total 99 100.0 182 100.0 362 100.0 96 100.0 Subjective: 92 3 92 2 92.9 3.0 92.9 2.0 158 86.8 5.5 89.6 3.3 237 89 258 78 65.5 24.6 26 65 33 55 27.1 67.7 34.4 57.3 Contralateral weakness 10 163 6 Objective: Normal 71.3 21.5 Contralateral impairment of motor power was generally associated with some loss of superficial sensibility (table 78). At debridement 148 patients were noted to have weakness; at the time of follow-up only 27 of these (18 percent) did not complain of weakness, and another 14 were found to have no paresis on examination. It may, therefore, be concluded that in penetrating wounds of the head, a hemi- paresis noted just after wounding has about a 25-percent chance of clearing up almost completely. However, motor impairment at the time of wound- ing was either overlooked at that examination or developed later, for 160 patients were noted to have some paresis at the follow-up examination. 67

Table 77.—Correlation of Motor Disturbances With Location of Wounding Location of wounding Motor disturbance Frontal Parietal Temporal Occipital Num- ber Per- cent Num- ber Per- cent Num- ber Per- cent Num- ber Per- cent Total 246 100.0 372 100.0 163 100.0 176 100.0 Subjective: No symptoms 176 51 185 43 71.5 20.7 75.2 17.5 207 135 226 120 55.6 36.3 60.8 32.3 102 40 120 31 62.6 24.5 73.6 19.0 133 29 134 27 75.6 16.5 76.1 15.3 Contralateral weak- ness Objective: Normal Contralateral weak- ness Table 78.—Correlation of Motor Findings With Impairment of Superficial Sensation Finding Total Superficial sensation Impaired Other Normal Paralyzed 34 124 2 578 1 32 83 2 38 2 Impaired 1 40 Other Normal 2 538 Unknown 1 Total 739 155 4 580 Of the 148 men stated to have paresis at debridement, 96 were noted in the discharge records to have some weakness at that time. At follow-up 84 percent of these were found to have motor impairment. Of the 52 who were considered normal at discharge, 21 had paresis at the time of the follow-up examination. Fourteen men had weakness at discharge and at follow-up, but were not so noted at the time of debridement, while 47 other men had weakness at follow-up which was not noted in any of the Army records. It was hoped that an analysis with reference to the status at follow-up, of the 148 patients noted to have a hemiparesis at the time of wounding, would give some indication of factors favorable and unfavorable in prognosis. For the purpose of this study, a residual weakness at follow-up of at least 20 units difference in dynamometer readings of the 2 grips, or a difference of 10 units in favor of the nondominant hand, was arbitrarily taken to be the 68

criterion for residual weakness. Patients were considered to have no residual weakness if the difference of dynamometer readings of the 2 grips was less than 10 units. This residual nonparalyzed group consisted of only 24 men, or 16 percent of the men with an initial hemiparesis. This figure is a little lower than might be expected from the 25-percent recovery rate estimated above. Russell (110), however, noted recovery of motor function in more than half of the initially paralyzed cases. There is no apparent or statistically significant difference in the residual paralyzed and nonparalyzed groups relative to the factors of wounding— site of wounding, size of cranial defect, and depth of wound—or to the fac- tors associated with the initial debridement—time of debridement and skill of surgeon. It is of interest, although not significant statistically, that the group with no residual weakness had a higher percentage (83.3 percent) of men without complications of debridement than the hemiparetic group (67.4 percent of 86 patients). The factors associated with cranioplasty are the same in the two groups. There is no difference in the pneumoencephalographic abnormalities of the two series. In the early electroencephalographic studies there are both more focal (62.2 percent) and generalized (42.2 percent) abnormalities in the paralyzed group than in the nonparalyzed group (27.2 and 18.1 percent). However, in the follow-up electroencephalograms this difference is not so apparent, the proportions that were normal being 41.9 percent and 47.8 percent, respectively. The two groups seem to have the same type and frequency of posttraumatic symptoms. Aphasia is more common in the group with residual weakness (34 percent) than in the second group (17 percent), although the latter contains a higher percentage of left-sided wounds (83.3 percent vs. 52.6 percent). Epilepsy seems to be more fre- quent in the paralyzed than in the nonparalyzed group (53.7 percent vs. 33.3 percent). The two classes do not seem to be distinguishable on the basis of intelligence or personality. This suggests that the factors favoring recovery were either not those examined or that the influence of several factors together was important. Certainly there is no evidence that factors in treatment within the range of the present study modify the course appreciably. Disturbances of the motor system may be manifested by weakness, spasticity, atrophy, or changes in reflex activity. Because in wounds of the brain the involvement of the motor system is of the upper motor neuron type, spastic paresis with increased deep reflexes and pathological superficial reflex responses is usually found. However, the degree of involvement of each of these does not run absolutely parallel so that, although paresis may be used as a prototype for correlations with other phenomena, it is worthwhile con- sidering some of the other characteristics of upper motor lesions in relation- ship to the degree of paresis. The tone of the paretic muscles varied from hypotonic to hypertonic. About half of the patients with objective weakness had normal tone, but of the more severely paralyzed men, 28 of 34 had hypertonia (table 79). Augmentation of the appropriate tendon reflexes, usually considered a manifestation of increased tone, was present in 67 of the 70 hypertonic patients and in a number of patients in whom increased tone could not be 69

demonstrated clinically. It was, however, not present in all patients having paresis. In fact, decreased reflexes were noted in paretic extremities having normal (five cases) or decreased tone (three cases). Alterations in tone were frequently accompanied by abnormalities of deep sensation: 54 of 70 men with hypertonic paresis had hypesthesia, as did 8 of 13 men with hypo- tonic limbs. Table 79.—Correlation of Motor Power With Tone Finding Tone, side contralateral to wound Hypotonia Hypertonia Rigidity Normal Other and unknown Total 3 9 28 39 1 2 2 3 1 34 124 578 2 1 Normal 1 73 574 2 Other Unknown 1 Total 13 70 5 648 3 739 Tone, side ipsilateral to wound 1 33 112 34 124 578 2 1 7 5 1 575 2 Other 2 1 Total 10 6 720 3 739 Muscular atrophy was less commonly found than hypertonicity or hyper- reflexia, being noted in only 62, or approximately one-fourth of the paretic patients (table 80). It was present, however, in 32 of the 34 patients with severe weakness. Usually there was an associated alteration in tone: Of some 70 patients with hypertonic and paretic limbs, 46 had atrophy, and of 13 patients with hypotonic weakness, 8 had atrophy. Although somewhat more commonly seen in parietal lobe lesions, it did occur with lesions of other regions (table 81). Atrophy was generally associated with superficial sensory impairment (56 of 63 men), although the reverse was not true. (Only 56 of 154 men with superficial sensory disturbances had atrophy.) L. SOMATOSENSORY DISTURBANCES Paresthesias, such as numbness or feeling of the member being dead, are the sensory symptoms mentioned by about 15 percent of the patients in this series. These disturbances, as may be seen in table 82, are usually on the side contralateral to the wound, but may involve one member or one side of the face. The distal type of sensory impairment (ulnar or radial dis-

Table 80.—Correlation of Motor Power With Atrophy Finding Atrophy None Present Other Unknown Total Paralyzed 2 32 34 Impaired 94 28 2 124 Normal . 576 2 578 Other 2 2 1 1 Total 672 62 2 3 739 Table 81.—Relationship of Atrophy to Site of Wounding Location of wounding Atrophy Frontal Parietal Temporal Occipital Num- ber Per- cent Num- ber Per- cent Num- ber Per- cent Num- ber Per- cent Total 251 100.0 372 100.0 187 100.0 176 100.0 Contralateral extremities . . 21 8.4 54 14.5 14 7.5 8 4.5 Table 82.—Somatosensory Disturbances Impaired Impaired Impaired stereog- nosis Location Pares- thesias superficial sensation deep sensation None 584 561 618 634 Face: Contralateral ... 8 Ipsilateral 4 Arm: Contralateral 34 28 23 56 Leg: Contralateral 4 4 1 3 18 13 18 5 Ipsilateral 2 3 2 0 Arm and leg: Contralateral. . . 33 77 64 27 Ipsilateral 5 10 5 3 Entire side: 27 3 Other 16 5 4 2 Unknown 4 4 5 7 739 739 739 739 630802—62 6

tribution), although present in some patients shortly after wounding, was not noted in this series at the follow-up; stocking or glove paresthesias did occur. The presence of such paresthesias correlated positively with the severity of wounding, being present in practically 50 percent of the patients with a severe head wound (table 83). All factors relating to severity of wounding, such as brain laceration, diameter of wound, depth of wounding, complications, debridement, period of unconsciousness, neurological deficit, residual foreign body, and type of healing, influence the incidence of pares- thesias. Wounds of the parietal area are more likely to give rise to sensory disturbances than those of other regions of the head (table 84). Table 83.—Correlation of Sensory Disturbances With Severity of Wounding R-I, jroup Disturbance 1 i " \ I i i Num- ber Per- cent Num- ber Per- cent Num- ber Per- cent Num- ber Per- cent Total 99 100.0 182 100 0 362 100.0 96 100 0 Contralateral: Paresthesia 1 1.0 13 7. 1 62 17. 1 44 45 8 3 3.0 10 5.5 54 14.9 51 53. 1 Table 84.—Correlation of Sensory Disturbances With Location of Wounding Location of wounding Disturbance Frontal Parietal Temporal Occipital Num- ber Per- cent Num- ber Per- cent Num- ber Per- cent Num- ber Per- cent Total 251 100.0 372 100.0 187 100.0 176 100.0 Contralateral: 35 41 13.9 16.3 96 99 25.8 26.6 37 33 19.8 17.6 25 25 14.2 14.2 Hypesthesia Paresthesias may or may not be associated with demonstrable sensory alterations. In none of the patients having facial paresthesias alone could sensory changes be demonstrated in the face. Paresthesias of the arm or leg alone were associated with sensory disturbances in approximately 50 percent of cases, but if both were involved the incidence rose to 75 percent. Of the 72

30 patients having paresthesias of the face, arm, and leg, 28 had impairment of sensation. The association of paresthesias and motor disturbances was of the same order as for paresthesias and sensory alterations. About half of the patients with paresthesias did not complain of weakness. Dysesdiesias of the face or of both arms or both legs were rarely associated with paresis (2 of 13 cases in each category). Paresthesias of the arm or leg were accompanied by weakness in 75 percent of cases. Of the 27 patients having paresthesias of the entire side, 26 had some weakness. The presence of paresthesias was not significantly associated with ab- normal findings in the personality inventory. It is apparent that disturb- ances of deep sensibility and astereognosis closely parallel those of the superficial sensibilities. Of 154 men with superficial sensory disturbances, 101 had impaired deep sensibility, and only 11 with normal superficial sensation had impairment of deep sensibility. Of the 154 men with super- ficial sensory disturbances, 84 had astereognosis. Of the 113 men with impaired deep sensibility, 82 had astereognosis as contrasted with only 12 of 621 men with normal deep sensation. Astereognosis was also closely associated with motor impairment. Of 123 patients with some degree of weakness, 52 had astereognosis, as did 28 of 32 paralyzed patients. It was also closely correlated with disturbances of tone, being present in 50 of 70 hypertonic patients and in 7 of 13 hypotonic patients. M. URINARY DISTURBANCES Urinary disturbances were encountered in only 21 cases. In the early stages of a cerebral injury, bladder disturbances are common, but they usually disappear in a few weeks. They may consist of an urgency or inability to urinate. Goldstein (55) and others have discussed the cortical centers mediating bladder function. The lateral cortical representation in the arm and leg area does not seem to be so important in producing urinary dis- turbances as the paracentral region which, if injured bilaterally, gives rise to a paralytic bladder with overflow incontinence. N. SEXUAL DISTURBANCES Relatively few patients complained of sexual disturbances. Impotence occurred in 60 cases and some increase in sexual desire was reported by 4 men. Various other complaints referable to sexual appetite were men- tioned in 14 instances. The great majority of patients, some 641, main- tained that there was no change in their sexual appetite. There seemed to be a definite relationship betwen the severity of the injury and the presence of decreased potency (table 85). However, although a slightly greater percentage of patients having frontal lobe involvement suffered from sexual complaints than those having injuries of other regions, the difference was not statistically significant. It is noteworthy that the presence of sexual disturbances correlates well in the personality inventory only with psychasthenia. Sexual disturbances have been noted in previous reports of cerebral injuries, but few detailed reports are available. Usbeck (128) mentions such difficulties in his series. Meyer (87) discusses the problem, indicating that decreased erection, weak 73

bo •S e I 9s .M "C 3 •B Q e 5 a W) CO SI o ^ 0 O so O-* d . * . • • D 2 r^ »-H f-> z V "# eu NO ^-.Tf ^0 u OX r- i-I ^-c 1 3 a o i d o oo K m b S T!-.* Csl CM ^- tN eg a d i 1 7 c os ON O U"l ^ 6 ON A ON 00 »-H eN b 00 O O »-iTH NO Csl J3 *— 1 ^— i B s a o O O O O I r^ «sj ',.; ON ^H it Os OS ° *" V £ Q 3 C o t^ T-H in so I ON sd 00 '.*' -— , £ 00 • 0 H 4J m .* so en S r- so § 3 in 1 * cd f-j '•rt S ° • S oi C '« C 1 No symptom Impotence a Increased de Other and u 74

orgasm, or premature ejaculation are the most common causes of poor sexual relationships. He reports that 81 of 100 head-injured patients ex- perienced these difficulties. Perhaps the explanation of the relatively few cases from military wounds lies in the fact that these disturbances are much more frequent in older people. Meyer believes that they are more common following wounds of the orbitofrontal or hypothalmic regions than other parts of the brain. 0. DISCUSSION Although wounds of the head and brain are generally considered as local or focal cerebral lesions, it is emphasized in this analysis that such violence has a much wider distribution than merely to the area below the site of cranial impact. The relative frequency of effects on a part of the brain remote from the violence, and the failure to demonstrate the correlation of site of wounding with cerebral functions which appear to be represented in small cortical foci, indicate a widespread effect of the head trauma. This generalized effect of the craniocerebral injury is as important in the sequelae as the local damage. In fact, certain disabling symptoms seem to be more dependent upon the general than the local injuries. Thus the posttraumatic syndrome, the mental disturbances, certain cranial nerve impairments, and sexual alterations, correlate with general rather than local factors. On the other hand, the disturbances of sensation and motor power are related more specifically to regional damage, and to a lesser extent with general factors of cerebral impairment. The degree of recuperation of a patient from a head wound, while de- pendent upon the severity of wounding, the location of the injury, and factors in repair, is also bound up with the preinjury mental and personality status of the patient. It is of great interest that individuals of low intelli- gence and neurotic adjustment do not recover from a brain injury as rapidly or as completely as more intelligent and better adjusted individuals. Although intelligence and mature personality may not necessarily be related, in general they seem to be associated and are strong factors in combating the stresses involved in cerebral injuries. As a rule, men with higher intelligence and nonneurotic personalities were able to effect satisfactory occupational, economic, and social adjustments, even with a severe neuro- logical deficit, while patients of subnormal intelligence and neurotic makeup were unable to adjust well in any sphere, even in the absence of an overt neurological deficit. ft is of interest that none of the head-injured men in this study have developed extrapyramidal diseases, brain tumors, multiple sclerosis, etc., which have occasionally been attributed to trauma. As Leonhardt (78) has emphasized, if rigid criteria must be met before suggesting a traumatic etiology for such conditions, the number of cases which might be so con- sidered dwindles. 73

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 Follow-Up Study of Head Wounds in World War II, by a. Earl Walker and Seymour Jablon
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