Physiogenesis and Psychogenesis in The 'Post-Concussional Syndrome'
Physiogenesis and Psychogenesis in The 'Post-Concussional Syndrome'
Physiogenesis and Psychogenesis in The 'Post-Concussional Syndrome'
Review Article
460
POST-CONCUSSIONALSYNDROME 461
Pie-traumatic factors and financial stability, his occupational satisfactions
and dissatisfactions, may powerfully determine his
First, there are aspects already present before response to injury and to recovery therefrom.
the injury occurred (Table I). Age alone will be Moreover, we may see the ‘¿scapegoat motive' in
important, in more than one respect. The ageing action, whereby the injury serves as a pivotal
brain is less resilient to organic insult, and the experience on which to pin the blame for pre-existing
ageing person less adaptable to its effects. Among worries and unhappiness. This shifting of the blame
adults, rising age has proved to be associated with may be seen to operate both in the patient's mind
diminished chance of returning to work (Heiskanen and sometimes in that of his attendants. Yet the pre
& Sipponen, 1970), increased memory difficulty existing problems may quite often be more intrusive
(Russell, 1932), an increased incidence of anxiety and and directly relevant to his disability than any aspect
fears (Adler, 1945), and increased mortality (Kerr of the injury itself.
et a!, 1971). Studies of children have shown a It is also important to recognise that disturbing
different spectrum of disabilities compared with life events may be operating surreptitiously in an
those occurring in adults, certainly with the classical entirely similar manner. Seizer et a! (1968) were able
‘¿post-concussional
symptoms' figuring less frequently to show an excess of personal crises and conflicts in
(Black et a!, 1969). the lives of drivers causing fatal accidents during the
Pre-existing problems such as arteriosclerosis or months before these occurred. No less than 20% had
alcoholism will add further to the ageing factor. had an acutely disturbing experience during the
Remarkably little research attention appears to have preceding 6 hours. Whitlock et a! (1977) similarly
been given to the influence of alcoholism despite found a significant excess of such items as moving
its high prevalence in head-injured populations. house, marital separations, serious discord, or
Thus Waller (1968), investigating road deaths in changes of work in the recent lives of victims of
California, found that 58% of drivers, 47% of accidental injury. Thus, far from occurring in an
passengers, and 36% of pedestrians had alcohol in emotional vacuum, accidents are prone to occur just
the blood, most with levels exceeding the legal when the person already has to cope with other
maximum for drivers. The effects of a chronic high sources of conflict and upheaval.
alcohol intake in delaying reparative processes within
the central nervous system are now appreciated, from
laboratory experimental studies (West et al, 1982). Pen-traumatic factors
With regard to mental constitution, we must All of the above occurs as the prelude. The accident
consider genetic propensity to neuroses, depression, then imparts both physical and psychological damage
and even the major psychoses. Such liability may be (Table I). The brain damage itself is partly transient,
obvious when there is already a history of psychiatric partly permanent, in part demonstrable and in part
illness. Both the physical and the psychological forever elusive. It is now essential, for example, to
traumas of the injury may thus be operating on a think in terms not only of structural disruption,
particularly vulnerable person. The personality, or but of changes in circulation, changes in brain
in Symonds' (1937) phrase the “¿kindof head that metabolism, and perhaps far-reaching changes in
is injured―, can be crucially important to the neurotransmitter function. The old ‘¿molecular
processes of rehabilitation. disturbance of neuronal function', postulated by
early writers (Oppenheim, 1889), has a fresh scientific
This was strikinglyillustratedin the caseof a youth respectability. For example, considering stroke, it may
who sustained minor but definite frontal-lobe be noted that Robinson et a!(1984) now suspect wide
damage. He had had a stormy adolescencewith spread noradrenergic brain dysfunction as playing
problemsof addictionand irresponsibletrends. The an important role in the genesis of post-stroke
injury occurred when he was emerging from such
difficultiesand showingclear evidenceof maturing depression.
towards a stable lifestyle. Following the injury he With new techniques, moreover, there is more
became grossly psychopathic. Here one could argue awareness of subclinical structural damage imme
that more than most he had stood in need of intact diately after injury. Jenkins et a! (1986), for example,
frontal lobe functions. His premorbid constitution scanned 50 patients with magnetic resonance imaging
had had a powerfulinfluencein shapinghisresponse (MRI) during the first few days, showing twice
to the injury. the yield of lesions that could be detected with
computerised axial tomography (CT). Cortical
Pre-existing psychosocial difficulties are notoriously contusions could sometimes be identified when there
prone to be overlooked. The patient's domestic had been no loss of consciousness. Deep white-matter
462 LISHMAN
lesions (seen in 15 patients with MRI, compared with possible to show that disability tends to differ from
only 1 on CT) were sometimes present when one broad category of accident to another —¿whether
concussion had last for only 5 mm. on the roads, at work, or in the home (Brain, 1942;
The more readily definable contribution of coarse Adler, 1945; Miller, 1966).
brain lesions has been extensively researched. Both Next, there is the iatrogenic factor. In the early
the severity of such damage and its principal post-injury phase, the patient is vulnerable and often
locations within the brain are known to affect both highly suggestible to the treatment he or she receives
cognitive and broader behavioural sequelae, as and how much is explained to him or her.
reviewed, for example, by Lishman (1973) and in
detail by Newcombe (1983). Other physical damage, A policewoman of 22 sustained a minor blow on the
particularly to the vestibular apparatus, can dictate head when travelling on duty in a car. Continuing
important symptoms without being immediately headache led to skull X-ray which showed some
obvious. increased convolutional markings. A CT scan
was therefore undertaken in case a pre-existing
Considering pen-traumatic factors of a psycho hydrocephalus had been exacerbated. This was
logical nature, the purely emotional shock can be normal but the foramen magnumseemedenlarged.
immense, some accidents occurring in terrifying A myelogramwas therefore in turn carried out to
circumstances that remain alive in the patient's exclude any possibility of abnormality at the cranio
memory. The ordeal of coming close to death, the cervical junction and was also normal. Throughout
destruction of the ‘¿myth
of personal invulnerability', the sixweeksof investigationher headachessteadily
can itself dictate prolonged invalidity. This has been worsened—¿and were still troublesome some three
well documented in studies of persons surviving years later. Her attention had indeed been firmly
focused on her early symptoms.
floods, fires, and other disasters that have not injured
the head at all.
Post-traumatic factors
A 50-year-oldman remained severelydisabled for When the acute phase of the injury is over, the
six years following an accident in which his lorry patient has to adjust to what has occurrred (Table
had jack-knifed on the motorway, causing a pile I). Intellectual impairments may be marked in degree
up of casualties. His degree of depression and
withdrawal was such that he was considered by some or of a very subtle nature, sometimes so subtle
observersto be demented.He had regressedto total that they are easily overlooked. The “¿changed
dependenceon his wifewho had to washand shave organism―,in Goldstein's (1942, 1952) terms, may
him. Yet close enquiries about the nature of the find it difficult to cope. Much will depend on how
accident showed that he had not been rendered far the disability is overt and what allowances
unconscious, and that the likelihood of any head accordingly are made. Physical disability will have
trauma had been very slight indeed. He had an impact of its own, with deformities or scars
respondedcatastrophicallyto the circumstancesof possibly having a disproportionate influence on the
the ordeal (Lishman, 1973). patient's mental state. Epilepsy can represent a
serious added burden.
Added to this, head injury may have a special The emotional repercussions may be closely tied
meaning to the patient —¿ he may fear the conse to the above or follow more directly. Depression is
quences of ‘¿concussion',and worry about the an ever-present risk. Guilt may be highlighted,
long-term import of early symptoms. The post or important losses sustained. Sometimes the reper
traumatic amnesic gap sometimes serves a para cussions will build as chains of causal sequences over
doxical protective function in saving the patient from a considerable period of time:
awareness of the more disturbing details of his
injury. A man of 30, for example, was injured by a falling
Not surprisingly, the circumstances of the accident ladder, which struck him behind the ear. A period
can also be important. The setting may have been of intense vertigo and vomiting was followed by
peculiarly conducive to fear, anger, or resentment. postural instability. He becamephobic of walking
The circumstances may have special significance, as far or of travelling, lost his job, and took to working
when a reckless driver has injured his family or a in a public house nearby. He was depressed and
began drinking heavily.
workman has been forced against his will to use Examination 18 months later still showed evidence
faulty equipment. Exploring the details surrounding of labyrinthine damage and his phobias were easily
the accident can be rewarding in revealing such demonstrable.Bythen, however,he had falleninto
circumstances (Pilowsky, 1985). And even ignoring debt, and had quarrelledwith his wifewho had left
highly individual determinants of this nature, it is him (Lishman, 1978).
POST-CONCUSSIONAL SYNDROME 463
75 50 (a)
n 50 25
0'
Co
C
u
a, a,
°- 25 0,
@0
26 14 30 90
C
a,
0
a, (b)
0. 50
2614 30 90
essentially indistinguishable from those who had This survey of several research approaches
made complete recoveries. Psychosocial aspects has thus revealed a number of contradictions.
were the factors that seemed influential in dis Associations which emerge in one study may fail to
tinguishing between the post-concussional and appear in another. There is sometimes evidence of
recovered patients —¿
marital status, social class, type organic influences, sometimes mainly of psychosocial
of accident (industrial, etc.), and any previous history variables. When both are looked for together,
of psychiatric illness. However, an organic contri both are sometimes observed. Altogether, we can
bution could still be pinpointed —¿ visual symptoms summarise the types of evidence brought forward as
(diplopia and blurring) and anosmia, persisting after follows, dealing first with the organic then the non
the acute stage had passed, were commoner in the organic contributions. It is assumed that grossly
post-concussional than in the recovered group. obvious organic causes such as subdural haematoma
or hydrocephalus have already been excluded by
5. Lishman (1968) suitable screening procedures.
The penetrating head injuries from World War II
that were analysed illustrate yet another approach. Organic evidence
These were evaluated retrospectively and in a much
Evidence was provided first of all for the ‘¿clustered
less discriminating manner. No attempt was made
symptom complex' itself. The very pervasiveness of
to evaluate psychosocial factors, but symptoms were headache, dizziness, and fatigue from the early stages
viewed in relation to several indices of brain damage.
(Table II) suggests an organic process at work. Some
Of 670 soldiers with penetrating injuries, 144 showed
50% of patients can be expected to experience such
marked psychiatric disability 1—5 years later. In 71
symptoms, and, in the great majority, they can be
of these, there were persisting complaints of
expected to die away with time. There is evidence,
headache, dizziness, fatigue, or sensitivity to noise.
moreover, that several of these complaints may be
This ‘¿somatic
complaints' group could be compared
commoner after head injury than injury to other
with the remainder. On several indices of brain
body parts. McMillan & Glucksman (1987) found
damage (depth of penetration of injury, amount of
that headache, dizziness, fatigue, irritability, and
brain tissue destroyed, length of post-traumatic
sensitivity to noise and light were all significantly
amnesia), such patients consistently emerged as commoner after minor head injury than after
having the milder injuries. They had shown less
orthopaedic injuries, mostly to the upper limbs.
intellectual impairment. And such symptoms
Certain relationships between early evidence of
clustered repeatedly with other symptoms that
brain damage, particularly to brain stem and
appeared to owe little if anything to any organic
basal brain regions, and the development of post
aetiology (e.g. difficulty with concentration,
concussional symptoms were observed. Lidvall et al
depression, and anxiety).
(1974) found that otological dysfunction predicted
the later development of dizziness; Rutherford et al
6. Dencker (1958, 1960)
(1977) showed an association between frequency of
This remarkable study adopted a strict case control symptoms and early headache, diplopia, or anosmia.
approach. Dencker collected 36 monozygotic twin Some, although certainly not all, investigations have
pairs and 81 dyzygotic pairs in which only one of found a positive association with indices of severity
the twins had had a head injury. They were all of injury, such as duration of post-traumatic amnesia,
examined 3—25years later (mean 10 years) and or evidence of intellectual impairment (e.g. Keshavan
symptom profiles compared. The head-injured twins et a!, 1981). In these last respects, different studies
were inferior on a variety of tests of intellectual have, however, given remarkably different results.
function, usually with rather subtle defects, as might Other investigations have sought directly for
have been expected. But no differences were found evidence of cerebral dysfunction among post
between members of individual monozygotic pairs concussional patients, using a number of experimental
in classical post-concussional symptoms. The mono techniques. Taylor & Bell (1966) observed slowing of
zygotic pairs proved to be more concordant than the cerebral circulation time in patients with post-con
dyzygotic for an impressive range of symptoms, cussional symptoms, most being studied at 4-8 weeks
including headache, dizziness, sensitivity to noise after injury. Brain-stem auditory-evoked responses
and light, even subjective memory impairment. have been found to be delayed, even in patients with
These, then, seemed to owe more to constitutional very mild injuries who are free from other neuro
factors, by way of genetic make-up, than to any logical abnormalities (Rowe & Carlson, 1980;
brain damage that had occurred. Noseworthy et a!, 1981; Montgomery et a!, 1984).
POST-CONCUSSIONAL SYNDROME 467
Waddell & Gronwall (1984) were able to demon such as stresses antedating and surrounding the
strate lowered thresholds for tolerance to light, injury are related to the chance of developing
and possibly to sound also, using objective tests symptoms, as is the anxiety engendered by the
administered 1—3weeks after injury. accident and attaching to early complaints. Such
Slowed information processing has been shown matters are difficult to measure with precision, but
repeatedly. Gronwall & Wrightson (1974) used a nonetheless the associations have emerged fairly
serial addition test, revealing impairments at 1—2 clearly. ‘¿Neuroticism'in the personality, a history
months that progressively resolved thereafter. of psychiatric illness, and demographic variables such
McMillan & Glucksman (1987) confirmed such a as sex and marital status have been shown to be
finding at 1 week, even though tests of inteffigence influential. Even from shortly after the injury,
and memory were unimpaired. MacFlynn eta! (1984) Rutherford eta! (1977) found that a feeling of blame
found similar delays on a four-choice reaction-time towards an employer was related to the frequency
test at 24 hours and 6 weeks after injury. Ewing eta! of symptoms.
(1980), in an interesting study, exposed patients to Other investigations reinforce these findings.
hypoxia a year or more after minor injuries, and Studies from the second World War, for instance,
found that after such a period they still performed underlined the similarities between head-injured and
less well than control subjects on memory and non-head-injured soldiers seen in army neurosis units
vigilance tasks. (Lewis, 1942; Guttmann, 1946). They seemed
Such observations confirm the presence of some equivalent to a remarkable degree in terms of
subtle alteration of cerebral function shortly after family and personal histories of neurotic disability,
injury, which is occasionally still detectable well personality type, and even range of symptoms. Lewis
afterwards. They have, however, tended to rely on (1942) concluded that the “¿long-lastingrelatively
normal uninjured control subjects for assessment, intractable post-concussional syndrome is apt to
rather than directly comparing patients with and occur in much the same person as develops a
without post-concussional symptoms following head psychiatric syndrome anyway―. Dencker's (1958,
injury. We are left, in consequence, uncertain about 1960) study of twins, as previously indicated, gives
the relationship between such demonstrated abnorm strong support for such a view.
alities and the genesis of the post-concussional Guttmann (1946) considered that environmental,
symptoms. The most we can find are impressionistic social, and psychological factors were usually
statements; Taylor & Bell (1966) reported that operative when post-concussional complaints were
symptoms of headache, dizziness, and poor effort long maintained. Among 300 patients, he observed
tolerance could often be seen to subside in parallel that headache persisting at 6 months had usually been
with return of the circulation times to normal, and precipitated by psychological causes. Ruesch &
Gronwall & Wrightson (1974) observed that the Bowman (1945) made several observations on a large
slowing of mental function tended to be more severe group of civilian head-injured patients; those with
and long drawn out in the presence of complaints post-concussional symptoms who lacked obvious
of headache, fatigue, and difficulty with con signs of brain damage resembled non-head-injured
centration. MacFlynn et a!, (1984), however, were neurotic patients very closely; the longer the
unable to detect any relationship between their symptoms persisted, the more multiple and diffuse
reaction-time measures and the presence or number they became; and whereas in the acute stages
of post-concussional complaints. complaints were more frequent when there was
It remains possible, therefore, that some at collateral evidence of brain damage, in those with
least of these experimental observations of post long-lasting symptoms this situation was reversed —¿
concussional symptoms are revealing concomitants the complaints were more prominent when brain
rather than aetiologically relevant aspects of cerebral damage appeared to be lacking.
dysfunction. It should also be noted that the vast
majority of these investigations have been carried out Synthesis
during the early post-injury phase, most within
several weeks of the occurrence of the injury. In the foregoing survey, both physiogenic and
psychogenic causes have emerged for the ‘¿post
concussional syndrome'. The evidence for each set
Non-organic evidence
of factors appears to be compelling, and we are led
There is as much evidence for non-organic influ to think in terms of a complex interaction. Must it
ences as for cerebral dysfunction in the syndrome. then be concluded that the search for greater clarity
The studies already reviewed showed that factors is a hopeless task? One possibility would be that both
468 LISHMAN
sets of factors inevitably operate together and those collateral damage to impose the invalid role. As the
aspects demonstrated are those that are measured weeks go by, however, the symptoms are destined
most carefully. Another could be that the genesis of to recede, by a natural process of healing towards
the syndrome differs from one individual to another, the status quo. If he is able to feel untroubled by
some patients responding to cerebral dysfunction and them, and if left undistrubed by his environment,
others to psychological influences. recuperation will in favourable cases be complete.
In appraising the detailed evidence it seems There are obstacles, however, to this natural process
possible to advance a short way further than this, ofresolution, anditwould seem likelythat, in patients
while accepting that the situation is indeed very with the milder forms of injury, these obstacles are
complex. An important aspect appears to hinge on mainly of a psychological nature. They may lie, for
the time course followed by the symptoms. As noted instance, in the patient's mental constitution, his
earlier, the post-concussional syndrome is not a static tendency to worry unduly, to condition too rapidly,
matter, but one which tends to decline markedly, and or to build anxiety around his symptoms. Or they
in some respects to alter, according to the time may lie in the handling he receives in the early days
elapsed since injury. This applies both in the short and the attention that he is encouraged to focus on
term and the long-term view. The investigations them. Obstacles may emerge in the form of other
reviewed above have varied greatly along this time sources of distress —¿
domestic difficulties, financial
continuum. Thus those that have pointed to organic hardship, resentment about the origins of the
influences have in general been undertaken within accident itself. There may be the need to struggle to
a few weeks or months of injury —¿ e.g. those cope too early, or to face an uncongenial job. He
showing altered cerebral circulation, delayed evoked may become significantly depressed. Later there may
responses, impaired information processing, or be conflict over compensation. If the obstacles
relationships to early neurological impairments. By are substantial, there may be secondary neurotic
contrast, those that have highlighted non-organic developments, founded in anxiety, and sometimes
factors have mostly dealt with patients in the chronic destined to be long-lasting. The symptoms of the
later stages —¿
those drawing comparisons with non post-concussional syndrome provide, indeed, the
head-injured neurotic patients, uninjured twins, or ideal nexus for neurotic elaboration —¿
in contrast to
those showing no trace of relationship with severity physical disability, they are subjective, unverifiable,
of injury or indices of brain damage. Many of these and irrefutable, and there is no way that the sufferer
latter studies have been conducted on that very small can reassure himself that they have disappeared.
proportion of patients who still complain of Thus, the longer after the accident that post
symptoms many months or even years after the concussional symptoms persist, the more evidence
injuries have occurred. Guttmann's (1946) patients, that non-organic factors play a part is gained.
for example, had been injured 6 months earlier, Complaining patients studied shortly after the
Lishman's (1968) were followed up at 1-5 years and accident will form a different population from those
Dencker's (1958, 1960) at 3—25years. still complaining after several months or years. With
Such evidence is far from watertight, but in sum time, those with an uncomplicated and purely organic
total it emerges as reasonably impressive. When the contribution to their disability willbe lost to the sample,
numerous studies concerning the post-concussional and an increasing proportion will have secondary
syndrome are carefully considered, the time factor neurotic developments. Ultimately, indeed, in mildly
after injury appears to be markedly influential in the injured patients, the organic cerebral contribution
associations we observe. may give way almost completely, and we will be left
Thus a model may be tentatively formulated, with patients virtually all of whom are suffering from
which could be tested with a properly designed conflict, depression, and anxiety.
prospective investigation. The model proposes that In conclusion, therefore, there is certainly an inter
the cerebral dysfunction engendered by head injury play of factors in the genesis of the post-concussional
commonly yields a nuclear group of symptoms, syndrome, with an intertwining of organic and non
headache, dizziness, and fatigue being the central organic contributions. But this interplay is time
group. At the outset, these are firmly organic in dependent. Over many weeks and months there is a
origin. In many respects, the less severe the injury, shifting balance, as the patient's innate proclivities, and
the more troublesome they may be to the patient —¿ his individual problems and conflicts, affect the initial
he will be aware of them more acutely when symptoms of cerebral dysfunction. This model needs
consciousness is regained rapidly, and will be careful testing and exploration in properly designed
attempting to cope while they are still severe. Also, prospective investigations. The identification of the
more will be expected of him, as there will be less obstacles —¿ in general, and in the individual
POST-CONCUSSIONALSYNDROME 469
patient —¿
is the essential prelude to decisions about LIsH@ri, W. A. (1968) Brain damage in relation to psychiatric
where treatment can most effectively be directed. disability after head injury. British Journal ofPsychiatry, 114,
373—410.
—¿ (1973) The psychiatric sequelae of head injury: a review.
lam indebted to DrsM. D. KopelmanandT. M. McMillanforhelpful diagnosis. Journalofthelrish MedicalAssociation, 71, 306-314.
comments on the manuscript and to Mrs P. Mott for preparing it. MCMILLAN, T. M. & GLUcKSMAN,E. E. (1987) The neuro
psychology of moderate head injury. Journal of Neurology,
Neurosurgery and Psychiatry, 50, 393—397.
References MACFLYNN, 0., MONTGOMERY, E. A., FEWrON, 0. E &
Rurmaroan, W. (1984) Measurement of reaction time following
ArXER, A. (1945) Mental symptoms following head injury. minor head injury. Journal of Neurology, Neurosurgery and
Archivesof Neurologyand Psychiatry,53, 34-43. Psychiatry, 47, 1326—1331.
BLACK, P., JarFalEs, J. 3., BLUMER, D., Wai.u@a, A. & WALKER, MIu.aR, H. (1966) Mental after-effects of head injury. Proceedings
A. E. (1969) The post-traumatic syndrome in children. In The of the Royal Societyof Medicine,59, 257-261.
Late Effects of Head Injury, ch. 14(edsA. E. Walker, W. F. MoNTGoMERY, A., FENTON,0. Q. & MCCLEU.AND,R. 3. (1984)
Caveness & M. Critchley). Springfield, Illinois: Thomas. Delayed brainstem conduction time in post-concussional
BRAIN,W. R. (1942) Discussion on rehabilitation after injuries to syndrome. The Lancet, i, 1011.
the central nervous system. Proceedings of theRoyal Society of NEWCOMBE, F. (1983) The psychological consequences of closed
Medicine,35, 302—305. head injury: assessment and rehabilitation. Injury, 14,
DENCKER,S. J. (1958) A follow-up study of 128 closed head 111—136.
injuries in twins using co-twins as controls. Acta Psychiatrica NOSEWORThY, 3. H., MILLER, 3., Mu@y, T. 3. & REGAN, D
et NeurologicaScandinavica(suppl. 123), 1—125. (1981) Auditory brainstem responses in post concussion
—¿ (1960) Closed head injury in twins. Archives of General syndrome. Archives of Neurology, 3$, 275-278.
Psychiatry, 2, 569—575. OPPENHEIM,H. (1889) Die Trawnatischen Neurosen. Berlin.
EwING, R., McCARThY, D., GRONWALL, D. & WRIGHTSON, P. Pii.owsxy, I. (1985) Cryptotrauma and ‘¿accidentneurosis'. British
(1980) Persisting effects of minor head injury observable during Journal of Psychiatry, 147, 310—311.
hypoxic stress. Journal of CllnicoiNeuropsychology, 2,147-155. ROBINSON, R. 0., Kuaos, K. L., STAIta,L. B., RAO, K. & PRICE,
Gou@ni, K. (1942) After Effects of Brain Injuries in War. New T. R. (1984) Mood disorders in stroke patients. Importance of
York: Grune and Stratton. location of lesion. BraIn, 107, 81-93.
—¿ (1952) The effect of brain damage on the personality. Rowa, M. 3. & CARLsON,C. (1980) Brainstem auditory evoked
Psychiatry, 15, 245-260. potentials in postconcussion dizziness. Archives of Neurology,
GRoI@IwAu., D. & WRlowrsoN, P. (1974) Delayed recovery of 37, 679—683.
intellectual function after minor head injury. The Lancet, ii, RUESCH, J. & BOwMAN, K. M. (1945) Prolonged post-traumatic
605—609. syndromes following head injury. American Journal of
Gurmwri, E. (1946) Late effects of closed head injuries: Psychiatry, 102, 145—163.
psychiatric observations. Journal of Mental Science, 92, 1-18. RussELL,W. R. (1932) Cerebral involvement in head injury. Brain,
HEISKANEN, 0. & Sippopami, P. (1970) Prognosis of severe brain 55, 549—603.
injury. Acta Neurologica Scandinavica, 46, 343-348. RimaaaroRD, W. H., MERRETr,J. D. & MCDONALD,3. R. (1977)
Jerecmis,A., TEASDALE, 0., H@ay, M. D. M., MACPHERSON, P. Sequelae of concussion caused by minor head injuries. The
& ROwAN,3. 0. (1986) Brain lesions detected by magnetic Lancet, 1, 1—4.
resonance imaging. The Lancet Ii, 445—446. SELZER, M. L., ROGERs, 3. E. & KEari, 5. (1968) Fatal accidents:
JoNEs, R. K. (1974) Assessment of minimal head injuries: The role of psychopathology, social stress, and acute
indications for in-hospital care. Surgical Neurology, 2, 101-104. disturbances. American Journal of Psychiatry, 124,1028-1936.
KAY, D. W. K., KERR, T. A. & LASsMAN, L. P. (1971) Brain STEADMAN, J. H. & GRAHAM, 3. 0. (1970) Head injuries: an
trauma and the post.concussional syndrome. The Lancet, ii, analysis and follow-up study. Proceedings of the Royal Society
1052—1055. of Medicine,63, 23-28.
KELLY, R. & SMITh, B. N. (1981) Post-traumatic syndrome: Smiopms,C. P. (1937)Mental disorder followinghead injury.
another myth discredited. Journal of the Royal Society of Proceedings
of theRoyalSocietyof MedIcine,30, 1081-1092.
Medicine, 74, 275—277. TARSH,M. 3. & RoYsroN, C. (1985) A follow-up study of accident
KaRa, T. A., KAY, D. W. K. & L@'.snwi, L. P. (1971) neurosis. British Journal of PsychIatry, 146, 18-25.
Characteristics of patients, type of accident, and mortality in TAYLOR,A. R. & BEI.L, T. K. (1966) Slowing of cerebral circulation
a consecutive series of head injuries admitted to a neurosurgical after concussional head injury. The Lancet, ii, 178-180.
unit. British Journal of Preventive and Social Medicine, 25, WADDELL, P. A. & GRONWALL, D. M. A. (1984) Sensitivity to light
179—185. and sound following minor head injury. Acta Neurologlca
KE5IIAvAN, M. S., CHANNABASAvANNA,S. M. & REDDY, G. N. Scandinavica,69, 270—276.
(1981) Post-traumatic psychiatric disturbances: patterns and WALLER, J. A. (1968) Holiday drinking and highway fatalities.
predictors of outcome. British Journal of Psychiatry, 13$, Journal of theAmerican Medical Association, 206, 2693-2697.
157—160. W@si, 3. R., LiNE, M. D., DaMum, R. M., P@@mit,E. S.,
LEwis, A. 3. (1942) Discussion on differential diagnosis and AuU@w@, R. L., CA5SEU.,M. & BLAcK,A. C. (1982) Lesion
treatment of post.contusional states. Proceedings of the Royal induced sprouting in the rate dentate gyrus is inhibited by
Society of Medicine, 35, 607-614. repeated ethanol administration. Science, 21$, 808-810.
LIDVALI., H. F., LINDER0Th, B. & NORLIN, B. (1974) Causes of the WHITLOCK, F. A., STou., 3. R. & REKHDAHL, R. 3. (1977) Crisis,
post-concussional syndrome. Acta Neurologica Scandinavica, life events and accidents. Australian and New Zealand Journal
Suppi. 56, 1-144. of Psychiatry,11, 127—132.
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