Physiogenesis and Psychogenesis in The 'Post-Concussional Syndrome'

Download as pdf or txt
Download as pdf or txt
You are on page 1of 11

British Journal of Psychiatry (1988), 153, 460—469

Review Article

Physiogenesis and Psychogenesis in the


‘¿Post-ConcussionalSyndrome'
W. A. LISHMAN

The aetiological factors relevant to the development of post-concussional symptoms are


reviewed. From the numerous studies carried out to date, it would appear that both
physiogenic and psychogenic influences are important in their genesis. However, where
mild-to-moderate injuries are concerned, organic factors are chiefly relevant in the earlier
stages, whereas long-continued symptoms are perpetuated by secondary neurotic
developments, often of a complex nature.

Sir Aubrey Lewis (1942), referring to the post TABLE I


concussional syndrome, described it as “¿that
common, Factors relevant to psychiatric disability
dubious, psychopathic condition - the bugbear of the
1. Pre-traumatic
clear-minded doctor and lawyer―.In this forceful
Age
declaration, he encapsulated the strong divisions of Cerebral arteriosclerosis
opinion that have surrounded the nosological status, Alcoholism
and especially the genesis, of the syndrome since Mental constitution
before the turn of the century. Such uncertainties Genetic vulnerability
persist today. Previous psychiatric illness
Central to most descriptions are headache and Personality (including being prone to accidents)
dizziness, but to these may be added abnormal Pre-existing psychosocial difficulties
fatiguability, insomnia, sensitivityto noise, irritability, Domestic
and emotional instability. Anxiety and depression are Financial
Occupational
often prominent. Difficulties with concentration and Recent life events
memory may feature strongly among the complaints,
and some degree of overt intellectual impairment may 2. Pen-traumatic
on occasion be detected. With this mixture of quasi Brain damage
organic and subjective symptoms, variously reported, Transient (contusion, oedema, hypoxia, raised intra
it is scarcely surprising that the concept lacks clarity and cranial pressure, circulation)
that its aetiology has remained in doubt. Nevertheless Permanent (amount, location)
its ubiquity following even minor blows to the head, Otherphysicaldamage(skull,scalp,vestibularapparatus)
and the regularity with which it features among claims Emotional impact and meaning
for compensation, have ensured that it persists as an Fear of accident
important subject for medical interest and debate. Fear of early symptoms
Circumstances of accident
A striking feature in the literature is the disparity Setting
between those who argue for physiological or for Significance
psychological causation. Some see it as founded in Type(road trafficaccident,industrial,domestic,sport)
subtle cerebral pathology, while others adduce latrogenic (early information, management, investigations)
evidence that its roots may lie in conflict and anxiety.
Psychiatric disability following head injury is often 3. Post-traumatic
ripe for such divisions of opinion, since undoubtedly Intellectual impairment
the injury imparts at a blow both physical and Other impairments (physical disabilities, deformity, scars)
emotional trauma. Before focusing on the ‘¿post Epilepsy
concussional syndrome' (‘post-traumaticsyndrome') Emotional repercussions of accident (including depression)
directly, some of the principal aetiological forces at Ensuing psychosocial difficulties
Domestic
work when the head has been injured are reviewed. Financial
They include organic, psychological, social, even Occupational
cultural factors, all of which deserve close Compensation and litigation
consideration.

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

In examples such as this we see the gradual build-up TABLE II


of ensuing psychosocial difficulties, which make their Relative incidenceof post-traumatic complaints
own clear contributions to the patient's mental state.
Interruption of education or threats to a career can RutherfordLidvallKeshavanTotaletaletaletal(1977)(1974)(1981)Follow-up
likewise have profound consequences on the patient's
life: monthsTotal
period 6 weeks0-3
months3
A boy of 18 was injured just prior to taking up his 1458360288Percentage
patients
place at art college. He had been an excellent student
and had won the place against competition. showingHeadache
Attempts to cope, however, led to repeated failures, 25584739Dizziness
quarrels within the family, and increasing loss of 15473027Fatigue
self-esteem. He took numerous jobs of a simple 9373723Anxiety
labouring nature, usually losing them quickly 19232822Insomnia
through boredom. He developed a pattern of 15NK3721Sensitivity
abscondingfrom homeon drinkingspreesand often NK'73017noiseDifficulty
to
came into conflict with the law. Four years after the
injury he had made an excellent physical recovery 830815concen
with
but was still completelyadrift.
trationIrritability
Tarsh & Royston (1985) have documented the 9131712Subjective
powerful influences of changes within the family 816810memoryimpairmentDepression
structure in contributing to prolongation of
disability - overprotection from family members 6NKNK6Any
resulting in childlike dependence, and upheavals in
the normal family hierarchies and roles. 514665521.
of above
The patient often becomes deeply involved in
processes of litigation. Litigation is not an easy path NK= not known.
to follow; hopes are aroused, doubts engendered, and
conflicting advice is received from lawyers and doctors.
The nature of the
The whole process conspires towards a state of chronic
post-concusslonalsyndrome
conflict and often long-drawn-out frustration. The
repeated rehearsal of symptoms before a variety of Table II shows the relative incidence of complaints
audiences, some encouraging, some sceptical, does in three series of head-injured patients, all carefully
not help the patient to be clear about what he is truly studied during the early weeks or months following
experiencing. When symptoms are of a predominantly injury. Most of the injuries had been of a relatively
subjective nature it is hardly surprising that he will mild nature. Rutherford et al's (1977) patients had
often fail to keep them in perspective. There is now been admitted overnight to an observation ward, and
evidence that the so-called ‘¿compensationneurosis' the symptoms were determined from a checklist
cannot be expected to resolve, in all cases, once the administered at 6-weeks follow-up examination.
litigation is ended (Steadman & Graham, 1970; Kelly Lidvall et al's (1974) patients had been admitted to
& Smith, 1981).Many patients,
indeed,remain hospital with relatively mild injuries and co-operated
chronically disabled in the long-term. fully by the second day; symptoms described at any
The above influences generate, reinforce, or time during the next 3 months were noted. Keshavan
perpetuate, post-concussional psychiatric disability, et al's (1981) series consisted of patients admitted
including the post-concussional syndrome. Examin consecutively to an emergency service, and followed
ation of such a number of contributory factors com up at 3 months. In addition to the 10 main symptoms
prehensively is especially difficult with a syndrome listed in the table, others that are not infrequently
containing several well-recognised components, all mentioned include sensitivity to light as well as to
of which may not necessarily share the same sound, decreased alcohol tolerance, and impairment
determining forces. The syndrome, moreover, is not of sexual interest and performance.
a static entity, but prone to change with time —¿
over A close concordance for most symptoms is
the days, weeks, even very many months succeeding observed among these three series —¿ headache
the injury. Different factors may come into operation heading the list, then dizziness, fatigue, anxiety, etc.
in relation to different components during rehabili To a striking extent, these symptoms are subjective,
tation and recovery. and not directly accessible to observers. A high
464 LISHMAN

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

Number of days after the trauma


25

Fio. I Percentage of patients reporting one or more post


concussional symptoms on various occasions during the observation
period (reprinted with permission from Lidvall et a!, 1974).
26 14 30 90
proportion of patients are affected during this early Number of days after the trauma
period, barely half, even of those with quite mild
injuries, having no symptoms.
Lidvall et al's (1974) study has particular impor Fio. 2 Differing time courses of headache and anxiety, as
reported on various occasions during the observation period. (a)
tance to consideration of the symptoms' time course. headache; (b) anxiety (reprinted with permission from Lidvall eta!,
All patients suffering concussive head injury from 1974).
the Stockholm area were included, provided they
were able and willing to co-operate with question
naires by the second day after injury. These were exclusive cluster was formed from headache,
then followed up prospectively with careful docu dizziness, fatigue, and difficulty in concentration.
mentation of symptoms at regular intervals until At 2 weeks, this cluster persisted, but a second had
3 months had elapsed. Eighty-three patients were appeared, consisting of difficulty with concentration
studied in this fashion (Fig. 1). There was a marked and anxiety. At 1 month, anxiety became coupled
and continuing decline in the percentage of patients with headache and fatigue. At 3 months, the
displaying one or more post-concussional symptoms, prominent cluster consisted of anxiety and headache.
from 73°loat 2 days to 24% at 3 months, the fall It seems, therefore, that, at first, the syndrome is
being particularly marked during the first post-injury dominated by headache and dizziness, but that over
week. Thus, there is a fundamental problem in quite a short period of time, it becomes more
understanding the aetiology —¿ different groups of polymorphous. Anxiety becomes prominent in the
patients will often be studied at different points along later clusters.
this course. Different symptoms, moreover, may In the longer term, such changes doubtless
follow different time gradients. Headache (and continue. Jones (1974) traced 80% of a large group
dizziness also), forexample, tended tobegradually less of over 4000 patients discharged from an emergency
frequently reported, the fall being quite precipitous department after minor head injuries not requiring
after starting at 50% (Fig. 2, Lidvall et al, 1974). admission, and tested the time course of their
Anxiety, by contrast, tended to increase from the 6th symptoms. Forty-two per cent had become asympto
to the 14th day (the week after the majority of matic within 3 weeks of their injuries; 57% continued
the patients were discharged from hospital), and with symptoms, mostly headache and dizziness,
irritability followed a similar course. It may safely for at least 2 months. But at 1-year follow-up
be concluded that different processes are likely to investigation, only 1% were still symptomatic and
underlie such differing time courses. continuing to seek medical advice. Of these 36
Lidvall et al (1974) were also able to examine the patients, a few had had complications, but the great
clusters which the symptoms formed with one majority had not. Twenty were re-examined in
another, i.e. the basis on which syndromes are hospital, and no physical causes for symptoms
designated. Just after the injury, a large and almost discovered.
POST-CONCUSSIONAL SYNDROME 465

It is therefore important to note that very different 2. Rutherford et al (1977)


populations of patients with post-concussional
A consecutive group of 145 mild head injuries in
symptoms are encountered, according to whether
Belfast were followed, and the symptoms experienced
they are studied weeks, months, or years after the 4 and 6 weeks after the accidents charted. Seventy
head injury has occurred. A study of Jones' (1974) four patients complained of one or more post
patients at 3 weeks would have given vastly different concussional symptoms. The number of symptoms
results from any study conducted at 1 year —¿
those
encountered was significantly higher in females than
still complaining would represent a tiny percentage males, and tended to rise, although non significantly,
only of those who would have been encountered with age and with length of post-traumatic amnesia.
earlier. Any causative factors unearthed could not
A strong influence was seen in relation to type of
be expected to apply equivalently. accident —¿
significantly more symptoms emerging
when blame could be attached to an employer or a
Aetiological investigations large impersonal organisation, than in patients who
blamed themselves or ‘¿Acts of God'. However,
Some of the investigations undertaken are now evidence of a possible organic factor was again
reviewed, to see the ways in which the various found. When examination at 24 hours had disclosed
aetiological factors have been explored. It will be headache, diplopia, anosmia, or other abnormality
apparent how markedly the studies differ on a range on neurological examination, the symptom rate
of significant parameters - the type of injury studied, proved to be significantly higher 6 weeks later.
its severity, the aetiological factors chosen for Evidence for both organic and non-organic com
scrutiny, and certainly the time elapsed since injury. ponents in the genesis of the symptoms was thus
Ideally, all aetiological factors should be measured adduced.
simultaneously and at repeated intervals during
recovery, to gain a just appreciation of their relative
3. Keshavan et al (1981)
values, and, most importantly, of how they might
sometimes operate in conjunction with one another. An analogous investigation in India was reported,
No such large-scale survey seems to have been involving 60 consecutive head-injury admissions
undertaken, but several smaller investigations are to an emergency service. The number of post
nonetheless informative. concussional symptoms experienced by patients at
3-months follow-up examination was noted. It may
1. Lidvall et al (1974) be significant that the injuries here were probably
somewhat more severe, in that the symptom rate was
A group of 83 head-injured patients were followed found to correlate significantly with the duration of
prospectively for 3 months, and the 38 who post-traumatic amnesia, and with the presence
developed ‘¿post-concussionalsymptoms' compared of intellectual deficits. But it was also strongly
with those without. The females and the unskilled associated with scores on premorbid neuroticism,
workers were particularly at risk. No relationship was derived from relatives' accounts. By contrast it
found with length of post-traumatic amnesia or the was striking to observe how clearly physical and
presence of intellectual impairment, neither when the social disability correlated with the organic factors
post-concussional group was considered as a whole, measured (PTA and intellectual deficits), but
nor when any individual symptom was considered not with the index of pre-traumatic neuroticism.
in isolation. Care was taken to measure early Nevertheless, both organic and non-organic influ
attitudes and stresses, with a series of questionnaires, ences were again upheld in relation to the genesis of
and significant relationships emerged. Mental stress the post-concussional symptoms.
at work and in the home was commoner in the post
concussional group. From the earliest stages, these
4. Kay et al (1971)
patients had had more anxiety about the accident,
more worries about other ailments, and more A retrospective case-note review of 474 patients
fears that they had sustained serious and possibly admitted to a neurosurgical unit was carried out.
permanent brain damage. All such factors suggested Brain damaged (n = 61), ‘¿post-concussional'
(n = 94),
pen-traumatic or secondary psychogenesis. Never and recovered groups (n = 268) could be discerned
theless, an organic factor could be discerned —¿ 3—6months later. The remaining 51 patients had
a strong relationship persisted between early evidence died. The post-concussional group had shown less
of otological dysfunction and the ultimate develop severe injuries than the brain-damaged group, and
ment of dizziness. indeed on a composite score of severity were
466 LISHMAN

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.

Acknowledgements PsychologicalMedicine, 3, 304—318.


—¿ (1978) Psychiatric sequelac of head injuries: problems in

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.

W. A. Lishman, MD, DSc, FRCP, FRCPsych,Professor of Neuropsychiatry, Institute of Psychiatry, De


Crespigny Park, Denmark Hi!!, London SES 8AF
Physiogenesis and psychogenesis in the 'post-concussional
syndrome'.
W A Lishman
BJP 1988, 153:460-469.
Access the most recent version at DOI: 10.1192/bjp.153.4.460

References This article cites 0 articles, 0 of which you can access for free at:
http://bjp.rcpsych.org/content/153/4/460#BIBL
Reprints/ To obtain reprints or permission to reproduce material from this paper, please write
permissions to [email protected]

You can respond /letters/submit/bjprcpsych;153/4/460


to this article at
Downloaded http://bjp.rcpsych.org/ on December 5, 2016
from Published by The Royal College of Psychiatrists

To subscribe to The British Journal of Psychiatry go to:


http://bjp.rcpsych.org/site/subscriptions/

You might also like