Case Study: Bipolar Disorder After Head Injury
KAPIL SAYAL, M.RC.PSYCH.,TAMSIN FORD, M.R.C.PSYCH.,AND RODERIC PIPE, M.R.C.PSYCH.

ABSTRACT

A case of bipdar disorder subsequent to a mild head injury in a 1Syear-old girl is reported. Review of the literatureindicates
that this is an extremely rare outcome. Lack of adequate follow-up studies makes it difficult to accurately predict type and
severlty of psychiatric wtcorne.Assessment and management involves ongoing consideration of both organic and psycho-

social factors even after initial negative investigations. ./. Am. Aced. Chi@Ado/esc. Psychiatry; 2OO0, 39(4):52=28.

Key

Words: head injury, adolescent, mania, bipolar disorder, psychosoda1factors.

Head injuries and their sequelae are one of the most common reasons for emergency admission to the hospital. As
intensive care facilities improve, many of those who in the
past would have died of a head injury now survive
(Gillberg, 1995). Their incidence among children is
increasing, accounting for 25% of all head injuries.
Those between the ages of 15 and 24 are at highest risk
(Livingston and McCabe, 1990). Psychiatric disturbance
after a childhood head injury is a well-recognized phenomenon, although much less predictable than cognitive
outcome (Chadwick, 1985). However, mania or bipolar
disorder h e r head injury is rare, even in adults (McAllister,
1992). We describe the management of a 15-year-old girl
who presented with manic symptoms shortly after a head
injury and discuss the issues raised with regard to the etiology, course, and prognosis of her illness.

chiany#Denmark Hill London SE5 %AEEngkad e-maiL.k.sqaI@op.kcLar.uk.
0890-8567/00/3904-052502000 by the Amcriun Audcmy of Child
and Adolescent Psychiatry.

well academically and was described as being hardworking with high standards.
A.B. presented 4 weeks after a head injury which she
sustained when she fell fiom her bicycle. The fall was not
witnessed directly, and she may have lost consciousness for
several minutes. She had posttraumatic amnesia for 5
hours and retrograde amnesia for 2 hours. Initially she was
drowsy, slow to respond, and disoriented in time but
oriented in place and person. A skull x-ray was normal. She
was admitted for observation for 3 days, and during this
time she described olfactory hallucinations on 2 occasions.
At discharge she was M y oriented but had unequal pupils.
During the following 3 weeks A.B. was tired,lost interest
in activities, had poor self-care, slept excessively, and worried about not remembering the accident. The M y were
then involved in a uaffic accident with no reported injuries.
That evening she became overtalkative, slept poorly, and
was agitated and fearfll. She was admitted to a pediatric
ward where she was distractible, with pressured speech,
elated and labile mood, and grandiose thoughts. A cranial
computed tomography (
0
scan revealed no abnormalities. She began a regimen of oral chlorpmmazineup to 300
mg/day but remained agitated, &inhibited, and thoughtdisordered. She acknowledged difficulties in thinking, and
hearing voices, but was unable to elaborate.
The patient was transferred to an adolescent psychiatric
unit, where she improved in the following 2 weeks; her
psychotic features resolved completely. An EEG was normal. A magnetic resonance imaging (MRI) scan showed
small lesions caudal to the right amygdala (Fig. l), right
putamen (Fig. 2), and to the right of the pituitary gland.
It was unclear whether this represented hematomas secondary to the head injury or whether a spontaneous bleed
had led to the fall.

J . AM. ACAD. C H I L D ADOLESC. PSYCHIATRY, 39:4. APRIL 2000

525

CASE REPORT

A.B. is a 15-year-old girl with a history of anorexia
nervosa (13-kg weight loss, overvalued ideas about shape
and weight, and amenorrhoea) 2 years previously. This
occurred secondary to peer pressure about her appearance and exam stress. She was monitored by her general
practitioner and improved after her exams. She had no
developmental or physical health problems, and there
was no family history of m e n d illness. She functioned
Accqtrd October 26 1999.
From the B a h h and Maudt.+y Hopitah, London.
The anthorr thank Profisor Eric Taybr, Dr Eric Fombonnr, and Dr Isobel
Heymanf i r commenting on the manuscript.
C o r m p o h c e ta Dr Say4 Dqamncnt of Chiki&hiany. Institute of I3y

SAYAL E T AL.

Fig. 2 Magnetic resonance imaging scan showing hemorrhage along the
antcrolatcral aspcct of the right putamen.

Fig. 1 Magnetic resonance imaging scan showing hemorrhage immcdiatcly
caudal to the right amygdala.

executive Syndrome (Wilson et al., 1996), showed subtle
signs of a dysexecutive syndrome with difficulties in tasks
involving planning and organization.
Before discharge AB. experienced short-lived episodes
of low mood reflecting increased insight into her illness
and concern about weight increase. Discharge recommendations were made with respect to continuing carbamazepine and chlorpromazine under neuropsychiatric review,
individual and family work, and minimizing initial academic pressures, in order to reduce the risk of relapse of
psychosis, depression, and anorexia.

Soon after a reduction in the chlorpromazine dose, A.B.
relapsed; she became distractible and perplexed, with irritable mood, pressure of speech, flight of ideas, ideas of reference, and thought disorder. During this episode there
was no clinical evidence of a conhional state. Following
expert neuropsychiauic advice that these manic symptoms
might represent ictal phenomena, she began a regimen of
cabamazepine (gradually increased to 800 mg/day). Her
symptoms abated after 2 weeks but returned with similar
intensity 2 weeks later. Over the following month she
gradually improved but experienced residual irritability
and lability of mood. A second EEG was normal, and a
second MRI showed appearances consistent with partial
resolution of the earlier hemorrhagic abnormalities. Carotid and invasive angiography revealed no abnormalities,
clarifjring that trauma had caused the hemorrhage. Metabolic disorders were excluded (investigationsincluded routine hematology and biochemistry, lysosomal enzymes,
and urinary vanillylmandelicand organic acids). Psychometry, including the Behavioural Assessment of the Dys-

Before we discuss the case, we will highlight some of
the methodological difficulties inherent in this area.Many
studies fail to control for preinjury factors, despite evidence that children with externalizing behavioral disturbance are more likely to sustain a head injury (Chadwick,
1985), and few studies involve non- or other-injured controls. According to the severity criteria used by Max et al.
(1998), A.B. would be considered to have a mild traumatic brain injury (i.e., a Glasgow Coma Scale [Teasdale
and Jennett, 19741 score of at least 13 and a normal brain

526

J . AM. ACAD. CHILD ADOLESC. PSYCHIATRY, 3 9 : 4 . APRIL 2 0 0 0

DISCUSSION

B I P O L A R D I S O R D E R A F T E R HEAD INJURY

CT scan), and the posttraumatic amnesia was also relatively short. However, a severe mental illness followed.
There are difficulties in extrapolating to children findings from the adult literature, especially in relation to
types of injury and forces involved. The etiology of head
injuries and subsequent mortality varies with age, which
has implications for the interpretation of pathological
findings (Livingston and McCabe, 1990; Sollee and
Kindon, 1987). It is also possible that there is a differential
impact on emerging cognitive abilities and personality
according to age at the time of injury (Saa et al., 1997).
Although the psychiatric outcome seems more variable
than the cognitive outcome (Chadwick, 1985), there is little doubt that moderate or severe head injury is associated
with an increased risk of psychological disturbance (Brown
et al., 1981; Chadwick, 1985; Max et al., 1997b; Rutter
et al., 1980).The sequelae of mild head injury in children
are more controversial. A review of mild head injury in
children reported that two thirds of studies failed to demonstrate any disability, and methodologically “strong”
studies were associated with no subsequent morbidity
(Saa et al., 1997, p. 123). In A.B.’s case,the psychological
and physical features in the 3 weeks following the initial
head injury suggest either a postconcussional disorder or
a major depressive episode. Her presentation after the traffic accident involving the family had features suggestive
of a delirium with perceptual abnormalities. Despite the
lack of impact of this second accident, the acceleration/
deceleration forces involved may have had a cumulative
effect with the initial head injury.The subsequent psychotic
illness with fear and perplexity was unusual in that it developed out of a confusional state, but then relapsed despite
the confusional state improving.The characteristicfeatures
of a manic illness and the episodes being preceded and
followed by depressive symptoms led to a diagnosis of
bipolar disorder.
The range of disorders seen after head injury is similar
to those in noninjured children, with a predominance of
conduct and emotional disorders (Brown et al., 1981;
Chadwick, 1985; Max et al., 1997a,b; Oddy, 1993; Rutter
et al., 1980), although there is an excess of hyperkinetic
disorder and socially disinhibited behavior (Chadwick,
1985).Very few cases of mania occurring secondary to a
head injury in children or adolescents have been reported
(Cohn et al., 1977;Joshi et al., 1985; Khanna and Srinath,
1985; Max et al., 1997c).
Evidence suggests that in adulthood, secondary mania
is associated with the full range of head injury and has a
similar course to primary mania, but that there may be a

higher relapse rate and irritability is commonly the predominant affect Uorge et al., 1993; McAllister, 1992).
One series of 20 patients presenting with mania after
closed head injury reported that 50% had clinical seizures
(Shukla et al., 1987). In A.B.’s case, investigations revealed
no evidence of seizures, although her clinical presentation
was highly suggestive of seizures. The olfactory hallucinations may have represented subclinical seizures, perhaps
involving irritation of the mesial temporal cortex.
There are lower rates of family and past psychiatric disorder in secondary mania compared with primary mania
or secondary depression Uorge et al., 1993; Starkstein
et al., 1987). The former is associated with injury to the
right hemisphere, in particular to the limbic system or
related structures (Jorgeet al., 1993; Robinson et al., 1988;
Starkstein et al., 1987, 1990). A.B.’s injury is in keeping
with this. One study of secondary mania found a high
incidence of frontal subcortical atrophy in those without
a family history (Robinson et al., 1988). A greater depletion of biogenic amines has been demonstrated &er insults
to the right rather than the left hemisphere (Starkstein
et al., 1990). Secondary mania may be rare because it
requires the unlikely combination of genetic loading or
anterior subcortical atrophy with greater amine depletion
(Starkstein et al., 1990). For the case described, the close
temporal proximity of the head injury as a risk factor and
the absence of Family history of affective disorder suggest
a relatively good prognosis.
The case described emphasizes the need for clinical
management to be guided by clinical features in preference
to investigationswith normal results. Early contusions following a head injury may not be seen on CT scanning, and
a normal CT and EEG do not rule out an organic contribution to the etiology.
While the severity of the injury seems the most important predictor of psychiatric disorder (Max et al., 1997a),
pre- and postinjury intellectual function, the child‘s and
the family’s psychiatric history, and current psychosocial
circumstances are risk factors (Brown et al., 1981; Max
et al., 1997a ; Rutter et al., 1980). Follow-up studies suggest that difficulties fluctuate predictably over time (Oddy,
1993). Subtle cognitive deficits may combine with behavioral problems, leading to significant educational and
social handicap, despite the preservation of global intellectual function (Chadwick, 1985; Klonoff et al., 1993).
“In other words, it is not only the kind of injury that matters, but the kind of head” (Symonds [I9371 ref. in
McAllister [1992], p. 399).

J . A M . ACAD. C H I L D A D O L E S C . PSYCHIATRY, 39:4. APRIL 2 0 0 0

527

SAYAL E T AL.
REFERENCES
Brown G, Chadwick 0. ShafTcr D. Runcr M.Traub M (1981). A prospmivc
study of children with h a d injuries. Ill: psychiatric scquclae. nycholMrd
11:63-78

Chadwick 0 (1985), Psychological squclac of h a d injury in children. Dn,
Mrd Child Nruml27:72-75
Cohn CK, Wright JR, DcVaul RA (1977). Post head trauma syndrome in an
adolcsccnt trcatcd with lithium carbonate: case report. Dis New Syst
38:630-631

Gillbcrg C (1995). Traumatic brain injury and its ncuropsychiatric scquclac.
In: Cliniral Child Nrumpychiatty, Gillbcrg C, cd. N m York: Cambridgc
University Pras. pp 274-278
Jorgc RE, Robinson RG. Starkstcin SE, Arndt SV, Former AW. Gcislcr FH
(1993). Secondary mania following traumatic brain injury. Am J PJYchiany 150:916-921
Joshi P, G p o m l i JA. Coylc JT (1985). Efktivc managcrncnt with lithium of
a pcnistcnt, post-traumatic hypomania in a 10 year old child.JDn, &huu
Pr&n 6:352-354
Khanna S, Srinath S (1985). Symptomatic mania after head injury. CllnJ h y cbiutty 30:236-237

Klonoff H, Clark C, Klonoff PS (1993), Long term outcomc of head injuries:
a 23 ycar follow up study of children with head injuria. JNrumlNrummrg
Aychiatty 56:41&415
Livingston MG. McCabc RJR (1990), Psychosocial conxqucnccs of h u d
injury in children and adolcsccnts: implicationsfor rchabilitation.Pcdiutri&n 17255-261
Max JE, Kodc SL Smith WL ct al. (1998). Psychiatric disordcn in childrrn and
a d o l w n t s aftcr scvcre traumatic brain injury: a controlled study. J Am
Acud ChildAablcrc pryrhiany 37832-840

Max JE, Sharma A. Qurashi MI (1997a), Tnumatic brain injury in a child psychiatry inpatient population: a controlled study. J Am Arad Child A h k

Bychiany 36: 1595-1601
Max JE, Smith WL, Sato Y ct al. (1997b), Traumatic brain injury in children
and adolesccnts: psychiatric disordcn in thc fint thm months. JAm Acud
Child A h k &rhiatry 36:94-102
Max JE, Smith WL, Sato Y cf al. (1997~).Mania and hypomania following
traumatic brain injury in children and adolescents. Nrumrarr 3:119-126
MdUlitcr T W (1992), Ncuropsychiatricscquclac of head injuries. hychiurr
CIin N o d Am 15:395-413
Oddy M (1993). H a d injury during childhood.Nrumpr)rhollRrhabil3:301-320
Robinson RG, Boston JD, Srarkstcin SE, PriaTR (1988). CMnpvison of mania
and depmion Acr bnin injury: auslhaon. Am JAy-bimy 145:172-178
Runcr M. Chadwick 0,Shafir D, Brown G (1980). A prospmivc study of
c h i i l k with h a d injuries, I: design and mcthods. rjrhorMcd 10:633445
SaQ r! Zaucha K, McClary C, Light R, Asarnow R, Beckcr D (1997). Mild
head injury in children and adolcsccnts: a mim of studia (197C1995).
Ryrhol Bull 122:107-13 1
Shukla S. Cook BL. Mukhcjct S,Godwin C, Miller MG (1987), Mania following h a d trauma. Am JAychiutty 144:93-96
Sollct ND, Kindon DJ (1987). I a t c r a l i d brain injury and bchaviour pmblcms in children.J A b ~ r n
ChildRyrhoI15:479-490
Starkstcin SE, Maybcrg HS. Bcnhicr ML c t al. (1990). Mania aftcr brain
injury: ncumndiological and mctabolic findings. Ann Nrum127652-659
Starkstcin SE, Pcarlson GD. Boston J, Robinson RG (1987), Mania aftcr
brain injury. Arrh Nruml44:1069-1073
T d c G. Jcnncn B (1974), Ascsmcnt of coma and impaired consciousnas: a practical d c . Lancer 2:81-84
Wilson BA, Alderman N, Burgcss PW,Emslic H, Evans JJ (1996). &huuimtml
Arumnrnt of the L?ysae~~tiw
SyUlmmr. Bury St Edmunds, UK: Thama
Valley Tat Company Limited

Traumatic Brain Injury in High School Athletes. John W. Powcll, PhD, ATC, Kim D. Barber-Foss, MS, ATC

C o n m : T h c potential xriousncss of mild traumatic brain injury (MTBI) is increasingly r r c o g n i d ; however, information on the
frequency of MTBI among high school athlcta is limited. 0bjem"UCTo identify thc typc, frcqucncy, and severity of MTBI in selmcd
high school sports activities. Daign: Observational cohon study. M n g and Purticpunts: Two hundred forty-six certified athletic
trainers recorded injury and exposure data for high school vanity athletes participating in boys' football, wrestling, baseball and field
hockey, girls' volleyball and softbal, boys' and girls' basketball, and boys' and girls' soccer at 235 US high schools during 1 or more of
the 1995-1997 academic years. Muin Ou~~omcMrruum:
Rates of rcportcd MTBI. defined as a head-injud player who was removed
from participation and evaluated by an athletic trainer or physician prior to rrturning to participation. National incidence figures for
MTBI as0 wcre atimatcd. Rrsultr: Of 23 566 reported injuries in thc 10 sports during the 3-ycar study period, 1219 (5.5%) WCK
MTBIs. Of thc MTBIs, football accounted for 7 3 (63.4%) of cases;wrestling, 128 (10.5%); girls' soccer, 7 6 (6.2%); boys' soccer,
69 (5.7%); girls' basketball, 63 (5.2%); bays' basketball, 5 1 (4.2%); softball, 25 (2.1%); baseball, 15 (12%);fidd hockey, 13 (1.1%);
and voll+all, 6 (0.5%). Thc injury rates per 100 player-seasons were 3.66 for football, 1.58 for wrrstling, 1.14 for girls' rocccr, 1.04
for girls' basketball, 0.92 for boys'soccer, 0.75 for boys' basketball, 0.46 for softball, 0.46 for field hockey, 0.23 for baseball, and 0.14
for volleyball.T h e median time lost from participation for all MTBIs was 3 days.There were 6 cases of subduralhematoma and intracranial injury reported in football. Baxd on these data, an atimatcd 62 816 cam of MTBI occur annually among high school MTsity athlcta participating in thesc sports,with football accounting for about 63% of cam.Conrlrrrirom;Rates of MTBI vary among
sports and nonc of thc 10 popular high school sports we studied is without thc occurrence of an MTBI. Continued involvcmcnt of
high school sports sponsors, researchers, medical professionals, coacha, and sports participants is csscntial to help minimiv the risk
of MTBI. J A M A 1999;282:958-963. Copyright 1999, Amcrican Medical Association.

528

J . AM. ACAD. C H I L D ADOLESC. PSYCHIATRY, 3 9 : 4 , APRIL ZOO0