Movement Disorders

Vol. 7, No. 3, 1992, pp. 263-272,

0 1992 Movement Disorder Society

Dy stonia Following Head Trauma: A Report of Nine

Patients and Review of the Literature

Joachim K. Krauss, "Mohsen Mohadjer, ?Dieter F. Braus, SAjay K. Wakhloo, Fritz Nobbe,
and §Fritz Mundinger

Departments of Neurosurgery and "Stereotaxy and Neuronuclear Medicine, Neurosurgical Clinic, TFDepartment of
Neuropathology, and $Section of Neuroradiology, Albert Ludwigs Universitat; and §St. Josefs Krankenhaus,
Freiburg, Germany

Summary: We report nine patients who developed dystonia following head

trauma. The most frequent form was hemidystonia only (six patients). One
patient presented with hemidystonia plus torticollis, one with bilateral
hemidystonia and one with torticollis only. Seven patients sustained a severe
head injury, and two had a mild head injury. At the time of injury, six were
younger than 10 years, two were adolescents, and the patient with torticollis
only was an adult. Except in the patient with torticollis only, the onset of
dystonia varied considerably from months to years. All patients with hemidys-
tonia had posthemiplegic dystonia of delayed onset. Seven out of 8 patients
with hemidystonia had lesions involving the contralateral caudate or putamen,
as demonstrated by CT and MR. The patient with hemidystonia plus torticollis
had no lesion to the basal ganglia, but a contralateral pontomesencephalic
lesion. Response to medical treatment was generally poor. Functional stereo-
tactic operations were performed in seven patients. A variety of factors may be
responsible for the vascular or nonvascular posttraumatic basal ganglia lesions,
which may lead to dystonia. The pathophysiology seems to be more complex
than thought previously. We believe that dystonia following head injury is not
as rare as is assumed. Awareness of its characteristics and optimized diagnos-
tic procedures will lead to wider recognition of this entity. Key Words:
Hemidystonia-Torticollis-Head injury-Posttraumatic movement disor-
der-Stereotactic surgery-Basal ganglia lesions.

Head trauma is a well established (1) but infre-
quent cause of movement disorders. Dystonia
(hemidystonia and torticollis) following head injury
is considered to be unusual (2). Since the report on
a patient with presumably posttraumatic dystonia
by Austregesilio in 1928 (3), only few detailed re-
ports on patients with this condition have been pub-
lished (4-2 1).
So far, there has been no large series on dystonia
following head trauma. To focus better this uncom-
- history of dystonia or neurological disease. Exclu-
Videotape segments accompany this article.
Address correspondence and reprint requests to Dr. J. K.
Krauss at Neurochirurgische Universitatsklinik, Hugstetter Str.
55, D-7800 Freiburg, Germany.
mon movement disorder we reviewed the literature
and studied the clinical features, the mechanism of
trauma, the effect of medical and surgical therapy,
the course and clinicopathologicalcorrelations with
neuroradiological findings in a series of 9 patients.
PATIENTS AND METHODS
In all patients reported here, dystonia was the
predominant symptom. None suffered from meta-
bolic disorders or intoxications; none had a family
sion criteria were: complications like fat embolism
or asphyxia; meningoencephalitis; an unusually
long delay after mild head trauma in adults (>lo

263
264 J . K . KRAUSS ET AL.

years); decerebration rigidity or fixed “dystonic
postures” in spastic hemiparesis; long-term neuro-
leptic treatment prior to the onset of dystonia.
Trauma was considered to be severe with a Glas-
gow Coma Scale (GCS) of <8, coma for > 1 day, or
posttraumatic amnesia for >1 week. All patients
were filmed or videotaped. CT scans were routinely
taken in all patients. MR was carried out if lesions
were not found or could not be definitively estab-
lished. Dystonia was quantified in three grades of
severity (1, moderate; 2, marked; 3, severe) and
was qualified by appearance (spontaneous andlor
on action, and mobile spasms or athetosis). The ac-
companying hemiparesis was graded from 0 to 4 (0,
full strength; 1, mild weakness; 2, marked weak-
ness; 3, minimal effect of movement; and 4, plegia).
Seven patients underwent a functional stereotactic
operation; two were operated on twice. Outcome
was graded from 0 to 4, taking into consideration
pre- and postoperative film demonstrations, medi-
cal reports, examinations and interviews of the pa-
tients, their relatives and attending physicians (0,
no movement disorder; 1 , marked improvement
ranging from 50% to 90%; 2, moderate of 30-50%;
3, minimal improvement; 4, no notable change).
All patients were followed up at various times,
with one to seven follow-up examinations; eight
were followed up in 1990 or in 1991, when we con-
ducted the study.
RESULTS
The study consisted of seven men and two
women (Table 1). The mean age at trauma of pa-
tients developing hemidystonia was 8 years (range,
3-16 years), the patient with torticollis only was 36
years old. Head trauma was mild in two: no loss of
consciousness in patient 9, who fell from a height of
2.5 meters landing on his left neck and shoulder,
and obtundation for 2 h in patient 2. The remaining
seven patients had sustained a severe head injury.
Duration of unconsciousness and clouded con-
sciousness ranged from a few days to several
months (patient 6). Six patients were victims of au-
topedestrian accidents, partly with high decelera-
tion forces. Closed head injury was found in eight
patients, open head injury in one. Skull fractures
were detected by X-ray in patients 1, 3, 5 , and 8. In
four patients, craniotomies were performed: in pa-
tient 3, a large left frontal hematoma was evacuated
(1966); in patient 1 , a brain prolapse was resected
(1957); in patient 4, a vaguely described right pari-
eto-occipital hemorrhagic contusion or hematoma
was removed (1940); in patient 5, a left epidural
hematoma was trephinated, evacuated, and drained
(1971).
In patient 8, CT scans 2 days after the trauma
showed multiple contusions and generalized edema,
but no bleeding, contusions, or low-density lesion
in the basal ganglia. Intracranial pressure was mon-
itored and controlled; however, CT 2 weeks later
showed an increase in generalized edema. X-ray
and CT scans of the head and the cervical spine in
patient 9, taken 2 days after the trauma as well as
several controls were unremarkable.
Patient 5 had a polytrauma with fracture of the
left hip and myositis ossificans of the right quadri-
ceps muscle. All other patients had no significant
lesions of the extremities.

TABLE 1. Clinical features of nine patients with dystonia following head injury
Latency of
Age at Severity Posttraumatic and onset Age at Duration Hemiparesis Dystonia
Patient Gender trauma of trauma hemiparesis” of dystonia study of dystonia Distribution at study” at studyb
1 F 7 S 4 1 year 40 31 years HD . R:A.Le.(Fa),
I~ I_
1 3
2 F 9 M 3 4 years 50 37 years HD . L:A,Le 1 3
M 6 S 3 months 30 24 years HD . R:A,Le,(Fa),(T) 1 2
M 3 S 3 years 53 47 years HD . L:A,Le,(Fa),(T) 1 2
M 13 S 6 months 32 18 years HD . R:A,Le,(Fa),(T) 1 L
M I S 9 21 >I0 years HD . R:A,Le,(Fa),(T) 2 2
HD . L:A 1 1
M 4 S 3 6 months (HD) 28 23 years (HD) HD . R:A,Le,(Fa),(T) 1 1
6 years (TC) 17 years (TC) TC 1
M 16 S 2 years 2s 9 years HD . R:A,Le,(Fa) 1 1

M 36 M 2 days 38 12 months TC -
“ Seventy of hemiparesis graded from 0 to 4: 0, full strength; 1, mild weakness; 2, marked weakness; 3, weakness with only minimal effect of movement;
4, plegia.
Grading of severity of dystonia: 1, moderate; 2, marked; 3, severe.
S, severe; M , mild; HD, hemidystonia; TC, torticollis; R, right; L, left; A, arm; Le, leg; Fa, face; T, trunk.

Movement Disorders, Vol. 7, No. 3, 1992

 D YSTONIA FOLLOWING HEAD TRAUMA 265

Initial hemiplegia was found in two, and severe

hemiparesis in four patients-concerning the limbs
which developed dystonia later on. Patient 8 had a
marked left and a mild right hemiparesis. Patients 1 ,
3, 5 , and 6 had aphasia. Two patients had seizures.
The mean delay of onset of hemidystonia after
trauma was 20 months (range, 3 months for patient
3, to 4 years for patient 2). Torticollis in patient 9
became manifest 2 days after the trauma. Torticollis
in patient 7 was diagnosed several years after the
hemidystonia, which was noted 6 months after the
head injury. Hemidystonia increased up to 3 years,
whereas hemiparesis improved.
The mean age of patients with hemidystonia at
study was 35 years (range, 21-53 years), the patient
with torticollis only was 38 years old. Two patients
exhibited severe psychological and cognitive alter-
ations; four had disturbed memory and concentra-
tion. Patient 6 had ataxia, patient 4 vertical gaze
palsy, and patient 5 palilalia. Muscle tone at rest
varied, but constant findings were discrete hyper-
tonicity and increased deep tendon reflexes. Hemi-
hypaesthesia was evident in five patients.
Four patients had right, two left hemidystonia, FIG. 1. Clinical presentation of patients with posttraumatic dys-
one bilateral hemisdystonia, one torticollis only tonia. a: Patient 7 with right-sided hemidystonia and torticollis
before stereotactic operations. b Same patient at follow-up in
with inclination to the left and rotation to the right, 1990. c: Patient 1 . d: Patient 4, who presented with marked athe-
and one right hemidystonia combined with torticol- tosis. e: Patient 3. f: Patient 5.
lis with inclination of the head to the right and ro-
tation to the left side (Fig. 1). The arm was more
affected than the leg, in two restricted to a dystonic bined therapies. Seven patients had no benefit from
big toe. The face was involved in seven patients and treatment with the following drugs, neither as
trunk with scoliosis in five. Dystonia at first admis- monotherapy nor in combination: chlormezanon,
sion (patients 6 and 7 are counted twice) was mod- tiapride, biperiden, haloperidol, clonazepam,
erate in three patients, marked in five, and severe in memantine, trihexyphenidyl, pimozide, tetrabena-
three. Ipsilateral hemiparesis with mild weakness zine, diphenylhydantoin, methyldopa, bamipine,
was present in all patients with hemidystonia, only and levopropylhexedrin. Patient 2 had subjective
patient 6 had marked weakness on the right side. improvement with dantrolene sodium, high-dosed
Spontaneous dystonia intensified by action and mo- diazepame, and bromazepame; patient 8 improved
bile spasms or athetoid movements were found in with trihexyphenidyl, but worsened with tetrabena-
all. The picture in patient 4 was dominated by athe- zine and pimozide. Five patients had subjective im-
tosis. The mean duration of hemidystonia at study provement after physical therapy.
was 27 years (range, 9 4 7 years). In patient 9, tor- As response to medication was poor, stereotactic
ticollis faded following injections of botulinum A surgery had been performed in seven patients (Ta-
toxin. Other movement disorders were present in ble 2). Electrocoagulations were done in the con-
patients 6 (right-sided choreoathetosis and jerks on tralateral zona incerta (Zi) and/or nuclei of the
intentional movements), 7 (right intention tremor), ventrolateral thalamus (VL): Voa, Vop, and Vim,
and 8 (hypomimia and mild akinesia). according to Hassler. In three patients, additional
The response to various medications was as- target points were the medial pulvinar, and in one
sessed. As some patients took different drugs for a the globus pallidus after previous coagulations in
period of >40 years, it was difficult to evaluate ex- the VL. The technique is described in detail else-
actly the response to various dosages or to com- where (22). Two patients were operated on twice,

Movement Disorders, Vol. 7, No. 3, 1992

266 J . K . KRAUSS ET AL.

TABLE 2. Data of stereotactic surgery in seven patients

Age at Improvement Time of
stereotaxic Duration (postoperative, postoperative
Patient oueration of dystonia Procedure Side effects > 3 years)a follow-up
1 I18 9 years EC: Zi + Vo-Base (L) Transient depression 22 years
I1 19 10 years EC: GP (L)
2 28 14 years RI + EC: Zi, Vo-Base, Vim (R) Transient increase of 4 22 years
left hemiparesis
3 20 14 years EC:Zi, Vo-Base, Vim, Vop (L) Transient increase of 3 9 years
right hemiparesis
4 29 23 years EC:Zi, Vo-Base (R) - 4 24 years
5 16 2 years EC:Zi, Pulv. med (L) Transient increase of 3 16 years
right hemiparesis
6 21 > 10 years EC:Zi, Voa, Vop, Pulv. med (L) - ? 1 month
I I14 9 years (HD), EC:Zi, Pulv. med (L) TC = 1 14 years
3 years (TC) (
I1 16 11 years (HD), EC:Vop (L) Transient increase HD = 4
5 years (TC) right hemiparesis
~~ ~

Outcome after stereotactic surgery was graded on a scale from 0 to 4: 0 indicates no movement disorder; 1, marked improvement;
a
2, moderate improvement; 3, minimal improvement; 4, no notable change.
EC, electrocoagulation; RI, implantation of radionuclide; L, left; R, right; Zi, zona incerta; Vo, nucleus ventralis oralis thalami; Voa
and Vop, nucleus ventralis oralis anterior and posterior thalami; Vim, nucleus intermedius thalami; GP, globus pallidus; Pulv. med.,
pulvinar medialis thalami.

spaced by an interval of 7 and 30 months, respec-
tively. Additionally, a radionuclide was implanted
in one case (in 1968). Duration of hemidystonia at
stereotactic surgery varied from 2 to 23 years, with
a mean of 12 years. The age ranged from 14 to 29
years, with a mean of 21 years. Five patients had
transient side effects: four increased hemiparesis
improving after days to weeks, and one depression.
There were no side effects on long-term follow-up.
In all patients, dystonia improved immediately after
operation. In patient 1, there was a significant relief
of foot dystonia, whereas the arm improved only
minimally. Nevertheless, over a period of 3 years,
hemidystonia increased again in all patients. An ex-
cellent lasting effect on torticollis was achieved af-
ter the first operation in patient 7 over a period of 14
years (Fig. 1). At the recent follow-up (1990/91),
hemidystonia was unchanged compared to preoper-
atively in three patients and was improved to a cer-
tain degree in three.
The patients were followed up for an average of
18 years (range, 9-24 years). One patient was lost to
follow-up. At the time of the study, seven lived with
their families, one in an asylum. All but one were
working. Three of the younger male patients regu-
larly engaged in sports.
CT scans were performed in all. In five patients,
stereotactic surgery had been performed in the pre-
CT era. The focal lesions in the VL, subthalamic
region (STR), or pulvinar were detected in all cases
operated on as corresponding to the target points
that had been calculated (Tables 2 and 3). In those
who were operated on in the pre-CT era, the small
circumscribed lesions were “subtracted” from the
traumatic lesions. Thus, preoperative lesions of the
VL of course cannot be excluded. This is of impor-
tance, as the preoperative CT scan of patient 6
showed a small lesion in the VL. MR scans were
obtained in three patients. All patients had focal
lesions, except patient 9 with torticollis only. In this
patient, MR scans could not be obtained. Details of
the findings are given in Table 3. All patients with
hemidystonia had contralateral hemiatrophy. In
five patients cortical/subcortical large low-density
lesions were found, in two with extension to the
anterior parts of the lateral basal ganglia. Lesions of
the contralateral caudate were found in four, defi-
nite lesions of the putamen in seven. Similarly dis-
tributed lesions of caudate, anterior internal cap-
sule, and putamen were found in four patients (Fig.
2). Patient 6 with bilateral hemidystonia had bilat-
eral putaminal lesions (Fig. 2). Predominantly pal-
lidal lesions were detected in two patients. In pa-
tient 8, bilateral pallidal lesions were found only
by MR, extending to the posterior putamen contra-
lateral to the movement disorder. In patient 5 ,
CT demonstrated a pallidal lesions, but damage
to the posterior basal putamen could be detected
reliably only after coronal MR scans (Fig. 3).
Patient 7 with hemidystonia plus torticollis and

Movement Disorders, Vol. 7, N o . 3, 1992

 DYSTONIA FOLLOWING HEAD TRAUMA 267

TABLE 3 . Neuroradiological .findings in nine patients with posttraumatic dystonia

Low-density focal lesions (in CT) Lesions due to
stereotactic
Patient Examination General findings Cortedsubcortex Basal ganglia operations
~

1 CT L frontal osteoplasticl L frontalhigh-frontal L Caudate-anterior L STRIGP

osteoclastic trephination
Cerebellar atrophy
L hemiatrophy with
marked enlargement of
frontal horn + cella
media
R frontal cortical atrophy
CT R hemiatrophy with
marked enlargement of
frontal horn + cella
media
CT L frontal osteoplastic
trephination
L hemiatrophy
R fronto-parietal cortical
atrophy
4 CT R occipitotemporo-
parietal trephination
R hemiatrophy with
marked dilatation of
lateral ventricle
L frontotemporo-
parietal atrophy
CT + MR Atrophy of vermis
L hemiatrophy
CT Enlarged cerebello-
medullary cistern
Mesencephalic atrophy
L hemiatrophy with
marked enlargement of
frontal horn + cella
media
I CT + MR Cerebellar atrophy
Cavum Vergae
L hemiatrophy
R frontoparietal cortical
atrophy
8 CT + MR Bilateral frontal cortical
atrophy
9 CT Brain and cervical
Spinal cord: normal
extending to basal
ganglia@ X 5 x 5)
R Subcortical high-frontal
(1.5 X 1.5 X 1.5)
L frontopolar/fronto-
lateral extending to
basal ganglia (7 x 2 x
3.5)
R occipitotemporo-
parietal extending to
posterior part of lateral
ventricle (5 x 5 x 5.5)
L temporaVtemporo-
polar (4 x 3.5 x 2.5)
L frontal (5 x 2 x 2) and
(1 x 1 x I )
R temporolateral (2 x 1 X CT: 0
1) and frontolateral (2 X MR: lesions of pallidum L
1 x 2)
internal capsule
putamen
R Caudate-anterior R VL/STR
interior capsule- (hyperdense pellet)
putamen (4 x 1 x 1.5)
L Caudate-anterior L VL/STR
internal capsule
putamen-pallidum
R Putamen-posterior R VLlSTR
internal capsule (1.5 x
1 x 1.3)
L Pallidum-posterior L VL/STWpulvinar
internal capsule (I X 1
x 1)
MR: Lesion of posterior
basal putamen
L Caudate-anterior ?
internal capsule
putamen (3 x 1 x 1.5)
L ventrolateral thalamus
(0.5 x 0.5 x 0.5)
R anterior internal capsule
putamen (1 x 0.5 x I )
R cerebellar peduncle (0.5
X 0.5 X 0.5)
L Tegmentum pontis et VL/STR/pulvinar
mesencephali
MR: Longish lesion with
extension from
subthalamic region to
superior cerebellar
peduncle (including
tractus tegmentalis
centr.)
> R (0.5 x 0.5 x 1)
extending to left
putamen

STR, subthalamic region; VL, nucleus ventrolateralis thalami; GP, globus pallidus.

intention tremor had no lesions of the contralateral DISCUSSION

caudate, putamen, pallidum, or thalamus, but a
longish pontomesencephalic lesion. MR demon-
strated that the lesion was located in the contralat-
era1 mesencephalic and pontine tegmentum (Fig. 4).
It extended to the STR, but not to the thalamus, and
could be differentiated clearly from the stereotactic
lesions.
We observed two distributions of dystonia fol-
lowing head injury: hemidystonia and torticollis.
The predominance of males correlates well with
findings that craniocerebral trauma occurs more of-
ten in male infants (70%) than in female (30%) (23).
According to the available data reported previously

Movement Disorders, Vol. 7, No. 3, I992

268 J . K . KRAUSS ETAL.
all but four patients (1 1,16,19,20) with posttrau-
matic hemidystonia were infants or adolescents.
In contrast to isolated previous reports on
hemidystonia after mild head trauma (9), even with-
out loss of consciousness (7,8,10-13,15,16), all pa-
tients of the present series except one sustained a
severe head trauma. There were no previous or
concomitant injuries of the dystonic limbs, which
may have been involved in induction of dystonia
(24,25). In the patient with torticollis only, how-
ever, a “peripheral” lesion may also be causative
(26).
All patients had “posthemiplegic dystonia” with
delayed onset. Delay did not correlate with the ini-
tial severity of hemiparesis, nor with the severity of
the trauma. Dystonia progressed while paresis re-
gressed. Hemidystonia may present already one
day after head trauma (9) but delay may take as long
as 6 years (14). Delayed type of onset and young age
suggest that the movement disorder represents an
evolving process in neuronal plasticity and is due to
neuronal reorganization (27), possibly due to neu-
ronal sprouting (14). Delayed onset is longer in chil-
dren than in adults (28).
It has recently been stated that dystonic hemipa-
resis following severe head injury does not have a
specific neuroanatomical basis (19). By contrast,
we found focal lesions in all patients of this study
Movement Disorders, Vol. 7, No. 3, 1992
FIG. 2. Upper row: CT scans of
patient 6 before stereotactic oper-
ation. Left low-density lesion of
caudate, anterior internal capsule
and putamen corresponding to
supply of lateral lenticulostriate
branches of middle cerebral ar-
tery and small lesion of ventrolat-
era1 thalamus. On the right side
lesion of anterior putamen. Lower
row: Similar type of right-sided
low-density lesion in patient 2
(sides are reversed). Note the pel-
let placed stereotactically.
who presented with hemidystonia. As we proposed
earlier (29), MR-especially coronal slices-should
be applied to detect smaller lesions of the basal gan-
glia, especially of the putamen, when CT findings
are doubtful. Pathoanatomical correlations (as de-
termined by neuroradiological findings) in patients
with hemidystonia following head trauma are simi-
lar to those reported for secondary hemidystonia
due to other causes (15,16). Lesions of the caudate
and putamen, as well as thalamic, but presumably
not pallidal lesions may be responsible for dystonia
(15). In patients younger than 18 years at trauma
with hemidystonia later on, lesions of the contralat-
era1 caudate, putamen, or pallidum have been re-
ported (7,9,10,12,13,15). We found lesions of the
contralateral caudate andfor putamen in seven pa-
tients with hemidystonia, and an additional lesion in
the thalamus in one. It has been proposed (30) that
dystonia also may be produced by abnormal re-
sponses of descending inhibitory supraspinal path-
ways. This may account for the mild hemidystonia
of patient 7 of the present study, who had no lesion
of the basal ganglia, but of the contralateral mesen-
cephalic and pontine tegmentum.
The neuroanatomical basis for symptomatic tor-
ticollis following brain damage is not well known.
One patient reported previously had a putaminal
lesion detected by MR (6). In another patient,
 D YSTONIA FOLLOWING HEAD TRAUMA 269

A ley car at the age of 34 this patient developed right-

sided hemiathetosis. After his death at age 65, au-
topsy revealed a large cystic lesion extending from
the left Sylvian fissure to the partly destroyed cau-
date, putamen, and pallidum. Some authors feel
that the patients reported by Strich in 1956 may
have had dystonia (34), but according to the clinical
description they had postures as seen in decorticate
rigidity.
We suppose that pathophysiological mechanisms
leading to basal ganglia lesions in posttraumatic
B dystonia are more complex than assumed previ-
ously. Primary as well as secondary damage may be
of importance. Neuroradiological examinations in
the early posttraumatic phase only rarely have been
reported. They may show hypodense (7), hemor-
rhagic (6,7), or no (19) lesions of the basal ganglia.
It is remarkable that some of the basal ganglia
lesions in posttraumatic hemidystonia correspond
to vascular supply. Lesions in the present series
correlate most often to the supply of the anterior
C
(plus posterior) group of the lateral lenticulostriate
branches of the middle cerebral artery (35,36).
Stretch of branches by rotating forces may lead to

A B

FIG. 3. Axial and coronal SE 600117 MR images of patient 5

(hemidystonia). A Axial image through lower part of basal gan-
glia shows the posttraumatic pallidal defect extending to poste-
nor part of the putamen and the lesion after stereotactic surgery
in the subthalamic region. B,C: Coronal images show clearly
defined lesions of the posterobasal putamen.

brain stem auditory evoked potentials suggested a

pontomesencephalic damage (4). There is some ev- c D
idence that brainstem lesions may be associated
with torticollis. In animals, it has been produced
experimentally by pontomesencephalic lesions
(31,32). Patients with retrocollis suffering from pro-
gressive supranuclear palsy show only little putam-
inal changes, but extensive damage of pretectal and
tegmental areas (33). We propose that the lesion in
patient 7 may represent a clinicopathological corre-
lation for torticollis.
Apart from Thomas’ published in 1932, there FIG. 4. Axial and coronal SE 600/17 MR images of patient 7
(hemidystonia plus torticollis). A,B: Coronal images show the
are no reports on postmortem examinations in post- longish extension of the pontomesencephalic tegmental lesion.
traumatic dystonia (20). After being struck by a trol- Note persisting cavum Vergae. C,D: Axial images.

Movement Disorders, Vol. 7, No. 3, 1992

270 J . K . KRAUSS ET AL.
traumatic injuries (7). Lesions located posteriorly
cover the area of the anterior choroidal artery. Yet
not all lesions correspond to vascular supply.
It is conceivable that the basal ganglia had been
damaged also secondarily due to the ipsilateral
space-occupying lesions found in 4 patients of the
present study. It was proposed that brain swelling
may lead to compression of basal arteries to the
tentorium with secondary hypoxemia (37). But hyp-
oxia may also produce damage following topistic
patterns (38). This may be modified by an increase
in glutamate (39), which accumulates after head in-
jury (40). As selective vulnerability can show “stri-
atal types” of lesions (38,41), it may explain lesions
not corresponding to vascular territories.
Prognosis of posttraumatic dystonia is poor. An
atypical case with Meige-syndrome, retrocollis, and
bilateral athetosis showed remission under therapy
with carbamazepine (17). Spontaneous improve-
ment of torticollis was reported 3 days after onset
(7).
Medication in secondary dystonia often is inef-
fective (16,42). In posttraumatic dystonia limited
benefit with trihexyphenidyl ( 6 ) , carbamazepin (4)
and combined treatment with piribedil, dantrolene
and clonazepame (13) and with phenytoin and tri-
hexyphenidyl (18) has been reported. In pure post-
traumatic torticollis, botulinum A toxin may be the
therapy of first choice (26).
Two uncommon cases with relief of posttrau-
matic dystonia were reported. Alleviation of tor-
ticollis was achieved in a historical case resecting a
“right parietal cicatrix” (3,however, resulting in
postoperative hemiparesis. Hemidystonia due to a
subdural hematoma could be treated by evacuation
of the hematoma (21).
Stereotactic surgery has been reported to be ef-
fective in primary and secondary dystonia (22,43-
47). Patients with posttraumatic hemidystonia have
been mentioned, but not evaluated separately with
long-term follow-ups. In the series of Andrew et al.
(44) only three of 11 patients with secondary dysto-
nia could be followed up for more than I year.
Richardson (19) reported that nine of 12 patients
with a “significant dystonic element of hemiplegia”
improved after contralateral ventrolateral and/or
pulvinar cryothalamectomies; however, duration of
follow-up was not stated. Good results were also
reported in two single cases (8,9). But it has also
been stated that relief was only mild or transient
(16). One of the reasons explaining this discrepancy
might be the duration of follow-up. The patients of
Movement Disorders, Vol. 7, No. 3 , 1992
our study had a marked reduction of dystonia im-
mediately after the operation. However dystonia
worsened again later on. The improvement did not
correlate with the transient increase of hemiparesis
in four of the patients, nor with the choice of com-
bination of target points.
It remains unclear which patients with basal gan-
glia lesions will develop movement disorders. Jel-
linger (41) stated that unilateral vascular lesions to
the striatum only rarely may result in chorea or dys-
tonia. We did not find dystonia in contemporary
multipatient studies on traumatic hematomas in the
basal ganglia (48,49), acute tissue tear hemorrhages
frequently involving the basal ganglia (50), diffuse
axonal injury (51), on mild (52,53) or severe (54)
head injuries, on outcome and rehabilitation after
craniocerebral trauma in children (23 3 - 5 7 ) , nor in
a prospective 5-year follow-up study on head inju-
ries in children (58).
There may be various explanations for this: the
studies were conducted for other purposes, dysto-
nia could not be differentiated clearly from spastic-
ity, because of the long delay of onset the move-
ment disorder was missed at follow-up, it was not
seen in the etiological context or posttraumatic dys-
tonia indeed is very rare. As all descriptions of post-
traumatic dystonia so far derive from retrospective
data, no figures on the incidence of this movement
disorder can be given. We believe that awareness of
its occurrence will lead to its being diagnosed more
often.
Predisposing factors for hemidystonia in the
present series were young age at trauma, coupled
with structural lesions of the contralateral striatum
or pontomesencephalic tegmentum, initially severe
hemiparesis with remission over a longer period and
contralateral cerebral hemiatrophy. Yet only a pro-
spective study focusing on the subject may outline
additional prerequisites for the development of
posttraumatic dystonia.
Acknowledgment: We wish to thank H. Forster, G. HIS-
ter, G . Benz, K. Roskamm, and V . Sonntag-O’Brien for
technical assistance and preparation of the manuscript,
and the patients and their families for cooperating in this
study.
LEGENDS TO VIDEOTAPE’
Segment 1: This segment, recorded in April 1981,
shows patient 3 some days prior to the stereotactic
The sequences originally were recorded on a movie-camera.
 DYSTONIA FOLLOWING HEAD TRAUMA
operation. At the age of 6 years, he sustained a
severe head injury. Initially, he had a right-sided
hemiplegia. During recovery, 3 months after the
head trauma, hemidystonia developed while the
hemiplegia improved. The dystonia is increased on
action. While walking the arm is hyperextended and
held backwards.
Segment 2: One week postoperatively, there is
marked improvement of the hemidystonia, concern-
ing the spontaneous appearance as well as the in-
duction by action. There is a slight increase of the
mild preoperative hemiparesis. While walking the
hyperextension of the arm is not present anymore.
Segment 3: This segment shows the patient on the
last follow-up examination in June, 1990, at the age
of 30. There is still some improvement of the
hemidystonia. This is obvious particularly at rest
and while extending the arm. While concentrating
and on action the dystonia is pronounced again. Af-
ter clenching the fist volitionally it is quite hard for
the patient to open it. But on the whole dystonia is
still slightly improved compared to preoperatively.
The arm becomes hyperextended, when the patient
is walking in place.
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