Neurol Med Chir (Tokyo) 41, 306¿312, 2001

Delayed, Transient Neurological Deterioration
After Mild Head Injury
—Case Report—
Eiichirou URASAKI, Hideoki YASUKOUCHI, Akira YOKOTA,
and Yoshihiro ARAGAKI*
Department of Neurosurgery, University of Occupational and Environmental Health,
Kitakyushu, Fukuoka; *Aragaki Neurosurgical Hospital, Kitakyushu, Fukuoka

Abstract
A 16-year-old boy presented with delayed, transient neurological deterioration 18 days after mild head
injury. Left hemiparesis and left homonymous hemianopsia appeared after right frontal contusional
and mild subdural hematomas subsided. Neuroimaging examinations including cerebral angiography,
magnetic resonance imaging, and single photon emission computed tomography showed vasodilation
and hyperemia in the right cerebral hemisphere. The present case is not typical of acute ``juvenile head
trauma syndrome,'' but may represent a possible pathophysiology of the delayed type of transient neurological deterioration after mild head injury.
Key words: mild head injury,
hyperemia, status epilepticus

neurological deterioration,

Introduction

with subdural and contusional hematomas, and
hemispheric hyperemia.

Delayed, transient neurological deterioration
characterized by headache, vomiting, clouded
consciousness, hemiparesis, cortical blindness, or
seizures occasionally occurs after mild head injury
in children and adolescents. This syndrome has
been called ``juvenile head trauma syndrome''
(JHTS).7,8,25,27,29) Almost all of the symptoms characteristically appear within 48 hours, usually within
several hours, after craniofacial injury.7,8,25,27,29)
JHTS has recently been classified into acute and
delayed types on the basis of whether symptoms appear before or after 48 hours.27) However, any difference in the pathophysiologies for these types has not
been identified.
Traumatic subdural hematoma sometimes causes
delayed neurological deterioration more than 10
days after head injury.1,24) The underlying condition
is suspected to be cerebral edema or swelling due to
disturbed cortical venous return.1,24) We describe an
interesting case of delayed and transient neurological deterioration after mild head injury associated
Received
2001

September 7, 2000;

Accepted

juvenile head trauma syndrome,

Case Report
A 16-year-old boy, with no past personal or family
history of epilepsy or migraine, struck the occipital
area of his head on the ground after falling from a
2 m high wall while playing on a school ground (day
0). He did not lose consciousness but was admitted
to a nearby hospital 3 hours after the accident because of continuous headache. Neurological examination found no abnormalities except for headache,
and his score on the Glasgow Coma Scale (GCS) was
the full 15 points. Skull radiography showed no fracture, but computed tomography (CT) detected an
equivocal acute subdural hematoma in the right
frontal lobe. The severity of the headache increased
on the following evening, and he suffered nausea
and vomiting. He was transferred to our department
on day 3.
On admission, headache and nausea were the only
positive neurological symptoms, and his GCS score
again was 15. CT showed a right acute subdural
hematoma, 5-mm thick, and a contusional hematoma in the right frontal base accompanied by mild

April 4,

306

Neurological Deterioration After Mild Head Injury
midline shift. Conservative therapy using glycerol,
an antiemetic, and an analgesic was given, and his
symptoms gradually subsided. Electroencephalography (EEG) on day 6 showed only mild, lazy activities in the right anterior and middle temporal regions (Fig. 1). Follow-up CT (day 12) showed that
the subdural and contusional hematomas had almost disappeared, and hospital discharge was planned. His headache sometimes recurred, but was
well controlled by oral administration of an analgesic.
He complained of progressive weakness in the left

Fig. 1

Electroencephalograms recorded on days 6,
23, 32, and 128 (upper row) after head injury
and on day 20 (lower row) when right
hemiparesis
and
right
homonymous
hemianopsia appeared. Delta waves on day
20 and alpha wave suppression on days 23
and 32 are present predominantly in the
right cerebral hemisphere. No spikes or
sharp wave activities were recorded.

Neurol Med Chir (Tokyo) 41, June, 2001

307

upper extremity on day 18, with positive Barr áe's
sign (4/5). CT showed a post-contusional low density
area in the right frontal base, slight right subdural
fluid collection, and midline shift. Left hemiparesis
including the face (upper 3/5, lower 4/5, face 4/5)
became objectively apparent on days 19 and 20.
Dysesthesia of the left extremities and left homonymous hemianopsia were also present. Angiography
on day 19 showed vasodilation of the M3 portion and
the peripheral branches of the middle cerebral artery on the right as compared with the left (Fig. 2A,
B), and vertebral angiography showed dilation of the
right posterior cerebral artery trunk and right
posterior temporal branch (Fig. 2C). No vasospasm
was detected in the proximal or distal portions of the
cerebral arteries. The capillary and venous phases

Fig. 2

Left (A) and right (B) carotid angiograms
showing relative vasodilation of the M3 portion and peripheral branches in the territory
of the right middle cerebral artery. Vertebral
angiograms (C) showing vasodilation of the
right posterior cerebral artery trunk and
right posterior temporal branch.

E. Urasaki et al.

308

showed a slight increase in capillary brush and
slight dilation of the cortical veins in the right
cerebral hemisphere, but the cerebral circulation
time was almost equal for both hemispheres (not
shown). Magnetic resonance (MR) imaging on day
19 showed high intensity, thick cortical ribbons
along the gray matter of the right cerebral
hemisphere on the T2-weighted image (Fig. 3A),
which appeared iso-intense on the T1-weighted image. Many flow voids were present in the gray matter. These findings were compatible with vasodilation and cortical hyperemia. Hyperemia in the right
cerebral convexity was confirmed on day 20 by
single photon emission computed tomography
(SPECT) with technetium-99m-ethyl-cysteinatedimer (Fig. 3B). EEG findings on day 20 showed
diffuse delta activities, predominantly in the right
cerebral hemisphere (Fig. 1), but no spikes or sharp
waves were detected. A generalized convulsive seizure occurred on day 21. Oral administration of val-

Fig. 3

proic acid at 800 mg/day was started after this seizure and was discontinued at discharge (day 33).
Transient neurological deterioration continued for a
week. The neurological symptoms gradually subsided and disappeared on day 25. EEG on days 23 and
32 showed that the delta wave had disappeared but
that the alpha wave was still suppressed in the right
centro-parieto-occipital and temporal regions
(Fig. 1). Follow-up MR imaging showed residual
hyperintense cortical ribbons in the right
hemisphere on day 37, and normality on day 91 after
injury (Fig. 4). The EEG on day 128 was normal
(Fig. 1).

Discussion
Prolonged ictal paralysis and cortical blindness are
occasional forms of nonconvulsive simple partial
seizure.2,3,16,28,32,33) The convulsive seizure that occurred 2 days after the onset of symptoms, and the

T2-weighted magnetic resonance images on day 19 (A) showing a flow void and hyperemia in
the right cerebral hemisphere. Single photon emission computed tomography images (B)
showing apparent hyperemia in the right cerebral hemisphere.

Neurol Med Chir (Tokyo) 41, June, 2001

Neurological Deterioration After Mild Head Injury

Fig. 4

309

Follow-up magnetic resonance images on days 37 (A) and 91 (B) showing gradual normalization of hyperemia in the right cerebral hemisphere.

post-traumatic clinical course together with the neuroimaging findings required us to exclude the diagnosis of status epilepticus of the nonconvulsive type.
Cerebral angiography has detected vascular
hyperemia, capillary brush, and early draining veins
in patients with status epilepticus,17,21,34) which are
compatible with the increased blood flow in SPECT
that is generally seen in status epilepticus.11,16,32)
Neuroimaging signs of transient abnormalities in
patients with status epilepticus characteristically involve a focal area either in the white matter or in the
combined white and gray matter, appearing as low
density areas by CT, and as decreased signal intensity on T1-weighted images and/or increased signal
intensity on T2-weighted ones by MR imaging,
without a mass effect.9,13,31) Such changes are
thought to be due to vasogenic edema induced by
hyperemia. Increased oxygen consumption in the
cortical epileptogenic zone and the resulting hypoxia are assumed to lead to an accumulation of CO2
and lactic acid, which in turn causes vasodilation,
loss of autoregulation, and increased cerebral blood

Neurol Med Chir (Tokyo) 41, June, 2001

flow.13,17)
Such neuroradiological findings mentioned above
were similar to those of the present case, but no EEG
findings to support the diagnosis of epilepsy were
obtained. EEG findings of status epilepticus may be
normal when the epileptic focus is small11) or deep in
the brain structure. However, the diffuse slow waves
in the entire unilateral hemisphere found in our case
without epileptic discharges tended to exclude status epilepticus.
Vasospasm was not the direct cause of delayed
neurological deterioration in our patient, although
hypoperfusion, hyperemia, and vasospasm are well
known factors in neurological deterioration after
head injury.5,12,18–20,22,23,26,30) Complete neuroimaging
examinations including CT and MR imaging,
cerebral angiography, and SPECT during the period
of neurological deterioration found no traces of
vasospasm.
The time course in this case is unique because,
except for occasional headache, the neurological
symptoms appeared after a far longer interval than

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E. Urasaki et al.

in previously reported cases of JHTS in which the
delay between head injury and the onset of the neurological episodes varied from several seconds,
minutes, and hours up to 2 days,7,8,25,27,29) and the
episodes lasted from several minutes to several days.
Presumably, the majority of the acute type of JHTS,
especially those at intervals of several seconds or
minutes, involve electrical and/or neuronal
reflex phenomena such as cortical spreading
depression25,29) or a trigeminovascular response, because these phenomena appear immediately after
the input of stimuli.7,27) Our case cannot be classified
as the acute type of JHTS.
Vasoconstriction and hypoperfusion may be
causes of neurological deterioration, as partial
peripheral arterial obliterations were found in two
cases of JHTS by cerebral angiography performed
on the 7th and 2nd days after onset of the hemiparesis.8) Cerebral angiography found no abnormalities
in six of 37 patients with JHTS.25) In contrast, investigation of migraine suggested that vasodilation and
hyperemia are the underlying causes of JHTS, but
there was no radiological evidence.27) The present
case did not fit the profile of typical acute JHTS, but
our findings suggest that vasodilation and hyperemia are the baseline conditions for some cases of
delayed neurological deterioration after mild head
injury.
CT showed mild subdural and contusional hematomas in our patient, but no abnormalities in most
reported cases of JHTS.6,7,25,29) CT found no pathological abnormalities in nine of 12 cases of JHTS.27)
Exceptional CT findings in one case with diffuse
cerebral swelling and in another with hemispheric
swelling after mild head injury were considered to
reflect vasodilation and not edema.29) JHTS probably
includes a variety of pathological states.29)
Subdural hematoma is sometimes associated with
delayed neurological deterioration 10 or more days
after head injury.1,24) Cerebral hemispheric swelling
and ischemia due to disturbed cortical venous flow
may be the causes of this neurological
deterioration.1) Cerebral angiography in our patient
showed no such abnormal findings of the cerebral
venous system when the neurological deterioration
occurred. SPECT showed decreased cerebral blood
flow in a patient with subacute subdural
hematoma.1) Our patient suffered subacute neurological deterioration similar to these subdural hematoma cases,1,24) but harbored different pathological
conditions, such as vasodilation and hyperemia.
Disturbed cerebral autoregulation after mild head
injury was recently found in 28% of patients with
GCS 13–15, who had poor or absent functioning of
cerebral autoregulation.10) This finding suggests that

hyperemia is involved in mild head injury, although
the majority of patients regain normal autoregulation.7,8,25,27,29)
Post-traumatic hyperemia can be divided into
malignant and benign types depending on the association with intracranial hypertension.4,12–15,19,23,26,27)
Analysis of intracranial pressure and cerebral
blood flow in 59 patients with moderate or severe
head injuries showed that the median duration of
hyperemia associated with intracranial hypertension was longer (median 6 days, range 1–14 days)
than that of hyperemia without intracranial hypertension (median 2.5 days, range 0–5 days).12) Our
findings indicate that certain cases of mild head injury may represent a more delayed or prolonged
hyperemia phase linked to a favorable outcome.
Hyperemia also frequently occurs focally or
globally in the unilateral hemisphere, when cortical
contusion and laceration or subdural hematoma are
present, respectively.18,26) Hyperemia in our case
was interpreted as the benign hemispheric type induced by metabolic recovery from the damage done
by the mild contusional and subdural hematomas.
The benign type of hyperemia is considered to be
secondarily induced by metabolic demands on the
release of metabolic mediators during reestablishment of membrane ionic homeostasis after head injury.12,26)
Delayed neurological deterioration after mild
head injury involves a variety of pathological causes
from early neuronal reflex phenomena to late
cerebral edema due to hyperemia or ischemia. The
baseline condition may be disturbed autoregulation
of cerebral vasoreactivity. The present case can be
classified as the delayed type of JHTS, or subacute
subdural hematoma, in which neurological deterioration is caused by hyperemia as a result of ``overregulation'' during the recovery from head injury.
Immature autoregulation may be a factor in such
delayed neurological deterioration after head trauma.

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Address reprint requests to: E. Urasaki, M.D., Department
of Neurosurgery, University of Occupational and Environmental Health, 1–1 Iseigaoka, Yahata Nishi–ku,
Kitakyushu, Fukuoka 807–8555, Japan.

Neurol Med Chir (Tokyo) 41, June, 2001