J Neurosurg 72:813-815, 1990

Delayed traumatic intracerebral hematomas: "Sp/itApoplexie"
Report of two cases
HENRY ELSNER, M.D., DANIELE RIGAMONTI, M.D., GREGORY CORRADINO, M.D.,
ROBERT S C H L E G E L ~ JR., M.D., AND JOHN JOSLYN, M.D.

Divisions of Neurological Surgery and Neuroradiology, University of Maryland Medical System,
Baltimore, Maryland
~" Two patients who suffered a head trauma experienced sudden clinical deterioration more than 1 week after
their injury. The initial computerized tomography (CT) scan demonstrated a small hematoma underlying a
depressed skull fracture in one patient and a small interhemispheric subdural hematoma in the other. Both
patients had made a complete recovery and follow-up CT scans were normal when clinical deterioration
suddenly occurred. Both patients developed a large intracerebral hematoma and underwent emergency
evacuation of the mass. The first patient recovered with the exception of a moderate hemiparesis and dysphasia,
but the second patient died.
Delayed traumatic intracerebral hematomas have been described in the literature. Since the advent of CT
scanning, the incidence of this phenomenon has been estimated as between 1.7% and 7.4% of closed head
injuries. In 1891, Otto Bollinger described four patients who suffered head injury, followed days to weeks later
by death from an apoplectic event. His criteria for diagnosis of "traumatische Sp~it-Apoplexie" included the
absence of preexisting vascular disease, a definite history of trauma, an asymptomatic interval of at least
several days, and an apoplectic episode. These two cases reemphasize the existence of Sp~it-Apoplexie as a rare
clinical condition. In the presence of CT findings of even small traumatic intracerebral or extracerebral
hematomas, the possibility of this late complication should be kept in mind.

KEY WORDS

"

Sp~it-Apoplexie

S

INCE the development o f computerized tomograplay (CT), the occurrence o f delayed traumatic
intracerebral h e m a t o m a has been well documented. Many of these hematomas occur in a subacute
fashion 24 to 48 hours after the initial trauma. "Sp~itApoplexie" was described in 1891 by Otto Bollinger. 2
He reported four cases of delayed traumatic intracerebral and intraventricular hematomas which occurred
2 to 4 weeks after mild head injury and resulted in
death. In each case, the patients were recovering well
and experienced a sudden apoplectic episode followed
by death, hence the term "spat" (or late) apoplexy.
At the University of Maryland Hospital and the
Maryland Institute for Emergency Medical Services
System (MIEMSS) approximately 800 patients are evaluated by the Neurosurgery Service for closed head
injury each year. Approximately 150 of these patients
have a CT finding of intracranial pathology. In the past

J. Neurosurg. / Volume 72~May, 1990

9 delayed traumatic hematoma

9 hematoma

year, two patients experienced apoplectic events while
recovering from head injury, a p h e n o m e n o n consistent
with Bollinger's initial description o f "Sp/it-Apoplexie. "2 A review o f the clinical course of these two
patients as well as an appraisal of the pertinent literature
on this entity form the subject of this report.

Case Reports

Case 1
This 29-year-old m a n suffered a left frontal depressed
skull fracture with underlying cerebral contusion after
being struck in the head with a blunt object. On admission he was awake and alert but aphasic. He had no
m o t o r deficit. He underwent operative elevation o f the
fracture and closure of the dural laceration. Follow-up
CT scans confirmed the presence o f the small contusion
underlying the craniectomy area. Ten days after the
813

H. Elsner, et at.
event he was found in his r o o m unresponsive. An
emergency C T scan demonstrated a large intracerebral
h e m a t o m a in the area of the previously noted contusion. Preoperative studies ruled out the presence of
coagulopathy and he underwent emergency evacuation
o f the h e m a t o m a via a left frontotemporal craniotomy.
At discharge, a fair recovery characterized by the return
o f some m o t o r power had already begun. The aphasia
remained dense.
Case 2
This 15-year-old girl had been involved in a motorvehicle accident. At the time o f admission, she was
combative but did not show any evidence of focal
deficit; CT scanning (Fig. 1 left) demonstrated an interhemispheric subdural hematoma. Angiography several
days later demonstrated no vascular lesion. She was
treated conservatively and made a complete recovery.
On the 14th day after injury, the day of her planned
discharge from the hospital, she experienced a seizure
and rapidly lapsed into a coma with extensor posturing
and a unilateral fixed and dilated pupil; CT scanning
(Fig. 1 right) demonstrated the presence o f bilateral
intracerebral and intraventricular hemorrhage. Coagulation studies were within normal limits. The patient underwent craniotomy and evacuation of the hematoma
but developed severe diffuse brain edema. She never
regained neurological function and died 2 days later.
Discussion
The four cases o f death after a delayed apoplectiform
episode following head trauma described by Bollinger 2 met the following criteria: 1) a definite history of
trauma; 2) an asymptomatic interval; 3) an apoplectic
event; and 4) absence of vascular disease. Based on
experimental data previously gathered by Duret, 6 Bollinger suggested that cranial trauma caused softening
of the brain involving the wall o f an artery with eventual rupture of the vessel, necrosis, and hemorrhage.

Scheinker 15 suggested the role o f posttraumatic vasoparalysis as an alternative initial factor in the genesis
of the hematoma. 8 Vasoparalysis accompanied by dilatation of the capillaries with accumulation of toxic
metabolites would precipitate an increase in capillary
permeability, perivascular edema, and hemorrhage.
Coalescence o f multiple areas of diapedetic hemorrhage would create large traumatic intracerebral hematomas? ~ After the original description, m a n y authors
reported several cases meeting Bollinger's criteria. 4'5~~'~2
This subject was reviewed in 1970 by Morin and
Pitts. ~ They included a review of patients with an
apoplectic episode occurring after an asymptomatic period of less than 120 days. In total, they collected 24
cases from the literature and added three of their own.
This review pointed out the following facts: 1) severity
of the injury was in most cases minor, usually without
fracture and with only a brief period of unconsciousness; 2) the asymptomatic interval was usually less than
30 days; 3) "Sp/it-Apoplexie" seemed to affect predominantly younger people in whom arteriosclerotic disease
did not appear to be a factor, although a few cases
occurred after the fourth decade; 4) sudden hemiplegia
(an u n c o m m o n presentation in the young age group)
appeared to be the prominent presentation in these
patients; and 5) pathologically, the posttraumatic intracerebral hematoma most commonly affected structures
other than the basal ganglia, as was demonstrated by
Courville and Blomquist? Morin and Pitts also stressed
the need to differentiate delayed posttraumatic hematomas from those due to the unrecognized presence of
a vascular malformation or tumor.
Challenging the previous authors, Baratham and Dennyson ~maintained that Bollinger's original description 2
was unsatisfactory because apoplexy is a term of dubious validity, not denoting a specific pathological entity.
They questioned the relevance of trauma when the lucid
interval is prolonged, inferring that it may have been
purely fortuitous. They also explained the relatively
high incidence o f "Sp/it-Apoplexie" in the young by

FIG. 1. Case 2. Left Pair." Nonenhanced computerized tomography (CT) scans obtained on admission
showing an interhemispheric subdural hematoma. Right Pair: Nonenhanced CT scans obtained on the 14th
day after injury showing bilateral intracerebral hemorrhage.
814

J. Neurosurg. / Volume 7 2 / M a y , 1990

Delayed traumatic intracerebral hematomas: "Sp/it-Apoplexie"
stating that this group is m o r e prone to injury than
elderly patients. However, 14 of their 21 patients in
thct had an asymptomatic interval of less than 48 hours
and the majority of patients were in the seventh decade,
a group quite different from Bollinger's cases.
Since CT has been available, the m a n a g e m e n t of
head t r a u m a patients and the understanding of the
pathology o f head injuries have been greatly improved
by the recognition o f different types of posttraumatic
hematomas. F r o m a m o n g 656 cases, Diaz, et al., 4 presented nine patients with delayed h e m a t o m a s in whom
the interval from cranial injury to the development of
the h e m a t o m a varied from 8 hours to 13 days. However, all of their cases differed from Bollinger's classic
description 2 in that the patients who had initial negative
CT scans did not have an asymptomatic interval. The
25 cases described in 1984 by Ninchoji, et aL, ~3differed
from the classic traumatic "Sp/it-Apoplexie" syndrome
because they lacked a symptom-free interval and an
apoplectic episode. The patients who "talk and deteriorate" after severe closed head injury usually do so
within the first 48 hours ~4 and should not be included
in the category discussed here. Fukamachi, et al., 7 reviewed 84 cases and described four subtypes of posttraumatic intracerebral hematomas, none of which
matched the entity originally described by Bollinger.
We report two cases that seem to fall into the group
of true "Sp~it-Apoplexie" cases. Both patients were
young and had a definite a s y m p t o m a t i c interval. The
onset of their s y m p t o m s was precipitous, in fact apoplectic, and no coagulation abnormality was detected
(as has been noted in some delayed h e m a t o m a s reported
in the literature 9) or preexisting vascular abnormality
found. Their clinical course was characterized by complete neurological recovery and by resolution of the
initial lesion seen on CT prior to the development of
the apoplectic event, which occurred in both cases more
than a week after the original trauma.
M a n y years after its original description, we are still
at odds in trying to explain the pathogenesis of this
entity, but we believe that traumatic "Sp~it-Apoplexie"
should remain a clinical entity. Although we cannot
provide any clues to help neurosurgeons in detecting
these patients in advance, we r e c o m m e n d that the existence of this condition be kept in mind, especially in
view of its potential medicolegal implications.

J. Neurosurg. / V o l u m e 72 / M a y , 1990

References

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698-706, 1972
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457-470
3. Courville CB, Blomquist OA: Traumatic intracerebral
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15. Scheinker M: Cited in Reference 7
Manuscript received August 9, 1989.

Address reprint requests to." Daniele Rigamonti, M.D.,

Division of Neurosurgery, University of Maryland Hospital,
22 South Greene Street, Baltimore, Maryland 21201.

81 B