J Neurol (1991) 238:420-426

Journal of

Neurology
© Springer-Verlag 1991

Cervical intramedullary cavernous angioma
with MRl-proven haemorrhages
H. M. Mehdorn and D. Stolkc
Neurochirurgische Universit~tsklinik, Weimarer Strasse 8, W-2300 Kiel 1, Federal Republic of Germany
Received September 6, 1990 / Received in revised form November 28, 1990 / Accepted January 21, 1991

Summary. T w o c o n t r a s t i n g cases of cervical i n t r a m e d u l lary c a v e r n o u s a n g i o m a in y o u n g f e m a l e p a t i e n t s a r e rep o r t e d . O n e p a t i e n t h a d a 3 - y e a r course of step-wise p r o gressive t e t r a p a r e s i s ; at e a c h o f the five e v e n t s i n t r a m e d u l l a r y b l e e d i n g f r o m a c r y p t i c v a s c u l a r m a l f o r m a t i o n at
C6-7 level was d i a g n o s e d b y M R I . T h e o t h e r p a t i e n t p r e s e n t e d with o n e e p i s o d e w h i c h l e d to M R I diagnosis o f a
v a s c u l a r m a l f o r m a t i o n at the C2 level. B o t h p a t i e n t s
e v e n t u a l l y u n d e r w e n t c o m p l e t e surgical excision of the
a n g i o m a with s u b s e q u e n t s t e a d y i m p r o v e m e n t of the
n e u r o l o g i c a l deficit.
Key words: S p i n a l c a v e r n o m a - M a g n e t i c r e s o n a n c e imaging - A r t e r i o v e n o u s m a l f o r m a t i o n

Introduction
In 1912, surgical r e m o v a l of an i n t r a m e d u l l a r y spinal
c a v e r n o u s a n g i o m a b y G a r r 6 [30] f o l l o w e d by i m p r o v e m e n t of t h e p a t i e n t ' s B r o w n - S 6 q u a r d s y n d r o m e was rep o r t e d . Until 1985, only an additional 11 surgically t r e a t e d
cases w e r e r e p o r t e d [3, 4, 9, 11, 13, 22, 29, 30, 33] in the
l i t e r a t u r e (see T a b l e 1). H o w e v e r , since 1986, 20 f u r t h e r
cases h a v e b e e n r e p o r t e d , i n d i c a t i n g that spinal cavernomas occur more frequently than previously thought
[2, 5, 19, 24, 27, 28, 3 4 - 3 8 , 41]. W e r e p o r t two a d d i t i o n a l
p a t i e n t s w h o h a d i n t r a s p i n a l c a v e r n o u s a n g i o m a s diagn o s e d a f t e r t h e y b e c a m e s y m p t o m a t i c with e p i s o d e s of
i n t r a m e d u l l a r y b l e e d i n g s . T h e c o n t r a s t in the d i a g n o s t i c
a n d t h e r a p e u t i c m a n a g e m e n t o f the two p a t i e n t s p r o m p t e d this r e p o r t . O n e p a t i e n t h a d s u f f e r e d five h a e m o r r h a g e s , p r o v e n by m a g n e t i c r e s o n a n c e i m a g i n g ( M R I )
( a n d this m a y r e p r e s e n t the n a t u r a l h i s t o r y of t h e dise a s e ) , b e f o r e she was r e f e r r e d to us for t h e r a p y , while
t h e o t h e r o n e was t r a n s f e r r e d for t h e r a p y after the first
bleeding episode.
Offprint requests to." H. M. Mehdorn

Case reports
Case l

At the time of first bleed in July 1987, this female patient was aged
29 years; she suffered an acute onset of pain in the right arm extending along the C7 dermatome; after a few days, she noticed
spasticity in the digits IV and V of her right hand, and was unsuccessfully treated by an orthopaedist, subsequently referred to a
neurologist and underwent MRI. The first MRI (Fig. la), performed 2 weeks after the acute onset of symptoms, showed a small, anteriorly located intense signal lesion surrounded by a low-intensity
rim, at the level of C6-7, and additionally a low intensity line just
below the lesion; angiography was normal, so the diagnosis of cryptic arteriovenous malformation, possibly a cavernous angioma, was
made. A repeat MRI study (Fig. Ib), performed 3 months after the
initial bleeding and after her symptoms had completely resolved,
showed a low-intensity lesion at the site of the previous haemorrhage, partially surrounded by an iso-intense lesion, indicating that
the haemorrhage had resolved (leaving haemosiderin and/or vessels) and that the cavernoma itself was revealed. However, 1 year
after the first haemorrhage (October 1988), she developed the
same symptoms as described above, and underwent repeat of MRI
(Fig. lc). Again, the high-intensity lesion was present, at the site of
the previous low-intensity area, suggestive of another haemorrhage. At this time, the mass effect of the lesion was less obvious
than on the first MRI scan: the subarachnoid space anterior and
posterior to the spinal cord was still present, shown well on the
axial slice, which also shows the location of the haemorrhage.
Again, the symptoms resolved completely. In 1989, when another
episode of haemorrhage had occurred, she complained of increase
of her pain (in the C7 distribution), but also noted some difficulty
in her gait suggestive of disturbed proprioceptive sensation. At this
time, the Tl-weighted image (Fig. ld) showed a high-intensity signal through the entire sagittal diameter of the spinal cord, and the
nearly iso-intense lesion seemed to be pushed backwards from its
previous position. Application of gadolinium-DTPA did not yield
any additional information. Spinal angiography was performed to
exclude any other vascular disease of the spinal canal and was
negative. In May 1990, she experienced progressive, step-wise
worsening of gait after acute onset of pain to the point that she became unable to walk; also, progressive weakness of her left and to
a lesser degree of her right hand became evident. MRI performed
after this episode showed, on T2-weighted images, mixed signal intensities in the core of the lesion surrounded by the tow-intensity
rim, and again this lesion was seen nearly through the entire sagit-

421

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422

Fig. la-h. Case 1. a Initial MRI after
spinal cord haemorrhage, July 1987. b
MRI 3 mouths after the initial haemorrhage, patient at this time neurologically
intact (TR SE 1000/TE 30). c Recurrent
haemorrhage, October 1988 (300/30). d
Recurrent haemorrhage, October 1989,
incomplete improvement (477/30). e, f
Recurrent haemorrhage, May 1990, incomplete improvement (2800/80). g, h
Recurrent haemorrhage, July 1990

423

Fig. 2a-c. Case 2. MRI performed
15 h after the initial clinical
manifestation of the bleeding.
a Sagittal Tl-weighted image shows
the typical mixed appearance of
the cavernoma with haemorrhage
in the dorsal part of the spinal cord
at C2; aedema extends upwards to
the pons as well as downward for
one segment, h Sagittal T2weighted multi-echo/gradient echo
image, e Horizontal image through
the maximum extension of the
cavernoma

tasl diameter of the spinal cord (Fig. le, f). The patient's neurological deficit remained unchanged (minor paresis of flexion and extension of her left fingers, increase other leg jerks, hypaesthesia in
the dermatome C8 left).
Two months later, another episode of intramedullary bleeding
occurred. This time, the motor deficit progressed, and a dissociated sensory deficit below D6 in the right and D12 in the left lower
extremities developed. While on dexamethasone, she developed
spastic-atactic gait to the point that she was not able to walk on her
own, and had urinary incontinence. This time, MRI (Fig. lg, h)
showed a major haemorrhage in her cervical medulla extending
over the major part of the coronal diameter and, in the sagittal
projection, nearly completely in the left part of the medulla. At
this time, the patient agreed to surgery, and she was referred to
our department. At surgery, laminotomy from C4 to D1 was performed; under the microscope, the dura was opened longitudinally, and the arachnoid membrane was dissected. Between the exit
of the left dorsal roots of C7-8, a red-yellowish mass appeared
under the pial layer. Bipolar coagulation and incision led to the
intramedullary cavity of haemorrhages of various age which was
evacuated, and a mulberry-shaped tumour of about 1 cm length
was removed. Histological examination confirmed the MRI diagnosis of cavernous angioma. Her postoperative course was uneventful; her neurological deficit slowly improved over the ensuing
4 months.

Case 2
This 35-year-old female suffered from acute onset of radicular pain
in the neck, increasing over the day and followed by nausea and
vomiting, as well as a tingling sensation in the right arm and leg.
Upon admission in an other hospital, she had only a slight rightsided hemiparesis; her cranial nerves were normal. Lumbar puncture revealed no abnormality. Cranial computed tomography was
normal. A few hours after admission, she developed right-sided
hemiparesis and paraesthesias as well a weakness in her left hand.
Sensory deficit was below DI on the right and D3 on the left.
There was urinary incontinence. MRI (Fig. 2a-c) showed a lesion
suggestive of a cavernous angioma at the level of C2 with recent
haemorrhage; an intramedullary area of decreased signal intensity
in Tl-weighted image extended up to the pons suggestive of haemosiderin deposits. It should be noted that she had never presented
with any clinical episode suggestive of previous haemorrhage.
After a few days on dexamethasone, a cavernoma was removed
in a fashion similarly to the one described above. The postoperative neurological status showed steady improvement to the point

that she became able to walk with help, 2 weeks after surgery, and
became essentially neurologically normal within 4-months.

Discussion
Incidence
T h e true i n c i d e n c e o f spinal c a v e r n o u s a n g i o m a s is unk n o w n . A s can b e s e e n in T a b l e 1, t h e n u m b e r of r e p o r t ed surgical series since t h e first surgical t r e a t m e n t in
1912 until 1985 is v e r y s m a l l , in a d d i t i o n to a few a u t o p s y
r e p o r t s of p a r t i a l l y a n t e m o r t e m u n d i a g n o s e d d i s e a s e
[10, 16, 19, 32, 38]. K r a y e n b ~ h l a n d Y a s a r g i l [14] r e p o r t ed o n l y a single c a v e r n o m a in a series o f 568 spinal tum o u r s s e e n o v e r a p e r i o d o f 25 y e a r s , r e p r e s e n t i n g 4 . 3 %
of t h e i r i n t r a d u r a l a n g i o m a s . P i a a n d D j i n d i j i a n [22] rep o r t e d 2 spinal c a v e r n o m a s ( 3 % o f t h e i r spinal i n t r a dural arteriovenous malformations). McCormick and
N o f z i n g e r [18] d e s c r i b e d 1 cervical c a v e r n o m a in an
a u t o p s y series o f 48 " c r y p t i c " v a s c u l a r m a l f o r m a t i o n s ;
r e v i e w i n g t h e l i t e r a t u r e , t h e y f o u n d 18 s p i n a l " c r y p t i c "
v a s c u l a r m a l f o r m a t i o n s a m o n g 308 l o c a t e d in t h e c e n t r a l
n e r v o u s s y s t e m , a n d a p p r o x i m a t e l y 31% o f t h e i n t r a c r a nial " c r y p t i c " v a s c u l a r m a l f o r m a t i o n s w e r e c a v e r n o m a s
[17]. R e c e n t l y , a r e p o r t f r o m t h e N e w Y o r k N e u r o l o g i cal I n s t i t u t e [19] s t a t e d t h a t spinal c a v e r n o m a s r e p r e s e n t e d 5 . 1 % of the i n t r a m e d u l l a r y t u m o u r s t r e a t e d at this ins t i t u t i o n b e t w e e n 1980 a n d 1987. O w i n g to r e f i n e m e n t of
d i a g n o s t i c p r o c e d u r e s , p a r t i c u l a r l y to t h e a p p l i c a t i o n o f
M R I to diseases of the spinal cord, intraspinal c a v e r n o m a s
a r e d i a g n o s e d n o w with i n c r e a s i n g f r e q u e n c y , so t h a t a
re-appraisal of diagnostic steps and therapeutic options
should be considered.

Clinical presentation
T h e n a t u r a l history of central n e r v o u s system c a v e r n o m a s
with r e g a r d to t h e f r e q u e n c y of clinically d i s t i n g u i s h a b l e
h a e m o r r h a g e has b e e n u n c e r t a i n , a l t h o u g h e s s e n t i a l l y all
h i s t o l o g i c a l l y e x a m i n e d cases s h o w e d e v i d e n c e o f h a e -

424
morrhage [31]. Spinal cavernomas present clinically in
the way already described by Schultze [30] in 1912; painful attacks may be followed by neurological deficits, frequently in the way of Brown-Sdquard paresis [2, 5, 19,
30]; as in our own case 1). The neurological deficit may
resolve at least partially while under corticosteroids.
Step-wise progression of conservatively treated disease
may lead to paraparesis and sensory deficits with or without bladder/bowl dysfunction. The clinical course of spinal cavernomas resembles, frequently, that of multiple
sclerosis. This diagnosis has previously often been made
in these patients [19, 29] until a mass effect by enlarging
cavernomas led to myelographic appearance of the lesion [5, 9, 19]. The clinical differential diagnosis of this
slowly progressive disease further includes other vascular disease of the spinal canal such as Foix-Alajouanine's
disease [1, 7]. This clinical course may take from 1 week
to 25 years (most frequently 2 - 4 years) until the diagnosis is established. Occasionally, sudden onset of a massive deficit may lead to early diagnosis (our case 2). If
the cavernoma is located on the surface of the spinal
cord or the bleeding breaks through the pial layer, it may
present as subarachnoid haemorrhage [11, 34]; rarely, its
presentation is that of a spinal tumour causing hydrocephalus [24].
The summary of published cases shows a female preponderance (1.8:1) and a maximum age of onset of symptoms in the early twenties to thirties.

Diagnostic procedures
The first successfully operated case was diagnosed only
clinically [30]; over the next 70 years, myelography was
often misleadingly normal and usually only helpful [4, 5,
9, 19, 21] after several bleeding episodes had occurred leading to a mass effect of the cavernoma with its surrounding haematoma. MRI nowadays is the first diagnostic tool for suspected lesions of the spinal cord. The
MRI appearance of intracranial cavernous angiomas has
recently been well described [12, 15, 25, 27], and its
characteristics also apply to the cavernomas in the spinal
cord [2, 5]. On T2-weighted images, most frequently
mixed signal intensity lesions are seen with a reticulated
appearance and a prominent surrounding rim of decreased
signal intensity (see Figs. 1, 2). While this central portion is thought to reflect the presence of methaemoglobin, the surrounding low intensity rim represents haemosiderin deposits, indicating previous haemorrhages. T1weighted images are less sensitive for the detection of
cavernomas. Smaller lesions may appear only as signal
.hypointensity or mixed signal intensity (Fig. 1). However,
it should be r e m e m b e r e d that the MRI appearance of
cavernomas is non-specific and may also be present in
other types of cryptic vascular malformations of the central nervous system with histological evidence of previous haemorrhage and even in small haemorrhagic tumours. In the patients presented here, the diagnosis of
an intramedullary bleeding from a cryptic vascular malformation was clear, based on the MRI findings. Although
in case 1 the cavernoma itself which was removed at surgery had not increased in size when compared with the

lesion initially detected 3 years previously, the mass effect due to haematoma formation had remarkably increased; growth of cerebral cavernomas due to haematoma and capsule formation has been previously reported [23] and may also be responsible for the eventual detection by repeatedly performed myelography [4, 5, 9,
19, 21].
In case 2, MRI performed immediately following the
dramatic onset of tetraparesis showed the irregularly
shaped lesion at the level of C2, as well as the surrounding high-intensity signal extending up to the pons, suggestive of central haemosiderin deposits; this strongly
suggests previous silent haemorrhages.

Therapy
Most of the previously reported case have been characterized by a step-wise progression of the neurological deficit, and myelography performed after the initial events
frequently has been unable to show any lesion. This
meant that worsening of the neurological status had to
be followed without a means of intervening surgically.
However, our case 1 shows on MR1, for the first time, a
close correlation of the clinical progression of the neurological deficit and the expanding nature of the lesion,
due to recurrent haemorrhages. This case may serve as a
particularly impressive example to demonstrate the natural history of the disease, and it should help to clarify
the therapeutic options.
Conservative therapy was only of temporary benefit,
as in many reported cases, and was unable to stop the
progression of the neurological deficit. Only surgical removal of the cavernoma offers a way to stop progression
and to reduce the neurological deficit. Of the reported
31 cases, 17 were reported improved following removal
of the cavernoma, and 8 remained unchanged. Only 5
patients were reportedly permanently worse postoperatively, and 2 of them had undergone only incomplete removal of the lesion. Surgical removal of the cavernomas
was thought to be complete in both cases presented here,
because pathological vascular structures were clearly demarcated from surrounding spinal cord tissue by haemosiderin laden glial scar tissue. MRI scans were not performed in the early postoperative course and should be
considered for later follow-up studies in order to prove
the absence of abnormal vascular structures (suggestive
of residual vascular malformation) within the glial scar.
The usual approach to the spinal cord is posterior or
posterolateral laminotomy or laminectomy or hemilaminectomy. Laminotomy with re-insertion of the temporarily
removed posterior segments of the vertebral arches (important particularly in young patients to prevent late
sequelae of laminectomy) has been performed in both
cases presented here. While one might have questioned,
in the early phase of case 1, the possibility of complete
removal of an anteriorly located cavernoma, the anterior
approach to the spinal cord should also be considered
possible nowadays with the use of temporary spondylectomy and microsurgical techniques, similarly to microsurgical removal of cavernomas in other regions such as
the brain stem [6, 20, 40].

425

Final comments
M u l t i c e n t r i c i t y a n d familial o c c u r r e n c e of c a v e r n o m a s
have b e e n r e p o r t e d . I n 1 6 - 5 0 % of p a t i e n t s who b e c o m e
s y m p t o m a t i c b e c a u s e of i n t r a c r a n i a l c a v e r n o m a s , addit i o n a l c a v e r n o m a s of the c e n t r a l n e r v o u s system or elsew h e r e have b e e n d e t e c t e d [8, 12, 25, 39]. T h e familial
o c c u r r e n c e of c a v e r n o m a s a n d the familial association
with o t h e r vascular a b n o r m a l i t i e s also has b e e n n o t e d
u p o n several occasions [4, 2 5 - 2 7 , 29], a n d its true i m p o r t a n c e should b e c o m e clear with m o r e w i d e s p r e a d applic a t i o n of M R I diagnostics. T h e n , the q u e s t i o n will arise
w h e t h e r a s y m p t o m a t i c c a v e r n o m a s should be c o n s i d e r e d
for r e m o v a l .

Conclusion
A c u t e p a i n f u l spinal cord n e u r o l o g i c a l deficit, particularly in a y o u n g f e m a l e p a t i e n t , s h o u l d be suggestive of
i n t r a m e d u l l a r y h a e m o r r h a g e a n d be d i a g n o s e d i m m e d i ately by M R I . T h e typical a p p e a r a n c e of c a v e r n o m a o n
T 2 - w e i g h t e d images is that of m i x e d i n c r e a s e d signal int e n s i t y in the c e n t r e a n d l o w - i n t e n s i t y r i m suggestive of
p r e v i o u s silent h a e m o r r h a g e s . Surgical r e m o v a l of the
c a v e r n o m a should b e the t r e a t m e n t of choice in o r d e r to
stop the n a t u r a l course of the disease which is characterized b y r e p e a t e d h a e m o r r h a g e s a n d step-wise progression of the deficit.

Acknowledgements. Professors/Drs. Felix (Berlin), Hornung, Ktihne, Blttmm (Essen) supplied the MRI scans of case 1; Professor
Hebestreit (Lfidenscheidt) the MRI scans of case 2. Drs.Urban,
Tenfelde and Gallenkamp kindly referred the patients for therapy.

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