Neuroradiology (1998) 40: 51±53
Ó Springer-Verlag 1998

G. K. Bejjani
R. G. Rizkallah
F. Tzortidis
A. S. Mark

Received: 9 December 1996
Accepted: 28 May 1997

G. K. Bejjani × R. G. Rizkallah × F. Tzortidis
Department of Neurosurgery,
George Washington University Medical
Center, Washington, DC, USA
A. S. Mark
Department of Neuroradiology,
Washington Hospital Center,
Washington, DC, USA

)

G. K. Bejjani ( )
2150 Pennsylvania Avenue NW,
Suite 7-420, Department of Neurosurgery,
George Washington University,
Washington, DC 20037, USA
Tel. (2 02) 9 94-22 10;
fax (2 02) 9 94-99 44;
e-mail gbejjani @ gwis2.circ.gwu.edu

D IA G N O S T I C N E U RO R A D IO L O GY

Cervical spinal cord injury during cerebral
angiography with MRI confirmation:
case report

Abstract We report the first case of
MRI-documented cervical spinal
cord injury during cerebral angiography. A 54-year-old woman underwent an angiogram for subarachnoid hemorrhage. Her head
was secured in a plastic head-holder.
At the end of the procedure, she was
found to have a left hemiparesis.
MRI revealed high signal in the cervical spinal cord. The etiology may
have been mechanical due to patient
positioning, or toxic, from contrast
medium injection in the vessels
feeding the spinal cord, or a combination of both.

Key words Angiography, cerebral ×
Spinal cord, injury × Magnetic
resonance imaging \sg

Introduction

Case report

Complications of cerebral angiography are generally
classified as local, due to injury to the arteries, nerves or
surrounding structures at the injection site; systemic,
due to reactions to the contrast medium; neurological,
due to subintimal dissection, embolization of atherosclerotic plaques or air; and neurotoxic and others [1, 2].
Myelopathy has been reported when the contrast
medium was injected inadvertently into the spinal cord
feeders during aortography, bronchial and intercostal arteries angiography, and spinal angiography [3±12]. There
have been three cases of myelopathy following cerebral
angiography, all in the pre-MRI era, and due to contrast
medium injection into the spinal cord arteries [13±15].
We report the first case of MRI-documented cervical
cord injury following cerebral angiography.

A 54-year-old woman presented with acute headache and neck
stiffness. She reported neck pain and bilateral hand weakness a few
weeks prior to the event. Her past medical history included hypertension.
The patient was admitted after CT revealed diffuse subarachnoid hemorrhage and hydrocephalus. A cerebral angiogram
was normal. MRI of the neck revealed cervical spondylosis at the
C4±5, C5±6 and C6±7 levels, with canal stenosis (Fig. 1). After two
weeks of observation the patient was discharged.
Two months later she underwent a repeat cerebral angiogram
as an outpatient. On arrival she was anxious and hypertensive. She
was premedicated with intravenous diazepam. Sublingual nifedipine and intravenous labetalol were used to control her blood
pressure. Her head was secured and taped in a plastic head-holder.
The right common femoral artery was cannulated using the Seldinger technique and a 6 F sheath was inserted. Using a 5.5 F catheter, selective catheterization and angiography of both internal

52

There was no evidence of intracranial damage, but a lesion was
seen in the cervical spinal cord between C3 and C7 with high signal
intensity on T2, consistent with edema (Fig. 2).
The patient improved neurologically over the following days and
was discharged to a rehabilitation facility after 1 week. Six weeks
later, following complete neurological recovery, she underwent a
decompressive cervical laminectomy with a very good outcome.

Discussion

Fig. 1 Sagittal T2-weighted image of cervical spine before angiography revealing spinal stenosis at C4 to 7
carotid and the left vertebral arteries was performed. A total of
150 cc of contrast medium (Hexabrix and Conray 60) was used.
The patient received additional intravenous labetalol during
the procedure to control her blood pressure, with minimal success:
despite a total of 110 mg of labetalol, the diastolic blood pressure
persisted in the 100±130 mm Hg range.
About 45 min after the beginning of the procedure, the patient
started complaining of neck and back pain and heaviness in both
arms, which we attributed to anxiety. She received an additional
dose of diazepam and the procedure was continued. At the completion of the procedure, the patient was found to have a left
hemiparesis, more marked in the arm, involving mainly the triceps
and the intrinsic muscles of the hand.
CT showed no evidence of ischemic or hemorrhagic stroke.
Two days later, cerebral and cervical spine MRI was obtained.

In series published during the past two decades, the rate
of persistent neurological complications of cerebral angiography varies between 0 % and 5.7 %, most series
reporting a rate lower than 1 % [2, 16, 17].
In a review in 1966, Killen and Foster [18] proposed
three mechanisms of injury to the spinal cord during
angiography: direct injection of contrast medium into
the subarachnoid space; occlusion of critical spinal arteries by aortic dissection; and neurotoxicity of the contrast medium; they found the last of these to be responsible of the majority of complications (54 of 60
cases). The exact mechanism by which contrast medium
is toxis to neural tissue is not well known. Multiple factors seem to interact, including disruption of the bloodbrain barrier by hyperosmolar agents, vasomotor changes, sludging of blood flow, and alteration of the coagulation pathways [14, 19]. We have traced only three
cases of myelopathy following cerebral angiography, all
during the pre-MRI era [13±15]. In two the myelopathy
occurred following injection of contrast medium into
the thyrocervical trunk [14, 15], the third following injection into the left subclavian artery [13]. The contrast
media used were Renografin-60 (methylglucamine and

Fig. 2 a Sagittal T2-weighted image 2
days after the angiogram. Diffuse increase in signal intensity in the cord is
seen at the stenotic level. This is confirmed by an axial image (b)

2a

2b

53

sodium diatrizoate) [14], 60 % methylglucamine iothalamate [15] and tri-iodide acetylaminobenzoate of methylglucamine [13].
More than one mechanism can be invoked to explain
the cord injury in our patient, including contrast medium
toxicity and mechanical compression; a combination is a
possibility. Although the left vertebral artery was injected,
contrast medium was not injected into the thyrocervical
trunk, but might have reached the spinal cord through the
anterior spinal artery. The concomittant presence of cervical spondylosis, and high signal in the spinal cord within
the spondylotic area point to neck positioning as a possible
etiology. Two other factors favor positioning as being responsible: the head was taped in an uncomfortable position, and the patient's complaints were addressed by giving
more sedatives, which could decrease the protective mechanism of the tone of the paraspinal muscles.
Positioning of the head has not been reported as a
mechanism of spinal cord injury in patients undergoing
cerebral angiography, but it is a well known complication
of neck positioning and manipulation during surgical
procedures, including acoustic neurinoma resection in
the sitting position [20], posterior cervical laminectomy

[21], and hyperlordotic positioning for lumbar surgery
[22]. Spinal cord injury can also occur in patients with
cervical spondylosis during induction of anesthesia [23].
In these cases, drug-induced muscle paralysis causes increased mobility of the cervical spine, which may lead to
cervical cord injury when the neck is extended for intubation, due to anterior compression by bony spurs and
posterior compression by infolding of the ligamentum
flavum [24]. Myelopathy will be due to either direct cord
compression and/or ischemia by compression of the
neural vascular structures; these are the same mechanisms that are thought to underlie the pathogenesis of
spinal cord disorders associated with cervical spondylosis
[25]. In awake patients the paraspinal muscle tone prevents extremes of position and subsequent spinal cord
injury. This protective mechanism is lost during general
anesthesia when muscle relaxants are used [23], and or in
trauma [26]. In our case, sedation and securing the head
in an uncomfortable position may have overcome the
protective mechanisms and caused the spinal cord injury.
The mechanical compression of the spinal cord and its
vessels might have slowed the circulation and favored the
toxic effect of the contrast medium.

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