802

J Neurol Neurosurg Psychiatry 1998;64:802–805

SHORT REPORT

Intracranial haemodynamics during attenuated
responses to electroconvulsive therapy in the
presence of an intracerebral aneurysm
A Viguera, G Rordorf, R Schouten, C Welch, L J Drop

Department of
Psychiatry
A Viguera
R Schouten
C Welch
Department of
Neurology
G Rordorf
Department of
Anesthesia and
Critical Care,
Massachusetts General
Hospital, and
Departments of
Anaesthesia,
Psychiatry, and
Neurology, Harvard
Medical School,
Boston, Massachusetts
02114, USA
L J Drop
Correspondence to:
Dr LJ Drop, Department of
Anesthesia, Massachusetts
General Hospital, Boston
Massachusetts 02114.
Telephone 001 617 724
3278; fax 001 617 726 7536;
email
drop@helix.mgh.harvard.edu
Received 13 May 1997 and
in revised form 6 October
1997
Accepted 20 October 1997

Abstract
Objectives—This report describes successful anaesthesia and electroconvulsive
therapy (ECT) in a patient with an unruptured basilar artery aneurysm. ECT is
associated with a hyperdynamic state
characterised by arterial hypertension,
tachycardia, and considerably increased
cerebral blood flow rate and velocity.
These responses pose an increased risk for
subarachnoid haemorrhage when an intracranial aneurysm coexists.
Methods—A 54 year old woman presented
for ECT. She had a 20 year history of
major depression which was unresponsive
to three diVerent antidepressant drugs.
There was also an unruptured 5 mm
saccular aneurysm at the basilar tip,
which had been documented by cerebral
angiography, but its size had remained
unchanged for the previous four years.
After she declined surgical intervention,
she gave informed consent for ECT. During a series of seven ECT sessions middle
cerebral artery flow velocity was recorded
by a pulsed transcranial Doppler ultrasonography system. She was pretreated
with 50 mg oral atenolol daily, continuing
up to the day of the last ECT and immediately before each treatment, sodium nitroprusside was infused at a rate of 30
µg/min, to reduce systolic arterial pressure to 90–95 mm Hg.
Results—Systolic flow velocity during the
awake state ranged from 62–75 cm/s,
remaining initially unchanged with sodium nitroprusside infusion. After induction
of
anaesthesia
(0.5
mg/kg
methohexitone and 0.9 mg/kg succinylcholine), flow velocities decreased to 39–54
cm/s, reaching maximal values of 90 cm/s
(only 20% above baseline) after ECT.
These flow velocities recorded post-ECT
were considerably below the more than
twofold increase recorded when no attenuating drugs were used. Systolic arterial blood pressure reached maximal
values of 110–140 mm Hg and heart rate
did not exceed 66 bpm. Rapid awakening
followed each treatment, no focal or global

neurological signs were apparent, and the
patient was discharged in remission.
Conclusion—In a patient with major depression and a coexisting intracerebral
saccular aneurysm who was treated with
ECT, the combination of â blockade with
atenolol and intravenous infusion of sodium nitroprusside prevented tachycardia
and hypertension, and greatly attenuated
the expected increase in flow velocity in
the middle cerebral artery.
(J Neurol Neurosurg Psychiatry 1998;64:802–805)
Keywords: electroconvulsive therapy; blood pressure;
hypertension; blood vessels; aneurysm

The two principal therapeutic options for
major depression are antidepressant drugs and
electroconvulsive therapy (ECT). The current
standard practice oVers ECT to patients with
disabling depressive symptoms or with life
threatening depression and urgent need for
intervention. In view of an ECT related hyperdynamic state with large increases in cerebral
blood flow rate1 2 and velocity,3 and arterial
hypertension,4 the risk of major intracerebral
complications is high when an intracranial
aneurysm coexists.5 6 Case reports are not
available showing intracranial haemodynamics
during ECT with the use of attenuating drugs.
In a patient with a known 5 mm intracranial
aneurysm at the basilar tip we closely monitored arterial pressure and middle cerebral
artery (MCA) flow velocity by transcranial
Doppler sonography before, during, and after
ECT when attenuating drugs were administered. â adrenergic blockade was produced
with oral atenolol and intravenous sodium
nitroprusside was used to manage the anticipated arterial hypertension.
Case report
A 54 year old woman with a 25 year history of
major depression was admitted with recurrent
unipolar illness of eight months in duration,
which was unresponsive to antidepressants,
including venlafaxine, lithium, and fluoxetine.
Because a course of ECT had been successful
20 years earlier, she asked to be treated in the
same manner. Of special interest was an
unruptured intracranial aneurysm, the size of

Cerebral haemodynamics and electroconvulsive therapy

803

Data obtained with invasive pressure monitoring. Shown in several sections, from left to right are data obtained in the patient awake at baseline, awake but
after the start of sodium nitroprusside infusion, after induction of anaesthesia and muscular relaxation (indicated by arrows for methohexitone and
succinylcholine), and after application of the ECT stimulus. At the top are ECG traces, below them, corresponding in time, traces of arterial pressure and
middle cerebral artery flow velocity. The V lead of the ECG is in the V-5 position. The recording speed used for the arterial trace was 5 mm/s; that for the
ECG was 25 mm/s. The last section shows data obtained after the sodium nitroprusside infuson was turned oV.

which had not changed over the previous four
years. There was no history of headache and no
hypertension. She smoked a pack of cigarettes
each day. Physical examination showed no
focal neurological signs; current blood pressure
readings were 110/70 mm Hg. An ECG
showed a sinus rhythm of 88 beats/min. A
complete blood count and coagulation profile
were normal. A cerebral angiogram showed a 5
mm aneurysm at the basilar tip, but the patient
firmly declined the surgical intervention recommended by the neurosurgical consultant.
She was anxious to receive unilateral ECT, and
gave informed consent.
To reduce the tachycardia and hypertension
anticipated with ECT,4 7 the patient was
pretreated with 50 mg atenolol orally a day; this
treatment continued up to and including the
day of the last ECT. During the two first ECT
sessions, arterial pressure was continuously
monitored from an indwelling radial artery
catheter and recorded on a multichannel direct
writing recorder via a calibrated pressure
transducer. A long indwelling central venous
cannula was inserted via an antecubital vein for
accurately metered infusion of sodium nitroprusside. However, because of the risk of complications associated with multiple radial artery
cannulations, we recorded non-invasive arterial
pressure measurements (Dinamap, Criticon,
Tampa, FL, USA) during the subsequent five
treatments. For the same reason, central
venous cannulation was not used after the second treatment and sodium nitroprusside was
then administered via a large bore peripheral
venous line. During the third and later
treatments, non-invasive blood pressure meas-

urements and leads II and V5 of the ECG were
recorded by a patient monitor (SpaceLabs,
Redmond-Wash) and a microcomputer with
customised software, allowing simultaneous
real time display of all data at the bedside both
in tabular and graphical formats (v time) and
data storage. Systolic and mean middle cerebral artery blood flow velocities were measured intermittently with a pulsed 8 mHz Doppler ultrasound probe, which was anchored in a
frame strapped on the head to allow a left temporal window at a depth of 40–50 mm from the
surface. The emitting area of the transducer
was about 10 times that of the cross sectional
area of the middle cerebral artery in adults.
The signal quality was adjusted according to
the typical high pitch sound and the sonographic wave form. Measurements were recorded during the awake state at baseline, during the awake state but after the start of sodium
nitroprusside infusion, after induction of anaesthesia, and continuously starting immediately before the application of ECT up until
three minutes after the seizure. Because the
patient was cooperative while awake and only
slight movements of the feet were noted as evidence of a generalised seizure after anaesthesia
and muscular paralysis, high fidelity recordings
of middle cerebral artery blood flow velocity
were obtained.
General anaesthesia was induced with
methohexitone (0.75 mg/kg) and muscular
paralysis was produced by succinylcholine
(0.75 mg/kg), and these drug doses were
constant for the series of treatments. The lungs
were ventilated with 100% oxygen via a face
mask at a rate of 8–10 breaths/min until

804

Viguera, Rordorf, Schouten, et al

spontaneous breathing resumed. With the use
of a face mask, end tidal CO2 values could not
be reliably measured. However, in the presence
of an endotracheal tube, such manual ventilation may be expected to yield end tidal PCO2
values ranging from 30–40 mm Hg. Immediately before each treatment sodium nitroprusside was infused by an adjustable infusion
pump at a constant rate of 30 µg/min to lower
systolic blood pressure from a range of
120–125 mm Hg to 90–95 mm Hg, a 20%
change (figure). This vasodilator dose was constant during the series of treatments. Taking
the absence of a foot sole reflex as evidence of
adequate muscular relaxation, ECT was then
administered by a unilateral brief pulse stimulus (average, 55 Ws) which was followed by a
modified seizure averaging 40 seconds.
Middle cerebral artery flow velocity measurements together with an invasive pressure
recording (figure) were representative for all
treatments. In the awake state at baseline
systolic blood flow velocity ranged from 62 to
75 cm/s; similar values were observed initially
during sodium nitroprusside infusion. After
induction of anaesthesia but immediately
before ECT, systolic middle cerebral artery
blood flow velocity decreased to 39–54 cm/s.
After the application of the ECT stimulus peak
middle cerebral artery flow velocities reached
maximal values of 90 cm/s—that is, not more
than 20% above baseline awake values. Immediately after ECT, systolic arterial blood
pressure returned to control or only slightly
above (range: 110–140 mm Hg); and heart rate
did not exceed 66 bpm. Rapid awakening
followed each treatment; no focal or global
neurological signs were found at any time, and
cranial nerve examination remained normal.
The patient was discharged in remission after a
series of seven treatments.
Discussion
Although the presence of a saccular aneurysm
at the basilar tip posed an important risk for
major cerebrovascular complications including aneurysm rupture and cerebral vasospasm,
we successfully administered ECT to this
patient who was unresponsive to three diVerent antidepressant drugs. The intracranial
haemodynamic consequences of ECT are
unknown when hypertension and tachycardia
are attenuated. Without attenuation, however,
a previous study conducted in 92 patients has
shown that ECT is associated with a more
than twofold increase in middle cerebral artery
blood flow velocity.3 Such a major increase
may be explained by cerebral vascular narrowing caused by greatly increased plasma catecholamine concentrations, by electrical
stimulation,8 or by increased cerebral blood
flow rate,1 2 which occurs because of flowmetabolism coupling.9 The small increase in
middle cerebral artery flow velocity (by only
20%) we consistently observed, therefore, was
all the more striking. ECT is known to be
associated with a hyperdynamic state, with
tachycardia4 and increased systolic arterial
pressure by 34%4 and a twofold increase in

cardiac output.7 Such hypertension is of major
concern when an intracerebral aneurysm is
present, as it causes increased wall stress in the
aneurysm. However, although augmented wall
stress may lead to aneurysm growth or
rupture, and although arterial hypertension is
recognised as a risk factor, a direct correlation
between aneurysm rupture and acute hypertension is not established.10 Of a total of 250
postmortem examinations, hypertension was
present in 37% when an intracranial aneurysm
had ruptured, but in 43% when an intracerebral aneurysm was found incidentally.10
Nevertheless, because the risk of acute subarachnoid haemorrhage was real in this patient
and its rate of growth unpredictable,11 control
of blood pressure and heart rate was sought.
To reduce blood pressure and hold it steady,
we selected sodium nitroprusside because of
its short duration of onset and action. Its
potent cerebral vasodilator properties may
explain the small changes in middle cerebral
artery flow velocity despite increased blood
flow rate1 2 and vascular narrowing8 expected
with increased blood catecholamine concentrations. In addition, systemic pressure
changes were small and pretreatment with
atenolol by mouth resulted in minimal
changes in heart rate. It is recognised that in
the current patient no hypertension was
present before ECT and therefore, that the
drug regimen instituted and the successful
outcome we found may not apply to all
patients with intracranial aneurysms presenting for ECT.
This case report raises two principal questions. Firstly, what conditions predict intracranial aneurysm rupture? The answer is that predictors are unreliable. Studies in patients with
asymptomatic aneurysms have established
bleeding rates of 2.0%12 and 1.5% a year.13 Risk
factors include cigarette smoking, use of oral
contraceptives, and possibly chronic hypertension. Aneurysm size (smaller v >10 mm in
diameter) is also a risk factor for bleeding.14
Although no bleeding occurred in 102 patients
with intracranial aneurysms with diameters<10 mm,14 small asymptomatic aneurysms may bleed.11 Aneurysm enlargement is a
strong predictor for rupture.15
Secondly, what mechanisms are involved in
aneurysm rupture? The answer is elusive. It is
well established that wall stress in an aneurysm
is augmented by increased blood pressure.
However, Weir16 proposed that development or
growth of a saccular aneurysm may be related
to disintegration or focal weakness of the elastic layer secondary to ceaseless pounding of the
arterial pulse wave. Such a mechanism may
explain the location of saccular aneurysms at
the apices of vascular bifurcations, where
structural fatigue may be produced by the
dissipation of kinetic energy or turbulence,
which develops with excessive flow velocity.17
Thus flow velocity may be a determinant of
stress at the site of the aneurysm.17 However,
this case report shows that its anticipated
sharp increase3 did not occur with a regimen
of â blockade and sodium nitroprusside.
Further study of intracranial and systemic

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Cerebral haemodynamics and electroconvulsive therapy

haemodynamics under conditions of hyperdynamic states and diVerent attenuating drugs
will be necessary to establish the safety of ECT
in the presence of intracranial aneurysms.
We thank Mr Glen Pelikan from SpaceLabs (Redmond, Washington) for the use of the SpaceLabs PCExpress patient monitor.
1 Plum F, Posner JB, Troy B. Cerebral metabolic and circulatory responses to induced convulsions in animals. Arch
Neurol 1968;18:1–13.
2 Posner JB, Plum F. Cerebral metabolism during electrically
induced seizures in man. Arch Neurol 1969;20:388–95.
3 Saito S, Yoshikawa D, Nishihara F, et al. The cerebral hemodynamic response to electrically induced seizures in man.
Brain Res 1995;673:93–100.
4 Castelli I, Steiner LA, Kaufmann MA, et al. Comparative
eVects of esmolol and labetalol to atenuate hyperdynamic
states after electroconvulsive therapy. Anesth Analg 1995;
80:557–61.
5 Fink M. Convulsive therapy. Theory and practice. New York:
Raven Press, 1979:219.
6 Task Force Report of the Am Psychiatric Association. The
practice of electroconvulsive therapy. Recommendations for
treatment, training and privileging. Washington, DC: American Psychiatric Association, 1990:58.
7 Wells DG, Davies CG. Hemodynamic changes associated
with electroconvulsive therapy. Anesth Analg 1987;66:
1193–5.

8 Johansson B, Somlyo A. Electrophysiology and excitationcontraction coupling. In: Geiger S, ed. Handbook of physiology. The cardiovascular system. Vol 2. Vascular smooth muscle. Bethesda: American Physiological Society, 1980:301–
23.
9 Plum F, DuVy TE. The couple between cerebral metabolism and blood flow during seizures. In: Ingvar DH, Lassen
NA, eds. Brain work. Copenhagen: Munksgaard, 1975:
197–214.
10 McCormick WF, Schmalstieg EJ. The relationship of
arterial hypertension to intracranial aneurysms. Arch Neurol 1977;34:285–7.
11 Schievink WI, Piepgras DG, Wirth FP. Rupture of
previously documented small asymptomatic saccular intracranial aneurysms. Report of three cases. J Neurosurg
1992;76:1019–24.
12 Rosenkorn J, Eskesen V, Schmidt K. Unruptured intracranial aneurysms. An assessment of the annual risk of rupture
based on epidemiological and clinical data. Br J Neurosurg
1988;2:369–78.
13 Wiebers DO, Whisnant JP, O’Fallon WM. The natural history of unruptured intracranial saccular aneurysms. N Engl
J Med 1981;304:696–8.
14 Wiebers DO, Whisnant JP, Sundt TM, et al. The
significance of unruptured intracranial saccular aneurysms.
J Neurosurg 1987;66:23–9.
15 Zack DJ, Russell DB, Miller DR. Fortuitously discovered
intracranial aneurysms. Arch Neurol 1980;37:37–41.
16 Weir B. Aneurysms aVecting the nervous system. Baltimore:
Williams and Wilkins 1987:671–92.
17 Sekhar LN, Heros RC Origin, growth and rupture of
aneurysms: a review. Neurosurgery 1981;8:248–60.

HISTORICAL NOTE

Schroeder van der Kolk: the soul and epilepsy
Jacobus Schroeder van der Kolk (1797–1862)1
showed his intellectual abilities when a student
at Groningen. He became Professor of
Anatomy and Physiology at Utrecht in 1826.
More than 100 scientific contributions followed. They were devoted to the management
of the mentally ill in asylums to which he had
devoted his labours, clinical studies of neurology, lung diseases, blood disorders, embryology, zoology and later in his life he considered
philosophical issues of the nature of the soul.
His major work was entitled Body and Soul in
which he described psychic processes and
material disorders as the outcome of a higher
spirit (spiritus animalis).
His writings, evolved from primitive Galenic
ideas, have to be seen in their historical
context; but throughout he emphasised the
miraculous aspects of natural history, and of
life itself. He initiated investigations of the
causes of disease using morbid anatomy,
publishing an important work Anatomy of the
Cord and Medulla.
Van der Kolk performed autopsies and used
a primitive microscope on the brains of epileptics. His conclusions were given in the
Sydenham Lecture of 1859, On the minute
structure and functions of the medulla oblongata
and the proximate causes and rational treatment of

epilepsy. He found “dilatation of the veins which
appeared filled with blood in the cortex,
medulla and spinal cord”. The medulla
“showed a fatty degeneration with albuminous
intracellular fluid.” Those who bit their
tongues during a fit had dilated vessels feeding
the hypoglossal nucleus whereas those without
a bitten tongue had dilated vessels of the vagal
nucleus.
“The first cause of epilepsy . . . is exalted
sensibility and excitability of the medulla
oblongata. . . .” These caused the medulla to be
“liable to discharge upon itself” and these discharges caused spasms in blood vessels leading
to hyperaemia followed by involuntary reflex
movements . . .” Frequent or repeated fits
caused inflammation of the cortex leading to
“incurable dementia” due to “thickening and
dilatation of blood vessels.”2
This problem of the prime seat of the epileptic fit was a major source of controversy.3 4 The
distinguished American neurologist Hammond cited van der Kolk’s work in his A treatise
on the diseases of the nervous system (1871), and
claimed “no one has been more thorough in
the search for the essential cause of epilepsy
than he.”
continued on page 812