The Journal of ECT
18(2):99–102 © 2002 Lippincott Williams & Wilkins, Inc., Philadelphia

Case Report

Successful ECT in a Patient with Intracranial Venous Angioma
Parviz Malek-Ahmadi, M.D., and Allan T. Hanretta, M.D., Ph.D.
Department of Neuropsychiatry, School of Medicine, Texas Tech Health Sciences Center, Lubbock, Texas, U.S.A.

Summary: The 1990 American Psychiatric Association (APA)
Task Force report on electroconvulsive therapy (ECT) suggests
that there is an increased risk of complications in patients with
intracranial vascular masses. There have been only a few published
reports on the use of ECT in these patients. In this case report, an
additional case is described that used ECT in the treatment of
major depression in a 72-year-old patient with a venous angioma
involving the left cerebellum. Brain imaging studies, neurosurgery,
cardiology, and orthopedic consultations were obtained prior to
ECT. Blood pressure was monitored closely throughout the course
of ECT. Prior to each ECT, antihypertensive medication was given
in addition to other pretreatment medications. Consistent with previously published reports, the patient did not experience any neurological deterioration or adverse effects. A brief review of the
literature on the use of ECT in patients with venous angioma and
other intracranial vascular masses is presented.

diovascular status was assessed by a cardiology consultation
and by monitoring blood pressure and pulse during ECT and
throughout the hospitalization. Pretreatment with an antihypertensive medication is described. The patient was successfully treated with ECT with a good response and no
adverse events.
CASE REPORT
A 72-year-old retired male with a diagnosis of major
depression, recurrent, with psychotic features (DSM-IV
296.34) (2), was referred to our in-patient facility for recurrence of his depressive symptoms. He had a history of multiple psychiatric admissions since age 40 when he first developed depression. On admission, his depression had a
2-month duration and was associated with discontinuing his
psychotropic medications because “they did not help
[him].” He had been stable on amitriptyline for 6 years prior
to his relapse, and was subsequently given trials of nefazodone with nortriptyline and olanzapine. Lithium had been
added to his medication regimen for a brief period of time.
He had a past history of unsuccessful trials of mirtazapine,
doxepin, bupropion, imipramine, gabapentin, and divalproex, and was unable to tolerate side effects associated
with sertraline and paroxetine.
After his admission, due to the severity of his depressive
symptoms, presence of delusional thinking, and failure to
respond to trials of antidepressants (venlafaxine, citalopram,
mirtazapine, trazodone, amitriptyline) and risperidone, ECT
was considered. His consideration of ECT also was based,
in part, on the distress associated with weight loss from
between 30 and 40 lb prior to admission, and on his mother’s history of having had ECT with a good response.
The patient’s medical history was significant for
asthma, adenocarcinoma of prostate with transurethral resection of the prostate, right orchiectomy, mild mitral valve
prolapse, “mild” arrhythmias, and multiple surgeries including vasectomy, appendectomy, cholecystectomy, and two
lumbar laminectomies. He had previously been treated with
diltiazem for chest pain and arrhythmias. His family history

Key Words: Venous angioma—Intracranial vascular masses—
Hemorrhage—Major depression—Electroconvulsive therapy.

INTRODUCTION
Intracranial vascular masses do not pose an “absolute”
contraindication to treatment with electroconvulsive therapy
(ECT), as reported by the 1990 APA Task Force on ECT,
but may present an increased risk for serious complications
such as rupture/hemorrhage, or increased intracranial pressure (1). There is a paucity of published reports on ECT in
patients with vascular masses and even fewer reports on
patients with venous angioma. Recommendations by several authors include monitoring and treating elevated blood
pressure during ECT.
This case report provides an additional case to support
the safety of the use of ECT in patients with venous angioma. Assessment of the venous angioma was through
neuroimaging studies and neurosurgical consultation. Car-

Received November 15, 2001; accepted June 12, 2002.
Address correspondence and reprint requests to Dr. P. Malek-Ahmadi,
Department of Neuropsychiatry, School of Medicine, Texas Tech University Health Sciences Center, Lubbock, TX 79430, U.S.A.

99

DOI: 10.1097/01.YCT.0000027709.14566.2C

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P. MALEK-AHMADI AND A. T. HANRETTA

was significant for bipolar disorder (in one brother) and, as
previously noted, for depression in his mother, who had had
a good response to ECT.
A particular concern regarding the use of ECT was the
patient’s history of magnetic resonance imaging (MRI) of
the head in 1995 with “findings compatible with a venous
angioma involving the left cerebellar hemisphere,” “most
likely a prominent venous angioma.” There were no other
significant abnormalities.
A pre-ECT work-up consisted of a complete blood
count with differential, serum chemistry, thyroid function
tests, and urinalysis. Plasma cholinesterase was 4,751 IU/L
(reference range: 4,970–11,120 IU/L). Dibucaine inhibition
was 89.2% (reference range: 85–93%) An electrocardiogram (ECG) revealed normal sinus rhythm, and chest films
were unremarkable. Entire spine films indicated lumbar levoscoliosis and degenerative changes through the cervical,
thoracic, and lumbar spine, with narrowing of several disc
spaces. Mild anterior wedging of the midthoracic vertebrae
was also noted, but no fractures or subluxation. Spirometry
showed normal pulmonary parameters.
Due to the history of venous angioma, a repeat MRI of
the head (with and without contrast) and a magnetic resonance angiogram (MRA) of the brain were taken prior to
ECT. The MRI indicated a 12 × 28 mm venous angioma
in the left cerebellar hemisphere (Fig. 1A and B). The
MRA, in contrast, did not reveal any significant stenosis,
vascular malformations, or aneurysms involving the intracranial vasculature. Venous angiomas are not usually detected by MRA (3).

The pre-ECT work-up included consultations from neurosurgery, cardiology, orthopedic surgery, and internal
medicine. The neurosurgery consultant noted the venous
angioma as “small” and without an indication of hemorrhage. There were no identified neurological abnormalities
on examination. The consultant felt that the increased risk of
hemorrhage secondary to increased intracranial pressure
and/or increased blood pressure during ECT would be controlled with sedation (anesthesia), and that the overall risk
would be minimal. A second opinion psychiatry consultation was concurrent with the neurosurgery consultation approving ECT and recommended “working with the attending anesthesiologist to keep [the patient’s] blood pressure
low during the process.” A cardiology consultant evaluated
the patient, and a treadmill stress test was interpreted as
normal with no significant ECG changes and a normal
blood pressure response to exercise and no significant arrhythmias. A prior echocardiogram had indicated a mild
mitral valve prolapse. Orthopedic evaluation noted arthritis
of the cervical, thoracic, and lumbar spines, with no orthopedic contraindication to proceeding with ECT. An internal
medicine consultant initiated a work-up for the patient’s
weight loss and reported no identifiable increased risk
for ECT.
ECT anesthesia consisted of glycopyrrolate 0.2 mg,
methohexital 50 mg, succinylcholine 95 mg, and 100% oxygen. The patient’s baseline blood pressures prior to the first
ECT were in the low normal range. To minimize elevated
blood pressure in potentiating the risk of hemorrhage with
venous angioma, the patient’s blood pressures were closely

FIG. 1. A and B: Magnetic resonance imaging with contrast indicates a venous angioma involving the left cerebellar hemisphere.

J ECT, Vol. 18, No. 2, 2002

SUCCESSFUL ECT IN A PATIENT WITH INTRACRANIAL VENOUS ANGIOMA

monitored throughout his hospitalization and during each
ECT. However, his low baseline blood pressure warranted
caution with the use of antihypertensive medication that
could result in compromising cardiac perfusion. Subsequently, nitroglycerin, two sprays (0.8 mg) sublingually,
were given prior to anesthesia induction at the time of the
first ECT, and blood pressure was monitored closely. A
pulse oximeter was used to monitor pulse rate and oxygen
saturation. A brief pulse stimulator Thymatron DG (Somatics, LLC, Lake Bluff, IL, U.S.A.) delivered the stimulus.
After discussing the risks and benefits of unilateral versus
bilateral ECT, the patient requested the latter. He was given
ECT on a three-times-a-week schedule. After adequate neuromuscular blockade was reached, as assessed by deep tendon reflexes in the extremities, the stimulus was delivered
using the Thymatron DG apparatus with a percent energy
set at 65% (frequency ⳱ 70 Hz, duration ⳱ 2.4 s, number
of pulses ⳱ 336, charge ⳱ 302.4 mC, current ⳱ 0.9 Amps,
pulse width ⳱ 1.0 ms). Seizure activity was monitored by
electroencephalogram (EEG) and each stimulus resulted in
adequate seizure durations ranging from 26 to 57s.
The first ECT resulted in a 26 s seizure, therefore the
energy was increased to 70% (frequency ⳱ 70 Hz, duration
⳱ 2.8 s, number of pulses ⳱ 392, charge ⳱ 352.8 mC,
current ⳱ 0.9 Amps, pulse width ⳱ 1.0 ms) for each of the
remaining six ECTs. The percent energy (70%) was selected
on the basis of the recommendation made by the manufacturer. The patient’s peak blood pressure during seizure with
the first ECT was 270/100 mmHg with a pulse of 114. The
cardiology consultant recommended diltiazem 240 mg a day
and 4 hours prior to each of the remaining six ECTs. Subsequent to the addition of diltiazem, peak blood pressures
occurring during the last six ECTs ranged from 160 to 200
mmHg for systolic blood pressures and from 98 to 128
mmHg for diastolic blood pressures, and pulses ranged from
95 to 127 bpm. The patient tolerated ECT well without
complications.
The eighth ECT was canceled after the patient developed shortness of breath the previous evening, which responded to treatment with bronchodilators (ipratropium and
albuterol). The patient had a history of asthma. An ECG
indicated normal sinus rhythm with first-degree atrioventricular block. The patient agreed to discontinue ECT. His
depression had responded maximally to ECT. The consultant cardiologist recommended avoiding tricyclic antidepressant medications. Subsequently, the patient was started
on a prophylactic trial of citalopram 20 mg at bedtime and
olanzapine 7.5 mg at bedtime for depression.
A post-ECT MRI of the head was requested for comparison with the pre-ECT MRI to assess the venous angioma. However, the patient declined the post-ECT MRI
based on his concern regarding the cost of this procedure. A
neurological exam was negative for focal neurological deficits. His mental status examination (without using any in-

101

strument) did not reveal any cognitive impairment. Since
his discharge, he has done very well as an outpatient on
citalopram 20 mg daily and olanzapine 7.5 mg at bedtime.

DISCUSSION
Intracranial vascular malformations include capillary
malformations, cavernous angiomas, arteriovenous malformations (AVM), and venous angiomas (3).
Typically, a venous angioma consists of several small
abnormal veins. Histologically, the walls of these veins are
hyalinized and contain very few muscle fibers (4).
Most venous angiomas are asymptomatic and incidentally discovered. Saito and Kobayashi suggested that intracranial venous angiomas are of low clinical significance (5).
However, in some patients they can cause headaches, convulsions, and hemorrhage (6). According to Rothfus et al.,
cerebellar venous angiomas are more likely to rupture.
After hypertension, angiomatous malformations are the
second most common cause of spontaneous cerebellar hemorrhage (7).
Electrically induced seizures induce an acute hemodynamic response resulting in elevation of blood pressure (8).
Therefore, in patients with intracranial vascular masses,
ECT-induced elevation of blood pressure should always be
of some concern. However with adequate control of blood
pressure, ECT has been safely administered to patients with
intracranial aneurysms. Table 1 contains a summary of the
published case reports on the use of ECT in patients with
intracranial aneurysms (9–16).
With respect to venous angiomas, we could find only
two published case reports on the use of ECT in patients
with this type of intravascular malformation. In 1986,
Greenberg et al. described the use of ECT in a 24-year-old
male patient with bipolar disorder (depressed) and a venous
angioma in the left parietal lobe. The angioma was detected
by CT, standard cerebral angiography, and MRI. The patient, who had not responded to drug therapy, was given 12
right unilateral ECTs (on a three-times-a-week schedule)
with improvement. For the first ECT, a nitroprusside intraarterial line was established. The patient tolerated the treatments without complications. Repeat CT and MRI 18 days
following the last treatment remained unchanged (17).
More recently, Salaris et al. described a 50-year-old female patient with bipolar disorder and a 3.6 × 4.5 cm left
cerebellar angioma. The patient had previously been given
two courses of ECT (three and four ECTs, respectively).
The first course was terminated due to emergence of migraine headaches and ataxia. The second course had to be
discontinued due to migraine headaches, hypertension, and
ataxia. MRI studies following each course showed no effect
on angioma (16).
Severe depressive symptoms persisted after a 12-month
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P. MALEK-AHMADI AND A. T. HANRETTA

TABLE 1. ECT in patients with intracranial aneurysms: summary of case reports
Authors
Husum et al., 1983 (9)
Drop et al., 1988 (10)
Bader et al., 1995 (11)
Bader et al., 1995 (11)
Farah et al., 1996 (12)
Najjar and Guttmacher, 1988 (13)
Najjar and Guttmacher, 1988 (13)
Viguera et al., 1998 (14)
Hunt and Kaplan, 1998 (14a)
Gardner and Kellner, 1998 (15)
Salaris et al., 2000 (16)

Patients

Aneurysms

Number of
ECTs

Antihypertensive agents
used before each ECT

42-year-old
70-year-old
37-year-old
45-year-old
60-year-old
66-year-old
51-year-old
54-year-old
83-year-old
75-year-old
74-year-old

Internal carotid artery (surgically repaired)
Middle cerebral artery, internal carotid artery
Anterior communicating artery (retrospective diagnosis)
Internal carotid artery
Posterior cerebral artery
Middle cerebral artery
“Paraophthalmic”
Basilar artery
Internal carotid artery
Posterior communicating artery
Internal carotid artery

10
11
9
6
6
12
9
7
3
7
12

Hydralazine and propranolol
Nitroprusside
None
Esmolol
None*
Esmolol
Esmolol
Atenolol and nitroprusside
Propranolol
Nitroglycerin and enalapril
Esmolol/labetalol

*For anesthesia, propofol was used to maintain blood pressure stability.

period, so the authors administered a third course of 10 right
unilateral ECTs without complications. The patient was pretreated with esmolol 30–50 mg and/or labetalol 0–50 mg.
She was also given hydrocortisone 20 mg orally following
each treatment. The patient responded well to ECT without
complications. Computed tomography scan or MRI was not
conducted following the index course of ECT (16).
Naturally occurring seizures do not appear to have a
deleterious effect on intracranial venous angiomas. Wendling et al. reported three patients with intracerebral angioma and seizures without resulting in an hemorrhagic
event (18). Numaguchi et al. studied 11 patients with intracranial venous angioma. One patient with a venous angioma
in the right frontal lobe had “convulsive seizures” and was
treated with antiepileptic drugs (19). In a retrospective
study, Garner et al. examined the natural history of venous
angioma in 100 patients over a period of 14 years. In 23
patients, seizures were the presenting manifestations requiring treatment with antiepileptic drugs (20).
In our experience, patients with venous angiomas may
be safely treated with ECT. Neuroimaging studies and a
neurosurgery consultation should be part of the pre-ECT
work-up. In patients with coexisting hypertension, proper
dose adjustment of antihypertensive agents must be made.
ECT-induced elevation of blood pressure should be controlled with appropriate antihypertensive agents. For patients with intracranial aneurysms undergoing ECT, it has
been suggested that diastolic and systolic blood pressures
during treatment should be kept below 100 and 180 mmHg,
respectively (11). Pretreatment with nitroprusside infusion
may preclude blood pressure peaks outside the recommended range. However, as Najjar and Guttmacher have
pointed out, pretreatment with antihypertensive agents does
not always prevent acute elevation of blood pressure induced by ECT, although such elevation is not associated
with morbidity (13). Ultimately the decision to proceed with
ECT should be made after a careful assessment of a
risk/benefit ratio relevant to any high-risk patient.
J ECT, Vol. 18, No. 2, 2002

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