In performing the endoscopic fenestration of a large sphenoid

mucocele extending into the temporal and infratemporal fossa

using a sublabial, transmaxillary approach, we conclude that the
computer-assisted navigation facilitated surgery by providing
three-dimensional orientation during approach to the cyst.
REFERENCES
1. Delfini R, Missori P, Iannetti G, Ciappetta P, Cantore G. Mucocele of the
paranasal sinus with intracranial and intraorbital extension: report of 28 cases.
Neurosurgery 1993; 32: 901906.
2. El-Fiki ME, Abdel-Fattah HM, El-Deeb AK. Sphenoid sinus mucocele with
marked intracranial extension: a more common phenomenon in the third world?
Surg Neurol 1993; 39: 115119.
3. Nicolai P, Redaelli LO, Tomenzoli D, Maroldi R, Antonelli AR. Sphenoid
mucocele with intracranial invasion secondary to nasopharyngeal acinic cell
carcinoma. Head and Neck 1991; 13: 540544.
4. Nugent GR, Sprinkle P, Bloor BM. Sphenoid sinus mucoceles. J Neurosurg
1970; 32: 443451.
5. Kato A, Yoshimine T, Hayakawa T et al. A frameless, armless navigation system
for computer assisted neurosurgery . J Neurosurg 1991; 74: 845849.
6. Brenner A, Brunei P Delitala A, Greco R, Chiappetta F. Frontoethmoidal
osteoma complicated by intracranial mucocele and hypertensive
pneumocephalus: case report. Neurosurgery 1995; 36: 12371238.
7. Ching HS, Lindsay KW, OReilly BF. Intracranial mucoceles with midline fusion
defects. J Neurol Neurosurg Psychiatry 1996; 61: 428429.
8. Diaz F, Latchow R, Duvall AJ, Quick CA, Erickson DL. Mucocele with
intracranial and extracranial extension. J Neurosurg 1978; 48: 284288.
9. Holness RO, Attia E. Osteoma of the frontoethomoidal sinus with secondary
brain abscess and intracranial mucocele: case report. Neurosurgery 1994; 34:
920923.
10. Lunardi P, Missori P, Lorenzo ND, Fortuna A. Giant intracranial mucocele
secondary to osteoma of the frontal sinus: report of two cases and review of the
literature. Surg Neurol 1993; 39: 4638.
11. Matsuno A, Yoshida Y, Masugi N, Eguchi M. Sphenoid sinus aspergillosis
presenting abducens nerve palsy and visual field impairment: a case report.
Neurol Surg 1992; 20: 799804.
12. Pompili A, Mastrostefano R, Caroli F et al. Mucocele of neurosurgical interest:
clinical considerations on five cases. Acta Neurochir (Wien) 1990; 102:
114121.
13. Shady JA, Bland LI, Kazee AM, Pilcher WH. Osteoma of the frontoethmoidal
sinus with secondary brain abscess and intracranial mucocele: case report.
Neurosurgery 1994; 34: 920923.
14. Schroeder HW, Gaab MR, Niendorf WN. Neuroendoscopic approach to
arachnoid cysts. J Neurosurg 1996; 85: 293298.
15. Zamorano L, Chavantes C, Dujovny M, Malik G, Ausman J. Stereotactic
endoscopic interventions in cystic and intraventricular brain lesions. Acta
Neurochir Suppl (Wien) 1992; 54: 6976.
16. Manwaring KH, Manwaring ML, Moss SD. Magnetic field guided endoscopic
dissection through a burr hole may avoid more invasive craniotomies. A
preliminary report. Acta Neurochir Suppl (Wien) 1994; 61:3439.
17. Rhoten RL, Luciano MG, Barnett GH. Computer-assisted endoscopy for
neurosugical procedures: Technical Note. Neurosurgery 1997; 40: 632638.
Intense and recurrent
dj vu experiences
related to amantadine
and phenylpropanolamine
in a healthy male
Tero Taiminen
1
, Satu K. Jskelinen
2
Departments of
1
Psychiatry and
2
Clinical Neurophysiology, Turku University
Central Hospital, Turku, Finland
Summary We report a case of a 39-year-old caucasian healthy
male physician who developed intense and recurrent dj vu expe-
riences within 24h of initiating concomitant amantadinephenyl-
propanolamine treatment against influenza. Dj vu experiences
terminated on discontinuation of medication. Findings in temporal
epilepsy suggest that mesial temporal structures, including hip-
pocampus, are related to paramnesic symptoms. On the other
hand, previous case reports have confirmed that both amantadine
and phenylpropanolamine alone, and particularly in combination,
can induce psychotic symptoms due to their dopaminergic activity.
The authors suggest that dj vu experiences may be provoked by
increased dopamine activity in mesial temporal structures of the
brain. 2001 Harcourt Publishers Ltd
Journal of Clinical Neuroscience (2001) 8(5), 460462 2001 Harcourt Publishers Ltd
DOI: 10.1054/jocn.2000.0810, available online at http://www.idealibrary.com on
Keywords: amantadine, phenylpropanolamine, paramnesia,
dj vu, dopamine
Received 20 April 2000
Accepted 8 June 2000
Correspondence to: Tero Taiminen MD, PhD, Associate Professor of
Psychiatry, Department of Psychiatry, University of Turku, Rak. 9, III krs.,
Kunnallissairaalantie 20, FIN-20700 Turku, Finland. Tel.: ;358 2 2692577;
Fax: ;358 2 2692528; E-mail: tero.taiminen@utu.fi
INTRODUCTION
Amantadine, originally used in the treatment and prophylaxis of
influenza infection, has at present also many indications in neu-
ropsychopharmacology. It has proved beneficial in Parkinsons dis-
ease, drug-induced Parkinsonism, traumatic head injury, dementia,
multiple sclerosis, cocaine withdrawal, neuroleptic-induced sexual
dysfunction, and depression.
13
Amantadine is a dopamine-releasing
agent and antagonist of the M-methyl-D-aspartate (NMDA) gluta-
mate receptor, and it has noradrenergic, serotonergic, monoaminox-
idase A blocking, and dopa decarboxylase stimulating properties.
1,4
Although high doses of amantadine can cause hallucinations, the
prevalence of psychotic symptoms with amantadine as an antiviral
agent is probably less than 1 percent.
5
Phenylpropanolamine is a sympathomimetic alpha-1-agonist
drug contained in numerous nasal decongestants and appetite
supressants. Phenylpropanolamine is sometimes characterized as a
weak amphetamine-like agent, and a range of adverse psychiatric
reactions attributed to it have been reported, including paranoid
and manic psychosis.
6
Dysmnesic symptoms include illusion of recognition, subjec-
tively inappropriate impressions of familiarity of the present with
460 Taiminen et al.
Journal of Clinical Neuroscience (2001) 8(5) 2001 Harcourt Publishers Ltd
JOCN-169.QXD 8/14/01 6:33 PM Page 460
an undefined past.
7
They are generally known as dj vu (visual
recognition) experiences, but false recognition can also be pre-
dominantly auditory (dj entendu) or cognitive (dj pens). The
anatomical compartment and the neurotransmitter systems
involved in the development of dj vu experiences is not exactly
known. Based on symptoms and findings in temporal epilepsy,
mesial temporal structures have been suggested to be involved in
the formation of dysmnesic symptoms.
8
Transient separate dj vu
experiences are common in the general population. In the survey
among 2500 university students, more than 90% had experienced
dj vu on at least one occasion, and 17% did so at least once per
week.
9
On the other hand, frequent and prolonged dj vu experi-
ences may be related with a neurologic or psychiatric disorder.
Dysmnesic symptoms often take place in association with com-
plex partial seizures of temporal lobe epilepsy, and the occurrence
of dj vu experiences is also increased in dissociative disorders,
depression and schizophrenia.
7,10,11
Here, we report a case of a 39-year-old caucasian man who
developed intense and recurrent dj vu experiences during a 10-
day course of amantadine concomitant with phenylpropanolamine
against influenza.
CASE REPORT
A 39-year-old caucasian male physician previously acquainted
with the authors contacted us to report a phenomenon he thought
we would find interesting. The subject gave his written informed
consent for the presentation of the case history. Four weeks before
contacting us, the subject caught type A influenza, which was at
that time epidemic in Finland. The subject had been in his usual
state of good physical and psychological health until falling ill. He
developed typical symptoms of moderate fever (-38.5C), myal-
gia, rhinitis, cough and prostration. The subject went on sick
leave, and, in hopes of alleviating the viral infection, started a
course of amantadine hydrochloride 100 mg twice a day for 10
days. The subject had never used amantadine previously. During
the amantadine medication, he also used phenylpropanolamine
hydrochloride 25mg twice a day (slow-release tablet) as a decon-
gestant. The subject had used short courses with the same phenyl-
propanolamine preparation six times previously during the past 15
years without any side-effects.
On the next day after initiating amantadine and phenyl-
propanolamine combination therapy, the subject started to experi-
ence several intense dj vu experiences per hour, each lasting
from a few seconds to minutes. Experiences were all-inclusive
occurring in every sensory modality. The subject did not find
dj vu incidents unpleasant, rather amusing and puzzling. He
suspected that amantadine might be causing dj vu experiences,
but, because he did not find them annoying, he decided to con-
tinue the medication. Few times he woke up during the night and
had an intense feeling of dj vu regarding the dream he had just
had. He did not report amnesia, psychiatric symptoms or any other
type of paramnesia except illusion of recognition during the
amantadine course. The subject recovered from the viral infection
within 10 days without any complications. After discontinuing
amantadine and phenylpropanolamine dj vu experiences ceased
on the same day.
The subject had no family history of major psychiatric disorder
or epilepsy. He had no history of head traumas, febrile convul-
sions, epilepsy, or remarkable somatic disease. He had had short-
lasting dj vu experiences few times before in his life, but his
recollections about them were vague. The subject had had type A
influenzas three times previously, and the most recent infection
did not differ from previous ones except in regard to dj vu
experiences. Four weeks after the dj vu episode the subject was
screened with the Structured Clinical Interview for DSM-IV Axis
I and II Disorders (SCID I and II; 12, 13) by the first author. He
did not meet diagnostic criteria for any life-time or past-month
DSM-IV disorder, and his character was social. The subject had
not had any dj vu experiences between cessation of amantadine
phenylpropanolamine combination and screening interview. To
investigate subjects life-time tendency for dissociation, he
answered to the Dissociative Experiences Scale questionnnaire
(DES; 14). His DES-score was only 2.8, which is below mean
score in the general population.
14
DISCUSSION
To our knowledge, this is the first report on possible association
between psychotrophic medication and intense and recurrent
dj vu experiences in a healthy subject. We find it unlikely that dj
vu experiences would have been caused by viral infection for
three reasons. First, the subject had had influenzas with similar
symptoms three times previously without paramnesia. Second,
general medical condition of the subject was not exceptionally bad
during the viral infection. He did not find himself exhausted, his
temperature was only moderate, and he did not have insomnia.
Third, dj vu experiences were restricted to the periods of med-
ication. Therefore, we find it probable that dj vu experiences
were related to medication. Because the subject had used phenyl-
propanolamine previously without side effects, the probable cause
for dj vu experiences is either amantadine alone, or amantadine
phenylpropanolamine combination.
Both amantadine and phenylpropanolamine facilitate dopamin-
ergic neurotransmission in brain, and may thus expose a patient
to psychotic symptoms.
5,6,15
Moreover, Stroe et al.
14
reported a
case of confusive psychosis in a healthy 28-year-old female taking
prescribed doses of amantadine concomitant with phenylpropanol-
amine. The authors hypothesized that these two drugs can com-
plement each others dopaminergic and hence psychotogenic
effects.
15
Sno et al.
11
have argued that dj vu experiences,
depersonalisation and delusional reduplicative paramnesia form a
continuum of increasing psychopathology. It seems plausible that
this continuum may be related to increasing dopamine activity.
Recent evidence suggests that high dopamine D
2
receptor density
may be associated with social desirability.
16
Our subject has a
very social character, which may have made him particularly vul-
nerable to hyperdopaminergic symptoms. On the other hand, lack
of risk factors for psychosis have probably protected him from the
loss of reality testing.
6
Findings in temporal epilepsy suggest that
mesial temporal structures, including hippocampus, are related to
dysmnesic symptoms.
8
Recent animal studies indicate that hip-
pocampal dopamine systems are involved in spatial working
memory.
17
Taken together, we hypothesize that recurrent dj vu
experiences of our subject were related to hyperdopaminergic
dysfunction in mesial temporal structures.
REFERENCES
1. Huber TJ, Dietrich DE, Emrich HM. Possible use of amantadine in depression.
Pharmacopsychiatry 1999; 32: 4755.
2. Nickels JL, Schneider WN, Dombovy ML, Wong TM. Clinical use of
amantadine in brain injury rehabilitation. Brain Inj 1994; 8: 709718.
3. Valevski A, Modai I, Zbarski E, Zemishlany Z, Weizman A. Effect of
amantadine on sexual dysfunction in neuroleptic-treated male schizophrenic
patients. Clin Neuropharmacol 1998; 21: 355357.
4. Deep P, Dagher A, Sadikot A, Gjedde A, Cumming P. Stimulation of dopa
decarboxylase activity in striatum of healthy human brain secondary to
NMDA receptor antagonism with a low dose of amantadine. Synapse 1999; 34:
313318.
Intense and recurrent dj vu experiences related to amantadine and phenylpropanolamine in a healthy male 461
2001 Harcourt Publishers Ltd Journal of Clinical Neuroscience (2001) 8(5)
JOCN-169.QXD 8/14/01 6:33 PM Page 461
5. Flaherty JA, Bellur SN. Mental side effects of amantadine therapy: its spectrum
and characteristics in a normal population. J Clin Psychiatry 1981; 42: 344345.
6. Marshall RD, Douglas CJ. Phenylpropanolamine-induced psychosis: potential
predisposing factors. Gen Hosp Psychiatry 1994; 16: 358360.
7. Neppe VM. The psychology of dj vu: have I been here before? Johannesburg:
Witwaterstrand University Press, 1983.
8. Fish DR. Psychic seizures. In: Engel J, Pedley TA, eds. Epilepsy: a
comprehensive textbook. Volume 1. Philadelphia: Lippincott-Raven, 1997;
543548.
9. Ardila A, Nino CR, Pulido E, Rivera DB, Vanegras CJ. Episodic psychic
symptoms in the general population. Epilepsia 1993; 34: 133140.
10. Richardson TF, Winokur G. Dj vu as related to diagnostic categories in
psychiatric and neurosurgical patients. J Nerv Ment Dis 1968; 146: 161164.
11. Sno HN, Linszen DH, De Jonghe F. Dj vu experiences and reduplicative
paramnesia. Br J Psychiatry 1992; 161: 565568.
12. First MB, Spitzer RL, Gibbon M, Williams BW. Structured Clinical Interview
for DSM-IV Axis I Disorders Patient Edition (SCID-I/P, Version 2.0, 4/97
revision). New York: Biometrics Research Department, New York State
Psychiatric Institute, 1997.
13. First MB, Spitzer RL, Gibbon M, Williams BW, Benjamin L. Structured
Clinical Interview for DSM-IV Axis II Personality Disorders (SCID-II). New
York: Biometrics Research Department, New York State Psychiatric Institute,
1997.
14. Bernstein EM, Putnam FW. Development, reliability, and validity of a
dissociation scale. J Nerv Ment Dis 1986; 174: 727735.
15. Stroe AE, Hall J, Amin F. Psychotic episode related to phenylpropanolamine
and amantadine in a healthy female. Gen Hosp Psychiatry 1995; 17: 457458
(letter).
16. Laakso A, Vilkman H, Kajander J, Bergman J, Haaparanta M, Solin J, Hietala
J. Prediction of detached personality in healthy subjects by low dopamine
transporter binding. Am J Psychiatry 2000; 157: 290292.
17. Wilkerson A, Levin ED. Ventral hippocampal dopamine D
1
and D
2
systems
and spatial working memory in rats. Neuroscience 1999; 89: 743749.
Intraaneurysmal
embolization of an
unruptured basilar tip
aneurysm associated
with moyamoya disease
Kenji Kagawa
1
, Masayuki Ezura
1
, Reizo Shirane
2
, Akira
Takahashi
3
, and Takashi Yoshimoto
2
1
Department of Neuroendovascular Therapy, Kohnan Hospital, Sendai,
Japan,
2
Department of Neurosurgery, Tohoku University School of Medicine,
Sendai, Japan,
3
Department of Neuroendovascular Therapy, Tohoku
University School of Medicine, Sendai, Japan
Summary We describe a patient with moyamoya disease associ-
ated with an unruptured basilar tip aneurysm which was treated by
endovascular embolization using Guglielmi detachable coils
(GDCs). A 53-year-old man presented with left hemiparesis persist-
ing for 3 months before admission. Cerebral angiography revealed
occlusion of the bilateral middle cerebral arteries and the left ante-
rior cerebral artery, stenosis of the right anterior cerebral artery, and
basal moyamoya vessels. In addition, a saccular small aneurysm
was seen at the top of the basilar artery. The aneurysm was com-
pletely embolized by intraaneurysmal GDCs. Direct surgical clipping
is often selected for the treatment of posterior fossa aneurysms in
moyamoya disease. However, complete clipping is usually difficult
due to the difficulties in operative technique associated with moy-
amoya disease. We suggest that the endovascular treatment using
GDCs is comparatively safe and effective for the treatment of surgi-
cally difficult aneurysms in patients with moyamoya disease. 2001
Harcourt Publishers Ltd
Journal of Clinical Neuroscience (2001) 8(5), 462464 2001 Harcourt Publishers Ltd
DOI: 10.1054/jocn.2000.0806, available online at http://www.idealibrary.com on
Keywords: cerebral aneurysm, moyamoya disease, endovascular
treatment, embolization, Guglielmi detachable coils
Received 1 November 1999
Accepted 9 June 2000
Correspondence to: Kenji Kagawa, Department of Neuroendovascular
Therapy, Kohnan Hospital, 4-20-1, Nagamachi-Minami, Taihaku-ku, Sendai,
982-8523, Japan. Tel.: ;81 22 248 2131; Fax: ;81 22 304 1641
INTRODUCTION
Moyamoya disease is often associated with intracranial ane-
urysms, and reports of such cases increased in number recently.
The incidence of intracranial aneurysms in patients with moya-
moya disease was reported from 5% to 15%.
14
With the recent
increment of reports of such aneurysms treated surgically, devel-
opmental mechanisms and etiologies have gradually become
obvious.
5
Regarding sites of occurrence, two types of aneurysms
are found in this disease.
24,68
Cerebral aneurysms can be classi-
fied into the peripheral artery aneurysms in the moyamoya vessels
or collateral circulation, and major artery aneurysms in the circle
of Willis. Generally, peripheral artery aneurysms are considered
to be pseudoaneurysms, occurring in the fragile moyamoya ves-
sels in the basal ganglia, and rupture of pseudoaneurysms fre-
quently causes intraventricular or intracerebral hemorrhage, but
pseudo-aneurysms can be gradually reduced and may completely
disappear.
1,2,6
Major artery aneurysms are true aneurysms, occur-
ring in the posterior circulation in about 5060% of those associated
with moyamoya disease.
2,9
Increased hemodynamic stress in the
posterior circulation due to occlusion or stenosis of the internal
carotid artery may contribute to the development of this type of
aneurysm,
1,10,12
and the resultant increased blood flow often causes
enlargement and rupture of these aneurysms with time.
3,1214
Spontaneous disappearance of true aneurysms is extremely rare.
8,12
Ruptured aneurysms associated with moya-moya disease contribute
to the poor clinical outcome. Therefore, treatment to prevent rupture
is very important. However, it is difficult to perform radical surgery
on aneurysms around the circle of Willis associated with moyamoya
disease. In recent years, intravascular procedures have been used to
treat such directly inaccessible aneurysms.
We describe a case of unruptured basilar tip aneurysm asso-
ciated with moyamoya disease manifesting as ischemic attack
and treated with intraaneurysmal embolization using Guglielmi
detachable coils (GDCs).
CASE REPORT
A 53-year-old man presented with left hemiparesis. The patient
visited a nearby hospital. Cerebral angiography demonstrated moya-
moya disease and an aneurysm at the top of the basilar artery.
Three months later, the patient was referred to our hospital for the
treatment of both moyamoya disease and unruptured aneurysm.
The patients parents and older brother had suffered from cerebral
infarction. The patients past history was not contributory.
On admission, the patients consciousness was clear, but slight
left hemiparesis including face was noted. Magnetic resonance
imaging (MRI) revealed a dotted line-like watershed infarction in
the deep white matter of the right cerebral hemisphere. Right
carotid angiography demonstrated occlusion of the middle cere-
bral artery, stenosis of the anterior cerebral artery, and sparse
moyamoya vessels in the base of the brain (Fig. 1). Left carotid
angiography showed occlusion of the middle cerebral and anterior
462 Kagawa et al.
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JOCN-169.QXD 8/14/01 6:33 PM Page 462