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Remission of essential hypertension following decompression of a giant aneurysm of the right vertebral artery
Remission of essential hypertension following decompression of a giant aneurysm of the right vertebral artery Hiroshi Okudera MD* Shigeaki Kobayashi MD* Kazuhiko Kyoshima MD* Kenichiro Sugita MD** Departnlrnt of Neurosurger;,4 Shinshu University School of Medicine. Drparrmtmt of N&osurgery,*” Nagow I’nivrrsitx, ,Japat~.
_.
_
We report a case with giant aneurysm of the right vertebral artery in which remission of essential hypertension occurred following surgical decompression. The patient presented with a history of progressive gait disturbance and essential hypertension over a period of 4 years and 10 years respectively. Computerised tomography scan demonstrated a giant thrombosed aneurysm in the right vertebral artery. The aneurysm was trapped and decompressed
to reduce the
neurological deficits. Post-operatively, the gait disturbance recovered with complete remission of the long standing essential hypertension. Neuroscience
~Journ;ll of(Xnical
Keywords:
Essential
1994, 1 (4):277-279
hypertension,
Giant
0 I,ottgtnati
aneurysm,
Microvascular
decompression,
Vertebral
artery
disclosed
a completely
Introduction Recently,
compression
nerves
cranial
proposed
of the
root
zone
of the left
vertebral
artery
has been
aneurysm
entry
IX and X by a looping
as one of the sure pathogeneses
hypertension.
‘-’ In the
unexpected
patient
remission
hypertension
occurred
giant aneurysm
here,
standing
an
essential
after surgical decompression
of the right vertebral
in the right vertebral
thrombosed
artt’rv.
for essential
presented
of long
angiography
of the
artery.
Operation With the patient in the lateral position, craniectomy
was made.‘,4
seen behind
the right cranial
a right suboccipital
large hard aneurysm
was partly
nerves IX and X, which had
Case report This
57-year-old
man
initially
paresis and hypaesthesia been
diagnosed
as having
headache,
ataxic
developed;
arachnoid
haemorrhage.
blocker
gait, slight there
slight
left hemi-
admission.
essential
treated with calcium-channel gradually
noticed
1 year before
He had
hypertension
and
for 10 years. Recently
dysphagia
and hoarseness
was no episode
of sub-
Examination The
patient
86/min, chest
was well
and blood
pressure
and
abdomen
neurological
findings
reflex,
moderate
hypaesthesia.
nourished. were
was 162/102 normal.
on admission
truncal
ataxia,
Computerised
His pulse
rate
mmHg.
The
included
The
abnormal absent
left hemiparesis
tomographic
(CT)
gag and scan
revealed a large round mass of 25 mm in diameter
without
midline
1). The
shift
of the medulla
oblongata
Fig. 1 Computerised tomography scan at the medulla level. The giant right vertebral aneurysm is demonstrated as round high density mass.
was
(Fig.
1. Clin. Neuroscience
Volume
1
Number
4
October
1994
277
Essential hypertension
Case reports
been
elevated
was trapped artery.
by the aneurysm
by clipping
Following
isolation
aneurysmotomy aneurysm.
80%
removed.
the elevation normalised.
aneurysm
and distal vertebral
of the lower
was made
About
carefully
(Fig. 2). The
the proximal to reduce
cranial
nerves,
the mass of the
of the intraluminal
clots
were
At the final stage of the clot removal,
of the right
cranial
nerves
IX and X was
Removal of the bottom part of the aneurysmal
wall was abandoned ventrolateral
because
it had lightly adhered
to the
aspect of the medulla.
Post-operative
course
Post-operatively, improved
the
neurological
over several
weeks
also normalised
within
remained
normotensive
without
years later because
deficits
gradually
and the systemic
pressure
arterial
a few days. The medication
patient
and died 2
of gastric cancer.
Discussion Pathogenesis 1974, mental
investigations
central
nervous
neurogenic
that the Cl
medulla
oblongata
control
of integration
zone
tractus solitarius
of arterial
innervation
autonomic
from
paired.
of essential nerves
both
which
volume.
hypertension
Anatomically,
observation,
tracti
solitarii
they stressed
of the vagus nerves
the animal
they
that
is the
was asym-
that
pulsatile compression
might
be causative
study in hypertensive
compression nerve. In the
of and
using
their
pathogenesis
“3 14, l5 The hypothesis
retrospectively.
output
directly
case, the aneurysm
compressed
of the medulla.
the rostra1 ventrolateral
medulla
hypertension
as demonstrated
in humans
Although
several
observation, angiographical
in animals.g,11
mention
study, animal
study, the number
surgical model
observation
and
of cases is insufficient
to explain all about essential arterial hypertension. careful
right
plays a role in causing
literatures
microanatomical
the
It may suggest that
and investigation
the entity of ‘neurogenic
Further
would be necessary hypertension’
and
Received 24 August 1993 Accepted for publication 11 November 1993
of essential
was supported
by an
and normotensive
16.17Until today, there hypertension
have been
caused by the arterial
of the REZ of the right XI and Xth cranial reported
cases
with essential
hypertension
relieved by neurovascular decompression, compression of the left REZ was mainly caused by an arterial 10op.~~, 16z1’ Compression
by a contralateral
mass lesion
such as the
vertebral aneurysm has not been documented. In the case with a large mass lesion in the posterior fossa, structural shift by the lesion may cause compression of the REZ of the left cranial nerves 1X and X, even if the lesion is
J. Clin. Neuroscience
Volume 1
and offprint requests:
Hiroshi Okudera MD, Department of Neurosurgery, Shinshu University School of Medicine, 3-l-l Asahi, Matsumoto, Nagano 390, Japan. Tel: 81 263 35 4600 (ext 5358) Fax: 81 263 37 0480
the
clinical
to the leftventrolateral
angiographic
no reports on essential
cardiac
experiment
proposed
hypertension.
278
portion
Correspondence
of cranial nerves with
would increase
From
device,
medulla,
ventrolateral
to establish
IX and X1-6. I’? and
nuclei
However,
distribution
balloon
to have
its pathogenesis.
of the root entry
and the left vagus nerve was the major control
the left heart
patients
for
in right side. In the present
was found
on the basis of surgical results that the left side
symmetrically
stroke
region
pressure.”
all the somatic and sensory function
metrical
by
in the rat9 and
of the medulla was sensitive to compression. central
caused
brainstem
decompression
of the left cranial
speculated
the
and his group have reported
cases with remission
(REZ)
between
area of the rostra1 ventrolateral
Jannetta
micro-vascular
experi-
hypertension.
hypertension
was a critical
In neurosurgery, clinical
have reported
and neurogenic
of the nucleus
concluded
is still unclear. Since
on the relationship
system
They demonstrated stimulation
Fig. 2 Drawing showing the intra-operative findings. The large hard aneurysm was observed behind the right cranial nerves IX and X. The aneurysm was located lateral to the root entry zone (REZ) of the right cranial nerves IX and X, which had been elevated by the aneurysm.
located
of essential hypertension
Reid and his colleaguesal’
following
caused by right VA aneurysm
Number 4
References 1. Fein JM, Frishman W. Neurogenic hypertension related to vascular compression of the lateral medulla. Neurosurgery 1980;6:615-22. 2. Jannetta PJ. Neurovascular compression in cranial nerve and systemic disease. Ann Surg. 1980;192:518-25. 3. Jannetta PJ. Cranial nerve vascular compression syndromes (other than tic douloureux and haemifacial spasm). Clin Neurosurg 1981;28:445-56. 4. Jannetta PJ, Gendell HM. Neurovascular compression associated with essential hypertension. Neurosurgery 1978;2:165. 5. Jannetta PJ, Gendell HM. Clinical observations on essential hypertension. Surg Forum 1979;30:431-32. 6. Jannetta PJ, Segal R. Neurogenic hypertension: Etiology and surgical treatment. 1. Observations in 53 patients. Ann Surg 1985;201:381-91. 7. Sugita K, Kobayashi S, Takemac T, Tanaka Y, Okudera H, Ohsawa M. Giant aneurysms of the vertebral artery. Report of five cases. J Neurosurg 1988;68:960-66.
October 1994
Essential hypertension
caused by right VA aneurysm
8.
Rcis DJ. Doba N. ‘I‘hc central nervous system and tt~rogenic hypertension. Prog Cardiovasc Dis 1974;17:51-71.
9.
R&s D,J. The nucleus tractus soliatrius and experitnrntal ttcurogenic hypertension: evidence for a central neural imbalance hypothesis of hypertensive disease. Adv l{iochem Psvchophar tnacol 1981;28:409-20. Kcis IIJ. Brain-stem mechanisms governing resting and t-eflex tone of precapillary vessels..J Cardiovasc Pharntacol 398.5:7 (Suppl. 3):s160-66. Kcis QJ, Ruggiero DA. Morrison SF. The Cl area of the I astral ventrolateral medulla oblongata. A critical brainstem region for control of resting and reflex itttegration of arterial pressure. Am J Hypertens I989:2:363S-374s. Naraghi R. &ah MR. Ll’alter GF, Kleinberg B. Arterial l~pertension and ncurovascular compression at the ~entct-lateral medull,t. A comparative microanatomical and p;tthologiral stud\,. ,J. Nettrosurg 1992:77: 103-12.
10.
1 I.
12.
Case report
13. .Jannetta PJ, Segal R, Wolfson SK, DLI~OVI~~ M, Scmba A. (:ook EE. Neurogenic hypertension: etiology and surgical treat ment. II. Observations in a ttonhtmlan primate model. Ann Surg 198.5;202:253-6 I. 1.4. Segal R. Gendell HM. Canfield D. Dujovny M,.Janncrt;t F’J. (:ardiovascular response to pttlsatilc pressurtapplied to ventrolateral medulla. Surg Forutl~ 1979:30:433-35. 15. Segal R. Jannetta F’J, Wolfso~~ SE;,Jr.. Dujovnv M. Cook IX. Implanted pulsatile balloon devict, for &lulatiott of ttcuro-vascular compression syndt-otiie5 in anittials.,J Neurosurg 1982;57:646-50. 16. Kleineberg B, Becker H. (;aab MK. N~~urovasculat compression and essential hypcrtcnsion. .In angiographic study. Neuroradiologv I!)9 I ;M:Z-8. 17. Kleineberg B, Becker H. Gash MR.‘Naraghi R. Essential hypertension associatrd with tteurovascular compression: Angiographic tindings. Ncurosttrgerv 19'.tz:30:834-41.
J. Clin. Neuroscience
Volume
1
Number
4
October
1994
279
_.
_
We report a case with giant aneurysm of the right vertebral artery in which remission of essential hypertension occurred following surgical decompression. The patient presented with a history of progressive gait disturbance and essential hypertension over a period of 4 years and 10 years respectively. Computerised tomography scan demonstrated a giant thrombosed aneurysm in the right vertebral artery. The aneurysm was trapped and decompressed
to reduce the
neurological deficits. Post-operatively, the gait disturbance recovered with complete remission of the long standing essential hypertension. Neuroscience
~Journ;ll of(Xnical
Keywords:
Essential
1994, 1 (4):277-279
hypertension,
Giant
0 I,ottgtnati
aneurysm,
Microvascular
decompression,
Vertebral
artery
disclosed
a completely
Introduction Recently,
compression
nerves
cranial
proposed
of the
root
zone
of the left
vertebral
artery
has been
aneurysm
entry
IX and X by a looping
as one of the sure pathogeneses
hypertension.
‘-’ In the
unexpected
patient
remission
hypertension
occurred
giant aneurysm
here,
standing
an
essential
after surgical decompression
of the right vertebral
in the right vertebral
thrombosed
artt’rv.
for essential
presented
of long
angiography
of the
artery.
Operation With the patient in the lateral position, craniectomy
was made.‘,4
seen behind
the right cranial
a right suboccipital
large hard aneurysm
was partly
nerves IX and X, which had
Case report This
57-year-old
man
initially
paresis and hypaesthesia been
diagnosed
as having
headache,
ataxic
developed;
arachnoid
haemorrhage.
blocker
gait, slight there
slight
left hemi-
admission.
essential
treated with calcium-channel gradually
noticed
1 year before
He had
hypertension
and
for 10 years. Recently
dysphagia
and hoarseness
was no episode
of sub-
Examination The
patient
86/min, chest
was well
and blood
pressure
and
abdomen
neurological
findings
reflex,
moderate
hypaesthesia.
nourished. were
was 162/102 normal.
on admission
truncal
ataxia,
Computerised
His pulse
rate
mmHg.
The
included
The
abnormal absent
left hemiparesis
tomographic
(CT)
gag and scan
revealed a large round mass of 25 mm in diameter
without
midline
1). The
shift
of the medulla
oblongata
Fig. 1 Computerised tomography scan at the medulla level. The giant right vertebral aneurysm is demonstrated as round high density mass.
was
(Fig.
1. Clin. Neuroscience
Volume
1
Number
4
October
1994
277
Essential hypertension
Case reports
been
elevated
was trapped artery.
by the aneurysm
by clipping
Following
isolation
aneurysmotomy aneurysm.
80%
removed.
the elevation normalised.
aneurysm
and distal vertebral
of the lower
was made
About
carefully
(Fig. 2). The
the proximal to reduce
cranial
nerves,
the mass of the
of the intraluminal
clots
were
At the final stage of the clot removal,
of the right
cranial
nerves
IX and X was
Removal of the bottom part of the aneurysmal
wall was abandoned ventrolateral
because
it had lightly adhered
to the
aspect of the medulla.
Post-operative
course
Post-operatively, improved
the
neurological
over several
weeks
also normalised
within
remained
normotensive
without
years later because
deficits
gradually
and the systemic
pressure
arterial
a few days. The medication
patient
and died 2
of gastric cancer.
Discussion Pathogenesis 1974, mental
investigations
central
nervous
neurogenic
that the Cl
medulla
oblongata
control
of integration
zone
tractus solitarius
of arterial
innervation
autonomic
from
paired.
of essential nerves
both
which
volume.
hypertension
Anatomically,
observation,
tracti
solitarii
they stressed
of the vagus nerves
the animal
they
that
is the
was asym-
that
pulsatile compression
might
be causative
study in hypertensive
compression nerve. In the
of and
using
their
pathogenesis
“3 14, l5 The hypothesis
retrospectively.
output
directly
case, the aneurysm
compressed
of the medulla.
the rostra1 ventrolateral
medulla
hypertension
as demonstrated
in humans
Although
several
observation, angiographical
in animals.g,11
mention
study, animal
study, the number
surgical model
observation
and
of cases is insufficient
to explain all about essential arterial hypertension. careful
right
plays a role in causing
literatures
microanatomical
the
It may suggest that
and investigation
the entity of ‘neurogenic
Further
would be necessary hypertension’
and
Received 24 August 1993 Accepted for publication 11 November 1993
of essential
was supported
by an
and normotensive
16.17Until today, there hypertension
have been
caused by the arterial
of the REZ of the right XI and Xth cranial reported
cases
with essential
hypertension
relieved by neurovascular decompression, compression of the left REZ was mainly caused by an arterial 10op.~~, 16z1’ Compression
by a contralateral
mass lesion
such as the
vertebral aneurysm has not been documented. In the case with a large mass lesion in the posterior fossa, structural shift by the lesion may cause compression of the REZ of the left cranial nerves 1X and X, even if the lesion is
J. Clin. Neuroscience
Volume 1
and offprint requests:
Hiroshi Okudera MD, Department of Neurosurgery, Shinshu University School of Medicine, 3-l-l Asahi, Matsumoto, Nagano 390, Japan. Tel: 81 263 35 4600 (ext 5358) Fax: 81 263 37 0480
the
clinical
to the leftventrolateral
angiographic
no reports on essential
cardiac
experiment
proposed
hypertension.
278
portion
Correspondence
of cranial nerves with
would increase
From
device,
medulla,
ventrolateral
to establish
IX and X1-6. I’? and
nuclei
However,
distribution
balloon
to have
its pathogenesis.
of the root entry
and the left vagus nerve was the major control
the left heart
patients
for
in right side. In the present
was found
on the basis of surgical results that the left side
symmetrically
stroke
region
pressure.”
all the somatic and sensory function
metrical
by
in the rat9 and
of the medulla was sensitive to compression. central
caused
brainstem
decompression
of the left cranial
speculated
the
and his group have reported
cases with remission
(REZ)
between
area of the rostra1 ventrolateral
Jannetta
micro-vascular
experi-
hypertension.
hypertension
was a critical
In neurosurgery, clinical
have reported
and neurogenic
of the nucleus
concluded
is still unclear. Since
on the relationship
system
They demonstrated stimulation
Fig. 2 Drawing showing the intra-operative findings. The large hard aneurysm was observed behind the right cranial nerves IX and X. The aneurysm was located lateral to the root entry zone (REZ) of the right cranial nerves IX and X, which had been elevated by the aneurysm.
located
of essential hypertension
Reid and his colleaguesal’
following
caused by right VA aneurysm
Number 4
References 1. Fein JM, Frishman W. Neurogenic hypertension related to vascular compression of the lateral medulla. Neurosurgery 1980;6:615-22. 2. Jannetta PJ. Neurovascular compression in cranial nerve and systemic disease. Ann Surg. 1980;192:518-25. 3. Jannetta PJ. Cranial nerve vascular compression syndromes (other than tic douloureux and haemifacial spasm). Clin Neurosurg 1981;28:445-56. 4. Jannetta PJ, Gendell HM. Neurovascular compression associated with essential hypertension. Neurosurgery 1978;2:165. 5. Jannetta PJ, Gendell HM. Clinical observations on essential hypertension. Surg Forum 1979;30:431-32. 6. Jannetta PJ, Segal R. Neurogenic hypertension: Etiology and surgical treatment. 1. Observations in 53 patients. Ann Surg 1985;201:381-91. 7. Sugita K, Kobayashi S, Takemac T, Tanaka Y, Okudera H, Ohsawa M. Giant aneurysms of the vertebral artery. Report of five cases. J Neurosurg 1988;68:960-66.
October 1994
Essential hypertension
caused by right VA aneurysm
8.
Rcis DJ. Doba N. ‘I‘hc central nervous system and tt~rogenic hypertension. Prog Cardiovasc Dis 1974;17:51-71.
9.
R&s D,J. The nucleus tractus soliatrius and experitnrntal ttcurogenic hypertension: evidence for a central neural imbalance hypothesis of hypertensive disease. Adv l{iochem Psvchophar tnacol 1981;28:409-20. Kcis IIJ. Brain-stem mechanisms governing resting and t-eflex tone of precapillary vessels..J Cardiovasc Pharntacol 398.5:7 (Suppl. 3):s160-66. Kcis QJ, Ruggiero DA. Morrison SF. The Cl area of the I astral ventrolateral medulla oblongata. A critical brainstem region for control of resting and reflex itttegration of arterial pressure. Am J Hypertens I989:2:363S-374s. Naraghi R. &ah MR. Ll’alter GF, Kleinberg B. Arterial l~pertension and ncurovascular compression at the ~entct-lateral medull,t. A comparative microanatomical and p;tthologiral stud\,. ,J. Nettrosurg 1992:77: 103-12.
10.
1 I.
12.
Case report
13. .Jannetta PJ, Segal R, Wolfson SK, DLI~OVI~~ M, Scmba A. (:ook EE. Neurogenic hypertension: etiology and surgical treat ment. II. Observations in a ttonhtmlan primate model. Ann Surg 198.5;202:253-6 I. 1.4. Segal R. Gendell HM. Canfield D. Dujovny M,.Janncrt;t F’J. (:ardiovascular response to pttlsatilc pressurtapplied to ventrolateral medulla. Surg Forutl~ 1979:30:433-35. 15. Segal R. Jannetta F’J, Wolfso~~ SE;,Jr.. Dujovnv M. Cook IX. Implanted pulsatile balloon devict, for &lulatiott of ttcuro-vascular compression syndt-otiie5 in anittials.,J Neurosurg 1982;57:646-50. 16. Kleineberg B, Becker H. (;aab MK. N~~urovasculat compression and essential hypcrtcnsion. .In angiographic study. Neuroradiologv I!)9 I ;M:Z-8. 17. Kleineberg B, Becker H. Gash MR.‘Naraghi R. Essential hypertension associatrd with tteurovascular compression: Angiographic tindings. Ncurosttrgerv 19'.tz:30:834-41.
J. Clin. Neuroscience
Volume
1
Number
4
October
1994
279