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HELLENIC NEUROSURGERY
JANUARY - APRIL 2009, Volume 16, Number 1

CONTENTS
EXPERIMENTAL STUDY
A model for reproduction of experimental spinal cord injury................................................................................... 6
K. Violaris, E. Siotou, K. Kouzounias, T. Siozos, N. Skoulios, P. Sakellariou, I. Mpaltas,
V. Katsaridis, K. Nanassis

Clinical Studies
Multimodality neuromonitoring using intraparenchymal brain catheters.
A safe interventional procedure.................................................................................................................................... 13
P.G. Papanikolaou, K. Barkas, A. Venetikidis, K. Damilakis, G. Georgoulis, T.S. Paleologos,
E. Hatzidakis, T. Kyriakou
A study on possible anti-inflammatory function of serotoninergic antidepressants
in the treatment of chronic low back or cervical pain............................................................................................... 17
N. Sakellaridis, A. Kandyli, H. Gialouri, Ch. Kelesis, S. Gazi, K. Koniari, K. Tempos, L. Gregorakos

CASE REPORTS
Remission of glossopharyngeal neuralgia after radiofrequency thermocoagulation
of Gasserian gagglion in a patient with trigeminal and glossopharyngeal neuralgia........................................... 24
B. Christodoulou, G. Drositis, E. Dimitrakoudi, I. Baltas
Treatment of an acute interhemisphric subdural hematoma and review of the literature................................... 30
V. Panagiotopoulos, C. Kollatos, S. Raftopoulos, D. Konstantinou


- 2009, 16, 1

....................................................... 6
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experimental STUDY

2009, 16(1):6-12
HELLENIC NEUROSURGERY 2009, 16(1):6-12

A model for reproduction of experimental

spinal cord injury
ABSTRACT
AIM: This study was designed to develop an experimental model of rat spinal
cord contusion. METHODS: Incomplete cord injury was produced by a weightdrop device. Cord contusions were created at the level of eleventh thoracic
vertebrae after laminectomy. Rats were divided in three groups, L group with
animals undergoing laminectomy and no cord damage, and two groups of
different severity injuries (A and B), each containing ten animals. Neurological
examinations followed until six weeks after trauma. RESULTS: Group L
animals, undergoing laminectomy and no cord injury, had no neurological
deficits. Group A animals, bearing cord injuries of medium severity, presented
higher neurological scores than group B animals, which underwent heavier
cord contusions. Results of animals for each group separately presented minor
diversion. CONCLUSION: This device can be used in rat experimental studies
that require cord contusions. The method is accurate and injuries can de
reproduced with minor diversion. The apparatus has the capability to create
injuries of different severity.

Konstantinos Violaris1,
Eleni Siotou2,
Konstantinos Kouzounias4,
Thomas Siozos2,
Nikolaos Skoulios1,
Pavlos Sakellariou2,
Ioannis Mpaltas2,
Vasilios Katsaridis2,
Kimon Nanassis3

Nikosia General Hospital,

Cyprus
2
Papanikolaou General Hospital,
Thessaloniki
3
A Neurosurgery clinic, Aristotle
University, Thessaloniki
4
Navy Hospital, Athens
1

Key words: spinal cord, spinal cord injury, experimental model, contusion

INTRODUCTION
Spinal trauma is a common cause of severe disability in modern societies.
Acute spinal cord injury brings patients in an awful position as recovery of
lost ability in these cases is rare4. Injured axons of central nervous system
are not capable to regenerate7 and existing methods to restore lost neuronal
links are yet to be discovered8,9. Complete spinal cord injury, or transection,
(anatomical or functional) inhibits any hopes for neurological improvement
in man9. Functional improvement can only be seen in patients with incomplete SCI (such as contusion type).
Many experiments on the subject of SCI are conducted around the world.
Various models have been proposed with different animals. Frequently, rats
are used in animal models10,14,15. The main advantage of the rat model is that

:
Konstantinos Violaris
Neurosurgeon,
Neurosurgery Department, Nikosia
General Hospital, Cyprus
Tel.: 0035796717283
E-mail:

experimental spinal cord injury 7

the natural history of SCI mimics that of man20,22,25. In

rats with functional or anatomical cord transection,
no recovery is expected. On the contrary, rats with
incomplete cord injury may show some recovery of
locomotion17,21,24.
Although numerous studies concerning SCI have
been performed, various matters trouble scientists dealing with this subject11,12. For instance, the mechanism
for the production of injury must be reliable and easy
to use. Minimal animal preparation and minimal anesthesia time are desirable. Repetition of equal impact
SCI with the least possible variance is essential for
comparison across research groups16,20. Characteristics
of the cord contusion (severity, diameter, depth, time
of dura compression) must be strictly controlled by
the conductor of the experiment. Accurate repetition of cord trauma is crucial for standardization of
the experiments that would enable reliable testing of
neurological recovery of animals after SCI and the
effectiveness of therapeutic protocols5,9,14.
In addition, the apparatus inflicting the contusion
should have the ability to create multiple grades of
injury, since SCI in humans also appear with a range
of intensities. Controlled grading creation of SCI is
significant. The mechanism should have the potential
to produce SCI of designed intensity escalating from
minor cord contusion to functional transection, so
that the whole range of these lesions can be studied.

MATERIALS AND METHODS:

The injury model
A weight-drop contusion injury model was developed based on previous evidence1,2,22. Adult male
Fisher rats (8-12 weeks old), and weighing 300-350
grammars were individually housed in clear cages in
a controlled environment at a constant temperature of
21 C and humidity of 5010% with food and water
available at libitum. The animal room was on 12/12
hour light/dark cycle. All experimental procedures
and protocols were in accordance with the European
Council Directive 86/609 as well as the national and
institutional guidelines for animal care.
Rats were anesthetized by intraperitoneal injection
of hydrated chloral 4% (1 milliliter/100 grammars of
body weight). Dorsal surface of thoracic vertebrae 9-11
was exposed by dissection of overlying muscles. Spinal

process, ligaments and laminae of tenth and eleventh

thoracic vertebrae (th11 and th10) were removed with
fine instruments under magnification. The level of
th11 was recognized by the mammillary process of
th11, which can be seen protruding above the level of
rostral vertebral processes. Laminectomy of th11 was
performed to give full exposure of the dorsal surface
of the cord.
Contusion was carried out by a weight drop device.
Animals were divided into groups L (laminectomy
only, with two animals), A (ten animals) and B, also
containing ten animals. Group A animals underwent
a cord contusion created with a mass of 12 grammars
falling from a height of 10 centimetres. According to
previous research, severity of spinal cord injury created
with these standards is characterized as severe incomplete10,25. Group B animals underwent a heavier cord
injury, but not functional cord transaction, as a mass
of 20 grammars was left to drop from the same height.
The device (Figure 1) consisted of a metal tube
with adjustable height, containing at its lower end a
piston made of plastic. This piston acted as the interface
among the falling mass and the dorsal surface of the
cord. The cylinder was held perpendicularly over the
spinal cord by a three point stereotactic system that
allowed precise positioning. The weight, consisting of
a cylinder, was left to drop in the tube at an adjustable
height above the upper surface of the retracted piston.
The tube was lowered towards the surface of the cord
by the manipulator, with the piston very carefully

Figure 1. The apparatus used for the creation of cord contusions on rats.

placed on the dura matter over the dorsal surface of

the cord. The piston itself weighed 1grammar and did
not constrict the cord. The piston interface between
the falling mass and the cord had an important role
in succeeding accurate reproducible SCI, because it
could be accurately placed before the dropping of the
weight and then it provided directional stability during the impact. The piston could not compress the
dorsal surface of the cord more than 4 millimetres in
depth. The diameter of the compressing surface of the
piston was 3 millimetres. It was made out of plastic so
that it would cause a type of contusion injury and not
transection to the cord. After careful positioning of
the apparatus, the weight was left to drop. The drop
apparatus and the supporting rods were removed immediately following impact. After that, muscle fascia
and skin were sutured over the laminectomy site and
the animal was allowed to recover from anaesthesia
in a fit environment. Precautions were taken so that
animals would undergo as little as possible pain and
suffering. The bladder and bowel were controlled
manually by the animal carer, until the rats gained
control of urination defecation.
The falling weight has a velocity and kinetic energy
at impact that depends on its mass and the height that is
left to drop10,25. With this device, creation of repeatable
contusions is relatively easy, since it delivers a constant
force to the cord with a consistent contact speed22.
Neurological tests followed the creation of SCI,
beginning 48 hours post trauma, and were repeated at
1 week, 2 weeks, 4 weeks and 6 weeks after the injury.
Clinical evaluation-BBB test
The BBB test, by Basso, Beattie and Bresnahan2
was used for the evaluation of neurological progress
of the rats. This test was specifically designed for the
clinical examination of rats with SCI. It is a comprehensive scale of rats various levels of hind limbs and
body motion and coordination after SCI. The test
divides the ranking of motion behaviour of the rat
into 21 levels starting with 0 for no motion, and 21 for
normal walking. During this test, various parameters
such as movement of joints, walking with support from
hind limbs, coordination of forelimbs and hind limbs,
placement of foot, movement of tale and stability of
the body are examined. Writers divide the period of
recovery into primary (0-7), medium (8-13) and late
phase (14-21). The severity of SCI determines weather

, . 16, 1, 2009

the animal will progress to the first, second or third

phase and the time needed for this recovery.
Tests were performed by two examiners, trained
and experienced with the BBB test. The examinations
were blind (examiners did not have knowledge of
the identity of the animal). In cases where two given
scores were significantly different, the test was taken
again. Every examination lasted four minutes and all
tests were videotaped. During examination tests, the
highest score that rats achieved was noted. First test
was performed 48 hours after the injury and after that,
regular evaluations followed. Animals were examined
at 48 hours, 1 week, 2 weeks, 4 weeks and 6 weeks
after trauma.

RESULTS
Examination tests were performed at 48 hours, 1
week, 2 weeks, 4 weeks and 6 weeks after SCI. Average score of hind limbs for each animal was estimated
for the calculation of the rats total score. After that,
average of each group every given examination were
estimated. Description of movement behaviours that
follows correlates with scores achieved by the majority
of animals of both groups.
Group L animals (laminectomy only) presented
no neurological deficit.
On the examination two days after trauma, group
A and B animals presented with very slight motion of
one hind limb joint (the hip). On the test performed one
week after SCI, group A animals had a slight improvement, presenting extensive to moderate movement in
two joints (av. 2.21). Group B animals improved very
little, having movement of one or two joints (av. 1.4).
Two weeks after SCI, group A animals presented with
a minor improvement of their neurological outcome,
showing extensive movement of two joints of hind limbs
(av. 2.41). On the other hand, group B animals improved
also to some extent, exhibiting moderate movement
in two joints (av. 2.1). Four weeks after trauma, group
A animals presented again with higher rankings than
group B animals and showed wide movement of all
three joints of hind limbs (av.7.62). Animals of group
B improved slightly (av. 3.5) and were able to move all
three joints of hind limbs at a moderate degree. On
six weeks test, group A animals improved even more
and with an average score 12, were able to take often
or constant hind limbs steps with rare coordination of

experimental spinal cord injury 9

hind limbs and fore limbs. Animals of group B also

had higher scores and could show extensive motion
of two hind limb joints and moderate motion of the
third joint (av. 5.71). Average results of group A and
group B animals are given on tables 1 and 2.
The results of group A and group B had considerable differences. On the examination 48 hours post
SCI, both group animals had slight hind limb movement. On the examination 1 week post trauma, little
improvement was noticed for both group, with group A
animals achieving slightly better scores (2.21-1.4). Two
weeks after SCI, minor improvement was again seen in
both groups (2.41-2.1). On tests taken four weeks post
trauma, group A presented with significant improvement and achieved an average score of 7.62. Group B
animals also improved but their progress was slight
(av. 3.5) compared to group A. Six weeks after trauma,
group A animals presented with essential progress of
the locomotion of hind limbs (av. 12). Group B animals
improved also, but not as fine as group A animals5.71.
On the period from two weeks until six weeks post
trauma, group A animals presented with remarkable
improvement. Significant improvement at this certain
Table 1. Average neurological rankings of group A
and group B animals (BBB test).
Group
A average

Group
B average

2 days post SCI

1.08

1.05

1 week post SCI

2.21

1.4

2 weeks post SCI

2.41

2.1

4 weeks post SCI

7.62

3.5

6 weeks post SCI

12

5.71

Time of test

time period was also noted by other writers2 for rats

with contusions of similar intensity. On the same period, group B animals also advanced but their progress
was notably inferior. Group B animals never achieved
taking steps, or even plantar placing of a foot on the
floor. Their final average score shows that they did
not reach the second phase of recovery, as described
by the BBB test.
On the contrary, the majority of group A animals
were able to take often or constant hind limbs steps
and even showed coordination of hind limbs and fore
limbs rarely, reaching the higher steps of the second
phase of recovery on the BBB test.

DISCUSSION
For many years, numerous experiments are conducted around the world, studying various parameters
on the consequences of SCI. All these experimental
studies about SCI require a mechanism for the creation of cord injury.
Many different mechanisms of experimental SCI
have been proposed, with each of these devices having different orientations. Some of them try to imitate
the biomechanical way cord injuries are produced in
human. Others focus on the accuracy of the model.
A description of commonly mentioned models for
creating SCI follows.
1. Transection or semi-transection of spinal cord
with a surgical scalpel5,18,19, after laminectomy.
This method causes a totally controlled and easily reproducible injury. The disadvantage of the
method is that this kind of SCI is not often seen
in humans.
2. Placement of a surgical aneurysm clip on the SC

Table 2. Graphic demonstration of average neurological rankings of group A and group B animals (BBB test).

10

after laminectomy15,22. This causes acute compression of the SC. The severity of SCI can be controlled
by the period the clip stays on the cord.
3. Compression of the cord with a controlled dilatation of a balloon, placed in the epidural space15.
Severity of SCI is determined by the time of compression and by the size of balloon dilatation. This
apparatus tries to mimic some kind of SCI such as
cord compression in cases of spine fractures.
4. Placement of a mass in the epidural space1, left there
for certain time. Severity depends on the period
of compression. This apparatus also imitates the
production of SCI in human.
5. Compression of dura matter and spinal cord by a
mass that is directed by the function of an electromagnetic field23. This model was created in order
to produce SCI in a similar way that SCI is created
in human.
6. Falling of a mass, forcing an impact to compress
the spine, without previous laminectomy. This apparatus also mimics injuries often seen in human
patients. It requires minimal surgical preparation for
the animal. With this model, accurate reproduction
of equal severity injuries is not so easy13. This is a
significant disadvantage for this SCI production
concept.
7. Compression of exposed dura by an impact which
receives the force from a dropping mass after
laminectomy6,9. In our study an apparatus based
on this model was used. The severity of injury
can be determined by parameters such as the
mass of dropping weight or the height the mass is
dropped6,8. This method requires longer surgical
preparation but reproducible injuries are easily
achieved. In some experiments with weight-drop
devices, clinical and pathological results are not
aligned with the reported trauma impact, as that
is determined by the weight mass and the height
that is dropped from6,8,9,14. This disagreement could
be explained by the fact that different parameters
of the experiment, such as the kind of animal, air
resistance and frictional contact with the wall of
the drop tube may differ. Severity of impact depends on the release of kinetic energy but also on
the momentary change of the energy of the mass
as it compresses the cord. This quick release of
energy is called impulse, as described by Blight and

, . 16, 1, 2009

Decrescito3. According to these writers3, severity

of contusion is determined by the impulse, even
when different heights and weights are used. Even
when total kinetic energy is equal, impulse in fact
sets the clinical outcome of the impact. Time of
compression of the cord by the piston is important
for calculating the impulse of injury with this apparatus. This study3 suggests that the impulse of
weight drop contusion should be accounted as
a complicated mechanism, rather than just the
calculation of height and weight. Nevertheless, it
seems possible that setting strict constants on the
experiments parameters, may actually achieve accurate impulse of the force, similar clinical results
and related pathological results8,14.
In order to prove the sufficiency of the system, based
on previous data, we performed a laminectomy of th10
and th11 with no contusion on two animals ( group L)
and we used two groups of animals with spinal cord
contusions of different intensity at the level of th11;
Group A, with a contusion of medium severity; and
Group B, with a contusion of heavier intensity, but not
functional transection. Rats underwent neurological
evaluation at certain time points after the creation of
cord contusion. On the test 48 hours post injury, all
animals had very slight movement of hind limbs. In all
the rest examinations until six weeks after SCI, group
A animals achieved higher scores than group B. The
results of individual animals in each group did not
have great deviations.
Our study aimed on producing a device that could
create experimental contusion type injuries on rats
spinal cord. The apparatus was designed to create accurate impacts on the dura matter and subsequently
the thoracic spinal cord. The hitting point was perfectly
controlled. Control of the piston allowed strict confirm
of the depth of cord contusion, so that incomplete
cord damage would be created. The diameter of the
contusion on the cords surface was equal to the pistons
diameter and subsequently the same in all the examined
segments. Intensity of impact was set by the mass of
the dropping weight and the height it was dropped.
Neurological results, conducted according to the
BBB test, showed that group A animals suffered a cord
lesion less intense than group B. The manipulation of
the apparatus parameters determined the impact of
SCI. We showed that the device is capable to produce
cord injuries of graded severity easily. The apparatus

experimental spinal cord injury 11

is adjustable to different injury impacts, according to

the purpose of the experiment.
To conclude, we believe that this weight drop device
may be a useful tool for researchers who investigate

SCI. It is easy to use and highly accurate. These characteristics make this weight-drop device a reliable
mechanism for experiments regarding SCI that need
repeatable, contusion type cord injuries.

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fuction after spinal cord hemisection in newborn and

23. Stokes BT, Noyes DH, Behrmann DL. An electromechanical spinal injury technique with dynamic sensitivity. J
Neurotrauma 9(3):187-95, 1992.
24. Windle WF. Concussion, contusion, and severance of
the spinal cord. Pages 205-217 in W.F. Windle, Ed. The
spinal cord and its reaction to traumatic injury. Dekker,
New York, 1980.
25. Wrathall JR, Pettegrew RK, Harvey F. Spinal cord contusion in the rat: production of graded, reproducible, injury
groops. Exp Neurol 88: 108-122, 1985.

 2009, 16(1):13-16
HELLENIC NEUROSURGERY 2009, 16(1):13-16

Clinical study

, .
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.: 213 2077203
: 6974383283
Fax: 2105714442
e-mail: p.g.papanikolaou@gmail.com

14

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16

, . 16, 1, 2009

SU M M A RY
Multimodality neuromonitoring using intraparenchymal brain catheters.
A safe interventional procedure
Papanikolaou P.G., Barkas K., Venetikidis A., Damilakis K., Georgoulis G., Paleologos T.S.,
Hatzidakis E., Kyriakou T.
Neurosurgical Department, General Hospital of Nikaia Piraeus, Athens, Greece

Prevention of secondary brain ischemia is the major goal of neurosurgical intensive care for critical patients
with head injury or subarachnoid hemorrhage. Brain multimodality monitoring is essential for neurosurgical
intensive care. Our experience on use of intraparenchymal brain monitoring catheters is presented. Data of 54
patients was analyzed. All were catheterized for intracranial pressure, brain tissue oxymetry and microdialysis (3 catheters via the same burr hole). Additionally, 5 of them were catheterized for regional cerebral blood
flow as well via a second burr hole. In all cases the catheterization procedure took place on bed. There were
no rebarkable complications caused by catheterization and monitoring procedure. In 2 cases there were small
white matter contusions at three-lumen guides trajectory. In other 2 cases there were catheters tip contamination without clinical signs of infection. In 5 cases there was fracture of catheters or of the three-lumen guide
during insertion. As a conclusion, use of intraparenchymal brain monitoring catheters is a safe, practical and
reliable technique with a brief learning curve.
Key words: brain monitoring, intraparenchymal catheters, safety, reliability

1. Arabi Y, Memish ZA, Balkhy HH, et al: Ventriculostomyassociated infections: incidence and risk factors. Am J
Infect Control 33:137-43, 2005.

cerebral oxygenation in patients with severe head injuries:

brain tissue PO2 versus jugular vein oxygen saturation.
J Neurosurg 85:751-7, 1996.

2. Davis JW, Davis IC, Bennink LD, et al: Placement of intracranial pressure monitors: are normal coagulation
parameters necessary? J Trauma 57:1173-7, 2004.

8. Narotam PK, Morrison JF, Nathoo N: Brain tissue oxygen

monitoring in traumatic brain injury and major trauma:
outcome analysis of a brain tissue oxygen-directed therapy.
J Neurosurg 111:672-82, 2009.

3. Ehtisham A, Taylor S, Bayless L, et al: Placement of external

ventricular drains and intracranial pressure monitors by
neurointensivists. Neurocrit Care 10:241-7, 2009.
4. Harris CH, Smith RS, Helmer SD, et al: Placement of
intracranial pressure monitors by non-neurosurgeons.
Am Surg 68:787-90, 2002.
5. Hillered L, Persson L, Nilsson P, et al: Continuous monitoring of cerebral metabolism in traumatic brain injury:
a focus on cerebral microdialysis. Curr Opin Crit Care
12:112-8, 2006.
6. Hutchinson PJ, Menon DK, Czosnyka M, et al: Monitoring cerebral blood flow and metabolism, In : Head Injury,
Reilly PL, Bullock R (eds), Hodder Arnold, London, 2005,
pp : 215-245
7. Kiening KL, Unterberg AW, Bardt TF, et al: Monitoring of

9. Presciutti M, Schmidt JM, Alexander S: Neuromonitoring

in intensive care: focus on microdialysis and its nursing
implications. J Neurosci Nurs 41:131-9, 2009.
10. Sorani MD, Hemphill JC 3rd, Morabito D, et al: New
approaches to physiological informatics in neurocritical
care. Neurocrit Care 7:45-52, 2007.
11. Stiefel MF, Spiotta A, Gracias VH, et al: Reduced mortality rate in patients with severe traumatic brain injury
treated with brain tissue oxygen monitoring. J Neurosurg
103:805-11, 2005.
12. Vajkoczy P, Roth H, Horn P, et al: Continuous monitoring
of regional cerebral blood flow: experimental and clinical validation of a novel thermal diffusion microprobe. J
Neurosurg 93:265-74, 2000.


Clinical Study

2009, 16(1):17-23
HELLENIC NEUROSURGERY 2009, 16(1):17-23

. 56
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 19

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20

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 21

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22

, . 16, 1, 2009

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SU M M A RY
A study on possible anti-inflammatory function of serotoninergic antidepressants
in the treatment of chronic low back or cervical pain
Sakellaridis N., Kandyli A., Gialouri H., Kelesis Ch., Gazi S., Koniari K., Tempos K., Gregorakos L.4
Departments of Neurosurgery, Rheumatology, Internal Medicine and 4University Department
of Intensive Care, KAT National Hospital, Attica, Greece

Our purpose is to study if there is anti-inflammatory function of serotoninergic antidepressants in chronic low
back or cervical pain. Patients are included, who have low back or cervical pain of at least 6 months duration,
whose neuroradiological investigation has shown no need for operative or other special treatment and who
have failed in the usual conservative treatment. We use many inflammatory indexes and especially CRP. We
treat these patients with fluoxetine. We reevaluate them at one and three months. We statistically analyze our
data for 39 patients. CRP was improved in 6 of them. Paired t-test result for CRP before and after treatment is
p=0,22. This result is not statistically significant. We discuss the relevant bibliography.
Key words: Low back pain, cervical pain, serotoninergic anti-depressants, CRP, inflammatory indexes

1. Abdel-Salam OM, Nofal SM, El-Shenawy SM. Evaluation

of the anti-inflammatory and anti-nociceptive effects
of different antidepressants in the rat. Pharmacol Res
48(2):157-65, 2003.
2. Ariciolu F, Buldanliolu U, Salanturolu G et al. Evaluation of antinociceptive and anti-inflammatory effects of
venlafaxine in the rat. Agri 17(4):41-6, 2005.

population. Psychosom Med 66(5):679-83, 2004.

7. Ford DE, Erlinger TP. Depression and C-reactive protein in US adults: data from the Third National Health
and Nutrition Examination Survey. Arch Intern Med
164(9):1010-4, 2004.

3. Bianchi M, Sacerdote P, Panerai AE. Fluoxetine reduces

inflammatory edema in the rat: involvement of the pituitary-adrenal axis. Eur J Pharmacol 263(1-2):81-4, 1994.

8. Gebhardt K, Brenner H, Sturmer T et al. The course of

high-sensitive C-reactive protein in correlation with pain
and clinical function in patients with acute lumbosciatic
pain and chronic low back pain - a 6 months prospective
longitudinal study. Eur J Pain 10(8):711-9, 2006.

4. Elovainio M, KeltikangasJarvinen L, Pulkki-Raback L,

et al. Depressive symptoms and C - reactive protein: the
cardiovascular risk in young Finns study. Psychol Med
36:797-805, 2006.

9. Kim SK, Jung I, Kim JH. Exercise reduces C-reactive

protein and improves physical function in automotive
workers with low back pain. J Occup Rehabil 18(2):218-22,
2008.

5. Clauw DJ, Crofford LJ. Chronic widespread pain and

fibromyalgia: what we know, and what we need to know.
Best Pract Res Clin Rheumatol 17(4):685-701, 2003.

10. Kuo HK, Yen CJ, Chang CH et al. Relation of C-reactive

protein to stroke, cognitive disorders, and depression
in the general population: systematic review and metaanalysis. Lancet Neurol 4(6):371-80, 2005.

6. Douglas KM, Taylor AJ, OMalley PG. Relationship between depression and C-reactive protein in a screening

11. Loucks EB, Berkman LF, Gruenewald TL et al. Relation

 23

of social integration to inflammatory marker concentrations in men and women 70 to 79 years. Am J Cardiol
97(7):1010-6, 2006.
12. Mohan V, Deepa R, Velmurugan K et al. Association of
C-reactive protein with body fat, diabetes and coronary
artery disease in Asian Indians: the Chennai Urban Rural
Epidemiology Study (CURES-6). Diabet Med 22(7):86370, 2005.
13. OBrien S, Scott L, Dinan T. Antidepressive therapy and
C-reactive protein levels. Br J Psych 188: 449-452, 2006.
14. Roumestan C, Michel A, Bichon F et al. Anti-inflammatory
properties of desipramine and fluoxetine. Respir Res 8:35,
2007.
15. Staiger TO, Gaster B, Sullivan MD et al. Systematic review
of antidepressants in the treatment of chronic low back
pain. Spine 28(22):2540-5, 2003.
16. Toker S, Shirom A, Shapira I et al. The association between burnout, depression, anxiety, and inflammation

biomarkers: C-reactive protein and fibrinogen in men

and women. J Occup Health Psychol 10(4):344-62, 2005.
17. Vahdat SM, Vahdat SZ, Moshtaaghi M et al: The relationship between depression and serum ferritin level. Eur J
Clin Nutr 61: 532535, 2007.
18. Von Kanel R, Hepp U, Kraemer B et al. Evidence for
low-grade systemic proinflammatory activity in patients
with posttraumatic stress disorder. J Psychiatr Res 41(9):
744-752, 2007.
19. Wolfe F. The C-reactive protein but not erythrocyte
sedimentation rate is associated with clinical severity in
patients with osteoarthritis of the knee or hip. J Rheumatol
24(8):1486-8, 1997.
20. Yaron I, Shirazi I, Judovich R et al. Fluoxetine and amitriptyline inhibit nitric oxide, prostaglandin E2, and
hyaluronic acid production in human synovial cells and
synovial tissue cultures. Arthritis Rheum 42(12):2561-8,
1999.

 2009, 16(1):24-29
HELLENIC NEUROSURGERY 2009, 16(1):24-29

CASE REPORT

,
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.-Fax: 2313030284
: 6977707178
E-mail: cvassilis@gmail.com

 25

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, . 16, 1, 2009

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SU M M A RY
Remission of glossopharyngeal neuralgia after radiofrequency thermocoagulation of
Gasserian gagglion in a patient with trigeminal and glossopharyngeal neuralgia
Christodoulou B.1, Drositis G.1, Dimitrakoudi E.2, Baltas I.3
1

Private Clinic Bioclinic Thessaloniki Greece, 2 A Department of Neurology, Ahepa Hospital, Thessaloniki Greece,
3
Department of Neurosurgery G Papanikolaou Hospital, Thessaloniki Greece.

A 59-year- old man developed simultaneous left trigeminal and glossopharyngeal neuralgia. Episodes initiated
three years before the operation. MRA showed compression of the left trigeminal nerve by the left superior
cerebellar and loop of the left vertebral arteries. The left glossopharyngeal nerve was also compressed by the
left vertebral artery. Patient initially was treated by carbamazepine with little effect, requiring increase in daily
dosage. After a period of response, patient deteriorated and topiramate, baclofen and pregabalin was added.
Because of history of myocardial infarction, patient denied major surgery of microvascular decompression. He
underwent percutaneous radiofrequency thermocoagulation of Gasserian gagglion. Three days after the operation patient became free of symptoms from trigeminal neuralgia and fifteen days later from glossopharyngeal
neuralgia. One year postoperatively the patient is pain free. We conclude that percutaneous radiofrequency
thermocoagulation may be applied for simultaneous trigeminal and glossopharyngeal neuralgia if craniotomy
is contraindicated.
Key words: trigeminal neuralgia, glossopharyngeal neyralgia, percutaneous radiofrequency thermocoagulation.

1. Cheng-Yuan W, Meng F, Xu Shu, et al. Selective percutaneous radiofrequency thermocoagulation in the

treatment of trigeminal neuralgia: report of1860 cases.
Ch Med J 117: 467-70, 2004
2. Childs A, Meaney J, Ferrie C, et al. Neurovascular compression of the trigeminal and glossopharyngeal nerve:
three case reports. Arch Dis Child 82:311-15, 2000
3. FrommG, Terrence C, Chattha A, et al. Role of inhibitory
mechanisms in trigeminal neuralgia. Neurology 31:683687, 1981
4. Fromm G, Terrence C, Maroon J. Trigeminal neuralgia.
Current concepts regarding etiology and pathogenesis.

Arch Neurol 41: 1205-07, 1984

5. Greenstein B, Greenstein A. Color atlas of neuroscience.
Neurophysiology, 2000, pp222-230
6. Love S, Coacham H. Trigeminal neuralgia: Pathology
and Pathogenesis. Brain 124:2347-2360, 2001
7. Nurmikko T, Eldridge P. Trigeminal neuralgia. Pathophysiology, diagnosis and current treatment. Br J Anaesth
87:117-32, 2001
8. Rasminsky M. Ectopic generation of impulses and crosstalk in spinal nerve roots of `dystrophic mice. Ann Neurol
3: 3517, 1978
9. Rengachary S, Ellenbongen R. Principles of Neurosurgery.

 29

2nd ed., 2005, pp 777-783

10. Rosen T. Trigeminal neuralgia and glossopharyngeal
neuralgia. Neurol Clin 22:185-206, 2004
11. Rosenkopf K. Current concepts concerning the etiology
and treatment of trigeminal neuralgia. Cranio 7: 312-8,
1984
12. Sekhar L, Fessler R. Atlas of Neurosurgical Techniques.
Brain, 2006
13. Sessle B. Acute and chronic craniofacial pain: Brainstem
mechanisms of nociceptive transmission and neuroplasticity and their clinical correlates. Crit Rev Oral Biol Med
11: 57-91, 2000

14. Sessle B. Neural mechanisms and pathways in craniofacial

pain. J Neurol Sci 26: 7-11, 1999
15. Smith KJ, McDonald WI. Spontaneous and mechanically
evoked activity due to central demyelinating lesion. Nature
286: 1545, 1980
16. Warren H, Kotsenas A, Czervionke L. Trigeminal and
concurrent glossopharyngeal neuralgia secondary to
lateral medullary infarction. AJNR 27: 705-07, 2001
17. Vago-Glossopharyngeal and geniculate Neuralgia. In
Youmans Neurological surgery, Van Loveren H, Tew J,
Thomas G. Saunders, 3rd Edition., vol 6, 3944-45, 1990

 2009, 16(1):30-38
HELLENIC NEUROSURGERY 2009, 16(1):30-38

CASE REPORT

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SU M M A RY
Treatment of an acute interhemisphric subdural hematoma and review of the literature
Panagiotopoulos V.1, Kollatos C.2, Raftopoulos S.1, Konstantinou D.1
1

Department of Neurosurgery of University Hospital of Patras, 2Medical school of University of Patras

Interhemispheric subdural hematoma (ISH), a collection of blood within the interhemispheric fissure is one
of the rare forms of intracranial hemorrhages following head injury. It is more frequent in male adults over
50 years old, especially those with blood clotting disturbances. Acute ISH is classically presented with specific
neurological abnormalities, such as disturbances of consciousness, hemiparesis or more often with the Falx
Syndrome after a post-traumatic delay of several hours. CT scan is the diagnostic tool of choice for ISH.

 37

Treatment may be conservative management for stable patients without deterioration of the level of consciousness or craniotomy in case of progressive deterioration. We present a case of successful surgical removal of an
extended fronto-temporo-occipital acute ISH of traumatic origin and we perform a review of the literature.
Key words: Acute interhemispheric subdural hematoma, falx syndrome, head injury.

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