Clinical Neurology and Neurosurgery 115 (2013) 2207–2212

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Clinical Neurology and Neurosurgery

journal homepage: www.elsevier.com/locate/clineuro

Case report

Entrapment of temporal horn: First case of bilateral occurrence and

review of literature
Corrado Iaccarino a,b,∗ , Antonio Romano a,b , Vania Ramponi a,b , Davide Nasi c ,
Massimo Maggi d , Rosario Pascarella d , Reza Ghadirpour a,b , Franco Servadei a,b
a
Neurosurgery-Neurotraumatology Unit, Emergency Department, University Hospital of Parma, Parma, Italy
b
Emergency Neurosurgery Unit, Neuromotor Department, IRCCS “Arcispedale Santa Maria Nuova” of Reggio Emilia, Reggio Emilia, Italy
c
Clinic of Neurosurgery, Department of Neurological Sciences, Polytechnic University of Marche, Ancona, Italy
d
Neuroradiology Unit, Diagnostic Imaging and Laboratory Medicine Department, IRCCS, “Arcispedale Santa Maria Nuova” of Reggio Emilia, Reggio Emilia,
Italy

a r t i c l e i n f o

Article history:
Received 25 February 2013
Received in revised form 1 June 2013
Accepted 9 June 2013
Available online 11 July 2013

Keywords:
Hydrocephalus
Shunt insertion
Frameless neuronavigation
CSF dynamic
Ventricle malformation

1. Introduction 2. Case report

The entrapped temporal horn is a rare entity, caused by an
obstruction of the trigone of the lateral ventricle which seals off
the temporal horn from the rest of the ventricular system.
This form of focal hydrocephalus has been described in a variety
of diseases including central nervous system infections, hemor-
rhages, trauma, extra-axial or intra-axial tumors, postoperative
scarring within the trigone, neurosarcoidosis and xanthogranu-
lomatosis [1–20]. Clinical presentation is often with headache,
seizures, hemiparesis, and visual field deficits [9]. Within the
trapped temporal horn, the choroid plexus continues to produce
cerebro spinal fluid (CSF), resulting in progressive dilation; the
dilated temporal horn then behaves as a mass lesion [7].
Since 1947, thirty-six cases have been reported (Table 1) [1–20].
To the best of our knowledge this is the first case of bilateral
entrapped temporal horn.
∗ Corresponding author at: Neurosurgery-Neurotraumatology Unit, Emergency
Department, University Hospital of Parma, Parma, Italy. fax: +39 0521704634.
E-mail address: ciaccarino@ao.pr.it (C. Iaccarino).
A 50-year-old male patient with partial seizures was admitted to
our department for the first time, due to a one-month progressive
history of gait disturbance, subjective vertigo, and headache. A clin-
ical history of migraine, prostatic hypertrophy and celiac disease is
reported.
The patient reported a nine-year history of episodic migraine,
and partial seizures (alienation, right hand paresthesia). The
patient underwent clinical and neuroradiological follow-up under
antiepileptic therapy. A first CT scan repeated two years later dis-
closed no brain pathologies (Fig. 1A and B). The patient presented
fluctuating symptoms, so a first MRI was performed after further
three years. The MRI showed a bilateral enlarged septed temporal
horns, with a prevalence of the left side, with no contrast enhance-
ment, no mass effect (Fig. 1C). The stationary size of the temporal
horns was observed until emergency admission (Fig. 1D and E).
Upon admission an emergency CT scan disclosed a fur-
ther expansion of the temporal horns. MRI examination with
paramagnetic contrast confirmed the asymmetric dilatation
(right > left) of the temporal horns with intraventricular septa.
The ventricular content was isointense to CSF in all sequences
(Fig. 3A and B). There where no dependent changes of the remaining
portions of the ventricular system, the parenchyma and the

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2208 C. Iaccarino et al. / Clinical Neurology and Neurosurgery 115 (2013) 2207–2212

Table 1
Summary of reported cases from 1947 to 2013.

Author, year, source Sex, age Side Cause of entrapment Treatment

Cairns, 1947 [3] M, NR NR Penetrating wound Coagulation of plexus choroideus,

Smith, 1979 [17]
Maurice-Williams, 1986 [11]
Ofori-Kwakye, 1986 [13]
Schlitt, 1986 [15]
Yamamoto, 1987 [19]
Bruck, 1991 [2]
Tsugane, 1992 [18]
Watanabe, 1999 [20]
Coria, 2000 [5]
Parrent, 2000 [14]
Hamada, 2006 [6]
Maurya, 2007 [12]
Lyngdoh, 2007 [10]
Berhouma, 2008 [1]
Singh, 2010 [16]
Hervey-Jumper, 2010 [7]
Chen, 2011 [4]
Kamali, 2011 [8]
Krähenbühl, 2013 [9]
Present case, 2013
ventriculostomy into 3rd ventricle
M, 19 y NR Penetrating wound Resection of plexus choroideus
NR, 7 m NR Subependymal hemorrhage suspected None, diagnosed at autopsy
NR R Grade II WHO astrocytoma NR
NR R Mass of unspecified origin NR
NR R Meningioma NR
F, 23 y R Recurrent glioma Direct communication to the atrium
F, 35 y R Tuberculous meningitis VAS
F, 30 y L Removal of AVM VPS
F, 35 y R Cryptococcal meningoencephalitis EVS
F, 33 y L Neurosarcoidosis Drainage of trapped temporal horn and VPS
F, 2 y L Multiple streptococcal brain abscess VPS
M, 50 y L Xanthogranuloma of choroid plexus Removal
M, 35 y R Tuberculous meningitis EVS followed by VPS
F, 44 y R ␣ and ␤ streptococcal brain abscess EVS followed by VPS
M, 16 y L Intraventricular hemorrhage by AVM rupture VPS
F, 70 y R Intracranial surgery for a giant basilar aneurysm Conservative
M, 68 y R Cryptococcal meningitis Endoscopic fenestration of the choroidal
fissure
F, 7 m L Arachnoid cyst Endoscopic ventriculo-cyst-cysternostomy
F, 25 y L Intraventricular hydatid cyst Removal
M, 12 y L Intraventricular meningioma Removal
F, 15 y L Intraventricular meningioma Removal
M, 60 y L Intraventricular meningioma Removal followed by VPS
F, 42 y R Neurosarcoidosis Temporal tip lobectomy
F, 35 y R Neurocysticercosis Endoscopic removal
F, 35 y R Neurocysticercosis Removal
M, 47 y L Ependymoma in the left atrium Fronto-temporal shunt
F, 70 y R B-cell CNS lymphoma Fronto-temporal shunt
F, 69 y R Glioblastoma multiforme Fronto-temporal shunt
M, 41 y R Meningioma Temporal horn to prepontine cistern shunt
F, 25 y L Intraventricular hydatid cyst Removal
F, 8 y R Intraventricular hydatid cyst Cyst’s marsupialization
M, 15 m MH Postnatal CNS infection (haemophilus influenza) Endoscopic temporal ventriculocisternostomy
followed by VPS
F, 10 m R After resection of xanthogranulomatous lesion Endoscopic temporal ventriculocisternostomy
(Systemic juvenile xanthogranulomatosis)
F, 66 y L After resection of anaplastic glioma Endoscopic temporal ventriculocisternostomy
F, 15 y R After resection of CNS ganglioneuroblastoma Endoscopic temporal ventriculocisternostomy
M, 50 y L+R Septed temporal horns (?) Bitemporal horn-peritoneal shunt

AVM, Arteriovenous Malformation; CNS, central nervous system; EVS, external ventricular shunt; F, female; L, left; M, male; m, months-old; MH, multiloculated hydro-
cephalus; NR, not reported; R, right; VAS, ventriculoatrial shunt; VPS, ventriculoperitoneal shunt; WHO, world hearth organization; y: years-old.

subarachnoid spaces. The CSF dynamics study showed normal sys-
tolic and diastolic kinetics levels. The low flow in the posterior part
of the left ventricle was interpreted as a suspicious finding for com-
munication. T2* sequence showed no signs of previous bleeding.
Not restricted to the Diffusion Weighted Imaging (DWI) sequences.
During lumbar puncture the CSF pressure decreased from
21 mmHg to 12 mmHg after removal of 30 mL. The CSF appearance
was clear, fluid. The laboratory values of all the CSF components
were in normal range. The complete blood count, the C-reactive
protein (CRP) and the erythrocyte sedimentation rate (ESR) were
preoperative tested disclosing normal. In Table 2 the laboratory test
work up performed at admission and two days after operation are
summarized.
On neurological examination, he was alert, with ataxic gait, pro-
gressive headache. During the night he presented a partial seizure,
therefore surgery was planned for the day after.
frameless magnetic neuronavigation system (AxiEMTM , Medtronic
Inc., Boulder, CO, USA) the registration of the patient was accom-
plished.
Bilateral posterior parietal burr holes were then placed (Fig. 3D).
After bipolar coagulation of the dura mater and small pial cor-
ticectomies, an active neuronavigated stylet was inserted into the
catheters to ensure the placing shunt tubes under optical con-
trol on the neuronavigator’s monitor. After evident good flow of
CSF, 20 mL was collected for a new CSF physical–chemical and
culture examination. The two catheters were then joined using a
“Y” shaped connector with a single programmable valve (Hakim-
Medos CODMANTM ) then tunneled peritoneal tubing connected.
Prophylactic antibiotic injection was done at according to surgeon
preference.
2.2. Postoperative course

2.1. Operation Postoperative period was uneventful. The neurological deficits

Preoperatively, the trajectories of shunts insertion were planned
using neuronavigation station (Stealth Station S7TM , Medtronic
Inc., Boulder, CO, USA). After anesthesia induction, the patient was
placed supine with a slight cervical anterior flexion. The head of
the patient was not affixed in the Mayfield head holder. With
sudden disappeared after surgery. The CT scan confirmed correct
positioning of the catheters and the reduction of the temporal horns
volume (Fig. 3E and F). The postoperative laboratory values of CSF
components showed a xanthochromic color, protein 163 mg/dL
(n.v. 45–75 mg/dL), glucose 42 mg/dL (n.v. 45–75 mg/dL), lac-
tate 28.3 mg/dL (n.v. 10.8–18.9 mg/dL), white blood cells 3/␮L
 C. Iaccarino et al. / Clinical Neurology and Neurosurgery 115 (2013) 2207–2212 2209

Table 2
Preoperative and II day postoperive main laboratory tests work up is not suggestive for any inflammatory or infective process.

Preoperative II day postoperative Range

Liquor
Gross examination Clear, fluid Xantochromic
Glucose 40.0 mg/dL 42.0 mg/dL 45–75 mg/dL
Total protein 70.0 mg/dL 1620 mg/dL 45–75 mg/dL
Lactate 15.2 mg/dL 28.3 mg/dL 10.8–18.9 mg/dL
WBC count 2 cells/␮L 3 cells/␮L 0–5 cells/␮L
Gram stain Negative Negative
Culture
Aerobic bacteria Negative Negative
Anaerobic bacteria Negative Negative
Fungi Negative Negative

Blood
WBC count 5.210 cells/␮L 7.210 cells/␮L 4000–10,000 cells/␮L
RBC count 5.76 million cells/mcL 4.89 million cells/mcL 4.5–6 million cells/mcL
Hb 15.9 g/dL 14.1 g/dL 14–17.5 g/dL
Hematocrit 47.8% 41.2% 40–52%
MCV 88.6 fL 84.05 fL 80–95 fL
MCH 29.2 pg/cell 28.1 pg/cell 26–32 pg/cell
MCHC 33 g/dL 34.1 g/dL 32.5–36 g/dL
Platelets 241 cells/␮L 222 cells/␮L 150–450 cells/␮L
ESR 3 mm/h 15 mm/h 2–38 mm/h
CRP <1 mg/dL 17 mg/dL ≤1 mg/dL
PCT – <0.1 ng/dL <0.1 ng/dL
FTA-Abs Negative
PT 10.1 s – 9–13 s
PTT 26.7 s – 25–35 s
INR 1 – 0.8–1.2

CRP, C-reactive protein; ESR, erythrocyte sedimentation rate; FTA-Abs, fluorescent treponemal antibody – absorption; Hb, hemoglobin; INR, international normalized ratio;
MCH, mean corpuscular hemoglobin; MCHC, mean corpuscular hemoglobin concentration; MCV, mean corpuscular volume; PCT, procalcitonin; PT, prothrombin time; PTT,
partial thromboplastin time; RBC, red blood cells; WBC, white blood cells.

Fig. 1. (A) First CT scan performed in 2003 for migraine and partial seizures that disclosed no brain pathologies; (B) follow-up CT scan performed in 2005 confirmed absence of
hydrocephalus. Nevertheless a slight enlargement seems to be present in the temporal horns, with several septa, the neuroradiologist interpreted the findings as inconclusive
and produced a final negative report; (C) axial T1-w scan with gadolinium administration. The first MRI was performed in 2008 for fluctuating symptomatology (migraine, not
seizures) where an enlarged septed temporal horns with a prevalence of the left side were disclosed. No evidence of contrast enhancement, mass effect, neither dislocation
of cerebral sulci and internal capsule; (D) axial T1-w scan with gadolinium administration. The second MRI performed two years later showed a stable size of the temporal
horns. No change in neurological status is reported; (E) axial T1-w scan with gadolinium administration and Coronal T2-w scan of the MRI performed in 2012 after emergency
admission. An increase of dilatation of the temporal horns (with asymmetry right > left) despite previous MRI was disclosed.
2210 C. Iaccarino et al. / Clinical Neurology and Neurosurgery 115 (2013) 2207–2212

Fig. 2. The first CT scan performed in 2003 disclosed. (A) An enlarged fourth ventricle with a latero-lateral diameter of 16.9 mm; (B) A regular size of third ventricle and
foramen of Monro; (C) no evidence of aqueductal stenosis. A cerebral MRI performed in 2008, five years later the first CT scan disclosed; (D) a stable size of the fourth ventricle,
compared with the previous CT scan; (E) no evidence of third ventricle enlargement; (F) no evidence of aqueductal stenosis. The MRI performed at admission disclosed; (G)
a stable size of the fourth ventricle, with a diameter of 17 mm, compared to 16.9 mm of the first CT scan performed 9 years previously; (H) no further enlargement of third
ventricle respect to the previous MR and (I) no changes of the aqueduct.

(n.v. 0–5 cells/␮L), some red blood cells. The culture examination
showed no bacterial infection, neither fungine growth, even in the
preoperative and postoperative CSF samples.
Four months after surgery a complete seizure control was
achieved with the same preoperative antiepileptic therapy. No gait
disturbance neither migraine were reported.
3. Discussion
Entrapment of temporal horn was first termed in 1947 by Cairns
et al. [3]. To the best of our knowledge this is the first reported case
with a progressive enlargement of both trapped temporal horns.
Previously twelve cases of the left temporal horn and seventeen
cases of the right temporal horn entrapment were reported [1–20].
The entrapment is described due to choroids plexitis, intraven-
tricular hemorrhage, intraventricular hydatid cyst, intraventricular
arachnoid cyst, brain abscesses, cryptococcal meningitis, previ-
ous intraventricular surgery, neurosarcoidosis, neurocysticercosis,
intra and extraventricular meningiomas, xanthogranulomas of the
choroid plexus, systemic juvenile xanthogranulomatosis, gliomas
and B-cell CNS lymphoma [1–20]. In the presented case the exclu-
sion of both temporal horns is apparently not secondary to other
previous causes. The enlarged fourth ventricle occurred since the
first CT scan performed 9 years previously with a stable size showed
in the MRI performed at admission (Fig. 2A, D, and G). No evidence of
increasing of third ventricle or Sylvian aqueduct size was disclosed
during the neuroradiological follow-up (Fig. 2).
The developing of the ventricular enlargement after previous
normal CT scan might suggest a hypothetical infective process.
No exposition to any infectious pathogens, either endemic to his
region or by travel, was reported by the patient and his family. After
gadolinium administration no contrast enhancement of the ventri-
cular system was disclosed during the neuroradiological follow-up.
Laboratory tests confirmed no inflammatory condition.
Continued secretion of CSF by the choroid plexus within the
temporal horn leads it to expand when there is an obstruction of
the flow from the rest of the ventricular system. In the presented
case the intraventricular septa of both temporal horns disclosed
at MRI could support this hypothesis (Fig. 2A and B). The gait
disturbance appeared as onset of a neurological worsening, after
a nine-year history of migraine and partial seizures. During this
period a quite stationary clinical status was observed, despite the
neuroimaging studies disclosed the progressive enlargement of
the temporal horns. The enlargement was observed only at one
MRI after five years of observation, while a MRI two years later
showed no progressive increase of ventricular size (Fig. 1C and D).
Therefore this could be the explanation of a conservative choice in
the management of the patient before the first admission to our
observation.
Treatment could be performed endoscopically by communi-
cating the trapped space to the rest of the ventricular system or
opening the ventricular isolation into subarachnoid spaces. Also
the drainage of the isolated temporal horn could be achieved
via a shunt system including classically ventriculoperitoneal or
 C. Iaccarino et al. / Clinical Neurology and Neurosurgery 115 (2013) 2207–2212 2211

Fig. 3. (A) Axial T1-w scan with gadolinium administration performed after emergency admission confirmed the dilatation of the temporal horns (with asymmetry right > left)
associated to intraventricular septa (white arrows); (B) coronal T2-w scan with gadolinium administration. The temporal horns content is isointense to cerebro-spinal fluid
as in T1 sequences; (C) screenshot of the trajectory planning at preoperative neuronavigation planning (Stealth Station S7TM , Medtronic Inc., Boulder, CO, USA). On axial T1-w
scan the trajectory is planned to ensure the positioning of catheters through the entire length of the temporal horn (dot lines); (D) screenshot of the 3D model where the
entry points position (white arrows) are checked; (E) postoperative CT scan showed good positioning of the catheters; and (F) coronal reconstruction of postoperative CT
scan showed the reduction of the temporal horns volumes.

ventriculoatrial shunting. Recently internal shunting by stereotac- head of the patient in the same supine position for both burr holes
tic placement of a ventricular catheter to the frontal horn or to the (Fig. 3D). The magnetic neuronavigation system avoided the fixa-
prepontine cisterns have been described. However the manage- tion of the head in the Mayfield head holder, so the position was
ment of this rare condition is still under debate [9]. adapted to the different phases of the shunting procedure, and the
In nine cases the surgical treatment focused on the entrap- patient was kept in the same supine position for the peritoneal
ping cause [1,2,8,10,16]. In six cases an endoscopic procedure approach. The catheters insertion technique allows to minimize
was proposed: a fenestration of the choroidal fissure to avoid the CSF outflow, without risk of brainshift.
insertion of a device in the presence of infected CSF, a ventriculo-
cyst-cysternostomy in the prepontine cistern for a recurred
4. Conclusion
enlargement of an arachnoid cyst and temporal ventriculocister-
nostomy [6,9,14].
In all cases the entrapment of temporal horn is due to a sealing
The CSF diversion is the most common treatment: one external
off from ventricular system caused by extraventricular or intraven-
drainage, four cases of intraventricular shunting, one ventriculoa-
tricular causes. The enlargement of the entrapped temporal horn is
trial and nine ventriculo-peritoneal shunts [4,7,10,11,13,15,18–20],
secondary to the CSF production, therefore an aggressive treatment
including one case for recurrence of trapped temporal horn after
should always be considered also in patients with no progressive
endoscopic procedure [9].
symptoms. The frameless magnetic neuronavigation system allows
In the presented case the treatment was a placement of a bitem-
a safe and effective positioning of intraventricular catheters even
poral horn-peritoneal shunt. In cases of temporal horn entrapment
in case of complex trajectory, such as in this first case of bilateral
the ventricular anatomy is usually distorted. The neuronavigation
entrapment.
is advocated as helpful to determine the optimal location to per-
form the ventriculostomy, as reported in all but one endoscopic
cases. In the presented case an endoscopic bilateral approach could Disclaimer
have compromised the reliability of navigation, due to the brain-
shift secondary to CSF outflow and Ringer Lactate rinsing through The authors report no conflict of interest concerning the mate-
the endoscope. Moreover on preoperative imaging no clear evi- rials or methods used in this study or the findings specified in this
dence of a thinned wall between the temporal horn and basal CSF paper.
pathways was disclosed.
The authors used frameless neuronavigation technique, also
reported by Hervey-Jumper et al. [7], that took advantage to ensure References
the positioning of catheters through the entire length of the tem-
[1] Berhouma M, Abderrazek K, Krichen W, Jemel H. Apropos of an unusual and
poral horn, with the tip reaching the excluded septed parts of menacing presentation of neurosarcoidosis: the space-occupying trapped tem-
ventricle. The entry points position was low enough to keep the poral horn. Clinical Neurology and Neurosurgery 2009;111:196–9.
2212 C. Iaccarino et al. / Clinical Neurology and Neurosurgery 115 (2013) 2207–2212
[2] Bruck W, Sander U, Blanckenberg P, Friede LR. Symptomatic xanthogranu-
loma of choroid plexus with unilateral hydrocephalus. Journal of Neurosurgery
1991;75:324–7.
[3] Cairns H, Daniel P, Johnson RT, Northcroft GB. Localized hydrocephalus
following penetrating wounds of the ventricle. British Journal of Surgery
1947;55(Suppl. 1):187–97.
[4] Chen CC, Kasper EM, Zinn PO, Warnke PC. Management of entrapped temporal
horn by temporal horn to prepontine cistern shunting. World Neurosurgery
2011;(November) [Epub ahead of print].
[5] Coria F, Bahíllo Marcos E, Moral Blanco M, García Gutiérrez P, Ortiz Sáenz de
Santa María R. Late-onset isolated gelastic epilepsy secondary to entrapment
of the right temporal horn. Neurologia 2000;15(May (5)):204–7.
[6] Hamada H, Nonaka Y, Kusuka Y, Nakazaki H, Abdullah SH, Oi S. Huge arachnoid
cyst incorporating choroid plexus. Child’s Nervous System 2006;22:420–3.
[7] Hervey-Jumper SL, Ziewacz JE, Heth JA, Sullivan SE. Frontal-to-temporal horn
shunt as treatment for temporal horn entrapment. Journal of Neurosurgery
2010;112:410–3.
[8] Kamali NI, Huda MF, Srivastava VK. Intraventricular hydatid cyst causing
entrapped temporal horn syndrome: case report and review of literature. Trop-
ical Parasitology 2011;1(2):113–5.
[9] Krähenbühl AK, Baldauf J, Gaab MR, Schroeder HW. Endoscopic temporal ven-
triculocisternostomy: an option for the treatment of trapped temporal horns.
Journal of Neurosurgery: Pediatrics 2013;11:568–74.
[10] Lyngdoh BT, Giri PJ, Behari S, Banerji D, Chhabra DK, Jain VK. Intraven-
tricular meningiomas: a surgical challenge. Journal of Clinical Neuroscience
2007;14:442–8.
[11] Maurice-Williams RS, Choksey M. Entrapment of the temporal horn: a form of
focal obstructive hydrocephalus. Journal of Neurology, Neurosurgery & Psychi-
atry 1986;49(March (3)):238–42.
[12] Maurya P, Singh V, Prasad R, Bhaikhel K, Sharma V, Kumar M. Intraventricular
hydatid cyst causing entrapped temporal horn syndrome: a case report and
review of literature. Journal of Pediatric Neurosciences 2007;2(1 Suppl.):20–2.
[13] Ofori-Kwakye SK, Wang AM, Morris JH, O’Reilly GV, Fischer EG, Rumbaugh
CL. Septation and focal dilatation of ventricles associated with cryptococcal
meningoencephalitis. Surgical Neurology 1986;25(March (3)):253–60.
[14] Parrent AG. Endoscopically guided fenestration of the choroidal fis-
sure for treatment of trapped temporal horn. Journal of Neurosurgery
2000;93(November (5)):891–4.
[15] Schlitt M, Duvall ER, Bonnin J, Morawetz RB. Neurosarcoidosis causing ventri-
cular loculation, hydrocephalus, and death. Surgical Neurology 1986;26(July
(1)):67–71.
[16] Singh SK, Srivastava C, Ojha BK, Chandra A, Parihar A, Husain N. An unusual
cause of entrapment of temporal horn: neurocysticercosis. Neurology India
2010;58:814–5.
[17] Smith H, Moody D, Ball M, Laster W, Kelly Jr DL, Alexander Jr E. The trapped tem-
poral horn: a trap in neuroradiological diagnosis. Neurosurgery 1979;5(August
(2)):245–9.
[18] Tsugane R, Shimoda M, Yamaguchi T, Yamamoto I, Sato O. Entrapment of the
temporal horn: a form of focal non-communicating hydrocephalus caused by
intraventricular block of cerebrospinal fluid flow—report of two cases. Neu-
rologia Medico Chirurgica 1992;32:210–4.
[19] Yamamoto H, Matsukado Y, Nagahiro S. Entrapment of the temporal horn
which developed during antibiotic therapy for multiple brain abscess. Shoni
No Noshinkei 1987;12:415–21.
[20] Watanabe T, Katayama Y. Evaluation by magnetic resonance imaging of the
entrapped temporal horn syndrome. Journal of Neurology, Neurosurgery &
Psychiatry 1999;66(January (1)):113.