\documentclass[10pt]{article}

\usepackage{fullpage}
\usepackage{setspace}
\usepackage{parskip}
\usepackage{titlesec}
\usepackage[section]{placeins}
\usepackage{xcolor}
\usepackage{breakcites}
\usepackage{lineno}
\usepackage{hyphenat}





\PassOptionsToPackage{hyphens}{url}
\usepackage[colorlinks = true,
            linkcolor = blue,
            urlcolor  = blue,
            citecolor = blue,
            anchorcolor = blue]{hyperref}
\usepackage{etoolbox}
\makeatletter
\patchcmd\@combinedblfloats{\box\@outputbox}{\unvbox\@outputbox}{}{%
  \errmessage{\noexpand\@combinedblfloats could not be patched}%
}%
\makeatother


\usepackage{natbib}




\renewenvironment{abstract}
  {{\bfseries\noindent{\abstractname}\par\nobreak}\footnotesize}
  {\bigskip}

\titlespacing{\section}{0pt}{*3}{*1}
\titlespacing{\subsection}{0pt}{*2}{*0.5}
\titlespacing{\subsubsection}{0pt}{*1.5}{0pt}


\usepackage{authblk}


\usepackage{graphicx}
\usepackage[space]{grffile}
\usepackage{latexsym}
\usepackage{textcomp}
\usepackage{longtable}
\usepackage{tabulary}
\usepackage{booktabs,array,multirow}
\usepackage{amsfonts,amsmath,amssymb}
\providecommand\citet{\cite}
\providecommand\citep{\cite}
\providecommand\citealt{\cite}
% You can conditionalize code for latexml or normal latex using this.
\newif\iflatexml\latexmlfalse
\providecommand{\tightlist}{\setlength{\itemsep}{0pt}\setlength{\parskip}{0pt}}%

\AtBeginDocument{\DeclareGraphicsExtensions{.pdf,.PDF,.eps,.EPS,.png,.PNG,.tif,.TIF,.jpg,.JPG,.jpeg,.JPEG}}

\usepackage[utf8]{inputenc}
\usepackage[ngerman,english]{babel}



\usepackage{float}








\begin{document}

\title{WHEN LYMPHOMA HIDES IN THE CANAL.}



\author[1]{Daniele Zama}%
\author[2]{Egidio Candela}%
\author[2]{Gennaro Pagano}%
\author[1]{Francesco Venturelli}%
\author[1]{Fraia Melchionda}%
\author[3]{Francesco Toni}%
\author[2]{Mino Zucchelli}%
\author[2]{Andrea Pession}%
\affil[1]{IRCCS Azienda Ospedaliero-Universitaria di Bologna Policlinico S Orsola}%
\affil[2]{University of Bologna}%
\affil[3]{IRCCS Institute of Neurological Sciences of Bologna}%


\vspace{-1em}



  
  \date{May 21, 2024}


\begingroup
\let\center\flushleft
\let\endcenter\endflushleft
\maketitle
\endgroup





\selectlanguage{english}
\begin{abstract}
Primary intramedullary spinal cord lymphoma (PISCL) is a rare cause of
myelopathies. As PISCL is often underrecognized, delaying appropriate
treatment, we sought to describe its presentation. We report two
clinical cases of pediatric patients. The diagnosis of PISCL must be
considered in a patient with symptoms of acute myelopathies.%
\end{abstract}%



\sloppy


\section*{TITLE PAGE}

{\label{title-page}}

\section*{WHEN LYMPHOMA HIDES IN THE
CANAL.}

{\label{when-lymphoma-hides-in-the-canal.}}

Daniele Zama11 PhD, Egidio Candela2 MD, Gennaro Pagano2 MD*,Francesco
Venturelli1 MD, Fraia Melchionda1 PhD, Francesco Toni 3 MD, Mino
Zucchelli4 MD, Andrea Pession 1 PhD.

1 Pediatric Oncology and Hematology Unit ''Lalla Ser\selectlanguage{ngerman}àgnoli'', Department
of Pediatrics, University of Bologna, IRCCS Azienda Ospedaliera
Universitaria di Bologna

2 Specialty School of Paediatrics - Alma Mater Studiorum, University of
Bologna, Italy

3 Neuroradiology Unit, IRCCS Istituto Delle Scienze Neurologiche di
Bologna, Bologna, Italy

4 Pediatric Neurosurgery, Institute of Neurological Science, IRCCS
Bellaria Hospital, Bologna, Italy.

*Corresponding Author: Dr. Gennaro Pagano, Specialty School of
Pediatrics, Alma Mater Studiorum, University of Bologna, Bologna, Italy;
pagano8@gmail.com; Tel: +39-3914511185

\textbf{Abstract}

Primary intramedullary spinal cord lymphoma (PISCL) is a rare cause of
myelopathies. As PISCL is often underrecognized, delaying appropriate
treatment, we sought to describe its presentation. We report two
clinical cases of pediatric patients. The diagnosis of PISCL must be
considered in a patient with symptoms of acute myelopathies.

\textbf{Key words} : Primary intramedullary spinal cord lymphoma ,PISCL,
Myelopathies, Chemotherapy.

\textbf{CASE 1}

Mattia is a 6-year-old boy with no previous medical history. He came for
intermittent cramp-like abdominal pain in the last 48 hours, no fever,
vomiting or diarrhea. Since some signs of inflammation in the appendix
were found at an initial abdominal ultrasound scan, Mattia was sent to
Pediatric Emergency Room (PER). Physical examination showed signs of
acute abdomen. Therefore, he underwent a video-assisted trans-umbilical
appendectomy with histological confirmation of acute appendicitis. After
an initial clinical improvement, that allowed him to start walking
independently on postoperative day four, we observed a progressive
exacerbation of abdominal pain associated with difficulty in maintaining
the sitting position.

The next day we also noticed an intermittent tenderness in the lower
limbs and inability to keep the upright position and nocturnal enuresis.
During a neuropsychiatric evaluation, the patient reported that he did
not feel the urge to urinate and refused to leave autonomously the
wheelchair. The neurological evaluation highlighted the presence of
hypotonia and hyposthenia of the lower limbs, abolished patellar
osteotendinous reflexes, abnormal plantar reflex in bilateral toe
extension (Babinski sign). An electroneurography, a lumbar puncture and
a magnetic resonance imaging (MRI) have been recommended to complete the
diagnosis. The neurographic study showed only an asymmetry between left
and right. Lumbar puncture showed elevated protein level
(\textgreater{}700 mg/dl) in the cerebrospinal fluid, which supported
the suspect of a Guillain-Barre syndrome (GBS). Therefore, a treatment
with intravenous immunoglobulin at a dose of 0.5 g/kg/day was started.
The following day the clinical picture of the patient appeared
unchanged. An encephalic and spinal MRI was executed, showing an
epidural intracanal tissue located from D7 to D11, associated with
blurred signs of medullary suffering (Figure 1A and 1B).

An urgent surgical decompressive laminotomy on 5 levels was performed,
with removal of most of the pathological tissue (Figure 1C and 1D). The
histological examination reported a pre-B lymphoblastic lymphoma. Mattia
has been subsequently transferred to the Onco-hematology department to
undertake a specific chemotherapy treatment for the underlying disease.
High-dose steroid therapy with methylprednisolone succinate was
prescribed.

After surgery Mattia showed a persistent severe hypotonia in the lower
limbs, absence of spontaneous movements with weak patellar and Achilles'
osteotendinous reflexes and recovery of tactile sensitivity.

During the hospitalization, the initial paraparesis gradually improved
thanks to a targeted rehabilitation program. Distal motor deficiency was
associated with intestinal dysmotility, anal sphincter disfunction and
spastic neurogenic bladder. The initial difficulty in perceiving the
stimulus to defecate and the anal sphincter atony has progressively
improved, until resolution. Neurogenic bladder, characterized by an
increase in daily urinations with a small amount of urine and mintional
urge, was treated by oxybutynin. Intermittent catheterizations were
performed six times a day as prophylaxis of urinary tract infections.
The patient was found to have 3 asymptomatic bacteriuria, from catheter
urinary sample cultures, treated according to the antibiogram.
Currently, the number of daily urinations has partially reduced and
mintional urge has improved.

\textbf{CASE 2}

Luca is a 13-year-old boy admitted in the pediatric emergency room,
complaining hypoesthesia of the lower limbs, with increasing difficulty
in walking, during the last seven days.

About 25 days before, the boy reported difficulty in bending the head
after physical activity (weight throw). Due to persistent pain, he
underwent an orthopedic examination with cervical spine x-ray. The
imaging showed vertebral instability characterized by moderate
retrolisthesis of C3-C4 and C4-C5.

After a while, Luca began to complain paresthesiae of the lower limbs
associated with walking difficulties. Taping was removed, with immediate
benefit. After a few hours, however, paresthesiae and difficulties in
walking appeared again. Child neuropsychiatric evaluation was then
performed, but the neurological objective examination was negative.

After 48 hours the boy returned to the PER, complaining inability to
walk, with no pain in the lower limbs. At the physical examination he
was not able to keep the standing position. Lower limbs muscle
contractions were present intermittently for short intervals of time.
These muscles had normal consistency with no tenderness to the
palpation. Deep tendon reflex was present and symmetrical. No sphincter,
nor sensitive deficits were detected. After confirming a worsening of
the motor deficit, we decided for hospitalization.

On the following day, brain and spinal MRI were performed, with evidence
of an expansive intravertebral epidural lesion in the dorsal area,
extending from D1 to D3, which involves and widens the conjugation
foramina of the left side (Figure 2A and 2B). Additionally, there was
also another polylobed formation with similar characteristics in the
right mid-thoracic area along the costal margin line.

The patient therefore underwent an urgent neurosurgical intervention of
laminotomy and removal of the mass compressing the medulla (Figure 2 C
and 2D).

Histological examination showed an anaplastic large-cell ALK-positive
lymphoma. After surgery, the patient presented incomplete paraplegia. A
specific chemotherapy protocol was undertaken, followed by a
rehabilitative management, with the execution of daily exercise
sessions.

After the first discharge from the department of Pediatric
Oncohematology, following about 2 months of physiotherapy, Luca showed
an initial motility of the lower limbs with the possibility of loading.
Over time there has been a progressive improvement of the motor deficit,
until complete resolution. At present, he usually plays tennis.

\textbf{DISCUSSION}

We report the unusual cases of two children with symptoms suggestive for
acute myelopathy, who resulted both affected by Primary Intramedullary
Spinal Cord Lymphoma (PISCL). Though considered rare spinal canal
tumors, PISCL should always be included in the differential diagnosis of
acute myelopathy, because any delay in diagnosis and treatment could
significantly impact on the prognosis of this disease.

Among the oncological causes of compressive myelopathy in the pediatric
population, non- Hodgkin lymphomas (LNH) are the main group. LNHs are
represented by a heterogeneous group of malignant neoplasms of lymph
node tissue derived from the progenitors or mature B lymphocyte cells
or, with lower frequency, T lymphocyte cells. While in adult the
predominant subtype is low-grade, clinically indolent, lymphomas in
pediatric age are mainly high-grade and characterized by an aggressive
behavior (1). Extra nodal location in LNH of the child-adolescent, which
differs from that of the adult, is more frequent, with involvement of
the mediastinum, abdomen, head-neck district, bone marrow or central
nervous system (2). Symptoms often develop rapidly, over a period of 1-3
weeks (see Table 1 for signs and symptoms). The onset of
lymphadenopathy, with lymph nodes increased in size and indolent, is
common as well as compression symptoms on the surrounding structures.

Our two clinical cases emphasize how clinical presentation of LNH
frequently constitutes a challenge for the pediatrician because of the
variety of possible onset manifestations and the different types of
lymphomas and areas involved. For example: a chronic, deep, dull
abdominal pain, devoid of specificity and precise localization, can
characterize the onset of a LNH with primitively medullary localization.
The main cause of this clinical sign is the stimulation of the nerve
endings present in the wall of the bowel by the neoplasia (see Table 2
for red flags of PISCL).

However, acute abdominal pain is frequently a diagnostic challenge in
children due to the difficulty in correctly interpreting a nonspecific
symptomatology. Acute paraplegia in children is also a rare clinical
presentation of lymphoma, with signs and symptoms reflecting spinal cord
dysfunction. The 4 main etiological groups (see Table 3) of motor
paralysis and/or functional deficit of the lower limbs in pediatric age
consist of:

\begin{enumerate}
\tightlist
\item
  trauma (for example, from falls or road accidents);
\item
  vascular pathologies, including epidural spinal hematoma, caused by
  the rupture of epidural veins in correspondence of a locus minoris
  resistentiae following a sudden increase in intrathoracic or
  intra-abdominal pressure, due to efforts (even when of low intensity
  such as cough or defecation);
\item
  inflammatory diseases (including primary infections, abscesses,
  polyradiculoneuropathy and infection associated processes, such as
  transverse myelitis and encephalomyelitis);
\item
  compressions (tumors, syringomyelia) (11-12).
\end{enumerate}

According to an Australian case study, the most common cause of acute
flaccid paralysis of the lower limbs (up to 47\% of cases) is GBS (5).

Malignant compression of the spinal cord (MCSC), whether it is caused by
a primary tumor localization or as the consequence of a metastasis, can
be divided into two types, depending on location: extradural (the most
frequent in adults, extending from the vertebral bodies or from
structures external to the dura mater) and intramedullary (14). Despite
their impact on morbidity and mortality, only a small amount of data on
the incidence of the disease are available in the pediatric population.
Acute spinal cord compression can occur in a not negligible percentage
of children with cancer, often at the time of diagnosis (15). Tumors
associated with medullary compression in childhood are shown on table 4.

In an italian case study in pediatric oncology, motor deficit was the
onset symptom of MCSC in all patients, while pain was reported in 60\%
of cases and sphincter deficit in 43\% (3). MRI is the diagnostic
technique of choice in all cases when there is suspicion of medullary
involvement (3). This exam should be carried out as soon as possible
because the neurological prognosis is strongly related to the promptness
of spinal cord decompression surgery (11). Complications of spinal cord
compression, such as urinary dysfunction, fecal incontinence,
spasticity, painful syndromes and psychological sequelae are complex
problems for children and adolescents (13). According to the latest 2013
guidelines of the American Association of Neurological Surgeons and the
Congress of Neurological Surgeons, the use of glucocorticoids in acute
traumatic spinal cord injury is no longer recommended.

The American Academy of Emergency Medicine states that glucocorticoid
treatment remains an acceptable option. Many experts affirm that there
are compelling and undeniable data justifying the clinical use of
glucocorticoids, particularly in patients with incomplete lesions. The
molecule to be used should be methylprednisolone, administered
intravenously. The therapeutic scheme is:

30 mg/kg in bolus in 15 minutes

After 45', 5,4 mg/kg infused every hour for 23 hours. (18)

A bladder dysfunction can lead to difficulties in urination associated
with changes in intravesical pressure, an increased risk of infection
and kidney damage as well as a source of social distress. Urinary
symptoms can be very variable, ranging from an increase in urinary
frequency to a complete urinary retention. It is therefore mandatory to
perform a proper neurological examination (complete with evaluation of
sphincter function and reflexes), a mintional diary, to measure residual
post-mintional volumes and to execute urodynamic studies. Similarly, the
presence of neurogenic bowel can be a source of serious social distress
and skin impairment. Laxatives or anti-diarrheal drugs with pelvic floor
rehabilitation can improve sphincter control (14). On the other hand,
several studies show how neurological recovery in childhood is better
than in adulthood (6) thanks to the greater plasticity of the immature
spinal cord (7-8). In a recent work, the presence of residual muscle
activity in children, found in electromyography analysis of the motor
sites located below the level of injury, documents the existence of a
residual descending influence from the spinal motor circuits. This
observation, independently of its immediate functional relevance, can
represent an objective indicator of the potential recovery of both
intentional and postural motor function (16). Physiotherapy, following
damage to the spinal cord, is still one of the key processes in the
rehabilitation of the patient (9-10). Age at the time of diagnosis,
location and degree of spread of the spinal cord injury are the main
prognostic factors for the recovery of gait. Children under 5 years of
age, with incomplete injuries, located in thoracic or lumbar spine, have
the best chance of functional recovery thanks to physiotherapy (17).

\textbf{CONCLUSIONS}

A child presenting recent gait alterations or motor impairment, whether
or not associated with pain and sphincter deficit, especially if rapidly
progressive, must be promptly evaluated in the hospital. Root pain and
motor impairment may be the first signs of spinal compression. The rapid
onset and evolution of symptomatology have been an important warning
signal.

It is essential to know the possible clinical manifestations of
medullary compression in order to be able to recognize them and avoid
unsuitable treatments for patients.

\textbf{Authorship List}

Conceptualization: Daniele Zama, Egidio Candela, Gennaro Pagano,
Francesco Venturelli; data curation: Egidio Candela; formal analysis:
Daniele Zama, Egidio Candela. Neuroradiological images: Francesco Toni;
supervision: Fraia Melchionda, Mino Zucchelli, Andrea Pession;
validation: Andrea Pession; visualization: Egidio Candela; writing --
original draft: Egidio Candela, Gennaro Pagano, Francesco Venturelli;
writing -- review and editing: Daniele Zama, Fraia Melchionda, Mino
Zucchelli, Andrea Pession. All the authors have read and agreed to the
published version of the manuscript.

\textbf{Acknowledgments}

This research received no external funding and support.

\textbf{Conflict of Interest Statement}

The authors have no conflicts of interest to declare.

\textbf{Statement of Ethics}

Written informed consent was obtained from the patient for the
publication of these case reports and any accompanying images. Ethics
committee approval was not obtained because we report a clinical case of
only two patients, we have not included any identifiable information,
and we obtained written consent for publication from the patient's
parents according to the 1964 Helsinki Declaration and its later
amendments or comparable ethical standards. This retrospective review of
patient data did not require ethical approval in accordance with local
guidelines.

\section*{Bibliography}

{\label{bibliography}}

\begin{enumerate}
\tightlist
\item
  Morton LM, Wang SS, Devesa SS, et al. Lymphoma incidence patterns by
  WHO subtype in the United States, 1992-2001. Blood 2006; 107:265.
\item
  Principi N, Rubino A. Pediatria generale e specialistica. 2nd ed, Casa
  Editrice Ambrosiana; 2017
\item
  De Martino, L., Spennato, P., Vetrella, S. et al. Symptomatic
  malignant spinal cord compression in children: a single-center
  experience. Ital J Pediatr 2019; 45, 80.
\item
  Sharpe AN, Forsyth R. Acute paediatric paraplegia: a case series
  review. Eur J Paediatr Neurol. 2013 Nov;17(6):620-4.
\item
  Morris, A., Elliott, E., D'Souza, R., Antony, J., Kennett, M. and
  Longbottom, H. (2003), Acute flaccid paralysis in Australian children.
  Journal of Paediatrics and Child Health, 39: 22-26.
\item
  Parent S, Mac-Thiong JM, Roy-Beaudry M, Sosa JF, Labelle H. Spinal
  cord injury in the pediatric population: a systematic review of the
  literature. J Neurotrauma. 2011 Aug;28(8):1515-24
\item
  Fawcett JW, Curt A, Steeves JD, Coleman WP, Tuszynski MH, Lammertse D,
  et al. Guidelines for the conduct of clinical trials for spinal cord
  injury as developed by the ICCP panel: spontaneous recovery after
  spinal cord injury and statistical power needed for therapeutic
  clinical trials. Spinal Cord. 2007 Mar;45(3):190-205.
\item
  Edgerton VR, Tillakaratne NJ, Bigbee AJ, de Leon RD, Roy RR.
  Plasticity of the spinal neural circuitry after injury. Annu Rev
  Neurosci. 2004; 27:145-67
\item
  Calhoun CL, Schottler J, Vogel LC. Recommendations for mobility in
  children with spinal cord injury. Top Spinal Cord Inj Rehabil.
  2013;19(2):142-51
\item
  Benmelouka A, Shamseldin LS, Nourelden AZ, Negida A. A Review on the
  Etiology and Management of Pediatric Traumatic Spinal Cord Injuries.
  Adv J Emerg Med. 2019 Oct 10;4(2):e28..
\end{enumerate}

\par\null

\begin{enumerate}
\tightlist
\item
  New PW. A Narrative Review of Pediatric Nontraumatic Spinal Cord
  Dysfunction. \emph{Top Spinal Cord Inj Rehabil} . 2019;25(2):112-120.
\item
  Vogel LC, Betz RR, Mulcahey MJ. Spinal cord injuries in children and
  adolescents. Handbook of clinical neurology; vol. 109. p. 131e48
  Vinken PJ, Bruyn GW, editors; 2012
\item
  Ruppert LM. Malignant spinal cord compression: adapting conventional
  rehabilitation approaches. Phys Med Rehabil Clin N Am.
  2017;28(1):101--14.
\item
  Lewis DW, et al. Incidence, presentation, and outcome of spinal cord
  disease in children with systemic cancer. Pediatrics.
  1986;78(3):438--43.
\item
  Atkinson DA, Mendez L, Goodrich N, Aslan SC, Ugiliweneza B, Behrman
  AL. Muscle Activation Patterns During Movement Attempts in Children
  With Acquired Spinal Cord Injury: Neurophysiological Assessment of
  Residual Motor Function Below the Level of Lesion. Front Neurol. 2019
  Dec 20;10:1295
\item
  Donenberg JG, Fetters L, Johnson R. The effects of locomotor training
  in children with spinal cord injury: a systematic review. Dev
  Neurorehabil. 2019 May;22(4):272-287.
\item
  Cheung V, Hoshide R, Bansal V, Kasper E, Chen CC. Methylprednisolone
  in the management of spinal cord injuries: Lessons from randomized,
  controlled trials. Surg Neurol Int. 2015 Aug 24;6:142..
\end{enumerate}

Figures:

Figure 1. \textbf{Sagittal (A) and axial (B) T2 weighted images.}
Pre-operative picture shows epidural vertebral canal tissue (arrow heads
in A and asterisks in B), located from D7 to D11, slightly hyperintense
to the medullary nervous tissue. The lesion compresses and dislocates
the dural sac and its contents antero-laterally, towards the left (arrow
in B), with extension, through the right conjugation foramen, into the
adjacent cost-vertebral space (asterisk in A). An area of altered
signal, expression of medullary suffering, at level D11-D12 (arrows in
A) is associated.\textbf{Sagittal (C) and axial (D) T2 weighted images.}
Post-operative picture after the removal of the neoformation, with
resolution of the associated mass effect (arrowheads in C) and the area
of medullary suffering. Noteworthy is the prompt response to
chemotherapy of the extended component in the right costovertebral
space. Figure 2. \textbf{Sagittal T2 weighted (A) and T1 weighted images
after contrast administration(B).} Before surgery picture was
characterized by intravertebral epidural neoformation, located in the
D1-D3 tract (arrowheads in A and asterisks in B), characterized by a
signal similar to the that from the spinal cord in T2, because of high
cellularity, as well as by lower contrast impregnation (asterisks in B).
The lesion described engages almost entirely the spinal canal, with a
marked compressive effect on the dural sac and its contents (white
arrows in A), dislocated laterally to the left (black arrow in B). The
neoformation extends into the costovertebral adipose tissue through the
intervertebral foramina, on the left side.\textbf{Sagittal (C) and axial
(D) T2 weighted images.} Post-operative picture characterized by the
removal of the lesion (arrowheads in C), with a reduction of the
associated mass effect. On the post-operative phase, the spinal cord
early appears distorted by previous compression (arrows in C and D),
however, without radiological features of suffering.\selectlanguage{english}
\begin{longtable}[]{@{}l@{}}
\toprule
Asymptomatic peripheral lymphadenopathy Medullary infiltration (lymphoma
if the neoplastic medullary infiltrate is \textless{}25\%, otherwise
leukemia) with any secondary alteration of blood count.
Localization-dependent symptoms (e.g. abdominal pain, chest pain,
dyspnoea \ldots{}) Systemic symptoms: - evening fever or low-grade fever
night sweats weight loss (\textgreater{} 10\% in the past 6 months)
pruritus sine materia\tabularnewline
\bottomrule
\end{longtable}

\textbf{Table 1} : Main clinical manifestations of the LNH.\selectlanguage{english}
\begin{longtable}[]{@{}l@{}}
\toprule
\vtop{\hbox{\strut Radicular pain (cervical-brachial, abdominal,
lumbar-cruralgia, lumbar-sciatalgia)}\hbox{\strut Hypoesthesia of the
limbs (compression of the cervical cord can cause
weakness}\hbox{\strut extended to the 4 limbs. The most frequent
presentation is strength deficit at the lower limbs, usually
symmetrical, but sometimes, as in the compression of the cauda equina,
prevalent in one limb)}\hbox{\strut Progressive reduction of
sensitivity}\hbox{\strut Sphincter dysfunction}}\tabularnewline
\bottomrule
\end{longtable}

\textbf{Table 2} : Red Flags of warning signs and symptoms for LNH with
primarily medullary localization.\selectlanguage{english}
\begin{longtable}[]{@{}lll@{}}
\toprule
\begin{minipage}[t]{0.32\columnwidth}\raggedright\strut
\textbf{Congenital}\strut
\end{minipage} & \begin{minipage}[t]{0.32\columnwidth}\raggedright\strut
\textbf{Genetic disorders}\strut
\end{minipage} & \begin{minipage}[t]{0.32\columnwidth}\raggedright\strut
\textbf{Acquired}\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
Spinal dysraphisms Arnold-Chiari malformation Skeletal
Malformations\strut
\end{minipage} & \begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
Hereditary spastic paraplegia Spino-cerebellar ataxia
Adrenomyeloneuropathy Other leukodystrophies Spinal muscular
atrophies\strut
\end{minipage} & \begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
Traumas Degenerative disorders of the spine Metabolic pathologies
Vascular pathologies Inflammatory diseases (transverse myelitis)
Autoimmune diseases Infectious diseases Neoplastic diseases\strut
\end{minipage}\tabularnewline
\bottomrule
\end{longtable}

\textbf{Table 3} : Main causes of myelopathy in pediatric patients.\selectlanguage{english}
\begin{longtable}[]{@{}lllll@{}}
\toprule
\begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
\textbf{Neoplasms of the spinal cord}\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
\textbf{Neoplasms of the spinal cord}\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
\textbf{Neoplasms of the spinal cord}\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
\textbf{Neoplasms of the spinal cord}\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
\textbf{Neoplasms of the spinal cord}\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.19\columnwidth}\raggedright\strut
\textbf{Extradural}\strut
\end{minipage} & \begin{minipage}[t]{0.19\columnwidth}\raggedright\strut
\textbf{Extradural}\strut
\end{minipage} & \begin{minipage}[t]{0.19\columnwidth}\raggedright\strut
\textbf{Extradural}\strut
\end{minipage} & \begin{minipage}[t]{0.19\columnwidth}\raggedright\strut
\textbf{Intradural}\strut
\end{minipage} & \begin{minipage}[t]{0.19\columnwidth}\raggedright\strut
\textbf{Intradural}\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.19\columnwidth}\raggedright\strut
\textbf{Epidural}\strut
\end{minipage} & \begin{minipage}[t]{0.19\columnwidth}\raggedright\strut
\textbf{Osteo- cartilaginous}\strut
\end{minipage} & \begin{minipage}[t]{0.19\columnwidth}\raggedright\strut
\textbf{Peri-vertebral}\strut
\end{minipage} & \begin{minipage}[t]{0.19\columnwidth}\raggedright\strut
\textbf{Intramedullary}\strut
\end{minipage} & \begin{minipage}[t]{0.19\columnwidth}\raggedright\strut
\textbf{Extramedullary}\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
Leukemia Lymphoma PNET Germ cell tumors Lipoma\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
Ewing's sarcoma Osteo-sarcoma Osteoid osteoma Osteoblastoma Langerhans
cell histiocytosis Aneurismatic bone cysts Hemangioma Sacrococcygeal
Teratoma Lymphoma Leukemia\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
Neuroblastoma Ganglioneuroma PNET\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
Astrocytoma Ependymoma Ganglioglioma Lipoma\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
Neurofibroma Schwannoma Meningioma Malignant peripheral nerve sheath
tumors Myxopapillary ependymoma Dermoid/epidermoid cysts PNET Atypical
Teratoid Rhabdoid Tumors Lipoma\strut
\end{minipage}\tabularnewline
\bottomrule
\end{longtable}

\textbf{Table 4:} Main tumors that can cause spinal cord compression in
childhood.\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/FIG/FIG}

\end{center}
\end{figure}\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/FIH/FIH}

\end{center}
\end{figure}

\textbf{Hosted file}

\verb`Table 1.docx`  available at \url{https://authorea.com/users/372520/articles/613028-when-lymphoma-hides-in-the-canal}

\textbf{Hosted file}

\verb`Table 2.docx`  available at \url{https://authorea.com/users/372520/articles/613028-when-lymphoma-hides-in-the-canal}

\textbf{Hosted file}

\verb`Table 3.docx`  available at \url{https://authorea.com/users/372520/articles/613028-when-lymphoma-hides-in-the-canal}

\textbf{Hosted file}

\verb`Table 4.docx`  available at \url{https://authorea.com/users/372520/articles/613028-when-lymphoma-hides-in-the-canal}

\selectlanguage{english}
\FloatBarrier
\end{document}

