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\begin{document}

\title{Bilateral horizontal gaze palsy in an 8-year-old girl; rare case with
NDUFS4 gene mutation: a case report and literature review}



\author[1]{Mohammad Vafaee Shahi}%
\author[2]{Saeide  Ghasemi}%
\author[1]{Mehran  Beiraghi Toosi}%
\author[1]{Mahmoud Reza  Ashrafi}%
\author[1]{Reza Shervin  Badv}%
\author[3]{Alireza Tavasoli}%
\author[1]{Leila Tahernia}%
\affil[1]{Affiliation not available}%
\affil[2]{Iran University of Medical Sciences}%
\affil[3]{Natl Inst Genet Engn }%


\vspace{-1em}



  
  \date{May 30, 2024}


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\selectlanguage{english}
\begin{abstract}
Here, an 8-year-old girl is reported with bilateral horizontal gaze
palsy, ataxia and drowsiness. Brain MRI demonstrated dorsal midbrain,
bilateral putamen nuclei and cerebellar dentate nucleus involvement. MRS
revealed an elevated lactate peak which suggested a mitochondrial
disease. Finally, the molecular genetic test reported NDUFS4 gene
mutation%
\end{abstract}%



\sloppy


\textbf{Background}

Leigh syndrome (LS) is a rare and inherited heterogeneous disease which
is associated with progressive neurodegenerative brain damage. Diarrhea,
vomiting and dysphagia are usually the initial signs of Leigh syndrome
in infants. Clinically, it may be also associated with multiple
features, including brainstem symptoms, ataxia, hypotonia, dystonia,
respiratory insufficiency, pyramidal signs, lactic acidosis in blood or
cerebrospinal fluid and hypertrophic cardiomyopathy (1). It is usually
associated with cerebral hypotonia, movement and mental disabilities and
respiratory failure which results in death within 2-3 years (2).
Weakness of limbs and loss of sensation are also common in these cases
(3). Although the basic neuropathological features in affected children
are relatively similar, there is heterogeneity in clinical, genetic and
biochemistry findings. Therefore, early diagnosis of the disease is
essential to increase survival in affected patients.

The molecular mechanism underlying LS pathogenesis is mainly due to the
defects in mitochondrial respiratory chain enzymes (4). Recent evidences
have revealed that mutations in genes for the pyruvate dehydrogenase
complex, ATP synthase subunit-6, cytochrome-c oxidase, and subunits of
mitochondrial complex-I are responsible for LS (4, 5). NADH: ubiquinone
oxidoreductase, encoded by \emph{NDUFS4} gene, is a subunit of
mitochondrial complex-I which catalyzes the oxidation of NADH
(6).\emph{NDUFS4} gene is located in 5q11.2, which spans of eight exons.
This gene encodes a nuclear-encoded accessory subunit of the
mitochondrial membrane respiratory chain NADH dehydrogenase (complex I,
or NADH: ubiquinone oxidoreductase). Complex I removes electrons from
NADH and passes them to the electron acceptor ubiquinone. Mutations in
this gene can cause mitochondrial complex I deficiencies such as Leigh
syndrome. More than 35 different genes have been identified in the
mitochondrial respiratory chain that is associated with Leigh syndrome.
Nearly 25\% of Leigh disease mutations detected in the mitochondrial
genome. Here, this is the first case of LS from Iran with
\emph{NDFUS4}gene mutation presented with horizontal gaze palsy.

\textbf{Case presentation}

An 8-year-old girl was admitted to Rasool Akram hospital with bilateral
horizontal gaze palsy, ataxia and drowsiness. The gaze palsy was
initiated in the right eye during the last year and then gradually
affected the left eye during the previous month. She developed unsteady
gait, drowsiness, progressive ataxia, intention tremor and seizure
during the admission time. The past medical history of the patient
revealed that she was the first child of the family, from a
consanguineous marriage. She had also developmental milestone delay. She
had the history of seizure around 4 years ago, without current
medication therapy. The genetic background of the patient's family tree
is shown in figure 1. According to the pedigree, the case of 4-1 is the
first child of the family to be the result of kinship marriage. Her
grandmother (case 2-1) died of a brain tumor. In the case of 4-4, the
hand is paralyzed, which is found to be non-congenital and due to lack
of oxygen.

The vital signs were stable during her admission time. She was confused;
however, she responded to verbal stimulations. Horizontal gaze palsy was
detected in both eyes under ocular examinations, without any vertical
gaze palsy. Nystagmus was not observed during the examination .The
normal light reflection was detected in her pupils. Ocular examination
revealed retinal atrophy and pale disk in both sides. Cranial nerve
examination was normal. Deep tendon reflexes (DTR) were Brisk.
Cerebellar examination revealed positive tandem gait, intention tremor,
ataxic and wide based gait. The results of finger-to-nose and heel to
shin tests were detected normal. The biochemical test results, complete
blood count (CBC) and electrolytes were reported within the normal
ranges. Dorsal midbrain involvements were reported in brain Magnetic
resonance imaging (MRI) (Figure 2), which was provided one month ago out
of our center. Total abdominal and pelvic ultrasounds were performed in
order to rule out the possibility of organomegaly and malignancy.
Electroencephalography (EEG) was performed showing slowing background
activity prominent in posterior area without epileptiform discharges.

On the 5\textsuperscript{th} day of admission, the patient presented a
generalized tonic-clonic (GTC) seizure lasted for one minute.
Cerebrospinal fluid (CSF) was analyzed for cells, biochemical tests,
lactated dehydrogenase (LDH), and lactate contents that the results were
reported acceptable. Anti- Neuromyelitis optica antibody (NMO), IgG
index and oligoclonal bands (OCB) tests were performed for the
possibility of autoimmune diseases. A basic metabolic panel test was
performed for the assessment of serum ammoniac, lactate, pyruvate, and
amino acids content with high performance liquid chromatography (HPLC)
method. The possibility of specific metabolic syndromes was ruled out
with all normal metabolic results. The patient received biotin, Vitamin
B1, B\textsubscript{12} and Vitamin E to evaluate the possibility of
Wernicke-Korsakoff syndrome. However, no change in signs and symptoms
was observed following these treatments. Serum immunoglobulins were
evaluated in order to rule out the possibility of ataxia telangiectasia
and other immune deficiencies. The laboratory test results including
ANA; Anti-ds-DNA; serum complements (C3, C4, C5), SSA-Ro, SSA-LA; RPR;
AFP; Anti-GM Ab (IgM and IgA); \selectlanguage{greek}β\selectlanguage{english}2 glycoproteins; Anti-phospholipids;
Anti- cardiolipin (IgM and IgG); HLA (B5 and B51); and serum ACE were
within normal values. Therefore, the possibility of neuro-Behcet
disease, lupus erythematous, neuro-brucellosis, and neuro-sarcoidosis
was declined by detecting laboratory results. The infectious diseases
biomarkers were performed to rule out the possibility of infectious
diseases including HIV Ab, VDRL, Anti-toxoplasma Ab (IgM and IgG),
wright and 2ME. Wilson's disease was evaluated by 24-hour urine copper
test. Serum levels of vitamin B\textsubscript{12} and folic acid were
normal. Listeria infection was a recommended diagnosis due to midbrain
involvement. So, Ampicillin and Gentamycin was then started empirically.

On the 10\textsuperscript{th} day of admission, the second brain MRI was
performed with and without contrast for the second time (Figure 3).
Abnormal high signal flair and T2 lesions were detected in medulla,
Midbrain, bilateral putamen nuclei and cerebellar dentate nucleus.
Corticosteroid pulse therapy was started to resolve involved areas,
increased signal in midbrain, progressive ophthalmoplegia and
consequently the possibility of inflammatory lesions.

On the 15\textsuperscript{th} day of admission, Magnetic Resonance
Spectroscopy (MRS) demonstrated an elevated lactate peak in involved
areas which could indicate the possibility of mitochondrial disease
(Figure 4). Mitochondrial treatment cocktail (including Vitamin B2,
Vitamin B6, folic acid, L-carnitine and coenzyme Q) was prescribed for
the patient. Gaze palsy of the eyes, ataxia, tremor and ophthalmoplegia
were improved relatively. The patient was discharged with mitochondrial
treatment cocktail and oral prednisolone (1mg/kg/day). The patient was
examined again two weeks after discharge. The complete improvement was
observed in eye movements and gaze palsy; however, a mild intention
tremor and ataxia were detected during the examination time.
Unfortunately, ataxia and dysarthria gradually progressed despite use of
mitochondrial cocktail (including Vitamin B2, Vitamin B6, folic acid,
L-carnitine and coenzyme Q), and she lost the ability to walk after one
year. Whole exome sequencing was done to evaluate any genetic disorder.
In this work Whole exome sequencing technique revealed a novel variant,
c.474-478dup p. (Tyr160Cysfs*31), in NDUFS4 gene. This mutation leads to
a shift in the reading frame starting at codon 160 and could be
responsible for the symptoms of Leigh syndrome. The new frame reading
ends in a stop codon 30 downstream. Finally, the molecular genetic test
result showed mutation in \emph{NDUFS4} gene, confirming the diagnosis
of Leigh syndrome. Due to financial problems, the patient's parents did
not allow to performing sanger sequencing technique of themselves.

\textbf{Discussion}

Leigh syndrome is a rare progressive neurological disorder typically in
childhood that can be inherited as X-linked recessive, autosomal
recessive and mitochondrial trait. The incidence of this syndrome is
estimated approximately 2 in 100,000 births. Leigh syndrome may present
early in life with multiple characteristics such as weakness,
drowsiness, dystonia, psychomotor regression, cerebral hypotonia,
ataxia, developmental milestones delay, and signs of brainstem
involvement, seizures, visual loss and tachypnea. Some studies reported
the occurrence of sleep apnea syndrome and abdominal symptoms in these
patients (7). However, the exact mechanism is unknown. Progressive
respiratory failure is one of the main leading causes of mortality among
LS cases (8). Elevated blood and CSF lactate, as well as pyruvate levels
can be found upon laboratory tests analysis. However, neuroimaging is a
valuable tool for the diagnosis of Leigh syndrome (9).

The present case was referred to Rasool Akram Hospital with the chief
complaint of progressive gaze palsy and also ataxia, intention tremor
and drowsiness. Her ocular examination revealed retinal atrophy and pale
disk. In a recent study, Jabeen \emph{et al} ., (10) reported a
37-year-old female with Leigh syndrome who admitted with similar ocular
symptoms including bilateral horizontal gaze palsy and ataxic gait. The
ocular involvement is frequently reported in patients with Leigh
syndrome. Many patients with Leigh syndrome may suffer from
ophthalmoplegia, a condition which is associated with weakness or
paralysis of the muscles responsible for eyes movement (11). Some
studies have reported nystagmus, optic atrophy, ptosis, strabismus, and
pigmentary retinopathy in patients with Leigh syndrome (11, 12). Our
case had also a past medical history of delayed development and seizure.
Abnormal cerebellar test results were detected including abnormal tandem
gait, intention tremor and ataxic gait. Most of the reported LS patients
like the present case excluded infections, autoimmune diseases and
toxins as the causes of presented symptoms (12). The second brain MRI
reported dorsal midbrain, cerebellar dentate nucleus and bilateral
putamen nuclei involvement. These symptoms pointed towards a
neurodegenerative disorder. A basic metabolic panel test result showed
normal serum ammonia, pyruvate, and amino acids contents and normal
blood and CSF lactate. Magnetic resonance spectroscopy revealed an
elevated lactate peak in involved areas which suggested a possible
mitochondrial disease. Eventually, the molecular genetic test analysis
using Whole exome sequencing technique revealed a novel variant,
c.474-478dup p. (Tyr160Cysfs*31), in \emph{NDUFS4} gene. This mutation
leads to a shift in the reading frame starting at codon 160 and could be
responsible for the symptoms of Leigh syndrome. The new frame reading
ends in a stop codon 30 downstream. Therefore, genetic test result
confirmed the diagnosis of Leigh syndrome. Due to financial problems,
the patient's parents did not allow to performing sanger sequencing
technique of themselves. She initially responded significantly to
mitochondrial treatment cocktail and significant improvement was
observed in clinical symptoms. The complete improvement was observed in
eye movements and gaze palsy; however, a mild intention tremor and
ataxia were detected during the examination time. Unfortunately, ataxia
and dysarthria gradually progressed despite use of mitochondrial
cocktail and she lost the ability to walk after one year. Several
studies showed similar initially responses to mitochondrial treatment
cocktail (including Vitamin B2, Vitamin B6, folic acid, L-carnitine and
coenzyme Q) in different cases (10). Goldenberg \emph{et al} ., (7)
reported a 22-year-old woman with Leigh syndrome who had partial
deficiency in cytochrome C oxidase. They observed excellent response to
mitochondrial treatment cocktail.

Molecular genetic studies illustrated that Leigh syndrome can be
resulted from defects or mutations in mitochondrial enzymes such as
pyruvate dehydrogenase (\emph{PDHA1} gene mutations) (13), pyruvate
carboxylase (\emph{SURF1}gene mutations in nuclear genome), ATP synthase
subunit-6, cytochrome C oxidase, and subunits of complex-I (14). Recent
evidences identified 24 known mutations in mitochondrial genes and 21 in
nuclear genes in Leigh syndrome (15). Here, we found \emph{NDUFS4} gene
mutation which was associated with Leigh syndrome. This gene is a
nuclear-encoded accessory subunit of mitochondrial complex I (NADH:
ubiquinone oxidoreductase). This complex removes electrons from NADH and
transfers them to the electron acceptor ubiquinone. Therefore, mutations
in \emph{NDUFS4} gene can cause mitochondrial respiratory chain
deficiencies. In another study, Leshinsky-Silver \emph{et al} . (16)
reported a case with Leigh syndrome due to \emph{NDUFS4} mutation. The
patient developed predominant brainstem involvement. More recently,
Ortigoza-Escobar \emph{et al} ., (17) reported a patient with
\emph{NDUFS4} gene mutation related to Leigh syndrome.

These data has suggested that various symptoms and clinical features
could be found in Leigh syndrome. Variations in the disease severity and
the number of clinical features are probably due to different mutations
in mitochondrial genes. Therefore, further studies are necessary to
evaluate the relationship between genotype and phenotype. Our patient
was born from parents with consanguineous marriage; however, no evidence
of similar conditions was reported in his family. Since consanguineous
marriage is common in Iran, there may be a relationship between the
incidence of Leigh syndrome and consanguineous marriage. Therefore,
further considerations are required to evaluate the correlation.
Therefore, premarital genetic counseling and education may be helpful.

Leigh syndrome is a rare mitochondrial disease which is associated with
progressive neurological disorders. Our case presented with progressive
bilateral gaze palsy, ataxia, retinal atrophy, pale disk, unsteady gait,
intention tremor, and drowsiness. The brain MRI showed dorsal midbrain
and cerebellar dentate nucleus involvement. These symptoms pointed
towards a neurodegenerative disorder. MRS illustrated an elevated
lactate peak in involved area despite normal blood and CSF lactate which
indicated a mitochondrial disease. The genetic test analysis
revealed\emph{NDUFS4} gene mutation which confirmed the diagnosis of
Leigh syndrome.

\textbf{Conclusion}

Our findings indicated that various symptoms and clinical features can
be found in Leigh syndrome which could be probably due to different
mutations in mitochondrial genes. Therefore, appropriate clinical and
laboratory settings along with brain MRI, MRS and genetic test analysis
would be necessary for the early diagnosis. Our patient was born from
parents with consanguineous marriage, which highlighted the possible
relationship between familial marriage and incidence of Leigh syndrome.
Since consanguineous marriage is popular in Iran, premarital genetic
counseling and education may be helpful.

\textbf{Abbreviations:}

Leigh syndrome (LS), Cerebrospinal fluid (CSF), Magnetic resonance
imaging (MRI), Magnetic resonance spectroscopy (MRS), Nicotinamide
adenine dinucleotide hydrogen (NADH), Deep tendon reflex (DTR), Complete
blood count (CBC), Electroencephalogram (EEG), Generalized tonic clonic
(GTC), Lactate dehydrogenase (LDH), Anti-Neuromyelitis optica antibody
(NMO-Ab), High performance liquid chromatography (HPLC), Anti nucleotide
antibody (ANA), Anti- double stranded DNA (Anti-ds DNA), Anti-sj\selectlanguage{ngerman}ögren's-
syndrome- related antigen A (Anti-SSA-RO and SSA-LA), Rapid Plasma
Reagin (RPR), Alpha fetoprotein (AFP), Anti-ganglioside antibody
(anti-GM antibody), Serum Angiotensin converting enzyme (ACE), Human
immunodeficiency virus (HIV), Venereal disease research laboratory test
(VDRL), 2-mercaptoethanol Brucella agglutination test (2ME).

\textbf{Acknowledgements:}

Not applicable

\textbf{Declarations}

\textbf{Ethics approval and consent to participate:}

This case study was accredited by Ethical Committee of Iran University
of Medical Sciences. Written informed consent was obtained from the
parents of the patient for publication of this Case Report and any
accompanying images. A copy of the written consent is available for
review by the Editor of this journal.

\textbf{Consent for publication:}

The consent for publication of personal detailed data was obtained from
parents.

\textbf{Availability of data and material:}

The datasets used during the current case study are available from the
corresponding author on reasonable request.

\textbf{Competing interests} :

The authors declare no conflict of interest in preparing this case
presentation.

\textbf{Funding:}

This case presentation received no specific grant from any funding
agency in the public, institutions or not-for-profit sectors.

\textbf{Authors' contributions} :

VM, AM, BM, BR and TA analyzed and interpreted the patient data
regarding the neurologic disease. TL and GS performed follow up the
patient and were major contributors in writing the manuscript. All
authors read and approved the final manuscript.

\textbf{References}

1. Shrikhande DY, Kalakoti P, Aarif Syed MM, Ahya K, Singh G. A rare
mitochondrial disorder: Leigh sydrome - a case report. Ital J Pediatr.
2010;36:62.

2. Topçu M, Saatci I, Anil Apak R, Söylemezoglu F, Akçören Z. Leigh
Syndrome in a 3-Year-Old Boy with Unusual Brain MR Imaging and
Pathologic Findings. American Journal of Neuroradiology 2000;21:224-7.

3. Lake NJ, Bird MJ, Isohanni P, Paetau A. Leigh syndrome:
neuropathology and pathogenesis. J Neuropathol Exp Neurol.
2015;74:482-92.

4. Sofou K, et al. A multicenter study on Leigh syndrome: disease course
and predictors of survival. Orphanet Journal of Rare Diseases.
2014;9:52.

5. Shrikhande DY, Kalakoti P, Aarif Syed MM, Ahya K, Singh G. A rare
mitochondrial disorder: Leigh syndrome - a case report. talian Journal
of Pediatrics. 2010;62:36.

6. Scacco S, et al. Pathological Mutations of the Human NDUFS4 Gene of
the 18-kDa (AQDQ) Subunit of Complex I Affect the Expression of the
Protein and the Assembly and Function of the Complex. The Journal of
Biological Chemistry. 2003;278:44161-7.

7. Goldenberg PC, Steiner RD, Merkens LS, Dunaway T, Egan RA, Zimmerman
EA, et al. Remarkable improvement in adult Leigh syndrome with partial
cytochrome c oxidase deficiency. Neurology. 2003;60:865-8.

8. Barkovich AJ. Toxic and metabolic brain disorders. In:Pediatric
Neuroimaging. New York: Raven Press. 1995:55-106.

9. Hombal AG, Narvekar VN. Leigh's Disease (Subacute Necrotising
Encephalomyelopathy) - A Case Report. Ind J Radiol Imag. 2005;15:217-9.

10. Jabeen SA, Sandeep G, Rukmini Mridula K, Meena AK, Borgohain R,
Sundaram C. Adult-onset Leigh's disease: A rare entity. Ann Indian Acad
Neurol. 2016;19:140--2.

11. Grönlund MA, Andersson S, Åkebrand R, Seyedi Honarvar AK, Sofou K,
Darin N, et al. Ophthalmologic involvement in Leigh syndrome. Acta
Ophthalmologica 2017;95:e76-e.

12. Han J, Lee YM, Kim SM, Han SY, Lee JB, Han SH. Ophthalmological
manifestations in patients with Leigh syndrome. Br J Ophthalmol.
2015;99:528-35.

13. Matthews PM, Marchington DR, Squier M, Land J, Brown RM, Brown GK.
Molecular genetic characterization of an X-linked form of leigh's
syndrome. Ann Neurol. 1993;33:652-5.

14. Moslemi AR, Darin N. Molecular genetic and clinical aspects of
mitochondrial disorders in childhood. Mitochondrion. 2007;7:241-52.

15. Finsterer J. Leigh and Leigh-like syndrome in children and adults.
Pediatr Neurol. 2008;39:223-35.

16. Leshinsky-Silver E, Lebre AS, Minai L, Saada A, Steffann J, Cohen S,
et al. NDUFS4 mutations cause Leigh syndrome with predominant brainstem
involvement. Mol Genet Metab. 2009;97:185-9.

17. Ortigoza-Escobar JD, et al. Ndufs4 related Leigh syndrome: A case
report and review of the literature. Mitochondrion. 2016;28:73-8.

\textbf{Figures' titles}

\textbf{Figure 1:} The genetic background of the patient's family tree.
The case of 4-1 is the first child of the family to be the result of
kinship marriage. Her grandmother (case 2-1) died of a brain tumor. In
the case of 4-4, the hand is paralyzed, which is found to be
non-congenital and due to lack of oxygen.

\textbf{Figure 2:} The first brain MRI. (A): Axial brain MRI (flair)
showing hyper intensity in dorsal midbrain; (B): Axial brain MRI (T2)
showing hyper intensity in dorsal midbrain; (C): Axial brain MRI (DWI)
showing hyper intensity in dorsal midbrain; (D): Axial brain MRI (ADC
map) showing restriction in dorsal midbrain involvement

\textbf{Figure 3:} The second brain MRI. (A): Axial brain MRI (flair)
showing hyper intensity in dorsal midbrain; (B): Axial brain MRI (T2)
showing bilateral hyper intensity in putamen nucleus; (C): Axial brain
MRI (flair) showing hyper intensity in dorsal midbrain and dentate
nucleus of cerebellum; (D): Axial brain MRI (T1) showing hypo intensity
in dorsal midbrain

\textbf{Figure 4:} Magnetic resonance spectroscopy result. The result
demonstrated an elevated lactate peak in involved areas\selectlanguage{english}
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