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Abstract

  1. Top of page
  2. Abstract
  3. What this paper adds
  4. Definition
  5. Clinical features
  6. Case reports
  7. Differential diagnosis
  8. Treatment and outcome
  9. Summary and conclusion
  10. Acknowledgement
  11. References
  12. Supporting Information

Congential hemifacial spasm is a rare condition that is characterized by the occurrence of paroxysmal hemifacial contractions in neonates. We review the clinical, neurophysiological, neuroimaging, and histopathological findings, as well as the differential diagnosis, therapeutic approach, and outcome of all the described cases. Moreover, we report two new cases including the ictal video-electroencephalography recordings. Hemifacial spasm starts early in life, and is characterized by unilateral, involuntary, irregular tonic or clonic contractions of muscles innervated by the seventh cranial nerve. Hemifacial spasm is associated with eyelid blinking, and sometimes with breathing irregularities, hyperventilation, and/or other neurological manifestations (dystonic movements, nystagmus). Interictal and ictal video-electroencephalography did not reveal epileptiform abnormalities. In all cases, brain magnetic resonance imaging showed a mass involving the cerebellar peduncle, the cerebellar hemisphere, or the floor of the fourth ventricle. The semiology of the paroxysmal attacks is probably due to the activation of cranial nerve nuclei through intralesional hypersynchronous discharges, as shown by the intraoperative recordings and functional brain imaging described in the literature. We point out the importance of identifying such seizures in order to make an early diagnosis of the underlying cerebral lesion.


What this paper adds

  1. Top of page
  2. Abstract
  3. What this paper adds
  4. Definition
  5. Clinical features
  6. Case reports
  7. Differential diagnosis
  8. Treatment and outcome
  9. Summary and conclusion
  10. Acknowledgement
  11. References
  12. Supporting Information
  •  This report provides video-electroencephalography documentation of hemifacial spasm associated with eye blinking and autonomic symptoms in neonates.
  •  This article reviews all published cases of hemifacial spasm associated with a fourth ventricle mass.
  •  This article provide differential diagnosis, and physiopathological findings of hemifacial spasms.

Neonatal hemifacial spasm associated with a lesion in the fourth ventricle was first described in 1976 by Langston and Tharp.1 Since then, 20 children with this pathology have been reported (for references see Table I). These lesions produce paroxysmal and stereotyped attacks of hemifacial spasm and eye blinking associated with autonomic signs such as tachypnoea.2–9 The onset of attacks usually occurs in the first days of life in otherwise healthy infants.3,5–7,9–17 Intralesional electrical recordings and functional imaging studies have documented respectively, a hypersynchronous discharge and a hypermetabolism within the lesion and the brainstem nuclei,3,5–7,9 which is congruent with the peculiar semiology of the paroxysmal attacks. This condition is underestimated because it is rare and is insufficiently documented by video-polygraphic recordings, and it is therefore commonly misdiagnosed.

Table I.   Literature review of published reports of individuals with hemifacial spasms and posterior cranial fossa mass compared with the two individuals in this study
ReferenceSex/age at onsetPsychomotor developmentSeizure semiologySeizure frequencyTreatmentAge at surgeryPathological findings (localization)Outcome (time after surgery)
  1. aIndividual affected by Goldenhar syndrome. M, male; F, female; PB, phenobarbital; PHT, phenytoin; VPA, valproate; CBZ, carbamazepine; CZP, clonazepam; DZP, diazepam; AED, antiepileptic drugs; NP, not performed; NA, not available; FFV, floor of fourth ventricle; LTG, lamotrigine; LEV, levetiracetam; KD, ketogenic diet; TPM, topiramate; NZP, nitrazepan; CNZ, clonazepam; GBP, gabapentin; GVG, gamma-vinyl-GABA; CLB, Clobazam; BDZ, Benzodiazepine.

Langston and Tharp1M/6wksNormalLeft hemifacial spasm, right head deviation, left elbow flexion and extensionMultiple per dayPHT, CBZ5y 6moGangliogliomaLeft facial weakness, left arm clumsy, left nystagmus, seizure persistence (2y 6mo)
Jayakar and Seshia2M/1yMild incoordination, impaired parachute reflexLeft eyelid jerks, bilateral eye blinking, left hemifacial spasm, abnormal respiration, right and up eye deviation, right head deviation, involuntary movements of left armMultiple per dayPB, PHT, VPA, CBZ, CNZ, DZP, haloperidol, pyridoxine, biotin18moLow-grade dense fibrillary astrocytoma (left cerebellar)Mild incoordination of left arm, slight language delay, seizure free without AED (3y 6mo)
Flüeler et al.10F/1dNormalRight hemifacial spasm, right eyelid blinkingMultiple per day (cluster)CBZ, PHT, DZPNPNP (right middle and superior cerebellar peduncle)Seizure persistence (12y)
F/10moNystagmus, tremor, hypotoniaRight hemifacial spasmMultiple per day (cluster)NANPNP (right middle cerebellar peduncle)Seizure persistence (5y)
Bills and Hanieh11M/3wksNormalLeft hemifacial spasm, left gaze deviation, left upper limb dystonic movementsMultiple per dayPB, CNZ, PHT, CBZNAGanglioglioma (left superior cerebellar peduncle)Normal development, seizure free without AED (3mo)
Al-Shahawan et al.12F/1dPsychomotor delayRight hemifacial spasm, right arm flexion and right leg extensionMultiple per dayMultiple AED3yGanglioglioma (right middle and superior cerebellar peduncle)Seizure persistence (NA)
Harvey et al.3M/1dIntermittent gaze-evoked nystagmus, left mouth angle weaknessLeft hemifacial contraction, right head and eye deviation, nystagmoid jerks, autonomic dysfunctionMultiple per dayPB, CBZ, PHT pyridoxine, CNZ, GBP6moGanglioglioma (left cerebellar and middle and superior peduncle)Seizure free (NA)
McLone et al.13M/1dNormalShaking of upper extremities, eye flutteringMultiple per dayPB, PHT1moGangliomatous hamartoma (middle and superior cerebellar peduncle)Normal development, seizure free with PB (6mo)
Arzimanoglou et al.4M/6wksaMild axial hypotoniaLeft hemifacial spasm, eye blinking, left eye deviation, breathing irregularities, cough-like noiseMultiple per dayNANPNA (left cerebellar peduncle impinging fourth ventricle)Bilateral abnormal eye movements, seizure frequency unchanged (21y)
Chae et al.5M/1dNormalLeft hemifacial spasm, hyperventilation with or without vocalization, nystagmoid eye movements, eye blinking, tremulous movements of limbsMultiple per dayPB, VPA, CLB8moLow-grade ganglioglioma (left superior cerebellar peduncle)Mild ataxia, seizure free without AED (2y 6mo)
Delande et al.6F/1dNormalEyelid blinking, left hemifacial twitching, right nystagmoid movements, breathing irregularities, groansMultiple per day (cluster)Pyridoxine, CBZ, CNP, VPA, PB, PHT, GVG, steroids3yHamartoma (FFV; left superior cerebellar peduncle)Normal development, seizure free without AED (8y)
F/1dModerate ataxia, hypotoniaLeft hemifacial contraction, right head and eye deviation, eye blinking, eyelid nystagmoid jerks, breathing irregularities, left arm flexion and elevationMultiple per day (cluster)NA3yHamartoma (FFV; left middle and inferior cerebellar peduncle)Mild left hemiparesis, left abducens nerve deficit, seizure free without AED (1y)
Mesiwala et al.7M/1dNormalLeft eye blinking, extremity twitching, postural arching, shallow breathing, mouth chewing and pursing, arms and legs rowing movementMultiple per dayPB, CNZ, LTG, DZP, CBZ, LEV, KD, TPM7mo/8moGanglioglioma (left cerebellar displacing the fourth ventricle)Left hemifacial weakness, right hypertropia, right nystagmus, left mild hemiparesis, seizure free without AED (12mo)
Pontes-Neto et al.8F/2moNormalEyelid blinking, left hemifacial contraction, left gaze deviation, right nystagmus, breathing irregularities, diaphoresis, decreased temperature of left hemiface and armMultiple per day (cluster)PB, VPA, NZP1yHamartoma (FFV; left cerebellar peduncle; left pons)Normal development, seizure free without AED (2y)
Dagcinar et al.14F/1dNormalLeft hemifacial spasm, bilateral blinking, left head and eye deviation, left arm clonic contraction, impairment of consciousnessMultiple per day (cluster)CBZ, VPA, PB3moGanglioneurocytoma (left middle and superior cerebellar peduncle)Normal development, seizure free with PB (10mo)
Kulkarni et al.19M/2yNormalRight hemifacial spasm, right nystagmioid jerksMultiple per dayVPA, CLBNPNA (right cerebellar)Reduction of seizure frequency with AED
Minkin et al.15F/1dNormalLeft hemifacial spasm, left eyelid blinking, right nystagmoid eye movements, left head deviationMultiple per dayPB, VPA8moGangliocytoma (left superior cerebellar peduncle)Seizure frequency reduced by 95% after surgery (2y)
Hanani et al.16M/1dPsychomotor delay, hypotoniaLeft orbicularis oculi spasms, bilateral eyelid blinking, left hemifacial spasm, right eye deviationMultiple per dayCBZ, CNZ21moGanglioglioma (left middle cerebellar peduncle)Normal development, seizure free (3y)
Park et al.9M/1dNormalLeft hemifacial twitching, eye blinking, left eye deviation, breathing irregularitiesMultiple per dayPB, GVG, BDZ3moHamartoma (FFV; left cerebellar middle peduncle)Normal development, seizure free without AED (NA)
Zamponi et al.17M/2moNormalRight hemifacial spasm, eye blinking, myoclonusMultiple per dayVPA2yHamartoma (FFV; right superior cerebellar peduncle)Seizure free without AED (1y)
Participant 1F/1dMild axial, hypotoniaEyelid blinking, left hemifacial twitching, left nystagmoid movements, tachypnoeaMultiple per day (cluster)Pyridoxine, CBZNPNASeizure persistence (10mo)
Participant 2M/1dMild axial, hypotoniaEyelid blinking, right hemifacial twitching, right eye deviation, right limbs jerks, breathing irregularitiesMultiple per day (cluster)CZP, PB, GVG, CBZNPNASeizure persistence (9mo)

In this article, we review the clinical, neurophysiological, neuroimaging, and histopathological findings, as well as the differential diagnosis, therapeutic approach, and outcome of all previously reported cases. Moreover, we report in detail two new cases including the ictal video-electroencephalography (EEG) recordings.

Definition

  1. Top of page
  2. Abstract
  3. What this paper adds
  4. Definition
  5. Clinical features
  6. Case reports
  7. Differential diagnosis
  8. Treatment and outcome
  9. Summary and conclusion
  10. Acknowledgement
  11. References
  12. Supporting Information

Hemifacial spasm is defined as the unilateral, involuntary, irregular clonic or tonic contraction of muscles innervated by the seventh cranial nerve.18 It occurs most commonly in adults, and is due to facial nerve injury caused by a compression of the facial nerve by a vascular loop or a posterior fossa tumour, but may also occur without apparent cause. However, it is rare in children, in whom it is often associated with the presence of a mass in the fourth ventricle. Moreover, it seems that in children hemifacial spasm is due not to compression of a facial nerve, but to spread to the brainstem nuclei of an epileptic discharge originating within the lesion.

Clinical features

  1. Top of page
  2. Abstract
  3. What this paper adds
  4. Definition
  5. Clinical features
  6. Case reports
  7. Differential diagnosis
  8. Treatment and outcome
  9. Summary and conclusion
  10. Acknowledgement
  11. References
  12. Supporting Information

The clinical presentation is similar in all reported cases. The onset of episodes occurs at an early age, usually in the first days of life (12 out of 20 individuals reported), making this condition particular to the neonatal period; however, there are rare reports of a later onset, occurring within the second year.2,10 After onset, the frequency of episodes is high, with multiple attacks each day, sometimes in clusters, which could lead to feeding impairment.6,9 Hemifacial spasm is always ipsilateral to the lesion: it is described as an irregular tonic or clonic contraction of facial muscles, mainly involving the upper hemifacial muscles. It lasts less than 1 minute. Hemifacial spasm can be associated with other signs. Eye blinking that was mostly unilateral, but at times bilateral, was reported in 13 out of 20 published case. Tachypnoea has been reported in nine individuals.2–9 Deviation of the eyes and/or head towards the side of lesion was described in seven individuals.1,3,4,6,10,14–16,19 Myoclonus of the proximal lower and upper extremities was reported in one individual.17

Neurological examination was normal in 13 of the 20 reported individuals.3,5–7,9–17 In five, one or more of the following cerebellar signs were described: mild hypotonia,4,6,10,16 nystagmus,3,10 mild incoordination,2 and intention tremor.10 A general psychomotor delay was described in two infants.12,16

Case reports

  1. Top of page
  2. Abstract
  3. What this paper adds
  4. Definition
  5. Clinical features
  6. Case reports
  7. Differential diagnosis
  8. Treatment and outcome
  9. Summary and conclusion
  10. Acknowledgement
  11. References
  12. Supporting Information

A 10-month-old female and a 9-month-old male (participants 1 and 2, Fig. 1) with a fourth ventricle mass are reported. Both infants were born at term, after an uneventful pregnancy and delivery, to non-consanguineous parents. No family history of epilepsy or febrile seizures was reported. Soon after birth, both infants started to experience multiple episodes per day characterized by hemifacial twitching ipsilateral to the lesion. Bilateral eye blinking was constantly associated with the hemifacial spasm, predominantly on the same side. Episodes of hemifacial spasm were sometimes associated with ipsilateral eye deviation and tachypnoea. Episodes lasted for 20 to 30 seconds and occurred in clusters, during wakefulness or during sleep. An increase in episodes during feeding was reported, leading to eating impairment in one case. Neurological examination, performed at the ages of 45 days in one case and 30 days in the other, revealed a mild axial hypotonia in both individuals.

image

Figure 1.  (a) Participant 1. Seizure recorded at the age of 45 days by ambulatory video-electroencephalography. The seizure was characterized by sudden blinking of the left eye, followed by bilateral eye involvement, spasm of the left facial muscle (more evident over the area of the lower branch of the facial nerve), left eye lateral nystagmus, and tachypnoea. Video-electroencephalography shows more evident theta activity in the left hemisphere intermingled with left frontal artefacts due to eye blinking, without evidence of epileptiform abnormalities. The electromyography trace reveals repetitive brief jerks over the left orbicularis oris muscle during the first 10 seconds, followed by more pronounced tonic contractions. The breathing trace shows a tachypnoea persisting throughout the entire episode. (b) Participant 2. Seizure recorded at the age of 29 days. The child is awake and presents a paroxysmal blinking of the right eye that rapidly involves the contralateral eye. This is followed by right hemifacial spasm. Video-electroencephalography is characterized by low-voltage theta activity, as well as artefactual high-voltage delta waves. No epileptiform abnormalities are evident. The electromyography trace shows repetitive brief jerks over the right orbicularis oris, followed by a tonic contraction corresponding to the hemifacial spasm. (c–e) Participant 1. Magnetic resonance imaging at the age of 50 days revealed a mass arising from the floor and left wall of the fourth ventricle and fully occupying it. On an axial T2-weighted image (c), the mass is seen to be isohyperintense with the cerebellar cortex. On axial infrared (d) and sagittal spin-echo T1-weighted images, the lesion has an isointense signal (10 × 6 × 7mm). (f–h) Participant 2. Magnetic resonance imaging at the age of 30 days revealed a mass partially occupying the fourth ventricle, intimately associated with the right side of its floor and involving the right middle cerebellar peduncle. The lesion shows an isointense signal on axial turbo spin-echo T2-weighted (f), axial infrared (g), and sagittal spin-echo T1-weighted sequences (13 × 8 × 9mm).

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Video-EEG was performed in both children (Videos S1 and S2, supplementary material published online). Interictal EEG showed normal background activity; ictal EEG showed no epileptiform discharges during the episodes (Fig. 1a,b). Back-average analysis, performed only in the first individual, failed to detect a cortical potential as a counterpart of clinical facial spasm. Magnetic resonance imaging revealed in the first individual a mass arising from the left side of the floor of the fourth ventricle involving the left middle cerebellar peduncle without accompanying hydrocephalus (Fig. 1c–e), and in the second individual a well-defined mass, located on the right side of the floor of the fourth ventricle, involving the right cerebellar hemisphere and the adjacent middle cerebellar peduncle, which displaced the superior cerebellar peduncle upwards and the fourth ventricle to the left (Fig. 1f–h). Both lesions showed an isointense signal with cerebral cortex on T1-weighted sequences, and an isohyperintense signal on T2-weighted sequences with no gadolinium enhancement.

The first infant was treated with carbamazepine (20mg/kg/day), which resulted in a reduction, albeit not significant, in seizure frequency; the second infant was treated instead with clonazepam, phenobarbital, vigabatrin, and carbamazepine in various combinations but without effect. A neuropsychological assessment was performed in the first child at the age of 2 months and revealed a general quotient of 110 (Griffiths scale), although a mild deficit in visual attention was found. A second magnetic resonance study was performed in at the age of 6 months in the first infant and 3 months in the second, and showed unchanged findings. Because during follow-up both infants continued to experience multiple seizures per day, a surgical resection was planned for both individuals.

Electroencephalography findings

In 14 individuals, ictal EEG was reported to be normal, while in four cases slow waves (theta or delta waves) over the central regions were described.6–8 Frontal or temporal epileptiform activity was reported in two individuals,13,19 although in one of them it was uncertain whether this was an ictal or interictal activity.19 The absence of a cortical ictal potential as a counterpart to the clinical manifestations was confirmed in one of our individuals (case 1) by a back-average study. This finding suggests that the cortex is not primarily involved in the pathogenesis of these episodes, and thus the seizure type is of non-cortical origin.6

Some authors focused on the modification of polygraphic parameters such as breathing irregularities and eye blinking, suggesting that they are typical of these episodes (like other artefacts, such as contraction of frontal muscles).1,8,9,15

An intraoperative recording with an electrode implanted within the mass was performed in five of the reported cases, and showed paroxysmal rhythmic activity as usually seen in epileptic seizures.3,5–7,9 Thus, these episodes have been considered to be epileptic in nature. As the cortex is not primarily involved in the pathogenesis, these seizures may be considered to be of non-cortical origin.6

Neuroimaging findings

In previously reported cases, the magnetic resonance signal depended on the type of lesion. The radiological appearance of the lesions observed in our cases was suggestive of hamartoma: a slight hyperintense or isointense signal on T2-weighted and isointense signal on T1-weighted sequences, relative to the cortex, without gadolinium enhancement. In previously reported cases, ictal positron emission tomography and single photon-emission computed tomography studies documented respectively, hypermetabolism and hyperperfusion inside the lesion and in the brainstem nuclei, suggesting a spreading of the epileptic discharge to the brainstem, particularly to the nucleus of the seventh cranial nerve.3,5–9,16,19

Histopathological findings

Of 20 reported cases, histological diagnosis was available in 16 as follows: ganglioglioma in seven, gangliocytoma in two, hamartoma in five, gangliomatous hamartoma in one, and astrocytoma in one (Table I). All but one lesion (Table I)2 belonged to the group of dysplastic neuronal lesions,20 thus supporting the hypothesis that the hypersynchronous ictal discharge could arise from dysplastic neuronal cells inside the tumour. A histological analysis of our two participants will be performed at the time of surgery.

Physiopathological findings

When the first case of hemifacial spasm associated with a fourth ventricle mass was described, it was hypothesized that it could be due to the ‘compression of the genu of the facial nerve, located directly below the tumor in the floor of the IV ventricle’.1 Subsequently, since this hypothesis was not convincing because no mass effect on neighbouring structures was found, Harvey et al.3 suggested a different physiopathological mechanism and, after implanting two depth electrodes in the cerebellar hemisphere, they demonstrated the presence of an epileptic discharge and proposed the concept of cerebellar epilepsy. At a later date, Delande et al.,6 having recorded epileptic discharges inside the lesion with depth electrodes, strengthened the epileptic hypothesis and suggested that the origin of these attacks was within the lesion and not in the cerebellum. This was confirmed by other authors.7,9 Moreover, the lack of a clear-cut distinction between the lesion and the floor of the fourth ventricle and the disappearance of the episodes after resection or disconnection of the lesion are further elements that are highly suggestive of an intralesional epileptogenicity.1,3,5–9,11,13–17,19

Hemifacial spasm is the most evident feature of these attacks, but various other manifestations could be associated events if other cranial nerves are involved (i.e. autonomic dysfunction, deviation and nystagmic eye movements).6 Unilateral or bilateral blinking is frequently associated with hemifacial spasm. Among subcortical structures, blinking was reported to be produced by lesions in the fourth ventricle or in the ipsilateral cerebellar hemisphere.7 It has also been described in seizures of cortical origin caused by the activation of the mesial frontal region (rostral cingulated cortex) and the basal region of the temporal lobe.21,22 Also, in other models of epilepsies, such as epileptic spasms, subcortical structures, such as the basal ganglia and thalamus, seems to be involved in the genesis of seizures. Tachypnoea was hypothesized to be due to the activation of the vagal nucleus,6 despite no modifications of cardiac rhythm having been detected.

Differential diagnosis

  1. Top of page
  2. Abstract
  3. What this paper adds
  4. Definition
  5. Clinical features
  6. Case reports
  7. Differential diagnosis
  8. Treatment and outcome
  9. Summary and conclusion
  10. Acknowledgement
  11. References
  12. Supporting Information

Hemifacial spasm is a peripherally induced movement disorder characterized by clonic or tonic contractions of the facial muscles. It is usually unilateral and sporadic. In adults, hemifacial spasm predominantly affects females in the fourth and fifth decades of life.23 It may be primary (mainly attributed to vascular compression of the seventh cranial nerve in the posterior fossa) or secondary to facial nerve lesions, such as Bell’s palsy or traumatic facial nerve injury, or brainstem damage.24 The two forms share a number of features but may differ in clinical presentation (simultaneous involvement of the upper and lower facial muscles in secondary forms).25 In addition, several reports of familial hemifacial spasm have been documented.26 Even though some ophthalmological causes, such as accommodative esotropia, have been described,27 paediatric hemifacial spasm could also be due to facial nerve compression by vascular loop or brainstem masses. In neonates, neurovascular compression has never been reported, and in most cases hemifacial spasm is due to a posterior fossa mass. Rare cases of benign congenital hemifacial spasm have been reported.28 Neuroradiological studies, including brain magnetic resonance imaging and magnetic resonance angiography, combined with submillimetre magnetic resonance tomographic angiographic sections, are fundamental in differential diagnosis.29 Other involuntary facial movements, such as tardive dyskinesias, myokymia, tics, cranial dystonia, and psychogenic facial spasm, should be differentiated from hemifacial spasm.30

Treatment and outcome

  1. Top of page
  2. Abstract
  3. What this paper adds
  4. Definition
  5. Clinical features
  6. Case reports
  7. Differential diagnosis
  8. Treatment and outcome
  9. Summary and conclusion
  10. Acknowledgement
  11. References
  12. Supporting Information

Antiepileptic drugs are not effective in these cases. In 19 out of 20 previously reported cases, at least two antiepileptic drugs were administered without any effect except for an inconstant reduction in seizure frequency. Only resection or disconnection of the lesion can lead to remission of the attacks persisting also after drug withdrawal of drug treatment.1,5–9,11,17 When seizures occur many times a day and are disabling, treatment with multiple antiepileptic drugs is useless, as described in three individuals with neonatal hemifacial spasms who received eight antiepileptic drugs in combination,2,6,7 and surgery should be considered as early as possible. The timing of surgery is still controversial because of potential complications when surgery is performed at a young age. At the time of surgery, the age of individuals ranged from 3 months4,9 to 5 years 6 months.1 The neurological outcome was unremarkable in all cases except for three individuals with hemifacial weakness or mild hemiparesis1,6,7 and one individual5 with mild ataxia. Furthermore, in some cases radiosurgery should be considered for posterior cranial fossa tumours, as complete resection of the tumour may be difficult because of its close proximity to critical vascular and neural structures.31

Summary and conclusion

  1. Top of page
  2. Abstract
  3. What this paper adds
  4. Definition
  5. Clinical features
  6. Case reports
  7. Differential diagnosis
  8. Treatment and outcome
  9. Summary and conclusion
  10. Acknowledgement
  11. References
  12. Supporting Information

Clinical, neurophysiological, neuroimaging, and histopathological findings in all described cases of neonatal hemifacial spasms related to lesions of fourth ventricle suggest that these episodes should be considered epileptic in nature. Moreover, as neonatal hemifacial spasms are so rare and thus are not well known, we stress the importance of identifying this peculiar seizure semiology in the neonatal period in order to provide adequate treatment and correct prognosis.

Acknowledgement

  1. Top of page
  2. Abstract
  3. What this paper adds
  4. Definition
  5. Clinical features
  6. Case reports
  7. Differential diagnosis
  8. Treatment and outcome
  9. Summary and conclusion
  10. Acknowledgement
  11. References
  12. Supporting Information

We thank the staff of the Neurophysiology Unit of Bambino Gesù Children’s Hospital and the electroencephalography technicians Roberto Miliucci and Tiziana Fubelli.

References

  1. Top of page
  2. Abstract
  3. What this paper adds
  4. Definition
  5. Clinical features
  6. Case reports
  7. Differential diagnosis
  8. Treatment and outcome
  9. Summary and conclusion
  10. Acknowledgement
  11. References
  12. Supporting Information

Supporting Information

  1. Top of page
  2. Abstract
  3. What this paper adds
  4. Definition
  5. Clinical features
  6. Case reports
  7. Differential diagnosis
  8. Treatment and outcome
  9. Summary and conclusion
  10. Acknowledgement
  11. References
  12. Supporting Information
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