Thirteen-And-A-Half Syndrome

Allbon, Daniel; Hood, Ben

doi:10.1097/wno.0000000000000341

Cited by 15 publications

(9 citation statements)

References 7 publications

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“…Allbon and La Hood (20) reported in 2016 that a patient with a lymphoproliferative disease after renal transplantation had a group of cranial nerve symptoms. A 50-year-old man suddenly presented the right one-and-a-half syndrome with the right facial paralysis, the right lagophthalmos with absent corneal sensation and significant punctate epithelial erosions on the right cornea, accompanied by right facial numbness and right limbs and torso ataxia symptoms.…”

Section: Thirteen-and-a-half Syndromementioning

confidence: 99%

One-and-a-half syndrome with its spectrum disorders

Xue¹,

Zhang²,

Zhang³

et al. 2017

Quant. Imaging Med. Surg.

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One-and-a-half syndrome is a syndrome characterized by horizontal movement disorders of the eyeballs, which was first reported and named by Fisher in 1967. It presents a combination of ipsilateral conjugate horizontal gaze palsy (one) and ipsilateral internuclear ophthalmoplegia (INO) (a half). On the basis of the one-and-a-half syndrome, there are a series of related rare syndromes called the one-and-a-half syndrome spectrum disorders. This article reviews rare cases of one-and-a-half syndrome spectrum disorder, describes the clinical and pathological features of different syndromes, and summarizes their nomenclature. Quant Imaging Med Surg 2017;7(6):691-697 qims.amegroups.com Xue et al. One-and-a-half syndrome with its spectrum disorders horizontal conjugate movement of eyes. If the isolated side of PPRF is damaged, the eyes could not gaze at the lesion side, presenting the horizontal gaze palsy to the lesion side (6).The abducens nucleus is located in colliculus facialis, which is in the lower part of the pons and the bottom of the fourth ventricle (7). It contains two functionally distinct cell groups: the abducens motoneurons that innervate the lateral rectus muscle; the internuclear neurons which axons cross the midline and ascend via the contralateral MLF to oculomotor subnucleus and control the medial rectus (8). Therefore, the unilateral lesion of the abducens nucleus will also produce ipsilateral horizontal gaze paralysis.MLF are the longitudinal nerve fibers that locate on the back of the pons and are close to the front of the fourth ventricle, a part of which relating to horizontal gaze is from the side of the abducens nucleus to the contralateral oculomotor subnucleus (9). The lesion of unilateral pontine tegmentum can damage the ipsilateral MLF, causing the ipsilateral INO, and its clinical manifestations show the ipsilateral intraocular muscle paralysis and contralateral horizontal nystagmus when staring at the opposite side. If the damage does not involve the midbrain, the convergence reflex is integrated (10). One-and-a-half syndromeThe one-and-a-half syndrome is caused by a lesion of unilateral tegmentum of pons, causing damage to the PPRF (or abducens nucleus) and MLF ( Figure 2). The most common cause of one-and-a-half syndrome was cerebrovascular disease, and usually was brain stem lacunar infarction, followed by the demyelinating etiology (multiple sclerosis), and then the infectious cause including neurocysticercosis and brainstem encephalitis. Other uncommon causes were head trauma, brain stem tumor (primary or metastasis), astrocytomas, etc. (6,11). Therefore, the vast majority of one-and-a-half syndrome companied by other positioning signs is due to the different lesions of brainstem (3). Only a very small number of patients showed isolated one-and-a half syndrome, while the lesions are smaller and localized, such as brainstem cysticercosis, brainstem tuberculosis, brainstem cavernous hemangioma and the local hemorrhagic infarction of brainstem (12-15).We recently diagnosed a ...

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Section: Thirteen-and-a-half Syndromementioning

confidence: 99%

One-and-a-half syndrome with its spectrum disorders

Xue¹,

Zhang²,

Zhang³

et al. 2017

Quant. Imaging Med. Surg.

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“…[5] Subsequently, Eggenberger put forward eight-and-a-half syndrome (i.e., one-and-a-half syndrome plus ipsilateral peripheral seventh cranial nerve palsy) in 1998. [1] Accordingly, some new variants of eight-and-a-half syndrome have been successively proposed, such as “fifteen-and-a-half” syndrome (i.e., one-and-a-half syndrome plus bilateral seventh cranial nerve palsy proposed by Bae et al [6] ), nine syndrome (i.e., eight-and-a-half syndrome plus hemiplegia and hemidysesthesia presented by Rosini et al [2] ), and “thirteen-and-a-half” syndrome (i.e., eight-and-a-half syndrome plus ipsilateral fifth cranial nerve palsy introduced by Allbon et al [7] ). Although Rosini et al first proposed the concept of nine syndrome, [2] Uysal et al had previously reported a patient with the right pontine infarction who manifested as eight-and-a-half syndrome combined with transient hemiparesis, which should belong to atypical nine syndrome.…”

Section: Discussionmentioning

confidence: 99%

Atypical “nine” syndrome in bilateral pontine infarction

Cao

Wang²,

Xia³

et al. 2019

Medicine

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Rationale: “Nine” syndrome, that is “eight-and-a-half” syndrome associated with hemiplegia and hemidysesthesia, is a rare disorder. This study aimed to report a Chinese patient with acute bilateral pontine infarction manifesting as eight-and-a-half syndrome plus hemiplegia (atypical nine syndrome), and also the clinical and neuroimaging findings were explained and discussed with review of the literature. Patient concerns: A 79-year-old woman experienced sudden vertigo, nausea, vomiting, and weakness at her left arm and leg. The neurological examination disclosed her right horizontal gaze palsy, internuclear ophtalmoplegia (INO), and right-sided peripheral facial paralysis combined with slight left-sided hemiplegia, which were consistent with atypical nine syndrome. Diagnoses: Cranial magnetic resonance imaging (MRI) displayed acute multiple ischemic infarction, involving bilateral pontine tegmentum, basilar part of right paramedian pontine, and left cerebellar hemisphere. Intracranial MR angiography (MRA) revealed right middle cerebral artery occlusion, no clear visualization of bilateral vertebral arteries, and basilar artery hypoplasia with stenotic segments. Interventions: Thrombolysis could not be performed due to the time window. The patient was given low molecular weight heparin for anticoagulation because of posterior circulation and progressive stroke. Outcomes: The vertigo disappeared, and a notable improvement with minimal restriction in the right horizontal gaze and partial relief of her facial paralysis were found at discharge, while her left hemiparesis was fully resolved. No recurrence of cerebral infarction was observed during follow-up as well. Lessons: This case report with atypical nine syndrome is fairly rare. Nine syndrome may refer to the lesion located in unilateral tegmentum of the caudal pontine plus paramedian pontine, with an important localization value.

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“…It has been proposed that OAAH syndrome and the EAAH syndrome variants are all part of the same continuum involving paramedian pontine lesions . OAAH syndromes commonly may include other cranial nerves in approximately 75 per cent of cases .…”

Section: Discussionmentioning

confidence: 99%

“…Cases of OAAH in combination with ipsilateral lower motor neuron facial nerve (cranial nerve VII) palsies are called ‘eight‐and‐a‐half syndrome’ (EAAH: OAAH plus cranial nerve VII involvement), and were first described by Eggenberger in 1998 . Since then, different variants of EAAH syndrome have appeared in the ophthalmological literature such as: nine syndrome (EAAH syndrome plus hemiplegia), thirteen‐and‐a‐half syndrome (EAAH syndrome plus trigeminal nerve palsy), fifteen‐and‐a‐half syndrome (OAAH syndrome plus bilateral facial nerve palsies), sixteen‐and‐a‐half syndrome (EAAH syndrome plus vestibulocochlear nerve involvement), and even a twenty‐four‐and‐a‐half syndrome (EAAH syndrome plus bilateral vestibulocochlear nerve involvement) …”

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confidence: 99%