Vertical one-and-a-half syndrome (VOHS) is an uncommon presentation resulting from a unilateral thalamomesencephalic stroke with involvement of the rostral interstitial nucleus of the medial longitudinal fasciculus and posterior commissure. The artery of Percheron (aPe) is a branch of the posterior cerebral artery (PCA) and it is a variant that arises as a solitary trunk supplying both medial thalami and upper midbrain. A 78-year-old female patient, presented at the hospital emergency with approximately 12 hours of sudden onset of diplopia, associated with dizziness. Neurological exam revealed torsional nystagmus associated with bilateral upgaze palsy with limitation of infraduction on the left . We describe a rare case of VOHS associated with ischemic alterations at the MRI suggesting an aPe impairment. The conjugate gaze control lies anatomically at the midbrain at the central nervous system (CNS). This report describes a rare type of VOHS and brings a new insight on a possible aPe topography possibly causing this clinical presentation.

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Context: Neurosarcoidosis is common in 50-70% of cases of sarcoidosis, but polyradiculoptia in sarcoidosis is rare in 1.3% of cases. Case Report: a 48-year- old woman diagnosed with Sarcoidosis after skin, evolved with sporadic paresthesia of the lower limbs. The use of Methotrexate controlled the disease. However, she developed acute pancreatitis secondary to the treatment and suspended it. After 2 months, the patient presented paraparesis. In view of probable polyradiculoneuropathy, Human Immunoglobulin was administered. However, she evolved with mental confusion, flaccid tetraparesis and global arreflexia. CT of skull showed paramedian bridge hypodensity and left cerebellum, suggestive of vasculitis, and normal liquor. Methylprednisolone was administered. And despite the treatment, patient worsened with decreased level of consciousness and respiratory failure. MRI of skull showed hypersignal in bilateral temporal region, suggesting viral encephalitis secondary to immunosuppression, after methylprednisolone and immunoglobulin. Thus, Aciclovir was administered and there was improvement in the use of BIPAP. Discussion: Other differential diagnoses were considered: Guillain-Barré syndrome, inflammatory and chronic demyelinating polyneuropathies, spirochete infections, fungi or toxoplasmosis. The diagnosis of neurosarcoidosis is mainly due to MRI, high sensitivity and low specificity. Neural tissue biopsy is gold standard, but difficult to access. Conclusion: This clinical history shows an atypical involvement of the Central and Peripheral Nervous System for sarcoidosis: a viral encephalitis after polyradiculopathy and vasculitis treated.

Context: The acute paralysis of the vertical gaze is usually caused by a mesencephalic lesion because the control of the vertical conjugated gaze is found there; there are three main structures: the rostral interstitial nucleus of the medial longitudinal fascicle (riFLM), the Cajal interstitial nucleus and the posterior commissure (CP). The riFLM, contains burst neurons responsible for the saccades, projecting to the subnuclei of the upper rectum and inferior oblique to look upwards and subnuclei of the lower rectum and superior oblique to look downwards. The projections for the elevators appear to be bilateral, with axons probably crossing within the oculomotor nuclear complex and apparently not via CP; depressors, on the other hand, are ipsilateral. Case report: Female, 78 years old, hypertensive and diabetic, suddenly started with vertical diplopia and vertigo. Examination: Bilateral hypoactive photomotor reflex, bilateral paralysis of the vertical gaze upward, monocular paralysis downward and torsional nystagmus in the left eye. Resonance with restriction the diffusion of water molecules in both thalamus and in the right rostral midbrain. Conclusions: riFLM is vascularized by the posterior thalamus-subthalamic paramedian artery. A single artery, Percheron’s, provides both riFLM in 20% of the population and allows bilateral lesions from a single infarction. Unilateral infarction can also cause saccadic paralysis of the bilateral vertical gaze. The disjunctive disorders of the vertical gaze have two variants of the one and a half syndrome. One consists of bilateral paralysis of the gaze upwards and monocular paresis of the gaze downwards with an ipsilateral or contralateral lesion, described in thalamomesencephalic lesions, explanation for the exposed case. The other is due to bilateral mesodiencephalic infarctions. It is difficult to understand the relationship between topography and the vertical gaze circuit, showing that it is more complex than we imagine. It is probably an association of topographies, little described, but of paramount importance to be discussed and researched.

Context: Acute Disseminated Encephalomyelitis (ADEM) usually happens after an infectious event, vaccination reaction and with history of immunosuppression. Clinical features can be varied: headache, fever, seizure, blurred vision, ataxia, motor deficits and mental confusion. Case report: A 35-yearsold woman, in a social risk situation, complained about pain and blurred vision, history of cocaine abuse, victim of sexual and physical abuse and recent Measles vaccination. She had corneal ulcer with bilateral endophthalmitis and optic nerve infection. Despite intravitreal injections of Vancomycin + Ceftazidime, patient had to eviscerate the left eye. After surgery, patient evolved with mental confusion and paraparesis, CSF cell 69, lymphomonocyte, proteins 257, MRI showed central bulbar hyperintensity, lesions in the dentate nucleus and periaqueductal of gray substance in T2 / FLAIR, thoracic and lumbar spine with demyelinating pattern, extensive longitudinal myelitis. Patient obtained clinical improvement after treatment with Methylprednisolone 1gr for 5 days. It is important to discard other hypothesis: transverse myelitis, neuromyelitis optica, multiple sclerosis and systemic lupus erythematosus. The diagnosis is clinical and radiological with multifocal and confluent areas of hypersignal on MRI, CSF analysis reveals high protein and lymphocytic pleocytosis. Treatment with Methylprednisolone is the first choice and then Plasmapheresis. Conclusion: there are several risk factors for the development of ADEM correlated with a rapid and aggressive evolution in this patient.