Drooping of the upper eyelid (upper eyelid ptosis) may be minimal (1-2 mm), moderate (3-4 mm), or severe (>4 mm), covering the pupil entirely. Ptosis can affect one or both eyes. Ptosis can be present at birth (congenital) or develop later in life (acquired). Ptosis may be due to a myogenic, neurogenic, aponeurotic, mechanical or traumatic cause. Usually, ptosis occurs isolated, but may be associated with various other conditions, like immunological, degenerative, or hereditary disorders, tumors, or infections. Besides drooping, patients with ptosis complain about tired appearance, blurred vision, and increased tearing. Patients with significant ptosis may need to tilt their head back into a chin-up position, lift their eyelid with a finger, or raise their eyebrows. Continuous activation of the forehead and scalp muscles may additionally cause tension headache and eyestrain. If congenital ptosis is not corrected, amblyopia, leading to permanently poor vision, may develop. Patients with ptosis should be investigated clinically by an ophthalmologist and neurologist, for blood tests, X-rays, and CT/MRI scans of the brain, orbita, and thorax. Treatment of ptosis depends on age, etiology, whether one or both eyelids are involved, the severity of ptosis, the levator function, and presence of additional ophthalmologic or neurologic abnormalities. Generally, treatment of ptosis comprises a watch-and-wait policy, prosthesis, medication, or surgery. For minimal ptosis, Müller's muscle conjunctival resection or the Fasanella Servat procedure are proposed. For moderate ptosis with a levator function of 5-10 mm, shortening of the levator palpebrae or levator muscle advancement are proposed. For severe ptosis with a levator function <5 mm, a brow/frontalis suspension is indicated. Risks of ptosis surgery infrequently include infection, bleeding, over- or undercorrection, and reduced vision. Immediately after surgery, there may be temporary difficulties in completely closing the eye. Although improvement of the lid height is usually achieved, the eyelids may not appear perfectly symmetrical. In rare cases, full eyelid movement does not return. In some cases, more than one operation is required.

Lesions of the lower cranial nerves (LCN) are due to numerous causes, which need to be differentiated to optimize management and outcome. This review aims at summarizing and discussing diseases affecting LCN. Review of publications dealing with disorders of the LCN in humans. Affection of multiple LCN is much more frequent than the affection of a single LCN. LCN may be affected solely or together with more proximal cranial nerves, with central nervous system disease, or with nonneurological disorders. LCN lesions have to be suspected if there are typical symptoms or signs attributable to a LCN. Causes of LCN lesions can be classified as genetic, vascular, traumatic, iatrogenic, infectious, immunologic, metabolic, nutritional, degenerative, or neoplastic. Treatment of LCN lesions depends on the underlying cause. An effective treatment is available in the majority of the cases, but a prerequisite for complete recovery is the prompt and correct diagnosis. LCN lesions need to be considered in case of disturbed speech, swallowing, coughing, deglutition, sensory functions, taste, or autonomic functions, neuralgic pain, dysphagia, head, pharyngeal, or neck pain, cardiac or gastrointestinal compromise, or weakness of the trapezius, sternocleidomastoid, or the tongue muscles. To correctly assess manifestations of LCN lesions, precise knowledge of the anatomy and physiology of the area is required.

This is the first report of reversible cerebral vasoconstriction syndrome (RCVS) as a complication of a SARS-CoV-2 vaccination. A 38-year-old female developed visual impairment due to scotomas and thunderclap headache 18 days after the second shot of the Moderna SARS-CoV-2 vaccine. Multimodal cerebral MRI revealed an acute cortical ischemic lesion in the territory of the right posterior cerebral artery (PCA) on T2weighted images, diffusion-weighted imaging (DWI), apparent diffusion coefficient (ADC) maps and absence of the PCA on magnetic resonance angiography (MRA). RCVS was diagnosed as the cause of the ischemic lesion. RCVS partially resolved upon nimodipine and anti-seizure drugs within nine days. In conclusion, this case shows that a SARS-CoV-2 vaccination can be followed by RCVS, manifesting as headache, stroke, and epileptiform discharges, and responding favorably to nimodipine.

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Acute myocardial infarction (AMI) is a multifactorial disease influenced by environmental and genetic factors. The aim of this study was to assess the association of angiotensin II type 1 receptor (ATR1) gene polymorphisms with AMI as well as to evaluate the role of serum angiotensin-converting enzyme (ACE) activity and that of cardiac troponin I (cTnI) in Tunisian AMI patients. One hundred and eighteen AMI patients were compared to 150 healthy controls. ATR1 genotypes were determined by polymerase chain reaction restriction fragment length polymorphism (PCR-RFLP). The ATR1 A1166C polymorphism was significantly associated with AMI (p = 0.024). CC genotype and C allele frequencies were associated with increased AMI risk [CC vs. AC and AA: OR = 2.06; p = 0.045; 95 % CI (1.02-4.18); C vs. A: OR = 1.68; p = 0.004; 95 % CI (1.17-2.41)]. By multivariate logistic regression analysis, CC genotype, hypertension, diabetes, serum ACE activity and peak-cTnI were significant independent predictors of AMI. Increased serum ACE activity and cTnI peak levels were associated with the CC genotype in AMI patients. In conclusion, the ATR1 A1166C polymorphism is associated with AMI and the CC genotype associated with increased ACE activity and cTnI levels appear to predispose for AMI risk.