(1) Background: Reversible cerebral vasoconstriction syndrome (RCVS) encompasses a clinical and radiological diagnosis characterized by recurrent thunderclap headache, with or without focal deficits due to multifocal arterial vasoconstriction and dilation. RCVS can be correlated to pregnancy and exposure to certain drugs. Currently, the data on prevalence of RCVS in the postpartum period is lacking. We aim to investigate the prevalence of RCVS in the postpartum period and the rate of hemorrhagic complications of RCVS among the same group of patients; (2) Methods: We conducted the metanalysis by using the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA), and Meta-Analyses and Systematic Reviews of Observational Studies in Epidemiology (MOOSE) protocol. To analyze the Bias, we used the Ottawa Newcastle scale tool. We included only full-text observational studies conducted on humans and written in English. We excluded Literature Reviews, Systematic Reviews, and Metanalysis. Additionally, we excluded articles that did not document the prevalence of RCVS in the postpartum period (3). Results: According to our analysis, the Prevalence of RCVS in the postpartum period was 129/1083 (11.9%). Of these, 51/100 (52.7%) patients had hemorrhagic RCVS vs. 49/101 (49.5%) with non-hemorrhagic RCVS. The rates of Intracerebral Hemorrhage (ICH) and Subarachnoid Hemorrhage (SAH) were (51.6% and 10.7%, respectively. ICH seems to be more common than.; (4) Conclusions: Among patients with RCVS, the prevalence in PP patients is relativity high. Pregnant women with RCVS have a higher recurrence of hemorrhagic vs. non-hemorrhagic RCVS. Regarding the type of Hemorrhagic RCVS, ICH is more common than SAH among patients in the postpartum period. Female Sex, history of migraine, and older age group (above 45) seem to be risk factors for H-RCVS. Furthermore, recurrence of RCVS is associated with a higher age group (above 45). Recurrence of RCVS is more commonly idiopathic than being triggered by vasoactive drugs in the postpartum period.
Few studies have thoroughly evaluated the neuro-invasive effect of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, which may contribute to a wide range of sequelae from mild longterm effects like headaches and fatigue to severe events like stroke and arrhythmias. Our study aimed to evaluate the long-term neurological effects of coronavirus disease 2019 (COVID-19) among patients discharged from the hospital.In this systematic review and meta-analysis, we assessed the long-term neurocognitive effects of COVID-19. Post-COVID-19 neurological sequelae were defined as persistent symptoms of headache, fatigue, myalgia, anosmia, dysgeusia, sleep disturbance, issues with concentration, post-traumatic stress disorder (PTSD), suicidality, and depression long after the acute phase of COVID-19. Data from observational studies describing post-COVID-19 neurocognitive sequelae and severity of COVID-19 from September 1, 2019, to the present were extracted following the Meta-analysis of Observational Studies in Epidemiology (MOOSE) guidelines and Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) protocol with a consensus of three independent reviewers. A systematic review was performed for qualitative evaluation and a meta-analysis was performed for quantitative analysis by calculating log odds of COVID-19 neurocognitive sequelae. The odds ratio (OR) and 95% confidence interval (CI) were obtained and forest plots were created using random effects models.We found seven studies, out of which three were used for quantitative synthesis of evidence. Of the 3,304 post-COVID-19 patients identified, 50.27% were male with a mean age of 56 years; 20.20% had post-COVID-19 symptoms more than two weeks after the acute phase of infection. Among persistence symptoms, neurocognitive symptoms like headache (27.8%), fatigue (26.7%), myalgia (23.14%), anosmia (22.8%), dysgeusia (12.1%), sleep disturbance (63.1%), confusion (32.6%), difficulty to concentrate (22%), and psychiatric symptoms like PTSD (31%), feeling depressed (20%), and suicidality (2%) had a higher prevalence. In meta-analysis, COVID-19 patients with severe symptoms had higher odds of headache
Primary Central Nervous System Lymphoma (PCNSL) is a rare variant of Non-Hodgkin Lymphoma (NHL) representing 1–2% of all NHL cases. PCNSL is defined as a lymphoma that occurs in the brain, spinal cord, leptomeninges, or eyes. Efforts to treat PCNSL by traditional chemotherapy and radiotherapy have generally been unsuccessful as a significant proportion of patients have frequent relapses or are refractory to treatment. The prognosis of patients with Refractory or Relapsed (R/R) PCNSL is abysmal. The optimal treatment for R/R PCNSL is poorly defined as there are only a limited number of studies in this setting. Several studies have recently shown that ibrutinib, a Bruton tyrosine kinase (BTK) inhibitor, has promising results in the treatment of R/R PCNSL. However, these are preliminary studies with a limited sample size. In this systematic review, we explored and critically appraised the evidence about the efficacy of the novel agent ibrutinib in treating R/R PCNSL.
Megacephaly polymicrogyria, polydactyly, hydrocephalus (MPPH) is an extremely rare condition caused by a defect in the AKT3, CCND2, or PIKR2 genes. Although the prevalence of the syndrome is very low, there is a significant clinical and radiological variation in the syndrome. We present a case with MPPH admitted to the hospital due to an increase in seizure frequency. The patient had a history of cerebral palsy, global developmental delay, spasticity, and hypoglycemic episodes. MRI findings revealed ventriculomegaly, polymicrogyria, abnormal encephalon, and pachygyria. The addition of clobazam and alprazolam diminished the seizures' frequency and the patient's spasticity, respectively. To highlight the clinical and radiological variation of the syndrome, we review cases of MPPH with clinical and radiological variants. Pachygyria and cerebral palsy are new associations not previously described before in MPPH. Pachygyria and cerebral palsy could be worsening the seizures and the global delay in this patient. Hypoglycemic episodes are probably related to the AKT3 gene, promoting more glucose consumption. Spasticity is most probably related to an upper motor sign due to the patient's cerebral palsy. This case highlights the clinical and radiological variation of the syndrome. More cases of MPPH need to be described to consolidate the knowledge and have a better understanding of the clinical and radiological variation of the syndrome.
Parinaud’s syndrome involves dysfunction of the structures of the dorsal midbrain. We investigated the pathophysiology related to the signs and symptoms to better understand the symptoms of Parinaud’s syndrome: diplopia, blurred vision, visual field defects, ptosis, squint, and ataxia, and Parinaud’s main signs of upward gaze paralysis, upper eyelid retraction, convergence retraction nystagmus (CRN), and pseudo-Argyll Robertson pupils. In upward gaze palsy, three structures are disrupted: the rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF), interstitial nucleus of Cajal (iNC), and the posterior commissure. In CRN, there is a continuous discharge of the medial rectus muscle because of the lack of inhibition of supranuclear fibers. In Collier’s sign, the posterior commissure and the iNC are mainly involved. In the vicinity of the iNC, there are two essential groups of cells, the M-group cells and central caudal nuclear (CCN) group cells, which are important for vertical gaze, and eyelid control. Overstimulation of the M group of cells and increased firing rate of the CCN group causing eyelid retraction. External compression of the posterior commissure, and pretectal area causes pseudo-Argyll Robertson pupils. Pseudo-Argyll Robertson pupils constrict to accommodation and have a slight response to light (miosis) as opposed to Argyll Robertson pupils were there is no response to a light stimulus. In Parinaud’s syndrome patients conserve a slight response to light because an additional pathway to a pupillary light response that involves attention to a conscious bright/dark stimulus. Diplopia is mainly due to involvement of the trochlear nerve (IVth cranial nerve. Blurry vision is related to accommodation problems, while the visual field defects are a consequence of chronic papilledema that causes optic neuropathy. Ptosis in Parinaud’s syndrome is caused by damage to the oculomotor nerve, mainly the levator palpebrae portion. We did not find a reasonable explanation for squint. Finally, ataxia is caused by compression of the superior cerebellar peduncle.
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