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Stroke
Published in Henry J. Woodford, Essential Geriatrics, 2022
SAH should be suspected when there is a sudden onset of severe headache (‘worst ever') and will be detected in around a quarter of these people.96 The pain may be diffuse or localised. Additional suggestive features that may be present include neck pain, photophobia, nausea/vomiting and reduced consciousness. Sudden loss of consciousness may be the presenting feature. Focal neurological signs are occasionally present. A third nerve palsy can be caused by compression by an expanding, or bleeding, posterior communicating artery aneurysm.
Stroke and Transient Ischemic Attacks of the Brain and Eye
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Other features of SAH include: Vomiting (75%).Depressed consciousness (67%).Focal neurologic signs (15%).Intraocular subhyaloid hemorrhages (linear or flame-shaped hemorrhages in the preretinal layer (Figure 12.12) (14%).Epileptic seizures (7%).Delirium (1%).Radicular or precordial pain (spinal SAH).Severe hypertension.Electrocardiographic changes that can mimic those of acute myocardial infarction (MI).
General Medical Emergencies
Published in Anthony FT Brown, Michael D Cadogan, Emergency Medicine, 2020
Anthony FT Brown, Michael D Cadogan
Examine for focal neurological signs. Seizures and coma may develop later. Look for papilloedema, retinal haemorrhages, exudates and cotton-wool spots on funduscopy (grade IV retinal changes).
Reversible cerebral vasoconstriction syndrome
Published in Neuropsychological Rehabilitation, 2018
Michael Perdices, Geoffrey Herkes
Neurological complications and comorbidities can occur during the acute phase of RCVS, usually within days of symptom onset. Recurring thunderclap headaches are very common, up to 100% in some case series (Singhal et al., 2011). There may be focal neurological signs which are transient in most cases. Persistent (i.e., > 24 hour duration) focal neurological deficits may occur in approximately 30% and 2% of individuals with and without haemorrhagic complications, respectively (Ducros et al., 2010). However, the true prevalence of cerebral stroke/non-aneurysmal haemorrhagic events in these patients is unclear. Low rates of ischaemic stroke (7.8%) are reported in some case series, but no other type of haemorrhagic event (Chen et al., 2010b). By contrast, in the series of 89 patients reported by Ducros et al. (2010), approximately one third had at least one haemorrhagic complication, with chronic subarachnoid haemorrhage being the most common (30%). Variable rates of posterior reversible encephalopathy syndrome (9.1–38%) have been reported (Chen et al., 2010b; Singhal et al., 2011).
Sepsis-associated encephalopathy and septic encephalitis: an update
Published in Expert Review of Anti-infective Therapy, 2021
Simone C. Tauber, Marija Djukic, Johannes Gossner, Helmut Eiffert, Wolfgang Brück, Roland Nau
The presence of focal neurological signs is a strong indicator of SE. Important differential diagnoses of SE are focal CNS infections (e.g., multiple brain abscesses by Nocardia spp [144]. mimicking SME) and infectious vasculitis which can be caused by a wide range of infections including viruses, bacteria, parasites, and fungi [145–147]. Varicella zoster virus (VZV)-induced angiitis of the CNS can occur without Herpes zoster and without CSF pleocytosis, but lesions on brain MRI or CT are almost always visible [147]. SARS-CoV-2 virus infection, originally thought to be restricted to the respiratory system, affects multiple other organs including the central and peripheral nervous system. Neurologic manifestations of SARS-CoV-2 virus infection are caused by a variety of mechanisms, including virus-induced hyperinflammatory and hypercoagulable states, entry of the virus into the CNS, and postinfectious immune-mediated processes. Clinical manifestations include encephalopathy, encephalitis, acute disseminated encephalomyelitis, meningitis, ischemic and hemorrhagic stroke, venous sinus thrombosis, and endothelial injury, dysfunction of smell and taste, muscle injury, and Guillain-Barre syndrome [148]. In a large series 1683 of in-patients with SARS-CoV-2 virus infection, 23 (1.4%) developed cerebrovascular disease with an unfavorable functional outcome. In 17 patients (74%) cerebral ischemia and in 5 (22%) intracerebral hemorrhage predominated, one patient developed posterior reversible leukencephalopathy. Brain biopsies showed signs of thrombotic microangiopathy and endothelial damage, but no evidence of vasculitis or necrotizing encephalitis [149].
Neuropathological complications associated with hypertensive disorders of pregnancy
Published in Hypertension in Pregnancy, 2019
Adedayo Damilare Adekomi, Jagidesa Moodley, Thajasvarie Naicker
Symptoms of visual impairment occur in 25% of cases of severe PE and in about 50% of cases of eclampsia (13,14). The visual disturbances associated with preeclampsia/eclampsia include blurred vision, photophobia, photopsia, visual field defects, sudden inability to focus, and in severe cases, visual spots, diplopia, and complete blindness (13,15,16). These ocular anomalies could be attributed to focal or generalized arteriolar narrowing, posterior cerebral artery vasospasm with ischemia or to cerebral edema in the occipital area of the brain (17). The most prominent finding is terminal arteriolar vasospasm, associated with the development of systemic hypertension (18). Although retinal vasculature changes are more common, the conjunctive, choroid, the optic nerve, and visual cortex may be affected in severe PE (13). The neuropathological pathologies can be divided into: Cortical blindness which is thought to be due to posterior reversible encephalopathy syndrome (PRES) which usually resolves in the postpartum period;Serous retinal detachment which occurs in 1–3% of patients with preeclampsia/eclampsia. Most of these cases tend to occur in the postpartum period and they resolve spontaneously within a week of diagnosis and;Rare events such as Purtscher-like retinopathy (central vein occlusion and retinal/vitreous hemorrhages) (17). Assuming that PE is cause of the patients’ headache and or visual disturbances, treatment of the former will result in resolution of the latter. Persistent symptomology or atypical presentations of focal neurological signs should prompt the performance of advanced neuroimaging examination