Resolution of Acute Hydrocephalus and Migration of Neurocysticercosis Cyst with External Ventricular Drainage

Neurocysticercosis is endemic in the developing world, but is becoming more common in the US due to immigration. A 24-year-old man presented with acute hydrocephalus and headaches, nausea, and vomiting. Head CT revealed a 3rd ventricular cyst and immunological studies were suggestive of neurocysticercosis. EVD placement resulted in migration of the cyst interiorly and superiorly with return of normal CSF flow by MRI and resolution of symptoms. Review of this condition is important given increasing incidence in the United States

Paradoxical Emboli Secondary to Hepatic Pathology: Common or Coincidental?

Paradoxical cerebral emboli from cardiac and pulmonary sources are well described in the peer-reviewed literature. We outline a case with a hepatic etiology and describe diagnostic and management options. Though this paper represents the first documentation of such, we believe that transpulmonary shunting with concurrent paradoxical cerebral microemboli is more prevalent than recognized. We introduce this case report to compel practitioners to consider paradoxical emboli in selected cirrhotic patients since it can often be difficult to elicit subtle neurologic changes on clinical examination of patients with end stage liver disease

Stroke severity mediates the effect of socioeconomic disadvantage on poor outcomes among patients with intracerebral hemorrhage

BackgroundSocioeconomic deprivation drives poor functional outcomes after intracerebral hemorrhage (ICH). Stroke severity and background cerebral small vessel disease (CSVD) burden have each been linked to socioeconomic status and independently contribute to worse outcomes after ICH, providing distinct, plausible pathways for the effects of deprivation. We investigate whether admission stroke severity or cerebral small vessel disease (CSVD) mediates the effect of socioeconomic deprivation on 90-day functional outcomes.MethodsElectronic medical record data, including demographics, treatments, comorbidities, and physiological data, were analyzed. CSVD burden was graded from 0 to 4, with severe CSVD categorized as ≥3. High deprivation was assessed for patients in the top 30% of state-level area deprivation index scores. Severe disability or death was defined as a 90-day modified Rankin Scale score of 4–6. Stroke severity (NIH stroke scale (NIHSS)) was classified as: none (0), minor (1–4), moderate (5–15), moderate–severe (16–20), and severe (21+). Univariate and multivariate associations with severe disability or death were determined, with mediation evaluated through structural equation modelling.ResultsA total of 677 patients were included (46.8% female; 43.9% White, 27.0% Black, 20.7% Hispanic, 6.1% Asian, 2.4% Other). In univariable modelling, high deprivation (odds ratio: 1.54; 95% confidence interval: [1.06–2.23]; p = 0.024), severe CSVD (2.14 [1.42–3.21]; p < 0.001), moderate (8.03 [2.76–17.15]; p < 0.001), moderate–severe (32.79 [11.52–93.29]; p < 0.001), and severe stroke (104.19 [37.66–288.12]; p < 0.001) were associated with severe disability or death. In multivariable modelling, severe CSVD (3.42 [1.75–6.69]; p < 0.001) and moderate (5.84 [2.27–15.01], p < 0.001), moderate–severe (27.59 [7.34–103.69], p < 0.001), and severe stroke (36.41 [9.90–133.85]; p < 0.001) independently increased odds of severe disability or death; high deprivation did not. Stroke severity mediated 94.1% of deprivation’s effect on severe disability or death (p = 0.005), while CSVD accounted for 4.9% (p = 0.524).ConclusionCSVD contributed to poor functional outcome independent of socioeconomic deprivation, while stroke severity mediated the effects of deprivation. Improving awareness and trust among disadvantaged communities may reduce admission stroke severity and improve outcomes

Fibrinogen Chains Intrinsic to the Brain

We observed fine fibrin deposition along the paravascular spaces in naive animals, which increased dramatically following subarachnoid hemorrhage (SAH). Following SAH, fibrin deposits in the areas remote from the hemorrhage. Traditionally it is thought that fibrinogen enters subarachnoid space through damaged blood brain barrier. However, deposition of fibrin remotely from hemorrhage suggests that fibrinogen chains Aα, Bβ, and γ can originate in the brain. Here we demonstrate in vivo and in vitro that astroglia and neurons are capable of expression of fibrinogen chains. SAH in mice was induced by the filament perforation of the circle of Willis. Four days after SAH animals were anesthetized, transcardially perfused and fixed. Whole brain was processed for immunofluorescent (IF) analysis of fibrin deposition on the brain surface or in brains slices processed for fibrinogen chains Aα, Bβ, γ immunohistochemical detection. Normal human astrocytes were grown media to confluency and stimulated with NOC-18 (100 μM), TNF-α (100 nM), ATP-γ-S (100 μM) for 24 h. Culture was fixed and washed/permeabilized with 0.1% Triton and processed for IF. Four days following SAH fibrinogen chains Aα IF associated with glia limitans and superficial brain layers increased 3.2 and 2.5 times (p < 0.05 and p < 0.01) on the ventral and dorsal brain surfaces respectively; fibrinogen chains Bβ increased by 3 times (p < 0.01) on the dorsal surface and fibrinogen chain γ increased by 3 times (p < 0.01) on the ventral surface compared to sham animals. Human cultured astrocytes and neurons constitutively expressed all three fibrinogen chains. Their expression changed differentially when exposed for 24 h to biologically significant stimuli: TNFα, NO or ATP. Western blot and RT-qPCR confirmed presence of the products of the appropriate molecular weight and respective mRNA. We demonstrate for the first time that mouse and human astrocytes and neurons express fibrinogen chains suggesting potential presence of endogenous to the brain fibrinogen chains differentially changing to biologically significant stimuli. SAH is followed by increased expression of fibrinogen chains associated with glia limitans remote from the hemorrhage. We conclude that brain astrocytes and neurons are capable of production of fibrinogen chains, which may be involved in various normal and pathological processes

Development and Initial Testing of the Stroke Rapid-Treatment Readiness Tool

ABSTRACTNo instruments are currently available to help health systems identify target areas for reducing door-to-needle times for the administration of intravenous tissue plasminogen activator to eligible patients with ischemic stroke. A 67-item Likert-scale survey was administered by telephone to stroke personnel at 252 U.S. hospitals participating in the “Get With The Guidelines-Stroke” quality improvement program. Factor analysis was used to refine the instrument to a four-factor 29-item instrument that can be used by hospitals to assess their readiness to administer intravenous tissue plasminogen activator within 60 minutes of patient hospital arrival

Regulation of Cerebral Blood Flow

The control of cerebral blood flow is complex, and only beginning to be elucidated. Studies have identified three key regulatory paradigms. The first is cerebral pressure autoregulation, which maintains a constant flow in the face of changing cerebral perfusion pressure. Flow-metabolism coupling refers to the brains ability to vary blood flow to match metabolic activity. An extensive arborization of perivascular nerves also serves to modulate cerebral blood flow, so-called neurogenic regulation. Central to these three paradigms are two cell types: endothelium and astrocytes. The endothelium produces several vasoactive factors that are germane to the regulation of cerebral blood flow: nitric oxide, endothelium-dependent hyperpolarization factor, the eicosanoids, and the endothelins. Astrocytic foot processes directly abut the blood vessels, and play a key role in regulation of cerebral blood flow. Lastly, new research has been investigating cell-cell communication at the microvascular level. Several lines of evidence point to the ability of the larger proximal vessels to coordinate vasomotor responses downstream

Regulation of Cerebral Blood Flow

The control of cerebral blood flow is complex, and only beginning to be elucidated. Studies have identified three key regulatory paradigms. The first is cerebral pressure autoregulation, which maintains a constant flow in the face of changing cerebral perfusion pressure. Flow-metabolism coupling refers to the brains ability to vary blood flow to match metabolic activity. An extensive arborization of perivascular nerves also serves to modulate cerebral blood flow, so-called neurogenic regulation. Central to these three paradigms are two cell types: endothelium and astrocytes. The endothelium produces several vasoactive factors that are germane to the regulation of cerebral blood flow: nitric oxide, endothelium-dependent hyperpolarization factor, the eicosanoids, and the endothelins. Astrocytic foot processes directly abut the blood vessels, and play a key role in regulation of cerebral blood flow. Lastly, new research has been investigating cell-cell communication at the microvascular level. Several lines of evidence point to the ability of the larger proximal vessels to coordinate vasomotor responses downstream

Integrity of Cerebellar Fastigial Nucleus Intrinsic Neurons Is Critical for the Global Ischemic Preconditioning

Excitation of intrinsic neurons of cerebellar fastigial nucleus (FN) renders brain tolerant to local and global ischemia. This effect reaches a maximum 72 h after the stimulation and lasts over 10 days. Comparable neuroprotection is observed following sublethal global brain ischemia, a phenomenon known as preconditioning. We hypothesized that FN may participate in the mechanisms of ischemic preconditioning as a part of the intrinsic neuroprotective mechanism. To explore potential significance of FN neurons in brain ischemic tolerance we lesioned intrinsic FN neurons with excitotoxin ibotenic acid five days before exposure to 20 min four-vessel occlusion (4-VO) global ischemia while analyzing neuronal damage in Cornu Ammoni area 1 (CA1) hippocampal area one week later. In FN-lesioned animals, loss of CA1 cells was higher by 22% compared to control (phosphate buffered saline (PBS)-injected) animals. Moreover, lesion of FN neurons increased morbidity following global ischemia by 50%. Ablation of FN neurons also reversed salvaging effects of five-minute ischemic preconditioning on CA1 neurons and morbidity, while ablation of cerebellar dentate nucleus neurons did not change effect of ischemic preconditioning. We conclude that FN is an important part of intrinsic neuroprotective system, which participates in ischemic preconditioning and may participate in naturally occurring neuroprotection, such as “diving response”