Neurocysticercosis (NCC) is a specific form of cysticercosis that affects the central nervous system. It is caused by the tapeworm Taenia solium, which is often found in pigs. NCC is considered one of the “great simulator/mimickers” of other diseases. In this context, movement disorders (MDs) can occur in a small percentage of individuals with NCC. This review aims to evaluate the clinicoepidemiological profile, pathological mechanisms, and historical features of NCC-associated MD. Relevant reports in six databases were identified and assessed by two reviewers without language restriction. A total of 71 reports containing 148 individuals who developed an MD related to NCC were identified. NCC-associated MD included parkinsonism (n = 47), ataxia (n = 32), chorea (n = 18), dystonia (n = 13), tremor (n = 8), myokymia (n = 6), myoclonus (n = 4), ballism (n = 1), tics (n = 1), and others (n = 18). The mean and median ages were 36.58 (standard deviation: 20.51) and 35 years (age range: 1–88 years), respectively. There was a slight predominance of female sex (52.17%). On follow-up, 58.90% of the individuals had a full recovery; two deaths were reported. We believe that the majority of cases reported were only diagnosed because patients had classical clinical manifestations generally investigated by neuroimaging, resulting in incidental findings suggestive of NCC, which were later supported by laboratory examinations. Therefore, the association between NCC and MD is probably underreported. Clinicians should be wary of this association, mainly in endemic areas for cysticercosis.

Stroke remains a leading cause of adult death and disability. Poststroke rehabilitation is vital for reducing the long-term sequelae of brain ischemia. Recently, physical exercise training has been well established as an effective rehabilitation tool, but its efficacy depends on exercise parameters and the patient's capacities, which are often altered following a major cerebrovascular event. Thus, ischemic conditioning as a rehabilitation intervention was considered an “exercise equivalent,” but the investigation is still in its relative infancy. In this mini-review, we discuss the potential for physical exercise or ischemic conditioning and its relation to angiogenesis, neurogenesis, and plasticity in stroke rehabilitation. This allows the readers to understand the context of the research and the application of ischemic conditioning in poststroke rehabilitation.

Ischemia–reperfusion injury (IRI) is a series of multifactorial cellular events that lead to increased cellular dysfunction after the restoration of oxygen delivery to hypoxic tissue, which can result in acute heart failure and cerebral dysfunction. This injury is severe and would lead to significant morbidity and mortality and poses an important therapeutic challenge for physicians. Nitric oxide (NO) minimizes the deleterious effects of IRI on cells. NO donors, such as organic nitrates and sodium nitroprusside, are used systematically to treat heart failure, angina, and pulmonary hypertension. Inhaled NO gas was approved by the FDA in 1999 to treat hypoxic newborns, and its beneficial ameliorations reach outside the realm of lung disease. This review will summarize the clinical application of NO in IRI.

Chronic subdural hematoma (CSDH) is one of the most prevalent neurosurgical disorders. Patients with CSDH commonly present with altered mental status, focal neurological deficit, and/or headache. The first-line treatment for CSDH is surgical evacuation. Although the surgical procedures for CSDH have been considered relatively “straightforward,” they are not without any risk. The elderly are especially prone to show poor surgical outcomes. To make matters worse, many elderly patients are on anticoagulants and antiplatelet agents, increasing the risk of re-bleeding before and after surgery. These complications have led clinicians to search for nonsurgical alternatives. Dexamethasone should be used with caution for selected patients given its side effects. Tranexamic acid may be utilized as an adjunct therapy to surgery, but more randomized clinical trials are needed to evaluate its definitive efficacy. Interesting results of middle meningeal artery embolization (MMAE) have been reported from case studies. However, the risks associated with MMAE, including intracerebral hemorrhage, stroke, and vasospasm, have not been properly studied yet. The clinical benefits of atorvastatin and angiotensin-converting enzyme inhibitors are uncertain for CSDH. In conclusion, surgical intervention continues to be the first-line treatment while nonsurgical treatment options may be considered an adjunct therapy especially for recurrent hematoma or to reduce the volume of a hematoma.

OBJECTIVE: Acute ischemic stroke triggers complex neurovascular, neuroinflammatory, and synaptic alterations. This study explores whether blocking pro-inflammatory platelet-activating factor receptor (PAF-R) plus selected docosanoids after middle cerebral artery occlusion (MCAo) would lead to neurological recovery. The following small molecules were investigated: (a) LAU-0901, a PAF-R antagonist that blocks pro-inflammatory signaling; and (b) derivatives of docosahexaenoic acid (DHA), neuroprotectin D1 (NPD1), and aspirin-triggered NPD1 (AT-NPD1), which activates cell survival pathways and are exert potent anti-inflammatory activity in the brain. MATERIALS AND METHODS: Sprague-Dawley rats received 2 h MCAo and LAU-0901 (30 or 60 mg/kg, 2 h after stroke), NPD1, and AT-NPD1 (333 μg/kg), DHA (5 mg/kg), and their combination were administered intravenous at 3 h after stroke. Behavior testing and ex vivo magnetic resonance imaging were conducted on day 3 or 14 to assess lesion characteristics and lipidomic analysis on day 1. Series 1 (LAU-0901 + NPD1, 14d), Series 2 (LAU-0901 + AT-NPD1, 3d), and Series 3 (LAU-0901 + DHA, 1d). RESULTS: All combinatory groups improved behavior compared to NPD1, AT-NPD1, or DHA treatments alone. Total lesion volumes were reduced with LAU-0901 + NPD1 by 62% and LAU-0901 + AT-NPD1 by 90% treatments versus vehicle groups. LAU-0901 and LAU-0901 + DHA increased the production of vasoactive lipid mediators (prostaglandins: PGE₂, PGF_2-α, 6-keto-PGF_1-α, and PGD₂) as well an inflammatory regulating mediator hydroxyoctadecadienoic acid. In contrast, LAU-0901 and LAU-0901 + DHA decreased the production of 12-hydroxyeicosatetraenoic acid, a pro-inflammatory mediator. CONCLUSION: Combination therapy with LAU-0901 and selected docosanoids is more effective than the single therapy, affording synergistic neuroprotection, with restored pro-homeostatic lipid mediators and improved neurological recovery. Altogether, our findings support the combinatory therapy as the basis for future therapeutics for ischemic stroke.

Posterior reversible encephalopathy syndrome (PRES) is a neurological syndrome associated with headache, altered mental status, seizures, and visual disturbances and characterized by white matter vasogenic edema affecting predominantly the posterior occipital and parietal lobes of the brain. Neurological complications of blood transfusion are uncommon, and blood-transfusion-related PRES is seldom reported. We report here one such case of PRES. A 61-year-old Asian woman with chronic anemia presented with a history of fall, causing fracture of the left femur neck. As her hemoglobin was 5 g per deciliter, she was transfused with four units of packed cells in three consecutive days. At the time of admission, she was alert, normotensive, and afebrile. Later, she developed mild headache and had a generalized tonic-clonic seizure. Her brain magnetic resonance (MR) imaging showed edema in bilateral frontal lobes and parieto-occipital lobes with normal MR venogram, consistent with PRES. We described her disorder as blood-transfusion-related PRES. Immunologic, as well as non-immunologic complications of blood transfusion, are known but, PRES is rare. Cumulative effects of blood transfusion on blood flow, blood viscosity, endothelial dysfunction leads to blood-brain barrier dysfunction, which culminates into vasogenic edema and vasoconstriction despite normal systemic blood pressure, leading to blood-transfusion-related PRES.

Intraprocedural rupture (IPR) of an intracranial aneurysm is the most feared complication of primary and stent-assisted coiling because it carries a high risk of morbidity and mortality. The endovascular strategy applied to control IPR depends on the cause of the rupture and stage of the procedure. Rupture during primary or stent-assisted coiling is traditionally managed with the use of continued packing, balloon microcatheter placement, or in rare cases, with parent artery sacrifice. In this technical note, we describe the use of temporary coiling of the parent artery to control IPR in three cases. Temporary parent artery coiling creates a subocclusive state, resulting in aneurysmal blood flow reduction without interruption of blood flow to the distal territory. Flow reduction combined with the thrombogenicity of the previously deployed coils results in hemostasis. In the cases presented here, IPR occurred during the late stage of coiling. In each case, parent artery coiling was performed along with heparin reversal. After confirmation of hemostasis, the coils were retrieved to restore normal blood flow. We demonstrate that the technique of temporary parent artery coiling may be a safe and effective option for the management of IPR during primary or stent-assisted coiling.