Late-onset Rasmussen's encephalitis and long-term remission

2011 ◽  
Vol 13 (1) ◽  
pp. 88-91 ◽  
Author(s):  
Laura Kupila ◽  
Leena Jutila ◽  
Arto Immonen ◽  
Ritva Vanninen ◽  
Esa Mervaala ◽  
...  
Keyword(s):  
Late Onset ◽  
Rasmussen’S Encephalitis

Removal of a compressive mass causes a transient disruption of blood-brain barrier but a long-term recovery of spiny stellate neurons in the rat somatosensory cortex

2021 ◽  
pp. 1-17
Author(s):  
Tzu-Yin Yeh ◽  
Pei-Hsin Liu
Keyword(s):  
Somatosensory Cortex ◽  
Blood Brain Barrier ◽  
Dendritic Spines ◽  
Late Onset ◽  
Brain Barrier ◽  
Blood Brain ◽  
Afferent Fibers ◽  
Prolonged Recovery ◽  
Rat Somatosensory Cortex

Background: In the cranial cavity, a space-occupying mass such as epidural hematoma usually leads to compression of brain. Removal of a large compressive mass under the cranial vault is critical to the patients. Objective: The purpose of this study was to examine whether and to what extent epidural decompression of the rat primary somatosensory cortex affects the underlying microvessels, spiny stellate neurons and their afferent fibers. Methods: Rats received epidural decompression with preceding 1-week compression by implantation of a bead. The thickness of cortex was measured using brain coronal sections. The permeability of blood-brain barrier (BBB) was assessed by Evans Blue and immunoglobulin G extravasation. The dendrites and dendritic spines of the spiny stellate neurons were revealed by Golgi— Cox staining and analyzed. In addition, the thalamocortical afferent (TCA) fibers in the cortex were illustrated using anterograde tracing and examined. Results: The cortex gradually regained its thickness over time and became comparable to the sham group at 3 days after decompression. Although the diameter of cortical microvessels were unaltered, a transient disruption of the BBB was observed at 6 hours and 1 day after decompression. Nevertheless, no brain edema was detected. In contrast, the dendrites and dendritic spines of the spiny stellate neurons and the TCA fibers were markedly restored from 2 weeks to 3 months after decompression. Conclusions: Epidural decompression caused a breakdown of the BBB, which was early-occurring and short-lasting. In contrast, epidural decompression facilitated a late-onset and prolonged recovery of the spiny stellate neurons and their afferent fibers.

scholarly journals 1110. Very Late Onset Infections Amongst Long Term Survivors of Kidney Transplantation

2020 ◽  
Vol 7 (Supplement_1) ◽  
pp. S585-S585
Author(s):  
Harry Cheung ◽  
Marwan M Azar ◽  
Geliang Gan ◽  
Yanhong Deng ◽  
Elizabeth A Cohen ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Clinical Data ◽  
Opportunistic Infections ◽  
Late Onset ◽  
Retrospective Chart Review ◽  
Kidney Transplant Recipients ◽  
Increased Risk ◽  
Simple Logistic ◽  
Long Term Survivors

Abstract Background Kidney transplant recipients (KTR) are at increased risk for infections immediately post-transplant due to intense immunosuppression. However, this risk decreases over time as immunosuppression is tapered. The incidence of infection in KTR many years after transplant is not well characterized. The aim of this study was to describe these “very-late onset infections” (VLIs) ≥ 10 years after KT. Methods We performed a retrospective chart review of patients age ≥ 18 years who underwent KT between 2003 and 2009 and who survived ≥ 10 years post-KT. VLIs included opportunistic infections (OIs) and non-OIs. Demographics, comorbidities, immunosuppression, and clinical data for VLIs ≥ 10 years from KT were collected. Simple logistic regression was performed to determine characteristics associated with risk for VLIs. Results Of 332 KTR that met the inclusion criteria, the majority were male (62.0%), white (59.6%), and the largest proportion was transplanted between the ages of 50-59 (28.3%); 220 (67.9%) were on mycophenolate-based regimens. The mean Charlson Comorbidity Index (CCI) was 4.7 (S.D. 2.0). Of 332, 103 (31.0%) KTR experienced ≥ 1 VLI amounting to 187 episodes. Compared to those without VLI, KTR with VLI were more likely to have diabetes (p=0.005), cardiovascular disease (p=0.004), low ALC (p < 0.001) and require dialysis (p=0.002). Of 103 KTR with VLI, 16 (15.5%) had OIs, while 87 KTR (84.5%) had non-OIs, most commonly urinary tract infection (n=85, 45.5%), pneumonia (n=35, 18.7%) and gastrointestinal infection (n=18, 9.6%). The most commonly isolated pathogens were E. coli (n=30, 16%), K. pneumoniae (n=16, 8.6%), MSSA (n=7, 3.7%), and P. aeruginosa (n=7, 3.7%). Higher CCI, diabetes, dialysis, cerebrovascular, cardiovascular disease and lower ALC were associated with increased risk for VLI (p < 0.05), while living donor KTR was protective (p=0.04). Additionally, every 1 year after transplant was associated with an increased risk of VLI (OR=1.31, p < 0.001). Table 1: Demographics, comorbidities, immunosuppression, and clinical data for all patients Conclusion VLIs were common in long-term survivors of KT and included both conventional and opportunistic pathogens. Every additional year from transplant incurred additional risk for VLI, particularly for those with multiple co-morbidities and lower ALC. Disclosures All Authors: No reported disclosures

Long-term efficacy of alglucosidase alfa in late-onset Pompe disease

2017 ◽  
Vol 120 (1-2) ◽  
pp. S134
Author(s):  
Ans van der Ploeg ◽  
Paula Clemens ◽  
Robert J Hopkin ◽  
Katherine Kacena ◽  
Bernd-Jan Sanson ◽  
...  
Keyword(s):  
Pompe Disease ◽  
Late Onset ◽  
Term Efficacy ◽  
Alglucosidase Alfa

scholarly journals Identifying Activity Support Needs for individuals Aging With Disability: Subject Matter Expert Interviews

2020 ◽  
Vol 4 (Supplement_1) ◽  
pp. 600-600
Author(s):  
Lyndsie Koon ◽  
Megan Bayles ◽  
Elena Remillard ◽  
Wendy Rogers
Keyword(s):  
Subject Matter ◽  
Vision Loss ◽  
Cultural Practices ◽  
Late Onset ◽  
Mobility Impairment ◽  
Privacy Concerns ◽  
Target Populations ◽  
Need Support ◽  
Multi Method Approach

Abstract Technology designed to support aging-in-place for people with long-term disabilities begins with understanding the specific tasks that need support, and individual abilities, preferences, cultural practices, and privacy concerns. Such understanding is best achieved through a multi-method approach that includes direct, detailed assessments of representative users as well as individuals who work with or care for them. Our target users are people who identify as having a sensory or mobility impairment prior to the age of 50, including individuals aging with multiple sclerosis, late-onset hearing loss, and late-onset vision loss. In the present study, we are interviewing Subject Matter Experts (SMEs) to identify the scope of the challenges that should be explored in more depth. The SMEs include caregivers and medical professionals to identify challenges that the target populations experience in their everyday activities, advice about research adaptations, and recruitment ideas.

Treatment of tardive dyskinesia

1978 ◽  
Vol 16 (14) ◽  
pp. 55-56
Keyword(s):  
Tardive Dyskinesia ◽  
Late Onset ◽  
Psychiatric Patients ◽  
Term Treatment ◽  
Neuroleptic Drugs ◽  
Abnormal Movements ◽  
Long Term Treatment ◽  
The Face ◽  
Schizophrenic Patients

Neuroleptic drugs cause many forms of extra-pyramidal syndromes. One of these, tardive dyskinesia,1 occurs only after the patient has been taking the drug for some time (‘tardive’ refers to the late onset). The movements are involuntary and repetitive usually involving the face and tongue, but they may also affect the limbs and trunk. Tongue protrusion, licking and smacking of the lips, sucking and chewing movements, grimacing, grunting, blinking and furrowing of the forehead have all been described and attributed to long-continued medication with neuroleptic drugs of the phenothiazine, butyrophenone and thioxanthene groups. The patient can inhibit the movements, but anxiety makes them worse. Many of these symptoms were noticed in schizophrenic patients before neuroleptic drugs were introduced2 and they can occur in otherwise normal untreated elderly people. Nevertheless it is generally accepted that in most cases tardive dyskinesia is an unwanted effect of neuroleptic medication. Despite suggestions to the contrary, the abnormal movements are not necessarily associated with high dosage of neuroleptic drugs or with pre-existing brain damage.3 4 Tardive dyskinesia has been reported in 3–6% of a mixed population of psychiatric patients5 and over half of a group of chronic schizophrenics on long-term treatment.4 The more careful the neurological examination, the greater the apparent incidence.

scholarly journals Increased Cerebrospinal Fluid Production as a Possible Mechanism Underlying Caffeine's Protective Effect against Alzheimer's Disease

2011 ◽  
Vol 2011 ◽  
pp. 1-6 ◽  
Author(s):  
Peter Wostyn ◽  
Debby Van Dam ◽  
Kurt Audenaert ◽  
Peter Paul De Deyn
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cerebrospinal Fluid ◽  
Late Onset ◽  
Senile Plaques ◽  
Protective Effects ◽  
Caffeine Consumption ◽  
Neuroprotective Effects ◽  
Csf Production

Alzheimer's disease (AD), the most common type of dementia among older people, is characterized by the accumulation of β-amyloid (Aβ) senile plaques and neurofibrillary tangles composed of hyperphosphorylated tau in the brain. Despite major advances in understanding the molecular etiology of the disease, progress in the clinical treatment of AD patients has been extremely limited. Therefore, new and more effective therapeutic approaches are needed. Accumulating evidence from human and animal studies suggests that the long-term consumption of caffeine, the most commonly used psychoactive drug in the world, may be protective against AD. The mechanisms underlying the suggested beneficial effect of caffeine against AD remain to be elucidated. In recent studies, several potential neuroprotective effects of caffeine have been proposed. Interestingly, a recent study in rats showed that the long-term consumption of caffeine increased cerebrospinal fluid (CSF) production, associated with the increased expression of Na+-K+ATPase and increased cerebral blood flow. Compromised function of the choroid plexus and defective CSF production and turnover, with diminished clearance of Aβ, may be one mechanism implicated in the pathogenesis of late-onset AD. If reduced CSF turnover is a risk factor for AD, then therapeutic strategies to improve CSF flow are reasonable. In this paper, we hypothesize that long-term caffeine consumption could exert protective effects against AD at least in part by facilitating CSF production, turnover, and clearance. Further, we propose a preclinical experimental design allowing evaluation of this hypothesis.

scholarly journals Angiotensin-converting enzyme inhibition in the prevention and treatment of chronic renal damage in the hypertensive fawn-hooded rat.

1997 ◽  
Vol 8 (2) ◽  
pp. 249-259 ◽  
Author(s):  
G H Verseput ◽  
A P Provoost ◽  
B B Braam ◽  
J J Weening ◽  
H A Koomans
Keyword(s):  
Capillary Pressure ◽  
Enzyme Inhibition ◽  
Early Onset ◽  
Renal Damage ◽  
Late Onset ◽  
Converting Enzyme ◽  
Glomerular Hypertension ◽  
Converting Enzyme Inhibition

The spontaneously hypertensive fawn-hooded rat (FHH) develops accelerated albuminuria and focal glomerular sclerosis (FGS), leading to ESRD and shortening of lifespan. The FHH is characterized by moderate systemic hypertension, a relatively low afferent to efferent arteriolar resistance ratio, and glomerular hypertension. The FHH study presented here was designed to examine the efficacy of early-onset, late-onset, or early-temporary angiotensin I-converting enzyme inhibition (ACE-i) in ameliorating long-term hypertension and FGS, and improving survival, as well as to relate its protective efficacy to preexistent FGS and to reduction of glomerular pressure (PGC) Untreated rats developed hypertension and high PGC, and all (N = 22) except one died of ESRD within the 72-wk follow-up period. Early-onset (at 7 wk of age) ACE-i prevented development of systemic and glomerular hypertension, and it largely prevented proteinuria and FGS; all rats survived throughout the follow-up period. Rats treated with late-onset (22 wk) ACE-i were hypertensive and proteinuric at the start of ACE-i, and they showed beginning FGS. ACE-i corrected the hypertension, albuminuria, and PGC but could not fully prevent some hypertension, albuminuria, and FGS at the later stage. Early-temporary (7 to 22 wk) ACE-i adequately controlled blood pressure and development of FGS during therapy, but after withdrawal of ACE-i, systemic and glomerular hypertension developed as in untreated animals. This regimen postponed but did not control FGS development and early mortality. The results of this study indicate that: (1) early-onset ACE-i very effectively protects against development of renal damage in the FHH; (2) this protection is associated with normalization of the elevated glomerular capillary pressure; (3) ACE-i cannot completely prevent further development of previously established FGS, despite lowering glomerular capillary pressure; (4) early-temporary ACE-i has no long-term controlling effect on arterial and glomerular pressure, and it cannot control development of FGS.

scholarly journals Management Of Post Stroke Seizures

2017 ◽  
pp. 52
Author(s):  
Kavian Ghandehari
Keyword(s):  
Status Epilepticus ◽  
Elderly Patients ◽  
Bone Health ◽  
Late Onset ◽  
Stroke Patients ◽  
Anterior Circulation ◽  
Post Stroke ◽  
Antiepileptic Drug Treatment ◽  
New Generation

The incidence of seizures in relation to stroke is 8.9%, with a frequency of 10.6 and 8.6% in haemorrhagic and ischaemic stroke, respectively. In subarachnoid haemorrhage the incidence is 8.5%. Due to the fact that infarcts are significantly more frequent than haemorrhages, seizures are mainly related to occlusive vascular disease of the brain. The general view is to consider stroke-related seizures as harmless complications in the course of a prolonged vascular disease involving the heart and brain. Seizures can be classified as those of early and those of late onset in a paradigm comparable to post-traumatic epilepsy, with an arbitrary dividing point of two weeks after the event. Most early-onset seizures occur during the first day after the stroke. Late-onset seizures occur three times more often than early-onset ones. A first late-onset epileptic event is most likely to take place between six months and two years after the stroke. However, up to 28% of patients develop their first seizure several years later. Simple partial seizures, with or without secondary generalisation, account for about 50% of total seizures, while complex partial spells, with or without secondary generalisation, and primary generalised tonic–clonic insults account for approximately 25% each. Status epilepticus occurs in 12% of stroke patients, but the recurrence rate after an initial status epilepticus is not higher than after a single seizure. Inhibitory seizures, mimicking transient ischaemic attacks, are observed in 7.1% of cases. The only clinical predictor of late-onset seizures is the initial presentation of partial anterior circulation syndrome due to a territorial infarct. Patients with total anterior circulation syndrome have less chance of developing epileptic spells, not only due to their shorter life expectancy but also due to the fact that the large infarcts are sharply demarcated in these patients. The optimal timing and type of antiepileptic drug treatment for patients with post-stroke seizures is still a controversial issue. Prospective studies in the literature showed that immediate treatment after a first unprovoked seizure does not improve the long-term remission rate. However, because of the physical and psychological influences of recurrent seizures, prophylactic treatment should be considered after a first unprovoked event in an elderly person at high risk of recurrence, taking into consideration the individuality of the patient and a discussion with the patient and his/her family about the risks and benefits of both options latest studies regarding post-stroke seizure treatment showed that 'new-generation' drugs, such as lamotrigine, gabapentin and levetiracetam, in low doses would be reasonable. Although several studies suggest that seizures alter the functional recovery after a stroke, it remains difficult to determine whether or not the occurrence of a second seizure in an untreated stroke patient might hamper the overall outcome. However, repeated seizures and status epilepticus worsen the neurological and mental condition of stroke patienton The decision to initiate antiepileptic drug treatment after a first or a second post-stroke seizure should therefore be individualized, primarily based on the functional impact of the first seizure episode and the patient's preference. Several converging findings suggest that the majority of first-generation antiepileptic drugs, particularly phenytoin, are not the most appropriate choice in stroke patients because of their potential harmful impact on functional recovery and bone health, their suboptimal pharmacokinetic profile and interaction with anticoagulants or salicylates, their greater likelihood to be poorly tolerated, and the lack of level A evidence regarding their specific use in elderly patients. Among the new-generation drugs that do not interact with anticoagulants, antiplatelet agents, or bone health, lamotrigine and gabapentine are the only two drugs that proved to be more effective than immediate-release carbamazepine in elderly patients, providing level A evidence for their use in this indication. In addition, gabapentin remains the only drug that has been specifically evaluated in stroke patients, demonstrating a high rate of long-term seizure freedom. At present, low-dose lamotrigine or gabapentin appears to represent the optimal first-line therapy for post-stroke seizure and epilepsy in elderly patients or in younger patients requiring anticoagulants. However, low-dose extended-release carbamazepine might be a reasonable and less expensive option in patients with appropriate bone health who do not requiring anticoagulat. Based on the stroke management guidelines antiepileptic drugs should not be administered as preventive management in any type of stroke patients without seizure.  

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