scholarly journals Clinical and pathogenetic aspects of acute pancreatic encephalopathy

2021 ◽  
Vol 40 (4) ◽  
pp. 69-78
Author(s):  
Alla A. Strutsenko ◽  
Igor V. Damulin
Keyword(s):  
Acute Pancreatitis ◽  
Vascular Wall ◽  
Acute Onset ◽  
Neurological Symptoms ◽  
Psychomotor Agitation ◽  
Residual Symptoms ◽  
Hormonal Dysfunction ◽  
Pancreatic Encephalopathy ◽  
Fluctuating Course ◽  
The Brain

Pancreatic encephalopathy is a formidable complication of acute pancreatitis, significantly aggravating the course and increasing the mortality rate in this disease. For pancreatic encephalopathy, an acute onset and fluctuating course with subsequent cyclic progression are typical, and the severity of neurological symptoms may be directly dependent on the activity of the pancreatic process. The risk of having residual symptoms, primarily in the form of cognitive impairment, increases with repeated episodes of acute pancreatic encephalopathy. In the pathogenesis of pancreatic encephalopathy, an important role is played by a combination of enzymatic and hormonal dysfunction of the pancreas, systemic microcirculation disorders due to hypovolemia, typical for acute pancreatitis, and changes in glucose metabolism associated with the effects of secondary hepatocellular insufficiency and pancreonecrosis. Microscopically, gross changes in the vascular link are revealed in the form of plasmorrhages and diapedesic hemorrhages in the Virchow-Robin spaces and the white matter of the brain, desquamation and dystrophy of endothelial cells, swelling of the adventitia membrane, sludge of blood corpuscles, plasma impregnation and segmental necrosis of the vascular wall with predominant involvement and small caliber. The presence of pancreatic encephalopathy should be suspected if neurological symptoms are detected in patients with symptoms of acute pancreatitis, such as psychomotor agitation, visual and auditory hallucinations, delirium, followed by episodes of deafness, adynamia, drowsiness, up to a state of catatonia and coma. In most cases, psychomotor agitation is combined with manifestations of the syndrome of irritation of the meninges. Focal neurological symptoms, myoclonia, hyperkinesis may be associated with mental and general cerebral symptoms. Mortality in acute pancreatic encephalopathy is due to shock, hemorrhagic complications, ketoacidosis, fatty embolism of cerebral vessels or renal failure (bibliography: 35 refs)

scholarly journals Pancreatic encephalopathy: clinical, pathogenetic and diagnostic aspects

2017 ◽  
Vol 38 (4) ◽  
pp. 33-39
Author(s):  
I. V. Damulin ◽  
А. А. Strutsenko ◽  
P. P. Ogurtsov ◽  
N. V. Mazurchik
Keyword(s):  
Acute Pancreatitis ◽  
Latent Period ◽  
Carbohydrate Metabolism ◽  
Infectious Complications ◽  
Neurological Symptoms ◽  
Electrolyte Balance ◽  
Direct Proportion ◽  
Pancreatic Diseases ◽  
Diagnostic Aspects ◽  
Pancreatic Encephalopathy

Pancreatic encephalopathy occurs in 9–35% of patients with pancreatic diseases and is characterized by a variety of focal neurological symptoms. Neuropsychiatric disorders are observed both during the acute and latent period of the pancreatic diseases. The presence of pancreatic encephalopathy should be suspected if patients with symptoms of acute pancreatitis have neurological symptoms. The course of acute pancreatic encephalopathy is cyclical, fluctuating, being in direct proportion to the pancreatic process. Leading mechanism in the development of pancreatic encephalopathy is a combination of hyperenzymemia with insulin imbalance which leads to changes of water-electrolyte balance and carbohydrate metabolism. Infectious complications, that often accompany acute pancreatitis, lead to the increasing intoxication syndrome.

scholarly journals Acute pancreatitis complicated by encephalopathy

2020 ◽  
Vol 8 (6) ◽  
pp. 2319
Author(s):  
Rajat Jhamb ◽  
Anant Parasher ◽  
Ashish Baweja
Keyword(s):  
Acute Pancreatitis ◽  
Supportive Care ◽  
Male Patient ◽  
Neurological Deficit ◽  
Rare Complication ◽  
Neurological Symptoms ◽  
Metabolic Parameters ◽  
Focal Neurological Deficit ◽  
Altered Sensorium ◽  
Pancreatic Encephalopathy

Pancreatic encephalopathy is a frequently under-diagnosed and rare complication of acute pancreatitis. It denotes the occurrence of neuropsychiatric abnormalities in the setting of acute pancreatic inflammation, and presents with neurological symptoms that may persist even after the resolution of all metabolic parameters. Here we present the case of a 42 year old male patient presenting with altered sensorium and focal neurological deficit during the course of acute pancreatitis. The patient was treated conservatively, and later improved with supportive care.

scholarly journals Subarachnoid diverticulum associated with feline infectious peritonitis in a Siberian cat

2020 ◽  
Vol 6 (2) ◽  
pp. 205511692094147
Author(s):  
Christopher Hoey ◽  
George Nye ◽  
Angela Fadda ◽  
Janet Bradshaw ◽  
Emi N Barker
Keyword(s):  
Cervical Spinal Cord ◽  
Serum Biochemistry ◽  
Acute Onset ◽  
Neurological Deficits ◽  
Rt Pcr ◽  
Feline Infectious Peritonitis ◽  
Case Summary ◽  
Choroid Plexitis ◽  
The Brain ◽  
Feline Coronavirus

Case summary A 7-month-old Siberian cat was presented for investigation of acute onset multifocal neurological deficits. Neurological examination documented dull mental status and an ambulatory left hemiparesis. Serum biochemistry documented marked hyperglobulinaemia. MRI of the brain identified marked leptomeningeal contrast enhancement extending along the brainstem caudally to involve the cranial cervical spinal cord. MRI of the cervical spine further identified a subarachnoid diverticulum that extended from the level of the obex to the C2–C3 vertebrae. Cerebrospinal fluid quantitative RT-PCR was positive for the presence of feline coronavirus. Histopathology revealed pyogranulomatous meningitis and choroid plexitis, uveitis and nephritis. Relevance and novel information This article describes the first reported case of a subarachnoid diverticulum associated with feline infectious peritonitis.

scholarly journals A Rare Case of Spontaneous Arachnoid Cyst Rupture Presenting as Right Hemiplegia and Expressive Aphasia in a Pediatric Patient

Children ◽  
2021 ◽  
Vol 8 (2) ◽  
pp. 78
Author(s):  
Anne Bryden ◽  
Natalie Majors ◽  
Vinay Puri ◽  
Thomas Moriarty
Keyword(s):  
Cognitive Processing ◽  
Arachnoid Cyst ◽  
Memory Loss ◽  
Acute Onset ◽  
Word Finding ◽  
Outpatient Visits ◽  
The Family ◽  
History Of ◽  
Cyst Rupture ◽  
The Brain

This study examines an 11-year-old boy with a known history of a large previously asymptomatic arachnoid cyst (AC) presenting with acute onset of right facial droop, hemiplegia, and expressive aphasia. Shortly after arrival to the emergency department, the patient exhibited complete resolution of right-sided hemiplegia but developed headache and had persistent word-finding difficulties. Prior to symptom onset while in class at school, there was an absence of reported jerking movements, headache, photophobia, fever, or trauma. At the time of neurology consultation, the physical exam showed mildly delayed cognitive processing but was otherwise unremarkable. The patient underwent MRI scanning of the brain, which revealed left convexity subdural hematohygroma and perirolandic cortex edema resulting from ruptured left frontoparietal AC. He was evaluated by neurosurgery and managed expectantly. He recovered uneventfully and was discharged two days after presentation remaining asymptomatic on subsequent outpatient visits. The family express concerns regarding increased anxiety and mild memory loss since hospitalization.

Neurological symptoms of COVID-19

2021 ◽  
Vol 36 (4) ◽  
pp. 285-296
Author(s):  
Adriana Wawer ◽  
Agnieszka Piechal
Keyword(s):  
Nervous System ◽  
Viral Infections ◽  
Harmful Effect ◽  
Neurological Complications ◽  
Neurological Symptoms ◽  
Acute Respiratory Disease ◽  
Neurological Damage ◽  
Impaired Consciousness ◽  
Potential Impact ◽  
The Brain

Objective. Some viral infections can have a harmful effect on the functioning of the nervous system and can even cause serious neurological damage. This work aims to review the results of studies published so far concerning neurological complications in people infected with coronaviruses, especially SARS-CoV-2, and possible mechanisms responsible for nervous system damage. Literature review. Recently, there have been reports that coronaviruses, including SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2), cause acute respiratory disease, exhibit neurotropic properties and can also cause neurological symptoms. There are studies published showing that these viruses may penetrate to the brain and cerebrospinal fluid. Conclusions. Coronaviruses are still poorly understood, so it seems important to study the potential impact of SARS-CoV-2 infections on the nervous system. It seems appropriate that patients infected with SARS-CoV-2 should be early evaluated for neurological symptoms, including headache and impaired consciousness.

scholarly journals LOCKED-IN SYNDROME DUE TO MULTIPLE BRAIN STEM INFARCTIONS AND FOCI OF DEMYELINATION AFTER RADIATION THERAPY OF PITUITARY ADENOMA WITH ACROMEGALY

2018 ◽  
Vol 25 (3) ◽  
pp. 89-95
Author(s):  
L. G. Zaslavskii ◽  
E. A. Skorniakova ◽  
O. L. Zaslavskaia ◽  
S. G. Feofanova ◽  
E. A. Lomteva ◽  
...  
Keyword(s):  
Radiation Therapy ◽  
Pituitary Adenoma ◽  
Brain Stem ◽  
Vascular Wall ◽  
Pulse Therapy ◽  
Focal Lesion ◽  
Homozygous Mutation ◽  
Respiratory Disturbance ◽  
The Brain ◽  
Multiple Cerebral Infarctions

Locked-in syndrome (LIS) is a rare neurological disorder, usually appears as a result of the pons cerebellar damage, mostly after the brain stroke. Locked-in syndrome is characterized by the paralysis of skeletal muscles (respiratory, facial, pharyngeal, lingual and muscles of the extremities). Patient is unable to speak and breath, facial expressions and voluntary movements are also impossible. Acromegaly is a disease that can be described by the increase of the growth hormone (GH) and Insulin-like growth factor (IGF-1) and develops in most cases due to the pituitary adenomas. Pituitary adenoma (PA) can be treated by neurosurgical techniques, pharmaceutical and radiation therapy (RT). We present a clinical case of 33-year-old woman with PA-caused acromegaly, that developed muscle weakness, nausea, vomit and respiratory disturbance in a 2 months after the radiation therapy. Subacute comatose state was developed in the patient. MRI of the brain revealed a multi-focal lesion of the media-basal regions on both sides, frontal corpus callosum and brain stem. Differential diagnosis included an acute demyelination (SD, PML), viral encephalitis and vasculitis. Treatment included methylprednisolone pulse therapy and plasmapheresis. The consciousness cleared up, but there was no spontaneous breathing, tetraplegia persisted. Autoimmune and infectious diseases was excluded. The homozygous mutation PAI-1-675 4G/4G was found. In this case, acromegaly induced endothelial dysfunction was the pathogenesis factor of multiple cerebral infarctions and demyelinating lesions, as well as RT and its proven pathological influence on the vascular wall and the fibrinolytic system. The revealed thrombophilia was also a factor of multiple cerebral infarctions. A Potential combination of pathogenic factors in the development of cerebral should be taken into account in predicting complications of RT.

scholarly journals ОСНОВНІ НЕВРОЛОГІЧНІ СИМТОМИ ТА ЇХ ПОШИРЕННЯ У СОБАК

2016 ◽  
Vol 18 (3(71)) ◽  
pp. 240-243
Author(s):  
V. Fedorovych ◽  
L. Slivinska ◽  
N. Fedorovych
Keyword(s):  
Nervous System ◽  
Pathological Process ◽  
Neurological Symptoms ◽  
Nervous System Diseases ◽  
Anatomical Localization ◽  
Neurological Research ◽  
The Brain

As a result of the ambulatory reception it was investigated 12233 animals, of which 5653 (46.2%) were dogs. In the neurological research it had shown the symptoms of the nervous system damage in 653 dogs (11.5%). In particular it was found that paresis and paralysis (23.4%) were the most common neurological symptoms in dogs. Number of animals with inclination of head, ataxia, myoclonus and epileptiform state was respectively 19.8; 14.7; 11.7 and 10.5%. The manifestations of the nervous system damage as nystagmus, tremor and lameness were registered in accordance with 8.3; 4.4 and 4.1% of sick dogs. The least number of dogs were with a disorder of vision (2,8%) and hearing (0,3%), which was associated with the pathology of the nervous system. The above mentioned symptoms of the nervous system diseases do not occur as a symptom, but it was marked their combination – syndromes. The conducted neurological research makes it possible to establish the location of the pathological process in the departments of nervous system (neurons anatomical localization).As a result of the research and the results found that most dogs manifest the symptoms of damage to the brain and spinal mozkupaytiyi. Based on the results of verification of the diagnosis will be made using the methods of visual diagnostics. 

scholarly journals Acute onset neurological symptoms in Wilson disease after traumatic, surgical or emotional events

Medicine ◽  
2019 ◽  
Vol 98 (26) ◽  
pp. e15917
Author(s):  
Liang-Yong Li ◽  
Xiao-Qun Zhu ◽  
Wei-Wei Tao ◽  
Wen-Ming Yang ◽  
Huai-Zhen Chen ◽  
...  
Keyword(s):  
Wilson Disease ◽  
Acute Onset ◽  
Neurological Symptoms ◽  
Emotional Events

scholarly journals Identification and characterization of microglia/macrophages in the granuloma microenvironment of encephalic schistosomiasis japonicum

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Zhoubin Tan ◽  
Zhuowei Lei ◽  
Zhuo Zhang ◽  
Huaqiu Zhang ◽  
Kai Shu ◽  
...  
Keyword(s):  
Clinical Symptoms ◽  
Neurological Symptoms ◽  
Granuloma Formation ◽  
Post Injection ◽  
Mice Model ◽  
M2 Polarization ◽  
New Findings ◽  
New Perspective ◽  
Weight Decrease ◽  
The Brain

Abstract Background Egg-induced immune response and granuloma formation are thought to be the basis of central nervous system (CNS)-related clinical symptoms of Schistosoma japonicum. Microglia/macrophages are the major immune cells involved in detection and subsequent elimination of pathogens and injured tissue in the brain. However, little is known about their role in the pathogenesis of neuroschistosomiasis. The main purpose of the study is to clarify the pathological involvement of microglia/macrophages in the pathogenesis of neuroschistosomiasis (NS). Methods Staining techniques were applied to the granuloma tissues excised from 4 patients, as well as mice model which was established by microinjecting viable S. japonicum eggs into the brain. Clinical features of the patients and neurological symptoms in mice were also collected and analyzed in terms of their correlation with microglia/macrophages. Results Microglia/macrophages constituted the major portions of the granulomas surrounding the eggs in both all human cases and S. japonicum egg-injected mice. Granuloma persisted in all patients accompanied by unremitted neurological symptoms, while in mice granuloma formation initiated on day 3, peaked on day 7 and subsided on day 30 post injection with S. japonicum eggs. No neurological abnormalities were observed in egg-injected mice except for significant weight decrease on day 3 compared with saline-injected control. M1 polarization of microglia/macrophages was confirmed in egg-injected mice 3 days post injection and in all human cases. M2 polarization was absent in human patients despite the duration of complaints but dominated in the whole progression of egg-induced pathology in mice until the elimination of eggs and subsidence of neuroinflammation on day 30 post injection. Conclusions Microglia/macrophages participated actively in the granuloma microenvironment of encephalic schistosomiasis japonicum in both human and mice. The polarization pattern of microglia/macrophages coincided with the symptomatic features in human cases and S. japonicum egg-injected mice, indicating M2 instead of M1 activation as a probably more important mediator in the battle against egg-induced pathology and concomitant manifestations. These new findings will shed light on the pathogenesis of NS from a brand-new perspective, and may contribute to the immunotherapy development for such disease, favoring perhaps M2 polarization of microglia/macrophages as a feasible strategy.

scholarly journals High Parasite Burdens Cause Liver Damage in Mice following Plasmodium berghei ANKA Infection Independently of CD8+T Cell-Mediated Immune Pathology

2011 ◽  
Vol 79 (5) ◽  
pp. 1882-1888 ◽  
Author(s):  
Ashraful Haque ◽  
Shannon E. Best ◽  
Fiona H. Amante ◽  
Anne Ammerdorffer ◽  
Fabian de Labastida ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Liver Damage ◽  
Plasmodium Berghei ◽  
Clinical Symptoms ◽  
Neurological Symptoms ◽  
Experimental Cerebral Malaria ◽  
Content Type ◽  
Immune Pathology ◽  
The Brain

ABSTRACTInfection of C57BL/6 mice withPlasmodium bergheiANKA induces a fatal neurological disease commonly referred to as experimental cerebral malaria. The onset of neurological symptoms and mortality depend on pathogenic CD8+T cells and elevated parasite burdens in the brain. Here we provide clear evidence of liver damage in this model, which precedes and is independent of the onset of neurological symptoms. Large numbers of parasite-specific CD8+T cells accumulated in the liver followingP. bergheiANKA infection. However, systemic depletion of these cells at various times during infection, while preventing neurological symptoms, failed to protect against liver damage or ameliorate it once established. In contrast, rapid, drug-mediated removal of parasites prevented hepatic injury if administered early and quickly resolved liver damage if administered after the onset of clinical symptoms. These data indicate that CD8+T cell-mediated immune pathology occurs in the brain but not the liver, while parasite-dependent pathology occurs in both organs duringP. bergheiANKA infection. Therefore, we show thatP. bergheiANKA infection of C57BL/6 mice is a multiorgan disease driven by the accumulation of parasites, which is also characterized by organ-specific CD8+T cell-mediated pathology.

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