scholarly journals Answering the Call: The Influence of Neuroimaging and Electrophysiological Evidence on Rehabilitation

2007 ◽  
Vol 87 (6) ◽  
pp. 684-703 ◽  
Author(s):  
Lara A Boyd ◽  
Eric D Vidoni ◽  
Janis J Daly
Keyword(s):  
Functional Recovery ◽  
Diffusion Tensor ◽  
Central Nervous System Disease ◽  
Neurological Injury ◽  
Cortical Injury ◽  
Electrophysiological Data ◽  
Damage Models ◽  
System Disease ◽  
Positron Emission ◽  
The Brain

Functional recovery after brain damage or disease is dependent on the neuroplastic capability of the cortex and the nonaffected brain. Following cortical injury in the motor and sensory regions, the adjacent spared neural tissues and related areas undergo modifications that are required in order to drive more normal motor control. Current rehabilitation models seek to stimulate functional recovery by capitalizing on the inherent potential of the brain for positive reorganization after neurological injury or disease. This article discusses how neuroimaging and electrophysiological data can inform clinical practice; representative data from the modalities of functional magnetic resonance imaging, diffusion tensor imaging, magnetoencephalography, electroencephalography, and positron emission tomography are cited. Data from a variety of central nervous system disease and damage models are presented to illustrate how rehabilitation practices are beginning to be shaped and informed by neuroimaging and electrophysiological data.

scholarly journals A Case of Cerebral Vasculitis Associated with Ulcerative Colitis

2015 ◽  
Vol 2015 ◽  
pp. 1-5 ◽  
Author(s):  
Naveen Raj ◽  
Matthew Arkebauer ◽  
Barry Waters ◽  
Brucha Dickinson
Keyword(s):  
Ulcerative Colitis ◽  
Central Nervous System Disease ◽  
Altered Mental Status ◽  
Inflammatory Disorder ◽  
Cerebral Lesions ◽  
System Disease ◽  
Organ Systems ◽  
History Of ◽  
Inflammatory Bowel ◽  
The Brain

Ulcerative colitis (UC) is a chronic, debilitating condition characterized by inflammation of the colonic mucosa. It is regarded as a systemic inflammatory disorder that can affect a number of organ systems. Central nervous system disease associated with UC is a rare sequela of inflammatory bowel disease, occurring in less than 5% of cases. These manifestations include arterial and venous thrombosis, leukoencephalitis, seizures, and vasculitis. We present a case of a 61-year-old female with a two-year history of well-controlled ulcerative colitis, who developed altered mental status and weakness. On brain imaging, she was found to have cerebral lesions which were biopsied. Histopathology subsequently revealed coagulative necrosis and inflammation characteristic of vasculitis. Rheumatology serologies were negative, and the patient was started on steroids that dramatically improved her neurological function, with no residual deficits, and led to resolution of the brain lesions.

scholarly journals Immune Response-Mediated Protection of Adult but Not Neonatal Mice from Neuron-Restricted Measles Virus Infection and Central Nervous System Disease

1999 ◽  
Vol 73 (3) ◽  
pp. 1795-1801 ◽  
Author(s):  
Diane M. P. Lawrence ◽  
Melinda M. Vaughn ◽  
Alec R. Belman ◽  
Joan S. Cole ◽  
Glenn F. Rall
Keyword(s):  
Central Nervous System ◽  
Immune Response ◽  
Nervous System ◽  
Neurological Disease ◽  
Measles Virus ◽  
Central Nervous System Disease ◽  
Nervous System Disease ◽  
Antiviral Immune Response ◽  
System Disease ◽  
The Brain

ABSTRACT In many cases of neurological disease associated with viral infection, such as measles virus (MV)-induced subacute sclerosing panencephalitis in children, it is unclear whether the virus or the antiviral immune response within the brain is the cause of disease. MV inoculation of transgenic mice expressing the human MV receptor, CD46, exclusively in neurons resulted in neuronal infection and fatal encephalitis within 2 weeks in neonates, while mice older than 3 weeks of age were resistant to both infection and disease. At all ages, T lymphocytes infiltrated the brain in response to inoculation. To determine the role of lymphocytes in disease progression, CD46+ mice were back-crossed to T- and B-cell-deficient RAG-2 knockout mice. The lymphocyte deficiency did not affect the outcome of disease in neonates, but adult CD46+RAG-2− mice were much more susceptible to both neuronal infection and central nervous system disease than their immunocompetent littermates. These results indicate that CD46-dependent MV infection of neurons, rather than the antiviral immune response in the brain, produces neurological disease in this model system and that immunocompetent adult mice, but not immunologically compromised or immature mice, are protected from infection.

Rasmussen's Syndrome: Intractable Epilepsy and Progressive Neurological Deterioration From a Unilateral Central Nervous System Disease

CNS Spectrums ◽  
2001 ◽  
Vol 6 (5) ◽  
pp. 398,409-416 ◽  
Author(s):  
Paul R. Carney
Keyword(s):  
Central Nervous System ◽  
Cerebral Hemisphere ◽  
Antiviral Agents ◽  
Intractable Epilepsy ◽  
Central Nervous System Disease ◽  
System Disease ◽  
Chronic Encephalitis ◽  
Rasmussen’S Syndrome ◽  
The Brain ◽  
Severe Epilepsy

AbstractRasmussen's syndrome (chronic encephalitis with epilepsy) is a rare neurological disorder of unknown cause characterized by severe epilepsy, hemiplegia, dementia, and inflammation of the brain, and progressive functional and structural destruction of a single cerebral hemisphere. While one mechanism underlying the pathogenesis of Rasmussens encephalitis has been hypothesized to be mediated by production of excitotoxic GluR3 autoantibodies to the a-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptor, other neuropathological etiologies have also been indicated. Proposed therapies have included antiepileptics, steroids, antiviral agents, alpha-interferon, and immunoglobulin. The mainstay of therapy is surgical hemispherectomy. To date, no medical therapies have permanently halted neurologic deterioration.

scholarly journals Association of the Intronic Polymorphism rs3773364 A>G in Synapsin-2 Gene with Epilepsy Patients in Iraq

2021 ◽  
pp. 2169-2175
Author(s):  
Akram Jawad Hameedi ◽  
Asmaa Mohammed Saud
Keyword(s):  
Central Nervous System Disease ◽  
Healthy Individuals ◽  
Recurrent Seizure ◽  
System Disease ◽  
Intronic Polymorphism ◽  
Significant Difference ◽  
Pcr Rflp ◽  
Age Range ◽  
The Brain ◽  
Rflp Assay

     Epilepsy is a central nervous system disease which is characterized by a recurrent seizure that distinguishes it from other similar diseases. Epilepsy may occur due to defects in genes that encode some receptors in the brain. For this reason, this study aimed to understand the association between Synapsin-2 (SYN2) gene and susceptibility to epilepsy. Blood samples were collected from 40 volunteers, including 30 patients suffering epilepsy with an age range of 26-49 years old and 10 healthy individuals with an age range of 25-53 years old. The study sample involved 16 males and 14 females with epilepsy along with 6 males and 4 females healthy subjects.  DNA was isolated from the volunteers for PCR-RFLP assay. Genotyping of rs3773364 A>G SYN2 was conducted and the results refer to a highly significant difference in the distribution of AG genotype (P=0.0001), while there is no significant difference in the distribution of AA and GG genotypes, with p values of 0.1702 and 1.00, respectively. The results also showed that gender did not significantly affect the results when comparing patients with the control (p=0.0934). Our findings indicates that SYN2 rs3773364 A>G confers risk to epilepsy and may be implicated in epileptogenesis.

scholarly journals Naturally Occurring Eastern Equine Encephalitis in a Hampshire Wether

2005 ◽  
Vol 17 (3) ◽  
pp. 281-285 ◽  
Author(s):  
Rudy W. Bauer ◽  
Marjorie S. Gill ◽  
Rob P. Poston ◽  
Dae Young Kim
Keyword(s):  
Fluorescent Antibody ◽  
Clinical Signs ◽  
Central Nervous System Disease ◽  
Thiamine Hydrochloride ◽  
Antibody Testing ◽  
Tetanus Antitoxin ◽  
Eastern Equine Encephalitis ◽  
System Disease ◽  
Hind Limbs ◽  
The Brain

Eastern equine encephalitis (EEE) was diagnosed (postmortem) in a sheep with clinical signs attributable to a central nervous system disease. The sheep was febrile and initially had front limb incoordination, which progressed to paralysis of both front and hind limbs during a course of 2 days. The sheep maintained an alert attitude with the ability to eat up to the time of euthanasia. The only clinical pathologic abnormalities were neutrophilia and lymphopenia without appreciable leukocytosis, a moderate hyperglycemia, and an elevated creatine kinase. Treatment included hydrotherapy for lowering body temperature, intravenous fluids, thiamine hydrochloride, tetanus antitoxin, antibiotics, and corticosteroids. The only gross lesion at the time of necropsy was a wet glistening surface of the brain (leptomeninges). Microscopically, there was severe nonsuppurative meningoencephalitis, poliomyelitis, and polyradiculoneuritis with mild multifocal neutrophilic infiltration. The EEE virus was isolated from the brain, and subsequent fluorescent antibody testing for EEE was positive on cell culture.

scholarly journals The first RT-qPCR confirmed case of tick-borne encephalitis in a dog in Scandinavia

2020 ◽  
Vol 62 (1) ◽  
Author(s):  
Elina Andersson ◽  
Anna Kendall ◽  
Angelika Url ◽  
Angelika Auer ◽  
Michael Leschnik
Keyword(s):  
Serum Antibody ◽  
Clinical Signs ◽  
Central Nervous System Disease ◽  
Acute Onset ◽  
Case Presentation ◽  
System Disease ◽  
Tick Borne Encephalitis ◽  
Antibody Titres ◽  
Tick Borne Encephalitis Virus ◽  
The Brain

Abstract Background Tick-borne encephalitis (TBE) is a zoonotic neurological disease caused by tick-borne encephalitis virus (TBEV), a flavivirus endemic in parts of Europe and Asia. Seroconversion without signs of clinical disease is common in dogs and most of the cases previously described have been tentatively diagnosed by combining neurologic signs with serum antibody titres. Here, the first Scandinavian RT-qPCR-confirmed clinical case of TBE in a dog is reported. Case presentation A 4-year old castrated male Pointer Labrador cross was presented with acute-onset ataxia. During hospitalisation, the dog developed seizures. Despite aggressive treatment with steroids, antimicrobials and sedation/anaesthesia, there was continued deterioration during the following 24 h after admission and the dog was euthanised and submitted for necropsy. Histopathological changes in the brain were consistent with lymphoplasmacytic and histiocytic meningoencephalomyelitis. RT-qPCR examination of the brain was positive for TBEV, confirming infection. Conclusions Meningoencephalomyelitis caused by TBEV should be a diagnostic consideration in dogs presenting with clinical signs of central nervous system disease such as acute-onset ataxia and seizures in areas where TBEV-positive ticks are endemic. Clinical TBE may be underdiagnosed in dogs due to lack of specific testing.

scholarly journals IMMUNOPATHOGENESIS OF ACUTE CENTRAL NERVOUS SYSTEM DISEASE PRODUCED BY LYMPHOCYTIC CHORIOMENINGITIS VIRUS

1972 ◽  
Vol 135 (4) ◽  
pp. 860-873 ◽  
Author(s):  
Donald H. Gilden ◽  
Gerald A. Cole ◽  
Andrew A. Monjan ◽  
Neal Nathanson
Keyword(s):  
Choroid Plexus ◽  
Molecular Layer ◽  
Central Nervous System Disease ◽  
Lymphocytic Choriomeningitis ◽  
Lymphocytic Choriomeningitis Virus ◽  
Brain Nuclei ◽  
System Disease ◽  
High Virus ◽  
The Brain ◽  
Virus Carrier

A single dose of 150 mg/g of cyclophosphamide (CY), given 3 days after intracerebral (i.c.) inoculation of lymphocytic choriomeningitis (LCM) virus, protected over 90% of adult BALB/c mice against acutely fatal choriomeningitis. Surviving mice became persistently infected carriers, with high virus titers in blood and brain. Immunofluorescent examination of the brain showed that in CY-induced carriers infection was initially confined to the choroid plexus, ependyma, and leptomeninges, but over the next 30 days gradually spread to the neural parenchyma, most notably to the molecular layer of the cerebellum. By contrast, LCM virus-carrier mice produced by neonatal virus injection and examined as adults, showed a much less marked infection of choroid plexus and much more widespread infection of parenchyma, with a different distribution among brain nuclei, including heavy infection of the Purkinje cells of the cerebellum.

Meningoencephalitis in cats in Austria: a study of infectious causes, including Encephalitozoon cuniculi

2016 ◽  
Vol 19 (2) ◽  
pp. 171-176 ◽  
Author(s):  
Frank Künzel ◽  
Barbara Rebel-Bauder ◽  
Christine Kassl ◽  
Michael Leschnik ◽  
Angelika Url
Keyword(s):  
Central Nervous System ◽  
Unknown Origin ◽  
Central Nervous System Disease ◽  
Second Step ◽  
Encephalitozoon Cuniculi ◽  
Feline Infectious Peritonitis ◽  
System Disease ◽  
Ocular Disorders ◽  
Fungal Organisms ◽  
The Brain

Objectives Despite comprehensive diagnostics, the aetiology of meningoencephalitis (ME) in cats often remains undetermined. As a result of recently published surveys, Encephalitozoon cuniculi has gained growing importance in cats not only with ocular disorders, but also with central nervous system disease. Therefore, it was hypothesised that E cuniculi may be an underestimated pathogen in the development of feline non-suppurative and/or granulomatous ME. Methods As a first step, histopathological sections of the brain of cats with encephalopathy were retrospectively reviewed to identify cases of granulomatous ME. In a second step, an immunohistochemical screening for detection of E cuniculi was performed in cases with ME of unknown origin. Results In 59/89 (66.3%) cats with ME, an aetiologically relevant pathogen was detected. Forty-three of 89 (48.3%) cats had a diagnosis of feline infectious peritonitis. In 14/89 (15.7%) cats, protozoan cysts were identified and infection with Toxoplasma gondii was confirmed by immunohistochemistry (IHC) in all cases. In 2/89 (2.3%) cats with granulomatous ME, fungal organisms were identified. Thirty of 89 (33.7%) cats with ME of unknown origin that underwent IHC for the detection of E cuniculi remained negative. Conclusions and relevance The results of this study suggest that E cuniculi is unlikely to be directly associated with (non-suppurative and/or granulomatous) ME in cats in Austria.

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