parietal anormalencephalomalaciaassociated with schizophrenia: a case report.
Pan, Fen; Wang, Jun-Yuan; Xu, Yi; Huang, Man-Li
2017-03-01
Structural abnormalities of the brain are widely believed to contribute to the pathophysiology of schizophrenia. The parietal lobe is the center of multisensory integration, and abnormalities in this region may explain the clinical features of schizophrenia. However, some parietal casesencephalomalaciaSymptoms associated with schizophrenia have been described. The article presents the case of a 25-year-old schizophrenic patient with abnormal parietal position.encephalomalacia. The patient had a poor diet and frequently suffered from upper respiratory tract infections during childhood and adolescence. For 2 years he displayed severe schizophrenic symptoms, such as visual hallucinations. After examining all possible conditions, we determined that the patient had a change consistent with the diagnosis.encephalomalaciain the right parietal lobe and slight cerebral atrophy. The patient was prescribed olanzapine (10 mg daily). His symptoms improved significantly after antipsychotic treatment and were still well controlled one year later. This case suggested parietalencephalomalacia, which can be caused by inflammatory and infectious conditions in the first years of life and aggravated by malnutrition, may be related to the etiology of schizophrenia.
Prenatal diagnosis of the fetus.encephalomalaciaafter maternal diabetic ketoacidosis.
Con amor, Rosalyn; Lee, Amy; Matiasek, abril; Carter, William; Yagan, Marissa
2014-11-01
Prohibitedencephalomalaciain the developing fetus it is a rare and devastating neurological finding on radiological images. Diabetic ketoacidosis (DKA) in the mother can cause metabolic and vascular disorders that can cause fetal harm.encephalomalacia. Case We present the case of a 27-year-old pregnant woman with Class C White diabetes who developed CAD at 25 weeks' gestation. Four weeks after discharge from the hospital, an ultrasound examination revealed a distinct fetal cerebral ventricle. Subsequently, fetal magnetic resonance imaging (MRI) showed an extensive and symmetrical cyst.encephalomalaciaIt mainly affects both cerebral hemispheres. The pregnancy continued under close fetal and maternal supervision. The patient underwent a second cesarean section at 37 weeks of gestation. The baby remained in the neonatal intensive care unit for 1 month under the care of a multidisciplinary team of pediatric specialists. The postpartum course was complicated by general hypotonia, malnutrition, failure to thrive, and eventually required the use of anticonvulsants for recurrent seizures. She died at the age of 9 months as a result of an aspiration during a seizure. Discussion: Although maternal mortality from CAD has decreased, CAD continues to cause significant neurological complications in surviving fetuses.
Prenatal diagnosis of the fetus.encephalomalaciaafter maternal diabetic ketoacidosis
Con amor, Rosalyn; Lee, Amy; Matiasek, abril; Carter, William; Yagan, Marissa
2014-01-01
Prohibitedencephalomalaciain the developing fetus it is a rare and devastating neurological finding on radiological images. Diabetic ketoacidosis (DKA) in the mother can cause metabolic and vascular disorders that can cause fetal harm.encephalomalacia. Case We present the case of a 27-year-old pregnant woman with Class C White diabetes who developed CAD at 25 weeks' gestation. Four weeks after discharge from the hospital, an ultrasound examination revealed a distinct fetal cerebral ventricle. Subsequently, fetal magnetic resonance imaging (MRI) showed an extensive and symmetrical cyst.encephalomalaciaIt mainly affects both cerebral hemispheres. The pregnancy continued under close fetal and maternal supervision. The patient underwent a second cesarean section at 37 weeks of gestation. The baby remained in the neonatal intensive care unit for 1 month under the care of a multidisciplinary team of pediatric specialists. The postpartum course was complicated by general hypotonia, malnutrition, failure to thrive, and eventually required the use of anticonvulsants for recurrent seizures. She died at the age of 9 months as a result of an aspiration during a seizure. Discussion: Although maternal mortality from CAD has decreased, CAD continues to cause significant neurological complications in surviving fetuses. PMID:25452892
Semiautomated deep ballistic brain injury trajectory analysis.
Folio, Les; Solomon, Jeffrey; Biassou, Nadia; Fisher, Tatiana; Dworzak, Jenny; Raymont, Vanessa; Sinai, ninet; Wassermann, Eric M.; Grafman, Jordan
2016-01-01
Background: Penetrating head injuries (PHI) are common in combat operations, and in most cases, traces of the wounds are visible on computed tomography (CT). Objective To assess the correspondence between automated assessment of brain injury based on trajectory analysis and manual follow-up of brain injury.encephalomalaciain CT. Methods We analyzed 80 head CT scans with ballistic PHI from the Vietnam Head Injury Registry approved by the Institutional Review Board. Anatomical reports were generated based on the spatial coordinates of the projectile entry and the location of the final fragment. They were compared with manual records of the regions.encephalomalacia. Dice coefficients of similarity, kappa, sensitivity, and specificity were calculated to assess concordance. The time required for case analysis was also compared. Results The results show a high specificity of the anatomical areas identified by computed tomography using semi-automated anatomical estimates and manual monitoring of tissue damage. Reports of the anatomical region by radiologists and medical students were similar (Kappa 0.8, t-test p < 0.001). Modeling of the area of probable damage in the involved brain structures was sensitive (0.7) and specific (0.9) compared to manually traced structures. Semi-automated analysis was 9 times faster than manual tracking. Conclusions Our spatial model of the area of probable injury is close to the anatomical areas.encephalomalaciaof ballistic PHI with time savings compared to manual methods. The results show the potential for automated anatomical reports to complement the current practice of radiologists and neurosurgeons in the assessment of brain damage caused by penetrating bullets. PMID:23707123
Mo, Andrew Z; Asemota, Anthony O; Venkatesan, Arun; Ritzl, Eve K.; Njoku, Dolores B.; Sponsors: Paul D.
2017-12-01
Intraoperative neuromonitoring (IONM) is widely used to reduce postoperative neurological complications during scoliosis correction. IONM enables intraoperative detection of neurological spinal cord injuries and allows surgeons to react in real time. IONM failure rates can be as high as 61% in patients with cerebral palsy (CP). Factors that impair IONM signal quality or prevent IONJ in patients with cerebral palsy undergoing scoliosis correction have not been well described. We divided IONM data from 206 children with cerebral palsy who underwent surgical correction of scoliosis at an institution between 2002 and 2013 into 3 groups: (1) "no cues" if neither somatosensory evoked potentials (SSEPs) are activated; nor transcranial motor potentials (TcMEP) can be obtained; (2) "no sensory" if no interpretable SSEP is obtained independently of the interpretable TcMEP; and (3) "non-powered" if an interpretable TcMEP has not been obtained independently of an interpretable SSEP. We reviewed existing neuroimaging available for 93 patients and the neurological status of the entire cohort for these categories. Statistical analysis of univariate and multivariate associations was performed using logistic regression. The odds ratio (OR) was calculated at a significance level of P<0.05. Multivariate analysis showed a significant association between periventricular leukomalacia (PVL), hydrocephalus, andencephalomalaciawithout significant and interpretable signals. Focal PVL (Fig. 1) was associated with absence of motor (OR = 39.95; P = 0.04). Moderate hydrocephalus was associated with no cue (OR = 32.35; P < 0.01), no movement (OR = 10.14; P = 0.04), and no sensation (OR = 8.44; P = 0.03). Significant hydrocephalus (Fig. 2) was associated with absence of motor (OR = 20.46; P < 0.01) and absence of cues (OR = 8.83; P = 0.01). At last,encephalomalacia(Fig. 3) was associated with no motor (OR = 6.99; P = 0.01) and no signal (OR = 4.26; P = 0.03). Neuroanatomical findings in PVL, hydrocephalus andencephalomalaciaare important predictors of restricted IONM signals
Isolated cataplexy and REM sleep behavior disorder after Pontine stroke
Reynolds, Thomas Q.; Roy, Asim
2011-01-01
Cataplexy is a complex neurological phenomenon that occurs in the awake state, possibly as a result of poor pons and hypothalamus control over muscle tone. REM sleep behavior disorder (RSBD) is characterized by nonatonic REM sleep that manifests clinically as disruptive or harmful behaviors. We present a patient with cataplexy and RSBD after a bridge.encephalomalacia. The clinical presentation provides insight into the possible pathobiology of disorders of REM sleep regulation, both during wakefulness and sleep. Citation: Reynolds TQ; Roy A. Isolated cataplexy and REM sleep behavior disorder after stroke. J Clin Sleep Med 2011;7(2):211-213. PMID:21509338
Xiao, Lianxiang, Lin, Xiangtao, Cao, Jinfeng, Wang, Xueyu;
2011-09-01
Combined diphenoxylate (diphenoxylate and atropine) poisoning can cause toxic encephalopathy in children, and magnetic resonance imaging (MRI) of the brain has not been reported for this condition. The aim of the study is to analyze the results of MRI of the brain and to investigate the relationship between MRI characteristics and possible pathophysiological changes in children. Six children accidentally ingested the diphenoxylate compound, 4 male and 2 female, ranging in age from 20 to 46 months, with an average age of 33 months. The amount of atropine diphenoxylate ingested ranged from 6 to 30 tablets, each tablet containing 2.5 mg diphenoxylate and 0.025 mg atropine. These patients were referred to our hospital within 24 hours of receiving atropine diphenoxylate and underwent brain MRI within 24 to 72 hours of emergency treatment. The characteristics of conventional magnetic resonance were analyzed. These children and adolescents presented with a variety of symptoms of opioid intoxication and atropine toxicity. Brain MRI showed abnormally low signal intensity on T1-weighted images (T1WI) and abnormally high signal intensity on T2-weighted images (T2WI) and fluid-attenuated inversion images (FLAIR) in both cases; abnormally high signal intensity on T1WI, T2WI and FLAIR in 4 cases.encephalomalaciaobserved in 3 cases during follow-up. In the early stages of combined diphenoxylate poisoning in children, numerous extensive edema-necrotic and hemorrhagic-necrotic foci were observed in the basal ganglia, palis, and cerebellum, resulting in corresponding brain dysfunction withencephalomalacia. MRI in the early stages of this disease can provide evidence of brain damage and is beneficial for early diagnosis, treatment, and prognosis. Crown Copyright © 2010. Published by Elsevier Ireland Ltd. All rights reserved.
Cerebral neuropathology submitted under the Bovine Spongiform Encephalopathy Orders in Scotland.
Jeffreya, M.
10.10.1992
Bovine spongiform encephalopathy was not confirmed histologically in 225 of the 829 bovine brains presented for diagnosis. A number of previously described central nervous system disorders were observed in these brains, as well as disorders not previously recognized in the UK, including bilateral vacuolation of the substantia nigra, hippocampal sclerosis with chromatolysis and brainstem neuronal necrosis, focal symmetric disease .encephalomalaciaand meningoangiomatosis. Severe cerebellar dysplasia consistent with antenatal bovine viral diarrhea-mucosal disease virus infection or vascular mineralization of the basal ganglia were interpreted as congenital or age-related changes, respectively, and were not considered clinically significant.
Cognitive improvement after basal encephalocele repair.
Tulloch, Elizabeth; Palmer, Siobhan; Scott, Richard; Lozsadi, Dora; Martin, Andrew J. .
2018-06-01
We present the case of a 55-year-old woman with progressive memory impairment secondary to a transsphenoidal encephalocele affecting the dominant medial temporal lobe. Clinical deterioration was accompanied by radiographic progression in the size of the encephalocele and the associated lesion.encephalomalacia. As a result of a temporary craniotomy, the brain herniation was removed and the defect closed. Initial neuropsychological evaluation showed general cognitive impairment, but after the operation, memory and concentration improved. The standardized score reflected an improvement in perceptual skills and a related improvement in recall of complex figures. This is the first case report of improvement in memory in a patient after treatment for a basal encephalocele.
Neurological impairment in a twin who survived intrauterine fetal death in a twin: a case study.
Forrester, KR; Keegan, KM; Schmidt, JW
2013-01-01
It has been established that there is an increased risk of complications in twin pregnancies, including the risk of morbidity or mortality for one or both babies. Cerebral palsy and other related neurological deficits are also more common in twin pregnancies. This report investigated two cases of intrauterine death of a twin, after which the other managed to survive. In both cases, the surviving infant developed severe neurological sequelae. The disorders seen in these two cases include polycystic disease.encephalomalaciaand periventricular leukomalacia, as well as the subsequent development of cerebral palsy. In this case study, the predisposing factors, prevalence, pathophysiology, consequences, and future implications of these findings for research were investigated.
Primer informe de Angiostrongylus vasorum en un zorro rojo salvaje (Vulpes foxes) de Apulia (Italy).
Passantino, Józef; Marino, Fabio; Gaglio, Gabriela; Patruno, Róża; Lanteri, enero; Zizo, Nicole
2017-04-05
A wild red fox (Vulpes vulpes) (1/12) from Apulia (Italy) has been diagnosed with severe pulmonary carbidosis. We performed routine diagnostics on 12 dead foxes found in Puglia. Eleven of them presented alterations that resembled a vehicle collision. However, the remaining fox appeared to have died of other causes. In the autopsy catarrhal enteritis, hepatic steatosis, pulmonary congestion in some areas of constant consistency, cerebral hemorrhage and malacia were observed. Histopathology showed pulmonary bronchi containing mononuclear cells, thrombosis of several disseminated nematode larvae in the parenchyma, interstitial nephritis, interstitial myocarditis, encephalitis,encephalomalaciaand brain granuloma. The larvae isolated from the lung parenchyma were identified as first-stage larvae of Angiostrongylus vasorum. This is the first documented report of angiostrongylosis in a fox in southern Italy.
Aleutian disease: an emerging disease of free-ranging California striped skunks (Mephitis mephitis).
LaDouceur, EE B; Anderson , M. ; Ritchie , BW ; Ciembor, P; Rimoldi, G; Plaza, M; Plague, D; Clifford, Dallas; Giannitti, F. (1999).
2015-11-01
Aleutian disease virus (ADV, Amdovirus, Parvoviridae) infects mainly mustelids (mink and ferrets), but also other fur-bearing animals and humans. Three cases of Aleutian disease (AD) have been reported in captive striped skunks; however, little is known about the importance of EA in free-living carnivores. This article describes the pathology and spatiotemporal distribution of 7 AD cases in free-ranging striped skunks. All cases showed neurologic disease and were detected within 46 months (2010-2013) in a specific geographic region of California. Lesions included multisystem plasmacytic and lymphocytic inflammation (ie, interstitial nephritis, myocarditis, hepatitis, meningitis, pneumonia, and splenitis), glomerulonephritis, arteritis with or without fibrinous necrosis in various organs (ie, kidneys, heart, brain, and spleen), splenomegaly, ascites. / hydrocele and / orencephalomalaciawith cerebral microangiopathy. ADV infection was confirmed in all cases by specific polymerase chain reaction and/or in situ hybridization. The results suggest that AD is an emerging disease in free-ranging striped skunks in California. © Author(s) 2014.
Cho, Yang Je; Han, Sang Don; Song, Sook Keun; Lee, Byung In; hi kyoung
2009-06-01
Palilalia is a relatively rare pathological speech behavior that has been reported in various neurological and psychiatric disorders. We found a case of palilalia, echolalia and echopraxia-palipraxia as a phenomenon of paroxysmal epilepsy of the left frontal lobe. A 55-year-old right-handed man was admitted due to frequent episodes of rapid repetition of syllables. Video electroencephalography monitoring revealed stereotyped episodes of palilalia accompanied by rhythmic head movements and right arm posture with paroxysmal discharges in the left frontocentral area. He also had echolalia or echopraxia-pallipraxia, partially responding to the examiner's stimulus. Reveal magnetic resonance imagingencephalomalaciain the left superior frontal gyrus and paroxysm by single photon emission computed tomography showed hyperperfusion just above the lesion, corresponding to the left supplementary motor area (SMA) and basal ganglia. This result suggests that the neuroanatomical substrate involved in the generation of these behaviors in the form of convulsive phenomena may exist in the SMA of the left frontal lobe.
[Serious late-onset group B streptococcal infection. A case report].
Haase, Roland; Nagel, Frank; Hirscha, Wolfganga; sitka, ser
2003-01-01
Group B streptococcus (GBS) is a well-known cause of neonatal pneumonia, sepsis, and meningitis. Perinatal antibiotic prophylaxis for early-onset GBS infections has been used routinely since the beginning of the last decade, but effective prevention strategies for late-onset GBS infections are still lacking. A few hours after discharge from the long-distance maternity ward, a 3-week-old boy was admitted to our hospital for GBS meningitis with necrotizing meningitis.encephalomalacia. Maternal mastitis, not the baby's disease, was the cause of the first hospital admission. The clinical history and the negative smears and cultures of the mother for GBS led to the hypothesis of nosocomial infection. Risk-based perinatal screening and antibiotic prophylaxis, better follow-up, and better treatments have reduced the incidence and mortality of early-onset GBS infections, but perinatal prophylaxis has not affected late-onset GBS infections. Up to 40% of infants with late-onset meningitis develop neurologic sequelae. Vaccination of the mother with GBS multivalent conjugate vaccines is a novel strategy that may lead to passive protection of the infant. More studies are being done to test the effectiveness of the vaccines.
Eyelid swelling: a rare cause of a common symptom
Almeida, Cristina; Freitas, Cristina; Sales-Sanz, Marco; Ribeiro, Sarah
2017-01-01
We present the case of a 48-year-old patient who came to the emergency room due to swelling of the right eyelid of 3 days of evolution. She had suffered a minor injury to that eye a week earlier. He reported episodes of self-resolving right eyelid edema since the onset of a traumatic brain injury 5 years ago. The ophthalmological examination revealed a soft and painless swelling of the eyelid of the right eye. Computed tomography of the brain showed an area of discontinuity of the orbital roof with cerebral herniation and leakage of cerebrospinal fluid into the eyelid (blepharocele). MRI confirmed the CT result and revealed the frontal area.encephalomalacia. Ibuprofen (800 mg/day) is prescribed, which completely disappears in 20 days. She was evaluated in neurosurgery, with no indication for surgery due to resolution of the edema and absence of symptoms. Palpebral eyelids are a rare pathological entity that should be considered in the differential diagnosis of unilateral eyelid edema. It can be secondary to an orbital fracture or a congenital defect. PMID:28848682
Surveillance of bovine spongiform encephalopathy lesions in US cattle.
Millman, LD; Davis , AJ ; Jenny, Alabama; Fekadu, M; Whitfield, Georgia
1993-01-01
The emergence of bovine spongiform encephalopathy (BSE) as a new bovine disease between 1985 and 1987 led to increased worldwide interest in various aspects of human and animal spongiform encephalopathies. In the United States, part of the surveillance activities have been directed at prospective testing of bovine brain samples for BSE lesions. One area of focus was the collection of samples from cattle that were (1) two years of age or older, (2) had documented signs of neurological disease, and (3) were receiving a protein supplement as an essential part of intravenous administration. administration. ration. Another area of interest was the investigation of suspected rabies cases that did not present rabies. The third axis was obtaining the results of bovine neuropathology studies carried out in other state and regional laboratories. Samples were obtained by direct shipment or referral from other public health and veterinary diagnostic laboratories. Many cases were classified as (1) inflammatory lesions such as listeriosis, pseudorabies, brain abscesses, and indeterminate inflammatory conditions, (2) degenerative lesions such as polio,encephalomalacialead poisoning, Wallerian degeneration, siderocalcinosis, and lipofuscinosis, (3) neoplastic lesions such as meningioma and schwannoma, and (4) no significant change. In other cases, the results were reported as inflammation or no significant results. Of the 459 cases reported here, none contained lesions with typical BSE characteristics and distribution.
Kim, JiHye; Jeon, Tae Yeon; Rha, Jung Ho; Eo, Hong; Yoo, taki joven; Shu, Chang Hae
2011-01-01
Objective We analyzed the diffusion and perfusion characteristics of acute MELAS lesions (mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke episode) in a large series to investigate controversial changes in apparent diffusion coefficient (ADC) that have been reported in previous studies. Materials and methods We analyzed 44 new lesions during 28 stroke-like episodes in 13 MELAS patients. We performed a visual assessment of the MR images, including ADC and perfusion maps, ADC comparison between normal and abnormal areas, %ADC comparison between 44 MELAS lesions and 30 acute ischemic infarcts. In addition, the patterns of evolution in successive MR images were analyzed. Results Decreased, increased, and normal ADC were observed in 16 (36%), 16 (36%), and 12 (27%) lesions, respectively. The mean percentage of ADC was 102 ± 40.9% in MELAS and 64 ± 17.8% in acute vascular infarcts (p < 0.001), while perfusion imaging showed hyperperfusion in six acute MELAS lesions. In subsequent images, resolution, progression, and tissue loss were recorded in 10, 4, and 17 lesions, respectively. Conclusions Cytotoxic edema develops gradually after an acute stroke-like episode in MELAS patients and may overlap with hyperperfusion and angioedema. The edema may be reversible or may developencephalomalacia, suggesting irreversible damage. PMID:21228936
Prediction of chronic subdural hematoma in patients with minor head injuries
Han, Sang-beom; Piosenka, Shi-Hun; Ty, Jin-Young; Koh, Hyeon-Song; Kim, Seon-Hwan; Kwon, Hyon-jo
2014-01-01
Purpose Chronic subdural hematoma (CSDH) is a relatively common occurrence in neurosurgery. However, not all patients with CSDH develop after a minor head injury. In this study, we evaluated risk factors for post-traumatic CSDH. Methods Between January 2012 and December 2013, two hundred and seventy-seven patients were enrolled and analyzed in this study. Of these, 20 participants subsequently developed a minor head injury after CSDH. We also included 257 patients with minor head injury who did not develop CSDH during the same follow-up period as controls. We examined the risk factors associated with the development of CSDH after minor head injury. Results Advanced age (p=0.014), existing diabetes mellitus (p=0.010), arterial hypertension (p=0.026), previous cerebral infarction (p=0.035), antiplatelet agents (p=0.000), acute subdural hematoma in the convex zone ( p=0.035) =0.000). p=0.000),encephalomalacia(p=0.029) and a large distance between the skull and the brain parenchyma (p=0.000) were significantly correlated with the development of CSDH after trauma. Multivariate analysis showed that an independent risk factor for CSDH (hazard ratio 2.55, p = 0.000) was only the maximum distance between the skull and the brain parenchyma. Conclusions The possibility of developing CSDH in post-traumatic patients with identified risk factors should be considered. PMID:27169043
Paroxysmal EEG paradoxical lateralization in children with unilateral cerebroclastic lesions.
Garzon, Eliana; Gupta, Ajay; Bingaman, William; Sakamoto, Americ C; Lüders, Hans
2009-09-01
To describe the pattern of paradoxical lateralization in encephalographic EEG in children with unilateral damage to the cerebroclastic hemisphere acquired early in life. Of 68 children who underwent hemispherectomy between 2003 and 2005, video-EEG of the scalp and MRI of the brain were reanalyzed in six children with head EEG seizures inconsistent with clinical and imaging data. . Medical records were reviewed to determine clinical outcomes and seizure outcomes. The age of seizure onset ranged from 1 day to 4 years. The devastating change on MRI was an ischemic stroke in 2 cases, which was the consequence of infection.encephalomalaciain 2 and perinatal trauma and hemiconvulsive-hemiplegic syndrome in one patient. The paroxysmal EEG pattern was characterized by pronounced paroxysmal rhythms with complex spikes and 3 to 7 Hz waves or sharp beta waves (rapid paroxysmal) over the uninjured hemisphere (contralateral to the lesion). Video-EEG of the scalp was inconsistent, however decision was made based on other findings related to motor deficits (hemiparesis; 5 severe, 1 mild), seizure semiology (4/6), interictal EEG abnormalities (3/6) and one-sided. MRI lesion load for hemispherectomy. After 12 to 39 months of follow-up after surgery, five of the six patients were seizure-free and one had brief periods of staring. We describe the paradoxical lateralization of the EEG to the "good" hemisphere in children with unihemispheric cerebroclastic lesions. This EEG pattern is consistent with a seizure-free postoperative outcome, provided other findings and clinical studies are consistent with an abnormal hemisphere origin.
Hydrocephalus in the yellow-headed Amazon parrot (Amazona ochrocephala oratrix).
Keller, Krista A; Guzmán, David Sánchez-Migallon; Muthuswamy, Anantharaman; Forrest, Lisa J.; Steinberg, Howard; Sweet, Kurt; Petersen, Zofia
2011-09-01
A 37-year-old female yellow-headed Amazon parrot (Amazona ochrocephala oratrix) is presented after a 4-month behavior change and occasional episodes of dementia. Clinical signs on physical examination included ataxia, poor grip, and reluctance to move. MRI confirmed severe hydrocephalus without signs of cerebrospinal fluid obstruction. The bird received gradual doses of prednisolone over a 4-month period without episodes. Several attempts were made to stop treatment, but the disease relapsed. After 3.5 years of prednisolone maintenance treatment, the bird experienced a 5-hour episode of mental weakness and worsening neurological symptoms. Despite increasing the prednisolone dose and providing additional supportive care, the bird's condition deteriorated and it was decided to euthanize. Necropsy findings included severe hydrocephalus with significant loss of right brain parenchyma and no evidence of cerebrospinal fluid obstruction. Histological examination of the remaining brain parenchyma revealed a moderate multifocal cellular infiltrate;encephalomalacia; fibrosis; and hemosiderosis in the tissue adjacent to the dilated chambers. Other findings included vacuolar degeneration of the liver. The imaging diagnosis and the results of the postmortem examinations confirmed the diagnosis of ex vacuo hydrocephalus. To our knowledge, this is the first report of hydrocephalus in an Amazon parrot, as well as the first report of hydrocephalus in any bird species associated with long-term follow-up and long-term corticosteroid treatment.
FAQs
What are some facts about encephalomalacia? ›
Encephalomalacia is softening of the brain tissue which may lead to the brain changes and present with varied clinical manifestations. Most of the cases reported previously were in infants and children and almost all of them were related to neurological disorders.
What is the focus of encephalomalacia? ›Encephalomalacia is the softening or loss of brain tissue after cerebral infarction, cerebral ischemia, infection, craniocerebral trauma, or other injury. The term is usually used during gross pathologic inspection to describe blurred cortical margins and decreased consistency of brain tissue after infarction.
What effects does encephalomalacia have on the brain? ›These symptoms can include somnolence (extreme drowsiness), blindness, ataxia (wobbliness and lack of coordination), sleep walking, head pressing, circling, and, eventually, terminal coma. Also, depending on the location of the softened tissue, there can be different effects.
What are the different types of encephalomalacia? ›Cerebral softening, also known as encephalomalacia, is a localized softening of the substance of the brain, due to bleeding or inflammation. Three varieties, distinguished by their color and representing different stages of the disease progress, are known respectively as red, yellow, and white softening.
What are the risk factors for encephalomalacia? ›Encephalomalacia can be caused by stroke, or by severe brain swelling that interrupts cerebral blood flow. Removal of tumors may leave areas of brain softening, but one preventable cause is serious head trauma.
What are the long term effects of encephalomalacia? ›The long-term effects can be devastating. Any type of brain injury can result in significant motor and cognitive delays. It can result in different types of infections, and these injuries can have long lasting, permanent effects on children.
Can you heal encephalomalacia? ›After it is diagnosed, doctors will likely order a CT scan, which will help them determine when the softening began, and how much of the tissue has been lost to the condition. Currently, there is no cure for encephalomalacia. Once tissue in the brain is destroyed, there isn't a way to regain what's been lost.
How quickly does encephalomalacia progress? ›Multicystic encephalopathy can develop in a short time span (27 days after the incident in this study). As confessed by the perpetrator during police interrogation, abusive head trauma can be the result of a shaking incident alone.
What is encephalomalacia simple? ›a softness or degeneration of brain tissue, as caused by impairment of the blood supply; softening of the brain.
How do you fix encephalomalacia? ›There is no direct treatment or cure for encephalamalacia. However, doctors may attempt to treat the underlying cause of the condition, which cannot be reversed. In some cases, surgery may be performed to remove the part of the brain affected by the softening.
How bad is encephalomalacia? ›
Encephalomalacia after head trauma is a very serious condition with potentially lifelong consequences and residual motor, sensory and cognitive deficits. For more information, check out our 'Brain and Head Injury Fact Sheet'.
What is the presence of encephalomalacia? ›The terms "multicystic encephalomalacia" and "subcortical leucomalacia" (SCL) are used to describe the presence of areas of necrosis that develop into cystic lesions inside the brain. These lesions are generally due to severe asphyxia and/or hypotension.
Can encephalomalacia cause anxiety? ›It may have been precipitated by the frontal lobe encephalomalacia as right frontal lobe lesions are associated with disorganized behavior and anxiety [1], [2].
What does encephalomalacia look like on an MRI? ›Using MRI, encephalomalacia is recognized as a loss of brain matter and is typically isointense to cerebrospinal fluid on all sequences: T1 hypointense, T2 hyperintense, and FLAIR hypointense. However, encephalomalacia is very often associated with adjacent gliosis which is FLAIR hyperintense.
What is encephalomalacia with old insult? ›Encephalomalacia is an old term coined by pathologists to describe the macroscopic appearance of the brain following a variety of insults (e.g. cerebral infarction) and literally means "softening of the brain", as a result of liquefactive necrosis.
How long can a person live with encephalomalacia? ›Five children, three boys and two girls (mean age 57 days, range 8–142 days) who developed cystic encephalomalacia after inflicted traumatic brain injury were included. Survival ranged from 27 to 993 days.
How common is encephalomalacia in adults? ›In adults, although rare, cystic encephalomalacia can follow an acquired parenchymal brain injury such as infection [4], trauma [5], or infarction [6].
Is encephalomalacia a disability? ›Traumatic Brain Injury (TBI) or Encephalomalacia caused by head trauma can have a significant impact on your life, leaving you unable work or care for your self.