Controversial Final Years

2019 ◽  
pp. 451-478
Author(s):  
Stanley Finger
Keyword(s):  
Brain Damage ◽  
Strong Evidence ◽  
Cerebral Hemorrhage ◽  
Anterior Part ◽  
Brain Lesion ◽  
Georges Cuvier ◽  
Cortical Localization ◽  
The Brain

Gall remained a controversial figure throughout his life, which ended in Paris in 1828. In his later years, he continued to fight with Georges Cuvier, who had overseen the rejection of his and Spurzheim’s Mémoire to the Institut National in 1808, and with Cuvier’s protégé, physiologist Pierre Flourens. Flourens initially looked favorably on Gall’s doctrine, but during the 1820s his brain lesion experiments on birds and other animals were heralded by the French élite as strong evidence against cortical localization of function. Despite this formidable opposition, Gall did find a supporter of localization of function in physician Jean-Baptiste Bouillaud, who started reporting in 1825 that lesions of the anterior part of the brain are more likely to affect speech than posterior brain damage. Gall’s health began to fail a year later, when he was 68 and began to have strokes. After he succumbed to a cerebral hemorrhage in 1828, his body was buried in Paris’ Cimetiére du Pére-Lachaise, but not his skull, which was examined by his followers and added to his collection. Gall’s organologie, now regarded as phrénologie, now began an even steeper decline in France and throughout the Continent, although “popular phrenology,” with less emphasis on the underlying science, continued to be influential on British and American landscapes.

Rehabilitation of Attention

2003 ◽  
Vol 14 (3) ◽  
pp. 165-170 ◽  
Author(s):  
Ian H. Robertson
Keyword(s):  
Brain Damage ◽  
Dependent Plasticity ◽  
Attention Systems ◽  
The Brain

Abstract: In this paper, evidence is reviewed for separable attention systems in the brain, and it is argued a) that attention may have a privileged role in mediating experience dependent plasticity in the brain and b) that at least some types of attention may be capable of rehabilitation following brain damage.

Aetiologies and anatomy of confabulation

2017 ◽  
Author(s):  
Armin Schnider
Keyword(s):  
Brain Damage ◽  
Limbic Encephalitis ◽  
Artery Aneurysm ◽  
Anterior Communicating Artery ◽  
Brain Areas ◽  
Anatomical Basis ◽  
Korsakoff Syndrome ◽  
Hypoxic Brain ◽  
Degenerative Dementia ◽  
The Brain

What diseases cause confabulations and which are the brain areas whose damage is responsible? This chapter reviews the causes, both historic and present, of confabulations and deduces the anatomo-clinical relationships for the four forms of confabulation in the following disorders: alcoholic Korsakoff syndrome, traumatic brain injury, rupture of an anterior communicating artery aneurysm, posterior circulation stroke, herpes and limbic encephalitis, hypoxic brain damage, degenerative dementia, tumours, schizophrenia, and syphilis. Overall, clinically relevant confabulation is rare. Some aetiologies have become more important over time, others have virtually disappeared. While confabulations seem to be more frequent after anterior brain damage, only one form has a distinct anatomical basis.

Relief of facial pain after combined removal of precentral and postcentral cortex

1971 ◽  
Vol 34 (4) ◽  
pp. 537-543 ◽  
Author(s):  
Richard A. Lende ◽  
Wolff M. Kirsch ◽  
Ralph Druckman
Keyword(s):  
Facial Pain ◽  
The Other ◽  
Precentral Gyrus ◽  
Nerve Section ◽  
Content Type ◽  
Burning Pain ◽  
Cortical Localization ◽  
The Brain ◽  
Fine Print ◽  
Frontal Lobotomy

✓ Cortical removals which included precentral and postcentral facial representations resulted in relief of facial pain in two patients. Because of known failures following only postcentral (SmI) ablations, these operations were designed to eliminate also the cutaneous afferent projection to the precentral gyrus (MsI) and the second somatic sensory area (SmII). In one case burning pain developed after a stroke involving the brain stem and was not improved by total fifth nerve section; prompt relief followed corticectomy and lasted until death from heart disease 20 months later. In the other case persistent steady pain that developed after fifth rhizotomy for trigeminal neuralgia proved refractory to frontal lobotomy; relief after corticectomy was immediate and has lasted 14 months. Cortical localization was established by stimulation under local anesthesia. Each removal extended up to the border of the arm representation and down to the upper border of the insula. Such a resection necessarily included SmII, and in one case responses presumably from SmII were obtained before removal. The suggestions of Biemond (1956) and Poggio and Mountcastle (1960) that SmII might be concerned with pain sensibility may be pertinent in these cases.

scholarly journals UV-induced neuronal degeneration in the rat cerebral cortex

2021 ◽  
Author(s):  
Mariko Nakata ◽  
Masayuki Shimoda ◽  
Shinya Yamamoto
Keyword(s):  
Uv Irradiation ◽  
Neuronal Degeneration ◽  
Uv Light ◽  
Brain Lesion ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Heme Oxygenase 1 ◽  
Dependent Manner ◽  
Focal Brain Injury ◽  
The Brain ◽  
And Oxidative Stress

Abstract Irradiation with ultraviolet (UV) light on the cortical surface can induce a focal brain lesion (UV lesion) in rodents. In the present study, we investigated the process of establishing a UV lesion. Rats underwent UV irradiation (365 nm wavelength, 2.0 mWh) over the dura, and time-dependent changes in the cortical tissue were analyzed histologically. We found that the majority of neurons in the lesion started to degenerate within 24 hours and the rest disappeared within 5 days after irradiation. UV-induced neuronal degeneration progressed in a layer-dependent manner. Moreover, UV-induced terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) positivity and heme oxygenase-1 (HO-1) immunoreactivity were also detected. These findings suggest that UV irradiation in the brain can induce gradual neural degeneration and oxidative stress. Importantly, UV vulnerability may vary among cortical layers. UV-induced cell death may be due to apoptosis; however, there remains a possibility that UV-irradiated cells were degenerated via processes other than apoptosis. The UV lesion technique will not only assist in investigating brain function at a targeted site but may also serve as a pathophysiological model of focal brain injury and/or neurodegenerative disorders.

Arteriovenous malformations in the posterior fossa

1977 ◽  
Vol 47 (1) ◽  
pp. 50-56 ◽  
Author(s):  
Hiroshi Matsumura ◽  
Yasumasa Makita ◽  
Kuniyuki Someda ◽  
Akinori Kondo
Keyword(s):  
Arteriovenous Malformation ◽  
Brain Stem ◽  
Posterior Fossa ◽  
Arteriovenous Malformations ◽  
Cerebellopontine Angle ◽  
Anterior Part ◽  
Content Type ◽  
The Brain ◽  
Fine Print

✓ We have operated on 12 of 14 cases of arteriovenous malformation (AVM) in the posterior fossa since 1968, with one death. The lesions were in the cerebellum in 10 cases (three anteromedial, one central, three lateral, and three posteromedial), and in the cerebellopontine angle in two; in two cases the lesions were directly related to the brain stem. The AVM's in the anterior part of the cerebellum were operated on through a transtentorial occipital approach.

scholarly journals Zingiber officinaleMitigates Brain Damage and Improves Memory Impairment in Focal Cerebral Ischemic Rat

2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Jintanaporn Wattanathorn ◽  
Jinatta Jittiwat ◽  
Terdthai Tongun ◽  
Supaporn Muchimapura ◽  
Kornkanok Ingkaninan
Keyword(s):  
Cognitive Function ◽  
Cerebral Ischemia ◽  
Brain Damage ◽  
Focal Cerebral Ischemia ◽  
Infarct Volume ◽  
Neuroprotective Effect ◽  
Morris Water Maze Test ◽  
Brain Infarct ◽  
Ginger Rhizome ◽  
The Brain

Cerebral ischemia is known to produce brain damage and related behavioral deficits including memory. Recently, accumulating lines of evidence showed that dietary enrichment with nutritional antioxidants could reduce brain damage and improve cognitive function. In this study, possible protective effect ofZingiber officinale, a medicinal plant reputed for neuroprotective effect against oxidative stress-related brain damage, on brain damage and memory deficit induced by focal cerebral ischemia was elucidated. Male adult Wistar rats were administrated an alcoholic extract of ginger rhizome orally 14 days before and 21 days after the permanent occlusion of right middle cerebral artery (MCAO). Cognitive function assessment was performed at 7, 14, and 21 days after MCAO using the Morris water maze test. The brain infarct volume and density of neurons in hippocampus were also determined. Furthermore, the level of malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) in cerebral cortex, striatum, and hippocampus was also quantified at the end of experiment. The results showed that cognitive function and neurons density in hippocampus of rats receiving ginger rhizome extract were improved while the brain infarct volume was decreased. The cognitive enhancing effect and neuroprotective effect occurred partly via the antioxidant activity of the extract. In conclusion, our study demonstrated the beneficial effect of ginger rhizome to protect against focal cerebral ischemia.

Race and Rorschach Signs of Brain Damage in Cerebral Thrombosis

1966 ◽  
Vol 22 (2) ◽  
pp. 655-662 ◽  
Author(s):  
Ray B. Evans ◽  
Jessie Marmorston
Keyword(s):  
Myocardial Infarction ◽  
Brain Damage ◽  
Cerebral Thrombosis ◽  
The Brain ◽  
Item Scale

In an attempt to identify Rorschach signs which would differentiate the brain-damaged regardless of race, a study was made of 225 Caucasian and 127 Negro patients between 40 and 80 yr. of age. There was known brain damage (cerebral thrombosis) in 204 patients, and no known brain damage in 148 patients (myocardial infarction). Each of 31 Rorschach signs of cerebral impairment was studied to determine its power in discriminating Caucasian damaged from nondamaged and Negro damaged from nondamaged patients. A combination of 13 signs was thereby selected in which race did not appear to be a significant factor. The 13-item scale differentiated brain-damaged from nondamaged Caucasian, Negro, and combined Caucasian-Negro groups, all at levels below .001. The 13-item scale correctly classified 71% of the patients, compared with 73% when all 31 signs were used.

scholarly journals Three-dimensional cultured mesenchymal stem cells enhance repair of ischemic stroke through inhibition of microglia

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Yuejiao Li ◽  
Yankai Dong ◽  
Ye Ran ◽  
Yanan Zhang ◽  
Boyao Wu ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Ischemic Stroke ◽  
Proinflammatory Cytokines ◽  
Infarct Volume ◽  
Brain Lesion ◽  
Three Dimensional ◽  
Artery Occlusion ◽  
Rna Seq ◽  
The Brain

Abstract Background We show previously that three-dimensional (3D) spheroid cultured mesenchymal stem cells (MSCs) exhibit reduced cell size thus devoid of lung entrapment following intravenous (IV) infusion. In this study, we determined the therapeutic effect of 3D-cultured MSCs on ischemic stroke and investigated the mechanisms involved. Methods Rats underwent middle cerebral artery occlusion (MCAO) and reperfusion. 1 × 106 of 3D- or 2D-cultured MSCs, which were pre-labeled with GFP, were injected through the tail vain three and seven days after MCAO. Two days after infusion, MSC engraftment into the ischemic brain tissues was assessed by histological analysis for GFP-expressing cells, and infarct volume was determined by MRI. Microglia in the lesion were sorted and subjected to gene expressional analysis by RNA-seq. Results We found that infusion of 3D-cultured MSCs significantly reduced the infarct volume of the brain with increased engraftment of the cells into the ischemic tissue, compared to 2D-cultured MSCs. Accordingly, in the brain lesion of 3D MSC-treated animals, there were significantly reduced numbers of amoeboid microglia and decreased levels of proinflammatory cytokines, indicating attenuated activation of the microglia. RNA-seq of microglia derived from the lesions suggested that 3D-cultured MSCs decreased the response of microglia to the ischemic insult. Interestingly, we observed a decreased expression of mincle, a damage-associated molecular patterns (DAMPs) receptor, which induces the production of proinflammatory cytokines, suggestive of a potential mechanism in 3D MSC-mediated enhanced repair to ischemic stroke. Conclusions Our data indicate that 3D-cultured MSCs exhibit enhanced repair to ischemic stroke, probably through a suppression to ischemia-induced microglial activation.

scholarly journals GANGGUAN BERBAHASA PADA PENDERITA CEREBRAL PALSY SEBUAH KAJIAN LINGUISTIK KLINIS

2020 ◽  
Vol 6 (2) ◽  
pp. 175-186
Author(s):  
Agus Syahid
Keyword(s):  
Cerebral Palsy ◽  
Brain Damage ◽  
Language Disorders ◽  
Motor Center ◽  
The People ◽  
Children With Cerebral Palsy ◽  
The Brain ◽  
Motor Disturbances

This study describes language disorders in the people with cerebral palsy and what kind of treatments to people with cerebral palsy related to language disorders. Cerebral palsy is a series of disorders with problems regulating muscle movements where it is as a result of some damage to the motor centers in the brain. Damage to the motor center in the brain that causes cerebral palsy can occur prenatal (before birth), perinatal (during the birth), or even postnatal (immediately after birth). There are several main problems that are often found and faced by children with cerebral palsy, they are: (1) difficulty in eating and swallowing caused by motor disturbances in the mouth, (2) difficulty in speaking, (3) difficulty in hearing, and (4) language disorders.

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