scholarly journals EFFECT OF BASTI AND NASYA IN HEMORRHAGIC STROKE SPECIFICALLY ON BARTHEL INDEX, GRIP POWER AND NIH STROKE SCALE: A PILOT STUDY

2020 ◽  
Vol 11 (10) ◽  
pp. 33-36
Author(s):  
Jui V Gundo ◽  
Ashish A Thatere ◽  
Vaishali K Gajbhiye ◽  
Shweta P Deolekar ◽  
Prakash R Kabra

Cerebrovascular diseases include some of the most common and devastating disorders; ischemic stroke and hemorrhagic stroke. Intracranial hemorrhage usually results from rupture of blood vessel within the brain parenchyma but may also occur in patients with subarachnoid haemorrhage, if the artery ruptures into the brain substance as well as into the subarachnoid space. It produces neurological symptoms by producing mass effect on neural structures, from the toxic effects of blood itself or by increasing intracranial pressure. According to Ayurved hemorrhagic stroke can be linked with Urdhva Raktapitta. Chikitsa of Urdhva Raktapitta was Virechana and Adho Raktapitta was Vamana as stated by Charak. So initial management was planned to stabilize Prakupit Dosha and hence Basti and Nasya were selected in these 5 patients of pilot study. Observations and results obtained were encouraging and assessed on different parameters which are presented in full paper. The patients of acute hemorrhagic stroke (not less than 1yr) were selected on the basis of CT/ MRI of brain and sign- symptoms of stroke. Observation and results are mention by applying appropriate statistical tests. Clinically encouraging results were observed on signs and symptoms. Statistically significant results were observed on parameters. These results are presented in full paper in details. Combination of this Ayurvedic treatment can be helpful in treating the cases of hemorrhagic stroke however the study on the larger compound will be helpful to validate its effect on hemorrhagic stroke.

2021 ◽  
Vol 22 (1) ◽  
pp. 83-86
Author(s):  
O. A. Kicherova ◽  
◽  
L. I. Reikhert ◽  
O. N. Bovt ◽  
◽  
...  

In recent years, cerebral vascular diseases have been increasingly detected in young patients. It is due not only to better physicians’ knowledge about this pathology, but also to the improvement of its diagnosis methods. Modern neuroimaging techniques allow us to clarify the nature of hemorrhage, to determine the volume and location of intracerebral hematoma, and to establish the degree of concomitant edema and dislocation of the brain. However, despite the high accuracy of the research, it is not always possible to establish the cause that led to a brain accident, which greatly affects the tactics of management and outcomes in this category of patients. A special feature of the structure of cerebrovascular diseases of young people is the high proportion of hemorrhagic stroke, the causes of which are most often arterio-venous malformations. Meanwhile, there are a number of other causes that can lead to hemorrhage into the brain substance. These include disorders of blood clotting, and various vasculitis, and exposure to toxic substances and drugs, and tumor formations (primary and secondary). All these pathological factors outline the range of diagnostic search in young patients who underwent hemorrhagic stroke. Diagnosis of these pathological conditions with the help of modern visualization techniques is considered to be easy, but this is not always the case. In this article, the authors give their own clinical observation of a hemorrhagic stroke in a young patient, which demonstrates the complexity of the diagnostic search in patients with this pathology.


PEDIATRICS ◽  
1988 ◽  
Vol 82 (6) ◽  
pp. 931-934
Author(s):  
HENRY M. FEDER ◽  
EDWIN L. ZALNERAITIS ◽  
LOUIS REIK

Nervous system involvement in Lyme disease was originally described as meningitis, cranial neuritis, and radiculoneuritis,1-3 but Lyme disease can also involve the brain parenchyma. We describe a child whose first manifestation of Lyme disease was an acute, focal meningoencephalitis with signs and symptoms such as fever, headache, slurred speech, hemiparesis, seizure, and CSF pleocytosis. CASE REPORT A 7-year-old boy was hospitalized Aug 27, 1985, because of hemiparesis. Six weeks prior to admission he had vacationed at Old Lyme, CT. There was no history of rash or tick bite. He had been well until eight hours prior to admission when fever and headache developed.


Author(s):  
Tom Solomon ◽  
Benedict Michael

Neurological infections can be broadly subdivided into chronic/subacute and acute. Chronic/subacute infection usually presents with global cognitive decline, with the prototypical disease being progressive multifocal leucoencephalopathy due to infection with the JC virus in immunocompromised patients. Acute neurological infections can be defined microbiologically, by the nature of the pathogen; clinically, by the presenting signs and symptoms and initial CSF findings; or anatomically. The anatomical definitions are those occurring intracranially (‘meningitis’, where infection involves the meninges overlying the brain; ‘encephalitis’, where the brain parenchyma is involved; or ‘cerebral abscesses’) and those affecting the spinal cord (‘myelitis’). However, there is often both clinical and histological overlap between these syndromes; consequently, the terms ‘meningoencephalitis’ and ‘encephalomyelitis’ are often used. Patients with acute intracranial CNS infections provide the greatest challenge to general physicians, because urgent investigation and appropriate treatment can save lives; they therefore form the focus of this chapter.


2021 ◽  
Author(s):  
Karine Felipe Martins ◽  
Flávia Pascoal Teles ◽  
Amanda Fernandes de Sousa Oliveira Balestra ◽  
Isadora Rosa Maia

Background: Until the 70s, cerebrovascular diseases (CVDs) were neglected to the lack of resources. However, due to the advancement of technology, several imaging tests have appeared, such as magnetic resonance and computed tomography, which facilitated the diagnosis and the understanding of the pathophysiology of each disease. Objectives: The objective of this work is to identify the main CVDs signs and symptoms. Methods: An integrative literature review was carried out based on selected articles from Google Scholar, PubMed and SciELO, using the terms headache, cerebrovascular disease, neurology. Results: CVDs are characterized by causing damage to brain vessels, due to changes in blood flow momentarily or permanently in an area of the brain, allowing them to be classified as ischemic or hemorrhagic. In ischemic there is a blockage of blood flow and, consequently, of oxygen to areas of the brain, in hemorrhagic rupture of a vessel occurs and, with this, blood leakage. Therefore, it is necessary to recognize the signs and symptoms early, in order to prevent loss of neurological function, movements on one side of the body and the presence or absence of headaches in both patients, with ischemic CVD and hemorrhagic CVD prevent rapid loss of consciousness accompanied by severe headache. Such signs and symptoms associated with the patient’s family history and lifestyle can help in the diagnosis of this disease. Conclusion: Therefore, it is important to recognize the signs and symptoms of CVDs, in order to determine the treatment and advise the patient, which will guarantee a better prognosis.


Author(s):  
Yareeda Sireesha ◽  
Niloufer Ali ◽  
Mathukumalli Neeharika ◽  
Meena Angamattu Kanikannan

:Infarction of the basal ganglia after minor head injury �is a� well described entity .�Mineralising angiopathy� is a term to describe mineralisation along� the lenticulostriate vessels that predisposes infants to stroke,even after trivial head injury.(1)The prognosis in these children is excellent.The supratentorial compartment is relatively mobile in comparision to the fixed infratentorial compartment �offering greater shearing forces between the perforating vessels and the brain parenchyma following �an acute trauma.(2)The acute angulation of the lenticulostriate perforators is further responsible for its propensity of the basal ganglia for the insult.(3) The current report is unique as it presents a young boy with hemorrhagic stroke in the�� basal ganglia after a trivial trauma and �imaging findings suggestive of mineralising angiopathy


2021 ◽  
Author(s):  
Kiran Thakur ◽  
Emily H Miller ◽  
Michael D Glendinning ◽  
Osama Al Dalahmah ◽  
Matei Banu ◽  
...  

Many patients with SARS-CoV-2 infection develop neurological signs and symptoms, though, to date, little evidence exists that primary infection of the brain is a significant contributing factor. We present the clinical, neuropathological, and molecular findings of 41 consecutive patients with SARS-CoV-2 infections who died and underwent autopsy in our medical center. The mean age was 74 years (38-97 years), 27 patients (66%) were male and 34 (83%) were of Hispanic/Latinx ethnicity. Twenty-four patients (59%) were admitted to the intensive care unit (ICU). Hospital-associated complications were common, including 8 (20%) with deep vein thrombosis/pulmonary embolism (DVT/PE), 7 (17%) patients with acute kidney injury requiring dialysis, and 10 (24%) with positive blood cultures during admission. Eight (20%) patients died within 24 hours of hospital admission, while 11 (27%) died more than 4 weeks after hospital admission. Neuropathological examination of 20-30 areas from each brain revealed hypoxic/ischemic changes in all brains, both global and focal; large and small infarcts, many of which appeared hemorrhagic; and microglial activation with microglial nodules accompanied by neuronophagia, most prominently in the brainstem. We observed sparse T lymphocyte accumulation in either perivascular regions or in the brain parenchyma. Many brains contained atherosclerosis of large arteries and arteriolosclerosis, though none had evidence of vasculitis. Eighteen (44%) contained pathologies of neurodegenerative diseases, not unexpected given the age range of our patients. We examined multiple fresh frozen and fixed tissues from 28 brains for the presence of viral RNA and protein, using quantitative reverse-transcriptase PCR (qRT- PCR), RNAscope, and immunocytochemistry with primers, probes, and antibodies directed against the spike and nucleocapsid regions. qRT-PCR revealed low to very low, but detectable, viral RNA levels in the majority of brains, although they were far lower than those in nasal epithelia. RNAscope and immunocytochemistry failed to detect viral RNA or protein in brains. Our findings indicate that the levels of detectable virus in COVID-19 brains are very low and do not correlate with the histopathological alterations. These findings suggest that microglial activation, microglial nodules and neuronophagia, observed in the majority of brains, do not result from direct viral infection of brain parenchyma, but rather likely from systemic inflammation, perhaps with synergistic contribution from hypoxia/ischemia. Further studies are needed to define whether these pathologies, if present in patients who survive COVID-19, might contribute to chronic neurological problems.


Author(s):  
Tyler Martinez

Encephalitis is an inflammation of the brain parenchyma, typically due to a viral infection. Pure encephalitis will lack the signs and symptoms of meningeal irritation (eg, stiff neck and photophobia). New-onset seizures, cognitive deficits, new psychiatric symptoms, lethargy/coma, cranial nerve abnormalities, or movement disorders should alert the clinician to possible encephalitis. It is important to question the patient about foreign travel, immunocompromised state, and potential exposures. Empiric treatment for presumed viral encephalitis is with the antiviral acyclovir. Empiric broad-spectrum antibiotics are also typically given to cover for possible bacterial meningitis. If there are signs of elevated intracranial pressure (ICP), neurosurgical consultation should be obtained for possible decompressive craniotomy. Standard therapy for ICP (ie, hyperventilation, steroids, mannitol, hypertonic saline, and elevation of the head of the bed) should also be considered. The most concerning complication of encephalitis is the development of life-threatening cerebral edema with resultant brainstem compression and herniation.


1980 ◽  
Vol 53 (5) ◽  
pp. 698-702 ◽  
Author(s):  
Kazuo Miyasaka ◽  
Hidetoshi Takei ◽  
Mikio Nomura ◽  
Sinji Sugimoto ◽  
Toshimitsu Aida ◽  
...  

✓ Changes in the brain parenchyma and cerebrospinal fluid spaces were demonstrated in three cases of dural arteriovenous malformations by computerized tomography (CT). In various combinations, there were 1) vermiform or patchy enhancement after intravenous contrast infusion, 2) abnormal decreased density mainly in the white matter, 3) local mass effect, 4) hydrocephalus, 5) dilatation of the major venous sinus system, and 6) prominent vascular grooving of the skull inner table. Most of these changes were secondary to raised sinus pressure caused by arteriovenous shunt. It was also demonstrated by serial CT that some elements improved after artificial embolization or surgical excision of the malformations.


2006 ◽  
Vol 21 (1) ◽  
pp. 1-9 ◽  
Author(s):  
Francesco Maiuri ◽  
Paolo Cappabianca ◽  
Michelangelo Gangemi ◽  
Marialaura Del Basso De Caro ◽  
Felice Esposito ◽  
...  

Object The authors studied the expression of angiogenic and growth factors and various proliferative indices in cavernous angiomas of the brain. The goal was to define whether the often progressive clinical course of both sporadic and familial forms of the lesion is correlated with different expression of these factors. Methods Forty-three cavernomas of the brain were investigated with immunohistochemical studies and stained for four growth factors (vascular endothelial growth factor [VEGF], tenascin, transforming growth factor–β [TGFβ], and platelet-derived growth factor [PDGF]), and for Ki-67 and bcl-2. The intensity of expression was tested in all cases in the walls of cavernoma vessels, in the perivascular tissue, and in the perilesional brain parenchyma. Among the 43 cavernomas, 32 were stable and sporadic single lesions less than 2 cm in size, whereas 11 were cavernomas larger than 2 cm (up to 6 cm). These larger cavernomas had more aggressive behavior (documented growth in five cases, mass effect in eight, significant hemorrhage in four), familial occurrence (six cases), and/or multiple lesions (five cases). The expression of VEGF, tenascin, and PDGF in cavernomas did not significantly differ in the two groups of patients, whereas TGFβ expression was higher in the more aggressive forms of cavernomas. The expression of Ki-67 and bcl-2 was always absent in stable lesions, and it was positive in eight (72.7%) of 11 aggressive lesions. The perilesional brain parenchyma showed a significantly higher expression of TGFβ, PDGF, and tenascin in more aggressive cavernomas. Conclusions The familial occurrence and more aggressive clinical behavior of cavernous angiomas of the brain are associated with higher expression of Ki-67 and bcl-2 in the cavernoma tissue, as in other proliferative lesions. These features are also associated with higher expression of some growth factors (excluding VEGF) in the perilesional brain parenchyma, suggesting that the neighboring vasculature and glia may be predisposed to and recruited for further growth and progression.


Brain ◽  
2021 ◽  
Author(s):  
Kiran T Thakur ◽  
Emily Happy Miller ◽  
Michael D Glendinning ◽  
Osama Al-Dalahmah ◽  
Matei A Banu ◽  
...  

Abstract Many patients with SARS-CoV-2 infection develop neurological signs and symptoms, though, to date, little evidence exists that primary infection of the brain is a significant contributing factor. We present the clinical, neuropathological, and molecular findings of 41 consecutive patients with SARS-CoV-2 infections who died and underwent autopsy in our medical center. The mean age was 74 years (38–97 years), 27 patients (66%) were male and 34 (83%) were of Hispanic/Latinx ethnicity. Twenty-four patients (59%) were admitted to the intensive care unit (ICU). Hospital-associated complications were common, including 8 (20%) with deep vein thrombosis/pulmonary embolism (DVT/PE), 7 (17%) patients with acute kidney injury requiring dialysis, and 10 (24%) with positive blood cultures during admission. Eight (20%) patients died within 24 hours of hospital admission, while 11 (27%) died more than 4 weeks after hospital admission. Neuropathological examination of 20–30 areas from each brain revealed hypoxic/ischemic changes in all brains, both global and focal; large and small infarcts, many of which appeared hemorrhagic; and microglial activation with microglial nodules accompanied by neuronophagia, most prominently in the brainstem. We observed sparse T lymphocyte accumulation in either perivascular regions or in the brain parenchyma. Many brains contained atherosclerosis of large arteries and arteriolosclerosis, though none had evidence of vasculitis. Eighteen (44%) contained pathologies of neurodegenerative diseases, not unexpected given the age range of our patients. We examined multiple fresh frozen and fixed tissues from 28 brains for the presence of viral RNA and protein, using quantitative reverse-transcriptase PCR (qRT-PCR), RNAscope, and immunocytochemistry with primers, probes, and antibodies directed against the spike and nucleocapsid regions. qRT-PCR revealed low to very low, but detectable, viral RNA levels in the majority of brains, although they were far lower than those in nasal epithelia. RNAscope and immunocytochemistry failed to detect viral RNA or protein in brains. Our findings indicate that the levels of detectable virus in COVID-19 brains are very low and do not correlate with the histopathological alterations. These findings suggest that microglial activation, microglial nodules and neuronophagia, observed in the majority of brains, do not result from direct viral infection of brain parenchyma, but rather likely from systemic inflammation, perhaps with synergistic contribution from hypoxia/ischemia. Further studies are needed to define whether these pathologies, if present in patients who survive COVID-19, might contribute to chronic neurological problems.


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