scholarly journals Drug-induced ischemic stroke

2021 ◽  
pp. 42-49
Author(s):  
T. M. Ostroumova ◽  
O. D. Ostroumova ◽  
Yu. A. Filippova
Keyword(s):  
Ischemic Stroke ◽  
Drug Prescription ◽  
Cerebral Arteries ◽  
Sudden Onset ◽  
Prevention Measures ◽  
Drug Induced ◽  
The Central Nervous System ◽  
Acute Disturbance ◽  
Inflammatory Drugs ◽  
High Doses

Stroke is an acute disturbance of the blood supply to the brain, characterized by the sudden onset of focal neurological symptoms, which persists for more than 24 hours or leads to the death of the patient in a shorter period of time due to cerebrovascular pathology. In the world and in Russia, stroke remains one of the leading causes of death and disability. At the same time, ischemic stroke (IS) is more common – about 80% of cases. Many classes of drugs, such as oral contraceptives, nonsteroidal anti-inflammatory drugs, and various psychoactive substances, can contribute to the development of drug-induced IS (DI IS). Data upon the frequency of DI IS is limited. In part, this reflects the problem of identifying and confirming the causal relationship between drug prescription and the development of IS. DI IS risk factors include: abuse of caffeine and alcohol, older age, smoking, drug addiction, high doses of drugs containing provoking agents, the simultaneous use of several drugs, the presence of comorbid diseases. Adverse drug reactions develop due to the following pathophysiological mechanisms: cerebral embolism, vasoconstriction of cerebral arteries, vasculitis of the central nervous system, orthostatic hypotension. The management of a patient with a DI IS does not differ significantly from the management of a patient with IS of a different etiology and includes thrombolysis or mechanical thromboextraction (in the absence of contraindications), as well as rational methods of secondary prevention. It is necessary to completely cancel or reduce the dose of the drug, the use of which led to the development of a stroke. DI IS prevention measures include the choice of drugs with the lowest risk of its occurrence and the use of modern scales for assessing the risk of this phenomenon.

Some groups of drugs which use is associated with development of drug-induced atrial fibrillation

2021 ◽  
Vol 1 (11) ◽  
pp. 20-28
Author(s):  
O. D. Ostroumova ◽  
M. S. Cherniaeva ◽  
D. I. Bakhteeva ◽  
N. A. Arablinskiy ◽  
D. A. Sychyov
Keyword(s):  
Atrial Fibrillation ◽  
Bisphosphonate Therapy ◽  
Nandrolone Decanoate ◽  
Drug Induced ◽  
Genitourinary System ◽  
Increased Risk ◽  
The Central Nervous System ◽  
Inflammatory Drugs ◽  
High Doses ◽  
Cyclooxygenase 2 Inhibitors

Recently, more and more attention has been paid to the problem of drug‑induced (DI) atrial fibrillation (AF). It is known that the development of DI AF can be associated with the intake of cardiovascular and anticancer drugs, drugs that affect the central nervous system or respiratory organs. However, there are other drugs that can provoke DI AF, which practitioners are less aware of. This article is a review of the current literature on DI AF associated with the intake of other groups of drugs and individual drugs that are not included in the above groups. Analysis of the available literature has shown that the incidence of DI AF reaches 6.9% when taking zoledronic acid and 1.5% when taking alendronate, although data from different authors regarding the causal relationship between bisphosphonate therapy and the development of AF are ambiguous. The use of high doses of glucocorticosteroids (at a daily dose of ≥ 7.5 mg in terms of prednisolone) is also associated with an increased risk of AF (OR = 6.07; 95% CI: 3.90–9.42). Treatment with non‑steroidal anti‑inflammatory drugs is also associated with a higher risk of developing DI AF compared to those who do not use it – the incidence rate is 1.17 (95% CI: 1.10–1.24) for nonselective and 1.27 (95% CI: 1.20–1.34) for cyclooxygenase‑2 inhibitors. The literature contains a description of clinical cases of DI AF while taking immunosuppressants (azathioprine, methotrexate + etanercept, fingolimod, cyclosporine), drugs that affect the genitourinary system (vardenafil, sildenafil, yohimbine hydrochloride, hexoprenaline), local anesthetics, bupacaero testosterone, stanozolol, testosterone cypionate, nandrolone decanoate extraboline) and nicotine‑containing products (nicotine‑containing chewing gum).

scholarly journals Ischemic stroke with agraphestesia signal focus

2021 ◽  
Author(s):  
Ana Luísa Lopes Espínola da Costa Reis ◽  
Leonardo Henrique Gandolfi de Souza ◽  
Vitor Roberto Pugliesi Marques
Keyword(s):  
Atrial Fibrillation ◽  
Ischemic Stroke ◽  
Parietal Lobe ◽  
Cerebral Arteries ◽  
Sudden Onset ◽  
Neurological Deficits ◽  
Motor Deficits ◽  
Ischemic Event ◽  
The Right ◽  
Sensory Ability

Introduction: The ischemic stroke is one of the main causes of death and disability in Brazil. Among the main risk factors are age, atrial fibrillation (AF), diabetes, dyslipidemia and physical inactivity. The main etiology of stroke is cardioembolic, resulting in obstruction of the cerebral arteries by a thrombus of cardiac origin. The artery most affected in ischemic strokes is the middle cerebral artery. The stroke has main characteristics, with emphasis on the sudden onset of symptoms, involvement of a focal area, ischemia caused by obstruction of a vessel and neurological deficits depending on the affected area. Graphesthesia is defined as a cutaneous sensory ability to recognize letters or numbers traced on the skin. The loss of this sensory ability is known as agraphesthesia. Case Report: M.A.F.O. female, 78a, arrived at the UPA complaining of mental confusion. Patient denies previous stroke. Personal history of systemic arterial hypertension. Upon physical examination, the patient was conscious, self and disoriented and inattentive. He was able to repeat and evoke words, without measurable motor déficits. Left upper limb with agraphestesia. Computed tomography was requested, which showed an extensive hypodense area in the right parietoccipital region, which leads to the erasure of the furrows between the adjacent gyres, which may correspond to a recent ischemic event. Magnetic resonance imaging, diffusion-restricted area with correspondence on the ADC map, located in the right temporoparietal region inferring an acute ischemic event. An electrocardiogram was also requested, which showed an irregular rhythm, characteristic of atrial fibrillation, resulting in a diagnostic hypothesis of cardioembolic ischemic stroke. Discussion: The involvement of post-central ischemic gyrus lesions may correspond to paresthesia, anesthesia, hypoesthesia; the involvement of secondary and terciary areas of sensitivity in the upper parietal lobe, especially in the active movements of the hand and in the modalities of integrated sensitivity, their lesions may be clinically affected by: apraxias, dysgraphias, hemineglect, agraphestesia, stereoagnosia and spacial disorientation.

Drugs associated with drug-induced pancreatitis: focus on rarely discussed drugs

2021 ◽  
Vol 1 (29) ◽  
pp. 33-39
Author(s):  
A. V. Filippova ◽  
E. E. Pavleeva ◽  
O. D. Ostroumova
Keyword(s):  
Central Nervous System ◽  
Acute Pancreatitis ◽  
Acute Inflammation ◽  
World Health ◽  
Antitumor Drugs ◽  
Drug Induced ◽  
The World ◽  
The Central Nervous System ◽  
Inflammatory Drugs ◽  
Health Organization

More than 500 medicines are included in the database of the World Health Organization as drugs that can cause acute inflammation of the pancreas. Drug-induced acute pancreatitis develops against the background of taking many medications (statins, antitumor drugs, drugs for the treatment of diseases of the gastrointestinal tract, analgesics and anti-inflammatory drugs, antimicrobial, antiparasitic and antiviral drugs, drugs for the treatment of tuberculosis, diseases of the central nervous system, estrogens, calcium preparations, etc.) from different classes, while the clinical picture does not differ from pancreatitis of other etiology. Based on this, it is worth paying attention to the reasons that contributed to the development of this pathology. Therefore, one of the main principles of the diagnosis of drug-induced pancreatitis is a thorough collection of a pharmacological history. If you suspect that pancreatitis was caused by a drug, you should immediately stop using it and start traditional therapeutic treatment.

scholarly journals A Case of Turner Syndrome with Multiple Embolic Infarcts

2016 ◽  
Vol 8 (3) ◽  
pp. 199-203 ◽  
Author(s):  
Cindy W. Yoon ◽  
Eungseok Lee ◽  
Byung-Nam Yoon ◽  
Hee-Kwon Park ◽  
Joung-Ho Rha
Keyword(s):  
Ischemic Stroke ◽  
Magnetic Resonance ◽  
Turner Syndrome ◽  
Cerebral Arteries ◽  
Brain Mri ◽  
Brain Magnetic Resonance Imaging ◽  
Holter Monitoring ◽  
Sudden Onset ◽  
Embolic Stroke ◽  
Mri Findings

Only a few cases of Turner syndrome (TS) with ischemic stroke have been reported. Various arteriopathies of the cerebral arteries, including fibromuscular dysplasia, congenital hypoplasia, moyamoya syndrome, and premature atherosclerosis have been assumed to be the cause of ischemic stroke in TS. There has been no case report of a TS patient presenting with an embolic stroke pattern without any cerebral arteriopathy. A 28-year-old woman with TS was referred to our hospital because of abnormal brain magnetic resonance imaging (MRI) findings. She underwent brain MRI at the referring hospital because she experienced sudden-onset diffuse headache. Diffusion-weighted imaging revealed multiple acute embolic infarcts in different vascular territories. Intracranial and extracranial arterial disease was not detected on cerebral magnetic resonance angiography and carotid sonography. Embolic source workups, including transthoracic and transesophageal echocardiography, Holter monitoring, and transcranial Doppler shunt study, were all negative. Hypercoagulability and vasculitis panels were also negative. Our patient was diagnosed with cryptogenic embolic stroke. This is the first report of a TS patient with an embolic stroke pattern. Our case shows that ischemic stroke in TS could be due to embolism as well as the various cerebral arteriopathies documented in previous reports.

scholarly journals Ibuprofen-Induced Aseptic Meningitis in a Male Adolescent with Intracranial Hypertension and Visual Impairment: A Case Report

2021 ◽  
Vol 13 (1) ◽  
pp. 233-238
Author(s):  
Seyed Mohammad Mousavi Mirzaei ◽  
Zahra Ahmadi
Keyword(s):  
Visual Impairment ◽  
Intracranial Hypertension ◽  
Aseptic Meningitis ◽  
Rare Complication ◽  
Clinical Signs ◽  
Male Adolescent ◽  
Drug Induced ◽  
Blurred Vision ◽  
Inflammatory Drugs

Drug-induced aseptic meningitis (DIAM) is a rare complication of certain drugs, most commonly reported with ibuprofen use. The present study reports on a male adolescent with intracranial hypertension and visual impairment accompanied by DIAM. We present a 16-year-old male patient who after ibuprofen consumption displayed headache, fever, photophobia, and blurred vision following heavy exercises. Examination of cerebrospinal fluid showed a mononuclear pleocytosis and an increase in protein concentration. Other examinations had normal results. The development of common clinical signs following ibuprofen use reflected DIAM. The patient’s vision was found to improve with supportive care and stopping of the drug during follow-up. Given the widespread use of nonsteroidal anti-inflammatory drugs and the fact that these drugs are the most common cause of DIAM, the probability of occurrence of this event should be always kept in mind, and screening for autoimmune diseases in these patients is of great importance.

scholarly journals In Vivo and In Vitro Toxicodynamic Analyses of New Quinolone-and Nonsteroidal Anti-Inflammatory Drug-Induced Effects on the Central Nervous System

1999 ◽  
Vol 43 (5) ◽  
pp. 1091-1097 ◽  
Author(s):  
Hideki Kita ◽  
Hirotami Matsuo ◽  
Hitomi Takanaga ◽  
Junichi Kawakami ◽  
Koujirou Yamamoto ◽  
...  
Keyword(s):  
Brain Tissue ◽  
Threshold Concentration ◽  
Current Response ◽  
Drug Induced ◽  
Inhibition Ratio ◽  
New Quinolones ◽  
The Central Nervous System ◽  
Anti Inflammatory

ABSTRACT We investigated the correlation between an in vivo isobologram based on the concentrations of new quinolones (NQs) in brain tissue and the administration of nonsteroidal anti-inflammatory drugs (NSAIDs) for the occurrence of convulsions in mice and an in vitro isobologram based on the concentrations of both drugs for changes in the γ-aminobutyric acid (GABA)-induced current response in Xenopus oocytes injected with mRNA from mouse brains in the presence of NQs and/or NSAIDs. After the administration of enoxacin (ENX) in the presence or absence of felbinac (FLB), ketoprofen (KTP), or flurbiprofen (FRP), a synergistic effect was observed in the isobologram based on the threshold concentration in brain tissue between mice with convulsions and those without convulsions. The three NSAIDs did not affect the pharmacokinetic behavior of ENX in the brain. However, the ENX-induced inhibition of the GABA response in the GABAA receptor expressed in Xenopus oocytes was enhanced in the presence of the three NSAIDs. The inhibition ratio profiles of the GABA responses for both drugs were analyzed with a newly developed toxicodynamic model. The inhibitory profiles for ENX in the presence of NSAIDs followed the order KTP (1.2 μM) > FRP (0.3 μM) > FLB (0.2 μM). These were 50- to 280-fold smaller than those observed in the absence of NSAIDs. The inhibition ratio (0.01 to 0.02) of the GABAA receptor in the presence of both drugs was well-fitted to the isobologram based on threshold concentrations of both drugs in brain tissue between mice with convulsions and those without convulsions, despite the presence of NSAIDs. In mice with convulsions, the inhibitory profiles of the threshold concentrations of both drugs in brain tissue of mice with convulsions and those without convulsions can be predicted quantitatively by using in vitro GABA response data and toxicodynamic model.

Some Aspects of the Psychopharmacological Activity of Maprotiline (Ludiomil®): Effects of Single and Repeated Treatments

1978 ◽  
Vol 6 (6) ◽  
pp. 421-429 ◽  
Author(s):  
A Delini-Stula ◽  
E Radeke ◽  
A Vassout
Keyword(s):  
Nervous System ◽  
Chronic Treatment ◽  
Conditioned Fear ◽  
Conditioned Avoidance ◽  
Repeated Treatment ◽  
Antidepressant Effects ◽  
The Central Nervous System ◽  
Pre Treatment ◽  
High Doses ◽  
Psychopharmacological Activity

Three different aspects of the psychopharmacological activity of the antidepressant maprotiline were investigated: its influence on serotoninergic functions the effects produced by chronic treatment its central nervous depressant and anxiolytic properties. Study of the effects of maprotiline on 5-HTP-induced head-twitch in mice pre-treated with pargyline or on hyperpyrexia in rats provided no evidence that the drug interferes with serotonin-mediated functions in the central nervous system even after quite high doses. These findings corroborate the results of extensive neurobiochemical investigations, which failed to demonstrate any influence of maprotiline on the metabolism of serotonin. Chronic studies showed that classical effects of maprotiline such as antagonism against reserpine-induced ptosis or tetrabenazine-induced catalepsy do not change in their intensity after daily administration of the drugs in a dose of 30 mg/kg p.o.for 11 days. A new component of the action of the compound, not detectable after one single dose, seems to appear, however, after repeated treatment (8 days). This effect is manifested in the restoration of conditioned avoidance behaviour after its suppression by pre-treatment with reserpine. The same effect is produced by imipramine. It is suggested that this restorative effect may be due to an additional activation of the dopaminergic nervous system and may have a bearing on the appearance of clinical antidepressant effects. Maprotiline was found to potentiate central nervous depressant effects of drugs like chlorpromazine, phenobarbitone and propranolol. This affords further confirmation that, in addition to its antidepressant qualities, it possesses sedative actions. An anxiolytic component was also demonstrated in rats in which maprotiline suppressed the conditioned, fear-induced rise in body-temperature.

scholarly journals Cardiovascular and cerebrovascular risk with nonsteroidal anti-inflammatory drugs and cyclooxygenase 2 inhibitors: latest evidence and clinical implications

2017 ◽  
Vol 8 (6) ◽  
pp. 173-182 ◽  
Author(s):  
Andrea Fanelli ◽  
Daniela Ghisi ◽  
Pierangelo Lora Aprile ◽  
Francesco Lapi
Keyword(s):  
Term Treatment ◽  
Cyclooxygenase 2 ◽  
Thrombotic Risk ◽  
Long Term Treatment ◽  
Pressure Development ◽  
Inflammatory Drugs ◽  
Anti Inflammatory ◽  
High Doses ◽  
The Right ◽  
Meta Analyses

Observational studies and meta-analyses have shown that the administration of nonsteroidal anti-inflammatory drugs (NSAIDs), especially when prescribed at high doses for long periods of time, can potentially increase the risk of cardiovascular diseases. The increased thrombotic risk related to the use of NSAIDs is mainly due to their cyclooxygenase 2 selectivity. The dosage use, the formulation selected and the duration of the therapy are other factors that can significantly impact on the cardiovascular risk. In order to minimize the risk, prescription of the right drug based on the patient’s features and the different safety profiles of several NSAIDs that are available on the market is key for their appropriate administration. Despite the baseline cardiovascular and gastrointestinal risk of each patient, monitoring of patients is suggested for increases in blood pressure, development of edema, deterioration of renal function, or gastrointestinal bleeding during long-term treatment with NSAIDs.

Modification of Insulin Resistance

1956 ◽  
Vol 102 (428) ◽  
pp. 576-588 ◽  
Author(s):  
Edward Marley
Keyword(s):  
Deep Coma ◽  
Insulin Dosage ◽  
Insulin Resistant ◽  
Significant Difference ◽  
High Insulin ◽  
Insulin Coma ◽  
The Central Nervous System ◽  
Resistance To Insulin ◽  
High Doses ◽  
Special Instance

Sakel (1938a) drew attention to the difficulty of establishing satisfactory comas in a minority of patients attending for Deep Insulin therapy. This phenomenon has since been confirmed by other workers including Tillim (1938) whose patient received 500 units of insulin without the production of deep coma, by Hall (1940) who reported an instance in which 1,000 units of insulin was equally unsuccessful, by Reznikoff and Scott (1942) who described how neither 120 nor 1,000 units of insulin when injected intravenously produced any significant difference in hypoglycaemia in insulin resistant patients, and more recently by Fogarty (1953) whose case required 5,000 units of insulin for the production even of sopor. Other recorded examples of resistance to massive doses of insulin include those of Bantinget al.(1938) and Tennent (1944).Various explanations of this perverse response to insulin have been formulated, including that of Jones (1939) who proposed that resistance to insulin was both a problem of true insulin insensitivity and also of an anomalous response of the central nervous system to hypoglycaemia. Medunaet al.(1942) preferred to ascribe it to anti-insulin factors in the blood, but a more interesting interpretation derived from Freudenberg (1952) who suggested that if the effects of high insulin dosage employed in insulin coma treatment were regarded as a special instance of a stress response, then the fluctuations and differences in response could be equated in terms of the General Adaptation Syndrome of Selye. High doses were thus an index of an effective “alarm stage” characterized by a discharge from plentiful adrenocortical reserves.

Sign in / Sign up

Export Citation Format

Share Document