Mg Of Hydrocortisone Research Articles

Working memory performance and cognitive flexibility after dexamethasone or hydrocortisone administration in healthy volunteers

Several studies have shown that glucocorticoids can impair declarative memory retrieval and working memory (WM) performance. The aim of the present study was to investigate the impact of a high dose of hydrocortisone on WM, as well as to examine the effects of cortisol suppression via treatment with a high dose of dexamethasone (DEX). We hypothesized that hydrocortisone treatment results in an impaired cognitive function compared with placebo. We further expected that dexamethasone treatment is also followed by cognitive impairment, due to the hypothesis that very low levels of cortisol are also associated with alterations in memory performance. In a placebo-controlled study with a within-subject design, 16 healthy volunteers received placebo or 120mg of hydrocortisone (two boluses of 60mg) directly before neuropsychological testing or 4mg of DEX the day before testing. We did not find any effect of hydrocortisone on WM and cognitive flexibility, even though cortisol levels were high at the time of testing. Furthermore, we did not find any effect of DEX treatment on WM and reaction time in a cognitive flexibility test. However, cognitive flexibility was negatively correlated with adrenocorticotropin (ACTH) in the DEX condition. Our results found no clear effect of hydrocortisone and dexamethasone treatment on WM. These results emphasize the need for further research on the association between hypothalamic-pituitary-adrenal axis activity and cognition. These studies should investigate the hypotheses of dose-dependent associations in more detail and should also include analyses on ACTH and cognition.

Arthroscopic versus percutaneous release of common extensor origin for treatment of chronic tennis elbow

Lateral epicondylitis is a common orthopedic problem. Rest, activity modification, and conservative therapies are generally efficacious in relieving symptoms in the majority of patients; however, a small percentage of people will experience refractory pain and require surgical intervention to alleviate their discomfort. Surgical release of the common extensor origin can be done through an open, percutaneous, or arthroscopic approach. This prospective study includes 33 patients with chronic resistant lateral epicondylitis who had received conservative treatment including modification of activity and 2 injections of 80mg of hydrocortisone, for more than 6months, aiming to compare two different techniques of treatment. The first group included 14 patients with a mean age of 42years treated by arthroscopic release of common extensor origin. The second group included 19 patients with a mean age of 48years treated by percutaneous tenotomy. The mean follow up was 12months for the arthroscopic group and 10months for the percutaneous tenotomy group. The results were evaluated according to the Disabilities of the Arm, Shoulder and Hand (DASH) score and the visual analogue scale (VAS). In the first group (treated by arthroscopy), the average DASH score improved from 72 to 48 and the average VAS improved from 9.1 to 2. In the second group (treated by percutaneous tenotomy), the average DASH score improved from 70 to 50 and the average VAS improved from 9 to 2.1. Concerning patient satisfaction after surgery, in the first group 7 patients (50%) were pleased, 6 (42.85%) were satisfied and 1 case (7.14%) was not satisfied. In the second group, 7 patients (36.84%) were pleased, 10(52.63%) were satisfied and 2 cases (10.52%) were not satisfied. Both arthroscopic and percutaneous release of the common extensor origin can be effective in treatment of lateral epicondylitis. Arthroscopic treatment of lateral epicondylitis gives more favorable results than percutaneous tenotomy. Although technically more difficult than percutaneous tenotomy, arthroscopy has the advantage of visualization of the pathology and much better improvement of elbow functions.

Hydrocortisone impairs working memory in healthy humans, but not in patients with major depressive disorder

Several studies have shown that stress or the administration of glucocorticoids can impair hippocampus-based declarative memory retrieval and prefrontal dependent working memory performance in healthy subjects. Major Depressive Disorder (MDD) is often characterized by memory impairment and increased cortisol secretion. Studies indicate that the impairing effects of glucocorticoids on declarative memory performance are missing in patients with MDD. The purpose of our study was to investigate whether the finding of missing effects of acute cortisol administration on memory performance in MDD is also seen when examining prefrontal-based working memory. In a placebo-controlled study, 57 patients with MDD and 56 sex- and age-matched healthy control subjects received either placebo or 10 mg of hydrocortisone orally before memory testing. To test the verbal modality of working memory, the Word Suppression Test was applied with one negative and one neutral test part. After hydrocortisone intake, healthy subjects showed a significantly poorer working memory performance compared to placebo treatment when negative interference words were administered. In contrast, memory performance of MDD patients was not affected by hydrocortisone treatment. The missing effects of glucocorticoid administration on working memory in MDD might be interpreted in the context of reduced central glucocorticoid receptor function.

Perioperative management of an adult patient with childhood cerebral X-linked adrenoleukodystrophy

Perioperative management of an adult patient with childhood cerebral X-linked adrenoleukodystrophy

Acute effects of hydrocortisone on the human brain: An fMRI study

Cortisol is essential for regulating all cell types in the body, including those in the brain. Most information concerning cortisol's cerebral effects comes from work in nonhumans. This is a first effort to use functional magnetic resonance imaging (fMRI) to study the time course and locus of cortisol's effects on selected brain structures in resting humans. We repeatedly scanned 21 healthy young adults over 45 min to examine changes in the brain's activity 5 min before, and for 40 min after, an IV injection of 10mg of hydrocortisone (N=11) or saline placebo (N=10). At 15-18 min postinjection we observed in the hydrocortisone group reduced activity in the hippocampus and amygdala that reached a peak response minimum at 25-30 min postinjection (-1 Standard Deviation) relative to placebo. No such effect was seen in the thalamus. Functional MRI appears to be a safe, noninvasive method to study the time course and anatomical effects of glucocorticoids in the human brain.

Cortisol-induced effects on human cortical excitability

Cortisol may fulfill all criteria for a neuromodulator. However, it is not known whether it may rapidly influence motor system activity in humans. Circulating cortisol levels were manipulated by administration of a single intravenous dose of hydrocortisone or saline solution, on separate days, to study changes in corticospinal and motor cortical excitability. Motor-evoked potentials (MEPs) to single- and paired-pulse transcranial magnetic stimulation from the resting first dorsal interosseous muscle, and cortisol plasma levels were assessed before and after either a bolus of 20 mg of hydrocortisone or saline solution in seven healthy subjects. Mean cortisol plasma level rapidly rose, peaked between 5 and 10 minutes after hydrocortisone injection, to slowly decay afterward. Mean MEP amplitude significantly increased from preinjection levels, and mean standard deviation of MEPs significantly increased between 8-12 minutes postinjection. Short-intracortical inhibition, tested during the same period, was significantly decreased. No significant changes in the above measures were observed after saline solution administration. Our results suggest that high circulating levels of cortisol rapidly increase corticospinal excitability and reduce gamma aminobutyric acid activity, as measured by short-intracortical inhibition, in humans. These effects, lasting about 10 minutes, were observed within 15 minutes from the pharmacological intervention. They are therefore compatible with a nongenomic mechanism. These findings are important in view of the notion that a decrease in intracortical gamma aminobutyric acid activity appears to be a prerequisite for motor learning and plastic processes in the human motor cortex.

Effects of acute cortisol administration on autobiographical memory in patients with major depression and healthy controls

Overgeneral autobiographical memory has become a well established phenomenon within major depressive disorder (MDD). Neuroendocrinologically, MDD is often characterized by a dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis, i.e. hypercortisolemia and reduced feedback sensitivity. In healthy participants cortisol administration has been found to impair autobiographical memory retrieval. The purpose of this study was to compare the effects of acute cortisol administration on autobiographical memory in MDD patients with the effects observed in healthy controls. We hypothesized that in contrast to healthy control subjects acute cortisol administration would not affect autobiographical memory performance in MDD due to reduced central glucocorticoid sensitivity. In a placebo-controlled, double-blind crossover study, 16 patients with MDD and 16 healthy control subjects received a placebo or 10mg of hydrocortisone orally before autobiographical memory testing (AMT). In the placebo condition depressed patients performed poorer than controls. After hydrocortisone intake, healthy subjects reported significantly fewer specific memories on the AMT compared to placebo treatment. In contrast, memory specificity of MDD patients was not affected by hydrocortisone treatment. The present findings replicate previous findings of impaired autobiographical memory retrieval after hydrocortisone treatment in healthy subjects and of impaired AMT performance in depressed patients. We speculate that the missing acute impairing effect of hydrocortisone on autobiographical memory in depressed patients might reflect reduced central glucocorticoid sensitivity. However alternative explanations cannot be ruled out.

A vivid example of angioedema

Case reportA 68-year-old hypertensive woman, who had been using25 mg of carvedilol daily for the past 5 years, woke up withedema of the tongue and dyspnea. At the admission to therural hospital, 5 mg of hydrocortisone and 5 mg of dex-chlorpheniramine were given intravenously, and the patientwas sent to our department. It was learned from relatives ofthe patient that she had been given sublingual captopril inanother hospital where she had been treated the day beforefor hypertension. Additionally, it was reported that thepatient hadalsosufferedfromtongueedema intheprioryearafter using the same medication, sublingual captopril. Onphysical examination, she was alert, with vital signs: bloodpressure 130/80 mmHg, pulse rate 94 beats per minute,respiration rate 14 breathes per minute (Fig. 1). Inspiratorystridor was heard on auscultation, and the patient was notable to speak. She was breathing supplemental oxygen,placed on a cardiac monitor, and intravenous lines wereestablished. Therapy was commenced with 0.3 mg of a1:10,000 epinephrine subcutaneously, 40 mg methylpred-nisolone, 50 mg diphenhydramine administered intra-venously. Over the following 10 min, subcutaneous 0.3 mgof a 1:10,000 epinephrine was repeated a single time. Thetongue of the patient decreased in size and she became ableto speak. The patient stayed in the observation unit for 24 hand was discharged without any further problems.DiscussionAngiotensin-converting enzyme (ACE) inhibitors are fre-quently used in the treatment of hypertension. Side effectprofiles vary from minor allergic reactions to anaphylactic

Multiple Organ Failure Followed by Intrauterine Klebsiella Pneumoniae Infection Associated with Diabetes Mellitus

A 49-year-old semi-conscious woman was admitted due to fever and dehydration. Disseminated intravascular coagulation (DIC), renal dysfunction and diabetic ketoacidosis were detected. Whole body computed tomography showed multiple nodular lesions in bilateral lungs and kidneys indicating septic emboli, and intrauterine lesions. We diagnosed multiple organ failure followed by intrauterine infection due to untreated diabetes mellitus. Vaginal discharge and blood culture revealed Klebsiella pneumoniae. We used multi-antibiotics for sepsis, respirator at low tidal volume ventilation, 200mg of sivelestat sodium hydrate and 300mg of hydrocortisone for respiratory failure, gabexate mesilate and anti-thrombin III for DIC, transfusion for bleeding from uterus and regular insulin aiming for a blood glucose range of from 80 to 140mg/dl. When we extracted the myoma uteri, the patient's fever subsided and the C-reactive protein became negative. Treating diabetes mellitus is important for the prevention of severe infection.

Modeling a Negative Response Bias in the Human Amygdala by Noradrenergic–Glucocorticoid Interactions

An emerging theme in the neuroscience of emotion is the question of how acute stress shapes, and distorts, social-emotional behavior. The prevailing neurocircuitry models of social-emotional behavior emphasize the central role of the amygdala. Acute stress leads to increased central levels of norepinephrine (NE) and cortisol (CORT), and evidence suggests that these endogenous neuromodulators synergistically influence amygdala responses to social-emotional stimuli. We therefore hypothesized that amygdala responses to emotional facial expressions would be susceptible to pharmacologically induced increases in central NE and CORT levels. To specifically test this hypothesis, we measured amygdala activation to emotional faces using functional magnetic resonance imaging in 62 healthy subjects under four pharmacological conditions: (1) single oral dose of placebo, (2) 4 mg of the selective NE-reuptake inhibitor reboxetine (RBX), (3) 30 mg of hydrocortisone, or (4) both drugs in combination. We found that a decrease in amygdala activation to positive facial emotion was coupled with an increase in amygdala activation to negative facial emotion in the RBX-CORT combined challenge condition. In conclusion, a pharmacologically induced elevation of central NE and CORT levels in healthy subjects created a negative response bias in the amygdala that did not exist at baseline. Our results implicate a causative role of NE-CORT interactions in the emergence of a negative bias of cognitive and emotional functions which is germane in stress-related affective spectrum disorders.

Should we abandon corticosteroids during septic shock? No

With the publication of the results of the recent CORTICUS trial, stress ('low') doses of corticosteroids for the treatment of vasopressor-dependent septic shock in adults can still be considered controversial. The purpose of this narrative review is to elaborate the pros and cons of this treatment in clinical practice and to formulate clinical and research directions. The recent CORTICUS study only shows a beneficial effect of stress doses of corticosteroids in the time interval to shock reversal and not on mortality, potentially explained by an increased risk for superinfection. The mortality in the placebo arm was relatively low and lower than in earlier randomized studies in which stress doses of corticosteroids had a favorable hemodynamic effect and conferred a survival benefit in septic shock. Treatment by stress doses of corticosteroids should not be abandoned during septic shock. Additional studies are needed, however, to better delineate the patient group with the highest likelihood to benefit from this therapy, as a function of severity of illness, response to adrenocorticotrophic hormone testing or both. For now, results of the CORTICUS study should not change current clinical practice of administering 200-300 mg of hydrocortisone daily (in divided doses) in case of fluid and vasopressor-insensitive septic shock and rapid tapering of this treatment on the basis of a hemodynamic response.

Low-dose and high-dose adrenocorticotropin testing: indications and shortcomings

The 250 microg adrenocorticotropin test (high-dose test) is the most commonly used adrenal stimulation test, though the use of physiologic doses (1.0 microg or 0.5 microg/1.73 m) (low-dose test) has recently gained wider acceptance. These variants and the use of adrenocorticotropin test in the ICU, however, remain controversial. The validity of the low-dose test and the parameters for evaluation of high- and low-dose tests in different situations need reevaluation. In the last few years, numerous studies have used the low-dose test as a single test following previous findings that it is more sensitive and accurate than the high-dose test. It is used mainly in secondary adrenal insufficiency and after treatment with therapeutic glucocorticosteroids to define hypothalamo-pituitary-adrenal suppression. Unless there is a very recent onset of disease, the results are interpreted by most researchers as diagnostic. The treatment of relative adrenal insufficiency, based on delta cortisol, has not yielded proof of correlation between this diagnosis and better prognosis with glucocorticoid treatment. For interpretation of an adrenocorticotropin test, only peak - and not delta - cortisol should be used. The use of 240-300 mg of hydrocortisone daily in ICU patients, including septic shock, should be considered as pharmacologic, rather than as a replacement dose. Using the low-dose test for this purpose will lead to further misdiagnosis.

Correction of cortisol overreplacement ameliorates morbidities in patients with hypopituitarism: a pilot study

Hypopituitarism in adults is known to be associated with deleterious effects on body composition, lipid profile and quality of life (QoL). This was attributed to GH deficiency. The potential role of glucocorticoid overreplacement had never been investigated. To investigate whether reduction in glucocorticoid replacement dose to more physiological one could ameliorate the "AO-GHD"-attributed symptomatology in patients with hypopituitarism. Design Eleven patients with panhypopituitarism taking 20-30 mg/day of hydrocortisone, but on no GH replacement were switched to 10-15 mg of hydrocortisone daily. Both basally and 6-12 months later, their body mass index, body composition by dual-energy X-ray absorptiometry, lipid profile, and the score of quality of life, QOL-AGHDA were measured. Within 6-12 months of lower hydrocortisone dose, subjects lost an average of 7.1 kg of total body fat and 4.1 kg of abdominal fat. No changes were seen in lean body mass, bone mineral content and HOMA-IR. Plasma total cholesterol and triglyceride concentrations decreased significantly (< 0.05) and the QoL improved (P = 0.018). Our pilot study suggests that decreasing the glucocorticoid replacement dose to approximately 15 mg/day is beneficial in terms of patients' body composition, lipid profile and quality of life.

Hydrocortisone effects on cardiovascular variability in septic shock: A spectral analysis approach*

Septic shock may be associated with a loss in cardiovascular variability and adrenal dysfunction. To investigate the relationship between cardiovascular autonomic modulation and adrenal function during sepsis. Seventy-five volunteers with septic shock and six healthy volunteers were prospectively included in the study. Cardiovascular variability was assessed by spectral analysis of heart rate and diastolic blood pressure signals, which included computation of normalized low (LF(nu)) and high frequency (HF(nu)) components. Cardiovascular variability was investigated in patients and healthy volunteers immediately before and 1 hr after a single bolus of 50 mg of hydrocortisone (study phase I); in patients according to adrenal function (study phase II); and in patients with septic shock and adrenal insufficiency, before and 72 hrs after a treatment with 50 mg every 6 hrs of hydrocortisone and 50 microg daily of fludrocortisone or their placebos (study phase III). As compared to healthy volunteers, patients had decreased LF(nu)-HR (.16 +/- .05 vs. .23 +/- .07 p = .01) and LF(nu)-DBP (.18 +/- .11 vs. .28 +/- .02 p = .01) and, after hydrocortisone, they had a greater increase in LF(nu)-DBP (p = .01). As compared to patients with normal adrenal function, those with adrenal failure had decreased LF(nu)-HR (.1 +/- .01 vs. .2 +/- .15 p = .01) and LF(nu)-DBP (.008 +/- .01 vs. .14 +/- .22 p = .0003). In patients with adrenal failure, as compared to placebos, hydrocortisone plus fludrocortisone increased significantly LF(nu)-DBP (p = .02) and low frequency/high volume ratio (p = .009). In septic shock, the loss in cardiovascular variability is more marked in patients with adrenal insufficiency and is partly restored by exogenous administration of corticosteroids.

Another Look at Steroid Therapy for Septic Shock

Another Look at Steroid Therapy for Septic Shock

Corticosteroids in Septic Shock

As the balance of evidence regarding corticosteroid treatment for septic shock shifts once again toward the negative, the study by Sprung et al.1 in this issue of the Journal elicits a strong feeling of déjà vu. Will the historical fate of high-dose corticosteroids, which were largely abandoned when the benefit observed in early studies could not be replicated in larger trials,2,3 now befall “physiologic-dose” corticosteroids?The rationale for therapy with corticosteroids at a physiologic dose (i.e., 200 to 300 mg of hydrocortisone per day) originated in the observations that patients with septic shock who had a reduced response to . . .

Therapies for adrenal insufficiency

Adrenal insufficiency is a life-threatening disorder. In the treatment of adrenal insufficiency, it is essential to administer the optimal medication at the optimal dose. Glucocorticoids are the main therapeutic approach in all forms of adrenal insufficiency. The recommended protocol for maintenance therapy is 15 – 25 mg of hydrocortisone, divided into two or three separate doses. Patients with primary adrenal insufficiency generally receive mineralocorticoid replacement comprised of fludrocortisone 0.05 – 0.2 mg/day. Recently, dehydroepiandrosterone has been proposed as a new therapeutic approach, despite the lack of strong evidence for beneficial effects. Additional glucocorticoid supplementation should be administered in stressful states. During critical illness, inadequate or no temporary increase in the dose of the replacement glucocorticoid can lead to acute adrenal failure. When acute adrenal failure occurs, it becomes necessary to administer intravenous hydrocortisone.

Repeated successful induction of fertility after replacing hydrocortisone with dexamethasone in a patient with congenital adrenal hyperplasia and testicular adrenal rest tumors

To report repeated successful induction of fertility in an adult male patient with congenital adrenal hyperplasia (CAH) and testicular adrenal rest tumors (TART). Case report. Radboud University Nijmegen Medical Centre. A 23-year-old male CAH patient with bilateral TART and azoospermia. Changing glucocorticoid medication from 30 mg of hydrocortisone to 0.75 mg of dexamethasone (DXM) daily. Improved semen analysis. With the use of ultrasound screening, TART were detected in the 23-year-old patient. The semen analysis showed azoospermia. In an attempt to decrease tumor size and improve testicular function, his glucocorticoid medication was changed from hydrocortisone to an equivalent dosage of DXM. The azoospermia was quickly reversed, and his partner conceived within 7 months of stopping oral contraceptives. Due to his progressive weight gain and striae, his medication was changed back to hydrocortisone, and he again developed again azoospermia. Two years later, the patient started again with DXM at the same dosage. His sperm concentration increased with progressive weight gain. Seven months later his partner became pregnant for the second time; afterward, the DXM treatment was changed back to hydrocortisone. In male CAH patients with testicular adrenal rest tumors, infertility may be reversible by replacing hydrocortisone with short courses of an equivalent dosage of DXM.

Early Goal Directed Therapy for Septic Shock Is Feasible and Safe in Hematopoietic Stem Cell Transplant Patients.

Hematopoietic stem cell transplant (HSCT) patients are at high risk for infection that can quickly progress to septic shock and multi-organ failure at various stages of their HSCT, with very high mortality and morbidity. One intervention that showed impact on outcomes is early goal directed therapy (EGDT), in which optimizing peripheral tissue oxygen delivery to meet hemodynamic endpoints using monitored early aggressive fluid resuscitation, hemoglobin correction, and pressors led to significant improvement in mortality and morbidity. Since that study did not include any HSCT patients who are considered such a high risk group with poor organ reserve function, immune suppression, micro-vascular injury caused by chemotherapy, radiation, implementing this aggressive approach for these patients in septic shock can raise concern of worsening respiratory, hemodynamic status and the added risk of inserting a new central line for monitoring central venous pressure (CVP) and Central venous Oxygen saturation (ScvO2) as a functional measure of cardiac output and oxygen delivery. In a pilot study we've tested the feasibility and safety of using EGDT approach in our HSCT patients in septic shock who needed ICU admission. We treated 10 consecutive patients upon admission to the ICU. Ages ranged from 24–70 years, all the patients were hypotensive with no response to at least 1500 mls of fluid boluses and low dose dopamine on the floor(5–7 mic/kg/min). Most of them were oliguric and some of them were in mild to moderate hypoxemia and tachypnea at the time of ICU transfer. In our institution most of these patients have right atrial catheters that can be used for measurement of CVP and ScvO2 through blood draws. In a sequenced approach CVP was kept between 8–12 mm hg with aggressive fluid resuscitation, Hgb at 10 and ScvO2 above 70%, levophed was used only if systolic BP was less than 90 mm hg. Dobutamine was used only if the ScvO2 was less than 70% despite all the above measures. All patients received 100 mg of hydrocortisone every 8 hours X 3–6 doses (to optimize adrenal function). All patients tolerated the treatment well. The average time of need for pressors was less than 14 hours. The average time with ICU care was 2.2 days. No complications reported as a result of the intervention, no end organ damage, and no renal or respiratory complications despite an average amount of IV fluid given in the 1st 12 hours of around 6.4 liters. All patients survived that ICU admission. The early aggressive approach of optimizing hemodynamic parameters in HSCT patients in septic shock is feasible, safe and may result in improved outcomes of survival, less ICU time and less end organ damage.Patients CharacteristicsPatientDiagnosisBacteriaTransplant stateTime of ICU careLevophed time hours12 hours fluid intake mlsPS1ALLP Aerogenosapre-transplant1 day<128493PS2ALLnonepre-transplant2 days<125079HB3AMLCitribacter Freundii5 months post allo2 days<178026FD4ALLE coli8 years post allo2 days<125411JS5NHLXanthomanas65 days post allo1 daynone4361RN6Multiple myelomaSerratia MPre-transplant2 days<245007AA7AMLE ColiPre-transplant2 days<12 hours5904AT8AMLKlebsilla PneumoniaPre-transplant4 days<12 hours8000DW9Germ cell TumornoneDay 10 post auto4 days<12 hours8307FA10AMLStaph AureusDay 67 post MUD2 days<24 hours6130

Paraplégie à la suite d'une infiltration foraminale lombaire : revue de la littérature à partir d'un cas

Objectives We report a patient in whom paraplegia developed following transforaminal epidural injection of a corticosteroid and discuss the physiopathology of this complication, based on a literature survey. Case report A 40-year-old man presented with low-back pain and symptoms of L4 radiculopathy due to degenerative disc herniation resistant to conventional medical treatment. Computed tomography revealed posterolateral L4–L5 disc protrusion. A dosage of 125 mg of hydrocortisone was given by epidural transforaminal L4–L5 left injection under radioscopy guidance. Within minutes following the injection, intense pain developed in both legs, with T12 complete paraplegia. Emergency magnetic resonance imaging (MRI) 2 hours later did not reveal spinal cord abnormalities. The patient underwent immediate surgery consisting of excising the protruding disc and extensive L3–L5 laminectomy. MRI performed 3 months later did not reveal medullar abnormalities. Six months later, the patient continued to show slow neurologic improvement, permitting him to walk with crutches and to stop intermittent self-catheterisation. Discussion The occurrence of paraplegia following epidural transforaminal injection of corticosteroids is a rare complication. To our knowledge, only 5 similar cases have been described. Most of the authors proposed that the mechanism of this complication is ischemia of the terminal cone due to accidental suppression of medullary blood supply. Direct lesion of a medullar artery, arterial spasm, or corticosteroid-induced occlusion due to undetected intra-arterial injection could lead to this medullar infarction. Anatomical variations of the path followed by the Adamkievicz artery strongly support this hypothesis.