Introduction

Case report

Discussion

References

Abstract

Relative bradycardia (mild sinus bradycardia) is one of the major barriers for the effective treatment of hemodynamically unstable patients with heart failure and reduced cardiac output. We report a case of a man aged 58 years with an old broad anterior myocardial infarction and relative bradycardia (about 60 bpm) suffering from symptoms of congestive heart failure at rest in spite of optimal medical therapy, including the use of the inotropes. Transvenous atrial pacing during right heart catheterization indicated that an increase in heart rate (up to 80 bpm) improved hemodynamics immediately. Implantation of a pacemaker (atrial pacing of 80 bpm) was effective for stabilizing the heart failure symptoms. Transvenous atrial pacing during right heart catheterization is effective for estimating the optimal heart rate in patients with heart failure and relative bradycardia. <Learning objective: Temporary atrial pacing during right heart catheterization is effective for estimating the optimal heart rate in patients with refractory heart failure and relative bradycardia. We present a case of inotrope-dependent heart failure. Our findings, obtained through echocardiography and right heart catheterization, showed dramatic improvements in hemodynamic parameters following an increase in heart rate via a cardiac pacemaker. This case assesses the impact of optimal heart rate in severe heart failure with relative bradycardia.>

Introduction

Bradycardia is one of the exacerbating factors of heart failure, especially in patients with underlying heart disease [1]. Severe bradycardia that is clearly adversely influencing a patient’s hemodynamic status is an absolute indication for insertion of a permanent cardiac pacemaker. However, this is not necessarily true for heart failure patients with relative bradycardia. There are several reasons for this. Firstly, patients have no symptoms of bradycardia itself. Secondly, it is unclear whether augmentation of cardiac output by increasing heart rate is a sufficient indication for implantation of a pacemaker. Furthermore, the optimal dose of beta-blockers is also uncertain in such cases. Here we report a patient with severe heart failure and relative bradycardia in whom increasing the heart rate by atrial pacing (from 60 to 80 bpm) greatly improved his hemodynamics and symptoms.

INTRODUCTION

CASE REPORTS

DISCUSSION

CONCLUSION

REFERENCES

ABSTRACT

Idiopathic normal pressure hydrocephalus (iNPH) is a disorder of aging that is characterized by enlarged cerebral ventricles, gait apraxia, dementia, and urinary incontinence. iNPH is frequently misdiagnosed, in part because the symptoms resemble other neurological disorders, and because other associated symptoms have not been fully characterized. Importantly, iNPH has not previously been associated with stuttering, and shunting has not been shown to alleviate the symptom of stuttering. Here, the authors report two cases of patients with iNPH presenting with stuttering that resolved after ventriculoperitoneal (VP) shunt placement. Each patient presented with gait difficulty, incontinence, cognitive impairment and stuttering. Lasting improvements of the symptoms (including stuttering) were seen in both patients after CSF drainage procedures that included lumbar puncture, extended lumbar CSF drainage, placement of a VP shunt, and VP shunt revision.

INTRODUCTION

Normal pressure hydrocephalus (NPH) is a neurological disorder of aging that is characterized by enlarged ventricles, gait difficulty, incontinence, cognitive impairment, and normal (or only slightly elevated) intracranial pressure. Patients with NPH are diagnosed as having primary (idiopathic) or secondary NPH, based on the etiology of the disease. Secondary NPH can affect individuals of any age. Common causes are subarachnoid hemorrhage, head trauma and meningitis, all of which may lead to increased brain inflammation and fibrosis of CSF resorption pathways. Idiopathic NPH (iNPH) is most commonly seen in adults over the age of 60. The pathophysiology of iNPH is poorly understood. Proposed mechanisms suggest decreased cerebral blood flow, poor cerebral vascular autoregulation, and impaired CSF production, absorption, and turnover rate. The treatment for NPH, regardless of etiology, is the placement of a ventriculoperitoneal (VP) shunt . iNPH remains a difficult disease to diagnosis, given its late age of onset and the notable overlap of its presenting symptoms with other diseases of aging, including Lewy body dementia, Parkinson’s Disease, progressive supranuclear palsy, and Alzheimer’s Disease . To date, however, there are no reports that describe stuttering or dysarthria as presenting symptoms in iNPH. This case report describes two patients who presented with iNPH symptoms with stuttering, and who displayed sustained symptomatic improvement after VP shunt placement.

1- Background

2- Case representation

3- Conclusion

4- Ethics approval and consent to participate section

5- Consent for publication

References

Abstract

Background: Vascular malformations can present with hydrocephalus following external compression of ventricular outlet. This can be managed by a CSF diversion. Case presentation: We report a case of hydrocephalus secondary to a congenital venous anomaly treated successfully with cerebrospinal fluid diversion. Here we present a case to literature of a 57 years old male patient who had presented with hydrocephalus secondary to aqueductal obstruction by developmental venous anomaly. Patient underwent right ventriculoperitoneal shunt placement and post operative Computed Tomography showed reduction in size of bilateral lateral ventricles and third ventricle. Conclusion: Although developmental venous anomaly as a cause for hydrocephalus have been reported, we present one more case of hydrocephalus secondary to a congenital venous anomaly who was treated successfully with cerebrospinal fluid diversion.

Background

Aqueduct of Sylvius, a channel connecting third and fourth ventricle situated in the dorsal midbrain, surrounded by periaqueductal gray matter is the narrowest part of CSF pathway and the commonest site of CSF flow obstruction [1]. Commonest etiology for aqueduct cerebrospinal fluid flow obstruction include congenital stenosis and gliosis secondary to inflammatory conditions, tumors [2]. While vascular malformations form an infrequent cause of aqueductal obstruction, developmental venous anomalies are extremely rare with only about 10 cases reported so far [3]. Here we report a case of developmental venous anomaly in a 57 years old male causing obstruction of aqueduct of sylvius thereby causing hyrodephalus.

1. Introduction

2. Case report

3. Discussion

Declaration of Competing Interest

Appendix A. Supplementary data

Research Data

References

Abstract

Case: We present a case of common peroneal nerve entrapment following inside-out lateral meniscus repair in a collegiate-level football player. To our knowledge, there are a limited number of cases describing this injury pattern in the literature, with none describing such in a college athlete.

Conclusion: This case demonstrates that even with appropriate precautionary use of accessory portals and careful retraction, nerve entrapment can still occur, but with the identification and treatment of the compression, patients and even elite athletes can make a full recovery and return to their previous level of function.

Introduction

The common peroneal nerve (CPN, common fibular nerve) is the lateral branch of the sciatic nerve and originates from the L4, L5, S1, S2 nerve roots [1–3]. The CPN travels inferiorly and laterally from its origin at the apex of the popliteal fossa through the posterior compartment of the thigh along the medial border of the biceps femoris tendon and posterior to the lateral head of the gastrocnemius muscle. The nerve then enters the lateral compartment of the leg as it wraps around the fibular head and enters deep to the peroneus longus tendon before bifurcating into the deep peroneal nerve and the superficial peroneal nerve. The deep peroneal innervates the anterior compartment of the leg and provides sensation to the first web space; the superficial peroneal nerve innervates the lateral compartment of the leg and provides sensation to areas of the anterolateral lower leg and dorsal midfoot [1–3].

CPN palsies manifest most frequently as foot drop or difficulty ambulating, but the presentation may be varied depending on the location and severity of nerve injury [2]. The most common cause of CPN palsy is nerve compression, however traumatic events including knee dislocation, leg lacerations, or direct, blunt trauma are also common causes of CPN injury [2]. Iatrogenic injury is less common, but wellrecognized as a potential cause of nerve palsy particularly in surgeries about the knee, such as total knee arthroplasty or even resulting from routine, postoperative care such as the use of compression stockings [4–6]. There have only been a limited number of documented cases of common peroneal nerve palsy following meniscus repair [7–9], and no such reports have been documented in a collegiate athlete.

1. Introduction

2. Case report

3. Discussion

References

Abstract

The purpose of this case report is to describe the imaging and associated clinical features of an asymptomatic novel coronavirus pneumonia (COVID -19) patient outside WuHan, China. The principle findings are that in this patient with laboratory -confirmed COVID -19, CT findings preceded symptoms and included bilateral pleural effusions, previously not reported in association with COVID -19. The role of this case report is promotion of potential recognition amongst radiologists of this new disease, which has been declared a global health emergency by the World Health Organization (WHO).

Introduction

In Wuhan, China, in December 2019, a series of pneumonia cases of unknown etiology appeared, soon after diagnosed as being caused by a novel coronavirus initially titled 2019 novel coronavirus (2019 -nCoV) and subsequently officially named COVID -19 by the WHO on February 11, 2020 [1].

As of February 14, 2020, there are 49,053 laboratory -confirmed cases globally [2], 15 of which are in the United States [3]. There is a small but growing body of literature regarding the imaging findings of COVID -19, and the purpose of this case report is to describe the imaging and associated clinical features of an asymptomatic COVID -19 patient outside Wuhan, China, including an imaging finding previously not reported.

2- Case Report

3- Discussion

4- Conclusion

References

Introduction

Spontaneous coronary artery dissection (SCAD) is an underdiagnosed and rare cause of myocardial infarction (MI). SCAD is defined as the separation of the coronary artery wall by hemorrhage with or without intimal tear. SCAD causes acute coronary syndrome in 1.7% to 4% of cases [1]. We report a case of a patient with acute MI caused by SCAD with marked progression of dissection within 4 days and spontaneous healing in 2 months.

2- Case Report

A 47-year-old woman with a 4-day history of chest pain, which had begun directly after emotional stress (air travel), was transferred to our clinic from another hospital. The patient was normosthenic, had practiced gymnastics in youth, and had no signs of joint hypermobility syndrome or other connective tissue disorder. She had smoked for a long time and had arterial hypertension grade 2. She had never experienced chest pain before and was very active in her everyday life. An electrocardiogram upon admission to our clinic revealed a sinus rhythm with a 2 mm ST elevation in leads II, III, aVF, V3-V5, “-” and T V3-V5 (Figure 1). On echocardiography, an apex dyskinesis was found; the left ventricle ejection fraction was 56%. The level of cardiac troponin-I was 13.2 ng/mL, confirming the development of acute myocardial infarction. We analysed the first angiogram, which had been performed in another clinic. It revealed 70– 75% smooth extended narrowing in the middle segment of the left anterior descending artery, and no signs of atherosclerosis in the proximal segment of LAD or the remaining arteries were found. Side branches were absolutely normal as well (Figure 2). It looked like a subintimal hematoma. We repeated the coronary angiography upon admission on day 4; the extension of the culprit lesion to the distal segment of the LAD was observed (Figure 3). Because of the high risk of intima rupture, intravascular visualization was not performed. This finding on the second angiogram confirmed our initial suspicion and corresponded to SCAD type 2. Considering that the association of SCAD and FMD is a well-known fact, we performed angiography of the renal and carotid arteries [2].

Background: Polycythemia vera is a myeloproliferative disease that sometimes evolves to myelofibrosis, causing splenomegaly and neutropenia. In this case report, we describe a patient with polycythemia vera and unexplained neutropenia who later turned out to also have hairy cell leukemia. Case presentation: A middle-aged Caucasian man with polycythemia vera presented to our hospital with chronic mouth ulcers. Later he developed leukopenia and pancytopenia. Bone marrow biopsies showed fibrosis. Further morphological analyses of bone marrow and blood smears revealed probable transformation into acute myeloid leukemia. However, there were also cells indicating hairy cell leukemia. Morphological and immunohistochemical analyses later confirmed the presence of hairy cell leukemia in biopsies that had been present for 3 years. Treatment with cladribine temporarily reversed the patient’s neutropenia. Conclusions: Hairy cell leukemia may mimic development to myelofibrosis in patients with polycythemia vera.

Background

The BCR-ABL-negative myeloproliferative neoplasms (MPN) polycythemia vera, essential thrombocythemia, and primary myelofibrosis are characterized by excessive production of terminally differentiated and functional blood cells. They clinically overlap, because primary myelofibrosis sometimes presents with thrombocythemia and may be difficult to distinguish from essential thrombocythemia, whereas both essential thrombocythemia and polycythemia vera can progress to myelofibrosis [1]. All three entities have a risk of transformation to acute myeloid leukemia (AML). Polycythemia vera, essential thrombocythemia, and primary myelofibrosis are genetically characterized by clonal mutations in JAK2, CALR, or MPL. The MPN diseases are thought to arise from a somatically mutated hematopoietic stem cell that gives rise to all myeloid cells, B cells, and natural killer cells [2]. Patients with polycythemia vera usually live with the disease for many years, often decades, before it may transform into AML or secondary myelofibrosis [3]. The phase when polycythemia vera is about to transform to myelofibrosis is known as spent phase polycythemia vera and is characterized by reduced erythropoiesis and splenomegaly because of extramedullary hematopoiesis. More than 10% blasts in peripheral blood is unusual and may suggest a blast transformation to AML. Postpolycythemia myelofibrosis, and certainly AML, has a poorer prognosis than polycythemia vera and may therefore be considered for allogeneic stem cell transplant [4]. Hairy cell leukemia is a mature, indolent B-cell malignancy. Patients with hairy cell leukemia are characterized by fatigue, splenomegaly, and cytopenia, most often pancytopenia, and some patients may display bone marrow fibrosis [5]. The prognosis is good, and patients usually respond well to purine analogs such as cladribine or pentostatin [6, 7]. Mutation in the BRAF gene leading to a Val-to-Glu substitution in position 600 of the BRAF molecule (V600E) is probably the driving mutation in hairy cell leukemia [8], and a phase II trial testing the BRAF inhibitor vemurafenib in hairy cell leukemia showed promising results, with response in 25 of 26 patients [9]. We report diagnostic and therapeutic difficulties with a patient presenting with myelofibrosis secondary to polycythemia vera, further development to AML, and hairy cell leukemia. This case report illustrates that hairy cell leukemia in a patient with polycythemia vera may be interpreted as secondary myelofibrosis, that monocytopenia could have raised the suspicion of hairy cell leukemia earlier, and that AML does not always present with CD34-positive blasts.

AB, a 20-year-old woman with Down syndrome (DS) and moderate intellectual disability, was referred to a Down syndrome clinic for loss of skills. Her medical history was signifcant for atrial septal defect repair in infancy and Graves’ disease in remission for the last four years of medications. She presented with a one-year history of slowing in her general movements and with behavioral regression. Te family noted that her symptoms became more noticeable when she changed day programs from a less structured to a more demanding environment.Te change was implemented because she had been so successful the prior year. She previously spoke in full sentences, but now her speech was sof and limited to 1 or 2 words at a time. She had tremors that had increased signifcantly over a few months. Tese motor symptoms impacted her ability to complete activities of daily living. She had occasional bowel or bladder accidents if she was not able to get to a bathroom in time. Te patient exhibited some symptoms of depression, including decreased interest in activities and somber afect. Te decline in function did not appear to afect her comprehension as she was still able to follow conversations and directions as before, albeit more slowly. Neurological fndings were signifcant for paucity of expressive speech, hypophonia, decreased facial expression, slow gait, tremors, and cogwheel rigidity. Her motor fndings were more pronounced on the lef side. Extensive testing including complete blood count, celiac panel, thyroid panel, vitamin B12 level, HIV screen, complete metabolic panel, sedimentation rate, urine HVA/VMA, ANA, paraneoplastic panel, and myasthenia gravis antibodies was unremarkable. Her EEG showed mild difuse slowing consistent with her diagnosis of DS. An MRI of her brain showed cystic expansion of the cavum septum pellucidum and vergae, measuring 7.5 cm in greatest transverse dimension.Te lateral ventricles were enlarged and obstructed at the level of the foramina of Monro with no obvious periventricular interstitial edema (See Figure 1). Follow-up images three months, one year, and two years later remained stable. A CT scan of her brain did not show calcifcations. Developmental regression related to depression was initially suspected, leading to mental health interventions. Her psychiatrist started citalopram, which improved her afect and level of interest, but not her motor slowing. Te neurologist initiated carbidopa-levodopa 25 mg–100 mg three times daily for symptomatic treatment of extrapyramidal features. Tis led to an immediate and dramatic response with return to baseline motor function. Te patient had no side efects of treatment and sustained the response for a fairly long period on the same dose of carbidopa-levodopa. Follow-up examination eighteen months afer initiation of therapy showed recurrence of cogwheel rigidity and increase in tremors, requiring doubling of the dose of carbidopalevodopa and giving it four times a day.