A Rare Presentation of Neurobrucellosis in a 6-Year-Old Pediatric Patient with Sagittal Sinus Thrombosis.

Brucellosis is one of the most common zoonosis worldwide. It is still endemic in many regions of the world. A 6-year-old female was admitted to the emergency department (ED) due to a sudden change in consciousness, urinary incontinence, vomiting, and difficulty in walking. Neurological examination demonstrated abducens nerve paralysis, mild-to-moderate motor deficit in hemiparesis in the left arm. Brain magnetic resonance imaging showed a hemorrhagic focus at the right frontal lobe and thrombosis in the superior sagittal sinus of the brain. The diagnosis of neurobrucellosis was confirmed by identifying Brucella spp. in the blood culture on the day 6 of pediatric intensive care unit admission; thus, trimethoprim-sulfamethoxazole and rifampicin, and ceftriaxone were promptly initiated. Despite neuroprotective management and acetazolamide, the patient's neurological problems and high intracranial pressure (ICP) persisted. An external ventricular drainage tube and a Codman ICP monitor were placed to be on the consent vigilance of the patient's neurological condition. The patient's ICP continued to increase despite the current treatment regimen; therefore, a decompressive bitemporal craniectomy was performed. The ICP level of the patient returned to its normal range immediately after the craniectomy. The patient did not have any notable neurologic sequelae at the first-year follow-up. Neurobrucellosis is a rare complication of systemic brucellosis and may present as meningitis, encephalitis, myelitis, radiculitis, and/or neuritis. Herein, we describe a six-year-old girl with brucellosis complicated with cerebral vein thrombosis. This case illustrates the need for close monitoring of patients with unexplained neurological signs or symptoms for brucellosis in endemic areas.

Suspected bacterial meningoencephalomyelitis as the trigger or presentation of neuromyelitis optica spectrum disorder flare.

BACKGROUND: Suspected bacterial meningoencephalomyelitis as the presentation or trigger of neuromyelitis optica spectrum disorders (NMOSD) flare has not been reported in literature. CASE PRESENTATION: A 29 year old female, who has a history of neuromyelitis optica spectrum disorder (NMOSD) for 6 years, presented with symptoms of meningitits, encephalitis, myelitis, headache and fever. Cerebrospinal fluid analysis revealed pleocytosis (1131 × 106/L [83% neutrophils]) and a glucose level of 39.6 mg/dl. Magnetic resonance imaging revealed lesions in the cervical cord, medulla, right frontal-parietal lobe, and corpus callosum. Serum anti-aquaporin-4 (AQP-4) antibody was positive. An initial diagnosis of bacterial meningoencephalomyelitis was considered. Despite broad-spectrum antimicrobial therapy, her neurologic symptom continued to deteriorate. Intravenous gamma immunoglobulin and methylprednisolone was initiated, which improved her symptoms rapidly. CONCLUSION: Suspected bacterial meningoencephalomyelitis as the presentation or trigger of NMOSD flare was considered in our case. Literature review revealed that bacterial meningitis-like presentation was a rare presentation in the attack phase of NMOSD. Corticosteroid therapy should be initiated in such cases.

A case report of community-acquired Pseudomonas aeruginosa pneumonia complicated with MODS in a previously healthy patient and related literature review.

BACKGROUND: Pseudomonas aeruginosa is an unusual pathogen in community-acquired pneumonia, especially in previously healthy adults, but often indicates poor prognosis. CASE PRESENTATION: We report a previously healthy patient who developed severe community-acquired pneumonia (CAP) caused by P. aeruginosa. He deteriorated to septic shock and multiple organ dysfunction syndrome (MODS) quickly, complicated by secondary hematogenous central nervous system (CNS) infection. After 1 month of organ support and antipseudomonal therapy, he had significant symptomatic improvement and was discharged from hospital. During treatment, the pathogen developed resistance to carbapenems quickly and the antibiotic regimen was adjusted accordingly. CONCLUSIONS: According to our case and related literature review, we conclude that more attention should be paid to community-acquired Pseudomonas aeruginosa pneumonia, because of its rapid progression and poor prognosis.

Nocardial spinal epidural abscess with lumbar disc herniation: A case report and review of literature.

RATIONALE: Nocardial spinal epidural abscess is rare. The diagnosis is often difficult to make and, if delayed, poses a high risk of long-term disability. Nocardial spinal epidural abscess with severe lumbar disc herniation has not previously been reported. PATIENT CONCERNS: A 50-year-old man presented with progressive lumbago and leg pain for 6 weeks after receiving acupuncture therapy, and then the patient suddenly occurred urine retention after walking. DIAGNOSES: Clinical examination revealed sign of cauda equina syndrome. Magnetic resonance imaging (MRI) revealed a Lumbar(L)4 to L5 disc herniation, L3 to Sacrum(S)1 epidural abscess, and L2 to S1 paravertebral abscess. The causative organism was Nocardia farcinica. INTERVENTIONS: An urgent paravertebral abscess debridement and right L4 to L5 laminectomy were performed. Simultaneously, the disc tissue protruding into the spinal canal was removed, as well as irrigation and drainage. And antimicrobial treatment was continued for 12 months. OUTCOMES: Fortunately, the patient was able to walk with a cane and urinate autonomously without a catheter, although this remained difficult 7 days after surgery. After 1 year of treatment, the patient has recovered completely and returned to work. LESSONS: Nocardial spinal epidural abscess with severe lumbar disc herniation is extremely rare. Pain from spinal degenerative diseases often masks the early symptoms of spinal infection. It's worth noting that invasive treatment of spine is a way of causing spinal nocardial infection.

Multi-systemic melioidosis: a clinical, neurological, and radiological case study from Hainan Province, China.

BACKGROUND: Melioidosis is a tropical disease caused by Burkholderia pseudomallei (B. pseudomallei). It can infect any organ system and lead to multiple abscesses. A few studies reported that central nervous system (CNS) is also involved. We present a diabetic patient with multi-systemic melioidosis that affected the CNS, thorax, and spleen. The aim was to study the clinical and radiological features of melioidosis and enhance understanding of the disease. CASE PRESENTATION: A 38-year-old male presented with cough and expectoration mixed with blood for several days. Chest computed tomography (CT) showed a patchy opacity in his left lung, and multiple low-density lesions in his spleen. After 10 days of antibiotics treatment, his clinical symptoms improved and he was discharged from the hospital. But 8 months later, the patient experienced sudden onset of left limb weakness and seizure and was re-admitted to the hospital. Brain CT indicated a low-density lesion over the right frontal lobe, and magnetic resonance imaging (MRI) indicated a well-enhanced lobulated lesion with multiple diffusion restriction areas in the lesion. He had a neuronavigation-guided open surgery but no malignancy was found. B. pseudomallei was cultured from the operative samples. After 4 months of systemic and intraventricular antibiotic administration treatment, he recovered complete consciousness with left hemiparesis. CONCLUSIONS: Multi-systemic melioidosis may present atypical clinical, neurological, and radiological manifestations. It is extremely important to accurately diagnose before treatment is selected. CNS melioidosis in early stage manifests similar symptoms to malignancy or stroke. It might mislead to a false diagnose. Diffusion weighted imaging (DWI) can help in differentiate abscesses from cystic tumours.

Brain Abscess of Basal Ganglia Presenting with Persistent Hiccups.

BACKGROUND: Brain abscesses are well-known to neurologic surgeons with well-recognized presentations, which include seizures, neurologic deficit, and headache. Rare symptoms may lead to a delay in diagnosis, which can be life threatening in the setting of a brain abscess. CASE DESCRIPTION: We present the case of a 46-year-old male with intractable hiccups found to have an abscess of the right basal ganglia. The brain abscess was treated by frameless stereotactic-guided aspiration. The patient's hiccups improved after surgical aspiration and medical management. CONCLUSIONS: A comprehensive literature review confirmed brain abscess as a rare cause of intractable hiccups. In addition, there are few reports of lesions of the basal ganglia causing intractable hiccups. Aspiration and medical therapy resulted in resolution of the hiccups. Knowledge of the hiccup reflex arc and unusual presentation of basal ganglia lesions may shorten time to diagnosis.

[Acute disseminated encephalomyelitis presenting as an acute urinary febrile retention]. / Un cas d'encéphalomyélite aiguë disséminée post-infectieuse découvert devant une rétention vésicale fébrile.

INTRODUCTION: MRI should be performed in the presence of an acute febrile urinary retention, when septic and obstructive causes are eliminated. We report a case of post-infectious probable acute disseminated encephalomyelitis (ADEM) with a mostly spinal cord tropism of involving Campylobacter. CASE REPORT: A 32-year-old man with no medical history was admitted for an acute febrile urinary retention. He reported severe diarrhea 3 days before. Clinical course was then complicated by a progressive tetraparesis predominating in the lower limbs. Medullar MRI showed thoracic myelitis. A five-day course of intravenous corticosteroids allowed a full recovery of both the motor and urinary symptoms. Fecal culture isolated Campylobacter sp. Final diagnosis was post-bacterial ADEM. CONCLUSION: Clinical findings and MRI allow clinicians to suspect acute disseminated encephalomyelitis. This hypothesis implies to actively look for recent infections or vaccinations preceding the clinical presentation.

[Ocular syndromes in patients with neurobrucellosis].

OBJECTIVE: To investigate the clinical features of ocular syndromes in patients with neurobrucellosis. METHOD: This is a retrospective series case study. The clinical data of 5 patients with neurobrucellosis, who were treated in Department of Neurology, Beijing Tongren Hospital, Captical Medical Uinversity, from May 2009 to January 2015, were collected. Their epidemiological information, clinical manifestation, laboratory and radiologic examination, therapy and prognosis were analyzed. RESULTS: Among the five patients, there were 3 males and 2 females, and their ages ranged from 20 to 67 years. The median age was 25 years. All patients had ever exposed to sheep. 1 patient lived close to a slaughterhouse and 2 patients lived in epidemic areas of brucellosis. 5 patients presented with binocular vision loss, 8 eyes with fundus edema, 3 patients with ophthalmoplegia;4 patients with fever,4 patients with headache,3 patients with neck stiffness,1 patient with movement and sensation disorders. Cerebrospinal fluid (CSF) pressure elevated, white cell number and protein increased with glucose reduction were detected respectively in 3 cases. While, CSF chloride decreased in 2 cases. Serum agglutination test for brucella was positive in 5 patients. Serum brucella culture was positive in 1 patient and CSF brucella culture was positive in 1 patient. Brain magnetic resonance imaging (MRI) showed that the optic nerve was involved in 3 patients,the meninges were involved in 1 patient and the brain white matter was involved in 1 patient. The combination of rifamycin, tetracycline, ceftriaxone sodium or quinolone were given to all patients and showed appreciated effects. CONCLUSIONS: The clinical features of ocular syndromes are atypical in patients with neurobrucellosis. Vision loss and ophthalmoplegia are more common to be seen. Neurobrucellosis should be considered when patients with ocular signs and other system symptoms without a definite diagnosis.

Chronic Meningitis Complicating Intracranial Hypertension in Neurobrucellosis: A Case Report.

In neurobrucellosis, even though meningitis is encountered frequently, chronic intracranial hypertension is a rare manifestation. Early diagnosis and treatment is very important for the prevention of permanent visual loss secondary to poststasis optic atrophy in these cases. We report a case that presented with permanent visual loss secondary to intracranial hypertension in neurobrucellosis. Our goal is to draw attention to the consideration of neurobrucellosis in cases with papilla stasis, even in the absence of neurological findings in endemic areas.

An unusual case of neurobrucellosis presenting as demyelination disorder.

Brucellosis is a public health problem in most countries in the Mediterranean. Involvement of the central nervous system is seen in 4-13% of patients with brucellosis. A 13-year-old girl was admitted because of gait disturbance, diplopia, and dizziness. Her complaints began about 1.5 years ago. The second symptomatic episode repeated about three months ago and the third two months ago. In total, attacks repeated 3 times over 1.5 years. The magnetic resonance imaging (MRI) and the clinical features mimicked multiple sclerosis. The patient was given pulse steroid treatments. After steroid treatment, her gait disturbance and diplopia improved over the short term. Following positive developments, her symptoms recurred. The tests were repeated; the MRI showed increasingly high signal abnormalities, and Brucella melitensis was grown in cerebrospinal fluid. The patient was started on an oral combination of rifampin, doxycycline, and ciprofloxacin. MRI findings improved markedly after nine months of treatment. Although neurobrucellosis is associated rarely with demyelination in adults, this finding has not been reported previously in children or adolescents. Additionally, this case is the first in terms of involvement of the corpus callosum in neurobrucellosis. In this article, we present an unusual case of neurobrucellosis.

Kaleidoscopic presentation of neurobrucellosis.

Brucellosis remains an important public health problem especially in the underdeveloped countries as well as the Middle East. It may be a "master mimic" leading on to grave diagnostic dilemmas. Chronic neurobrucellosis is seldom associated with signs and symptoms of toxaemia due to multi organ dysfunction. We report the case of a 23-year-old man who presented with fever of 8 weeks associated with ascending weakness of lower limbs and sensorineural type of hearing loss of 6 weeks duration with prominent systemic findings in the form of hepatosplenomegaly and significant loss of weight. He responded well to treatment with combination antimicrobials with clinicoradiological resolution after 6 months of therapy. Even though a rare complication of brucellosis, neurobrucellosis causes significant morbidity if not promptly recognised and treated. Favourable outcomes can be achieved in neurobrucellosis with appropriate protracted polymicrobial antibiotic therapy as was illustrated in our patient.

Pathophysiology of bacterial infection of the central nervous system and its putative role in the pathogenesis of behavioral changes.

Invasion of the central nervous system (CNS) by microorganisms is a severe and frequently fatal event during the course of many infectious diseases. It may lead to deafness, blindness, cerebral palsy, hydrocephalus, cognitive impairment or permanent neurological dysfunction in survivors. Pathogens can cross the blood-brain barrier by transcellular migration, paracellular migration and in infected macrophages. Pathogens may breach the blood-brain barrier and be recognized by antigen-presenting cells through the binding of Toll-like receptors. This induces the activation of nuclear factor kappa B or mitogen-activated protein kinase pathways and subsequently induces leukocyte infiltration and proliferation and the expression of numerous proteins involved in inflammation and the immune response. Many brain cells can produce cytokines, chemokines and other pro-inflammatory molecules in response to bacteria stimuli; as a consequence, polymorphonuclear cells are attracted and activated, and release large amounts of superoxide anion and nitric oxide, leading to peroxynitrite formation and oxidative stress. This cascade leads to lipid peroxidation, mitochondrial damage and blood-brain barrier breakdown, contributing to cellular injury during neuronal infection. Current evidence suggests that bacterial CNS infections can play a role in the etiopathogenesis of behavioral disorders by increasing pro-inflammatory cytokines and bacterial virulence factors. The aim of this review is to summarize the current knowledge of the relevant pathophysiologic steps in CNS infections.

Pathophysiology of bacterial infection of the central nervous system and its putative role in the pathogenesis of behavioral changes

Invasion of the central nervous system (CNS) by microorganisms is a severe and frequently fatal event during the course of many infectious diseases. It may lead to deafness, blindness, cerebral palsy, hydrocephalus, cognitive impairment or permanent neurological dysfunction in survivors. Pathogens can cross the blood-brain barrier by transcellular migration, paracellular migration and in infected macrophages. Pathogens may breach the blood-brain barrier and be recognized by antigen-presenting cells through the binding of Toll-like receptors. This induces the activation of nuclear factor kappa B or mitogen-activated protein kinase pathways and subsequently induces leukocyte infiltration and proliferation and the expression of numerous proteins involved in inflammation and the immune response. Many brain cells can produce cytokines, chemokines and other pro-inflammatory molecules in response to bacteria stimuli; as a consequence, polymorphonuclear cells are attracted and activated, and release large amounts of superoxide anion and nitric oxide, leading to peroxynitrite formation and oxidative stress. This cascade leads to lipid peroxidation, mitochondrial damage and blood-brain barrier breakdown, contributing to cellular injury during neuronal infection. Current evidence suggests that bacterial CNS infections can play a role in the etiopathogenesis of behavioral disorders by increasing pro-inflammatory cytokines and bacterial virulence factors. The aim of this review is to summarize the current knowledge of the relevant pathophysiologic steps in CNS infections.