Campylobacter jejuni subdural hygroma infection in a 2-year old boy: case report and a brief literature review.

BACKGROUND: Campylobacter jejuni is a common cause of acute gastroenteritis, but central nervous system infections are rare manifestations of Campylobacter infection. Therefore, C. jejuni trauma-related subdural hygroma infection in children is poorly described in the literature. CASE PRESENTATION: We described a 2-year old boy with lobar holoprosencephaly presenting with subdural hygroma following head trauma. C. jejuni infection was confirmed from a subdural hygroma sample by culture as well as by DNA sequencing of a broad range 16S rDNA PCR product. Cerebrospinal fluid from the ventriculoperitoneal shunt remained sterile. Combined neurosurgical and antimicrobial treatment led to complete recovery. Review of the literature showed that the most common manifestation of Campylobacter central nervous system infection is meningitis, mostly in neonates, and subdural hygroma infection was described for only one case. CONCLUSIONS: Subdural hygroma infection caused by C. jejuni is a rare clinical condition in children. Molecular methods represent an important tool for the detection of rare or unexpected pathogens. No standard recommendations for antimicrobial treatment of C. jejuni subdural space infection in children are available, but meropenem treatment combined with surgery seems to be an effective approach.

Subdural contrast effusion during endovascular therapy: case report.

Accumulation of contrast medium in the subdural space after diagnostic intraarterial contrast administration is a rare observation. The authors report the case of a subdural contrast effusion (SCE) presenting during endovascular treatment of an intracranial dural arteriovenous fistula (DAVF) mimicking an acute subdural hematoma. Differentiation between the two by computed tomography (CT) or intraprocedural Dyna CT and early neurological examination can be crucial for patient management. We believe that repeated large-volume contrast injections via large-bore intermediate catheters into the territory of an (even partly) occluded DAVF may induce leakage of contrast medium into the extravascular subdural space thereby causing a SCE.

Imaging of bridging vein thrombosis in infants with abusive head trauma: the "Tadpole Sign".

OBJECTIVES: Abusive head trauma (AHT) in infants is usually diagnosed using a multi-disciplinary approach by investigating the circumstances and identifying morphological indicators, for example, subdural hematomas (SDHs), subdural hygromas (SDHys), retinal haemorrhages and encephalopathy. The present morphological study investigates the incidence, radiological characteristics and non-radiological co-factors of bridging vein thrombosis (BVT) in infants with AHT. METHODS: From 2002 to 2013, computed tomography (CT) and magnetic resonance imaging (MRI) material of 628 infants aged 0-2 years were analysed retrospectively. If available, medicolegal expert opinions were additionally considered. Cases with SDHs and/or SDHys were identified and systematically evaluated as to the presence and characteristics of BVT. RESULTS: SDHs and/or SDHys were present in 29 of the 81 cases exhibiting morphological abnormalities in the initial CT. Among these, 11 cases (40%) had BVT (mean age = 5.0 months). BVT could be best depicted in the T1-weighted spin echo and T2*/susceptibility-weighted MRI. In one case, BVT could be depicted indirectly using time-of-flight MR venography. The predominant (73%) BVT shape was found to be tadpole-like ("Tadpole Sign"). CONCLUSIONS: In the absence of appropriate accidental trauma, BVT appears to be a strong indicator of AHT. Therefore, the BVT/Tadpole Sign represents compelling cause to search for other signs of AHT. KEY POINTS: • BVT is an excellent indicator of AHT in SDH/SDHy cases. • Accidental trauma must be ruled out before diagnosing AHT. • The Tadpole Sign appears to be the most characteristic shape of BVT. • BVT can be depicted using CT, MRI and MR venography. • The Tadpole Sign suggests searching for other signs of AHT.

Neuropsychological examination detects post-operative complications in idiopathic normal pressure hydrocephalus (iNPH): report of two cases.

Subdural fluid collections (SFC) are characteristic complications of shunting for idiopathic normal pressure hydrocephalus (iNPH). This report presents two shunted iNPH patients with clinically silent postoperative SFC, detected after abnormal neuropsychological findings. These cases highlight the value of neuropsychological assessment in the routine postoperative assessment of iNPH.

A calvarial acute subdural hematoma migrating into the spinal canal in a young male.

It is not common for an acute subdural hematoma (SDH) in the supratentorial region to show rapid resolution or migration during the clinical course. In this report, we present a rare case where the SDH in the supratentorial region was observed to rapidly migrate into the lumbar spinal canal, leading to severe radiculopathy. A 20-year-old male patient was admitted to the emergency department with severe headache after head trauma. The patient's overall condition was good, whereas his Glasgow Coma Scale score was 15 and blood pressure was normal. He had vomited 3 times after the onset of pain. No stiff neck was found, and the computed tomography showed an ASDH over the outer layer of the right hemisphere, causing a 7- to 8-mm shift. During the follow-up, the headache regressed and eventually resolved after 12 hours; however, another severe pain occurred in the lumbar region and in both legs. The pain worsened over time, progressing to sciatica in both legs. Acute SDH associated with a minor head trauma may migrate from the supratentorial compartment into the spinal canal by the help of elastic cerebral tissues in young adults and children.

Subdural hygroma accompanied by parenchymal and subarachnoid haemorrhage after epidural analgesia in an obstetric patient.

BACKGROUND: Anaesthetists need to know the different causes of persistent headache or a change in level of consciousness following epidural analgesia for labour. Failure to recognise these neurological complications can lead to delayed diagnoses, with subsequent serious implications. METHODS: We present a patient who was re-admitted for postural headache resulting from an unrecognised dural puncture during an epidural for pain relief while in labour. During the interview, the patient confirmed drug use (cocaine), so she was evaluated by a psychiatrist with possible post-partum psychosis or drug withdrawal syndrome. Afterwards, the patient deteriorated neurologically, showing impaired consciousness and seizures. RESULTS: The cranial computed tomography showed bilateral frontoparietal subdural collections with intraparenchymal and subarachnoid haemorrhaging. She improved by burr hole drainage of subdural hygroma and a blood patch. CONCLUSIONS: Neurological signs should alert the clinician to the possibility of subdural collection and other possible complications such as sinking of the brain in order not to delay the request for imaging tests for diagnoses and effective treatments.

Headache secondary to intracranial hypotension.

Intracranial hypotension is known to occur as a result of spinal cerebrospinal fluid (CSF) leaking, which may be iatrogenic, traumatic, or spontaneous. Headache is usually, but not always, orthostatic. Spontaneous cases are recognized more readily than in previous decades as a result of a greater awareness of clinical presentations and typical cranial magnetic resonance imaging findings. An underlying disorder of connective tissue that predisposes to weakness of the dura is implicated in spontaneous spinal CSF leaks. CT, MR, and digital subtraction myelography are the imaging modalities of choice to identify spinal CSF leakage. Spinal imaging protocols continue to evolve with improved diagnostic sensitivity. Epidural blood patching is the most common initial intervention for those seeking medical attention, and may be repeated several times. Surgery is reserved for cases that fail to respond or relapse after simpler measures. While the prognosis is generally good with intervention, serious complications do occur. More research is needed to better understand the genetics and pathophysiology of dural weakness as well as physiologic compensatory mechanisms, to continue to refine imaging modalities and treatment approaches, and to evaluate short- and long-term clinical outcomes.

Hypothalamic dysfunctions as a late consequence of surgical opening of the lamina terminalis. A controversial hypothesis.

BACKGROUND: Opening of the lamina terminalis is often used in surgery of the optico-chiasmatic region. Consequently, alteration of cerebral-spinal fluid (CSF) dynamics can occur after this manoeuvre, thus potentially translating into clinical complications. Herein, we describe 2 cases in which clinically relevant hypothalamic dysfunctions developed after few days opening of the lamina terminalis both patients showed mild to moderate preoperative hydrocephalus which improved postoperatively. CASES DESCRIPTION: In a patient with ruptured aneurysm of the basilar bifurcation, opening of the lamina terminalis was performed prior to acute-stage clipping. On postoperative day 7th, the patient developed significant subdural hygroma, mild disturbances of consciousness and increase of ADH concentration. These clinical features resolved only following subdural hygroma drainage and ventricular-peritoneal shunting. One previously operated patient in whom the lamina terminalis had been opened to remove a sizeable parasellar tumour showed a similar post-operative course. In this patient, sole subdural hygroma drainage was not an effective treatment, and the patient died subsequently for complications related to long-standing, though mild, hypothalamic dysfunction. CONCLUSIONS: Our experience may suggest that hypothalamic dysfunctions should be reminded as a possible, although rare, complication following the opening of the lamina terminalis. This clinical condition, if not properly managed, may contribute to trigger severe life-threatening complications.

Contralateral subdural effusion after decompressive craniectomy in patients with severe traumatic brain injury: clinical features and outcome.

BACKGROUND: Contralateral subdural effusion (SDE) is usually considered as an uncommon complication after decompressive craniectomy (DC) for head trauma. This complication may need more aggressive treatment because of its tendency to cause midline shift and neurologic deterioration. In this article, we present our experience with this group of patients and discuss the diagnosis and management of this entity. METHODS: This study included 13 patients with severe traumatic brain injury who developed contralateral SDE after DC. Clinical and radiographic information was obtained through a retrospective review of the medical records and the radiographs. RESULTS: The average time from the procedure of DC to the diagnosis of contralateral SDE was 13 days. Deterioration of clinical condition or appearance of new symptoms/signs related to the contralateral SDE was noted in four patients. In the remaining nine patients without apparent clinical deterioration, the contralateral SDE was discovered on routine computed tomography scan. Six patients were treated conservatively and the contralateral SDE resolved gradually. In six patients who underwent burr hole craniectomy to evacuate the SDE, the operation had successfully drained the SDE in four patients. Two patients received subsequent subduroperitoneal shunt to manage the reaccumulation of SDE. In one patient, subduroperitoneal shunt and cranioplasty were performed simultaneously to treat the SDE. Subsequently, six patients (46.2%) developed hydrocephalus and underwent ventriculoperitoneal shunt operation. CONCLUSIONS: Contralateral SDE may not be a rare complication after DC. Its diagnosis may be delayed or missed when it is asymptomatic or the clinical condition of the patient masks its clinical manifestations. It may be reasonable to repeat a computed tomography scan to detect contralateral SDE 2 weeks to 3 weeks after DC, irrespective of the clinical condition. In addition, posttraumatic hydrocephalus is a common late consequence in these patients. Close surveillance in these patients is indicated to prompt appropriate management.

Arachnoid cysts of the middle cranial fossa accompanied by subdural effusions--experience with 60 consecutive cases.

BACKGROUND: Subdural effusions (SDEs) can complicate arachnoid cysts of the middle cranial fossa (ACMFs). While there is a consensus that at least in adults asymptomatic ACMFs should not be operated, those with concomitant subdural and/or intracystic effusions are clinically apparent in the majority of cases and should be surgically treated. But it remains unclear, which surgical procedure is best. METHODS: Since 1980, 60 out of 343 patients with an ACMF presented with accompanying SDEs. Four categories of SDEs were differentiated radiologically. This collective was controlled in a follow-up study up to 60 months after conservative or operative treatment by clinical and radiological means. RESULTS: In 54 of the 60 patients, we saw an indication for surgical treatment. Twenty-nine patients received a burr hole, 13 cases were treated by craniotomy, seven by endoscopical means, three patients underwent shunting and two combined procedures. Six patients were treated conservatively. An excellent final clinical outcome was observed in 55 cases. While craniotomy succeeded best to reduce the cyst volume in postoperative CT, the final clinical outcome did not differ significantly compared with burr hole trepanation. CONCLUSIONS: Patients with small effusions can be treated conservatively in selected cases. Based on our experience, we prefer a differentiated therapy. As first procedure, burr hole and subdural drainage were performed, leaving the cyst alone, seeming sufficient for the majority of cases. Craniotomy or endoscopical means should be reserved as treatment of choice for special cases, depending on category and acuteness of SDE and size/localisation of the ACMF.

[Delayed pseudomeningocele as a result of penetrating injury: case report]. / Delici kesici alet yaralanmasina bagli geç gelisen psödomeningosel: Olgu sunumu.

Pseudomeningocele is cerebrospinal fluid collection in an extradural area after meningeal tear. The size of the defect in the dura-arachnoid, the pressure of spinal fluid, and the resistance of the soft tissue presumably determine the size of the pseudocyst. The main symptoms are often: headache, neck pain and myelopathic and radicular signs. Pseudomeningocele is diagnosed by myelography, sonography, computed tomography, and magnetic resonance imaging. We present a case of intraoperative identification nerve root entrapment by pseudomeningocele cyst and postoperative recovery of a patient's neurologic deficit.

Spinal imaging findings in spontaneous intracranial hypotension.

OBJECTIVE: spontaneous intracranial hypotension is a syndrome of postural headaches that arises as a result of CSF leakage and without previous lumbar puncture. The purpose of this study was to review and describe the spinal imaging findings of this entity. MATERIALS AND METHODS: The spinal MRI and CT myelographic imaging findings of 13 patients with spontaneous intracranial hypotension were retrospectively reviewed. Spinal images were evaluated for spinal fluid collections, dural enhancement, dilated epidural veins, a thickened or enlarged ventral lateral epidural venous plexus, high T2 signal intensity between the spinous processes of C1 and C2 (C1-C2 sign), structural abnormalities, canal attenuation or cord compression, and active contrast extravasation. When available, brain MRI findings were reviewed. Surgical correlation was made in the cases of four patients. RESULTS: The patients were found to have spinal fluid collections (11 of 13 patients), dural enhancement (eight of 10 patients undergoing contrast administration), dilated epidural veins (10 of 13 patients), an enlarged epidural venous plexus (nine of 13 patients), C1-C2 sign (seven of 13 patients), structural abnormalities (four of 13 patients), canal attenuation or cord compression (five of 13 patients), and active contrast extravasation (four of 13 patients). CONCLUSION: Spinal imaging is likely to show one or more findings in patients with spontaneous intracranial hypotension and may be of particular value to patients with equivocal clinical or brain imaging findings and patients who need surgery. Encountering these findings on spinal images may suggest the diagnosis of spontaneous intracranial hypotension and therefore can influence patient treatment.

Diagnostics and treatment of spontaneous intracranial hypotension.

OBJECTIVE: Intracranial hypotension is a frequently misdiagnosed syndrome which is caused by reduced intracranial cerebrospinal fluid (CSF) pressure due to spontaneous spinal CSF leakage. We present our series of intracranial hypotension regarding especially the required diagnostic imaging and the treatment. METHODS: A retrospective analysis was performed on 8 patients (5 males, 3 females, mean age 49 years) with postural and non-postural headache due to spinal CSF collection. RESULTS: Cranial MRI showed diffuse pachymeningeal gadolinium enhancement in all cases. CSF leakage detected by gadolinium-enhanced MR cisternography could be either diffuse (n=5) or precisely located around a dural tear (n=3). All but one leakages were located at the thoracic spine. In 6 patients 40-65 mL of blood were injected through epidurally placed drainages. In 1 patient, a dural tear was sealed with fibrin glue and fat. One patient refused surgical intervention. One epidural haematoma had to be revised. 5 of 7 patients showed excellent results. CONCLUSION: Gadolinium-enhanced MR cisternography best revealed CSF leaks. In the majority of patients with spontaneous intracranial hypotension, complete recovery may be achieved via a midthoracic epidural blood patch with minimal complications.

Symptomatic Subdural Hygroma and Hydrocephalus following Chiari I Decompression.

BACKGROUND: The aim of the present case report is to describe an unusual complication of foramen magnum decompression (FMD) for the Chiari 1 hindbrain malformation and its successful management with non-operative measures. METHODS: A 2-year-old girl with the Chiari 1 malformation underwent FMD, including suboccipital craniotomy, C1 laminectomy and durotomy without opening the arachnoid. RESULTS: After initial postoperative improvement, the patient deteriorated, developing subdural hygromas and hydrocephalus. These were treated successfully with observation and acetazolamide. CONCLUSIONS: Subdural hygromas may complicate FMD. A slit valve opening in the arachnoid might be part of the pathophysiology. While surgical intervention may be necessary in some circumstances, non-operative measures may be effective as well.

[The role of biology in the diagnosis of cerebrospinal fluid leaks]. / Place de la biologie dans la prise en charge des brèches ostéoméningées.

Cerebrospinal fluid leakage is a rare but critical condition with a substantial risk of intracranial infection, therefore its diagnosis and treatment is of major importance. CSF leakage diagnostic can be a challenging problem. Nephelometric measurement of beta-trace protein in the liquorrhoea is a non-invasive and fast method that can be used for CSF leakage diagnosis. It should kept in mind, however, that the cut-off of 1.1 mg/L is not suitable for patients with bacterial meningitis and those with a reduced glomerular filtration rate. Complementary use of beta-trace protein assay and beta2-transferrin detection is therefore recommended.

[Diagnosis and management of ENT conditions responsible for acute community acquired bacterial meningitis]. / Recherche et prise en charge de la porte d'entrée ORL des méningites aiguës bactériennes communautaires.

Only few epidemiological studies evaluate the role of ENT infections in meningitis. A retrospective review of data shows that the frequency of ENT infections is estimated at 25% in adults and children. Meningitis may occur during otological and nasosinusal infections. Acute otitis media and mastoiditis are the most common ear infections responsible for meningitis. Chronic otitis (cholesteatoma) are rarely involved. In case of acute rhinosinusitis, frequently responsible frontal and ethmoidal locations are investigated by nasal endoscopy and CT scan. A CSF leak originating mostly from anterior skull base or middle ear, either posttraumatic or spontaneous, may also be associated with meningitis. The management of ENT infections begins with antibiotics. Drainage may be discussed when identification of the bacteria is needed or if the medical treatment seems inefficient. In case of a CSF leak, closure of the defect is performed according to its location and size after evaluation by imaging (CT scan, MRI).

Understanding Subdural Collections in Pediatric Abusive Head Trauma.

Life-threatening physical abuse of infants and toddlers is frequently correlated with head injuries. A common variant of the abusive head trauma is the shaken baby syndrome. The present review article sheds light on subdural collections in children with abusive head trauma and aims at providing a recent knowledge base for various medical disciplines involved in diagnostic procedures and legal proceedings. To this end, the different subdural collection entities are presented and illustrated. The pathophysiologic background is explained. Differential and age-diagnostic aspects are discussed and summarized by tabular and graphic overviews. Two problematic constellations frequently occurring during initial CT investigations are evaluated: A mixed-density subdural collection does not prove repeated trauma, and hypodense subdural collections are not synonymous with chronicity. The neuroradiologic analysis and assessment of subdural collections may decisively contribute to answering differential diagnostic and forensic questions. In addition to more reference data, a harmonization of terminology and methodology is urgently needed, especially with respect to age-diagnostic aspects.

Imaging of skull base cerebrospinal fluid leaks in adults.

Cerebrospinal fluid (CSF) leak occurs when there is an osseous and dural defect at the skull base, with direct communication of the subarachnoid space to the extracranial space, usually a paranasal sinus. Recognition of the leak site and source and appropriate treatment are necessary to avoid rhinorrhea or otorrhea, low-pressure headaches, and meningitis, known complications of CSF leak. The imaging evaluation has evolved over the past several decades. Description of current techniques available to direct treatment options, including multidetector thin-section computed tomography, and imaging recommendations are presented.

Spontaneous spinal cerebrospinal fluid leaks.

Spontaneous intracranial hypotension is an uncommon but not rare cause of new onset daily persistent headaches. A delay in diagnosis is the norm. Women are affected more commonly than men and most are in the fifth or sixth decade of life. The underlying cause is a spontaneous spinal cerebrospinal fluid (CSF) leak. Typically the headache is orthostatic in nature but other headache patterns occur as well. Associated symptoms are common and include neck pain, a change in hearing, diplopia, facial numbness, cognitive abnormalities and even coma. Typical imaging findings consist of subdural fluid collections, pachymeningeal enhancement, pituitary hyperaemia and brain sagging, but magnetic resonance imaging may be normal. Myelography is the study of choice to identify the CSF leak but is not always necessary to make the diagnosis. Treatment consists of bedrest, abdominal binder, epidural blood patching, percutaneous fibrin glue injection or surgical CSF leak repair. Outcomes have been poorly studied.

Case report: spontaneous intracranial hypotension in association with the presence of a false localizing C1-C2 cerebrospinal fluid leak.

BACKGROUND: Spontaneous intracranial hypotension is an increasingly recognized cause of new-onset, daily, persistent headaches. Although these headaches are similar to post-lumbar puncture headaches, characteristic differences include intracranial pachymeningeal enhancement, subdural fluid collections, and downward displacement of the brain. The identification of upper cervical epidural fluid collections as a false localizing sign in patients with SIH has provided significant insight into the selection of management options. CASE DESCRIPTION: We review a case of a 57-year-old woman who presented to our institution with progressive orthostatic headaches relieved by recumbency. The patient had no recent history of lumbar puncture, spinal, or intracranial procedure. The patient isolated the onset of symptoms to 3 weeks prior, when she was lifting heavy items in her home, and was diagnosed with SIH. Subsequently, she was found to have a C1-C2 epidural fluid collection. After much diagnostic consideration and review of the literature, the collection was defined as a false localizing sign; and the patient eventually underwent a lumbar EBP with complete resolution of her symptoms. CONCLUSIONS: Upper cervical fluid collections in patients with SIH often represent a false localizing sign. Conservative management should be instituted; and if unsuccessful, a lumbar EBP should be performed. It is important to note that C1-C2 fluid accumulations may not provide the actual leak site in patients presenting with SIH. This understanding prevents therapy from being unintentionally directed at C1-C2.