Assessment of patients with a suspected cardioembolic ischemic stroke. A national consensus statement.

OBJECTIVES: Several cardiovascular, structural, and functional abnormalities have been considered as potential causes of cardioembolic ischemic strokes. Beyond atrial fibrillation, other sources of embolism clearly exist and may warrant urgent action, but they are only a minor part of the many stroke mechanisms and strokes that seem to be of embolic origin remain without a determined source. The associations between stroke and findings like atrial fibrillation, valve calcification, or heart failure are confounded by co-existing risk factors for atherosclerosis and vascular disease. In addition, a patent foramen ovale which is a common abnormality in the general population is mostly an innocent bystander in patients with ischemic stroke. For these reasons, experts from the national Danish societies of cardiology, neurology, stroke, and neuroradiology sought to develop a consensus document to provide national recommendations on how to manage patients with a suspected cardioembolic stroke. Design: Comprehensive literature search and analyses were done by a panel of experts and presented at a consensus meeting. Evidence supporting each subject was vetted by open discussion and statements were adjusted thereafter. Results: The most common sources of embolic stroke were identified, and the statement provides advise on how neurologist can identify cases that need referral, and what is expected by the cardiologist. Conclusions: A primary neurological and neuroradiological assessment is mandatory and neurovascular specialists should manage the initiation of secondary prophylactic treatment. If a cardioembolic stroke is suspected, a dedicated cardiologist experienced in the management of cardioembolism should provide a tailored clinical and echocardiographic assessment.

Giant prolactinoma presenting as a skull base tumor with erosion of the cervical vertebrae: pronounced responsiveness to dopamine agonist treatment.

Giant prolactinomas are rare and usually associated with symptoms attributable to hypopituitarism and compression of juxtasellar structures such as the cranial nerves of the cavernous sinus and the optic chiasm. Occasionally, they masquerade as skull base tumors with atypical symptoms. We describe a patient who presented with a low-energy trauma in the neck region that led to the initial diagnosis of a large skull base tumor eroding the cervical vertebrae. After stabilizing surgery, the patient responded to dopamine agonist therapy with normalization of serum prolactin levels and pronounced reduction in tumor volume.

Prolactinoma-associated headache and dopamine agonist treatment.

AIM: The aim of this article is to investigate the phenotype and etiology of prolactinoma-associated headache as well as present and discuss the plausible pain-relieving effect of dopamine agonist treatment. METHODS: In this case-based audit we included 11 patients with prolactinomas and one patient with idiopathic hyperprolactinemia presenting with headache that subsequently improved or resolved after dopamine agonist treatment. RESULTS: A significant ipsilateral location of tumor mass and reported headache symptoms was observed (p = 0.018). After dopamine agonist treatment seven out of 12 patients became pain free within 2.5 months; after one year of treatment 11 out of 12 reported headache improvement or resolution. Average tumor volume reduction after treatment was 47 ± 22% during 9.5 ± 8.4 months of follow-up. There was no significant association between headache relief and tumor shrinkage (p = 0.43) or normalization of serum prolactin (p = 1.00), respectively. CONCLUSIONS: 1) The significant association between lateralization of tumor and headache suggests a mechanical origin of the headache, 2) headache responded to dopamine agonist treatment in most patients, and 3) our observations encourage future prospective controlled trials to investigate the role of hyperprolactinemia in the pathogenesis of headache as well as the therapeutic effects of dopamine agonists.

Absent 18F-FDG Uptake in the Brain-Unsuspected Brain Death.

Brain death is the complete, irreversible cessation of brain function, including the capacity for brainstem, respiratory, and vegetative activities. It is a clinical diagnosis that can be supplemented with brain perfusion imaging. Absent cerebral blood flow can be visualized with CT angiography or perfusion scintigraphy. F-FDG PET/CT, visualizing glucose uptake, is another approach that has been shown to indicate brain death in small case series. We here present a case with unsuspected absent F-FDG uptake and thus no metabolic activity, in the brain. The patient was declared brain dead later the same day.

Imaging occult lesions in the cervical spine facet joints.

Discrete injuries in the lower cervical spine facet joints have been reported in studies of motor vehicle crash victims. We conducted a detailed investigation of these joints from 20 motor vehicle crash fatalities and 22 decedents due to nontraumatic causes, using conventional radiology, computed tomography, and magnetic resonance imaging to examine whether the diagnostic imaging procedures could identify injuries in the facet joints. The diagnostic imaging procedures identified facet joint fractures in 4 of the 19 trauma cases with computed tomography having the highest sensitivity and obtaining good correlation with findings from the microscopical evaluation. No diagnostic imaging procedure could reliably evaluate the integrity of the synovial folds or the joint spaces for bleeding despite microscopical evidence of such findings in these structures in a large proportion of the motor vehicle crash fatalities. This study emphasizes the need for scientific evidence of validity and reliability of advanced diagnostic imaging procedures in forensic settings, in particular, with regard to occult soft tissue lesions, and cautions uncritical use of negative results from these procedures until such evidence has been produced.

Non-fatal injuries to the cervical spine facet joints after a fatal motor vehicle crash: a case report.

Injuries to the lower cervical spine facet joints may be identified in people killed in road traffic crashes. However, many of these injuries are not identified on diagnostic imaging procedures despite histological evidence of injury. This case report illustrates possible non-lethal pathological conditions in the facet joints following fatal road traffic trauma. The cervical spine segments C4 to C7 were removed en bloc and examined with magnetic resonance imaging, computed tomography and conventional radiology. The specimen was fixated in alcohol, embedded in methylmethacrylate, and divided into 3 mm thick parasaggital slices from where 10 microm thick sections were produced and evaluated with light microscopy. Injuries identified on microscopy included haemarthrosis, capsular avulsion, synovial fold contusions and subchondral fractures. None of the injuries were detected on diagnostic imaging or at routine autopsy. Discrete injuries to the cervical spine facet joints were identified using supplemental histological procedures in this case report. Post-mortem diagnostic imaging did not reveal these injuries and future studies should investigate the nature, prevalence and clinical relevance of such lesions.

Hypertensive microbleed as a transient ischemic attack mimic.

Cerebral microbleeds have acquired increased attention as a silent marker of small vessel disease that carries an increased risk of hemorrhage. The etiology is believed to be either hypertension or amyloid deposition. Here, we present a case with a patient whose transient focal symptom most likely was due to the occurrence of an acute microbleed, indicating that not all microbleeds are silent and that the cause of a transient ischemic attack is not always ischemic.

[Cranial diabetes insipidus in Wegener's granulomatosis]. / Central diabetes insipidus ved Wegeners granulomatose.

We describe three cases of cranial diabetes insipidus (CDI) caused by Wegener's granulomatosis (WG). Panhypopituitarism was the presenting symptom in one patient. Magnetic resonance imaging (MRI) showed enlargement of the pituitary gland with an intrasellar mass lesion and absence of posterior pituitary lobe hyperintensity. Follow-up MRI disclosed reduction of the intrasellar lesion but sustained loss of posterior lobe hyperintensity. The patients still have CDI despite a marked clinical response to the treatment of WG. Pituitary dysfunction may be the presenting symptom as well as a complication of WG.