Julie Mack

Anatomy and development of the meninges: implications for subdural collections and CSF circulation

The dura is traditionally viewed as a supportive fibrous covering of the brain containing the dural venous sinuses but otherwise devoid of vessels and lacking any specific function. However, review of the embryology and anatomy reveals the dura to be a complex, vascularized and innervated structure, not a simple fibrous covering. The dura contains an inner vascular plexus that is larger in the infant than in the adult, and this plexus likely plays a role in CSF absorption. This role could be particularly important in the infant whose arachnoid granulations are not completely developed. Although subdural hemorrhage is frequently traumatic, there are nontraumatic conditions associated with subdural hemorrhage, and the inner dural plexus is a likely source of bleeding in these nontraumatic circumstances. This review outlines the development and age-specific vascularity of the dura and offers an alternative perspective on the role of the dura in homeostasis of the central nervous system.

The neuropathology of infant subdural haemorrhage

Subdural haemorrhage (SDH) in the infant has a different pattern from that seen in the older child and adult. It is usually a widespread, bilateral, thin film, unlike the thick, space-occupying and often unilateral clot seen in older children and adults after trauma. Whether both arise by the same mechanism is unknown, but it seems unlikely. Most SDH is said to be due to trauma but in infants there are other, atraumatic causes. Birth is also important; recent MRI studies show an incidence of almost 50% in asymptomatic neonates. Traumatic SDH is said to result from rupture of bridging veins but new insights into the anatomy of infant dura suggest a dural origin for thin film subdural bleeding in young babies. Acute SDH usually rapidly resolves, but sometimes develops into a chronic fluid collection. Healing of SDH is by formation of a granulating membrane which may confer vulnerability to rebleeding, either spontaneously or after an otherwise innocuous event. SDH has a particular significance as one of the features of the triad (together with retinal haemorrhage and encephalopathy) associated with non-accidental injury. As the possibility of non-accidental injury is often first raised by a radiologic report of subdural bleeding, it becomes critically important in the interpretation of the scan appearances to understand the unique physiology and anatomy of the infant dura.

Pediatric and adolescent breast masses: a review of pathophysiology, imaging, diagnosis, and treatment.

OBJECTIVE Pediatric breast masses are relatively rare and most are benign. Most are either secondary to normal developmental changes or neoplastic processes with a relatively benign behavior. To fully understand pediatric breast disease, it is important to have a firm comprehension of normal development and of the various tumors that can arise. Physical examination and targeted history (including family history) are key to appropriate patient management. When indicated, ultrasound is the imaging modality of choice. The purpose of this article is to review the benign breast conditions that arise as part of the spectrum of normal breast development, as well as the usually benign but neoplastic process that may develop within an otherwise normal breast. Rare primary carcinomas and metastatic lesions to the pediatric breast will also be addressed. The associated imaging findings will be reviewed, as well as treatment strategies for clinical management of the pediatric patient with signs or symptoms of breast disease. CONCLUSION The majority of breast abnormalities in the pediatric patient are benign, but malignancies do occur. Careful attention to patient presentation, history, and clinical findings will help guide appropriate imaging and therapeutic decisions.

Breast cancer screening controversies: who, when, why, and how?

Mammographic screening is effective in reducing mortality from breast cancer. The issue is not whether mammography is effective, but whether the false positive rate and false negative rates can be reduced. This review will discuss controversies including the reduction in breast cancer mortality, overdiagnosis, the ideal screening candidate, and the optimal imaging modality for breast cancer screening. The article will compare and contrast screening mammography, tomosynthesis, whole-breast screening ultrasound, magnetic resonance imaging, and molecular breast imaging. Though supplemental imaging modalities are being utilized to improve breast cancer diagnosis, mammography still remains the gold standard for breast cancer screening.

Hematoma Formation During Breast Core Needle Biopsy in Women Taking Antithrombotic Therapy

OBJECTIVE The purpose of this study was to compare hematoma formation after breast core needle biopsy performed on patients undergoing and those not undergoing concurrent antithrombotic therapy. SUBJECTS AND METHODS A prospective assessment of core needle biopsies (stereotactic, ultrasound guided, or MRI guided) performed on patients enrolled between September 2011 and July 2012 formed the basis of this study. Postprocedure mediolateral and craniocaudal mammograms were evaluated for the presence and size of hematomas. Patients were clinically evaluated for complications 24-48 hours after the procedure through telephone call or face-to-face consultation. Needle size, type of biopsy, and presence of hematoma and documented complications were correlated with use of antithrombotic agents (including aspirin, warfarin, clopidogrel, and daily nonsteroidal antiinflammatory medications). RESULTS No clinically significant hematomas or bleeding complications were found. Eighty-nine of 617 (14.4%) non-clinically significant hematomas were detected on postprocedure mammograms. The probability of development of a non-clinically significant hematoma was 21.6% for patients taking antithrombotics and 13.0% for those not taking antithrombotics. Concurrent antithrombotic therapy and larger needle gauge were significant factors contributing to the probability of hematoma formation. The volume of the hematoma was not related to needle gauge or presence of antithrombotic therapy. CONCLUSION No clinically significant hematomas were found. Because there are potential life-threatening risks to stopping antithrombotic therapy before breast biopsy, withholding antithrombotic therapy for core needle breast biopsy is not recommended because the incidence of non-clinically significant hematoma is low.

The pathophysiology of brain swelling associated with subdural hemorrhage: the role of the trigeminovascular system

IntroductionThis paper reviews the evidence in support of the hypothesis that the trigeminal system mediates brain swelling associated with subdural bleeding. The trigeminovascular system has been extensively studied in migraine; it may play an important but under-recognized role in the response to head trauma. Nerve fibers originating in trigeminal ganglion cells are the primary sensors of head trauma and, through their collateral innervation of the intracranial and dural blood vessels, are capable of inciting a cascade of vascular responses and brain swelling. The extensive trigeminal representation in the brainstem initiates and augments autonomic responses. Blood and tissue injury in the dura incite neurogenic inflammatory responses capable of sensitizing dural nerves and potentiating the response to trauma.DiscussionThe trigeminal system may provide the anatomo-physiological link between small-volume, thin subdural bleeds and swelling of the underlying brain. This physiology may help to explain the poorly understood phenomena of “second-impact syndrome,” the infant response to subdural bleeding (the “big black brain”), as well as post-traumatic subdural effusions. Considerable age-specific differences in the density of dural innervation exist; age-specific responses of this innervation may explain differences in the brains response to trauma in the young. An understanding of this pathophysiology is crucial to the development of intervention and treatment of these conditions. Antagonists to specific neuropeptides of the trigeminal system modify brain swelling after trauma and should be further explored as potential therapy in brain trauma and subdural bleeding.

Mast cells in the human dura: effects of age and dural bleeding.

BackgroundAnimal studies have shown that the dura mater contains mast cells. We investigated the density of mast cells in the human dura mater, and the changes associated with subdural haemorrhage (SDH).MethodsSamples of the human dura were stained with tryptase antibody and were examined for mast cells. We used control cases with no dural bleeding (n = 9) and cases of fresh (n = 24) and old (n = 18) dural haemorrhage.ResultsMast cells were easily found in dural samples. The mean density in controls (11.05 cells per mm2) was less than that in fresh SDH (15.69), which was less than that in old SDH (23.09).ConclusionsSubdural haemorrhage is associated with an increase in dural mast cell density, and the density increases as the haematoma ages. We hypothesise that dural mast cells may contribute to neurogenic inflammation and the clinical features of subdural haemorrhage.

“Shaken baby syndrome” and forensic pathology

The concept of shaking baby syndrome (SBS) and the ‘‘triad’’ of encephalopathy, subdural hemorrhage (SDH), and retinal hemorrhage (RH) have become, as Dr. Byard [1] states, a hotly debated topic. SBS has come under increased scrutiny as our understanding of the mechanisms underlying the physiologic responses of neonates and infants continues to evolve. The triad can be secondary to trauma, but many forensic pathologists consider that impact is necessary to account for the signs and symptoms; as a consequence, the term SBS has been replaced by ‘‘shaken impact’’ syndrome or the more nondescript ‘‘abusive head trauma.’’ The issue is not whether or not shaking is injurious; Finnie’s experiment [2] clearly shows that smaller animals can die from repeated shaking. Instead, the issue is whether shaking alone can generate the forces associated with bridging vein rupture and SDH described in experimental models of SDH [3]. It is now well established that bridging vein rupture is not the only source of SDH in infants [4–6]. RHs also have multifactorial etiology [7, 8]. The small intradural vessels of the parasagittal dura, the falx, and tentorium are more extensive in young babies, and these vessels can leak to produce intradural and subdural hemorrhage. The extensive valveless plexus within the intracranial dura connects with the venous plexus of the spine and together form the craniospinal venous system [9]; the function of this system is not fully understood, though it is known to be involved in the maintenance of intracranial pressure, and affected by posture and respiration. This brings us to the possible role of hypoxia in SDH. While hypoxia on its own is not enough to produce SDH, there is a strong association between hypoxia and SDH [5, 6]. Additional factors such as increased venous pressure or coagulation disorders may serve to extend an intradural hemorrhage (IDH) into a thin-film SDH over the hemispheres and along the dural folds. Pathologists who do large numbers of perinatal autopsies see the close association between hypoxia and IDH/SDH [10]. Critics who sustain that the trauma of delivery has not been accounted for ignore the fact that with current obstetric care, traumatic tears of the falx or tentorium are extraordinarily rare [5]. In fact the ‘‘trauma’’ of delivery is one of hypoxia and increased intracranial pressures and not one of traumatic acceleration/deceleration. Geddes et al. [11] were the first to report that the microscopic changes seen in the brain of infants who died of inflicted head injury were hypoxic-ischemic rather than traumatic. The lack of traumatic changes in the brain made them suggest an alternative pathway for the findings of SDH and RH [12]. Since then other authors have postulated neck injury as the event that precipitates apnea and results in hypoxic changes of the brain [13]. Most of the current literature lumps together children under 2–3 years of age; however, the anatomy of the dura of infants below the age of 6 months is very different from an infant of age 2. Age-dependent changes in the cardiovascular, respiratory, immune, and coagulation systems, as well as individual variation in maturation, need to be considered when evaluating the triad in infants. We agree that ascribing intention to a combination of symptoms is absurd. While lethal craniocerebral trauma seems appropriate [1], this does not include the children This comment refers to the article available at DOI 10.1007/s12024013-9514-7.

Don’t blame the messenger: a response to Debelle et al and the Royal College of Paediatrics and Child Health

Instead of acknowledging the clear lessons of the Swedish Agency for Health Technology Assessment and Assessment of Social Services (SBU’s) review, Debelle et al 1 choose to attack the messenger for delivering news about the impoverished state of the medical literature on shaken baby syndrome/abusive head trauma. They criticise the SBU’s literature search, but fail to put forward the body of …

Infants dying suddenly and unexpectedly share demographic features with infants who die with retinal and dural bleeding: a review of neural mechanisms.

The cause of death in infants who die suddenly and unexpectedly (sudden unexpected death in infancy [SUDI]) remains a diagnostic challenge. Some infants have identified diseases (explained SUDI); those without explanation are called sudden infant death syndrome (SIDS). Demographic data indicate subgroups among SUDI and SIDS cases, such as unsafe sleeping and apparent life‐threatening events. Infants dying suddenly with retinal and dural bleeding are often classified as abused, but in many there is no evidence of trauma. Demographic features suggest that they may represent a further subgroup of SUDI. This review examines the neuropathological hypotheses to explain SIDS and highlights the interaction of infant oxygen‐conserving reflexes with the brainstem networks considered responsible for SIDS. We consider sex‐ and age‐specific vulnerabilities related to dural bleeding and how sensitization of the dural innervation by bleeding may influence these reflexes, potentially leading to collapse or even death after otherwise trivial insults.