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Autor: Bogdan Istrate
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This paper tries to summarize different clinical aspects and causes of intracerebral bleeding in pediatric and neonate neuropa-thology. Because in the pediatric population the intracranial bleeding comprises complicated mechanisms and the monitoring of little patients is still difficult, here with some example’s help is already given a “little key” in the diagnosis which can contribute as a useful tool for pediatric neurology practitioner, when a intracerebral mass bleeding occur.



Spontaneous subarachnoid hemorrhage is most commonly caused by a ruptured aneurysm in the pediatric population, also true in adults (Meyer-Heim, 2003).

Which other causes could be mentioned? There it can be included: ruptured arteriovenous malforma-tions, tumors, recreative drugs use, vasculitis, coagu-lophaties, meningoencephalitis, iatrogenic causes and benign perimesencephalic subarachnoid hemorrhage (Westra, 2008).



Trauma could be considerate also as a cause of iso-lated subarachnoid hemorrhage in the pediatric popu-
lation.Contrary, when a history of accidental trauma could suggest the causative agent, non-accidental trauma should be taken in consideration as well. Most interesting is the fact that subarachnoid hemorrhage was found in 8% of accidental traumas and 31% of non-accidental traumas (Reece R.M et al,2000). Non-accidental trauma could affect all pediatric groups but is most frequently in children less than 3 years with a peak incidence under 1 year of age.

The child is unable to speak, and other symptoms are: lethargy, irritability, seizures, increased or de-creased tonus, breathing abnormalities, and apnea. If the skull fractures and retinal and/or subdural hemor-rhages occur along with a poor history of events, then could be considered as a key point for the diagnosis. In infants with enlarged extra-axial spaces an increased risk for subarachnoid hemorrhage might be present. Trauma is responsible also in causing intracranial an-eurysms, as well as arterial dissections, leading in this way to an extensive subarachnoid hemorrhage. The hemorrhage secondary to the rupture of traumatic aneurysms or arterial dissections results in diffusing of blood in subarachnoid space with a predominance in the basal cisterns, which sometimes slowly tends to clear.



Trauma accounts for 5-39% of all pediatric intra-cranial aneurysms. Possible etiologies of intracranial aneurysms: Alagille syndrome (paucity of the inter-lobular bile ducts with various cardiovascular abnor-malities), sickle cell anemia, irradiation, HIV/AIDS, thalassemia, tuberous sclerosis, Marfan syndrome, syphilis, Moya Moya disease, pseudoxanthoma elasti-cum, type IV collagenophaty, fibromuscular dysplasia, hypertension, coarctation of the aorta, a1 anti-trypsin deficiency.

Immunocompromised patients: Staphylococcus, Streptococcus, Candida and Phycomycetes.

Intracranial aneurysms in pediatrics could also be caused by changes in the arterial flow, extracellular matrix, degradation/repair of the arterial wall. The ruptured aneurysms in children ^ acute onset give symptoms like: severe headache, nausea, vomiting, meningism, seizures, tense fontanel (in children un-der the age of 18 months) and cranial nerve deficits. Lethargy is most frequent encountered symptom. In the same time, it was reported that pediatric an-eurysms have a predilection for the internal carotid artery bifurcation, the middle cerebral artery and the posterior circulation.



Arteriovenous malformation is less common source of spontaneous pediatric subarachnoid hemor-rhage. These malformations could also be combined with an intraparenchymal hemorrhage. Most arte-riovenous malformations encountered in pediatric population are Speltzer-Martin grades 1-3 (Hillman, 2001).

Signs and symptoms: headache, nausea, vomiting, lethargy, when only subarachnoidian hemorrhage is
present. Arteriovenous malformations with neurolog-ical signs and symptoms are secondary to the location of the intraparenchymal hemorrhage.


Perimesencephalic non-aneurysmal subarachnoid hemorrhage

Here we talk now about a distinct type of sub-arachnoid hemorrhage in pediatrics which, unfortu-nately is not well diagnosed and recognized.

Radiographically: pattern of hemorrhage restrict-ed to the perimesencephalic or prepontine cisterns (with/without extension into the sylvian or interemi-spheric fissure) in combination with a normal angio-gram; serial head CT scans; MRI and Angiography of brain and cervical spine.

Clinically: invariable excellent prognosis.

Biologically: complete blood count, serum electro-lytes, liver function tests, coagulation study and drog screen.

Onset clinical pediatric presentation: headache, nausea, vomiting, neck pain.

Physical examination reveals -lethargy and nuchal tenderness

  • arousable of voice and follow simple com-mands
  • examination of cranial nerves, sensory and motor functions.

The clinical entity of this type of hemorrhage is not yet defined, but a venous or capillary source of bleeding could be implicated (Anderson, 2002).The possibility of a pontine capillary telangiectasia and a primary intracranial hematoma of the basilar artery should be suggested as a etiologic abnormalities.

Coagulopathies: Intracerebral bleeding of term neonate due to the protein coagulation system defi-ciency.
Intracerebral hemorrhage in a term neonates with vitamin K deficiency is the major cause of coagu-lopathy-induced intracranial bleeding (Fischer et al, 2010). The most common manifestation during the neonatal period is thrombosis of the A.cerebri media or sinus thrombosis, leading to extended trombophil-iac screening in these patients.

Patophysiology. Hereditary thrombophiliac dis-eases could be sometimes a cause for postpartum intracerebral bleeding in term neonates. Asphyxia whether in utero, perinatally or postnatally may lead also to intracerebral hemorrhage.

Patomolecular causes: vitamin K deficiency, protein S deficiency, anticoagulant enzyme-activated protein C (APC) molecular defects.

Protein S deficiency is rare but severe hereditary thrombophiliac disease.

Neonatal seizures, Intracranial hematoma and subarachnoid hemorrhage in full-term infants.

During the first days of life intracranial hemorrhage is a frequent cause of convulsions in the full-term infant. If cerebrospinal fluid is bloody and there is no evidence of asphyxia, infection or acute metabolic disease, then a presumptive diagnosis of primary subarachnoid hemorrhage is already made. Remains interesting, the aspect when infants appear remarkably well in the intercritical period and their outcome is usually good. Usually we can see in infants seizures and a bloody cerebrospinal fluid.

Laboratory: hematocrit, serum calcium, magnesium,glucose, urea electrolytes.

Lumbar puncture: could produce hemorrhagic cerebrospinal fluid with: xantochromic supernatant, increased percentage of erythrocytes, leukocytes, polymorphonucleocytes, lymphocytosis and mono-histiocytosis. Glucose and protein level might be also determined a well cultures for the bacteria.

Physical examination could reveal:

  • infant awake and alert:
  • normal/abnormal head circumference
  • negative/positive transillumination findings
  • soft anterior fontanelle
  • evidence/not evidence of external trauma or suture diastasis.
  • Moro embrace reflex could be assymetrical with slow and delayed adduction of the left upper ex-tremity
  • palmar and plantar grasps could weak.

Commonly this cortical pathology in the full-term infants may produce clonic seizures. If a trauma/accidental trauma occurs we must think at intracranial hematoma.



Intracerebral bleeding at different stages of the childhood occurs with various forms of manifesta-tions and sometimes with common signs and symptoms. Sometimes seizures accesses are responsible for triggering a intracranial hemorrhage in full-term infants. Carefully evaluations and management of
neonates and children suspected or confirmed with intracrerebral hemorrhage should be performed with accurate and specific guidliness.



  1. Meyer-Heim A, Boltshauser E (2003) Spontaneous intracranial hemorrhage in children: aetiology, presentation and outcome. Brain Dev 25:416-421.
  2. D.L.Westra, A.R.T.Colohan (2008) Pediatric subarach-noid haemorrhage. Acta Neurochir.Suppl.104:401-405.
  3. Reece RM, Sege R (2000) Childhood head injuries: accidental or inflicted? Arch of Pediatr.Adolesc.Med. 154:11-15.
  4. Hillman J (2001) Population-based analysis of arteriove-nous malformation treatment.J.Neurosurg.95: 633-637.
  5. Richard C.Anderson, Jonatan Baskin, Neil A.Feldstein (2002) Perimesencephalic Nonaneurysmal Subarachnoid Hemorrhage in the Pediatric Populatuon: Case report and Review of the Literature. Pediatr.Neurosurg.37:258-261.
  6. Doris Fischer, Luciana Porto, Hildegard Stoll, Christof Geisen, Rolf L.Schloesser (2010) Intracerebral Mass Bleeding in a Term Neonate: Manifestation of Hereditary Protein S Deficiency with a New Mutation in the PROS1 Gene. Neonatology 98:337-340.


Correspondence to:
Department of Cardiovascular diseases, Faculty of Medicine, Katholieke University of Leuven, Belgium