MIDLINE CAVITY - keywords
midline cavity
references to midline cavities
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Anderson NG, Laurent I, Cook N, Woodward L, Inder TE (2005) Growth Rate of Corpus Callosum in Very Premature Infants. Am J Neuroradiol 26:2685–2690.
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Liss L, Mervis L (1964) The ependymal lining of the cavum septi pellucidi: a histological and histochemical study. J Neuropathol Exp Neurol 23:355–367
LoeserJD, Alvord EC (1968) Agenesis of the corpus callosum. Brain 91:553–570.
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Mehta NM, Hartnoll G (2001) Congenital CMV with callosal lipoma and agenesis. Pediatr Neurol 24:222-4.Meizner I, Barki Y, Tadmor R, Katz M (1988) In utero ultrasonic detection of fetal arachnoid cyst. Journal of Clin Ultrasound 16:506–509.
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Oteruelo FT (1986) On the cavum septi pellucidi and the cavum Vergae. Anat Anz. 162(4):271-8.
Pavone P, Barone R, Baieli S, Parano E, Incorpora E, Ruggieri M (2005) Callosal anomalies with interhemispheric cyst: expanding the phenotype. Acta Paediatrica 94:1066-1072.
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midline crossing
internal cerebral vein
value of ultrasound
cavum veli interpositi
There are several types of midline cavity in the newborn that can be differentiated with ultrasound.
The quadrigeminal cistern is a normal echofree area (1-3 mm wide) behind an echoic line between the plexus of the third ventricle and the vermis. It is often a very small hypoechoic area, certainly without mass effect. A cyst of the quadrigeminal cistern (larger and possibly compressing other tissue) thus lies behind the lower third ventricle ventricle and the tectum. This cistern contains the posterior cerebral and posterior choroidal arteries, the IVth cranial nerve and the great vein of Galen. There is a direct lateral communication with the retrothalamic cistern behind the pulvinar. The thickness of the echoic zone overlying the colliculi (normally no more than 3 mm) often increases in case of subarachnoid haemorrhage.
vestigial
membrane ?
corpus callosum
commissure sequence
cavum Vergae
ACC + IHC
typical cases
>
size of the cavities
fetal onset
From viable age until near term almost all newborns have a visible cavum septi pellucidi. A sagittal section through the anterior fontanelle quite often shows an echopoor zone more caudally, behind and above the superior colliculi, under the splenium of the corpus callosum. Follow-up of some of these ‘cysts’ allows to observe that they do not grow but remain visible for months. Options: cavum Vergae, cavum veli interpositi (normal or dilated), quadrigeminal cyst (extended cistern), pineal cyst, arachnoid cyst. The doppler visualisation of the internal cerebral vein is important for differentiation: arachnoid and quadrigeminal cysts are below this vein.
Arachnoid cysts: Two thirds are supratentorial, especially in the temporal fossa and along the sylvian fissure. Location above the sella turcica, in the cerebellopontine angle, on the vermis and in the quadrigeminal cistern are less common.
Pineal cyst: Is a small midline cavity, exceedingly rare in the newborn.
Agenesis of the corpus callosum with interhemispheric cyst : Very large and erratic midline cysts can be seen with callosal agenesis.
arachnoid cyst
chance finding at PMA 31w
pineal cyst
midline cavities
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brain cavities
midline development
fornix
pineal cyst ?
cystic CSPellucidi
examples of typical midline cavities
haemorrhage CV
cystic cavum Vergae
asymmetrical leaflets
CVI versus CQ
normal 34 w PMA
absence one leaflet
septo-optic dysplasia
normal 24 w PMA
thick leaflets
unusual cavities
cisterna quadrigemina
cavum veli interpositit
(Loeser and Alvord 1986, O’Rahilly and Müller 1994, Norman et al. 1995, Barkovich et al. 1996 and 2001, Raybaud and Girard 1998)
Within the embryonic lamina terminalis a thick dorsal section, called the lamina reuniens of His, forms by embryonic day 41. It is an area in which preformed cell pathways (the sling created by processes from subependymal cells, migrated from the medial ventricle wall to the midline) attract axons across the midline. Early callosal fibers are repelled by the induseum griseum (superiorly) and by a glial wedge (inferiorly).
This crossing of fibers is preceded by the formation of a dorsal groove, the banks of which unite after degeneration of cells in its walls and the inlying meninges. In this area, called the commissural plate, will pass the hippocampal commissure as well as the fornix, the anterior commissure and the corpus callosum.
Glial cells proliferate from that area in the lamina reuniens. Some fornix fibers are already present before the corpus callosum forms.
The primitive area of hemisphere fusion will become the future septum pellucidum, containing cinguloseptal fibers from cingular cortex to
the choroid fissure below. These are pioneer
fibers from the cingulate cortex that guide callosal axons anteriorly, whereas hippocampal commissural axons guide callosal fibers posteriorly. Thick septal leaflets can be observed in conditions like megalencephaly.
Primordia of the fornix are first present in the commissural plate in the 9th week. Pioneer fibers of the anterior commissure (uniting both olfactory bulbs, amygdala and adjacent rhinal cortex) cross the midline in the 10th postconceptional week, one week later followed by those of the hippocampal commissure (between the crura of the fornix around one fifth of the fornical fibers cross in the mature brain).
Callosal connections form later. The callosal crossing intersects with the primitive subiculum leaving a small hippocampal part dorsal to it, later developing into induseum griseum and striae longitudinales. Growth of the corpus callosum in a rostro-caudal direction is the reason why fornix, psalterium (hippocampal commissure) and di-telencephalic junction are displaced occipitally and eventually end up covered by the corpus callosum.
development of the midline
The genu of the corpus callosum is present around 13 weeks, before the midportion. Cingulate sulcus and gyrus are visible by the 16th postconceptional week. The entire corpus callosum (rostrum, trunk and splenium) is complete around the 20th week. Some splenial swelling is present at viable preterm age. Latest completed part is splenium.
MRI demonstrated how genu and rostrum thicken in early infancy (around 2 to 3 months), whereas the splenium tends to swell around 5–8 months. Genu and splenium at the moment of birth of a term infant will be about 4 mm thick and the trunk about 2 mm.
Callosal myelination starts in the second month after term birth and progresses in a caudo-rostral direction (first around the isthmus that connects the rolandic areas and in splenium that connects visual cortices). Splenium acquires hyperintensity on T1W and hypointensity on T2W images around 3 months post term age. These changes in intensity reach the adult-like stage around 8 to 10 months, when rostrum and genu are finally myelinated. Eventually about half callosal axons acquire myelin. Arterial perfusion of the corpus callosum is from the ACA except for the posterior splenium irrigated by the PCA.
Callosal axons connect around 2% of associative neocortical areas of the hemispheres, with in addition a small fiber connection between the caudate heads. In phylogeny callosal size parallels neocortical size. Axons are mainly derived from cortical layer III. Most temporal cortex is excluded from it: temporal cortex is connected to the other side through the anterior commissure, together with amygdaloid nuclei, hippocampus, olfactory bulbs and insular cortex. Frontal lobes are interconnected through the rostrum, parietal lobes through the corpus, occipital lobes through the splenium. Both hetero- and homotopic connections exist, either excitatory or inhibitory. Tapetum is a collection of callosal fibers covering the lateral atrial wall. Excluded from this system are connections between striate visual cortex receptive of images away from the vertical meridian, and fibers between distal limb somatosensory areas.
The function of commissural axons through trunk and splenium is modulatory: co-operation between both hemispheres in somatosensory, visual and auditory impressions.
Individuals with callosal agenesis may have intellectual capacity in the low normal range, but are slower in linguistic, visual and tactile exercices that challenge interhemispheric transfer. They display deficits in rhyming, in the pronounciation of nonwords and in puzzling together abstract forms for instance. Agenesis of the corpus callosum does not prohibit differential hemispheric function (e.g. speech remains a left function as in the normal population). Section of the corpus callosum later in life causes more obvious signs of hemispheric disconnection as if separating the half-brains produces separate conscious systems. Then one is left with a dominant and a minor hemisphere.
midline cavities: summary
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massa commissuralis formed in banks of median telencephalic groove (glial cells and mesenchymal reaction)
lamina terminalis
callosal fibers commissurate on two different guides: the hippocampal commissure and the glial sling in the lamina reuniens
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ventral part of the lamina reuniens
anterior commissure
dorsal part of the lamina reuniens
hippocampal commissure
1 lamina reuniens in commissural plate
2 anterior commissure
3 lamina terminalis
4 fornix
5 hippocampal commissure
6 corpus callosum fibers posterior
7 corpus callosum fibers anterior, in the glial sling
8 future cavum septi pellucidi (initially open to the arachnoid space due to the fact that the rostrum is not formed)
9 chiasma opticum
M foramen of Monro
S septal nuclei
development of the midline: early fetal period
septal nuclei
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callosal commissure
Development of the “commissural plate” is in the massa commissuralis of the primordium hippocampi. Initially juxtaposition of the banks of the sulcus medianus and formation of the massa commissuralis occur in the infolded primordium hippocampi in the floor of the interhemispheric fissure.
This is followed by commissuration of the hemispheres by fibers of the corpus callosum and rostral extension of the massa commissuralis over the median groove. Then diastasis of the banks of the median groove shape lamellae of the septum pellucidum and form a closed cavum septi sealed off by the rostrum from the interhemispheric fissure.
The rostrum is not the last segment of the corpus callosum to develop. Rather, the lamina rostralis of the fetal rostrum is already present before genu and splenium (Kier and Truwit 1997). Additionally, the beaked segment of the rostrum develops concurrently with maturation of the genu. The cavum septi pellucidi is formed when the rostrum is complete, before that the space is open to extracerebral CSF.
development of the midline: cavum septi pellucidi et Vergae
commissuration sequence
Sequence of commissure formation in rodents (Wahlsten 1981).
midline at viable preterm age
Status of the midline at viable preterm age (background by Retzius 1896).
midline formation mechanisms and molecules
1 to send a cingulate pioneer axon ventrally toward the intermediate zone
2 turning toward the midline (choose internal capsule or corpus callosum)
3 cross at the corticoseptal boundary (funnelling)
4 dorsal turn at corticoseptal boundary of other side
5 locate neocortical target
6 locate correct layer and innervate
molecular players
- Slits (Slit 1,2,3 and their Robo receptors: repelling axons at the midline with a complex method depending on concentration and type of Robo receptors), Comm (inhibiting repulsion by Robo), Netrins (to floor plate after crossing), Ephrins, NF1A and B
- Wnt family (attraction to rostral after crossing), heparan sulphate proteoglycans
- Sema3F repelling from floor plate after crossing
- FGF and DRAXIN in the formation of midline glial structures
Corpus callosum develops for interhemispheric integration of sensory cortices, with more performance than anterior and hippocampal commissures of nonplacental mammals; reptiles have a large tectal commissure instead. Most likely eutherians needed this commissure for motor specialisation (fine motor control across the midline: to catch prey, move around at high speed on unveven surface). Specific motor cortex areas developed at the same time as corpus callosum, in eutherians about 100 million years ago.
Pioneering cingulate fibres use the axons of the HC across the midline; later in evolution additional rostral connections were formed in the lamina terminalis. Specialised glia secrete axon guidance cues, both of which may lead to callosal agenesis if impaired or absent (glia in the induseum griseum and the glial wedge are repellants and the midline zipper glia is an attractant); similar glial constructs exist for the anterior commissure and for the optic chiasm. Some neurons from the midline shape the subcallosal sling as an attractant. Pioneering axons from cingulum become later themselves guides for neocortical axons that fasciculate with them.
Corpus callosum (rostrum, trunk and splenium) is complete around the 15th week; splenium is fully grown by 20 weeks. Both commissural anchors are present until 14 w PMA.
Rakic and Yakovlev 1968.
Echogenicity differs between roof and floor of the corpus callosum.
The isthmus can be slightly less wide between corpus and splenium.
growth and shaping of the corpus callosum
28w PMA
membrane in cavum ?
cavum Vergae with a membrane
Uusally graphics of the midline cavities in development, do not show a membrane between cavum septi pellucidi and cavum Vergae; on occasion there is a well depicted dividing membrane (Feess-Higgins and Larroche 1987). It is not unusual to find partial membranes in the cavum Vergae.
Dandy 1931: CV cavum Vergae, CVI cavum veli interpositi, F fornix, LV lateral ventricle.
1 lateral ventricle
2 third ventricle
3 fornix
4 cavum septi pellucidi/cavum Vergae
5 cavum veli interpositi
6 internal cerebral vein
7 medial posterior choroidal artery
8 plexus
9 corpus callosum
fornix is above cavum veli interpositi
fornix is below cavum Vergae
columnae fornicis join but do not fuse
fornix targets:
precommissural: hypothalamus, septum, lateral dorsal thalamus
postcommissural: mammillary bodies
Doppler view (coronal) of the internal cerebral veins running along the inferolateral border of the cavum Vergae.
layering and spaces under the corpus callosum (with the internal cerebral vein)
Size of the midline cavities in fetal MRI (Jarvis and Griffiths 2020). Following formation, the cavities grow until around 30w PMA to their maximal size to dissappear in most fetuses near term.
The cavum Vergae never occurs alone (Oteruelo 1986). Noncommunicating midline cavities contain cerebrospinal fluid that filters through the septal laminae and is reabsorbed by capillaries and veins of the septa. In adults a persistent cavum septi pellucidi has neuropsychiatric relations. It is more common in boxers (Casson et al. 1984, Bogdanoff and Natter 1989).
large cavum Vergae
midline cavity size in the fetal period; persistence in adults
courtesy dr Schwartz, Essen
Cavum veli interpositi (space around choroid plexus forming the tela choroidea in the roof of the third ventricle) extends caudally into the pineal region beneath the splenium. The course of the internal cerebral veins is away from the splenium. The fornices are downwardly displaced with the presence of the cavum septi pellucidi (SP) and the cavum vergae (CV), resulting in a concave upper border of the cavum velum interpositum.
Cavum above the pineal gland carrying the choroid plexus and its vessels: the cavum of the veli interpositi (Retzius 1896).
cavum veli interpositi
temporal pole
suprasellar
pontocerebellar angle
Two thirds of arachnoid cysts are supratentorial, especially located in the temporal fossa and along the sylvian fissure. Position above the sella turcica, in the cerebellopontine angle, on the vermis and in the quadrigeminal cistern are less common. A cyst may rarely be located between the cerebral peduncles, over the cerebral convexity or interhemispherically. Usually it is a single cyst. In the posterior fossa, mostly located in the sagittal plane, they exert pressure on the aqueduct (behind the colliculi) or interfere with CSF circulation around the cerebellum, provoking hydrocephalus. It is difficult to distinguish an arachnoid cyst from a big cisterna magna because cysts can adapt their shape to the surrounding structures. Histological examination is the only robust way to confirm a diagnosis of arachnoid cyst.
arachnoid cyst
After perinatal subarachnoid haematoma a cyst may replace part of the temporal lobe, similar in imaging to an arachnoid cyst. Exceptionally there is association of large arachnoid cysts with cerebral hemiatrophy. Even for antenatal onset it is believed they result from injury to primitive leptomeninges, causing a split that gradually fills with fluid. Mature cysts may have lost communication with the arachnoid space.
quadrigeminal
Agenesis of the corpus callosum with interhemispheric cyst (McGahan et al. 1988, Griebel et al. 1995, Uematsu et al. 2000, Barkovich et al. 2001, Smith and Levine 2004, Pavone et al. 2005)
Very large and erratic midline cysts can be seen with callosal agenesis. The association of agenesis of the corpus callosum with giant dorsal interhemispheric cyst predicts mild to moderate decrease of cognitive, linguistic and behavioural function, although the occasional child may score average. Left expansion of this cyst weighs on language development. Over half of the children with callosal agenesis and giant midline cyst develop epilepsy. Some need repeated marsupialisation or drainage of expanding cysts in the first years of life.
septal agenesis for comparison ——>
callosal agenesis with interhemispheric cyst
Initial classification of callosal agenesis with interhemispheric cyst (salient features only, Barkovich et al. 2001)
type 1midline cyst is extension or diverticulation of third or lateral ventricle (LV) type 1a: communication with one LV or V3 or with a cephalocoele type 1b: dysgenesis of diencephalic nuclei with partial thalamic fusion, ACC total or partial mid or anterior part type 1c: microcephaly, total ACC and inferior vermis agenesis, wide communication with LVtype 2midline cyst loculated and not communicating with ventricle type 2a: multiloculated cyst on both sides of falx, complete ACC type 2b: with frontal PMG and subependymal heterotopia, cyst content different from CSF, walls contrast enhanced type 2c: with large subcortical heterotopia
brain cavities
A graphic summary of cavities in the newborn brain. In the differential diagnosis should be included:- porencephaly, schizencephaly
- vascular anomaly like vein of Galen malformation
- enlarged cavum septi pellucidi, cavum Vergae
- cavum veli interpositi
- tumour with cavitation.
pineal cyst
A pineal cyst is a unilocular cyst within the pineal gland, with a signal similar to that of CSF. Most pineal cysts (80%) are smaller than 1 cm in diameter; those larger than 1.5 cm can result in hydrocephalus due to compression of the aqueduct of Sylvius (Pereira et al. 2021). In most cases, pineal cysts present peripheral contrast (CT, MR) enhancement, due to the pineal parenchyma, and some contain calcifications. There can be extravasation of the contrast agent, the enhancement simulating a solid lesion, because the pineal parenchyma of the cyst lining has no blood-brain barrier. Pineal cysts are typically found in young adults (20-30 years of age) with a predilection for women (3:1 female to male ratio). They are seen in ~5% of brain MRIs and 20-40% of autopsy series. In high-resolution MRIs, a study found a prevalence of asymptomatic cysts in 23% of healthy subjects.
After perinatal subarachnoid haematoma a cyst may replace part of the temporal lobe, similar in imaging to an arachnoid cyst. Exceptionally there is association of large arachnoid cysts with cerebral hemiatrophy. Even for antenatal onset it is believed they result from injury to primitive leptomeninges, causing a split that gradually fills with fluid. Mature cysts may have lost communication with the arachnoid space.
https://pmc.ncbi.nlm.nih.gov/articles/PMC7863714/
septa in floor of corpus callosum
(Jovanov-Milosević et al. 2006)- transient cellular structures (septa) divide major fiber bundles
- the septa are composed of a GFAP reactive meshwork (glial fibers), neurons, and chondroitin sulphate immunoreactive extracellular matrix
- window of presence of callosal septa is 20 to 36 weeks PMA ; during the early postnatal period the callosal septa become thinner and shorter, lose their neuronal and chondroitin sulphate content
- ? rôle in guidance during intensive growth of callosal fibers in the human brain
- although not objectively measured, a difference in echogenicity between dorsal and ventral part of the corpus callosum is normal in preterms
The majority of axons within the PFP originate from neurons in the medial septum and diagonal band of Broca complex. These neurons project in a topographic manner to the cingulate cortex. The pioneering projections of the PFP and the corpus callosum arrive at the corticoseptal boundary at around the same developmental stage.
The relevance of cinguloseptal fibers in human fetal development is not known.
A perforating pathway (PFP) intersects the corpus callosum perpendicularly at the midline in the dorsoventral axis in mice (Tianzhi S et al. 2001); axons in either the PFP or the corpus callosum make different guidance decisions in the same region.
the cingulo-septal perforant path
septum is vestigial
A thick septum can be demonstrated in normal human fetuses in the early second trimester of gestation. Septal neuroblasts in humans do not mature as functional neurons with synaptic connections before regression begins, hence they do not develop functional importance. The cavum septi pellucidi arises as a pocket between the walls of the infolded primordial hippocampus, bridged by the developing corpus callosum. Beginning at about 15 weeks GA, the human septum begins to regress with loss of its neuronal progenitors but preservation of astrocytes, until it evolves into a pair of thin glial membranes with a space between them, the cavum. The septum persists as such until the early postnatal period when the cavum decreases in width and the membranes fuse into a single midline structure. The cavum is uniformly present in normal fetal brain of less than 36 weeks' gestation but by term only 36% of infants still exhibit a cavum.
A minority of adult brains, including the elderly, may show persistence of a thin cavum septi pellucidi.
In simple mammals, such as rodents, the septum remains a true neural structure. Medial septal projections in the rodent brain are the major cholinergic input into the hippocampus; septal axons synapse with somatostatin-containing GABAergic inhibitory interneurons to suppress seizure activity. Glutamatergic and GABAergic neurons also exist in rodent septal nuclei. Rodent septal nuclei secrete Reelin, similar to Cajal-Retzius neurons of the molecular zone of the cortical plate.
The septum in the mature brains of humans and other advanced mammals thus is an acellular phylogenetic evolutionary vestige still prominent as a complete and functional neural structure in lower vertebrates including simple mammals.
From a historical perspective, the septal fissure was named fünfte Hirnhöle by Burdach in 1822, later called ventriculus septi. The cavum septi pellucidi and cavum Vergae were redescribed by Tenchini in 1880, who noted that its incidence in preterm neonates was 100% (references in Sarnat 2021).
Dandy reported these cava from neurosurgical and postmortem observations in 1931. Unlike the ventricular system, the space between the two vertical leaves of the septa is not lined by ependyma, only by glial cell processes. The septum pellucidum in the late second and third trimesters is a pair of thin glial membranes containing no neurons or axonal pathways.
vimentin staining at 19 w PMA (Sarnat 2001)
common normal cavities in ultrasound
<—— cavum Vergae
<—— cavum veli interpositi
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