Search Results (15)

Idiopathic normal pressure hydrocephalus (iNPH) is a potentially reversible cause of gait disturbance and cognitive impairment in older adults, yet its diagnosis remains challenging and controversial. The core difficulty lies in distinguishing true hydrocephalus from ventricular enlargement secondary to cerebral atrophy or neurodegenerative disease, a distinction now recognized as non-binary. In many patients, ventricular enlargement reflects a continuum ranging from predominantly hydrocephalic iNPH to mixed pathological states combining impaired cerebrospinal fluid (CSF) dynamics and neurodegeneration. Conventional neuroradiological markers, including the Evans Index, the callosal angle, and the disproportionately enlarged subarachnoid-space hydrocephalus (DESH) pattern, provide useful qualitative guidance but are limited by their two-dimensional nature, interobserver variability, and poor sensitivity for differential diagnosis and outcome prediction. Over the past decade, advances in artificial intelligence-based brain volumetry (AI-BrV) have introduced a new paradigm for quantitative structural assessment. By enabling automated, anatomically precise, and reproducible three-dimensional quantification of ventricular and extraventricular CSF, cortical and subcortical gray matter, deep gray matter nuclei, and periventricular white matter, AI-BrV addresses many limitations of traditional imaging approaches. Beyond absolute volume measurements, AI-BrV enables the derivation of composite indices and ratios that may capture disease-specific structural phenotypes and better reflect the underlying pathophysiology of ventricular enlargement. Importantly, AI-BrV pipelines can be applied retrospectively to large legacy neuroimaging datasets and compared with extensive publicly available repositories, facilitating normative modeling, cross-disease analyses, and external validation of volumetric biomarkers. When integrated with clinical data and multivariable statistical or machine-learning frameworks, these approaches hold promise for improving patient selection, refining disease categorization, and supporting more rational decision-making regarding CSF diversion. In this context, AI-BrV offers a unifying framework for reconciling divergent clinical perspectives and advancing iNPH toward a more precise, reproducible, and evidence-based diagnostic and therapeutic paradigm. Full article

Background: Vascular risk factors (VRFs) are known to influence cerebral small vessel disease (cSVD) burden and progression. However, their specific impact on the presence and distribution of each cSVD imaging marker (white matter hyperintensity [WMH], perivascular spaces [PVSs], lacunes, and cerebral microbleeds [CMBs]) and their spatial distribution remains unclear. Methods: We conducted a retrospective analysis of 93 patients with lacunar stroke with a standardized investigational magnetic resonance imaging protocol using a 3T scanner. WMH and PVSs were segmented semi-automatically, and lacunes and CMBs were manually segmented. We assessed the univariable associations of four common VRFs (hypertension, hyperlipidemia, diabetes, and smoking) with the load of each cSVD marker. Then, we assessed the independent associations of these VRFs in multivariable regression models adjusted for age and sex. Spatial lesion patterns were explored with regional volumetric comparisons using Pearson’s coefficient analysis, which was adjusted for multiple comparisons, and by visually examining heatmap lesion distributions. Results: Hypertension was the VRF that exhibited stronger associations with the cSVD markers in the univariable analysis. In the multivariable analysis, only lacunes (p = 0.009) and PVSs in the basal ganglia (p = 0.014) and white matter (p = 0.016) were still associated with hypertension. In the regional analysis, hypertension showed a higher WMH load in deep structures and white matter, particularly in the posterior periventricular regions. In patients with hyperlipidemia, WMH was preferentially found in hippocampal regions. Conclusions: Hypertension was confirmed to be the VRF with the most impact on cSVD load, especially for lacunes and PVSs, while the lesion topography was variable for each VRF. These findings shed light on the complexity of cSVD expression in relation to factors detrimental to vascular health. Full article

Background/Objectives: Idiopathic normal-pressure hydrocephalus (iNPH) is a potentially reversible neurological disorder characterized by gait disturbance, cognitive impairment, and urinary incontinence. Its pathophysiology involves impaired cerebrospinal fluid (CSF) absorption, and recent research has highlighted the role of the glymphatic and meningeal lymphatic systems in this process. However, the factors that trigger the clinical manifestations of iNPH in subclinical cases remain poorly understood. Case Presentation: Herein, we report two rare cases of iNPH in which clinical symptoms only became apparent following systemic infections. An 82-year-old man presented with transient neurological deficits during a course of sepsis caused by Klebsiella pneumoniae. Neuroimaging revealed periventricular changes and mild ventricular enlargement. Shunting and a tap test led to significant improvements to both his gait and cognition. An 80-year-old man with a history of progressive gait disturbance and cognitive decline developed worsening urinary incontinence and acute cerebral infarction caused by Staphylococcus haemolyticus bacteremia. Magnetic resonance imaging revealed a ventriculomegaly with features of disproportionally enlarged subarachnoid space hydrocephalus and a corona radiata infarct. Clinical improvement was achieved after a ventriculoperitoneal shunt was placed. Conclusions: Our two present cases suggest that systemic inflammatory states may act as catalysts for the manifestation of iNPH in patients with predisposing cerebral ischemia or subclinical abnormalities in CSF flow, highlighting the need for higher clinical awareness of iNPH in older patients who present with neurological deterioration during systemic infections. Early diagnosis and timely shunting after appropriate infection control may facilitate significant functional recovery in such patients. Full article

Purpose: This study aims to create a deep learning (DL) model capable of accurately delineating the ventricles, and by extension, the periventricular space (PVS), following the 2021 EPTN Neuro-Oncology Atlas guidelines on T1-weighted contrast-enhanced MRI scans (T1CE). The performance of this DL model was quantitatively and qualitatively compared with an off-the-shelf model. Materials and Methods: An nnU-Net was trained for ventricle segmentation using both CT and T1CE MRI images from 78 patients. Its performance was compared to that of a publicly available pretrained segmentation model, SynthSeg. The evaluation was conducted on both internal (N = 18) and external (n = 18) test sets, with each consisting of paired CT and T1CE MRI images and expert-delineated ground truths (GTs). Segmentation accuracy was assessed using the volumetric Dice Similarity Coefficient (DSC), 95th percentile Hausdorff distance (HD95), surface DSC, and added path length (APL). Additionally, a local evaluation of ventricle segmentations quantified differences between manual and automatic segmentations across both test sets. All segmentations were scored by radiotherapy technicians for clinical acceptability using a 4-point Likert scale. Results: The nnU-Net significantly outperformed the SynthSeg model on the internal test dataset in terms of median [range] DSC, 0.93 [0.86–0.95] vs. 0.85 [0.67–0.91], HD95, 0.9 [0.7–2.5] mm vs. 2.2 [1.7–4.8] mm, surface DSC, 0.97 [0.90–0.98] vs. 0.84 [0.70–0.89], and APL, 876 [407–1298] mm vs. 2809 [2311–3622] mm, all with p < 0.001. No significant differences in these metrics were found in the external test set. However clinical ratings favored nnU-Net segmentations on the internal and external test sets. In addition, the nnU-Net had higher clinical ratings than the GT delineation on the internal and external test set. Conclusions: The nnU-Net model outperformed the SynthSeg model on the internal dataset in both segmentation metrics and clinician ratings. While segmentation metrics showed no significant differences between the models on the external set, clinician ratings favored nnU-Net, suggesting enhanced clinical acceptability. This suggests that nnU-Net could contribute to more time-efficient and streamlined radiotherapy planning workflows. Full article

Perivascular spaces (PVS) support metabolic clearance in the brain and are increasingly recognized as key contributors to dementia pathogenesis. Plasma-based biomarkers, such as glial fibrillary acidic protein (GFAP) and the amyloid β42/40 (Aβ42/40) ratio, show promise in dementia diagnosis but remain understudied in vascular cognitive impairment (VCI). VCI, a major global cause of cognitive decline, may be more prevalent in Southeast Asia. Despite its impact, it is underdiagnosed compared to Alzheimer’s, highlighting the need for early, reliable markers. This study aims to examine how these biomarkers relate to PVS burden and domain-specific cognitive outcomes in VCI. VCI was defined as global cognition as assessed by a Montreal Cognitive Assessment Score <26, along with the presence of confluent white matter hyperintensities (deep white matter hyperintensities score >2 or periventricular hyperintensities >3), and >1 lacuna. A total of 108 participants (mean age of 67.3 years, 51.9% female) were included. Multivariate ordinal regression assessed biomarker associations with PVS grade, adjusting for age and diastolic blood pressure. A Aβ42/40 ratio <0.05 and GFAP >54.1 pg/mL were used as biomarker thresholds to subgroup the participants, and the relationship between these thresholds and cognitive performance was analyzed. Elevated GFAP (p = 0.0438) and a reduced Aβ42/40 ratio (p < 0.01) were correlated with a higher PVS grade. In the subgroup with a low Aβ42/40 ratio, a greater PVS burden was associated with poorer executive function (p = 0.045, β = 0.612), while in those with high GFAP levels, it was linked to more pronounced impairments in learning and memory (p = 0.006, β = 0.375). A lower Aβ42/40 ratio and higher GFAP levels track greater PVS burden in VCI. PVS severity may be associated with domain-specific cognitive decline, highlighting the potential utility of these biomarkers in refining clinical assessments and monitoring disease progression. Full article

Background: To explore the performance of deep medullary vein (DMV) and magnetic resonance imaging (MRI) markers in different intracerebral hemorrhage (ICH) subtypes in patients with cerebral small vessel disease (CSVD). Methods: In total, 232 cases of CSVD with ICH were included in this study. The clinical and image data were retrospectively analyzed. Patients were divided into hypertensive arteriopathy (HTNA)-related ICH, cerebral amyloid angiopathy (CAA)-related ICH, and mixed ICH groups. The DMV score was determined in the cerebral hemisphere contralateral to the ICH. Results: The DMV score was different between the HTNA-related and mixed ICH groups (p < 0.01). The MRI markers and CSVD burden score were significant among the ICH groups (p < 0.05). Compared to mixed ICH, HTNA-related ICH diagnosis was associated with higher deep white matter hyperintensity (DWMH) (OR: 0.452, 95% CI: 0.253–0.809, p < 0.05) and high-degree perivascular space (PVS) (OR: 0.633, 95% CI: 0.416–0.963, p < 0.05), and CAA-related ICH diagnosis was associated with increased age (OR: 1.074; 95% CI: 1.028–1.122, p = 0.001). The DMV score correlated with cerebral microbleed (CMB), PVS, DWMH, periventricular white matter hyperintensity (PWMH), and CSVD burden score (p < 0.05) but not with lacuna (p > 0.05). Age was an independent risk factor for the severity of DMV score (OR: 1.052; 95% CI: 0.026–0.076, p < 0.001). Conclusion: DMV scores, CSVD markers, and CSVD burden scores were associated with different subtypes of ICH. In addition, DMV scores were associated with the severity of CSVD and CSVD markers. Full article

Cognitive impairment (CI) shares common cardiovascular risk factors with acute myocardial infarction (AMI), and is increasingly prevalent in our ageing population. Whilst AMI is associated with increased rates of CI, CI remains underreported and infrequently identified in patients with AMI. In this review, we discuss the evidence surrounding AMI and its links to dementia and CI, including pathophysiology, risk factors, management and interventions. Vascular dysregulation plays a major role in CI, with atherosclerosis, platelet activation, microinfarcts and perivascular inflammation resulting in neurovascular unit dysfunction, disordered homeostasis and a dysfunctional neurohormonal response. This subsequently affects perfusion pressure, resulting in enlarged periventricular spaces and hippocampal sclerosis. The increased platelet activation seen in coronary artery disease (CAD) can also result in inflammation and amyloid-β protein deposition which is associated with Alzheimer’s Dementia. Post-AMI, reduced blood pressure and reduced left ventricular ejection fraction can cause chronic cerebral hypoperfusion, cerebral infarction and failure of normal circulatory autoregulatory mechanisms. Patients who undergo coronary revascularization (percutaneous coronary intervention or bypass surgery) are at increased risk for post-procedure cognitive impairment, though whether this is related to the intervention itself or underlying cardiovascular risk factors is debated. Mortality rates are higher in dementia patients with AMI, and post-AMI CI is more prevalent in the elderly and in patients with post-AMI heart failure. Medical management (antiplatelet, statin, renin-angiotensin system inhibitors, cardiac rehabilitation) can reduce the risk of post-AMI CI; however, beta-blockers may be associated with functional decline in patients with existing CI. The early identification of those with dementia or CI who present with AMI is important, as subsequent tailoring of management strategies can potentially improve outcomes as well as guide prognosis. Full article

Background: Previous studies have demonstrated different MRI characteristics in Asian and Western patients with multiple sclerosis (MS). However, the number of studies performed on Thai patients is still limited. Furthermore, these studies were conducted before the revision of the McDonald criteria in 2017. Methods: A retrospective descriptive study was performed on Thai patients diagnosed with MS, according to the McDonald criteria (2017), in a tertiary care hospital in Thailand. Results: Thirty-two patients were included (twenty-seven female and five male patients). The mean age was 37.8 years. Most (28 patients) had relapsing remitting MS. Brain MRIs were available for all 32 patients, all of which showed abnormalities. The most common locations were the periventricular regions (78.1%), juxtacortical regions (75%) and deep white matter (62.5%). Dawson’s fingers were identified in 20 patients (62.5%). Tumefactive MS was noted in two patients. Gadolinium-enhancing brain lesions were noted in nine patients (28.1%). Optic nerve lesions were found in seven patients. Six of the seven patients showed short segmental lesions with predominant posterior-half involvement. Spinal MRIs were available for 26 patients, with abnormalities detected in 23. Most (11 patients) had lesions both in the cervical and in the thoracic spinal cord. In total, 22 patients (95.7%) showed lesions at the periphery, most commonly at the lateral column. Fifteen patients showed lesions shorter than three vertebral segments (65.2%). Enhancing spinal lesions were noted in 14 patients. Dissemination in space was fulfilled in 31 patients (96.9%). Conclusion: Some of the MRI findings in our study were similar to those of previous studies in Thailand and Asia, emphasizing the difference between Asian and Western MS. Full article

The correlation between cerebral small vessel disease (CSVD) and the outcomes of acute ischemic stroke (AIS) patients after endovascular therapy (EVT) remains elusive. We aimed to investigate the effect of combined white matter hyperintensities (WMH) and enlarged perivascular spaces (EPVS) as detected in magnetic resonance imaging (MRI) at baseline on clinical outcomes in patients with AIS who underwent EVT. AIS patients that experienced EVT were retrospectively analyzed in this single-center study. Using MRIs taken prior to EVT, we rated WMH and EPVS as the burden of CSVD and dichotomized the population into two groups: absent-to-moderate and severe. Neurological outcome was assessed at day 90 with a modified Rankin Scale (mRS). Symptomatic intracerebral hemorrhage (sICH), early neurological deterioration (END), malignant cerebral edema (MCE), and hospital death were secondary outcomes. Of the 100 patients (64.0% male; mean age 63.71 ± 11.79 years), periventricular WMHs (28%), deep WMHs (41%), EPVS in basal ganglia (53%), and EPVS in centrum semiovale (73%) were observed. In addition, 69% had an absent-to-moderate total CSVD burden and 31.0% had a severe burden. The severe CSVD was not substantially linked to either the primary or secondary outcomes. Patients with AIS who underwent EVT had an elevated risk (OR: 7.89, 95% CI: 1.0, 62.53) of END if they also had EPVS. When considering WMH and EPVS together as a CSVD burden, there seemed to be no correlation between severe CSVD burden and sICH, END, or MCE following EVT for AIS patients. Further studies are warranted to clarify the relationship between CSVD burden and the occurrence, progression, and prognosis of AIS. Full article

(1) Objective: to investigate the association between the total burden of cerebral small vessel disease (CSVD) and cognitive function in Parkinson’s disease (PD). (2) Methods: this retrospective study compared clinical and neuroimaging characteristics of 122 PD patients to determine the association between cognitive decline and total burden of CSVD in PD. All patients underwent brain MRI examinations, and their total CSVD burden scores were evaluated by silent lacunar infarction (SLI), cerebral microbleeds (CMB), white matter hyperintensities (WMH), and enlarged perivascular spaces (EPVS). The cognitive function was assessed by administering Mini-Mental State Examination (MMSE). Receiver-operating characteristic (ROC) curve and the area under the ROC curve (AUC) were performed to quantify the accuracy of the total burden of CSVD and PVH in discriminating PD patients with or without cognitive impairment. (3) Results: the PD patients with cognitive impairment had a significantly higher SLI, CMB, periventricular hyperintensities (PVH), deep white matter hyperintensities (DWMH), enlarged perivascular spaces of basal ganglia (BG-EPVS), and the total CSVD score compared with no cognitive impairment. Total CSVD score and MMSE had a significant negative correlation (r = −0. 483). Furthermore, total burden of CSVD and PVH were the independent risk factors of cognitive impairment in PD, and their good accuracy in discriminating PD patients with cognitive impairment from those with no cognitive impairment was confirmed by the results of ROC curves. (4) Conclusions: total burden of CSVD tightly linked to cognitive impairment in PD patients. The total burden of CSVD or PVH may predict the cognitive impairment in PD. Full article

Background and Objectives: Cerebral perivascular spaces (PVS) are part of the cerebral microvascular structure and play a role in lymphatic drainage and the removal of waste products from the brain. White matter hyperintensities (WMH) are hyperintense lesions on magnetic resonance imaging that are associated with cognitive impairment, dementia, and cerebral vascular disease. WMH and PVS are direct and indirect imaging biomarkers of cerebral microvascular integrity and health. In our research, we evaluated WMH and PVS enlargement in patients with normal cognition (NC), mild cognitive impairment (MCI), and dementia (D). Materials and Methods: In total, 57 participants were included in the study and divided into groups based on neurological evaluation and Montreal Cognitive Assessment results (NC group 16 participants, MCI group 29 participants, D group 12 participants). All participants underwent 3T magnetic resonance imaging. PVS were evaluated in the basal ganglia, centrum semiovale, and midbrain. WMHs were evaluated based on the Fazekas scale and the division between deep white matter (DWM) and periventricular white matter (PVWM). The combined score based on PVS and WMH was evaluated and correlated with the results of the MoCA. Results: We found statistically significant differences between groups on several measures. Centrum semiovale PVS dilatation was more severe in MCI and dementia group and statistically significant differences were found between D-MCI and D-NC pairs. PVWM was more severe in patients with MCI and dementia group, and statistically significant differences were found between D-MCI and D-NC pairs. Furthermore, we found statistically significant differences between the groups by analyzing the combined score of PVS dilatation and WMH. We did not find statistically significant differences between the groups in PVS dilation of the basal ganglia and midbrain and DWM hyperintensities. Conclusions: PVS assessment could become one of neuroimaging biomarkers for patients with cognitive decline. Furthermore, the combined score of WMH and PVS dilatation could facilitate diagnostics of cognitive impairment, but more research is needed with a larger cohort to determine the use of PVS dilatation and the combined score. Full article

Progressive forms of multiple sclerosis (MS) are associated with chronic demyelination, axonal loss, neurodegeneration, cortical and deep gray matter damage, and atrophy. These changes are strictly associated with compartmentalized sustained inflammation within the brain parenchyma, the leptomeninges, and the cerebrospinal fluid. In progressive MS, molecular mechanisms underlying active demyelination differ from processes that drive neurodegeneration at cortical and subcortical locations. The widespread pattern of neurodegeneration is consistent with mechanisms associated with the inflammatory molecular load of the cerebrospinal fluid. This is at variance with gray matter demyelination that typically occurs at focal subpial sites, in the proximity of ectopic meningeal lymphoid follicles. Accordingly, it is possible that variations in the extent and location of neurodegeneration may be accounted for by individual differences in CSF flow, and by the composition of soluble inflammatory factors and their clearance. In addition, “double hit” damage may occur at sites allowing a bidirectional exchange between interstitial fluid and CSF, such as the Virchow–Robin spaces and the periventricular ependymal barrier. An important aspect of CSF inflammation and deep gray matter damage in MS involves dysfunction of the blood–cerebrospinal fluid barrier and inflammation in the choroid plexus. Here, we provide a comprehensive review on the role of intrathecal inflammation compartmentalized to CNS and non-neural tissues in progressive MS. Full article

The proliferation of neural stem cells (NSCs)/neuronal precursor cells (NPCs) and the occurrence of postmitotic neuroblasts in the mesencephalic tegmentum of intact juvenile chum salmon, Oncorhynchus keta, and at 3 days after a tegmental injury, were studied by immunohistochemical labeling. BrdU+ constitutive progenitor cells located both in the periventricular matrix zone and in deeper subventricular and parenchymal layers of the brain are revealed in the tegmentum of juvenile chum salmon. As a result of traumatic damage to the tegmentum, the proliferation of resident progenitor cells of the neuroepithelial type increases. Nestin-positive and vimentin-positive NPCs and granules located in the periventricular and subventricular matrix zones, as well as in the parenchymal regions of the tegmentum, are revealed in the mesencephalic tegmentum of juvenile chum salmon, which indicates a high level of constructive metabolism and constitutive neurogenesis. The expression of vimentin and nestin in the extracellular space, as well as additionally in the NSCs and NPCs of the neuroepithelial phenotype, which do not express nestin in the control animals, is enhanced during the traumatic process. As a result of the proliferation of such cells in the post-traumatic period, local Nes+ and Vim+ NPCs clusters are formed and become involved in the reparative response. Along with the primary traumatic lesion, which coincides with the injury zone, additional Nes+ and Vim+ secondary lesions are observed to form in the adjacent subventricular and parenchymal zones of the tegmentum. In the lateral tegmentum, the number of doublecortin-positive cells is higher compared to that in the medial tegmentum, which determines the different intensities and rates of neuronal differentiation in the sensory and motor regions of the tegmentum, respectively. In periventricular regions remote from the injury, the expression of doublecortin in single cells and their groups significantly increases compared to that in the damage zone. Full article

The entry of blood-borne macromolecular substances into the brain parenchyma from cerebral vessels is blocked by the blood–brain barrier (BBB) function. Accordingly, increased permeability of the vessels induced by insult noted in patients suffering from vascular dementia likely contributes to the cognitive impairment. On the other hand, blood-borne substances can enter extracellular spaces of the brain via endothelial cells at specific sites without the BBB, and can move to brain parenchyma, such as the hippocampus and periventricular areas, adjacent to specific sites, indicating the contribution of increased permeability of vessels in the specific sites to brain function. It is necessary to consider influx and efflux of interstitial fluid (ISF) and cerebrospinal fluid (CSF) in considering effects of brain transfer of intravascular substances on brain function. Two pathways of ISF and CSF are recently being established. One is the intramural peri-arterial drainage (IPAD) pathway of ISF. The other is the glymphatic system of CSF. Dysfunction of the two pathways could also contribute to brain dysfunction. We review the effects of several kinds of insult on vascular permeability and the failure of fluid clearance on the brain function. Full article

Until noninvasive neuroradiological examinations were put into practice, the study of the septum pellucidum was only of interest to embryologists and anatomists. The septum pellucidum appears around the 10th–12th embryonic week and deepens around the 16th, forming the cavum septi pellucidi which radiology objectifies frequently and without correspondence with the determined clinical frame. The present study is based on a review of the literature (97 publications) and an anatomical series of 6057 cases (3396 males and 2661 females), with ages ranging from the 21st week of gestation to 95 years. All the cases come from a general hospital.To be included in the study, the individual had to be of known age and sex, and free from any clinical psychiatric syndrome. The volume of the lateral ventricles had to have been measured and the massa intermedia examined. All cases come from brains systematically autopsied in the Division of Neuropathology of the Geneva University Hospital between the years 1971 and 1976 inclusively, and all are free from affections, duly diagnosed, and come from the clinics of this same hospital. The cases used in the study fit the following criteria: (1) knowledge of age and sex; (2) knowledge of the capacity, in cc, of the two lateral ventricles; (3) notion of the presence or absence of the massa intermedia. The first stage of the septum pellucidum is made up of pluripotential stem cells which degenerate quite early, leaving a liquid between them. A number of hypotheses have been put forward to explain the origin of this liquid, without any agreement being reached. Our explanation for the appearance of this liquid is the following: as in every necrosis, the molecular concentration increases after the disintegration of the large protein molecules into amino acids; this concentration necessarily attracts liquid to equalise the oncological pressure. Cellular resorption is easier to study in the periventricular telencephalic matrix than in the resorption of the stem cells of the septum pellucidum, as it occurs a little later, and this makes the microglia, being nearer to maturity, easier to be recognised. The incidence of cavum septi pellucidi during the embryo-foetal phase is quite well-known by virtue of the various concordant results of different authors. In contrast, over the course of adult life, the results published are extraordinarily discordant; moreover, the cases presented are taken together, that is to say, globally. Our results, which take the succession of decades into account, indicate that the cavum septi pellucidi persists among adults in 1224 of the 6057 cases studied, this being an incidence of 20.2%. From 57.7% at birth, the incidence establishes itself quite early in life at around 16%, and this rate is maintained until old age.This stability from one decade to the next supports the hypothesis that the cavum septi pellucidi is resorbed at its own precise moment. 1224 cava septi pellucidi were found in men and 466 in women.This discrepancy works out to a male preponderance of around 3:2, a result which corresponds with the greater part of the literature. The rare documents that deal with hereditary speak against such an origin. The only homozygotes that carry cavum septi pellucidi are those that appear in Craig et al. (Mayo Clin Proc 1953;28:330–5). Just as for the cavum septi pellucidi, the agenesis of the massa intermedia is preponderant in males (x2 of 23,900, Morel [Acta Anatomica 1947;4:203–7]). In our series, it is approximately the same among cavum septi pellucidi carriers as it is in Morel’s series. In an anatomo-clinical and statistical study of the colloid cyst of the third ventricle, made up of 75 cases, found by Witzig (Acta Neurol Belg 1982;82:281–99) in a total of 13,389 autopsies, a very low incidence (0.46%) is noted with a clear male preponderance (62 men, 13 women, x2 of 8.99). In 40 of his cases, 7 were carriers of a cavum septi pellucidi, or 17.5%. This fact confirms the possible co-existence of these two dysgeneses near to one another, estimated by Moseley at 10%. This relation is significant, as each of the two can lead to a hydrocephalus, the origin of which is then to be determined by radiology. The terms cavum and cyst, frequently used to designate each other, are not the same on an anatomical level. The former must be reserved for an enclosed space of liquid content, whose wall does not form an epithelium. In contrast, the cyst, also an enclosed space, has its wall covered by an epithelium and its contents are not always liquid (cellular debris, mucus, squama, cholesterol, etc.). As far as the cavum septi pellucidi is concerned, if at the beginning of life it is indeed a cavum, in the course of life the immature cells bordering become modified and end up as genuine ependymocytes. Many authors have studied these cellular transformations and most of them currently acknowledge that the cavum can transform into a cyst. The seeming ability of a given cavum to expand does not relate to age but perhaps to sex (female predominance), either by genetic programming or hormonal factors. In the cases studied, the enlargement of the cavum septi pellucidi is independent of that of the lateral ventricles of the brain. The association “cavum septi pellucidi-hydrocephalus” has been recognised for a long time. In an attempt to determine this frequency, which is still approximate, we chose 42 publications of anatomo- clinical cases of cavum septi pellucidi, published separately or in small series. They supplied 91 cases. Among the extreme cases, 49 simultaneously show both cavum septi pellucidi and hydrocephalus (28 men, 21 women). When the hind portion of the cavum septi pellucidi is separated from the front by contact between trigona and the corpus callosum, it is referred to as cavum vergae. Certain authors contest its existence by assimilating it to the cavum septi pellucidi. It is, in fact, exceptional (only one case among the 7711 pneumoencephalographies of Finke and Koch [Dtsch Z Nervenheilk 1968; 193:154–7]). Our 4 cases added to the 12 found in the literature indicate a form of female predominance (11 women, 5 men). The correlation with hydrocephalus is vague. None of the 1224 cases studied displayed particular neurological or mental symptoms. In certain cases, where such symptoms exist, one can easily link them to other concomitant dysgeneses. The cavum septi pellucidi can provoke disorders if (a) it attains a certain width (generally given as 10 mm); (b) it is free of fenestration, that is to say, non-communicating; (c) it is expanding. The blocking of one or both of Monro’s holes (Sylvius’ duct in case of cavum vergae) manifests itself through a syndrome of intracranial hypertension and its accompanying symptoms.Among the latter, which are well-known, the various types of epilepsy and mental retardation are too widespread to be taken account of in this context. Moreover, following lesions to the trigona, which remain unproven, certain behavioural and emotional disorders have been linked to secondary lesions of the limbic lobes, also unproven. Singly or doubly partitioned, the septum pellucidum can be split in one or several places. These perforations, which connect the cavum septi pellucidi to the lateral ventricles, are given as fenestration. They are produced under various circumstances: (a) they often accompany the various cerebral atrophies and internal hydrocephalies; (b) they are produced as result of manipulations of the pneumoencephalography and often by certain types of cranio-cerebral traumatism, among which those brought on by boxing are well-documented. Expanding cava septi pellucidi are operated on by means of various neurosurgical operations which range from simple endoscopic fenestration to the placing of a shunt by conventional stereotaxis. Full article