Georgiana Munteanu

Cerebral venous sinus thrombosis (CVST) is an uncommon cerebrovascular disorder with heterogeneous manifestations and may occasionally precede the diagnosis of an underlying malignancy. We report the case of a 24-year-old man who presented with recurrent fever, headache, pharyngodynia, and systemic inflammation initially attributed to a sinonasal or odontogenic infectious process. He subsequently developed binocular horizontal diplopia, left abducens nerve palsy, papilledema, severe headache, and nausea. Neuroimaging demonstrated extensive CVST involving the left internal jugular vein, bilateral transverse sinuses, and superior sagittal sinus, without ischemic, hemorrhagic, or tumoral brain parenchymal lesions. Thrombophilia testing identified heterozygous prothrombin G20210A as the only established inherited thrombophilic factor. Despite initial neurological stabilization, the patient developed a rapidly recurrent frontal calvarial, epicranial, and cranio-dural lesion extending toward the superior sagittal sinus, without brain parenchymal involvement or imaging evidence of leptomeningeal disease. Initial morphological assessment suggested Langerhans cell histiocytosis. However, comprehensive histopathological and immunohistochemical reassessment demonstrated diffuse strong CD30 expression, nuclear and cytoplasmic ALK positivity, CD43 expression, and focal epithelial membrane antigen and granzyme B positivity, while CD1a and S100 were negative. These findings established the diagnosis of systemic ALK-positive anaplastic large cell lymphoma with secondary extra-axial cranio-dural involvement. Systemic staging demonstrated disseminated nodal disease and a noncontiguous cranio-dural extranodal lesion, consistent with stage IV disease. Treatment with anticoagulation and six cycles of brentuximab vedotin combined with cyclophosphamide, doxorubicin, and prednisone resulted in a favorable neurological and oncological outcome, with no metabolically active or residual enhancing disease on follow-up imaging. This case emphasizes the importance of continued etiological investigation in young patients with extensive CVST and an atypical clinical course, even when plausible infectious and inherited thrombotic risk factors coexist.

Background: The coexistence of systemic prothrombotic disorders, chronic thromboembolic pulmonary hypertension (CTEPH), chronic hypoxia, and cerebrovascular thrombosis creates complex diagnostic and therapeutic challenges. Case summary: We report the case of a 52-year-old woman with JAK2V617F-positive polycythemia vera, inherited thrombophilic abnormalities, recurrent pulmonary thromboembolism progressing to severe CTEPH, chronic hypoxemia, cerebral venous sinus thrombosis, and right vertebral artery occlusion. Management challenge: The case illustrates persistent thrombotic risk despite anticoagulation, the need for disease-directed cytoreduction, limited access to CTEPH-directed interventional treatment, neurological vulnerability despite preserved brain parenchymal integrity, and the narrow therapeutic margin created by the combined use of anticoagulant, cytoreductive, and pulmonary vasodilator therapy. Particular emphasis is placed on the competing risks of recurrent thrombosis and hemorrhagic complications, especially in the cerebrovascular territory. Conclusion: This case highlights the need for repeated multidisciplinary reassessment in patients with overlapping hematological, pulmonary, and neurological vascular disease. Improved survival in patients with severe multisystemic conditions may increase the clinical relevance of complex presentations requiring coordinated management. Further evidence is needed to support safer, more standardized treatment strategies for patients requiring simultaneous control of thrombosis, pulmonary vascular disease, myeloproliferation, hypoxia, and treatment-related bleeding risk.

Aphasia is a complex neurological syndrome that includes a multitude of signs and symptoms that describe a patient’s inability to use language (understanding and producing spoken and/or written language) after it has already been acquired, which is caused by cerebral lesions situated in the dominant (left) cerebral hemisphere in right-handed people. Aphasia has a prevalence of 25–30% in acute ischemic stroke (especially in arterial infarcts). In patients who suffered cerebral venous and dural sinuses thrombosis (CVST), aphasia has been noticed in almost 20% of cases, its presence being considered a negative predictive factor. We report the case of a 22-year-old right-handed woman with obesity and active smoking (10 cigarettes/day), undergoing treatment with oral contraceptives who presented to the Emergency Department with an intense headache, resistant to usual analgesic treatment, accompanied by language disorders onset within 24 h. The neurological examination was normal, except for language assessment, which revealed the severe impairment of the repetition domain (she was unable to repeat simple words), and difficulty in naming objects with some hesitations and mild comprehension difficulties (especially in complex orders). She underwent neuroimaging examinations at admission. Native Head Computed Tomography revealed spontaneous hyperdensity (parenchymatous hematoma) in the left temporal lobe. Cranial magnetic resonance imaging (MRI) confirmed venous infarction in the left temporal area and a hypointense signal on MRI T2*SW (susceptibility-weighted) in the region of the left lateral sinus and left jugular vein bulb, which confirmed the thrombosis at this level. Associated cortical vein thrombosis was diagnosed on indirect radiological grounds, since hemorrhagic transformation obscured the direct visualization of the adjacent cortical veins. MR venography was not performed at that time, but instead at the 1-month follow-up, MR venography confirmed the chronic, partial thrombosis of the left lateral sinus and left jugular vein bulb. Laboratory data demonstrated an elevated D-dimer and the presence of homozygosity for MTHFR C677T and PAI-1 4G/4G. Anticoagulation in the form of low-molecular-weight heparin was immediately started, followed by chronic treatment with oral anticoagulant (apixaban) and folic acid. The headaches resolved within three days, and her neurological examination was almost normal: the repetition continued being altered for complex phrases. We did not observe any left lateral sinus thrombosis recurrence, or other extra-cerebral embolic events (deep vein thrombosis or pulmonary embolism) during the follow-up year. The immediate anticoagulation since the admission resulted in a favorable outcome. Taking into consideration our interest in monitoring patients with aphasia secondary to CVST, we also analyzed data from the literature regarding the incidence of conduction aphasia and other aphasic syndromes in this CVST. Due to the limited number of articles identified in the last 21 years (2005–2026) in the literature, we concluded that conduction aphasia is an extremely rare clinical presentation in this kind of pathology and further studies should be conducted in order to identify significant statistical data.

Cerebral venous sinus thrombosis (CVST) is a rare form of stroke with heterogeneous clinical presentation and etiological profile. This study aimed to evaluate the demographic, clinical, imaging, etiological, treatment, and outcome characteristics of CVST in a Romanian population. We conducted a retrospective monocentric cohort study including 55 patients diagnosed over a six-year period in a tertiary neurological center. CVST accounted for 1.2% of all stroke cases, with an incidence of 13.75 per million per year. Gender distribution was relatively balanced, differing from international cohorts, and traditional female-specific risk factors were less prominent. Thrombophilia (68.6%) and infections (38.2%) were the most frequent etiologies. Younger patients were more frequently associated with thrombophilia, while a higher inflammatory response was observed in older individuals; additionally, female patients showed a higher prevalence of the MTHFR C677T mutation. Transverse and sigmoid sinuses were the most affected, while cavernous sinus involvement was more frequent than typically reported and associated with infections. At discharge, long-term anticoagulation was recommended in 67.3% of patients, tailored to underlying etiology and risk profile. Outcomes were favorable, with 70–80% achieving a modified Rankin Scale score ≤2 at discharge and over 90% at 90-day follow-up, despite inconsistent correlation with imaging findings. These results highlight the heterogeneous nature of CVST and the need for comprehensive, individualized evaluation and management.

Vascular cognitive impairment (VCI) includes any degree of cognitive impairment, from subjective cognitive decline to mild cognitive impairment, to dementia that shares a presumed vascular cause (stroke and/or vascular risk factors) alone or in combination (additive or synergistic interactions) with neurodegenerative pathology. The vascular contribution to dementia represents at least 20–40% of all dementia cases. On one hand, cognitive decline produced by an acute stroke is the most well-known type of VCI; on the other hand, different cerebrovascular diseases, especially subclinical cerebral white matter lesions and subclinical microinfarcts (representing types of cerebral small-vessel diseases), can determine insidious cognitive decline. The most important mechanism of VCI is chronic age-related dysregulation of cerebral blood flow. If vascular risk factors are detected in midlife, they envisage cognitive impairment later in life. In this chapter, we present recent data concerning the epidemiology, mechanisms, diagnostic criteria, neuroimaging features, and vascular risk factors of VCI.

Background: The Improved Health Care in Neurology and Psychiatry—Longer Life (IHCNP) study was an 18-month prospective, observational, non-interventional research study focused on patients with mild cognitive impairment (MCI) following ischemic stroke. Objectives: Our secondary analysis of the IHCNP data aimed to document the progression of MCI in this patient group. Methods: A total of 100 patients from Romania were recruited, all of whom underwent cognitive assessments using the Mini-Mental State Examination (MMSE), Montreal Cognitive Assessment (MoCA), and Rey Auditory Verbal Learning Test (RAVLT). Clinical evaluations were also conducted as part of the study. Baseline cognitive scores were recorded, and subsequent follow-ups documented cognitive changes over time. Results: At baseline, cognitive scores indicated mild impairment, with averages of MMSE 25.41, MoCA 23.27, and RAVLT 33.63. By the end of the study, patients exhibited a significant cognitive decline, with MMSE scores dropping by 8.7%, MoCA by 10.0%, and RAVLT by 29.5% (p < 0.0001 for all measures), reflecting the progressive nature of MCI post-stroke. Conclusions: These findings highlight the importance of early diagnosis and intervention to mitigate cognitive decline in post-stroke patients. The study underscores the need for ongoing cognitive monitoring to improve patient outcomes and manage MCI progression effectively.

Cerebral veins and dural sinus thrombosis (CVT) represents a rare cause of stroke. In adults, CVT has a higher frequency among cases with inherited thrombophilia, mostly women, patients with malignancy, or infections. Two pathophysiological mechanisms contribute to their clinical presentation: diminution of cerebrospinal fluid absorption and increase of venular and capillary pressure. Four major syndromes have been described as isolated or in combination: intracranial hypertension, focal neurological deficits, seizures, and encephalopathy. Non-enhanced CT (NECT) of the head is the most frequently performed imaging study in the emergency department. Features of CVT on NECT can be divided into direct signs (detection of venous clot within a venous channel) and, more frequently, indirect signs (such as cerebral edema or cerebral venous infarct). CVT diagnosis is confirmed with CT venography, which can be performed immediately after NECT, and detects the venous clot as a filling defect, or magnetic resonance imaging (MRI)/MR venography. Different imaging techniques may need to be combined to avoid pitfalls. Conclusions: CVT is a relatively rare disorder in the general population and due to its wide clinical spectrum is frequently misdiagnosed upon initial examination. The knowledge of variable clinical aspects and imaging signs will be essential in providing a timely diagnosis.

(1) Background: Cerebral venous and dural sinus thrombosis (CVT) rarely appears in the adult population. It is difficult to diagnosis because of its variable clinical presentation and the overlapping signal intensities of thrombosis and venous flow on conventional MR images and MR venograms. (2) Case presentation: A 41-year-old male patient presented with an acute isolated intracranial hypertension syndrome. The diagnosis of acute thrombosis of the left lateral sinus (both transverse and sigmoid portions), the torcular Herophili, and the bulb of the left internal jugular vein was established by neuroimaging data from head-computed tomography, magnetic resonance imaging (including Contrast-enhanced 3D T1-MPRAGE sequence), and magnetic resonance venography (2D-TOF MR venography). We detected different risk factors (polycythemia vera-PV with JAK2 V617F mutation and inherited low-risk thrombophilia). He was successfully treated with low-molecular-weight heparin, followed by oral anticoagulation. (3) Conclusions: In the case of our patient, polycythemia vera represented a predisposing risk factor for CVT, and the identification of JAK2 V617F mutation was mandatory for the etiology of the disease. Contrast-enhanced 3D T1-MPRAGE sequence proved superior to 2D-TOF MR venography and to conventional SE MR imaging in the diagnosis of acute intracranial dural sinus thrombosis.

Aphasia is an acquired central disorder of language that affects a person’s ability to understand and/or produce spoken and written language, caused by lesions situated usually in the dominant (left) cerebral hemisphere. On one hand aphasia has a prevalence of 25–30% in acute ischemic stroke, especially in arterial infarcts. On the other hand, cerebral venous and dural sinuses thrombosis (CVT) remains a less common and underdiagnosed cause of ischemic stroke (0.5–1% of all strokes). Aphasia has been observed in almost 20% of patients who suffered CVT. The presence of aphasia is considered a negative predictive factor in patients with stroke, severe language disorders corresponding to arduous recovery. Taking into consideration data from the literature, aphasia is also considered a predictive factor for patients with CVT; its absences, together with the absence of worsening after admission, are determinants of complete recovery after CVT. This review has as the principal role of gathering current information from the literature (PubMed database 2012–2022) regarding the clinical features of aphasic syndromes and its incidence in patients with CVT. The main conclusion of this review was that aphasic syndromes are not usually the consequence of isolated thrombosis of dural sinuses or cerebral veins thrombosis. The most frequent form of CVT that determines aphasia is represented by the left transverse sinus thrombosis associated with a posterior left temporal lesion (due to left temporal cortical veins thrombosis), followed by the superior sagittal sinus thrombosis associated with a left frontal lesion (due to left frontal cortical veins thrombosis). Only a few cases are presenting isolated cortical veins thrombosis and left thalamus lesions due to deep cerebral vein thrombosis. We also concluded that the most important demographic factor was the gender of the patients, women being more affected than men, due to their postpartum condition.

Giant cell arteritis (GCA) is a primary autoimmune vasculitis that specifically affects medium-sized extracranial arteries, like superficial temporal arteries (TAs). The most important data to be considered for the ultrasound (US) diagnosis of temporal arteritis are stenosis, acute occlusions and “dark halo” sign, which represent the edema of the vascular wall. The vessel wall thickening of large vessels in GCA can be recognized by the US, which has high sensitivity and is facile to use. Ocular complications of GCA are common and consist especially of anterior arterial ischemic optic neuropathies or central retinal artery occlusion with sudden, painless, and sharp loss of vision in the affected eye. Color Doppler imaging of the orbital vessels (showing low-end diastolic velocities and a high resistance index) is essential to quickly differentiate the mechanism of ocular involvement (arteritic versus non-arteritic), since the characteristics of TAs on US do not correspond with ocular involvement on GCA. GCA should be cured immediately with systemic corticosteroids to avoid further visual loss of the eyes.