Title: Cerebellar Tonsillar Herniation Following Acute Ischemic Stroke in Meningovascular Neurosyphilis: A Case ReportAbstract:   Introduction: Meningovascular neurosyphilis (MVNS) represents an uncommon manifestation of Treponema pallidum infection, potentially leading to stroke, cerebral edema, and elevated intracranial pressure. Cerebellar tonsillar herniation represents a rare yet critical complication with potentially life-threatening consequences. Timely diagnosis and intervention are critical to avert lethal consequences.Case Presentation: A 20-year-old female presented with headache, dizziness, and altered sensorium, which were preceded by a self-limiting genital lesion eight weeks prior. She exhibited disorientation without any focal neurological deficits. The MRI indicated a left thalamic infarct, while cerebrospinal fluid analysis validated the presence of meningovascular neurosyphilis. Intravenous ceftriaxone and corticosteroids were administered for her treatment. On the 14th day of hospitalization, the patient experienced a generalized seizure accompanied by a rapid deterioration in consciousness. Subsequent imaging revealed widespread cerebral edema and herniation of the cerebellar tonsils. Despite receiving supportive care, she ultimately died due to complications arising from brainstem compression and increased intracranial pressure.Conclusion: This case illustrates the significant consequences of MVNS resulting in infarction, cerebral edema, and tonsillar herniation in a young woman without a previous STD diagnosis. Early neuroimaging, cerebrospinal fluid analysis, and timely antimicrobial therapy are essential. The provision of IV penicillin and prompt surgical decompression are essential, particularly in resource-limited settings.Key Clinical Message: This case shows how a thalamic stroke caused by meningovascular neurosyphilis can quickly lead to cerebral edema and a tonsillar herniation. Neurological problems need to be diagnosed, treated, and decompressed surgically as soon as possible to avoid permanent damage.Keywords: Meningovascular neurosyphilis, ischemic stroke, cerebellar tonsillar herniationIntroduction:Syphilis, caused by Treponema pallidum, can progress to neurosyphilis at any stage. It is more prevalent in high-risk groups, including men who have sex with men and individuals with human immunodeficiency virus (HIV) 1. Early neurosyphilis may involve the meninges, cerebrospinal fluid (CSF), and vasculature 2; syphilitic meningitis and meningovascular forms are more common, and timely treatment along with earlier diagnosis can help prevent late progression to conditions such as tabes dorsalis 3.While most cases resolve spontaneously and remain asymptomatic, approximately 5% progress to meningitis, which may present with seizures, aphasia, hemiplegia, or confusion. Meningovascular neurosyphilis (MVNS), a sub-type, typically occurs as early as six months to seven years after primary infection 4. It causes vascular inflammation, ischemic infarction, cerebral edema, and increased intracranial pressure (ICP) 5.Cerebellar tonsillar herniation, an exceptionally rare but life-threatening consequence of elevated ICP, can result in brainstem compression, hydrocephalus, and fetal cardio-respiratory failure6. Timely recognition and neurosurgical decompression are essential to prevent irreversible injuries 7.We present a rare case of a 20-year-old female with neuro-psychiatric symptoms and altered sensorium, ultimately diagnosed with MVNS complicated by thalamic infarction, which progressed to diffuse cerebral edema and ultimately cerebellar tonsillar herniation. This case underscores the critical importance of early neuroimaging, CSF analysis, and prompt decompression to prevent life-threatening complications.Case History and Examination:A 20-year-old female presented to our hospital with a sudden onset of a dull headache localized to the parietal region. The patient reported dizziness, nausea, vomiting, and orbital pain. The patient presented with a history of multiple episodes of watery vomiting, devoid of bile or blood. The patient reported no fever, visual disturbances, or prior history of trauma, diabetes, or hypertension. The patient’s mother reported that eight months ago, the patient developed a painless, itchy lesion on her genitalia, which resolved spontaneously after two months without treatment. Two weeks ago, she had visited the emergency room with similar symptoms, which painkillers alleviated. The patient exhibited altered sensorium characterized by confusion, disorientation, amnesia, nervousness, personality changes, hostility, aggressive behaviors, hallucinations, and illusions. The patient’s temperature measured 98.9°F, with a pulse rate of 100 beats per minute, a respiratory rate of 20 breaths per minute, blood pressure recorded at 110/90 mm Hg, and oxygen saturation at 94% in room air. On physical examination, pupils were equal, measuring 4 mm in diameter, and exhibited reactivity to light. She experienced disorientation regarding time, place, and person. Motor examinations reveal that muscle bulk, tone, and power in both upper and lower limbs are within normal limits. The plantar reflex, along with other reflexes, was intact. We did not conduct the sensory examination. Aside from the neurological examination, the examination of other systems revealed no significant findings.Differential Diagnosis:At this point, given the patient’s presentation with altered mental status, headache, visual hallucinations, and a prior painless genital lesion, the most probable differential diagnoses included viral encephalitis, bacterial or tubercular meningoencephalitis, autoimmune encephalitis and cerebral vasculitis.

INTRODUCTION:Tuberculosis remains a significant global health burden, with central nervous system (CNS) involvement being a rare but serious manifestation. While pulmonary tuberculosis is the most common form, extrapulmonary manifestations can affect various organs and systems. The CNS involvement in developing countries constitutes nearly 10% of all tuberculosis patients [1]. Tuberculomas with compressive myelopathies without bone involvement are an even rarer occurrence. In the differential diagnosis of extensive spinal cord injuries, particularly in young patients with a history of pulmonary tuberculosis or tuberculous meningitis, it is important to consider the possibility of an intradural extramedullary tuberculoma [2].Here we will be discussing a case of intradural extramedullary tuberculosis of the thoracic spine, with progressive neurological dysfunction. Surgery aims to decompress the spinal cord and remove the tuberculoma, thereby relieving the pressure on the neural tissues and preventing further neurological deterioration [3-5]. The specific surgical technique employed depends on the location and extent of the tuberculoma.Following surgery, anti-tubercular therapy is initiated to target the underlying tuberculosis infection. This typically involves a combination of multiple anti-tuberculosis medications, such as isoniazid, rifampicin, ethambutol, and pyrazinamide [2]. The duration of anti-tubercular therapy may vary but generally lasts several months to ensure complete eradication of the infection. Continual postoperative monitoring assumes paramount importance in assessing neurological recovery and treatment response. Concurrently, physiotherapy and rehabilitation assume significance in facilitating the functional restoration and enhancing the overall quality of life [1].This report aims to discuss the diagnostic challenges, treatment strategy, and clinical outcomes, highlighting the importance of a multidisciplinary approach in managing this uncommon condition.

INTRODUCTION:Tuberculosis (TB) is still one of the most prevalent infections, especially in the developing world. The World Health Organisation (WHO) estimates that there are 8 million new cases annually [1,2]. Cough, sputum with or without haemoptysis, fever, and constitutional symptoms are the hallmark manifestations of an active tuberculosis infection. In patients with pulmonary TB, an increase in haemoglobin levels is regarded as an indicator of a positive response to treatment. Furthermore, Omar et al. found that a fall in platelet count, white blood cell (WBC) count, and erythrocyte sedimentation rate (ESR) were strong indications of clinical response [3]. Despite the possibility of an increase in white blood cells (WBC), which results in lymphocyte predominance, in clinical practice, eosinophilia is a usual finding that is self-limiting in moderate cases, but it is exceedingly infrequent in TB [4,5].Many allergic, viral, and neoplastic conditions may produce peripheral blood eosinophilia, necessitating a variety of examinations and subsequent therapy. Common causes of eosinophilia in children include infections with helminthic parasites, allergic diseases, malignancies, and adverse drug reactions [1,6]. One of the primary goals of the early evaluation is to identify an underlying cause that needs specific therapy. Even though difficulties linked with eosinophilia are more prevalent in individuals with higher eosinophil counts (>1500 eosinophils/uL), the peripheral blood eosinophil count does not accurately assess the risk of organ damage in each patient. A patient with modest peripheral blood eosinophilia may also have significant eosinophil organ involvement. Normal eosinophil counts in the human blood range between 0-350/mm3. This quantity accounts for between 1 and 3% of the differential leukocyte count [7]. Most reports of eosinophilia in tuberculosis describe local eosinophilia as opposed to peripheral eosinophilia [8]. To the best of our knowledge, reported cases are very rare. As a consequence, we describe one case of TB with considerable peripheral eosinophilia and the treatment outcome.

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Trauma or surgery to the lower limbs can cause fat from the marrow within the leg bones to enter the bloodstream and form an embolus. However, if there is cerebral involvement without any pulmonary or dermatological manifestations at diagnosis, it could delay identifying cerebral fat embolism (CFE).