To explore the clinical characteristics and long-term prognosis of nervus intermedius sectioning via a retrosigmoid approach for the treatment of nervus intermedius neuralgia (NIN). A total of 10 NIN patients treated at the First Affiliated Hospital of Fujian Medical University between May 2016 and October 2024 were included retrospectively. All patients underwent nervus intermedius sectioning through the retrosigmoid approach, with combined microvascular decompression (MVD) performed for those with concomitant trigeminal neuralgia (TN) or glossopharyngeal neuralgia (GN) based on intraoperative findings. Surgical efficacy was evaluated using the Barrow Neurological Institute (BNI) Pain Intensity Score, with a follow-up period of 14-109 months. Among the 10 patients [3 males, 7 females; mean age: (58.7±11.5) years; median disease duration: 3.0 years], pain was predominantly electric shock-like (6 cases, 60.0%) and stabbing (3 cases, 30.0%). Beyond typical deep ear pain (6 cases, 60.0%), pain also involved the periauricular area (4 cases, 40.0%), cheek (2 cases, 20.0%), root of tongue (1 cases, 10.0%) and 2/3 of the tongue (1 case, 10.0%). Intraoperative exploration identified offending vessels in 7 cases (anterior inferior cerebellar artery in 5 cases and posterior inferior cerebellar artery in 2 cases). The immediate postoperative efficacy rate (BNI Ⅰ-Ⅱ) was 90.0% (9/10). Over a mean follow-up period of (61.5±31.8) months, the long-term efficacy rate at the last follow-up was 70.0% (7/10). Complications included facial paralysis, taste impairment, and wound infection in 1 case each, with no instances of hearing loss or intracranial infection. Nervus intermedius sectioning is an effective treatment for NIN with a high immediate relief rate, although a certain risk of long-term recurrence remains. For patients with concomitant cranial neuralgias, nervus intermedius sectioning combined MVD can enhance overall therapeutic outcomes.

Neurofilament light chain (NfL) and glial fibrillary acidic protein (GFAP), established biomarkers of neuroaxonal injury and astroglial pathology, are frequently only assessed in blood, which limits conclusions regarding their origin. Bi-compartmental analyses of CSF and serum may help differentiate central or peripheral origin of biomarker elevation. Moreover, studies on NfL and GFAP in distinct neuroinfectious disease (NID) phenotypes, particularly those based on real-world cohorts, are limited. This retrospective monocentric study analyzed CSF and serum from patients with (meningo-)encephalitis/myelitis (TI+; n = 48), meningitis (TI-; n = 80), (cranial) nerve palsies/polyradiculitis (PND; n = 61), and 113 non-neuroinflammatory/non-neurodegenerative controls. A bi-compartmental model using scatter plots and simple linear regression was applied to assess the origin of blood biomarker levels and discriminate between central and peripheral pathology. CSF and serum NfL and GFAP z-scores were significantly higher in TI+ compared with TI- (CSF-GFAP p < 0.001/sGFAP p = 0.0083; CSF-NfL p = 0.003/sNfL p = 0.0004). TI+ and PND differed only in GFAP levels, which were higher in TI+ (CSF-GFAP p = 0.0049/sGFAP p = 0.003). The overall group effect (p ≤ 0.003) and principal findings remained significant after adjustment for age, sex, QAlb, and time since (symptom) onset to LP. Bi-compartmental analysis revealed simultaneous elevation of CSF and serum NfL in TI+, indicating predominantly central origin, whereas PND demonstrated a shift toward higher sNfL levels suggesting peripheral origin. Higher clinical severity (modified Rankin Scale 3-5) was associated with elevated serum and CSF GFAP and NfL (sGFAP p = 0.012/sNfL p = 0.002; CSF-GFAP p < 0.0001/CSF-NfL p = 0.0001), which also predicted unfavorable outcome at discharge (sGFAP p = 0.006/sNfL p = 0.004; CSF-GFAP p = 0.003/CSF-NfL p = 0.012). NfL and GFAP were associated with brain/myelon involvement in NID, predominantly reflecting central pathology. Despite strong CSF-serum correlations, bi-compartmental approaches provide additional insight into biomarker origin and disease compartment.

Paragangliomas are rare neuroendocrine tumors that can arise anywhere from the skull base to the pelvis, but most frequently occur in the head and neck, with the carotid body being the most common site. Subtypes are named according to site of origin, such as glomus tympanicum (behind tympanic membrane) and glomus jugulare (at or near jugular foramen). These tumors may cause cranial nerve deficits depending on location. The following case describes a 51-year-old male who first presented with long-standing right-sided facial paralysis who later developed progressive neurologic symptoms. Imaging revealed multiple head and neck tumors. A multidisciplinary tumor board diagnosed right glomus tympanicum, bilateral glomus jugulare, and bilateral carotid body paragangliomas based on "salt-and-pepper" imaging findings on MRI. Although surgical resection was considered, radiation therapy was ultimately recommended for all of his paragangliomas. The patient underwent radiation therapy with good response and annual surveillance is planned. Given the genetic predisposition for paragangliomas, genetic counseling is essential. Treatment remains individualized, though advances in therapy can improve standardization.

Background and Clinical Significance: Heerfordt syndrome (uveoparotid fever) is an uncommon extrapulmonary expression of sarcoidosis defined by parotid enlargement, uveitis, low-grade fever, and facial nerve palsy. It is identified in fewer than 1% of patients with biopsy-confirmed sarcoidosis, and the co-occurrence of bilateral seventh-nerve palsy with calcitriol-driven obstructive kidney injury has been reported only sporadically. Recognizing this metabolic-renal phenotype is clinically important because it is readily reversible yet easily missed when the chest radiograph is normal. Case Presentation: A 30-year-old man presented with four months of progressive bilateral parotid swelling, sicca symptoms, and intermittent blurred vision, preceded by a self-limited episode of bilateral simultaneous peripheral facial weakness; renal colic developed one month before admission. Evaluation showed parathyroid-hormone-independent hypercalcemia (peak corrected calcium 13.1 mg/dL), a serum angiotensin-converting enzyme level above 100 U/L, and acute kidney injury (creatinine 2.1 mg/dL) caused by bilateral upper-ureteric calculi with hydronephrosis. Posterior uveitis was confirmed ophthalmologically. Chest radiography and high-resolution thoracic computed tomography were unremarkable, with no hilar lymphadenopathy. Parotid gland biopsy demonstrated non-caseating epithelioid granulomas. Bilateral ureteric stenting and oral prednisolone 40 mg daily produced rapid normalization of serum calcium, recovery of renal function, and regression of parotid enlargement. Conclusions: This report characterizes a phenotype that combines bilateral simultaneous facial-nerve involvement, calcitriol-mediated hypercalcemia, and obstructive nephrolithiasis without coexistent pulmonary disease. It argues for early consideration of sarcoidosis whenever hypercalcemia, parotid enlargement, and cranial neuropathy occur together, and reinforces the reversibility of sarcoidosis-related renal injury when corticosteroids are introduced promptly.

Hemangiosarcomas (HSAs) are rare neoplasms in cats, with cutaneous and subcutaneous forms occurring more frequently than visceral HSAs and often associated with chronic ultraviolet radiation exposure. Herein, we report a case of vestibular syndrome secondary to subcutaneous hemangiosarcoma in a 2-year-old cat. The patient was presented with ataxia, proprioceptive deficits, cranial nerve palsy, mild nystagmus, and head tilt. The cat tested positive for feline leukemia virus (FeLV) and feline immunodeficiency virus (FIV), while complete blood count, serum biochemical profile, and albumin-to-globulin ratio were within normal limits. Based on the neurological findings and the absence of systemic abnormalities, central vestibulopathy was suspected. Corticosteroid therapy resulted in transient clinical improvement within 36 hours; however, 48 hours later, the cat developed vocalization and reduced consciousness. Due to the poor prognosis, euthanasia was elected. Necropsy revealed two dark-red subcutaneous nodules (∼1 cm) in the right thoracic region, multifocal omental nodules, and a red mass (3.2 × 2.7 × 1.3 cm) compressing and replacing part of the cerebellar parenchyma. Histopathologically, all nodules consisted of proliferating neoplastic endothelial cells forming irregular vascular channels filled with erythrocytes, consistent with hemangiosarcoma. Cerebellar metastasis accounted for the clinical signs of central vestibulopathy. Although meningoencephalitis is the most common cause of central vestibular disease in cats, neoplasms involving the cerebellum or brainstem should also be considered as differential diagnoses.