Lymphocytic hypophysitis (LYH), attributed to autoimmune mechanisms, typically causes multiple anterior pituitary hormone deficiencies, with corticotroph dysfunction occurring earliest; predominant thyrotroph dysfunction is uncommon. A 65-year-old woman presented with headache, fever, and diplopia. Laboratory tests revealed marked systemic inflammation and cerebrospinal fluid (CSF) pleocytosis. Pituitary magnetic resonance imaging (MRI) demonstrated diffuse enlargement and homogeneous contrast enhancement of the pituitary gland and stalk. Endocrinological evaluation showed paradoxically decreased thyroid-stimulating hormone (TSH) despite low thyroid hormone levels, contrasting with elevated adrenocorticotropic hormone (ACTH) levels. Endocrinological stimulation tests revealed a markedly blunted TSH response, with preserved gonadotropin and growth hormone responses, indicating predominant thyrotroph dysfunction despite preserved corticotroph function. Glucocorticoid therapy resulted in prompt improvement of clinical, laboratory, and MRI findings, with complete recovery of anterior pituitary functions. A presumptive diagnosis of LYH with reversible predominant thyrotroph dysfunction and meningitis secondary to direct extension of pituitary inflammation was established. This case demonstrates that LYH can present with atypical anterior pituitary hormone dysfunction, may be complicated by aseptic meningitis, and requires prompt glucocorticoid therapy for favorable outcomes.

Varicella-zoster virus (VZV) is a neurotropic alpha herpesvirus capable of producing a wide spectrum of CNS disease, ranging from aseptic meningitis and vasculopathy to encephalitis and myelitis. Less widely appreciated is its capacity to extend centrally along the trigeminal pathway into the brainstem, producing intra-axial spinal trigeminal tract involvement that may remain clinically silent or manifest only as a cranial neuropathy, particularly when cerebrospinal fluid (CSF) polymerase chain reaction (PCR) is negative. We describe an immunocompetent 41-year-old man who presented with herpes zoster of the left hemiface in a maxillary-mandibular (V2-V3) distribution, followed by an acute left lower motor neuron facial palsy, initially indistinguishable from Ramsay Hunt syndrome. In the absence of encephalopathy, limb weakness, or cerebellar signs, magnetic resonance imaging of the brain demonstrated linear non-enhancing fluid-attenuated inversion recovery (FLAIR) hyperintensity extending across the posterior pons, medulla, and upper cervical cord, corresponding to the course of the spinal trigeminal tract and nucleus. CSF showed lymphocytic pleocytosis with otherwise unremarkable biochemistry; both herpes simplex virus and VZV PCR were negative. The patient was managed with intravenous acyclovir for 14 days, alongside short-course corticosteroids and supportive care. A transient rise in serum creatinine was managed with hydration and close monitoring while full-dose acyclovir was continued, without acyclovir-related neurotoxicity. Recovery was marked, with the House-Brackmann grade improving from V to III over follow-up and corresponding radiological regression of the brainstem signal change. The picture is best understood as sequential trigeminal-then-facial cranial neuropathy with longitudinally extensive spinal trigeminal tract involvement attributable to centripetal VZV spread, rather than a rhombencephalitic clinical syndrome. Such a combination -- trigeminal-territory zoster with longitudinally extensive spinal trigeminal tract involvement and an isolated facial palsy -- has only rarely been reported. This case illustrates the diagnostic dilemma of PCR-negative VZV CNS disease and underscores the value of clinicoradiological correlation, early antiviral therapy, and close neurological surveillance when a peripheral facial palsy emerges in the setting of cephalic herpes zoster.

We report a case of immune-related aseptic meningitis (irAE meningitis) presenting with multiple cranial nerve symptoms during immune checkpoint inhibitor therapy for lung adenocarcinoma. A 72-year-old woman diagnosed with left lower lobe lung adenocarcinoma initiated combination therapy consisting of carboplatin, paclitaxel, bevacizumab, and atezolizumab. Paclitaxel was subsequently discontinued due to peripheral neuropathy, and maintenance therapy with bevacizumab and atezolizumab followed. Eight months after starting treatment (after four cycles of atezolizumab maintenance), the patient presented with a three-week history of dysgeusia, anosmia, trismus, and neck pain. Cerebrospinal fluid (CSF) analysis revealed lymphocytic and monocytic pleocytosis, while cytological examination showed no malignant cells and bacterial cultures were negative. Brain and neck magnetic resonance imaging (MRI) showed no alternative etiologies. Intravenous prednisolone led to a rapid resolution of all symptoms. The patient was diagnosed with irAE meningitis with concomitant cranial nerve involvement, including the olfactory (I), trigeminal (V), facial (VII), and/or glossopharyngeal (IX) nerves. Intravenous prednisolone led to a rapid resolution of all symptoms. Although irAE meningitis is a known rare adverse event, cases complicated by multiple cranial nerve symptoms are extremely uncommon. This case highlights the phenotypic diversity of neurotoxicity associated with immune checkpoint inhibitors.

Today, minimally invasive oxygen(O2)-ozone(O3) intramuscular lumbar paravertebral injections are used to relieve pain in conditions such as low back pain. Repeated paraspinal, peridural, or spinal O3 injections, when performed under non-aseptic conditions or not performed with proper technique, may carry a risk of parameningeal inoculation of bacteria resulting in meningitis and pneumocephalus. Although this treatment is well tolerated in most cases, the patient may sometimes develop rare but very serious complications. Our study presents a case of pneumocephaly and meningitis due to the injection of an intramuscular O2-O3 mixture directed into the subarachnoid space after dural puncture for the treatment of low back pain. Air-density lesions were detected in the temporal and frontal horns of the left lateral ventricle on the patient's computed tomography scan of the brain. The cerebrospinal fluid appeared slightly cloudy, with a leukocyte count of 4000/mm3, protein level of 483 mg/dL, glucose at 40 mg/dL, and chlorine at 113 mmol/L. Ensuring that ozone injection therapy is performed by qualified professionals and that strict aseptic precautions are taken before the procedure will prevent serious iatrogenic complications such as pneumocephalus and meningitis.

Viral central nervous system (CNS) infections in adults frequently remain unresolved after routine diagnostic testing. We applied probe-based viral metagenomic next-generation sequencing (vmNGS) to cerebrospinal fluid samples from adults with suspected CNS infection and negative conventional diagnostics in a retrospective multicentre study conducted in Spain between 2022 and 2023. Among 40 idiopathic cases, vmNGS detected viral sequences in 6 patients without evidence of coinfection: human pegivirus (HPgV, n=3), Toscana virus (TOSV, n=1), herpes simplex virus type 1 (HSV-1, n=1) and varicella-zoster virus (VZV, n=1). Two HPgV-positive patients were transplant recipients, with neurological disease occurring more than 2 years after transplantation, compatible with possible long-term viral persistence in immunocompromised hosts. TOSV genotype B was identified in a patient residing in central Spain, supporting consideration of TOSV in selected cases of unexplained aseptic meningitis during the vector season, including outside traditionally recognized Mediterranean coastal regions. Furthermore, the failure of syndromic panel testing to detect HSV-1 and VZV highlights the need for complementary diagnostic strategies when clinical suspicion remains high. Overall, the detection of unexpected viral sequences, together with missed clinically actionable infections, supports the use of complementary molecular testing in selected cases of unexplained CNS syndromes when routine diagnostics are negative. These findings highlight the added diagnostic value of vmNGS and provide sequence-level data for future studies of viral diversity and molecular epidemiology in neurological disease.

Aseptic meningitis is a clinical syndrome of meningeal inflammation without clear infectious aetiology. Drug-induced aseptic meningitis is a well-documented but poorly understood side effect of a variety of medications, and has rarely been described with the immunosuppressive and anti-inflammatory drug sulfasalazine. This report describes the case of a man in his 60s presenting with aseptic meningitis after commencing sulfasalazine for seronegative arthritis 1 month prior. Analysis of cerebrospinal fluid showed a predominantly mononuclear leucocytosis, slightly elevated protein, and normal glucose. Cerebrospinal fluid microscopy, culture, sensitivities, and polymerase chain reaction testing were negative for bacterial and viral causes of meningitis. The patient improved with cessation of sulfasalazine. Antimicrobial treatment was ceased with ongoing resolution of symptoms, supporting a diagnosis of sulfasalazine-induced aseptic meningitis. Clinicians should consider a diagnosis of sulfasalazine-induced aseptic meningitis when other aetiologies of meningitis have been excluded, particularly in the first weeks to months of commencing sulfasalazine.

Meningitis is the inflammation of the meninges with an associated abnormal cell count in the cerebrospinal fluid (CSF). Aseptic meningitis, defined by the lack of bacterial growth in cultures, is the most common form, with viruses being a frequent cause. Viral causes of meningitis have become more common as the prevalence of bacterial meningitis has decreased due to vaccinations, and viral meningitis is the most common form of meningitis in many countries. Viral meningitis typically presents with the acute onset of fever, headache, photophobia, neck stiffness, and often nausea and vomiting, although younger children may not show signs of meningeal irritation.  Appropriate and timely evaluation is critical as there are no reliable initial clinical indicators to differentiate bacterial and viral etiologies of meningitis. Viral meningitis is usually a self-limiting illness with a good prognosis. 

Intravenous immunoglobulin (IVIG) is an established therapy for immune-mediated neurological disorders and is generally well-tolerated, although rare neurological adverse effects have been reported. We describe a woman in her 40s treated with IVIG for suspected acute inflammatory demyelinating polyneuropathy following Campylobacter infection. Within 48 hours of therapy, she developed a headache and fever without meningism. Neuroimaging was unremarkable. Cerebrospinal fluid (CSF) analysis demonstrated marked pleocytosis with neutrophilic predominance, initially suggestive of bacterial meningitis. However, inflammatory markers and microbiological investigations were negative. Symptoms resolved rapidly following the discontinuation of IVIG without antimicrobial therapy. A diagnosis of IVIG-induced aseptic meningitis was made. This case highlights that IVIG can produce marked CSF pleocytosis mimicking bacterial meningitis and underscores the importance of clinical correlation to avoid unnecessary antimicrobial treatment.

CXCL12 is a chemokine acting via CXCR4 that plays a key role in inflammatory processes by regulating leukocyte migration and immune responses, making it an important focus of research in neuroinfections. In this study, the CXCL12 chemokine was evaluated as a potential diagnostic marker of different neuroinfections with particular emphasis on tick-borne encephalitis (TBE). A group of 214 patients with confirmed meningitis and/or encephalitis was included and divided according to etiology into TBE, aseptic meningitis, neuroborreliosis, and purulent meningitis. CXCL12 concentration and other inflammatory parameters were measured in cerebrospinal fluid (CSF). CXCL12 levels were compared with those of controls (N = 25) and analyzed statistically. In addition, serum was used to determine albumin concentrations. CXCL12 concentrations were significantly higher in patients with neuroinfections compared to controls and showed good diagnostic performance in the overall study group (AUC = 0.791), with a more moderate diagnostic performance observed in individual etiological groups, except in the purulent meningitis group, where the effect was not statistically significant, likely due to the small sample size. CXCL12 also demonstrated some utility in differentiating between specific etiologies; however, this effect was limited. Better diagnostic performance was observed when CXCL12 was combined with pleocytosis in a composite model differentiating between the TBE group and aseptic meningitis (AUC = 0.761). The presented results indicate the role of CXCL12 in neuroinflammation while simultaneously highlighting its potential in the development of novel diagnostic approaches for viral neuroinfections. Despite higher levels in TBE, its standalone diagnostic value is limited; however, it may enhance diagnostic accuracy when combined with other markers such as pleocytosis.