The special role of CXCL13 in Lyme neuroborreliosis: a case report

The diagnosis of chronic lyme neuroborreliosis can be a challenge even for experienced neurologists. The clinical picture may be multifaceted, including polyradiculitis to cranial nerve palsies, meningitis, encephalomyelitis, encephalopathy and peripheral neuropathy. We report on a patient presenting with basal leptomeningoencephalitis associated with vasculopathy where the chemokine CXCL13 in cerebrospinal fluid played an important diagnostic role.

The Impact of Hyponatremia on the Severity of Childhood Tuberculous Meningitis

Introduction: Hyponatremia and/or hypoglycorrhachia are commonly encountered biochemical derangements during the acute stage of childhood tuberculous meningitis (TBM). Few studies have explored the correlation between these derangements and the staging of TBM disease (severity), or explored their role as biomarkers for vascular ischemic events, hydrocephalus, or seizures.Methods: We aimed to identify the prevalence and the correlation between serum hyponatremia (mild, moderate and severe) and/or hypoglycorrhachia in relation to clinical TBM features such as stage of disease, seizures and stroke in children diagnosed with definite and probable TBM, between 1985 and 2015, at Tygerberg Hospital, Cape town, South Africa.Results: The prevalence of hyponatremia was 344 out of 481 (71.5%) patients; 169 (49.1%) had mild hyponatremia, 146 (42.4%) moderate hyponatremia and 29 (8.4%) severe hyponatremia. Children with severe hyponatremia had higher frequency of stroke [odds ratio (OR) 4.36, 95% confidence interval (CI) 1.24–15.35; p = 0.01], brainstem dysfunction (OR 7.37, 95% CI 2.92–18.61; p < 0.01), cranial nerve palsies (OR 2.48, 95% CI 1.04–5.91; p = 0.04) and non-communicating hydrocephalus (OR 2.66, 95% CI 1.09–6.44; p = 0.03). Children with moderate hyponatremia and mild hyponatremia compared to those without hyponatremia similarly were more likely to exhibit signs of brainstem dysfunction (OR 1.91, 95% CI 1.11–3.28; p = 0.02) and hydrocephalus (OR 3.18, 95% CI 1.25–8.09; p = 0.01), respectively. On multivariable analysis only brainstem dysfunction was significantly associated with severe hyponatremia [adjusted odds ratio (aOR) 4.46, 95% CI 1.62–12.30; p < 0.01]. Children with hypoglycorrhachia compared to normoglycorrhachia were more likely to have had longer symptom duration prior to admission (OR 1.87, 95% CI 1.09–3.20; p = 0.02), non-communicating hydrocephalus (OR 1.64, 95% CI 0.99–2.71; p = 0.05), higher cerebrospinal white cell counts (OR 3.00, 95% CI 1.47–6.12; p < 0.01) and higher CSF protein concentrations (OR 2.51, 95% CI 1.49–4.20; p < 0.01). On multivariable analysis raised CSF protein concentration >1 g/L was significantly associated with hypoglycorrhachia (aOR 2.52, 95% CI 1.44–4.40; p < 0.01). Death rates did not differ by sodium level category or presence of hypoglycorrachia, however an increasing trend of children that had demised was noted the more severe the sodium category.Conclusion: Hyponatremia and/or hypoglycorrhachia occur in more than two-thirds of children with TBM. Severe TBM disease complications such as brainstem dysfunction was associated with moderate hyponatremia, while severe hyponatremia was associated with brainstem dysfunction, stroke, cranial nerve palsies and non-communicating hydrocephalus. Cerebrospinal fluid (CSF) glucose depletion correlated with non-communicating hydrocephalus and increased CSF inflammation.

Lower Cranial Nerve Palsy due to Prevertebral Tuberculosis Infection

Prevertebral tuberculosis is a rare infectious disease that often affects immunocompromised patients in developing countries. We present the case of a patient who complained of headache, dysarthria, and dysphagia. Neurological examination revealed multiple cranial nerve palsies, including the hypoglossal, glossopharyngeal, and vagus nerves. Brain magnetic resonance imaging demonstrated an infiltrative lesion in the prevertebral space, and the biopsy revealed chronic inflammation. On suspicion of immune-mediated inflammation, the patient was treated with intravenous dexamethasone and oral prednisolone, with minimal response. Eleven months after the initial diagnosis, the patient’s neurological symptoms were aggravated, and we detected newly developed pulmonary tuberculosis. After the treatment of pulmonary tuberculosis, his neurological symptoms improved, and the imaging study demonstrated improvements. Although we lacked positive laboratory or biopsy results for tuberculosis, we suspect that the lesions were distant tuberculosis infections. Tuberculosis should be considered in patients with unknown infiltrative mass-like lesions in the prevertebral spaces.

Necrotising Otitis Externa Antibiotic therapy complications: A retrospective cohort analysis

Introduction: Necrotising otitis externa (NOE) is a serious, progressive infection of the external ear canal. If untreated, it can invade into temporal bone, skull-base and surrounding tissue resulting in cranial nerve palsies, neurological infections and death. Patients present with unremitting, severe otalgia, otorrhoea and oedematous ear canals containing granulation. Surgery has a limited role; the mainstay of treatment involves a long course of intravenous antibiotics. Currently, there is no data on the complications of antibiotic treatment for NOE. This project aims to provide evidence on the nature/frequency of severe treatment-related complications requiring a change in antibiotic regime. Methods: A retrospective 5-year cohort analysis was performed on 64 patients who were treated for confirmed NOE with intravenous antibiotic therapy. Clinical notes, blood results and antibiotic prescriptions were documented and analysed. Results: Average duration of treatment was 11 weeks (range=38 weeks). There was an average of 2.1 antibiotic regimes per patient with 10 cases requiring inpatient admission due to treatment-related complications. 63% of treatment changes were directly related to adverse effects of intravenous antibiotics. Drug allergy/intolerance (n=18) and clinical deterioration i.e. Lack of symptomatic improvement and/or worsening inflammatory markers (n=18), were the most common reasons for antibiotic change. Neutropenia, deranged liver function tests and acute kidney injury were also recognised adverse effects of treatment. Conclusion: This study provides the first evidence on the notable frequency of antibiotic-related complications in NOE patients. Larger, multicentre studies are required in the future to validate our findings and will better inform both clinicians and patients of the risks of treatment.

Bilateral Cranial Nerve VI Palsies in Cryptococcal Meningitis, HIV, and Syphilis: A Case Report

Introduction: Cranial nerve (CN) VI palsy is a common complaint seen in the emergency department (ED) and has a wide range of causes. Bilateral CN VI palsies are uncommon and appear to be associated with more severe complications. Case Report: A 29-year-old male presented to the ED from an ophthalmology office for diplopia, headache, and strabismus. He was found to have bilateral CN VI palsies and new-onset seizure in the ED. A lumbar puncture revealed cryptococcal meningitis. Additional tests revealed a new diagnosis of human immunodeficiency virus (HIV), acquired immunodeficiency syndrome (AIDS), and syphilis. Conclusion: Cryptococcal meningitis remains a life-threatening complication of HIV/AIDS. Coinfections with HIV, particularly syphilis, further complicate a patient’s prognosis as both can lead to devastating neurological sequelae. In cryptococcal meningitis, elevated intracranial pressure is a complication that can manifest as seizures, altered mental status, and cranial nerve palsies.

Unilateral Oculomotor Nerve Palsy Associated with Leptomeningeal Carcinomatosis and Intracranial Hypertension

Meningeal carcinomatosis is caused by cancer cells invading the meninges and can cause cranial nerve palsies or intracranial hypertension. Intracranial hypertension can present various symptoms such as headache, visual loss, diplopia and may rarely include unilateral cranial nerve palsy. We report a 57-year-old female with leptomeningeal carcinomatosis and intracranial hypertension who presented as unilateral oculomotor nerve palsy.