Isolated intracranial hypertension associated with COVID-19.

BACKGROUND: Headache is a frequent complaint in COVID-19 patients. However, no detailed information on headache characteristics is provided in these reports. Our objective is to describe the characteristics of headache and the cerebrospinal fluid (CSF) profile in COVID-19 patients, highlighting the cases of isolated intracranial hypertension. METHODS: In this cross-sectional study, we selected COVID-19 patients who underwent lumbar puncture due to neurological complaints from April to May 2020. We reviewed clinical, imaging, and laboratory data of patients with refractory headache in the absence of other encephalitic or meningitic features. CSF opening pressures higher than 250 mmH2O were considered elevated, and from 200 to 250 mmH2O equivocal. RESULTS: Fifty-six COVID-19 patients underwent lumbar puncture for different neurological conditions. A new, persistent headache that prompted a CSF analysis was diagnosed in 13 (23.2%). The pain was throbbing, holocranial or bilateral in the majority of patients. All patients had normal CSF analysis and RT-qPCR for SARS-CoV-2 was negative in all samples. Opening pressure >200 mmH2O was present in 11 patients and, in six of these, > 250 mmH2O. 6/13 patients had complete improvement of the pain, five had partial improvement, and two were left with a daily persistent headache. CONCLUSIONS: In a significant proportion of COVID-19 patients, headache was associated to intracranial hypertension in the absence of meningitic or encephalitic features. Coagulopathy associated with COVID-19 could be an explanation, but further studies including post-mortem analysis of areas of production and CSF absorption (choroid plexuses and arachnoid granulations) are necessary to clarify this issue.

Primary varicella infection presenting with headache and elevated intracranial pressure.

Primary varicella infection may be associated with neurologic complications, such as cerebritis and meningoencephalitis. Several cases of varicella infection with elevated intracranial pressure have been reported. We describe a 13-year-old immunocompetent girl who presented with a clinical picture of headaches and elevated intracranial pressure as the only manifestation of primary varicella zoster infection. The working diagnosis at first was pseudotumor cerebri based on complaints of headache of 2 weeks' duration, in addition to vomiting and papilledema, without fever or skin eruption. On lumbar puncture, opening pressure was 420 mmH2O, but mild pleocytosis and mildly elevated protein level ruled out the diagnosis of pseudotumor cerebri. Our patient had no history of previous varicella infection, and she did not receive the varicella zoster vaccine. Serology tests, done on admission and repeated 2 months later, suggested primary varicella infection. The literature on varicella infection associated with pseudotumor cerebri or elevated intracranial pressure is reviewed.

Relevance of intracranial hypertension control in the management of Cryptococcus neoformans meningitis related to AIDS.

PURPOSE: To evaluate the relationship between intracranial hyperpressure (HICP) and mortality in patients with cryptococcal meningitis related to AIDS (CMRA). METHODS: This was an observational retrospective study. Patients were treated according to the Infectious Diseases Society of America recommendations during the evaluation period (days 0, 3, 5 and after hospitalization). High intracranial pressure (HICP) was defined as ICP values of C250 mm H20. The correlation between HICP and mortality at each of the three time points considered was investigated. Statistical analysis on the descriptive parameters and on the probability of a "death" event (odds ratio, OR) at each of those three time points was performed using the statistical software program Epidata. RESULTS: Eighty patients were included in this study, of whom 53 (66.25 %) were male. The average age of the patients was 37.5 ± 8.1 (range 22­55) years. The median CD4?lymphocyte cell count was 35 (range 0­367) cells/ml. Among the entire patient cohort, 53 patients had a favorable outcome, and the mortality rate was 33.75 %. At baseline (day 0), 57 subjects (71.5 %) presented HICP, and these patients had a higher mortality rate than those with a normal ICP, but the difference did not reach statistical significance[OR 1.65, 95 % confidence interval (CI) 0.56­4.84]. On day 3, 41 of the patients presented HICP, and HICP at this timepoint was significantly associated with an increased risk of mortality (OR 4.35, 95 % CI 1.56­12.09). On day 5, 35(43.5 %) patients presented HICP, and HCIP at this time point was also significantly associated with higher mortality (OR 7.23, 95 % CI 2.53­20.14). CONCLUSION: The results of this study confirm an association between HICP and mortality in patients with CMRA and indicate that the control of ICP during the first 5 days of hospitalization is more important than managing HICP only at baseline.

Viral-induced intracranial hypertension mimicking pseudotumor cerebri.

BACKGROUND: Pseudotumor cerebri or idiopathic intracranial hypertension is characterized by normal spinal fluid composition and increased intracranial pressure in the absence of a space-occupying lesion. METHODS: This study describes a subgroup of 10 patients with the same typical presenting symptoms (headache, vomiting, and papilledema) but without nuchal rigidity, meningeal signs, or change in mental status. Patients had normal neuroimaging studies and intracranial hypertension but also pleocytosis in the cerebrospinal fluid, suggesting central nervous system infection. From the results it can be hypothesized that those children represent a unique subgroup of viral-induced intracranial hypertension when comparing their risk factors, clinical course, treatment, and outcome with 58 patients who had idiopathic intracranial hypertension. RESULTS: All patients with viral-induced intracranial hypertension presented with papilledema but none had reduced visual acuity or abnormal visual fields, compared with 20.7% of patients who had idiopathic intracranial hypertension. They also responded better to treatment with acetazolamide, needed a shorter duration of treatment (7.7 ± 2.6 months vs 12.2 ± 6.3 months, P = 0.03), and had no recurrences. CONCLUSIONS: The results suggest that children who fulfill the typical presenting signs and symptoms and all diagnostic criteria for pseudotumor cerebri other than the normal cerebrospinal fluid component may represent a unique subgroup of viral-induced intracranial hypertension and should be managed accordingly. The overall prognosis is excellent.

The peptide AF-16 and the AF protein counteract intracranial hypertension.

Intracranial hypertension develops after, for example, trauma, stroke and brain inflammation, and contributes to increased morbidity, mortality, and persistent neuropsychiatric sequelae. Nonsurgical therapy offers limited relief. We investigated whether the peptide AF-16 and the endogenous protein Antisecretory Factor (AF) counteracted abnormal fluid transfer by cells, and lowered raised intracranial pressure (ICP). Adult rats, infected with an encephalitogenic Herpes simplex virus (HSV-1), developed after 5 days' sickness of increasing severity. AF-16 rescued all rats while vehicle treatment only saved 20%. AF-16 from day 4 reduced the ICP in HSV-1-infected rats from 30.7 to 14.6 mmHg and all survived without sequelae. A standardised closed head brain injury in rats raised the ICP. Continuous and intermittent AF-16 kept ICP at an almost normal level. A single dose of AF-16 maintained the raised ICP after a TBI lowered during 3-9 h. The AF protein, enriched in egg yolk, similarly lowered the post-traumatically raised ICP in rats. AF-16 also lowered the ICP in rabbits with diffuse brain injury. We conclude that the peptide AF-16 and the AF protein offer new approaches to treat raised ICP with no side effects.

[Acute inflammatory polyradiculoneuropathy and membranous glomerulonephritis following Epbstein-Barr virus primary infection in a 12-year-old girl]. / Polyradiculonévrite aiguë et glomérulonéphrite extramembraneuse au décours d'une primo-infection à Epstein-Barr virus chez une patiente de 12 ans.

Acute inflammatory polyradiculoneuropathy, or Guillain-Barré syndrome (GBS), is characterized by peripheral nerve demyelination, which leads to rapidly progressive weakness, loss of sensation, and loss of deep tendon reflexes. It is a prototype of postinfectious autoimmune disease, whose pathophysiology is well described in the forms provoked by certain bacteria (molecular mimicry with Campylobacter jejuni), but remains unclear for the forms related to other organisms (cytomegalovirus, Epstein-Barr virus and other herpes group viruses, Mycoplasma pneumoniae). Glomerular lesions can be associated with the neurological symptoms and have also been described after various infections, independently of any signs of polyradiculoneuropathy. We report the observation of a 12-year-old girl who presented with Guillain-Barré syndrome with facial diplegia, ataxia, and intracranial hypertension following Epstein-Barr virus (EBV) primary infection. During the course of the neurological disease, membranous glomerulonephritis (MGN) was diagnosed. The neurological impairment was regressive within 6 months after intravenous immunoglobulin treatment followed by intravenous then oral corticosteroid administration. Viremia remained high more than 6 months after the onset of symptoms. Glomerulopathy progressed independently and finally required immunosuppressant medication with cyclosporine. EBV might be the factor that triggered the autoimmune disorders, as previously reported for systemic lupus erythematosus and multiple sclerosis in children. To the best of our knowledge, this association of 3 conditions (GBS, MGN, and EBV primary infection) has never been reported in the literature.