A Case of Severe Anti-N-Methyl D-Aspartate (Anti-NMDA) Receptor Encephalitis with Refractory Autonomic Instability and Elevated Intracranial Pressure.

Salehi N, Yuan AK, Stevens G, Koshy R, Klein WF.

BACKGROUND Anti-N-methyl D-Aspartate (anti-NMDA) receptor encephalitis is a rare autoimmune panencephalitis that typically presents with acute psychiatric disturbances and neurological deficits. Anti-NMDA receptor encephalitis is associated with certain tumors, most commonly ovarian teratomas. First-line therapy typically involves immunotherapy and tumor resection, if present, with up to 53% of patients experiencing improvement within 4 weeks. Cardiac arrhythmias and increased intracranial pressure have been reported in anti-NMDA receptor encephalitis, but these complications have usually been self-limited. CASE REPORT We report the case of a previously healthy, obese 21-year-old female who presented with acute encephalopathy.

Her psychiatric and neurological function rapidly deteriorated, warranting intubation and mechanical ventilation. Lumbar puncture was performed. Cerebrospinal fluid (CSF) opening pressure was elevated and a lumbar drain was placed. Infectious disease work-up was negative and anti-NMDA receptor antibodies were present in the CSF and serum. Initial treatment included intravenous immunoglobulin (IVIG) therapy, plasmapheresis, methylprednisolone, and bilateral salpingoophorectomy, without clinical improvement. Second-line immunotherapy with cyclophosphamide and rituximab was then administered. The patient also developed intermittent episodes of severe bradycardia and asystole that remained refractory to treatment and required placement of a permanent cardiac pacemaker. CONCLUSIONS Anti-NMDA receptor encephalitis presents with rapidly progressive psychiatric and neurologic dysfunction and can develop a severe and prolonged course with limited response to treatment. Patients can develop severe autonomic dysfunction with bradycardia and asystole that may require placement of permanent cardiac pacemakers. Elevated intracranial pressure may also be associated with anti-NMDA receptor encephalitis, and might contribute to the autonomic instability.

Am J Case Rep. 2018 Oct 12;19:1216-1221. doi: 10.12659/AJCR.911165.

Idiopathic intracranial hypertension following deep brain stimulation for Parkinson's disease

Authors: Finet P, Delavallée M, Raftopoulos C.

Idiopathic intracranial hypertension (IIH) is a syndrome characterized by an increased intracranial pressure of unknown origin arising mainly in overweight females. The typical symptoms of IIH are headaches and papilledema associated with visual disorders, which can often evolve to blindness. We describe the first patient who developed a clinical syndrome related to an IIH following a bilateral subthalamic deep brain stimulation (DBS) procedure for Parkinson's disease with the particularity that the clinical expression of the IIH syndrome was atypical because of the presence of intracerebral electrodes.

Source: PubMed

Acta Neurochir (Wien). 2015 Jan 28.

Management of raised intracranial pressure in children with traumatic brain injury

Authors: Kukreti V, Mohseni-Bod H, Drake J.

Increased intracranial pressure (ICP) is associated with worse outcome after traumatic brain injury (TBI). The current guidelines and management strategies are aimed at maintaining adequate cerebral perfusion pressure and treating elevated ICP. Despite controversies, ICP monitoring is important particularly after severe TBI to guide treatment and in developed countries is accepted as a standard of care. We provide a narrative review of the recent evidence for the use of ICP monitoring and management of ICP in pediatric TBI.

Free full text and source: PMC

Usefulness of intracranial pressure continuous monitoring in pseudotumor cerebri

Authors: Horcajadas Almansa A, Cordero Tous N, Román Cutillas A, Saura Rojas E, Jorques Infante A, Iáñez Velasco B, Sánchez Corral C.

OBJECTIVES: To analyse the usefulness of intracranial pressure (ICP) monitoring in pseudotumor cerebri (PTC).

MATERIAL AND METHODS: Ten patients with suspected PTC, but having incomplete criteria for the syndrome, on whom ICP monitoring was performed. Demographic, clinical and radiological data were collected, as well as ICP monitoring data and related complications. Results were evaluated 6months after surgery.

RESULTS: In relation to demographics, all patients were young females. Mean ICP was less than 250mmH2O in 5 of 8 patients with pathological monitoring. Most patients (62.5%) showed A waves; these were related with higher mean ICP, but not always with papilloedema. All recordings showed high amplitude B waves. Most pathological recordings showed wave amplitudes superior to 5mmHg. There were no complications related to the monitoring technique.

CONCLUSIONS: Clinical and lumbar opening pressure data are not enough to establish PTC diagnosis correctly, especially if patient has been treated previously. Monitoring using ICP is a valuable, safe tool, and very useful in this syndrome. Mean ICP could be normal even with pathological recordings. Morphological analysis is necessary to establish diagnosis. A and B waves are highly related to shunt response. Wave amplitude is related to brain compliance and to shunt response as well.

Impact of intracranial pressure monitoring on mortality in patients with traumatic brain injury: a systematic review and meta-analysis

Authors: Yuan Q, Wu X, Sun Y, Yu J, Li Z, Du Z, Mao Y, Zhou L, Hu J.

OBJECT Some studies have demonstrated that intracranial pressure (ICP) monitoring reduces the mortality of traumatic brain injury (TBI). But other studies have shown that ICP monitoring is associated with increased mortality. Thus, the authors performed a meta-analysis of studies comparing ICP monitoring with no ICP monitoring in patients who have suffered a TBI to determine if differences exist between these strategies with respect to mortality, intensive care unit (ICU) length of stay (LOS), and hospital LOS. METHODS The authors systematically searched MEDLINE, EMBASE, and the Cochrane Central Register of Controlled Trials (Central) from their inception to October 2013 for relevant studies. Randomized clinical trials and prospective cohort, retrospective observational cohort, and case-control studies that compared ICP monitoring with no ICP monitoring for the treatment of TBI were included in the analysis. Studies included had to report at least one point of mortality in an ICP monitoring group and a no-ICP monitoring group. Data were extracted for study characteristics, patient demographics, baseline characteristics, treatment details, and study outcomes. RESULTS A total of 14 studies including 24,792 patients were analyzed. The meta-analysis provides no evidence that ICP monitoring decreased the risk of death (pooled OR 0.93 , p = 0.40). However, 7 of the studies including 12,944 patients were published after 2012 (January 2012 to October 2013), and they revealed that ICP monitoring was significantly associated with a greater decrease in mortality than no ICP monitoring (pooled OR 0.56 , p = 0.0006). In addition, 7 of the studies conducted in North America showed no evidence that ICP monitoring decreased the risk of death, similar to the studies conducted in other regions. ICU LOSs were significantly longer for the group subjected to ICP monitoring (mean difference 0.29 ; p < 0.00001). In the pooled data, the hospital LOS with ICP monitoring was also significantly longer than with no ICP monitoring (MD 0.21 ; p = 0.01). CONCLUSIONS In this systematic review and meta-analysis of ICP monitoring studies, the authors found that the current clinical evidence does not indicate that ICP monitoring overall is significantly superior to no ICP monitoring in terms of the mortality of TBI patients. However, studies published after 2012 indicated a lower mortality in patients who underwent ICP monitoring.

Intracranial hypertension associated with obstructive sleep apnea: A discussion of potential etiologic factors

Authors: Wardly DE.

Obstructive sleep apnea has been shown to increase intracranial pressure, and to be a secondary cause of intracranial hypertension. There are a few theories that attempt to explain this relationship, however there is little data, and even less recognition among physicians that this actually occurs. This paper discusses multiple pieces of data, from anatomical correlates to biochemical information involving neuro-excitotoxicity, as well as hematologic factors and issues surrounding brain edema and blood-brain barrier dysfunction. A complex paradigm for how obstructive sleep apnea may lead to increased intracranial pressure is thus proposed. In addition, suggestions are made for how obstructive sleep apnea must as a result be managed differently in the setting of idiopathic intracranial hypertension.

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