Cerebral White Matter Edema Research Articles

Posterior reversible encephalopathy syndrome: An uncommon sequelae of Eclampsia

Posterior reversible encephalopathy syndrome (PRES) refers to a clinical neuro-radiologic entity with characteristic features on neuro-imaging depicting posterior cerebral white matter edema. Clinical symptoms include headache, visual disturbances, confusion, and seizures. We report six cases of acute PRES who had eclampsia and presented with recurrent episodes of convulsions and hypertension. Magnetic resonance imaging scan showed diffuse abnormal signal intensities involving deep white matter of occipital region. Follow-up examination after 2 weeks of conservative management, showed marked improvement clinically and on neuro-imaging following which patients were discharged in stable condition.

POS-505 Posterior Reversible Encephalopathy Syndrome in Dialysis Patients and Kidney Disease

Posterior reversible encephalopathy syndrome (PRES) is uncommon condition with characteristic neuroimaging findings of cerebral white matter edema. The clinical presentation varies in severity from headache, confusion, decreased consciousness, visual disturbances, and seizures. It can be fatal if unrecognized early, reversible in some cases, and recurrence is rare. There are few case series describing the potential risk factors and outcomes of PRES syndrome in dialysis patients. We studied the clinical-radiological features of PRES syndrome in dialysis patients and management outcomes.

Neuropathology of Spontaneous Hypertensive Encephalopathy in Cats.

Pathologic features of 12 cats with naturally acquired systemic hypertension and concomitant hypertensive encephalopathy were analyzed. All cats demonstrated acute onset of signs localized to the forebrain and/or brainstem, including stupor, coma, and seizures. All cats had systemic hypertension, ranging from 160 to 300 mm Hg. Gross lesions were identified in 4 of 12 cases, including caudal herniation of the cerebrum and cerebellum, sometimes with compression of the rostral colliculus and medulla. Histologically, all cases featured bilaterally symmetrical edema of the cerebral white matter. Associated vascular lesions, especially arteriolar hyalinosis, were also observed. Concurrent lesions were chronic tubulointerstitial nephritis (11/12 cases), adenomatous hyperplasia of the thyroid gland (4 cases), hypertensive choroidal arteriopathy (6 cases), and left ventricular hypertrophy (5 cases). This study demonstrates that the typical histologic manifestation of spontaneous hypertensive encephalopathy in cats is bilaterally symmetrical edema of the subcortical cerebral white matter.

Trastuzumab-Associated Posterior Reversible Encephalopathy Syndrome in a Patient With Metastatic Gastric Cancer

Introduction: Posterior reversible encephalopathy syndrome (PRES) is a clinical-radiographic syndrome of seizures, headache, altered mental status and posterior cerebral white matter edema on neuroimaging. The exact pathophysiology of PRES is unclear. However, blood brain barrier vascular endothelial dysfunction has been proposed. Trastuzumab is rarely reported as a cause of PRES. To our knowledge, this is second reported case of trastuzumab-associated PRES, and the first case in a gastric cancer patient. Case summary: A 51-year-old female with a history of hypertension and stage 4, HER-2 positive, gastric adenocarcinoma with peritoneal, bone and lymph nodes metastasis. She presented with an episode of tonic clonic seizure. She did not have any previous history of seizures. The patient was diagnosed with stage 4 cancer two years ago. She was started on trastuzumab, cisplatin and capecitabine for 3 cycles and continued trastuzumab till her presentation (last cycle was 4 weeks prior to presentation). Her vital signs and labs are shown in table 1. A Brain MRI w/wo contrast (figure 1) showed bilateral, symmetric areas of T2 FLAIR hyperintensity involving the occipital and posterior parietal lobes. There was no evidence of acute stroke, intracranial hemorrhage or intracranial metastasis. This was suggestive of PRES. A multi-disciplinary discussion involved medicine, neurology and oncology teams decided that PRES could be due to the toxic effect of trastuzumab or hypertension. They decided to discharge patient on levetiracetam, continue trastuzumab, strictly control the BP and repeat the MRI in 3 months. During that period, the patient's BP was controlled on multiple encounters with all readings < 140/90. A repeated brain MRI w/wo contrast showed persistent T2 FLAIR hyperintensity in the occipital and posterior parietal lobes suggestive of PRES. Trastuzumab was held for 1 month. The patient was admitted shortly with worsening epigastric pain and concern of disease progression. An EGD (figure 2) showed a large, malignant looking, partially obstructing mass in the gastric body with no active bleeding. She died after 2 days of cardiac arrest. Conclusion: PRES has been reported with some chemotherapeutic protocols. Whether the toxic effect of the chemotherapy alone or history of metastatic cancer is responsible is not fully understood. It is extremely important to rule out other common causes of PRES, especially poorly controlled hypertension.Figure: Brain MRI w/wo contrast. A) T2-TSE, B) T2- FLAIR sequence. Showing a bilateral, symmetric areas of T2 FLAIR hyperintensity involving the posterior parietal and occipital lobes. There was no evidence of acute stroke, intracranial hemorrhage, hydrocephalus, dural venous sinuses thrombosis or intracranial metastatic disease.Figure: EGD showing a large malignant looking, friable, fungating, ulcerated mass in the gastric body.Table: Table. Patient's vital signs and laboratory workup

Posterior Reversible Encephalopathy Syndrome After Ustekinumab Induction

Biological agents are frequently used in the management of inflammatory bowel disease, and understanding the potential adverse effects of these therapies is markedly important. We report a case of posterior reversible encephalopathy syndrome (PRES), a serious but often reversible neurological disorder, in a young patient with Crohn's disease following induction with ustekinumab. The patient is an 18 year-old Dominican female with Crohn's disease diagnosed 6 years ago with ileocolonic involvement and stricturing and fistulizing phenotype. Since diagnosis, her disease was managed in a step-up fashion with oral mesalamine, 6-mercaptopurine, methotrexate (MTX) and infliximab with periods of medication non-adherence. In the year leading up to presentation, she had multiple complicated hospitalizations due to active Crohn's disease. During this time, infliximab was increased to 10 mg/kg every 4 weeks and MTX was continued weekly. The patient presented to our hospital with abdominal pain after receiving an outpatient infliximab infusion. CT scan showed worsening small bowel disease with new enterocolic and enteroenteric fistulas. Serologic drug monitoring revealed detectable infliximab trough level and low titer anti-drug antibodies. Given the lack of clinical response, infliximab was stopped and ustekinumab (390 mg IV) was subsequently administered 1 week after the last MTX dose. Twelve days after ustekinumab induction, the patient had observed tonic-clonic seizures. Subsequent evaluation was notable for hyponatremia, and MRI brain showed bilateral foci of high signal intensity on T2/FLAIR imaging within the frontal, parietal and occipital lobes consistent with PRES. The patient was started on anti-epileptic medications, and had no further seizures or neurological deficits. Due to concern for PRES as cause of the seizure, ustekinumab was not continued. PRES is a rare and typically reversible neurological disorder that can present with headache, seizure, altered consciousness, and visual change, and may result in death. Neuroimaging reveals symmetric posterior cerebral white matter edema. Only one case of PRES was observed in the ustekinumab clinical trials for psoriasis and psoriatic arthritis, and no cases of PRES were seen during trials of ustekinumab for the management of moderate to severe Crohn's disease. To our knowledge this is the first case reported of PRES occurring after ustekinumab treatment in a patient with Crohn's disease.

Recurarization in a successfully managed case of posterior reversible encephalopathy syndrome (PRES) for emergency caesarean section

Posterior reversible encephalopathy syndrome (PRES) is a clinicoradiologic syndrome of headache, visual changes, altered mental status and seizures with radiologic findings of posterior cerebral white matter edema. It is seen in hypertensive encephalopathy, renal failure, and autoimmune disorders or in patients on immunosuppressants. We report a case of 24-year-old primigravida who presented at term with sudden onset hypertension, neurological deficits, and an episode of the visual blackout. Magnetic resonance imaging showed features suggestive of PRES. She was posted for emergency lower segment cesarean section. General anesthesia was administered and blood pressure managed with antihypertensives. Postoperatively, she developed acute respiratory depression after prophylactic administration of injection magnesium sulfate. This case highlights that good clinical acumen along with early neuroimaging helps in prompt diagnosis, treatment and prevention of long-term neurological sequelae in PRES and the anesthetic implications of administering magnesium sulfate in the immediate post neuromuscular block reversal phase.

Posterior reversible encephalopathy syndrome: An atypical postpartum complication

Posterior reversible encephalopathy syndrome (PRES) is presented by headache, altered mental status, blurring of vision, vomiting and seizure in conjunction with radiological finding of posterior cerebral white matter edema. Data suggest that most cases occur in young middle-aged with marked female preponderance, hypertension being the most common cause. In this case, it was diagnosed in a normotensive patient in the postnatal period that underwent cesarean section. The initial symptoms had misled toward a diagnosis of postdural puncture headache. Symptomatic treatment was started immediately in the ICU. This is an interesting case as the patient was a normotensive one without any other contributory factors and there was unanticipated delay in diagnosing the case until the time we could get a magnetic resonance imaging report.

Posterior reversible encephalopathy syndrome complicating macrophage activation syndrome in a patient with systemic juvenile idiopathic arthritis

Posterior reversible encephalopathy syndrome (PRES) is a distinct clinical entity presenting with a constellation of neurological symptoms and characteristic neuroimaging findings of posterior cerebral white matter edema. In adults, PRES has been associated with a variety of conditions and predisposing factors, including acute hypertension, preeclampsia or eclampsia, renal disease, sepsis, and exposure to immunosuppressants. The syndrome has been reported less frequently in children, with only one publication reporting the association of PRES with macrophage activation syndrome (MAS) in a patient with systemic onset juvenile idiopathic arthritis (SoJIA).

Reversible Posterior Encephalopathy Syndrome Secondary to Sunitinib

Reversible posterior leukoencephalopathy syndrome (RPLS) is clinical radiologic condition associated with neurological symptoms and cerebral white matter edema. It has been associated with uncontrolled hypertension, eclampsia, immunosuppressants, and more recently the use of antiangiogenic drugs. Sunitinib is an inhibitor of the vascular endothelial growth factor receptor widely used in the treatment of metastatic renal cell carcinoma (RCC). We report a rare case of RPLS occurring on therapy with sunitinib in a patient with RCC. Our aim is to highlight the importance of considering RPLS as a diagnostic possibility and to hold sunitinib for RCC patients presenting with neurologic symptoms.

A Pressing Headache

A Pressing Headache

Hypoxia-Induced Acute Mountain Sickness is Associated with Intracellular Cerebral Edema: A 3 T Magnetic Resonance Imaging Study

Acute mountain sickness is common among not acclimatized persons ascending to high altitude; the underlying mechanism is unknown, but may be related to cerebral edema. Nine healthy male students were studied before and after 6-h exposure to isobaric hypoxia. Subjects inhaled room air enriched with N(2) to obtain arterial O(2) saturation values of 75 to 80%. Acute mountain sickness was assessed with the environmental symptom questionnaire, and cerebral edema with 3 T magnetic resonance imaging in 18 regions of interest in the cerebral white matter. The main outcome measures were development of intra- and extracellular cerebral white matter edema assessed by visual inspection and quantitative analysis of apparent diffusion coefficients derived from diffusion-weighted imaging, and B0 signal intensities derived from T2-weighted imaging. Seven of nine subjects developed acute mountain sickness. Mean apparent diffusion coefficient increased 2.12% (baseline, 0.80+/-0.09; 6 h hypoxia, 0.81+/-0.09; P=0.034), and mean B0 signal intensity increased 4.56% (baseline, 432.1+/-98.2; 6 h hypoxia, 450.7+/-102.5; P<0.001). Visual inspection of magnetic resonance images failed to reveal cerebral edema. Cerebral acute mountain sickness scores showed a negative correlation with relative changes of apparent diffusion coefficients (r=-0.83, P=0.006); there was no correlation with relative changes of B0 signal intensities. In conclusion, isobaric hypoxia is associated with mild extracellular (vasogenic) cerebral edema irrespective of the presence of acute mountain sickness in most subjects, and severe acute mountain sickness with additional mild intracellular (cytotoxic) cerebral edema.

Patchy cerebral white matter edema in chronic renal failure

Bilateral patchy cerebral white matter edema was observed in two children with chronic renal failure. Uremia in one case and hypertension or hyponatremia in the other appeared to be the cause of the neurological and radiological findings.