Cerebral Fat Embolism: Clinical Presentation, Diagnostic Steps and Long-Term Follow-Up.

OBJECTIVE: Symptomatic cerebral fat embolism (CFE) is a rare complication that occurs after a traumatic injury or orthopaedic surgery and is diagnostically challenging. No data is currently available concerning long-term follow-up. METHODS: We identified from medical records 9 patients with CFE and revised the clinical signs and the diagnostic process. We then analysed long-term follow-up data, targeting clinical course after discharge, neurological impairment, and current quality of life, using the Barthel index and the modified Rankin Scale. RESULTS: All 9 patients initially showed severe neurological deficits, including disturbance of consciousness ranging from somnolence to coma. During the follow-up period for 3-58 months after the insult 2 patients had died. The 7 patients who remained alive had either recovered completely or showed only minor neurological deficits after rehabilitation. They were nearly independent in daily life and needed only minimal assistance. We performed the first brain biopsy in a patient with CFE. CONCLUSION: Most patients had a good outcome after long-term follow-up. In patients with an unexplained altered state of consciousness after a traumatic injury or an orthopaedic surgery, an MRI with diffusion-weighted imaging must be performed to uncover the characteristic pattern of disseminated hyperintense lesions in the white matter that are associated with CFE.

Two Cases of Severe Tick-Borne Encephalitis in Rituximab-Treated Patients in Germany: Implications for Diagnosis and Prevention.

Rituximab (RTX) has become a standard therapy for certain B cell malignancies and autoimmune diseases. We report 2 RTX-treated patients who developed severe tick-borne encephalitis virus (TBEV) infection. The inability to generate new antibody responses renders RTX-treated patients susceptible to TBEV, impedes laboratory diagnosis, and necessitates preventive vaccination in endemic areas.

Severe Cerebral Venous and Sinus Thrombosis: Clinical Course, Imaging Correlates, and Prognosis.

BACKGROUND: Severe cerebral venous-sinus thrombosis (CVT) is a rare disease, and its clinical course, imaging correlates, as well as long-term prognosis have not yet been investigated systematically. METHODS: Multicenter retrospective study. Inclusion criteria were CVT, Glasgow coma scale ≤9, and treatment in the intensive care unit. Primary outcome was death or dependency, assessed by a modified Rankin Score (mRS) >2 at last follow-up. RESULTS: 114 patients were included. At last follow-up (median 2.5 years), 38 patients (33.3 %) showed no or minor residual symptoms (mRS = 0 or 1), 12 (10.5 %) had a mild (mRS = 2), 13 (11.4 %) a moderate (mRS = 3), 12 (10.5 %) a severe disability (mRS = 4 or 5), and 39 (34.2 %) had died. In bivariate analysis, predictors of poor outcome were any signs of mass effect on imaging, clinical deterioration after admission, and age. In contrast, clinical symptoms on admission and parenchymal lesions per se, such as edema, infarction, or hemorrhage were not predictive. Multivariate predictors of poor outcome were an increase in National Institutes of Health Stroke Scale ≥3 after admission [odds ratio (OR) 6.7], bilateral motor signs in the further course (OR 9.2), and midline shift (OR 5.1). CONCLUSION: The outcome of severe CVT is almost equally divided between severe impairment or death and survival with no or only mild handicap. Specifically, space-occupying mass effect and associated neurologic deterioration seem to determine a poor outcome. Therefore, early detection and treatment of mass effect should be the focus of critical care.

Chest pain and paralysis after pulse prednisolone therapy an unusual case presentation of thyrotoxic periodic paralysis: a case report.

Thyrotoxic periodic paralysis is a disease characterized by recurrent episodes of paralysis and hypokalemia during a thyrotoxic state. Thyrotoxic periodic paralysis is a common complication of hyperthyroidism in Asian populations, but can affect other ethnic groups as well. Due to population mobility, Thyrotoxic periodic paralysis is increasingly common in Western countries. Early diagnosis and prompt treatment of the thyrotoxic state and potassium supplementation prevent life-threatening complications associated with hypokalemia and muscle weakness. We present a young Turkish man who developed acute flaccid paralysis after receiving pulse prednisolone therapy for treatment of Pityriasis versicolor. His muscle strength and serum potassium fully recovered after potassium replacement and treatment of the thyrotoxic state which was a consequence of underlying Graves' disease.

Neurological symptoms in aortic dissection: a challenge for neurologists.

Typically, aortic dissection has to be considered in patients with acute thoracic or abdominal pain and accompanying cardiovascular symptoms. Due to these clinical symptoms, neurologists have not been involved in the routine emergency management of aortic dissection. However, transient or permanent neurological symptoms at onset of aortic dissection are not only frequent (17-40% of the patients), but often dramatic and may mask the underlying condition. Especially in pain-free dissection (which occurs in 5-15%) with predominant neurological symptoms diagnosis of aortic dissection can be difficult and delayed. Affecting the outflow of supra-aortal, spinal as well as extremity arteries leads to a variety of neurological symptoms including disturbances of central or peripheral nervous system. Thrombolysis as an emergency stroke therapy without considering aortic dissection may be life-threatening for these patients. Routine chest X-ray and being alert to physical examination findings such as hypotension, asymmetrical pulses or cardiac murmur may reduce risk of delayed diagnosis or misdiagnosis. Neurological symptoms at onset or in the postoperative course of aortic dissection are not necessarily associated with increased mortality.

Neurological symptoms in type A aortic dissections.

BACKGROUND AND PURPOSE: Aortic dissection typically presents with severe chest or back pain. Neurological symptoms may occur because of occlusion of supplying vessels or general hypotension. Especially in pain-free dissections diagnosis can be difficult and delayed. The purpose of this study is to analyze the association between type A aortic dissection and neurological symptoms. METHODS: Clinical records of 102 consecutive patients with aortic dissection (63% male, median age 58 years) over 7.5 years were analyzed for medical history, preoperative clinical characteristics, treatment and outcome with main emphasis on neurological symptoms. RESULTS: Thirty patients showed initial neurological symptoms (29%). Only two-thirds of them reported chest pain, and most patients without initial neurological symptoms experienced pain (94%). Neurological symptoms were attributable to ischemic stroke (16%), spinal cord ischemia (1%), ischemic neuropathy (11%), and hypoxic encephalopathy (2%). Other frequent symptoms were syncopes (6%) and seizures (3%). In half of the patients, neurological symptoms were transient. Postoperatively, neurological symptoms were found in 48% of all patients encompassing ischemic stroke (14%), spinal cord ischemia (4%), ischemic neuropathy (3%), hypoxic encephalopathy (8%), nerve compression (7%), and postoperative delirium (15%). Overall mortality was 23% and did not significantly differ between patients with and without initial neurological symptoms or complications. CONCLUSIONS: Aortic dissections might be missed in patients with neurological symptoms but without pain. Neurological findings in elderly hypertensive patients with asymmetrical pulses or cardiac murmur suggest dissection. Especially in patients considered for thrombolytic therapy in acute stroke further diagnostics is essential. Neurological symptoms are not necessarily associated with increased mortality.