Spatial mapping of dynamic cerebral autoregulation by multichannel near-infrared spectroscopy in high-grade carotid artery disease.

The exact spatial distribution of impaired cerebral autoregulation in carotid artery disease is unknown. In this pilot study, we present a new approach of multichannel near-infrared spectroscopy (mcNIRS) for non-invasive spatial mapping of dynamic autoregulation in carotid artery disease. In 15 patients with unilateral severe carotid artery stenosis or occlusion, cortical hemodynamics in the bilateral frontal cortex were assessed from changes in oxyhemoglobin concentration using 52-channel NIRS (spatial resolution ∼2 cm). Dynamic autoregulation was graded by the phase shift between respiratory-induced 0.1 Hz oscillations of blood pressure and oxyhemoglobin. Ten of 15 patients showed regular phase values in the expected (patho) physiological range.Five patients had clearly outlying irregular phase values mostly due to artifacts. In patients with a regular phase pattern, a significant side-to-side difference of dynamic autoregulation was observed for the cortical border zone area between the middle and anterior cerebral artery (p < 0.05). In conclusion, dynamic cerebral autoregulation can be spatially assessed from slow hemodynamic oscillations with mcNIRS. In high-grade carotid artery disease,cortical dynamic autoregulation is affected mostly in the vascular border zone. Spatial mapping of dynamic autoregulation may serve as a powerful tool for identifying brain regions at specific risks for hemodynamic infarction.

Behind the screen: pseudobulbar symptoms after deep brain stimulation.

BACKGROUND: Thalamotomy was formerly used to treat different tremor syndromes. Nowadays, deep brain stimulation has become an established technique to treat -different movement disorders. The combination of these two stereotactic interventions is rare. CLINICAL PRESENTATION: We present a patient in which a right-sided tremor -syndrome with an underlying pathology of combined essential tremor and Parkinsonian tremor was successfully treated initially with a left-sided thalamotomy and subsequently with -bilateral deep brain stimulation in the subthalamic nucleus. RESULTS: Deep brain stimulation in the subthalamic nucleus resulted in hemidystonia, pathological laughing and crying, dysarthria and dysphagia, all due to dislocation of the stimulation electrodes contacting the internal capsule. After discontinuation of the high-frequency stimulation these side-effects disappeared, but were then reactivated by an LCD television in stand-by mode. CONCLUSION: In this report we discuss the pathophysiology of pseudobulbar symptoms and pathological laughing and crying in context of thalamotomy and dislocated DBS electrodes. Furthermore, we report on the occurrence that magnetic fields in the household have an impact on deep brain stimulation, even if they are in stand-by mode.

Roller coaster-associated subarachnoid hemorrhage--report of 2 cases.

The most common neurological injuries associated with roller coaster rides are subdural hematoma and cervical artery dissection. We report two cases of roller-coaster associated subarachnoid hemorrhage (SAH). A 40-year-old healthy man developed a strong, holocephalic headache during a roller coaster ride. SAH Hunt & Hess grade II and Fisher grade 3 was diagnosed. An underlying aneurysm of the anterior communicating artery was successfully treated with coil embolization. A 41-year-old female (smoker, otherwise healthy) experienced a sudden, strong headache and diplopia during a roller coaster ride. A perimesencephalic SAH (Hunt & Hess grade II, Fisher grade 3) was disclosed by a CT scan. No aneurysm was detected on angiography. Both patients were discharged without neurological disability. In conclusion, SAH is a rare but relevant differential diagnosis in cases of acute headache during roller coaster rides. Both aneurysmal and non-aneurysmal perimesencephalic SAH can occur. A combination of mechanical factors and excessive blood pressure rises in vulnerable persons is discussed.

IL-6 and MYC collaborate in plasma cell tumor formation in mice.

Interleukin-6 (IL-6) plays a critical role in the natural history of human plasma cell neoplasms (PCNs), such as plasma cell myeloma and plasmacytoma (PCT). IL-6 is also at the center of neoplastic plasma cell transformation in BALB/c (C) mice carrying a transgene, H2-L(d)-IL6, that encodes human IL-6 under control of the major histocompatibility complex H2-L(d) promoter: strain C.H2-L(d)-IL6. These mice are prone to PCT, but tumor development is incomplete with long latencies ( approximately 40% PCT at 12 months of age). To generate a more robust mouse model of IL-6-dependent PCN, we intercrossed strain C.H2-L(d)-IL6 with strains C.iMyc(Emu) or C.iMyc(Calpha), 2 interrelated gene-insertion models of the chromosomal T(12;15) translocation causing deregulated expression of Myc in mouse PCT. Deregulation of MYC is also a prominent feature of human PCN. We found that double-transgenic C.H2-L(d)-IL6/iMyc(Emu) and C.H2-L(d)-IL6/iMyc(Calpha) mice develop PCT with full penetrance (100% tumor incidence) and short latencies (3-6 months). The mouse tumors mimic molecular hallmarks of their human tumor counterparts, including elevated IL-6/Stat3/Bcl-X(L) signaling. The newly developed mouse strains may provide a good preclinical research tool for the design and testing of new approaches to target IL-6 in treatment and prevention of human PCNs.