F. Thoemke
University of Mainz
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Publication
Featured researches published by F. Thoemke.
Journal of Neurology, Neurosurgery, and Psychiatry | 2002
J. J. Marx; A. Mika-Gruettner; F. Thoemke; Sabine Fitzek; C Fitzek; Goran Vucurevic; P. P. Urban; Peter Stoeter; H. C. Hopf
Objectives: To evaluate the sensitivity of diffusion weighted magnetic resonance imaging (MRI) for the diagnosis of clinically suspected reversible ischaemic deficits of the brainstem. Methods: A total of 158 consecutive patients presenting with acute signs of brainstem dysfunction were investigated using EPI diffusion weighted MRI within 24 hours of the onset of symptoms. High resolution T1 and T2 weighted imaging was performed as a follow up after a median of six days Results: Fourteen of the 158 patients had a complete clinical recovery within 24 hours (transitory ischaemic attack (TIA)), and 19 patients recovered in less than one week (prolonged reversible neurological deficit (RIND)). Diffusion weighted MRI showed acute ischaemic deficits in 39% of patients with transient neurological deficits. The detection rate seemed to be higher in patients with longer lasting symptoms, but the difference between patients with TIA (29%) and RIND (47%) was not significant. Conclusions: Diffusion weighted MRI is a sensitive indicator of acute ischaemic brainstem deficits even in patients with reversible neurological deficit. Early identification of patients with TIA and increased risk of stroke may influence acute management and improve patient outcome.
Muscle & Nerve | 2001
Juergen J. Marx; F. Thoemke; Sabine Fitzek; Goran Vucurevic; Clemens Fitzek; A. Mika-Gruettner; P. P. Urban; Peter Stoeter; Hanns Christian Hopf
The aim of the study was to investigate the relation of the blink reflex R1 arc to known anatomical brainstem structures. Acute vascular brainstem lesions as identified by magnetic resonance imaging (MRI) of patients with isolated R1 pathology were superimposed into a stereotactic anatomical atlas using a new method of digital postprocessing. Isolated acute brainstem lesions were documented by diffusion‐weighted MRI in 12 of 24 patients with unilateral R1 pathology. The lesions were located in the ipsilateral mid‐ to lower pons. In three patients only, the lesion had partial contact with the principal sensory nucleus of the trigeminal nerve (PSN) on at least one level. In two patients, the lesion involved the medial longitudinal fasciculus. Most lesions were located medially and ventrally to the PSN on transverse slices. Our results underline the high localizing value of changes in the R1 component of the blink reflex in patients with ipsilateral pontine functional deficits. Although available physiological evidence suggests that the R1 component of the blink reflex traverses an oligosynaptic pathway, this MRI study does not support the view that synaptic transmission in the PSN subserves R1. The reflex arc probably descends more medially and ventrally on its course to the facial nucleus.
Journal of Neurology, Neurosurgery, and Psychiatry | 2004
J. J. Marx; G. D. Iannetti; A. Mika-Gruettner; F. Thoemke; Sabine Fitzek; Goran Vucurevic; P. P. Urban; P Stoeter; G. Cruccu; H. C. Hopf
Objectives: To study the incompletely understood sympathoexcitatory pathway through the human brain stem, using a new method of three dimensional brain stem mapping on the basis of digitally postprocessed magnetic resonance imaging (MRI). Methods: 258 consecutive patients presenting with acute signs of brain stem ischaemia underwent biplane T2 and EPI diffusion weighted MRI, with slice orientation parallel and perpendicular to a transversal slice selection of the stereotactic anatomical atlas of Schaltenbrand and Wahren, 1977. The individual slices were digitally normalised and projected onto the appropriate slices of the anatomical atlas. For correlation analysis lesions were imported into a three dimensional model of the human brain stem. Results: 31 of the 258 patients had Horner’s syndrome caused by acute brain stem ischaemia. Only four of the patients with Horner’s syndrome had pontine infarctions, 12 had pontomedullary lesions, and 15 had medullary lesions. Correlation analysis showed significantly affected voxels in the dorsolateral medulla but not in the pons. A statistical comparison with infarct topology in patients with medullary lesions but without Horner’s syndrome indicated that involvement of the medial and ventral part of affected voxels located in the ventrolateral medullary tegmentum was specific for Horner’s syndrome. Conclusions: Based on this first in vivo topodiagnostic study, the central sympathoexcitatory pathway probably descends through the dorsal pons before converging on specific generators in the ventrolateral medullary tegmentum at a level below the IX and X nerve exits.
Journal of Neurology | 2002
Juergen J. Marx; A. Mika-Gruettner; F. Thoemke; Sabine Fitzek; Clemens Fitzek; Goran Vucurevic; P. P. Urban; Peter Stoeter; Hanns Christian Hopf
Abstract The aim of this study was to evaluate the sensitivity of multimodal electrophysiological brainstem testing in the diagnosis of clinically suspected reversible ischemic deficits of the brainstem compared with diffusion weighted MR imaging. We investigated 158 consecutive patients presenting with signs of acute brainstem dysfunction. Serial electrophysiological brainstem tests including masseter reflex, blink reflex, masseter inhibitory reflex, AEP, MEP, EOG and the oculoauricular phenomenon were applied. In 14 of the 158 patients neurological deficits resolved in less than 24 hours, which was suggestive of a transitory ischemic attack (TIA), 19 patients had brainstem signs for more than 24 hours but less than 1 week, suggestive of a reversible ischemic neurological deficit (RIND). Electrophysiological data indicated acute functional brainstem lesions in 54,5 % of patients with transient clinical brainstem impairment. Lesion detection rate was significantly higher when combining electrophysiological data and MRI (60,4 %) than using acute brainstem abnormalities in diffusion weighted MRI alone (39,4 %). We conclude that diffusion weighted MRI and electrophysiological brainstem testing are complimentary sensitive indicators of acute brainstem lesions in patients with reversible neurological deficits. Correct identification of brainstem ischemia influences the therapeutic regimen and may improve patient outcome.
European Journal of Neurology | 2001
J. J. Marx; F. Thoemke; Sabine Fitzek; Goran Vucurevic; Clemens Fitzek; A. Mika-Gruettner; P. P. Urban; Peter Stoeter; H. C. Hopf
We investigated the reliability of a new digital post‐processing magnetic resonance imaging (MRI) technique in ischemic brain stem lesions to identify relations of the lesion to anatomical brain stem structures. The target was a medial longitudinal fasciculus (MLF) lesion, which was evident from ipsilateral internuclear ophthalmoplegia (INO). Sixteen patients with acute unilateral INO and an isolated acute brain stem lesion in T2‐ and EPI‐diffusion weighted MRI within 2 days after the onset of symptoms were studied. The MRI slice direction was parallel and perpendicular to a slice selection of a stereotactic anatomical atlas. The individual slices were normalized and projected in the digitalized atlas. The eye movement disorder was monitored by electro‐oculography. In all patients with clinical or subclinical electro‐oculographically documented INO and MRI proven brain stem infarction the lesion covered or at least partially overlapped the ipsilateral MLF at one or more atlas levels. We conclude that digital post‐processing MRI with normalizing and projecting brain stem lesions in an anatomical atlas is a reliable method to demonstrate the anatomical structures involved by the lesion. Combined with electrophysiological brain stem testing, this method may be a useful tool to identify incompletely understood pathways mediating brain stem reflexes or the generators of evoked potentials.
Cases Journal | 2009
Janina Sollors; Katrin Frauenknecht; Eike Schwandt; Harald D Mueller; Peter Stoeter; Johannes Blum; F. Thoemke
Neurocysticercosis is rare in Western Europe and a high degree of physician awareness is necessary for diagnosis. We describe a case of Neurocysticercosis with a single brain lesion acquired in Germany in which only surgical removal and subsequent histological examination allowed diagnosis whereas diagnostic investigation yielded no pathological findings.
Clinical Neurophysiology | 2007
J. J. Marx; F. Thoemke; G. Iannetti; Marianne Dieterich; P.Stoeter; H. C. Hopf; G. Cruccu
Here we review the essential brain stem circuitry generating saccades. In addition we develop a conceptual scheme for understanding how saccade speed is determined, and how saccadic oscillations (flutter and opsoclonus) are both prevented when fixation is required, and released in pathological circumstances. We introduce new ideas about how the ion channel kinetics of the membranes of brain stem burst neurons (which generate saccades) determine saccade properties with potential therapeutic implications. We illustrate these principles with videos of patients with various disorders of saccade speed, accuracy and stability.
Clinical Neurophysiology | 2007
C. Dierkes; F. Thoemke; Peter Stoeter; Marianne Dieterich; H. C. Hopf; J. J. Marx
reported in the original historical publications. Results: Ten of the 268 cases (3.7%) were matching the minimal clinical criteria of Wallenberg’s syndrome. In all of these patients MRI revealed brain stem infarction affecting the lateral medulla oblongata. Two patients fulfilled the clinical criteria of Babinski–Nageotte and two the criteria of Raymond–Cestan syndrome. One patient showed all signs of Weber’s syndrome. For none of the following classical brain stem syndromes a case matching the clinical criteria as reported in the original publications could be detected: syndromes of Avellis, Benedikt, Brissaud-Sicard, Cestan-Chenais, Dejerine-Spiller, Foville, Millard-Gubler, Nothnagel-Claude and Tapia. Discussion: With the exception of Wallenberg’s syndrome, none of the other historic descriptions of crossed brain stem syndromes seems to play a relevant role in clinical neurology. Wallenberg’s syndrome is a clinical correlate of classical lateral medullary infarction, which is a frequent area of ischemia due to the vascular architecture of the brain stem. In modern neurology, other syndromes may serve as theoretical constructions only, which may illustrate possible neuroanatomical allocations in the human brain stem.
Clinical Neurophysiology | 2007
Peter Stoeter; Goran Vucurevic; J. J. Marx; F. Thoemke
PJ. Central neuromodulation in chronic migraine patients with suboccipital stimulators: a PET study. Brain 2004;127:220–30. Denuelle M, Fabre N, Payoux P, Chollet F, Geraud G. Hypothalamic activation in spontaneous migraine attacks: a PET study. Cephalalgia 2005;25(10):858. May A, Bahra A, Buchel C, Frackowiak RS, Goadsby PJ. Hypothalamic activation in cluster headache attacks. Lancet 1998;352(9124): 275–8. Matharu MS, Cohen AS, Frackowiak RS, Goadsby PJ. Posterior hypothalamic activation in paroxysmal hemicrania. Annals of Neurology 2006;59(3):535–45. May A, Bahra A, Buchel C, Turner R, Goadsby PJ. Functional magnetic resonance imaging in spontaneous attacks of SUNCT: short-lasting neuralgiform headache with conjunctival injection and tearing. Annals of Neurology 1999;46(5):791–4. Rosen SD, Paulesu E, Frith CD, Frackowiak RS, Davies GJ, Jones T, et al. Central nervous pathways mediating angina pectoris. Lancet 1994;344(8916):147–50. Rosen SD, Paulesu E, Nihoyannopoulos P, Tousoulis D, Frackowiak RS, Frith CD, et al. Silent ischemia as a central problem: regional brain activation compared in silent and painful myocardial ischemia. Annals of Internal Medicine 1996;124(11):939–49.
Nervenarzt | 2004
J. J. Marx; F. Thoemke; A. Mika-Gruettner; Sabine Fitzek; Goran Vucurevic; P. P. Urban; Peter Stoeter; Marianne Dieterich; H. C. Hopf