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Biomedical subjects

C M Bütefisch

Publications and source records attributed to C M Bütefisch.

10 recordsLinked to original sources
PubMed2006

Neurobiological bases of rehabilitation.

The adult brain maintains the ability to reorganise throughout life. Motor cortical representations can reorganise rapidly in response to different stimuli. Important mechanisms for mediating reorganisation in the cerebral cortex involve the unmasking of existing, but latent, horizontal connections and modulation of GABAergic inhibition and synaptic efficacy. Interfering with these mechanisms can either block or enhance reorganisational processes. Following injury to the motor cortex alterations of the neurotransmitter system regulation, recruitment of additional undamaged brain areas even remote from the injury, and anatomical alterations such as axonal sprouting and synaptogenesis in the brain tissue surrounding the lesion or in the homotopic motor area of the non-affected hemisphere occur. The understanding of cortical reorganisation may enable us to apply principles of plasticity to the rehabilitation of patients after brain injury.

Amphetamine↗
PubMed2005

Recruitment of contralesional motor cortex in stroke patients with recovery of hand function.

In neuroimaging studies of stroke patients, coactivation may account for increased recruitment of bilateral motor areas when moving the affected limb. Here we studied eight patients after stroke with fMRI and simultaneous EMG. Bilateral recruitment of premotor and primary motor cortices was evident in five patients with strictly unilateral performance per EMG. Because patients had excellent motor recovery, this increased recruitment suggests an adaptive response to the infarct.

Adaptation, Physiological↗
PubMed2005

Functional activation within the PI-DWI mismatch region in recovery from ischemic stroke: preliminary observations.

In this study, we sought to investigate if brain tissue affected by ischemia can accommodate areas of activation related to restoration of brain function following ischemic stroke. In two patients perfusion imaging (PI) and diffusion weighted imaging (DWI) obtained in the acute phase after stroke was coregistered with BOLD imaging of brain functions acquired when profound recovery had occurred. Both patients suffered from thrombembolic brain infarction due to dissection of the internal carotid artery (ICA) characterized by a severe PI-DWI mismatch in the acute stage of stroke. Following ICA recanalization and clinical recovery BOLD imaging showed task-specific activation adjacent to the infarct lesion within the former PI-DWI mismatch area. The data in these two stroke patients provide evidence that brain tissue at risk of infarction as shown by the PI-DWI mismatch can survive and, thereby, constitute the major site underlying post-ischemic recovery.

Adult↗
PubMed2005

Reorganization of cerebral circuits in human brain lesion.

Recovery after focal brain lesions is supposed to be mediated by cerebral reorganization. Stroke is a powerful model to study these processes in the human brain, since middle cerebral artery infarction is a common neurological disease with a clearly defined onset of a lateralized sensorimotor deficit syndrome. Brain tumours constitute a further model differing from stroke by their slow lesion dynamics. Evidence from functional neuroimaging and transcranial magnetic stimulation will be presented showing that recovery of hand function is related to reorganization of local perilesional and large-scale circuits involving the contralesional hemisphere.

Adaptation, Physiological↗
PubMed2002

Enhancement of use-dependent plasticity by D-amphetamine.

In healthy individuals, motor training can elicit use-dependent plasticity. Here the authors studied six subjects in whom training alone failed to elicit this effect. Administration of a single dose of 10 mg of D-amphetamine preceding training led to use-dependent plasticity in a subgroup of these subjects. Using pharmacologic interventions to enhance the effects of motor training might help rehabilitative efforts in patients in whom training alone fails.

Adult↗
PubMed2002

Cholinergic influences on use-dependent plasticity.

Motor practice elicits use-dependent plasticity in humans as well as in animals. Given the influence of cholinergic neurotransmission on learning and memory processes, we evaluated the effects of scopolamine (a muscarinic receptor antagonist) on use-dependent plasticity and corticomotor excitability in a double-blind placebo-controlled randomized design study. Use-dependent plasticity was substantially attenuated by scopolamine in the absence of global changes in corticomotor excitability. These results identify a facilitatory role for cholinergic influences in use-dependent plasticity in the human motor system.

Administration, Cutaneous↗
PubMed2001

Mechanisms underlying human motor system plasticity.

There has been increased interest in the ability of the adult human nervous system to reorganize and adapt to environmental changes throughout life. This ability has been termed "plasticity." Plastic changes in the cerebral cortex have been studied: (a) as modifications of sensory or motor cortical representation of specific body parts (cortical maps, body representation level); and (b) as changes in the efficacy of existing synapses or generation of new synapses (neuronal or synaptic level). In this review, we describe paradigms used to study mechanisms of plasticity in the intact human motor system, the functional relevance of such plasticity, and possible ways to modulate it.

Animals↗
PubMed2000

Inherited prion encephalopathy associated with the novel PRNP H187R mutation: a clinical study.

OBJECTIVE: To describe a variant of prion encephalopathy associated with the recently identified H187R mutation in the prion protein (PRNP) gene. METHODS: The authors studied a multigenerational American family with nine affected individuals. Clinical examination included imaging, EEG, and CSF analysis with 14-3-3 protein testing. Histopathology was characterized by examination of a brain biopsy from an H187R mutation-positive patient. RESULTS: The disease in this family is caused by the PRNP H187R mutation and characterized by autosomal dominant inheritance, median age at disease onset of 42 years (range 33 to 50 years), and median duration of illness of 12 years (range 8 to 19 years). Clinical signs include progressive dementia, ataxia, myoclonus, and seizures. Histopathologic features consist of distinctive "curly" prion protein deposits with a strictly laminar distribution in the cerebral cortex and minimal astrogliosis in the absence of amyloid plaques or spongiosis. CONCLUSION: A variant of prion encephalopathy associated with the novel H187R mutation in the PRNP gene displays distinctive clinical and immunostaining characteristics that further expand the boundaries of human prion disease.

Adult↗
PubMed2000

Mechanisms of use-dependent plasticity in the human motor cortex.

Practicing movements results in improvement in performance and in plasticity of the motor cortex. To identify the underlying mechanisms, we studied use-dependent plasticity in human subjects premedicated with drugs that influence synaptic plasticity. Use-dependent plasticity was reduced substantially by dextromethorphan (an N-methyl-d-aspartate receptor blocker) and by lorazepam [a gamma-aminobutyric acid (GABA) type A receptor-positive allosteric modulator]. These results identify N-methyl-d-aspartate receptor activation and GABAergic inhibition as mechanisms operating in use-dependent plasticity in intact human motor cortex and point to similarities in the mechanisms underlying this form of plasticity and long-term potentiation.

Dextromethorphan↗