CIN Members

In 2007, the CIN started with 25 principal investigators as cluster applicants, as stipulated in the DFG call for bids. When the CIN cluster was approved further  scientists from a range of institutions were incorporated, to make up the 48 'founding members' of the CIN. Since the beginning of 2014 the CIN has consisted of over 80 scientists in total. The membership process involves an application to the steering committee in which the candidate outlines his or her scientific profile and submits a list of publications. The committee's decision is based purely on the scientific excellence of each candidate.

CIN Members

Prof. Dr. Hermann Ackermann

Organization: Hertie Institute for Clinical Brain Research


Otfried-Müller-Str. 27
72076 Tübingen

Phone number: +49 (0)7071 29 87529

Department: Dept. of General Neurology

Area: CIN Members

Scientific topic: Neurophonetics

Field of Research

  1. Blind subjects deploy visual cortex in order to better understand spoken language. (cooperation with E. Zrenner and A. Bernd, Centre for Ophthalmology, University of Tuebingen) Blind individuals may learn to comprehend ultra-fast synthetic speech at a rate of up to about 22 syllables per second (syl/s), exceeding by far the maximum performance level of normal-sighted listeners (8-10 syl/s). 
  2. Speech motor deficits in disorders of the cerebellum. Cerebellar disorders may give rise to a distinct syndrome of speech motor deficits, called ataxic dysarthria. In cooperation with L. Schöls, M. Synofzik and T. Lindig, Centre for Neurology, University of Tuebingen, we try to clarify whether the syndrome of ataxic dysarthria separates into various subtypes, depending upon which component of the cerebellum is predominantly compromised. 
  3. An evolutionary perspective on spoken language: vocal continuity between nonhuman and human primates. (cooperation with S. Hage, Department of Biology, University of Tuebingen, and W. Ziegler, Clinical Neuropsychology Research Group, Munich)  Any account of “what is special about the human brain” must specify the neural bases of our unique trait of articulate speech – and the evolution of these remarkable skills in the first place. Analyses of the disorders of acoustic communication following cerebral lesions/diseases as well as functional imaging studies in healthy subjects – together with paleoanthropological data – throw some light on the phylogenetic emergence of spoken language, pointing at a two-stage model of the evolution of articulate speech: (i) monosynaptic refinement of the projections of motor cortex to the brainstem nuclei steering laryngeal muscles (brain size-associated phylogenetic trend), and (ii) a subsequent "vocal-laryngeal elaboration" of cortico-basal ganglia circuitries, driven by human-specific FOXP2 mutations. A more extensive representation of laryngeal muscles within the basal ganglia should have allowed for the deployment of the vocal folds - beyond sound generation ("voice box") - as an “articulatory organ” which can be pieced together with orofacial gestures into holistic “motor plans”, controlling syllable-sized movement sequences. Among other things, this concept elucidates the deep entrenchment of articulate speech into a nonverbal matrix of vocal affect expression (emotive prosody) for which "gestural-origin theories" fail to account, and points towards age-dependent interactions between the basal ganglia and their cortical targets similar to vocal learning in songbirds. Thus, the emergence of articulate speech – often considered a sign of human superiority within the animal kingdom – appears to have involved the "renaissance" of an ancestral organizational principle (“evolutionary tinkering”).


  1. Using functional magnetic resonance imaging (fMRI), we were able to demonstrate for the first time that this exceptional skill correlates significantly with hemodynamic activation of several components of the central-visual system, including right-hemisphere primary visual cortex (V1). Whole-head fMRI analyses (14 blind, 12 sighted subjects) revealed activation clusters in right-hemisphere primary- visual cortex (V1), left fusiform gyrus (FG), bilateral pulvinar (Pv) – not visible – and supplementary motor area (SMA), in addition to perisylvian “language zones”. Magnetoencephalography (MEG) can further corroborate the suggestion of a crucial contribution of right-hemisphere V1 to this perceptual skill: cross-correlation analyses revealed enhanced phase-locking of MEG signals to syllable onsets during comprehension of ultra-fast speech in blind subjects.
  2. Patients with Friedreich ataxia or spinocerebellar ataxia (SCA3, SCA,6) have been analyzed so far. Reduced speaking rate and voice irregularities were found specifically related to ataxia in other domains (Brendel et al., submitted). In SCA-patients, by contrast, articulatory problems emerged as a predictor for ataxia severity.