The neural origin of many neurological and psychiatric symptoms is still largely unclear. Neuromodulation techniques, such as transcranial magnetic stimulation (TMS), deep brain stimulation (DBS) and MR-guided focused ultrasound (MRgFUS), are increasingly used to treat brain disorders. However, use of neuromodulation is currently limited to only a minority of the brain disorders, because in most of the disorders we still don’t know where and how to modify brain function to treat the symptoms.  

At Turku BrainLab, we try to solve this issue by leveraging unique clinical cohorts, causal brain lesions, state-of-the-art neuroimaging, and cutting-edge neuromodulation techniques. Our overarching aim is to develop new treatments for brain disorders, for which we are ideally positioned given our exceptional datasets, wide array of techniques and strong link to the university hospital. Our work covers a wide spectrum of brain disorders but has a special focus in movement disorders and addiction. 

Neurological and psychiatric symptoms are caused by disruption of normal brain function, but in most cases the exact localization in the brain is not known. Identification of the neural origin of the symptoms is critical for the development of new therapeutic options. With the current technology, we can target almost any part of the brain using invasive or noninvasive neuromodulation techniques. For example, DBS and MRgFUS of the basal ganglia for movement disorders and repetitive TMS of the prefrontal cortex for depression have proven highly efficacious, far exceeding the efficacy of pharmacological treatments, and highlighting the therapeutic potential of these techniques. However, the main challenge and the reason why these techniques cannot be used to treat all brain disorders is that we do not know which part(s) of the brain the symptoms originate from and should be targeted with treatment.  

Modern neuroimaging methods have allowed us to study the functions and malfunctions of the living human brain in greater detail than ever before. However, typical case-control studies are inherently limited by not being able to establish causal relationship between abnormal brain function and clinical symptoms. Thus, based on these studies, it is not possible to define which of the observed brain changes are causal and which are secondary/compensatory to the primary abnormality underlying the symptoms. 

Throughout the history of neurology, studying brain lesions has formed the foundation for establishing causal relationships between brain damage and symptoms. However, in most cases, locations of lesions causing the symptom do not overlap, leaving the localization unclear. Accordingly, brain disorders are currently conceptualized as disorders of brain networks and new neuroimaging techniques, such as lesion network mapping and disconnectome mapping, have provided tools to localize brain lesion to networks (Joutsa et al. Curr Opin Neurol 2022; Joutsa et al. Brain 2023). 

Together with our international colleagues, we have already mapped the causal brain circuits underlying, for example, parkinsonism (Joutsa et al, Brain 2018), dystonias (Corp et al., Brain 2019; Corp et al., Neurology 2022), tremor syndromes (Joutsa et al., Ann Neurol 2019; Younger et al., Neurology 2023), migraine (Burke et al. Brain 2020) and epilepsy (Schaper et al., JAMA Neurol 2023), and developed techniques to systematically identify treatment targets for neurological and psychiatric conditions (Joutsa et al., Ann Neurol 2018; Joutsa et al., Nat Med 2022). Combined with cutting-edge neuromodulation (TMS, DBS, MRgFUS) and neuroimaging (MRI, PET, SPECT) tools available at our hospital, we are ideally positioned to translate these findings towards new treatments.