Striatofrontal dysfunction

A striatofrontal dysfunction (also fronto-striatal dysfunction ) is used in neuroscience or in brain research when there are functional disorders of certain neuronal control circuits , the essential components of which are the striatum (part of the basal ganglia ) and the frontal lobe .

The relevant control loops are of fundamental importance for the function of the frontal part of the cerebral cortex ( frontal lobes ) and thus for the so-called executive functions . They play a key role in realizing and controlling the interaction of motivation, emotion, cognition and movement behavior in a neuronal manner. Dysfunctions (functional disorders) of these control circuits lead to an excess or insufficient supply of neurotransmitters (especially dopamine and norepinephrine ) in certain brain regions and result in disorders of the mental or behavioral functions mentioned.

Striatofrontale dysfunctions occur in areas such as Parkinson's and Huntington's disease and are also in tics , geriatric depression and dependence discussed (addiction). In the attention deficit / hyperactivity disorder , striatofrontal dysfunctions were also detected with the help of imaging procedures .

The causes of such malfunctions are diverse. Genetic and developmental factors often work together. In most cases, the consequences include a disruption of executive functions.

Striatofrontal (frontostriatal) control circuits

Networking of the nuclei in the basal ganglia system

Striatofrontal or frontostriatal control circuits (loops) emanate from the cerebral cortex and run via the basal ganglia and thalamus back to the cerebrum, essentially to the frontal lobe . Information reaches the striatum from almost the entire cerebral cortex as the entrance station for the basal ganglia (cortico-striatal connections with excitatory glutamatergic neurotransmission). Via the exit station of the basal ganglia , the substantia nigra pars reticulata (SNR) and the globus pallidus internus (GPI) , the end information processed by the basal ganglia ( inhibitory GABA -ergic neurotransmission) reaches the thalamus and from there with an excitatory glutamatergic connection back to the cortex, primarily to the frontal lobe.

A “direct excitatory connection” from the striatum to the initial structures (SNR and GPI) must therefore be distinguished from an “indirect inhibitory connection”. The striatum and the GPI are both GABAerg (inhibitory). Thus, a direct projection of the striatum to the GPI leads to an inhibition of the inhibition of the GPI, which results in an excitation of the thalamus / cortex.

The indirect connection is a little more complicated: the striatum inhibits the pallidum externum , which inhibits the subthalamic nucleus . Thus, the inhibition is again inhibited, with the result that the subthalamic nucleus is excited. This now has an exciting effect on the pallidum internum, which inhibits the thalamus and thus indirectly the cortex.

Through this interaction of exciting and inhibiting neurotransmission on the direct and indirect loops, the output modulation of the basal ganglia activity is, so to speak, on two opposing reins.

Striatofrontal dysfunction in ADHD

Left: brain activity of a person without ADD. Right: activity of a person with ADD

With the help of functional magnetic resonance imaging , a reduced activation in the right-sided prefrontal system as well as an increased frontal and reduced striatal activation (in so-called go / no-go tasks ) were found in ADHD patients .

With positron emission tomography (PET) a 8.1% decrease in glucose turnover in the left frontal lobe and with single photon emission computed tomography ( SPECT) a low blood flow in the frontal lobe and the striatum as well as an increased dopamine transporter concentration in the striatum were found.

In the dopaminergic system of ADHD patients, too many transporter proteins for dopamine are present in the presynaptic membranes , with the result that too much dopamine is transported back from the synaptic gap (see also synapse ) into the presynaptic nerve cell. This ratio is normalized by treatment with dopamine reuptake inhibitors such as methylphenidate , provided the person concerned is not a non-responder .

Striatofrontal dysfunction in Parkinson's syndromes

Disorders of the striatofrontal connections continue to be discussed in connection with Parkinson's disease and progressive supranuclear palsy .

literature

Johanna Krause , Klaus-Henning Krause : ADHD in adulthood. Symptoms - differential diagnosis - therapy . 4th complete act. and exp. Edition. Schattauer, Stuttgart 2014, ISBN 978-3-7945-2782-3 .
Ulrich Müller: The catecholaminergic modulation of prefrontal cognitive functions in humans (= MPI Series in Cognitive Neuroscience . Volume 26). Max Planck Institute for Neuropsychological Research, Leipzig 2002, ISBN 3-9807904-5-2 (also: Leipzig, Univ., Habil.-Schr., 2002).

Individual evidence

↑ Dougherty et al .: Dopamine transporter availability in patients with attention deficit hyperactivity disorder. In: The Lancet , Vol. 354, No. 9196, December 1999, pp. 2132-2133 ( PMID 10609822 ).
↑ Dreel et al .: Pharmacological effects of dopaminergic drugs on in vivo binding of [99mTc] TRODAT-1 to the central dopamine transporters in rats. In: Eur.J.Nucl.Med. Vol. 25, No. 1, January 1998, pp. 31-39 ( PMID 9396872 ).
^ Johanna Krause : SPECT and PET of the dopamine transporter in attention-deficit / hyperactivity disorder. In: Expert Review of Neurotherapeutics . Vol. 8, No. 4, April 2008, ISSN 1744-8360 , pp. 611-625 ( doi : 10.1586 / 14737175.8.4.611 , PMID 18416663 ).
^ Sarazin M. et al .: Procedural learning and striatofrontal dysfunction in Parkinson's disease . In: Mov Disord. , Vol. 17, No. 2, March / April 2002, ISSN 1531-8257 , pp. 265-273 ( PMID 11921111 ).
↑ Dubois B. et al .: Slowing of cognitive processing in progressive supranuclear palsy. A comparison with Parkinson's disease. In: Arch Neurol . , Vol. 45, No. 11, November 1988, pp. 1194-1199 ( PMID 3190499 ).

[1] Dougherty et al .: Dopamine transporter availability in patients with attention deficit hyperactivity disorder. In: The Lancet , Vol. 354, No. 9196, December 1999, pp. 2132-2133 ( PMID 10609822 ).

[2] Dreel et al .: Pharmacological effects of dopaminergic drugs on in vivo binding of [99mTc] TRODAT-1 to the central dopamine transporters in rats. In: Eur.J.Nucl.Med. Vol. 25, No. 1, January 1998, pp. 31-39 ( PMID 9396872 ).

[3] Johanna Krause : SPECT and PET of the dopamine transporter in attention-deficit / hyperactivity disorder. In: Expert Review of Neurotherapeutics . Vol. 8, No. 4, April 2008, ISSN 1744-8360 , pp. 611-625 ( doi : 10.1586 / 14737175.8.4.611 , PMID 18416663 ).

[4] Sarazin M. et al .: Procedural learning and striatofrontal dysfunction in Parkinson's disease . In: Mov Disord. , Vol. 17, No. 2, March / April 2002, ISSN 1531-8257 , pp. 265-273 ( PMID 11921111 ).

[5] Dubois B. et al .: Slowing of cognitive processing in progressive supranuclear palsy. A comparison with Parkinson's disease. In: Arch Neurol . , Vol. 45, No. 11, November 1988, pp. 1194-1199 ( PMID 3190499 ).