> Any increase in GABA will counteract the excitatory transmission of Glutamate. That is all that matters. No that is not all that matters. The main effect of tofizopam is unrelated to GABAergy, the fact it indirectly modulate GABA-A and potentiate benzos is a plus but its main effect come from atypical PDE inhibition. Look if klonopin is viable for you and solve your tinnitus that's great to hear. But for many people regular benzos are not a complete solution. Tinnitus is a multi-factorial condition and some people might get better results that other with a given medication.

> if you can explain how that works go right ahead Tinnitus is an excitatory overload localized in audition related neuron circuits. AKA too much glutamate (mGLURs, AMPA, NMDA, kainate). The brain is mostly a mixture of excitation (GLUT) and inhibition (GABA-A, B). By taking a classical benzo like klonopin you increase your GABA-A level which inhibit the overload of excitation (GLUT). That is why it works. You can also lower you glutamate levels independently of you GABA via an NMDA antagonist such as memantine. Those two mechanisms are the basic treatments to tinnitus. However there are more specific mechanisms (PDE, synaptotophics, calcium blockers, anti oxidants, bioenergetics) that can be complementary. Classical benzos and NMDA antagonists are not enough for some people with tinnitus.