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A Visit with Dr. Daniel AmenAuthor: Dr. Siegfried OthmerRecently we had occasion to revisit with Dr. Daniel Amen at his clinic in Newport Beach. His colleague Dr. Earl Henslin, a psychologist, happened to be giving a lecture that day on the relevance of brain regulation to relationships. It’s not always a matter of denial, avoidance, or resistance---it could simply be a matter of poor brain function. He reviewed the principal categories in which these problems are currently being compartmented in the Amen schema. There is, first of all, the matter of frontal lobe function governing attention, focus, planning, and forethought. Pharmacologic intervention here consists of the stimulant class of medications. The second major category is limbic function, and cingulate function is included here as well. Here we are dealing with moodiness and depression, as well as relationship and bonding issues. Pharmacologic support here is offered through the anti-depressants such as Effexor, Prozac, Celexa, Zoloft, and Paxil, as well as Serezone, Wellbutrin, Lexapro, SAM-E, St. John’s Wort, and 5-HTP. The third major category is temporal lobe function, and basal ganglia issues are lumped in here as well. This category includes pain, fear, panic, irritability, mood swings, headaches, muscle tension, perception, and issues of short and long-term memory. Pharmacologic support is offered here by the anti-convulsants, including Neurontin, Trileptal, Lomectal, Topamax, Depakote, and Gabitril, along with fish oil (for the fatty acids). The experience at the Amen clinic has been that out of the last 2000 SPECT scans that have been done, there were none that did not yield relevant information of therapeutic import. There were none that did not call for an alteration of the medication strategy. Of course people were referred to the Amen Clinic largely because the operative medication strategy was not adequate. In any event, Dr. Amen has reason to be quite satisfied with the impact he is having with his work. Interestingly, he also still has to assert himself within his own profession of child psychiatry, and there are colleagues in the land who will to this day have a PTSD reaction when one of their patients mentions Amen or SPECT. Henslin addressed the question of affordability. What happens to the mother on low income with four kids at home? A foundation was set up to provide funding for families in need, and not a long time later it had $100,000 in it. That’s Newport Beach… This does not solve the overall problem, of course, so the next level of remedy is simply to use the classification scheme that Dr. Amen has devised without the actual SPECT scan. After all, the SPECT has simply validated a systematic association of certain symptoms with certain deficits in the SPECT, and in such identification even the involvement of the basal ganglia has to be inferred. Once that association is in hand, however, it can be used directly to determine a medication strategy…or a neurofeedback protocol. It may therefore be time once again to make a mapping of the Amen subtypes into training strategies for neurofeedback. Dr. Amen’s Subsystems Checklist is to be found in his “Clinician’s Guide.” A number of neurofeedback therapists are already using the checklist and finding it useful. With such a mapping in mind, how do Dr. Amen’s basic schema line up with our worldview? There is the obvious general identification of the pre-frontal issues with our Fp1-Fp2 training. There is a general identification of mood issues (anxiety and depression) with frontal training (F3-F4 and F7-F8), and of the temporal lobe issues with standard T3-T4 training. So far so good. But cingulate function does not fall obviously into one domain or the other for us. We find presumptive cingulate function to be most responsive to our pre-frontal training. The connection of temporal lobe training with basal ganglia function is similarly ill-defined. We are up against the problem that neurofeedback in general does not lend itself well to localization-of-function models. This type of identification comes more easily to a pharmacological model where it is known what neurotransmitter system is being impacted. The model that emerges must be consistent with what we know about drug effects. Matters are less well delineated when it comes to neurofeedback. We don’t seem to have a single approach to basal ganglia issues. Whereas the Amen approach is more “nucleus-specific,” at least in this instance, our approach is more function-specific. We get at basal ganglia regulation through its various input functions: inhibitory control pre-frontally (for tics, as an example); frontal training (for initiation of movement in Parkinson’s, as an example); supplementary motor area (for speech articulation); parietal training (for spatial organization and orientation within space); and central training (for the regulation of activation and arousal, the set-point of motor excitability, and for the organization of somatosensory fields, an issue in Dystonia). But I am getting ahead of the story. Neurofeedback for Movement Disorders Lisa Tataryn recently gave a rousing talk to a Dystonia support group down in San Diego, after umpteen years of working successfully with movement disorders. Ripples carried up here to Los Angeles, so I was invited to talk to the local support group on the same topic. (So, that is how one gets to talk in a hospital setting; one talks to support groups. This launches the revolution from the bottom up.) As I gathered my materials, which are not as extensive as Lisa’s when it comes to movement disorders, it became apparent that we have a rather comprehensive remedy here. That is to say, we can do a lot of good for a large variety of conditions. Dystonia, first of all, is a syndrome of sustained or episodic muscle contractions that cause twisting, jerking, and repetitive movements or very abnormal postures. The category includes such conditions as Spasmodic Torticollis, or Cervical Dystonia, in which head position is significantly altered; Blepharospasm, in which eye blinks are frequent, exaggerated and forced; Paroxysmal and Myoclonic Dystonia; and Oromandibular Dystonia. Even writer’s cramp is included in this category. Dystonia is part of the larger category of movement disorders in which we may include all of the following: Parkinson’s, essential tremor, Tourette Syndrome (motor and vocal tics), Tardive Dyskinesia, Cerebral Palsy, Ptosis (forced eyelid closing), Temporomandibular Disorder and Bruxism, Nocturnal Myoclonus, Restless Leg Syndrome, and Periodic Leg Movement. In the larger scheme of things, one might even include motor seizures and hyperkinesis, which takes us back to the origin of this field in the regulation of motor function. We have seen clinical benefit for instances of all of these conditions, which suggests that an over-arching perspective should be adopted for movement disorders in general. And a number of these conditions have been historically regarded as amenable to peripheral biofeedback as well. But when we put all this information together, it is apparent that there is not just a narrow pathway here to the goal of improved motor control. A wide variety of techniques has achieved success. So it would be best to back-slide to our favorite more generalized model: 1) the regulation of brain timing is a distributed network function, and 2) any frequency-based neurofeedback or stimulation technique challenges the relevant mechanisms to mount an immediate response, in first instance, and to effect a strengthening of regulatory function over the longer term. Whatever structures are involved in the regulation of movementbe it the basal ganglia or the cerebellumwill be involved in the resulting reorganization. It is the accumulation of a wealth of clinical data that motivates the adoption of a general model of self-regulation. Much of cortex is oriented around the regulation of the motor act, and sub-cortical circuitry as well, so it should be no surprise that when we get that right, other things should fall into place as well. As Sherrington once said, “the motor act is the cradle of the mind.” All the requirements for the regulation of brain timing at the millisecond level are present in motor control loops. Get that right, and the consequences cannot be merely localized. It is both amazing and heartening to find support for these views from a very unexpected quarter. In the following reference, the author projects that the benefits of Deep Brain Stimulation (DBS) should redound not only to the remediation of motor deficits but to the larger category of psychiatric and neurological conditions. DBS pre-empts the natural firing streams emerging from the sub-thalamic nucleus and imposes an artificial but more typical firing pattern on down-stream nuclei. The only mechanism that can be invoked here is the change in brain timing, and yet a variety of benefits is anticipated. One suspects that this projection was not cut from whole cloth, but rather follows from intriguing nuggets of evidence that must have already emerged from ongoing DBS studies, morsels that individually do not rise to the level of publishable material but collectively cannot be dismissed. If that is the case, then these would be instances of very delocalized consequences of a highly localized intervention. It appears that we will not be alone in moving toward an integrated model of brain function based on electrophysiology in general, and on timing and frequency-based models in particular. In: Expert Review of Neurotherapeutics Deep brain stimulation in the treatment of neurological and psychiatric
disease Dr. Siegfried Othmer |
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