Behavioral neurology refers to that sub-specialty of neurology (neurology being the investigation of the function and disorders of the nervous system, central and peripheral). that focuses on the way the brain thinks, learns, memorizes and behaves in the sense of directing social conduct, communicating and feelings as in the sense of anxiety, depression or obsessiveness. As a consequence of these interests, behavioral neurology overlaps into psychiatry. And for those psychiatrists who are very much interested into the neurology of behavior, they will refer to their specialty as neuropsychiatry. More than ever before, the use of specialized techniques permits identification of behavioral syndromes with greater precision, and the multiplicity of medicinal agents available to us increases considerably the possibility of improving brain function. What this means is to maximize the individual’s potential; i.e., people aren’t made any brighter than what they ever were or less anxious than they ever were. Rather, the glitch if one will, inside that person’s nervous system is minimized and as a consequence their intellectual and emotional potential, latent in the past, is now realized and actuated.
Dystonia is a central nervous system disorder so far as we know, usually coming from a dysfunction deep in the brain in the region called the basal ganglia, including its connections into the upper portion of the brainstem (the part of the brain that lies between the hemispheres of the brain and the spinal cord). There may be some spinal cord disorders, which may be affected in certain kinds of dystonia, but these appear to be in the minority. There are two categories of dystonic classification. Those that are primary or essential; that is they are not due to any injury to the brain like multiple sclerosis, stroke or other diseases, but rather are intrinsic to the way that nervous system operates. Secondary dystonia means the condition is due to some alteration of an otherwise normal nervous system due to an acquired disorder, changing the original functioning of the nervous system and producing over-activity in the muscles because of a brain or spinal cord relative over-activity and directing the muscles to be overactive. Most of the essential dystonias are thought to likely have some genetic mechanisms. But not all genetic disorders are multi-generational. That may be because of a new spontaneous genetic mutation that has occurred in that person or it may be that other family members may possess what is called a suppressor gene, which limits the expression of the dystonia gene. One of the nice things about essential dystonia, which appears at all ages but especially in adulthood and the most common form of dystonic mechanisms, is that it is almost always potentially reversible, since the brain is not dying (as occurs in Alzheimer’s disease, where nerve cells are shrinking and dying off, as they also do in Parkinsonism). A spontaneous improvement or response to therapy improve the probabilities that dystonic symptoms will lessen. However, once dystonia has occurred and then goes away, the patient continues to be at risk to have their symptoms recur.
There are several possibilities. One very rare reason why a person may not get a positive response is that they are genetically different; i.e., they have a resistance to the toxin so that it doesn’t weaken their muscles. That is extremely rare. What can happen are two things after several injections have occurred:
- The mechanism fatigues by which the toxin had been effective in the past – not antibody formation – just not as reactive and
- The antibodies have formed, and if they have formed, then the individual will lose the response to the A toxin and must wait for the clearance from the FDA for the B toxin, which we anticipate will be some time in the year 2000. It appears to be just as effective as A and as long of duration for benefit, but a higher frequency of induced dry mouth. There is no higher frequency of swallowing problems or neck weakness.
The other reason is that the individual receiving the injections may have gotten them in the wrong muscles. And to limit that possibility, EMG recordings are carried out to try to maximize the accuracy as to which muscles are most active and how can we cut those muscles down and give the patient the best possible outcome. Multiple channel EMG recordings before injection map out the areas of activation, and then the muscles are injected based on which are most active. Sometimes a conversion from the US made Botox™ to the British made Dysport™ results in improvement even though they are both botulinum toxin A (Botox™ is frozen, Dysport™ is refrigerated). Botulinum toxin B, by the way, is kept at room temperature whenever necessary, but it can be housed in a refrigerator, but it can’t be frozen.
Learning differences is a more appealing way and probably includes a larger proportion of the population than does the term learning disabilities. Disabilities was the term that was selected in 1969 when the Aid to All Handicapped Children Act was written and passed by Congress. The sense was that the child needed to be disabled before the school would provide special education services, as had been done for instance for children who have had motor coordination problems and required physical therapy for conditions like congenital hip problems or cerebral palsy. The difference implies that there is a distinct, unique style of learning for the person. But unless it is truly associated with some reduction in student performance in one of the academic areas, then it is not considered a learning disability. Changing the educational environment might help a learning difference; usually more than just a minor alteration in teaching strategy would be required for a learning disability. Although family history is important, it alone does not make the diagnosis for a child that is being seen. One wishes to observe the pattern of behaviors both in and out of school, particularly for attentional problems, which must be manifest in multiple environments. Additionally, one must have some sense of the overall intellectual potential of the person as well as specific academic achievement in certain academic areas such as reading, spelling and arithmetic. But motor skill deficits can also be assisted under Federal legislation. Thus students who write slowly as with muscle coordination difficulties, as are not rare in those with learning disabilities, could qualify for some adaptations such as untimed written exams and a reduction in written homework assignments. Quantitative neurological examination performed by us gives a picture of the subtle motor nervous system function as it may be altered in developmental disorders that intrude on a specific academic subject, attention or muscle coordination. Additionally, neuropsychological measures provide the specific cognitive deficit (i.e., thinking glitch) that may account for why the student of average or above intelligence is performing below average in a specific classroom subject. The physiological measures clarify whether or not by routine electroencephalogram alternative forms of medical management, such as those for seizure disorder, may be helpful. And whether by evoked potential studies (N100/P300) one can verify that there are the slow processing speeds that distinguish the special education from the general population. One must also be sensitive to the emotional state of the student, which may be primarily or secondarily at risk with anxiety, depression or obsessiveness; and which will require management if the student’s academic skills are to be maximized.
As a consequence, in this medical setting in addition to the usual IQ academic achievement discrepancy, we will be looking at the qualitative features of the student’s academic and neuropsychological makeup as part of the qualitative and quantitative assessment. This includes muscle coordination, brain physiology, and emotional status. On that basis not only is diagnosis much more accurate, but is multifaceted, allowing one to provide the most sensitive intervention – both educationally and medically.
Whether or not there is any treatment will depend upon the severity of the condition. And what the treatment will be will depend upon its type. At the very least, it requires understanding on the part of both the educational and home environment. The first steps are always behavioral – how can we make the classroom setting optimal for this learner to optimize his/her attention or specific skill acquisition in reading, spelling or arithmetic? From a medical standpoint, if these prove ineffective alone and severity is great enough, and also if one has a safe and can prove there is an effective form of treatment, then a variety of medicinal approaches may be of assistance.
For attentional problems, psychostimulants or other classes of medicine that favorably influence the metabolism of the transmitter in the brain called dopamine can be considered. These include Cylert, Ritalin, Dexedrine, Adderall, and Desoxyn among the stimulants; and among the non-stimulant agents, Wellbutrin, Prozac or Zoloft may simulate or facilitate dopamine metabolism while elevating mood in those who are depressed or assisting in obsessiveness in those with obsessive-compulsive symptoms. Their effect can be measured in the case of the psychostimulants (other than Cylert) in one hour and for Cylert in three days. In the case of psychotropic agents, results can be measured in a matter of two to four weeks. When specific problems occur in reading, there may be an advantage if there are attentional problems in the use of Cylert over Ritalin based on studies we have done in the recent past. But Cylert carries the risk of potentially injuring the liver, whereas the other stimulant agents do not. It also has the advantage that a single dose in the morning tends to last the entire day. This lessens the necessity of the student to take a medicine in school, which is something, particularly older children, dislike intensely.
Reading instruction research shows that phonological awareness training is essential, and in some instances helping brain processing speed of speech sounds as is fostered by the Fast Forward program can be attempted. But the agents Piracetam and Hydergine are agents which for some individuals facilitate verbal processing, i.e., speaking, and also in processing reading. These agents, however, take anywhere from two to four weeks to help. Agents which may be helpful to memory and sometime facilitate academic performance, are phosphatidl choline (trade name for one of the agents we have used called Phoschol 900). Its effectiveness in improving memory can be measured in one month’s time.
The exact age for a given individual varies, depending upon type and severity; i.e., language problems that are quite intense can be identified as early as 18 months and motor coordination problems by age two. But higher order skill problems in reading, arithmetic, spelling and penmanship may be more difficult to ascertain before the age of five, but are reasonably reliably identified between the ages of five and seven years. In adulthood, it is possible to identify any of the developmental disorders and to verify their biological nature. Encouragingly, these developmental disorders, the majority of which seem to be treatable in childhood, remain treatable through the lifespan of the person unless there has been some unusual injury or illness that may have damaged the nervous system. Developmental disorders of reading, attention, math and nonverbal communication are all potentially treatable throughout the lifespan of the individual. Dosages and agents change with age, and the prognosis is best when the severity is mild and when the disorder is not multiple; i.e., not several different types of learning or attention problems.
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