Brain Fluctuations, Disease States Affect Creative Dexterity

There is a neurophysiological noise in all of our heads that is only somewhat modified by the sights, sounds, and other stimuli around us. This activity is not random and reflects a variety of functional networks. Neurons within functional networks, such as those subserving oculomotor, sensorimotor, visual, and possibly even cognitive functions, spontaneously fire in the absence of sensory stimulation (even under the extreme condition of burst suppression level anesthesia (Nature 2007;447:83-6). This spontaneous neuronal ensemble activity begins prenatally, laying the groundwork for the cortical processing of anticipated sensory stimulation. Sensory stimulation modifies this activity, but in both experimental animal models and in humans, external stimulation accounts for around only 25% of the overall network function – meaning that intrinsic/spontaneous activity accounts for the majority of our cerebral activity (Nature 2004;431:573-8).

Alterations in our performance of a task can result from fluctuations in intrinsic cerebral activity. Fox and colleagues showed that an individual’s varying performance between trials on a simple button-pressing task was a result of this inherent variability in intrinsic activity (Neuron 2007;56:171-84). This led the authors to speculate that our normal, day-to-day variability in performing any task, whether it is a motor task like inserting a needle, a perceptual task like visually scanning and tactually palpating the lower back to find the L4-5 interspace, or a complex cognitive task like deciding whether a patient needs a spinal tap, might also reflect this phenomenon.

Recent evidence from a remarkable experiment in mice further supports the possibility that inherent variability in intrinsic cerebral activity can alter the performance of a task. Investigators conditioned transgenic mice to show fear in one particular environmental context (context A) by endowing them with a c-fos promoter that could be induced to activate in the presence of the drug CNO. This led to activation of the c-fos promoter in the neurons that were relevant for this specific memory (that is, fear conditioning in context A), meaning that the inducible drug (CNO) receptor was activated. Exposure to CNO could then reactivate this neuronal ensemble (ensemble A), the network underlying the context A memory. Next, the mice were fear conditioned in a different context, context B, so that they now had two distinct memories relevant to either context A or context B and related to two different neuronal ensembles (ensembles A and B). The mice were then tested for memory in context B with and without stimulating ensemble A. Of several possible anticipated outcomes only one emerged: the mice exhibited the learned freezing response but only in context B when injected with CNO (the ensemble A drug), indicating a hybrid memory. Thus manipulation of intrinsic brain dynamics influenced learning and encoding resulting in an entirely new memory composed of pieces of two other distinct memories (Science 2012;335:1513-6). Extending this phenomenon to our own experiences, it suggests that when we are exposed to a seemingly new context, elements within the new context that remind us of a prior experience (an old context) may in turn influence how we learn and remember the new context. In short, past experience influences new learning, and this can be further manipulated with drugs.

While our normal cerebral activity may fluctuate and be influenced by new experiences, our ability to execute a plan may be especially impaired by any of the many neurologic disorders of motor control and expression. For example, aphasia impairs our ability to communicate and so would affect our oratory and writing skills and our ability to learn (at least within the verbal modality) and teach.

Apraxia results from damage to supplementary motor and parietal cortices, brain regions involved with programming movement. Goal oriented movements, such as combing our hair or dressing, become confused and ineffective as if our limbs do not know what to do. The French neurologist Théophile Alajouanine reported that the famous composer Maurice Ravel in later life suffered from a degenerative brain disease that was shown on pneumoencephalography to cause asymmetric expansion of his lateral ventricles (potentially corticobasal degeneration) that initially robbed him of his ability to play music and eventually led to his death (Brain 1948;71:229-41). Different types of dementia also can produce varying effects on the ability to be expressive. Willem de Kooning, the famous 20th-century artist, developed Alzheimer’s disease, yet continued to paint with the disease. During the early stages of dementia he produced simpler work that retained a coherent style, according to art critics and contemporaries. However, as his dementia worsened, his paintings became increasingly simplified (Neuropsychologia 2004;42:1568-83). Frontotemporal dementia (FTD) affects our social skills, resulting in behavioral problems early in its course. A small subset of FTD patients have shown enhanced artistic skills, presumably as their behavioral disinhibition led them to produce less rule-constrained expression (Arch. Neurol. 2004;61:842-4).