facial muscles is initiated from the motor strip in the mid-portion of the
hemisphere—Dear Reader, if you touch your scalp above your ear, the bit
of brain about an inch deep from your finger is what controls your face on
the opposite side of where you are touching. DeLong’s big finding was that
there is a similar map of uniquely active cells in the basal ganglia; these
nerve cells are active with specific face, arm, and leg movements. His
1971 publication was^21 “very much a landmark,”^22 and greatly challenged
scientists’ preconceived notions about the role of the basal ganglia in
movement.
No sooner had DeLong published this classic paper than he returned to
academic clinical medicine, but instead of returning to Boston, he
transferred to Johns Hopkins, where he completed a three-year residency
in neurology. Donning the white lab coat of a resident, there can be no
doubt there were times of awkward role reversal when Dr. DeLong was
schooling his superiors on the function of the basal ganglia. Not
surprisingly, DeLong continued his research as a resident, and then stayed
on at Hopkins until 1989. In these years, DeLong and his team showed that
the basal ganglia “structures were not a funnel of diverse influences to the
motor cortex but rather components of a series of independent parallel
circuits, receiving from and sending information to specific cerebral
cortex. And, another big surprise, the circuits were not only involved in
movement but also in cognition and emotion.”^23 In short, Mahlon DeLong
had decoded the deepest parts of the brain, finally understanding why a
malady like Parkinson’s disease simultaneously causes shaking and
spasmodic tremors of the hands while freezing someone’s legs from
moving.
The brilliant scientists of the 19th century had positively no explanation
whatsoever for tremors, seizures, migraines, and brain infections. Santiago
Ramón y Cajal mapped the neural pathways he could see. The succeeding
wave of neuroscientists used electrodes to determine the firing patterns of
the neural cells, but what was needed was a mammalian model of PD that
would allow scientists to further illuminate the complex pathways of
movement disorders, and perhaps, miraculously, intervene surgically. No
one was thinking of a brain implant in 1982 ... that was the stuff of
science fiction. But Mahlon DeLong continued to hope for an animal
model to test his hypotheses, when he stumbled upon a report in Science