Part 1. What it means to move

After Parkinson’s disease, I discovered something strange.

On flat ground the first step will not come, yet in front of stairs the foot lifts.

At a narrow doorway the body freezes, yet draw a single line on the floor and I can step over it and walk again.

Starting from a standstill is hard, yet after shifting my feet in place a few times, I can sometimes move forward.

Once you have lived these moments, the simple explanations stop being enough.

“The muscles are weak.”

Then stairs should be impossible too.

“The legs are paralyzed.”

Then a single line on the floor could not revive movement.

My legs still have strength.

The problem seemed to lie less in producing force than in when and how that force is brought out.

Motor neuroanatomy begins with that question.

Chapter 1. Movement is not made by a single command

We tend to imagine that the brain sends a command to the muscles and the body moves.

Broadly, that is true.

A signal that starts in the motor cortex travels through the brainstem and spinal cord to the peripheral nerves and finally contracts the muscles.

The best-known of these pathways is the corticospinal tract.

So if the motor cortex or the corticospinal tract is badly damaged, strength drops and paralysis can follow.

But the core problem of Parkinson’s disease is usually not a severing of this road.

The main command line remains — yet starting a movement, scaling its size, and carrying it on automatically become difficult.

Here an important structure enters.

The basal ganglia.

The basal ganglia are not the final motor neurons that command muscles directly.

They are closer to a circuit that regulates which of many possible movements to select, how large to start it, and how much to suppress the unnecessary ones.

So when basal ganglia function falters, it is not strength itself but the selection and initiation of movement that goes wrong.

Chapter 2. I want to move, but the body does not move right away

Consider the utterly ordinary act of rising from a chair and walking.

We usually feel it as one action.

But in the brain, several processes run almost simultaneously.

Decide to stand.

Shift the body’s center forward.

Load the legs.

Adjust balance.

Choose the first step.

Set stride and speed.

And once walking has begun, the motion continues without consciously attending to every step.

Living with Parkinson’s disease taught me that this last part matters most.

Once I start walking I can walk a fair distance — but the start itself is sometimes the hard part.

In other words, the ability to move and the ability to initiate movement are not the same thing.

Miss this distinction, and Parkinsonian gait is easily mistaken for simple muscle weakness.

Chapter 3. The motor cortex does not act alone

The motor cortex is an important starting point, but it does not decide alone.

Before a movement is produced, several circuits tune the motor cortex’s activity.

There is the basal ganglia loop, the cerebellar loop, incoming sensory information, and the brainstem circuits for posture and gait, all working together.

Put simply: the motor cortex issues the command, but the surrounding circuits are continuously adjusting when, and how naturally, that command goes out.

I found an orchestra a helpful picture.

The muscles are the instruments.

The motor cortex can begin the performance.

But for the performance to flow, a system must coordinate tempo, dynamics, and entrances.

In Parkinson’s disease the instruments are not broken; it is closer to the coordination of the performance’s start and flow being shaken.

Chapter 4. Why do small movements keep getting smaller?

One of the signature motor symptoms of Parkinson’s disease is bradykinesia.

It is usually translated as slowness, but slowness alone falls short.

Not only speed but the size of movements and their maintenance across repetition are affected.

A movement may begin at a reasonable size and shrink with each repetition.

Handwriting that grows progressively smaller — micrographia — belongs to the same picture.

In walking, the stride shortens.

Arm swing diminishes.

Starting a movement takes time.

This is not because the muscles weaken with each attempt.

It can be understood as a problem in the brain’s automatic setting and maintenance of appropriate movement size.

That is why external instructions like “bigger” or “one big step” can sometimes genuinely change the movement in Parkinson’s disease.

The body is not incapable; the automatic regulation is shaken, so a conscious command can substitute for part of it.

Chapter 5. Automatic movement and deliberate movement are different

This distinction is fascinating in Parkinson’s disease.

Walking normally, we do not think each step.

Right foot.

Left foot.

Stride, fifty centimeters.

Swing the arms.

We do not calculate our way down the street. Once walking starts, much of it continues automatically.

Yet when automatized movement fails, giving the body an external target can restore it.

Step over a line on the floor.

Take one stair.

Match the beat of music.

Someone counts “one, two.”

At that moment, movement changes from mere automatic gait into deliberate movement with a target.

I came to see this difference as a key clue to why stairs are sometimes easier for me than flat ground.

On stairs, each step’s target is right before your eyes.

Where to place the foot is unambiguous.

Wide flat ground offers no such external target.

The brain must generate stride and rhythm on its own.

And in Parkinson’s disease, it is precisely that self-generation that can fail.

Chapter 6. Why does a single line move the foot?

When freezing strikes, trying to step over a line or an object on the floor can suddenly free the foot.

The first time, it feels uncanny.

A moment ago not one step would come — and a line appears, and the legs move.

Neuroanatomically, though, there is an important hint here.

External visual information has supplied a new target for movement.

A situation that demanded automatically generating “walking” turns into the concrete action

“step over that line.”

In that process, circuits that use external sensory information — visual cortex, parietal lobe, premotor areas — can participate more actively.

In other words, when one circuit is not working well, another circuit is used to route around it.

I began to understand this as a compensatory circuit.

Chapter 7. The paradox that stairs can be easier than flat ground

Tell someone unfamiliar with Parkinson’s disease,

“Flat ground is hard, but stairs are easier,”

and they may struggle to believe it — stairs usually demand more strength and balance.

But that is exactly the clue.

Being able to climb stairs means the necessary strength and the basic motor pathways are, to a fair degree, intact.

The problem may lie in automatically generating and sustaining steps on flat ground.

Stairs present a clear next target every time.

There is height, there is an edge, and where to place the foot is visually obvious.

As a result, the movement can shift away from reliance on automatic gait toward movement guided by external targets.

So each time I climb stairs, a strange thought comes:

“My legs are not unable to move.”

“The way movement is drawn out has changed.”

That difference meant a great deal to me.

Chapter 8. Finding the circuits that remain

In Parkinson’s disease, the motor circuits do not all vanish at once.

Some pathways become difficult; others remain relatively spared.

That is why cueing works.

Use a visual line.

Use rhythm.

Consciously enlarge the movement.

Change direction briefly.

March in place, then set off.

These methods do not cure the disease.

But they can be strategies for drawing movement out of the circuits that remain.

Living with Parkinson’s disease, I stopped seeing exercise as mere muscle training.

Exercise is sometimes the practice of finding and using the neural circuits that remain.

Closing Part 1

I used to think of movement first as a matter of muscles and motor nerves.

Parkinson’s disease taught me there is a process that comes before.

Select what to do.

Set the movement’s size.

Initiate.

Continue automatically.

Suppress what is unnecessary.

And, as the situation demands, call in other circuits.

Only when all of this meshes can we take a single step without thinking.

So now, when the first step will not come, I no longer think only

“My legs won’t move.”

I ask a slightly different question:

“Which motor circuit is blocked right now?”

And one question more:

“Then which other circuit can I use?”

Follow that question, and the next structure to meet becomes clear.

The basal ganglia.

Before the muscles that make movement directly —

the system that selects movement, permits it, and scales it.

In Part 2, we go inside.