3B: Movement Disorders

Question 1

Posterior parietal cortex

Answer 1

located posterior to sensorimotor cortex, it integrates sensory and motor portions of the brain, processes of body and objects in space, and controls eye movements. Lesions; Problems with visual-spatial coordination, problems with attention, neglect syndromes.

Question 2

Premotor cortex (PMA)

Answer 2

located just anterior to M1 and inferior to SMA, it controls postural/trunk and large limb muscles, the planning of actions based on sensory cues, and refinement of movements based on sensory input with cerebellum. Lesions: disruption of learned responses to visual cues.

Question 3

Supplementary motor area (SMA)

Answer 3

Located just anterior to M1 and superior
to PMA, it is involved in planning learned sequences of movements, activity just prior to
movement, and has strong connections with subcortical structures. Unilateral lesions:
disruption of learned sequences of movement; Bilateral lesions: blocks all movement;
Stimulation: creates strong urge to move

Question 4

Primary motor cortex (M1)

Answer 4

A strip of cortex just anterior to the central sulcus in the frontal lobes, where the primary control of motor movements occurs. M1 contains a body-based motor map similar to the somatotopic representation in S1. M1 controls the execution of movement. Lesions: spastic paralysis; Stimulation: executes a movement

Question 5

Corticospinal (C.S.) tract

Answer 5

the fibers that connect motor cortex through the spinal cord to motor neurons throughout the body

Question 6

Lateral corticospinal tract

Answer 6

– 80% of the C.S. axons cross to other side; these generally go to the limbs

Question 7

Anterior corticospinal tract

Answer 7

20% of the C.S. axons don’t cross; these generally go to the trunk

Question 8

Upper motor neurons

Answer 8

• originate in the M1 motor region of the cerebral cortex and carry motor information down to a specific spinal cord level. With damage to the upper motor neurons, the baseline inhibitory inputs from the cortex is lost, and the lower motor neurons are hyper-active, causing spastic muscles.

Question 9

Lower motor neurons

Answer 9

bring the nerve impulses from the upper motor neurons out to the muscles. The cell bodies are in the spinal cord and send axons to innervate sets of muscle fibers. When lower motor neurons are damaged, ‘function goes down.’ When the lower motor neurons don’t work, there is no way to send a signal to the muscles to tell them to contract. The muscles are flaccid (loose and floppy), and eventually atrophy due to loss of neurotrophic factors that the lower motor neurons also deliver to the muscle fibers.

Question 10

Somatotopic organization

Answer 10

organization that follows a map of the body (i.e., neighboring body parts have neighboring representations in cortex)

Question 11

Hemiplegia

Answer 11

Hemiplegia - total paralysis of the arm, leg, and trunk on the same side of the body, usually from lesions to M1

Question 12

Hemiparesis

Answer 12

weakness on one side of the body

Question 13

Anosognosia

Answer 13

a disorder where the patient is unaware of and denies their disability, often associated with paralysis and right dorsal parietal damage (also seen in Anton’s syndrome, eating disorders). Patients typically use confabulations to ‘explain’ why they have the symptoms.

Question 14

Confabulation

Answer 14

basically: lying unintentionally. More technically: a disturbance of memory, defined as the production of fabricated, distorted, or misinterpreted memories about oneself or the world, without the conscious intention to deceive. Certain types of damage to the parietal lobes can cause neglect syndromes that are associated with confabulation. The patient has anosognosia – thus is not aware that he/she has a deficit (e.g., paralysis) – and instead comes up with random/untrue reasons for why he/she doesn’t have an issue (like ‘I just don’t feel like moving’ instead of ‘I am paralyzed).

Question 15

Anton’s syndrome

Answer 15

blindness and anosognosia from dorsal occipital damage

Question 16

Hemispatial neglect

Answer 16

a syndrome where patients are unaware of the
world/themselves/objects/visual scene/etc. on one side of space, usually the left side from
damage to right posterior parietal cortex.

Question 17

Gerstmann’s syndrome

Answer 17

a syndrome where patients have finger agnosia (can’t identify what their fingers/toes are), problems with left/right differentiation, and problems with calculation and writing, It is usually caused by damage to inferior part of dominant parietal cortex or can be developmental

Question 18

Apraxia

Answer 18

a disorder of motor planning involving the loss of the ability to carry out learned purposeful movements, despite having the desire and the physical ability to perform the movements. There are several sub-types.

Question 19

Basal ganglia

Answer 19

a group of cell bodies below cortex interconnected with the cortex, thalamus and brainstem that is involved in motor control and also cognition, emotions, and learning; circuitry includes ‘direct’/excitatory and ‘indirect’/inhibitory pathways.

Question 20

Dopamine

Answer 20

a neurotransmitter that plays a key role in the basal ganglia motor circuit and the inhibitory and excitatory pathways. (It is also a key neurotransmitter in the arousal and reward systems.)

Question 21

Hypokinetic

Answer 21

characterized by decreased movement

Question 22

Hyperkinetic

Answer 22

characterized by increased movement

Question 23

Parkinson’s disease

Answer 23

a hypokinetic disease characterized by slowing or loss of movement (akinesia), muscle rigidity, and a ‘pill-rolling’ tremor at rest
–Cause: due to a loss of dopamine neurons in the basal ganglia that causes a decrease in activity in basal ganglia’s excitatory ‘direct’ pathway
–Treatments: include medication (L-Dopa), Fetal neural tissue graft, deep brain stimulation (DBS)

Question 24

Huntington’s chorea

Answer 24

– a hyperkinetic disease characterized by
–Cause: an autosomal dominant genetic mutation that causes proteins to build up
in and ultimately kill cortical neurons (especially in the inhibitory ‘indirect’ pathway of basal ganglia). This cell death is progressive and causes a decline in mental abilities (personality changes, memory issues, dementia) and
uncoordinated, jerky body movements (chorea), and eventually leads to death
(usually from malnutrition due to constant movement or other complications like
pneumonia)
–Treatments: genetic testing can identify disease risk (if you have the genetic mutation, you will get the disease); medications for symptoms (that reduce neural signaling); nutrition management; physical therapy)

Question 25

Hemiballismus

Answer 25

a relatively rare hyperkinetic disorder characterized by involuntary flinging motions of the extremities that increase with increased activity. Symptoms stop during sleep.
- Causes: due to damage of the inhibitory pathway of the motor loop, especially from damage to the subthalamic nucleus
-Treatments: Deep brain stimulation, surgery to remove more basal ganglia, drugs (that reduce neural signaling)