HST 722 Brain Mechanisms for Hearing and Speech Neural...

HST 722 – Speech Motor Control 1

HST 722Brain Mechanisms for Hearing and Speech

Neural Bases of Speech Motor Control

Frank [email protected]


Early Studies – Penfield and Colleagues

Wilder Penfield performed neurosurgery at the Montreal Neurological Institute in the 1940s and 1950’s.

Focal cerebral epilepsy – Injury to a brain area (e.g., stroke) can lead to abnormal activity in the immediate or surrounding gray matter. This abnormal activity may occur years after injury. A damaged cortical area that acts as a “self-discharging electrochemical unit” is called an epileptogenic focus.

From time to time, explosive discharges are released by this area; these discharges are called epileptic fits, characterized by loss of consciousness, contraction of many or all muscles, groaning, and frothing at the mouth.

In severe cases, the epileptogenic focus is removed via surgery. Penfield and colleagues used electrical stimulation to carefully map the cortical areas before performing such operations to try to minimize damage.


Cortical Stimulation Prior to Epilepsy Surgery

FIG. VII-l. Layout of operating room. The surgeon is filling in a sketch of the brain. In the background Dr. Jasper is seen recording an electrocorticogram behind the glass partition of the observing stand, while his associate, Dr. Guy Courtois, watches. The patient is seen fully conscious and comfortable, thanks to local analgesia, with the anesthetist, Dr. Andre Pasquet, who is acting as observer, beside him. Beyond the observer is the square window through which the photographs of the brain are taken by means of the mirror placed above the table.


Areas of the Brain Where Stimulation Has a Noticeable Effect

FIG. 111-1. Photograph of left hemisphere of the human brain.


Auditory cortex stimulation• Patient hears “ringing, humming, clicking, rushing, chirping, buzzing,

knocking, or rumbling. He is never under the impression that he has heard words, nor music, nor anything that represents a memory.”

Somatosensory cortex stimulation• Patient “reports a sensation of tingling or numbness, or of movement in

some particular part. But he is never under the impression that he has touched an external object. He considers it an artifact, not an ordinary sensation.”

Visual cortex stimulation• “what the patients see is much more elementary than things seen in ordinary

life… [they see] flickering lights, colors, stars, wheels, blue-green and red colored disks … a long white mark, shadow moving, black wheel, etc.”

Motor cortex stimulation• “the patient may be astonished to discover that he is moving his arm or leg.

He may be surprised to hear himself vocalizing, but he never has the impression that he has willed himself to do these things.”


Effects of Direct Cortical Stimulation on Speech

FIG. VIII-1. Vocalization, which is a sustained or interrupted vowel cry, has been produced by stimulation at these points in the left hemisphere.


FIG. VIII-2. Vocalization has occurred during stimulation at these points in the right hemisphere.


FIG. VI11-3. Electrical interference has produced interference with speech at these points in the left hemisphere. When the electric current has been applied to other areas, such as the frontal pole or the occipital lobe, no difficulty in speech has been noted. The types of disturbance are given in subsequent figures.


Motor Cortex and Movement Control

“Motor cortex” used to refer to either primary motor cortex (Brodmann’sArea 4, M1) or both Area 4 and Area 6 (supplementary motor area,premotor cortex).

Area 4 stimulation produces movements with lowest currents of any area in the brain.

Some commands to the fingers, hand, and speech articulators are mediated by direct connections from motor cortex (BA 4) to the spinal cord or brain stem motoneurons.

However, most motor output commands involve subcortical structures such as the red nucleus and cerebellum.


The Motor Homunculus

• In humans, the speech articulators and fingers have very large primary motor cortex representations

• The somatosensory and motor homunculi are approximately aligned with each other

• Corresponding parts of primary somatosensory cortex and primary motor cortex are interconnected


Figure 38.3 Sites controlling an individual muscle are not located together but are distributed over a wide area of motor cortex. Intracortical microstimulation was used to identify sites in monkey primary motor cortex at which low-threshold stimulation evoked electromyographicactivity (indicating monosynaptic connections) in a shoulder abduction muscle (middle head of deltoid muscle) and a wrist extensor muscle (extensor carpi radialis; ECR). Topographic maps of the identified sites reveal overlap between shoulder and wrist representations. The maps were constructed based on the inverse of the threshold (1/threshold) in microamperes, with the peaks representing approximately 1/3 microamps and the valleys 1/40 microamps (From Humphrey DR, Tanji J. 1991. In: DR Humphrey, HJ Freund (eds.). Motor Control: Concepts and Issues, pp 413-443. New York: Wiley.)

PNS p. 759


Basal Ganglia and Cerebellum in Movement Control


The Basal Ganglia


Basal Ganglia-Thalamo-Cortical Loop


The basal ganglia are important for movement selection and initiation,perhaps by providing a gating signal back to cortex to cause a planned movement to be produced, and by inhibiting the gating signals for unwanted movements.


Parkinson’s Disease

Parkinson’s disease is the result of damage to the substantia nigra pars compacta, which supplies the neurotransmitter dopamine to the input partof the basal ganglia (the striatum, composed of the caudate nucleus and the putamen). Symptoms include:

• Rigidity• Tremor • Lessened muscular power• Slowness of movement with movement initiation difficulty

(bradykinesia)• Abnormally small movements (hypometria), including

micrographia• Fast gait with small steps

[See INS Dictionary of Neuropsychology]


Huntington’s Disease

Another disease of the basal ganglia, Huntington’s disease (formerly called Huntington’s chorea), has symptoms that are different from, and in some ways opposite to, those of Parkinson’s disease:

• Patients exhibit excess, or unsuppressed, movements, referred to as chorea (from the Greek word for “dance”).

• Patients later suffer from dementia and other psychiatric disorders.• Chorea can be preceded by a period of depression (up to 10 years

before onset of movement disorder).

Huntington’s disease is associated with severe atrophy in the striatum, particularly the head of the caudate nucleus. It has been suggested that the neuropsychological aspects of Huntington’s disease might be the result of compromised prefrontal cortex operation (the frontal lobe is heavily interconnected with the striatum, particularly the head of the caudate nucleus).



Direct and Indirect Pathways of the Basal Ganglia

Pathways through the basal ganglia are often broken into a direct (striatum->GPi) and indirect(striatum->Gpe->STN->Gpi) pathway.

The output of the basal ganglia (Gpi) is inhibitory, as are the direct projections from striatum to GPi.

Excess activation in the direct pathway facilitates movement; excess activation in the indirect pathway inhibits movement.


Difference Between Parkinson’s and Huntington’s Diseases

Parkinson’s disease can be characterized as a shift in the balance of activity toward the indirect pathway, thus inhibiting movement. This occurs due to differential effects of dopamine on the direct and indirect pathways.

Thus, lesions or disruptive stimulation (deep brain stimulation, DBS) of the subthalamic nucleus (STN) or GPi can actually help relieve Parkinson’s symptoms.

Huntington’s disease can be characterized as a shift in the balance of activity toward the direct pathway, thus causing excess movement.

Pink pathways are excitatory; gray are inhibitory


CerebellumThe cerebellar cortex has a very regular and well-studied structure:


Ataxia

Greek meaning: without order.

Ataxia is characterized by abnormal movement, including errors in range, direction, timing, and force (“coordination”) of motor activity. Components of ataxia include trouble decomposing movements into component parts, incorrect movement distance (dysmetria), and tremor.

Ataxia is usually the result of damage to the cerebellum.

Ataxic dysarthria – slurred, slow, and uncoordinated speech caused by cerebellum damage (patients often appear to be inebriated).



The Cerebellum as a “Side Loop”

Figure 42-6 Synaptic organization of the basic cerebellar circuit module. Mossy and climbing fibers convey output from the cerebellum via a main excitatory loop through the deep nuclei. This loop is modulated by an inhibitory side loop passing through the cerebellar cortex. This figure shows the excitatory (+) and inhibitory (-) connections among the cell types.


Learning in the cerebellar side loop results in the tuning of motor commands:

This accounts for the role of the cerebellum in maintaining smooth, well-coordinated movements.

Cerebellarcortex

Tunableside-loop

Motorcommand

Input from cortex

HST 722 – Speech Motor Control 24PNS, p. 757

<= Somatotopic organization of the medial and lateral motor cortex in the monkey, showing the arm and leg representations. (ArSi, arcuate sulcus, inferior limb; ArSs=arcuate sulcus, superior limb; CS=central sulcus; M1 =primary motor cortex; PMd=dorsal premotor area; PMv=ventral premotor area; PS=precentral sulcus; SGm=superior frontal gyrus, medial wall;SMA=supplementary motor area; pre-SMA = presupplementary motor area; SPcS=superior precentral sulcus.) (From Dum and Strick 1996.)

Premotor Cortical Areas


PNS p. 760


Onset times from Kalaska & Crammond (1992):


The medial premotor area (medial BA 6), is called the supplementary motor area (SMA) and is important for the planning of internally generated movements and mental rehearsal:


Brodmann’s areas 8 (frontal eye fields) and 44/45 (Broca’s area) can be considered to be premotor areas specialized for eye movements (area 8) and speech (areas 44/45).

44/45

8


Rizzolatti et al. (1998):Classical definitions of motor cortex highlight 2 or 3 functionally and cytoarchitectonically distinct areas: primary motor cortex (BA 4), premotor cortex (lateral BA 6), and supplementary motor area (SMA; medial BA 6).

More recent studies indicate a more complex organization, with at least seven distinct motor cortical areas in the frontal lobe of the macaque monkey (F1-F7).

Rizzolatti et al. (1998) Fig. 1

Global Organization of Motor Circuits


The motor areas are interconnected with distinct parietal areas to form several somewhat separate motor circuits with different functionalities.

Rizzolatti et al. (1998) Fig. 1

Global Organization of Motor Circuits (cont’d)


Separate circuits for reaching (VIP/F4) and grasping (AIP/F5):


PF – F5c Circuit

Motor properties of F5c neurons same as F5ab neurons, but visual properties differ: F5c neurons will respond when monkey observes another individual performing an action similar to that coded by the neuron (e.g., grasping, placing, or manipulating objects).

⇒“Mirror neurons”

PF neurons have similar visual properties.


Prefrontal Lobe – F6 Circuit

Unlike other motor areas, F6 (pre-SMA) has few connections with parietal lobe, instead connecting with frontal lobe areas BA 46 (dorsolateral prefrontal cortex) and the rostral cingulate cortex (BA 24c).

Seems to be involved in control of motor processing in the parieto-frontal circuits rather than in sensorimotor transformations.

May also play an important role in sequence organization (Tanjiand colleagues).


Possible Human – Monkey HomologuesHuman: Monkey:

Matching colors indicate possible homologues

HST 722 Brain Mechanisms for Hearing and Speech Neural...

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