brainstem and motor cortex

contralateral innervation

right side of brain goes with left sides movements and vice versa

brainstem

• houses reticular activation formation

• cranial nerves synapse with CNS (UMNs to LMNs) at cranial nerve nuclei (III-VII)

• superior to inferior: midbrain, pons, medulla

midbrain

• superior section of brainstem

• houses afferent and efferent pathways

• houses cranial nerve nuclei

• houses substantial nigra

• controls pupil size, auditory reflexes, and reflexive eye movement

substantia nigra

part of brain that produces a neurotransmitter called dopamine (brain needs this to function normally

pons

• middle structure of brainstem

• houses afferent and efferent pathways

• houses cranial nerve nuclei

• houses respiratory center

• swallow center

• controls autonomic rhythm of respiration

medulla

• Inferior section of brainstem

• Houses afferent and efferent pathways

• Houses cranial nerve nuclei

• Point of decussation of UMNs coursing to spinal nerves.

• Also Swallow Center

• Also houses Respiratory Center

• Controls: Autonomic respiratory activity, Heart rate, Blood pressure

cortical representation of body

• The finer the movement of the body parts- the more cortex is dedicated/needed to generating motor plans for this body part.

• The more gross the movement of the body parts- the less cortex is dedicated/needed to generate motor plans.

closed head injury

the skull was not penetrated – brain has been damaged inside the skull (generally large parts of the brain have been damaged ex: car wrecks, falls, etc.)

open head injury

skull has been penetrated, and the brain has been damaged (generally impacts a certain area only, ex: gunshot wound to the head)

what is the cerebellum often called

little brain

role of the cerebellum

• ALL ABOUT MOTOR MOVEMENT

• Equilibrium (eyes, ears,  brain), posture, and…

• Timing of movement

  • Synchronization individual components of movements

• Scales and Coordinates muscle contractions in both:

  • Stereotyped (repetitive) movement (e.g., gait)

  • Non stereotyped movement (e.g., reaching for something)  

• Error Control Device

• Monitors ongoing motor plans

  • Compares intent of movement, with motor plans, afferent info, and makes adjustments

    Corrects for overshooting and undershooting; compensates forerrors before they occur. (as in reaching for something).

• Receives ongoing sensory information concerning activity and compares that information to intention and makes corrections as needed. (compares action to intent)

• The more rapid, alternating, sequential, or precise the activity the more cerebellar function is required

• For speech - allows smooth flow of movement from one articulatory position to the next.

cerebellar anatomy

• Two hemispheres

  • Cerebellar hemispheres have contralateral connections to thalamus and cerebral hemispheres.

• Connect at midline - Vermis

• Attached at Pons via peduncles

• Information arrives via middle and inferior cerebellar peduncles, connects to pathways from: the spinal cord, vestibular system, motor control areas

• Superior cerebellar peduncle- Purkinje cells- primary cerebellar output

• Output from cerebellum travels via superior cerebellar peduncle to reach the spinal cord, thalamus, and cerebral cortex.

CVA

vertobrobasilar artery supplies cerebellar arteries

toxicity in cerebellar pathologies

• hypercapnia

• chronic ETOH

progressive cerebellar degeneration

Friedrich’s

Cerebellum lesion effects

• Decomposition of movement into component parts

• Errors in rate and range of movement

• Errors in speech are likely when you have cerebellum lesions

• Dysmetria: Patients overshoot or undershoot what they’re reaching for

• Cerebellar Lesion Effects

  • Speech may sound as if person is inebriated

  • Ataxic dysarthria*- damage to the cerebellum

  • Difficulty regulating movement, but not paralysis

  • Broad based discoordinated gait

  • Hypotonia(low muscle tone)

ataxic dysarthria

damage to the cerebellum

signs of ataxia

clumsy and uncoordinated movements

ataxic dysarthria speech characteristics and patient complaints

• drunk sounding speech

• biting tongue or cheek

• speech deteriorates inordinately with alcohol

  Speech Characteristics:

• excessive loudness

• irregular articulatory breakdowns

• irregular AMRs

• Distorted vowels - tongue not in right place

• excess/equal stress

• prolonged phonemes

role of basil ganglia

• Assist in regulating/refining raw motor plans assembled at cortex

• Inhibit extraneous involuntary movements

• Modulate automatic movement

  • Arm swinging during gait

  • Automatic facial expressions

  • Postural stretch reflexes (anti-gravity reflexes)

primary functions of basal ganglia

• (IAP)-Regulate muscle tone.

• (IAP)-Posture- static muscle contraction.

• (DAP)-Dampen/modulate extraneous movements in raw volitional motor plans.

• Also involved in new motor learning and motor initiation

anatomy of the basal ganglia

• Has functional connections to substantia nigra

• Three primary components

  • Striatum

    • 1. Caudate nucleus

    • 2. Putamen

  • 3. Globus Pallidus

    • Internal

    • External 

clinical manifestations of basil ganglia involvement

• Clinical manifestation (fig 15-1)

  • vary depending on specific structures or loops affected

  • Which varies according to specific pathology (etiology)  

• Damage to BG or circuitry

  • Not spastic or flaccid paralysis

  • Loss of automatic BG inhibition of motor control

  • Release of hyperkinesias (INVOLUNTARY MOVEMENT)

  • Athetosis, ballism, chorea, tremor, dystonia, myoclonus, etc…

• Hypokinesia- Inappropriate inhibition (reduction in tone, force, ROM) of volitional movements. 

hypertonia

too much muscle tone

hypotonia

too little muscle tone

hyperreflexia

too many reflexes

hyporeflexia

too little reflexes

hyperkinesia

too much involuntary movement

hypokinesia

too little volitional movement

hyperkinetic dysarthria

speech disorder caused by too much involuntary movement

hypo kinetic dysarthria

speech disorder caused by too little volitional movement

some diseases of the basil ganglia

• parkinson’s disease

• huntington’s chorea

• Wilson’s disease

• progressive supra nuclear palsy

Parkinson’s Disease

• Death of substantia nigra

• Dysfunction of BG

• Onset usually unilateral

• Release of involuntary tremors (hyperkinesia)

• Prognosis varies but usually about 10-15 years post onset

• Overinhibition of voluntary movements (hypokinesia)

Parkinson’s disease characteristics

• Shuffling gait

• Tremors present

• Hypomimia- blank facial expression

• Hypokinetic dysarthria

hypokinetic dysarthria

• Dysarthria is something that you hear, you can’t see itbut you might see the hypokinesia that causes it but cannot see the dysarthria. Dysarthria is a speech disorder.

• More homogenous presentation than hyperkinetic dysarthria

speech characteristics of hypokinetic dysarthria

• Monopitch

• Monoloud

• Breathy voice*

• Low pitch

• Reduced Stress

• Variable rate

  • Short rushes of speech*

• Increase rate of speech*

• Imprecise consonants

  • Articulatory blurring

hyperkinetic dysarthria

• Damage to the basal ganglia can lead to this

• Any hyperkinesia which interrupts or inhibits normal speech

• Will vary according to the hyperkinesia type and intensity that is affecting speech.

• Can present in a myriad of ways

General dysarthria characteristics:

mixed hypo-hyperkinetic dysarthria

• Combined

  • Hypokinesia- reduction in volitional movement affecting speech

  • Hyperkinesia- Addition of nonvolitional movement speech