Final- Neuroscience

Higher centers of motor control

involved in voluntary movements; long descending tracts that come from the cortex/brainstem (UMN->LMN)

Long descending tracts

UMN end on LMN; movement, posture, muscle tone, and reflexes are controlled by a balance of these; parallel pathways with overlapping complementary function

Motor cortex

located in the frontal lobe; premotor area/cortex->supplementary motor areas-> primary motor cortex (M1, main motor area); receives info from somatosensory areas, other frontal lobe areas, association areas, basal ganglia, cerebellum (ALL INFO SENT HERE FOR APPROPRIATE MOTOR RESPONSE)

premotor area/cortex

anterior to M1, located laterally; involved in motor planning, controls trunk and girdle muscles (shoulder/hips)

supplementary motor area/cortex

anterior to M1, located medially; involved in initiation of movement, orientation of eyes/head, planning bimanual/sequential movements, motor planning

primary motor cortex

in front of central gyrus (precentral gyrus); controls contralateral voluntary movements, especially fine movements of hands and face; somatotopic organization (homunculus)

somatotopic organization

same orientation as sensory; medial=LE, lateral=face, in between=UE

descending systems

split into dorsolateral system and ventromedial system; named for orientation in the spine

dorsolateral system

included tracts: lateral corticospinal, rubrospinal, corticobulbar; involved in limb flexion, fine movements (of the distal muscles), voluntary movements; originate from cortex/brainstem and descend to LATERAL ventral horn (for distal muscles)

ventromedial system

included tracts: anterior/ventral corticospinal, vestibulospinal (medial and lateral); involved in posture, gross limb movements, automatic movements (postural control), originate from brainstem/cortex and descend to MEDIAL ventral horn (for proximal muscles)

Lateral Corticospinal Tract functions

dorsolateral tract involved in voluntary control of distal muscles needed for precise movement and fractionation; suppress or inhibit reflex activity (UMN)

Lateral Corticospinal Tract pathway

one long neuron (dorsolateral tract) that originates at the motor area of the cortex-> descends through internal capsule/brainstem-> decussates at pyramids of medulla-> through lateral funiculus-> terminates at spinal cord interneurons or LMN

fractionation

ability to activate individual muscles independently of other muscles

Ventral/anterior corticospinal tract function

ventromedial tract that controls neck, shoulders, trunk muscles

ventral/anterior corticospinal tract pathway

originates in cortex motor areas-> descends ipsilaterally through internal capsule-> anterior funiculus of spinal cord. NO DECUSSATION HERE, but BILATERAL fibers exist (run along both sides with majority on the ipsilateral side for ipsilateral control)

corticobulbar tract function

dorsolateral tract same as lateral corticospinal tract function but in the face muscles

corticobulbar tract pathway

dorsolateral tract that originates in motor areas of the cortex-> projects to and terminates on cranial nerves of different brainstem areas (pons, medulla); some terminate contralaterally and some bilateral depending on area of the face controlled

brainstem in motor control

regulates postural equilibrium (vestibular) and act reflexively to stimuli in response to descending information (motor info) from cortex and cerebellum

vestibulospinal tract

has both medial and lateral portions in ventromedial system; involved in postural control; originates in the brainstem (vestibular nuclei)

reticulospinal tract

included in both medial and lateral systems; involved in postural control and gross motor movement; originates in the brainstem

rubrospinal tract function

dorsolateral tract that works closely with the lateral corticospinal tract to control distal muscles (upper limb flexors) and suppress/inhibit reflex activity

rubrospinal tract pathway

dorsolateral tract that originates at the red nucleus of the brainstem-> immediately decussates-> descends to LMN and spinal cord

Brainstem reflexes

concerned with posture, head alignment, body with respect to gravity; seen in developing infants but is integrated in adults, return of these reflexes suggests damage to brain/cortex (inhibitory info is not reaching the body)

integration

process by which reflex becomes inhibited by descending pathways

Asymmetrical tonic neck reflex (ATNR)

stimulus- head is rotated

response- arm is aBducted and extended on the same side of rotation and arm is aDducted and flexed at the elbow on the opposite side of the rotation

ATNR integration/persistence

should be integrated by six months in waking state; persistence of the reflex will impact hand eye coordination, ability to cross midline, bilateral integration (differentiated and integrated use of both sides of the body)

Symmetrical Tonic Neck Reflex (STNR)

stimulus: head flexion (1) or extension (2)

Response: 1. arms flex, legs extend

2. arms extend, legs flex (arms will follow head, legs will do the opposite)

STNR integration and persistence

should be integrated between 8 and 11 months; pertinence of the reflex will impact integration of lower and upper body, sitting posture, muscle tone, and hand eye coordination

Upper motor neuron lesions

P: lesion in cortex, brainstem, spinal cord area where descending tracts travel through

S: paresis/paralysis, inadequate recruitment of LMNs, loss of fractionation, atypical reflexes

Babinski reflex

Stimulus: sole of foot is stroked

Response: extension of big toe and toes fan out

typically present in infants but should be integrated by 2 years. persistence beyond this suggests damage to corticospinal tract

cerebral palsy

E: maternal infection, hypoxia, trauma, fetal stroke

P: atypical development of areas of brain responsible for movement (or damage to these areas)

S: difficulties with movement, posture, balance (symptoms become more apparent/more complex with growth) (muscle tone affectation points to where damage has occurred in brain)

often with co-occurring conditions (ID, seizures, vision impairment, S/L deficits)

P: variable, non-progressive

spastic cerebral palsy

characterized by spastic hypertonia; common contractures (body stiffness, toe walking, scissor walking); classified by body impact (hemiplegia, paraplegia, tetraplegia); damage to the cortex

hypotonic cerebral palsy

• Low muscle tone "floppy"

• Little/no ability to move

• Unknown damage site

dyskinetic cerebral palsy

fluctuating tone, characterized by involuntary movements (choreiform/jerky, athetoid/slow); potential damage to the basal ganglia

Mixed cerebral palsy

spastic in some areas and dyskinetic in other areas

ataxic cerebral palsy

no atypical muscle tone but incoordination and shakiness during voluntary movements

diplegia

lower extremities are more affected than upper extremities

scissor gait

seen in spastic CP; internal rotation of feet, legs walking on top of each other (hip adductors are tight)

cerebral palsy treatment

physical therapy, OT, speech, drugs, surgery

Constraint-Induced therapy (CIT)

short term intense treatment (for CP) that involves constraint of non0involved are and intensive movement practice on involved arm; highly effective when used with other treatments

botox

possible pharmaceutical CP treatment, Botulinum toxin is injected to therapeutically relax the muscle and reduce muscle rigidity/spasticity

dorsal rhizotomy

possible surgical CP treatment; cuts overactive dorsal roots to reduce muscle tone by reducing input

baclofen

possible pharmaceutical CP treatment; muscle relaxant drug that reduces stiffness from spasticity

basal ganglia structures

caudate nucleus, putamen (striatum nucleus in yellow), globus pallidus, subthalamic nucleus, substantia niagra

Basal ganglia role

link between idea of movement and motor expression (regulates movement); controls movement from initiation to completion; regulates muscle contraction, force, sequencing; has no direct connection to the spinal cord

dyskinesia

motor disorder involving loss of voluntary control and regulation of movement (includes hyper/hypo variations)

hyperkinesia

increased movement, Huntington's disease

hypokinesia

decreased movement, Parkinson's disease

Huntington's Disease

E: hereditary neurodegenerative disease (50% chance of passing it on)

P: degeneration in many areas including cortex/striatum results in disinhibition of motor thalamus/PPN

S: involuntary, jerky movements (Chorea); dementia, cognitive problems (impulse control, memory, difficulty learning), personality changes (HYPERKINESIA)

P: fatal and progressive

Treatment with drugs, but heavy side effects

dementia

loss of intellectual capacity due to loss/damage to neurons

Parkinson's Disease

P: degeneration of nigrostriatal dopaminergic pathways (striatum and substantia niagra)-> death of dopamine producing cells in substantia niagra and GABA producing cells in PPN (pons structure)-> less dopamine/GABA

S: hypokinesia- decrease in ROM, lack of automatic movements, bradykinesia (slow movements); rigidity, gait impairments (shuffling/festinating gait), resting tremors, non-motor symptoms (psychosis, dementia, etc.)

P: variable but progressive

Treatments for Parkinsons

medication: drugs that replace dopamine (Ldopa) or act as dopamine agonist; surgery: deep brain stimulation, destructure surgery, neuronal transplantation; OT can help with adaptations and diet/exercise

Parkinson's disease on/off phenomenon

symptoms will suddenly appear with no warning even after high doses of medicine; happens because something blocked the absorption of medicine in the brain; dramatic change (the condition changes daily)

Dyskinetic Cerebral Palsy

P: damage to basal ganglia

S: atypical movements, posture, tone; involuntary sustained muscle contractions; chorea (jerky movements); athetosis (slow, writhing movements)

(card is on here twice)

cerebellum

coordinates skilled voluntary movements (compares actual output to intended movements and adjusts as necessary); controls equilibrium and muscle tone through connections with vestibular system; participates in motor learning; outputs are vital but there is no direct connection to the SC (other structures first)

Cerebellum dysfunction

ataxia (truncal, limb, gait); dysarthria (speech), nystagmus

ataxia types

truncal: postural instability

gait: unsteady, staggering gait

limb: uncoordinated limbs

Dysdiadochokinesia

product of limb ataxia; inability to perform rapidly alternate movements

dysmetria

product of limb ataxia; inability to accurately move an intended distance; checked with finger to finger/nose test; includes hypo (undershooting) and hyper (overshooting) components

action tremor

product of limb ataxia; shaking of limb during voluntary movement

ataxic cerebral palsy

P: damage to cerebellum

S: low muscle tone, poor coordination, poor movements; walking/fine motor difficulties, shaky/unsteady movement

different levels of severity

card is on here twice

brain hemispheres

connected by the corpus callosum; left and right have different functions and structures (speech example); creativity depends on both sides

split brain patients

corpus callosotomy-> process of sectioning the corpus callosum first performed in 1940 to treat severe epilepsy (electrical signals could not flow between hemispheres)

speech and hemispheres

right hemisphere does not produce or comprehend speech so it sends signals across the corpus callosum for left hemisphere to pull all information together

language

use of complex abstract symbols to represent perception of world; handled by the lateral surface of the LEFT hemisphere

Wernicke's area

responsible for recognition and comprehension of language; temporal lobe

Broca's area

responsible for producing coherent speech; frontal lobe

arcuate fasciculus

pathway connecting Broca's and Wernicke's areas

language pathway

primary auditory cortex-> secondary auditory cortex-> Wernicke's area-> arcuate fasciculus-> Broca's area-> oral and throat cortex

alexia

lost/diminished ability to comprehend written language

agraphia

lost/diminished ability to produce written language

aphasia

disorder of language expression/comprehension

Wernicke's aphasia (receptive)

hearing is in tact but comprehension of word meanings is lost; often results in word salad production, meaningless words, paraphasia; often unaware the the impairment; often exists with other conditions (alexia, agraphia, sensory issues, contralateral homonymous hemianopia)

Broca's aphasia (expressive)

results from frontal lobe damage; difficulty expressing one's self using language; no comprehension difficulties but production of language; no language output, habitual phrase use, emotional speech, slow/deliberate speech, telegraphic speech; usual aware of errors and existence of the condition (frustration occurs); co-occurs with difficulty reading aloud, writing impairment, right side hemiplegia (frontal lobe damage)

conduction aphasia

results from damage to arcuate fasciculus; comprehension of written and spoken speech is intact; can range from substitution paraphasia to meaningless words in written and spoken language

global aphasia

results from extreme lesion to left lateral cerebrum; inability to use language in any form

right hemisphere language responsibilities

prosody, pragmatics (social cues, timing, influences), understanding metaphors/humor, inference

prosody

element of speech which includes linguistic functions such as intonation, stress, rhythm

Aprosodia

disorder of prosody caused by damage to Right Broca's area, Right Wernicke's area

Right Wernicke's area

interprets nonverbal signs from other people; damage will result in difficulty understanding nonverbal communication

Right Broca's area

provides instruction for producing nonverbal communication; emotional gestures, speech intonation; damage will result in difficulty producing nonverbal motor responses

perception

interpretation of sensation into meaningful forms; deficits mean that sensation is still intact; deficits are associated with right hemisphere damage

agnosia

inability to identify objects when using a specific sense even though the discriminative ability of that sense is in tact

astereognosis

inability to recognize objects by touch manipulation alone, despite intact discriminative somatic sensations (tactile agnosia)

visual agnosia

inability to visually recognize objects despite having intact vision

auditory agnosia

inability to auditorily recognize objects despite being able to hear

right lesion: interferes with interpretation of environmental sounds

left lesion: inability to understand speech (Wernicke's area)

Prosopagnosia

type of visual agnosia; face blindness; inability to visually identify people's faces; can describe facial features and interpret emotional facial expressions and can recognize objects

unilateral neglect

failure to report/respond to stimuli presented contralaterally to brain lesion (hemi-inattention); tendency to behave as one side of the body/space does not exist; personal/spatial

co-occurs with visual deficits (CHH) and anosognosia

implications for ADLs

test with line cancelation (bisection) test

anosognosia

lack of awareness/insight into condition; denial of symptom severity

visual perception

ability to interpret information from visible light

visuospatial perception

ability to perceive/react to size, distance, depth aspects of environment

schema

a mental representation of some aspect of the world; internal awareness of body and relationship of body parts to each other

form discrimination

ability to perceive differences among objects and positional aspects of objects; difficulty results in inability to distinguish between similar geometric shapes (square or rectangle? M or N? words like house, hose, horse)

figure ground

ability to differentiate foreground and background forms or objects

spatial relations

relating objects to each other or to self

topographical orientation

ability to determine location and route to location; difficulty results in topographical disorientation

tests of visual perceptual skills (TVPS)

visual discrimination, visual foreground, visual closure, visual spatial relations

apraxia

knowledge of how to perform skilled movements is lost; intact sensation, muscular strength, coordination, understanding

developmental dyspraxia

impairment in ability to plan or carry out skilled nonhabitual motor acts in correct sequence (not due to brain damage); congenital

constructional apraxia

difficulty drawing, building, assembling objects