Neuroanatomy and

Neurophysiology

Sensory Motor• Afferent

• Vision• Kinesthesia• Olfaction• Hearing• Taste• Pain• Temperature• Touch• Balance

• Efferent• Glands• Muscle• Organs

• Circulation• Digestion• Respiration• Excretion• Reproduction

,Viscera

Dendrite

Cell Body

Axon

Boutons contain:

-neurotransmitters for excitation or inhibition of response

-mitochondria for energy generation and protein development

Presynaptic neurons

Postsynaptic neurons

Meningeal Lining

protective and nutritive function

Cortex=Bark

6 layers of cells

Pyramidal motor cells

Non Pyramidal sensory cells

Broadman’s Map

1,2,3,4,6,8,17,18,22, 41,42,44,45

Fissure

Gyri

Sulci

Frontal Lobe precentral gyrus supplemental motor area inf. frontal gyrus= pars operculum= Broca’s Area

Parietal Lobe postcentral gyrus supramarginal gyrus angular gyrus

Temporal Lobe superior temporal gyrus

Heschl’s Gyrus Wernicke’s Area

Occipital Lobe calcarine sulcus

Corona Radiata

Myelinated Fibers

Projection to and from cortex to

brain stem, spinal cord – Corona Radiata

Association links regions of same

hemisphere Short connect one gyrus to the next Long interconnect lobes of the brain of the same hemisphere- arcuate fasciculus

Commissural from one location on one hemisphere to the corresponding location in the other –corpus callosum

Subcortical Structures

Basal Ganglia

Control of background movement initiation of movement

patterns

Lesions basal ganglia = extrapyramydal dysfunction including hypokenetic and hyperkenetic dysarthria

Cerebrovascular System

Carotid Division ext&int carotid Int. carotid = Ant. Cerebral a. Mid. Cerebral

a.

Vertebral Division ant&post spinal a.

basilar arteries = sup/ant cerebellar a. post cerebral a.

Cerebralvascular Obstruction• Thrombosis is a stationary obstruction• Embolus is a traveling clot that obstructs• Aneurysm is a dilation or ballooning of a vessel wall which can

cause a rupture into surrounding space• Congenital, AVM• Trauma• CVA, TIA

Anatomy of the Brainstem

II

Olfactory I Reaches the brain without going through thalamus

Olfactory cortex in pyriform lobe and hippocampal formation

CN II Optic Nerve

CN III oculomotor CN IV Trochlear CN VI Abducens

CN V Trigeminal Sensory/motor 3 branches opthalmic: transmits sensory information from skin of the upper face maxillary: transmits sensory information from the middle face

mandibular: sen/mot sensory from lower face, kinesthetic/proprioceptive sense of m. of mastication, sen. ant. 2/3 of tongue & floor of mouth (pain/temp), motor innervates m. of mastication, tensor tympani and veli palatini, mylohyoid, ant. belly of digastric

UMN Damage: increased jaw jerk reflex

LMN Damage: atrophy/weakness of affected side, jaw pulls to unaffected side on closure bilateral-jaw hangs open

TVP damage: hypernasality

Upper face innervated bilaterally

Lower face contralateral

Efferent for facial m. Afferent: -taste ant. 2/3 tongue

-sublingual/submandibular glands

UMN damage: no upper face paralysis LMN damage: upper/lower face paralysis on side of lesion

VII CN S/M

Facial

VIII CN S/M

Vestibulocochlear

IX CN S/M

Glossopharyngeal

Part of Pharyngeal Plexus

Efferent stylopharyngeus

Afferent taste posterior 1/3 tongue, soft palate

Pain, temp., touch posterior 1/3

X CN

Vagus S/M

Pharyngeal, superior, and laryngeal branches important in voice, speech, and swallowing

Lesions can cause: Lack of sensation in pharynx Lack of muscle function: palate, pharynx, vocal fold, esophagus

Large autonomic role

IX CN

Accessory MPart of pharyngeal plexus for innervation of larynx, pharynx, and soft palate

Sole innervation for trapezius and SCM

XII CN

Hypoglossal MInnervation for the motor function of the tongue

Each hypoglossal nucleus served by contralateral corticobulbar tract (L) UMN damage = (R) tongue weakness (L) LMN damage = (L) tongue weakness

Fibers of the Corticobulbar Tract decussate prior to reaching the hypoglossal nucleus, therefore (L) UMN damage/ (R) LMN damage = (R) tongue weakness

Dorsal Root + Ventral Root = Spinal Nerve = Dorsal & Ventral Rami

Branches of ventral rami go to sympathetic ganglia, nuclei of ANS

Efferent neurons of dorsal and ventral rami go to motor end plates/muscle synapse

Spinal Reflex Arc

UMN: commands from upper brain levels that activate or inhibit muscle function by synapsing with LMN

LMN: dendrites and soma within the spinal cord,axons/components that communicate with muscle fiber

Neuron within ventral gray matter is LMN or Final Common Pathway

UMN/LMN• LMN Damage: muscle weakness or complete paralysis,

reflexes not intact• UMN Damage: muscle weakness or complete paralysis,

reflexes intact because a spinal arc reflex is a LMN process

AST Tract: transmits info. On sense of light touch from spine to thalamus

Ipsilateral: sensations on the same side as they enter the cord

Contralateral: sensations on the opposite side as they enter the cord

Decussate: cross the midline

Corticospinal Tract

Pyramidal Tract

Voluntary Movement

Modification of Reflexes

Visceral Activation

Two neuron pathway consisting of an UMN

and LMN

Corticobulbar Tract

Arises from: cortical cells in lateral aspects of pre central gyrus premotor/somesthetic regions of parietal lobe

Axons will: branch/decussate at different levels of brainstem synapse with nuclei of CN

Sensory Information: facilitate/inhibit transmission to thalamus

Serves: CN for speech

Higher Functioning• Primary activity areas: receive information from senses,

extract info.• Adjacent higher order areas of processing (secondary,

tertiary,quaterary): info. compared to other info. received and stored associated with modality

• Association areas: highest level of cognitive processing

Motor Function• Identify target: tongue tip to alveolar ridge

• Spacial orientation: integration of information of body parts in space

• Posterior parietal lobe receives information from thalamus, cerebellum, basal ganglia

• Develop plan to achieve target behavior• Premotor region, area 6, anterior to motor strip plans the action,

receives info from areas 1,2,3 re location of muscles and joints• SMA, area 6 sup. & med., preparatory speech act, initiation of

speech act

• Execute plan: muscle movement with accurate timing force and rate• Area 4 execution of voluntary movement

Motor System Lesions• Dysarthria: speech disorder arising from paralysis, muscular weakness,

and dyscoordination of speech musculature

• Flaccid Dysarthria: LMN damage of CN, dysphonia due to VF paralysis, fasciculations, hypotonia, reflexive responses reduced or absent

• Spastic Dysarthria: UMN bilateral damage to pyramidal or extrapyramidal tracts, hyper-reflexia, hypertonia• UUMN: less devastating than bilateral

Motor System Lesions• Ataxic Dysarthria: Damage to the cerebellum &/or brainstem

vestibular nuclei• Loss of coordination, unable to achieve articulatory target,

problems in coordination of rate, range, and movement• Dysdiadochokinesia• Dysprosody

Motor System Lesions• Hypokenetic Dysarthria: paucity of movement, inhibited initiation of

movement, reduced ROM, rigidity, pill rolling hand tremor• Damage to BG &/or substantia nigra (SN)

• SN produces Dopamine (DA) which balances acetylcholine (Ach), decreased DA results in inhibited initiation of motor function

• Speech rushed, reduced duration of speech sounds, monopitch, monoloudness

Motor System Lesions• Hyperkenetic Dysarthria:Extraneous involuntary movement caused by BG

circuit damage• Subthalamic N. damage: inhibition to GP is lost resulting in Ballism (uncontrolled

flailing)• BG damage: if Ach is decreased and DA increased choreiform, involuntary

twitching and movements, result• Tics: rapid movements of small groups of muscle fibers• Tremors: rhythmic contractions• Athetosis: slow, writhing movements• Dystonia: involuntary movement to a posture, posture held briefly

Motor System Lesions

• Mixed Dysarthria: Damage to more than one of the controlling systems• S/F: found in ALS, disease of UMN & LMN• S/A: found in MS, UMN and cerebellum • S/A/hypo: Wilson’s disease (hepatolenticular

degeneration)

Motor System Lesions• Apraxia/Dyspraxia: A dysfunction of motor planning in the absence of

muscular weakness or dysfunction• SMA damage: difficulty in initiating speech• Dominant insular cortex damage: verbal dyspraxia (loss of fluency and groping

behavior, ability to contract musculature voluntarily is impaired) • Oral apraxia: inability to perform non speech oral gestures

• Supramarginal Gyrus damage: verbal apraxia affecting long and complex sentences

Hemispheric Specialization

• Left Hemisphere• Lateral Fissure is longer• Planum Temporale (HG) is larger• Generally functional dominance for L/S• Processes consonant transitions and stop consonant

bursts in (R) handed • Process of analysis, favored discrete, sequential, brief

duration or rapidly changing information• Spoken/written language perception & production

Hemispheric Specialization

• Right Hemisphere• Spatial and holistic elements

• Face recognition• Speech intonation• Melody, tonal information• Perception of form• Intention of speaker

Lesion Studies• Speech and Language Areas

• Wernicke’s Area (22): receptive or fluent aphasia• Relatively normal flow of speech• Has syntax • Does not understand what is said • Verbal paraphasias (substitution of words)• Neologisms (new word), jargon, word salad• Cannot repeat

Lesion Studies• Broca’s Aphasia: lesions to 44,45, operculum of frontal-

parietal, insula, supramarginal gyrus of parietal lobe• Difficulty with the planning of speech• Non fluent aphasia• Expressive abilities severely limited• Usually retain auditory and visual input

Lesion Studies• Global Aphasia: Damage to both Wernicke’s and Broca’s

Area and some sub cortical structures• Both receptive and expressive functions are severely impaired

Lesion Studies• Conduction Aphasia: lesion of arcuate fasiculus connecting Broca’s and

Wernicke’s area• problem with repetition of words

• Anomia: difficulty naming objects• Thalamic damage, cortical and subcortical structures

Lesion Studies• Dyspraxia: : inability to program the articulators for

voluntary speech and non speech movements• Frontal lobe insular cortex damage: difficulty producing simple

gestures with articulators (executive dyspraxia)• Supramarginal gyrus damage: difficulty sequencing more

complex articulatory gestures ( planning dyspraxia)

Lesion Studies• TBI/Right Hemisphere Damage

• Decision making• Problem solving• Judgment• Response inhibition• Pragmatics• Emotional lability• Personality characteristics• Communication of emotion, intent, humor• Abstract information• Frontal- response inhibition

Lesion Studies

• Parahippocampal region• Learning complex tasks• Remembering information received through sensory

modalities

• Hippocampus• Bilateral produce profound short term memory

deficit• Unilateral produce milder deficit• Removal of (L) difficulty remembering verbal

information