Medical Neuroscience

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Chapter 3-2

1. Glia

Structural matrix

Astrocyte foot processes form part of blood-brain-barrier (BBB)

Vascular basement membrane & vascular endothelial cells with tight junctions

Form glia limitans

Maintain neuronal environment

Regulate extracellular potassium concentration

Reuptake of peptide neurotransmitters & glutamate

Produce growth factors

Insulate and prevent cross talk of neuron


Form & maintain myelin in CNS

Contribute myelination of 100 or more internodes
Schwann cells

Myelination of PNS

Similar capacity to astrocytes

Secrete extracellular matrix in dorsal root ganglia and peripheral nerves

Become phagocytes under injury or inflammation

Secrete neurotrophic factors

Ependymal cells

Line ventricles and central canal

Cilia circulate CSF

Form choroids plexus of ventricles = make CSF


Multiply at injury site

Differentiate into brain macrophages

Clear debris & mediate immunologic responses

Antigen presentation

Targeted by HIV

Chapter 3-3

1. Major loci of stem cells in adult CNS
Subependymal zone of ventricular system

Telencephalon to central canal

Dentate gyrus of hippocampal formation

Neural parenchyma

2. Normal brain functions that rely on continuous supply of new neurons
Olfactory bulb

Routine turnover of granule cells by precursor cells in subependymal zone

Hippocampal formation

Neural precursors in dentate gyrus

Ongoing process of new fact memories
3. Brain degeneration effects on neural precursor cells
Generation of time- and location-specific signal molecules

Regulate proliferation, migration, and differentiation of neural precursors

Extension of axons and dendrites to appropriate locations

Chapter 3-4

1. Major components of blood-brain barrier
Vascular basement membrane

Astrocytic foot processes coat of blood vessels & pial surface

Vascular endothelial cells

Tight junctions

Perivascular macrophages (from pericyte = mesenchymal cell)
*complete absence of fluid-phase endocytosis & restricted receptor-mediated endocytosis
2. Function of BBB
Isolate CNS from molecular and cellular constituents of blood

Ionic homeostasis in CNS

Exclude microorganisms & leukocytes

Selective permeability of metabolites and nutrients

CSF composition = low white blood cell (<5/cu mm), no red blood cells, low protein (<45 mg/dL)
3. BBB windows
Circumventricular organs

High vascularity and gaps between endothelial cells

Hypothalamus & pituitary gland

Limited receptor-mediated endocytosis (Ion channels)

Insulin & leptin

Lipid-soluble substances

Corticosteroids, estrogen, & testosterone

Active & facilitative transport

Amino acids & glucose
4. Breakdown of BBB
Viral, bacterial, or fungal infection of meninges

Facilitate lipid-insoluble antibiotics passage into CNS

Meningeal carcinomatosis

Damage glucose transporter by cancer

Increased gap junctions = MRI

* Mannitol disrupt barrier to allow drug enter brain tissue

Chapter 3-5

1. Cytoarchitectonic organization of cerebral cortex
Comprised of six layers of neurons

Regional variation in cortical layers

Layer III

Outer pyramidal cells

Long axons (projection)

Project to ipsilateral cortex or across opposite hemisphere

Transverse anterior commissure & corpus callosum

Layer IV

Inner granular cells

Receives information from thalamus (target of afferent thalamocortical fibers)

Layer V

Inner pyramidal cells

Long axon (projection)

Project outside cerebral cortex (include basal ganglia, thalamus, brainstem, & spinal cord)

2. Projection neuron & interneuron
Projection neurons

Extensive dendritic arborization

Large cell bodies

Long axons

Important for information processing between structures


Small dendritic arborizations

Small cell bodies

Short axons

Project short distances (between cortical layers & spinal cord layers)

Local information processing
3. Cytoarchitectonic structure of hippocampus
3 layer cortex

Connect with parahippocampal gyrus & other structures (amygdala, septal nuclei, thalamus)

Consist of dentate gyrus & pyramidal neurons (CA region)
4. Cytoarchitectonic structure of cerebellum
3 layer cortex

Molecular layer – Purkinje cell layer – Granule cell layer

5. Hippocampus & cerebellum functions

Encode memories via connection of pyramidal neurons to thalamus/basal forebrain to cortex

Susceptible to ischemia = amnesia

Parahippocampal cortex to dentate cells to pyramidal cells (of hippocampus proper) to cerebral cortex

Define space-time envelope of muscle contractions

Cerebral cortex & spinal cord to granule cell to molecular layer (parallel fibers) to purkinje cells

Chapter 3-6

1. Cytoarchitectonic structure of spinal cord & dorsal root ganglia
Dorsal horns = sensory neurons

Intermediate zone = preganglionic autonomic neurons (terminate in autonomic ganglia)

Ventral horns = motor neurons (terminate in muscles)
Dorsal root ganglion

Axons bifurcate

1) Dorsal root – spinal nerve – peripheral nerve – sensory receptor

2) Neuron in dorsal horn or up spinal cord to synapse

Chapter 3-7

1. Peripheral nerve structure
Contain both afferent & efferent fibers = myelinated and unmyelinated

Endoneurium = fibroblasts and collagen

Perineurium = connective tissue

Epineurium = adipocytes, nerve bundles, and blood vessels

Regenerate due to epineurium (effective barrier)
Chapter 4-1
1. Neurotransmitter processing

Biogenic amine synthesis

Enzymes concentrated at axon terminal

Neuropeptide synthesis

Enzymes concentrated in rER at cell body

Neuropeptide transported to axon terminal


Stored in 50-100 nm synaptic vesicles

Concentrated at axon terminal


Voltage-sensitive channels

Influx of calcium from depolarization

Synaptic vesicles fuse with plasma membrane


Neurotransmitter (ligand) bind to receptor

Excitatory (glutamate) or inhibitory (GABA)

G-proteins or voltage-sensitive ligand-gated ion channels


Enzymatic catabolism (acetylcholinesterase)

Reuptake and catabolism (dopamine)

Diffusion out of synaptic cleft and reuptake (glutamate)

Chapter 4-2

1. Synthesis and catabolism of glutamate
Glutamate = major excitatory neurotransmitter

Synthesized from a-ketoglutarate (TCA cycle)

Catabolized by reverse route or decarboxylated into GABA

Action terminated by carrier-mediated reuptake system & diffusion

2. Major locations of glutamatergic neurons
Intrahemispheric connections

Interhemispheric connections

Corticobulbar (cortex to brainstem)

Corticospinal (cortex to spinal cord)

3. Two major functions of glutamate and its receptors
Bind to ligand-gated sodium channels (AMPA & kainite receptors)

Open transmembrane protein channel

Sodium enter

Postsynaptic membrane depolarize

4. Seizures, migraine, and stroke
Glutamate = excitatory neurotransmitter

Paroxysmal discharge = seizure

Spreading depression of Leao = 3 mm/min

Depression of cortical neuronal activity

Chapter 4-3

1. Synthesis and catabolism of GABA
GABA = principal inhibitory neurotransmitter of interneurons

Synthesized from glutamate via glutamic acid decarboxylase (GAD)

Catabolized by GABA-transaminase

Yield glutamate & succinate semialdehyde

Converted to succinate = TCA cycle

Action terminated by carrier-mediated presynaptic reuptake system & diffusion

2. GABA function and receptor
Mediate neural signaling = hyperpolarize postsynaptic neuron = inhibition

GABAA & GABAC receptor = poteniate Cl- conductance

GABAB receptor = potentiate K+ conductance
3. GABAergic neurons location

Globus pallidus

Purkinje cells (cerebellum)
4. GABA-mimetic drugs as anticonvulsants
Moderation of gluatamatergic effects on sodium & chloride channels
5. Alcohol withdrawal syndrome
Alcohol = chronic potentiation of GABAergic neurotransmission

Downregulation of GABA receptors

Withdraw = deficient of GABA-mediated inhibition

Seizures, agitation, tremulousness

Lorazepam = potentiates GABAA receptors

Increase Cl- channel opening = inhibition

Chapter 4-4

1. Glycinergic neuronal location and function
Glycine = second most widespread inhibitory neurotransmitter




Spinal cord

Open chloride channels

2. Interference of glycinergic neural transmission
Limit inhibition of neurons

Uninhibited firing of motor neurons

Risus sardonicus

Increase muscle tone

Chapter 4-5

1. Peptide neurotransmitter synthesis, transportation, and degradation
Neuropeptides = within-system modulatory neurotransmitters

Produced by proteolytic cleavage of large precursor proteins

Proteins synthesized by rER in cell body

Transported to presynaptic terminal

Degraded by extracellular proteases
2. Receptor downregulation (tolerance and dependence)
Chronic intensive stimulation

Reduction in receptor density (at postsynaptic sites)

Reduce sensitivity of target neuron
3. Ligand non-specificity
Opioid drugs bind endorphin and enkephalin receptors throughout nervous system

Produce side effects from nonspecificity

Chapter 4-6

1. Synthesis and degradation of catecholamines
Rate-limiting step = tyrosine hydroxylase

Become dopaminergic, noradrenergic, or adrenergic

Depends on presence of enzymes

Degraded by monoamine oxidase (MAO) & catechol-O-methyltransferase (COMT)

Eliminated in urine

Action terminated by transporter system reuptake

Chapter 4-7

1. Synthesis and degradation of serotonin
Rate-limiting step = tryptophan hydroxylase

Tryptophan – 5-hydroxytryptophan – serotonin

Degraded by MAO only

Eliminated in urine

Chapter 4-8

1. Major dopamine systems

Tuberoinfundibular system

Originate in hypothalamus

Inhibits pituitary secretion of prolactin

Nigrostriatal/mesolimbic systems

Substantia nigra and ventral tegmental area
2. Specific dopamine receptor blocker
Haloperidol = nonspecific D2 blocker

Block mesolimbic system

Side affects = block dorsal striatum
3. Modulatory biogenic amine neurotransmitters
Wide host of functionally disparate targets

Each amine neuron has over a million synapses

Less variability in firing rates

Regulate signal-to-noise ratio

4. Parkinson’s disease, dyskinesias, and psychosis
Parkinson’s disease

Progressive loss of dopaminergic neurons

Located in substantia nigra

Reduced dopamine levels in putamen

L-Dopa cross BBB


Involuntary muscular movements

Over-stimulation of dopamine


Over-stimulation of dopamine

Dopamine receptor antagonist
5. Depression
Limbic system

Has heavy serotonergic and noradrenergic projections

Low serotonin levels

Prozac = inhibit serotonin reuptake

6. Migraine
CN V activation and gasserian ganglion

Vasodilatation of microvasculature


Inhibit release of vasoactive proteins

Chapter 4-9

1. Synthesis and degradation of acetylcholine
Synthesized by hydrolysis of phosphatidylcholine of cell membranes

Degraded by acetylcholinesterase in synaptic cleft

Reuptake by high-affinity system
2. Cholinergic neurons within CNS

Midbrain reticular formation

Basal ganglia

Basal forebrain

3. Disorders of neuromuscular junction
Myasthenia gravis

Acetylcholine receptors destroyed by autoimmune mechanism

Decreased sensitivity to acetylcholine

Weakness of limbs and mucles

Eaton-Lambert syndrome


Toxin disrupt acetylcholine vesicles from fusing with presynaptic membrane

Ocular and systemic muscular weakness

4. Memory formation and Alzheimer’s disease
Anticholinergic drugs

Inhibit acetylcholine in neural connectivity in cerebral cortex

Limit memory formation
Cholinomimetic drugs

Inhibit acetylcholinesterase

Increase half-life of acetylcholine

Limit decline in neurodegenerative process


Area of Release



Substantia nigra & Ventral tegmental area

Prolactinoma (Tubero-infundibular)

Parkinsons (Substantia Nigra)

Schizophrenia (mesolimbic)


Locus coeruleus


Tuberomammilliary nucleus of hypothalamus


Raphe nucleus


Reticular formation

Basal ganglia

Basal forebrain



Myesthenia Gravis


Alzheimer’s Disease




Corticobulbar projections


Spreading depression







Basal ganglia

Cerebellum (Purkinje cells)



Anxiety disorders




Spinal cord

Tetanus (lockjaw)


Postsynaptic Effect


Rate-limiting Step in Synthesis

Removal mechanism

Receptor Type



Choline + acetyl CoA



D: nAchR
InD: mAchR*






D: NMDA, AMPA, Kainate GluR
InD: mGluR












D: GlyR

Catecholamines (epinephrine, norepinephrine, dopamine)



Tyrosine hydroxylase

Transporters, MAO, COMT

All are indirect, but have different receptors.

Serotonin (5-HT)



Tryptophan hydroxylase

Transporters, MAO




Histidine decarboxylase





Mitochondrial oxidative phosphorylation + glycolysis

Hydrolysis to AMP and adenosine


Excitatory + Inhibitory

Amino acids

Synthesis and transport


*n (nicotinic) & m (muscarinic)
Cholinergic System

CNS = modulator

PNS = signaler & modulator

Nicotinic cholinergic receptor = excitatory

Neuromuscular junctions

Muscarine cholinergic receptor = inhibitory

Heart, smooth muscle, exocrine glands

Glutamatergic System

Non-essential amino acid

Do not cross BBB

Fast & slow excitatory

NMDA receptor = voltage gated Mg2+ blocking system

Require co-agonist = NMDA

Mg2+ block hyperpolarization; not depolarization

GABAergic System

Fast & slow inhibitory


GABA-A & GABA-C receptors = chloride

GABA-B receptors = potassium

Not an essential metabolite = not part of proteins

Glucose – Glutamate (TCA) – GABA (with enzyme and co-factor)

Co-factor = Vitamin B6

Glycinergic System

Inhibitory = hyperpolarization by chloride

Derived from diet and serine


Inhibit SNAREs & SNAPs = glycine can’t be release

Biogenic Amine System

Modulatory – excitatory

Five amines








B12, folate, SAMe

Chapter 5-2

1. Action potential
Excitatory neurotransmitter = glutamate

Bind ligand-gated sodium channel receptors

Sodium flow down its electrical & concentration gradients

Depolarize membrane = excitatory postsynaptic potential (EPSP)

Exceed threshold

Initiation phase = high increase in sodium conductance

Depolarization phase

Accumulation of positive charge (sodium ions) = inactivate sodium channel

Simultaneously open voltage-sensitive potassium channels

Repolarization phase

Absolute refractory period = immune to any action potentials


Relative refractory period
2. Neural transmission
Depolarization opens voltage-gated sodium channels adjacent

Succession of action potentials

Opens N-type voltage-sensitive calcium channels at axon terminal

Chapter 5-3

1. Spatiotemporal summation of neurons
Neuronal action potentials are spatially weighted and over time

Chapter 5-4

1. Propagation of unmyelinated axons
Current is attenuated by resistance and capacitance

Unmyelinated action potentials = 1m/sec

2. Myelin and action potential propagation
Capacitance of myelinated axon is less

Undergo salutatory conduction

3. Conduction block from myelin destruction
Multiple sclerosis

Lesions form = recurrent autoimmune inflammatory attach at myelin

Remyelination reduces capacitance and leakiness
Guillain-Barre syndrome

Autoimmune response for myelin antigen

Occur after infection

Inflammatory damage to myelin in PNS

Chapter 5-5

1. Sodium-potassium pump
Sodium and chloride increase within cell from membrane permeability

Restored by S/P pumps = require ATP

Sodium out = potassium in

Division 2

Chapter 6-6

1. Motor unit
Combination of one -motoneuron and its muscle fiber
2. -motoneuron somatotopic organization
Located in ventral horn of spinal cord

Form column of cells in ventral horn

Dendritic tree in ventral horn and junctional zone

Axons through ventral roots – spinal nerves – peripheral nerves – muscle fibers

Medial ventral horn

Supply axial and proximal limb muscles

Lateral ventral horn

Supply peripheral limb muscles

3. Trophic influence of -motoneuron

Neighboring -motoneurons sprout axon to muscle

Chapter 6-2

1. Recruitment
With increased force from muscles

Incease in small -motoneurons firing

Increase numbers of larger -motoneurons

Slow rates then fast rates (in maximal force)

2. Electromyography
Amplitude and duration of motor unit potentials

Recruitment patterns

Lou Gehrig’s Disease

Fasciculation potentials

Irregular, broad, high amplitude, multiphasic potentials

Chapter 6-3

1. Reflex arc with -motoneuron and Ia sensory afferent projections
Group Ia afferents

Terminate in annulospiral endings of nuclear region

Rate of muscle stretch

Group II afferents

Terminate in intermediate region

Muscle length

Myotatic reflex arc

Muscle stretches = stimulate sensory nerves

Excitatory input to a-motoneuron = resist stretching force

Prevent further muscle lengthening

2. Upper motor neuron and lower motor neuron lesions

Lower motor neuron lesions

Cause hyporeflexia

Higher motor neuron lesions

Presynaptic inhibition lost


Hyperactive deep tendon reflexes = increased dynamic tone

Augmented length-dependent resistance = increased static tone

3. Jacksonian principle
Higher centers bring sophistication to neuronal processing and inhibit lower centers
4. Golgi tendon organs and type Ib afferent fibers
Feedback to -motoneuron

Increased muscle fiber tension = increased inhibitory to -motoneuron

Information to CNS

Ib afferent inhibit motoneuron of homonymous and heteronymous muscles

Excite neurons to antagonist muscle

Chapter 6-4

1. Spinal agonist-antagonist circuits and ventral horn

Group Ia afferents excite -motoneurons

Homonymous muscles

Synergistic (agonist) muscles

Inhibitory interneurons – to -motoneurons of antagonist muscles

Nociceptive flexion reflex afferent fibers

Group III & IV = muscles

Group A & C = skin

Excite flexor -motoneurons

Inhibit extensor -motoneurons

Reflex inhibited by cerebral and brainstem systems
2. Babinski sign and triple flexion responses
Extensor plantar response

Right foot stimulated, great toe extends (goes up)

Normal = great toe curls down

Damage to cerebral cortex and medullary reticular formation

Disinhibition of nociceptive flexion reflex

Triple flexion response

Flexion at ankle, knee, and hip
3. Spastic catch
Clasped knife reflex

Disinhibition of Golgi tendon organs sensitive to muscle tension

4. Signs of lesions and localization
Deep tendon reflexes

C5-C6 = biceps, brachioradialis

C7 = triceps

L2-L4 = knee jerks

S1 = ankle jerks

Chapter 6-5

1. Distributed representation of the motor system
Movement by multiple systemic interaction

Cortical – brainstem – spinal – segmental


Precise with great speed in production of internal movements

Slow with reactive movements

Incapable of two simultaneous movement programs

Brainstem & spine

Great reactive speed

2. Renshaw cells
Regulation of information processing in motor systems of spinal cord

Glycinergic inhibitory interneurons

Synapse on homonymous and heteronymous -motoneurons

Dampen neural noise not related to sensory stimulation or motor action

Chapter 6-6
1. Ventromedial & lateral tract groups
Ventromedial tracts

Innervate axial & limb girdle musculature

Actions of axial and proximal muscle groups & posture and tone

Lateral corticospinal tract

Major lateral tract

Innervate distal musculature

Precision movements of distal extremities (hands)

Ventromedial tracts

Except tectoreticulospinal tract

Favor extensor tone (antigravity)

Lateral corticospinal tract = minimal on tone

Most synapse with interneuron of ventral horn or junctional zone

Interneuron synapse to - & -motoneurons and Group Ia & II


Lateral corticospinal tract synapse directly to - & -motoneurons in arm and hands

CONTRA = 90% @ medullary pyramidal decussation

IPSI = 10%
2. Lesions on balance pathways
Vestibulospinal system

Antigravity tone maintenance, posture, & balance

Parkinson’s disease
3. Decorticate and decerebrate patients with lesions of pons and above pons
Decerebrate posturing = lesion at pons

Disinhibition of vestibulospinal and caudal pontine reticulospinal systems

Profound extensor tone

Decorticate posturing = lesion at or above level of midbrain

Disinhibition of cortical drive to brainstem motor systems

Flexion and pronation of upper extremity

Extension of lower extremity
4. Spinal shock and chronic spinal cord lesions
Spinal shock = acute lesion

Flaccid muscle tone

Absent deep tendon reflexes

No plantar responses

Chronic lesions of motor systems

Hyperactive muscle stretch reflexes

Increased deep tendon reflexes

Extensor plantar responses


Vestibulospinal tract

Antigravity tone


Medullary & Pontine Reticulospinal tracts

Travel down brainstem and spinal cord – terminate at spinal segments

Flexor (medullary) & extensor (pontine) muscle tone


Immobilize proximal portion of extremities

Tectoreticulospinal tract

Deep superior colliculus – a- & g-motoneurons in cervical spinal cord

Deep layer = visual, auditory, and somatosensory input

Superficial layer = define targets for movement

Reactive movements of eyes and head

Lateral Corticospinal tract

Pyramidal cells of BA 4

Execution of precise movements (especially the hands)

Independent finger movement

Chapter 6-7

1. Bladder function and bowel control
Innervated by ANS
Detrusor muscle = empty bladder

Parasympathetic control

Inhibition = pontine reticular formation via pontine reticulospinal tract

Internal sphincter muscle = restrict urine through bladder neck

Lower motor neuron bladder = lesions of spinal cord, sacral parasympathetic, paravertebral ganglia

Detrusor = large, flaccid bladder, poor emptying

Sphincter = overflow incontinence during increase abdominal pressure

Upper motor neuron bladder = lesions above nerves innervation detrusor

Detrusor = small capacity, spastic bladder

Sphincter = difficulty emptying bladder, urgency incontinence

Chapter 6-8

1. Major components of cerebral motor system
Precentral gyrus = pyramidal neurons of layer V

Afferent to BA 4 = Premotor cortex and supplementary motor area (IPSI)

Receive input from muscle spindles

Area 4 & 6 = input from VL nucleus of thalamus (relay to putamen and cerebellum)

Basal ganglia & cerebellum = consultants to cerebral cortical systems
2. Corticospinal tract
BA 4 – corona radiata – genu and internal capsule – cerebral peduncles – basis pontis

Longitudinal fibers of ventral pons – medullary pyramids – decussation of pyramids (90% cross)

Dorsolateral of contralateral spinal cord (90%) & ventromedial of ipsilateral spinal cord (10%)

Exit on interneurons or -motoneurons in ventral horn

3. Major brainstem and spinal cord input from corticospinal projections
Corticobulbar fibers

Terminate on interneurons of cranial nerve motor nuclei from midbrain to medulla

Red nucleus

Pontine and medullar reticulospinal centers

4. Somatotopic organization of corticospinal system
Brainstem and spinal cord

Face fibers = medial

Leg fibers = lateral

Arm fibers = intermediate

Extensive fibers for face and upper extremities
5.Cerebral lesions and its involvement in arm and hands
Common infarction of middle cerebral artery distribution even with collaterals

Arm and face regions of motor homunculus

Corticospinal and corticobulbar fibers travel through corona radiata

Except in periventricular region

No somatotopic organization of corticobulbar/corticospinal fibers
6. Microscopic representation of movements in area 4
Corticospinal system = supervisory system

Suppress background muscle tone of other systems

Collateral projections

Deep superior colliculus (tectospinal tract)

Red nucleus (rubrospinal tract)

Pontine and medullar reticular formation (reticulospinal tracts)

Each corticospinal fiber project to -motoneurons of principal target muscle, inhibitory neurons, etc
7. Supplementary motor area and dorsolateral premotor cortices
Supplementary motor area = parasagittal

Generation of practiced movement sequences

Premotor area = dorsolateral

Development of movement sequences

Receive visual and somatosensory cortices

Chapter 6-9

1. Major structures of basal ganglia
Caudate nucleus


Globus pallidus

Substantia nigra pars reticulata (SNPR)

Substantia nigra pars compacta (SNPC)

Subthalamic nucleus (STN)

2. Two major basal ganglia circuits

Cortex – striatum – GPi/SNPR – thalamus – cortex


Cortex – STN – GPi/SNPR – thalamus – cortex

Glutamate = excitatory

Cortical neurons project to striatum & STN

STN neurons

Thalamic neurons relaying back to cortex

GABA = inhibitory

Striatum neurons

GPi/SNPR neurons
3. Lesion locus of diseases
Parkinson’s disease

Striatal dysfunction = putamen

Loss of dopamine

Hypophonia = quiet voice

Hypokinesia = small movements

Festination = fall forward

Pill-rolling = tremor of forearm and hand

Akinesia = silent and immobile

Bradykinesia = slow to execute commands

Huntington’s disease

Frontal lobe and basal ganglia (caudate nucleus)

Lack of inhibition = primarily direct route

Inappropriate behavior

Chorea = lilting gait


Globus pallidus = carbon monoxide poisoning

Lack of inhibition = direct route

Uncontrollable inappropriate movements

Constant, sinuous, writhing movements of arms, hands, head, and legs

Chorea during walking


Stroke to subthalamic nucleus

Loss of excitatory input from STN to cells of GPi = loss of inhibition to Vlo

Paroxysmal surges in area 4 = violent movements

Loss of indirect basal ganglia pathway

Chapter 6-10

1. Four major cerebellar subsystems and function
Vermis = midline

Linked to fastigial nucleus

Intermediate zone = paramedian

Linked to interpositus nucleus

Hemispheres = lateral

Linked to dentate nucleus

Flocculonodular lobe

Linked to vestibular nuclei

Purkinje cells = inhibitory

Project to cerebrum, brainstem, and spinal cord

Inferior cerebellar peduncle

Spinal cord afferents enter cerebellum

Middle cerebellar peduncle

Afferent projections from cerebrum relay by basis pontis

Superior cerebellar peduncle

Cerebellar projections to cerebrum\

2. Lesions of cerebellum
Degeneration of cerebellar vermis

Chronic alcohol

Unbalance in legs

Hand coordination is fine

Paraneoplastic cerebellar degeneration of Purkinje cells

Strength normal

Hypermetric saccades = eye movements jerky

Dysmetria = unable to hit target with finger

Truncal titubation = swing side to side while sitting

Chapter 7-1

1. Major somatosensory receptors

Physical sense of position and movement of limbs

Group Ia & II afferent systems

Proprioception in proximal extremities (arms)

Ruffini endings

Proprioception in distal extremities (hands)

Collagen fibrils in skin


Superificial dermis

Merkel disks

Slow adapting receptors

Skin deformation

Meissner’s corpuscles

Rapidly adapting

Movement of skin (slippage)

Deep dermis

Ruffini endings

Slow adapting receptors

Detect skin stretch

Hands and feet

Pacinian corpuscles

Rapidly adapting

Vibratory stimuli

Range 0o to 40o & 30o to 48o

Cross at body temperature 37o

Detect absolute temperatures 30o to 48o


Mechanical/thermal nociceptors

High intensity stimuli

Rapid transmit to CNS via lightly myelinated A

Highly localized pain

Polymodal nociceptors

High intensity mechanical stimuli

Exogenous chemical stimuli

Endogenous chemical stimuli

Thermal stimuli

Slow transmit to CNS via unmyelinated C fibers

Poorly localized

Visceral pain system

Stretch or distention

Transmit to CNS via DRG & CN X

Chapter 7-2

1. Protopathic and epicritic systems

Temperature and pain

Small, slow conducting fibers

Low spatial and temporal dispersion

Lateral spinothalamic tract


Proprioception, touch, and vibration

Large myelinated fibers

High spatial and temporal resolution

Dorsal & dorsolateral columns

2. Dorsal root ganglia
Spinal cord levels more rostral than vertebral levels from cranial to caudal

No dendrites


Receptive fields

Low threshold, large-diameter, epicritic fibers = small (hands)

High threshold, small-diameter, protopathic fibers = large


Region of skin supplied by one dorsal ganglion

3. Spinal segmental neural systems, spinal cord, and brainstem pathways
Protopathic sensory fibers

Enter dorsally by Lissauer’s tract

A and C fibers of protopathic system

Terminate at lamina I & II

Crosses anterior commissure to contralateral ventrolateral white matter

Ascend spinothalamic tract

Brainstem & thalamus

Medullary, pontine, & midbrain reticular formations

Arousal and muscle impact from pain

Periaqueductal gray matter

Regulation of pain

VPL of thalamus

Localization and quantitative analysis of pain

Epicritic sensory fibers

Enter ipsilateral dorsal column

Enter dorsal horns to ventral regions


Travel uncrossed rostrally in ipsilateral dorsal column

Dorsal column nuclei at cervico-medullary junction

Gracile fasciculus (T6) & cuneate fasciculus

Chapter 7-3

1. Primary somatosensory cortex and association cortex
Occupies nearly all postcentral gyrus

First Somatosensory Area (SI)

Brodmann’s Area

Sensory Afferents



Muscle & nociceptive (via thalamus)




Slowly & rapidly adapting cutaneous input (via thalamus)





Slowly and rapidly adapting cutaneous from area 3b



Cutaneous from area 3b

Nociceptive and muscle from area 3a

Position, size, 3-D shape


Second somatosensory area

Projections from thalamus

Shape & texture

Linked by transcallosal connections

2. Graphesthesia and localization
Graphesthesia = ability to identify numbers traced on the body surface

Afferents ascend via dorsal columns

BA 5 & 7 = somatosensory from area 2

BA 7 = visual association

Chapter 7-4

1. Trigeminal peripheral trajectories
Nuclei in trigeminal ganglion

Floor of cavernous sinus


Forehead – eyebrows – eye – nose

Meninges & dura of supratentorial compartment

Superior orbital fissure


Central face – lateral nose – upper lip – cheeks – mouth

Foramen rotundum


Chin – lower lip – mandible – floor of mouth – tongue

Foramen ovale

2. Three major brainstem trigeminal nuclei
Spinal nucleus of V

Caudal pons to C2 of spinal cord

Merge with lamina I & II of dorsal horn

Project across brainstem to trigeminothalamic tract

Travel dorsal to medial lemniscus = reticular formation & periaqueductal gray

Terminate in VPL of thalamus

Chief sensory nucleus of V

Epicritic fibers

Lateral pons rostral to spinal nucleus

Project rostal to trigeminothalamic tract

Terminate in contralateral VPL nucleus of thalamus

Relay cells in VPL project to postcentral gyrus

Via genu of internal capsule & corona radiata

Motor nucleus of V

Muscles of masatication & extraocular muscles

Mesencephalic nucleus of V

Lateral midbrain

Jaw reflexes

3. Headaches
Trigeminal terminals in meninges & microvasculature

Pain due to destruction of meninges

Chapter 7-5
1. Two major anti-nociceptive descending spinal cord systems
Serotonergic system

Inhibitory interneurons = enkephalinergic – -opioid – dynorphin receptors

Synapse to nociceptive C fibers

Synapse to excitatory interneurons of nociceptive relay transmission

Synapse to spinothalamic tract fibers


Serotonergic & nonserotonergic fibers

Raphe magnus nucleus & ventromedial medulla from periaqueductal gray

Noradrenergic system

Locus ceruleus

DLPT (pontine)

Target 2-noradrenergic receptors

Potassium ionophore
2. Gate control theory of pain modulation
Nociceptive C fiber transmission suppression

By enhance myelinated fiber afferent transmission

Inhibitory neurons in dorsal horn = input from myelinated peripheral nerves

Nerve stimulators to treat pain

3. Pain perception and pain experience
Suffering = afferent nociceptive transmission

Cerebrum and limbic system

Attach value to the experience

Chapter 7-6

1. Ectopic impulse
Spontaneous generation of action potentials

Sites of axonal demyelination

High density of voltage-sensitive sodium channels in demyelinated membrane

Depolarization outlasts refractory period

Antidromical impulse

Postherpetic neuralgia = local reactivation of herpes zoster

Follow dermatomes
2. Suppression of ectopic impulse generation
Phenytoin = binds inactivated voltage-sensitive sodium channels

Inhibit action potentials and ectopic impulse generation

3. Dorsal root ganglion follow nerve injury
Increased density of sodium channels in  neurons

Low threshold, fast conduction, non-nociceptive

Enhancement of sodium channels conductivity

Increased growth factors in neurons, Schwann cells, and macrophages

Induce vasculation of dorsal root ganglion

Increased expression of 1-noradrenergic receptors

Polymodal nociceptive afferent neurons

Chapter 7-7

1. Wind-up
Central sensitization

Hypersensitivity to pain in dorsal horn

Constant release of glutamate by C fiber nociceptive afferent endings

Co-transmittors = substance P & CGRP

Strengthen connections between nociceptive afferent fibers & dorsal horn neurons
2. Pathologic learning
Chronic input from nociceptors & central cells

Repetitive transmission of ascending nociception

Expansion of receptive fields

Loss of specificity by neurons

Chapter 8-2

1. Olfactory apparatus and targets in cerebrum
Receptor cells

Between cribriform plate and mucosa of nasopharynx

Olfactory expithelial cells synapse within olfactory bulb

Olfactory glomerulus – olfactory tract

Terminate in pyriform cortex of amygdala and entorhinal cortex

Projections to orbitofrontal cortex via thalamus

Chapter 8-3

1. Extraocular muscles and levator palpebrae

Control of Ocular Movements

Cranial Nerve



Action on Eye



Superior rectus


Inferior rectus


Medial rectus


Inferior Oblique



Levator palpebra

Elevation of upper eyelid

Pupillary sphincter

Pupillary constriction



Superior oblique





Lateral rectus


Chapter 8-4

1. Conjugate horizontal eye movements
Neural yoking mechanisms

Abducens project to contralateral Oculomotor nucleus via MLF

Contraction of LR & contralateral MR
2. Internuclear ophthalmoplegia (INO)
Normal abduction of one eye

Deficient adduction of contralateral eye

Lesion between oculomotor & abducens nuclei

MLF lesion or multiple sclerosis

3. Vertical eye movements
Trochlear nuclei = SO

Oculomotor nuclei = IR & IO

4. Near triad


Pupillary constriction

Ocular vergence

Pretectal area = superior colliculi

Direct contraction of MR without MLF

5. Vestibulo-ocular reflex
Vestibule of inner ear = constant signal to medial vestibular nucleus

Tonic inhibitory input to abducens nuclei & midbrain vertical eye movement network

Head turns to opposite side = tonic vestibular input reduced

Eyes deviate to side of reduced input

6. Voluntary & reflexive gaze mechanisms & orienting responses
Gaze = conjugate movement (saccades)

Frontal eye fields & superior colliculi

Smooth pursuit
Superficial superior colliculi = directed & reactive saccadic eye movements
Paramedian pontine reticular formation (PPRF)

Frontal eye fields & superior colliculi project to PPRF

Activity in LEFT frontal eye field = Firing of RIGHT abducens nucleus

Conjugate saccadic movements to right

7. Ocular smooth pursuit
Temporal & parietal lobes – frontal eye fields & brainstem – IPSI vestibular nuclei – IPSI FN cerebellar lobe –

IPSI abducens

Smooth pursuit in LEFT hemisphere = control smooth pursuit to LEFT
8. Optokinetic & vestibular nystagmus
Mixture of saccades & smooth pursuit

Optokinetic = target moving

Vestibular = subject moving

Chapter 8-5

1. Motor component of CN V
Located in lateral pontine tegmentum = Junction of middle and caudal pons

Follows mandibular division of CN V

Innervate muscles of mastication

Lesion = inability to thrust mandible to contralateral side

Bilateral supranuclear innervation

Lesions of hemispheres = no effect on mastication

Chapter 8-6

1. Motor nuclei of CN VII, IX, and X

Located in entrolateral tegmentum of caudal pons

Enter IAC – stylomastoid foramen

Muscles of facial expression

Dorsal = lower face (CONTRA via corticobulbar)

Ventral = upper face (BI via corticobulbar)


Nucleus ambiguous = swallowing (dependent)

Paramedian rostral medulla – dorsal to inferior olive

Bilateral via corticobulbar tract

CN IX = stylopharyngeus

CN X = muscles of pharynx, larynx, & palate

2. Upper & lower motor neuron CN VII palsy
Upper motor neuron

Weakness of muscles of facial expression in LOWER face

No dysfunction in upper face

Lower motor neuron

Weakness of entire hemiface
3. Corneal reflex
V1 trigeminal afferent fibers = unmyelinated & nociceptive

Spinal nucleus of V = project to reticular formation = CN VII nuclei (BI) motoneurons = efferent

4. Somatosensory function of CN VII, IX, and X

Solitary tract = sensation in pharynx & afferent to nucleus ambiguous (swallow)


Innervate middle ear, external auditory meatus, & pinna

Pain, temperature, & touch

Project to CN V via spinal nucleus

5. Taste functions of CN VII, IX, and X
Nucleus Solitary

CN VII = anterior 2/3 tongue

CN IX = posterior ½ tongue

CN X = taste to epiglottis

6. Autonomic efferent functions of CN VII, IX, and X
Salivatory Nucleus

CN VII = lacrimal gland, nasal and oral mucous membranes, sublingual, & submandibular glands

CN IX = parotid salivary gland

Dorsal Efferent Nucleus of Vagus

CN X = parasympathetic to thoracic & abdominal viscera
7. Visceral autonomic afferent functions of CN IX and X

Baroreceptor at carotid sinus


Baroreceptor in left ventricle of heart & aortic arch

Project to medullary cardiovascular center

Chapter 8-7

1. Pathway of CN XI
Exit between dorsal and lateral roots – through foramen magnum – jugular foramen

Innervate sternocleidomastoid and trapezius muscles

Superficial of posterior triangle of neck


Chapter 8-8

1. Hypoglossal nerve CN XII
Nucleus = dorsomedial medullary tegmentum

Exit lateral to medullary pyramid – hypoglossal foramen

Form major part of lingual nerve

Innervate muscles of tongue and salivary glands

Supranuclear innervation of hypoglossal nuclei = CONTRA hemisphere

Supranuclear lesions = tongue deviates to opposite side

Infranuclear lesions = tongue protude to side of lesion

Supranuclear Innervation of Cranial Nerve Motor Nuclei

Cranial Nerve

Supranuclear Innervation




Eye movements


Smooth Pursuit





BI – redundant



Lower face

BI – redundant





BI – dependent


Head turning (sternocleidomastoid)

Shoulder shrug






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