Download Key Points: Neuroscience Exam #2 Lecture 16 and 17: Development of

Key Points: Neuroscience Exam #2
Lecture 16 and 17: Development of the NS I and II  see David’s study guide
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Day 18: prechordal plate and notochord signal overlying ectoderm to differentiate into
neuroepithelia cells
o Begins at the CRANIAL end of the embryo and proceeds caudally
o Forms the neural plate  every NS structure is derived from the neural plate and formation
ends at the end of the 4th week
o Neural groove will become the ventricular system of brain and central canal of SC
Day 22: neural plate invaginates in the midline to form the neural groove
o Cells in the lateral lip of the neural groove will proliferate in a process known as neuralation
o As the neural plate cells proliferate, they create folds lateral to the neural groove (these
grow upward and inward)
 As the neural fold develop, neural crest cells begin to differentiate at the crest of
the folds  these will migrate out and form many structures of the PNS as well as
others
 DRG and sympathetic chain ganglia and enteric ganglia  allows you to
interact with you environment
 Teath, CT around the eye, cilliary muscles, septum in the heart, pharyngeal
arch cartilage (hyoid), dermis and hypodermis of the face and neck, adrenal
medulla (sympathetic chain ganglia-like), schwann cells, enteric ganglia,
arachnoid and pia matter, melanocytes
o Albinism is caused by defect in neural crest migration
o
o
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They eventually meet in the midline at day 22 in the region that the 1st 5 somites
The closure forms a hollow tube: neural tube (ectoderm)  the closure proceeds cranially
and caudally in both directions
Day 24: cranial neuropore closes
Day 28: caudal neuropore closes; both neural tubes are closed
o Closure of the neuropores coincides with the establishment of a vascular circulation for the
neural tube. The walls of the neural tube thicken to form the brain and spinal cord
o Anytime the neuropores do not close, you end up with an open NS and parts can be missing
th
4 week (29 days): embryo undergoes flexure of the cranial region to define developing brain
regions (only regions bc they have not differentiated yet)
o Prosencephalon= forebrain
o Mesencephalon= midbrain
o Rhombencephalon= hindbrain
Brain development:
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Certain transcription factors (Shh, BMP) determine how the NS will be spatially organized
The neural tube must form and close appropriately for things to develop in the right places
o The neural tube in the spinal cord region keep dividing inward until all that is left is the small
central canal
3 primary brain vesicles:
o Prosencephalon= forebrain
o Mesencephalon= midbrain
o Rhombencephalon= hindbrain
o
As the brain starts to develop, certain flexures form and separate the compartments
 Cervical flexure between spinal cord and medulla
 Medulla= not as distinct as the SC  tela choroidia forms roof of 4th
ventricle
o General and special somatic and visceral afferent nuclei form
o General and special somatic and visceral efferent nuclei form
 Not special somatic efferent
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o Sulcus limitans separates 4th ventricle and medulla
Pontine flexure
Midbrain flexure between midbrain region and forebrain
Patterning: there are opposing gradients that give your ventral and dorsal segments of the spinal
cord  this is how we get functionally efficient organization of the SC  makes sure axons go in the
right place
o Alar= dorsal (sensory)  BMP mainly
o Basal= ventral (motor)  Shh mainly
Lecture 18: Sensory receptors and pathways
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Sensory receptor types, functions, associated axonal fiber types (e.g., Aβ), rapidly adapting vs. slowly
adapting mechanoreceptors
o Mechanoreceptors are stimulated by mechanical displacement of some tissue of the body
which includes both tactile and position sensations
 One continues the on and offset of stimuli and one is doing continued presence
 Rapidly adapting (RA) mechanoreceptors adapt quickly and signal a change in a
stimulus (e.g., onset or offset) or movement
 Meissner corpuscles (touch; flutter)
 Pacinian corpuscles (pressure; vibration)
 Slowly adapting (SA) mechanoreceptors signal the continued presence, and
intensity, of a stimulus
 Merkel disks (touch)
 Ruffini endings (detects steady pressure)

Thermoreceptors detect heat and cold (changes in temperature – thermal)
Nociceptors (pain receptors) are activated by any factor that damages the tissue (noxious
stimuli)
o Proprioceptors: knowledge of joint/limb position; information on muscle length, position
and tension
 Proprioceptors found in the muscle spindles and GTO  not found in skin
 A-alpha and beta fiber types
o Non-hairy skin
o Hairy skin (Glabrous)
 Thick epidermis
 Thin epidermis
 Sweat glands
 Sebaceous glands.
 Meissner corpuscles
 Hair follicle receptors
 Higher receptor density
 Ruffini endings
 Lower receptor density
o See slides for fiber types:
 A-beta= (mechanoreceptors of skin) meisner’s corpuscles, merkel receptor for
superficial touch AND pacinian corpuscles and ruffini endings for deep touch and
vibration
 A-delt= (thermo and nocioceptors for skin) free nerve endings for pain and temp
(cool)
 C-fibers= free nerve endings for pain, temp(warm), and itch
o Free nerve endings in the skin are modality specific and can detect either pain or touch or
pressure or temperature
Receptor potentials
2-point discrimination and receptive fields
o Receptive fields: the area that would stimulate one nerve would constitue its receptive field
o 2-point discrimination: determines how sensitive an area of your body is  how far apart do
they have to be in order to determine that there are two stimuli
 On your back, there is a greater distance than in the finger and tongue
 Larger distance= less dense sensory innervation
 Smaller distance= more sensitive
o
o
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Know your pathways – I could lesion anything
Brown Sequard syndrome
Lecture #19: Spinal reflexes- Atance
Intro to reflexes:
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Reflex= reaction of muscles or glands to a stimulus mediated by simple neuronal circuits consisting
of a sensory neuron, one or more interneurons, and a motor neuron
o Interneuron relays the info to the motor neuron to withdraw from the stimulus
Types of reflexes:
o Somatic reflex: skeletal muscle
 Innate reflexes= patellar reflex
 Developed reflexes= learned over time  driving, hitting a baseball
o Autonomic reflex (visceral): increase HR, sweating, etc
Processing site: interneurons can be in the spinal cord or in the brain
Purpose of reflexes: Reflexes are automatic, stereotyped responses that prevent us from having to
think about all the little details required from day to day living
o Posture, locomotion, protection, visceral activity
Spinal reflexes:
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Delayed awareness: spinal reflexes occur without immediate conscious awareness  you will feel
pain later bc it has to go up to higher centers
Reflex suppression: reflexes can be suppressed by conscious thought (higher centers)
o You can hold on to a pot of boiling water in order to save a child from getting burnt
Purpose of spinal reflexes:
o Once you make a decision to walk, we no longer need to use higher centers to continue
walking  perpetuation of activity is via central pattern generators (rhythmic patterns)
o Reflexes work to continue to maintain balance and reestablish your walking pattern
o Decerebrate animals (where brain and spinal cord has been cut) can still walk due to
reflexes and central pattern generator
o Clinical: testing reflexes can determine level of the lesion (hyper or hypo-reflexive)
Muscle spindles give info about length of muscle and GTO give info about the tension on the muscle
o provide continuous, subconscious feedback to the spinal cord, cerebellum, and cortex
o they also play a role in proprioception (where your body is in space)
 knowledge of the position of your fingers on an object give you a better idea of
what the object is easier than just brushing it across your fingers
o Muscle spindle anatomy
 Extrafusal fibers allow the muscle to contract
 Intrafusal fibers are involved in sensation and on the inside of the muscle spindle
 Spindle is encapsulated
 Gamma motor neurons supply the intrafusal fibers and alpha motor neurons
innervate the extrafusal fibers
 Two types of γ-motor neurons supply the contractile regions of the
intrafusal fibers
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 Dynamic γ-motor neurons supply the bag fibers (arranged randomly)
 Static γ-motor neurons supply the chain fibers (arranged in a chain)
o Muscle spindle function: sensory
 Providing info on the length of the muscle by determining how much the muscle is
stretched
 Determine info based on dynamic and static stretch response
o Static= measure of the amount of stretch
 Type II are sensitive to the amount of stretch but not the
rate; when tension is released, these are quite of AP
o Dynamic= how fast is the stretch occurring
 Type Ia are sensitive to change in rate of stretch
o Muscle spindle function: motor
 If a muscle gets stretched, the immediate response is going to want to contract
 If there is a contraction reflexively of the extrafusal fibers via alpha motor neuron in
response to the stretch in the intrafusal fibers, there must be a co-activating
contraction from gamma motor neurons of the intrafusal fibers in order to continue
to monitor stretch in that muscle
 If there was not a concurrent contraction, then the intrafusal fibers could no
longer monitor stretch in that muscle  this is why gamma motor neuron
activation is so important to allow the intrafusal fibers to do their stretchsensing work
o Stretch reflex
 Reciprocal inhibition of the antagonist must occur so that the reflex can work
properly
 Dynamic vs static
 Type I= dynamic  initial contraction
 Type II= static  to slow the reflex down and control it after the initial
response
 If the muscle spindles are damaged, the muscle contraction is not as smooth and
controlled
o Goli tendon organs: encapsulated and embedded in the tendon  will serve 10-15 muscle
fibers
 Type IB serves the GTO  determines the amount of tension based on the amount
on the amount of collagen fiber displacement
 These are inflexible and non-adapting
 There is an interneuron in the SC and there is an inhibitory neuron that causes
reflexive relaxation
 Relaxation of a muscle in response to a buildup of tension
 The GTO is also working to balance out the stretch and relax inputs
Flexor-relfex
o You must have a counterbalance between withdraw and maintaining balance
 Called crossed extensor reflex: One would flex to withdraw and the other leg
extensors would contract to keep balance
o After-discharge= allows you to maintain withdraw bc the spinal reflex fatigues very quickly
o
Reverberatory Circuits= allows you to stay away from a stimulus after withdrawing initially
Lecture #20: Cortical brainstem control of motor function
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Primary motor cortex, premotor area, and supplementary motor area function.
o PMA: intention to perform a movement and selection of a movement based on external
events
o SMA: involved in programming complex sequences of movements and coordinating bilateral
movements, especially selecting movements based on remembered sequences of
movements.
o Premotor & supplementary motor areas help in planning movement; precise control of
complex sequences of voluntary movements. Receive projections from:
 Prefrontal cortex (decision making)
 Parietal association areas (spatial relationships between body & external world)
o The brainstem also comes into play through a collective group of tracts that give inputs to
body movements
 Vestibular nuclear complex (balance: lateral subdivision; positioning of head &
neck: medial subdivision)
 Reticular formation (affects the body position, coordination)
 Red nucleus (exerts control over tone of distal flexor muscles)
 Superior colliculus (initiates orienting movements of the head and eyes; saccades)
Alpha and gamma motor neurons.
o Alpha MN supply the extrafusal fibers in muscle; they contact them directly and are called
lower motor neurons
 Means by which the NS can exert control over body movements
o Gamma MN supply contractile portions of the intrafusal fibers inside the muscle spindle
 Alpha-gamma coactivation helps sense changes in load during movement
UMN vs. LMS: what are they, what lesions of each would result in.
o UMN= where the command for movement begins (precentral gyrus) until it synapses with
LMN in the ventral horn of the SC
o LMN= after synapse in the ventral horn, the nerves exit the SC and travel to the effector
Sign
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UMN lesions: CP, TBI, stroke, MS, LMN lesions: poliomyelitis, lesions
corticospinal tract injury
near spinal cord
weakness
YES
YES
atrophy
No
Yes
fasiculations
no
Yes
reflexes
Increased: hyperreflexia
Decreased: hyporeflexia
tone
Increased: hypertonia
Decreased: flaccid
o Fasciculation: abnormal muscle twitches due to spontaneous muscle activity
o Increased resistance to passive stretching of muscles (spasticity, hypertonia) vs. reduced
resistance to passive stretching (hypotonia)
Medial and lateral motor systems: Location of termination within the spinal cord, general function
of each in motor control.
Pathway
Site of origin
Site of termination
Function in motor
control
Primary motor cortex
and supplementary
area
Medial VST: med and
inf vestibular nuclei
Lateral VST: lat
vestibular nucleus
Pontine and medullary
reticular formation
Cervical and thoracic
cord – sends out
bilateral projections
Med VST: cervical and
upper thoracic
Lat VST: entire cord
Control of bilateral
axial and girdle muscles
Reticulospinal
Superior colliculus
Cervical cord
Lateral systems
Lateral corticospinal
Precentral gyrus
Entire cord
Rubrospinal
Red nucleus
Cervical cord
Medial systems
Anterior corticospinal
Vestibulospinal
Tectospinal
Entire cord
Med VST: positioning
of the head and neck
Lat VST: balance
**maintain position
Automatic posture and
gait-related
movements
Orientation based on
auditory stimuli
Movement of
contralateral limbs
Movement of
contralateral limbs;
tone of distal flexor
muscles
o
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Somatotopy in the ventral horn:
 most medial= axial muscles
 posterior= flexors
 most lateral= limbs
 anterior= extensors
Motor functions of the cranial nerves, what lesions of each would result in.
o Motor nuclei are more medially and sensory nuclei are more lateral
o CN 3 (oculomotor), 7 (facial), 9 (glossopharyngeal), and 10 (vagus) are involved with the
parasympathetics
o Somatic motor: extraocular muscles and intrinsic tongue muscles
 Occulomotor, trochlear, abducens, and hypoglossal nerves and brainstem nuclei
o Brachial motor: muscles of mastication, facial expression, middle ear, pharynx (swallowing),
larynx (voicebox), SCM, upper portion of trap
 Brainstem nuclei and CN: Motor nucleus of CN 5 (trigeminal), facial nucleus (CN 7facial), nucleus ambiguous (CN 9, 10- glossopharyngeal, vagus), accessory spinal
nucleus (CN 11- accessory)
o Corticobulbar tract= leads to the motor neurons in the brainstem nuclei (5, 7, 12)
 Nuclei stimulate muscles of the face that are under the finest control (lip and
tongue muscles) and muscles of the jaw and pharynx
 Distributes bilaterally  exception= facial nucleus for lower face which receives
contralateral projections (causes Bell’s palsy findings)
CN
Oculomotor (3),
trochlear (4),
abducens (6)
Function
3= most eye movements; PS pupil
constriction/lens
4= down and out
Lesion
3= eye tracking problems; pupil
dilation
4= would deviate up and in
**Trigeminal motor
(5)
Facial nerve (7)
Glossopharyngeal (9)
6= Abducts the eye lat in a
horizontal direction
Brachial motor root supplies
muscles of mastication- bilateral
projections
Brachial motor controlling muscles
of facial expression- contralateral
projection
Stylopharyngeus elevates the
pharynx during talking and
swallowing, and contributes (with
CN X) to the gag reflex
Brachial motor= all pharyngeal
muscles of the larynx
Recurrent laryngeal nerve= intrinsic
laryngeal muscles (almost all)
Supplies SCM (rotates to opp side)
and upper trap
6= eye would deviate medially
Weakness of the jaw  can be
partially compensated for due to
bilateral projections
UMN lesion= muscle weaknessforehead spared
LMN lesion= muscle weakness of
entire half of face
Dysphagia, speech difficulties
Danger of injury during surgery 
causes temporary voice disturbance
and laryngeal spasm
** Hoarseness after surgery is a sign
Spinal Accessory (11)
Pt would have weakness turning head
away from lesion and couldn’t shrug
shoulders (ipsalateral weakness)
Hypoglossal (12)
Tongue movements
Tongue would deviate toward side of
lesion; contra=UMN, ipsa=LMN
** UMN control reaching the trigeminal motor nucleus is bilateral  meaning that unilateral lesions in
the motor cortex or corticobulbar tract usually cause little deficit in the jaw movement bc it is partially
compensated for
Vagus (10)
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Upper vs. lower motor neuron facial weakness.
o Facial nucleus has two divisions: upper face= bilateral projections and lower face=
contralateral projections
o UMN lesions spare the forehead due to bilateral projections of the UMN to the forehead
and orbicularis oculi
 Orbicularis oculi muscle closes the eyelid
o LMN lesions affect the entire half of the face and do not spare the forehead because there is
no longer some ipsilateral cortical input remaining to help innervate (and spare) the
forehead
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Any clinically relevant details mentioned.
Lecture #21: Basal Ganglia
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Know the components of the basal ganglia, functional relevance, and circuitry involved
o Basal ganglia are a collection of gray matter nuclei located deep in the white matter of the
cerebral hemispheres
 Basal ganglia + Thalamus
 Movement
 Cognition
 Emotion
 Motivation
o Striatum= caudate and putamen
 Receives all input to the basal ganglia
 Cortico-striate fibers run from the cortex to the striatum
 Putamen= Mainly motor and somatosensory cortex
 Movements, bodily positions
 Caudate= Mainly association cortex
 Cognition
 Bilateral damage of the head of the caudate nucleus= can completely
change someone’s personality  caudate is closely associated to the
association cortexes
 Ventral striatum (nucleus accumbens)
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 Limbic cortex, hippocampus, amygdala
 Initiating drive-related behaviors
o Lenticular nucleus= globus pallidus and putamen
 Globus pallidus has an internum (medial) and externum (lateral)
o Subthalamic nucleus (diencephalon)
o Substantia nigra (rostral midbrain)
 Pars compacta: (closely packed) widespread modulatory dopaminergic inputs to BG
 INPUT CENTER
 Pars reticulata: (loosely packed) BG output
 OUTPUT CENTER
Associated vasculature
o ACA= nucleus acumbens and head of caudate nucleus
o Anterior choroidal artery= globus pallidus
o Perforating branches of the MCA= striatum
o Perforating branches of PCA and post communicating= substantia nigra and subthalamic
nucleus
Direct and indirect pathways involving the basal ganglia
o Inputs to the BG:
 Corticostriatal  cortex to striatum  motor, somatosensory, association, and
limbic cortex
 Putamen= most important input nucleus for motor control pathways
o Most are excitatory and use glutamate
 Substantia nigra pars compacta  another important input
 Dopaminergic nigrostriatal pathway (substantia nigra to striatum)=
excitatory to some cells and inhibitory to others
o Outputs to the BG:
 Substantia nigra pars reticulata  conveys info for the head and neck
 Internal segment of the globus pallidus  conveys info for the rest of the body
 These pathways are inhibitory and use GABA
 There is a constant tonic inhibition by these output systems
 Both pathways go to the thalamus (ventral lateral nucleus- VL and ventral anterior
nucleus- VA) via thalamic fasciculus
o Internal connections in the BG: go from striatum to the internal segment of the globus
pallidus (GPi) or substantia nigra pars reticulata (SNPr)
 Direct: straight from striatum  GPi or SNPr
 Free the thalamus from its state of tonic inhibition by GPi and SNPr
 Net effect= excitation of the thalamus
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Indirect (takes a detour): striatum  external segment of globus pallidus (GPe) 
subthalamic nucleus  GPi or SNPr
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o
Net effect= inhibition of the thalamus (resulting in
inhibition of movements through connections back to the cortex
4 main categories of internal connections: mostly inhibitory
o
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Disinhibition= striatum inhibits GPi and SNPr through excitation from the cortex which
inhibits the tonic inhibition by GPi and SNPr on the thalamus  thus the net effect is
excitation of the thalamus
Know the movement disorders, including Parkinson’s disease, Huntingdon’s chorea, Sydenham’s
chorea, chorea, athetosis, and hemiballism.
o BG disorders can produce either hypokinetic or hyperkinetic movement disorders
o Parkinson’s disease (hypokinetic): rigidity, slowness, and marked difficulty initiating
movements
 Loss of dopaminergic neurons in the SNPc (nigrostriatal projections)
 Ultimately results in decerased input from the thalamus (VL) to the cortex
o
o
o
 hypokinetic (direct pathway problems)
 Characterized by asymmetrical “pill-rolling”, resting tremor, and bradykinesia
(extreme slowness of movement), rigidity, and shuffling, stooped, flat-footed gait
 Tremor diminishes during voluntary movement and increases during
emotional stress
 SNPc D1 and D2 are degenerated  causes more tonic inhibition of the GPi 
causes decreased excitation of the thalamus to the cortex  hypokinetic disorder
 Rx= administer levodopa (L-dopa) to help alleiviate some sx
 Deep brain stimulation= implantation of electrodes to the GPi or
subthalamic nuclei to help replace abnormal activity with normal activity
Huntington’s disease (hyperkinetic): uncontrolled involuntary movements producing a
random pattern of jerks and twists
 Can’t produce coordinated movement; progressive - usually choreiform (irregular,
spasmodic, involuntary movements of the limbs or facial muscles) - movement
disorder, dementia, and psychiatric disturbances, ultimately leading to death.
 CAG repeats in tandem
 The pathologic hallmark is progressive atrophy of the striatum, especially involving
the caudate nucleus (degenerated).
 Caudate nucleus degenerated  decreasing inhibitory influence on GPe and that
makes its own inhibitory inputs more active  less excitatory input from
subthalamic nucleus and more inhibitory from GPe  causes inhibition of GPi (tonic
inhibition)  less tonic inhibition= excitation of the thalamus  increased
excitation of the cortex= hyperkinetic disorder
Rigidity from BG disorders is called “lead pipe rigidity” bc the spasticity is more continuous
throughout attempts to bend the limb
Look through other disorders briefly  not tested
Lecture #22: Pathophysiology of genetic neuronal diseases
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Know the signs & symptoms of each disorder discussed
Know the genetic mutation involved, what issues this causes, and how
Know the inheritance of each disorder
Disease
Signs and Sx
Fabry
Disease
Think: dark
skin spots
and eye
issues
Episodes of pain (hands
and feet), clusters of dark
spots on skin
(Angiokeratomas),
decreased ability to sweat,
corneal opacity, retinal and
conjuctival issues, GI
issues, tinnitus, hearing
loss
SAUSAGE-LIKE vessels in
conj
Along with associated
conditions… Dystonia,
chorea, flailing of limbs,
inability to walk, behavioral
disturbances (selfmutilation)
The infant’s diapers=
orange-colored crystal-like
deposits (“orange sand”),
pink or reddish urine
(hematuria), kidney
stones/failure, dysphagia,
aspiration, aggressiveness
Lesch-Nyhan
Syndrome
Think:
behavioral
problems
and high uric
acid
NiemannPick Disease
Think:
Lipids and
enlarged
spleen/liver
Maple Syrup
Urine
Disease
Think: poor
feeding, AA
build-up,
brain toxicity
B= non-neurological
A= neuro deterioration
C= seizures
Hepatosplenomegaly,
macular cherry red spots,
foamy cytoplasm
histologically due to lipids
Poor feeding, vomiting,
lethargy, developmental
delay, seizures, hypotonia,
intramyelinic edema,
vasogenic edema
Genetic
mutation
GLA gene that
responsible for
making alphagalactosidase A
Mutation causes…
Inheritance
build-up of a particular type
of fat
(globotriaosylceramide, or
GL3) in the body's cells 
can eventually lead to MI,
kidney damage, and stroke
X-linked
HPRT1 gene: a
severe
deficiency of
the enzyme
hypoxanthine
phosphoribosyl
transferase 1
(HPRT1)
Purines are broken
down but NOT
recycled: overproduction
X-linked
recessive
Type A and B=
SMPD1
Type C= NPC1
or NPC2
abnormal lipid metabolism
causes harmful amounts of
lipids to accumulate in the
spleen, liver, lungs, bone
marrow, and brain
Autosomal
recessive
BCKDHA,
BCKDHB, DBT,
and DLD genes
Abnormal AA processing
and prevent breakdown of
leucine, isoleucine, and
valine (toxic to brain)
Autosomal
recessive
and accumulation of uric
acid which can cause can
cause gouty arthritis
(arthritis caused by an
accumulation of uric acid in
the joints), kidney stones,
and bladder stones; low
levels of dopamine
Lecture #23: hypothalamus
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Identify the structure of the hypothalamus, including the major hypothalamic nuclei and areas.
o Lowest level of the diencephalon, situated below the thalamus
 Bilaterally symmetric structure split by the 3rd ventricle
 Region sitting right below the thalamus
 Connects through the infundibulum to the pituitary
 Pituitary tumors can compress a part of the
optic chiasm and cause bitemporal hemianopia
o Parts of the hypothalamus based on what is below it:
 Preoptic (most rostral)  before being above the optic
chiasm
 ACA and ant com art
 Supraoptic= above the optic chiasm
 ACA and ant com art
 Area above the tuber cinereum
 PCA and post com art
 Posterior part= above the mammillary bodies  most caudal
 PCA and post com art
 Lateral hypothalamus= supplied by lenticulostriate art from MCA and choroidial
branches
Outline the major functions of the hypothalamus and its nuclei/areas.
o Major functions: HEAL
 Homeostasis, endocrine control, autonomic control, limbic mechanisms
 Neural and neurohumoral (direct hormone control) functions
 The hypothalamus serves as an integrator of autonomic, endocrine, emotional, and
somatic functions
 Nodal point in pathways concerned with homeostasis
 Coordinates drive-related behaviors
o Afferent connections (things coming in)
 Hippocampus to hypothalamus (periventricular nucleus and mammillary body) via
fornix  important for limbic system
 Afferent fibers from olfactory areas to preoptic nucleus and dorsomedial nuclei via
medial forebrain bundle
 Amygdala to hypothalamus via stria terminalis  emotion, fear
 Visceral afferent fibers to hypothalamus via peduncle of mammillary bodies
o Efferent connections (things leaving)
 Dorsal longitudinal fasciculus to parasympathetic nuclei
 Mamillotegmental tract to tegmentum of midbrain
 Then relayed to midbrain reticular formation
 Mediates autonomic info between hypothalamus, CN nuclei, and SC
 Hypothalamic-hypophyseal tract to pituitary
 Anterior (adenohypophysis  outgrowth of the ectodermal cells of
pharynx)
o Direct vascular link to directly release
hormones

 Could be releasing hormones or inhibiting hormones)
o Optic chiasm in front of it
Posterior (neurohypophysis  buds down from diencephalon)
o Needs a neuronal signal and then can release
hormones no direct release
o
o
o
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Mammillary bodies on the posterior end
Supraoptic and paraventricular (on either side of the lateral
ventricle) have large neurosecratory cells that produce two
hormones depending on need
 ADH or vasopressin: increase the reabsorption of water in
the kidney and decrease production of urine
 Neurotransmitter function: helps in controlling
circadian rhythms
 Oxytocin: Causes contraction of uterine and mammary
smooth muscle; important in parturition and milk letdown
Hypothalamic nuclei
Medial has three subdivisions (anterior-supraoptic, middle-tuberal, and posterior-mammillary) and
lateral has one
o Parasympathetic= anterior and med
o Sympathetic= lateral and posteromedial
o
o
o
o
o
Circadian rhythms= suprachiasmatic nucleus ant and med
 Master clock for circadian rhythms, direct retinal projections (getting info about
daylight), melatonin receptors
Temperature
 Preoptic (ant-medial): lowers body temp  anterior= A/C helps to cool you down
 Promotes heat loss (sweating, behavioral) and prevent heat production
 Lesion= hyperthermia in a warm environment
 Posterior nuclei= raises body temp
 Promote heat production (shivering, behavioral) and prevent heat loss
 Lesion= hypothermia in cold environments
Feeding and thirst
 Lateral= initiate feeding based on glucose levels and thirst when dehydrating
 Lesion= loss of desire to eat (aphasia)  possible underlying cause to
anorexia and very little fluid intake (adipsia)
 Medial- tuberal zone= satiety center  inhibits food intake stimulated by high
glucose levels
 Lesion= compulsive overeating (hyperphagia) or overdrinking (polydipsia)
Sexual behaviors
 Medial-preoptic nucleus= control sexual dimorphism involving hormonal influences
on maturation
 Contains high density of GNRH producing neurons which synthesize large
peptides that are directed at target cells in the anterior pituitary
Oxytocin/vasopressin
 Medial-supraoptic
 Paraventricular and Supraoptic Nuclei
 Neurosecretory cells whose axons project to posterior pituitary
 Secrete oxytocin and vasopressin
 Systemic feedback to hypothalamus via circumventricular Organs (OVLT, Organum
Vaculosum Lamina Terminalis, and SFO, subfornical organ)


Predict the role and mechanisms of the hypothalamus as it relates to thirst, hunger, temperature
regulation, and the defense mechanism.
Distinguish some of the basic disorders associated with hypothalamic dysfunctions
Lecture #24: thalamus diencephalon  thalamus= major subdivision of the diencephalon (hugging the
third ventricle)


Thalamic anatomy
o Boundries:
 Most rostral= lamina terminalis (contains organum vasculosum which regulates
osmolarity of blood
 Rostral and dorsal= anterior comminsure
 Caudal= posterior commissure
 Anterior pole= interventricular foramen
 Lateral boundry= internal capsule that divides it from the putamen
 medial edge= 3rd ventricle
 caudal to post commissure on top of tectum= pineal gland
 above/dorsal= lateral ventricle
 below/ventral= roof of hypothalamus
o Medial to lateral in horizontal section:
 Third ventricle, thalamus, internal capsule, putamen
o Caudate and putamen hugging thalamus in horizontal section
o Massa intermedia= connects right and left thalamus
o Hypothalamic sulcus= separates thalamus and hypo
Describe the thalamic nuclei and their functional significance
o Thalamus= gateway to the cortex
 Gateway that has some transforming properties  can modulate signals based on
inputs from many sources
o Internal medullary lamina= Y shaped white matter tract that divides the thalamus into the
medial, anterior, and lateral groups
1. Intralaminar nucleus:
 Central median nucleus= part of ARAS
o Afferents from globus pallidus, reticular formation, and sensory
pathways
o Efferents to stratium (caudate and putamen)
 Parafascicular nucleus= similar connections
o Nonspecific: Connect with cortical areas that have broader functional implications such as
association and limbic cortices
2. Anterior nuclear group
 Main connectivity to cingulate cortex
3. Medial nuclear group (whole group is dorsal medial group
4. Lateral nuclear group (has dorsal and ventral tier and lateral and medial geniculate
nucleus
 Lateral dorsal nucleus and
o Also connectivity to cingulate cortex


Lateral posterior nucleus
o Connectivity to sensory association cortex of parietal lobes
 Pulvinar: huge chunk of posterior thalamus
o largest thalamic nucleus in humans and has extensive connections
with parietal-occipital-temporal (POT) association cortex
 Visual cortical areas
 Posterior parietal cortex
 Cingulate, posterior parietal, premotor and prefrontal
cortex
 The pulvinar also has extensive input from the superior
colliculus important in the initiation of saccades, regulation
of visual attention, and orientation behavior
Describe the major “inputs” and “outputs” of the “specific” thalamic nuclei
o Specific nuclei: from the ventral tier of the lateral nuclear group and lateral and medial and
lateral geniculate nuclei
 Almost all projections are ipsalateral when going to the cortex (more on the specific
nuclei)
 Ventral tier
 Ventral anterior nucleus (association motor)
o Receive inputs from BG and originate in the GPi and also SNPr
o Motor  projects to premotor and supplementary motor cortex
 VA nucleus is an important part of the mechanism by which
the BG exerts influence on normal movement
 Ventral lateral nucleus  motor info
o Receives inputs from BG and originate in the GPi and also SNPr
 Also receives input from the dentate nucleus of the
cerebellum
o Motor  projects to primary motor cortex (precentral gyrus)
 Ventral posterior nucleus  sensory info
o Lateral subdivision (VPL)
 Receives inputs from PCML and spinothalamic inputs from
LE and UE and projects to primary sensory cortex
(postcentral gyrus)
 Fine touch and proprioception (PCML)
 Pain and temp (spinothalamic)
o Medial subdivision (VPM)
 Receives input from the face from the trigeminal nucleus
and projects to primary sensory cortex (postcentral gyrus)
 Fine touch and proprioception from face (principle
sensory nucleus)
 Pain and temp (spinal trigeminal nucleus)
 Lateral geniculate nucleus  visual
 Projects to primary visual cortex (upper and lower banks of the calcarene
sulcus)



Medial geniculate nucleus  auditory
 Projects to auditory cortex of temporal lobe
o Also receives input from inferior colliculus of midbrain via inferior
brachium
Review and describe the arterial blood supply to the thalamus
o MCA and PCA send up perforating branches to regions of the thalamus
Thalamic lesions & related functional deficits
o The deficits are related to which nuclei is affected
o Posterior lesion: sensory defects, abnormal sensation
o Thalamic (Dejerine-Roussy) syndrome: thalamic stroke leads to innocuous stimulus
perceived as very painful (allodynia) – severe contralateral pain. Can be worsened by
emotional distress.
o VA/VL lesion: motor disturbances due to connections with globus pallidus, cerebellum
o Dorsomedial, Anterior lesions: disorders of consciousness, alterations in personality,
decreased motivation, indifference to pain (less specific deficits)
Lecture #25: limbic system



Big picture:
o Fornix: From hippocampus to hypothalamus, mammillary bodies and septal nuclei
o Stria Terminalis (ST): from Amygdala to red nucleus, septal nuclei & nucleus accumbens
o cingulum loop: fibers run around the cingulum into parahippocampal cortex then into
hippocampus
o Limbic structures handle both conscious and unconscious processes related to emotion,
memory, and basic drives (hunger, thirst, sex, etc.)
Clinically relevant points
o *Note damage to hippocampus, fornix and mammillary bodies all cause memory loss
o Korsakoff’s psychosis:Damage to mammillary bodies (hippocampus->fornix->MBs) and
Dorsomedial nuclei of thalamus
 Chronic alcoholics
 Vitamin B1 defficiency
 Anterograde amnesia
 Inability to form new declarative memories
 Make up answers as they go along to conceal memory loss (confabulatory
syndrome)
o Kluver-Bucy: bilateral temporal lobe damage  hypersexuality, absence of emotional
reactions and fear
 Man with child porn after surgery for seizures
Know the major limbic structures and functions described.
o Cingulate gyrus
 Stimulation elicits:
 Autonomic responses
 Aggression if anterior cingulate involved
 Damage results in:

o
o
o
o
Greatly diminished emotional responses and may result in problems
remembering the order of events, or akinetic mutism (looks and acts like a
coma but you aren’t)
 Subgenual (knee of the corpus collosum) cingulate
 Active during sadness
 Hyperactive in major depression
Medial Prefrontal cortex
 Executive functions, working memory, planning, emotion regulation, foresight.
Reciprocal inhibitory connections with the amygdala
Amygdala  can see with a coronal section through the uncus
 Associated with fear conditioning in animals
 Stimulation in humans generates predominantly negative emotions (sadness, fear
and anxiety) but also some positive
 Links perception of objects with appropriate emotional responses, particularly in
types of danger  snowman video
 Sensory cortex and thalamus inform amygdala about the outside world
 Lesions= bilateral destruction  memory deficit that impairs ability to
learn/remember an appropriate emotional response; have difficulty recognizing fear
or understanding the concept of fear
 They are not afraid and their body won’t react as if they are afraid
Hypothalamus
 When stimulated in the lab:
 Medial hypo= panic attack sx in humans
 Lateral= predatory aggression in cats
 Dorsal-medial= stress response activated
 Mammillary bodies
 Receive majority of input from the hippocampus (memory area) through the
fornix  damage= impairs memory
Hippocampus: HM and memory
 Bilateral removal= sever anterograde amnesia and some retrograde
 Amnesia only in declarative memories and not in learning new
skills/procedures
 Involved in moving some types of memory from short to long-term storage
 Hippocampus is a curved sheet of cortex folded into the medial surface of the
temporal lobe in three distinct zones:
 Dentate gyrus (looks like teeth)
 Hippocampus proper
o Dentate gyrus and hipp prop look like 2 interlocking Cs
 Subiculum
 Alveus= hippocampal equivalent of subcortical white matter)



Contains inputs and outputs to/from hippocampus
Form a fiber bundle called the fimbria (“fringe”) of
the hippocampus
 Fimbria in turn becomes the crus (“leg”) of the
fornix
 Parahippocampal gyrus
o Fornix: he leg of each fimbria joins at the midline to form the body of the fornix
 Travels out of the hippcampus, loops around, then heads anterior and dives down to
form columns of fornix, heading to mammillary bodies, septal nuclei, and nucleus
accumbens
 Damage to fonix causes impairment of spatial memory
 Receives projections from the hippocampus through the fornix and from the
amygdala through the stria terminalis.
 Projects to the Ventral Tegmental Area (reward pathway). Also sends return
projections to the hippocampus and amygdala
o Septal nuclei: stimulation causes varying degrees of sexual arousal and compulsion to
masturbate
o Dorsomedial, anterior nuclei of the thalamus
 Hippocampus projects to anterior nucleus via the cingulum, Amygdala to
Dorsomedial Nucleus via the Ventral Amygdalaofugal pathway
Input-output relationships of limbic structures, focusing on amygdala, hippocampus
o Amygdala
 Major nuclei:
 Central: Connected with hypothalamus, brainstem nuclei (e.g., PAG)
o Emotional responses
 Basolateral: continuous with parahippocampal cortex, extensively
connected with other cortical areas (prefrontal, insula, entorhinal, etc.)
o motor response to fear based on learned associations
 Medial: Connected with olfactory system (bulb & cortex), relatively small in
humans
 Inputs:
 Central: Visceral sensory inputs
o Hypothalamus, septum,PAG, project to central nucleus
 Basolateral: sensory info from thalamus, visual, auditory, somatosensory,
and gustatory project BL nucleus
o Levels of physical/emotional comfort/discomfort in the anterior
cingulate and insula project to basolateral nucleus
 Medial: Olfactory bulb & cortex project to medial nucleus through olfactory
tract
 Major Inputs arrive via:
o stria terminalis (from hypothalamus and septal nuclei to central
nucleus)
o ventral amygdalofugal pathway (from thalamus, anterior cingulate
cortex to basolateral; from hypothalamus to central nucleus)
o

directly from temporal lobe cortex and hippocampus (to BL) (not
pictured)
o From the olfactory bulb to the central nucleus and medial nucleus
 Outputs: Fibers leave through Stria Terminalis and Ventralamygdalofugal pathway
to reach many of the same areas
 Stria terminalis= connects amygdala to septal nuclei in the hypothalamus
 VAF= connects amygdala to septum, PAG, brainstem, DM thalamus, and
substantia inomonata
 Amygdala connections to hypothalamus, brainstem initiate emotional
responses such as fear and aggression
 Outputs to ventral striatum, modulate reward seeking, modulates
reproductive drives. No time for romance when you are being chased by a
bear
 Outputs to sensory cortical areas heighten awareness
 Outputs to PAG and spinal cord prime defensive reflexes
o Hippocampus:
 Outputs: through fornix to the hypothalamus, mammilary body and septal nuclei
 Mainly arise in the subiculum or hipp proper and mainly project diretly back
to entorhinal cortex/parahippocampal cortex (most anatomically
prominent pathway is through the fornix)
 Near the interventricular foramen, some fibers branch off in front of the
anterior commissure and are called the pre-commissural fornix, terminating
in septal nuclei
 Remaining fibers (post-commissural fornix) terminate in, mammillary body,
anterior thalamic nucleus, and hypothalamus
 Inputs (afferents):
 Primary source of afferents to hippocampus is entorhinal cortex
(parahippocampal cortex)
o EC receives some olfactory inputs, lots of association cortex inputs
(posterior cingulate gyrus,orbital cortex, multimodal areas of
frontal, parietal, temporal lobes)
 Modulatory cholinergic inputs from septal nuclei (S) reach hipp through
fornix
o Also direct inputs from amygdala
 Hippocampal commissure connects contralateral hippocampus to share info
between one another
Describe the components and flow of information in the Papez circuit
o Hippocampus  through fornix  mammillary bodies (memory processing)  ant nucleus
of thalamus  cingulate gyrus
Lecture #26: Cerebellum

Clinically relevant details
Cerebellum has NO DIRECT connections to LMN’s  indirect effect of LMN (higher center)
Lesions of cerebellum, association cortex, and BG would be problems with coordination
(ataxia) rather than weakness (as with problems in the motor cortices)
 Ataxia that you see will be ipsalateral to the side of the lesion (double cross)
 Midline lesions of the cerebellar vermis or flocculonodular lobes mainly cause
unsteady gait (truncal ataxia) and eye movement abnormalities
 Lesions lateral to the cerebellar vermis mainly cause ataxia of the limbs
(appendicular ataxia)
 Cerebellum receives inputs and error signals and the cerebellum can correct them
based on the input it receives
 Primarily motor even though it receives a lot of sensory input as well
Tests to determine cerebellar lesions:
o Finger-nose test  tests for intact cerebellum
 Can be done to determine if someone is drunk
o Complex movements involves in speaking can also be affected: scanning speech (normal
flow/rhythm disrupted; successive syllables emerge slowly, separated)
o Rebound Phenomenon
 Patient, with eyes closed, told to move arm against resistance of examiner
 Examiner releases arm, forcefully “rebounds” toward patient (hypermetria)
o Truncal Ataxia: Lesions confined to the cerebellar vermis affect primarily the medial motor
systems. Patients with such lesions therefore often have a wide-based, unsteady
“drunklike” gait
o Appendicular ataxia: Lesions of the intermediate and lateral portions of the cerebellar
hemisphere affect the lateral motor systems. Therefore, these patients have ataxia on
movement of the extremities
Vascular supply to cerebellum:
o
o



 AICA is where the peduncles are
Major cerebellar anatomical regions, layers, excitatory vs. inhibitory parts of circuitry
o Folia= folds in cerebellum (similar to gyri in cortex)
o
o
o
o
o
o
1.
2.


Anterior lobe
Posterior lobe
Primary fissure= separates ant and post lobes (seen on mid-sagital cut)
Flocculonodular lobe= shown in ventral view  includes flocculus and nodular lobes
Posterolateral fissure= separates Flocculonodular lobes
Left hemisphere and Right hemisphere
Lateral hemisphere= motor planning in extremities  lat corticospinal tract
Paravermis (intermediate hemispheres)= intermediate portion of the lateral hemisphere
a. Distal limb corrdination  lat CS and rubrospinal tracts
3. Vermis= midline structure that connects the two hemispheres
o Middle, superior, and inferior peduncles= for the cortex to communicate with the
cerebellum
Cerebellar nuclei: Don’t Eat Greasy Food (lateral to medial)
o Dentate nucleus (only one that you can see grossly)
 Receive projections from the lateral cerebellar hemispheres
 Active just before voluntary movements  motor planning
o Emboliform nucleus and Globose nucleus (connected functionally)
 Receives inputs from intermediate part of the lateral
hemisphere
 Active during and in relation to that movement 
error correction system (a way to get better at a
task)
o Fastigial nucleus
 Receives inputs from the vermi
Major inputs/outputs
o Key points:
 Inputs arrive to cerebellar cortex (green, excitatory)
 Cerebellar cortex projects to deep cerebellar nuclei (red,
inhibitory)
 Deep nuclei project to output targets (green, excitatory)
o Cerebellar cortex: MPG (from outside to inside)
 Molecular layer
 Mostly composed of axons and dendrites
 Purkinje cell layer: only output from the cerebellar cortex
 Inhibitory in their projections: GABA
 They have intricate dendritic trees that branch out to the cortex
 Granule cell layer
 Each sends out a projection through the parallel fibers and can then project
to the dendritic trees of the purkinje cells (transversely oriented)
o Cerebellar cortex:
 Climbing fibers: associated ONLY with inferior olive  in a question,
CF are linked with inferior olive

A single climbing fiber winds around the dendritic tree of each Purkinje cell
making thousands of excitatory synapses




Most powerful excitatory input in the nervous system
CFs arise ONLY from contralateral inferior olivary nucleus
Destruction of inferior olive has acute effects similar to destruction of the
entire (contralateral) cerebellar hemisphere
Mossy fibers: everything that doesn’t come from inf olivary nucleus
will come in via mossy fibers


o
Mossy fibers terminate on dendrites of granule cells – less direct effect on
Purkinje cells bc they reach out to granule cells first
o Order to reach purkinje cells: Mossy fiber  granule cell  parallel
fiber  Purkinje cell
All of the input into the purkinje fibers are excitatory (ignore GABA to purkinje) and
all output carried by purkinje fibers to the efferent connections is inhibitory
Cerebellar inputs:
 Pontocerebellar tract: Cerebral cortex (motor/premotor/ somatosensory cortex)
projects to cerebellum via pontine nuclei
 Pontine nuclei receive inputs from ipsilateral cerebral cortex (orange),
project to contralateral cerebellum through massive MCP
 Can see the middle cerebellar peduncles and pontocerebellar fibers in the
mid pons section
 Gives the cortex some feedback as to what action it should perform next
 Spinocerebellar pathway (anterior and posterior)
 Particularly vulnerable to damage bc they travel on the lateral-most edge of
the SC
 Post= inferior cerebellar peduncle
 Ant= superior cerebellar peduncle
 Lesion= Friedreich’s ataxia  intention tremor from spinocerebellar tract
problems
o
o
Intention tremor= over and under-correcting movement and not
direct movement  finger-to-nose test
Cerebellar outputs:
 Major output= superior cerebellar peduncle to the ventrolateral
nuclei of thalamus (bc it has to go through this in the thalamus to
go to the motor cortex)

Dentate nucleus  superior cerebellar peduncle at superior cerebellar peduncle
decussation  VL nucleus of thalamus  primary motor cortex  LMN in ventral
horn of spinal cord
 Deficits would be ipsalateral bc inputs to the cortex and back down cross
twice  cerebellum to cortex crosses then cortex to SC (corticospinal)
crosses again
 Involved in motor planning
 Cerebellum gives extra info so that we can generate better motor outputs
 Interposed nuclei (Emboliform and Globose nucleus)  superior cerebellar
peduncle  VL nucleus of thalamus  motor cortex
 Deals with error-correction (golf game)  controlling ongoing
movements of extremities
 Fastigial nucleus (don’t worry about details of pathway)  goes to VL and cortex
also eventually
 Proximal trunk movements and eye movements
 Bilateral projections  allows for compensation with lesions
Lecture #27: Cerebrum

Lobes of the cerebral hemispheres and the functions of each
o Frontal: voluntary motor and personality (Broca’s area)
 The frontal cortex is involved in “executive” function, i.e., the process of making
decisions about how an individual will conduct themselves.
 Phineus Gage
o Parietal: Postcentral Gyrus; tactile and proprioceptive inputs
 Inferior parietal lobule: language comprehension; Wernicke’s area
 Remainder of parietal cortex: spatial orientation, directing attention
o Temporal: learning, memory, hearing (primary auditory cortex)
 In the 50’s; HM had progressively worse seizures; experimental (bilateral) removal
of medial temporal lobe, including amygdala, most of hippocampus and
parahippocampal gyrus
 Profound anterograde amnesia
 Unable to add new words to his vocabulary, remember people after 1953,
or recall events after surgery
 Ability to keep track of his internal state was impaired (amygdala)
 After eating/drinking he remained hungry/thirsty
o Occipital: visual info
o Limbic: motivation, emotion, arousal, memory
o

Insular cortex: Involved in taste, emotion, consciousness, homeostatic regulation,
perception, motor control, self-awareness, cognition, interpersonal experience
Histological organization of the cortex (which cortical regions are characterized by particularly
prominent cortical layers, e.g., layer V for motor cortex).
o Small pyramidal neurons (layer III) have axons that terminate in the cortex. These form
“association” fibers.
o Layer IV is the granular layer – receives thalamic inputs, so this is the layer where large
sensory tracts terminate (e.g., DCML/PCML, spinothalamic/anterolateral).
o Large pyramidal neurons project out of the cortex. These form the fibers of, for example,
corticobulbar and corticospinal tracts – layer V
Type of information/BA
Prefrontal association (46)
Primary visual cortex (4)
Primary motor cortex (17)



Primary/largest layer
Layer III
Layer IV
Layer V
Main connections
Cortical-cortical
Inputs from thalamus
Sends outputs to subcortical structures
Know main Brodmann’s areas.
o Brodmann’s areas are different based on what the section looks like histologically
o Area 4 = primary motor cortex
o Areas 1, 2, 3 = primary somatosensory cortex
o Areas 41, 42 = primary auditory cortex
o Area 17 = primary visual cortex  hugging calcarene sulcus
o Area 44, 45 (left hemisphere) = Broca’s speech and language area  opercularis and
triangularis near inferior frontal gyrus
o Area 22 (left hemisphere) = Wernicke’s area  posterior portion of superior temporal gyrus
Somatotopic organization of the somatosensory cortex and primary motor cortex; cortical vascular
supply.
o Density of distribution of sensory receptors determines the representation in the
somatosensory cortex
 Different types of receptors can give us an overall picture of our environment
o Imaging of the brain for professionals and amateurs: more diverse and random for amateurs
and more focal and practiced for professionals
Basal ganglia location, vascular supply
o BG considered part of the cerebrum: group of subcortical nuclei
o Largest components include: caudate nucleus, putamen, globus pallidus (internum and
externum)
 Caudate hugs the lateral ventricle
 From lateral to medial: putamen, globus pallidus, internal capsule, thalamus
 Ant limb of IC separates head of caudate from putamen
 Post limb of IC separates thalamus from putamen and globus pallidus
o Exert indirect effects on motor control, e.g., via VA and VL thalamic nuclei, reticular
formation of brainstem
 Important in facilitating appropriate motor actions, inhibiting unwanted movements
 Determines how much excitation the cortex will have by controlling motor output
o


Main categories of white matter fiber tracts that connect cortical areas.
1. U (arcuate) fibers: connect two adjacent gyri
2. Association fibers: span and connect several gyri
 Playing the piano would require many different inputs from many different areas 
shows the need for association fibers
3. Commissural fibers: travel to the opposite hemisphere, terminate in functionally related
cortex
 Ant and post division
 Corpus collosum
4. Projections fibers: leave the cortex (e.g., corticospinal fibers)
 Internal capsule
 Corticobulbar (motor innervation to the face) pass through the genu
 Corticospinal and somatosensory fibers pass through the posterior limb
Recognize the somatotopic organization of fibers traversing the internal capsule (above); vascular
supply
o MCA in particular dives out from the insula and provides supply (putamen and globus
pallidus and a ton of cortex)
o PCA and ACA (caudate) also play a role
Vasculature
MCA
ACA
Anterior
choroidal
PCA
Areas impacted
Putamen and globus pallidus and a
ton of cortex (face representation
in postcentral gyrus)
Caudate and ant limb of IC
Post limb and genu of IC
thalamus
Lecture #28: physiology of sleep
Lesion would cause…
Movements and body position (GP); sensory
deficits in face, trunk, arm
Cognition; sensory deficits in the leg
Corticospinal and corticobulbar pathway
deficits (motor weakness in extremities and
face)
Tons of deficits depending on nuclei effected
Lecture #30: Motor pathways integration



Know your lesions! Given a set of symptoms, be able to localize a lesion based on some process of
elimination and associated symptoms. These give clues. Your patient is like a mystery you have to
solve.
Know whether you’d be ipsi/contra (whether the lesion is on the same side or opposite side of the
body relative to the motor deficits observed).
Know UMN (upper motor neuron) lesion signs versus LMN (lower motor neuron) lesion signs (slide
5)
Sign
weakness
atrophy
fasiculations
reflexes
tone





UMN lesions: CP, TBI, stroke, MS,
corticospinal tract injury
YES
No
no
Increased: hyperreflexia
Increased: hypertonia
LMN lesions: poliomyelitis, lesions
near spinal cord
YES
Yes
Yes
Decreased: hyporeflexia
Decreased: flaccid
Know where corticobulbar and corticospinal tracts are running within the internal capsule.
o Corticobulbar (facial motor)= genu
o Corticospinal= post limb
Know the vasculature that would be associated with a given lesion.
o Anterior choroidal artery  post limb and genu of IC  corticospinal affected
Is the lesion a vascular event or a tumor? (fast, acute onset vs. slow, gradually worsening)
Know the terminology of slide 27/28. Also, do NOT memorize slide 8.
o Plegia= total paralysis  quadri= all 4 limbs, para= both legs or both arms, hemi= one side
o Paresis= motor weakness  quadri, para, hemi
o Thrombosis= occlusion of vessels
o Infarction= area of tissue undergoing necrosis due to restricted blood and O2
o Hemorrhage= bleeding into nervous tissue
o Acute event  vascular
o Tumor  chronic
o Relapsing and remitting  something like MS (can show up in a different part of the body)
For the descending lateral and medial pathways, still know the main function for each and where
each would be located in a C7 cross-section of the spinal cord (i.e., if given a lesion, what would be
impacted).
o Lateral systems: descending pathways  descend contralaterally  deficits tend to show
marked deficits on one side
 Lateral corticospinal: pre-central gyrus  post limb of IC  through cerebral
peduncle  through basal pons  through pyramid  pyramidal decussation at
the spinomedullary junction  descends through lat corticospinal tract  synapses
in ventral horn of SC
 Rubrospinal: tone over flexor muscles
 red nucleus (this is the origin bc there are several inputs coming into the red
nucleus to create this descending pathway)  crosses immediately at
o
ventral tegmental decussation in midbrain  travels through rubrospinal
tract  LMN in ventral horn
Medial systems: mainly descend ipsalaterally or bilaterally  less obvious defects when
lesioned bc they have bilateral projections
 Ant corticospinal: trunk muscles
 Motor cortex  ant CS tract  terminates bilaterally at the level of the
effector
 Vestibulospinal: postural adjustments; positioning of head and neck
 Balance: Lateral vestibular nucleus in pons  descends ipsalaterally 
Travels through ventral part of lateral funiculus  excitatory projections to
ventral horn of entire spinal cord
 Position of head and neck: medial V nucleus in the medulla  descends
bilaterally  Bilateral projections to cervical, upper thoracic spinal cord
(head and neck)
 Reticulospinal: Posture, gait-related movements
 Reticular formation at pons (medial) or medulla (lateral)  ipsilaterally
through reticulospinal tract  Terminates in ventral horn
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Tectospinal: orient head and eyes to (only contralateral medial system!)
 Superior colliculus  crosses immediately through the dorsal tegmental
decussation, in midbrain  tectospinal tract  ventral horn
Lecture #31: Sensory pathways integration
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Know these pathways:
o PCML pathway: proprioception and discriminative touch
 DRG  dorsal horn  travels up medial gracile (LE) or lateral cuneate (UE) 
decussates at internal arcuate fibers in medulla  becomes the medial lemniscus
pathway and travels through pons and midbrain  thalamus (VPL)  postcentral
gyrus in parietal lobe (medial for LE and lateral for UE)
o Anterior and lateral spinothalamic tracts:
 Ant= pressure and crude touch
 Lat= pain and temp
 DRG  ventral horn  decussated immediately through ventral white commissure
and joins contralateral spinothalamic tract  VPL of thalamus  postcentral gyrus
o Trigeminothalamic pathway: sensory info from face
 CN 5 fine touch and proprioception enters via principle sensory nucleus at mid-pons
 decussate and travel to VPM in the thalamus
 Spinal trigeminal nucleus at caudal pons brings in pain and temp from face  VPM
in thalamus
o Spinocerebellar (ant and lat): unconscious proprioception  lesions= ataxia
 Ant= decussate immediately  LE info ascends contralaterally to enter cerebellum
through sup cerebellar peduncle
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Post= synapse in Clark’s nucleus  ascend ipsalaterally and enter cerebellum
through inf cerebellar peduncle
Lecture #29: higher cortical function
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Functions (and the effects of lesions to) primary motor, supplementary motor, premotor areas,
frontal eye fields
Corticospinal pathway, and UMN vs. LMN damage
Know Brodmann’s areas for visual, auditory, somatic sensory, motor, and speech areas
Recognize the cortical areas important for language. Compare and contrast Broca’s, Wernicke’s,
conduction, and global aphasias, etc., and know the vascular lesion likely to produce each deficit.
Recall the cortical area important for spatial relations, and hemispatial neglect (hemineglect).
Identify the functions of the prefrontal association cortex.
Any other clinically relevant details (e.g., prosopagnosia)
Compare the major differences in hemispheric function in humans