 Introduction: principles of neurolocalization

 The somatosensory pathways

 The spinal cord
 The cerebral hemispheres
 Differential diagnosis in neurology is based on
two main components determined rom the
clinical history and physical examination:
 The localization of the neuroanatomic origin(s) of
the patient’s symptoms and signs
 The time course over which these symptoms and
signs have arisen and evolved
 Localization is the process of determining
where in the nervous system the patient’s
disease process is occurring:
 Is the problem in the CNS, the PNS, or both?
 Within the CNS, is there a lesion in the brain, brainstem,
cerebellum, or spinal cord?
 More precisely, where is the lesion within those
structures?
 Within the PNS, is the lesion at the level of one or
more spinal roots, dorsal root ganglia, peripheral
nerves, muscles, or at the NMJ?
 Time course in neurologic diagnosis: determining
what the problem is
 The time course of symptom onset and evolution may be
described as
 Sudden/hyperacute (over seconds to minutes): vascular
 Acute (over hours to days): infections, inflammatory,
metabolic, etc
 Subacute (over days to weeks to months): infections,
inflammatory, etc
 Chronic (over months to years): neoplastic,
neurodegenerative diseases, etc
 NB: metabolic abnormalities, drugs, and toxins can cause
neurologic dys unction over nearly any time course
 The cerebral hemispheres are where the motor
pathways originate, and where the somatosensory
pathways terminate
 The left cerebral hemisphere controls the motor
functions of the right side of the body, and vice
versa
 Motor:
 The corticospinal tracts send motor information from the
cortex to the spinal cord
 Sensory :
 The anterolateral (or spinothalamic) tracts and
 The dorsal (or posterior) column pathways
 The Corticospinal Tracts (Pyramidal System)
 The CST are the final output of the motor system
 The convey the action plan to the alpha motor
neurons of the anterior horns of the spinal cord
 The AHC, in turn, relay the signals to move the
muscles by way of peripheral nerves
 Each CST begins in the motor cortex, which is
located in the precentral gyrus (anterior to the
central sulcus)
 The motor cortex is organized by the region of the
body it controls
 CST
 Cortex (frontal lobe)
 Corona radiata
 Internal capsule
(posterior limb)
 Brainstem: cerebral
peduncles of the
midbrain, basis pontis,
and medullary
pyramids
 Cervicomedually
junction: Crosses to the
contralateral side at the
lower medulla (>85%)
 Lateral CST
 CST…
 Synapse on alpha
motor neurons in the
AHC
 Axons of the alpha
motor neurons leave
the ventral/anterior
spinal cord via
ventral roots and
enter peripheral
nerves to travel to
muscles
 The pyarmidal motor system is a two-neuron
system
 First-order neurons have their cell bodies in the
motor cortex
 Their axons travel through the internal capsule,
brainstem, and spinal cord (CST)
 Upper motor neurons
 Second-order neurons have their cell bodies in the
AHC of the spinal cord
 Their axons travel in peripheral nerves
 Lower motor neurons
 UMN: the neurons of the CNS component in
the brain/brainstem/ spinal cord (i.e., the CST)
 LMN: the neurons of the PNS component
(AHC through the ventral roots into peripheral
nerves)
 Lesions in the CST in the brain and brainstem
cause contralateral weakness
 Lesions on one side of the spinal cord cause
ipsilateral weakness
 UMN lesion  LMN
 Tone: increased  Hyporeflexia or
(spastic) areflexia
 DTR: increased  Flaccid
(exaggerated)  Atrophy (decreased
 Plantar: extensor/up muscle bulk)
going/Babniski sign  Fasciculation
present
 Hoffmann sign
present
 Pronator drift present
 Pronator drift (can be present acutely)
 The arms are held outstretched with the palms up
and fingers spread
 The hand may begin to close and the arm may begin
to pronate and drift downward with UMN lesion
 NB:
 With parietal lesions, the affected arm may drift
upward due to impaired proprioception
 UMN pattern of weakness (can be present
acutely)
 The upper extremity extensors are weaker than the
flexors (DDx: radial nerve palsy)
 I.e., the arm is stronger when flexing the elbow
compared to extending the elbow
 The lower extremity flexors are weaker than the
extensors
 I.e., the leg is stronger when extending the knee
compared to flexing the knee
 The Corticobulbar Tracts
 The muscles of the face, tongue, larynx, and
pharynx also have UMN and LMN
 The upper motor neurons arise from the motor
cortex and travel with the CST as the corticobulbar
tracts
 However, the corticobulbar fibers terminate in their
respective cranial nerve nuclei (c0ntralateral) in the
brainstem
 The lower motor neurons arise in the cranial nerve
nuclei and travel in the cranial nerves
 The sensory pathways begin in the periphery and
end in the brain
 Sensory information from the skin (light touch,
pressure, pain, temperature, vibration) and from
the muscle spindles and the Golgi tendon organs
(proprioception) travels arrive in the dorsal root
ganglia
 At the entrance to the spinal cord, somatosensory
information is “sorted” into two pathways:
 The spinothalamic tracts (the anterolateral tracts): pain
and temperature information
 The dorsal columns: proprioception and vibration
information
 Light touch information travels in both pathways
 Both sensory pathways
ascend through the
spinal cord and
brainstem to arrive at the
VPL nucleus of the
thalamus
 The thalamus transmits
this somatosensory
information to the
somatosensory cortex in
the postcentral gyrus,
just posterior to the
motor strip
 Sensory homunculus
 Postcentral gyrus and
posterior part of the
paracentral lobule
 NB: the location and
amount of cortex
assigned to the
processing of sensory
information from a
particular part of the
body
 Two systems:
 Dorsal columns (convey joint position sense,
vibration sense, and light touch senses)
 Spinothalamic tracts (convey pain, temperature, and
crude touch senses)
 Both cross to transmit sensory information
from one side of the body to the contralateral
cerebral hemisphere
 However, the sites of crossing differ
 The dorsal column system
crosses in the medulla, just
superior to the crossing of the
CST
 Unilateral lesions of the dorsal
column pathway from the upper
medulla and superiorly affect
contralateral sensation
 Unilateral lesions from the lower
medulla through the spinal cord
affect ipsilateral sensation
 This pattern essentially mirrors
that of the corticospinal tracts
 The anterolateral tracts cross
immediately after entering the
spinal cord (they actually
cross over the course of a few
spinal levels)
 Unilateral lesions anywhere in
this pathway affect contralateral
sensation
 A small patch of ipsilateral pain/
temperature loss involving the
spinal levels over which the tract
crosses may also be observed)
 Brainstem
 In the brainstem, the corticospinal tracts
travel in the anterior (ventral) portion,
whereas the sensory pathways are
predominantly dorsolateral
 Brainstem lesions can cause crossed
signs:
 Weakness and/or sensory changes in the
face ipsilateral to the lesion but in the
contralateral body
 NB: Nearly all cranial nerves control
ipsilateral functions in the head
 Crossed signs: since brainstem lesions
affect the not-yet-crossed CST and the
already-crossed ascending sensory tracts
 Lamination of the long tracts in
the spinal cord
 The arrangement of fibers within a
pathway
 For the corticospinal, anterolateral,
and dorsal column pathways, this
refers to where the arm, leg, and torso
fibers run
 CST
 As the corticospinal tracts descend from
the brainstem, arm fibers synapse on
LMN in the cervical cord before leg
fibers
 Hence, the CST fibers are laminated
such that the arm fibers are medial and
the leg fibers are lateral
 The dorsal column fibers from
the feet and legs enter the
spinal cord at the lumbar and
sacral levels, and are pushed
medially by the addition of
trunk and arm fibers as the
tracts ascend
 The dorsal columns are thus
laminated with the legs medial
and the arms lateral
 The spinothalamic tracts’ feet
and leg fibers cross to the
contralateral side and are pushed
laterally as subsequent crossing
fibers or the trunk and arms
push them aside and layer more
medially
 The spinothalamic tracts are thus
laminated with the arms medial and
the legs lateral like the corticospinal
tracts (similar to CST)
 Brown-Séquard
(Hemicord) Syndrome
 Ipsilateral weakness
below the level of the
lesion
 Ipsilateral loss of
vibration sense and
proprioception below
the level of the lesion
 Contralateral loss of
pain and temperature
sensation below the
level o the lesion
 Anterior Cord Syndrome
 Involves nearly the entire
cross sectional area of the
spinal cord with the
exception of the dorsal
columns
 Motor function and pain and
temperature sensation are
impaired below the level of
the lesion
 Both upper and lower motor
neuron signs may be seen
 Occurs most commonly due
to infarction in the territory
of the anterior spinal artery
 Central Cord Syndrome
 Occurs most commonly
due to syrinx- usually in
the cervical spinal cord
 The closest structure to
the central canal is the
anterior commissure
where the anterolateral
tracts cross
 The upper extremity
spinothalamic fibers
affected first
 “Cape-like” distribution
of sensory deficits
(dissociated sensory loss)
 Subacute Combined
Degeneration
 Selective involvement of
the dorsal columns and
CST
 Most commonly caused by
vitamin B12 deficiency;
other causes include
copper in the setting of
excess zinc ingestion ;
vacuolar myelopathy
 Concurrent myelopathy
and neuropathy
 Tabes dorsalis in syphilis
affects the dorsal column
and dorsal roots
 Spinal Cord Pathways For Bowel And Bladder Control
 The pathways for bowel and bladder control also pass through
the spinal cord
 Acute spinal cord pathology causes flaccidity of the bowel and
bladder (as well as in cauda equina syndrome)
 Urinary retention with overflow incontinence
 Constipation due to decreased bowel motility and incontinence
due to decreased rectal tone
 Spasticity develops over time with chronic spinal cord lesions
 Bladder becomes spastic/hyperrefexic: it contracts too much,
leading to urgency and incontinence
 Increased bowel and rectal tone- leading to constipation
(generally requiring physical stimulation of the rectum for a
bowel movement to occur)
 The hemisphere contralateral to the side o
handedness is considered the dominant
hemisphere
 The hemisphere ipsilateral to the side o
handedness is considered the nondominant
hemisphere
 Most patients are right-handed, so their left
hemisphere is the dominant hemisphere
 Language dysunction is most commonly due to
lesions in the dominant (usually left) hemisphere,
whereas neglect is most commonly due to lesions
in the nondominant (usually right) hemisphere
(causing left -sided neglect)
 Arterial Supply Of The Cerebral Hemispheres
 Paired internal carotid arteries (the anterior
circulation) and
 Arise from the CCA
 The right CCA arise from the brachiocephalic trunk and
directly from the aortic arch on the left
 Each carotid artery ultimately gives rise to MCA and
ACA
 Each internal carotid artery also gives rise to an
ophthalmic artery (supplies the retina) and an anterior
choroidal artery (supplies the posterior thalamus and
internal capsule)
 Paired vertebral arteries (the posterior circulation)
 Arise from the subclavian arteries
 Join to form the basilar artery at around the level of the
pontomedullary junction
 End by giving off the posterior cerebral arteries (PCAs)
at the level of the upper midbrain
 PCAs supply the occipital lobes and inferior and
medial temporal lobes
 Before giving rise to the PCAs, the vertebrobasilar
system gives off three paired circumferential arteries
that supply the lateral brainstem and cerebellum: SCA,
AICA, and PICA.
 The anterior circulation and posterior
circulation are linked by the posterior
communicating arteries
 The ACAs are linked by the anterior
communicating artery
 These connections form the circle of Willis on
the inferior surface of the brain
 Not all patients have a complete circle of Willis,
and some patients have anatomic variants
 The Vascular Territories of the ACA, MCA, and
PCA
 The PCAs supply the occipital lobes, inferior medial
temporal lobes, and the thalami
 The MCAs supply the lateral surface of the frontal,
temporal, and parietal lobes
 The ACAs supply the medial surface of the frontal
and parietal lobes
 Watershed
(Borderzone)
Territories
 They are the regions at
the border of two
arterial territories
 The common teaching
is that borderzone in
arction is due to
hypoperfusion; other
causes include emboli
arriving at the end-
arterial territories
 Infarction in the Watershed (Borderzone)
Territories
 Infarction in the MCA-ACA borderzone can cause
proximal arm and leg weakness with preserved
strength distally in the hands and feet
 If bilaterally, it causes what is called the “person in a
barrel” syndrome
 Bilateral infarction in the MCA-PCA watershed
region results in deficits in visual attention (e.g.,
Balint’s syndrome: optic ataxia, ocular apraxia, and
simultanagnosia)
 Clinical Syndromes Associated With Cerebral
Vascular Territories
 MCA Territory Infarction
 The MCA territory includes the majority of the cerebral
hemisphere
 The functional regions supplied by the MCA include
the motor and premotor regions, somatosensory cortex,
the frontal eye fields, the language areas, parietal
regions responsible for spatial attention, and the
superior and inferior radiations of the visual pathways
as they pass through the parietal and temporal lobes,
respectively
 MCA strokes cause contralateral face and arm weakness
much more so than leg weakness
 Left MCA syndrome: right hemiplegia and hemisensory
loss, aphasia, gaze deviation toward the left, and right
homonymous hemianopia
 Right MCA syndrome: left hemiplegia and hemisensory
loss, left-sided neglect, gaze deviation to the right, and
left-sided homonomyous hemianopia
 The MCA stem gives off the lenticulostriate penetrating
branches that supply the basal ganglia and internal
capsule
 Complete contralateral hemiparesis (pure motor lacunar
syndrome
 ACA Territory Infarction
 ACA strokes cause contralateral leg weakness and
sensory loss more so than face and arm weakness
and sensory loss
 Cognitive changes such as abulia
 Occlusion o both ACAs simultaneously can cause
acute paraplegia
 Azygous ACA: both ACAs arise from a common
trunk
 The ACAs can also be compromised by subfalcine
herniation
 Recurrent Artery of Huebner Territory
Infarction
 A branch of the ACA that supplies the head of the
caudate and the adjacent internal capsule
 Contralateral hemiparesis and/or movement
disorder
 Anterior Choroidal Artery Territory Infarction
 Arises directly from the ICA and supplies the
posterior thalamus and the internal capsule
 Contralateral visual field defects, contralateral
hemiparesis, and/or contralateral hemisensory loss,
and can also cause cortical signs
 PCA Territory Infarction
 Contralateral homonymous hemianopia or superior
quadrantanopia, impaired short-term memory, inability
to read with spared ability to write (alexia without
agraphia- left inferior temporal lesion), decreased ability
to recognize faces (prosopagnosia- right inferior temporal
lesion), and/or changes in cognition and/or level of
arousal if thalamic is affected
 PCA territory strokes are generally considered posterior
circulation strokes
 Fetal PCA: when one or both PCAs arise from the ICAs
rather than the top of the basilar artery (anterior
circulation)
 Artery of Percheron: when both thalami are both supplied
by a single artery that arises from the PCA
 Lacunar Strokes
 Caused by occlusion of small penetrating arteries affecting the
subcortical white matter (internal capsule), subcortical gray
matter (BG, thalamus), or anterior pons
 Pure motor stroke: unilateral hemiparesis/hemiplegia due to
involvement of the posterior limb of the internal capsule or the
anterior pons
 Pure sensory stroke: unilateral hemisensory loss due to
involvement of the VPL/VPM nuclei of the thalamus
 Ataxia-hemiparesis: unilateral hemiparesis/hemiplegia (due to
involvement of the corticospinal tract) with ataxia in the weak
limb(s) due to lacunar stroke in either the internal capsule or
the anterior pons
 Dysarthria–clumsy hand: dysarthria and unilateral upper limb
ataxia; localization is the same as or ataxia-hemiparesis
 Spatial Attention and Praxis
 Attention
 The parietal lobe plays roles in awareness of the body
in space, spatial reasoning, and mathematical
processing
 The projection from the occipital lobe superiorly to the
parietal lobe (the dorsal stream)- the “where” pathway:
 Visual information is processed here to determine where
things are in space with respect to the body
 Lesions here can cause neglect: the patient is unaware of
one half of the world
 Neglect is more common with lesions in the nondominant
parietal lobe (the right parietal lobe) causing left sided
neglect
 Unilateral neglect:
 The loss of conscious awareness for the left side of
the perceptual and mental space
 Different, but simple bedside paper-and-pencil tests:
 Ask to bisect a line segment
 They misbisect it to the right of the objective midpoint;
 Ask to cross out line segments printed on a sheet of
paper (Albert’s test)
 They omit to cross out a number of left-side segments;
 Ask to draw a clock face
 They omit, misarrange, or distort left-side details
 Examination findings in patients with neglect may
include
 Simultagnosia (extinction) of the contralateral side
 The mildest manifestation of a right parietal lesion
 Primary sensory modalities are intact
 The patient fails to appreciate the stimulus on the involved
side or fails to see the stimulus in the involved visual
hemifield
 Tactile agnosia (astereognosia)
 Lesion: posterior–inferior portion of the parietal lobe
(postcentral gyrus).
 Lack of awareness of deficits (e.g., not acknowledging that a
paretic limb is weak), and inability to recognize the neglected
body parts as one’s own in severe cases
 Gerstmann’s syndrome:
 Due to lesions in the
angular gyrus of the left
parietal lobe can cause
 Characterized by left-
right confusion, inability
to count (acalculia),
inability to name the
fingers (finger agnosia),
and inability to write
(agraphia)
 Praxis
 Apraxia: parietal lesions can cause difficulty
performing a complex learned action
 There are several types of apraxia:
 Limb-kinetic apraxia: loss of dexterity in performing
actions
 Ideational apraxia: inability to conceive of the idea of
how to accurately perform an action (caused by lesions
of the left parietal lobe)
 Ideomotor apraxia: inability to convert an idea about
how to do something into a motor plan (caused by
lesions of the left parietal lobe)
 Recognition Memory
 Memories are internal representations of sensory
experiences
 Lesions of the medial temporal lobes can cause amnesia
 The flow of visual information inferiorly to the temporal
lobe (the ventral stream)- the “what pathway:”
 Visual information is processed here to determine what
things are (recognition memory)
 The dominant inferior temporal lobe houses the visual word
form area necessary for reading (alexia- inability to read)
 The nondominant inferior temporal lobe houses the face
recognition area (prosopagnosia- inability to recognize
familiar faces)
 In the most severe cases patients cannot even recognize their
own face in the mirror
Ventral (occipitotemporal) stream: fusiform and lingual gyri; involved in the
analysis of color and shape of the object.
Unilateral lesions: ontralateral hemiachromatopsia (loss of color perception in
the contralateral visual hemifield)
Bilateral (or rarely right-sided) lesions: visual agnosia (prosopagnosia and
object agnosia)
 The inferior frontal gyrus houses Broca’s area for
speech production
 Wernicke’s area for speech recognition lies at the
junction of the auditory cortex (superior temporal
gyrus) and the parietal cortex
 However, in some patients, language may localize
to the right hemisphere
 Dominant hemisphere
 Situated on the left side of the brain in > 90% of right
handed people and also in about two-third of left handed
people
 Lesions in and around Broca’s and Wernicke’s
areas lead to speech disturbances (aphasia)
 The aphasias can be categorized based on the
patient’s ability to produce speech, comprehend
speech, and repeat words and phrases
 Broca’s aphasia (nonfluent, expressive, or motor
aphasia)
 The primary deficit is in production of speech
 I.e., effortful speech with frequent errors
 Comprehension is largely preserved
 In the most severe Broca’s aphasias, the patient is mute
 The patient cannot repeat phrases stated by the examiner
but can comprehend (transcortical motor aphasia-
repetition is preserved)
 Wernicke’s aphasia (receptive, fluent or
sensory aphasia)
 Comprehension is impaired
 Nonsensical speech
 Repetitions is impaired (transcortical sensory
aphasia- repetition is preserved)
 Global aphasia
 Both production and comprehension are impaired
 Mixed transcortical aphasia- if repetition is
preserved
Global Aphasia
 Conduction aphasia
 A patient’s only language
deficit is repetition
 Conduction between
Wernicke’s area and
Broca’s area (via the
arcuate fasciculus) is
disrupted
 Most commonly due to
stroke in the left MCA
territory stroke
 Other functions of the Frontal lobes
 Executive functions including working memory, decision
making, abstract reasoning, and emotional processing
 Frontal lobe lesions can cause
 Abulia (decreased initiative, motivation, speech, and
emotional response),
 Behavioral disinhibition, and/or impairments in any of the
above executive functions
 Thalamus
 The thalami are positioned on either side of the third
ventricle, just superior to the midbrain
 The thalamus is a collection of nuclei
 Four basic types of circuitry pass through thalamic
nuclei en route to the cortex:
A. Sensory pathways
 All sensory pathways synapse in the thalamus, which
transmits sensory information to the respective
sensory cortices
 Smell is the only sensory modality that reaches the
cortex before the thalamus
B. Motor control pathways
 The ventral anterior (VA) and ventral lateral (VL) nuclei o
the thalamus participate in cortical–basal ganglia–cortical
loops and cerebellar–cortical pathways
C. Consciousness/arousal pathways
 These pathways begin in the brainstem reticular
activating system and project to both thalami, which in
turn project diffusely throughout the cortex
D. Cognition/emotion pathways
 Corticocortical loops pass through the thalamus, playing
roles in diverse cognitive functions
 E.g., the circuit of Papez which participates in memory
and emotion: hippocampus→ fornix→mamillary
bodies→anterior nucleus of the thalamus→anterior
cingulate→entorhinal cortex→hippocampus
 Lesions in the thalamus:
 Contralateral sensory loss; contralateral
hemiparesis/hemiplegia
 Larger lesions can cause decreased level of
consciousness
 Generally, lesions of the thalamus can “do anything”
(i.e., cause any type of deficit), including causing
“cortical” signs (e.g., aphasia, neglect, cognitive
deficits) and eye movement abnormalities (in part
due to effects on nearby midbrain pathways or eye
movements)
 Basal Ganglia
 The BG include the caudate, putamen, globus
pallidus, and subthalamic nucleus
 The striatum: caudate and putamen together
 The lentiform nuclei: putamen and globus pallidus
together
 The BG are part of circuits that initiate and
coordinate movements
 BG dysfunction leads to movement disorders (e.g.,
Parkinson’s disease)
 Disorders Of Visual Cognition
 Visual information rom the primary visual cortex (at the
occipital pole) is transmitted superiorly to the parietal
lobe or spatial processing (the “where” pathway) and
transmitted inferiorly to the temporal lobe or object
identification/ recognition (the “what” pathway)
 The left “what” pathway (inferior temporo-occipital
region )
 Specialized for processing of visual word forms
 Inability to read (alexia), alexia without agraphia
 The right “what” pathway (inferior temporo-occipital
region )
 Specialized for processing of faces
 Inability to recognize faces (prosopagnosia)
 Balint Syndrome
 Lesions of the bilateral parieto-occipital junctions
 This syndrome is characterized by a triad of signs
that are maniestations of deficits in visual attention:
 Optic ataxia
 Ocular apraxia
 Simultanagnosia
 Cortical Blindness and Anton Syndrome
 Bilateral posterior cerebral artery strokes can lead to
cortical blindness: the eyes and optic nerves still work
 I.e., normal pupillary light reflexes
 However, the brain cannot decode visual information
 Anton syndrome
 Some patients with cortical blindness are unaware that
they are blind and may deny being unable to see
 Charles Bonnet Syndrome
 “Release” hallucinations in a patient with bilateral visual
loss of any cause
 These hallucinations are generally of small people, are not
threatening to the patient, and the patient usually knows
they are not real
 Overview Of Brainstem Anatomy
 A “spinal cord or the head and neck”
 In addition to somatic sensory information, the
brainstem also receives vestibular, auditory, taste,
and visceral sensory information
 Motor functions of the brainstem include control of
ocular, pupillary, facial, laryngeal, pharyngeal, and
visceral musculature
 There are five general categories of structures:
 The descending motor pathways for the extremities and
torso (CST)
 The ascending somatosensory pathways from the
extremities and torso (dorsal columns and spinothalamic
tracts)
 The cranial nerve nuclei and associated structures
 The cerebellar peduncles
 The RAS and ascending neurotransmitter-specific
projection pathways: substantia nigra (dopamine), locus
coeruleus (norepinephrine), median raphe nuclei
(serotonin), pedunculopontine nuclei (acetylcholine)
 The following principles apply at all three levels of
the brainstem
 The CST run in the anterior (ventral) aspect of the
brainstem
 The somatosensory pathways for the extremities and
torso are most often posterior (dorsal) within the
brainstem (except in the mid-medulla where the medial
lemnisci are medial and extend anteriorly
 The cranial nerve nuclei are all posterior (dorsal)
 The motor cranial nerve nuclei are closest to the midline, and
their cranial nerves emerge medially/anteriorly (except CN 4)
 The motor cranial nerve nuclei innervating skeletal muscle
are at the midline: CNs 3, 4, 6, and 12
 The motor cranial nerve nuclei innervating branchial muscles
are more lateral: CN 7, CN 5, and CNs 9 and 10
 The sensory and special sensory cranial nerve nuclei
are all more lateral than the motor cranial nerve
nuclei: sensory nuclei of CN 5, vestibular and
cochlear nuclei (CN 8), and nucleus solitarius (for
taste and visceral sensation)
 The cerebellar peduncles all arise from the
posterior/dorsal brainstem
 The ascending neurotransmitter-specific projection
pathways are found throughout the brainstem, but
the RAS is at the level of the midbrain
 The Cerebellar Peduncles
 The inferior cerebellar peduncles connect the
medulla to the cerebellum
 The middle cerebellar peduncles connect the pons to
the cerebellum
 The superior cerebellar peduncles connect the
cerebellum to the upper pons
 The Arterial Supply of the Brainstem
 Brainstem has three levels
 One pair of circumferential arteries per level of the
brainstem:
 Superior cerebellar arteries (SCAs) or the midbrain
 Anterior inferior cerebellar arteries (AICAs) or the
pons
 Posterior inferior cerebellar arteries (PICAs) or the
medulla
 The SCAs and AICAs
arise from the basilar
artery and the PICAs from
the vertebral arteries
 The anterior spinal artery
ASA) arises from the
vertebral arteries and
supplies the medial
medulla and anterior
spinal cord
 At the level of the pons
and midbrain, the midline
basilar artery supplies the
medial brainstem through
penetrating branches
 Clinical Applications Of Basic Brainstem
Anatomy
 Crossed Signs Due to Brainstem Lesions
 Throughout most of the brainstem, lesions lead to
contralateral weakness and/or sensory symptoms in
the extremities
 With the exception of CN 4, all cranial nerves project
ipsilaterally (hence, unilateral lesions cause ipsilateral
sensory and/or motor symptoms in the face
 Medial Versus Lateral Brainstem Syndromes
 The descending CST are anterior and medial throughout
the brainstem
 The motor cranial nerve nuclei for skeletal muscle are
posterior and medial and their associated cranial nerves
exit anteriorly and medially except CN 4
 The sensory and special sensory cranial nerve nuclei are
dorsolateral in the brainstem
 Lesions of the medial brainstem cause predominantly
motor symptoms and signs
 Lesions of the dorsolateral brainstem cause
predominantly sensory and special sensory symptoms
and signs; cerebellar symptoms
 The cerebellar peduncles are positioned on the
dorsal/dorsolateral aspects of the brainstem