● Structure
○ reflections in dura matter where meningeal and periosteal layers split
● Function
○ return blood from cerebral veins to internal jugular vein
● Main examples
○ superior sagittal sinus
◆ superior to falx cerebri
◆ tributary of the confluence of sinuses
○ inferior sagittal sinus
◆ inferior to falx cerebri
◆ tributary to the straight sinus
○ cavernous sinus
◆ lateral to the sella turcica
◆ tributary of the transverse sinus and sigmoid sinus
◆ contains CN III, IV, V1, V2, VI, and internal carotid
◆ clinical correlate
◇ cavernous sinus thrombosis
■ spread of infection from superficial and deep face to cavernous sinus
■ present with symptoms relating to compression of cranial nerves
□ CN VI usually affected first
▲ patient cannot abduct eye
● Clinical importance
○ venous sinus thrombosis → increases intracranial pressure
◆ obstruction → increases venous pressure
◆ consequences include:
◇ decreases capillary perfusion pressure
◇ impairs blood brain barrier → vasogenic edema
◇ impairs CSF reabsorption
◇ brain parenchymal damage
◇ venous hemorrhage
◆ causes include:
◇ prothrombotic diseases
■ e.g., factor V leiden mutation, protein C or S deficiency, antithrombin deficiency
◇ oral contraceptives (OCP)
◇ pregnancy
◇ malignancy
• Venous plexus flanking the pituitary/sella turcica on both sides
◦ cranial nerves (CN) III, IV, V1, V2, and VI pass through the cavernous sinus
CN III, IV, V1, and V2 are found in a fibrous sheath found on the lateral walls of the cavernous sinus
CN VI is medial, close to the internal carotid artery
no fibrous sheath
prone to inflammation due to it being surrounded by blood
◦ carotid siphon (internal carotid artery) and sympathetic fibers that travel in the carotid plexus also pass through the cavernous sinus
• Receives blood from the cerebral, opthalmic, and emissary veins
◦ provides pathway for infection to reach intracranial structures
Cavernous Sinus Syndrome
• Introduction
◦ lesion of the cavernous sinus that affects its contents
can affect an isolated nerve, or all of them
can be secondary to:
malignancy
local spread or metastasis
internal carotid artery aneurysm within the cavernous sinus
bacterial infection → thrombosis
aseptic thrombosis
fungal (e.g., mucormycosis)
• Presentation
◦ physical exam
ophthalmoplegia
compression of CN III, IV, and VI
fixed-dilated pupil (CN III compression)
ophthalmic sensory loss
compression of V1
maxillary sensory loss
compression of V2
Horner syndrome
disruption of ocular sympathetic
Artery Syndrome Presentation
Anterior Spinal artery • Medial medullary syndrome • Ipsilateral paralysis of hypoglossal nerve
• Contralateral hemiparesis of the upper and lower extremity
• Medial lemniscus (↓ contralateral vibration and proprioception)
Posterior inferior cerebellar artery (PICA) • Lateral medullary syndrome • Ipsilateral manifestations
◦ facial loss of pain and temperature
◦ ataxia (arm and leg, gait)
◦ hoarseness
◦ dysphagia
◦ Horner syndrome
• Contralateral manifestations
◦ pain and temperature hemisensory loss
• Nausea, nystagmus, vomiting, vertigo
Anterior inferior cerebellar artery (AICA) • Lateral pontine syndrome • Ipsilateral manifestations
◦ facial paralysis
◦ loss of lacrimation
◦ reduced salivation
◦ loss of corneal reflex
◦ loss of sensation of the anterior 2/3rd of the tongue
◦ Horner syndrome
◦ sensorineural hearing loss
◦ loss of facial pain and temperature
• Contralateral manifestations
◦ pain and temperature hemisensory loss
Posterior cerebral artery - • Contralateral homonymous hemianopia with macular sparing
Middle cerebral artery - • Contralateral manifestations
◦ facial paralysis and sensory loss
◦ upper extremity weakness and sensory loss
◦ hemineglect (if stroke is in non-dominant hemisphere)
◦ aphasia (if stroke is in dominant hemisphere-Broca's area)
Anterior cerebral artery - • Contralateral manifestations
◦ lower extremity weakness and sensory loss
Posterior communicating artery - • Ipsilateral compression leading to CN III palsy
◦ down-and-out, mydriasis
Lenticular striate artery - • Contralateral manifestations
◦ motor hemiparesis
◦ hemisensory loss
• Lack of cortical signs
◦ no aphasia, neglect
Basilar artery • Locked-in syndrome • Quadriplegia
• Preserved reticular formation
• Intact vertical eye movement
• Intact blinking
Anterior communicating artery - • Can compression of optic chiasm
◦ bitemporal hemianopia
• If rupture, ischemia in anterior cerebral artery territory
Introduction
• Spinal nerves
◦ 31 pairs
8 cervical
12 thoracic
5 lumbar
5 sacral
1 coccygeal
◦ vertebral exit
C1-C7 exit via intervertebral foramina above corresponding vertebra
all other nerves exit via intervertebral foramina below corresponding vertebra
• Spinal cord termination
◦ adults
spinal cord ends at L1-L2
becomes cauda equina
subarachnoid space extends to lower border of S2
see Lumbar puncture topic
• Pathology
◦ vertebral disk herniation
nucleus pulposus herniates posteriolaterally through annulus fibrosis
most commonly occurs between L5 and S1
cauda equina affects S2-S5 nerve roots
◦ spinal cord syndromes
anterior cord syndrome
ischemia affecting region supplied by anterior spinal artery (anterior 2/3 of spinal cord)
Spinal Cord Pathways
• Sensory pathways
◦ dorsal columns
function
ascending pressure, vibration, discriminative touch, and proprioceptive sensation
subdivisions
fasciculus cuneatus
upper body and extremities
fasciculus gracilis
lower body and extremities
pathway
1st order neuron
sensory nerve ending → dorsal root ganglion (location of cell body) → spinal cord → ipsilateral ascent in dorsal column → synapse in ipsilateral nucleus in medulla (cuneatus or gracilis)
2nd order neuron
ipsilateral nucleus in medulla → decussates in medulla → contralateral ascent in medial lemniscus → synapse in VPL of thalamus
3rd order neuron
VPL of thalamus → sensory cortex
◦ Spinothalamic tract
◦
function
ascending pain and temperature sensation
pathway
1st order neuron
sensory nerve ending → dorsal root ganglion (location of cell body) → spinal cord → synapse in ipsilateral gray matter of spinal cord
2nd order neuron
ipsilateral gray matter of spinal cord → decussates at anterior white commissure → contralateral ascent in spinothalamic tract → synapse in VPL of thalamus
3rd order neuron
VPL of thalamus → sensory cortex
• Motor pathways
◦ lateral corticospinal tract
function
descending voluntary motor control of contralateral limbs
pathway
1st order neuron (upper motor neuron)
cell body in primary motor cortex → ipsilateral descent through internal capsule → decussation at caudal medulla (pyramidal decussation) → contralateral descent in lateral corticospinal tract → synapse at cell body of anterior horn in spinal cord
2nd order neuron (lower motor neuron)
leaves anterior horn of spinal cord → synapses at neuromuscular junction
anterior spinal artery strokes leads to
loss of deep tendon reflexes and flaccid weakness acutely after the stroke
hyperreflexia and spascity days to weeks following a strok
Brainstem
Overview
Introduction
• The brainstem is composed of the midbrain, pons, and medulla
Brainstem Structures
Structure Cranial Nerves Comments
Midbrain (Mesencephalon) • Oculomotor nerve (CN III) • Reticular activating system
• Trochlear nerve (CN IV) ◦ involved in arousal and alertness
◦ lesion can lead to coma
• Superior colliculus
◦ conjugate vertical gaze center
◦
• Inferior colliculus
◦ auditory information processor
• Parinaud's syndrome
◦ due to compression of dorsal midbrain and pretectal area (e.g., pinealoma, hydrocephalus)
lesions the superior colliculus
◦ conjugate vertical gaze palsy
Pons (Metencephalon) • Trigeminal nerve (CN V) • Medial longitudinal fasciculus
• Abducens nerve (CN VI) ◦ lesion leads to intranuclear ophthalmoplegia (INO)
• Facial nerve (CN VII)
• Vestibulocochlear nerve (CN VIII)
Medulla (Myelencephalon) • Glossopharyngeal nerve (CN IX) • Vasomotor center
• Vagus nerve (CN X) • Respiratory center
• Hypoglossal nerve (CN XII) • Area postrema
◦ incomplete blood-brain barrier
◦ chemoreception of toxins
triggers nausea and vomiting
• Medial lemniscus
◦ formed by decussating fibers of the nucleus gracillis and cuneatus
• Pyramids
◦ contain corticospinal tracts
most decussate in the caudal medulla
• Olives
◦ send fibers through the inferior cerebellar peduncle
◦ distinguishing feature of medull
Introduction
• Main components
◦ caudate
◦ putamen
◦ globus pallidus
◦ subthalamic nucleus
◦ substantia nigra
• Function
◦ initiation of movement and gross movement control
• Direct pathway in relation to dopamine (DA)
◦ DA stimulates D1 receptors on the striatum
leads to inhibition of the globus pallidus internus (GPi)
thalamus becomes disinhibited
sends excitatory input into the cortex
• Indirect pathway in relation to DA
◦ DA stimulates D2 receptors on the striatum
prevents inhibitory input to the globus pallidus externus (GPe)
allows GPe to inhibit the subthalamic nucleus (STN)
prevents GPi from inhibiting the thalamus
thalamus sends excitatory input into the cortex
• Role in disease
◦ parkinson's disease
degeneration of the dopaminergic neurons in the substantia nigra pars compacta (SNc)
decreased excitation of the direct pathway, and decreased inhibition of the indirect pathway
net result: decreased movement
due to decreased thalamic excitation
◦ hemiballismus
lesion to the STN
leads to contralateral spasmodic movement of the extremities
◦ huntington's disease
striatal neuron degeneration
impairs inhibition of GPe, allowing it to inhibit STN
leads to hyperkinetic movemen
● Function
○ to smoothly coordinate movement
○ to play a role in motor planning and balance
● Anatomy
○ the cerebellum is derived from the metencephalon and is found
◆ dorsally to the pons and rostral medulla which are attached by cerebellar peduncles
◇ between the cerebellum and this portion of the brainstem you will find the
■ fourth ventricle
○ the cerebellum contains
◆ the vermis and flocculonodular lobes which play an important role in
◇ proximal and truncal muscle control (vermis)
◇ vestibulo-ocular control (flocculonodular lobes)
◆ cerebellar hemisphere can be divided into
◇ intermediate hemisphere which plays an important role in
■ distal appendicular muscle control
◇ lateral hemisphere which plays an important role in
■ motor planning
◆ cerebellar peduncles
◇ superior cerebellar peduncles
■ mainly carries output signals
◇ middle and inferior cerebellar peduncles
■ mainly carries input signals to the cerebellum
○ deep cerebellar nuclei can be arranged from lateral → medial as
◆ Dendate nuclei
◆ Eboliform
◆ Globos
◆ Fastigial
◆ mnemonic: "Dont Eat Greasy Food"
● Circuitry
○ input
◆ brain (via the pontocerebellar and climbing fiber) to the cerebellum via the
◇ middle cerebellar peduncle
◆ spinal cord (via the spinocerebellar and climbing fibers) to the cerebellum via the
◇ inferior cerebellar peduncle (there are exceptions)
◆ vestibular system to the cerebellum via
◇ juxtarestiform body (in the inferior cerebellar peduncle)
output
all cerebellar outputs are carried by Purkinje cells which synapse in the
deep cerebellar nuclei or vestibular nuclei
which deep cerebellar nuclei the Purkinje cell synapse with is dependent on where the Purkinje cell arose from
Purkinje cells from
lateral cerebellum synapse to the dendate nucleus which
exits the cerebellum via the superior cerebellar peduncle → contralateral VL of the thalamus → motor cortex and supplementary motor areas to influence the corticospinal system for motor planning
intermediate cerebellum synapses to the eboliform and globose nucleus
exits the cerebellum via the superior cerebllar pendcuncle → contralateral VL of the thalamus → motor cortex and supplementary motor areas to influence the lateral corticospinal tract
vermis synapses to the fastigial nucleus
eventually influencing the medial motor system
flocculonodular lobe synapses to the vestibular nucleus
eventually leading to vestibulo-ocular control
● Clinical correlate
○ cerebellar disorders typically results in
◆ nausea, vomiting, and vertigo
◆ slurred speech
◆ uncoordinated limb movements
◇ dysmetria (under- or over-shooting towards a target)
◇ dysrhythmia
◆ unsteadiness
○ lesion localization
◆lesions to the vermis results in
◇ truncal ataxia
◆lesions to the flocculonodular lobe results in
◇ eye movement abnormalities
◆ lesions to the cerebellar hemispheres results in
◇ ipsilateral ataxia
● Physical exam
○ physical exam maneuvers to test the cerebellum include
◆ finger-to-nose and heel-to-shin test
◆ finger tapping
◆ rapid alternating movement
◆ gait testing
◇ truncal ataxia can present with
■ a wide-based and unsteady gait
◆ testing for ocular dysmetria and nyastagmus
Overview
Introduction
• Basic principle
◦ the parasympathetic and sympathetic nervous system control the pupil
parasympathetic fibers lead to pupillary constriction (miosis)
sympathetic fibers lead to pupillary dilation (mydriasis)
as well as controlling the
superior tarsal muscle
elevates the upper lid
smooth muscle orbitalis
prevents eye sinking into the orbit
facial and neck cutaneous arteries and sweat glands
• Miosis
◦ light enters the eye which activates
retinal ganglion cells that will project axons into the optic nerve → optic chiasm → optic tract and then reach the
pretectal nucleus
◦ fibers from the pretectal nucleus project to the Edinger-Westphal nucleus
pre-ganglionic parasympathetic fibers exit the Edinger-Westphal nucleus and synapse in the
ciliary ganglion
◦ post-ganglionic parasympathetic fibers from the ciliary ganglion innervate the
pupillary constrictor muscles causing uniform bilateral miosis
• Mydriasis
◦ sympathetic fibers from many hypothalamic nuclei descend and reach T1 and T2 spinal cord levels
pre-ganglionic sympathetic fibers exit the T1 and T2 spinal cord level to join the paravertebral sympathetic chain (via the white ramus) and
synapse to the superior cervical ganglion
◦ post-ganglionic sympathetic fibers ascend via the carotid plexus of the internal carotid artery, goes through the cavernous sinus, and synapses to the
pupillary dilator muscle
Select Pupillary Defects
Pupillary Defect Comments
Horner syndrome • Pathogenesis inolves impairment in sympathetic pathways to the eye and face which results in
◦ ptosis
secondary to impaired innervation into the upper lid smooth muscles
◦ miosis
secondary to impaired innervation into the pupillary dilator muscles
◦ anhidrosis
Marcus Gunn pupil • Describes an afferent pupillary defect resulting in
◦ the affected eye is not sensitive to the light
there is minimal or absent pupillary constriction of the affected eye to light
• A lesion may affect
◦ eye
◦ retina
◦ optic nerve
• Afferent pupillary defects can be detected with
◦ swinging flashlight test which will show
the affected pupil dilate when exposed to the penlight
Argyll Robertson pupil • A type of light-near dissociation where
◦ the eye does not constrict in response to light as much as it does with accomodation
• Associated with neurosyphilis
Adie's myotonic pupil • A type of light-near dissociation where
◦ the eye does not constrict in response to light as much as it does with accomodation
• Secondary to
◦ degeneration of the
ciliary ganglion
postganglionic parasympathetic neuron
TOPIC
Overview
Introduction
• Basic principle
◦ the parasympathetic and sympathetic nervous system control the pupil
parasympathetic fibers lead to pupillary constriction (miosis)
sympathetic fibers lead to pupillary dilation (mydriasis)
as well as controlling the
superior tarsal muscle
elevates the upper lid
smooth muscle orbitalis
prevents eye sinking into the orbit
facial and neck cutaneous arteries and sweat glands
• Miosis
◦ light enters the eye which activates
retinal ganglion cells that will project axons into the optic nerve → optic chiasm → optic tract and then reach the
pretectal nucleus
◦ fibers from the pretectal nucleus project to the Edinger-Westphal nucleus
pre-ganglionic parasympathetic fibers exit the Edinger-Westphal nucleus and synapse in the
ciliary ganglion
◦ post-ganglionic parasympathetic fibers from the ciliary ganglion innervate the
pupillary constrictor muscles causing uniform bilateral miosis
• Mydriasis
◦ sympathetic fibers from many hypothalamic nuclei descend and reach T1 and T2 spinal cord levels
pre-ganglionic sympathetic fibers exit the T1 and T2 spinal cord level to join the paravertebral sympathetic chain (via the white ramus) and
synapse to the superior cervical ganglion
◦ post-ganglionic sympathetic fibers ascend via the carotid plexus of the internal carotid artery, goes through the cavernous sinus, and synapses to the
pupillary dilator muscle
Select Pupillary Defects
Pupillary Defect Comments
Horner syndrome • Pathogenesis inolves impairment in sympathetic pathways to the eye and face which results in
◦ ptosis
secondary to impaired innervation into the upper lid smooth muscles
◦ miosis
secondary to impaired innervation into the pupillary dilator muscles
◦ anhidrosis
Marcus Gunn pupil • Describes an afferent pupillary defect resulting in
◦ the affected eye is not sensitive to the light
there is minimal or absent pupillary constriction of the affected eye to light
• A lesion may affect
◦ eye
◦ retina
◦ optic nerve
• Afferent pupillary defects can be detected with
◦ swinging flashlight test which will show
the affected pupil dilate when exposed to the penlight
Argyll Robertson pupil • A type of light-near dissociation where
◦ the eye does not constrict in response to light as much as it does with accomodation
• Associated with neurosyphilis
Adie's myotonic pupil • A type of light-near dissociation where
◦ the eye does not constrict in response to light as much as it does with accomodation
• Secondary to
◦ degeneration of the
ciliary ganglion
postganglionic parasympathetic neuron
Select Central Nervous System Lesions
Lesion Clinical Features
Frontal lobe • Frontal lobe lesions can result in disinhibition and an impairment in
◦ judgment
◦ orientation
◦ concentration
◦ frontal release signs
◦ magnetic gait
• Frontal eye field (FEF) lesions can result in
◦ eye deviation towards the side of the lesion
an example is a stroke affecting the FEF
Parietal lobe • Lesions affecting the
◦ dominant parietal (usually the left) cortex results in Gerstmann's syndrome
agraphia
acalculia
finger agnosia
right-left confusion
◦ non-dominant (usually the right) parietal cortex results in
contralateral hemineglect
distortion of perceived space
extinction
Temporal lobe • Lesions affecting the superior temporal lobe (Wernicke area) can result Wernicke aphasia and a right superior quadrant visual defect
• Lesions affecting limbic structures can result in deficits in
◦ consolidation and behavioral changes
• Seizures in the medial temporal lobe limbic structures results in
◦ emotions such as
fear
◦ deja vu
◦ olfactory hallucinations
• Bilacteral lesions in the amygdala results in
◦ Kluver-Bucy syndrome
Brainstem • Lesions affecting the
◦ superior colliculus
Parinaud syndrome
◦ reticular activating system
decreased consciousness and coma
◦ basal ganglia
resting tremor
chorea
athetosis
◦ medial longitudinal fasciculus
internuclear ophthalmoplegia
◦ paramedian pontine reticular formation
eyes look aways from the side of the lesio
TOPIC
Overview
Introduction
• Function
◦ to secrete oxytocin and vasopressin into systemic circulation
recall that the posterior pituitary (or neurohypophysis) have their neuronal cell bodies in the hypothalamus
• Anatomy
◦ embryology
derived from an evagination of the floor of the forming ventricular system
◦ the pituitary gland resides within the sella turcica
underneath the sella turcica is the sphenoid sinus allowing
a transphenoidal surgical approach to access the pituitary fossa
the pituitary fossa is laterally bounded by the cavernous sinus
◦ the pituitary gland lies inferiorly to the optic chiasm
pituitary tumors compressing the optic chiasm results in a
bitemporal hemianopia
• Clinical correlate
◦ central diabetes insipidus
secondary to vasopressin (ADH) deficiency and can result from
neurosurgery
head trauma
malignancy affecting the pituitary-hypothalamic region
◦ syndrome of inappropriate ADH
secondary to ADH excess and can results from
meningitis
head trauma
pulmonary disorders (e.g., pneumonia and small cell lung cancer)
medication side effects (e.g., selective-serotonin reuptake inhibitors, carbamazepine, and cyclophosphamide)
ADH-secreting tumor