Neuroanatomy Flashcards
Thalamic blood supply
Primarily PCA + branches (some anterior supply laterally (anterior choroidal->LGN)
Paramedian
Tuberothalamic (PCOM branch)
Inferolateral
Posterior choroidal
Anterior thalamic syndrome
Perseverations, superimposition of unrelated information, apathy, amnesia, emotional facial paresis
Paramedian thalamic syndrome
Disinhibition, loss of self activation, and amnesia, vertical gaze paresis - thalamic dementia
Inferolateral thalamic syndrome
Ataxia, hypesthesia, executive dysfunction (pure sensory, sensiromotor, Dejerine-Roussy)
Posterior thalamic
Hypoesthesia, homonymous horizontal sectoranopsia, aphasia, neglect
Field cuts in LGN
Anterior choroidal
Lateral choroidal form posterior choroidal of posterior circulation
Anterior thalamic nuclei
Anterior, lateral dorsal
Medial thalamic nuclei
Medial dorsal
Lateral thalamic nuclei
VA, VL, VPM/VPL, LGN, MGN, pulvinar
Intralaminar thalamic nuclei
Midline thalamic nuclei - adjacent to third ventricle
Reticular
Thin layer surround thalamus
Thalamic relay nuclei: specific vs non-specific vs intralaminar vs reticular
Specific: unique functional and anatomic correlate to projection (e.g., retina,anterior visual pathway->LGN->occiptal cortex)
Non-specific: pulvinar receives input from multiple sensory modalities (SS, vision) and project to parietal, temporal and occipital association areas
Diffuse relay nuclei with other deep structures (BG, brainstem)
Reticular nucleus - inhibitory intrathalamic, reciprocal projections
What generates sleep spindles
Reticular nucleus
What special sense bypasses the thalamus?
Olfactory
Thalamic nuclei involved in sensory processing
Thalamic nuclei involved in motor control
Thalamic nuclei involved in oriented towards behaviorally relevant stimuli
Thalamic nuclei involved in emotional processing
Intralaminar nuclei
What causes thalamic dementia?
Infarct of paramedian artery or other lesion of DM nucleus
Bilateral thalamic infarcts from single occlusive event?
Artery of Percheron
Which thalamic nuclei does not project to the cortex?
Reticular nucleus - gates stimuli, generates sleep spindles
Which thalamic nuclei does not project to the cortex?
Reticular nucleus - gates stimuli, generates sleep spindles
STN
The only excitatory nuclei from the basal ganglia
Basal ganglia prefrontal circuit
Basal ganglia limbic circuits
BG hypodensities and calcifications are common in what condition?
MELAS
Where do you see bilateral putamen necrosis?
Methanol poisoning
Sxs from BG lesions 2/2 perinatal ischemia may be delayed for…?
7-14 years
BG are prominently affected in what condition?
Leigh’s syndrome
STN lesions result in…?
Contralateral ballismus
Spinal nerve
Formed by the junction of the anterior and posterior roots at the level of the neural foramen (which is just beyond the dorsal root ganglion).
– The anterior roots contain lower motor neuron axons from the anterior horn cells
– The posterior roots contain axons from the sensory cell bodies in the dorsal root ganglion
Spinal Root / Vertebrae Relationships above L1/L2
C1-C7 roots exit through the neural foramina above the corresponding vertebrae
– 1st cervical nerve exits the spinal canal between the Atlas and the occiput and does not project to the skin
The 8th cervical nerve exits the spinal canal between C7 and T1 vertebrae.
– There is no C8 vertebra
All other spinal nerves exit through the neural foramina beneath the vertebrae of their same number
– From T1-L1/2, directly off the spinal cord
– Below L1/2, from the cauda equina
Spinal nerve roots exiting below L1/L2
Below L1/2 in the cauda equina, the nerve roots are organized to exit the spinal canal.
– The nerve root exiting below its vertebrae is quite lateral.
– The nerve root that will be exiting below the next caudal vertebrae is central lateral
– The remaining nerve roots are cental.
Neural foraminal stenosis and disc herniation effects above L1/L2
Neural foraminal stenosis affects the nerve root exiting at that level.
Disc herniation above the conus medullaris affects the nerve root exiting at that level.
Above the C7 vertebrae, the inferior vertebrae for either neural foraminal stenosis or disc herniation correlates with the nerve root affected
- The C5 nerve root is impinged by C4/5 neural foraminal stenosis or disc herniation.
The C8 nerve root is impinged by C7/T1 neural foraminal stenosis or disc herniation.
From T1/2-L1/2, the superior vertebrae for either neural foraminal stenosis or disc herniation correlates with the nerve root affected
- The T5 nerve root is impinged by T5/6 neural foraminal stenosis or disc herniation.
Neural foraminal stenosis and disc herniation effects above L1/L2
Neural foraminal stenosis affects the nerve root exiting at that level.
Typical centro-lateral disc herniation at the level of the cauda equina affects the nerve root exiting 1 vertebral segment below that level.
Far lateral disc herniation at the level of the cauda equina affects the nerve root exiting at that level.
The L5 nerve root is impinged by an L4/5 centro-lateral disc herniation, L5/S1 far lateral disc herniation or L5/S1 neural foraminal stenosis
Radiculopathies
Classically present with neck or low back pain that radiates in the distribution of a nerve root
– Sensory symptoms are often vague because the dermatomes overlap. Focal severe sensory loss argues against a radiculopathy.
– Weakness of the muscles that receive innervation from that nerve root are usually mild to moderate in severity. Complete muscle paralysis is uncommon because the myotomes overlap.
Structural: Herniated discs, Spondylosis, or Mass lesions (metastases, abcess) - common in C5-C7, L5, S1
Infiltration: Carcinoma, Lymphoma, Sarcoid
Infection: Lyme, VZV, CMV, HSV
Infarction: Vasculitis, DM
Demyelination: Early GBS
Spinal nerve sympathetic component
The second order sympathetic neurons arise from the intermediolateral column from T1- L2.
Each spinal nerve from T1-L2 contains sympathetic axons that leave the spinal nerve in a white communicating ramus to enter the sympathetic chain.
– Sympathetic axons synapse at that level or ascend and descend in the sympathetic chain.
All spinal nerves receive third order sympathetic neurons from the sympatheic chain via a gray communicating ramus.
Spinal nerve sensory and motor
Each spinal nerve divides into a
Ventral primary ramus which innervates
-Plexus of a limb: anterior segment sensory receptors, limb / anterior trunk muscles
Dorsal primary ramus which innervates: posterior segment sensory receptors, paraspinal muscles (involvement of paraspinal muscles on EMG is specific but not sensitive for either a spinal nerve (radiculopathy) or anterior horn cell disease)
Conus vs cauda equina lesions
Spinal segments and nerves
There are 31 spinal segments and nerves
– 8 Cervical
– 12 Thoracic
– 5 Lumbar
– 5 Sacral
– 1 Coccygeal
Vertebral bodies
There are 33 vertebral bodies
– 7 Cervical
– 12 Thoracic
– 5 Lumbar
– 5 Sacral
– 4 Coccygeal
Spinal cord vs vertebral segments
Spinal Cord vs. Vertebral Body Levels
C1 cord at C1 Vertebral Body
C8 cord at C7 Vertebral Body
T1 cord at T1 Vertebral Body
T12 cord at T8 Vertebral Body
L1-L5 between T9 and T11 Vertebral Bodies
S1-S5 between T12 and L2 Vertebral Bodies
Spinal cord and vertebral column development
In the 1st Trimester, the spinal cord is the same length as the vertebral column
During fetal development and early childhood, the vertebral column grows while the spinal cord does not grow at same rate
– The spinal cord “migrates” upward
– In the Newborn, the spinal cord ends at L3 – In the Adult, the spinal cord end at L1/2.
Spinal cord tracts
Desending tracts
Appendicular Movement
Lateral Corticospinal tract
Rubrospinal tract
Lateral Vestibulospinal tract
Corticospinal tract decussation at the medulla
80-90% of axons cross in the medullary pyramids prior to forming the lateral corticospinal tract
– Axons to the upper extremity are more medial and anterior in the pyramid and cross rostral to the legs
– 2% of axons do not cross and enter the lateral corticospinal tract
8% of axons do not cross and enter the anterior corticospinal tract
Hemiplegia Cruciata
A lesion in the rostral medial medullary pyramid effecting the upper extremity axons after they have crossed and the lower extremity axons before they cross.
– This results in arm weakness ipsilateral to the lesion and contralateral leg weakness.
Lateral corticospinal cord in the spinal cord
Lateral Corticospinal tract
Descends posteriorly in the lateral compartment of the spinal cord.
– The arm fibers are medial and the leg fibers are lateral.
Synapses on the lower motor neurons in the anterior horn.
– Flexor muscles are medial in Rexed lamina IX and extensor muscles are lateral
Any lesion in the spinal cord, produces ipsilateral weakness.
Rubrospinal tract
Another appendicular movement tract
– Originates from the red nucleus in the midbrain.
– Decussates in the midbrain and descends just ventral to the lateral corticospinal tract in the lateral compartment
– Terminates in the cervical spinal cord
– Partially mediates upper limb flexion
Lateral Vestibulospinal tract
Another appendicular movement tract
– Originates from the lateral vestibular nucleus
– Descends ipsilaterally in the ventral compartment
– Synapses on interneurons that decussate at that level to innervate bilateral medial anterior horn cells that control balance and stimulates appendicular extension
– Partially mediates arm and leg extension
Ventral Corticospinal tract:
Descending axial tract
– Remains ipsilateral in the ventral compartment
– Stimulates axial movement
Tectospinal tract
Descending axial tract
– Originates from the deeper layers of the superior
colliclus.
– Decussate in the dorsal tegmentum and descend in the medial dorsal portion of the ventral compartment of the brainstem.
– Terminates in the cervical spine
– Mediates movement of the neck and upper trunk (probably in coordination with eye movements.
Medial Vestibulospinal tract
Descending axial tract
– Originates from the medial vestibular nucleus and descends bilaterally.
– Also mediates movement of the neck and upper trunk (probably in coordination with eye movements.
Pontine and Medullary Reticulospinal tracts
Descending axial tract
– Receives input from premotor cortex
– Originate in the pontine and medullary reticular formation, respectively
– Descends ipsilaterally in the vental compartment.
– Mediate automatic movement (e.g. maintain posture).
Anterolateral tracts - arms and legs
The lateral spinothalamic tract originates from sensory receptors for temperature and pain. Leg fibers are lateral and arm fibers are medial.
DCML - arms and legs
Arms lateral in cuneate fascilus and legs medial in cuneate gracilis
Spinocerebellar tracts - arms and legs
Dorsal spinocerebellar tract
– Large diameter axons from the legs and trunk synapse on Clarke’s nucleus (C8-L2) in the medial intermediate zone of the ventral horn.
– The axons from Clarke’s nucleus ascend ipsilaterally in the lateral column (lateral to the corticospinal tract).
Cuneospinocerebeller tract (The dorsal spinocerebellar tract for the arms) – Large diameter axons from the arms ascend to the medulla in the cuneatus fassicle of the dorsal columns but bypass the cuneatus nucleus to synapse on the accessory cuneate nucleus.
In the medulla, these axons enter the cerebellum via the inferior cerebellar peduncle.
Spinocerebellar tracts - spinal border cells
Ventral spinocerebellar tract
– Originates from spinal border cells in the thoracic and lumbar ventral horn
– These axons decussate in the ventral commisure and ascend the spinal cord in the lateral column (lateral to the ALS).
Rostral spinocerebellar tract (the Ventral spinocerebellar tract for the arms)
– Originates from spinal border cells in the cervical ventral horn. Also decussate in the ventral commisure to join the ventral spinocerebellar tract.
These axons enter the cerebellum via the bilateral superior cerebellar peduncles. Some fibers decussate again, while others do not.
Blood supply to spinal cord
The spinal cord is supplied by a single anterior spinal artery and a pair of posterior spinal arteries.
– These arteries arise from the vertebral arteries.
The anterior spinal artery supplies the anterior 2/3of the cord, which includes the anterior horn, ALS, and corticospinal tracts.
The posterior spinal arteries supply the dorsal columns.
The spinal arteries narrow in the thoracic cord (may even be noncontiguous).
As a result, the spinal arteries can be divided into 3 longitudinal segments based on their blood supply
– C1-T2: supplied by radicular arteries from the vertebral and ascending cervical arteries
– T3-T7: spinalarteriesfromT3-T7aresuppliedby radicular arteries from intercostal arteries
– T8-conus: suppliedby radicular arteries from the artery of Adamkiewicz
Blood flow to these segments is reconstituted by radiculomedullary arteries.
The radiculomedullary arteries originate from radicular arteries.
Radicular arteries
Radicular arteries originate from segmental arteries, which include the ascending cervical, intercostal, lumbar, and sacral arteries.
There are thirty-one pairs of radicular arteries, each passing through the neural foramina to supply each spinal nerve, the vertebral body and the dura via a small dural branch.
Only 6 to 10 radicular arteries have radiculomedullary branches
– Their exact number and anatomic location is quite variable.
Spinal AVMs
Oculosympathetics
Aniscoria
Physiologic (same in dark/light)
Small pupil (greater in dark) - Horner’s
Large pupil (greater in light) - CN III
None in PURE afferent disease! This has APD
Testing for Horner’s - confirming the dx
Topical cocaine is used to confirm the clinical diagnosis of ocular sympathetic denervation, or Horner Syndrome (HS). Cocaine blocks re-uptake of norepinephrine (NE) by sympathetic nerve terminals in the iris dilator muscle, transiently increasing its concentration in the synaptic junction. Norepinephrine activates alpha1 receptors in the iris dilator to cause pupil dilation. In HS, cocaine fails to dilate the affected pupil as much as the unaffected pupil, but its indirect action makes it a weak dilator, and the test can give equivocal results. Cocaine is also a controlled substance and therefore difficult to obtain. A practical and reliable alternative to cocaine is apraclonidine, an ocular hypotensive agent that has a weak direct action on alpha1 receptors and therefore minimal to no clinical effect on the pupils of normal eyes. Patients with HS have denervation supersensitivity of the alpha1 receptors in the iris stroma of the affected eye, making the pupil dilator responsive to apraclonidine. In patients with HS, reversal of anisocoria occurs after bilateral instillation of apraclonidine 1% or 0.5%.
Cocaine
Urine drug test for cocaine will be positive for a few days after testing (5)
Apraclonidine
Denervation must be present long enough for receptor upregulation to have occurred (14) Positive tests have been noted within hours of a carotid dissection but the onset of denervation sensitivity are variable (15) False negatives can occur in the setting of acute Horner syndrome or in long-standing cases if strict “reversal of anisocoria” criteria used (16, 17) Apraclonidine has limited use in pediatric Horner syndrome due to the risk of CNS and respiratory depression (18)
https://www.ophthalmologyreview.org/articles/horner-syndrome-pharmacologic-diagnosis
Horner’s localization
HYDROXYAMPHETAMINE
Hydroxyamphetamine remains a useful tool for localization of the lesion once a diagnosis of Horner syndrome has been confirmed (20). However, it is limited by accessibility and some considerations detailed below. Since it’s still tested (and important to understand from a mechanistic and historical perspective), you still need to know how it works and what it does.
Mechanism of action: increases the release of norepinephrine from the presynaptic neuron (21). In intact presynaptic (3rd order, postganglionic) neurons, this results in pupil dilation; if this neuron is not intact, the pupil does not dilate.
Note anisocoria (which pupil is small, which pupil is larger)
Instill 1 drop of hydroxyamphetamine (1%) in each eye
Wait 45-60 minutes
Re-evaluate anisocoria
Results:
In patients with normal pupils, there is a symmetric 2 mm dilation of each pupil (anisocoria remains) (22).
In patients with Horner syndrome, the reaction is based on whether or not there is an intact 3rd-order (postganglionic) neuron (23):
Both pupils dilate: intact 3rd-order neuron (localizes to 1st- or 2nd-order neuron)
Only non-Horner pupil dilates: not intact 3rd-order neuron (localizes to 3rd-order neuron)
https://www.ophthalmologyreview.org/articles/horner-syndrome-pharmacologic-diagnosis
Tonic pupil
Adie tonic’s pupil denotes a pupil with parasympathetic denervation that constricts poorly to light but reacts better to accommodation (near response)
Light-near dissociation causes
Pupils in coma
Metabolic - small, reactive
Midbrain - mid position, fixed
Pons - pinpoint
Third nerve (uncal) - dilated, fixed
Pupils in coma
Metabolic - small, reactive
Midbrain - mid position, fixed
Pons - pinpoint
Third nerve (uncal) - dilated, fixed
CN IV
Innervates superior oblique - acts to depress, best in ADduction
Inferior oblique
CN III
Action elevation, best in ADduction
Actions of extraocular muscles
Aberrant regeneration of the third nerve
Lid/gaze dyskinesis: retraction on downgaze, adduction
Pupil/gaze dyskinesis: constriction on downgaze, convergence/adduction
Indicates trauma, compressive etiology
Aberrant regeneration of the third nerve
Lid/gaze dyskinesis: retraction on downgaze, adduction
Pupil/gaze dyskinesis: constriction on downgaze, convergence/adduction
Indicates trauma, compressive etiology
Fourth nerve palsy signs
If nerve - ipsilateral eye, if nucleus/fascicle before decussation- contralateral eye
Bincoular, vertical/oblique diplopia, worse in contralateral and down gaze
Fourth nerve palsy often presents with a head tilt away from the affected eye.
With ipsilateral head tilt, the medial utricle is excited.
The medial utricle projects to the contralateral trochlear and oculomotor nucleus through the MLF.
With ipsilateral head tilt, the ipsilateral eye elevates (sup rectus) and intorts (sup rectus and sup oblique) while the contralateral eye depresses (inf rectus) and extorts (inf rectus and inf oblique)
The ocular counterrolling reflex (top) causes a compensatory cyclorotation of both eyes to maintain the subjective visual vertical. On left head tilt, the right eye infraducts and excyclotorts and the left eye supraducts and incyclotorts relative to the position of the head and true vertical. Head velocity signals are encoded by the semicircular canals. The eyes maintain this position tonically because of otolithic inputs from the utricle and saccule on the side of the lower ear. In a right superior oblique palsy (middle right), the right eye is extorted because of the lack of intorsion from the paretic superior oblique. Increased activity to the other intorter—the right superior rectus—causes a hypertropia that worsens when more intorsion is demanded by tilting the head to the right (middle left). A left ocular tilt reaction caused by abnormalities in the vertical vestibulo-ocular reflex projections from the left vestibular system causes a left hypotropia with bilateral torsion in the direction of head tilt (lower right). For each eye, the line through the cornea represents the torsional vertical axis.
Sixth neve palsy
Binocular, horizontal diplopia
Increased in ipsilateral gaze
Worse at distance
Skew deviation
Vertical misalignment
Hypertropia
Midbrain - ipsilateral
Medulla - contralateral
Skew deviation
Vertical misalignment
Hypertropia
Midbrain - ipsilateral
Medulla - contralateral
Downbeat, periodic alternating nystagmus
Localization: cervicomedullary junction,
Downbeat - Clonazepam, lioresal, gabapentin
Periodic alternative - lioresal, phenytoin
Upbeat
Localization: cerebellum, pontomesencephalic, pontomedullary
Convergence retraction
Localization: dorsal midbrain
Brun’s
Localization: cerebellopontine angle
Seesaw
Parasellar>>midbrain
Treatment: Lioresal, clonazepam
Oculopalatal myoclonus
Treatment: Valproic acid, gabapentin
Superior oblique myokymia
Treatment: Carbamazepine, gabapentin
Oculomasticatory myorhythmia
Treatment: CTX
Dx and tx of benign positional vertigo
https://geekymedics.com/dix-hallpike-and-epley-manoeuvres-osce-guide/
Ear down/torsional direction tells you which ear is affected
If upbeat - right PC, if downbeat right AC
Opsoclonus
Features and Causes of Opsoclonus
Dramatic involuntary conjugate multidirectional saccades (saccadomania)
Differs from flutter (no vertical component)
Causes:
- Paraneoplastic (neuroblastoma, anti-Ri, anti-Hu antibodies)
- Postinfectious, encephalitis
- May be benign in neonates
CRAO
Inherited retionpahties - leukodystrophies (Tay-Sachs, Niemann-Pick)
Cherry red spot
Inherited retionpahties - VHL
AD
Retinal angiomas, cerebellar hemangioblastoma
Inherited retionpahties - Kearns-Sayre syndrome
Mitochondrial disorder
Retinal degeneration, chronic progressive external ophthalmoplegia, cardiac conduction defects
Inherited retionpahties - Tuberous sclerosis
Autosomal dominant
Retinal hamartoma, epilepsy, adenoma sebaceum, renal angiomyolipoma, cardiac rhabdomyoma, ungual fibroma
Inherited retionpahties - SCA type 7
AD
Retinal degeneration and progressive ataxia
Acute papilledema
Chronic papilledema with hemorrhages resolved and “champagne cork gloss”
Pseudopapilledema
IIH
Foster Kennedy Syndrome
Optic nerve swelling and contralateral optic nerve pallor Intracranial mass (i.e., subfrontal meningioma) causing compressive optic neuropathy and papilledema
Optic neuritis
Nonarteric ischemic optic neuropathy
Nonarteric ischemic optic neuropathy
Ischemic optic neuropathy
Inflammatory optic neuropathy
Temporal arteritis
Compressive optic neuropathy
Optic neuropathy and neoplasms
Leber’s hereditary optic neuropathy
Mitochondrial, maternal inheritance (11778)
9:1 male predominance
Age 20-30
Painless sequential visual loss
Hyperemia, mild swelling, telangiectasias
Leber’s hereditary optic neuropathy
Mitochondrial, maternal inheritance (11778)
9:1 male predominance
Age 20-30
Painless sequential visual loss
Hyperemia, mild swelling, telangiectasias
Kjer’s dominant optic atrophy
Temporal excavation
Childhood presentation, insidious onset, then stable course
OPA gene mutation
Toxic/nutritional optic neuropathies
Painless, insidious, symmetric
Centrocecal scotoma
Causes: Tobacco-alcohol, B12, ethambutol, amiodarone
Optic nerve hypoplasia
Surrounding visible sclera
Evaluate for: Septo-optic dysplasia (DeMorsier’s syndrome)
– Absent septum pellucidum – Endocrine abnormalities – Cortical heterotopia
Superior disc hypoplasia associated with maternal diabetes
Chiasmal field deficits
Junctional scotoma
Inferior nasal fibers carries visual inferior from superior temporal visual field of contralateral optic nerve
Visual fields in LGN - anterior choroidal vs posterior choroidal
Optic radiations
Optic radiations
Occipital field defects
Macular sparing
The favored explanation for why the center visual field is preserved after large hemispheric lesions is that the macular regions of the cortex have a double vascular supply from the middle cerebral artery (MCA) and the posterior cerebral artery (PCA). If there is damage to one vascular pathway, like in the case of a MCA or PCA stroke, there is still another blood supply that the macular portions of the visual cortex can rely on. Vision in the center of the visual field is then preserved whereas vision in peripheral areas is lost due to the resulting infarct.
Cortical layers
I – molecular (aka tangential) layer. Abuts pia. Consists of horizontal cell axons and dendrites from pyramidal cells in other layers. NO CELL BODIES
II - external granular layer. Granule cell dendrites from molecular layer and axons to deeper layers.
III - external pyramidal (suprastriate) layer. 2 sublayers of pyramidal cells 1) superficial-medium cells (ipsilateral) 2) deeper-large cells (contralateral). dendrites reach to layer I, and axons to other cortical areas.
IV - internal granular layer (external band of Baillarger). stellate cells which mediate between inputs from other areas to pyramidal dendrites and axons, and from pyramidal dendrites and axons. Often divided into two sublayers IVa and IVb. External band of Baillarger is dense horizontal plexus of myelinated fibres in this layer.
V - internal pyramidal layer. pyramidal cells intermingled with granule and Martinotti cells. The dendrites of the large-sized pyramidal cells reach to layer I, the dendrites of the small-sized pyramidal cells reach only to layer IV, or stay within layer V.
VI – polymorphic layer (aka multiform or fusiform layer). Consists of spindle cells with axons perpendicular to the cortical surface. Larger ones send dendrites to layer I and smaller ones to layer IV.
White matter cortical connections
Projection fibers to and from the cortex - internal/external capsule
Commissural Fibers between hemispheres - anterior and posterior commissure and corpus callosum
Association Fibers between cortical areas within a hemisphere - arcuate fascilius, U fibers
Nucleus accumbens
Seen where the caudate and putamen are not divided by the anterior limb of the internal capsule
Septal nuclei and Nucleus Basalis of Meynert
Amygdala
Hippocampal formation
Papez circuit
Developmental of ventricle system
Ventricular System
Begins as a hole or space in the middle of the developing nervous system that runs from the most rostral end (lamina terminalis) down through the spinal cord
As the brain vesicles grow, the ventricular system grows and expands along with it.
BBB
Regulated interface between the peripheral circulation and the CNS
Components include endotheilial tight junctions, basal lamina, astrocyte processes
Tight junction is an intricate complex of transmembrane (junctional adhesion molecule-1, occludin, and claudins) and cytoplasmic (zonula occludens-1 and -2, cingulin) proteins linked to the actin cytoskeleton
A small number of regions in the brain (circumventricular organs, pineal gland) do not have a blood–brain barrier
Generally permeable to smaller, lipophillic molecules
Impermeable to most macromolecules, microorganisms
Specific activated transport for glucose and amino acids
Parasympathetic nervous system
Cell bodies located in the brain and sacral (S2-4) spinal cord
– Axons exit via cranial or sacral nerves and synapse with neurons located in a ganglion that is integrally associated with the target organ/viscera (Long pre-synaptic and short post-synaptic)
– Sacral paraspympathetic innervation includes bladder, ureter, kidneys, rectum, and colon beyond the left colonic flexure
Parasympathetic nervous system
Cell bodies located in the brain and sacral (S2-4) spinal cord
– Axons exit via cranial or sacral nerves and synapse with neurons located in a ganglion that is integrally associated with the target organ/viscera (Long pre-synaptic and short post-synaptic)
– Sacral paraspympathetic innervation includes bladder, ureter, kidneys, rectum, and colon beyond the left colonic flexure
Sympathetic nervous system
The second order sympathetic neurons arise from the intermediolateral column from T1-L2.
Each spinal nerve from T1-L2 contains sympathetic axons, which can either
– Leave the spinal nerve in a white communicating ramus to enter the sympathetic chain to either synapse at that level or ascend and descend in the sympathetic chain.
– Continue on to synapse in collateral ganglia (celiac, superior mesenteric, and inferior mesenteric ganglia) near their target.
All spinal nerves receive third order sympathetic neurons from the sympatheic chain via a gray communicating ramus.
CERVICAL spinal nerves do not have white rami, but they do have grey rami
Recall that there are eight cervical nerves -> eight sets of grey rami.
The cervical ganglia have undergone fusions
– superior cervical ganglion joins to C1-4
– middle cervical ganglion connects to C5 and C6
– inferior cervical ganglion connects to C7 and C8
Spinal nerves below L2 do not have white rami, but they do have grey rami
All presynaptic fibers for ganglia L3-5 and S1-4 enter the lateral chain via white rami of L1,L2.
Unlike with the cervical ganglia, there has been no fusion between any of the lumbosacral series
The coccygeal ganglia merge into a single midline ganglion.