Neuroanatomy cortex Ventricles CN I-VI Flashcards
Spina Bifida
Neural tube fails to close
Happens around 4th week
Anterior Closure; day 25; Anencephaly
Posterior Closure; day 27; Meningocele
Glial Cells
Oligodendrocytes: Form Myelin
Astrocytes: Support, Nutrition, Vasoconstriction/dilation, removal of K+ and neurotransmitters from synapse, part of BBB; Release Glutamate (Excitatory)
Microglia: CNS Immune defense; Phagocytosis, Antigen presenting to T-Cells
BBB
CNS is Immune privileged due to BBB
Epithilial Tight jxn
Basement membrane
Astrocytes
Cereberal Cortex
Neocortex and Allocortex
NeoCortex
6 cell layers: Molecular External Granular External Pyramidal Internal Granular Internal Pyramidal Multiform/Fusiform
AlloCortex
ArchiCortex: Thalamus; 3 cell layers
PaleoCortex: Olfactory cortex
Frontal Lobe functions
1) Movement:
Motor Cortex
Lesion = Contralateral Spastic Hemiparesis
Premotor area
Motor planing and sequencing
Frontal eye field
Lesion = Ipsilateral eye deviation
2) Language and speech:
Broca’s area = Left inferior central Gyrus (Opercular part)
Lesion = nonfluent aphasia
3) Cognition and Personality:
Dorsal Lateral Frontal Cortex
Executive function, problem solving, Abstract, working memory
Supplemental Motor Area and Anterior Cingulate Gyrus
Lesion = Akinetic Mutism
4) Behavior, motivation, judgement:
Orbitofrontal Cortex
Social Behavior, impulsiveness
Lesion = frontal relase signs (grasp, suck), abulia
Parietal Lobe function
2 important functions:
1) Sensory Cortex and Sensory integration
2) Spatial body map in enviornment
Parietal Lobe lesions
Dominant Lobe (left): Gerstmann's syndrome: Right-left confusion, Finger agnosia, acalculia, agraphia
Non Dominant Lobe:
Contralateral Sensory neglect, Construction apraxia, dressing apraxia, denial of deficit (anosognosia)
Bilateral Lobe lesion:
Balint’s syndrome: Ocular Ataxia, Oculomotor apraxia, Simultanagnosia.
Temporal Lobe functions
1) Auditory Cortex : Gyrus of Heschl
2) Language:
Dominant (Left): Comprehension, Wernicke’s area
Non-Dominant (right): Prosody (rhythm)
3) Visual recognition: Ventral “what” pathway
Lesion = Prosopagnosia (inability to recognize faces)
4) Hippocampus: Longterm memory consolidation
Bilateral Lesion = Kluver-Bucy syndrome.
5) Olfactory cortex
Lesion = Anosmia
Kluver Bucy Syndrome
Lesion of bilateral Hippocampus (Temporal Lobe)
Hyperphagia,
Hypersexuality,
Visual Agnosia
Gerstmann’s Syndrome
Lesion of Dominant Parietal Lobe Right-Left Confusion Finger Agnosia Agraphia Acalculia
Occipital Lobe functions
1) Cortical Visual Perception (Visual cortex)
2) Color discrimination
Unilateral Occipital lobe damage
Contralteral Homonymous Hemianopsia
Bilateral Occipital Cortex lesion
Cortical Blindness.
If a/w denial and confabulation = Anton Syndrome
Left Occipital lobe lesion
Involving the splenium of Corpus Callosum
Alexia without Agraphia (a disconnection syndrome)
can not read but can write. disconnection between visual and motor cortex and the memory/name recall area.
Foster-Kennedy Syndrome
caused by Frontal Lobe tumor
Compression of one Optic nerve = visual field loss
Increased ICP = Papiledema
Compression of CN I = anosmia
CN I
Olfactory
Does not join brain stem ( CN I and II)
Does not relay through Thalamus
CN III
Occulomotor
Travels through Cavernous Sinus
Somatic part Innervates:
Levator Palpebrae (Opens the eye)
Superior Rectus, Inferior Rectus, Medial Rectus, Inferior Oblique
Visceral part:
Parasympathetic nerves to Iris Sphincter from
Edinger-Westphal Nucleus
Constricts the Pupil.
CN III
Occulomotor
Travels through Cavernous Sinus
Arises from Midbrain
Somatic part Innervates:
Levator Palpebrae (Opens the eye)
Superior Rectus, Inferior Rectus, Medial Rectus, Inferior Oblique
Visceral part:
Parasympathetic nerves to Iris Sphincter from
Edinger-Westphal Nucleus
Constricts the Pupil.
Pupil Sparing CN III Palsy
Most likely Diabetes Neuropathy.
May also be vasculitis, atherosclerosis.
Central Fibers are damaged.
CN III Palsy with Contralateral Hemiparesis
Midbrain Corticospinal Tract Infarct.
(Corticospinal Tract Decussate at Medulla)
Contralateral UMN hemiparesis and Ipsilateral CN III Palsy
CN IV
Trochlear
Travels through Cavernous Sinus
Innervates:
Superior Oblique
Long course; therefore, isolated Neuropathy common
Diabetes, Trauma, HTN, Atherosclerosis
CN IV
Trochlear
Travels through Cavernous Sinus
Arises from Midbrain
Innervates:
Superior Oblique
Long course; therefore, isolated Neuropathy common
Diabetes, Trauma, HTN, Atherosclerosis
CN VI
Abducent
Travels through Cavernous sinus
Arises from Caudal Pons
Innervates:
Lateral Rectus
Most Common isolated CN Nerve palsy due to long course
causes: SAH, Trauma, elevated ICP, Meningitis
CN VI Palsy
Vertical Diplopia
Estropia (eye adducted)
Duane Syndrome
Congenital absence of CN VI
Mobius Syndrome
underdevelopped CN VI and VII
Facial paralysis and inability to move the eyes
Pontine infarct
at Middle Cerebellar Peduncles
Can Affect Corticospinal tract and CN VI:
Contralateral UMN Hemiparesis
CN VI palsy (horizontal diplopia, Estropia)
Pupilary Constriction
Parasympathetic
CN III Via Edinger-Westphal Nuclei
Ciliary Ganglion as the relay Nucleus
Pupilary Dilation
Sympathetic
Via Internal Carotid Artery
Pupilary Dilation
Sympathetic
Carried on the Internal Carotid Artery
Marcus Gunn Pupil
Relative Afferent Pupilary Defect (RAPD)
Light into good eye both pupils constrict (Direct and Consensual)
Light into the bad eye. Light is not detected due to the lesion of the Optic nerve, etc.
Therefore both Pupils Dilate.
Argyll-Robertson Pupil
Light-Near dissociation
a/w Neurosyphilis of midbrain
Pupils Accomodate but Do not react to light
pupil constrict with near vision but do not constrict with light
Adie’s Myotonic Pupil
Degeneration of Ciliary Ganglion or post Ganglionic neurons.
Mid-Dilated Pupil
Poorly reactive to light
Dorsal Midbrain Syndrome
Parinaud’s Syndrome
Damage to dorsal midbrain
- Upgaze paralysis
- Light-Near dissociation in mid-dilation (Pseudo Argyll-Robertson)
- Eyelid Retraction (Collier’s sign)
- Conjugate downgaze in primary position (Setting Sun sign)
Horner’s Syndrome
Sympathetic denervation (Carried on Internal Carotid Art)
Miosis
Ptosis
Hemi (face) Anhydrosis