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Neuro Path, Brainstem Rule of 4:
IMG_2018, See Narcolepsy in Psych…
Neuro Path
Opthamology
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2. Bitemporal hemianopia
(pituitary lesion, optic chiasm)
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4. Upper quadrantanopia
(contralateral temporal lesion, MCA)
- Upper quadrantopia is seen in contralateral temporal lesions
- Right upper quadrantopia specifically is associated with Wernicke's aphasia
5. Lower quadrantanopia
(contralateral parietal lesion, MCA)
6. Hemianopia with macular sparing
(contralateral occipital lesion, PCA)
7. Central scotoma (eg, macular degeneration)
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Common brain lesions
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Dorsal midbrain (pretectal area of midbrain, "tectum")
Parinaud syndrome
- stroke, hydrocephalus, pinealoma →
- vertical gaze palsy
- pupillary light-near dissociation (Argyll-Robertson pupil)
- lid retraction
- convergence-retraction nystagmus
- See Pupillary light reflex image above
Reticular activating system (midbrain)
- consciousness (sleep/wakefulness)
- see basilar stroke; if RAS affected → coma
Cerebellar lesions
Cerebellar vermis (midline cerebellar lesion)
- affects axial and proximal movement → wide-based, "drunken sailor" gait (truncal ataxia)
- nystagmus
- degeneration associated with chronic alcohol use
Cerebellar hemispheres (lateral cerebellar lesion)
- affects voluntary movement of extremities → intention tremor, limb ataxia, loss of balance
- damage to cerebellum → ipsilateral deficits (fall toward side of lesion)
Red nucleus (midbrain)
- decerebrate + decorticate
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Spinal lesions
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Tabes dorsalis
1, 3° syphilis
- broad-based ataxia
Syringomyelia
- see entry under embryo, FA 506
Vitamin B12 deficiency/Subacute combined degeneration (SCD) 
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Friedreich ataxia
• most common hereditary form of ataxia
• auto recessive mutation in frataxin gene → degeneration of posterior columns spinocerebellar tracts
• symptoms usually begin in adolescence, leads to shortened lifespan
• symptoms include: progressive ataxia, dysmetria, dysarthria
• compare to vitamin E deficiency
Neurodenegerative disorders
- see separate coggle on these
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Common CN lesions
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CN 7 lesion (Bell's palsy)
- know this vs. UMN and LMN face lesions, FA pg. 550
CN 3 damage/palsy
- FA 561
- ischemic stroke, uncal herniation, PCom aneurysm ("down and out"), cavernous sinus thrombosis, midbrain stroke
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Demyelinating disorders
Central (CNS)
Multiple sclerosis
- autoimmune; CD4/Th cells activated against CNS (can be triggered by EBV, HHV-6, UV radiation, ↓ vitamin D, smoking → recruit macrophages/microglia, CD8 T cells, and B cells → extensive inflammation → damages BBB → ↑ inflammatory cell recruitment into the CNS (with the vessel wall remaining intact, unlike in CNS vasculitis) → demyelination (focal, with partial preservation of axons; acute plaques) → loss of axons + atrophy of oligodendrocytes (chronic plaques) → gliosis → inadequate remyelination
- acute plaques:
- patchy demyelination
- axonal sparing
- Histo: perivenular inflammatory infiltrates with autoreactive T cells and macrophages against myelin (infiltrating macrophages contain myelin debris)
- recruitment of B lymphocytes to the perivascular spaces → formation of myelin-specific antibodies
- chronic plaques
- necrosis (neuronal death)
- astrocytes hypertrophy and hyperplasia (ie, glial scar)
- most CNs unaffected (because CNS affected and CNs are peripheral nerves) except CN 2 because 2 is the only CN derived from diancephalon (all other CNs derived from neural crest)
- Diagnosis:
- ↑ IgG and myelin basic protein in CSF
- periventricular plaques are commonly seen as hyperintense lesions on T2- weighted MRI of the brain and spinal cord
- Oligoclonal IgG bands represent the IT production of immunoglobulins and are highly sensitive for multiple sclerosis
(but NOT specific; seen in any CNS disease involving humoral immunity like vasculitis or infection)
e.g. cerebral vasculitis (CV) can resemble MS with neurologic deficits that may wax and wane, and oligoclonal bands can be seen. BUT patients with CV typically develop severe headache, and systemic symptoms (eg, fever, fatigue, night sweats) are common
- Presentation/symptoms:
- episodic, progressive neurologic deficits that may involve multiple anatomic regions within the CNS (ie, separated in space and time)
- optic neuritis (presents as transient blurred vision and eye pain with movement) with Marcus Gunn pupil
- internuclear ophthalmoplegia (INO) due to lesions in medial longitudinal fasciculus
- cerebellar dysfunction (e.g. intention tremor, broad-based gait, ataxia, etc.)
- Lhermitte sign (electrical sensations down the back/limbs with neck flexion)
- sensory/motor symptoms (e.g. arm numbness and tingling)
- fatigue
- Uhthoff phenomenon (symptoms worsen with heat/increased body temperature (eg, exercise, bathing) due to slowing of neuronal conduction in unmyelinated nerves)
- Urge incontinence is most common, BUT as the disease progresses, the bladder can become atonic and dilated, leading to overflow incontinence
- dyssynergic defecation (if the internal or external anal sphincter or, more commonly, the puborectalis muscle fails to relax, stool remains in the rectal vault despite attempts to initiate bowel movements (dyssynergia), resulting in chronic constipation)
- can compress trigeminal nerve root → trigeminal neuralgia
- Associations:
- most often Caucasian women in 20s-30s
- HLA-DRB1
- more common in those who grew up farther from the equator (cold climates, also USA, Europe) and with low vitamin D levels
- smoking
Peripheral (PNS)
Guillain-Barré syndrome (GBS)
- CN deficits (because CNs are peripheral nerves)
Acute inflammatory demyelinating polyneuropathy
- most common subtype of GBS
Osmotic demyelination syndrome/central pontine myelinolysis
- can cause "locked in" syndrome
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Progressive multifocal leukoencephalopathy (PML)
Others
- Krabbe disease (lysosomal storage disease)
- metachromatic leukodystrophy (lysosomal storage disease)
- adrenoleukodystrophy (peroxisome disease)
Embryological/Congenital
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Syringomyelia
- see entry under spinal cord lesions, FA 548
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Misc.
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Heat stroke (see fever vs. heat stroke, FA pg. 534)
Diabetic neuropathy
- usually peripheral ("glove and stocking" distribution); affects the feet first (longest nerves); moves up; by the time it affects the knees it will start affecting the hands (around same length nerves)
- also involves autonomic degeneration (e.g. GERD, gastroparesis (see GI), diabetic diarrhea)
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Brain Hemorrhage
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Intracranial hemorrhage
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Subdural hematoma
- rupture of bridging veins (happens in the elderly, alcoholics, shaken baby syndrome) → collection of blood under dura mater (dura still attached to skull)
- DOES cross suture lines; thus it will be concave/crescent-shaped ("banana shaped")
- venous bleed, so builds more slowly; can take several days, weeks, or even months after initial injury for patient to present (venous system is the lower pressure, storage vascular system, so venous bleeds bleed at a slower rate), but it can also be acute
- "suB = Banana shaped"
Subarachnoid hemorrhage
- "worst headache of my life," "thunderclap headache"
- Xanthochromia (yellow CSF due to presence of bilirubin; usually a result of hemoglobin breakdown that occurs within 12 hours after bleeding into the CSF)
Intraparenchymal hemorrhage
- can be caused by ischemic stroke
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Otology (ear)
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Vertigo
- see the mindmap sheet I made
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Central vertigo
- e.g. posterior circulation stroke
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Meningitis
- see micro for most info
Bacterial meningitis
- Neutrophilic predominance
- WBC > 1000
- Glucose < 45 (low glucose, bacteria "eat" it)
- Protein > 250 (high protein)
Viral meningitis
- lymphocytic predominance
- WBC < 500
- glucose is normal or slightly low
- protein < 150
Fungal/TB meningitis
- can also cause low glucose
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Ischemic brain disease
Ischemic stroke
Watershed infarcts (due to severe hypoperfusion)
- watershed zones also common sites of brain metastases
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Anterior circulation
- If total anterior circulation stroke:
• Hemiplegia
• Homonymous Hemianopia
• Higher cortical dysfunction
- If partial anterior circulation stroke:
• 2/3 of above
ACA
- Contralateral hemiparesis/hemiplegia + hemisensory loss (lower limb)
- Can have urinary incontinence (frontal lobe has frontal micturition center)
- Behavioral symptoms (frontal lobe affected)
- Reemergence of primitive reflexes (these are inhibited by a mature frontal lobe)
- Can be compressed by subfalcine/cingulate herniation
- These strokes are rare because of collateral circulation from the anterior communicating artery (ACom, near optic chiasm in Circle of Willis); BUT rupture of berry aneurysms in ACom can cause an ACA stroke (compression as opposed to rupture can cause other symptoms)
MCA (parietal lobe + some of frontal lobe)
- commonly thrombotic or embolic strokes (due to atherosclerosis)
- can also be due to rupture of berry aneurysm
- contralateral hemiparesis/hemiplegia + hemisensory loss (face + upper limb; remember cortical spares the forehead!)
- Cortical signs (hemineglect, aphasia, visual field changes)
- Different effects depending on whether dominant or nondominant parietal cortex (right handed people are left hemisphere dominant)
- MCA can also cause a lesion in the frontal eye fields (eyes will look towards the lesion, away from the hemiparesis)
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Posterior circulation
- isolated homonymous hemianopia
- Cerebellar syndrome (gait ataxia, dysarthria, etc.; can also have central vertigo)
- loss of consciousness
PCA
- affects occipital lobe
- isolated visual field problems (visual field changes with no other changes)
- different effects depending on whether dominant or nondominant occipital lobe is affected
Dominant occipital (usually L; and splenium or corpus callosum)
→ alexia without agraphia (cannot read what you write)
Nondominant occipital (usually R)
- prosopagnosia (face blindness
- contralateral homonymous hemianopia with macular sparing
(Image shows left side homonymous hemianopia with macular sparing, so this would point to a right sided occipital lesion)
Why macular sparing?
→ the very tips of the occipital cortices are where input of macular vision is received; this area has dual blood supply from MCA and PCA and thus forms a watershed zone, protecting macular vision when only one of the major cerebral vessel distributions is affected
Basilar a. "locked in" syndrome
- affects lower midbrain, pons, and medulla
- makes sense, since pontine arteries and many others come off basilar
- corticospinal (+ corticobulbar) tract affected
- causes "locked in" syndrome → quadriplegia + loss of face, mouth, and tongue movements (bulbar palsy) + loss of horizontal eye movements (can only blink and vertically move eyes)
- Reticular activating system (RAS) controls consciousness (arousal/wakefulness) and is in the midbrain; if affected → coma, if RAS spared → consciousness preserved
Pons affected?
• NOTE: These are unlikely to come from basilar artery strokes (locked-in could come from that), but just listing them here so you remember what happens with a lesion in the pons
Paramedian pontine reticular formation (PPRF) lesion
- Eyes look away from brain lesion (toward side of hemiplegia)
- Can have loss of horizontal eye movements (if bilateral?)
- does this have something to do with the ocular nuclei?
Central pontine myelinosis/Osmotic demyelination syndrome
- see under "demyelinating disorders"
Inferior cerebellar a.
- both come off the basilar
Anterior inferior cerebellar a. (AICA)
- facial nucleus effects are specific to AICA lesions
Lateral pontine syndrome
- facial nucleus affected → ipsilateral facial paralysis (like Bell's), ↓ lacrimation, ↓ salivation, ↓ taste from anterior 2/3 of tongue; also hyperacusis (more sensitive to ordinary sounds)
- vestibular nuclei affected → vomiting, vertigo, nystagmus
- spinothalamic tract, spinal trigeminal nucleus affected → ↓ pain/temp sensation (ipsilateral face, contralateral body)
- sympathetic fibers affected → ipsilateral Horner's
- middle and inferior cerebellar peduncles affected → ipsilateral ataxia, dysmetria
- labyrinthine artery affected → ipsilateral sensorineural deafness, vertigo
Posterior inferior cerebellar a. (PICA)
- comes off vertebral a.
- nucleus ambiguus effects are specific to PICA lesions
“Don’t pick a (PICA) horse (hoarseness) that can’t eat (dysphagia).”
Lateral medullary (Wallenberg) syndrome
- Nucleus ambiguus affected (CN 9, 10, 12) → dysphagia, hoarseness, ↓ gag reflex, hiccups
- vestibular nuclei affected → vomiting, vertigo, nystagmus
- lateral spinothalamic tract, spinal trigeminal nucleus affected →
↓ pain/temp sensation (ipsilateral face, contralateral body)
- sympathetic fibers affected → ipsilateral Horner's
- inferior cerebellar peduncle affected → ipsilateral ataxia, dysmetria
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Aneurysms
Saccular/berry
- Rupture → subarachnoid hemorrhage
ACom
- Near optic chiasm in Circle of Willis
- Compression → bitemporal hemianopsia, visual acuity deficits (pushing on optic chiasm)
- Rupture → ACA stroke signs
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PCom "(down and out" eye)
- PCom is very close to CN 3 (see picture) so PCom berry rupture → ipsilateral CN3 palsy → "blown pupil," ptosis, "down + out" eye
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Primary brain tumors
Adult
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Oligodendroglioma• "fried-egg" on histo
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Note on why hyperventilation helps decrease ICP:
- CO2 vasodilates; if someone has ↑intracranial pressure → ↓ hyperventilate → ↓PaCO2 → vasoconstriction (because ↓ vasodilation) → ↑ cerebral vascular resistance → ↓ cerebral blood volume → relieved ICP
Brainstem Rule of 4:
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- See Narcolepsy in Psych Coggle (even though it's a neuro problem...)
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- add stroke notes mindmap
- add dizziness/vertigo notes mindmap (simlipfy it)
- add in BATS Drink Blood mnemonic for sleep stages
- add tracks sheet (DCML, corticospinal, etc.)
- add in an example problem or 2 that you do from the michigan site: https://www.med.umich.edu/lrc/neurologic2016/
- add in CN reflexes sheets (add the relevant one to the entry for Parinaud syndrome)
- add in notes/explanation in ipad FA for MLF lesion/INO
- add in anything else you took lots of notes on
- add more info to all the things like epidural hematoma etc.
- look through Zonkoo neuro and add in info, e.g. add info red nucleus under the entry in common brain lesions etc.
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1 - most common location for berry aneurysms (ACom)
2 - 2nd most common location
Note:
Unilateral defects generally occur before the optic chiasm; bilateral defects generally occur beyond/after the optic chiasm (chiasm is where the optic nerves cross)
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Marcus Gunn Pupil:
- aka Relative Afferent Pupillary Defect
- loss of pupillary light reflex in affected eye
- EXAMPLE: Marcus Gunn/RAPD in left eye:
- Shine light in right eye → both eyes constrict (consensual response intact)
- Shine light in left eye → both eyes dilate
- This tells you the problem is not an isolated ocular one e.g. cataracts because the eye constricted properly on consensual response; therefore the problem is with the optic nerve (left optic nerve in this case)
Internuclear ophthalmoplegia (INO)
- caused by lesion in medial longitudinal fasciculus (MLF)
- MLF has tracts connecting CN 6 + 3, coordinates eyes to move in the same direction
- MLF is highly myelinated (must communicate very quickly so eyes move at the same time) → hence affected in MS
- lesions may be unilateral or bilateral; if bilateral, more likely due to MS or stroke
- NORMAL function of MLF tracts:
CN 6 (innervates lateral rectus m.) → activates ipsilateral lateral rectus m. (contracts it) → stimulates the contralateral CN 3 (via MLF) to contract contralateral medial rectus m. (adduct contralateral eye, so both eyes will look in the same direction
e.g. L CN 6 → L lacteral rectus contracts (abducts) + R MLF tells R CN 3 to contract medial rectus → R eye adducts → both eyes look left
- ABNORMAL function of MLF tracts (example with R MLF lesion):
L CN 6 → L lacteral rectus contracts (abducts) but R MLF cannot tell R CN 3 to contract medial rectus → R eye does not adduct + L eye nystagmus
- I think of it as, the eye that wanted to abduct is indecisive; it wanted to look left in this case, but when the R eye wouldn't join it was like I don't know if I should....so it goes back and forth → nystagmus
- Thus INO causes Ipsilateral adduction failure, Nystagmus Opposite
- R MLF lesion → R eye fails to adduct, L eye nystagmus
- L MLF lesion → L eye fails to adduct, R eye nystagmus
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- DCML + corticospinal cross in medulla
- Spinothalamic crosses immediately