66. NeuroIntervention Radiology



Neurointerventional Radiology

Principals
- aneurysms - dome needs to be protected

Embolizations
- liquid embolic agent or embospheres
- liquid agest are onyx, glue, and squid

Onyx (superbond)
- onyx touches blood and solidifies
> black color
> if near skin causes black tattoo
- needs DMSO in catheter before placing onyx (otherwise clot catheter)
> DMSO smell terrible

Glue (NBCA)
- looks like onyx, but do not stain the skin (in facial AVMs)
> solidifies w/ blood & saline, so use D5W (flush D5W)
- mix (glue & oil, ratio 3:1) (higher ratio - low coagulation time)
- radiopaque

Squid
- smaller particle size when compared to onyx

Embospheres
- mix liq & microspheres
- transient embolization

Stents
Extracranial stenting
- extracranial carotid artery stenting (CAS)
> precise (open cell)
> xact (closed cell)
> cristallo (hybrid)

Precise
-non-tapered (equal diameter)
>6 mm x 40 mm

Xact
-tapered (can change size)
>6-8 mm x 40 mm

Intracranial stenting
- intracranial: atlas, onyx stent, cardiology stents, and flow diverting stents

Atlas
-deploy-open, no radioforce

Onyx
- pressure ballon
> pressure seen in the hand
- stent can be messed up w/ size due to atherosclerosis

Cardiology stent
- higher radioforce
- not common in SNC because SNC has small adventia and intima

Flow divert stent
- higher metal (30%) when compared to other stents (17%)
- pipeline, FRED, surpass, silk vista baby
- close aneurysm by itself


Coils
- many brands
- diameter (1st number) and length (2nd number)
- coil the way that they like

Closure devices
- 4 main devices
> Perclose (suture-mediated)
> Minks (extravascular sealant)
> Angioseal (intravascular sealant)
> CELT (mechanical non-suture)

Perclose
- suture
- subcutaneous venous bleeding (no pulsatile)

Mynx
- collage and plug, with a tiny little bump in the artery, which dissolves with time
- less robust closure (5-6 French in diagnostic procedure)

Angioseal
- deploys a plastic foot plated
- problem is atherosclerotic plaques, wrong anatomic positioning leading to bleeding (not closing)




CELT
- deploy a small disc sitting in the artery inside & outside
- can deploy in other places, causing ischemia
- radiopaque, can be localized



65. NeuroSonology


NeuroSonology


Carotid US
- memorize velocities
- most important parameter is ICA PSV; the others are additional
> for results, described based on what parameter was used
- colors are related to flame: blue high velocity (turbulent flow)


Angle
- most appropriate is 60 degrees interfere velocities

Transcranial Doppler (TCD)


64. Diplopia

Diplopia!
Charles Wheatstone (1802 – 1875)
Royal Medal of the Royal Society for binocular vision explanation
"...cause of the single appearance of objects seen by both eyes..."

2) EOM anatomy

3) Approach Is it true diplopia, or is it a blurry vision? - mono vs bi - other neurologic symptoms - CNs palsies - screen GCA & thyroid disease

4) Mono vs Bi Monocular "close one eye does not resolve" - pinhole, if normal - refractory; abnormal - cortical - dry eyes & refractory error Binocular "close either eye solves problem"

5) Other neurological symptoms
Yes, help to localize lesion
No, isolated diplopia

6) Isolated diplopia
a. How are the two images positioned? How does distance affect diplopia?
b. what field makes it worse? or improve it?
c. moving head correct the vision?
d. pain w/ eye movement?

7) CN palsies
- causes vasculopathy & tumors, specifics
aneurysm (CN III), congenital trauma (CN IV), cranial pressure (CN VI)

8) Double vision CN III: DV, others: droopy eyelid, pupil asymmetry CN IV: DV vertical or diagonal CN VI: DV horizontal INO: DV horizontal changing sides
9) Oculomotor palsy
For further localization of CN III
1. Nuclear lesion - bilateral incomplete ptosis 2. Complete or partial lesion of the nerve trunk - sup & inf divisions 3. Superior division of the third nerve - palpebrae & SR 4. Inferior division of the third nerve - all other muscles of CN III
9.1. CN III palsy- DV, others: droopy eyelid, pupil asymmetry

9.2. CN III palsy- DV, others: droopy eyelid, pupil asymmetry

9.3. CN III palsy
- DV, others: droopy eyelid, pupil asymmetry

9.4. Nuclear oculomotor nerve palsy- bilateral ptosis + L CN palsy features (SR palsy)

9.5. CN III palsy Trunk lesion involving sup and inf visions - sup div SR and palpebra - inf div rest

10) Trochlear palsy- Trochlear palsy versus skew deviation> skew deviation improves w/ laying down (vestibular system issue)

10.1. CN IV - 3-step test

10.2. CN IV- primary gaze hypertropia at the affected side - worsening at contralateral gaze - tilt head to the same side to increase hypertropia *contralateral dorsal exit

10.3. CN IV palsy - Always do 3-step test + head tilt; otherwise, you will miss it - MDR for degree - 4th CN vs skew!

10.4. CN IV palsy - 3-step test

10.5. Maddox Rod Test

11) Abducens palsy
11.1. CN VI palsy

11.2. CN VI palsy

195. Accepted

63. Peripheral Neuropathy

Peripheral Neuropathy
John Fothergill (1712 – 1780)
First, to describe neuropathic pain

2) Approach
- System
- Distribution
- Onsent
- Comorbidities & medications
- Basic labs & EMG

3) What system is involved (motor, sensory, autonomic, or mixed)?
a. Sensory involvement
- Positive neuropathic sensory symptoms – suggest acquired polyneuropathy
> prickling, tingling, asleep-like numbness
- Pain – suggests Small fiber neuropathy due to toxic, metabolic, ischemic, or idiopathic cause
> electric shock, burning, freezing, tightness, throbbing, allodynia (discomfort or pain to apparently painless stimuli), hyperalgesia (exaggerated pain response)
> often accompanied by reduced or absent sensation of pinprick or temperature
- Negative neuropathic sensory symptoms – suggest acquired or inherited cause
> loss of sensation, imbalance

b. Motor involvement
- Often combined with sensory symptoms:
- Motor > Sensory: Immune-mediated like GBS & CIDP
- Sensory > Motor: In many other polyneuropathies, especially length-dependent neuropathies caused by metabolic or toxic disorders

c. Autonomic involvement
- Symptoms include lightheadedness, syncope, diarrhea, constipation, postprandial bloating, early satiety, urinary complaints, erectile dysfunction, abnormal or absent sweating, and dry mouth and eyes.

4) Where (distribution of nerve involvement)?
a. Distal (length-dependent) and symmetric: metabolic, toxic, inherited, or idiopathic
b. Not length-dependent and asymmetric: immune-mediated or infectious

5) When (onset and course)?
Acute (<1 month) and subacute (1-2 months): immune-mediated or Infectious process
Chronic (>2 months): inherited, metabolic, toxic, or idiopathic

6) What setting – review of comorbidities and medications?
Common causes of acquired polyneuropathies.
Positive family history of high arched foot or hammer toes – Charcot Marie Tooth (CMT) Disease i.e., Hereditary Sensory and Motor Neuropathy

7) Electrodiagnostic test
Define – distribution and extent of neuropathy
Differentiate – axonal and demyelinating or mixed process
Limitation – normal in small fibre neuropathy (skin biopsy is helpful in these cases)

8) Blood tests
a. For distal symmetric neuropathy:
CBC, BMP (Cr, Ca), A1c, TSH, HIV, HCV, B12, folate, and SPEP

b. Specific:
Metabolic/toxic:
Elevated MCV: alcoholism, vitamin B12 deficiency
Thiamine deficiency: alcoholism, bariatric surgery
Urine heavy metals: Heavy metal intoxication
Thyroid function tests: Hypothyroid neuropathy (rare)

Inflammatory:
CBC: mononeuritis complex
Markers or vasculitis or systemic inflammation (ESR, ANCA, RF, ANA, cryoglobulins): Vasculitis, Cryoglobulinemic neuropathy (Hepatitis C)
CSF: protein elevation in AIDP and CIDP

Neoplastic/Paraneoplastic:
Paraneoplastic serology: especially subacute and severe neuropathy in smokers
Chest X-ray and other imaging for cancers: Small cell lung cancer and other malignancies
CSF cytology: carcinomatous or lymphomatous polyradiculopathy

Infections:
CSF: pleocytosis
Lyme titres (serum, CSF): Lyme neuroborreliosis
HIV testing: HIV-associated neuropathy
Hepatitis C (Cryoglobulin testing): Hepatitis C – mixed cryoglobulinemia

62. Guillain-Barre syndrome

Guillain-Barre syndrome
Georges Charles Guillain (1876-1971)
Jean Alexandre Barré (1880-1967)
André Strohl (1887-1977)

“diagnosed two soldiers with a condition similar to Landry paralysis”

2) Definition
“acute immune-mediated polyneuropathies”

3) Epidemiology
C. jejuni – MC infectious etiology
M. pneumoniae – MC in children
*Others: HEV, CMV, EBV

Prodrome
- Respiratory MC in Europe and North America
- Diarrheal MC in Asia

4)Time
“should not progress more than 4 weeks”
*consider acute on CIDP, if > 3 relapses or more than 8 weeks

5) Diagnostic criteria
Req
- progressive weakness
- hyporeflexia (appears within 1 wk)

Sup
- prog over 4 weeks
- symmetry
- mild sensory
- CN involvement
- autonomic dysfunction
- pain
- elevated CSF protein
- EMG features

6) GBS classification
- based on clinical and neurophysiological features

7) GBS variants
- axonal
- localized
- Miller Fisher syndrome

8) Axonals
- AMAN & AMSAN
- AMAN 2 patterns of recovery: quick (conduction block resolution) or slow (extensive axonal degeneration)

9) Miller Fisher syndrome
- triad ophthalmoplegia, ataxia, and areflexia
- Bickerstaff brainstem encephalitis: MFS + impaired consciousness and paradoxical hyperreflexia

10) Pathogenesis
- molecular mimicry
- neural target
- AIDP vs AMAN
> AIDP: multifocal perivascular and endoneurial T-cell infiltration, prox and distal (weak BBB)
> AMAN: anti-ganglioside binding, complement activation & MAC

11) LP & EMG & MRI
- LP before IVIG because alters WBC & protein count
- EMG should be later repeated
- Spinal MRI w/ thickening and enhancement of intrathecal spinal nerve roots

12) Ganglioside target

13) Treatment
Prompt Neuro ICU
- dysautonomia, bulbar dysfunction, severe or rapidly worsening weakness, and evolving respiratory distress
- GBS scale > 4

Dysautonomia
- profound dysautonomia at intubation

IVIg versus PLEX
- repeating IVIg or PLEX for absence of clinical response after initial treatment for GBS provides no additional benefit

14) Erasmus GBS outcome score (EGOS)

61. Saccadic intrusions

Saccadic intrusions!
Louis Émile Javal (1839 – 1907)
“during reading… eyes do not move continuously along a line of text, but make short rapid movements (saccades) intermingled with short stops (fixations)”

2) Normal vs abnormal
Normal saccades - help fixation
Saccadic intrusions - interrupt fixation

*In the absence of quantitative eye movement recordings, simply counting gaze fixation breaks (>9/min) may suffice

3) Types of saccadic intrusions

Square wave jerks (SWJ)
Macrosquare wave jerk
Macrosaccadic oscillations
Saccadic pulses
Ocular flutter
Opsoclonus
Voluntary nystagmus or flutter

*defined by eye position, amplitude (size), and velocity

4) Saccadic intrusions ≠ nystagmus ≠ saccadic dysmetria
Saccadic intrusions
-omnipause neuron def
-pause cell dysfunction (fast-fast)
Nystagmus
-neural integrator def
-leaky integrator (fast-slow)
Saccadic dysmetria
-cerebellum def
-eye over/undershoot before landing on target

5) Square wave jerks (SWJ) aka Gegenrucke
- 0.5 to 5 degrees
- intersaccardic interval (200 msc)

5.1. SWJ
-most common saccadic intrusion
- intersaccadic interval
- fixate on the camera, sir! But saccades interrupt fixation

5.2. SWJ
≠ nystagmus: no slow phase

5.3. SWJ
- healthy individuals, usually elderly
- long intersaccardic interval


5.4. SWJ
- intersaccadic interval

6) Macrosquare wave jerk
- > 5 degrees
- 2-3 Hz
- intersaccardic interval (200 msc)
- burst occurrence (vary amplitude)
- monocular vision suppression

6.1. MSWJ



7) Macrosaccadic oscillations
- inc-dec amplitude
- intersaccardic interval (200 msc)
- burst occurrence

7.1. MSO
- intersaccadic interval
- variable amplitude

8) Saccadic pulses
- small-amplitude saccades away from fixation followed by a rapid drift back
- “flutter in pulses”

9) Flutter
- horizontal saccades
*microflutter can have vertical & torsional
- no intersaccadic interval

9.1. Ocular Flutter
- fixation, fast-fast component
- horizontal
- no intersaccadic interval (back-to-back horizontal oscillatory movements)

9.2. Ocular flutter
- burst horizontal fast-fast moves with no intersaccadic interval
- "pause" neurons usually prevent saccadic oscillations during fixation by inhibiting "bursts" neuron firing
> saccadic intrusion - pause neuron lesion

9.3. Ocular flutter
- short eye movements (avoiding fixation) to prevent flutter initiation

9.4. Ocular flutter
- horizontal fast-fast
- occur at primary gaze
- can not be elicited by eye movement

9.5. Benign ocular flutter
- challenging to assess fixation
> color and bright stationary object
- subjectively assess oscillopsia
> feeding

10) Opsoclonus
- multidirectional, horizontal, vertical, and torsional saccadic oscillations
- no intersaccadic interval

10.1. Opsoclonus in the oscilloscope screen
"die in the eye and record eye movements"
- multidirectional
- varied amplitude
- no intersaccadic interval

10.2. Opsoclonus (saccadomania)
- all directions fast-fast component
- worsen w/ convergence
10.3. Opsoclonus
- 1st patient with opsoclonus due to anti-Ri in setting of breast cancer

10.4. Opsoclonus
- multidirectional
- fast-fast component
- no intersaccadic interval

10.5. Opsoclonus
- ramdon caotic saccades
- occurring at fixation

10.6. Opsoclonus
- multidirectional
- fast-fast component
- no intersaccadic interval

10.7. Opsoclonus
-multidirectional

10.8. Opsoclonus
- multidirectional
- no intersaccadic interval

11) Voluntary flutter/nystagmus
“ability to induce nystag & flutter”
- high frequency (usually, > 15 Hz)
- duration < 30 sec
- precipitated by convergence
- superimposed by smooth-tracking
*psychogenic: convergence effort, facial grimacing, eyelid flutter

11.1. Voluntary Ocular Flutter
≠ from ocular flutter:
- convergence elicits flutter
- unsustained
- near triad cause miosis

11.2 Voluntary ocular flutter
- stop w/ closing eyes
- eyelid flutter
- forcing convergence to occur flutter
> patient did not notice that she was purposefully converging for this to occur



60. Pourfour du Petit Syndrome

Pourfour du Petit Syndrome
The reverse Horner syndrome!
François Pourfour du Petit (1664–1741)
- 1st to describe

2) Definition
“ipsilateral mydriasis, hyperhidrosis, and eyelid retraction”

3) Pathophysiology
"oculosympathetic chain irritation causing the clinical signs of hyperactivity of the sympathetic pathway"
- causes are the same as those for Horner syndrome

4) Management
- resolve spontaneously
- clonidine
- sympathectomy

5) PPS cases
5.1 PPS associated with a cervical vertebral anomaly
- noticed at physical exercise (2 floors of stairs, two times, an go..)
5.2. PPS

5.3. PPS associated with internal carotid artery dissection
- hyperhidrosis
- eyelid retraction
- Fig b shows improvement after botox

5.4. Horner syndrome & Pourfour du Petit syndrome associated with oesophagostomy tube placement in a cat
First developed Horner syndrome (a); Later, Pourfour du Petit syndrome (b)

5.5. PPS after medullary thyroid carcinoma surgery
A) Day 5 after thyroid surgery, with right mydriasis and ipsilateral upper eyelid retraction. 
B) Follow-up 2 months after thyroid surgery, with complete resolution

5.6. PPS associated with thyroid CA

5.7. PPS due to ipsilateral IJV distention

5.8. PPS associated with cluster headache

59. Upper and Lower Motor Neuron Lesions

Upper and Lower Motor Neuron Lesions

1) Summary
- STORM Baby

Tone
- depends on gamma motor neuron

Reflex
- hyperreflexia (loss of UMN comand)

Mass
- disuse atrophy
- denervation atrophy (loss of continuous ACh release)

Babynski
- child (normal - UMN are not till myelinated)

Fasciculations (Denervation hypersensitivity)
- loss LMN --> loss ACh release --> muscle increase production of ACh receptors (any hit can cause fasciculations)

2) UMN lesions
Acute manifestations
- Spinal shock
- Relative sparing trunk
Late manifestations
- Babinski sign
- Spasticity
- Hyporeflexia of superficial reflexes
- Contralateral or ipsilateral involvement
- Involvement below the lesion
- Decorticate posture
- Decerebrate posture

3) Spinal shock
- Hypotonia and loss of all reflexes on contra-lateral side
- Gamma-motor neurons by stretching muscle spindle bodies, activate alpha-motor neurons leading to extrafusal muscle contraction.
- In upper motor neuron lesion, supraspinal excitatory input to gamma-neurons is lost.

4) Relative sparing of trunk muscles
- Trunk muscles are bilaterally innervated by anterior corticospinal tract, so that a lesion of one side of the tract has minimal/ imperceptible manifestations.
- Distal muscles, fingers, toes, fine articulations and flexors more than extensors are handled by lateral corticospinal tract and affected more.

5) Babinski sign
- It is a primitive response present normally in newborns.
- The extensor response is modified to flexor response by developing corticospinal tract.
- Upper motor neuron lesion results in reappearance of primitive extensor response.

6) Spasticity 
- Increased muscle tone, hyperactive stretch reflexes, and clonus.
- Due to removal of inhibitory influences exerted by cortex on postural centers of vestibular nuclei and reticular formation.

7) Hyporeflexia of superficial reflexes
- Superficial reflexes are absent in infants and appear after about 6 months to 1 year.
- Their appearance may depend upon the myelination of the corticospinal tract.
- Hence, in upper motor neuron lesion, superficial reflexes may be lost.
- It may even be absent in normal individuals, hence, correlation with other corticospinal signs is necessary.

8) Contralateral or ipsilateral involvement
Pyramidal decussation occurs at the level of medulla-spinal cord junction.
Lesion above pyramidal decussation leads to contralateral signs.
Lesion below pyramidal decussation leads to ipsilateral signs.
Involvement below the lesion
Damage of UMN below the level of lesion

9) Decorticate posture
- Occurs in UMNL above the red nucleus – hence, rubrospinal tract still working.
- This leads to release of cortical inhibition of the rubro-, reticulo-, and vestibulospinal tracts. In this circumstance, the action of rubrospinal tract supercedes that of the reticulo- and vestibulospinal tracts, which results in arm flexion at the elbows and lower extremity extension, so-called decorticate posturing.

10) Decerebrate posture
- Occurs in UMNL below the red nucleus – hence, rubrospinal tract not working.
- This releases inhibition of the reticulo- and vestibulospinal tracts, which results in extension of the neck and all four limbs, so-called decerebrate posturing.

11) LMN lesions
- Ipsilateral involvement
- Involvement at the level of lesion
- Flaccid paralysis, loss of deep tendon reflexes, and hypotonia
- Muscle atrophy
- Fasciculations and fibrillations

12) Ipsilateral involvement
- Lower motor neuron comprises of motor neurons in the anterior neurons and the fibers originating from them, which innervates the skeletal muscles.
- These fibers go uncrossed to the same side.

13) Involvement at the level of lesion
- Damage of LMN at the level of lesion.

14) Flaccid paralysis, loss of deep tendon reflexes, and hypotonia
- Loss of efferent limb in monosynaptic stretch or deep tendon reflexes
- Information from motor cortex doesn’t reach muscles due to defect in Lower motor neuron – leading to flaccid paralysis
- Loss of gamma and alpha motor neurons lead to decrease in baseline Ia and alpha motor neuron discharge – leading to hypotonicity 

15) Muscle atrophy
- Denervation (deprived of necessary trophic factors)
- Disuse

16) Fasciculations and fibrillations
- Damaged α-motor neuron → Spontaneous action potential → Motor unit fires → Visible twitching of muscle fibers group (fasciculations)
- Increased excitability of muscle fibers due to denervation → Spontaneous contraction of single muscle fiber visible in EMG (fibrillations)

194. Accepted

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