1 ⼀NEUROLOGY I Flashcards

(265 cards)

1
Q

identify

A
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2
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A
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3
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A
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4
Q

A: MIOS seen in Younger pts indicates ⬜

B: MIOS seen in OLDER pts indicates ⬜

C: What is the purpose of the MLF

A

[MIOS-MLF Internuclear Ophthalmoplegia Syndrome]

1) Younger pts= Multiple Sclerosis
2) Older pts= [Pontine a. lacunar stroke]

________________

MLF coordinates CN3 with CN6

________________

Image: Left MIOS

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5
Q

CP for [MIOS-MLF Internuclear Ophthalmoplegia Syndrome] (3)

A

[MIOS-MLF Internuclear Ophthalmoplegia Syndrome]

*[Impaired ADDuction of affected eye]

+

[Normal ADDuction of affected eye during [near reflex convergence]

+

*[Nystagmus of UNaffected eye when attempting to ABduct]👣

Image: L MIOS

👣{(2/2 [Abducens CN6] overfiring in an attempt to stimulate [Oculomotor CN3]}

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6
Q

1st line tx for Heat Stroke is ⬜, which should be used to ⬇︎core body temperature by ⬜C/min .

Describe it

________________

List 3 adjunct Heat Stroke therapies

A

[augmentation of EVAPORATIVE COOLING] ; [0.2C/min]

(naked pt is sprayed with tepid (warm) water mist or pt is covered in wet sheet – while large fans circulate air ➜ ⇪ evaporative heat loss)

________________

ice water lavage / ice packs / cold IVF

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7
Q

3 main causes of pinpoint pupils

A
  1. Opiate OD
  2. Pontine lesion destroying sympathetic fibers
  3. Cholinergic eyedrops for Glaucoma
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8
Q

3 Main causes of Spinal Cord Compression

A
  1. DJD Disc Herniation (Smoking risk factor)
  2. [Epidural Staph a. Abscess (think IV drug user vs DM)]
  3. Tumor (Prostate/Renal/Lung/Breast/Multiple Myeloma mets)

Dx = MRI, Positive Straight Leg, Classic S/S

DJD=Degenerative Joint Disease

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9
Q

6 major causes of Syncope

A

MVC BSD

  1. ⬇︎ Cardiac Output (Valvular Dz/HOCM/Pulm HTN/PE/Tamponade/myxoma/aFib)
  2. Bradyarrhythmia (SA Node dysfunction/AV Block)
  3. [VANS - Vasovagal Autonomic Neurocardiogenic Syncope]
  4. Dehydration
  5. Stroke
  6. Metabolic (⬇︎Glucose vs ⬇︎Na+)

OBTAIN ECHOS ON ANY PT WITH SUSPICIOUS SYNCOPE!

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10
Q

A patient taking metoclopramide develops involuntary next flexion known as ⬜

Tx? (2)

A

[Torticollis Dystonia] ; [Benztropine IV 🆚 Diphenhydramine IV]

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11
Q

A pt complains of inabilty to recognize previously known faces

What is this called? ; Where is the lesion?

A

[ProsoPagnosia visual agnosia] ; BL Temporo-Occipital

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12
Q

a. Tx for PostFall syndrome (2)

_________________

b. What is PostFall syndrome?

A

a.
-URGENT PHYSICAL THERAPY(to ⇪ mobility which ➜ ⇪ functionality)
-URGENT BEHAVIORAL THERAPY(to improve thinking/behavior about falls)

_________________

b. maladaptive fear of falling after a fall that ➜ restricted mobility ➜ functional decline in the elderly

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13
Q

Describe the 4 main sx for [Brown Sequard Syndrome]

A

1.[DCP: Ipsilateral 2TVP loss]

2.[LateralCST: Ipsilateral [UMN (Weak MESH)]

3.[STT: Contralateral Pain/Temp loss 2 LEVELS BELOW ORIGINAL LESION]

4.[+/- Horner’s MAP](if hemisection is above T1 since this → oculosympathetic pathway damage)

|💡 Brown Sequard = SpinalHemisection

🖊2TVP-2point/Touch/Vibration/[Position Proprioreception]

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14
Q

Causes of [Brown Sequard Syndrome] - 3

A
  1. [(Extramedullary Tumor]
  2. Trauma
  3. [DJD Disc Hernation (Smoking risk factor)]
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15
Q

A: Describe Opsoclonus-Myoclonus Syndrome

B: What Childhood tumor is it associated with?

A

A: [Non-Rhythmic Conjugate Eye mvmnts] with myoclonus= “Dancing Eyes and Feet

B: Neuroblastoma (onset 2 y/o)

Arises from Neural crest

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16
Q

PCiiH [Pseudotumor Cerebri Idiopathic Intracranial HTN] Dx - 3

A

1st: [CT to r/o space occupying lesion]

➜ 2nd: [Lumbar Puncture with opening pressure >250 mmH20 (from ⬇︎Arachnoid villi CSF absorption)]

3rd: [MRI +/- MRV revealing BL tortuous Optic N]
* _________________*
* This HA will make you go Blind!*

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17
Q

Papilledema is a ctx to Lumbar puncture

When is ⊕Papilledema not a ctx to Lumbar puncture? Explain

A

[PCiiH (Pseudotumor Cerebri Idiopathic Intracranial HTN)];

As long as there are no signs of obstructive/noncommunicating hydrocephalus or mass, then it is ok

LP with CSF opening pressure > 250 mmH20 = PCIIH

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18
Q

[Pseudotumor Cerebri Idiopathic Intracranial HTN] Clinical Presentation - 4

A

PCiiH girls like to VAPE

  1. [Vision ∆ +/- papilledema]
  2. [Abducens CN6 palsy]
  3. Pulsatile Tinnitus
  4. [Eye-blinding HA (worst at sleeping times) & with head position ∆]
    * This HA will make you go Blind!*
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19
Q

What is Wallerian Degeneration?

A

Degeneration of Axons after trauma, but in the setting of [preserved perineurium and epineurium] which later acts as scaffolding to allow axonal sprouting and regeneration within the PNS

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20
Q

Describe the Lacunar Syndrome CP

A

👀
lenticulostriate vessels perfuse [BTiC]

1A: {[Basal GangliaSubthalamic nc] → [CTLHemiballismus & involuntary writhing]}

1B: {[ThalamuSVPL]→[CTL Sensory Stroke]}

1C: {[internal CapsulePOST limb/Corona Radiata]-→ [CTLMotor stroke(ataxia|clumsy hand-dysarthria)]}

👀Lacunar Stroke= [Thrombotic HTN Arteriolosclerosis & Thrombotic microatheromas] of lenticulostriate vessels (BTiC) –> [cystic infarcts < 15 mm] –> Lacunar Syndrome
VPL=VentroPosteroLateral nc

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21
Q

List the n. roots associated with Common Peroneal n.

A

L4-S2

foot is dropPED (Peroneal Everts & Dorsiflexes)

  • Commonly caused by L5 Radiculopathy*
  • Dx: Knee MRI vs EMG*
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22
Q

List the n. roots associated with Tibial n.

A

L4-S3 (Three)

can’t walk on TIPtoes (Tibial Inverts & Plantarflexes)

Commonly caused by L5 Radiculopathy

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23
Q

What are the functions of the Common Peroneal n. -2

A

L4-S2

foot is dropPED (Peroneal Everts & Dorsiflexes)

_________________

🔬 Commonly caused by L5 Radiculopathy
🩺 Knee MRI vs EMG

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24
Q

What are the functions of the Tibial n. (2)

A

L4-S3 (Three)

can’t walk on TIPtoes (Tibial Inverts & Plantarflexes)

Commonly caused by L5 Radiculopathy

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25
CP of **Craniopharyngioma****s** - 3 \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Demographic?-2
1. BiTemporal Hemianopsia 2. HA 3. Pituitary Hormonal Deficiencies (i.e. ⬇︎Libido) Demographic: **MOSTLY KIDS**, but some adults
26
A: What is **Cheyne-Stokes Breathing**? B: What is this breathing associated with? - 3
A: Cyclic breathing in which apnea is followed by [INC and then DEC tidal volumes] all the way up until the next apneic period B: 1. [**Advanced** CHF] 2. [Comatosed BL metabolic encephalopathy] 3. Elderly during sleep
27
[Myasthenia Gravis] Tx-4
**P DDD F** ## Footnote 1st: [Pyridostigmine AChesterase inhibitor] 2nd: Cyclosporine 3rd: Thymectomy 4th: \*\*[Intubate + Plasmapharesis + IVIG + Steroids] if Crisis \*\*
28
Pts with Myasthenia Gravis may develop Myasthenia CRISIS, which presents clinically as ⬜ !!! What are precipitants of this?-3
**P DDD F** Respiratory Failure! Precipitants = FIS: 1. Fluoroquinolones 2. Infection 3. Surgery *Crisis Tx: [Intubate + Plasmapharesis + IVIG + Steroids]*
29
[**LEMS** - Lambert Eaton Myasthenic Syndrome] etx
[Autoimmune attack against (Presynpatic Ca+ channel)--\> No ACh release]
30
[Myasthenia Gravis] Clinical Presentation (5)
"*Give me Mya's* **P DDD F**" [**P**tosis [**D**iplopia from Disconjugate gaze] **D**ysarthria-*bulbar dysfunction* **D**ysphagia w/nasal regurgitation-*bulbar dysfunction* [**F**ATIGABLE progressive Weakness Muscularly (Extraocular/RESP/Proximal/limbs/worst w/repetition/impvd with rest)] *Tx: Pyridostigmine AChesterase inhibitor*
31
[Myasthenia Gravis] Dx-5
P DDD F 1. **ACh R Ab Assay** 2. **MuSK** (**Mu**scle-**S**pecific tyrosine **K**inase) **Ab Assay** (only if #1 is neg) 3. [**Tensilon Edrophonium**]--\> Improves all sx 4. **Ice Pack** to eyelids --\> Improves Ptosis by inhibiting ACh breakdown at NMJ 5. *BE SURE TO GET **CT CHEST** AFTER DX TO COVER FOR THYMOMA, POSSIBLE THYMECTOMY!!!!*
32
[**LEMS** - Lambert Eaton Myasthenic Syndrome] Clinical Presentation - 3
1. **Weakness of [Proximal limbs and trunk]** mimicking myopathy, better with exercise 2. Autonomic sx (Dry mouth /Orthostasis / Impotence) 3. ⬇︎Deep Tendon Reflexes
33
[Myasthenia Gravis] etx \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Demographic?-2
Autoantibodies block and degrade [**postsynpatic** _nicotinic_ ACh Receptors]] --\> [⬇︎ motor end plate potential] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *[Women 20-30] [Men 60-80] yo*
34
Migraine etx \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ How are the Trigeminal nerves associated-2 \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ ## Footnote "***VTAP** the migraine BEFORE it comes, and **SEND** it on its way when it does!"*
Genetic [GainOfFunction mutation in *excitatory NMDA receptor*]--\>burst of cerebral activity _when triggered_---\>hyperemia (*usually occipital lobe*)--\> aurasx. Burst is followed by **Cortical Depolarization** tht has slow but deliberate forward advance --\> Triggers Trigeminal pathway Trigeminal afferents : 1. send impulses--\>[Brain Stem APCTZ] & hypothalamus--\> Nausea/Photophobia/Phonophobia 2. retroactively depolarize--\>release of substance P --\> neurogenic inflammatory pain + vasoDilation
35
A: **Primary CNS Lymphoma** is the ⬜ most common cause of ⬜ in HIV pts B: What *virus* is this associated with? C: What WBCs would you expect to see in the brain tissue
A: **2nd** most common cause of **ring enhancing lesions** in HIV pts (*1st = Toxoplasmosis Gondi*) B: **EBV** C: B-lymphocytes
36
*Pontine*[Basilar Artery] occlusion CP
Locked In Syndrome!!! | *LIS🔒={**[✅QB VP] but [⛔HO]**}* ## Footnote [**Q**uadriplegia w intact consciousness]
37
PCA occlusion CP-4
1. [CTL Homonymous Hemianopiawith macular sparing (*K in image*)] 2. Visual hallucinations 3. [Alexia with NO agraphia]Dominant Hemisphere involvement 4. [DOPeOculomotor CN3 involvement] ## Footnote 🔎[DOPe= Down & Out + Ptosis + eyeDilated]
38
ACA occlusion CP-3
1. CTL Weakness worst in LE 2. CTL Numb worst in LE 3. Urinary Incontinence
39
AICA occlusion CP-4
*Somewhat like [PICA Lateral Medullary Syndrome of Wallenberg]* 1. Hearing Loss 2. FACE Paralysis (Similar to Bells Palsy) 3. Ipsilateral ⬇︎Facial Pain/Temp 4. CTL ⬇︎BODY Pain/Temp
40
PICA occlusion causes what syndrome? what other vessel abnormality can cause the same CP?
*This is AKA [PICA Lateral Medullary Syndrome of Wallenberg]* **Intracranial Vertebral A occlusion** = MOST COMMON CAUSE OF THIS!
41
ALL Elderly should be screened for "*Falls* " ⬜ a year with ⬜. How do you manage patients with ⊕*Fall* screen? (2)
once; [inquiry on how many (*if any*) falls they've had] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ ▶if fall screen ⊕ → assess gait/balance with [psGUGT (postural stability “Get Up and Go” test)] ▶ … --*(if psGUGT also ⊕)*--\> [extensive “fall” workup](image) * * * psGUGT: *Without assistance, pt stands from armless chair, walks short distance, turns around, returns to chair and sits down again.* [If **unsteady/difficulty** = ⊕ result]
42
# ALL Elderly should be screened for "Falls " ⬜ a year with ⬜. *Patient has ⊕fall screen → ⊕psGUGT → requires elderly [extensive fall workup] now* Describe the 6-part differential that outlines *elderly* [extensive fall workup]
once; [inquiry on how many (*if any*) falls they've had] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
43
All patients (especially elderly) s/p **FALL** require ⬜ by a ⬜ for the purposes of ⬜
[home safety assessment] ; occupational therapist \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ optimizing HOME safety and ADL
44
Altered Mental Status workup -7
**GOT** **CLUB** 1. G[Glucose level ➜ Thiamine B1 f/b glucose admin (dextrose **IV**)] 2. Oxygen level 3. T3/T4 level 3. B12 level 4. Lumbar puncture 5. [UDS/CMP/CBC] 6. CT head
45
Although Parkinson's disease is a clinical diagnosis *< *E + 2S **-** R - X* >*, what's the most important supportive feature for confirming the diagnosis?
excellent response to dopaminergic tx (Levodopa/Carbidopa) ## Footnote ⊡established PD = < *E + 2S **-** R - X* >
46
# [Parkinson's Disease] is a ⬜ diagnosis Diagnosing Parkinson's Disease consist of 4 criteria blocks Name them
clinical \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ < ***ESRX*** > critertion 1. {[**E**ssential (for PD)] = *AKA "PARKINSONISM"* } 2. [**S**upportive (of PD)] 3. [**R**edFlags (atypical for PD)] 4. e**X**clusion (excludes PD dx)] ## Footnote ⊡established PD = < *E + 2S **-** R - X* >
47
# [Parkinson Disease] = ⬜ diagnosis made of 4 criteria blocks < *ESRX* > the [< *E* > criteria(AKA ⬜ )] = ⬜, and is made of what 3 items?
clinical ; \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ < *ESRX* > ⭐[< *E* >ssential (for *any* Parkinson Disease diagnosis) = AKA "*parkinsonism​*​"] ▶requires ([**P** or **R**] ▶requires (+ **K**) | *E*ssential (for PD) = [ (**P**|**R**) **+K** ] ## Footnote **PRK** = -**P**ill Rolling resting tremor -**R**igiditiy cogwheel -brady**K**inesia \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ ⊡established PD = < *E + 2S **-** R - X* >
48
# [Parkinson Disease] = ⬜ diagnosis made of 4 criteria blocks < *ESRX* > the < *S* > criteria = ⬜, and is made of what 3 items?
clinical ; \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ < *ESRX* > ⭐[< *S* >upportive (of PD diagnosis)] ▶[Excellent response to levodopa/Carbidopa = MOST IMPORTANT SUPPORTIVE FEATURE] ▶Asymmetric limb findings (tremor, rigidity) ▶Olfactory dysfxn ## Footnote ⊡established PD = < *E + 2S **-** R - X* >
49
# [Parkinson Disease] = ⬜ diagnosis made of 4 criteria blocks < *ESRX* > the < *R* > criteria = ⬜, and is made of what 6 items?
clinical ; \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ < *ESRX* > ⭐[< *R* >ed Flags (atypical for PD diagnosis)] ▶ [early **A**reflexia posturally (recurrent falls) ▶early SEVERE orthostatic hypOtension] ▶ [early bulbar dysfxn (dysarthria)] ▶ having NO [nonmotor signs] (i.e. having NO sleep ∆ is atypical for PD ) ▶ Symmetric findings ▶Hyperreflexia ## Footnote ⊡established PD = < *E + 2S **-** R - X* >
50
# [Parkinson Disease] = ⬜ diagnosis made of 4 criteria blocks < *ESRX* > the < *X* > criteria = ⬜, and is made of what 5 items?
clinical ; \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ < *ESRX* > ⭐[< *X* >clusionist (automatically eXcludes Parkinson Disease diagnosis)] ❌vertical palsy ❌[cerebellar sx(*GRINDRR*) ] ❌cortical sensory loss ❌worsening aphasia ❌[pt taking antidopaminergic rx (ie haloperidol)] ## Footnote ⊡established PD = < *E + 2S **-** R - X* >
51
# [Parkinson Disease] = ⬜ diagnosis made of 4 criteria blocks < *ESRX* > What is the diagnostic criterion arrangement neccessary to diagnose a patient with [**ESTABLISHED** Parkinson's Disease] ?
clinical \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ < *E + 2S **-** R - X* >
52
# [Parkinson Disease] = ⬜ diagnosis made of 4 criteria blocks < *ESRX* > What is the diagnostic criterion arrangement neccessary to diagnose a patient with [**probable** Parkinson's Disease] ?
clinical \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ < *e + (s **≥**r) - x* >
53
Alzheimer's Dz etx (5)
Alzheimers etx = **NaTPO** ①. **N**eurofibrillary tangles = intracell hyperphosphorylated insoluble tau cytoskeleton = [ ⇪ Neurofib tangles = ⇪ Alzheimer dementia] + ② . ⭐**a**ccumlation of {**β-amyloid** *(derived from [cleavage of **chromo 21** t.A.P.P.]*} in: 2a. **T**emporal lobe early on ➜ [Neuritic Senile plaques] 2b.{[**P**arietal & occipital] lobe cerebral blood vessels} ➜ [P\o Spontaneous Hemorrhages📷] 2c .{hipp**O**campus & [Basal nc. of meynert]} ➜ defective [{O\B} Choline AcetylTransferase] ➜ [⬇︎ {O\B} ACh] ➜ {Alzheimer [**CLAV** ➜ **HANDU**]sx} 🖊{P\o} = {[Parietal & occipital]} | 🖊{O\B} = {hipp**O**campus & [Basal nc. of meynert]} ## Footnote 🩺**NaTPO** ↪ [**CLAV** ➜ **HANDU**]sx 👓*t.A.P.P.* = transmembrane Amyloid Precursor glycoProtein
54
*An Unconscious, Unresponsive patient with unremarkable vitals and normal Deep Tendon Reflex presents c/f coma* ▶How do you differentiate true coma from psychogenic coma? * * * ▶ Explain (2)
obtain **VCR** [⊕**VCR** = NO true COMA] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ **▶** [**V**estibular **C**aloricstimulation **R**eflex] = tests' [oculovestibular *brainstem* and *cortex* reflex] by irrigating auditory canal with cold water. ▶[⊕**VCR** = NO true COMA] = irrigating auditory canal with cold water ➜ {[conjugate slow deviation of gaze to side of cold water (*brainstem*)] ➜ [saccadic correction to midline (*cortex*)]} = [COMATOSED BRAINS CAN NOT DO THIS] =[⊕**VCR** = NO true COMA] = [⊕psychogenic Coma]
55
[Parkinson Disease Tx] can cause psychosis due to ⬜ How do you manage this? -2
dopaminergic activation of mesolimbic pathway \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ {DEC [PD Tx] dosage (starting with least potent)} --(if sx persist)--\> [add D2 R Blocker (Quetiapine/Clozapine/PimaVanserin)]
56
Aside from CSF analysis revealing ⬜3, name the typical manifestations of [Herpes Simplex Encephalitis] -6
- [⇪ **P**rotein] - [⇪ **W**BC lymphocyte pleocytosis] - [⇪ RBC (from temporal lobe destruction)] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *encephalitis* sx = **FAVORS**: [**F**ocal neuro ∆ *(aphasia, hemipLegia, hemiparesis)*] , ⭐**A**MS⭐, **V**omiting, **O**uch HA, **R**eally hot fever, **S**eizure ## Footnote *⭐= [encephalitis AMS] distinguishes encephalitis from meningitis*
57
Atomoxetine Indication
**Non**Stimulant ADHD Rx
58
Benzos can cause an *uncommon* SE known as **Paradoxical Agitation**. Describe this
[⬆︎Agitation, confusion and disinhibition] within a hour of benzo admin. GIVING MORE BENZOS WILL WORSEN THIS!
59
Benztropine & Trihexyphenidyl are in what class of drugs? \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ How can pts on these develop Retro-Orbital HA during OD?
Anticholinergics; OD can --\> Acute Glaucoma --\> RetroOrbital HA(from pupil Dilation and cyclopLegia) ## Footnote *Blind as a bat, Dry as a bone, Hot as a hare, Mad as a hatter, Red as a beet, Bowel & Bladder lose their tone, and the Heart runs alone*
60
Between DM, Smoking and HTN, which carries the GREATEST STROKE Risk?
**HTN**
61
# Both Mannitol and [Hypertonic Saline (3%/5%/23%)] are used to ⬇︎ ICP List the differences in using Hypertonic saline? - 4
1. HTS Anti-Inflammatory 2. [HTS does NOT cross into interstitial space like Mannitol ( Mannitol causes Rebound Edema!) ➜ 3. ➜ HTS eventually expands systemic volume 4. HTS **ONLY** given via Central line | HTS = Hypertonic Saline
62
Brachial Plexus damage of [lower Trunk {(C8) (T1)}] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ **clinical presentation?**
[klumpke palsy claw hand]
63
Brachial Plexus damage of [long thoracic {(C5)(C6)(C7)} n ] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ **clinical presentation? -2**
1. [winged scapula] 2. [inability to **AB**duct shoulder \> 90º]
64
Brachial Plexus damage of [Axillary {(C5)(C6)} n] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ clinical presentation?
[Deltoid paralysis]
65
Brachial Plexus damage of [Radial {C5⼀T1} n] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ clinical presentation? -2
1. [Saturday night palsy wrist drop] 2. [No Tricep Reflex]
66
Brachial Plexus damage of [Radial {C5⼀T1} n] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ causes -3
1. [Crutches/Axilla damage] 2. [anteroLateral⼀**pFSF**] 3. Midshaft Humerus ## Footnote 👓{[anteroLateral⼀**pFSF**] = {[anteroLateral⼀**p**roximal humerus displacement] iTSo [**F**OOSA **S**upracondylar **F**x]}
67
Brachial Plexus damage of [Axillary {(C5)(C6)} n] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ causes -3
1. [Surgical NECK humerus] 2. [ANTERIOR humerus displacement] 3. Shoulder Injury
68
Brachial Plexus damage of [long thoracic {(C5)(C6)(C7)} n ] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ **causes -3**
- STABS - [MASTECTOMY] - [AXILLARY NODE DISSECTION]
69
*Brain Death is a clinical diagnosis and involves [absent cortex functions] and [absent brain stem functions]* What are the legal complications of disabling artificial life support for a pt who is newly diagnosed with Brain Death?
None - Brain death is a legally acceptable definition of death
70
*Brain Death is a clinical diagnosis and involves absent cortical and brain stem reflexes* In correct diagnostic order, name the 5 Criteria Blocks used to diagnose Brain Death?
**(*****"CNaPL"*****​)** ## Footnote [**5****C**linical (*evidence of **_C_**NS catastrophe, NO **_C_**onfounders, NO **_C_**hemicals-drug intox, \>36**_C_**, **_C_**ore\>100 SBP*)] [**5****N**euro exam(*coma, NO cortex rflx, NO brainstem rflx, NO rooting/sucking rflx, spinal rflx ok*)] ➜ [**4a**ncillary testing if (C) (N) (P) inconclusive] = [EEG isoelectric line] vs [EEG NO SSensory activity] vs [EEG NO brainstem activity] vs [NO intracranial blood flow] [**3****P**ulmonary aPnea test (*Preoxygenate ➜ disconnect ventilator = positive if NO spontaneous breath x 8m + PaCO2\>60 + arterial pH\<7.28]* [**L**ocal requirements]
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*Brain Death is a clinical diagnosis and involves [absent cortex reflexes] and [absent brainstem reflexes]* There are 5 Criteria Blocks (**CNaPL**) used to diagnose Brain Death \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ ▶ Describe the [**C**linical] criteria block (5)
**(*****"CNaPL"*****​)** [ **5****C**linicalprerequisites] * *[**_C_**NS catastrophic evidence is present],* * *[NO **_C_**onfounders of CNS_metabolic ∆]* * *[NO **_C_**hemicals_sedatives/drug intox/poisoning*] * *\>36**_C_**,* * ***_C_**ore\>100 SBP*)]
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*Brain Death is a clinical diagnosis and involves [absent cortex reflexes] and [absent brainstem reflexes]* There are 5 Criteria Blocks (**CNaPL**) used to diagnose Brain Death \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ ▶ Describe the [**N**euro exam] criteria block (5)
**(*****"CNaPL"*****​)** ## Footnote [**5****N**euro exam(*coma, NO cortex rflx, NO brainstem rflx, NO rooting/sucking rflx, spinal rflx ok*)]
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*Brain Death is a clinical diagnosis and involves [absent cortex functions] and [absent brain stem functions]* There are 5 Criteria Blocks (**CNaPL**) used to diagnose Brain Death \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ ▶ Describe the [**a**ncillary testing] criteria block (4)
**(*****"CNaPL"*****​)** ## Footnote ➜ [**4a**ncillary testing⼀if (**C**)| (**N**) |(**P**) inconclusive ] = *(positive if)*... [*EEG* isoelectric line] + [*EEG* NO SomatoSensory activity] + [*EEG* NO brainstem activity] + [NO intracranial blood flow]
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*Brain Death is a clinical diagnosis and involves [absent cortex reflexes] and [absent brainstem reflexes]* There are 5 Criteria Blocks (**CNaPL**) used to diagnose Brain Death \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ ▶ Describe the [**P**ulmonary aPnea test] criteria block (3) \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ ▶▶What 3 factors prevent this test from being done?
**(*****"CNaPL"*****​)** [ **3****P**ulmonary aPnea test * Preoxygenate * ➜Pull vent ( disconnect ventilator) * ➜ ➜ Positive = [(NO spontaneous breath x 8m) + PaCO2\>60 + arterial pH\<7.28] ] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ ❌if active drug intoxication ❌if heart disease ❌if lung disease
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*Brain Death is a clinical diagnosis and involves absent cortical and brain stem reflexes* There are 5 Criteria Blocks (**CNaPL**) used to diagnose Brain Death \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ ▶ Explain the Order these criteria blocks should be followed when diagnosing brain death
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On EEG, what is a [burst suppression pattern]? \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ What does it indicate? (2)
isoelectric periods punctuated by high amplitude activity \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ - Deep Coma - Anesthesia
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# *pt exhibits ⊕Deep Tendon Reflexes* T or F: this finding effectively r/o brain death
FALSE | {[🧠 Death*Reflexes*] = [(⊕Spinal Cord) ➖Cortex ➖Brainstem ➖Suck/root]} ## Footnote ....because **[Spinal Cord reflexes*(i.e. Deep Tendon Reflex)*] are still intact** during Brain Death →
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Bromocriptine MOA \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Indication
[PostSynapticDopamine🟢 (ergot)] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Parkinson's
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Carbamazepine side effects -3
1. [bone marrow suppression (neutropenia)] 2. SIADH hypOnatremia 3. AntiCholinergic
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[Carpal Tunnel Syndrome] etx
**BILATERAL** Median n Compression by the [Flexor Retinacular Transverse carpal ligament] --\> Peripheral **mono**neuropathy + [ABductor pollicis brevis atrophy] ## Footnote * [Flexor Retinaculum Transverse Carpal ligament] can be surgically incised for relief* * CARPAL TUNNEL STARTS uL and --\> BL*
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Carpal Tunnel Syndrome Clinical Presentation - 6
1. [Paresthesia vs Pain with **Median n. Distribution** worst at night] 2. CARPAL TUNNEL STARTS uL and --\> BL 3. {[Thenar (ABP, FBP, O_P,)] atrophy* [ABductor Pollicis Brevis] atrophy ➜ (⬇︎flexion/ ⬇︎ABduction/ ⬇︎Opposition*)]} 4. Tinel Sign (tapping over flexor surface ⬆︎ sx) 5. Phalen Sign (flexing Wrist ⬆︎ sx) 6. HOH Sign (Hand over Head ⬆︎ sx)
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*Pregnancy is associated with Carpal Tunnel* What should these particular pts also be worked up for?
**Preeclampsia** ## Footnote *CARPEL TUNNEL starts uL and then --\> BL*
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[Carpal Tunnel Syndrome] dx ## Footnote *excluding clinical s/s*
Nerve Conduction studies ## Footnote *EMG is not necessary for Carpal Tunnel Syndrome*
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[Carpal Tunnel Syndrome] tx - 5
1. **[WRIST SPLINT** (sx \< 10 mo)] 2. Remove exacerbating factors 3. NSAIDs 4. CTS injection -IF MODERATE 5. [Flexor Retinaculum Transverse Carpal ligament] can be surgically incised for relief - IF SEVERE ​ \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *wrist splint maintains wrist in neutral position to avoid movements that narrow the tunnel more*
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Risk factors for Carpal Tunnel Syndrome - 4
1. Obesity 2. [Pregnancy (*c/s Preeclampsia*)] 3. DM 4. hypOthyroidism ## Footnote *CARPEL TUNNEL STARTS uL and --\> BL*
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[Conus Medullaris Syndrome] etx \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Clinical Presentation - 7
(Compression of S2 - S4 n. roots @ Conus Medullaris) --\> \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ "**RIM sara**!?" 1. [**R**eflexia: HYPER]reflexia (*Cauda Equina has hypOreflexia)* 2. [**I**ncontinence EARLY] 3. **M**otor weakness SYMMETRICALLY 4. **s**addle anesthesia 5. **a**nocutaneous reflex loss 6. **r**adiculopathy 7. [**a** MRI, CTS IV and Neurosurg consult = tx]
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[cauda equina syndrome] etx \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Clinical Presentation - 7
(Compression of S2 - S4 n. roots @ Cauda Equina) --\> \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ "**RIM sara**!?" 1. [**R**eflexia: hypO]reflexia (*Conus Medullaris has HYPERreflexia)* 2. [**I**ncontinence LATE] 3. **M**otor weakness Asymmetrically 4. **s**addle anesthesia 5. **a**nocutaneous reflex loss 6. **r**adiculopathy 7. [**a** MRI, (CTS IV) and Neurosurg consult = tx]
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What Spinal Columns are affected in [Subacute Combined Degeneration]?-3 ​ \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ How do this manifest?-3
[Su**BAC**ute Combined Degeneration] [Demyelinating lesions] in 3 **Thoracic** Spinal Columns: 1. [Dorsal--\> Loss of 2TVP] 2. [Lateral CST --\> UMN *Weak MESH*] 3. [Spinocerebellar --\>Ataxia] * FriEdreich Ataxia affects the SAME 3 columns*
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Causes of [Subacute Combined Degeneration] (3)
[Su**BAC**ute Combined Degeneration] 1)**B**12 Deficiency (demyelinates peripheral nerves also) 2.**A**IDS/HIV 3.**C**opper deficiency * Affects Dorsal / Lateral CST / Spinocerebellar Tracts (Combined)*
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# B12 deficiency is common in the elderly In the elderly B12 deficiency can present as ⬜ and [Subacute Combined Degeneration]. How do you address this?
Dementia ; \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ SX REVERSIBLE WITH B12 SUPPLEMENTATION ## Footnote 🩺SAC = demyelination of DCP/ CST-L, /SpinoCerebellar tracts
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Central Pontine Myelinolysis dx (2) \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ tx (3)
1. [Brain MRI: demyelinating lesions] 2. [CP: rapid Na+ correction of *hrhh* → delayed paralysis days later] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ - irreversible - supportive care - eye computer interface ## Footnote *🔎hrhh = high risk hypOtonic hypOnatremia*
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# Central Pontine Myelinolysis → ⬜ syndrome Name the clinical features of this syndrome(6)
**_LOCKED IN SYNDROME_** \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *"CPM, you have the* **QB-VP** but no **HO** for him" ⊕ ✅[**Q**uadriplegia w intact consciousness {LOCKED IN SYNDROME}] ✅[**B**link reflex(*upper CN intact*)] ✅[**V**ertical EOM(*upper CN intact*)] ✅[**P**upilllary reflex(*upper CN intact*)] ⊝ ⛔[**H**orizontal EOM(*lower CN paralyzed*)] ⛔[**O**ral movements(*lower CN paralyzed*)]
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Central Pontine Myelinolysis etx (4)
1a. *hrhh* = {[prolonged hypOnatremia≤120] x ≥2 days} 1b. Rapid correction of *hrhh* ➜ 1c. [osmotic shock → oligodendrocyte death → demyelination → 🔒LIS \_\_\_\_\_\_\_\_OR_\_\_\_\_\_\_\_\_ ## Footnote *2 Also can be caused by {Pontine (infarct) io\ [Basilar Artery (occlusion)]}* \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_x\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ 🔒LOCKED IN SYNDROME{***[✅QB VP] but [⛔HO]**} *🔎hrhh = high risk hypOtonic hypOnatremia*
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*Cerebral Palsy is a group of clinical syndromes generally characterized as \_\_\_\_\_\_* How does it present? - 3
Nonprogressive motor dysfunction (Prematurity\>EtOH = RF) ; ## Footnote "Cerebral Palsy is a *young*, *SAD** **BUM**" 1. **B**L equinovarus club feet (image) 2. {[UMN (**W**eak **MESH**)sx] *LE \>UE*} 3. Mental Retardation *Greatest RF = prematurity ( \< 32 wks gestation)*
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*Cerebral Palsy is a group of clinical syndromes generally characterized as \_\_\_\_\_\_* What are the 3 types? What's the greatest risk factor for Cerebral Palsy?
Nonprogressive motor dysfunction ; ## Footnote Cerebral Palsy is just **SAD** 1. **S**pastic 2. **A**taxic 3. **D**yskinetic Greatest RF = prematurity ( \< 32 wks gestation) but EtOH is second
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*Cerebral Palsy is a group of clinical syndromes generally characterized as \_\_\_\_\_\_* If Cerebral Palsy is suspected, what diagnositc test should be obtained and why?
Nonprogressive motor dysfunction ; brain MRI ; look for etx (periventrivcular leukomalacia or malformation)
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Classic signs of Fetal Alcohol Syndrome - 4
"FAS had drunk mama's baby looking like a **MULE**" 1. **M**icrocephaly 2. **U**pper THIN Lip 3. **L**ong smooth Philtrum 4. **E**yes have short Palpebral fissures
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clinical course for Guillain Barre syndrome (3)
[ascending motor weakness progressive over 2 wks(+/- paralysis) ] ➜ [plateau x 2-4 wks] ➜ [spontaneous recovery over months] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *tx (plasma Xchange/ IVIG ) shortens course duration by 50%*
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Describe **Pseudoexacerbation** of Multiple Sclerosis
[**SLUM** **SiiiN**] Infection in MS pt --\>⬆︎ Body temp --\> ⬇︎Conduction in [Remyelinated healed CNS areas] --\> clinically **APPEARS** to be MS exacerbation BUT REALLY ISN'T! *Image: T1 MRI Black Holes Dx*
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Clinical Manifestation of **Multiple Sclerosis** (9)
Charcot classic triad of MS is a [**SLUM** **SiiiN**] ! ## Footnote **S**ensory sx (think BL Trigeminal Neuralgia) **L**hermittes sign = "electric tingling" down spine into arm & legs when chin is touched to chest **U**hthoff phenomenon (sx ⬆︎ during heat) **M**otor sx **S**canning Speech [**I**nternuclear Ophthalmoplegia (MIOS)] / **I**ntention Tremor / **I**ncontinence **N**euritis Optic - (uL eye pain + vision loss + Marcus Gunn afferent pupillary defect) = ALSO RISK FACTOR
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Demonstrate Sensory Innervation of the Hand Ulnar nerve \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Median nerve \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Radial nerve
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Subarachnoid Hemorrhage is most commonly due to ⬜ \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Clinical Presentation (6)
[Berry Saccular Aneurysm] rupture \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ 1. **“worst HA of my life” ⼀*****sudden severe thunderclap HA different from previous*** 2. Nausea 3. Vomiting 4. LOC 5. meningismus 6. [focal neuro ❌]
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# Subarachnoid Hemorrhage Risk Factors (5)
1. HTN 2. Sympathomimetic drugs 3. Smoking 4. EtOH 5. fHX ## Footnote ✏️*Xanthochromia= yellow tinted CSF due to hgb degradation products*
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# Subarachnoid Hemorrhage ▶ ⬜ within ⬜ hours of sx onset is the initial preferred test for SAH diagnosis – - - - followed by secondary test ⬜ if initial test is negative. For secondary test, ⬜ confirms diagnosis of SAH
[Noncontrast Head CTwithin 2-6h sx] ; [LP confirmatory[ > 6h sx] ⼀*to document [+/- Xanthochromia] (if CT negative)*] ; **XANTHOCHROMIA** \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *Xanthochromia= yellow tinted CSF due to hgb degradation products*
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Clinical Presentation for **Diabetic Ophthalmoplegia** (3) \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Etx?
DM --\> [Oculomotor CN3 **CENTRAL** ischemia] 1. *Ipsilateral* Down & Out Eye 2. Ptosis (from Levator Palpebrae paralysis) 3. **NORMAL PERRL** (since Parasympathetic fibers are spared)
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# transverse myelitis acute myelopathy dx? \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ tx? | *SURE*
dx: GadiliniumMRI _________________ tx: [(CTSHD)]3d ⼀*give for confirmed TMAM via MRI and if high suspicion for compressive CA myelopathy* * SURE sx*
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# Patient presents with Paralysis what's your Workup? (4)
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Clinical presentation of [transverse myelitis acute myelopathy] (4)
*SURE* 1. **S**ensory level (demarcated sensory loss up to specific point) 2. **U**rinary retention 3. [**R**apid developing LE weakness *s/p URI/trauma/CA*] 4. **E**xam [hypOreflexia and flaccidity] ➜ [hyperreflexia and spasticity] *dx = MRIGad*
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clinical presentation of [Complex Regional Pain Syndrome] (6)
1. patient S/P RECENT JOINT INJURY 2. now p/w joint **POOP** 3. joint **burning** 4. joint **edema** 5. joint **skin ∆** 6. joint **⬇︎ROM** ## Footnote *etx: INC sensitivity of sympathetic nerves*
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sx of Meningoencephalitis (7)
"*MeningoEncephalitis* **N**eeds **FAVORS**" **N**uchal rigidity = *Meningo-* **FAVORS** = -*encephalitis* \_\_\_\_\_\_\_\_\_\_\_\_\_\_ **FAVORS**: [**F**ocal neuro ∆ *(aphasia, hemipLegia, hemiparesis)*] , ⭐**A**MS⭐, **V**omiting, **O**uch HA, **R**eally hot fever, **S**eizure
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*Viral* Etiologies of Meningoencephalitis include (⬜3) with treatment (⬜2)
1. [Herpesvirus*(HSV)*] 2. [Arbovirus*(West Nile Virus)*] 3. [Enterovirus*(Coxsackie Virus)*] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ -Acyclovir for HSV -Supportive Care ## Footnote 📄"*MeningoEncephalitis* **N**eeds **FAVORS**"
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*PML Clinically Presents like Multiple Sclerosis* Describe **PML-P**rogressive **M**ultifocal **L**eukoencephalopathy (3)
* Opportunistic infection by [John Cunningham Polyoma Virus]----\> [PML **multiple white** matter lesions] * demonstrated as (***Hyperintense Flair on radiology***) * --\> Death vs. Severe Neuro injury ## Footnote ⚡ *PML is also a RARE side effect of some drugs -- in [JCP virus⊕] pts*
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*PML (**P**rogressive **M**ultifocal **L**eukoencephalopathy) Clinically Presents like Multiple Sclerosis* How is **PML** related to the drug, Natalizumab?
PML is also a potential **Rare Side Effect** of Natalizumab (MS drug) in pts who are [ JCP Virus⊕] ## Footnote *Usual Demographic: HIV pts (reversal of immunosuppresion stops JC Polyoma virus progression)*
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Concussion is defined as [⬜ -3]
{any [neuro❌(brief Confusion, Amnesia +/- LOC)] that occurs i\ [mild TBI **without intracranial structural injury]**} \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *note: it is nml for concussion sx to wax/wane as pt returns to activity*
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# Concussion = [neuro disturbance io\mild TBI with NO structural damage] Concussion Management? (2)
[REST ≥24H] ➜ [gradual return to activity with progression titrated to tolerance] *note: it is nml for concussion sx to wax/wane as pt returns to activity*
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Congenital Torticollis etx
**Malpositioning of Head in Utero vs During birth** --\> constant contraction of SCM--\>Lateral Neck swelling ## Footnote *Torticollis also possible in Adults*
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CP for Chemotherapy Peripheral Neuropathy - 3
1. {***Symmetrical* STOCKING GLOVE*(onset fingers/toes-spreads proximally)* ** ➜ 2. [Loss of SenTor [(S:pain/temp)/(M:weakness)]:} 3. [*early*Loss of ankle jerk reflex] ## Footnote *Drug Culprits: Cisplatin / Paclitaxel / Vincristine* *🔎SenTor = Sensory & MoTor*
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CP of Cerebellar Damage - 7
Cere is def on **GRINDRR** **G**ait Ataxia {[vermis → truncal ataxia] / [hemisphere → limb ataxia IPSILATERAL]} **R**apid alternating mvmnt impairment **I**ntention tremor/Dysmetria IPSILATERAL (hemisphere) **N**ystagmus IPSILATERAL (medial AND Lateral Vermis) **D**ysarthria (Lateral Vermis only) **R**ebound phenomenon (pt hits themself in face if flexing bicep and examiner releases arm-*image*) **R**eflex Pendular (knee swings \>4x after Deep tendon reflex is elicited) *Vermis is midline*
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Alcoholic cerebellar degeneration causes damage to the ⬜ \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ How can you differentiate Alcoholic cerebellar damage from other causes of cerebellar damage?
[Purkinje cells of cerebellar vermis (→ truncal ataxia & dysarthria)] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Alcoholic cerebellar damage **LEAVES LIMB COORDINATION (cerebellar *hemisphere*) INTACT** (no intention tremor) | *Cere is def on **GRINDRR*** ## Footnote *cerebellum:* *-vermis(central)❌ ➜ [truncal ataxia + dysarthria]* *-hemisphere(Lateral)❌ ➜ {[Limb ataxia IPL(intention tremor/loses balance toward lesion)]*
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cp of [Medial Medullary syndrome] -(3)
1. [ hypoglossal CN12 nc❌ →IPL tongue weak *deviates toward lesion ("you lick your wounds")*] 2. [medial lemniscus❌ → CTL FaceBodynumb(2TVP loss) ] 3. [Lateral CST*Pyramidal Tract*❌ → CTL bodyweak(hemiparesis)] ## Footnote [(AsA❌) +(VA❌)] → [medial medullary syndrome]
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cp of [Lateral Medullary syndrome of Wallenberg] -(6)
**VSINSY** **V**estibular = [VDNV]sx [**S**tG *Spinal triGeminal*] = [IPL face pain/temp loss] **I**nferior cerebellar Peduncle = ataxia **N**ucleus ambiguus = {[dysgag *(gag reflex⬇︎)*] , dysphonia, dysphagia} [**S**TT *SpinoThalamic Tract*] = [CTL BODY pain/temp loss] **Y**sYmpathethetic descending fibers = [IPL Horners] ## Footnote VDNV = Vertigo/Diplopia/Nausea/Vomiting
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Brachial Plexus damage of [Upper Trunk {(C5)(C6)} n] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ clinical presentation?
[Erb Palsy Waiter's Tip]
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Brachial Plexus damage of [Upper Trunk {(C5)(C6)} n] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ cause
[Baby Delivery lateral neck pull]
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DDx for Clostridium Botulinum - 4
*Also consider...* 1. Myasthenia Gravis 2. Atypical Guillain Barre 3. Tick Paralysis 4. Brain Stem infarct *Adult tx: Equine Heptavalent Antitoxin (passive immunity)*
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*DDx of Neuromuscular Weakness has 5 origins* Describe **Upper Motor Neuron** causes of Neuromuscular weakness - 4
1. Vasculitis 2. Leukodystrophy 3. Mass 4. VitB12 deficiency
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*DDx of Neuromuscular Weakness has 5 origins* Describe **Anterior Horn Cell** causes of Neuromuscular weakness - 4
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Deficiency of what INC risk for Restless Leg syndrome? \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *unpleasant LE sensation at night or during rest, relieved by moving* ​
IRON ## Footnote *(dx = FerriTin ≤75 )* \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *other RF: Pregnancy/Uremia/DM/MS/[anti:MDD|Psychotics|Emetics]* *1st line tx = Gabapentin*
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Define Coma (6)
1. **Unarousable** sleep state + 2. **Unresponsive** sleep state 3. [brainstem reflexes] intact 4. [Spinal reflexes] intact 5. 2/2 diffuse cortex depression 6. can progress to vegetation / full recovery / brain death
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*DELIRIUM IS A MEDICAL EMERGENCY* Based on consciousness, how do you differentiate Delirium from Dementia ?
Delirium = CONSCIOUSNESS RAPIDLY FLUCTUATES \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ ​Dementia = consciousness intact *note: return of Primitive reflexes is normal in Dementia*
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Describe Athetosis ; What disease is it seen in?
Slow, writhing mvmnts of hands & feet often occuring **with** Chorea (*Choreoathetosis*) ; Huntington's
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What are the **TRAUMATIC LUMBAR PUNCTURE** CSF lab ranges Glucose Protein WBC count RBC count
**GPW-R** **G** ⇪ **P** ⇪ **W** ⇪ **R**BC 6K \< *Traumatic LP (without xanthrochromia)* \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *xanthochromia = discoloration of CSF 2/2 hgb breakdown that appears within 2-12h of SAH*
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What are the **Normal** CSF lab ranges Glucose Protein WBC count RBC count
**GPW****-R** **G**lucose: 40-70 **P**rotein: \<40 **W**BC: 0-5 **R**BC: \< 6K \< *Traumatic LP*
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Describe CSF analysis for **TB** meningitis Glucose Protein WBC
[**G** low \< 45] [**P** High 100-500] [**W** High 100-500]
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Describe CSF analysis for **Cryptococcal Neoformans** meningitis Glucose Protein WBC
[**G** low\< 40] [**P** Up \>40] [**W** Up \<50 (Lymphocytes)] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ + CSF opening pressure \> 250 || Occurs in advanced HIV || Dx = India Ink Prep or Antigen test
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Describe CSF analysis for **Bacterial** meningitis Glucose Protein WBC
[**G** low\< 40] [**P** High \>250\*] [**W** UBER HIGH \>1,000] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *\*G might be higher & P might be lower if pt s/p abx pretx*
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Describe CSF analysis for **Guillain Barre**: Glucose Protein WBC count
[**P** UBER HIGH 45-1,000] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ normal **G** / **W**
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Describe CSF analysis for **Viral** meningitis Glucose Protein WBC count
[**P** HIGH\<150] [**W** HIGH 10-500 (Lymphocytes)] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ normal **G** *Note: HSV = ⬆︎Protein and ⬆︎ RBC also from temporal lobe destruction*
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Dementia with Lewy Bodies (DLB) CP - 3
DLB at the **DMV** 1. **D**ementia/confusion periodically*(tx = Rivastigmine)* 2. **M**ichaelJFox Parkinsonism (PARK + hamp) tht **does NOT respond to dopaminergic tx** 3. **V**isual Hallucinations*(tx = SGA)* ## Footnote ✏️*Lewy Body= [**LABS** (**L**ewy **α**-synuclein **B**odie**S**)] that are Eosinophilic intracytoplasmic accumulations*
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Pts with [Dementia with Lewy Bodies (DLB)] are extremely sensitive to _____ and it may cause what side effects?-3
DLB at the **DMV** ## Footnote ANTIPSYCHOTICS \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ - Dementia INC - MichaelJFox PARK INC - autonomic dysfunction
140
Describe En-Bloc Gait \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ What type of ataxia is this?
Minimal mvmnt of head while walking w/staggering gait \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Vestibular Ataxia ## Footnote *Will be accompanied w/Vertigo & Nystagmus*
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[Essential *(Physiologic)* Tremors] clinical features (7)
1.benign [**12-14 Hz** **high freq**] action tremor 2.occurs posturally (i.e. when holdings arms out); 3.worst with action 4.activated w/emotion 5.activated w/caffeine 6.[BUE/voice/head] 7. Auto DOM
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Describe the "Clasp Knife" phenomenon \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ What disease is this related to?
**Rapid SPASTIC** **RESISTANCE** to passive mvmnt of limb \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ UMN (Weak ME**S**H) Pyramidal Tract dz * Pyramidal Tract = Corticospinal and Corticobulbar* * Pronator Drift also indicates Pyramidal Tract Dz*
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Px for Migraine HA - 4
**VTAP** the migraine BEFORE it comes, and **SEND** it on its way when it does! 1. **V**erapamil 2. **Topiramate** 3. **A**mitryptyline 4. **P**ropranolol
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Tx for Acute Migraine HA - 4
**VTAP** the migraine BEFORE it comes, and **SEND** it on its way when it does! 1. **S**umatriptan 2. **E**rgots (Bromocriptine) 3. **N**SAIDs 4. **D**2 R Blockers (Metaclopramide/Prochlorperazine)
145
Describe the **Character** for the HA: Migraine Cluster (3) Tension (2)
Migraine = **POUND** = [**P**ounding/**O**ne Day-3 day Duration/**U**nilateral/**N**ausea/**D**isabling] + photo vs. phonophobia & [flashing dots aura] Cluster = [Excruciating, sharp & steady] *(100% O2 tx)* Tension = Dull & tight
146
Describe the **Duration** for the HA: Migraine Cluster Tension
Migraine = **POUND** = [**P**ounding/**O**ne-3 Day Duration /**U**nilateral/**N**ausea/**D**isabling] + photo vs. phonophobia & [flashing dots aura] Cluster = 15 - 90 MINUTES *(100% O2 tx)* Tension = 30 min to 7 DAYS!!!! (*Tammy's Entire Work Week*)
147
Describe *tube* presentation of a traumatic CSF lumbar puncture
Elevated RBC in 1st tube, followed by declining numbers of RBC with each successive tube
148
Frontotemporal Pick's Dementia Sx -2
Prounouced Frontal & Temporal lobe atrophy --\> [**Socially inappropriate** Behavior] + aphasia *OCCURS MORE IN FEMALES!!!*
149
Demographic of Frontotemporal Pick's Dementia? \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Mode Of Inheritance
50-60 yo Females \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ AUTO DOM | *Alzheimers \>60 yo* ## Footnote *Socially inappropriate behavior + aphasia*
150
Describe Neuroleptic Malignant Syndrome - 5
RARE SE of Any Dopamine Blocker (Antipsychotics vs. GI meds) that --\> **FEVER** - [**F**ever \> 40C] - **E**ncephalopathy (Confusion) - **V**itals unstable (INC HR / RR / BP from autonomic dysfunction) - **E**nzymes ⬆︎ (CPK) - [**R**igitidy lead pipe] (Tremor)
151
Diagnostic Criteria for Febrile Seizure - 5
1. 3 mo - 6 yo 2. Temp \> 38C 3. No hx of **A**febrile seizures 4. No CNS infection 5. No acute metabolic cause of seizure (*pt would have dehydration*) *Tx = Reassurance only!*
152
Diagnostic criteria for Nightmare Disorder - 4
1. **M**akes recurrent awakenings 2. re**M**embers their nightmare 3. **M**anageable (CAN be consoled) upon awakening 4. **M**ind is alert upon awakening ## Footnote -*Night**M**ares occur during RE**M*** -*Night**M**ares are developmentally normal for kids*
153
Diaphragmatic paralysis can be easily confused with ⬜ because they both cause ⬜ . What's the most common cause of bilateral diaphragmatic paralysis?
CHF; orthopnea \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ ALS
154
# Subarachnoid Hemorrhage Dx (5)
1st: [**NONCONTRAST HEAD CT** *(ideally within 6-12h of sx)*] 1b. CT⊕ ➜ Cerebral angiography to identify bleeding source \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ 2nd: CT⊝ ➜ REQUIRES [Lumbar Puncture confirmation *(ideally \>6h from sx)*]\*\* 2b. LP⊕ =[**xanthochromia = CONFIRMS DIAGNOSIS**] but other findings= [⇪ opening pressure]/[⇪ RBC in all 4 CSF tubes] 2c. LP⊝ = r/o SAH
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# Subarachnoid Hemorrhage Why do negative [Noncontrast Head CT] have to be followed with a negative ⬜ before SAH can be ruled out conclusively \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Ideally when should this subsequent test be done and why?
[Lumbar Puncture confirmatory *(ideally \>6h from sx)*]\*\* \*\*(*some bleeds are outside ideal 6-12h CT window and/or are too small for CT)* \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ perform LP \> 6h from sx onset since.. *[CSF blood can take up to 6h to degrade and form Xanthochromia = LP ideal\>6h from sx]*
156
Dx for Creutzfeldt Jakob disease - 6
1. [PRNP prion protein] genetic testing 2. EEG Biphasic vs Triphasic **sharp wave complexes** 3. Postmortem brain biopsy 4. ⬆︎CSF 14-3-3 proteins 5. MRI Cortical Ribbons 6. MRI basal ganglia hyperintensity
157
Dx for VitB12 deficiency - 3
1. [⬆︎ **Methylmalonic Acid levels**] 2. CBC showing Macrocytic Anemia 3. Serum Vitamin levels
158
Which drugs are used to treat Multiple Sclerosis Exacerbation?-2
**1st: High Dose** **IV** **Methylprednisolone** 2nd: (Refractory): Plasmapheresis
159
Which drugs are used to treat Multiple Sclerosis maintenance?-3
Maintenance: **1. [β-interferon]** **2. [Glatiramer acetate]** 3.Natalizumab
160
Dx for **Multiple Sclerosis** - 5 \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Which diagnostic is the *preferred* test for MS? Which diagnostic is the *backup* test (used in equivocal cases) for MS?
1. T2 MRI: [**Periventricular** white matter demyelinating plaques with lipid laden macrophages] *= PREFERRED TEST* 2. [CSF Oligoclonal IgG bands = *backup test*] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ 3. T1 MRI Black holes 4. Clinical (SLUM SiiiN) 5. Visual conduction velocity test *Sx will be disseminated in time and space*
161
What do [{MS**⊕**}[Pregnant pts] and [{MS**⊕ **}[NONPregnant pts] have in common? \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ What additional risk does having MS pose for pregnant patients? (2) *MS: Multiple Sclerosis*
SAME TREATMENT for MS Exacerbation ⼀*[Methylprednisolone IV High Dose] is used for MS Exacerbation in Pregnant patients and Non-Pregnant MS patients* *\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_* 1. [MS⊕ Pregnants] have INC risk for [assisted delivery (cesarean/vacuum/forceps)] 2. [MS⊕ Pregnants] have INC risk of their infant developing MS as well
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[Pregnant MS⊕] typically have {[**⬜** lower | HIGHER] *MS activity*} during pregnancy and {[**⬜** lower | HIGHER] *MS activity*} during postpartum ## Footnote *MS: Multiple Sclerosis*
lower; HIGHER
163
**Normal Pressure Hydrocephalus** Sx (3) \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Which is earliest to present?
⬇︎CSF absorption --\> **Wobbly**, Wet & Wacky! ## Footnote [ **Wobbly** magnetic frontal gait apraxia] = EARLIEST CLINICAL FINDING] Wet (Urinary Incontinence from compressing periventricular cortico-cortical white fibers traveling to sacral micturition center) Wacky (memory loss)
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**Normal Pressure Hydrocephalus** characteristics - 4
**Wobbly**, Wet & Wacky! 1. Idiopathic 2. Episodic *⇪ in CSF pressure* 3. Normal *Pressure Hydrocephalus that Does not ⬆︎ SubArachnoid space volume* 4. Elderly
165
What's the only imaging modality for diagnosing Alzheimer's Disease? \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Which areas does it reveal this in? - 3
**CLAV --\> HANDU** PET scan revealing [**PIB**-Pittsburgh Compound B] binding to β-amyloid and being taken up in 1. PreFrontal 2. Temporal 3. Parietal ## Footnote **NaTPO** = [**CLAV** ➜ **HANDU**]sx
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**Early** Findings of Alzheimer's - 4
**CLAV --\> HANDU** **C**ognitive PROGRESSIVE ⬇︎ **L**anguage ⬇︎ **A**nterograde immediate memory loss **V**isualspatial disorientation (lost in ur own neighborhood) *Onsets after 60 yo* ## Footnote **NaTPO** = [**CLAV** ➜ **HANDU**]sx
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Clinical Criteria for diagnosing Alzheimer's -5
*Alzheimer pts wear Alzheimer [**GOWNS**]* 1. **G**OE 2 Cognitive deficits 2. **O**nsets after 60 yo 3. **W**orsening Memory 4. **N**o other Systemic/Neuro DO to cause cognitive defects 5. [**S**ound (Consciousness intact)] ## Footnote {**NaTPO** = [**CLAV** ➜ **HANDU**]sx per [**GOWNS**]}
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**Late** Findings of Alzheimer's - 5
**CLAV --\> HANDU** **H**allucinations **A**gnosia (lack of insight regarding deficits) **N**euro ∆ (seizure/myoclonus) **D**yspraxia (difficulty w previously Learned Motor task) **U**rinary Incontinence *Onsets after 60 yo* ## Footnote **NaTPO** = [**CLAV** ➜ **HANDU**]sx
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Alzheimer's tx - 7 \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Which medication should be used last?
CLAV --\> HANDU **DR TAG MR** *Alzheimer* 1. Donepezil - *AChnesterase inhibitor* 2. Tacrine - *AChnesterase inhibitor* 3. Rivastigmine - *AChnesterase inhibitor* 4. Galantamine - *AChnesterase inhibitor* 5. Memantine - *NMDA R Blocker: **USE LAST*** 6. Respite Care for Caregivers (ex: Adult day program) 7. Atypical antipsychotics - Olanzapine vs Risperidone (for acute psycosis) ## Footnote **NaTPO** = [**CLAV** ➜ **HANDU**]sx
170
[*early* Neurosyphilis] typically presents during the ⬜ syphilis stage. How does it present? -3
2nd; [**M**eningo-Vascular*(Meningitis vs CVA)*] | POST**U**veitis*MOST COMMON Sx❗️* | **T**innitus ## Footnote *prodrome ➜* **MUT** ➜ **DAT**
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[*LATE* Neurosyphilis] presents during the ⬜ syphilis stage. How does it present? -3
3rd ; **D**ementia |**A**rgyll Robertson Pupils | [**T**DPCD(⊕Romberg, ⊝DTR)] | *TDPCD: Tabes Dorsalis Posterior Column Disease* ## Footnote *prodrome ➜* **MUT** ➜ **DAT**
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Explain [Relative Afferent Pupillary Defect]
**partial** optic n vs retinal lesion --\> pupils BOTH constrict when light is shown in normal eye BUT when light is *swung* to **lesioned** eye BOTH eyes Dilates since lesioned eye has ⬇︎ afferent input
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Recall the Pupillary pathway beginning with light entering the eye (5)
## Footnote 1. Light enters retina 1 eye and that [Optic CN2] **uL** sends signal to [midbrain-SUP colliculus -pretectal nuclei] 2. "cross" decussates to... 3. → activate **BOTH** [Edinger Westphal nuclei]! BUT... 4. → **each** EWN sends its own **IPL** [efferent preganglionic parasympathetic outflow] to its **IPL** ciliary ganglion via [Oculomotor CN3] 5. that IPL ciliary ganglion uses short ciliary nerves to activate the pupillary sphincter muscle = *Miosis*
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*Edinger Westphal nucleus provides* ⬜ *to the* ⬜ *ganglion* CP of a pt with R damaged EW nucleus
PreGanglionic [ParaSympathetic efferent OUTflow] to ciliary ganglion **R** (Ipsilateral) FIXED DILATED pupil not reactive to light
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*Essential Tremor is a [ (BUE/Head/Voice) Action Tremor]* What are the 3 clinical exacerbants of Essential Tremor?
1. Hyperthyroid 2. Lithium 3. Valproic Acid
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Etx of Parkinsons Disease
[**LABS** (**L**ewy **α****-**synuclein**B**odie**S**)] accumulation in [substantia nigra pars compacta] --\>degeneration --\> ⬇︎Dopamine release and ⬇︎ stimulation of Striatum which --\> allows [Globus pallidus internal] to continuously inhibit [VA/VL Thalamus from stimulating motor cortex]
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# The Basal Ganglia consist of what 5 things? Recall the ____ Basal Ganglia pathway for movement starting with Cortex a. DIRECT (5) b. InDirect (5)
"**C**an **P**retty **G**ays **S**ound **S**mart?" -**C**audate -**P**utamen -**G**lobus Palidus -**S**ubthalamic nucleus -**S**ubstantia Nigra
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Explain how a Physician should approach the discussion of [Brain Death Diagnosis] and [Organ Donation]
1st: [Brain Death Dx] = Physician \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ **Later: [Organ Donation] = [OPO (Organ Procurement Organization)]**
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Explain how collateral blood flow to a "complete" circle of willis help prevent ischemic CVA/TIA?
**[External Carotid: Ophthalmic A]** can retrogradedly perfuse [Circle of Willis] when Internal Carotid is blocked
180
Fall has 3 main etiologies ( ⬜ , ⬜ or ⬜ ) \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ What are the 10 crucial points of medical history to work up Fall?
Mechanical 🆚 Syncope 🆚 Seizure \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ **HANDSTAMPED** **H**x Syncope? **A**ssociated symptoms **N**umber of episodes **D**uration **S**etting **T**ime until recovery **A**cknowledged/Witnessed? **M**edical hx **P**rodrome? **E**pilepsy hx **D**rug use? | "All *Fall* pts should be **HANDSTAMPED** by a MD"
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Febrile seizures present day ⬜ of illness, are a common complication of high fever a/w ⬜, and onset between ⬜ y/o \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ What is the prognosis for children with febrile seizure (3)
1 ; viral infection ; [3 months - 6 yo] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ -typically [benign course (does not require *abortive* tx)] - but 30% will have **≥1 recurrence** - and 30% will also have INC risk for **Epilepsy**
182
*Usually Simple Partial Seizures originate in a **single** hemisphere* **Simple** Partial Seizures may present as what 3 things?
1. Motor ∆ (head turning) - no LOC 2. Sensory ∆ (paresthesias)- no LOC 3. Autonomic ∆ (sweating)- no LOC
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For cp, what are 2 ways to differentiate [NRSADSleepTerror] from [RSRBD]? ## Footnote *RSRBD = REM Sleep Related Behavioral Disorder*
# Output "I love Ruby" [NRSADSleep Terror] = SUDDEN, INCONSOLABLE **N**on**R**EM **S**leep **A**rousal(**D**isorder)*] \_\_\_\_\_\_\_\_*vs*\_\_\_\_\_\_\_\_\_ [**R**SRBD= **R**EM = *"**R**eally "acting out dreams"*] ## Footnote *NRSAD = Non-REM Sleep Arousal Disorder* *RSRBD = REM Sleep Related Behavioral Disorder*
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The 3 types of dream disorders are ⬜, NRSAD and ⬜ \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Describe characteristics of NRSAD (5) ## Footnote *NRSAD = Non-REM Sleep Arousal Disorder*
RSRBD | NRSAD | NightMareDisorder \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ NRSAD 1. [recurrent **incomplete** awakenings from NonREM sleep] 2. ... complicated by DREAM AMNESIA ...that presents as either 3. [NRSAD*SleepWalking*(blank face/unresponsive to awakening)] or 4. [NRSAD*SleepTerrors*(abrupt autonomic arousal/unresponsive to consoling) ] 5. [self limited to ≤2y after onset (give benzo qhs if severe)] | Sleepwalking and SleepTerrors are both qualifiers (types) of NRSAD ## Footnote *NRSAD = Non-REM Sleep Arousal Disorder* *RSRBD = REM Sleep Related Behavioral Disorder*
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# NRSAD dx has 2 types = must be qualified as either ⬜ or ⬜ What is the clinical progression of NRSAD (3) ## Footnote *NRSAD = Non-REM Sleep Arousal Disorder*
[SleepWalkingNRSAD] ; [SleepTerrorNRSAD] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ -onset 4-12 yo -➜ **RESOLVES SPONTANEOUSLY ≤ 2 YEARS FROM ONSET** -(if SEVERE = low-dose benzo qhs)
186
# It is common for AIDS pts with Cryptococcal n. meningitis to develop ⇪ ICP due to ⬜ ➜ ⬜ sx For pts with recurrent sx of ⇪ ICP from [Cryptococcal n meningitis], how is this treated?
[high CSF fungal burden clogging arachnoid villi] ➜ ⬇︎ CSF outflow ➜ ⇪ ICP ; [**HEAD**sx ] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ [serial LP *until sx resolve*] ## Footnote ✏️ICPsx = **HEAD** = [**H**eadache \ [**E**ye papilledema/vision change] \ **A**MS \ [**D**ont eat_NV]
187
Friedreich Ataxia involves Degeneration of the ⬜ , ⬜ and ⬜ spinal columns.
Fri**E**dreich Ataxia involves Degeneration of the [**Dorsal**, **Lateral CST** and **SpinoCerebellar** spinal columns] ## Footnote * Fri**E**drecih is **Frat**astic! He's your fav. **twisted** **frat** brother, always **studdering** and **falling**, but has a **sweet**, **big heart*** * etx = [auto recessive Chromo 9 GAA repeat] → impaired [frataxin (iron binding protein)] which → widespread mitochondrial impairment → sx* *SuBACute Combined Degeneration affects SAME 3 columns*
188
Functions of the Obturator n.-2
1. MOTOR Leg ADDuction 2. SENSORY medial thigh \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *usually from pelvic trauma or surgery*
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**GCS**(**G**lasgow **C**oma **S**cale) predicts Prognosis of what 4 things? \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ The 3 components are **EVM** (**E**yes/**V**erbal/**M**otor) Describe the [**V**erbal Response] component (5)
* GCS prognosis'* *Brain **CHIT*** 1. **C**oma 2. **H**emorrhage (SAH) 3. **I**nfection (bacterial meningitis) 4. **T**rauma \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ **EVM** = **E**yes / **V**erbal / **M**otor
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**GCS**(**G**lasgow **C**oma **S**cale) predicts Prognosis of what 4 things? \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ The 3 components are **EVM** (**E**yes/**V**erbal/**M**otor) Describe the [**E**yes] component (4)
* GCS prognosis'* *Brain **CHIT*** 1. **C**oma 2. **H**emorrhage (SAH) 3. **I**nfection (bacterial meningitis) 4. **T**rauma \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ **EVM** = **E**yes / **V**erbal / **M**otor
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**GCS**(**G**lasgow **C**oma **S**cale) predicts Prognosis of what 4 things? \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ The 3 components are **EVM** (**E**yes/**V**erbal/**M**otor) Describe the [**M**otor] component (6)
* GCS prognosis'* *Brain **CHIT*** 1. **C**oma 2. **H**emorrhage (SAH) 3. **I**nfection (bacterial meningitis) 4. **T**rauma \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ **EVM** = **E**yes / **V**erbal / **M**otor
192
What's the marker for [Glioblastoma astrocytoma]?
**GFAP**
193
HemiNeglect Syndrome
Stroke in **[*NonDominant* Parietal cortex])** --\> Neglect of anything on the CTL side ## Footnote *Most R handed have [L hemisphere Dominance] = HemiNeglect Syndrome will occur if [NonDom (R) parietal ❌]➜ [pt neglects entire OPPOSITE (L) side]* *It's opposite for L handed*
194
What Dx should you suspect in a *Young HIV pt witih Dementia*? \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Pgn?
[**AIDS Dementia** HIV Encephalopathy]= slow cognitive & behavioral decline with POOR PGN . *Note: This presentation is Similar to [SuBACute Combined Degeneration]* | *HIV _Leuko_Encephalopathy is same thing but with White matter instead*
195
Homocystinuria tx -2?
[Pyridoxine B6] + AntiCoag ## Footnote 🔬*MOA = auto recessive [Cystathionine synthase] deficiency --\> Thromboembolism--\> Stroke*
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Homocystinuria dx-2
[Homocysteine⬆︎] and [Methionine⬆︎] ## Footnote *etx = auto recessive [Cystathionine synthase] deficiency --\> Thromboembolism--\> Stroke*
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Homocystinuria Clinical presentation-5
**{1. Stroke -h}** **{2. Retarded -h}** **{3. Fair*(Fair Hair /Fair Eyes)* -h}** \_\_\_\_\_\_\_\_*vs*\_\_\_\_\_\_\_\_\_ 4.[Marfanoid habitus (elongated limbs, arachnodactyly, scoliosis)] - MH 5.Ectopia Lentis - MH | *auto recv [Cystathionine synthase] deficiency --\> Clotting--\> Stroke* ## Footnote *MH = MARFAN and HOMOCYSTINURIA* *h = homocystinuria only*
198
How are HTN and DM mngmnt related to Acute CVA/TIA - 2
BP \> 185/110 in setting of stroke can --\> ICH - so Use Labetalol & Hyperglycemia augments brain injuries (*so ONLY use **Non**Dextrose IVF*)
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# [transverse myelitis] and [Guillain Barre Syndrome] both p/w LE paralysis How do they differ in \_\_\_\_\_\_ a. Motor b. Sensory
200
# [transverse myelitis] and [Guillain Barre Syndrome] both p/w LE paralysis How do they differ in \_\_\_\_\_\_ a. autonomics b. Cranial Nerves c. EMG/nerve conduction velocity
201
# [transverse myelitis] and [Guillain Barre Syndrome] both p/w LE paralysis How do they differ in \_\_\_\_\_\_ a. MRI b. CSF
202
How is Carotid Artery Dissection associated with Horner Syndrome?
Carotid A Dissection --\> **Partial** Horner (Ptosis + Miosis only) 2/2 postganglionic sympathetic fiber damage
203
Name the most important things to do when administering tPA to a stroke patient? (3)
1.STRICT IV BP CONTROL{[< 180/110 *before tPA*] [< 180/105 *after tPA* ] ## Footnote (avoid HTN to ⬇︎risk of hemorrhagic conversion but avoid hypOtension to maintain perfusion to the ischemic penumbra) \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ 3.wait ≥24h before ANY BLOOD THINNER
204
What test is used to determine definitive tx for Normal Pressure Hydrocephalus? \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Describe the test​
• MFLT (Miller Fisher Lumbar Tap) test = predicts if VPS placement will be helpful (and worth surgical risk) for definitive treatment in a NPH patient • (GCbaseline ➜ [CSF MFLT] ➜ GCIMPROVED ➜ VPS)​ \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *VPS = VentriculoPeritoneal Shunt // (G/C=Gait/Cognition )* ​
205
Why is a [rapid bedside dysphagia screening] required for Acute Stroke patients?
Stroke patients (especially if +dysarthria) have ⇪ risk for oropharyngeal dysphagia and aspiration = CAN NOT RECEIVE ANY MEDS BY MOUTH (like ASA) until [rapid bedside dysphagia screening performed]
206
How do you manage Ischemic Stroke? (4)
207
How do you treat Febrile Seizure? -3
1. 🟩**REASSURANCE** 2. 🟩APAP for fever 3.*🟨[abortive tx if ≥5 min]*
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How do you treat *Refractory* Serotonin Syndrome
Cyproheptadine (antihistamine with anti-serotonergic properties)
209
*prior to diagnosing Dementia, reversible causes of Cognitive impairment must be r/o* How do you workup Cognitive impairment ? (10)
210
how does hyperventilation reduce intracranial pressure?
*(reduce to 25-30 mmHg)* hyperventilation ➜ DEC pCO2 ➜ cerebral arteriole vaso**constriction** ➜ DEC ICP
211
How does Papilledema present in pts with Pseudotumor Cerebrii Idiopathic Intracranial HTN?
transient vision loss when changing head positions that last a few seconds Can --\> Vision Loss!
212
What role does Steroids play in [Intracerebral processes(tumor, infection, trauma)] ?
*CTS* DEC **edema** /swelling (in intracerebral processes 2/2 to *C*A|*T*umor|*S*ickness_infxn) | *"**S**top **M**y **H**ead **S**welling (**C**ancer) !"*
213
How is the [Oculocephalic Dolls eye Reflex] used to assess brainstem function?
Eyes should **remain stationary** **and fixed** as head is rotated = normal brain stem function ## Footnote "Dolls Eyes a NORMAL GUY" (Dolls Eyes = Brainstem intact)
214
How is [Apolipoprotein E] related to Alzheimers (2)
✔︎ ApoE2*"brings you 2 safety"* = actually DEC Alzheimer risk \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ ✔︎ ApoE**4***"is bad **4** you!"* --\> impairs synthesis and clearance of AB-amyloid ---\> INC risk for **LATE** onset Alzheimers ## Footnote **NaTPO** = [**CLAV** ➜ **HANDU**]sx
215
How long does it take pts with Subdural hematoma to have sx? Why is this a problem for elderly?
1-2 days; Elderly may have insidious subdural bleeds for weeks after injury --\> Confusion/Somnolence/HA/FOCAL Neuro ∆ ## Footnote *Image: L **Chronic** Subdural Hematoma*
216
DDx for patient p/w [1/2 facial paralysis*(with ⊝ forehead sparing)*] ?
[**Lyme** serology 1st] ➜ [**P7BP**Bells palsy (dx of exclusion!)] ## Footnote ⚠️{[⊕**S**paring*of forehead* ] = [⊕**S**troke*in patient* ]!}
217
What causes [Lateral ventricle frontal horn] enlargement in Huntington's disease?
\*\***Gross Caudate atrophy**\*\* ## Footnote [AUTO DOM [Chromo 4 CAG repeats]] ---\> Degeneration of (**Caudate** nc. inside the ((**I**)ndirect Striatum w/ [**Gross Caudate atrophy**] ) --\> [⬇︎ GABA release] *"Hunting **4** food is way too aggressive & dancey"*
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Huntington's Dz Clinical Presentation (2)
* "Hunting 4​ food is way too **aggressive** & **dancey**"* 1st: **Aggressive** Dementia w/ strange behavior 2nd: **Dance**-like Choreoathetosis (dancing/writhing movements) * AUTO DOM = Affects BOTH sexes equally!!*
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Etx of Huntington's Disease
[AUTO DOM [Chromo 4 CAG repeats]] ---\> Degeneration of (**Caudate** nc. inside the ((**I**)ndirect Striatum w/ [Gross Caudate atrophy] ) --\> [**⬇︎ GABA release** /⬇︎ACh release / but ( ⇪ dopamine releasae) ] ## Footnote *"Hunting **4** food is way too aggressive & dancey"*
220
Identify ; Which are Lenticulate and which are Striatum?
*"**G**ay **P**eople **C**ook!" = Basal Ganglia* ***G**ay **P**eople=Lenticulate // **P**eople **C**ook= Striatum* * eg = **G**lobus Pallidus * es = **P**utamen * d = **C**audate
221
In Neurology, evoked potentials are used to identify what?
silent CNS lesions
222
The 3 types of dream disorders are ⬜, NRSAD and ⬜ \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Name the primary characteristics of [NRSAD: Sleep Terrors] ? (4)
RSRBD | NRSAD | NightMareDisorder \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Sleep terrors are : 1. NRSAD (NonREM) 2. accompanied with recurrent incomplete awakenings 3. can NOT be consoled upon wakening 4. **S**eems to forget the dream = Dream Amnesia/No Dream Recall ## Footnote *NRSAD = Non-REM Sleep Arousal Disorder*
223
# *identify (12)*
224
# *identify (21)*
225
A: Identify Boxes (4) B: Clinical Presentation for lesion at A? B? C? D?
| A=[central scotoma 2/2 macular degeneration] ## Footnote 👓when image hits 1º visual cortex, it is *upside down* and *R-L reversed* #visual field defect.hemianopia.Meyer loop
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A: Identify Boxes (4) B: Clinical Presentation for lesion at E? F? G? H C: Explain how [H] is special (*** )?
C: [**H**] is actually {[**K**]-{CTL Homonymous Hemianopia*with macular sparing*} if [PCA occluded]
227
# *identify (14)*
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# cp for conduction aphasia? (3) What areas of the brain are involved in **CONDUCTION** Aphasia? - 4
⛔[**VERY POOR** Repetition](CAN NOT REPEAT phrases such as *"No ifs, ands or buts"*) but ✔︎ intact speech fluency ✔︎ intact comprehension ## Footnote 1. Arcuate Fasciculus = MOST COMMON 2. Supramarginal Gyrus 3. Auditory Cortex 4. Large Posterior Perisylvian area
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What is Kluver-Bucy syndrome?
**[BL Amygdala❌ (associated with HSV1)]** → *hyper*disinhibited behavior*(hypersexual, hyperphagia, hyperorality)*
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In patients with lesions of the *PPRF*, Eyes stare [⬜ opposite | toward] the *PPRF* lesion | *PPRF = Paramedian Pontine Reticular Formation*
opposite
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In patients with a {*Frontal Eye Field* lesion}, Eyes stare [⬜ opposite | toward] the {*Frontal Eye Field* lesion}
toward | *"eyes Front Toward me!"*
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# pt present s/p trauma to the **BL Hippocampus** lesions of **BL Hippocampus** → ⬜
anterograde amnesia (inability to make **new** memories)
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clinical features of Cerebral "Watershed Zones" (4)
✔︎ areas between [ACApz & MCApz] and ✔︎ areas between [MCApz & PCApz] ✔︎ susceptible to [irreversible brain damage io\ischemic hypoxia] *(Cerebellum, Neocortex, Hippocampus - also)* ✔︎ [WZ❌ → upper arm weakness and/or upper leg weakness] | [pz🔎perfusion zone]
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**MCA (Middle Cerebral Artery)** A: What 5 sites does MCA perfuse? (5) B: For each site, list Sx when compromised(*i.e. Stroke)* (5)
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**AsA (ANT spinal Artery)** A: What all does it perfuse? (3) B: Sx if compromised(*i.e. Stroke)* (3)
## Footnote [(AsA❌) +(VA❌)] → [medial medullary syndrome]
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# clinical features epidural hematoma (6)
1. fx of temporal bone 2. → rupture of [middle meningeal artery (from Maxillary artery)] 3. → Lucid interval f/b [hyperdense biconvex/lentiform epidural hematoma w transtentorial herniation] + DO3P 4. [⛔ suture linesXing] 5. [ ✅ falxXing] 6. [✅ tentoriumXing] ## Footnote *🔎DO3P = ["DOPe" Oculomotor CN3 Palsy]* *🔎Xing = Crossing*
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Why is the period after a SubArachnoid Hemorrhage important? (2)
[*3d s/p SAH*] can → 1. [cerebral vasospasm (tx = Nimodipine)] 2.***repeat***SAH
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3 most common locations for [Intraparenchymal HTN Hemorrhage]
1. basal ganglia 2. internal capsule(Charcot Bouchard ruptured aneurysm of lenticulostriate) 3. lobar
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# Irreversible brain damage begins after ⬜ min of hypoxia Which areas of the brain are most susceptible to [hypoxic-irreversible brain damage] during 🔲 < *ischemic* stroke? (4) > \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ <*hemorrhagic* stroke? >
5; ## Footnote *ischemic*: "Clots Never Help Watershed"[hippocampus|neocortex|cerebellum|watershed] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *hemorrhagic*: basal ganglia
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A: Name the 3 types of *ischemic* stroke B. What type of necrosis develops from *ischemic* stroke?
"**THE** *ischemic* stroke, smh" [**T**hrombotic🆚**H**ypoxic🆚**E**mbolic] ## Footnote b. Liquefactive
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post [*ischemic* stroke] management ⼀ (6)
**BALTIC** 1. [(**A** SA + ADP R Blocker)*DAPT* ] 2. [**B** P control ♨]x *24h* 3. [**C**arb (Glucose) control] 4. [**L**]ipid control 5. [**I** nvestigate possible causes (CTA h/n, Carotid US, TTE)] 6. [**T**reat possible causes (afib)] ## Footnote *🔎DAPT = [Dual AntiPlatelet Therapy (ASA + ADP R Blocker)]* ♨[(< 180/105*[if thrombolytic given]*)] vs [< 220/110 *[if thrombolytic NOT given]*) ]*24h*
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# pt presents with r/o ischemic stroke How long does it take 🔲 to detect cerebral **ischemic** changes? -NCHC -MRI ## Footnote *🔎NCHC = NonContrast Head CT*
NCHC: [6-24HOURS] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ MRI: [3-30min]
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# There are ⬜# [Spinal Cord Nerves] total describe the arrangement of [Spinal Cord *Nerves*] around the [Spiny Vertebra *Bone*] -3
*31* \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ 1. {[C1-C7🅽 ] 🅽 sits *above* 🄱} 2. {C8🅽 exits [*below* C7 bone]} 3. [ALL OTHER: 🄱 sits *above* 🅽 ] ## Footnote *🔎🅽= [Spinal Cord 🅽erves]* *🔎🄱= [Spiny Vertebra 🄱one]* ⚡ {C8🅽 exits [*below* C7 bone] and [*above* T1 bone]}
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▶In adults, spinal cord extends to ⬜ vertebra(e), ▶ [Subarachnoid space (which contains CSF)] extends to ⬜ vertebra(e).
[L1🄱 - L2🄱]; [S2🄱 (lower border)] ## Footnote *🔎🄱= [Spiny Vertebra 🄱one]* 💡**Lumbar Puncture*[L3🄱 - L5🄱]*
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Where are lumbar punctures performed?
L3🄱 - L5🄱 | (at level of caudal equina) ## Footnote *🔎🅽= [Spinal Cord 🅽erves]* *🔎🄱= [Spiny Vertebra 🄱one]*
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# *fill-in-blank (18)*
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Diaphragm pain and Gallbladder pain are referred to the ⬜ via the ⬜ nerve
R shoulder ; phrenic
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# Name physioanatomic significance for following dermatomes: a. L1 b. S2-S3-S4 c. T10 d. T4 e. T7
a. inguinal ligament = L1 b.[*"S2,3,4 ⼀my |**Dick** **FEELS**| |**HARD**|⼀and my |**HOLE** |**wants more**|*" ✏️] c. umbilicus (site for early appendicitis referred pain) = T10 d. @ nipple = T4 e. @ xiphoid process = T7 ## Footnote ✏️{[*"S2,3,4*S2-S3-S4 *⼀my Dick Feels***[Penis sensation]** *Hard***[Penis Erection]** *⼀and my hole***[anal wink reflex]** *wants more!**[anal wink only S3-S4)]** "* ] = [penis sensation, penis Erection, (anal wink reflexS3-S4 only) ,]}
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Nerve root(s) for Cremasteric reflex
L1🅽 ,L2🅽 | *"L1,L2 his testicles move"* ## Footnote [*"S2,3,4 ⼀my **DICK** **FEELS** **HARD**⼀and my **HOLE** **wants more***"]
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What are Primitive reflexes? (2) \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Name them (6)
✔︎ [infantile reflexes *(present before Frontal Lobe dvlops)* ] that dissolve by 1 y/o after Frontal Lobe develops ✔︎ may reemerge with Frontal Lobe❌
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Brimonidine MOA (2)
[⬇︎aqueous humor **synthesis**(⬇︎IOP)]α2🟢 | for Glaucoma
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Pilocarpine is a ⬜*MOA* sometimes used in emergency Glaucoma tx. Why?
{[**miosis and cyclospasm(ciliary m CTN)**][Muscarinic🟢*Direct* cholinomimetic]} | *(carbachol has same MOA)* ## Footnote 📝**Pilocarpine = [very effective(via cyclospasm)**] at opening trabecular meshwork into canal of Schlemm *🔎CTN = Contraction*
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# clinical features Von Hippel Lindau (4) | disease
1. hemangioblastoma in retina/brain stem/cerebellum/spine 2. angiomatosis 3. BL renal cell carcinoma 4. PHEOCHromocytoma
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*Describe the likely regions involved for the following deficits* ## Footnote A: Weakness of Face and UE B: Weakness of LE C: Numbness of Face and UE D: Numbness of LE
A: CTL Precentral MCA territory (*Face and UE weak*) B: CTL Precentral ACA territory (*LE weak*) C: CTL PostCentral MCA terrtory (*Face and UE numb*) D: CTL PostCentral ACA territory (*LE numb*)
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Describe how an action potential occurs (5)
**RANHP** {**R**esting}: [-70mV resting potential (maintained with Na+/K+ pump)] becomes more positive (via preceding Na+ influx) {**A**ction Potential: ➜ at [-55mV = action potential occurs] {[**N**a+ infux stop with K+ efflux start] *at +30mV* = repolarization}: ➜ at [+30 mV] = [voltage gated Na+ influx stops] and [K+ voltage gated K+ efflux starts] → membrane becomes more negative = repolarization {**H**yperpolarization}: 4. ➜ [K+ efflux] occurs more negative than [-70mV resting potential] = HYPERPOLARIZATION {**P**ump} → eventually climbs up to [-70mV resting potential] via Na+/K+ pump
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Describe how NTS is released from presynaptic nerve terminals (11)
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describe Malignant Hyperthermia (4)
***m**alignant* ***hyper***thermia 1.**m**uscle contraction + **hyper**thermia 2.{succinylcholine & [inhaled anesthetics (except N2O)} are causes 3.[rare hereditary condition] 4.potentially fatal ## Footnote ✏️inh*a*led *ane*sthetics = *-ane* (halothane, Sevoflurane, etc)
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Tx for Huntington's Disease (3)
1.[(Tetrabenazine + reserpine)*(inhibits VMAT → limits dopamine vesicle packaging and dopamine release)* ] 2.[ Haloperidol(D2 R Blocker)] ## Footnote etx = chromo 4 CAG repeat → caudate nc atrophy→ ⬇︎GABA, / ⬇︎ACh / ⇪dopamine] *"Hunting **4** food is way too aggressive & dancey"*
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[Glioblastoma Astrocytoma] Radiographic Findings - 2
1. **Butterfly lesion** from crossing Corpus Collosum 2. Midline shift from Lateral Vt Compression ## Footnote *GBM is usually a HIGH GRADE Astrocytoma*
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A: List the n. roots associated with [inferior Gluteal n.] B: Associated Injury (2) C: Sensory deficit D: Motor Deficit
**[inferior Gluteal nerve]** A: L4-S2 B: ❗️[Supero*medial**"[(Up) and (In)] ➜ IS A SIN!"* Butt injection] ❗️[POST Hip dislocation] C: none D. 🔧 [No Thigh Extension] ## Footnote "[(up) and (in) *IS A SIN*] < BUTT > [*WITHOUT A DOUBT INJECT* **(UP)** and **(OUT)**!]" "All Butt Injections go **Up** and **Out** (SuperoLateral)"
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A: List the n. roots associated with [SUP Gluteal n.] B: Associated Injury (2) C: Sensory deficit D: Motor Deficit (2)
**[SUP Gluteal nerve]** A: L4-S1 B: {[(up) and (in) *IS A SIN*] Superomedial Butt injection} vs. [POST Hip dislocation] C: none D: 🔧[Trendelenburg CTL hip drop *(hip drop points opposite the lesion)*] 🔧[No Hip ABduction] ## Footnote "[(up) and (in) *IS A SIN*] < BUTT > [*WITHOUT A DOUBT INJECT* **(UP)** and **(OUT)**!]" "All Butt Injections go **Up** and **Out** (SuperoLateral)"
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etx of stroke is classified into what 5 categories?
1. Large vessel 2. small vessel 3. cardioembolic 4. cryptogenic 5. [Other (vasculitis/drug/infxn/PFO/dissection/paradoxical)]
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# When localizing a stroke lesion, use the 7pt-Neuroaxis Name the 7 points of the Neuroaxis
1) Brain 2) Spinal Cord 3)ANT Horn [of Spinal Cord] 4) ROOTS [from ANT Horn of Spinal Cord] 5) Peripheral Nerves 6)NMJ 7)Muscle ________ [Use the 7-star Neuroaxis to locate stroke lesions]
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As apart of (BALTIC - post stroke mgmt) you have to (I)nvestigate etx _________________________________ Name 4 common stroke imaging workup and why they're indicated
-[MRI brain] = determines stroke distribution pattern -[CTA head/neck] = evaluates vessel abnormalities -[TTE] = looks for embolic etx (PFO/valvular❌/clot) -[Telemetry] = looks for afib/arrhythmia
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absolute contraindications to receiving [tPA thrombolysis] -7
1. active brain bleeding 2. active internal bleeding 3. prior brain bleed (hemorrhagic stroke) 4. Platelets < 100K 5. INR > 1.7 6. HTN > 185/110 7. major surgery recently