1 ⼀NEUROLOGY I Flashcards
identify
A: MIOS seen in Younger pts indicates ⬜
B: MIOS seen in OLDER pts indicates ⬜
C: What is the purpose of the MLF
[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
CP for [MIOS-MLF Internuclear Ophthalmoplegia Syndrome] (3)
[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]}
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
[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
3 main causes of pinpoint pupils
- Opiate OD
- Pontine lesion destroying sympathetic fibers
- Cholinergic eyedrops for Glaucoma
3 Main causes of Spinal Cord Compression
- DJD Disc Herniation (Smoking risk factor)
- [Epidural Staph a. Abscess (think IV drug user vs DM)]
- Tumor (Prostate/Renal/Lung/Breast/Multiple Myeloma mets)
Dx = MRI, Positive Straight Leg, Classic S/S
DJD=Degenerative Joint Disease
6 major causes of Syncope
MVC BSD
- ⬇︎ Cardiac Output (Valvular Dz/HOCM/Pulm HTN/PE/Tamponade/myxoma/aFib)
- Bradyarrhythmia (SA Node dysfunction/AV Block)
- [VANS - Vasovagal Autonomic Neurocardiogenic Syncope]
- Dehydration
- Stroke
- Metabolic (⬇︎Glucose vs ⬇︎Na+)
OBTAIN ECHOS ON ANY PT WITH SUSPICIOUS SYNCOPE!
A patient taking metoclopramide develops involuntary next flexion known as ⬜
Tx? (2)
[Torticollis Dystonia] ; [Benztropine IV 🆚 Diphenhydramine IV]
A pt complains of inabilty to recognize previously known faces
What is this called? ; Where is the lesion?
[ProsoPagnosia visual agnosia] ; BL Temporo-Occipital
a. Tx for PostFall syndrome (2)
_________________
b. What is PostFall syndrome?
a.
-URGENT PHYSICAL THERAPY
-URGENT BEHAVIORAL THERAPY
_________________
b. maladaptive fear of falling after a fall that ➜ restricted mobility and functional decline in the elderly
Describe the 4 main sx for [Brown Sequard Syndrome]
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]
Causes of [Brown Sequard Syndrome] - 3
- [(Extramedullary Tumor]
- Trauma
- [DJD Disc Hernation (Smoking risk factor)]
A: Describe Opsoclonus-Myoclonus Syndrome
B: What Childhood tumor is it associated with?
A: [Non-Rhythmic Conjugate Eye mvmnts] with myoclonus= “Dancing Eyes and Feet”
B: Neuroblastoma (onset 2 y/o)
Arises from Neural crest
PCiiH [Pseudotumor Cerebri Idiopathic Intracranial HTN] Dx - 3
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!*
⊕Papilledema is a ctx to Lumbar puncture
When is ⊕Papilledema not a ctx to Lumbar puncture? Explain
[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
[Pseudotumor Cerebri Idiopathic Intracranial HTN] Clinical Presentation - 4
PCiiH girls like to VAPE
- [Vision ∆ +/- papilledema]
- [Abducens CN6 palsy]
- Pulsatile Tinnitus
- [Eye-blinding HA (worst at sleeping times) & with head position ∆]
* This HA will make you go Blind!*
What is Wallerian Degeneration?
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
Describe the Lacunar Syndrome CP
👀
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
List the n. roots associated with Common Peroneal n.
L4-S2
foot is dropPED (Peroneal Everts & Dorsiflexes)
- Commonly caused by L5 Radiculopathy*
- Dx: Knee MRI vs EMG*
List the n. roots associated with Tibial n.
L4-S3 (Three)
can’t walk on TIPtoes (Tibial Inverts & Plantarflexes)
Commonly caused by L5 Radiculopathy
What are the functions of the Common Peroneal n. -2
L4-S2
foot is dropPED (Peroneal Everts & Dorsiflexes)
_________________
🔬 Commonly caused by L5 Radiculopathy
🩺 Knee MRI vs EMG
What are the functions of the Tibial n. (2)
L4-S3 (Three)
can’t walk on TIPtoes (Tibial Inverts & Plantarflexes)
Commonly caused by L5 Radiculopathy
CP of Craniopharyngiomas - 3
________________
Demographic?-2
- BiTemporal Hemianopsia
- HA
- Pituitary Hormonal Deficiencies (i.e. ⬇︎Libido)
Demographic: MOSTLY KIDS, but some adults
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:
- [Advanced CHF]
- [Comatosed BL metabolic encephalopathy]
- Elderly during sleep
[Myasthenia Gravis] Tx-4
P DDD F
1st: [Pyridostigmine AChesterase inhibitor]
2nd: Cyclosporine
3rd: Thymectomy
4th: **[Intubate + Plasmapharesis + IVIG + Steroids] if Crisis **
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:
- Fluoroquinolones
- Infection
- Surgery
Crisis Tx: [Intubate + Plasmapharesis + IVIG + Steroids]
[LEMS - Lambert Eaton Myasthenic Syndrome] etx
[Autoimmune attack against (Presynpatic Ca+ channel)–> No ACh release]
[Myasthenia Gravis] Clinical Presentation (5)
“Give me Mya’s P DDD F”
[Ptosis
[Diplopia from Disconjugate gaze]
Dysarthria-bulbar dysfunction
Dysphagia w/nasal regurgitation-bulbar dysfunction
[FATIGABLE progressive Weakness Muscularly (Extraocular/RESP/Proximal/limbs/worst w/repetition/impvd with rest)]
Tx: Pyridostigmine AChesterase inhibitor
[Myasthenia Gravis] Dx-5
P DDD F
- ACh R Ab Assay
- MuSK (Muscle-Specific tyrosine Kinase) Ab Assay (only if #1 is neg)
- [Tensilon Edrophonium]–> Improves all sx
- Ice Pack to eyelids –> Improves Ptosis by inhibiting ACh breakdown at NMJ
- BE SURE TO GET CT CHEST AFTER DX TO COVER FOR THYMOMA, POSSIBLE THYMECTOMY!!!!
[LEMS - Lambert Eaton Myasthenic Syndrome] Clinical Presentation - 3
- Weakness of [Proximal limbs and trunk] mimicking myopathy, better with exercise
- Autonomic sx (Dry mouth /Orthostasis / Impotence)
- ⬇︎Deep Tendon Reflexes
[Myasthenia Gravis] etx
________________
Demographic?-2
Autoantibodies block and degrade [postsynpatic nicotinic ACh Receptors]] –> [⬇︎ motor end plate potential]
_____________________
[Women 20-30] [Men 60-80] yo
Migraine etx
________________
How are the Trigeminal nerves associated-2
________________
“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 :
- send impulses–>[Brain Stem APCTZ] & hypothalamus–> Nausea/Photophobia/Phonophobia
- retroactively depolarize–>release of substance P –> neurogenic inflammatory pain + vasoDilation
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
Pontine[Basilar Artery] occlusion CP
Locked In Syndrome!!!
LIS🔒={[✅QB VP] but [⛔HO]}
[Quadriplegia w intact consciousness]
PCA occlusion CP-4
- [CTL Homonymous Hemianopiawith macular sparing (K in image)]
- Visual hallucinations
- [Alexia with NO agraphia]Dominant Hemisphere involvement
- [DOPeOculomotor CN3 involvement]
🔎[DOPe= Down & Out + Ptosis + eyeDilated]
ACA occlusion CP-3
- CTL Weakness worst in LE
- CTL Numb worst in LE
- Urinary Incontinence
AICA occlusion CP-4
Somewhat like [PICA Lateral Medullary Syndrome of Wallenberg]
- Hearing Loss
- FACE Paralysis (Similar to Bells Palsy)
- Ipsilateral ⬇︎Facial Pain/Temp
- CTL ⬇︎BODY Pain/Temp
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!
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]
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]
_________________
All patients (especially elderly) s/p FALL require ⬜ by a ⬜ for the purposes of ⬜
[home safety assessment] ; occupational therapist
_________________
optimizing HOME safety and ADL
Altered Mental Status workup -7
GOT CLUB
- G[Glucose level ➜ Thiamine B1 f/b glucose admin (dextrose IV)]
- Oxygen level
- T3/T4 level
- B12 level
- Lumbar puncture
- [UDS/CMP/CBC]
- CT head
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)
⊡established PD = < E + 2S - R - X >
[Parkinson’s Disease] is a ⬜ diagnosis
Diagnosing Parkinson’s Disease consist of 4 criteria blocks
Name them
clinical
_________________
< ESRX > critertion
1. {[Essential (for PD)] = AKA “PARKINSONISM” }
2. [Supportive (of PD)]
3. [RedFlags (atypical for PD)]
4. eXclusion (excludes PD dx)]
⊡established PD = < E + 2S - R - X >
[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)
Essential (for PD) = [ (P|R) +K ]
PRK =
-Pill Rolling resting tremor
-Rigiditiy cogwheel
-bradyKinesia
_________________
⊡established PD = < E + 2S - R - X >
[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
⊡established PD = < E + 2S - R - X >
[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 Areflexia 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
⊡established PD = < E + 2S - R - X >
[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)]
⊡established PD = < E + 2S - R - X >
[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 >
[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 >
Alzheimer’s Dz etx (5)
Alzheimers etx = NaTPO
①. Neurofibrillary tangles = intracell hyperphosphorylated insoluble tau cytoskeleton = [ ⇪ Neurofib tangles = ⇪ Alzheimer dementia]
+
② . ⭐accumlation of {β-amyloid (derived from [cleavage of chromo 21 t.A.P.P.]} in:
2a. Temporal lobe early on ➜ [Neuritic Senile plaques]
2b.{[Parietal & occipital] lobe cerebral blood vessels} ➜ [P\o Spontaneous Hemorrhages📷]
2c .{hippOcampus & [Basal nc. of meynert]} ➜ defective [{O\B} Choline AcetylTransferase] ➜ [⬇︎ {O\B} ACh] ➜ {Alzheimer [CLAV ➜ HANDU]sx}
🖊{P\o} = {[Parietal & occipital]}
🖊{O\B} = {hippOcampus & [Basal nc. of meynert]}
🩺NaTPO ↪ [CLAV ➜ HANDU]sx
👓t.A.P.P. = transmembrane Amyloid Precursor glycoProtein
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]
_________________
▶ [Vestibular Caloricstimulation Reflex] = 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]
[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)]
Aside from CSF analysis revealing ⬜3, name the typical manifestations of [Herpes Simplex Encephalitis] -6
- [⇪ Protein]
- [⇪ WBC lymphocyte pleocytosis]
- [⇪ RBC (from temporal lobe destruction)]
_________________
encephalitis sx = FAVORS: [Focal neuro ∆ (aphasia, hemipLegia, hemiparesis)] , ⭐AMS⭐, Vomiting, Ouch HA, Really hot fever, Seizure
⭐= [encephalitis AMS] distinguishes encephalitis from meningitis
Atomoxetine Indication
NonStimulant ADHD Rx
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!
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)
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
Between DM, Smoking and HTN, which carries the GREATEST STROKE Risk?
HTN
Both Mannitol and [Hypertonic Saline (3%/5%/23%)] are used to ⬇︎ ICP
List the differences in using Hypertonic saline? - 4
- HTS Anti-Inflammatory
- [HTS does NOT cross into interstitial space like Mannitol ( Mannitol causes Rebound Edema!) ➜
- ➜ HTS eventually expands systemic volume
- HTS ONLY given via Central line
HTS = Hypertonic Saline
Brachial Plexus damage of
[lower Trunk {(C8) (T1)}]
________________
clinical presentation?
[klumpke palsy claw hand]
Brachial Plexus damage of
[long thoracic {(C5)(C6)(C7)} n ]
________________
clinical presentation? -2
- [winged scapula]
- [inability to ABduct shoulder > 90º]
Brachial Plexus damage of
[Axillary {(C5)(C6)} n]
________________
clinical presentation?
[Deltoid paralysis]
Brachial Plexus damage of
[Radial {C5⼀T1} n]
________________
clinical presentation? -2
- [Saturday night palsy wrist drop]
- [No Tricep Reflex]
Brachial Plexus damage of
[Radial {C5⼀T1} n]
________________
causes -3
- [Crutches/Axilla damage]
- [anteroLateral⼀pFSF]
- Midshaft Humerus
👓{[anteroLateral⼀pFSF] = {[anteroLateral⼀proximal humerus displacement] iTSo [FOOSA Supracondylar Fx]}
Brachial Plexus damage of
[Axillary {(C5)(C6)} n]
________________
causes -3
- [Surgical NECK humerus]
- [ANTERIOR humerus displacement]
- Shoulder Injury
Brachial Plexus damage of
[long thoracic {(C5)(C6)(C7)} n ]
________________
causes -3
- STABS
- [MASTECTOMY]
- [AXILLARY NODE DISSECTION]
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
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”)
[5Clinical (evidence of _C_NS catastrophe, NO _C_onfounders, NO _C_hemicals-drug intox, >36_C_, _C_ore>100 SBP)]
[5Neuro exam(coma, NO cortex rflx, NO brainstem rflx, NO rooting/sucking rflx, spinal rflx ok)]
➜ [4ancillary testing if (C) (N) (P) inconclusive] = [EEG isoelectric line] vs [EEG NO SSensory activity] vs [EEG NO brainstem activity] vs [NO intracranial blood flow]
[3Pulmonary aPnea test (Preoxygenate ➜ disconnect ventilator = positive if NO spontaneous breath x 8m + PaCO2>60 + arterial pH<7.28]
[Local requirements]
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 [Clinical] criteria block (5)
(“CNaPL”)
[ 5Clinicalprerequisites]
- [_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)]
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 [Neuro exam] criteria block (5)
(“CNaPL”)
[5Neuro exam(coma, NO cortex rflx, NO brainstem rflx, NO rooting/sucking rflx, spinal rflx ok)]
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 [ancillary testing] criteria block (4)
(“CNaPL”)
➜ [4ancillary testing⼀if (C)| (N) |(P) inconclusive ] = (positive if)…
[EEG isoelectric line]
+
[EEG NO SomatoSensory activity]
+
[EEG NO brainstem activity]
+
[NO intracranial blood flow]
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 [Pulmonary aPnea test] criteria block (3)
_________________
▶▶What 3 factors prevent this test from being done?
(“CNaPL”)
[ 3Pulmonary 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
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
On EEG, what is a [burst suppression pattern]?
_________________
What does it indicate? (2)
isoelectric periods punctuated by high amplitude activity
_________________
- Deep Coma
- Anesthesia
pt exhibits ⊕Deep Tendon Reflexes
T or F: this finding effectively r/o brain death
FALSE
{[🧠 DeathReflexes] = [(⊕Spinal Cord) ➖Cortex ➖Brainstem ➖Suck/root]}
….because [Spinal Cord reflexes(i.e. Deep Tendon Reflex)] are still intact during Brain Death →
Bromocriptine
MOA
_________________
Indication
[PostSynapticDopamine🟢 (ergot)]
_________________
Parkinson’s
Carbamazepine side effects -3
- [bone marrow suppression (neutropenia)]
- SIADH hypOnatremia
- AntiCholinergic
[Carpal Tunnel Syndrome] etx
BILATERAL Median n Compression by the [Flexor Retinacular Transverse carpal ligament] –> Peripheral mononeuropathy + [ABductor pollicis brevis atrophy]
- [Flexor Retinaculum Transverse Carpal ligament] can be surgically incised for relief*
- CARPAL TUNNEL STARTS uL and –> BL*
Carpal Tunnel Syndrome Clinical Presentation - 6
- [Paresthesia vs Pain with Median n. Distribution worst at night]
- CARPAL TUNNEL STARTS uL and –> BL
- {[Thenar (ABP, FBP, O_P,)] atrophy [ABductor Pollicis Brevis] atrophy ➜ (⬇︎flexion/ ⬇︎ABduction/ ⬇︎Opposition)]}
- Tinel Sign (tapping over flexor surface ⬆︎ sx)
- Phalen Sign (flexing Wrist ⬆︎ sx)
- HOH Sign (Hand over Head ⬆︎ sx)
Pregnancy is associated with Carpal Tunnel
What should these particular pts also be worked up for?
Preeclampsia
CARPEL TUNNEL starts uL and then –> BL
[Carpal Tunnel Syndrome] dx
excluding clinical s/s
Nerve Conduction studies
EMG is not necessary for Carpal Tunnel Syndrome
[Carpal Tunnel Syndrome] tx - 5
- [WRIST SPLINT (sx < 10 mo)]
- Remove exacerbating factors
- NSAIDs
- CTS injection -IF MODERATE
- [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
Risk factors for Carpal Tunnel Syndrome - 4
- Obesity
- [Pregnancy (c/s Preeclampsia)]
- DM
- hypOthyroidism
CARPEL TUNNEL STARTS uL and –> BL
[Conus Medullaris Syndrome] etx
________________
Clinical Presentation - 7
(Compression of S2 - S4 n. roots @ Conus Medullaris) –>
________________
“RIM sara!?”
1. [Reflexia: HYPER]reflexia (Cauda Equina has hypOreflexia)
2. [Incontinence EARLY]
3. Motor weakness SYMMETRICALLY
4. saddle anesthesia
5. anocutaneous reflex loss
6. radiculopathy
7. [a MRI, CTS IV and Neurosurg consult = tx]
[cauda equina syndrome] etx
________________
Clinical Presentation - 7
(Compression of S2 - S4 n. roots @ Cauda Equina) –>
________________
“RIM sara!?”
1. [Reflexia: hypO]reflexia (Conus Medullaris has HYPERreflexia)
2. [Incontinence LATE]
3. Motor weakness Asymmetrically
4. saddle anesthesia
5. anocutaneous reflex loss
6. radiculopathy
7. [a MRI, (CTS IV) and Neurosurg consult = tx]
What Spinal Columns are affected in [Subacute Combined Degeneration]?-3
_________________
How do this manifest?-3
[SuBACute Combined Degeneration]
[Demyelinating lesions] in 3 Thoracic Spinal Columns:
- [Dorsal–> Loss of 2TVP]
- [Lateral CST –> UMN Weak MESH]
- [Spinocerebellar –>Ataxia]
* FriEdreich Ataxia affects the SAME 3 columns*
Causes of [Subacute Combined Degeneration] (3)
[SuBACute Combined Degeneration]
1)B12 Deficiency (demyelinates peripheral nerves also)
2.AIDS/HIV
3.Copper deficiency
* Affects Dorsal / Lateral CST / Spinocerebellar Tracts (Combined)*
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
🩺SAC = demyelination of DCP/ CST-L, /SpinoCerebellar tracts
Central Pontine Myelinolysis
dx (2)
_________________
tx (3)
- [Brain MRI: demyelinating lesions]
- [CP: rapid Na+ correction of hrhh → delayed paralysis days later]
_________________
- irreversible
- supportive care
- eye computer interface
🔎hrhh = high risk hypOtonic hypOnatremia
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”
⊕
✅[Quadriplegia w intact consciousness {LOCKED IN SYNDROME}]
✅[Blink reflex(upper CN intact)]
✅[Vertical EOM(upper CN intact)]
✅[Pupilllary reflex(upper CN intact)]
⊝
⛔[Horizontal EOM(lower CN paralyzed)]
⛔[Oral movements(lower CN paralyzed)]
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_________
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
Cerebral Palsy is a group of clinical syndromes generally characterized as ______
How does it present? - 3
Nonprogressive motor dysfunction (Prematurity>EtOH = RF) ;
“Cerebral Palsy is a young, *SAD** BUM”
- BL equinovarus club feet (image)
- {[UMN (Weak MESH)sx] LE >UE}
- Mental Retardation
Greatest RF = prematurity ( < 32 wks gestation)
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 ;
Cerebral Palsy is just SAD
- Spastic
- Ataxic
- Dyskinetic
Greatest RF = prematurity ( < 32 wks gestation) but EtOH is second
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)
Classic signs of Fetal Alcohol Syndrome - 4
“FAS had drunk mama’s baby looking like a MULE”
1. Microcephaly
2. Upper THIN Lip
3. Long smooth Philtrum
4. Eyes have short Palpebral fissures
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%
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
Clinical Manifestation of Multiple Sclerosis (9)
Charcot classic triad of MS is a [SLUM SiiiN] !
Sensory sx (think BL Trigeminal Neuralgia)
Lhermittes sign = “electric tingling” down spine into arm & legs when chin is touched to chest
Uhthoff phenomenon (sx ⬆︎ during heat)
Motor sx
Scanning Speech
[Internuclear Ophthalmoplegia (MIOS)] / Intention Tremor / Incontinence
Neuritis Optic - (uL eye pain + vision loss + Marcus Gunn afferent pupillary defect) = ALSO RISK FACTOR
Demonstrate Sensory Innervation of the Hand
Ulnar nerve
________________
Median nerve
________________
Radial nerve
Subarachnoid Hemorrhage is most commonly due to ⬜
_________________
Clinical Presentation (6)
[Berry Saccular Aneurysm] rupture
_________________
- “worst HA of my life” ⼀sudden severe thunderclap HA different from previous
- Nausea
- Vomiting
- LOC
- meningismus
- [focal neuro ❌]
Subarachnoid Hemorrhage
Risk Factors (5)
- HTN
- Sympathomimetic drugs
- Smoking
- EtOH
- fHX
✏️Xanthochromia= yellow tinted CSF due to hgb degradation products
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
Clinical Presentation for Diabetic Ophthalmoplegia (3)
_________________
Etx?
DM –> [Oculomotor CN3 CENTRAL ischemia]
- Ipsilateral Down & Out Eye
- Ptosis (from Levator Palpebrae paralysis)
- NORMAL PERRL (since Parasympathetic fibers are spared)
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*
Patient presents with Paralysis
what’s your Workup? (4)
Clinical presentation of
[transverse myelitis acute myelopathy] (4)
SURE
- Sensory level (demarcated sensory loss up to specific point)
- Urinary retention
- [Rapid developing LE weakness s/p URI/trauma/CA]
- Exam [hypOreflexia and flaccidity] ➜ [hyperreflexia and spasticity]
dx = MRIGad
clinical presentation of [Complex Regional Pain Syndrome] (6)
- patient S/P RECENT JOINT INJURY
- now p/w joint POOP
- joint burning
- joint edema
- joint skin ∆
- joint ⬇︎ROM
etx: INC sensitivity of sympathetic nerves
sx of Meningoencephalitis (7)
“MeningoEncephalitis Needs FAVORS”
Nuchal rigidity = Meningo-
FAVORS = -encephalitis
______________
FAVORS: [Focal neuro ∆ (aphasia, hemipLegia, hemiparesis)] , ⭐AMS⭐, Vomiting, Ouch HA, Really hot fever, Seizure
Viral Etiologies of Meningoencephalitis include (⬜3)
with
treatment (⬜2)
- [Herpesvirus(HSV)]
- [Arbovirus(West Nile Virus)]
- [Enterovirus(Coxsackie Virus)]
_________________
-Acyclovir for HSV
-Supportive Care
📄”MeningoEncephalitis Needs FAVORS”
PML Clinically Presents like Multiple Sclerosis
Describe PML-Progressive Multifocal Leukoencephalopathy (3)
- Opportunistic infection by [John Cunningham Polyoma Virus]—-> [PML multiple white matter lesions]
- demonstrated as (Hyperintense Flair on radiology)
- –> Death vs. Severe Neuro injury
⚡ PML is also a RARE side effect of some drugs – in [JCP virus⊕] pts
PML (Progressive Multifocal Leukoencephalopathy) 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⊕]
Usual Demographic: HIV pts (reversal of immunosuppresion stops JC Polyoma virus progression)
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
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
Congenital Torticollis etx
Malpositioning of Head in Utero vs During birth –> constant contraction of SCM–>Lateral Neck swelling
Torticollis also possible in Adults
CP for Chemotherapy Peripheral Neuropathy - 3
- {**Symmetrical STOCKING GLOVE(onset fingers/toes-spreads proximally) ** ➜
- [Loss of SenTor [(S:pain/temp)/(M:weakness)]:}
- [earlyLoss of ankle jerk reflex]
Drug Culprits: Cisplatin / Paclitaxel / Vincristine
🔎SenTor = Sensory & MoTor
CP of Cerebellar Damage - 7
Cere is def on GRINDRR
Gait Ataxia {[vermis → truncal ataxia] / [hemisphere → limb ataxia IPSILATERAL]}
Rapid alternating mvmnt impairment
Intention tremor/Dysmetria IPSILATERAL (hemisphere)
Nystagmus IPSILATERAL (medial AND Lateral Vermis)
Dysarthria (Lateral Vermis only)
Rebound phenomenon (pt hits themself in face if flexing bicep and examiner releases arm-image)
Reflex Pendular (knee swings >4x after Deep tendon reflex is elicited)
Vermis is midline
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
cerebellum:
-vermis(central)❌ ➜ [truncal ataxia + dysarthria]
-hemisphere(Lateral)❌ ➜ {[Limb ataxia IPL(intention tremor/loses balance toward lesion)]
cp of [Medial Medullary syndrome] -(3)
- [ hypoglossal CN12 nc❌ →IPL tongue weak deviates toward lesion (“you lick your wounds”)]
- [medial lemniscus❌ → CTL numb(2TVP loss) ]
- [Lateral CSTPyramidal Tract❌ → CTL weak(hemiparesis)]
[(AsA❌) +(VA❌)] → [medial medullary syndrome]
cp of [Lateral Medullary syndrome of Wallenberg] -(6)
VSINSY
Vestibular = [VDNV]sx
[StG Spinal triGeminal] = [IPL face pain/temp loss]
Inferior cerebellar Peduncle = ataxia
Nucleus ambiguus = {[dysgag (gag reflex⬇︎)] , dysphonia, dysphagia}
[STT SpinoThalamic Tract] = [CTL BODY pain/temp loss]
YsYmpathethetic descending fibers = [IPL Horners]
VDNV = Vertigo/Diplopia/Nausea/Vomiting
Brachial Plexus damage of
[Upper Trunk {(C5)(C6)} n]
________________
clinical presentation?
[Erb Palsy Waiter’s Tip]
Brachial Plexus damage of
[Upper Trunk {(C5)(C6)} n]
________________
cause
[Baby Delivery lateral neck pull]
DDx for Clostridium Botulinum - 4
Also consider…
- Myasthenia Gravis
- Atypical Guillain Barre
- Tick Paralysis
- Brain Stem infarct
Adult tx: Equine Heptavalent Antitoxin (passive immunity)
DDx of Neuromuscular Weakness has 5 origins
Describe Upper Motor Neuron causes of Neuromuscular weakness - 4
- Vasculitis
- Leukodystrophy
- Mass
- VitB12 deficiency
DDx of Neuromuscular Weakness has 5 origins
Describe Anterior Horn Cell causes of Neuromuscular weakness - 4
Deficiency of what INC risk for Restless Leg syndrome?
_________________
unpleasant LE sensation at night or during rest, relieved by moving
IRON
(dx = FerriTin ≤75 )
_________________
other RF: Pregnancy/Uremia/DM/MS/[anti:MDD|Psychotics|Emetics]
1st line tx = Gabapentin
Define Coma (6)
- Unarousable sleep state +
- Unresponsive sleep state
- [brainstem reflexes] intact
- [Spinal reflexes] intact
- 2/2 diffuse cortex depression
- can progress to vegetation / full recovery / brain death
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
Describe Athetosis ; What disease is it seen in?
Slow, writhing mvmnts of hands & feet often occuring with Chorea (Choreoathetosis) ; Huntington’s
What are the TRAUMATIC LUMBAR PUNCTURE CSF lab ranges
Glucose
Protein
WBC count
RBC count
GPW-R
G ⇪
P ⇪
W ⇪
RBC 6K < Traumatic LP (without xanthrochromia)
_________________
xanthochromia = discoloration of CSF 2/2 hgb breakdown that appears within 2-12h of SAH
What are the Normal CSF lab ranges
Glucose
Protein
WBC count
RBC count
GPW-R
Glucose: 40-70
Protein: <40
WBC: 0-5
RBC: < 6K < Traumatic LP
Describe CSF analysis for TB meningitis
Glucose
Protein
WBC
[G low < 45]
[P High 100-500]
[W High 100-500]
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
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
Describe CSF analysis for Guillain Barre:
Glucose
Protein
WBC count
[P UBER HIGH 45-1,000]
_________________
normal G / W
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
Dementia with Lewy Bodies (DLB) CP - 3
DLB at the DMV
- Dementia/confusion periodically(tx = Rivastigmine)
- MichaelJFox Parkinsonism (PARK + hamp) tht does NOT respond to dopaminergic tx
- Visual Hallucinations(tx = SGA)
✏️Lewy Body= [LABS (Lewy α-synuclein BodieS)] that are Eosinophilic intracytoplasmic accumulations
Pts with [Dementia with Lewy Bodies (DLB)] are extremely sensitive to _____ and it may cause what side effects?-3
DLB at the DMV
ANTIPSYCHOTICS
________________
- Dementia INC
- MichaelJFox PARK INC
- autonomic dysfunction
Describe En-Bloc Gait
_________________
What type of ataxia is this?
Minimal mvmnt of head while walking w/staggering gait
_________________
Vestibular Ataxia
Will be accompanied w/Vertigo & Nystagmus
[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
Describe the “Clasp Knife” phenomenon
________________
What disease is this related to?
Rapid SPASTIC RESISTANCE to passive mvmnt of limb
________________
UMN (Weak MESH) Pyramidal Tract dz
- Pyramidal Tract = Corticospinal and Corticobulbar*
- Pronator Drift also indicates Pyramidal Tract Dz*
Px for Migraine HA - 4
VTAP the migraine BEFORE it comes, and SEND it on its way when it does!
- Verapamil
- Topiramate
- Amitryptyline
- Propranolol
Tx for Acute Migraine HA - 4
VTAP the migraine BEFORE it comes, and SEND it on its way when it does!
- Sumatriptan
- Ergots (Bromocriptine)
- NSAIDs
- D2 R Blockers (Metaclopramide/Prochlorperazine)
Describe the Character for the HA:
Migraine
Cluster (3)
Tension (2)
Migraine = POUND = [Pounding/One Day-3 day Duration/Unilateral/Nausea/Disabling] + photo vs. phonophobia & [flashing dots aura]
Cluster = [Excruciating, sharp & steady] (100% O2 tx)
Tension = Dull & tight
Describe the Duration for the HA:
Migraine
Cluster
Tension
Migraine = POUND = [Pounding/One-3 Day Duration /Unilateral/Nausea/Disabling] + photo vs. phonophobia & [flashing dots aura]
Cluster = 15 - 90 MINUTES (100% O2 tx)
Tension = 30 min to 7 DAYS!!!! (Tammy’s Entire Work Week)
Describe tube presentation of a traumatic CSF lumbar puncture
Elevated RBC in 1st tube, followed by declining numbers of RBC with each successive tube
Frontotemporal Pick’s Dementia
Sx -2
Prounouced Frontal & Temporal lobe atrophy –>
[Socially inappropriate Behavior] + aphasia
OCCURS MORE IN FEMALES!!!
Demographic of Frontotemporal Pick’s Dementia?
________________
Mode Of Inheritance
50-60 yo Females
________________
AUTO DOM
Alzheimers >60 yo
Socially inappropriate behavior + aphasia
Describe Neuroleptic Malignant Syndrome - 5
RARE SE of Any Dopamine Blocker (Antipsychotics vs. GI meds) that –> FEVER
- [Fever > 40C]
- Encephalopathy (Confusion)
- Vitals unstable (INC HR / RR / BP from autonomic dysfunction)
- Enzymes ⬆︎ (CPK)
- [Rigitidy lead pipe] (Tremor)
Diagnostic Criteria for Febrile Seizure - 5
- 3 mo - 6 yo
- Temp > 38C
- No hx of Afebrile seizures
- No CNS infection
- No acute metabolic cause of seizure (pt would have dehydration)
Tx = Reassurance only!
Diagnostic criteria for Nightmare Disorder - 4
- Makes recurrent awakenings
- reMembers their nightmare
- Manageable (CAN be consoled) upon awakening
- Mind is alert upon awakening
-NightMares occur during REM
-NightMares are developmentally normal for kids
Diaphragmatic paralysis can be easily confused with ⬜ because they both cause ⬜ . What’s the most common cause of bilateral diaphragmatic paralysis?
CHF; orthopnea
_________________
ALS
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
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]
Dx for Creutzfeldt Jakob disease - 6
- [PRNP prion protein] genetic testing
- EEG Biphasic vs Triphasic sharp wave complexes
- Postmortem brain biopsy
- ⬆︎CSF 14-3-3 proteins
- MRI Cortical Ribbons
- MRI basal ganglia hyperintensity
Dx for VitB12 deficiency - 3
- [⬆︎ Methylmalonic Acid levels]
- CBC showing Macrocytic Anemia
- Serum Vitamin levels
Which drugs are used to treat Multiple Sclerosis Exacerbation?-2
1st: High Dose IV Methylprednisolone
2nd: (Refractory): Plasmapheresis
Which drugs are used to treat Multiple Sclerosis maintenance?-3
Maintenance:
1. [β-interferon]
2. [Glatiramer acetate]
3.Natalizumab
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?
- T2 MRI: [Periventricular white matter demyelinating plaques with lipid laden macrophages] = PREFERRED TEST
- [CSF Oligoclonal IgG bands = backup test]
_________________ - T1 MRI Black holes
- Clinical (SLUM SiiiN)
- Visual conduction velocity test
Sx will be disseminated in time and space
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
_________________
- [MS⊕ Pregnants] have INC risk for [assisted delivery (cesarean/vacuum/forceps)]
- [MS⊕ Pregnants] have INC risk of their infant developing MS as well
[Pregnant MS⊕] typically have {[⬜ lower | HIGHER] MS activity} during pregnancy and {[⬜ lower | HIGHER] MS activity} during postpartum
MS: Multiple Sclerosis
lower; HIGHER
Normal Pressure Hydrocephalus Sx (3)
_________________
Which is earliest to present?
⬇︎CSF absorption –> Wobbly, Wet & Wacky!
[ 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)
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
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
- PreFrontal
- Temporal
- Parietal
NaTPO = [CLAV ➜ HANDU]sx
Early Findings of Alzheimer’s - 4
CLAV –> HANDU
Cognitive PROGRESSIVE ⬇︎
Language ⬇︎
Anterograde immediate memory loss
Visualspatial disorientation (lost in ur own neighborhood)
Onsets after 60 yo
NaTPO = [CLAV ➜ HANDU]sx
Clinical Criteria for diagnosing Alzheimer’s -5
Alzheimer pts wear Alzheimer [GOWNS]
1. GOE 2 Cognitive deficits
2. Onsets after 60 yo
3. Worsening Memory
4. No other Systemic/Neuro DO to cause cognitive defects
5. [Sound (Consciousness intact)]
{NaTPO = [CLAV ➜ HANDU]sx per [GOWNS]}
Late Findings of Alzheimer’s - 5
CLAV –> HANDU
Hallucinations
Agnosia (lack of insight regarding deficits)
Neuro ∆ (seizure/myoclonus)
Dyspraxia (difficulty w previously Learned Motor task)
Urinary Incontinence
Onsets after 60 yo
NaTPO = [CLAV ➜ HANDU]sx
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)
NaTPO = [CLAV ➜ HANDU]sx
[early Neurosyphilis] typically presents during the ⬜ syphilis stage. How does it present? -3
2nd;
[Meningo-Vascular(Meningitis vs CVA)] | POSTUveitisMOST COMMON Sx❗️ | Tinnitus
prodrome ➜ MUT ➜ DAT
[LATE Neurosyphilis] presents during the ⬜ syphilis stage. How does it present? -3
3rd ; Dementia |Argyll Robertson Pupils | [TDPCD(⊕Romberg, ⊝DTR)]
TDPCD: Tabes Dorsalis Posterior Column Disease
prodrome ➜ MUT ➜ DAT
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
Recall the Pupillary pathway beginning with light entering the eye (5)
- Light enters retina 1 eye and that [Optic CN2] uL sends signal to [midbrain-SUP colliculus -pretectal nuclei]
- “cross” decussates to…
- → activate BOTH [Edinger Westphal nuclei]! BUT…
- → each EWN sends its own IPL [efferent preganglionic parasympathetic outflow] to its IPL ciliary ganglion via [Oculomotor CN3]
- that IPL ciliary ganglion uses short ciliary nerves to activate the pupillary sphincter muscle = Miosis
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
Essential Tremor is a [ (BUE/Head/Voice) Action Tremor]
What are the 3 clinical exacerbants of Essential Tremor?
- Hyperthyroid
- Lithium
- Valproic Acid
Etx of Parkinsons Disease
[LABS (Lewy α-synucleinBodieS)] 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]
The Basal Ganglia consist of what 5 things?
Recall the ____ Basal Ganglia pathway for movement starting with Cortex
a. DIRECT (5)
b. InDirect (5)
“Can Pretty Gays Sound Smart?”
-Caudate
-Putamen
-Globus Palidus
-Subthalamic nucleus
-Substantia Nigra
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)]
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
Fall has 3 main etiologies ( ⬜ , ⬜ or ⬜ )
_________________
What are the 10 crucial points of medical history to work up Fall?
Mechanical 🆚 Syncope 🆚 Seizure
_________________
HANDSTAMPED
Hx Syncope?
Associated symptoms
Number of episodes
Duration
Setting
Time until recovery
Acknowledged/Witnessed?
Medical hx
Prodrome?
Epilepsy hx
Drug use?
“All Fall pts should be HANDSTAMPED by a MD”
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
Usually Simple Partial Seizures originate in a single hemisphere
Simple Partial Seizures may present as what 3 things?
- Motor ∆ (head turning) - no LOC
- Sensory ∆ (paresthesias)- no LOC
- Autonomic ∆ (sweating)- no LOC
For cp, what are 2 ways to differentiate [NRSADSleepTerror] from [RSRBD]?
RSRBD = REM Sleep Related Behavioral Disorder
Output “I love Ruby”
[NRSADSleep Terror] = SUDDEN, INCONSOLABLE NonREM Sleep Arousal(Disorder)*]
________vs_________
[RSRBD= REM = “Really
“acting out dreams”]
NRSAD = Non-REM Sleep Arousal Disorder
RSRBD = REM Sleep Related Behavioral Disorder
The 3 types of dream disorders are ⬜, NRSAD and ⬜
_________________
Describe characteristics of NRSAD (5)
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. [NRSADSleepWalking(blank face/unresponsive to awakening)] or
4. [NRSADSleepTerrors(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
NRSAD = Non-REM Sleep Arousal Disorder
RSRBD = REM Sleep Related Behavioral Disorder
NRSAD dx has 2 types = must be qualified as either ⬜ or ⬜
What is the clinical progression of NRSAD (3)
NRSAD = Non-REM Sleep Arousal Disorder
[SleepWalkingNRSAD] ; [SleepTerrorNRSAD]
_________________
-onset 4-12 yo
-➜ RESOLVES SPONTANEOUSLY ≤ 2 YEARS FROM ONSET
-(if SEVERE = low-dose benzo qhs)
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 ; [HEADsx ]
_________________
[serial LP until sx resolve]
✏️ICPsx = HEAD = [Headache \ [Eye papilledema/vision change] \ AMS \ [Dont eat_NV]
Friedreich Ataxia involves Degeneration of the ⬜ , ⬜ and ⬜ spinal columns.
FriEdreich Ataxia involves Degeneration of the [Dorsal, Lateral CST and SpinoCerebellar spinal columns]
- FriEdrecih is Fratastic! 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
Functions of the Obturator n.-2
- MOTOR Leg ADDuction
- SENSORY medial thigh
________________
usually from pelvic trauma or surgery
GCS(Glasgow Coma Scale) predicts Prognosis of what 4 things?
________________
The 3 components are EVM (Eyes/Verbal/Motor)
Describe the [Verbal Response] component (5)
- GCS prognosis’* Brain CHIT
1. Coma
2. Hemorrhage (SAH)
3. Infection (bacterial meningitis)
4. Trauma
________________
EVM = Eyes / Verbal / Motor
GCS(Glasgow Coma Scale) predicts Prognosis of what 4 things?
________________
The 3 components are EVM (Eyes/Verbal/Motor)
Describe the [Eyes] component (4)
- GCS prognosis’* Brain CHIT
1. Coma
2. Hemorrhage (SAH)
3. Infection (bacterial meningitis)
4. Trauma
________________
EVM = Eyes / Verbal / Motor
GCS(Glasgow Coma Scale) predicts Prognosis of what 4 things?
________________
The 3 components are EVM (Eyes/Verbal/Motor)
Describe the [Motor] component (6)
- GCS prognosis’* Brain CHIT
1. Coma
2. Hemorrhage (SAH)
3. Infection (bacterial meningitis)
4. Trauma
________________
EVM = Eyes / Verbal / Motor
What’s the marker for [Glioblastoma astrocytoma]?
GFAP
HemiNeglect Syndrome
Stroke in [NonDominant Parietal cortex]) –> Neglect of anything on the CTL side
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
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
Homocystinuria tx -2?
[Pyridoxine B6] + AntiCoag
🔬MOA = auto recessive [Cystathionine synthase] deficiency –> Thromboembolism–> Stroke
Homocystinuria dx-2
[Homocysteine⬆︎] and [Methionine⬆︎]
etx = auto recessive [Cystathionine synthase] deficiency –> Thromboembolism–> Stroke
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
MH = MARFAN and HOMOCYSTINURIA
h = homocystinuria only
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 NonDextrose IVF)
[transverse myelitis] and [Guillain Barre Syndrome] both p/w LE paralysis
How do they differ in ______
a. Motor
b. Sensory
[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
[transverse myelitis] and [Guillain Barre Syndrome] both p/w LE paralysis
How do they differ in ______
a. MRI
b. CSF
How is Carotid Artery Dissection associated with Horner Syndrome?
Carotid A Dissection –> Partial Horner (Ptosis + Miosis only) 2/2 postganglionic sympathetic fiber damage
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 ]
(avoid HTN to ⬇︎risk of hemorrhagic conversion but avoid hypOtension to maintain perfusion to the ischemic penumbra)
_________________
3.wait ≥24h before ANY BLOOD THINNER
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 )
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]
How do you manage
Ischemic Stroke? (4)
How do you treat Febrile Seizure? -3
- 🟩REASSURANCE
- 🟩APAP for fever
3.🟨[abortive tx if ≥5 min]
How do you treat Refractory Serotonin Syndrome
Cyproheptadine
(antihistamine with anti-serotonergic properties)
prior to diagnosing Dementia, reversible causes of Cognitive impairment must be r/o
How do you workup Cognitive impairment ? (10)
how does hyperventilation reduce intracranial pressure?
(reduce to 25-30 mmHg)
hyperventilation ➜ DEC pCO2 ➜ cerebral arteriole vasoconstriction ➜ DEC ICP
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!
What role does Steroids play in [Intracerebral processes(tumor, infection, trauma)] ?
CTS DEC edema /swelling (in intracerebral processes 2/2 to CA|Tumor|Sickness_infxn)
“Stop My Head Swelling (Cancer) !”
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
“Dolls Eyes a NORMAL GUY” (Dolls Eyes = Brainstem intact)
How is [Apolipoprotein E] related to Alzheimers (2)
✔︎ ApoE2“brings you 2 safety” = actually DEC Alzheimer risk
_________________
✔︎ ApoE4“is bad 4 you!” –> impairs synthesis and clearance of AB-amyloid —> INC risk for LATE onset Alzheimers
NaTPO = [CLAV ➜ HANDU]sx
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 ∆
Image: L Chronic Subdural Hematoma
DDx for patient p/w
[1/2 facial paralysis(with ⊝ forehead sparing)] ?
[Lyme serology 1st] ➜ [P7BPBells palsy (dx of exclusion!)]
⚠️{[⊕Sparingof forehead ] = [⊕Strokein patient ]!}
What causes [Lateral ventricle frontal horn] enlargement in Huntington’s disease?
**Gross Caudate atrophy**
[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”
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!!*
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) ]
“Hunting 4 food is way too aggressive & dancey”
Identify ; Which are Lenticulate and which are Striatum?
“Gay People Cook!” = Basal Ganglia
Gay People=Lenticulate // People Cook= Striatum
- eg = Globus Pallidus
- es = Putamen
- d = Caudate
In Neurology, evoked potentials are used to identify what?
silent CNS lesions
The 3 types of dream disorders are ⬜, NRSAD and ⬜
_________________
Name the primary characteristics of [NRSAD: Sleep Terrors] ? (4)
RSRBD | NRSAD | NightMareDisorder
_________________
Sleep terrors are :
- NRSAD (NonREM)
- accompanied with recurrent incomplete awakenings
- can NOT be consoled upon wakening
- Seems to forget the dream = Dream Amnesia/No Dream Recall
NRSAD = Non-REM Sleep Arousal Disorder
identify (12)
identify (21)
A: Identify Boxes (4)
B: Clinical Presentation for lesion at A? B? C? D?
A=[central scotoma 2/2 macular degeneration]
👓when image hits 1º visual cortex, it is upside down and R-L reversed
#visual field defect.hemianopia.Meyer loop
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 Hemianopiawith macular sparing} if [PCA occluded]
identify (14)
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
- Arcuate Fasciculus = MOST COMMON
- Supramarginal Gyrus
- Auditory Cortex
- Large Posterior Perisylvian area
What is Kluver-Bucy syndrome?
[BL Amygdala❌ (associated with HSV1)] → hyperdisinhibited behavior(hypersexual, hyperphagia, hyperorality)
In patients with lesions of the PPRF, Eyes stare [⬜ opposite | toward] the PPRF lesion
PPRF = Paramedian Pontine Reticular Formation
opposite
In patients with a {Frontal Eye Field lesion}, Eyes stare [⬜ opposite | toward] the {Frontal Eye Field lesion}
toward
“eyes Front Toward me!”
pt present s/p trauma to the BL Hippocampus
lesions of BL Hippocampus → ⬜
anterograde amnesia (inability to make new memories)
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]
MCA (Middle Cerebral Artery)
A: What 5 sites does MCA perfuse? (5)
B: For each site, list Sx when compromised(i.e. Stroke) (5)
AsA (ANT spinal Artery)
A: What all does it perfuse? (3)
B: Sx if compromised(i.e. Stroke) (3)
[(AsA❌) +(VA❌)] → [medial medullary syndrome]
clinical features
epidural hematoma (6)
- fx of temporal bone
- → rupture of [middle meningeal artery (from Maxillary artery)]
- → Lucid interval f/b [hyperdense biconvex/lentiform epidural hematoma w transtentorial herniation] + DO3P
- [⛔ suture linesXing]
- [ ✅ falxXing]
- [✅ tentoriumXing]
🔎DO3P = [“DOPe” Oculomotor CN3 Palsy]
🔎Xing = Crossing
Why is the period after a SubArachnoid Hemorrhage important? (2)
[3d s/p SAH] can →
1. [cerebral vasospasm (tx = Nimodipine)]
2.repeatSAH
3 most common locations for [Intraparenchymal HTN Hemorrhage]
- basal ganglia
- internal capsule(Charcot Bouchard ruptured aneurysm of lenticulostriate)
- lobar
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;
ischemic: “Clots Never Help Watershed”[hippocampus|neocortex|cerebellum|watershed]
_________________
hemorrhagic: basal ganglia
A: Name the 3 types of ischemic stroke
B. What type of necrosis develops from ischemic stroke?
“THE ischemic stroke, smh”
[Thrombotic🆚Hypoxic🆚Embolic]
b. Liquefactive
post [ischemic stroke] management ⼀ (6)
BALTIC
1. [(A SA + ADP R Blocker)DAPT ]
2. [B P control ♨]x 24h
3. [Carb (Glucose) control]
4. [L]ipid control
5. [I nvestigate possible causes (CTA h/n, Carotid US, TTE)]
6. [Treat possible causes (afib)]
🔎DAPT = [Dual AntiPlatelet Therapy (ASA + ADP R Blocker)]
♨[(< 180/105[if thrombolytic given])] vs [< 220/110 [if thrombolytic NOT given]) ]24h
pt presents with r/o ischemic stroke
How long does it take 🔲 to detect cerebral ischemic changes?
-NCHC
-MRI
🔎NCHC = NonContrast Head CT
NCHC: [6-24HOURS]
_________________
MRI: [3-30min]
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 🅽 ]
🔎🅽= [Spinal Cord 🅽erves]
🔎🄱= [Spiny Vertebra 🄱one]
⚡ {C8🅽 exits [below C7 bone] and [above T1 bone]}
▶In adults, spinal cord extends to ⬜ vertebra(e),
▶ [Subarachnoid space (which contains CSF)] extends to ⬜ vertebra(e).
[L1🄱 - L2🄱];
[S2🄱 (lower border)]
🔎🄱= [Spiny Vertebra 🄱one]
💡*Lumbar Puncture*[L3🄱 - L5🄱]
Where are lumbar punctures performed?
L3🄱 - L5🄱
(at level of caudal equina)
🔎🅽= [Spinal Cord 🅽erves]
🔎🄱= [Spiny Vertebra 🄱one]
fill-in-blank (18)
Diaphragm pain and Gallbladder pain are referred to the ⬜ via the ⬜ nerve
R shoulder ; phrenic
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
✏️{[“S2,3,4S2-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) ,]}
Nerve root(s) for
Cremasteric reflex
L1🅽 ,L2🅽
“L1,L2 his testicles move”
[“S2,3,4 ⼀my DICK FEELS HARD⼀and my HOLE wants more”]
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❌
Brimonidine
MOA (2)
[⬇︎aqueous humor synthesis(⬇︎IOP)]α2🟢
for Glaucoma
Pilocarpine is a ⬜MOA sometimes used in emergency Glaucoma tx. Why?
{[miosis and cyclospasm(ciliary m CTN)][Muscarinic🟢Direct cholinomimetic]}
(carbachol has same MOA)
📝Pilocarpine = [very effective(via cyclospasm)] at opening trabecular meshwork into canal of Schlemm
🔎CTN = Contraction
clinical features
Von Hippel Lindau (4)
disease
- hemangioblastoma in retina/brain stem/cerebellum/spine
- angiomatosis
- BL renal cell carcinoma
- PHEOCHromocytoma
Describe the likely regions involved for the following deficits
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)
Describe how an action potential occurs (5)
RANHP
{Resting}: [-70mV resting potential (maintained with Na+/K+ pump)] becomes more positive (via preceding Na+ influx)
{Action Potential: ➜ at [-55mV = action potential occurs]
{[Na+ 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
{Hyperpolarization}: 4. ➜ [K+ efflux] occurs more negative than [-70mV resting potential] = HYPERPOLARIZATION
{Pump} → eventually climbs up to [-70mV resting potential] via Na+/K+ pump
Describe how NTS is released from presynaptic nerve terminals (11)
describe Malignant Hyperthermia (4)
malignant hyperthermia
1.muscle contraction + hyperthermia
2.{succinylcholine & [inhaled anesthetics (except N2O)} are causes
3.[rare hereditary condition]
4.potentially fatal
✏️inhaled anesthetics = -ane (halothane, Sevoflurane, etc)
Tx for Huntington’s Disease (3)
1.[(Tetrabenazine + reserpine)(inhibits VMAT → limits dopamine vesicle packaging and dopamine release) ]
2.[ Haloperidol(D2 R Blocker)]
etx = chromo 4 CAG repeat → caudate nc atrophy→ ⬇︎GABA, / ⬇︎ACh / ⇪dopamine]
“Hunting 4 food is way too aggressive & dancey”
[Glioblastoma Astrocytoma] Radiographic Findings - 2
- Butterfly lesion from crossing Corpus Collosum
- Midline shift from Lateral Vt Compression
GBM is usually a HIGH GRADE Astrocytoma
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:
❗️[Superomedial”[(Up) and (In)] ➜ IS A SIN!” Butt injection]
❗️[POST Hip dislocation]
C: none
D.
🔧 [No Thigh Extension]
”[(up) and (in) IS A SIN] < BUTT > [WITHOUT A DOUBT INJECT (UP) and (OUT)!]”
“All Butt Injections go Up and Out (SuperoLateral)”
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 <sup>*(hip drop points opposite the lesion)*</sup>]
🔧[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)"
etx of stroke is classified into what 5 categories?
- Large vessel
- small vessel
- cardioembolic
- cryptogenic
- [Other (vasculitis/drug/infxn/PFO/dissection/paradoxical)]
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]
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
absolute contraindications to receiving [tPA thrombolysis] -7
- active brain bleeding
- active internal bleeding
- prior brain bleed (hemorrhagic stroke)
- Platelets < 100K
- INR > 1.7
- HTN > 185/110
- major surgery recently
