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1
Q

Differentiate b/w UMN and LMN lesion

A

UMN: increased reflexes, tone, positive babinski, no atrophy and no fasiculations

LMN: decreased reflexes, tone, muscle bulk, positive fasiculations and absent babinskis

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2
Q

What 3 mechanisms can result in NMJ dysfxn

A
  1. blockage or nicotinic receptors (eg myesthenia gravis)
  2. reduced ACh released eg botulism
  3. inactivated of ACh by irreversible binding. Eg organophosphate tox
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3
Q

what investigations should you order in a weak pt

A 
lytes esp Ca/mg/PO4
CK
TSH
urine + renal fxn
consider LP
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4
Q

List 6 myopathies

A

1 polymyositis

  1. dermatomyositis
  2. Rhabdomyolisis
  3. PMR
  4. metabolic (hypokalemia)
  5. Periodic paralysis (familial or thyrotoxic)
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5
Q

What is myesthenia gravis?

A

Autoimmune blockade/destruction of nicotinic ACh receptors at NMJ causing decreased number available.

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6
Q

What will happen to a pt with myesthenia gravis when an icebag is placed on ptotic eyelid

A

Improves it b/c cold temporarily inhibits acetylcholinesterase therefore incr ACh available at synaptic cleft.
Apply x 2 min if improves at least 2mm it is diagnostic

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7
Q

what is a myesthnic crisis

A

resp failure in MG pt

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8
Q

What drugs (10) and conditions (5) can ppt a MG crisis

A 
Drugs: 
sedatives
1. diazepam
2. ketamine
3. NM blocking agents
4. lidocaine

Cardiovascular

  1. BB
  2. CCBs
  3. quinidine
  4. lidocaine
  5. procainamide

Antibiotics

  1. aminoglycosides
  2. tetracyclines
  3. clindamycin
  4. polymxin B
  5. fluoroquinolones
  6. colistin

Other

  1. phenytoin
  2. NM blockers
  3. corticosteroids
  4. thyroid replacement
  5. anticholinergics
  6. diuretics
  7. statins

Conditions:

  1. sepsis
  2. pregnancy
  3. cessation of anticholinesterases
  4. aspiration
  5. surgery
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9
Q

What is the FVC or NIF threshold for intubation in Myesthenic crisis

A

FVC: LT 15ml/kg

NIF

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10
Q

What are the S/S of botulism

A
  1. CN/bulbar muscle dysfxn (diplopia, dysarthria, dysphagia)
  2. NMJ dysfxn
    descening, symmetric, flaccid paralysis
  3. antimuscarinic sx
    (urinary retention, dry skin, temp, mydriasis)
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11
Q

what is the treatment of botulism

A

Heptavalent botulinum antitoxin

infant: BabyBIG (IV human botulism IG)

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12
Q

what conditions can cause flaccid paralysis

A 
GBS
botulism
MG
Eaton-Lambert syndrome
tick paralysis
polio
diptheric polyneuropathy
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13
Q

Describe Wallenberg syndrome

A

occlusion of PICA
loss of pain/temperature to ipsilateral face and contralaateral body. Paralysis of palate and pharynx/larynx causing dysphonia/dysarthria
Horner’s syndrome: (ptosis, miosis, anhidrosis) on ipsilateral side

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14
Q

what is internuclear opthalm

oplegia

A

pathognomonic of MS
weakness of one side CN 3 with adduction.
Indicates interruption of medial lo gitudinal fasiculus on side of CN III weakness

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15
Q

Describe a CN III palsy

A

pupil is down and out with associated ptosis

if pupil sparring (as in microvascular ischemia) there may not be meiosis

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16
Q

How doe an UMN lesion present?

A

Hyperreflexic with +ve Babinski
Weakness causing pronator drift
spacticity to extension of UE and flexion of LE

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17
Q

How does a LMN lesion present?

A

Hyporeflexic with flaccidity and muscle cramps and fasciculation

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18
Q

Where is the lesion?

Unilateral weakness with a combo of hand/leg with ipsilateral facial involvement

A

○ Lesion in contralateral cerebral cortex of CSTs forming the internal capsule
○ Senosry defects common on same side
○ Equal weakness to face/hand/leg more likely to be subcortical in internal capsule
○ Sudden onset= hemorrhage or ischemia
Gradual onset = demyelination or neoplasm

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19
Q

Where is the lesion?

Unilateral weakness: combo of arm/hand/leg with contralateral facial involvement

A

○ Brainstem leasion or vertebrobasila insufficiency
○ CN exam necessary, look for:
§ Ptosis (CN III)
§ Facial droop with forehead invilvement (VII nucleus)

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20
Q

Where is the lesion:

Unilateral limb weakness with no facial involvement

A

○ Lesions of:
§ Medial, contralateral cerebral homonculus
§ Discrete interanal capsule/brainstem lesion involving only 1 corticospiral tract
§ Brown-Sequard menicord syndrome if patient also has contralateral hemobody pain and temperature sensory disturbances below level of motor weakness

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21
Q

Where is the lesion:

bilateral weakness of upper extremities only

A

Central cord syndrome
○ Pinprick sensory loss
○ Light touch sensation intact (posterior columns)
○ Caused by: cervical spine hyperextension injuries and syringomyelia

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22
Q

Define seizure.

A
  • Episode of abnormal neurologic activity caused by an inappropriate electrical discharge of brain neurons
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23
Q

List causes of secondary seizures.

A
  • Intoxication
  • Poisoning
  • Encephalitis
  • Encephalopathy
  • Organ failure
  • Metabolic disturbances
  • CNS infections
  • Cerebral tumors
  • Pregnancy (eclampsia)
  • Supratherapeutic levels of anticonvulsants
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24
Q

List causes of vertigo

A 
PERIPHERAL
BPPV
vestibular neuritis
Labyrinthitis
Meniere's dz
FB in ear canal
AOM
perilymphatic fistula
trauma (labyrinth concussion)
motion sickness
acoustic neuroma

CENTRAL CAUSES

infection (encephalitis, meningitis, brain abscess)
vertebral basilar insufficiency
subclavian steel syndrome
cerebellar hemorrhage or infarction
vertebral basilar migraine
post-traumatic injury (temporal bone #)
postconcussive syndrome
temporal lobe epilepsy
tumor
MS

SYSTEMIC CAUSES
DM
hypothyroidism

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25
List 4 red flags in vertigo:
``` · ANY neurological deficit · Inability to walk without support · Direction-changing nystagmus · Total ipsilateral hearing loss · *Nelson et al. WestJEM. 2009;10(4):273-77 ```
26
List vestibulotoxic medications and drugs.
- Aminoglycosides - Anticonvulsants - Alcohols - Quinine - Quinidine - Minocycline
27
Acute vestibular syndrome
``` Top 2 causes are stroke and MS Syndrome consists of: N/V >24hrs Acute onset Gait instability Nystagmus Head motion intolerance ```
28
What is the characteristic triad of Meniere’s disease?
1. Progressive Hearing loss with episodes 2. Vertigo 3. Tinnitus
29
What is the SN of a plain CT head to detect acute infarction, especially in the posterior fossa?
- 16% | - Yield of CTA lesst han 3%
30
Describe the findings of a HINTS exam that suggest infarct
HINTS to INFARCT Impulse negative Fast alternating Test of skew positive (refixation)
31
Describe the components of the HINTS exam (Stroke 2009;40:3504):
1. Horizontal Head impulse test (h-HIT): a. Tests the vestibulo-ocular reflex b. Rapid, passive head rotation from lateral (10-20 degrees) to centre c. Head turned left à testing right VOR (vestibuloocular) d. Head turned right à testing left VOL e. Normal (Negative h-HIT): equal & opposite eye movement that keeps the eyes stationary in space f. Abnormal (Positive h-HIT): head rapidly rotated TOWARD the affected side of VOR dysfunction, results in the inability to maintain fixation during head rotation, requiring a corrective gaze shift once head stops moving g. A positive h-HIT indicates vestibular pathology à ie vestibular neuritis h. A negative h-HIT may signify a central lesion such as pontine stroke! 2. Nystagmus: a. Horizontal nystagmus beats in only 1 direction, increasing as gaze is in direction of nystagmus fast phase b. Other nystagmus: central pathology 3. Skew deviation: a. Vertical ocular misalignment that results form a right to left imbalance of vestibular tone b. Performed by alternate cover test: alternately occluding each eye with eyes focused on central target c. Normal: eyes remain motionless d. Abnormal: refixation saccade after removal of the cover, eyes move up or down, in opposite directions. e. Also can test by upwards gaze è will have diplopia 4. Benign HINTS: Abnormal h-HIT, directional fixed horizontal nystagmus, absent skew 5. Dangerous HINTS: Normal h-HIT, direction changing nystagmus, skew deviation present)
32
What is the DDx of headache diagnoses
``` CRITICAL SAH CO poisoning Temporal arteritis Bacterial meningitis/encephalitis Glaucoma Increased ICP ``` ``` EMERGENT Shunt failure Traction H/A Tumor/mass Subdural hematoma Mountain sickness ``` ``` Sinusitis Brain abscess Anoxic H/A Anemia Hypertensive crisis ``` ``` NON EMERGENT Migraine Vascular Trigeminal neuralgia Post-lumbar puncture Dental problem TMJ disease Tension H/A cervical strain Cluster H/A Febrile H/A Non neuro infection source HTN Effort dependent or coital H/A ```
33
Differentiate monocular vs binocular diplolpia:
onocular (15%): o Double vision that persists in one affected eye even when the other eye is closed o Related to distortions in light path - Binocular (85%): o Double vision that resolves when either eye is closed o Result of misalignment in the visual axis o Wide range of causes from eye to brainstem  
34
List 8 don’t/can’t miss causes of diplopia:
Critical: - Basilar artery thrombosis - Botulism - Basilar meningitis - Aneurysm ``` Emergent: - Vertebral dissection - Myasthenia Gravis - Wernicke’s encephalopathy Cavernous sinus process ```
35
List 5 causes of urgent diplopia:
- Brainstem tumor - Opthalmoplegic migraine - Miller-Fisher Syndrome - Ischemic neuropathy (microvascular) - GBS - Orbital myositis - MS - Orbital apex mass - Thyroid myopathy (Grave's)
36
What bedside tests can be used to diagnose Horner’s in the case of incidental anisocoria?
Apraclonidine: causes reveral of anasicoria. Horner's pupil is extra sensitive to alpha -1 stimulation causing it to dilate whereas the normal eye is more sensitive to alpha-2 and causes it to constrict
37
What 8 things can cause acute emergent weakness that may affect respiration (Box 107-1)?
Infection: - tick paralysis - polio - diptheria - botulism Toxic: - seafood: paralytic shellfish toxin, puffer fish - metals: arsenic, thallium Autoimmune - MG - GBS - chronic demyelination PM Metabolic Dyskalemic syndromes -hypoPO4, hypoMg, porphyria
38
What is GBS?
- Acute inflammatory demyelinating polyneuropathy - Others forms: o Acute motor axonal neuropathy next most commonly seen form, most common in Asians o Miller Fisher and acute sensory axonal neuropathy
39
What is the clinical presentation of GBS?
- Days to weeks after acute illness - Sx: o Symmetrical weakness o Distal > proximal “ascending weakness” o Variable sensory findings o Decreased DTRs o 50% have autonomic dysfunction or CN involvement (VII most common) o 30% experience respiratory failure (more if tongue weakenss)
40
List 4 organisms associated with GBS:
- Campylobacter - CMV - EBV - Mycoplasma pneumoniae
41
List demyelinating polyneuropathies
GBS - acute inflammatory demyelinating polyradiculoneuropathy - acute motor axonal neuropathy - miller-fisher syndrome Chronic inflammatory demyelinating polyradiculoplexoneuropathy Malignancy HIV infection Buckthorn Diptheria
42
What does CSF analysis show with GBS?
- Markedly elevated CSF protein with mild pleiocytosis - Highly Specific - Normal does not rule out GBS
43
What is the treatment for GBS?
- Assessment of respiratory function: FVC o FVC <20mL/kg, negative inspiratory pressure <30cmH20 = need intubation reatment options o Plasma exchange or IVIG 400mg/kg/day x 5 days
44
What is mononeuropathy multiplex, and what are 6 conditions that cause it (Box 107-7)?
- Asymmetrical sensorimotor, distal > proximal neuropathy ``` Systemic vasculitis: - Polyarteritis nodosa - RA - SLE - Sjogrens syndrome Nonsystemic vasculitis Sarcoid Diabetes Mellitus ``` ``` Toxic (lead) Transient (polycythemia vera) Cryoglobinemia )Hep C) Infectious - Lyme - HIV Neoplastic: - Paraneoplastic - Direct infiltration ```
45
What are the findings of ALS (Box 107-8)?
UMN signs - Hyperreflexia - spasticity - positive Babinski's LMN - fasiculations - cramos - distal weakness (assymetrical) - atrophy Combined UMN/LMN - dysarthria - dysphagia - resp compromise
46
Pathophysiologically, what 3 mechanisms can result in NMJ dysfunction?
1. Blockade of nicotinic receptors eg myasthenia gravis 2. Reduced ACh released eg. botulism o Affects both nicotnic and muscarinic receptors o Anticholinergic sx: decr VA, urinary ret, inr: HR,temp,dry 3. Inactivation of acetylcholinesterase by irreversible binding, resulting initially in hyperstimulation followed by paralysis eg organophosphate toxicity
47
List disorders that affect the NMJ, and the classic Sx of these disorders:
- MG: block nicotinic ACh Rs - Botulism: inhibit pre-synaptic Ach release - Eaton-Lambert - Tick paralysis - Sx: o Ptosis o Dysphagia o Diploplia o Dysarthria o Weakness o NO sensory changes
48
What is myasthenia Gravis (MG)?
- Autoantibodies block nicotinic ACh receptors at the NMJ - Form autoantibodies against receptor or muscle specific tyrosine kinase - Result: destruction of nicotinic ACh receptors à reduced total # available
49
What is Lambert-Eaton myasthenic syndrome?
- Rare. Paraneoplastic syndrome, 50% associated with lung SCC - Compared to MG: weakness improves with repeated stimulation: more ACh in synapse to bind receptors - Sx: improving weakness with use, hyporeflexia, autonomic dysfunction (dry mouth) - Rx: Treat cancer +/- IVIG
50
What is a myasthenic crisis?
- Respiratory crisis with respiratory failure | 15-20% of MG patients
51
List 5 conditions and 10 drugs things that can precipitate a myasthenic crisis (Box 108-2):
``` Conditions: - Pregnancy - Infection - Surgery - Aspiration - Cessation of anticholinesterases   Medications:   Sedative / Anasthetics - Diazepam - Ketamine - Lidocaine - NM blocking agents   Cardiovascular: - BBs - CCBs - Quinidine - Lidocaine ``` ``` Meds (con’t)   Antibiotics: - Aminoglycosides - Tetracyclines - Clindamycin - Polymxin B - Colistin - Fluoroquinolones   Other: - Phenytoin - NM blockers - Corticosteroids - Thyroid replacement - Anticholinergics - Diuretics - Statins ```
52
Outline your approach to the patient in myasthenic crisis:
Determine need for intubation IVIG 1g/kg identify and address precipitants & stop cholinergics
53
Describe the pathophysiology of botulism:
- Botulism toxin binds irreversibly to the pre-synaptic neuron, inhibits the release of ACh from presynaptic membrace - Acts in peripheral nerves and cranial nerves - Blocks voluntary AND autonomic functions - As new receptors are regenerated, Sx improve
54
What are the Sx of botulism?
- Onset Sx 6-48 after injestion of botulism toxin +/- Sx gastroenteritis - CN & bulbar muscle dysfunction o First to be affected o Diploplia, dysarthria, dysphagia - NMJ dysfunction o Descending, symmetric, flaccid paralysis - Antimuscarinic Sx: o Urinary retention o Dry skin elevated temperature o Mydriasis
55
How is infantile botulism different from adult?
- Adult = ingestion of toxin - Infantile = ingestion of spores that germinate in the high pH of the infant GI tract and produce toxins - Sx: constipation, poor feeding, weak cry, lethargy
56
What is tick paralysis?
- Ixovotoxin injected during tick feeding from Rocky Mountain Wood Tick (Dermacentor Veriabillis) - Decrease the release of ACh at NMJ, also reduces nerve conduction speeds - +/- Fixed dilated pupils - Acute, ascending, flaccid motor paralysis - Management: Removal of tick, supportive care until Sx resolution
57
Provide a list of 6 conditions that can cause ascending flaccid paralysis:
- GBS - Myasthenia gravis - Eaton-Lambert syndrome - Tick paralysis - Poliomyelitis - Botulism - Diptheritic polyneuropathy
58
What are the skin findings in Dermatomyositis?
``` Periorbital heliotrope (usu. photosensitive) 2. Erythema and swelling of the extensor surfaces of joints ```
59
What electrolyte abnormalities can cause muscle weakness?
- Hypokalemia - Hyperkalemia - Hypocalcemia - Hypercalcemia - Hypermagnesemia - Hypophosphatemia
60
What endocrinopathies can cause acute painless myopathies?
- Hypothyroid - Parathyroiud Adrenal glands
61
What syndromes can cause periodic paralysis?
- Familial periodic paralysis :hypokalemic or hyperkalemic - Thyrotoxic periodic paralysis - Asian men most commonly affected - AD disorders
62
How should you manage a patient with periodic paralysis?
- Hypokalemic: results form shifting, NOT whole body depletion!! o Fluid to redistribute K o Small doses of K PO - Thyrotoxic: o Sx with hyperthyroid à likely from overactive Na/K ATPase and intracellular shifting o Treatment of the thyrotoxicosis treats the paralysis and hypokelamia Propranolol

Neurology (6 decks)

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