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MBB2 Flashcards

1
Q

Describe pathophysiology of MG

A

Antibodies block AchR

Accelerated internalization and degradation of AchR

Complement-mediated lysis of post-synaptic membrane (see simplification of postsynaptic folds, this reduced number AchR)

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2
Q

clinical features MG

A 
Head drop (neck extensor weakness)
Ocular: ptosis, binocular double vision
Facial: hanging jaw sign, snarling smile
Mouth: difficulty chewing, dysphagia, dysarthria, hypophonia 
Dyspnea (resp muscles)
Proximal limb > distal
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3
Q

What are sensation and reflexes like in MG?

A

Normal!

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4
Q

MG weakness _____ with activity

A

increases

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5
Q

MG most common presenting symptom is?

A

OCULAR - ptosis, double vision

(less commonly, oropharyngeal, limb muscles
rarely, head drop, SOB)

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6
Q

MG age of onset?

A

Young Females 20-24

Older Males 70-74

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7
Q

What is MG crisis

A

Respiratory Muscle Failure
& Upper Airway Compromise

leads to aspiration

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8
Q

Describe basis and indication for Ice Test

A

indicated for ptosis
acetylcholinesterase enzyme has decreased activity at cold temp; ice pack will increase Ach availability and temporarily improve ptosis

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9
Q

Describe Tensilon (edrophonium chloride) test

A

indicated for ptosis, ophthalmoplegia
Tensilon is a short-acting acetylcholinesterase inhibitor, causes transient increase in Ach availability at NMJ

in MG, transiently improves ptosis and diplopia

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10
Q

Does serum titer of AchR antibody correlate with disease severity?

A

No

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11
Q

Disorder associated with thymus problems (thymoma, thymic hyperplasia)

A

Myasthenia Gravis

70% of AchR-Ab positive patients have thymic hyperplasia
10% AchR-Ab MG have thymoma (hence must do chest CT to check for this)

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12
Q

Treat Myasthenic crisis with?

A

PLEX or IVIG

may need mechanical respiratory support

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13
Q

List some precipitation factors of Myasthenic crisis

A 
Tapering rapidly immune modulators
Aspiration
Drugs 
Infection
Surgery
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14
Q

2 forms of LEMS

A 
paraneoplastic 
primary autoimmune (no identified tumor)
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15
Q

Most LEMS have antibodies against ______

A

P/Q type calcium channel

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16
Q

Most common type of cancer associated w/ paraneoplastic LEMS?

A

Small Cell Lung Cancer

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17
Q

Risk factors for paraneoplastic LEMS

A

median age 60
male
smoking
weight loss

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18
Q

Non-tumor LEMS affects what age and gender?

A

30 & 60yo

female more

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19
Q

What is the pathogenesis of LEMS?

A

P/Q VGCC antibody blocks Ca2+ influx

less Ach released at NMJ

muscle weakness

Ach is also neurotransmitter between pre- and post-ganglionic neurons so LEMS also results in autonomic dysfunction!

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20
Q

3 clinical features of LEMS

A 
proximal weakness (gradual onset)
- can extend to bulbar and distally

Areflexia
*with post-exercise facilitation

Autonomic dysfunction (from decr Ach)

  • dry mouth
  • constipation
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21
Q

What is motor facilitation? In what disease do you see it?

A

seen in LEMS

Exercise or HIGH-freq stimulation
keeps Ca channels in presynaptic membrane open longer, so more Ca influx, more Ach release –> transient amplification of muscle response

Contracting muscles transiently increases reflexes

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22
Q

Describe cancer screening process for LEMS

A

Chest CT - for SCLC
if negative, PET scan for other cancers
if still negative, screen every 3 months for at least 2 years

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23
Q

Treatments that can be used in LEMS (4)?

A

AchE inhibitors (less effective than in MG)

3,4-DAP
somehow increases Ca influx

Longterm immunsuppressants (prednisone, azathioprine)

IVIG/PLEX for severe or rapidly progressive LEMS

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24
Q

Botulinum toxin works by?

A

Cleaves SNARE protein important for vesicle docking and fusion. –> no ACh released into NMJ

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25
Q

List 4 UMN signs

A

weakness
increased tone (spasticity)
hyperreflexia
pathological reflexes (babinksi & hoffman’s)

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26
Q

List 4 LMN signs

A

atrophy
decreased tone
reduced reflexes
fasciculation

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27
Q

in a nerve conduction study, myelin corresponds to _______ and axon/cell body corresponds to _______

A

myelin - conduction speed

axon/cell body - amplitude

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28
Q

Duchenne muscular dystrophy inheritance? mutation?

A

XLR

dystrophin gene mutation (most are due to deletions)

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29
Q

Two big causes of mortality in duchenne’s

A

cardiomyopathy

respiratory failure

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30
Q

duchenne’s manifests at what age with what symptoms?

A

age 2
(before age 5)

proximal weakness
clumsiness
toe walking, waddling gait, can’t run
Pseudohypertrophy of calves

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31
Q

3 potential treatments for duchenne’s?

A

Supportive - PT, bracing, surgery
Prednisone
Gene therapy (not super effective)

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32
Q

What is difference between Duchenne and Becker muscular dystrophy?

A

both are XLR dystrophinopathies but Becker is less severe, later onset, cardiomyopathy less common

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33
Q

Fascioscapulohumeral muscular dystrophy inheritance pattern? mutation? hallmark symptom?

A

AD
DUX4 gene, chromosome 4q

weakness of FACE, neck, shoulder, (peroneal); prominent scapular winging

4 qute ADmiral DUX (ducks) can’t move their face and wings

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34
Q

delay in relaxation after a muscle contracts is called ___

A

myotonia

ex: takes a while to relax after handshake
hatchet face

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35
Q

Emery-Dreifuss can be inherited as

A

XLR,
AD,
AR

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36
Q

Type 1 Myotonic Muscular Dystrophy inheritance pattern? mutation?
**
clinical signs?

A

AD
CTG repeat on chrom 19 (DMPK gene)

Respiratory insufficiency (diaphragm/intercostal weakness
Endocrine abnormalities
DISTAL muscle weakness

frontal Balding

Cardiac (1st degree heart block, sudden cardiac death)

Cataracts

19-year-old dumb RED balding CAT with a bad heart is gasping for air

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37
Q

Type 2 Myotonic Muscular Dystrophy inheritance pattern? mutation?

A

AD
CCTG repeat ZNF9 gene chromosome 3

proximal muscle involvement
cataracts

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38
Q

Myotonia Congenita is characterized by? Is due to mutation in ___gene.

A

generalized myotonia without weakness

CLCN1 gene

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39
Q

In myotonia congenita, muscles stiffness is worse with _____ and relieved with ____

A

cold, inactivity

relieved by exercise

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40
Q

AD myotonia congenita is called

A

Thomsen disease

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41
Q

AR myotonia congenita is called

A

Becker disease

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42
Q

Type II / Pompe disease = deficient ___

A

acid maltase

muscle weakness, resp difficulty

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43
Q

Type III / Cori disease = deficient ___

symptoms?

A

glycogen debranching enzyme

myopathy

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44
Q

Type V / McArdle disease = deficient ___

symptoms?

A

myophosphorylase deficiency

exercise intolerance, rhabdomyolysis

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45
Q

Type VII / Tarui disease = deficient ___

symptoms?

A

PFK deficiency

exercise intolerance, muscle gramping

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46
Q

childhood onset lipid storage disease presents with

A

myopathy
encephalopathy
cardiomyopathy
hepatomegaly

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47
Q

adult onset lipid storage disease presents with

A

fatigability
muscle pain
myoglobinuria

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48
Q

in dermatomyositis, deposition of ____ leads to muscle ischemia

A

complement

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49
Q

25% of dermatomyositis associated with ___

A

malignancy

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50
Q

_____ is the most common myopathy in patients >50

A

inclusion body myositis

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51
Q

which inflammatory myopathy affects men more than women?

A

inclusion body myositis

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52
Q

which inflammatory myopathy does NOT respond to immunomodulating therapy (ie steroids)?

A

inclusion body myopathy

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53
Q

inflammatory myopathy with elevated CD8

what other marker?

what symptoms?

A

polymyositis

symmetric proximal weakness dev over weeks to months
bulbar symptoms
+ANA

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54
Q

symptoms of inclusion body myositis?

A

weak quads and finger flexors, ankle dorsiflexors (often asymmetric)

dysphagia, facial weakness

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55
Q

What do you expect to see in CSF with Guillaine Barre?

A

cyto-albumino dissociation (elevated protein without elevated WBC)

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56
Q

Describe symptoms and course of Guillaine Barre

A 
subacute onset after GI or URI
ascending sensory symptoms
motor weakness
reduced reflex
symptoms worst within 4 weeks onset
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57
Q

GBS treatment

A

PLEX or IVIG

most have good recovery

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58
Q

diagnostic indications for LP?

therapeutic indications for LP?

A

diagnostic:

  • measure CSF pressure
  • for lab studies
  • inject dye/radioactive tracer to see if blockage in circulation

therapeutic:

  • give anesthetics or chemo
  • reduce CSF pressure
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59
Q

LP needle inserted between which vertebrae? ____ used as a landmark

A

L3-L4 interspace

iliac crest

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60
Q

acute indications for LP?

chronic/subacute indications for LP?

A

acute

  • suspect meningitis or encephalitis
  • suspect subarachnoid hemorrhage
  • suspect demyelinating neuropathy like GBS

chronic

  • eval chronic infection (neurosyphilis, CJD)
  • suspect other meningial process (carcinomatous meningitis, neurosarcoid)
  • evidence of Multiple Sclerosis
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61
Q

LP contraindications

A
  • incr ICP due to mass lesion and/or edema
  • obstruction hydrocephalus
  • coagulopathy or therapeutic anticoagulation
  • thrombocytopenia
  • spinal epidural abscess
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62
Q

Normal opening pressure of CSF is

A

100-180 mmH20

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63
Q

normal CSF glucose is?

A

60

or ~2/3 of serum glucose

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64
Q

what is Xanthochromia?

A

yellow color in CSF due to bilirubin (lysed RBCs after SAH)

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65
Q

how to differentiate between Xanthochromia from SAH traumatic tap?

A

centrifuge it - if traumatic tap, CSF will become clear and colorless

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66
Q

ALS is due to loss of _____ (motor or sensory) neurons in _______ and ______

A

motor; brain and spinal cord

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67
Q

Does ALS have sensory symptoms?

A

no

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68
Q

Is most ALS sporadic or familial?

A

most is sporadic

5-10% familiali
SOD1
C9orf72
TDP43

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69
Q

EMG in ALS shows?

A

widespread denervation in multiple segments

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70
Q

ALS survival is ____(time) from time of onset. Most die from ____

A

2-4 years

respiratory failure

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71
Q

Two medications for ALS and how they work

A

Rilutek
-block glutamatergic activation

Radicava (endaravone)
free radical scavenger, slows disease progression

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72
Q

_____ can mimic ALS

A

Cervical Disc Disease

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73
Q

Most of blood supply to spinal cord is provided by ___

A

anterior spinal artery

posterior columns supplied by a pair of psosterior spinal arteries

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74
Q

Descending tracts are ______

A

motor

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75
Q

Ascending tracts are _______

A

sensory

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76
Q

Biceps and brachioradialis reflex mediated by ___ nerve root

A

C6

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77
Q

Triceps reflex mediated by ___ nerve root

A

C7

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78
Q

knee jerk reflex mediated by ___ nerve root

A

L3/L4

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79
Q

ankle jerk reflex mediated by _____ nerve root

A

S1

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80
Q

4 cardinal symptoms of Parkinson’s

A

bradykinesia
resting tremor
rigidity
festinating gait (shortened accelerated steps)

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81
Q

Dopamine binding to D2 results in

A

inhibition of indirect pathway (more movement)

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82
Q

activation of _____ (in the nigrostriatial pathway) leads to inhibition of movement

A

subthalamic nucleus
SNr
GPi

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83
Q

Dopamine binding to D1 results in

A

stimulation of direct pathway (more movement)

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84
Q

Side effects of medical treatment of Parkinsons

A
  • Dyskinesia
  • On-Off response (abrupt transient fluctuations in severity of parkinsonism
  • Psychosis (too much dopamine causes visual hallucinations)
  • Orthostatic hypotension
  • Nausea
  • Somnolence
  • Impulse control disorder (gambling, hypersexuality)
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85
Q

What is the on-off phenomenon in PD?

A

PD patients cycle between freezing (off), too much movement (on), and normal

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86
Q

Where can you put Deep Brain Stimulation to treat Parkinson’s?

Advantages of each location?

A

STN - greater decr in medications

GPi is usually default

  • less depression than STN
  • better for cognition
  • better for falls
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87
Q

Essential tremor is what type of tremor?

A

active

  • holding a utensil, sipping or pouring from a cup
  • writing
  • fine motor tasks
  • can also get tremor of head, voice, legs, or tongue
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88
Q

What is dystonia?

  • tx focal dystonia?
  • tx generalized dystonia (5)?
A

movement disorder with involuntary contractions of opposing muscles –> stereotyped twisting movements and abnormal postures

focal dystonia: botulinum injections for

generalized dystonia:

  • anti-cholinergics
  • muscle relaxants
  • benzos
  • carbidopa/levo? (there’s a rare form of dystonia b/c not enough dopamine, usu in kids)
  • DBS
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89
Q

what is paratonia? what is it usually caused by?

A

unable to relax

cause: frontal lobe lesion

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90
Q

what is tone?

List the 4P’s of tone

A

resistance of muscle to PASSIVE movement of a joint

Position at rest
Palpation
Passive movement
Posture

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91
Q

what is weakness?

A

loss of muscle POWER (when testing muscle power, pt asked to resist)

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92
Q

What are two types of hypotonia? How are they different?

A

Spasticity - velocity dependent (the more you pull, the more resistance). HYPERACTIVE STRETCH REFLEX

Rigidity - equal resistance regardless of movement direction and velocity

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93
Q

spasticity caused by ____ lesions

A

UMN

loss of UMN suppression of spinal cord reflex

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94
Q

Charcot Marie Tooth affects ____ Nervous System.

-symptoms?

A

Peripheral

hereditary loss of myelin
–> FOOT DROP, atrophy, contracture, hammertoes, champagne neck legs, high foot arch (affects legs first)

negative sensory sxs - numbness, sensory ataxia, trouble w balance
affects distal more

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95
Q

Congenital causes of Cerebral Palsy?

A

Periventricular Leukomalacia (damage to white matter; maternal infection, fetus injury, unknown)

Cerebral dysgenesis (abnormal brain growth)

Intracranial hemorrhage
(fetal stroke, maternal HTN, maternal infection)

Hypoxic ischemic encephalopathy

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96
Q

Brown-Sequard syndrome leads to what deficits?

A

Loss of pain/temp on contralateral side

Ipsilateral Loss of motor (acutely flaccid paralysis, then spasticity/hyperreflexia)

Ipsilateral Loss of fine touch/ proprioception/vibration

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97
Q

cause of subacute combined degeneration + symptoms?

A

B12 deficiency
involves dorsal column and lateral corticospinal tract

dorsal column –> balance problems

lat corticospinal –> stiffness, spasticity

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98
Q

Causes of anterior spinal cord infarction + symptoms?

A

hypoperfusion or emboli

BL loss pain/temp
initial flaccid paralysis, then spasticity

vibratory sensation intact

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99
Q

VITAMIN D mnemonic for differentials

A 
Vascular
Infections
Trauma/Toxic
Autoimmune
Metabolic 
Inflammatory
Neoplastic
Dengenerative
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100
Q

Name gross and microscopic findings of ALS

A

Gross:

  • shrunken/atrophic anterior nerve roots
  • brain usu normal but may see atrophic precentral gyrus (dt disappearing UMN)

Microscopic
-degen of myelinated fibers in corticospinal tract
-loss of motor neurons w/ reactive astrogliosis
-cytoplasmic eosinophilic Bunina Bodies
affects motor cortex, brainstem, and spinal cord

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101
Q

Spinal Muscular Atrophies are due to degeneration of ____

A

LMNs

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102
Q

Spinal muscular atrophy inheritance pattern?

Genetic mutation?

A

AR

SMN1, chromosome 5

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103
Q

Werdnig-Hoffmann Disease symptoms

A

aka SMA1, floppy baby syndrome

symptoms manifest abruptly in first months of life, quickly progress to respiratory failure

death within two years without mechanical vential

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104
Q

what is the most common genetic cause of infant death?

A

spinal muscular atrophy

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105
Q

two most common triggers of Guillain-Barre syndrome? (aka AIDP- acute inflammatory demyelinating polyneuropathy )

A 
campylobacter jejuni (30%)
cytomegalovirus (10%)
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106
Q

poliomyelitis

  • cause
  • symptoms
  • histo characteristics
A
  • lytic infection of LMNs
  • small RNA viruses in Enterovirus genus
  • flaccid paralysis (usually temporary but can be permanent)
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107
Q

friedrich’s ataxia

  • inheritance pattern?
  • mutation?
  • age of onset
  • symptoms
  • associated conditions
A

childhood- toddlers/teens
AR, expansion of GAA in frataxin (FXN) gene, chromosome 9

degeneration of

  • posterior column (vibratory sense, proprio)
  • lateral corticospinal (spastic paralysis)
  • spinocerebellar (ataxia)

assoc w/ DM and cardiomyopathy

Friedrich is Fratastic, he’s your favorite frat brother, always staggering and falling but has a sweet big heart.

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108
Q

on histology, Chronic Inflammatory Demyelinating Polyneuropathy has __

A

recurrent demyelination and remyelination with onion bulb formation

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109
Q

cause of Charcot Marie Tooth type 1

A

duplication of a region on chrom 17 that includes peripheral myelin protein 22 (PMP22) gene

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110
Q

histology of CMT1

A

recurrent demyelination and remyelination with onion bulb formation (similar to CIDP)

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111
Q

what primary CNS neoplasm is classically seen at bottom of spinal cord

A

myxopapollary ependymoma

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112
Q

gene altered in tuberous sclerosis

A

TSC1 (hamartin)

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113
Q

gene altered in frontal lobar degeneration & ALS

A

TDP-43

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114
Q

Name 4 drugs/toxins can induce myopathies

A

steroids
statins
colchine
ethanol

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115
Q

List 5 non-movement symptoms of Parkinson’s

A 
memory problems/hallucinations
mood symptoms (depression, anxiety)
sleep problems
choking on food 
dysautonomia (BP drops, ED, constipation, problems emtpying bladder, etc)
116
Q

list three signs of bradykinesia

A

masked facies
decreased movement
soft voice
small handwriting

117
Q

diagnostic criteria for Parkinson’s?

A

Parkinsonism
+responds to Sinemet
+no evidence of PD mimics

*no labs or studies needed

118
Q

carbidopa inhibits ____

A

DOPA decarboxylase in the periphery

119
Q

List 3 medications for essential tremor

A

don’t need to tx UNLESS it’s bothering pt!!

Propranolol
Primidone (anti-sz med)
Topiramate (anti-sz med)

120
Q

If meds don’t work for a debilitating essential tremor, can place Deep Brain Stim in ____

A

Ventral intermediate nucleus of THALAMUS (which is relay point from cerebellum to rest of brain)

121
Q

What are three antipsychotics that do NOT worsen parkinsonism

A

Quetiapine (seroquel)
Pimavanserin
Clozapine

122
Q

What is Lewy Body Dementia

A

Parkinsonism
+ hallucinations
+dementia within ONE YEAR of onset of parkinsonism

123
Q

what is multiple system atrophy

A

Parkinsonism and/or ataxia
+PROFOUND early dysautonomia (major orthostatic hypotension, urinary retention, ED, constipation, gastroparesis, severe peripheral neuropathy)

124
Q

what drugs can induce parkinsonism?

A

antipsychotics or antiemetics that block dopamine

  • risperidone
  • haliperidol
  • promethazine
125
Q

what is progressive supranuclear palsy?

A

Parkinsonism
+early gait instability/falls
+limited vertical gaze
+frontal cognitive signs (cry or laugh randomly)

is a sporadic tauopathy

126
Q

what is corticobasal degeneration?

A

Parkinsonism
+profound asymmetry
+weird stuff (alien limb, limb apraxia, rest AND action tremor, etc)

onset in 60s

127
Q

list 6 drug classes that for parkinson’s and an example of each

A
  1. levodopa/carbidopa (sinement)
  2. dopamine receptor agonists (pramiprexole, ropinirole, rotigotine, apomorphine, bromocriptine)
  3. COMT inhibitors (entacapone)
    - decreases peripheral metabolism of levodopa, making it last longer
  4. MAO-B inhibitors (selegiline, rasagiline)
  5. amantidine
    - unclear moa
    - just helps quiet dyskinesias
  6. anti-cholinergics?
128
Q

list 3 indications for DBS in parkinson’s

A

must have previous good response to levodopa!!
current symptoms are limiting patient
failed all optimized med therapy

signific on-off fluctionations,
signific dyskinesias,
no significant cognitive/uncontrolled mood symptoms

129
Q

Huntington’s disease inheritance and genetic cause?

A

AD

CAG repeat, chromosome 4

shows anticipation- more repeats in subsequent generations which leads to earlier onset and more likely passed on

130
Q

symptoms of Huntington’s

A
  • movement disorders - esp CHOREA- fidgety, wiggly
  • psych issues
  • cognitive decline
131
Q

4 symptoms in ataxia

A

nystagmus
dysarthria
limb coord problems
wide based unstable gait

132
Q

what is myoclonus
what part of brain can problem be in

first line tx?
second line tx?

A

quick shock-like jerks
cortex, brainstem, or spinal

first line: CLONAZEPAM

second line:
valproate (depakote)
levetiracetam (keppra)

133
Q

what is a tic?

A

repetitive movements/sounds that interrupt normally activity

have urge to do it, are uncomfortable until they do it

134
Q

what are diagnostic criteria for Tourettes?

A

2 or more motor tics
AND
at least 1 vocal tic

beginning BEFORE age 18 and present for more than 1 YEAR

not due to other causes

135
Q

treatment for Tourettes?

A

tx ONLY IF BOTHERSOME

  • remove stimulants (like adderall)
  • SSRIs
  • alpha-2 agonists
  • antipsychotics (risperidone)
  • VMAT-2 inhibitors (tetrabenazine)
  • behavior mod therapy
136
Q

How are Functional Movement Disorders diagnosed?

A

H&P

totally variable, paroxysmal (goes away and comes back), distractible & not consistent with known movement disorders

Stress to pt that they are NOT CRAZY and NOT FAKING IT, symptoms are real and outside of their control

137
Q

treatment for functional movement disorders?

A

no meds (unless for triggers)

treat triggers: psych/CBT/pain etc

retrain motor movements/brain (PT, OT, speech T)

138
Q

what is vonsattel grading?

A

used for path staging of Huntington Disease

0-1: no gross changes but see microscopic changes
4: complete atrophy of caudate, putamen, globus pallidus

139
Q

which movement disorders are Tau-opathies?

which are alpha-synuclein-opathies/?

A

tau:
Progressive Supranuclear Palsy and
Corticobasal degeneration

alpha synuclein:
parkinson’s
multiple system atrophy

140
Q

difference between Lewy Body Dementia and Parkinson’s Disease dementia? similarity?

A

BOTH have lewy bodies on histology
pathologically look THE SAME

Lewy body dementia = dementia and movement disorder onset in the same year

Parkinson’s disease dementia = have movement disease for a long time, then progress to dementia

141
Q

how do COMT and MAO-B inhibitors work to treat parkinson’s disease?

A

they inhibit dopamine degradatoin

142
Q

why is dopamine not useful in treating parkinson’s disease?

A

it does not cross the blood-brain barrier and generates peripheral side effects

143
Q

difference between hypoxia and anoxia

A

hypoxia- deprivation of O2

anoxia- COMPLETE deprivation of O2

144
Q

what is ischemia

A

inadequate blood flow

145
Q

pale infarcts are due to ____ occlusion

A

thrombotic (from plaque rupture, which exposes subendothelial collagen leading to thrombus formation)

146
Q

epidural hematoma etiology

A

trauma –> skull fracture –> lacerated middle meningeal artery which separates dura from skull and blood accumulates

147
Q

etiology of subdural hematoma

A

damage to bridging veins going from cortex to venous sinuses

**brain moves differently than the surrounding skull, this movement can tear the bridging veins

148
Q

Describe how an acute vs chronic subdural hematomas would present + possible causes

A

Acute

  • present unconscious, NO lucid interval
  • trauma

Chronic

  • slow neurologic decline due to repeated bleeding and slow growth of hematoma
  • elderly w/ brain atrophy _ GLF (can stretch and tear veins)
  • minor trauma
149
Q

etiology of amyloid angiopathy

A

amyloid deposits in blood vessel wall –> lobar hemorrhages

150
Q

list three causes of intraparenchymal hemorrhage

A
  • HTN
  • amyloid angiopathy
  • vascular lesions/malformations (ex AVM)
151
Q

list and describe 4 types of edema in CNS

A
  • vasogenic - BBB breakdown
  • cytotoxic - cellular swelling
  • interstitial- obstructive hydrocephalus
  • osmotic - plasma too dilute
152
Q

4 common signs of cerebellar tonsillar herniation

A
  • intractable HA
  • head tilt
  • neck stiffness
153
Q

uncal herniation results in what symptoms

A
  • ipsilateral paralysis
  • ipsilateral CN 3 compression –> pupil fixed and dilated, eye down and out
  • posterior cerebral artery compression
154
Q

central herniation / duret hemorrhage

A

downward herniation of bl temporal lobes
pons pushed down -> pressure on small vessels -> petechial hemorrhage in medial pons

fatal usu

155
Q

enhancing mass crossing corpus callosum - what are 3 things on differential?

A
  1. glioblastoma
  2. CNS lymphoma
  3. really really bad MS
156
Q

difference between stroke and TIA

A

acute loss of focal brain or monocular function

stroke symptoms >24h

TIA symptoms <24h with NO ischemic changes on imaging

157
Q

role of adenosine in sleep/wake

A

adenosine inhibits activity in basal forebrain –> sleep homeostatic drive

158
Q

how does caffeine work to keep us awake?

A

is an adenosine receptor antagonist

159
Q

sleep onset occurs with ___ Core Body Temp

160
Q

what time is CBT at a minimum

A

2 hours before waking

161
Q

what type of light has greatest phase shifting effect

A

short wavelength (~460nm) blue light

162
Q

to cause a phase delay, how should you time light exposure?

to cause phase advance?

A

phase delay- light 3-4h after CBT minumum

phase advance- light 2-4h before CBT min

*light in middle of day has relatively little effect

163
Q

what part of the brain is “pacemaker” of the entire circadian system?

A

suprachiasmatic nucleus (SCN)

164
Q

melatonin is secreted by

A

pineal gland

165
Q

what is process C?

what is process S?

A

process C = circadian ALERTING signal

process S = homeostatic drive for sleep

166
Q

moa Ramelteon, Tasimelteon

A

MT1 and MT2 receptor agonists

approved for treating insomnia (Ramelteon) and non-24h sleep/wake disorder (Tasimelteon)

167
Q

when are melatonin levels high? low?

A

high at night (dim light melatonin onset is 2-3h before bedtime)
low during daylight

168
Q

describe pathway of how light reduces melatonin secretion

A

light stimulates MERGs which has axons to SCN via RetinoHhypothalamic tract. ERGs release glutamate which stimulates the SCN to release GABA.

GABA inhibits PVN (paraventricular nucleus) of hypothalamus, shutting down pathway that makes melatonin.

169
Q

what is the molecular basis of endogenous circardian rhythms?

A

clock and bmal1 are transcribed in the AM. the proteins form hetermodimers (CLOCK-BMAL1) that bind promoter regions of per and cry genes –> stim PER and CRY productino.

Per and Cry proteins get broken down but so much is made that they accumulate and form heterodimers, which go into the nucleus. There, PER-CRY inhibits CLOCK-BMAL1 –> negative feedback; reduces PER and CRY production in the PM

as PER and CRY levels get very low, per and cry gene activation begins again in AM and repeat

170
Q

describe pathway by which melatonin increases in absence of light

A

without light, no MERG stimulation, no SCN stimulation. PVN disinhibited –> stimulate intermedioalateral cell column (ICC), which releases Ach –> stim superior cervical ganglion, which releases NE –> stimulate pineal gland.

171
Q

what is sundowning?

  • patient population
  • timing
  • symptoms
  • cause
A

institutionalized pts w/ dementia

agitation in late afternoon/early evening

  • anxiety
  • confusion
  • pacing, wandering
  • visual and auditory hallucinations

due to DEGENERATION of SCN

tx include late afternoon/evening bright light exposure , avoid daytime napping with planned activities, scheduled daytime routines. antipsychotics

172
Q

what is Free Running Sleep Disorder
what pt population is it often seen in
two possible treatments

A 
sleep progressively delayed each day
blind individuals (no MERG cells); free running rhythm in absence of light entrainment

Melatonin before desired bedtime
Tasimelteon

173
Q

Two explanations for why headaches with brain tumors?

A
  1. Mass pressing on dura, which is innervated by trigeminal nerve
  2. Mass causing obstructive hydrocephalus
174
Q

genetic factors affecting survival in oligodendrogliomas

A

1p and 19q deletion

175
Q

genetic factors affecting survival in gliomas

A

MGMT methylation in tumor

silences MGMT, which repairs DNA damaged by chemo, thus conferring chemo resistance

176
Q

which brain tumors can NOT just be observed?

A

High/Low Grade Gliomas
Metastatic Carcinoma
Cerebral Lymphoma

these are the same ones that can’t undergo stereotactic radiosurgery bc no focal target

177
Q

whic brain tumor can’t be surgically resected

A

cerebral lymphoma

178
Q

which brain tumors can’t be biopsied

A

Pilocytic Astrocytoma (usu locations not suitable for bx ex optic chiasm/tract, posterior fossa)

Metastatic Carcinoma (surg removal preferred)

pituitary adenoma (location not amenable)

179
Q

which brain tumors CAN undergo chemo

A

High/Low Grade Glioma

Cerebral Lymphoma

180
Q

classic tetrad symptoms of meningitis

A

fever
AMS
headache
nuchal rigidity

181
Q

bacterial meningitis - what type of WBC in CSF

how about viral

A

bacterial- PMNS (ex neutrophils)

viral - mononuclear

182
Q

Which drug is particularly useful for treating acute episodes of akinesia in a Parkinson’s
patient and should be co-administered with an anti-emetic?

A

apomorphine

183
Q

Huntington Disease

(3) meds to minimize movement disorder symptoms?
(3) meds to treat psychosis/disruptive behavior?

A

movement:

  • VMAT inhibitor (tetrabenazine)
  • Ach precursor (choline, lecithin; not super effective)
  • Antipsychotics (D2 receptor antagonists- Haloperidol, Quetiapine)

Psychosis
-Atypical antipsychotics (quetiapine, olanzapine, risperidone)

Depression- SSRIs - anitdepressants that DO not have anti-muscarinic activity (don’t wan’t to decrease cholinergic tone!)

184
Q

Tetrabenazine

  • what used for
  • MOA
  • side effects
A

Huntington’s

reversible VMAT-2 inhibitor (to decr dopaminergic tone)

side effects: depression, incr suicide risk!

185
Q

2 meds to chelate Cu in Wilson’s disease

A

Penicillamine

  • potential cross-reactivity for penicillin
  • SE: marrow suppression, N/V

Trientine

  • if can’t tolerate penicillamine
  • side effects: Fe deficiency, muscle spasms, rash
186
Q

Benzodiazepines and Baclofen act on which receptor types, to reduce muscle spasms and spasticity?

A

Benzos - GABA-A agonist

Baclofen- GABA-B agonist

187
Q

Tizanidine

  • usage
  • drug type
  • side effects
  • drug interactions
A

reduces spasticity (ex MS, cerebrovascular lesions)

alpha-2 agonist (unclear MOA, other a2 agonists don’t work as well)

SE: drowsiness, hypotension, dry mouth, muscle weakness

metabolized by CYP1A2
fluroquinolones inhibt CYP1A2, would increase Tizanidine levels

188
Q

Dantrolene

  • usages
  • MOA
  • side effects
A

spasticity, MS, spinal cord trauma, Malignant Hyperthermia

RyR antagonist- inhibits Ca induced CA released from SR

specific for skeletal muscle

SE: generalized muscle weakness, sedation, hepatotoxicity, hepatitis

189
Q

What is status epilepticus?
How should you intervene?

At what time point can it lead to long-term consequences (inclu neuronal death, injury)

A

Seizures for more than 5 minutes
INTERVENE! initiral tx w/ IV Lorazepam is key

More than 30 minutes will have long term consequences

190
Q

most common cause of status epilepticus in cihldren?

in adults?

A

children- fever/infection

adults - stroke

(other: metabolic abnml, TBI, brain neoplasm, withdrawal, cerebral anoxia)

191
Q

3 ways hyperexcitable networks are generated?

A

excitatory axonal sprouting

loss of inhibitory neurons

loss of excitatory neurons that drive inhibitory neurons

192
Q

what is the most imp study for diagnosis, prognosis and treatment of epilepsy

193
Q

what is the Kindling model

A

in mice- repeated subthreshold stimuli over time leads to abnormal neuronal pathway in which subthreshold stimulus leads to spontaneous seizures

posisble mechanism of epileptogenesis (unclear applicability to humans)

194
Q

highest incidence of seizures occurs when

A

early childhood & late adulthood

195
Q

what is a seizure

A

clinical manifestation of abnormal, excessive excitation and synchornization of a population of cortical neurons

196
Q

what is epilepsy

A

tendency toward UNPROVOKED recurrent seizures

197
Q

what is epileptogenesis

A

sequence of events that converts normal neuronal network into hyperexcitable network

198
Q

common causes of epilepsy in

  • children
  • young adults
  • elderly
A

children- fever, metabolic, congenital

young adults - trauma, tumor

elderly- stroke, tumor, degenerative

199
Q

carbidopa improves peripheral side effects of levodopa, but exacerbates ____

A

psychiatric symptoms

200
Q

which drug for parkinsonism can cause hepatic failure

201
Q

what two drug classes can be used as monotherapy in parkinson’s early on?

A

Dopamine agonists (bromocroptine, ropinarole, pramipexole, rotigotine)

MAO-B inhibitors (selegeline, rasageline)

202
Q

what type of ionic currents are excitatory?

inhibitory?

A

excitation:
-inward Na+, Ca2+

inhibition

  • inward Cl- (GABA-A receptor)
  • outward K+ (GABA-B receptor)
203
Q

pathophysiology of MS

A

peripheral immune cell infiltration

  • -> CNS immune cell activation
  • -> BBB disruption
  • -> intrathecal IgG synthesis
204
Q

how is MS defined pathologically?

A

presence of inflammatory demyelination in CNS in the absence of infection

is an immune-mediated inflammation targeting OLIGODENDROCYTES

demyelination w/ incomplete remyelination

205
Q

MS demyelination has predilection for what location? why?

A

periventricular regions

-there is a confluence of veins here; lesions start here in the post-capillary venules and spread out

206
Q

what are meningeal lymphoid follicles

A

areas of B cell activation in MS

207
Q

CNS capillaries have tight junctions. So where can immune cells from blood enter the CNS

A

via CNS perivascular space (in the post-capillary venules)

208
Q

TWO key features of MS?

A
  • lesional inflammatory activity / simultaneous presence of active and inactive lesions
  • relapsing remitting clinical course
209
Q

what are oligoclonal bands in CSF and what is their significance?

A

indicates intrathecal synthesis of IgG - clonal proliferation of B cells and establishment of an adaptive immune response in CNS

210
Q

What does gadolinium contrast enhancement indicate?

A

gadolinium contrast leaking into brain parenchyma means BBB compromised.

gadolinium enhancement of an MS lesion indicates ACTIVE INFLAMMATION

211
Q

how is MS diagnosed?

A

NO single test.

based on presence of CNS lesions disseminated in SPACE and TIME

+typical clinical presentation
+excluded alt diagnoses

212
Q

List (7) clinical presentations of MS

A
  • optic neuritis (painful blurred vision)
  • myelitis (BL weakness/numbness, urinary dysfunction)
  • cerebellitis (ataxia)
  • brainstem syndrome (diplopia, vertigo, dysphagia, dysarthria, incoord, n/wk)
  • hemisphereic snydrome (hemoparesis, hemianesthesia, visual field cut, word finding diff)
  • syndrome duration >24h in ABSENCE of fever or infection

typically followed by remission regardless of treatment

213
Q

(3) medications for MS and their MOA?

A
  1. Fingolimid is a sphingosine-1-phosphate receptor modulator that prevents immune cell egress from lymph nodes (must have S1P chemotactic gradient)
  2. Natalizumab is an antibody against alpha4 integrin (needed for immune cells to migrate to CNS)
  3. Ocrelizumab is a CD20 antibody, depletes all B cells
214
Q

What locations does neuromyelitis optica affect?

what is the cause?

A

-spinal cord (“myelitis”)
-optic nerves
LIMITED brain involvement

NMO IgG - a pathogenic antibody that targets aquaporin 4 –> loss of aquaporin 4 on astrocyte endfeet

215
Q

how is Neuromyelitis Optica diagnosed

A

relapsing optic neuritis & acute myelitis

at least 2 of the following:

  • contigous spinal cord MRI lesion extending down 3 or more vertebral segments
  • brain MRI does not meet criteria for MS
  • NMO IgG (aquaporin 4) seropositivity
216
Q

4 core clinical criteria for lewy body dementia

A
  • fluctuating attention/concentration
  • recurrent, detailed visual hallucinations
  • REM sleep disorder
  • Parkinsonism
217
Q

indicative biomarker for lewy bdoy dementia

A

reduced dopamine transporter uptake in basal ganglia

218
Q

Triad of Normal Pressure Hydrocephalus

A

Wet (incontinence)
Wacky (dementia)
Wobbly (gait)

219
Q

cause of normal pressure hydrocephalus? how is diagnosis confirmed?

A

*is due to failure of CSF drainage system

confirmed w/ imaging and LP

may reverse with shunt

220
Q

what is pseudodementia?

-signs?

A

severe depression that resembles dementia

fhx, prior hx, subacute onset likely precipants, depressive sxs
AMOTIVATIONAL exam

221
Q

What kind of necrosis does cortex undergo?

which cortical layers are most vulnerable

A

laminar necrosis

layers 3, 4, 5

222
Q

when does anoxic-ischemic encephalopathy occur?

what three clinical syndromes can result?

A

cardiopulm arrest

  • man in the barrel syndrome
  • parkinsonism
  • action myoclonus
223
Q

what is one cause of Osmotic Demyelination Syndrome?

A

rapid correction / overcorrection of chronic hyponatremia

  • causes water to leave brain
  • corticospinal tracts become demyelinated
224
Q

CO toxicity causes necrosis where?

A

globus pallidus

225
Q

Methanol toxicity affects?

A

retina (degen retinal ganglion cells)

if severe- BL putamen necrosis, focal WM necrosis

226
Q

Neuro symptoms of vit B12 deficiency

A
  • ataxia
  • LE n/t
  • progression to LE spastic weakness
  • complete paraplegia may occur later on in course - if reaches this point, recovery is poor
227
Q

what 2 marine toxins can cause temperature reversal

A

brevetoxin

ciguatoxin

228
Q

what marine toxins inhibit Na+ channel

which ones activate Na+ channel

A

inhibit

  • tetrodotoxin (puffer fish)
  • saxitoxin (dinoflagellates)

activate:

  • brevetoxin
  • ciguatera
229
Q

what does domoic acid act on

A

glutamate receptor agonist

-GI -> neuro -> memory impairment, can last years

230
Q

CT/MRI imaging not indicated in recurrent migraines unless??

A
  • recent substantial change in HA pattern
  • hx seizures
  • focal neuro signs/symptoms
231
Q

what is most dangerous, primary or secondary HA?

232
Q

dull, achy, BL, nonpulsating pain
episodic
sensation of pressing/tightening

not worse with physical activity
no N/V

may have photophobia OR phonophobia (noth both)

no prodrome or aura

msk component

A

tension HA

233
Q

criteria for chronic Tension Type Headache

A
  • occurs at least 15 days/month for more than 3 months
  • lasts hours or may be continous

at least TWO of following:

  • BL
  • pressing/tight (nonpulsating) quality
  • mild.mod intensity
  • not aggravated by routine phys activity

AND

  • no more than one of photophobia, phonophobia, or mild nausea
  • no mod or severe nausea, no vomiting
  • not due to another disorder
234
Q

Tension HA pathophys

A

a manifestation of abnormal neuronal sensitivity and pain facilitation

posisble hypersnesitivity of myofascial nociceptors
or neurons in trigeminal nucleaus

235
Q

TTH treatment

A

OTC analgesics

but if freq or chronic, consider preventatives:

  • SSRI
  • tricyclic antidepressant
  • muscle relaxant

nonmedication

  • manage stress
  • biofeedback to promote muscle relaxation
236
Q

Cluster HA

A 
Men
Genetic 
Circadian and annual periodicity 
1 every other day - 8 daily
clusters lasting 2wks - 3 months

Severe unilateral pain
Autonomic features - ex Horner’s, congestion/rhinorrhea, lacrimation, sweating, ptosis, conj injection

237
Q

Tx for acute cluster HA

A

O2 mask

inject sumatriptan

238
Q

Cluster headache - pathophysiology

A
  • activ of posterior hypothalamic grey matter
  • parasympathetic overacvitiy
  • sympt dysfunction, secondary to activation of trigeminal-parasymp reflex
239
Q

diagnostic criteria of trigeminal neuralgia

A

Paraoxysmal attacks of pain lasting seconds-2 min affecting at least one div of CN V
-pain intense, sharp, superficial or stabbing and/or precipitated from trigger areas or by trigger factors (talking, eating, brushing teeth - anything that involves face movement)

Attacks are sterotyped in each patient

No neuro deficity

Not attributed to another disorder

240
Q

what workup should be done in trigeminal neuralgia?

what treatments

A

MRI to look for lesion impinging on trigeminal nerve

Preventive Meds (carbamazepine, gabapentin most common)

Surgery

  • decompression (in applicable)
  • ABLATION on trigeminal ganglion! face all numb
241
Q

recurrent attacks lasting 4-72 hours

unilateral, pulsating pain
aggravated by routine activity
n/v
photphobia/phonophobia

A

migraine without aura

242
Q

how does migraine prevalence change with age

A

most common in teens/20s
worsen in 30s/40s
improve later in life

243
Q

migraine

  • risk factors?
  • protective factors
A

risk

  • hormones
  • chronobiologic changes
  • drugs
  • diet (tyramine, smoked foods, red wine)
  • sensory input
  • stress, trauma

protective

  • healthy lifestyle
  • hydrated
244
Q

Describe the pathway of a migrainte

A
  1. originates deep in brain
  2. electrical impulses spread
  3. changes in nerve cell activity and blood flow –> symptoms like visual disturbance, n/t, dizziness
  4. chemicals in brain (CGRP, substance P, NKA) cause blood vessel DILATION and INFLAMMATION of surrounding tissue
  5. inflammation irritates the TRIGEMINAL NERVE, resulting in severe or throbbing pain
245
Q

list three specific migraine treatments

A

Dihydroergotamine (DHE)
Triptans
CGRP inhibitors (preventive)

246
Q

Triptans

  • mechanism
  • site of action
  • what can they be used for
A

5HT-1 (serotonin) receptor AGONIST

works at interface between trigeminal nerve endings and blood vessel walls

migraines
cluster headaches

247
Q

most common cause of nonepidemic fatal encephalitis in US

A

HSV1

most pts who get CNS complications are actually in good health!

248
Q

HSV encephalitis affects what part of brain

A

fronto-temporal lobe(s)

249
Q

diabetic acidosis is strong risk factor for what fungus

A

rhinocerebral mucormycosis

250
Q

what 3 fungal infections often seen in untreated HIV infection

A
  • cryptococcus
  • coccidiodes
  • histoplasma
251
Q

CSF findings in fungal meningitis

A

lymphocytic pleocytosis, elevated protein,

mildly depressed glucose

252
Q

what is most common helminithis CSN infection?

what is it caused by?

what is the presentation?

A

CSN Cysticercosis

ingestion of larvae of pork tapeworm Taenia solium

chronic or acute HA, seizures, focal neuro deficits, subacute meningitis, or hydrocephalus

CT/MRI scan with cysts

CSF may have EOSINOPHILS

253
Q

CSF with eosinophils should make you think?

254
Q

treating parasitic CNS infections?

A

supportive

  • anti seizure meds
  • steroids if needed
  • shunting for mass effect and hydrocephalus if needed
255
Q

HIV dementia cause?

what does endstage look like

A

viral invasion of parencyhmal cells. secondary neuronal loss

akinetic mute with fetal posturing

256
Q

PML (Progressive Multifocal Leukoencephalopathy)

  • cause
  • what increases risk
  • what can it resemeble
  • CSF findings
  • treatment
A
  • JC virus
  • immunsuppression (virus normally contained) & use of monoclonal Ab therapies like Natalizumab (MS, crohn’s)
  • virus reactivates and infects oligodendrocytes –> multifocal areas of demyelination = resembles MS

CSF

  • mild lymphocytic pleocytosis
  • eleva protein
  • normal glucose
  • JC virus+

No treatment except for underlying immunosuppression

257
Q

list at least four meds that can prevent migraines

A
  • anticonvulsants
  • antidepressants
  • beta blockers- Propranolol, Timolol
  • CCBs
  • NSAIDs
258
Q

CGRP inhibitors

A

are monoclonal antbodies, prevent migraines

Fremanezumab - bind CGRP

Erenumab - bind CVRP receptor

259
Q

definition chronic migraine

A

headache at least 15 days/month, symptoms meet criteria for migraine on 8 or more of those days

preventive meds
Botox
wean off prn analgesics

260
Q

gross anatomical changes in aging brain

A
  • overall reduced weight
  • narrowing gyri, widening sulci
  • ventricle dilation
  • widening subarachnoid space

leads to memory impairments common with normal aging

261
Q

role of microglia and neuroinflammation on normal aging of CNS

A

normally microglia switch between resting surveillance / activated state

in older brain, once activated, harder to switch back to surveillance state. stays in an intermediate “primed” state. once there is a trigger, become SUPER-activated –> amplified cytokine production

  • -> elevated ROS prod
  • -> prolonged inflamm state

neurotoxic!!

262
Q

why is the nervous system uniquely vulnerable to aging?

A

-nervous tissue does NOT divide!

263
Q

describe the type of neuron loss in aging / histo changes

A

NOT just a generalized loss of neurons

instead, atrophy or loss of larger neurons that have high energy requirements - soma and dendrites shrink back; reduced complexity of the dendritic tree, decreased spine density, reduced excitatory input

264
Q

which neurons are uniquely susceptible in aging?

why? (4 reasons)

A

dopaminergic neurons

  • dopamine gets oxidized to ROS
  • neuromelanin (responsible for the pigment) sequesters Fe, which generates ROS
  • mitochondrial DNA deletion levels highest
  • local microglial activation
265
Q

where are reductions in white matter most common in aging?

A

prefrontal

temporal

266
Q

three sources of ROS production

how are ROS inactivated?

A

leaked from cell respiration in mitochondria
made by phagocytes
degradation of dopamine

inactivated by:

  • antioxidants (dietary)
  • superoxide dismutase, catalase
267
Q

reason why brain is uniquely susceptible to ROS damage?

A
  • high energy demand, high O2 consumption
  • abundant peroxidizable FAs
  • high Fe levels (potent ROS catalyst)
  • low levels of antioxidants and related enzymes
  • dopamine oxidation
268
Q

harmful effects of ROS?

A

lipids: lipid peroxidation makes toxic aldehydes
DNA: causes double strand breaks, base mod, alter gene expression
protein: oxidation causes loss of function, misfolding, aggregation

269
Q

GCS Eye

A

4 - spontaneous
3 - voice
2 - stimulation
1 - no opening

270
Q

GCS Verbal

A 
5 - oriented
4 - confused
3 - inappropriate
2 - incomprehensible
1 - none
271
Q

GCS Motor

A 
6 - obeys commands
5 - localizes
4 - withdraws to pain
3 - decorticate posturing
2 - decerebrate posturing 
1 - none
272
Q

Injury where increases risk of Autonomic dysreflexia?

273
Q

what is autonomic dysreflexia

what is most common cause

what is treatment

A

life threatening reaction to noxious stimuli below level of injury

  • elevated BP
  • bradycardia
  • flushing/sweating above level of injury
  • goosebumps below level of injury

Bladder distention

(also: constipation, fecal impaction, fractures, pressure injury)

Treatment: remove stimulus!!!
can temporarily tx with meds if needed

274
Q

upper trunk lesionn

  • location
  • symptoms
A

Cf, C6

  • prox arm muscles
  • infraspinatus
  • deltoid
  • biceps
  • supinator (waiter’s tip)

sensory deficit over lateral arm (C5, C6 dermatome)

275
Q

lower trunk lesion

  • location
  • symptoms
A

C8, T1

  • hand muscles (of median, ulnar and radial innervation)
  • interossei, thenar, hypothenar, EIP

sensory deficit over medial arm r

276
Q

how is lateral cord lesion diff from upper trunk lesion

A

similar to upper trunk lesion but spares the deltoid

277
Q

medial cord plexopathy

A

ulnar N

extended sensory deficit

278
Q

posterior cord affects what nerves

A

axillary nerve

radial nerve

279
Q

acute brachial plexus neuritis (parsonage-turner syndrome)

  • cause
  • symptoms
A

autoimmun

subacute severe shoulder/arm pain, followed by weakness

can affect any portion or individual proximal branches

280
Q

Erb palsy

A

neck lateral traction - affects upper trunk

281
Q

Klumpke palsy

A

arm upward extension - affects lower trunk

282
Q

thoracic outlet syndrome

A

compression of subclavian artery and lower trunk

–> hand munscle atrophy

283
Q

radiculopathy

  • sensory symptoms
  • motor symptoms
  • how to confirm
A

radiating pain
numbness in dermatome

weakness in muscles of myotome
reduced reflex at affected level

EMG and MRI

284
Q

Anti-epileptics that are hepatic inducers?

A

PCBOT

Phenytoin
Carbamazepine
Barbiturates
Topiramate

285
Q

Anti-epileptics that are mainly renally excreted?

A

Gabapentin
Levetiracetam
Topiramate (lesser extent)

286
Q

if you rly suscpet a subarachnoid hemorrhage but CT is negative, what next

287
Q

familial intracranial aneurysm syndrome (FIA)

A

two first thru thirddegree relatives have intracranial aneurysms

MBB (2 decks)

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