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Clin Med > Neurology > Flashcards

Neurology Flashcards

1
Q

Two types of injuries for TBI

EX of both

A

PRIMARY: direct result of initial trauma–gross result
EX–fx, cerebral contusion, vascular disruption

SECONDARY: results from the evolution of the initial injury or complications, damage on a molecular level—-what we aim to minimize
EX: hypoxia, ischemia, cerebral edema, IntracranialHTN

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2
Q

Cushings triad

A
  • hypertension
  • bradycardia
  • irregular respirations
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3
Q

CCP=

A

cerebral perfusion pressure=MAP-ICP

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4
Q

normal CPP

A

b/w 70 and 90 mmHg

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5
Q

list the primary HA

A
  • tension
  • migrane w/ or w/o aura
  • cluster
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6
Q

What is a secondary HA

-list the examples

A

-account for small percent of HA
-sequelae of another disease process (EX: incr ICP)
EX:
-SAH
-ICH from tumor, trauma or idiopathic
-hypertensive crisis
-acute glaucoma
-sinus infection
-TMJ
-temporal arteritis
-meningitis

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7
Q

MC HA?

A

PRIMARY—90%

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8
Q

HA caused by?

A

traction, displacement and inflammation or distention of the pain-sensitive structures in head or neck

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9
Q 
Head HX questions: 
H
E
A
D
A

H:

  • how severe is your headache scale 1-10
  • how did this HA start–gradual, sudden,
  • how long have you had this HA

E:

  • ever had HA before?
  • ever had a HA this bad before?
  • ever have HA like this one in the past?

A:

  • any other s/s before or during HA?
  • any other s/s right now?

D:

  • desc the quality of pain
  • desc location of pain
  • desc where pain radiates
  • desc any other medical problems
  • desc your use of meds
  • desc any hx of trauma or medical or dental procedurs
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10
Q

HA differentials by time course: list the HA for each timeline

  1. Acute onset
  2. Subacute onset
  3. Chronic
A
  1. SAH, carotid/vertebral dissection, meningitis or encephalitis, glaucoma, acute iritis
    * less common: lumbar puncutre, HTN encephalopathy, coitus
  2. Giant cell (temporal) arteritis, intracranial mass (tumor, subdural hematoma), trigeminal neuralgia,
  3. migraine, med overuse, cluster, tension, cervical spine disease, sinusitis, dental disease
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11
Q

List the HA red flag S/S

A
  • thunderclap onset
  • worsens with coughing, sneezing, straining, worse at night,
  • increasing in frequency
  • new HA in 50+ with no HX
  • New HA in CA PT
  • HA+ Fever
  • new HA in immunocomp PT
  • HA + focal neruologic signs
  • HA + Seizures
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12
Q

what disease processes can cause Thunderclap HA

A

VASCULAR PATHOPHYSIOLOGY

  • intracranial hem (SAH)
  • HTN emergency
  • venous sinus thrombosis
  • Cervical artery dissection
  • pituitary apoplexy
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13
Q

HA worse at night, worse with coughing/sneezing/straining/
or
increasing in severity

A

ELEVATED ICP

  • tumor
  • hydrocephalus
  • idiopathic intracranial HTN
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14
Q

New HA in older adult 50+ w/ no prior hx

A

MASS LESION INFLAMMATION DISEASE:

  • tumor
  • giant cell arteritis
  • primary CNS vasculitis
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15
Q

New HA in PT with hx of CA

…what do we think of?

A

METASTASIS

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16
Q

new HA in immunocomp PT

A

OPPORTUNISTIC INFECTION

  • toxoplasmosis
  • primary CNS lymphoma
  • cryptococcal (fungal) meningitis
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17
Q

HA + fever

A

INFECTION

  • meningitis
  • cerebral abscess
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18
Q

HA + seizures

A

FOCAL LESION

  • tumor
  • infection
  • hemorrhage
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19
Q

HA + focal neuro signs

A

FOCAL LESION

  • tumor
  • infection
  • hemorrhage
  • ischemic stroke
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20
Q

Which HA is MC in women

A

tension and migraine

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21
Q

main differences b/w s/s of:

-tension vs migrane w/o aura HA

A

tension: nonpulsatile, dull pain, bilateral, no n/v photophobia or phonophobia, s/s not worsen w/ activity
migraine: pulsatile, unilateral, YES: n/v, photophobia and phonophobia, s/s worsen with activity

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22
Q

list the 5 prophylactic drug therapies to prevent/reduce freq of migraine HA

A
  1. BB–propranolol
  2. CCBs–verapamil
  3. TCAs–amitriptyline
  4. anticonvulsants–valporic acid and topiramate
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23
Q

Indications for Head CT w/ HA

A
  1. prior to LP
    - abnorm neuro exam
    - ams
    - abnm fundoscopic exam
    - meningieal signs
  2. Emergent–conduct prior to leaving office/ED
    - abnm neuro exam
    - ams
    - thunderclap HA
  3. Urgent–scheudled prior to leaving office/ED
    - HIV pos PT (MRI is preferred)
    - age 50+ with normal neuro exam
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24
Q

MC aura

A

VISUAL

-scotomata—flashing lights

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25
Q

Name the classic CSF findings for:

  1. MS
  2. Guillain Barre
  3. Bac Meningitis
  4. Viral meningitis
  5. Fungal or TB meningitis
  6. Idiopathic intracranial HTN
  7. SAH
A
  1. High IGG (oligoclonal bands)
  2. High protein with normal WBC count
  3. High protein, incr WBC (polymorphonuclear neuts) and decr glucose
  4. Normal glucose, incr WBC (lymphocytes)
  5. Decr glucose, increase WBCs (lymphocytes)
  6. incr CSF pressure otherwise normal findings
  7. Xanthochromia, blood in CSF
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26
Q

younger PT diagnosed with Trigeminal neuralgia.. what do we want to r/o or be suspicious of?

A

Multiple sclerosis

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27
Q

cranial nerve palsy and can technically be classed as a LMN disorder?

A

Bell’s Palsy

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28
Q

first line tx for abortive care of acute migraine

A 
NSAIDS****
or
acetominophen 
or 
Excederin
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29
Q

first line tx for acute tension HA

A

NSAIDs ** + local heat
or
other analgesics

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30
Q

first line tx for acute cluster HA

A

100% oxygen
and
SQ Sumatriptan

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31
Q

1st line for cluster HA prophylaxsis

A

Verapamil

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32
Q

First line tx for Pseudotumor cerebral aka idiopathic intracranial HTN?

A

Acetazolamide (diuretic) + wt loss

*can use furosemide as adjunct

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33
Q

First line tx for trigeminal neuralgia

A

Carbamazepine PO —anticonvulsant

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34
Q

If Bell’s palsy is caught in the first 72 hours, what is FL tx?

A

-Prednisone
or
acyclovir+Prednisone (glucocorticos)

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35
Q

what is the MC type of intracranial hem caused by a ruptured cerebral aneurysm?

A

SAH
or
intracerebral hemorrhage

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36
Q

Intracranial hemorrhages divided into two classes:

-list what is in each class

A
  1. Extra-axial hemorrhage–occurs outside the brain tissue
    - epidural
    - subdural
    - subarachnoid
  2. Intra-axial hemorrhage–occurs inside brain tissue
    - intracerebral hemorrhage (aka hemorrhagic stroke)
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37
Q

what causes a subarachnoid hemm?

A

-cerebral aneurysm rupture

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38
Q

another term for intracerebral hemorrhage?

A

hemorrhagic stroke

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39
Q

Hemorrhagic strokes are often secondary to?

A

HTN

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40
Q

two types of weakened BVs can cause hemorrhagic stroke

A
  • aneurysms

- AV malformations

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41
Q

Ischemic strokes: three (two mainly) types defined and which is more common

A

Thrombotic stroke (2/3)–caused by blood clot that develops in the BVs inside brain

-Embolic (1/3)–caused by blood clot or plaque debris that develops elsewhere in the body–then travels to one of BVs in brain via blood stream (AFIB is COMMON)

third: hypoxia… hypotension and poor cerebral perfusion… border zone infarcts…there is no vascular occlusion but can lead to infarcted areas
* concept for watershed infarct**

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42
Q

Stroke s/s are ipsilateral or contralateral to the part of the brain affected?

A

contralateral (side of the body with s/s is opposite side of brain affected)

  • right sided s/s=left side stroke
  • left sided s/s=right side stroke
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43
Q

Define TIA

A

TRANSIENT ISCHEMIC ATTACK

-neuro deficits w/o acute infarct that lasts >24 hours

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44
Q

Four main “types” of intracranial hemorrhages

*which can be classified under hemorrhagic stroke?

A

Bleeding inside the brain

  1. epidural
  2. subdural
  3. subarachnoid
  4. intracerebral hem

***last two can also be classified under hemorrhagic stroke

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45
Q

where is the bleeding in a epidural hematoma?

A

space b/w skull and dura

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46
Q

MCC of epidural hematoma

A

middle meningeal artery rupture

*assoc w/ temporal bone fracture

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47
Q

define hemiparesis

A

muscle weakness or partial paralysis on one side

*also called hemiplegia

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48
Q

Uncal herniation

  • define
  • can develop secondary to?
A 
CNIII palsy... ipsilateral eye of injury is: 
-fixed
-dilated
-blown 
CAN DEVELOP DUE TO: 
-epidural hematoma
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49
Q

on CT, does the epidural hematoma cross suture lines?

A

NO

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50
Q

CT RESULTS: biconvex “lens shape” hyperdense in temporal area

A

epidural hematoma

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51
Q

First line tx for epidural hematoma

A

hematoma evacuation
OR
craniotomy

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52
Q

MCC of subdural hematoma

A

rupture of cortical bridging VEINS

post blunt force trauma

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53
Q

subdural hematoma is bleeding where

A

space b/w dura and arachnoid membranes

**bridging veins rupture

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54
Q

CT: concave/crescent shape bleed that does cross suture lines

A

Subdural Hematoma

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55
Q

First line tx for subdural hematoma

A
  1. if PT is stable and CT doesnt show signs of herniation (midline shift <5mm)… OBSERVE
  2. +s/s of incr ICP or midline shift is >5mm…. SURGERY
    - burr hole trephination
    - surgical evacuation
    - decompression craniotomy
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56
Q

Subarahchnoid hemorrhage is where

A

space b/w arachnoid membrane and pia mater

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57
Q

MCC of subarachnoid hem?

-other commmon cause

A

rupture saccular (berry) aneurysm —75% cases for nontraumatic

other:
- trauma
- AV malformations

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58
Q

mortality rate for nontraumatic SAH

A

50%

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59
Q

thunderclap HA

A

SAH

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60
Q

Xanthochromic CSF results?

A

SAH

*CSF is yellow to pink

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61
Q

TX options for SAH

A
  • BEDREST*
  • Nimodipine to reduce cerebral vasospasms
  • Labetalol to lower BP
  • surgical coiling or clipping
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62
Q

MCC overall for intracerebral hem?

second MCC?

A

HTN from angiopathy from systemic HTN–number one

Cerebral amyloid angiopathy (disease of BV)

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63
Q

MCC for intracerebral hem in:

  • eldery?
  • kids?
A

elderly–> cerebral amyloid angiopathy

kids–>AV malformation

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64
Q

with intracerebral hem, how do we want to lower BP?

A

GRADUALLY

IV BBs or CCBS or hydralazine

  • labetalol
  • nicardipine
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65
Q

tx for intracerebral hem

A

SUPPORTIVE
-gradual BP reduction

Reduce ICP and prevent incr ICP

  • raising bed 30 degrees
  • limit IV fluids
  • BP management
  • Analgesia
  • sedation
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66
Q

what is the 3rd MCC of death in the US?

A

Cerebrovascular accident—stroke

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67
Q

hemorrhagic stroke–another name for it?

A

intracerebral hemorrhage

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68
Q

two types of hemorrhagic stroke

A
  • intracerebral hem

- SAH

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69
Q

bulging weakened area in the wall of an artery in brain

  • what is it?
  • what does it result in?
A

CEREBRAL ANEURYSM

  • can result in abnormal widening or ballooning
  • weak spot=risk for rupture/bursting
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70
Q

which BV layer is affected in cerebral aneurysm?

A

muscular layer of the artery wall is thin….

-so instead of three layers, now the BV only has two

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71
Q

which arteries in the brain can develop an aneurysm?

mc where

A

ANY OF THEM

MC in the front part of brain

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72
Q

MC type of aneurysm

A

Berry or saccular aneurysm

80-90%

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73
Q

when are cerebral aneurysms diagnosed?

A

usually not diagnosed until they rupture….

but sometimes PT can have s/s before rupture.. and then aneurysm will be dx on CT

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74
Q

S/S of a cerebral aneurysm

-that did not rupture

A 
If large enough, will cause: 
HA or pain behind or near one eye 
vision deficits 
eye movement deficits 
**can cause s/s if its pressing on adjacent structure.. like eye or nerves OR cause s/s from tiny leaks
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75
Q

MC initial symptom of a cerebral aneurysm?

A

if it RUPTURED

  • sudden/thunderclap HA
  • SAH
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76
Q

s/s of SAH

A 
worst HA of my life 
stiff neck/nuchal rigidity 
n/v 
changes in mental status----like drowsiness 
dilated pupils 
\+LOC 
loss of coordination 
photophobia 
coma 
death
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77
Q

how to diagnose Cerebral aneurysm

*gold standard?

A

CT scan WITH contrast ****
MRI
GOLD STANDARD–angiography
*but dont start with that.. usually start with CT

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78
Q

where is berry aneurysm located

-where on arteries does it form?

A

in the circle of willis
-anterior communicating artery–MC

forms at the “Y” segment or bifurcation of arteries and branches of large arteries at base of brain…. aka circle of willis

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79
Q

RF for cerebral aneurysm

A

smoking
htn
hypercholesteremia
ETOH

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80
Q

Herald bleed

A

cerebral aneurysm leak

  • 40% in PTs
  • less severe but atypical HA
  • focal neuro s/s from pressure on brain or CNs
  • occur 1-3 weeks prior to severe SAH
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81
Q

TX for cerebral aneurysm

A

surgery

-clipping or coiling

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82
Q

what is brain arteriovenous malformation

-cause?

A

tangle of abnormal BVs
-connecting arteries and veins

  • rare
  • idiopathic.. most ppl are born with them
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83
Q

s/s of AVM

A

asympto usually—until rupture–about 1/2 of cases are asympto until rupture

w/o hemorrhage s/s:

  • seizures–>usually partial seizures (11-13%)
  • acute hemiparesis/muscle weakness one side and other focal neuro deficits
  • HA (0.2%)
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84
Q

in about 1/2 of PTs with AVM.. what is the first sign?

A

intracranial hemorrhage!

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85
Q

gold standard for AVM diagnosis, tx plannning, and follow-up after tx

A

angiography

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86
Q

what is the most dangerous congenital vascular malformation and why?

A

AVM

  • potential to cause intracerebral hem and epilepsy
  • AVM will grow as PT gets older
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87
Q

usual presenting age for AVM

A

10-40

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88
Q

RF for AVM

A

male

fam hx

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89
Q

Complications with AVM

A
  1. hemorrhage
  2. reduced o2 to brain–blood rushes quickly through AVM–moves so fast that some brain tissue not oxygenated
  3. Brain damage–as body grows, the AVM grows bc it recruits more arteries to supply blood–growing AVM eventually displaces or compresses part of brain
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90
Q

do we see midline shift with large AVMs?

A

no, because AVM is SLOW growing.. so the brain has time to adjust and move around without being pushed

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91
Q

diagnostic tests for AVM

A

CT WITH Contrast
MRI/MRA
cerebral angiography

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92
Q

TX for AVM

A

main goal of tx is to prevent hemorrhage **

  1. surgical resection of tangled mass
  2. endovascular emoblization that blocks feeding arteries to AVM
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93
Q

ruptured AVM can cause….

A
  • strokes (1-2% of all)
  • cause 3% of strokes in young adults
  • cause 9% of all SAH
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94
Q

what is TIA

A

transient ischemic attack

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95
Q

how long does TIA usually last

complete resolution of s/s?

A

no more than 24 hours
can be as little as few minutes
*resolution of s/s: within 1 hour

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96
Q

TIA of ophthalmic artery?

A

Amaurosis fugax

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97
Q

which artery is affected in amaurosis fugax?

A

TIA in the internal carotid

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98
Q

what is test of choice for definitive TIA?

A

conventional angio

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99
Q

with TIA, do we want to lower the BP?

A

NO!

unless it is >220/120

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100
Q

what is contraindicated in management of TIA

A

thrombolytics

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101
Q

first line tx for noncardiogenic TIA

A

ANTIPLATELET TX:

ASA***
clopidogrel

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102
Q

Percent of stroke after TIA?

A

30% risk within 5 years of TIA

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103
Q

ABCD2 Score Assessment

A
  • TIA
  • assesses risk of stroke w/in 3-90 days post stroke
  • **highest risk for stroke is days after TIA
  • PT gets one pt for each of the following:

A: age>60
B: BP >140/90
C: Clinical s/s (one PT for slurred speech and two PTs for unilateral weakness)
D: Duration (one PT for >10 mins and 2 points for >60mins)
D: diabetes

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104
Q

when do we allow permissive HTN and why?

A

with TIA and ischemic stroke PT
*bc their brain is used to having higher pressure, so if we drop it too fast, perfusion drops as well

**hemm stroke we want to drop the BP

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105
Q

ABCD2 scoring
0-3points=?
4-5 points=?
6-7points=?

A

0-3= 3.1% 90 day stroke

4-5= 9.8% 90 day stroke

6-7= 17.8% 90 day stroke

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106
Q

most modifiable and significant RF for stroke

A

HTN

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107
Q

aphasia

A

diff speaking or understnad speech

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108
Q

apraxia

A

inability to perform purposive actions

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109
Q

ataxia

A

loss of full control of bodily movements

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110
Q

with ischemic stroke, why can the CT be normal w/in first 24 hours?

A

bc it takes 24 hours for brain tissue death to show on CT

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111
Q

most accurate diagnostic test to diagnose stroke?

A

MRI

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112
Q

best initial diagnostic test for stroke?

A

CT w/o contrast

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113
Q

immediate tx for ischemic stroke?

A

allteplase

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114
Q

contras for alteplace?

A

BP 185/110 or higher;
recent bleeding;
bleeding disorder,
recent trauma.

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115
Q

can give alteplase how long after intial s/s of stroke

A

3

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116
Q

who can get thrombolytic tx for ischemic stroke up to 4.5 hours??

A

-less than 80 YO
<25 on NIH stroke scale
no DM with previous stroke

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117
Q

when is mechanical thrombectomy indicated?

A

within 24 hours of s/s onset

for large artery occlusion in anterior circulation

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118
Q

long term management ischemic stroke

A
  1. antiplatelet therapy: ASA, clopidogrel or dipyridamole
    * not started until 24 hours after Alteplace*
  2. Statin therapy regardless of their LDL
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119
Q

If PT is already on ASA prior to stroke… what is the long-term mangement plan?

A

either add on Dipryidamole or switch to clopidogrel

120
Q

when to lower BP with ischemic stroke

A

if BP is over 185/110 and thrombolytics are to be administered
OR
BP over 220/120 and no plan to use thrombolytics

121
Q

lacunar stroke?

-locations

A

small lesions that are under 5mm in diameter that occur in short penetrating (tiny arteries) arteries of

  • basal g
  • pins
  • cerebellum
  • internal capsule
  • thalamus
  • deep cerebral white matter

DEEP STRUCTURES*

122
Q

diff b/w ischemic stroke and lacunar stroke

A

LACUNAR: in the tiny tiny vessels deep in brain
ISCHEMIC: larger vessels

123
Q

TX for lacunar stroke

A

ASA and RF modifications

***no anticoagulation indicated **

124
Q

CT shows: small, punched-out hypodense areas?

A

Lacunar Stroke

125
Q

dysarthria

A

slurred speech

126
Q

MC presenting s/s for lacunar stroke?

A

dysarthria with clumsy hand (clumsy hand syndrome)

-PURE motor or PURE sensory deficits can be seen too

127
Q

classic territory for watershed infarct

A

between MCA and ACA
or
MCA and PCA

128
Q

typical pathway for movement

A

primary motor cortex–brainstem–spinal cord—nerves—innvervate skel muscles

129
Q

two main motor function categories

A

Upper motor neurons

lower motor neurons

130
Q

decussation area

A

corticospinal tract
-area where motor nerves “switch” to the opposite side of body

why person who has stroke on L side has R sided s/s**

131
Q

Upper motor neurons run from……

A

primary motor cortex down to the VENTRAL (anterior) horn of SC via corticospinal or pyramidal tract

132
Q

what tract does UMNs run on?

A

corticospinal or pyramidal tract

133
Q

what tract do the UMNs innervating cranial nerves run on?

A

corticobulbar tract

134
Q

Pthway for UMNs innervating CNs

A

primary motor cortex–cranial nerve nuclei–brainstem

*corticobulbar tract

135
Q

Lower motor neurons run from…

A

VENTRAL (anterior) horn of SC to the target muscle

136
Q

LMNs innervating the head and shoulders are found

A

in the CNs

137
Q

usual complaints from PTs with motor deficits

A 
weakness 
heaviness 
stiffness
clumsiness 
impaired muscle control 
diff executing movements
138
Q

during PE of patients with motor complaints, what is something very imp to look at?

A 
the MUSCLE 
appearance 
-wasting? 
-atrophy? 
-spasm? 
tone 
muscle power 
cordinationg 
reflexes 
gait
139
Q

Monoplegia/monoparesis

A

paralysis or severe weakness of muscles in one limb

140
Q

hemiplegia/hemiparesis

A

weakness/paralysis in both limbs (and something the face) on one side of the body

141
Q

paraplegia/paraparesis

A

weakness/paralysis of both LEGS

142
Q

quadriplegia/quadriparesis

A

weakness/paralysis of all four limbs

143
Q

term for paralysis or severe weakness of muscles in one limb

A

monoplegia or monoparesis

144
Q

term for weakness/paralysis in both limbs (and something the face) on one side of the body

A

hemiplegia/hemiparesis

145
Q

term for weakness/paralysis of both LEGS

A

paraplegia paraparesis

146
Q

term for weakness/paralysis of all four limbs

A

quadriplegia or quadriparesis

147
Q

S/S of UMN lesion

A

weakness or paralysis

  • hypertonia/spasticity
  • incr tendon reflexes
  • extensor plantar (babinski) response
  • loss of superficial adbominal reflexes
  • little if any muscle atrophy
148
Q

weakness or paralysis

  • hypertonia/spasticity
  • incr tendon reflexes
  • extensor plantar (babinski) response
  • loss of superficial adbominal reflexes
  • little if any muscle atrophy
A

S/S of UMN lesion

149
Q

S/S of LMN lesion

A 
weakness or paralysis 
*wasting and fasciculations or invovled muscles 
*hypotonia or flaccidity 
*loss of tendon reflexes 
normal abdominal and plantar reflexes 
little if any muscle atrophy
150
Q 
weakness or paralysis 
*wasting and fasciculations or invovled muscles 
*hypotonia or flaccidity 
*loss of tendon reflexes 
normal abdominal and plantar reflexes 
little if any muscle atrophy
A

LMN lesion s/s

151
Q

motor neuron disorders are character by degeneration of…….

A

anterior horn cells in SC**, motor nuclei of lower cranial nerves in the brain stem and corticospinal and corticobulbar pathways

152
Q

list the motor disordes

A 
ALS 
polio 
MS 
tetanus 
GBS 
Myasthenia gravis
153
Q

list the movement disorders

A 
tremors 
essential (familial) tremor 
tics 
Gilles de la tourette syndrome 
parkinson
154
Q

invol rhythmic oscillation of one or more body parts. May occur at rest, posture, and action and can be part of the cerebellar syndrome

A

tremor

155
Q

define tremor

A

invol rhythmic oscillation of one or more body parts. May occur at rest, posture, and action and can be part of the cerebellar syndrome

156
Q

irreg random rapid low amplitude semi-purposelful dance-like movements

A

chorea

157
Q

define chorea

A

irreg random rapid low amplitude semi-purposelful dance-like movements

158
Q

simultaneous contractions of agonsit and anatagonist muscles causing patterned sustained postures and irregular repetitive movements

A

dystonia

159
Q

define dystonia

A

simultaneous contractions of agonsit and anatagonist muscles causing patterned sustained postures and irregular repetitive movements

160
Q

sudden lightening like random jerks or sudden inhibition of on-going muscle activity

A

myoclonus

161
Q

define myoclonus

A

sudden lightening like random jerks or sudden inhibition of on-going muscle activity

162
Q

constellation of hyopkinetic symptoms such as bradykinesia, rigidity, postural instability and resting tremor

A

parkinson

163
Q

motor activity as a voluntary effort to relieve uncomfortable sensations

A

akathisia

164
Q

define akathisia

A

motor activity as a voluntary effort to relieve uncomfortable sensations

165
Q

Parkinson tremor:

  • distribution
  • what makes it worse and better
  • body part affected
  • writing?
  • progressive or sudden
  • fam hx
  • other neuro s/s with it
  • drugs that help
A

tremor present at rest “rolling pill”.. increases with walking and decreases with posture holding or action

asymmetric distribution

hands and legs usually affected

small and illegibile writing

progresive course

less common hx in fam

other s/s–bradykinesia, rigidity, loss of postural reflxes

drugs that make it better–levodopa, anticholinergics

166
Q

Essential tremor:

  • distribution
  • what makes it worse and better
  • body part affected
  • writing?
  • progressive or sudden
  • fam hx
  • other neuro s/s with it
  • drugs that help
A

posture holding or action increases

symmetric distrib

hands, head, voice distrib

tremulous writing seen

stable or slowly progressive

often related to fam hx

no other s/s seen with it

drugs that make better: ETOH, propranolol and primidone

167
Q

ALS is neurodegeneration of what

A

anterior horn cells

why sensation is not affected

168
Q

ALS affected LMN or UMN?

A

BOTH

*why it causes progressive motor dysfunction

169
Q

CM for ALS

A
  • asymmetric limb weakness (MC presenting symp)
  • bulbar symptoms: diff chewing, dysphagia, dysarthria, aspiration
  • cognitive impairment–frontotemporal dysfunction
170
Q

MC presenitng symp for ALS

A

asymmetric limb weakness

171
Q

“bulbar” symptoms means

A

muscles that control swallowing, speaking, chewing etc

  • diff in:
  • chewing
  • swallowing
  • speech
  • aspiration
172
Q

what functions are spared with ALS

A

sensory
voluntary eye movement
spinchter control
sexual function

173
Q

PE findings for ALS

A

mix of UMN and LMN s/s is hallmark

UMN:

  • muscle stiffness
  • hyperreflexia
  • spasticity
  • weakness

LMN:

  • muscle atrophy
  • hyporeflexia
  • muscle contractions/fasciculations
174
Q

diagnose ALS?

results?

A

electromyography–shows loss of neural improvement and reinnervation in muscle groups

175
Q

electromyography results–shows loss of neural improvement and reinnervation in muscle groups

A

ALS

176
Q

Management for ALS

A
  1. Riluzole–reduces glutamate accumulation in neurons
    * *only known drug to impact ALS by reducing progression up to six MOs
  2. Edaravone–free radical scavenger that helps in early-stage disease
  3. symptom managment:
    - drooling: muscarinic anticholinergic drugs
    - braces/walkers/wheelchairs
    - diet–usually progresses to liquid diet…. then progresses to tube feedings bc of dysphagia
    - ventilation– towards the end of disease
177
Q

What is the MC cause of death for ALS?

A

respiratory failure

178
Q

prognosis for ALS

A

fatal w/in 3-5 years of diagnosis

**resp failure MC cause of death

179
Q

what are some of the MC presenting s/s of MS?

A 
sudden blurred vision with 
-decreased acuity 
or
-double vision
-paresthesias (numbness/tingling) in extremities, ataxia, fatigue and focal motor s/s 
*trigeminal neuralgia 
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
*sensory loss 
*optic neuritis 
*weakness
*fatigue **
*paresthesias
180
Q

what is MS

A

autoinflammatory disease causing

  • demyelination
  • neuronal loss
  • scarring within white matter of brain + SC
181
Q

what is commonly seen with MS/typical complaint

A

visual disturbances over many yrs

182
Q

PT demographic we think of for MS

A

WOMEN and young adults 20-40 YO

183
Q

three types of MS

*MC?

A
  1. relapsing-remitting disease (MC..85%)–episodic exacerbations
  2. Progressive disease–progressive decline w/o acute exacerbations
  3. Secondary progressive–relapsing/remittent that becomes progressive
184
Q

prevalence of MS rises with ?

A
  • increasing distance from equator

* vit d may play a role?

185
Q

patho of MS

A

focal and scattered areas of demyelination

-triggered by immune response directed against myelin self-antigens

186
Q

clinical manifestation for MS

A

initally— the sudden blurry vision or double vision or loss of vision

sensory disturbances: pain, parathesias 
weakness 
motor deficits--gait and balance problems 
-fatigue 
-SC s/s--bladder or bowel dysfunction
187
Q

Uhthoff’s phenomenon–what is it ?

seen with?

A

Seen with MS

*worsening s/s with heat –excerise, fever, hot tubs, weather

188
Q

PE findings for MS

A
  • UMN–hypertonia and hyperreflexia and spasticity along with upward babinski sign
  • Lhermitte’s sign–neck flexion causes lightening shock pain rad down to spine and legs
  • cerebellar–Charcot’s neurologic triad: nystagmus, staccato speech, intentional tremor
  • optic neuritis with Marcus-Gunn pupil
  • Internuclear opthalmoplegia–inability to adduct eye on the side of lesioin w/ nystagmus in the other eye

SC s/s–bladder, bowel or sexual dysfunction

189
Q

what is -Lhermitte’s sign

seen with?

A
  • -neck flexion causes lightening shock pain rad down to spine and legs
  • seen with MS
190
Q

what is Charcot’s neurologic triad and seen with what disease

A

: nystagmus, staccato speech, intentional tremor

MS!

191
Q

Marcus-Gunn pupil.. what is it

seen with?

A

pos swinging light test

MS!!!

192
Q

what is -Internuclear opthalmoplegia and what is it seen with

A

–inability to adduct eye on the side of lesioin w/ nystagmus in the other eye

MS

193
Q

PE: UMN s/s, Lhermitte’s sign, Charcot’s neurologic triad, optic neuritis with Marcus-Gunn pupil, Internuclear opthalmoplegia and SC s/s

A

MS

194
Q

is MS autoimmune?

A

YES

195
Q

what is a strong sign of MS

A

internuclear ophthalmpleiga

-inability to adduct the eye on side of lesion w/ nystagmus on the other eye

196
Q

life expectancy for MS?

A

near normal

197
Q

major long term problem with MS?

A

optic neuritis

198
Q

CSF in MS shows–

A

increased IGG
oligoclonal bands
myelin fragments

199
Q

CSF shows increased IGG
oligoclonal bands
myelin fragments

what disease

A

MS

200
Q

cerebellar involvement in MS is manifested by?

A 
tremors 
ataxia 
babinski sign 
nystagmus 
staccato speech
201
Q

how do we diagnose ms

A

mainly clinical
*MRI with gadolinium—BEST INITIAL TEST most accurate too

LP

202
Q

hallmark findings on MRI with MS

A

hyperintense white matter plaques

203
Q

MRI shows hyperintense white matter plaques

A

MS

204
Q

Oligoclonal bands in csf indicates?

A

MS

205
Q

Management for acute episode of MS?

A

FIRST LINE–IV glucocorticos high dose

2nd–plasmapheresis if not responsive to glucos

206
Q

Managment for prevention of relapse and progression of MS?

A

1st line–Beta Interferon (anti-inflamm) or Glatiramer (immunodilators)
2nd–Natalizumabe (monoclonal antiobody) or Terifluomide

  • for fatigue: Amantadine-antiviral
  • for spasticity: Diazepam or Baclofen
207
Q

other than MRI, what are the diagnostic criteria for MS

A
  1. two episodes or attacks of s/s

2. two diff areas of CNS involved

208
Q

what kind of nerves does the tetanus toxin travel?

A

along motor nerves

209
Q

tetanus toxin interferes with? results?

A

release of GABA

results: motor nerve hyperactivity and severe muscle spasms

210
Q

incubation pd for tetanus toxin

A

3-21 days

211
Q

MC presenting s/s of tetanus

A

Trismus–lockjaw

212
Q

puncture wounds most susceptible to?

A

tetanus

213
Q

s/s of tetanus

A

lock jaw
local muscle spasms
neck or jaw stiffness
dysphagia
spasm of facial muscles–CONTORTED SMILE
PAINFUL muscle spasms and rigidity progress to involve both axial and limb musculature
—-can cause apneic episodes and hyperextended posturing (opisthotonos)

214
Q

contorted smile or spasm of facial muscles

A

tetanus

215
Q

LT complications of tetanus

A

epneic episdoes
layngospasm and autonomic dysfunction
hyperextended posturing

216
Q

TX for tetanus

A

hospitalize–need monitoring for resp/circulatory function

Neutralize toxin–tetanus immunoglobulin
Metronidazole for 7-10 days
diazepam to tx painful muscle spasms

217
Q

Prognosis of tetanus

A

fatality rate 10-60%

of PTs who recover–95% have no long-term sequelae

218
Q

Prevention for tetanus

A

Tdap

219
Q

DtaP schedule

  1. how many doses in total?
  2. schedule?
A

FIVE DOSES IN TOTAL

2 MO 
4 MO 
6MO 
15-18MO 
4-6 YO
220
Q

tDap booster given when? (4)

A
  • 11-12 YO get a booster….afterwards it is every 10 years
  • pregnant
  • after major injury IF last booster was 5 yrs ago or longer
221
Q

what are adults given who never had tetanus vaccine before? scheduling??

A

Tetanus immune globulin 250U AND initiation of tetanus toxoid vaccine:

  • second dose b/w wk 4-8
  • third dose given 6-12 MO after second
222
Q

tetanus immune globulin given to who?

A

PT with contaminated wound and NO vacc hx

223
Q

MS is demylelination of nerves in_____

GBS is demyelination in______

A

MS–CNS

GBS—PNS

224
Q

desc the weakness manifestatios seen with GBS

A

symmetric

ascending

225
Q

acquired autoimmune demyleinating polyradiculopathy of the PNS?

A

GBS

226
Q

patho for GBS

A

autoantibody attacks myelin sheath of PNS AFTER AN INFECTION

227
Q

Ascending paralysis begins where?

A

in the distal limbs

228
Q

etiology for GBS

A

INCREASED INCIDENCE POST INFECTIONS:

  • *****Campylobacter jejuni (MC)
  • other GI infectinons
  • Resp infections
  • CMV
  • epstein-barr virus
  • HIV
  • Mycoplasma infections
  • Immunizations (BOARDS LIKE THIS ONE)**
  • postsurgical
229
Q

CM for GBS

A

often stars with symmetrical ascending weakness and sensory changes (paresthesias, pain)
**starts in distal lower extrems first

  • can develop weakness of resp muscles and bulbar muscles
  • dysphagia

NO CNS S/S SINCE THIS IS PNS!!!!!!
*so no bowel or bladder incontinence

230
Q

what LT s/s can occur with GBS

A

autonomic dysfunctions can lead to death via impaired respirations via dia paralysis or aspiration pneumonia bc of aphagia

231
Q

PE findings for GBS

A

LMN

  • decreased tendon reflexes
  • flaccid paralysis
  • weakness

Sensory deficits

CN palsies—CN VII

Autonomic dysfunction:

  • tachycardia
  • arrhythmias
  • HTN or hypot
  • breathing problems
232
Q

how do we diagnose GBS

A

Electrophysiologic (nerve conduction) studies

***LP: HIGH protein with normal WBC

233
Q

CSF results: HIGH protein with normal WBC?

A

GBS

234
Q

TX for GBS

A

First line: Plasmaphoresis or IV immune globulins (IVIG)

  • prepare for mechanical ventilation
  • NO STEROIDS***
235
Q

What is contraindicated in tx of GBS?

A

steroids

236
Q

prognosis for GBS

A

most recover within 1 year

237
Q

patho for mysasthenia gravis

A

BLOCKADE to NM transmission:

autoantibodies attack nicotinic ACH rec–>fluctuating weakness–easy fatiguability of vol muscles

238
Q

MC age and gender population for Myasthenia gravis?

A

YOUNG women <40 ***

older men >50 but less common

239
Q

strong associationg with______ in Myasthenia gravis

A

abnormal THYMUS gland–75%

240
Q

CM for myasthenia gravis

A
  • generalized weakness: WORSENED WITH REPEATED MUSCLE USE….activity cannot be maintained
  • Ocular weakness: diplopia & ptosis (pupils spared)
241
Q

Hallmark complaint of Myasthenia gravis?

A

fatiguability

  • worsens during the day or after PDs of prolonged use
  • improved with rest
  • BOARDS LOVE: weakness in everyday activities like brushing hair**
242
Q

pathway of weakness for Myasthena gravis?

A

proximal to distal weakness:

  • eyes: ptosis usually FIRST
  • face: weak chewing
  • limbs: easily fatigued with movement exercise
243
Q

Myasthenia crisis

A

resp muscle weakness leds to resp failure

244
Q

MC first presenting s/s of Myasthenia gravis?

A

diplopia and ptosis

*****ocular weakness

245
Q

Diagnostic testing for Myasthenia gravis

A

ACH receptor antibodies**–initial test of choice

Electrophysiology testing–most accurate test

Edrophonium (Tensilon) test: when drug given, obvious improvement in muscle strength–lasts for 5 mins

ice pack test=place on eyelids for ten mins.. improves s/s

CXR, CT or MRI–done in all PT to detect thymus gland abnormalities

246
Q

gold standard to diagnose MG?

A

Electrophysiology testing

247
Q

best initial test for diagnose of MG? (OUTPT)

A

ACH receptor antibodies

248
Q

Best initial test for diagnose of MG (emergent setting)

A

Edrophonium/Tensilon test

249
Q

TX for severe or crisis of MG?

A

Plasmaphoresis or IVIG

250
Q

Long term tx for MG

A

FIRST LINE: acetylcholinesterase inhibitors (Pyridostigmine or Neostigmine)

2nd LINE: corticos

  • thymectomy–even if thymus is NORMAL—-good to do when medication doesnt work
  • avoid meds that exacerbate MG
251
Q

what medications are known to exacerbate MG?

A

Fluoroquinolones
Aminoglycosides
BBs

252
Q

tremor is enhanced by? Disappears when?

A
  • emotional stress

- disappears during stress

253
Q

define static or rest tremor

EX

A

tremor occurs when limb/muscle is at rest

EX: parkinson tremor

254
Q

Define postural tremor
EX
how to see this tremor?

A

tremor when skel muscle is sustained in a posture—may continue during movement but DOES NOT INCREASE with movement
*to see this tremor, ask the PT to hold out arms and hold the position

EX: essential tremor, physiologic tremor

255
Q

Define intention or kinetic tremor
EX
-how to see this tremor?

A

no tremor at rest
but tremor starts during movement
EX: MS, chronic ETOH, cerebellar disease

**have PT do rapid finger to nose movements

256
Q

tremor seen in ms?

A

intention or kinetic tremor

257
Q

essential tremor is what kind of tremor

A

intentional postural tremor

258
Q

MC kind of postural tremor

A

essential

259
Q

up to _____% of essential tremor cases are familial

A

50%

260
Q

list some activies affected by essential tremor

A
  • eating/drinking
  • writing and drawing
  • getting dressed
  • shaving
  • tying shoes
  • **when performing activities
261
Q

Parts of the body an essential tremor affects

A 
one or both hands
head 
voice 
or 
some combo of these 
**legs usually spared
262
Q

PE for essential tremor

A

finger to nose testing–tremor will increase at the end

***NO TREMOR AT REST

263
Q

DX for essential tremor

A

clinical

  • r/o other causes
  • fam hx
264
Q

TX for essential tremor

1st 2nd 2rd line agents

A

1st: Propranolol–severe cases or situational (stress)
2nd: Primidone (anticonvulsant) if propranolol not helpful
3rd: Benzo: Alprazolam

ETOH!!! can provide transient relief

265
Q

what makes essential tremor worse?

A 
stress 
anxiety 
caffeine 
stimulants 
emotional stress 
*intentional movement
266
Q

sudden, recurrent, quick, coordinated abnormal movements that can usually be imitated w/o difficulty

A

Tics

267
Q

can tics be surpressed voluntarily?

A

yes. .but for short pds of time

* doing so may cause anxiety

268
Q

what worsens tics

what makes it better

A

Worsen with:
-stress

diminish during

  • voluntary acitivity or menal concentration
  • sleep
269
Q

idiopathic movement disorder characterized by vocal tics, motor tics, and OCD

A

Tourette Disorder

270
Q

what is the leading cause of acute AMS

A

bac meningitis

271
Q

idiopathic disease due to loss of dopaminergic neurons in substania nigra

A

Parkinson disease

272
Q

loss of dopaminergic neurons in Parkinson disease leads to failure of?

A

ACH inhibition in basal ganlgia

*affects dopamines ability to initiate movement

273
Q

ACH is what type of NT?

Dopamine is what type of NT?

A

ACH=excitatory

Dopamine=inhibitory

274
Q

common age of onset for parkinson

A

45-65YO

275
Q

Parkinson triad

A
  • resting tremor (pill rolling)
  • bradykinesia–slow movements
  • muscle rigidity (cogwheel rigidity)
276
Q

ALL resting tremors are ____disease until proven otherwise

A

PARKINSON

277
Q

what is the second most common neurodegenerative disease?

what is the first

A

FIRST: dementia
SECOND: PD

278
Q

PD is characterized by?

A

tremor
hypokinesia
rigidity–increased resistance to passive movement (cogwheel..flexed posture)
abnormal gait and posture

279
Q

what is often the first s/s of Parkinson?

A

resting/pill rolling tremor

280
Q

bradykinesia

A

slowness of VOLUNTARY movement
AND
decreased autonomic movement (lack of swinging arms when walking and a shuffling gait)

281
Q

is there muscle weakness and hyper/hypo tendon reflexes in PD?

A

NO

  • no weakness
  • tendon reflexes normal
282
Q

what is a later finding in about 50% of PD cases?

A

dementia

283
Q

what improves the pill rolling tremor

A

initiation of voluntary movement
intentional movememnt
sleep

284
Q

pill rolling/resting tremor: asymmetric or symmetric?

A

begins asymmetric… usually one limb or one side of body… and then as diseases progresses will become generalized

285
Q

explain facial involvement in PD

A 
"fixed" facial expression 
immobile face 
-widended palpebral fissure 
"masked facies" 
decreased blinking 
*seborrhea is a common skin condition
286
Q

Myerson’s sign

A

tapping the bridge of nose repetitively causes sustained blink

287
Q

tapping the bridge of nose repetitively causes sustained blink
seen with?

A

Myerson;s sign

PD

288
Q

DX for PD

A

clinical

  • no lab tests or physiologic testing for dx
  • can R/O structural abnormalities with MRI

POST-MORTEM HISTOLOGY: only time we can officially dx

  • Lewy bodies
  • loss of pigment cels in susbtantia nigra
289
Q

TX for PD

  1. most effective
  2. what is 1st line
  3. drug to use if tremor only s/s
  4. Drug used in early cases wth mild s/s
A
  1. Levodopa-carbidopa–but long term use wears off after 10 years.. why we wait to start this drug until older >65 YO
  2. Dopamine agonist–Bromocriptine (>65YO)
  3. Anticholinergics–Trihexyphenidyl (does not help w/ bradykinesia)
  4. Amantadine–increases dopamine
290
Q

what happens if you pull the shoulders back of a PD PT?

A

they will fall or take step backwards

*bc they have postural instability

291
Q

typical age of onset for tourette?

A

childhood (4-6)

292
Q

MC gender for tourette?

A

M>W

293
Q

MC intitial presenting symp for Tourette?

A

motor tic–involving head, face or neck

  • blinnking
  • shrugging
  • head thrusting
  • sniffling
294
Q

DX criteria for tourette

A

Multiple motor or 1+ vocal tics for >1 year

Onset prior to age 18

295
Q

TX for tourette?

-first line

A

Most dont need pharmacotherpay
*habit reversal therapy is FIRST LINE aka CBT

Pharmaco:

  1. Dopamine blocking agents: Tetrabenzaine
  2. Alpha 2 adrenergics: Clonidine (sedating)
  3. Clonazepam for adjunct tx
296
Q

TX for refractory cases of tourette?

A

deep brain stimulation

Clin Med (52 decks)

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