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
2
Q
Cushings triad
A
- hypertension
- bradycardia
- irregular respirations
3
Q
CCP=
A
cerebral perfusion pressure=MAP-ICP
4
Q
normal CPP
A
b/w 70 and 90 mmHg
5
Q
list the primary HA
A
- tension
- migrane w/ or w/o aura
- cluster
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
7
Q
MC HA?
A
PRIMARY—90%
8
Q
HA caused by?
A
traction, displacement and inflammation or distention of the pain-sensitive structures in head or neck
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
10
Q
HA differentials by time course: list the HA for each timeline
- Acute onset
- Subacute onset
- Chronic
A
- SAH, carotid/vertebral dissection, meningitis or encephalitis, glaucoma, acute iritis
* less common: lumbar puncutre, HTN encephalopathy, coitus - Giant cell (temporal) arteritis, intracranial mass (tumor, subdural hematoma), trigeminal neuralgia,
- migraine, med overuse, cluster, tension, cervical spine disease, sinusitis, dental disease
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
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
13
Q
HA worse at night, worse with coughing/sneezing/straining/
or
increasing in severity
A
ELEVATED ICP
- tumor
- hydrocephalus
- idiopathic intracranial HTN
14
Q
New HA in older adult 50+ w/ no prior hx
A
MASS LESION INFLAMMATION DISEASE:
- tumor
- giant cell arteritis
- primary CNS vasculitis
15
Q
New HA in PT with hx of CA
…what do we think of?
A
METASTASIS
16
Q
new HA in immunocomp PT
A
OPPORTUNISTIC INFECTION
- toxoplasmosis
- primary CNS lymphoma
- cryptococcal (fungal) meningitis
17
Q
HA + fever
A
INFECTION
- meningitis
- cerebral abscess
18
Q
HA + seizures
A
FOCAL LESION
- tumor
- infection
- hemorrhage
19
Q
HA + focal neuro signs
A
FOCAL LESION
- tumor
- infection
- hemorrhage
- ischemic stroke
20
Q
Which HA is MC in women
A
tension and migraine
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
22
Q
list the 5 prophylactic drug therapies to prevent/reduce freq of migraine HA
A
- BB–propranolol
- CCBs–verapamil
- TCAs–amitriptyline
- anticonvulsants–valporic acid and topiramate
23
Q
Indications for Head CT w/ HA
A
- prior to LP
- abnorm neuro exam
- ams
- abnm fundoscopic exam
- meningieal signs - Emergent–conduct prior to leaving office/ED
- abnm neuro exam
- ams
- thunderclap HA - Urgent–scheudled prior to leaving office/ED
- HIV pos PT (MRI is preferred)
- age 50+ with normal neuro exam
24
Q
MC aura
A
VISUAL
-scotomata—flashing lights
25
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
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
26
younger PT diagnosed with Trigeminal neuralgia.. what do we want to r/o or be suspicious of?
Multiple sclerosis
27
cranial nerve palsy and can technically be classed as a LMN disorder?
Bell's Palsy
28
first line tx for abortive care of acute migraine
```
NSAIDS****
or
acetominophen
or
Excederin
```
29
first line tx for acute tension HA
NSAIDs **** + local heat
or
other analgesics
30
first line tx for acute cluster HA
100% oxygen
and
SQ Sumatriptan
31
1st line for cluster HA prophylaxsis
Verapamil
32
First line tx for Pseudotumor cerebral aka idiopathic intracranial HTN?
Acetazolamide (diuretic) + wt loss
*can use furosemide as adjunct
33
First line tx for trigeminal neuralgia
Carbamazepine PO ---anticonvulsant
34
If Bell's palsy is caught in the first 72 hours, what is FL tx?
-Prednisone
or
acyclovir+Prednisone (glucocorticos)
35
what is the MC type of intracranial hem caused by a ruptured cerebral aneurysm?
SAH
or
intracerebral hemorrhage
36
Intracranial hemorrhages divided into two classes:
| -list what is in each class
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)
37
what causes a subarachnoid hemm?
-cerebral aneurysm rupture
38
another term for intracerebral hemorrhage?
hemorrhagic stroke
39
Hemorrhagic strokes are often secondary to?
HTN
40
two types of weakened BVs can cause hemorrhagic stroke
- aneurysms
| - AV malformations
41
Ischemic strokes: three (two mainly) types defined and which is more common
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****
42
Stroke s/s are ipsilateral or contralateral to the part of the brain affected?
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
43
Define TIA
TRANSIENT ISCHEMIC ATTACK
| -neuro deficits w/o acute infarct that lasts >24 hours
44
Four main "types" of intracranial hemorrhages
*which can be classified under hemorrhagic stroke?
Bleeding inside the brain
1. epidural
2. subdural
3. subarachnoid
4. intracerebral hem
***last two can also be classified under hemorrhagic stroke
45
where is the bleeding in a epidural hematoma?
space b/w skull and dura
46
MCC of epidural hematoma
middle meningeal artery rupture
| *assoc w/ temporal bone fracture
47
define hemiparesis
muscle weakness or partial paralysis on one side
| *also called hemiplegia
48
Uncal herniation
- define
- can develop secondary to?
```
CNIII palsy... ipsilateral eye of injury is:
-fixed
-dilated
-blown
CAN DEVELOP DUE TO:
-epidural hematoma
```
49
on CT, does the epidural hematoma cross suture lines?
NO
50
CT RESULTS: biconvex "lens shape" hyperdense in temporal area
epidural hematoma
51
First line tx for epidural hematoma
hematoma evacuation
OR
craniotomy
52
MCC of subdural hematoma
rupture of cortical bridging VEINS
| post blunt force trauma
53
subdural hematoma is bleeding where
space b/w dura and arachnoid membranes
| **bridging veins rupture
54
CT: concave/crescent shape bleed that does cross suture lines
Subdural Hematoma
55
First line tx for subdural hematoma
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
56
Subarahchnoid hemorrhage is where
space b/w arachnoid membrane and pia mater
57
MCC of subarachnoid hem?
| -other commmon cause
rupture saccular (berry) aneurysm ---75% cases for nontraumatic
other:
- trauma
- AV malformations
58
mortality rate for nontraumatic SAH
50%
59
thunderclap HA
SAH
60
Xanthochromic CSF results?
SAH
| *CSF is yellow to pink
61
TX options for SAH
* ****BEDREST*****
- Nimodipine to reduce cerebral vasospasms
- Labetalol to lower BP
- surgical coiling or clipping
62
MCC overall for intracerebral hem?
second MCC?
HTN from angiopathy from systemic HTN--number one
Cerebral amyloid angiopathy (disease of BV)
63
MCC for intracerebral hem in:
- eldery?
- kids?
elderly--> cerebral amyloid angiopathy
kids-->AV malformation
64
with intracerebral hem, how do we want to lower BP?
GRADUALLY
IV BBs or CCBS or hydralazine
* labetalol
* nicardipine
65
tx for intracerebral hem
SUPPORTIVE
-gradual BP reduction
Reduce ICP and prevent incr ICP
- raising bed 30 degrees
- limit IV fluids
- BP management
- Analgesia
- sedation
66
what is the 3rd MCC of death in the US?
Cerebrovascular accident---stroke
67
hemorrhagic stroke--another name for it?
intracerebral hemorrhage
68
two types of hemorrhagic stroke
- intracerebral hem
| - SAH
69
bulging weakened area in the wall of an artery in brain
- what is it?
- what does it result in?
CEREBRAL ANEURYSM
* can result in abnormal widening or ballooning
* weak spot=risk for rupture/bursting
70
which BV layer is affected in cerebral aneurysm?
muscular layer of the artery wall is thin....
| -so instead of three layers, now the BV only has two
71
which arteries in the brain can develop an aneurysm?
| mc where
ANY OF THEM
| MC in the front part of brain
72
MC type of aneurysm
Berry or saccular aneurysm
| 80-90%
73
when are cerebral aneurysms diagnosed?
usually not diagnosed until they rupture....
| but sometimes PT can have s/s before rupture.. and then aneurysm will be dx on CT
74
S/S of a cerebral aneurysm
| -that did not rupture
```
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
```
75
MC initial symptom of a cerebral aneurysm?
if it RUPTURED
- sudden/thunderclap HA
- SAH
76
s/s of SAH
```
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
```
77
how to diagnose Cerebral aneurysm
| *gold standard?
CT scan WITH contrast ******
MRI
GOLD STANDARD--angiography
*but dont start with that.. usually start with CT
78
where is berry aneurysm located
| -where on arteries does it form?
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
79
RF for cerebral aneurysm
smoking
htn
hypercholesteremia
ETOH
80
Herald bleed
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
81
TX for cerebral aneurysm
surgery
| -clipping or coiling
82
what is brain arteriovenous malformation
| -cause?
tangle of abnormal BVs
-connecting arteries and veins
* rare
* idiopathic.. most ppl are born with them
83
s/s of AVM
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%)
84
in about 1/2 of PTs with AVM.. what is the first sign?
intracranial hemorrhage!
85
gold standard for AVM diagnosis, tx plannning, and follow-up after tx
angiography
86
what is the most dangerous congenital vascular malformation and why?
AVM
* potential to cause intracerebral hem and epilepsy
* AVM will grow as PT gets older
87
usual presenting age for AVM
10-40
88
RF for AVM
male
| fam hx
89
Complications with AVM
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
90
do we see midline shift with large AVMs?
no, because AVM is SLOW growing.. so the brain has time to adjust and move around without being pushed
91
diagnostic tests for AVM
CT WITH Contrast
MRI/MRA
cerebral angiography
92
TX for AVM
main goal of tx is to prevent hemorrhage ****
1. surgical resection of tangled mass
2. endovascular emoblization that blocks feeding arteries to AVM
93
ruptured AVM can cause....
- strokes (1-2% of all)
- cause 3% of strokes in young adults
- cause 9% of all SAH
94
what is TIA
transient ischemic attack
95
how long does TIA usually last
| complete resolution of s/s?
no more than 24 hours
can be as little as few minutes
*resolution of s/s: within 1 hour
96
TIA of ophthalmic artery?
Amaurosis fugax
97
which artery is affected in amaurosis fugax?
TIA in the internal carotid
98
what is test of choice for definitive TIA?
conventional angio
99
with TIA, do we want to lower the BP?
NO!
| unless it is >220/120
100
what is contraindicated in management of TIA
thrombolytics
101
first line tx for noncardiogenic TIA
ANTIPLATELET TX:
ASA***
clopidogrel
102
Percent of stroke after TIA?
30% risk within 5 years of TIA
103
ABCD2 Score Assessment
- 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
104
when do we allow permissive HTN and why?
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
105
ABCD2 scoring
0-3points=?
4-5 points=?
6-7points=?
0-3= 3.1% 90 day stroke
4-5= 9.8% 90 day stroke
6-7= 17.8% 90 day stroke
106
most modifiable and significant RF for stroke
HTN
107
aphasia
diff speaking or understnad speech
108
apraxia
inability to perform purposive actions
109
ataxia
loss of full control of bodily movements
110
with ischemic stroke, why can the CT be normal w/in first 24 hours?
bc it takes 24 hours for brain tissue death to show on CT
111
most accurate diagnostic test to diagnose stroke?
MRI
112
best initial diagnostic test for stroke?
CT w/o contrast
113
immediate tx for ischemic stroke?
allteplase
114
contras for alteplace?
BP 185/110 or higher;
recent bleeding;
bleeding disorder,
recent trauma.
115
can give alteplase how long after intial s/s of stroke
3
116
who can get thrombolytic tx for ischemic stroke up to 4.5 hours??
-less than 80 YO
<25 on NIH stroke scale
no DM with previous stroke
117
when is mechanical thrombectomy indicated?
within 24 hours of s/s onset
| for large artery occlusion in anterior circulation
118
long term management ischemic stroke
1. antiplatelet therapy: ASA, clopidogrel or dipyridamole
* **not started until 24 hours after Alteplace***
2. Statin therapy regardless of their LDL
119
If PT is already on ASA prior to stroke... what is the long-term mangement plan?
either add on Dipryidamole or switch to clopidogrel
120
when to lower BP with ischemic stroke
if BP is over 185/110 and thrombolytics are to be administered
OR
BP over 220/120 and no plan to use thrombolytics
121
lacunar stroke?
| -locations
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
diff b/w ischemic stroke and lacunar stroke
LACUNAR: in the tiny tiny vessels deep in brain
ISCHEMIC: larger vessels
123
TX for lacunar stroke
ASA and RF modifications
| ***no anticoagulation indicated ****
124
CT shows: small, punched-out hypodense areas?
Lacunar Stroke
125
dysarthria
slurred speech
126
MC presenting s/s for lacunar stroke?
dysarthria with clumsy hand (clumsy hand syndrome)
| -PURE motor or PURE sensory deficits can be seen too
127
classic territory for watershed infarct
between MCA and ACA
or
MCA and PCA
128
typical pathway for movement
primary motor cortex--brainstem--spinal cord---nerves---innvervate skel muscles
129
two main motor function categories
Upper motor neurons
lower motor neurons
130
decussation area
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
Upper motor neurons run from......
primary motor cortex down to the VENTRAL (anterior) horn of SC via corticospinal or pyramidal tract
132
what tract does UMNs run on?
corticospinal or pyramidal tract
133
what tract do the UMNs innervating cranial nerves run on?
corticobulbar tract
134
Pthway for UMNs innervating CNs
primary motor cortex--cranial nerve nuclei--brainstem
| *corticobulbar tract
135
Lower motor neurons run from...
VENTRAL (anterior) horn of SC to the target muscle
136
LMNs innervating the head and shoulders are found
in the CNs
137
usual complaints from PTs with motor deficits
```
weakness
heaviness
stiffness
clumsiness
impaired muscle control
diff executing movements
```
138
during PE of patients with motor complaints, what is something very imp to look at?
```
the MUSCLE
appearance
-wasting?
-atrophy?
-spasm?
```
```
tone
muscle power
cordinationg
reflexes
gait
```
139
Monoplegia/monoparesis
paralysis or severe weakness of muscles in one limb
140
hemiplegia/hemiparesis
weakness/paralysis in both limbs (and something the face) on one side of the body
141
paraplegia/paraparesis
weakness/paralysis of both LEGS
142
quadriplegia/quadriparesis
weakness/paralysis of all four limbs
143
term for paralysis or severe weakness of muscles in one limb
monoplegia or monoparesis
144
term for weakness/paralysis in both limbs (and something the face) on one side of the body
hemiplegia/hemiparesis
145
term for weakness/paralysis of both LEGS
paraplegia paraparesis
146
term for weakness/paralysis of all four limbs
quadriplegia or quadriparesis
147
S/S of UMN lesion
weakness or paralysis
* hypertonia/spasticity
* incr tendon reflexes
* extensor plantar (babinski) response
* loss of superficial adbominal reflexes
* little if any muscle atrophy
148
weakness or paralysis
* hypertonia/spasticity
* incr tendon reflexes
* extensor plantar (babinski) response
* loss of superficial adbominal reflexes
* little if any muscle atrophy
S/S of UMN lesion
149
S/S of LMN lesion
```
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
```
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
```
LMN lesion s/s
151
motor neuron disorders are character by degeneration of.......
anterior horn cells in SC****, motor nuclei of lower cranial nerves in the brain stem and corticospinal and corticobulbar pathways
152
list the motor disordes
```
ALS
polio
MS
tetanus
GBS
Myasthenia gravis
```
153
list the movement disorders
```
tremors
essential (familial) tremor
tics
Gilles de la tourette syndrome
parkinson
```
154
invol rhythmic oscillation of one or more body parts. May occur at rest, posture, and action and can be part of the cerebellar syndrome
tremor
155
define tremor
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
irreg random rapid low amplitude semi-purposelful dance-like movements
chorea
157
define chorea
irreg random rapid low amplitude semi-purposelful dance-like movements
158
simultaneous contractions of agonsit and anatagonist muscles causing patterned sustained postures and irregular repetitive movements
dystonia
159
define dystonia
simultaneous contractions of agonsit and anatagonist muscles causing patterned sustained postures and irregular repetitive movements
160
sudden lightening like random jerks or sudden inhibition of on-going muscle activity
myoclonus
161
define myoclonus
sudden lightening like random jerks or sudden inhibition of on-going muscle activity
162
constellation of hyopkinetic symptoms such as bradykinesia, rigidity, postural instability and resting tremor
parkinson
163
motor activity as a voluntary effort to relieve uncomfortable sensations
akathisia
164
define akathisia
motor activity as a voluntary effort to relieve uncomfortable sensations
165
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
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
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
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
ALS is neurodegeneration of what
anterior horn cells
| *why sensation is not affected*
168
ALS affected LMN or UMN?
BOTH
| *why it causes progressive motor dysfunction
169
CM for ALS
- asymmetric limb weakness (MC presenting symp)
- bulbar symptoms: diff chewing, dysphagia, dysarthria, aspiration
- cognitive impairment--frontotemporal dysfunction
170
MC presenitng symp for ALS
asymmetric limb weakness
171
"bulbar" symptoms means
muscles that control swallowing, speaking, chewing etc
* diff in:
- chewing
- swallowing
- speech
- aspiration
172
what functions are spared with ALS
sensory
voluntary eye movement
spinchter control
sexual function
173
PE findings for ALS
mix of UMN and LMN s/s is hallmark
UMN:
- muscle stiffness
- hyperreflexia
- spasticity
- weakness
LMN:
- muscle atrophy
- hyporeflexia
- muscle contractions/fasciculations
174
diagnose ALS?
| results?
electromyography--shows loss of neural improvement and reinnervation in muscle groups
175
electromyography results--shows loss of neural improvement and reinnervation in muscle groups
ALS
176
Management for ALS
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
4. 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
What is the MC cause of death for ALS?
respiratory failure
178
prognosis for ALS
fatal w/in 3-5 years of diagnosis
| **resp failure MC cause of death
179
what are some of the MC presenting s/s of MS?
```
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
what is MS
autoinflammatory disease causing
- demyelination
- neuronal loss
- scarring within white matter of brain + SC
181
what is commonly seen with MS/typical complaint
visual disturbances over many yrs
182
PT demographic we think of for MS
WOMEN and young adults 20-40 YO
183
three types of MS
| *MC?
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
prevalence of MS rises with ?
- increasing distance from equator
| * vit d may play a role?
185
patho of MS
focal and scattered areas of demyelination
| -triggered by immune response directed against myelin self-antigens
186
clinical manifestation for MS
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
Uhthoff's phenomenon--what is it ?
| seen with?
Seen with MS
| *worsening s/s with heat --excerise, fever, hot tubs, weather
188
PE findings for MS
- 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
what is -Lhermitte's sign
| seen with?
- -neck flexion causes lightening shock pain rad down to spine and legs
- seen with MS
190
what is Charcot's neurologic triad and seen with what disease
: nystagmus, staccato speech, intentional tremor
MS!
191
Marcus-Gunn pupil.. what is it
| seen with?
pos swinging light test
| MS!!!
192
what is -Internuclear opthalmoplegia and what is it seen with
--inability to adduct eye on the side of lesioin w/ nystagmus in the other eye
MS
193
PE: UMN s/s, Lhermitte's sign, Charcot's neurologic triad, optic neuritis with Marcus-Gunn pupil, Internuclear opthalmoplegia and SC s/s
MS
194
is MS autoimmune?
YES
195
what is a strong sign of MS
internuclear ophthalmpleiga
| -inability to adduct the eye on side of lesion w/ nystagmus on the other eye
196
life expectancy for MS?
near normal
197
major long term problem with MS?
optic neuritis
198
CSF in MS shows--
increased IGG
oligoclonal bands
myelin fragments
199
CSF shows increased IGG
oligoclonal bands
myelin fragments
what disease
MS
200
cerebellar involvement in MS is manifested by?
```
tremors
ataxia
babinski sign
nystagmus
staccato speech
```
201
how do we diagnose ms
mainly clinical
*MRI with gadolinium---BEST INITIAL TEST most accurate too
LP
202
hallmark findings on MRI with MS
hyperintense white matter plaques
203
MRI shows hyperintense white matter plaques
MS
204
Oligoclonal bands in csf indicates?
MS
205
Management for acute episode of MS?
FIRST LINE--IV glucocorticos high dose
2nd--plasmapheresis if not responsive to glucos
206
Managment for prevention of relapse and progression of MS?
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
other than MRI, what are the diagnostic criteria for MS
1. two episodes or attacks of s/s
| 2. two diff areas of CNS involved
208
what kind of nerves does the tetanus toxin travel?
along motor nerves
209
tetanus toxin interferes with? results?
release of GABA
| results: motor nerve hyperactivity and severe muscle spasms
210
incubation pd for tetanus toxin
3-21 days
211
MC presenting s/s of tetanus
Trismus--lockjaw
212
puncture wounds most susceptible to?
tetanus
213
s/s of tetanus
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
contorted smile or spasm of facial muscles
tetanus
215
LT complications of tetanus
epneic episdoes
layngospasm and autonomic dysfunction
hyperextended posturing
216
TX for tetanus
hospitalize--need monitoring for resp/circulatory function
Neutralize toxin--tetanus immunoglobulin
Metronidazole for 7-10 days
diazepam to tx painful muscle spasms
217
Prognosis of tetanus
fatality rate 10-60%
| of PTs who recover--95% have no long-term sequelae
218
Prevention for tetanus
Tdap
219
DtaP schedule
1. how many doses in total?
2. schedule?
FIVE DOSES IN TOTAL
```
2 MO
4 MO
6MO
15-18MO
4-6 YO
```
220
tDap booster given when? (4)
- 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
what are adults given who never had tetanus vaccine before? scheduling??
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
tetanus immune globulin given to who?
PT with contaminated wound and NO vacc hx
223
MS is demylelination of nerves in_____
| GBS is demyelination in______
MS--CNS
| GBS---PNS
224
desc the weakness manifestatios seen with GBS
symmetric
| ascending
225
acquired autoimmune demyleinating polyradiculopathy of the PNS?
GBS
226
patho for GBS
autoantibody attacks myelin sheath of PNS AFTER AN INFECTION
227
Ascending paralysis begins where?
in the distal limbs
228
etiology for GBS
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
CM for GBS
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
what LT s/s can occur with GBS
autonomic dysfunctions can lead to death via impaired respirations via dia paralysis or aspiration pneumonia bc of aphagia
231
PE findings for GBS
LMN
- decreased tendon reflexes
- flaccid paralysis
- weakness
Sensory deficits
CN palsies---CN VII
Autonomic dysfunction:
- tachycardia
- arrhythmias
- HTN or hypot
- breathing problems
232
how do we diagnose GBS
Electrophysiologic (nerve conduction) studies
*******LP: HIGH protein with normal WBC
233
CSF results: HIGH protein with normal WBC?
GBS
234
TX for GBS
First line: Plasmaphoresis or IV immune globulins (IVIG)
* prepare for mechanical ventilation
* ***NO STEROIDS******
235
What is contraindicated in tx of GBS?
steroids
236
prognosis for GBS
most recover within 1 year
237
patho for mysasthenia gravis
BLOCKADE to NM transmission:
| autoantibodies attack nicotinic ACH rec-->fluctuating weakness--easy fatiguability of vol muscles
238
MC age and gender population for Myasthenia gravis?
YOUNG women <40 *******
older men >50 but less common
239
strong associationg with______ in Myasthenia gravis
abnormal THYMUS gland--75%
240
CM for myasthenia gravis
* generalized weakness: WORSENED WITH REPEATED MUSCLE USE....activity cannot be maintained
* Ocular weakness: diplopia & ptosis (pupils spared)
241
Hallmark complaint of Myasthenia gravis?
fatiguability
* worsens during the day or after PDs of prolonged use
* improved with rest
* **BOARDS LOVE: weakness in everyday activities like brushing hair******
242
pathway of weakness for Myasthena gravis?
proximal to distal weakness:
- eyes: ptosis usually FIRST
- face: weak chewing
- limbs: easily fatigued with movement exercise
243
Myasthenia crisis
resp muscle weakness leds to resp failure
244
MC first presenting s/s of Myasthenia gravis?
diplopia and ptosis
| *****ocular weakness
245
Diagnostic testing for Myasthenia gravis
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
gold standard to diagnose MG?
Electrophysiology testing
247
best initial test for diagnose of MG? (OUTPT)
ACH receptor antibodies
248
Best initial test for diagnose of MG (emergent setting)
Edrophonium/Tensilon test
249
TX for severe or crisis of MG?
Plasmaphoresis or IVIG
250
Long term tx for MG
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
what medications are known to exacerbate MG?
Fluoroquinolones
Aminoglycosides
BBs
252
tremor is enhanced by? Disappears when?
- emotional stress
| - disappears during stress
253
define static or rest tremor
| EX
tremor occurs when limb/muscle is at rest
| EX: parkinson tremor
254
Define postural tremor
EX
how to see this tremor?
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
Define intention or kinetic tremor
EX
-how to see this tremor?
no tremor at rest
but tremor starts during movement
EX: MS, chronic ETOH, cerebellar disease
**have PT do rapid finger to nose movements
256
tremor seen in ms?
intention or kinetic tremor
257
essential tremor is what kind of tremor
intentional postural tremor
258
MC kind of postural tremor
essential
259
up to _____% of essential tremor cases are familial
50%
260
list some activies affected by essential tremor
- eating/drinking
- writing and drawing
- getting dressed
- shaving
- tying shoes
* **when performing activities
261
Parts of the body an essential tremor affects
```
one or both hands
head
voice
or
some combo of these
**legs usually spared
```
262
PE for essential tremor
finger to nose testing--tremor will increase at the end
| ***NO TREMOR AT REST
263
DX for essential tremor
clinical
* r/o other causes
* fam hx
264
TX for essential tremor
| 1st 2nd 2rd line agents
1st: Propranolol--severe cases or situational (stress)
2nd: Primidone (anticonvulsant) if propranolol not helpful
3rd: Benzo: Alprazolam
ETOH!!! can provide transient relief
265
what makes essential tremor worse?
```
stress
anxiety
caffeine
stimulants
emotional stress
*intentional movement
```
266
sudden, recurrent, quick, coordinated abnormal movements that can usually be imitated w/o difficulty
Tics
267
can tics be surpressed voluntarily?
yes. .but for short pds of time
| * doing so may cause anxiety
268
what worsens tics
| what makes it better
Worsen with:
-stress
diminish during
- voluntary acitivity or menal concentration
- sleep
269
idiopathic movement disorder characterized by vocal tics, motor tics, and OCD
Tourette Disorder
270
what is the leading cause of acute AMS
bac meningitis
271
idiopathic disease due to loss of dopaminergic neurons in substania nigra
Parkinson disease
272
loss of dopaminergic neurons in Parkinson disease leads to failure of?
ACH inhibition in basal ganlgia
| *affects dopamines ability to initiate movement
273
ACH is what type of NT?
| Dopamine is what type of NT?
ACH=excitatory
| Dopamine=inhibitory
274
common age of onset for parkinson
45-65YO
275
Parkinson triad
- resting tremor (pill rolling)
- bradykinesia--slow movements
- muscle rigidity (cogwheel rigidity)
276
ALL resting tremors are ____disease until proven otherwise
PARKINSON
277
what is the second most common neurodegenerative disease?
what is the first
FIRST: dementia
SECOND: PD
278
PD is characterized by?
tremor
hypokinesia
rigidity--increased resistance to passive movement (cogwheel..flexed posture)
abnormal gait and posture
279
what is often the first s/s of Parkinson?
resting/pill rolling tremor
280
bradykinesia
slowness of VOLUNTARY movement
AND
decreased autonomic movement (lack of swinging arms when walking and a shuffling gait)
281
is there muscle weakness and hyper/hypo tendon reflexes in PD?
NO
* no weakness
* tendon reflexes normal
282
what is a later finding in about 50% of PD cases?
dementia
283
what improves the pill rolling tremor
initiation of voluntary movement
intentional movememnt
sleep
284
pill rolling/resting tremor: asymmetric or symmetric?
begins asymmetric... usually one limb or one side of body... and then as diseases progresses will become generalized
285
explain facial involvement in PD
```
"fixed" facial expression
immobile face
-widended palpebral fissure
"masked facies"
decreased blinking
*seborrhea is a common skin condition
```
286
Myerson's sign
tapping the bridge of nose repetitively causes sustained blink
287
tapping the bridge of nose repetitively causes sustained blink
seen with?
Myerson;s sign
| PD
288
DX for PD
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
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
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
what happens if you pull the shoulders back of a PD PT?
they will fall or take step backwards
| *bc they have postural instability
291
typical age of onset for tourette?
childhood (4-6)
292
MC gender for tourette?
M>W
293
MC intitial presenting symp for Tourette?
motor tic--involving head, face or neck
* blinnking
* shrugging
* head thrusting
* sniffling
294
DX criteria for tourette
Multiple motor or 1+ vocal tics for >1 year
| Onset prior to age 18
295
TX for tourette?
| -first line
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
TX for refractory cases of tourette?
deep brain stimulation
