Neurology Flashcards
1
Q
ascending paralysis (rubbery legs) delayed DTRs (hypo, areflexia) peripheral nerve involvement (tingling dyesthesia) Bulbar weakness myelin damage
A
GBS
2
Q
Axon hillock is rich in
A
sodium
3
Q
Most common cause of acute paralysis
Acute/Subacute
Symmetric limb weakness with absent or reduced DTR
Widespread inflamm demyelination 2 to hypersensitivity (autoimmune) reaction
Potentially reversible condition (90%)
A
GBS
4
Q
Age
Axonopathy
Autonomics
A
Poor prognosis in GBS
5
Q
GBS pathophy
Immune response to nonself antigen misdirecting host nerve tissue through resemblance of epitope
A
Molecular mimicry
Ganglioside - myelin sheath attack
Antiganglioside antibody (GM1)
6
Q
GBS is related to antecedent infections:
A
C jejuni infection GM1 antiganglioside CMV EBV Mycoplasma Lymphoma Rabies and swine vaccine
7
Q
Classical form of GBS
A
Demyelinating
Acute Inflammatory Demy PN
Worldwide distrib
8
Q
Axonal form
A
Acute motor axonal PN
Acute motor sensory PN
China, Japan, Mexico
9
Q
Ataxia
Areflexia
Ophthalmoplegia
AntiGQ1b IgG antibody
A
Miller Fisher
10
Q
AIDP vs AMAN
A
AMAN more of children, AIDP equal AMAN also in C jejuni 80 Site of attack AMAN: nodes of ranvier (mac demyelination and lympho infiltration) AIDP: Schwann cell (axonal loss)
11
Q
GBS criteria for diagnosis
A
Ascending symmetrical motor paralysis Max deficit in 4 weeks peaking at 2 Areflexia EMG NCV abnormality CSF - elevated CSF protein 100-1000 CSF cell count less than 10 Cytoalbuminologic dissociation
12
Q
Electrodiagnostic medicine finding earliest feature in AIDP
A
Prolonged F wave latency
Distal motor latency
13
Q
GBS mx
A
IV Ig
Plasma exchange
Supportive (pneumonia and DVT prophy)
Monoclonal antibody
14
Q
IVIg in GBS
A
shortens duration of course
15
Q
Most common form of progressive motor neuron disease
Most devastating of neurodegen disorders
A
ALS
16
Q
ALS rf
A
Pesticide, insecticide
Smoking
Service in military
17
Q
ALS hallmark
A
Death of LMN and UMN
Selective loss of fxn then both
18
Q
ALS affects
A
Anterior horn cell
also polio
19
Q
If LMN predominantly:
A
Bulbar palsy (brainstem) SMA
20
Q
Upper MN
A
Pseudobulbar palsy
Primary lateral sclerosis
21
Q
insidious developing asymmetric weakness
distal first
ms wasting
atrophy, twitching, fasciculation, small muscle groups
hyperactivity of reflex
dysarthria and exaggerated motor expression of emotion
A
ALS
22
Q
ALS develops concurrently with
A
frontotemporal dementia
23
Q
ALS pathogenesis
A
Superoxide dismutase 1 SOD1 mutation
AD
24
Q
Drug that lengthens survival of ALS
Diminishes glutamate release
A
Riluzole
Nausea, dizziness, weight loss and LFTs
25
Leakage or rupture of congential aneurysm on circle of willis, angioma
Headache, stiffness, loss of consciousness
SAH
26
Most common cause of SAH is
head trauma
| ruptured saccular aneurysm
27
Perimesencephalic cistern, benign
Idiopathic SAH
28
Annual risk of rupture in >/= 10 mm
0.5-1%
<10 0.1%
29
Giant aneurysm >2.5cm risk of rupture
6% in 1st year
30
Most common locations of sacular aneurysm
Terminal ICA
MCA bifurcation
Top of basilar artery
31
Distal to first bifurcation of major arteries in circle
due to bacterial endocarditis becoming septic degeneration
Mycotic aneurysm
32
85% of ruptured aneurysms are at
anterior circulation
| ACom, MCA
33
In aneurysm development, this disappears at base of neck
internal elastic lamina
34
Greatest risk of rupture
>7mm diameter
Top of basilar
Origin of PCom (oculomotor palsy)
35
SAH is associated with severe headache with exertion in
45%
36
Four major causes of delayed neurologic deficit
1 rerupture
2 vasospasm
3 hydrocephalus
4 hyponatremia
37
Major cause of delayed morbidity and death SAH
Vasospasm
38
vasospasm tx
Nimodipine for 21 days
signs appear 4-14 days mean 7 days
39
Hunt and Hess grading 1
Mild headache
Normal mental status
No CN/Motor finding
40
Severe headache
Normal mental status
Cranial nerve deficit
H & H Type II
41
Somnolent
Confused
Cranial nerve and mild motor deficit
H & H Grade III
42
Stupor
Moderate to severe motor def
Intermittent reflex posturing
H & H Grade IV
43
Coma
Reflex
Flaccid
H & H Grade V
44
Fisher grade is
based on radiologic thickness of SAH on CT scan
45
Indicated only if CT scan not available at time of suspicion
Lumbar puncture
46
Yellowing of spinal fluid in SAH at
6-12 h peaking in intensity at 48h
Xanthochromia
47
SAH dx
Four vessel angiography
CT angiogram (alternative)
48
SAH hyponatremia may occur during
ECG may reveal:
1st two weeks
ST segment and T wave or prolonged QRS
changes similar to mi
49
Eliminates risk of rebleeding
| Assoc with neurologic morbidity
Clipping
50
Endovascular SAH technique
platinum coil through femoral catheter
Thrombosis and walling off circulation
Coiling
51
2nd leading cause of death worldwide
Abrupt onset of neurologic deficit that is attributable to a focal vascular cause
Clinical manif are variable:
Location
Blood vessel involved
Stroke
52
Most of the time abrupt onset within minute (maximal symptom within minutes)
Cardioembolic
53
Normal cerebral blood flow
50-55 ml/100g brain
54
Core infarct
<12 ml/100g / min
55
Electrically silent, structurally intact, potentially salvageable area of viability surrounding ischemic core
Penumbra
| 18 - 35 ml/100g / min
56
Area between normal brain and penumbra
Benign oligemia
57
Histologic effect are similar to hypoxia and anoxia
Hypoglycemia
58
Zone of neurons most sensitive to hypoxia
CA-1 of hippocampus pyramidal cell
59
Reduction in blood flow lasting longer than several seconds
| Neuro symptoms manifest due to lack of glycogen
Cerebral ischemia
60
Cessation of blood flow lasting more than a few minutes
| Death of brain tissue
Cerebral infarct
61
Causes of generalized/global infarction
Hypotension
| Cardiac arrest
62
Cause of focal infarction
Atherosclerosis
Arteriolosclerosis
Embolism
Vasculitis - CTD SLE, TB Meningitis
63
Virchow’s triad
Bood flow stasis
Hypercoagulability
Endothelial dysfunction
64
Hypotension resulting in generalized ischemia is felt especially in
Arterial border zone pattern
Watershed area
After a few days: Wedge shaped hemorrhagic infarct usually between MCA and ACA
Subject to reduction in blood flow
If patient dies immediately, no microscopic change
65
Cardiac arrest leading to diffuse neuronal necrosis of the cerebral and cerebellar cortices
More severe within sulci than gyri
Inc in severity from frontal and temporal to occipital lobe
Laminar necrosis
Hippocampus
Purkinje of cerebellum
66
Spectrum of change accompanying acute CNS hypoxia/ischemia
Earliest morphologic marker of neuronal death
Hallmark of acute neuronal injury
Red neuron
| acute neuronal injury
67
Red neurons are seen after irreversible hypoxic/ischemic insult:
12-24 hours
68
Hyperacute CT findings
```
Loss of grey-white matter interface
Obscuration of lentiform nucleus
Dense MCA sign (sludging of flow due to thrombus)
Insular ribbon size
Sulcal effacement
```
69
CT scan should be carried out in suspected stroke within
30 mins
70
Infarct ensues within
4-10 mins
71
Blood flow restored to ischemic tissue before significant infarct develops
Not time bound
No neuroimaging evidence of infarct
ABCD2 scoring system
Transient ischemic attack
72
Block of central retinal artery
or from blockage of internal carotid (ophthalmic)
leading to transient monocular blindness of ipsilateral eye
Amaurosis fugax
73
Ischemic but reversibly dysfunctional tissue surrounding a core area of infarct
Saving this is goal of revasc therapy
Ischemic penumbra
74
Infarct Pathogenesis
```
Hypoxia/Anoxia
Altered Na/K ATPase pump (cellular swelling)
Glutamate activation
Calcium influx
Ischemic injury (red neuron, vacuolation cell death karyorrhexis >1d)
Inflammation-edema (>3d)
Macrophage (>5d)
Liquefaction cavity (>1w)
Glial proliferation (>1w)
```
75
Nitric oxide synthase
Vasodilation
Angiogenesis
Neural development
Enzyme catalyzing production of nitric oxide from arginine
76
Contralateral hemiparesis and hemisensory loss
Face and UE > LE
Aphasia (Wernicke, Broca, Conduction) if infarct involves dominant cerebral hemisphere left parietal and temporal
Homonymous hemianopsia
Paralysis of conjugate gaze to opposite side
MCA syndrome
77
C/l hemiparesis and hemisensory
LE> UE
Urinary incontinence (medial frontal micturition center)
Contralateral grasp, sucking and Gegenhalten (paratonic rigidity)
Abulia, slowness, delay
Impairment of gaze and stance
ACA syndrome
78
```
C/l hemiparesis and hemisensory loss
Homonymous hemianopsia, amnesia
Unformed visual hallucination
Pendular hallucinosis
Complex hallucination
```
Peripheral PCA syndrome
79
```
Thalamic pain syndrome Dejerine-Roussy
Sensory loss
Spont pain and dysthesia
Claude syndrome
Weber syndrome
```
Central PCA syndrome
80
Constellation of B long tract (motor and sensory)
Signs of cranial nerve dysfunction
Cerebellar dysfunction
Quadriparesis
Basilar Artery distribution
81
Preserved consciousness
Quadriplegia
Only eyes are able to move
Locked in syndrome
82
Lacunes
Little lakes
20% of strokes due to arteriolar sclerosis (lipohyalinosis)
Small vessel stroke
Multiple small 3mm to 2cm old cavitary infarct
Basal ganglia and thalamus
Rf: hypertension and age
83
Pure motor hemiparesis (face-arm-leg)
Post limb of internal capsule or pons
84
Pure sensory stroke
ventral thalamus
85
Ataxic hemiparesis
Ventral pons and internal capsule
86
Dysarthria and clumsy hand or arm
Ventral pons or genu of internal capsule
87
Most significant cause of cardioembolic stroke
Nonvalvular non rheumatic atrial fib
88
CHADSVASC Score
Risk of stroke for px with AF
89
Cerebral autosomal dominant arteriopathy with subcortical infarct and leukoencephalopathy originates from
CADASIL
thrombus
90
Stroke tx goal
Reverse brain injury
1 medical support
2 IV thrombolysis
91
BP goal
reduce if
Permissive hypertension
BP >220/120
concomitant MI
BP > 185/110 and thrombolytic therapy anticipated
92
Glucose goal
140-180 mg/dl
93
IV thrombolysis
Cut off:
RTpA
Dose: 0.9mg/kg, maximum 90mg
0.6/kg in Japan and Asian countries
3 - 4.5h
94
Alternative or adjunct tx for acute stroke ineligible for or with contraindications to thrombolytics
Failed vascular recanalization with IV
Endovascular revascularization
95
Only antiplatelet for effective acute treatment of ischemic stroke
Prevents early recurrence <14d less death/disability at 6 mos
160mg at 4 weeks CAST
300 mg at 2 weeks IST
Risk of bleeding: 2/700
96
Accounts for 10% of strokes
High in blacks and Asian
Caused by
Intracerebral hemorrhage
HTN most common
Coagulopathy
Sympathomimetic
Cerebral amyloid angiopathy (elderly)
97
ICH dx
highly sensitive
highly specific
Determines bleeding location
Finding
Non contrast CT
hyperdensity
98
Most common site of hypertensive hemorrhage
```
Putamen
Globus pallidus
Thalamus
Cerebellar hemisphere
Pons
```
99
Primary CA that metastasize in brain
```
Lung
Breast
Skin/Melanoma
Kidney
GI
```
100
Transformation of prior ischemic infarct
Basal ganglion
Subcortical region
Lobar
101
Drugs causing ICH
Amphetamine
| Cocaine
102
Pathology of hypertensive ICH
Lipohyalinosis fibrinoid necrosis
| Charcot Bouchard microaneurysm
103
Sites of deep penetrating arteries
```
Basal ganglia (lenticulostriate) putamen
Thalamus
```
104
<10 secs
Microaneurysm
<6 h expansion. 38-40% expand in 24h most in 6 hr
<3 days early edema (cytotoxic, glutamate, thrombin, fibrin)
105
Pontine stroke
Narcotic overdose
Optic overdose
Pinpoint pupil
106
BP control in hypertensive ICH
130-150/160
107
Target MAP for stroke
110-130 mmHg
108
Lab value elevated in pseudoseizure
prolactin
not in true seizure
109
Most common tumor in cerebellopontine angle in adult
Schwannoma
110
Bilateral schwannoma
Neurofibromatosis type 2
